Skeletal Injury in the Child

Third Edition
Springer
New York
Berlin
Heidelberg
Barcelona
Hong Kong
London
Milan
Paris
Singapore
Tokyo
John A. Ogden, MD
Director of Orthopaedics, Atlanta Medical Center, Consultant,
Scottish Rite Children’s Hospital, Atlanta, Georgia

Skeletal Injury in the Child

Third Edition

With Forewords by Robert N. Hensinger, MD,

and Newton C. McCollough, III, MD

With 1436 Figures

13
John A. Ogden, MD
Director of Orthopaedics
Atlanta Medical Center
303 Parkway Drive, NE
Atlanta, GA 30312, USA

Library of Congress Cataloging-in-Publication Data

Ogden, John A. ( John Anthony),
Skeletal injury in the child / John A. Ogden.—3rd ed.
p. cm.
Includes bibliographical references and index.
ISBN 0-387-98510-7 (hard cover : alk. paper)
1. Pediatric orthopedics. 2. Fractures in children. 3. Children—
Wounds and injuries. I. Title.
[DNLM: 1. Bone and Bones—injuries. 2. Bone Development.
3. Fractures—in infancy & childhood. WE 200 034s 1999]
RD732.3.C48036 1999
617.4¢71044¢083—dc21
DNLM/DLC
for Library of Congress 98-51165
CIP

Printed on acid-free paper.

© 2000 Springer-Verlag New York, Inc.

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 To Dali
who has provided immense support
throughout the editions of this life work.

To Stephanie
for providing experience in the diagnosis and treatment
of the type 7 epiphyseal injury on her trampoline.

To John III
for trying hard to get a fracture
and leaving the space marbles on the stairs
so that Dad could have one instead.

To Tyler-Davis
for bringing up the rear and trying equally hard
to challenge his environment.
Perhaps you can make the next edition (hopefully not).

To Myke Tachdjian
colleague and pioneer in pediatric orthopaedics,
and most of all, a dear friend.
You are very much missed by all of us who care for children.
Foreword

It is remarkable that Dr. Ogden has created a third edition of Skeletal Injury in the
Child. It seems just a short time since the publication of the first (1982) and second
(1990) editions. The previous texts have been so comprehensive that it is difficult
to imagine he could add more information to the existing chapters and create
additional new chapters.
One of the new chapters concerns the multiply-injured child, who presents an
increasing problem in management. More children are surviving because of
modern methods of emergency transportation and resuscitation. As a conse-
quence, a significant number with extensive head and thoracoabdominal injuries
are presenting to the emergency room, posing difficult problems in the coordi-
nation of care and timing of selective aspects of management. Survival rates are
improving. Most of these children have concomitant musculoskeletal injury,
which must be effectively treated because of the survival potential.
There is a new chapter on abnormal healing and growth plate disruption, with
particular emphasis on bony bridge resection. Our ability to recognize epiphyseal
bars has greatly improved. Now, we can better anticipate and recognize growth
arrest before it becomes extensive. Dr. Ogden has provided many helpful sugges-
tions on how best to document and approach these physeal injury complications.
More and more children are intensively involved in a wide variety of high per-
formance athletics with resultant injuries. These are not limited to acute traumatic
injury but include repetitive and stress-induced problems in the immature skele-
ton. The new chapter on the pediatric athlete covers many of these injuries. Other
injuries related not only to sports but to nonathletic injury mechanisms are
covered in the regional chapters.
An overview of the operative and nonoperative approaches in fracture man-
agement is introduced early in the book. For many years surgical treatment was
avoided and conservative measures were recommended. More recently, surgical
reduction has become extremely popular and is ready to be placed in its proper
context. Dr. Ogden has had an extensive referral practice for the management of
difficult children’s fractures, which brings to the text an unusual assortment of
injuries and fractures and their management.
A chapter deals with the variety of new diagnostic imaging technologies such
as magnetic resonance imaging, computed tomography (CT), and three-
dimensional reconstruction of CT scans, all of which have been incorporated
throughout this wonderfully illustrated text. Dr. Ogden has also provided new
pathologic material as it applies to specific anatomic regions. His selection of illus-
trations helps the physician focus on these problems. A unique contribution to
the text is his interesting use of material from immature animals, carefully chosen
to illustrate and better understand similar injuries in the young human.
This is a huge undertaking, even when it is done by a consortium of authors.
It is even more so when it is done by an individual. However, Dr. Ogden has style
and consistency that provides a smooth, flowing text and lack of repetition. He is
a unique individual with an excellent understanding of the effect of trauma on

vii
viii Foreword

the immature skeleton. He has devoted his entire professional life, research, and
clinical interests to the problems of skeletal injury to children, and this text
continues a personal reflection of that interest and dedication.
This book is an important resource for anyone who manages musculoskeletal
injuries of childhood. I think it is essential to emergency room physicians, pedi-
atric and general orthopaedists, radiologists, pediatric residents, and students, all
of whom can profit by having this text available to them. It is a wonderful corre-
lation of anatomy, pathology, and diagnostic imaging of skeletal injury involving
the child. There is no other text on fractures that has been more helpful to me
or that I have found to be more comprehensive on this subject. This book is my
first choice when faced with a unique or challenging problem in skeletal injury.
Dr. Ogden is to be congratulated.

Robert N. Hensinger, MD
Chairman of Orthopaedics
University of Michigan
Past President, AAOS
Ann Arbor, MI
Foreword

In the third edition of Skeletal Injury in the Child, Dr. Ogden enlarges the scope of
the immensely comprehensive second edition of this text. New chapters covering
the subjects of polytrauma, growth plate disorders and their treatment, the pedi-
atric athlete, and an overview of nonoperative and operative approaches to chil-
dren’s fracture care enrich this classic text even further.
Many chapters in this new edition have been enhanced by the use of new diag-
nostic imaging technology, especially magnetic resonance imaging and three-
dimensional reconstruction of fractures. Beyond the addition of new subjects and
material, each chapter includes even more examples of rare injuries and addi-
tional pathologic material.
The third edition of this monumental work will serve as an even greater
resource for those involved in the care of children’s fractures. The exhaustive
coverage of each topic makes this book truly unique and an invaluable source of
reference.

Newton C. McCollough III, MD

Director of Medical Affairs
Shriners Hospitals for Children
Past President, AAOS
Tampa, FLT

ix
Preface to the Third Edition

Childhood and adolescence are times of individual evolution. A growing mind

needs to explore the external environs and to experiment with societal challenges.
Taunting wildlife as a young Maasai may seem markedly different than trying to
attain a 180° flip off a skateboard ramp in Atlanta; but both youngsters are
responding to specific challenges provided by the conditions under which they
live. These and a multitude of other opportunities, whether a recognized envi-
ronmental risk or an accident, bring about the potential for injury. Such trauma
frequently involves the growing skeleton.
Writing a book such as this and subsequently revising it has been a challenging
endeavor each time. Revision is necessary as diagnostic methodology, treatment
techniques, and further understanding of the biology of trauma to the immature
musculoskeletal system evolve. Particularly, magnetic resonance imaging (MRI)
and three-dimensional imaging of both computed tomography (CT) and MRI
scans have become significant diagnostic tools that allow better appreciation of
the extent of intraosseous and cartilaginous injury.
A single author obviously puts forth an individual concept (hardly authorita-
tive) concerning the many and preferred methods of diagnosis and treatment.
However, my written thoughts and concepts are hardly uniquely my own. I am
indebted to family, friends, students, residents, fellows, teachers and colleagues
throughout the planet who have provided intellectual interchange, education,
philosophy, anecdotes, and unusual cases that have coalesced to create the
concept of each edition of this book.
This concept had always been dual. First, there is significant emphasis on a sci-
entific basis, namely the inclusion of developmental and pathologic (traumatic)
anatomy and histology to emphasize the nuances of musculoskeletal injury prior
to skeletal maturity. Techniques of reduction, whether surgical or nonoperative,
must be undertaken only after considering the biologic principles and the dynam-
ics of childhood injury. Second, a heavy emphasis on illustrative material gives an
atlas-type format to the chapters, which can visually assist the physician, no matter
what his or her specialty may be, when looking for a comparable case to solve an
enigmatic radiograph.
Increasing trends in operative management are evident throughout this third
edition. These methods often serve to control fractures more effectively, allowing
quicker rehabilitation and fewer complications than “time-honored” conservative,
nonoperative approaches. Many of these “older” methods, which are often accept-
able, are retained, as some readers of this book do not have ready access to the
equipment that allows certain diagnostic and surgical approaches. Many parts of
the world still must rely on traction and casting because of limitations within the
available medical system.

John A Ogden, MD
Atlanta, GA

xi
Preface to the Second Edition

Since the publication of the first edition of this book, pediatric orthopaedics,
including trauma, has grown immensely as a subspecialty. Appreciation of the
anatomic and physiologic differences between children and adults has led to a
proliferation of information in the pediatric and orthopaedic literature. The
Shriners Hospitals for Crippled Children have supported my continued morpho-
logic research into developmental skeletal biology. This particularly has allowed
the study of pediatric chondroosseous injury in depth.
Updating concepts of cause, treatment, and biologic response to both contin-
ues the basic premise of this textbook—namely, the creation of a comprehensive,
meaningful scientific rationale for the logical treatment of skeletal injury to the
infant, child, and adolescent.
Accordingly, each chapter has been extensively revised to include pertinent new
clinical and research information. Utilization of this expanding database should
enable the physician to diagnose specific chondroosseous injury accurately,
understand its natural history, treat the patient properly, and prevent common
complications.
John A. Ogden, MD
Tampa, FL

xiii
Preface to the First Edition

Injury and the subsequent reparative response of the developing skeleton are fre-
quently disparate from the mature skeleton. This book is an outgrowth of a desire
to attain a morphologic understanding of the nuances of pediatric orthopaedic
trauma. As clinicians, we have a tendency to focus on specific injuries, often ignor-
ing trauma mechanisms and the relevance of underlying anatomy to both the
initial injury and long-term consequences.
This book introduces the principles of diagnosis and treatment of fractures
in children in a manner that first establishes a solid foundation of anatomy
and pathomechanics on which treatment principles are based. Developmental
anatomy is an overlooked facet of children’s injuries, primarily because of the
paucity of morphologic material available for use as source material. The unique
opportunity to include the resources of the Skeletal Growth and Development
Study Unit at Yale University allowed the inclusion of much material. In particu-
lar, I have attempted to translate the anatomic details into a form that has prac-
tical value. I believe that the emphasis on normal structure and function and the
mechanisms of response to trauma is essential to good clinical practice.
Decision making in orthopaedics is experience-dependent in that it requires a
proper mental set for what is normal for the given anatomic part at a particular
age. Because of the lack of available anatomic material, the orthopaedist must rely
on whatever resources he or she can muster for normal references for most of
development. One can more readily accept the importance and significance of
basic anatomic developmental changes if they are presented in close relation to
current clinical situations in which the information is germane.
This work is primarily a clinical textbook, although discussions encompass
aspects of skeletal developmental biology, particularly the response to trauma. My
hope is that this book provides the medical student, the resident, and the prac-
ticing physician a logical and progressive plan of approach to children’s fractures
and allows ready storage retrieval and utilization of knowledge concerning each
of the specific regions of injury. Because the study of orthopaedics must be a life-
long process, this book is intended to serve both as an introduction to the study
of skeletal injury and a basic text for continuing study. Hopefully, it will also have
import to pediatricians, general practitioners, and radiologists. The orientation is
to furnish a reference book that comprehensively covers the field of muscu-
loskeletal trauma in the child and provides adequate information for both the
specialist and the resident physician.
I have tried to develop a text for the teaching of basic and applied anatomy,
mechanisms, concepts, and principles that are applicable to each area of injury
in the pediatric patient. The factual and patient material has been carefully
selected to support an understanding of these concepts and principles. In doing
so I have attempted to integrate a scientific basis with the art of medicine. The
test of the value of this book will be its effectiveness in stimulating further insight
into the diagnosis and care of patients who face a lifetime of challenge. If this has
been achieved, the work will have been worth the effort.

John A. Ogden, MD
New Haven, CT

xv
Acknowledgments

As is previous editions, the morphologic and histologic studies have evolved

because of the progressive support of the Carl Henze Foundation, the National
Easter Seals Research Foundation, the National Institutes of Health, the AO/ASIF
Foundation, the Shriners Hospitals for Children, and the Skeletal Educational
Association. The opportunity to assist in orthopaedic care and to assess “natural”
aspects of trauma in skeletally immature animals at Busch Gardens Zoological
Park in Tampa, Florida and The Disney Corporation, Orlando, Florida is also
much appreciated.
The illustrations have been accomplished by Janet Barber, Patty Barber, Deby
Forrester-Gyatt, and Nina Sutherland. Appreciation is extended to the National
Library of Medicine for providing microfilm of Poland’s classic treatise on epi-
physeal injuries to produce the engravings used at the beginning of each chapter.
The anatomic and histologic materials have been diligently prepared by Tim
Ganey, PhD, Walter McAllister, and John Jacobs. Claire Keneally, Linda Pugh, and
Fay Evatt have continued to compile comprehensive bibliographic material and
patient databases. The multiple revisions have been tirelessly undertaken by
Carolyn Massey. Pam Smith, RN, has been extremely helpful in getting patients
back for follow-up studies. I also wish to thank my associates, G. Lee Cross, MD
and Douglas F. Powell, MD for their sincere cooperation during the preparation
of this text.
To cover the breadth of pediatric musculoskeletal injury, one can rely heavily
on individual experience. However, no one orthopaedist has seen or will be
likely to see every nuance of childhood fractures and dislocations. Accordingly,
the illustrative cases in this book comprise not only my own patients but gener-
ous contributions from orthopaedic surgeons throughout the world. To each
and every one of you I extend my sincere thanks and appreciation for those
additional fracture examples that have made this volume as comprehensive as
possible. If I have inadvertently failed to mention a contributor, please accept my
apologies.

Edward Abraham, MD David Aronson, MD

R.S. Adler, MD James Aronson, MD
Jae In Ahn, MD M. Azouz, MD
Michael D. Aiona, MD Thomas Bailey Jr., MD
Behrooz A. Akbarnia, MD Elhanan Bar-On, MD
Edward Akelman, MD Ian R. Barrett, MD
Javier Albiñana, MD James H. Beaty, MD
Daniel Albright, MD Michael Bell, MD
James Albright, MD A. Benaroya, MD
Benjamin L. Allen Jr., MD James T. Bennett, MD
Jorge Alonso, MD Henri Bensahel, MD
Jack T. Andrish, MD Randall R. Betz, MD
Peter F. Armstrong, MD R. Dale Blasier, MD

xvii
xviii
Eugene E. Bleck, MD
Walther H. Bohne, MD
G. Bollini, MD
J. Richard Bowen, MD
Christian F. Brunner, MD
Robert Bucholz, MD
Steven Buckley, MD
Stephen W. Burke, MD
Michael T. Busch, MD
Michael Cadieux, MD
Robert M. Campbell, MD
Aloysio Campos da Paz Jr., MD
S. Terry Canale, MD
Timothy P. Carey, MD
Allen Carl, MD
Henri Carlioz, MD
Norris C. Carroll, MD
William Carson, MD
Anthony Catterall, MD
Jack C.-Y. Cheng, MD
Michael Clancy, MD
Jane E. Clark, MD
William G. Cole, MD
Sherman S. Coleman, MD
Christopher L. Colton, MD
D.P. Conlan, MD
James J. Conway, MD
Daniel R. Cooperman, MD
Howard P. Cotler, MD
M.A.C. Craigen, MD
Alvin H. Crawford, MD
John C. Crick, MD
Robert J. Cummings Jr., MD
M. Dallek, MD
C. Dartoy, MD
Jon R. Davids, MD
Thomas A. DeCoster, MD
Peter A. DeLuca, MD
Julio dePablos, MD
G. Paul DeRosa, MD
Dennis P. Devito, MD
Luciano Dias, MD
Alain Dimeglio, MD
Thomas DiPasquale, DO
John P. Dormans, MD
James Drennan, MD
Denis S. Drummond, MD
D.M. Drvarich, MD
Prof. Jean Dubousset, MD
Morris O. Duhaime, MD
Michael G. Ehrlich, MD
Robert E. Eilert, MD
John C. Eldridge, MD
Marybeth Ezaki, MD
Albert B. Ferguson Jr., MD
Miguel Ferrer-Torrelles, MD
Elwyn C. Firth, BVSc
Mr. John Fixsen, F.R.C.S.
Bruce K. Foster, MD
Mark Frankel, MD
Acknowledgments
Michael Frierson, MD
James G. Gamble, MD
Timothy Ganey, PhD
Sarah J. Gaskill, MD
Seth Gasser, MD
Benjamin A. Goldberg, MD
Michael J. Goldberg, MD
J. Leonard Goldner, MD
M. Goodharzi, MD
Alfred D. Grant, MD
David Gray, MD
Neil E. Green, MD
Thomas Green, MD
Walter B. Greene, MD
J.R. Gregg, MD
Paul P. Griffin, MD
Harry J. Griffiths, MD
Kenneth J. Guidera, MD
Stephen Gunther, MD
Jeffrey F. Hassbeck, MD
John E. Hall, MD
John E. Handelsman, MD
Göran Hansson, MD
H.T. Harcke, MD
Y. Hasegawa, MD
P. Havranek, MD
Douglas M. Hedden, MD
D. Heilbronner, MD
Stephen D. Heinrich, MD
William L. Hennrikus Jr., MD
Robert N. Hensinger, MD
T. Herbert, MD
John A. Herring, MD
Frederick Hess, MD
John E. Herzenberg, MD
George Hirsch, MD
M. Mark Hoffer, MD
Louis C.S. Hsu, MD
G. Inoue, MD
R.P. Jakob, MD
Peter Jokl, MD
Eric T. Jones, MD
Lyle O. Johnson, MD
Ali Kalamchi, MD
James R. Kasser, MD
Theodore E. Keats, MD
Douglas K. Kehl, MD
Armen S. Kelikian, MD
David Keller, MD
Mr. J.A. Kenwright, F.R.C.S.
S.A. Khalil, MD
Gerhard N. Kiefer, MD
Richard E. King, MD
Thomas F. Kling Jr., MD
Steven Kopits, MD
K. Kozlowski, MD
Leon M. Kruger, MD
Ken N. Kuo, MD
Prof. Anders F. Langenskiöld, MD
Jack Lawson, MD
Acknowledgments xix

Louis J. Lawton, MD Mercer Rang, MD

David Leffers, MD A.H.C. Ratliff, MD
Wallace R. Lehman, MD Glen Rechtine, MD
Edward L. Lester, MD Kent A. Reinker, MD
Mervyn R. Letts, MD Thomas S. Renshaw, MD
Terry R. Light, MD Lee H. Riley, MD
Richard E. Lindseth, MD Veijo A. Ritsila, MD
W.E. Linhart, MD John M. Roberts, MD
Randall T. Loder, MD Charles Rockwood, MD
Stephen J. Lombardo, MD Dennis R. Roy, MD
John E. Lonstein, MD Sally Rudicel, MD
Sheila M. Love, MD Dietrich Schlenzka, MD
Wood Lovell, MD Robert S. Siffert, MD
John D. Lubahn, MD George W. Simons, MD
John P. Lubicky, MD Nicte Shier, MD
G. Dean MacEwen, MD Stephen R. Skinner, MD
Jay Malghem, MD James A. Slavin, MD
Henry J. Mankin, MD Clement B. Sledge, MD
Arthur E. Marlin, MD John Smith, MD
Keith M. Maxwell, MD Kwang S. Song, MD
Shirley McCarthy, MD Wayne O. Southwick, MD
Newton C. McCollough, MD Donald P. Speer, MD
J.P. McConkey, MD Philip Spiegel, MD
Douglas W. McKay, MD Lynn T. Staheli, MD
Brian McKibbin, MD Carl L. Stanitski, MD
Peter L. Meehan, MD Deborah F. Stanitski, MD
Malcolm B. Menelaus, MD Howard Steel, MD
Leslie C. Meyer, MD David B. Stevens, MD
Lyle J. Micheli, MD Stephen J. Stricker, MD
Y. Mikawa, MD Allen M. Strongwater, MD
James P. Milgram, MD Yoishi Sugioka, MD
Edward A. Millar, MD J. Andy Sullivan, MD
Dan Morrison, DO Mark D. Suprock, MD
Raymond T. Morrissy, MD Michael Sussman, MD
Colin F. Moseley, MD David H. Sutherland, MD
Scott J. Mubarak, MD Mihran O. Tachdjian, MD
Peter L. Munk, MD Claudia Thomas, MD
P. Nimityongskul, MD George Thompson, MD
Roy M. Nuzzo, MD Vernon T. Tolo, MD
William Obremsky, MD Paul D. Traughber, MD
William L. Oppenheim, MD Stephen J. Tredwell, MD
Kahlevi Österman, MD S. Troum, MD
Michael B. Ozonoff, MD Chester M. Tylkowski, MD
Dror Paley, MD Keith D. Vanden Brink, MD
Arthur M. Pappas, MD John L. VanderSchilden, MD
Klausdieter Parsch, MD David Vickers, MD
M.R. Patel, MD Pascual Vincente, MD
Sir Dennis Paterson Prof. Heinz Wagner
Jaari Peltonen, MD Janet Walker, MD
Hamlet A. Peterson, MD Arthur Walling, MD
G. Pietu, MD Stephen A. Wasilewski, MD
A. Piña-Medina, MD Peter M. Waters, MD
Peter Pizzutillo, MD Hugh G. Watts, MD
Ignacio V. Ponseti, MD Dennis S. Weiner, MD
Shlomo Porat, MD Stuart L. Weinstein, MD
Jean-Gabriel Pous, MD Dennis R. Wenger, MD
Andrew K. Poznanski, MD James J. Wiley, MD
Charles T. Price, MD Kaye E. Wilkins, MD
George T. Rab, MD Peter Williams, MD
Ellen M. Raney, MD David J. Zaleske, MD
xx Acknowledgments

I would also like to extend my sincere gratitude to all the residents and fellows
with whom I have had the honor and pleasure to work over the past 30 years.
Many of you have eagerly sought out and provided additional cases.
The staff at Springer-Verlag, ably led by Esther Gumpert, has been invaluable
in putting all the pieces together.

John A Ogden
Atlanta, 6A
Contents

Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vii
Robert N. Hensinger, MD
Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
Newton C. McCollough, III, MD
Preface to the Third Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . x
Preface to the Second Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi
Preface to the First Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xii
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii

Chapter 1
Anatomy and Physiology of Skeletal Development . . . . . . . . . . . . . . . . . . . . 1

Chapter 2
Injury to the Immature Skeleton . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

Chapter 3
The Child with Multiple Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69

Chapter 4
Treatment Concepts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86

Chapter 5
Diagnostic Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

Chapter 6
Injury to the Growth Mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147

Chapter 7
Management of Growth Mechanism Injuries and Arrest . . . . . . . . . . . . . . 209

Chapter 8
Biology of Repair of the Immature Skeleton . . . . . . . . . . . . . . . . . . . . . . . . 243

Chapter 9
Open Injuries and Traumatic Amputations . . . . . . . . . . . . . . . . . . . . . . . . . 269

Chapter 10
Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 311

Chapter 11
Fractures in Pediatric Growth Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346

xxi
xxii Contents

Chapter 12
Pediatric Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399

Chapter 13
Chest and Shoulder Girdle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419

Chapter 14
Humerus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 456

Chapter 15
Elbow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 542

Chapter 16
Radius and Ulna . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 567

Chapter 17
Wrist and Hand . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 650

Chapter 18
Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 708

Chapter 19
The Pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 790

Chapter 20
Hip . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 831

Chapter 21
Femur . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 857

Chapter 22
Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 929

Chapter 23
Tibia and Fibula . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 990

Chapter 24
Foot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1091

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1159
1
Anatomy and Physiology
of Skeletal Development
Engraving of a distal femoral physeal fracture. (From Poland J.
Traumatic Separation of the Epiphysis. London: Smith Elder, 1898)
ompared to the relatively static, mature bone of adults,
C there are highly variable structural and functional
response differences, both physiologic and biome-
chanical, in immature, developing bones that render them
susceptible to different patterns of fracture and modes of
healing. Even the types of fracture within any given imma-
ture bone demonstrate temporal (chronobiologic) varia-
tions that correlate closely with the progressive anatomic
changes affecting the epiphysis, physis, metaphysis, and di-
aphysis at both macroscopic and microscopic levels. The key
to understanding children’s musculoskeletal injuries lies ini-
tially in an adequate appreciation of the anatomy and the
physiology of the multiple chondro-osseous components of
the developing skeleton and particularly how these compo-
nents change with time as growth progresses from the
extremely biologically resilient skeleton of the newborn to
the much more rigid skeleton of late adolescence.
Bone Development
All skeletal structural elements initially form as mesen-
chymal cellular condensations during the embryonic
period.8,73,104,120,140,143,145,146,149,154,160,161,207,219 Some of these cel-
lular groupings modulate to fibrocellular tissue and ossify
directly to form membranous bone. This is characteristic of
the cranial and most facial bones, as well as of the initial for-
mation of the clavicle. In contrast, the appendicular and
axial skeletal elements are derived from initial transforma-
tion of the mesenchymal model into a cartilaginous model
and its subsequent transformation into an ossified structure
by two discrete processes: (1) formation of an osseous collar
around the midportion of the cartilaginous anlage, with sub-
sequent vascular invasion to form the primary ossification
center; and (2) a later, usually postnatal, vascular-mediated,
osseous transformation of the chondroepiphysis to form a
discrete secondary epiphyseal ossification center. This pro-
gressive, integrated replacement of the antecedent cartilage
model by osseous tissue is termed endochondral ossification.
These two basic types of osseous tissue formation—
membranous and endochondral—refer only to the primary
pattern of development of each individual structural unit,
whether a femur or a phalanx. Subsequent growth of any par-
ticular unit after this initial differentiation may involve dis-
crete, juxtaposed, or interspersed areas of both basic patterns
within the same bone. Endochondrally derived bones gen-
erally undergo intramembranous ossification by appositional
bone growth from the periosteum. Similarly, membrane-
derived bone may undergo subsequent growth and elonga-
tion by a modified endochondral process (e.g., the clavicle).
Membranous Bone Formation
Primary membranous bone formation occurs in the cranial
and facial bones and, in part, in the clavicle and mandible
(which also subsequently develop epiphyses and physes). In
1
2 1. Anatomy and Physiology of Skeletal Development

contrast, the endochondrally derived axial and appendicu-

lar bones become involved in membranous bone formation
secondarily.
The membrane-derived bones are formed from conden-
sations of mesenchymal tissue that are the structural ana-
logues of the presumptive bone, similar to the cartilaginous
precursor of an endochondral bone. At a presumably genet-
ically determined site of presumptive primary ossification,
small groups of cells differentiate and aggregate into short,
randomly directed cellular strands. These cells elaborate a
fibrous intercellular matrix that is calcified and subsequently
ossified to form the primary trabeculae. Ossification rapidly
spreads from the primary ossification center so relatively FIGURE 1-2. Osteomyelitis involving the right humerus of a 10-
large areas are ossified. The subsequent trabecular orienta- month-old infant. Extensive subperiosteal (membranous) reactive
tion within these laminar sheets of bone is a direct response bone, the involucrum (I), surrounds the minimally visible endo-
to applied mechanical stresses, internal and external, to the chondral shaft (S), comprising both metaphyses and diaphysis.
developing fetus. The surfaces thicken to form discrete sub- This bone, if totally deprived of its blood supply, may form a
chondral plates (Fig. 1-1). During the first decade of life sequestrum of dead bone.
these membrane-derived plates are extremely resilient and
capable of absorbing considerable energy without fracturing.
They may also deform, injuring the underlying cranial con-
Caffey’s disease or osteomyelitis, in which the entire original
tents, and then “spring back” to the normal shape without
diaphysis may become sequestrated, with the elevated perios-
fracturing.
teum forming a totally new shaft (involucrum) that is mem-
The clavicle is the first fetal bone to ossify, followed rapidly
branous, rather than endochondral, in origin (Fig. 1-2). The
by the mandible.160 Both bones eventually form hyaline
replacement process also may be seen when portions of the
cartilage at the ends and convert, in part, to endochondral
diaphysis are removed for use as bone graft. This membra-
ossification, but only after primary intramembranous ossifi-
nous ossification process is an absolutely essential step in
cation is well under way. This subsequently appearing carti-
physiologic fracture healing, especially in children.3 Borgi et
lage, sometimes referred to as secondary cartilage, becomes
al. showed an interesting clinical situation of a 6-year-old who
responsible for directed longitudinal growth and joint
lost the entire radial diaphysis during an open injury.12 The
formation.
wound was débrided and the limb immobilized. Within 6
All the axial and appendicular skeletal elements are
months this child had completely regenerated the diaphysis
involved in membranous ossification. The diaphyseal cortex
through periosteal new bone formation.
of any developing tubular bone is progressively modified by
Tumor bone formation is a rapid elaboration of membra-
specialized mesenchyme that differentiates into the perios-
nous bone that is naive bone formation completely unre-
teum and perichondrium, investing the chondro-osseous
sponsive to biomechanical demands (Fig. 1-3). Initially
model. This peripheral periosteal process of membrane-
formed membranous bone and endochondral bone are
derived bone is dramatic in childhood disease states, such as
elaborated as a biomechanically reactive process that must be
subsequently modified to create bone capable of accommo-
dating to the applied stresses. This process is compromised
in certain pediatric diseases. For example, juvenile rheuma-
toid arthritis is associated with progressive displacement of
biomechanically nonreactive bone to create deformation of
the membranous and endochondral bone to create the
phenomenon of acetabular protrusion.

FIGURE 1-1. Typical membranous bone formation of a cranial
bone. The outer table has undergone recent rapid appositional
growth. The interface of this table with the older, remodeled bone
is readily evident.
Endochondral Ossification
Endochondral bone formation is the primary osseous
formation process of axial and appendicular skeletal
components, and it may recur in selected areas of any
established bone during the normal process of fracture
repair (i.e., formation and maturation of cartilaginous
callus).143–146,148,149,152,153,155,157,160 Succinctly, this type of bone
formation is the continuous replacement of preexistent car-
tilaginous tissue by osseous tissue. The overall process is a
continuum that may be divided arbitrarily into a number of
steps (Fig. 1-4).
1. Formation of a highly cellular mesenchymal condensa-
tion, the basic anlage
Anatomic Regions
FIGURE 1-3. Reactive membranous bone formation from a Ewing’s
sarcoma. This bone is formed without any response to local bio-
mechanical demands. It may be referred to as “naive” bone.
2. Increased extracellular matrix formation to create
precartilage
3. Extensive ground substance elaboration to form the
chondral anlage, with selective hypertrophy of the central
chondrocytes
4. Further intercellular, interstitial, and extracellular
enlargement of the entire chondral anlage, with selective
hypertrophy of the central chondrocytes
5. Formation of a trabeculated primary bone collar, asso-
ciated periosteum, and vascular supply around the pre-
sumptive diaphysis
6. Increased intracellular and extracellular biochemical
activity, especially in the hypertrophic central chondrocytes,
leading to calcification of the cartilage
7. Penetration of the primary osseous collar by fibrovas-
cular tissue, part of which becomes the nutrient artery
8. Central replacement of cartilage by bone, initially
around the area of vascular invasion, followed by extension
of the process (including the bone collar) longitudinally
toward each end of the anlage; this forms the primary ossi-
fication center, which becomes the diaphysis and metaphy-
ses (Figs. 1-5, 1-6)
9. Establishment of an orderly arrangement in the ossi-
fication growth mechanism (physis) and an actively remod-
eling metaphysis
10. Vascularization of the chondroepiphyses by cartilage
canal systems
11. Appearance of one or more secondary ossification
centers within the chondroepiphyses (primarily a postnatal
process)
3
FIGURE 1-4. Endochondral bone formation: (A) mesenchymal
anlage; (B) central chondrification. (C) central cartilage hypertrophy;
(D) formation of the primary bone collar; (E) vascular irruption to
form the primary ossification center; (F) development of contiguous
endochondral and membranous ossification, and well-established
physeal cytoarchitecture; (G) cartilage canal formation within the
epiphysis; (H) diaphyseal remodeling and cavitation, and formation
of the epiphyseal preossification center; (I) formation of the sec-
ondary ossification center; (J) formation of accessory epiphyseal
ossification centers (e.g., greater trochanter). See text for details.
On cursory examination, nontubular bones seem to have
patterns of endochondral ossification different from those of
the major and smaller tubular (longitudinal) bones. However,
when analyzed, it becomes evident that each of these bones
is undergoing the same basic endochondral ossification
process, with it being reorganized to conform to the specific
contours of each particular bone. End-plate ossification of the
vertebral centrum during adolescence closely resembles the
process in a tubular bone, whereas the neural arch grows prin-
cipally by periosteal appositional growth. The growth poten-
tial in the end-plates affects the ability to restore vertebral
height after compression fracture with a wedge deformity or
to fill in an area with new bone in chronic anterior stress syn-
dromes such as Scheuerman’s disease. There are selected
areas at each end of the neural arch that function as growth
regions: the spinous processes and the neurocentral synchon-
droses (Fig. 1-7). The scapula also may be conceived of as
undergoing functionally and morphologically rearranged
endochondral ossification along the vertebral border,
acromion, coracoid, and glenoid. The calcaneus forms a pos-
terior chondroepiphysis with a secondary ossification center,
creating a situation similar to the end of a tubular bone.
Anatomic Regions
The major long bones of a child may be divided into several
distinct anatomic areas: diaphysis, metaphysis, epiphysis, and
physis (Figs. 1-6, 1-7). Each of these regions is prone to
4 1. Anatomy and Physiology of Skeletal Development

A B
FIGURE 1-5. (A) Endochondral derived bone is located centrally, evident and demarcates the greater contribution of the distal
and linear membranous-derived bone is located at the edges. (B) physis to overall longitudinal growth. Postnatal remodeling
Appearance of the two bone derivation patterns in the metacarpals usually removes these vestiges of the two mechanisms of bone
at 7 months’ gestation. The nutrient vessel in metacarpal 3 is formation.

FIGURE 1-6. (A) Characteristic regions of growing tubular bone.
(B) Metaphyseal–diaphyseal unit of osseous tissue is derived from
two basic patterns of bone formation. The endochondral bone may
be thought of as two conical structures, apex-to-apex, capable of
enlarging through physeal growth at the bases of the cones. Each
cone may develop at a relatively independent rate, although both
are integrated through the periosteal continuity. Membranous bone
(stippled regions) progressively fills the “gap” between the conical,
endochondral growth regions. (C) As the shaft progressively
enlarges longitudinally and latitudinally by the aforementioned
basic bone formation patterns, remodeling changes both the
macroscopic and the microscopic appearances. A, formation of
dense cortical (lamellar) bone by osteon maturation; B, formation
of trabecular endosteal bone (of membranous derivation); C, for-
mation of the fatty–erythropoietic marrow cavity essentially devoid
of bone; D, peripheral metaphyseal cortex and remodeling; E, for-
mation of trabecular endosteal bone (of endochondral derivation).
(D) Radiograph showing the basic anatomic regions of a develop-
ing bone. E, epiphysis; Eoc, epiphyseal ossification center; M,
metaphysis; D, diaphysis. Note the differences between the
porous, thin metaphyseal cortex (solid arrow) and the thick di-
aphyseal cortex (open arrow).
Anatomic Regions
FIGURE 1-7. Modified endochondral bone formation in nontubular
bones. (A) Vertebral body (sagittal section). (B) Scapular blade
(spine and acromion are white). Note the diaphyseal (D), epiphy-
seal (E), and metaphyseal (M) analogues. Subperiosteal membra-
nous bone plays a less important role in the postnatal development
of these bones than the major tubular bones.
certain patterns of injury, with this intrinsic susceptibility
changing as the physiologic and biomechanical capacities of
each region change with postnatal developmental modifica-
tions at the macroscopic and microscopic levels.2,57,144,193,194
These four major regions originate, and subsequently
become modified, as a result of the basic endochondral ossi-
fication process; they are supplemented by membranous
bone formation along the shaft, especially along the di-
aphysis (Fig. 1-8).
Diaphysis
The diaphysis comprises the major portion of the cortical
osseous tissue of each long bone. It is primarily a product of
periosteal, membranous osseous tissue apposition around
the original endochondral model and of endosteal remod-
eling and bone formation (Figs. 1-6, 1-8). It eventually leads
to the progressive and complete replacement of the primary
ossification center and primary spongiosa, with the latter
also being replaced by secondary spongiosa modeling and
remodeling in the metaphyseal region.
At birth the diaphysis is comprised principally of fetal,
woven bone, which is characteristically lacking in haversian
systems. The neonatal femoral diaphysis is the only area
exhibiting significant change from this fetal osseous state to
more mature (lamellar) bone with its various, constantly
changing osteon systems. Periosteally mediated, membra-
nous, appositional bone formation with concomitant
endosteal remodeling characterizes the postnatal period. It
leads to enlargement of the overall diameter of the shaft,
variably increased width of the diaphyseal cortices, and for-
mation of the marrow cavity. Mature, lamellar bone with
intrinsic, but constantly remodeling, osteonal patterns pro-
gressively becomes the dominant feature. This process is
mechanically responsive. A defect, such as a screw hole or
fenestration for bone biopsy, locally alters this biomechani-
cal responsivity and changes the fracture risk.53,132,137,163 A
toddler may push the reactive limits of such bone and easily
develop a stress fracture (see Chapters 12, 23). This early
bone is extremely vascular. When analyzed in cross section it
appears much less dense than the maturing bone of older
children, adolescents, and adults (Fig. 1-9). Subsequent
growth leads to increasingly complex haversian (osteonal)
systems and to the elaboration of increasing amounts of
5
extracellular matrix, decreasing the relative porosity and
increasing its hardness.4,5,7 The changing ratio of laminar
(fetal) to lamellar (haversian) bones affects childhood
fracture patterns: bowing, greenstick, complete, or commi-
nuted. In rare situations greenstick fractures may occur in
young adults.32
Periosteum
In comparison to mature (adult) bone, the periosteum is
much thicker, more vascular, more loosely attached to the
underlying diaphysis, and capable of more rapid callus for-
mation in response to similar injury (Figs. 1-10, 1-11). The
periosteum, rather than the bone, serves as the origin for
most muscular fibers along the metaphysis and diaphysis. It
allows growth of bone and muscle units to be coordinated,
a factor that would be impossible if all muscles attached
directly to a specific region of the developing bone. Excep-
tions include attachments of some adductor fibers into the
medial distal femoral metaphysis. This attachment probably
explains the irregularity of ossification seen in this area and
is often misdiagnosed as a neoplastic or traumatic response
(see Chapter 21).
Poussa et al. showed that periosteal grafts placed in chon-
drotrophic environments first formed cartilage but rapidly
transformed into bone. This was in contrast to previous
experiments that showed that free periosteal grafts placed in
a muscular bed formed bone directly without intermediate
cartilage.168–170
Metaphysis
The metaphyses are variably contoured flares at each end
of the diaphysis. Their major characteristics are decreased
thickness of the cortical bone and increased amounts of tra-
becular bone comprising both primary and secondary spon-
giosa. Extensive remodeling centrally and peripherally
causes the primary spongiosa, which is a direct result of
endochondral ossification, to be transformed into more
mature secondary spongiosa, a process that involves oste-
olytic, osteoclastic, and osteoblastic activity. The metaphyses
thus exhibit considerable bone turnover compared to other
regions of the bone. These active processes normally cause
increased uptake of radionuclides in a typical bone scan.
Like the diaphysis, the metaphyseal cortex also changes
with time. Relative to the confluent diaphysis the metaphy-
seal cortex is thinner and has greater porosity (i.e., trabecu-
lar fenestration). These cortical fenestrations (Fig. 1-12)
contain fibrovascular soft tissue elements that connect meta-
physeal marrow spaces with the subperiosteal regions.49 The
metaphyseal cortex exhibits greater fenestration near the
physis than the diaphysis, with which it gradually blends as
an increasingly thicker, denser type of bone. As temporal lon-
gitudinal growth continues, cortical fenestration decreases
and the overall width of the cortex increases, creating a
greater morphologic transition between the juxtaphyseal
and the juxtadiaphyseal cortices. The metaphyseal region
does not develop significant haversian systems until skeletal
maturity approaches. These microscopic anatomic changes
6 1. Anatomy and Physiology of Skeletal Development
FIGURE 1-8. (A) Humerus of a juvenile humpback whale showing
juxtaposition of endochondral derived bone, which is longitudinally
oriented toward each physis (thin arrows). This bone is demarcated
(curved open arrows) from the membranous bone formed by the
periosteum. The small open arrows show a growth slowdown line
in both endochondral and membranous bone, which probably
demarcates prenatal and postnatal bone development. The aster-
isk (*) indicates the juxtaposition of the apices of the two endo-
appear to be directly correlated with changing patterns of
fracture occurrence and undoubtedly influence the occur-
rence of torus (buckle) fractures, in contrast to complete
metaphyseal or epiphyseal/physeal fractures.141
Another microscopic anatomic variation in the metaphysis
may be seen at the juxtaposition of primary spongiosa with
the hypertrophic region of the physis. In most rapidly
growing bones the trabeculae tend to be oriented longitu-
dinally (Fig. 1-13). However, in shorter growing bones, such
chondral cones (see Fig. 1-9B). (B) Histologic macrosection of the
humerus from a fetal humpback whale demonstrating the two basic
patterns of bone formation in a long bone. (C) Higher-power view
of the juxtaposed ossification processes. P, periosteum, with
arrows indicating membranous bone; E, endochondral bone; Ep,
epiphysis; Pc, perichondrium, which is histologically indistinguish-
able from the periosteum and in continuity with it.
as the metacarpals and phalanges, the trabecular origin is
more predominantly horizontal. As growth decelerates
during adolescence, a similar, more horizontal orientation
may be seen even in the major long bones. These variations
in trabecular orientation affect the responsiveness of various
metaphyseal regions to abnormal stress and predispose to
certain fracture modes (see Chapter 6).
Whereas the periosteum is attached relatively loosely to
the diaphysis, it becomes more firmly fixed in the metaph-
Anatomic Regions
FIGURE 1-9. Transverse sections of the femoral diaphyseal cortex
at 2 months (A) and 8 months (B). The pattern of bone architec-
ture varies considerably around the circumference, a factor that
must be considered when performing biomechanical tests on
ysis due to the continuity of fibrous tissue through the meta-
physeal fenestrations (Fig. 1-12); and it is densely attached
to the physeal periphery through continuity of collagen
fibers (the microskeleton of soft tissues). Experimentally, it
is necessary to sever the metaphyseal/physeal periosteum to
FIGURE 1-10. Mid-shaft humeral fractures in a neonate (A) and a
9-year-old child (B) showing significant differences in the rates of
subperiosteal and callus ossification 4 weeks following the fracture.
The injury is almost completely healed in the neonate, whereas
little roentgenographically evident reparative bone appears in the
older child.
7
developing bone. The initial cortical bone is extremely porous but
rapidly becomes less so as osteon formation commences. The
laminar pattern of the new bone formation is readily evident in B
(arrows).
duplicate epiphyseal fractures easily. This intermingling of
endosteal and interosseous fibrous tissues with the periosteal
tissue imparts considerable, additional biomechanical
strength to the region. The periosteum attaches densely to
the peripheral physis, blending into the zone of Ranvier, and
to the epiphyseal perichondrium. The metaphyseal cortex
extends to the physis and continues as the osseous ring of
Lacroix (Fig. 1-12).
FIGURE 1-11. (A) Subperiosteal bone (arrows) forming in the
“intact” sleeve following comminuted femoral diaphyseal fracture.
(B, C) Progressive maturation of subperiosteal bone (arrows) in a
similar case of an open injury with traumatic extrusion of a frag-
ment of the diaphysis.
8 1. Anatomy and Physiology of Skeletal Development
B C
A
FIGURE 1-12. Histology of the metaphysis. (A) Fenestrated meta-
physis with significant cellularity between the bone and periosteum.
(B) Step-like pattern reflects episodic growth spurts (saltation and
The porosity of the metaphyseal cortex is retained until
adolescence in many bones. This fenestrated cortex is readily
evident in dry bone specimens (Fig. 1-14). The gradation
from porous metaphyseal bone to dense diaphyseal cortex
creates a biologic “stress riser” that is undoubtedly a factor
in the torus (buckling) fracture.
As in the diaphysis, there are limited significant direct
muscle attachments to the metaphyseal bone. Instead,
muscle fibers blend primarily into the overlying periosteum.
Epiphysis
At birth, with the exception of the distal femur, each epiph-
ysis is a completely cartilaginous structure at both ends of
each long bone; including the small longitudinal bones of
the hands and feet. This cartilaginous structure is termed
the chondroepiphysis, and the corresponding ossifying
structure is termed the chondro-osseous epiphysis or, simply,
epiphysis.
At a time characteristic for each of these chondroepiphy-
ses, one or more secondary centers of ossification appear
and enlarge until virtually the entire cartilage model has
been replaced by bone at skeletal maturity, when only artic-
ular cartilage remains. As the ossification center expands, it
undergoes structural modifications. Particularly, the region
adjacent to the physis forms a distinct subchondral plate
parallel to the metaphysis, creating the roentgenographi-
cally characteristic physeal line. Certain chondroepiphyses
exhibit varied appearances of the ossification centers, a
factor that must be considered to diagnose fractures of these
stasis) prior to any extensive remodeling. (C) Maturing metaphy-
seal bone in a 6-year-old boy.
regions appropriately. This point is particularly important
with elastic injuries, usually termed osteochondroses (e.g.,
Legg-Perthes, Panner’s and Kohler’s lesions). The distal
humerus shows an extremely variable pattern of ossification,
beginning with a small, solitary center of ossification within
the capitellum during the first year, a center in the medial
epicondyle at 3–6 years, multiple ossification foci in the
trochlea at approximately 7–8 years, and a focus in the lateral
epicondyle during adolescence. The appearance and pro-
gressive development of the secondary center of ossification
within any chondroepiphysis plays a role in the susceptibil-
ity of the region, including the adjacent physis and metaph-
ysis, to variable fracture patterns. As the osseous tissue
expands, the ossification center imparts increasing rigidity to
the more resilient epiphyseal cartilage. Type l growth mech-
anism injuries commonly affect infants with unossified or
minimally ossified epiphyses. In contrast, once a discrete sub-
chondral plate forms, the type 2 growth mechanism injury
becomes prevalent. The large capitellar center coupled with
late-appearing trochlear ossification is undoubtedly a
mechanical factor in the high rate of type 3 and 4 fractures
of the lateral condyle.
The expanding ossification center always has a shell of sub-
chondral bone. This bone has probably the thickness of an
eggshell but exhibits an intricate trabecular network. Both
the shell of subchondral bone and the contained trabecular
bone are in a high state of mechanically responsive turnover.
The portion of the subchondral shell apposed to the articu-
lar surface cartilage significantly thickens and mechanically
adapts as skeletal maturation is reached.52 This bone has
some microfenestrations but morphologically is more like
Anatomic Regions
A articular and epiphyseal hyaline cartilages.
B
FIGURE 1-13. (A) Minimal longitudinal orientation of physeal cells
in a phalanx. (B) Accentuated elongation of physeal cell columns
and comparable longitudinal orientation of the primary spongiosa
in a distal femur. Note the progressive change from the primary to
secondary spongiosa.
dense cortical bone.39 This anatomic structure affects joint
mechanics.48,139,162 Disruption (fracture) may significantly
alter the regional biomechanics.52,138,187 This same phenom-
enon of a cortical shell surrounding trabecular bone typifies
the developing vertebral body and affects the mechanics of
each vertebra.58,70,196
9
When the hyaline cartilage of the chondroepiphysis first
forms, there are no demonstrable macromorphologic dif-
ferences between the cells of the joint surface and the
remainder of the hyaline cartilage. At some point, however,
a finite cell population stabilizes and becomes functionally
different from the remaining epiphyseal cartilage. These two
cartilage types are different physiologically and, by implica-
tion, biomechanically and biochemically. If a core of articu-
lar and hyaline cartilage is removed, turned 180°, and
reinserted, the transposed hyaline cartilage eventually forms
bone at the joint surface. The transposed articular cartilage,
in contrast, remains completely cartilaginous and becomes
surrounded by the enlarging secondary ossification center.135
Thus under normal circumstances articular cartilage does
not appear capable of ossification. As skeletal maturity is
reached, a tidemark develops as a demarcation between the
An important aspect of the aforementioned experiment is
an explanation of nonunion of certain fractures, such as
those of the lateral condyle of the distal humerus, in which
the fragment may be rotated up to 180°, causing the articu-
lar surface to lie against metaphyseal and epiphyseal bone.
Union does not occur in such a situation because the artic-
ular surface is incapable of any osteogenic response, an
essential component of bone healing. This type of nonunion
FIGURE 1-14. Distal fibula from a 7-year-old child. Note the exten-
sive porosity of the metaphyseal (M) cortex, compared to the dense
diaphyseal (D) cortex.
10
has been attributed incorrectly to the fragment being sur-
rounded by synovial fluid, which allegedly prevents union.
However, this same fluid does not seem to prevent union of
osteochondral defects and other types of epiphyseal frac-
tures in which no significant displacement or rotation
occurs. In these instances, the apposed nonarticular surfaces
are capable of an appropriate conjoint osteogenic or chon-
drogenic healing response (or both).
Physis
The growth plate, or physis, is the essential mechanism of
endochondral ossification.55,68,84–86,96,114,116,127,158,176,182,188 For
many physes the basic structural contour remains similar
throughout development. For others there are major
changes in contour, which is particularly true in the proxi-
mal humerus and proximal femur, the physes of which
change from initially transverse to highly contoured struc-
tures as they grow. The contour of the distal femur also cha-
nges from transverse to quadrinodal (see Chapter 21).
Because the contours are undergoing constant change, frac-
ture pattern susceptibilities also change. The greater the
undulation, the greater the risk of variable fracture propa-
gation culminating in localized growth damage.2
Because the physeal cartilage remains radiolucent, except
in the final stages of physiologic epiphysiodesis, the roent-
genographic appearance of the physis must be inferred from
the metaphyseal contour, which follows the physeal contour
closely. The changing size of the epiphyseal ossification
1. Anatomy and Physiology of Skeletal Development
center more effectively demarcates the physeal contour
of the epiphyseal (germinal layer) side. As the
secondary center of ossification enlarges and approaches
the physis, the originally spherical shape of the ossification
center flattens and gradually develops a contour that paral-
lels the metaphyseal contour. Similar contouring also occurs
as the ossification center approaches the lateral and subar-
ticular regions of the epiphysis. The region of the ossifica-
tion center juxtaposed to the physis forms a discrete
subchondral bone plate through which the epiphyseal
vessels penetrate to reach the physis. This subchondral plate
surrounds the entire ossification center.
From a macroscopic viewpoint, there are two basic types
of growth plate: discoid and spherical. The pattern of bone
formation may be slightly different.16 Most primary physes of
the major long bones are discoid. They are characterized by
a relatively planar area of rapidly differentiating and matur-
ing cartilage that grades imperceptibly from the epiphyseal
hyaline cartilage. The primary function of the physis is to
cause rapid longitudinal growth. Initially, most discoid
physes are transversely planar; but as they respond to subse-
quent growth and biomechanical stresses, they assume char-
acteristic contouring while retaining this basic planar nature.
Additionally, small interdigitations of cartilage termed mam-
millary processes (Fig. 1-15) extend into the metaphyseal
bone. Contouring and mammillary processes contribute to
the intrinsic stability of the physis against shearing forces.
Discoid (planar) growth plates also may be found between
the metaphysis and an apophysis, which may be defined as
an epiphyseal/physeal extension subjected primarily to
FIGURE 1-15. (A) Sagittal cut of a proxi-
mal femur from a 9-year-old boy. The
physis has an irregular, convoluted
pattern, with a mammillary process
extending into the metaphysis (arrow).
(B) Histologic section from an 8-year-old
girl with similar convolutions and a mam-
millary process (arrow).
Anatomic Regions
FIGURE 1-16. Major patterns of endochondral
growth. Longitudinal growth occurs in the cell
columns, which may be divided on the basis of
physiologic function (growth, maturation, trans-
formation, remodeling) or histologic structure
and appearance. Two relatively independent
vascular systems supply the two sides of the
physis. Additional branches supply a specialized
region, the zone of Ranvier, where undiffer-
entiated mesenchymal cells (M) give rise to
chondroblasts. The periosteum (PO) and peri-
chondrium (PC) are continuous in this region.
Metaphyseal cortex also extends into this
region, becoming the osseous ring of Lacroix
(ORL), which acts as a peripheral restraint to the
cell columns but does not impede latitudinal
growth of the adjacent zone of Ranvier or the
more external periosteum and perichondrium.
tensile, rather than compressive, forces. The tibial tuberos-
ity typifies such a structure. Instead of the normal columnar
cytoarchitecture (Fig. 1-16), tension-responsive structures
are characterized by variable amounts of fibrocartilage that
apparently represent a microscopic structural adaptation of
the physis to the high tensile forces imparted by the quadri-
ceps mechanism.156
In the short, tubular bones (metacarpals, metatarsals, pha-
langes), two discoid physes and contiguous chondroepiphy-
ses initially form; but with subsequent skeletal growth, only
one end remains a true chondroepiphysis and physis,
becoming the primary mechanism for longitudinal growth
of each bone (Fig. 1-17). The metaphyseal bone tends to
have more transverse septa than comparable regions of
major long bones, in addition to the usual longitudinal
pattern of the primary spongiosa. Although this difference
may impart a greater degree of resistance to shear fractures,
it is primarily a reflection of relative rates of longitudinal
growth and metaphyseal remodeling. In contrast, the epi-
physeal hyaline cartilage of the opposite end of these small
longitudinal bones is replaced relatively rapidly, until only a
small amount remains between the articular surface and the
metaphysis. The associated physis assumes a spherical
contour with decreased cell column length underneath the
articular cartilage. This spherical physis contributes mini-
mally to longitudinal growth, but it does allow contoured
expansion of the phalangeal head.
11
An epiphyseal ossification center rarely appears in the epi-
physis associated with such a spherical growth plate,
although a structural variation, the pseudoepiphysis, is some-
times encountered. This occurs most commonly in the distal
end of the thumb metacarpal, where it should be considered
a normal variant. The pseudoepiphysis is not a true ossifica-
tion center but, rather, an upward and subsequently expan-
sile enlargement of metaphyseal ossification.82,150,151 It does
not appear to be subject to fracture, as are true physes; but
radiologically it may mimic a fracture in an acutely injured
child. These cartilage remnants may act as stress risers to
predispose children to distal phalangeal fractures (see
Chapter 17).
The spherical growth plate, which is the growth mecha-
nism of the epiphyseal ossification center (Fig. 1-18), is also
found in the small bones of the carpus and tarsus. By pro-
gressive centrifugal expansion, each spherical growth plate
gradually assumes the contours of the particular bone or epi-
physis. In the epiphysis, this enlargement of the secondary
ossification center leads to juxtaposition of part of the spher-
ical growth plate against the primary discoid physis, creating
a bipolar growth zone (Fig. 1-19). A bipolar growth zone also
may be found in the acetabular triradiate cartilage and
between the proximal tibial and tuberosity ossification
centers.
The physis has a characteristic and essentially unchanging
basic cytoarchitecture from early fetal life until skeletal mat-
12
FIGURE 1-17. Histologic section of the first toe from a 3-month-old
girl showing distal phalanx (DP), proximal phalanx (PP), and distal
metatarsal (MT). The distal phalanx exhibits only one epiphysis
and has a transversely oriented physis (T). The proximal phalanx
also has a transversely oriented physis (T) at its proximal end. The
transverse physis (T) of the metatarsal is also evident. Both struc-
tures eventually develop secondary ossification centers. At the
FIGURE 1-18. (A) Spherical ossification developing in the capital
femoral epiphysis. Cells around the periphery of the ossific nucleus
have the histologic appearance of foreshortened cell columns
similar to a longitudinal growth physis. This type of growth plate
(i.e., spherical) does not contribute to an increase in the size of the
epiphysis. Instead, it represents a mechanism, or replacement, of
the epiphyseal cartilage, which contributes to the overall increase
in size through both interstitial and peripheral (perichondral)
growth. The arrows indicate the centrifugal direction of ossification
expansion. (B) Multifocal ossification centers in the trochlear region
of the distal humerus of a 9-year-old boy. Contrast these with the
more mature ossification center in the capitellum.
1. Anatomy and Physiology of Skeletal Development
distal end of the proximal phalanx, a spherical (curvilinear) physis
(SP) is developing. Much of the epiphyseal cartilage will be
replaced by bone, without concomitant longitudinal growth of the
shaft. Contributions to the growth of the overall length of a phalanx
or metatarsal (or metacarpal) from such a physis are less than
those from the transversely oriented physis at the other end. A
sesamoid bone (S) is evident underneath the metatarsal head.
uration.51,73,74 However, in the absence of functioning skele-
tal muscle, fetal growth plate structure and function
change.75 There is a specific reduction in the size of the pro-
liferative zone. The hypertrophic zone tends to remain the
same width.
Differences among the physes, which are reflections of
growth rates and biomechanical stresses, may be found in
the relative numbers of cells in each zone, the overall height
of the physis, and any specific cellular modification, such as
replacement of the zone of hypertrophic cartilage by a
zone of fibrocartilage. These basic patterns may be analyzed
upon either their functional or morphologic characteristics
(Fig. 1-16).
The zone of growth is directly involved in both longitudi-
nal and latitudinal (diametric) expansion of the bone. It is
the area of most concern with any fracture involving the
growth plate, as damage to cells in this zone, in contra-
distinction to other zones of the physis, may have serious,
long-term consequences for normal growth patterns. This is
the cellular zone in which new cell formation occurs.
The resting and dividing cells are intimately associated with
blood vessels of the epiphysis (a factor discussed in detail
later in this chapter). Additional cells also may be added
peripherally through a specialized region surrounding the
physis, the zone of Ranvier. This zone contains fibrovascular
tissue, undifferentiated mesenchymal tissue, differentiated
epiphyseal and physeal cartilage, and the osseous ring of
Lacroix (Fig. 1-16). Adjacent to the resting cell layer is the
layer of active cell division. Mitoses occur in both longitudi-
nal and transverse directions, although principally the
former, leading to the earliest evidence of cell column for-
mation. In an active growth plate, such as the distal femur,
these cell columns may comprise half of the overall height
of the physis.228 The randomly dispersed matrix of the resting
and dividing regions becomes longitudinally oriented
between the columnar cells.54 In transverse section this
region of the physis has a honeycomb-like appearance
(Fig. 1-20).
Tensegrity 13

A B
FIGURE 1-19. (A) Bipolar growth zone that develops between the other areas, such as the triradiate cartilage of the acetabulum,
epiphyseal ossification center (EOC) and the metaphysis. Germi- longitudinal growth may occur from both sides (arrows). Note the
nal cells (G) are present on both sides of this plate, but significant germinal cells (G).
longitudinal growth occurs only on the metaphyseal side. (B) In

The next functional area is the zone of cartilage matura- Safran et al. studied five patients (skeletally immature)
tion. Increased extracellular matrix is formed in this zone, who had a cemented endoprosthetic replacement of the
principally between cell columns, rather than between suc- proximal tibia because of a malignant tumor.184 In each
cessive cells in a given column (which remain separated by patient the cement column fractured, allowing continuing
a thin transverse septum). This matrix is comprised of a dis- physeal growth. The estimated force to cause this growth was
tinct type of collagen (type X) that appears specifically 584 newtons/cm2.
related to endochondral ossification.222 Elastic fibers may
also be present.76 The extracellular matrix exhibits cell-
mediated biochemical changes, becoming metachromatic Periphysis
and then calcifying, a necessary prelude to ossification.55 The
Oestrich and Ahmad coined the term periphysis for the zone
chondrocytes hypertrophy and eventually are replaced by
of Ranvier, the ring of Lacroix, and the contiguous mem-
osteoblasts.42,97
branous bone they produce.142 The periphysis may be 1–3
The final functional zone is that of cartilage transforma-
mm wide and may have a radiographic step-off due to
tion. The cartilage matrix must be sufficiently calcified to
latitudinal growth in a periodic, rather than continous,
allow vascular invasion by the metaphyseal vessels, which
manner.124 It should not be confused with a corner fracture
break down the transverse cartilaginous septa to allow inva-
of child abuse.
sion of the mature cell columns.97 Perivascular osteoblastic
Rodriquez et al. assessed changes following excision of the
cells lay down primary spongiosa along the preformed inter-
perichondrial ring.180 The most evident changes were an
columnar matrices (Fig. 1-21). This cartilage–bone compos-
enlargement of the growth plate at the exposed surface that
ite is remodeled, removed, and replaced by a more mature,
grew in an abnormal direction and bending of the bone. No
secondary spongiosa eventually containing no remnants of
regeneration of the perichondrial ring occurred. These
the cartilaginous precursor.
changes support the role of the ring in the mechanical con-
The regions of cellular hypertrophy and transformation,
straint of the physis and the induction of bone formation by
which appear to be structurally weak, are the regions most
the hypertrophic cartilage at the level of the absent peri-
often involved in physeal fractures (see Chapter 6). With
chondrial ring.
certain diseases, such as rickets, the hypertrophic zone may
be greatly widened because the matrix fails to calcify. It pre-
vents capillary invasion from the metaphysis, so the hyper-
trophic zone cannot be replaced by osseous tissue. Addition Tensegrity
to the hypertrophic cartilage zone continues, resulting in a
progressively wider region that becomes more mechanically The aforementioned cellular (microstructure) and tissue–
unstable and may eventually result in epiphyseal displace- organ (macrostructure) shapes and evolving changes rely on
ment through both fracture and progressive plastic defor- a complex interaction between the genetic program for skele-
mation (see Chapters 5, 16). More specific aspects of physeal tal morphology and the interaction of the normal and abnor-
failure are discussed in Chapter 6. mal genotype with external (environmental) demands.
14
A B
C
FIGURE 1-20. Transverse sections of the upper hypertrophic zone (A), lower hypertrophic zone (B), and primary spongiosa (C).
Interestingly, the biomechanical interaction of the genotype
with the external and internal physical demands seems to
follow a common theme from the structure of a molecule to
the toddler struggling to learn to walk.
A universal set of basic building rules seems to guide the
design of organic structures, from simple carbon com-
pounds to complex cells and tissues.101–103 Understanding
what the component molecules of bone or cartilage tissue
might be does little to explain how the whole complex system
works and particularly how the chondro-osseous skeleton
changes and adapts as the child grows. Nature appears to
apply common assembly rules at any level. These rules may
be deduced from the recurrence (at scales from molecular
to macroscopic) of certain geometric patterns. This phe-
nomenon involves components that merge to form increas-
ingly larger, stable structures often having new biologic or
biomechanical properties that could not necessarily have
1. Anatomy and Physiology of Skeletal Development
been predicted from the characteristics of their individual
parts. It is defined as self-assembly. In the skeleton, large mol-
ecules self-assemble into cellular components (organelles),
which self-assemble into cells (e.g., osteocytes, chondrocytes,
fibroblasts), which self-assemble into tissues (e.g., bone,
cartilage, ligament), which self-assemble into organs (e.g.,
femur, radius, cuneiform). The result is a skeleton organized
heirarchically as tiers of systems within systems.223 This
common system of encompassing architecture is referred to
as tensegrity. This term basically refers to a system that stabi-
lizes itself mechanically because of the way in which tensional
and compressive forces are distributed and balanced
throughout the structure.
Tensegrity structures become mechanically stable not
because of the strength of individual members but because
of the way the entire structure distributes and balances
mechanical stresses. This concept is often used when plan-
Collagen
FIGURE 1-21. Growth patterns of typical endochondral bones. (A)
The two primary patterns for physeal growth are longitudinal (elon-
gation of cell columns) and latitudinal (diametric). (B) The devel-
oping ossification center enlarges by interstitial growth between
rudimentary columnar cartilage. (C) Such interstitial growth (elab-
oration of extracellular matrix) also occurs in the physis. In addi-
tion, there are peripheral areas of appositional growth. (D) Once a
relatively mature epiphyseal ossification center is present, latitudi-
nal development of the physis is limited essentially to appositional
growth, which occurs primarily from the zone of Ranvier.
ning realignment osteotomies following fracture malalign-
ment. It is probably the underlying basis for the seemingly
spontaneous correction of a dorsal angular deformity of a
distal radial metaphyseal fracture in a 10-year-old.
Tensegrity structures fall into two categories. The first are
rigid structures that can bear tension or compression. Each
strut is oriented to constrain each joint to a fixed position to
bring stability to the whole structure. The framework of a
Buckminster Fuller geodesic dome is an excellent example.
The second category includes structures that stabilize
through prestress. Compression-bearing rigid structures are
connected by other structures that bear only tension. Within
the structure these components complexly interact. Com-
pression-bearing rigid struts stretch (tense) the flexible,
tension-bearing components, and these tension-bearing
members interactively compress the rigid struts. The
counteracting forces equilibrate, thereby stabilizing the
structure.103
In the tensegrity model the internal structure of any cell’s
cytoskeleton, which is basically composed of three units
termed microfilaments, microtubules, and intermediate fil-
aments, may be geometrically transformed by an alteration
of physical forces transmitted across a cell surface.223 A frac-
ture is a macroalteration of organ dynamics that causes cel-
lular reaction (i.e., cellular biomechanical change). Many of
the enzymes and other substances that affect or control
protein synthesis, energy conversion, and growth in a cell are
physically attached to, and effectively immobilized on, the
cytoskeletal elements. Any change in cytoskeletal geometry
15
and mechanics therefore could affect or initiate the
appropriate biochemical reactions necessary to respond to
the fracture at the cellular level. This includes release of
previously immobilized molecules into the extracellular
milieu.
In an interesting experiment living cells were forced to
assume different shapes (spherical or flattened) by placing
them on islands of extracellular matrix.101,102 The modifica-
tion of cell shape affected the expression of various genetic
(nuclear controlled) patterns. This occurs because the
nucleus also changes shape as the cell changes shape. The
flatter the cell, the more likely it is to divide. In contrast,
rounded cells that were prevented from spreading activated
a death program (apoptosis). This action is evident in the
hypertrophic zone of the growth plate as a prelude to ossifi-
cation. Cells that were neither too extended (flat) nor too
retracted (round) differentiated in a tissue-specific manner.
Mechanical restructuring of the cell apparently tells the cells
what to do.36 Flattening tells the cell that more cells are
needed to cover the surrounding substrate (as during wound
repair) and that cell division is necessary. Sphericity indicates
the presence of too many cells and not enough matrix, sig-
naling the cessation of division. Unresponsive continuation
of division probably leads to tumor formation. Somewhere
between these cellular extremes, normal tissue function is
established and maintained.
Collagen
The orientation of collagen fibers in the growth plate and
contiguous structures of a growing long bone is character-
ized by five major groups of collagen fibers: transphyseal
(longitudinal), perichondrial-periosteal (longitudinal), epi-
physeal (radial), perichondrial ring (circumferential), and
metaphyseal bone (circumferential).190,201,206
Transphyseal collagen fibers extend from the calcified
cartilage in the metaphysis across the growth plate and into
the epiphyseal cartilage and secondary ossification center.
The transphyseal fibers interdigitate with radially oriented
epiphyseal fibers that lie between the secondary ossification
center and the zone of resting cells. Longitudinally oriented
collagen fibers predominate in the perichondrium–perios-
teum. In the primary spongiosa, bone collagen is oriented
obliquely and circumferentially on the longitudinal septa of
calcified cartilage. Circumferentially oriented collagen fibers
occur within the perichondrial groove and in the perichon-
drium–periosteum directly over the groove. The peri-
chondrial ring is the largest and most prominent of these
circumferential groups. All of these patterns create a
mechanically responsive microskeleton for the developing
bone.
Collagen fiber groups of the perichondrial–periosteal
complex achieve firm insertion into the epiphyseal cartilage
and interdigitation with the radial epiphyseal fiber group at
the periphery of the physis. Disruption of the perichon-
drial–periosteal fibers surgically or pharmacologically
reduces the resistance to separation through the physis.
Substitution of an abnormal collagen–fiber matrix, such as
scar or bone, at the periphery of the physis following injury
16
may result in partial growth arrest. This growth disturbance
may be viewed as a pathologic morphogenetic influence by
abnormal collagen fibers that cannot be removed by local
physiologic mechanisms but may be removed surgically. Clin-
ical and experimental results following circumferential inter-
ruption of the periosteum indicate that proliferation of
chondrocytes of the growth plate places the collagen fibers
of the perichondrium–periosteum under tension, providing
a specific stimulus to longitudinal osteogenesis of the
periosteal bone cylinder while at the same time inhibiting
further formation of endochondral bone. The perichondr-
ial–periosteal fiber group is a mechanical linkage for a
negative feedback loop in the physiologic control of growth-
plate proliferation.190
Tensile forces mediated by collagen fibers exert important
morphogenetic influences on the normal and pathologic
development of an immature bone and may provide the
physiologic mechanism for the Heuter-Volkmann and Wolff
laws of bone growth. The vectors and interrelations of the
collagen fiber systems are consistent with such morpho-
genetic roles. Selective manipulation of collagen fiber archi-
tecture may provide precise therapeutic methods to control
normal and pathologic bone growth.201,206
Bone Growth
Patterns of Physeal Growth
Characteristically, the growth of the tubular bones is consid-
ered a longitudinal phenomenon,50 although expansion
can, and must, occur in other significant directions. Cer-
tainly, appositional growth (widening) has been described
for the diaphysis and metaphyses through the combined
mechanisms of periosteal osteogenesis and endosteal remod-
eling. The physis also may expand in a diametric, or lat-
itudinal, fashion (Fig. 1-21).92 This occurs by cell division
and matrix expansion within the physis (interstitial growth)
and by cellular addition peripherally at the zone of Ranvier
(appositional growth).155
Interstitial growth of the discoid physis appears related
directly to enlargement of the secondary center of ossifica-
tion. When the epiphysis is completely cartilaginous or
contains only a small, spherical ossification center, the bio-
logically plastic cartilage does not present a total mechani-
cal barrier to interstitial expansion of the juxtaposed physis.
Both regions appear to undergo integrated interstitial
expansion; but with increasing development of the epiphy-
seal ossification center, a discrete subchondral bone plate
forms. Further interstitial expansion of the physis is effec-
tively precluded in areas directly apposed to the subchondral
plate. Latitudinal expansion thus becomes progressively
limited to appositional growth from the peripheral zone
of Ranvier as the subchondral bone plate enlarges. Once
the ossification center has expanded to the epiphyseal
margin, relatively minor damage to the peripheral zone
of Ranvier may lead to rapid formation of an osseous
bridge, severely limiting growth potential latitudinally and
longitudinally.
Expected growth rates at various ages are as follows.171,172
1. Anatomy and Physiology of Skeletal Development
Age Expected growth rate (cm/year)
Months 1–6 18–22
Months 6–12 14–18
Year 2 11
Year 3 8
Year 4 7
Years 5–10 5–6
Control of Growth
The factors affecting cell division within the physis are
not completely understood.10,55,77,112,181,182,183,204,226 The physis
appears to respond to various hormones, with cartilage
growth being stimulated by thyroxine, growth hormone, sul-
fation factor, and testosterone. Estrogen appears to have a
greater effect on stimulating the growth of already differ-
entiated osseous tissue, and it may slow cartilage growth,
primarily or secondarily, by affecting the periosteum and
subchondral bone on either side of the physis (see Physio-
logic Epiphysiodesis, below).186
Simmons has shown a definite circadian pattern to longi-
tudinal growth,198 which may reflect diurnal variations
of hormones. Mechanical factors, such as the intrinsic
tension within the periosteal sleeve, also may affect
growth rates.43,90,167,205 Disruption of this periosteal sleeve
and increased vascularity may be important factors in
the longitudinal overgrowth that often accompanies
fractures.54,87,106,115,177–179,202,222
Einhorn et al. showed that when one bone of the skeleton
is injured others experience an osteogenic response.56 This
may be seen in tibial overgrowth following femoral frac-
ture (in which there is well-recognized overgrowth). They
thought that a circulating osteogenic factor might be
responsible.
Saltation Concept
Lampl et al. studied human growth of infants from birth to
21 months.121 They showed that growth in length occurred
by discontinuous aperiodic saltatory spurts. These bursts of
growth ranged from 0.5 to 2.5 cm and were separated by
periods of no measurable growth ranging from 2 to 63 days.
Their data suggested that 90–95% of normal development
during infancy is growth-free. Length accretion is a distinctly
saltatory process of incremental bursts punctuating back-
ground stasis. Such spurt growth could help explain tod-
dlers’ fractures. Because the growth spurts occurred during
short (£24 hours) intervals, the lengthened bone and mass
increase would not have had time to adapt effectively to the
toddler’s activities, thereby predisposing to microinjury,
stress fracture, or plastic deformation.
Metaphyseal Changes
The metaphysis is the site of extensive osseous remodeling,
both peripherally and centrally. The metaphyseal cortex con-
sists of fenestrated, modified, trabecular bone on which the
periosteum elaborates new membranous bone to thicken the
cortex progressively (Fig. 1-14). Similar but less extensive
Bone Growth
FIGURE 1-22. Extensive modeling and remodeling leads to the
development of trabecular bone orientation that conforms to major
stress patterns within the developing bone. Note particularly how
the trabecular bone streams “upward” from the calcar toward the
capital femoral physis (compression response). The tension
response is evident “streaming” from the metaphysis of the greater
trochanter along the upper femoral neck and into the capital
femoral metaphysis.
endosteal bone formation occurs. As this region thickens,
the trabecular bone is invaded progressively by the diaphy-
seal osteon systems, a process not unlike osteons travers-
ing the fracture site during primary bone healing (see
FIGURE 1-23. Harris growth arrest or slowdown lines. (A) Three-
year-old child suffering from malnutrition (kwashiorkor) and mild
rickets. At the time of the first onset of disease a transverse line
was laid down (arrows). The child was treated in a hospital, pro-
vided with dietary supplements, and grew more rapidly. He died a
year later from Salmonella enteritis. Note the relative growth con-
17
Chapter 8). This converts peripheral trabecular bone (woven
or fiber) to lamellar bone (osteonal), which has different
biomechanical properties. A torus (buckle) fracture occurs
only in a metaphyseal region with a trabecular cortex. Cen-
trally, a considerable amount of trabecular reorientation and
remodeling occurs (Fig. 1-22).118 This is an area of intense
osteoblastic activity, a factor readily evident on a bone scan
in a child. This osteoblastic activity also explains the rapid
healing of fractures through the metaphysis. This transi-
tional area of bone formation and remodeling, which is con-
tinuously changing and responding to biologic stresses, is
one of the most susceptible regions of the developing skele-
ton to fracture. The distal humeral and distal radial metaph-
yses are certainly the most commonly involved areas.
Many bones exhibit transversely oriented, dense trabec-
ular patterns in the metaphysis.147 These patterns usually
duplicate the appropriate physeal contour (Fig. 1-23). They
often appear after generalized illnesses or even after local-
ized processes within the bone (e.g., osteomyelitis). Appar-
ently, they represent a temporary slowdown of normal
longitudinal growth rates during the illness and are often
referred to as Harris “growth slowdown or arrest” lines.
Because of the slowdown, as the trabeculae of the primary
spongiosa form, they become more transversely than longi-
tudinally oriented, creating a temporary subchondral thick-
ening in the primary spongiosa. Once the illness is over,
normal longitudinal growth rates resume, and the primarily
longitudinal trabecular orientation is restored. The thick-
ened, transverse plate is left behind, to be gradually remod-
eled as primary spongiosa becomes secondary spongiosa and
medullary cavity. These particular metaphyseal changes are
discussed further in Chapters 5 and 6.
Physiologic Epiphysiodesis
Physiologic epiphysiodesis refers to the normal, gradual re-
placement of the physis during adolescence. The process
tributions of the trochanteric, neck, and capital femoral regions.
(B) Harris growth arrest line in the distal femur of a 10-year-old
boy (arrows). This line occurred with the onset of leukemia. Sub-
sequent growth occurred over the next 14 months while the boy
was on chemotherapy. The disease recurred shortly before death,
and a second line of growth slowdown is occurring at the physis.
18
commences with the formation of small osseous bridges
between the epiphyseal ossification center and the metaph-
ysis and ends with complete replacement of the cartilaginous
physis by osseous tissue.83,113,145,148 This transversely oriented
replacement may be evident radiographically at any age
(even during adulthood), although it is usually progressively
remodeled until no longer evident. Each physis appears to
have its own pattern of closure, a factor that predisposes dif-
ferent physes to certain types of fractures (e.g., the Tillaux
fracture of the lateral distal tibia) (see Chapter 23).
Histologically, several significant changes occur during
normal epiphysiodesis. Similar changes also must occur in
damaged physes, although usually in more localized regions
of the physis. The juxtaphyseal subchondral bone plate
thickens. A similar thickening of the metaphyseal bone
also occurs, with formation of the transverse osseous septa
instead of the more characteristic longitudinal trabeculae.
The basic cellular arrangement of the physis does not
change significantly while these osseous plates initially are
forming. However, there is a distinct slowdown and cessation
of cellular proliferation, and the biochemistry is altered, with
progressive calcification and mineralization extending into
the germinal and resting zones to form multiple tide lines.
The cell columns are rapidly replaced as they are progres-
sively calcified. The extension of ossification from both sides
leads to eventual perforation of the physis in several areas by
small osseous bridges. Ossification then progresses outward
from these perforations, replacing the cartilage and leaving
an osseous physeal ghost, comprised of coalesced, thickened,
subchondral plates of the metaphysis and epiphysis; it is
readily evident on roentgenograms. Usually the process
starts centrally and proceeds centrifugally, so small remnants
of the physis may be found peripherally. Certain physes,
however, show altered patterns. In particular, the distal tibial
physis closes first over the middle and medial regions and
subsequently over the lateral region, a factor that leads to
certain types of fracture (see Chapter 23).
A B
FIGURE 1-24. (A) Remnant of thickened subchondral bone
(physeal ghost) in a 48-year-old man. This bone does not always
remodel and disappear. (B) MRI of a 43-year-old man showing the
1. Anatomy and Physiology of Skeletal Development
Physiologic epiphysiodesis begins earlier in females than
in males; and like the appearance of primary and second-
ary ossification centers, it follows a reasonably predictable
sequence from bone to bone. The earlier closure in the
female appears to be the direct effect of estrogenic com-
pounds that accelerate cartilage replacement and osseous
maturation versus the effect of androgenic compounds,
which stimulate cartilage growth and matrix elaboration.
The times of both the onset and the completion of fusion
are influenced significantly by sex hormones. Girls undergo
the process earlier than boys, but the relative sequence by
which physes undergo closure is the same in both sexes (see
Chapter 5 for closure patterns).
Vasculature
Developing bone, both osseous and cartilaginous compo-
nents, is extremely vascular.14,15,20,123,125,126,145,148,213–216 The peri-
osteum contains multiple small vessels that play a role in
osteogenesis and contribute to the increasingly complex
haversian systems of the maturing diaphyseal cortex. The
endosteal surface of the diaphysis receives blood through
the nutrient artery, a major vessel that sends branches to
each metaphysis and throughout the diaphysis. The epiph-
ysis receives its blood supply from vessels that penetrate and
ramify through the cartilage. These two major circula-
tory patterns—epiphyseal vessels and metaphyseal vessels—
appear to be functionally and anatomically separate. In fact,
they may remain relatively separate even after the growth
plate closes, as may be shown in magnetic resonance imaging
(MRI) studies in adults (Fig. 1-24). The physis derives a
blood supply from three regions: epiphyseal vessels, metaph-
yseal vessels, and perichondral vessels from the zone of
Ranvier.
Epiphyseal circulation varies significantly in conjunction
with development and enlargement of the secondary ossifi-
physeal ghost and gradation signal changes in the epiphysis and
metaphysis. They indicate continued separation of the vascularity
of these two regions even into adulthood.
Vasculature 19

FIGURE 1-25. (A) Penetration of cartilage

canals into the capital femoral epiphysis.
The vessels in these canals distribute
throughout the epiphyseal cartilage and
send selected branches to the germinal
zone of the physis (arrow). (B) Higher-power
view (20¥) of two adjacent cartilage canal
systems. They are both reasonably well
demarcated from the surrounding cartilage.
Much of the canal is occupied by undiffer-
entiated, perivascular mesenchyme (M).
Each canal usually has a central artery, one
or more veins, and a peripheral capillary
network. (C) India ink injection of a terminal
cartilage canal unit. Note the “glomerular”
structure of the capillaries peripheral to the
central artery (A).

cation center.71,119 Vessels distribute through the chon-
droepiphysis as specialized structures termed cartilage
canals (Fig. 1-25). These canals course throughout the chon-
droepiphysis and send branches to the resting/germinal
zones of the physis.19,81 Infrequently, these small vessels com-
municate across the physis, anastomosing with the metaphy-
seal circulation. These particular transphyseal vessels may be
found in the larger epiphyses, are usually more frequent
near the peripheral than the central regions, and become
less frequent as the secondary ossification center enlarges.
By the time the subchondral plate forms, these “crossing”
vessels are no longer present centrally.
The cartilage canals contain a central artery, one or more
accompanying veins, and a capillary complex that surrounds
the larger, central vessels (Fig. 1-25). The capillary network
forms a glomerular tuft that serves as the end-arterial ter-
mination of each canal system. These canals have several
important functional and morphologic characteristics: (1)
they supply discrete regions of the epiphysis and physis,
where there are no significant intraepiphyseal anastomoses;
(2) the mesenchymal (perivascular) tissue within the canals
may serve as a source of chondroblastic cells for the contin-
ued interstitial enlargement of the chondroepiphysis; (3) the
canals are surrounded by differentiating hyaline cartilage
containing hypertrophic cells and that may form an internal
structural network prior to ossification; and (4) the canals
play an integral role in the formation of the secondary
center of ossification (Fig. 1-26).19,71,72,227
Once the secondary center of ossification begins to
enlarge, changes commence within the epiphyseal cir-
culation. Several cartilage canal systems may contribute to
enlargement of the ossification center, creating anastomoses
between canal systems that were initially end-arterial. The
secondary center enlarges and forms a subchondral plate,
with small vessels penetrating this plate to supply the physis.
This circulatory pattern retains a territorial (end-arterial)
pattern.61 If a segment of the epiphyseal vasculature is com-
promised, temporarily or permanently, the zones of growth
associated with those vessels cannot undergo appropriate
cell division. Unaffected regions of the physis continue lon-
gitudinal and latitudinal growth, leaving behind the affected
region (Figs. 1-27, 1-28). The growth rates of the cells directly
adjacent to the infarcted area are more mechanically com-
promised than cellular areas farther away, resulting in an
angular growth deformity.
The perichondrial vascular network courses circumferen-
tially around each physis. This circulatory pattern is variable,
as dictated by individual epiphyseal anatomy. The small
20
FIGURE 1-26. Role of the cartilage canals in the formation of an
epiphyseal ossification center. (A) Preossification center formation
with hypertrophy of the epiphyseal cartilage surrounded by several
cartilage canals (cc). A portion of the capillary glomerulus (cg) is
present within the hypertrophied cartilage. This vessel is analogous
FIGURE 1-27. Epiphyseal and metaphyseal circulatory patterns. (A)
Epiphyseal circulation vessel (E-vessel) enters the epiphysis and
distributes to the enlarging epiphyseal ossification center. It also
either directly supplies the germinal cells of the physis or crosses
the subchondral plate to reach the physis. (B) If the E-vessel is cut
off, the germinal cells are deprived of nutrition and either decrease
or cease the cell division necessary for longitudinal growth. The
contiguous parts of the physis with good vascularity continue to
grow, leading to eccentric growth. (C) Metaphyseal circulation (M-
vessels) is derived from both central (nutrient artery) and periph-
eral sources and is essential to vascular invasion of the
hypertrophic regions of the physis. (D) If the M-vessels are dis-
rupted, as with a metaphyseal fracture, the physis continues to
grow and increases the height of the cell columns while adjacent
regions maintain normal structure. This leads to remnants of car-
tilage that extend into the metaphysis (see Fig. 1-40A,B). Because
the germinal cells are normally supplied there is no growth angu-
larity, but the physis is abnormally thick in the involved regions.
Normal physeal thickness in such areas is replaced rapidly once
metaphyseal circulation is reestablished.
1. Anatomy and Physiology of Skeletal Development
to the irruption artery that initiates primary ossification in the fetus.
If this vessel is not functional, secondary (epiphyseal) ossification
may be delayed. (B) Early formation of bone within the epiphyseal
ossification center (eoc). Portions of the cartilage canals (cc) are
sending small vessels into this structure.
vessels of this system may provide peripheral circulation to
the epiphysis, physis, and metaphysis. The most important
branches supply the zone of Ranvier (Fig. 1-29). The func-
tional integrity of these vessels is essential to continued appo-
sitional growth at the periphery of the physis. Disruption of
the perichondrial circulation, which may occur with certain
physeal injuries (e.g., fracture, burn, radiation), may lead to
isolated areas of ischemia along the periphery of the physis
and subsequent eccentric growth with premature, localized
epiphysiodesis.
Metaphyseal circulation is derived from two sources: the
nutrient artery, which supplies the central region; and the
perichondral vessels, which supply the peripheral regions
(Fig. 1-27C,D). The terminal portions of both systems form
a series of loops that penetrate between trabeculae to reach
the margin of the hypertrophic zone of the physis. The
venular side of the loop enlarges to form a sinusoid.203
Interruption of metaphyseal circulation has no effect on
initial chondrogenesis and subsequent cartilage maturation
within the physis, but subsequent transformation of cartilage
to bone is blocked. This causes widening of the affected area
as more cartilage is added to the cell columns (in a hyper-
trophic mode), but none is replaced by bone (Fig. 1-27D).
Once metaphyseal circulation is reestablished, the widened,
provisionally calcified region is penetrated rapidly and ossi-
fied, returning the physis to normal width. This mechanism
is seen with fractures of the physis and less frequently
with fractures of the metaphysis. The metaphyseal blood
supply is blocked temporarily by fracture-caused separation
or impaction, and usually at least 3–4 weeks are required for
its restoration. If the circulatory compromise has been
caused by a metaphyseal fracture, bone formation in the
ischemic portion of the metaphysis may increase temporar-
ily once revascularization occurs, leading to transient osseous
overgrowth and apparent sclerosis (Fig. 1-30). Compromise
of the metaphyseal circulation has a minimal effect on lon-
gitudinal and latitudinal physeal development, particularly
compared to the effects of epiphyseal circulatory compro-
mise. Limited weight-bearing while a fracture heals may lead
to relative osteoporosis in the region supplied by the metaph-
yseal vessels (Fig. 1-31).
Vasculature
The diaphyseal circulation has two sources: periosteal
branches and endosteal branches.126,136,189 The contributions
differ during development (Fig. 1-32) and are obviously
affected by fractures associated with periosteal stripping or
FIGURE 1-29. Vessel within the zone of Ranvier, juxtaposed to the
hypertrophic zone of the physis.
21
FIGURE 1-28. Impaired growth of the physis in a
section rendered ischemic by disseminated intravas-
cular coagulopathy. (A) Localized growth impairment.
(B) Histology of A. (C) Impaired physeal growth of a
lateral section of physis (arrow).
disruption of the nutrient artery. The tibia, in particular,
exhibits a relative decrease in vascularity with increasing
skeletal maturation, which may be a factor in delayed healing
during adolescence and adulthood.
Taylor and Palmer conducted detailed studies of blood
supply to the skin and underlying tissues.208 They found
that the blood supply was a continuous three-dimensional
network of vessels not only in the skin but in all tissue layers.
The anatomic territory of the source artery to such a region
gave rise to the angiosome concept.
Remodeling
On a developmental basis, cortical bone, which becomes the
dominant skeletal tissue by the time chondro-osseous matu-
ration is complete, may be categorized as either primary or
secondary bone. As described previously, primary bone may
be formed by endochondral ossification or subperiosteal
membranous deposition; and such bone is always the first
bone formed in any region. During subsequent growth and
even beyond skeletal maturation (as defined by closure of
the physes), there is a continuous process of osteoclastic
(and possibly osteocytic) resorption of existing primary bone
followed by osteoblastic deposition of new bone. These
remodeling processes may involve several generations of
bone absorption and accretion.105 All bone formed by the
process of bone resorption and subsequent bone deposition
is called secondary bone. The entire remodeling process is
vascular-dependent.
Three basic types of primary bone may be found in most
large mammals: (1) circumferential lamellar bone; (2)
woven-fibered bone; and (3) primary osteons. At birth the
differentiated metaphyseal and diaphyseal cortical bone con-
sists principally of woven-fibered bone, with a few areas such
22 1. Anatomy and Physiology of Skeletal Development

FIGURE 1-30. Sclerosis of the metaphysis consequent to fracture

(arrows). Because of temporary deprivation of the vascularity, the
metaphysis did not continue normal remodeling. With remodeling
of the still vascularized area and some osteoporosis resulting from
disuse of this segment distal to the fracture, a contrast is obvious
between the involved and uninvolved sections of the metaphysis
on either side of the fracture. This roentgenogram was obtained 3
weeks after the fracture and immobilization in a non-weight-
bearing, long leg cast. By 6 weeks after injury, the metaphysis was
the same throughout because the vascularity had been reestab-
lished.

FIGURE 1-32. Changing patterns of circulation in the canine femur

(A) and tibia (B) at birth, 4 months, and 1 year. Black indicates the
most intense circulation, with shades of gray representing lesser
amounts of blood flow. Note how the tibia, in particular, changes,
which may be a factor in the delayed healing as the patient grows
older.

FIGURE 1-31. Relative osteoporosis in a region supplied by the

metaphyseal vessels. This teenager had been non-weight-bearing
because of a proximal tibial fracture.
Vasculature
as the femur also having primary osteons. The width of mam-
malian long bone is increased during growth by the deposi-
tion of primary (membranous) bone along the subperiosteal
surface.62 The structure of this new bone varies considerably
among species and at different stages of development. In the
human this new bone normally consists of circumferen-
tial, laminar bone comprised of orderly collagen bundles,
whereas in more rapidly growing quadripedal species (which
usually reach skeletal maturity within 1–5 years) the more
common pattern consists of woven-fibered bone with ran-
domly arranged collagen bundles.146
Woven-fibered bone generally contains large, irregularly
shaped vascular spaces with osteoblasts on the surround-
ing bone surface. These osteoblasts deposit successive layers
(lamellae) of new bone, progressively diminishing the
caliber of each original vascular space. The resulting
anastomosing, convoluted areas of bone, occupying what
were previously vascular spaces, are called primary haversian
systems, or primary osteons. Primary osteons are usually, but
not always, parallel to the long axis of a bone. They may
contain one to several vascular canals, and they are always
surrounded initially by woven-fibered bone.13,33
The continuous process of remodeling that occurs
throughout chondro-osseous development constantly and
dynamically changes the architecture of each bone (Fig.
1-33).165 The remodeling process, initiated by the osteoclastic
resorption of bone, results in longitudinally oriented, anas-
tomotic tubular cavities. Osteoblasts on the surfaces of these
cavities then deposit successive layers of new bone with an
orderly fiber orientation. The caliber of each cavity is thereby
gradually reduced until only a small, single vascular canal
remains. The newly formed cylinders of bone are called
secondary haversian systems, or secondary osteons.30,59 Sec-
FIGURE 1-33. Extensive remodeling and distortion of a fibula
consequent to continual pressure from an expanding fibular
osteochondroma.
23
ondary osteons consist of concentric sheets of lamellar bone.
Unlike primary osteons, secondary osteons are bounded by
cement lines formed when osteoclastic activity is superseded
by osteoblastic bone formation. The irregular areas of bone
between secondary osteons, called interstitial bone, consist of
remnants of both the primary and the remodeled bone pre-
viously deposited in the area. Interstitial bone may consist of
woven-fibered bone, circumferential lamellar bone, portions
of primary osteons, or portions of secondary osteons. Modi-
fication and acceleration of these processes are essential to
the remodeling that affects fracture callus.56
The two principal bone types, woven-fibered and lamellar,
are a reflection of a skeletogenic response to various biologic
demands. As such, the fourth dimension, time, becomes
an integral factor in the progressive development of three-
dimensional bone structure. Woven-fibered bone, with or
without primary osteons, is formed during rapid bone devel-
opment and accretion. It is the normal bone of skeletal
growth and the initial responsive bone in fracture callus for-
mation.1 In contrast, lamellar bone, which may be found in
association with primary osteons, secondary osteons, and cir-
cumferential lamellar bone, is formed when the rate of bone
deposition is moderate or slow.
Salem et al. showed that immature trabecular bone
adapted readily to moderate exercise with changes evident
in geometric, biochemical, and biomechanical facets.185
Although directed at the effects of exercise regimens, these
data correlate with the effect of normal childhood activity
constantly pushing the limits of trabecular adaptability in the
epiphyseal ossification center and the metaphysis.
Bone Density
Dual photon absorptiometry and gadolinium radionuclide
studies showed that bone mineral density in a group of 17
children who sustained fractures of either the lumbar spine
or femoral neck was not significantly reduced.40 Bone
mineral density probably does not play a significant role in
children sustaining acute traumatic fractures.
Other authors have suggested that the extent of miner-
alization does have an effect on fracture susceptibil-
ity.35,66,78,122,159,191,220 Certainly, significant decreases in mineral
content do increase stress fracture incidence.67,134 The latter
situation is more likely to be present in children with chronic
disorders (see Chapter 11).
Pediatric bone has a lower mineral content than adult
bone, which partially accounts for its different mechanical
properties.128 Plasticity allows children’s long bones to absorb
more energy prior to fracture, and significant deformation
may persist after injury.
Most of the standard bone densitometry techniques used
in adults have limited applicability in children.88,89 Quantita-
tive digital radiography, also known as dual energy x-ray
absorptiometry (DEXA), however, has more potential for
evaluating metabolic bone disorders in children. Physical
handicaps such as myelomeningocele or even a simple
limp secondary to tarsal coalition may be associated with
decreased bone mineral density in children. Trabecular
bone is going to be affected first (epiphyseal ossification
center, metaphysis). Henderson et al. showed that with tibial
or femoral fractures there was a 3.3–4.3% decrease in bone
24
density in the immobilized limb. They did not believe it
would make a significant difference in the long term.88,89
Biomechanics
During normal childhood activity and growth, the develop-
ing chondro-osseous skeleton is subject to a complex pattern
of forces that may cause microdeformations of the bone,
usually followed by appropriate biologic response patterns,
such as replacement of epiphyseal and physeal cartilage by
osseous tissues, increased amounts of osseous tissue, chang-
ing trabecular orientation, and varying amounts of different
histologic types of bone. These local microdeformations are
referred to as strains, and the local force concentrations at
these points are termed stresses. The biologic relations
between stresses and strains at a particular point in the devel-
oping skeletal unit are governed by the material properties
of the local chondro-osseous and fibrous/fibro-osseous
tissues, the direction and magnitude of imposed loads,
and the geometric configuration of the region being
loaded.17,21,37,41,64,79,94,99,100,107,109,110,133,164,211,212,217,218,229
The effects of the normal biologic forces on the physis,
epiphysis, and metaphysis are minimally understood.230 The
development of the epiphyseal ossification center appears to
be controlled genetically and biomechanically, with both
affecting the molecular structure and components within
1. Anatomy and Physiology of Skeletal Development
the skeletal tissues. At a certain point in time, summated
joint reaction forces reach a maximum within a given region
of the chondroepiphysis, stimulating osteogenesis in an area
with appropriate, established vascular supply (i.e., cartilage
canals). If forces are abnormal, as with developmental hip
dysplasia or developmental dislocation of the head of the
radius, this ossification process may be delayed, irregular, or
eccentrically located. Similarly, if normal joint dynamics are
traumatically disrupted (e.g., Monteggia injury), subsequent
maturation of the ossification centers are rearranged. Phys-
iologic stress appears necessary for the continued, orderly
development of both the physis and the secondary ossifica-
tion center.
Stress is basically the internal resistance of bone and car-
tilage to acute or chronic deformation. It is not a directly
measurable physical phenomenon but may be considered
force applied per unit area. Rate of application of the force
is also important. Three types of stress are seen in develop-
ing bones under normal conditions: tension, compression,
and shear. If these stresses are increased beyond the physio-
logic response capacities of a given portion of the de-
veloping bone or cartilage, failure (fracture) may result.
Compression and tension forces normally act on bone at
various angles. The growth plate progressively develops
undulations and mammillary processes as a means of align-
ing the physis reasonably parallel or perpendicular to major
force patterns (Figs. 1-34, 1-35), whether compression or
FIGURE 1-34. Development of physeal undula-
tions in an “adolescent” giraffe. (A) Morphology.
(B) Radiology. These complex undulations are a
biologic reaction to minimize shearing and rota-
tional loads as the animal walks and runs. (C) In
a transverse section these undulations penetrate
the metaphysis like pegs.
 Biomechanics 25

FIGURE 1-35. (A) Separated epiphysis (bottom) and metaphysis (top) showing the
extensive pegging in a juvenile walrus. (B) CT scan of the distal tibia in a 10-year-
A old boy shows this same undulation process in a human.

tension. Similarly, developing trabecular patterns within the
metaphysis and epiphysis also seem to be a direct alignment
response to normal weight-bearing or functional stresses
(Fig. 1-36).38,98,173–175,199 Shear stress acts at any angle other
than 90°. Again, the undulations in the physis and the
appearance of fibrocartilage, rather than columnar cartilage,
appear to be biologic adaptations to minimize shear stresses.
Extrinsic forces acting on developing cartilage and bone
may therefore evoke a normal response (i.e., stimulation of
growth and remodeling) or an abnormal response (i.e.,
deformation or fracture failure), contingent on the magni-
tude, duration, and direction of the evocative forces and on
the rate at which the responsive tissue is loaded.
It is important to realize that there is a normal biologic
range of compression/tension response within each physis,
and that a given physis is responsive to more than one type
of stress.80,165,167,205 Within this physiologic limit, increased
tension or compression accelerates growth. Compression
appears to elicit a more rapid rate of growth than tension.
Beyond the physiologic limits of either stress, growth may be
significantly decreased or even stopped.80,91,117,195 This may
occur with certain physeal fractures (see Chapter 6).224 These
principles are often referred to as the Heuter-Volkmann law
of cartilage growth response.209
Ruysce, in 1713, demonstrated that a massive force was
required to separate the epiphysis from the metaphysis

FIGURE 1-36. In animals with knee flexion gait patterns, the bone formed by the physis of the tibial tuberosity is longitudinally oriented
to accommodate stress. (A) Radiology. (B) Morphology. (C) Histology.
26
because each epiphysis was firmly connected externally by
the periosteum and internally by the undulations and
mammillary processes existing between the metaphysis and
physis.166 In 1820 James Wilson showed that a longitudinal
force of 550 lb was required to detach the epiphysis from the
metaphysis; but if the periosteum was divided first, the force
required was only 119 lb.166
Bright and Elmore showed that both the age of the animal
and the direction in which the force was applied were sig-
nificant factors.13 The physis is most resistant to traction and
least resistant to torsion. Furthermore, the epiphysis can
probably be displaced at least 0.5 mm before any gross sepa-
ration begins. A more detailed description of physeal and
epiphyseal responses to injurious forces may be found in
Chapter 6.
In addition to the effects of extrinsic biomechanical forces
on growth plates, there is an intrinsic anatomic control
factor: the periosteum. The periosteum attaches directly and
firmly to the zone of Ranvier at each end of the developing
bone; it is attached more loosely to the diaphysis and
metaphysis. Experimental circumferential resection of a por-
tion of the periosteum may cause accelerated longitudinal
growth.43 It thus appears that the stimulus to longitudinal
growth caused by joint reaction forces may be tempered by
the intrinsic tensile restraint imposed by the periosteal sleeve
(cylinder). When this restraint is temporarily released, as
with a fracture, overgrowth may occur.
Major intrinsic factors also affect the response of devel-
oping bone and cartilage to potentially injurious forces:
(1) energy-absorbing capacity; (2) modulus of elasticity;
(3) fatigue strength; and (4) density. Each of these factors
is influenced by the changes that occur in develop-
ing bone over the period of progressive maturation. The
increasing size of the secondary center of ossification
affects the energy-absorbing capacity of the physis and
contributes to the greater incidence of physeal injuries
in older children. Increasing diaphyseal (and, less so,
metaphyseal) cortical width and the development of primary
and secondary osteons affect the modulus of elasticity
and relative density, thereby causing different fracture pat-
terns (e.g., greenstick versus complete).65,108 Much experi-
mental work still must be accomplished with developing
bone (rather than mature bone) to answer many of the
questions.
An understanding of the specific biomechanical changes
that take place during postnatal development makes it nec-
essary to relate changing function to changing morphology.
To date, there are only three brief studies on the mechani-
cal properties of children’s bones. Hirsch and Evans showed
that the tensile strength and the modulus of elasticity of
bone tissue from nine children (all under 2 months of age)
were less than those from similar bone tissue from a 14-year-
old.95 Vinz conducted a more comprehensive study showing
that tensile strength and modulus of elasticity increased
progressively throughout growth but that strain and fracture
patterns decreased slightly.221 Currey and Butter, using spec-
imens of femoral cortical bone from 18 subjects who were
2–48 years of age, conducted three-point bending tests.44–47
Compared to adult bone, they found that children’s bone
had a lower modulus of elasticity, lower bending strength,
and lower ash (mineral) content; it also reflected more
absorbed energy before breaking and tended to absorb more
energy after fracture propagation had started. The typical
1. Anatomy and Physiology of Skeletal Development
greenstick fracture surface required more energy for its
production than the relatively smooth surfaces of adult
fractures.
It is reasonable to suggest that progressive maturation of
porous cortical bone causes a gradual shift in the distribu-
tion of bone strength and stiffness in the various regions of
the bone, especially the metaphysis and diaphysis (Figs. 1-37,
1-38). In younger persons bone in the cortical center is prob-
ably the strongest and stiffest, although with aging (after
physiologic epiphysiodesis) there is gradual shift of strength
and stiffness toward the periosteal surface. In addition to
the varying porosity distribution, a definite, progressive
change also takes place in the osseous microstructure from
the endosteal to the periosteal surface as the child matures.
Bone near the endosteal surface undergoes more remodel-
ing and thus contains more osteons and osteon fragments.
However, inherent to such osteonal structure are numerous
cement lines that have been shown to be sites of weakness in
cortical bone.30 In contrast, bone near the periosteal surface
has undergone less remodeling and is often surrounded by
a layer of circumferential laminar bone containing few if any
cement lines.
Mechanical properties are determined by microstruc-
ture.22,23,76,225 The dynamic variations in microstructure
throughout cortical bone undoubtedly reinforce the
mechanical property distributions created by the porosity
gradients. The strongest type of bone is circumferential
lamellar bone, followed (in order of decreasing strength) by
primary laminar, secondary haversian, and woven-fibered
bone.
The effects of varying histology on bone mechanics have
also been studied.6,9,30,59,93,111,192,197 Maj investigated the corre-
lation between breaking load and collagen fiber orientation,
finding that bone cut longitudinally took three to six times
more applied force to break than similar bone cut tangen-
tially, transversely, or radially; that the breaking strength of
bone was proportional to the number of collagen fibers in
the plane of the applied force; and that the mechanical
anisotropy of bone depended on the distribution and direc-
tion of collagen fibers.129 Maj also found, with the exception
of the distal metacarpals, that the variation in porosity was
not specifically responsible for the variations in breakability
between different parts of the skeletal system. Toajari con-
FIGURE 1-37. Bone is relatively plastic when first formed. If sub-
jected to unusual forces it does not assume the genetically directed
shape. In this pelvis from a bedridden child with severe quadri-
plegic cerebral palsy, the asymmetric muscle involvement has led
to a distorted pelvic shape.
Biomechanics
A B C D
FIGURE 1-38. Bone forms within the periosteal sleeve during the
process of bone lengthening. (A) Early bone formation 4 weeks
after inception of lengthening. (B) Nine weeks later. Note the poor
osteogenic response in the fibula. (C) The fixator screws were
pulled out when the patient fell off a trampoline. The leg abruptly
cluded that the modulus of elasticity and the breaking
strength of bone were directly proportional and attributable
to the orientations and quantity of collagen fibers.210
Although these studies were directed specifically at bone,
they present concepts that seem applicable to failure of the
physis, as there are significant differences in collagen fiber
orientation among the various regions of the physis. Ascenzi
and Bonucci found that the ultimate tensile strength of a
single osteon system was found in the osteon in which most
of the collagen fibers were oriented parallel to the longitu-
dinal axis of the test specimens.4,5 Evans and Vincentelli also
thought that their experimental results showed that tensile
strength was related to the predominant direction of the
collagen fibers in the osteon.60 These studies gain further
import in the child, considering the fact that haversian
(osteon) systems must develop postnatally. Osteons with lon-
gitudinally oriented collagen fibers have stronger tension
than osteons with transversely oriented fibers, which have
stronger compression.
Children’s bone is susceptible to fracture in different
modes from adult bone, failing differently because of the fact
that the bones are in the process of forming and remod-
eling these various osteon systems. Young bone certainly
appears more porous on cross section, with the cortex having
a greater relative number of open osteon systems compared
to that in the adult (Fig. 1-9). These pores may have further
effects on the extension of a fracture line. Compact adult
bone principally fails in tension, whereas the more porous
nature of the child’s bone, particularly in the metaphysis,
allows failure in compression as well (especially in those
bones that go into greenstick failure or simple plastic
deformation).
Smith and Walmsley studied factors affecting the elasticity
of bone and found that the relation between the modulus of
elasticity during tension and during bending was highly
dependent on the vascular pattern in the bone, and that an
27
E
shortened owing to the plastic state of the biomechanically naive
bone. (D) The fixator was reattached, and most of the deformity
was corrected. (E) Final result after removal of the fixator and pro-
gressive weight-bearing.
adequate, functioning vascular supply was necessary to effect
a normal stress-pattern response.200 The usual equations
expressing the reactions of materials to tensile and bending
stresses are founded on the assumption that the experimen-
tal material is homogeneous. However, an obvious tissue dis-
continuity exists in the multiple, small, vascular canals in the
cortical, mature lamellar bone in the fenestrated cortical
bone of the metaphysis. The vascular pattern of bone varies
considerably, not only among species but among age groups
and throughout regions of a single bone. It is evident that
when a vascular gradient exists the value of Young’s modulus
of elasticity must vary progressively from the periosteal to the
endosteal aspect of bone and from the diaphysis to the
metaphysis. In some bone the vascular pattern is such that it
causes partial lamination of the tissues, as solid bone alter-
nates with relatively porous layers. This is more characteris-
tic of developing bone, particularly in the metaphysis. The
orientation of the irregular intertrabecular spaces shows a
distinct preferential orientation in which the intervening
bone is in the form of thin sheets that lie parallel to the bone
surface and have infrequent radial interconnections. Subse-
quently, primary osteons form within this vascular labyrinth.
The longitudinal vascular canals of these osteons lie within
the sites occupied by the original vascular spaces and are con-
sequently seen, in transverse section, to lie in rows parallel
to the bone surface. Areas of solid bone intervene between
adjacent vascular rows. In other regions, however, the vascu-
lar canals of the primary osteons undergo local enlargement
to form erosion cavities, and these cavities are subsequently
occupied by secondary osteons. Because this erosion phase
of the reconstruction and remodeling process usually pro-
ceeds eccentrically from the primary osteons, the canals of
the secondary osteons are not always aligned with the origi-
nal vascular planes. Consequently, as the remodeling process
becomes more extensive, the subdivision of the bone into
vascular/nonvascular laminae becomes progressively less dis-
28
tinct until, in many skeletally mature bones, it is no longer
discernible. This alternation of strong and weak layers par-
ticularly characterizes bone at the junction of the metaph-
ysis and diaphysis and probably renders this area more
susceptible to injury.
Cortical bone is stronger in compression than tension.
The shear strength for torsional loading about the longitu-
dinal axis is less than the tensile strength. Because secondary
haversian bone is an anisotropic material that is transversely
isotropic, it is stronger and stiffer in the longitudinal direc-
tion than it is in the transverse direction.30 Furthermore,
bone has poor fatigue resistance.
Classically, bone was considered a brittle material when
loaded in tension; but over the past few years it has become
evident that bone initially exhibits a type of ductile behavior.
That is, elongation of bone tissue under tensile or elongat-
ing loads may continue beyond 1% elongation, depending
on the age of the individual and the area of the bone.33,34
This may result in elongation of 2–7% of the overall length
of the bone. However, after elongation reaches about 3–4%,
continued elongation at the 2–7% level results in perma-
nent, plastic elongation (Fig. 1-39). Plastic deformation is
essentially irreversible. If a plastically deformed bone is sub-
sequently cyclically loaded, the total deformation increases
to a point at which the next load applied results in failure.
The clinical importance of this behavior of bone tissue is that
bone as a structure can sustain permanent damage, even
though no gross fracture or decrease in load-carrying capac-
ity is noted. Furthermore, such damaged bone tissue is
capable of sustaining a load virtually identical to that of the
previous cycle. When it has been loaded a sufficient number
of times at that level or slightly above that level, a fracture
may result. The only detectable damage during plastic defor-
mation appears to be the production of microvoids within
the osseous tissue.
Tensile behavior of bone tissue varies within an individual
from bone to bone and with age. The most dramatic change
is a decrease in the amount of total strain that bone tissue
FIGURE 1-39. Relation of osseous deformation (bowing) and force
(longitudinal compression). In the zone of elastic deformation, bone
deforms but springs back to its original contour (loop). Eventually,
the bone is overloaded (C) and develops acute permanent defor-
mation (bowing). If force increases beyond this point, fracture
results. In the child, remodeling brings a plastically deformed
bone back into the normal response zone of elastic deformation.
(Modified from Chamay,33 with permission.)
1. Anatomy and Physiology of Skeletal Development
can undergo. This amount decreases from almost 4% strain
capacity to slightly more than 2%; and the decrease occurs
gradually throughout adult life. It is possible that children
have a capacity for total strain even more than 4%, although
it has not been measured because of the minimum number
of specimens available.
Another significant change in the mechanical properties
of femoral bone tissue during deformation is the increase in
slope at the second region of loading, or the region of
fatigue. This increase probably reflects an increase in the
stiffness of bone collagen, again a factor that gradually
increases with age.9,30,93,197 Different bones exhibit different
capacities for plastic deformation and strength, even in
the same individual. For instance, between the third and
eighth decades of life femoral bone progressively exhibits
less plastic deformation and is somewhat weaker than tibial
bone.
Bending stress in developing tubular bone often causes
different patterns of incomplete fracture through only a
portion of the cortical circumference (Figs. 1-40 to 1-43).
The remaining cortex is grossly intact but in actuality prob-
ably has microfractures. This intact cortex is invariably plas-
tically deformed, whereas the fractured area has gone
through the phase of plastic deformation to complete
failure. Because plastic failure, by definition, means perma-
nent deformation, this has an effect on reducibility and
ability to maintain longitudinal alignment. Such greenstick
fractures usually must be completed, which is relatively easy
to do because the bone has already undergone a certain
degree of failure. Clinically, some bones undergo only plastic
deformation, causing increased bowing.130 This most likely
occurs in the radius, ulna, and fibula; although even the
femur may exhibit such bowing during early life.
In experimental work with puppies, bone subjected to
bending stress showed increased stiffness as the animal
aged.13 This finding reflects not only the increasing amount
of material in the cross section of the bone but also the
increasing strength of the bone tissue as well. The amount
of plastic deformation a bone can undergo decreases with
increasing age. Bone with thin cortices plastically deform to
a greater extent than bone with thick cortices, which invari-
ably has a better developed osteon structure.
Bending is not the only load situation that may cause per-
manent damage to bones without causing concomitant frac-
ture. Axial or compressive loads may cause permanent injury
even though no fracture is noticeable, even by roentgenog-
raphy. Because the predominant mode of loading of a long
bone is axial compression, it is not surprising that overload
conditions exist in which the compressive yield strength of
bone tissue is exceeded; and upon further increasing the
load, the tissue plastically deforms. Plastic deformation of
cortical bone under a compressive load is really a microfrac-
ture mechanism. These microfractures, owing to the large
shear stresses in oblique planes, may or may not coalesce into
larger shear cracks or buckling as is characteristic of the
torus fracture of the distal radius. Occurrence of compres-
sion overload does not appreciably reduce the load strength
of a bone during axial loading, but it may weaken the bone’s
response to a subsequent bending load. This may help
explain the phenomenon of refracture, which sometimes
complicates distal radial fractures.
Biomechanics 29

FIGURE 1-40. Deformation capacity of the

human neonatal ulna. (A) Bending was
applied toward the clamp. (B) Characteristic
degree of deformation in most of the bones,
with bowing beginning (arrow). These bones
characteristically spring back to their original
shape, but not always instantly. (C) Most
extreme deformation capacity in one speci-
men. Note the buckling (compression defor-
mation, C), which is occurring opposite the
tensile (T) deformation.

The compressive behavior of bone tissue is different from
tensile behavior. The application of a load again results in a
linear, reversible range and then a second, nonlinear, irre-
versible range. Failure occurs by a microfracture mechanism
within the tissue, with most of the microfracture character-
istically appearing at an approximately 35° angle to the
loading direction.176 Although the bone has undergone
microfracture in the compressive mode, it may still sustain
continued load application. In fact, it is possible to con-
tinue foreshortening the bone tissue by as much as 10–12%
of its total length and still have the tissue remain grossly
intact.
Bone fatigue, at least in adult bone, is a gradual damaging
process accompanied by a progressive increase in hysteresis
and loss of bone stiffness.24–31 The total number of cycles to
fatigue failure is influenced by the total strain range of the
individual bone specimen; it is not affected by the mean
strain itself. Bone has poor fatigue resistance. Furthermore,
mechanical fatigue damage accumulates more rapidly in the
compressive areas rather than the tensile areas of bone. If

FIGURE 1-41. (A) Torus fracture (arrow), a com-

pression failure pattern that occurs in children.
(B) Histology of a fracture, showing how the
cortex is deformed in a curvilinear fashion
(arrow) with mild cortical disruption.
30
FIGURE 1-42. Greenstick fracture in a 6-year-old who sustained a
traumatic forequarter amputation. (A) Radiograph. (B) Slab section
showing muscle entrapped in the fracture gap. (C) Histologic
section. (See Chapter 16, Monteggia Injuries, for additional illus-
trations of this injury.)
bone fatigue microdamage accumulates at a slow rate, bio-
logic remodeling can repair the damage and maintain the
structural integrity of bone. However, the creation of fatigue
microcracks could initiate an osteoclastic response in a
manner analogous to the first stage of fracture healing. The
subsequent removal of bone tissue by osteoclasts in a region
of bone that continued to be loaded with high cyclic stresses
may accelerate the accumulation of fatigue damage. In situ-
ations such as Legg-Perthes’ disease, microfailure and osteo-
clastic resorption and remodeling that cannot keep pace
with the biologic stress is undoubtedly a major factor in the
subsequent development of the classic subchondral fracture
that makes these children symptomatic.
The biologic response of bone to fatigue and microdam-
age may be influenced by the type of damage introduced.
Fatigue microdamage is markedly different for bone sub-
jected to repeated tensile stresses and that exposed to
repeated compressive stresses. Tensile fatigue tends to cause
failure at osteon cement lines and results in debonding of
1. Anatomy and Physiology of Skeletal Development
osteons from the surrounding interstitial bone. Compressive
fatigue, in contrast, causes formation of diffuse shear micro-
cracks throughout the bone that are oblique to the loading
direction.
In living bone the accumulation of damage may signifi-
cantly influence remodeling and growth characteristics.25
Living bone also responds differently to cyclic loads and
static loads. Severe cyclic loading may cause fatigue (stress)
fracture or bone hypertrophy. The hypertrophic response
may be greater in immature bone than in adult bone.
Fibrous Tissues
The dense fibrous tissues have a significant role in normal
function of the skeletal system. They exist in three principal
forms: tendon, ligament, and joint capsule. Each consists of
cells and an abundant extracellular matrix formed primarily
from densely packed collagen fibrils aligned to resist tensile
loads. Tendons transmit muscle forces to bone and fre-
quently have elaborate bursae or sheaths that provide low
friction gliding and retinacula or pulleys that direct the line
of pull. Ligaments and capsules restrain excessive joint
motion or displacement of the joint surfaces. Muscle con-
traction and joint shape provide much of the joint stability
under normal circumstances, but muscle cannot contract
rapidly enough to stabilize joints against unexpected loads.
Fiyio et al. studied tendon growth with markers.63 Intra-
tendinous elongation did not occur in the central region.
All growth occurred at the proximal and distal ends. The
skeletal end generally exhibited more growth than the
muscular end.
Each of the skeletal dense fibrous tissues has an extensive
vascular system. Diffusion through the tissue also may supply
nutrients, particularly in the sheathed portions of the
tendons. Despite their inert appearance, ligaments are meta-
bolically active. Prolonged immobilization adversely affects
their vascular supply, capacity for aerobic metabolism, and
strength. Immobilization also decreases the glycosaminogly-
can and water content and increases collagen turnover.18
After 6 weeks of immobilization, the restoration of normal
structure, composition, and strength may require 6 months
or more of normal activity. Greater than normal loading may
also alter the dense fibrous tissues. Training apparently
increases the strength, size, and collagen content of tendons
and ligaments in immature animals, and it may have similar
effects in mature animals, although these observations need
further study.18
As previously alluded to, the periosteum is attached rela-
tively loosely to the diaphysis, and its external surface serves
as the attachment (origin) of muscle units (both muscle
fibers and encircling mysial sheaths). The muscle tissues
usually do not originate directly from the developing osseous
surface; and with the exception of a few areas such as the
medial distal femur, they do not develop a direct relation-
ship with mature osseous tissue, although soft tissue compo-
nents contiguous with the muscle fibers may have fairly rigid
relationships. The most obvious example is the linea aspera.
Even in a child the periosteum is densely attached along this
structure and must be elevated by sharp dissection, in con-
trast to the ease with which most of the periosteum can be
elevated.
Fibrous Tissues 31

FIGURE 1-43. (A) Longitudinal cortical laminated splitting of a splitting within the intervening cortical segment. (C) Greenstick
fibula. (B) Torus buckling combined with longitudinal splitting of an injuries of the radius and ulna. Again, note how the ulna is frac-
ulna. Note the two levels of fracture and the additional longitudinal tured at two cortical levels (arrows).

In the metaphyseal region, the periosteum is more densely
attached to the underlying bone and blends continuously
into the epiphyseal perichondrium and physeal zone of
Ranvier. The latter regions are densely contiguous with the
underlying physeal and epiphyseal cartilage. Ligaments and
tendons insert, for the most part, into these fibrous and
fibrocartilaginous regions, and not directly into the osseous
tissue of the metaphysis or secondary ossification center (Fig.
1-44).131 Such attachment mechanisms not only allow active,
integrated growth of muscular and chondro-osseous struc-

FIGURE 1-44. Insertion of the patellar tendon (PT)

into the chondro-osseous epiphysis of the tibial
tuberosity. (A) Section from an 11-year-old with
early ossification center formation in the distal end
of the tuberosity. (B) More mature ossification in a
13-year-old. Note the blending of tendon fibers
into the hyaline cartilage and the continuity of the
tendon with the perichondrium–periosteum
complex (small arrows). As the epiphyseal ossifi-
cation center matures further, the tendon fibers
blend into fibrocartilage (FC), which then blends
into the ossification center. This is the initial step
in the formation of Sharpey’s fibers of an adult.
Ligament insertion into a chondrous or chondro-
osseous epiphysis is similiar to tendon insertion.
(C) Section from a 14-year-old showing extension
of the tendon toward the periosteum (solid arrows)
and tendon interfacing with developing bone
(open arrow) of the ossification center. Disruption
of this process may cause the Osgood-Schlatter
lesion (see Chapter 23).
32
tures, they permit a tensile-responsive unit, such as a liga-
ment or tendon, to insert into a similarly tensile-responsive
component of the developing skeleton, rather than directly
into bone, which is characteristically more susceptible to
failure during tension.63,69 Such an arrangement allows
progressive, rather than abrupt, gradations of moduli of
elasticity.
Only with progressive skeletal maturation, especially in the
epiphyses, do the characteristic Sharpey’s fibers develop.11
These are collagen continuities between tendon or ligament
and cortical bone. These differing and developing interre-
lationships between soft tissue and chondro-osseous compo-
nents are major factors in the tendency toward soft
tissue–bone interface avulsion in the adult and intraosseous
failure in a child (Fig. 1-45).231,232 For example, a child avulses
the tibial spine, whereas an adult avulses the cruciate liga-
ment, at the insertion or within the ligament proper. If skele-
tal chondro-osseous transformation progresses more rapidly
than the normal adaptive response patterns, failure may
result, as with the Osgood-Schlatter lesion (see Chapters
6, 23).
Injury of dense fibrous tissue initiates a complex sequence
of inflammation, repair, and remodeling that can, under
certain conditions, restore the essential properties of the
tissue. The repair tissue never exactly duplicates the struc-
ture and composition of uninjured tissue, however. Although
a variety of factors modify the repair process, loading and
functional demands placed on the repair tissue seem partic-
ularly important. Excessive demands may rupture or deform
reparative tissue, whereas carefully controlled motion and
loading applied at the appropriate time during the repair
sequence may decrease formation of dense adhesions,
increase the rate of repair, and improve the quality of the
reparative tissue.
FIGURE 1-45. (A) Insertion of the collateral ligaments into the peri-
chondrium (small arrow), while the pes anserinus extends distally
(large arrow). (B) When failure occurs the ligament usually sepa-
rates with an attached osseous fragment (arrow). Healing in this
situation is bone to bone, rather than fibrous ligament healing.
1. Anatomy and Physiology of Skeletal Development
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Injury to the Immature Skeleton
Engraving of a type 2 distal femoral growth mechanism injury.
(From Poland J. Traumatic Separation of the Epiphysis. London:
Smith Elder, 1898)
ractures and dislocations involving the developing
F skeleton may differ significantly from those of the
mature, adult skeleton.50 The first text dedicated to
these biologic differences was the classic work of Poland.25
This treatise attempted to collate historical vignettes with an
array of clinical and morphologic material and experience
throughout Europe. The principal emphasis was on epiphy-
seal injuries. Over the ensuing century and particularly
during the past 20 years there has been an increasing
amount of literature dedicated to a better understanding of
the acute and chronic effects of trauma to the immature
skeleton. Particularly, a number of textbooks have addressed
fractures and dislocations involving the growing chondro-
osseous skeleton.1–24,26–36 The increasing volume of literature
specifically addressing the immature skeleton is evident in
the reference sections of each ensuing chapter.
The pattern of injuries children may sustain via a certain
injury mechanism usually differs from that of adults and
so often requires different diagnostic and treatment algo-
rithms.320 These differences additionally vary during the pro-
gressive stages of chondro-osseous maturation and growth
until skeletal maturation is reached. Any primary physi-
38
cian (pediatrician, family practitioner), radiologist, or orth-
opaedist who is assessing, diagnosing, or treating skeletal
injuries in neonates, infants, children, or adolescents should
be familiar with the probable mechanism of injury, the cause,
the acute response, the appropriate treatment, and the long-
term biologic response of any injured skeletal component
(particularly when a growth mechanism is involved). The
appropriate, often age-related guidelines for the treatment of
the specific injury must be carefully considered.
Because these patients have their pliable formative and
productive years ahead of them, they should be treated with
skills based on both individual experience and a detailed
knowledge of the intrinsic capacities of repair and remodel-
ing of the growing skelton. When a treating physician relies
only on those principles of treatment applicable to injuries
of the mature (i.e., adult) skeleton, errors in judgment and
technique may progressively or eventually manifest in a per-
manent defect or deficit to the involved skeletal region and
an alteration or deprivation of normal function in the
involved limb. Any physician involved in the diagnosis or
treatment must be aware of obscure diagnoses such as a
toddler’s stress fracture or potential complicating factors
such as a compartment syndrome.135,245,261,318
Childhood injuries are a continual problem for treating
physicians and the entire social community. Accidents are
the leading cause of death and permanent disability among
children older than 1 year of age.* Trauma ranks second
only to acute infections for causing morbidity in the pedi-
atric age group and, more significantly, accounts for approx-
imately one-half of all deaths in children. About 15,000
children under 15 years of age die annually from accidental
injury in the United States alone. Accidental death during
childhood is usually due to shock, respiratory depression or
obstruction, or brain or brain stem drainage. The leading
causes of death include motor vehicle accidents, drownings,
burns, and exposure to toxic chemicals (poisons).
Another 19 million (3 in every 10 children) are injured
severely enough to seek hospital care. It has been estimated
* Refs. 15,22,33,40,45,52,64,66,68,69,73,76,78,84,87,92,97,98,109,116,
118,119,121,122,140,144,145,151,152,155,156,164,167,168,169,172,176,
177,181,184,191,193,197,201,202,207,209,212,216,221–226,247,269,
271,272,276,281,294,314,324,328,334,354,382,383,386,399,406.
2. Injury to the Immature Skeleton
that 47% of all patients receiving care in this nation’s emer-
gency rooms are under 14 years of age. One of four of these
children are treated because of violence or accidents. More
than 100,000 children are permanently crippled annually,
and another 2 million are temporarily incapacitated for 2
weeks or longer by accidents.66,216,217
Approximately 25% of all injury victims are in the
pediatric age group, and one in four injured children
may “require” a pediatric trauma center. A committed rela-
tionship between adult trauma surgeons and pediatric
internists is favorable for outcome if a pediatric surgeon is
unavailable.
More than 100,000 children are permanently crippled each
year as a result of accidents.110 Long-term morbidity is
directly related to the severity of any head and muscu-
loskeletal injuries.175,195 Fortunately, most injuries involving
children are minor. The common skeletal injuries are caused
most often by short distance falls resulting in a single extrem-
ity injury [usually the upper extremity (distal radius or distal
humerus) or the hand].
Cheng and Shen showed that approximately 13% of the
children being evaluated in the emergency department of
an urban teaching hospital had serious injuries.113 Gallagher
and colleagues152 showed a bimodal age distribution of trau-
matic injuries in children, the first during the first year of
life and the second being an increase through the adoles-
cent years. They showed a steady increase in the number of
age-associated injuries with respect to both total number
and severity.113
Although the exact incidence and rate of severe traumatic
injuries are not truly known, it has been shown in multiple
studies that the incidence increases as the child begins to
interact with the adult world, especially with motor vehi-
cles.162,167 Most injuries occur where young children spend
the most time, usually in or about the home, at school, or in
play areas.165 More than 40% of childhood accidents occur
in or around the home. For preschool children this rate may
be as high as 70%. Playgrounds are the site of more than 1
million injuries.290,359
Automatic garage door opening/closing devices may
cause serious injury to children.213,332 Such injuries can be
avoided by placing sensors that automatically stop closure
when motion or contact occurs.
Rivara et al. studied the risks of injury to children less than
5 years of age in day-care versus home-care settings.304 They
found that there was no change in the rate of injuries per
100,000 child-hours of exposure.
Wesson and Hu assessed 250 consecutive children hos-
pitalized with severe injuries.383 Altogether 217 survived,
although 190 of them (88%) had one or more functional
musculoskeletal limitations. A substantial portion of the
whole group had ongoing physical disabilities that limited
their participation in normal childhood or adolescent activ-
ities within the 6 months following their discharge, suggest-
ing a need for greater emphasis on the rehabilitation of
pediatric trauma patients and, specifically, greater attention
to the treatment of any extremity injury while the child
was hospitalized. Colombani et al. reviewed 267 children
with life-threatening multitrauma injuries and claimed that
full recovery from the life-threatening specific injury or
injuries was usual.121 Unfortunately, they neither defined
39
“life-threatening” nor described the injuries by any objective
injury-scoring system.
Backx et al. reviewed 233 patients with major trauma
admitted to a pediatric trauma center.65 The male/female
ratio was 1.7 : 1.0. The highest incidence of trauma occurred
during the spring months and was lowest during winter. Most
children (almost 80%) were injured between noon and mid-
night. Among them, 36% had musculoskeletal injuries. The
mean length of time spent for resuscitation and stabilization
in the trauma room was 49 minutes. The mean intensive care
unit (ICU) stay was 3.2 days, and the total length of hospi-
talization averaged 11.2 days.
Peclet et al. surveyed hospital admissions in an urban
children’s hospital (Children’s National Medical Center).281
Over a 3-year period 12.9% of the hospital admissions
were trauma-related. The average age was 5.5 years, and 64%
were boys. The mortality rate was 2.2%. In a Hong Kong
study of a population catchbasin of 1 million predominantly
ethnic Chinese, 35% of the children and adolescents seek-
ing care in the emergency room had trauma-related pre-
sentations, and 20% of the hospital admissions were
trauma-related.113
Annually 50,000 children are injured as pedestrians
in motor vehicle accidents.136 Motor vehicle-related trauma
remains the leading cause of death in children older than 1
year.296,300,397 Approximately 1800 die, 18,000 are admitted to
a hospital, and 5000 have significant long-term sequelae. The
physical, psychological, and economic burdens of traumatic
injury and death are enormous, not only for the young
victims but for their families and society as well.
The most common cause of multiple injury to children is a
motor vehicle accident, with the child an automobile occu-
pant or a pedestrian/cyclist. This statistic is well documented
in reports of multiply injured children.188 Among 376 multiply
injured children, motor vehicle-related accidents accounted
for 58% of the overall injuries and 76% of the severely injured
children.110 In one series there was a 91% incidence of motor
vehicle-related mechanism of injury.233 The incidence of
motor vehicle-related injuries increases with age. According
to the Injury Fact Book, deaths from motor vehicle accidents
are lowest from birth to 14 years (5.9/10,000 to 10/100,000
population), with the peak occurring in the 15- to 24-year age
group (26/100,000 to 45/100,000).66 Boys in this age group
have twice the mortality rate of girls.
Virtually all states have pediatric seat-belt restraint require-
ments for passenger vehicles to help prevent these deaths
and injuries.161,187,340,341,353,374,375 The introduction of com-
pulsory automobile safety seats or restraints for children
in Michigan led to a 25% reduction in the number of chil-
dren injured in automobile accidents. 376 These laws are
useful only if the restraint systems are used appropri-
ately.100,102,128,187,325,340,362,368,389,390 Modifications must be made
for children in body casts or in special-needs devices.101,141
Similarly, car seats for infants and toddlers are effective only
if they are properly used.196
In contrast, only a few states and other countries have
safety laws or restrictions for passengers of any age who
ride in the back of trucks. Woodward and Bolte reviewed
a 3- to 4-year period during which 40 patients sustained
injuries as a direct result of being a passenger in a cargo area
(bed) of a truck.398 The mean age of the patients was
40
7.75 years. Head trauma was the significant injury in most of
these patients. They concluded that until legislation is passed
and enforcement is effective children riding in the back of a
truck should (1) be restrained, (2) not stand while the truck
is in motion, (3) not sit on movable objects within the bed of
the truck, and (4) avoid movable cargo that could shift with
bumps and turns. With the increasing recognition of the
dangers of three-wheel all-terrain vehicles, legislation may,
and undoubtedly is, necessary to curtail this health hazard.
Skeletal trauma accounts for at least 10 to 15 percent of
these childhood injuries.* If all musculoskeletal tissues are
considered, they would constitute at least 40% of all child-
hood injuries. Such injuries include strains, sprains, tendon
disruption, muscle tears, and joint pain from injuries such
as bone bruising. The latter might be considered skeletal
injury without obvious radiologic abnormality (SKIWORA),
analogous to the phenomenon of spinal cord injury without
obvious radiologic abnormally (SCIWORA), discussed in
Chapter 18. Many of these radiographically “occult” injuries
may be diagnosed effectively with mag-netic resonance
imaging (MRI) (see Chapters 5, 6, 7). The occurrence of
such occult injury raises serious questions about selection cri-
teria for obtaining radiographs.197 What is applicable in the
adult may not be as efficacious in the child.
Mann and Rajmaira reviewed 2460 long-bone fractures in
children.241 Physeal injuries accounted for 30%. Girls with
physeal fractures were 1.5 years younger than boys with the
same type of fracture in the same location. Nonphyseal frac-
tures occurred twice as often in the upper extremity as in the
lower extremity.
Cheng and Shen reviewed the fracture patterns of 3350
children with 3413 limb fractures (spinal fractures were
excluded).113 The boy/girl ratio was 2.7 : 1.0 for all injuries. In
the adolescent group the boy/girl ratio rose to 5.5 : 1.0. Distal
radial fracture was the most common (19.8%), followed by
humeral supracondylar (16.6%) and forearm diaphyseal
(13.4%) fractures. When broken down by age, supracondylar
humeral fracture was most common in those 0–3 years old and
those 4–7 years old, accounting, respectively, for 28.9% and
31.2% of all limb fractures. Distal radial fractures occurred in
27.1% of the 8- to 11-year group and 23.3% of the 12- to 16-
year group. Open fractures were uncommon (2.2%). Green-
stick fractures were found in 5.3%. Seasonal variation
occurred, with more fractures during the summer and
autumn months. The open reduction rate was 10.1% in those
0–3 years old and rose to 34.0% in those 12–16 years old.
Young patients with multisystem injuries that may be or are
life-threatening (see Chapter 3) may experience failure to
diagnose less obvious fractures and dislocations, especially
during the acute resuscitative processes. Chan et al. reported
a 12% failure rate to diagnose even “significant” muscu-
loskeletal injuries in 327 patients.110 Even when an appro-
priate musculoskeletal injury diagnosis was made, the
tendency was to assign the injury a low priority, a factor that
could eventually lead to skeletal deformity and dysfunction.
Adequate fracture diagnosis and care must be an integral
part of the emergency and subsequent care of any multiply
injured child.23,287
* Refs. 75,83,90,104,133,139,173,178,182,225,232,242,243,246,262,
288,290,326,337,352,358,365,371–373,387,392,395,404.
2. Injury to the Immature Skeleton
Brainard et al. found the triad of head, pelvis, and knee
injuries traditionally associated with pediatric pedestrian
motor vehicle accident victims did not occur.96 They did,
however, find an association of femoral and pelvic fractures
and an ipsilateral dyad of an upper and lower extremity frac-
ture on the same side.
Oudjhane et al. reviewed 500 consecutively radiographed
acutely limping toddlers.278 Twenty percent (m = 100) had a
fracture as the underlying etiology; the fibula (m = 56) and
femur (m = 30) were most common, although pelvis and foot
fractures also occurred. There were 11 patients with
metatarsal fractures.
Early reviews developed primal concepts of approaches to
fracture treatment in children. Walking, in 1934, reviewed
patterns of healing and was one of the first to address con-
cepts of longitudinal overgrowth and remodeling of angular
deformities.377 Beekman and Sullivan, in 1941, reviewed 2094
long-bone fractures seen over 10 years (1930–1940) and pre-
sented many still usable basic principles for treating chil-
dren’s fractures.75 Wong explored cultural studies of fracture
incidence after comparing Indian (Asian), Malay, and
Swedish children.396
Rosenthal pointed out that many simple fractures can
be adequately managed, treated, and even reduced under
appropriate conditions in an office setting rather than
requiring the patient to go to an emergency room.318 Fur-
thermore, initial emergency treatment may be rendered in
the office for some injuries that require definitive manage-
ment in the hospital.49,179
Particularly, pediatricians tend to see patients with
greenstick and torus fractures because of the often innoc-
uous nature of the injury. They may also be involved
with patients who have undetected trauma due to abuse.
Treatment of these injuries must be based on knowledge of
not only the pathophysiology of the injury but also the ram-
ifications for complications, additional soft tissue injury,
and so on that might affect treatment. Obviously, treatment
of these injuries by the pediatrician or family practitioner
should be contingent on a feeling of “ease” during applica-
tion of a cast or splint. By assuming care of these patients,
rather than referring them to an orthopaedist, the primary
care physician thus assumes the same standard of care that
would be rendered by the orthopaedic specialist. Suboptimal
treatment (e.g., inappropriate reduction) or failure to rec-
ognize a complication (e.g., compartment syndrome)
exposes the primary care physician to liability at the same
level as the orthopaedist. The standard of care for fractures
and dislocations of the immature skeleton are the same
no matter whether the treatment is rendered by an
orthopaedist, family practitioner, or pediatrician. This same
liability holds for the interpretation of imaging studies. If
one assumes responsibility for reading radiographs, com-
puter tomography (CT) scans, or MRI, that individual is
liable for his or her action.
Prevention
Obviously an important parameter when dealing with child-
hood injury is to recognize injury patterns and, accordingly,
to devise measures to prevent injuries or at least lessen the
Basic Differences Between the Child and Adult Patient
likelihood of their happening.* The American Academy of
Pediatrics has a standing Committee on Accident and Poison
Prevention that has developed a number of position papers
and programs directed at the prevention of significant inju-
rious factors in children.54–60
Education of parents is integral to making children
aware of injurious factors in their environment.74,321 Rivara
et al. presented an interesting study showing that although
94% of parents did not believe that 5- to 6-year-old
children could reliably cross streets alone, one-third of the
parents allowed kindergarten-aged children to walk alone
to school.302 These authors thought that parental expecta-
tions for their child’s pedestrian skills were inappropriate and
might be a fruitful target for injury prevention programs.
Having appropriate leaflets and posters in the waiting
room may play an important role in this process.72 On a
national basis Sweden has enacted an array of changes affect-
ing traffic and childhood activities in an attempt to decrease
childhood injury, with a significant success in reducing the
injury rates.77,385
Rivara et al. showed that although factors in a child’s daily
living environment and socioeconomic background con-
tribute significantly to the risk of pedestrian injury little
reduction in the incidence of childhood pedestrian injuries
may be expected from any attempts to modify individual
behavior.300,305 The inability to assess distances and speeds
effectively and to localize sounds adequately, combined
with the normal impulsiveness of young children, results
in unsafe traffic or pedestrian behavior by most children
younger than 12 years, no matter what the socioeconomic
group.170,186,322,329,401 Teenagers probably are even more
unikely to respect the external milieu.
Basic Differences Between the
Child and Adult Patient
Patient History
Historical details of any injuries may be totally lacking, erro-
neous, or purposely deceptive. This is particularly true of the
battered or abused child. Frequently, no responsible adult
has witnessed the specific accident. Any child’s account of the
details of the accident often tends to be oversimplified,
halting, or incomplete. However, knowing how the injury
specifically occurred often enables the physician to anticipate
the full extent of the injury, including any important associ-
ated injuries. Appropriate treatment may be accomplished
much more satisfactorily when the physician has detailed
knowledge of the actual or probable mechanism of injury.
The variable lack of historical data on childhood injuries
usually requires that particular significance be attached to
the physical examination, which must thoroughly assess the
type of deformity, location, degree of concomitant soft tissue
swelling, and integrity of innervation and circulation. Physi-
cal examination, rather than historical data, often prevails in
the child.
* Refs. 120,143,204,205,236,237,244,254,317,342,343,348,355,369,370,
393.
41
Parental Involvement
An adequate discussion with the parents is often as impor-
tant as the treatment of their child’s injury. It is imperative
to establish not only a good doctor–child patient relation-
ship but also a satisfactory doctor–parent relationship, as the
parents are instrumental in carrying out the essentials of sub-
sequent care, especially rehabilitation. The troublesome
areas of diagnosis and treatment should and must be eluci-
dated in words the parents can comprehend. In a polyglot
society this communication often entails using a translator
capable of effectively communicating information between
physician and family regarding diagnosis, treatment, and
prognosis. However, the burden of responsibility for under-
standing the ramifications of the injury should be that of the
parent, not that of the physician, whose primary responsibility
is effectively treating the child. Whenever possible, parents
should bring a family member or friend who can adequately
translate.
The treating physician should be certain that the
parent(s) adequately understands the various aspects of the
injury, treatment, and prognosis. The parents should be
counseled regarding the parameters of acute care and about
any potential chronic or long-term problems. The doctor
should discuss the possibilities of limping, temporary loss of
full range of motion, nerve injury, loss of reduction after
initial treatment, and the need for remanipulation; adequate
follow-up care should be emphasized, in many cases until
skeletal maturity is attained to assess growth and remodel-
ing. Proper follow-up care is undoubtedly the most difficult
compliance factor, especially after the child appears out-
wardly normal several months after injury. Nonetheless, it is
the most significant element when anticipating and diag-
nosing subsequent problems of premature growth disrup-
tion or arrest during the early stages. During a growth spurt,
seemingly minor problems may rapidly assume major impor-
tance, especially when dealing with growth mechanism
injuries.
Childhood injury may lead to serious work and financial
problems for families.277,384 Long acute hospital stay and four
or more impairments are good predictors of potential family
difficulties. Some school systems are reluctant to accept
injured children back in school until they are free of casts.189
Such a problem also affects family dynamics.
Susceptible Child
Certain children seem to be accident-prone.62,79–81,91,117,
198,250,252,253,274,284
Wesson and Hu compared 92 injured chil-
dren to a control group with appendicitis.383 About 54% of
the minor-injury group and 71% of the major-injury group
had persistent physical limitations 12 months after injury
(none in the controls). Of the minor-injury patients, 38%
had preexisting behavioral disturbances, as did 14% of the
major-injury patients and 10% of the controls. The authors
noted a significant increase of maternal malice in the injury
groups compared to the controls. The family background
may be an important factor in accident-proneness.95,99,199
Loder et al. studied 52 children (2–16 years of age)
with extremity fractures.233 The family functioning was
usually normal; but there was a statistically significant
42
increase in the number of children with conduct problems,
psychosomatic complaints, and impulsive/hyperactive
behavior. There was a significant increase in children with
social competence problems as well, such as externalizing
behavioral problems.
The association of accident-proneness and hyperactivity is
being increasingly recognized as a major factor in accident
recidivism.127,240 Another risk factor may be left-handed-
ness.166,231,259 A patient sustaining an ankle injury or fracture
appears to be at greater risk for repeat injury. Karlsson et al.
found that the study group with former ankle fractures con-
tinued to have a twofold increased incidence of all types of
fracture.200
Bijur and colleagues showed that children with three
or more separate injury events reported between birth and
5 years of age were six times more likely to have three or
more injuries reported between 5 and 10 years of age
than children without early injuries.79 Children with one or
more injuries resulting in hospitalization before 5 years of
age were 2.5 times as likely to have one or more admissions
to a hospital for injuries after 5 years of age. Other predic-
tors of injuries between 5 and 10 years of age were male sex,
aggressive child behavior, young maternal age, and many
older and few younger siblings. Some authors have ques-
tioned whether the identification of accident-repetition qual-
ities or individuals has any effect whatsoever in preventing
further injury.131
Special Features
Multiple factors make fractures of the immature skeleton dif-
ferent from those of the mature skeleton. Fractures are more
likely to occur after seemingly minimal trauma. The perios-
teum is thicker, stronger, more resistive to displacement, and
more biologically active. Any specific diagnosis presents par-
ticular problems because of the variable radiolucency of the
incompletely ossified epiphyses. There is a distinct percep-
tion that if standard radiographic techniques do not demon-
strate musculoskeletal fracture the bone cannot possibly be
injured. However, as is shown in Chapter 5, radiographically
invisible or occult bone bruising and injury certainly may
occur, as can separations at the chondro-osseous interface of
the secondary ossification center and the epiphyseal carti-
lage. Some residual angular deformities may correct spon-
taneously, although not all do. Complications to the bone,
cartilage, and soft tissues tend to be fewer and different.
Methods of treatment receive different emphases, with
closed reduction often receiving the most emphasis. Joint
injuries, dislocations, or ligamentous disruptions are much
less common.
Injuries may involve specific growth regions, such as the
physis or epiphyseal ossification center, and may lead to
significant acute or chronic disturbances of growth. The
normal processes of bone remodeling in both the diaphysis
and the metaphysis of a growing child may progressively
realign many initially malunited fragments, making ab-
solutely accurate anatomic reductions less important in a
child than in an adult, although anatomic reduction should
be attempted whenever possible. The treating physician should
not unequivocally rely on “spontaneous” correction of an angular
rotational or bone length deformity.
2. Injury to the Immature Skeleton
Fractures variably stimulate longitudinal growth by differ-
entially affecting the blood supply to the metaphysis, physis,
and epiphysis and by disrupting the periosteum and its teth-
ering (restraint) mechanism on rates of longitudinal growth
of the physis.82 Therefore some mild degree of longitudinal
overriding with bayonet (side-to-side) apposition (approxi-
mately 1 cm) may be acceptable in certain age groups and
may even be desirable, particularly with fractures of the
femur or tibia. However, if such longitudinally aligned
(nonangulated) overriding is accepted, rotational alignment
should be anatomically corrected.
A group of 126 children with fractures of the femoral and
tibial diaphyses had a temporary growth acceleration that
reached a maximum at 3 months and returned to normal by
40 months in the tibia and by 50–60 months in the femur.
The maximum acceleration occurred with overlap (overrid-
ing) of the fragments, in contrast to end-to-end reduction.
The average increase in the femur was 0.7–0.8 cm and in the
tibia 0.3–0.4 cm. A fractured femur often was accompanied
by accelerated growth in the ipsilateral tibia. In contrast,
however, tibial fractures were not usually accompanied by
ipsilateral femoral overgrowth. Regardless of the child’s age
or the type of injury, it is unlikely that the final correction of
discrepancy in length will exceed 0.5–1.0 cm.293
Effect of Age
Bone healing is much more rapid during childhood because
of the thickened, extremely osteogenic periosteum and
the abundant blood supply to most osseous regions. The
younger the child, the more rapid are the usual callus
response and subsequent union. The dependence of healing
capacity on age is significant. At birth fracture healing is
remarkably rapid, but it becomes progressively less rapid
during childhood and adolescence. Healing of a femoral
shaft fracture in a newborn may take only 3 weeks, whereas
20 weeks is not an uncommon length of time in a teenager.
The rate of healing in the bone is directly related to the
osteogenic activity and reactive ability of the periosteum and
endosteum and to the relative maturity of the cortical bone
(i.e., a thick diaphysis versus a thin metaphysis).
After acute trauma it is appropriate to follow any child
until skeletal maturity to derive meaningful conclusions,
especially any ramifications for alterations of normal
growth. This principle applies to any study of the long-term
consequences of fractures in children. The common
tendency to cease follow-up care 6–12 months (if that long)
after the injury may result in subsequent presentation of
significant growth deformity and irate parents. Unfortu-
nately, such continued assessment is not the usual situation
in most practice situations. Parents also tend to discontinue
follow-up when the child appears to have recovered. The
physician should encourage long-term follow-up but must
also realize that it is not always practical or possible. Always
document any parental counseling regarding such potential
problems.
The age groups from infancy to adolescence have varying
injury patterns. Children also have certain reactions to
injury, such as a pseudoparalysis of the limb of a newborn in
response to a fracture of the shoulder girdle or proximal
femur. Knowledge of these aspects, when considered com-
Basic Differences Between the Child and Adult Patient
mensurate with the particular mechanism of trauma, is often
helpful for establishing the diagnosis and rendering the
most effective treatment and prognosis to the parents.
During periods of rapid growth children may twist or strain
an arm or leg, an “injury” that hardly seems to merit con-
sideration by the parent or the physician. However, this twist-
ing may cause chondro-osseous micro or macro failure,
particularly of the tibia, which is susceptible to occult frac-
ture in children 1–5 years of age (the “toddler’s fracture”).
Such injuries are not usually discerned on routine planar
radiographs.
The annual incidence of injuries is lowest during the first
year of life.301 The highest rates are during the next year (1–2
years), and in the age range 13–18 years. The boy/girl ratio
is most equal at 1 year (1.05 : 1.00), changing to 1.9 : 1.0 in
teenagers. The teenage boy has the highest susceptibility
to injury.206,231
Iqbal showed that upper limb fractures in children
were seven times more common than lower limb fractures,
and that the incidence of fractures was much higher
during the preschool period.192 The only fractures show-
ing a major variation from this pattern were forearm
fractures, which demonstrated a progressive increase with
increasing age, attaining maximal frequency during the pre-
pubescent period. In contrast, clavicular fractures were most
common during infancy and the preschool period but
became less frequent during the school years. Other studies
have shown that upper extremity fractures are three times
as common as lower extremity fractures in chil-
dren.192,216,217,290,384,387,399
The site, frequency, and nature of traumatic bone lesions
are all conditioned by the skeletal maturation of the
patient.123,169,218,289,293 The fetal bones, which are effectively
protected from external trauma by both the amniotic
fluid and thick uterine wall, are rarely traumatized (see
Chapter 11). However, chronic intrauterine stresses
operating on a fetus may cause changes in the shape of fetal
bones and joints, causing postural disorders such as prena-
tal bowing of the long bones, club feet, and developmen-
tal hip dysplasia. Localized deformations affecting the
mandible, facial bones, and skull bones may occur. During
birth, especially with breech deliveries, a wide variety of trau-
matic lesions may occur, including fractures of the shafts and
epiphyseal cartilages (e.g., distal humerus and proximal
femur). Common obstetric fractures involve the skull and
clavicles.34
Fractures are relatively rare during the first postnatal
year. However, multiple, especially severe fractures may be
the first indication of metabolic disorders or skeletal dyspla-
sia (e.g., hypophosphatemic rickets or osteogenesis imper-
fecta) and must be considered in the differential diagnosis of
any case of suspected child abuse. Most willful assaults (the
battered child) occur during the first 1–2 years of life. From
the age of 2 years on, particularly from the time the child
starts to walk, the most commonly fractured bones are the
clavicle and radius. The high incidence of radial fracture
continues into adolescence, although the pattern changes
from fractures of the shaft and distal metaphysis to fractures
of the distal physis. Fractures of the phalanges and
metacarpals are also common during the first 2 years while
the child is learning to walk.290 Such hand (metacarpal and
43
phalangeal) fractures remain frequent throughout child-
hood, although they are underemphasized in most studies
of fracture incidence.
It is important to realize that skeletal age and chronologic
age are not always synchronous. One need only observe the
range in sizes of children in a given school grade to realize
that rates of growth and maturation differ not only between
boys and girls but also among children of the same biologic
gender. Unfortunately, physical demands, especially sports
participation, are generally based only on chronologic age.
Thus a child born in December of a given year may be com-
pared with a child born in January of the same year. Thus
almost a year of maturational difference and, more impor-
tantly, size difference (height, body mass, or both) may be
present. Given the physical demands of any organized sport,
this may have a dramatic effect on musculoskeletal injury
susceptibility. Grouping based on chronologic age may put
certain children at serious risk for injury from “similar-aged”
but obviously physically larger peers.51 Efforts are being
made to quantify muscular development and strength.257,258
Such studies may lead to more effective structuring of child-
hood sports.
Particular consideration should be given to the adolescent
approaching skeletal maturity. Healing of fractures may be
more prolonged than in the younger child. Peer and adult
(parent, coach) pressure may encourage or “demand”
return to athletic activity before the individual is physically
or physiologically recovered. Remodeling of an injured bone
in an adolescent is less likely to correct malunion.263 Inter-
nal fixation of long-bone fractures in the polytraumatized
adolescent, particularly one with a femoral shaft fracture,
may decrease morbidity in such a patient. Ligament injuries
and joint dislocation become more common with the attain-
ment of skeletal maturity. In one study 40% of the injuries
during the 12th and 13th years occurred during sporting or
similar physical activites.107 The most common injuries were
sprains or strains followed by fractures or lacerations. Most
injuries were minor.
One of the most significant epidemiologic studies of chil-
dren’s injuries and fractures has been that of Langley and
associates.107,221–224,234 They studied a group of 1000 children
aged 1–15 years. They found, for each 2-year period, that
approximately 20% of the children were injured. Most
injuries were of soft tissues. Fractures slowly increased in fre-
quency from 16% of injuries in the 6- to 7-year group to 24%
in the 14- to 15-year group.
Landin and Nilsson showed that fractures are responsible
for 10–25% of all injuries in children and adolescents.216,217
The fracture rate in the Malmö study increased in children
of both genders up to the age of 11–12 years. It then
decreased in girls but further increased in boys to age 13–14
years. The figures showed that the accumulated risk of
having at least one fracture from birth to the age of 6 years
is 42% in boys and 27% in girls.
Season
Variation of fractures occurs by age, season of year (which
varies with regional climate patterns), cultural variations,
and environmental challenges.61 Rural patterns differ from
urban patterns. For example, multilating injury from farm
44
machines is more likely in a farm environment during plant-
ing and harvesting seasons, whereas falls from heights (mul-
tistory buildings) are more likely in the urban situation
during the summer months.
The exposure time to outdoor sports activities may be
greater for children who live in warm climates. However,
many concepts have failed to discern the reality of outdoor
cold sports (skiing, skating, sledding, toboganning) and
their attendant risks of injury.
With certain sports the climate has an effect. In subtropi-
cal parts of the United States (Florida, Texas, Arizona,
Southern California) sports such as baseball are often
played year-round. This makes the likelihood of certain
injuries, such as Little League elbow, much more likely
than in areas of the country with climates with short sport
seasons.
Activity Levels
Children generally approach life with relatively unbridled
exuberance. This factor must be considered in any plan of
treatment. Once pain subsides, any child or teenager tends
to forget that an extremity has been injured and quickly
returns to the usual levels of preinjury activity. Such rever-
sion to structured activity, however, may not be conducive to
continued fracture healing and biomechanically responsive
remodeling; furthermore, it may damage immobilization
devices.
Fracture etiology reflects levels of activity during growth.
Simple falls are the predominant cause in small children.
In older children playground equipment and sports-related
accidents are more common.
Sports and Recreational Injuries
Children are constantly exposed to recreational activities.
There is increasing impetus to participate in structured ath-
letics both during and after school. As such, the potential for
contact and noncontact injury increases.37,108,129,157,214,220,235,
248,276,285,364,366,378
As participation (and accordingly injury)
increases, the number of studies that document the
general and sports-specific injury patterns grows. Krist et al.
showed an increasing incidence of sports-related injuries,
rising from 14% of all injuries in the 6- to 10-year-old cohort
to 26% of all reported injuries in the 11- to 15-year-old
group.214 No sport seemed at higher risk than any other,
although certain injury patterns prevailed in certain sports
(see Chapter 12). Depending on the complexity of the
details of the analysis, fractures have comprised between 7%
and 26% of all reported injuries in childhood/adolescent
sports activities.
Childhood is also a time of increasing emphasis on com-
petitive individual and team sports, often with a greater drive
coming from the parents or coach rather than from the
child. Organized sports, which are progressively involving
girls and younger children (e.g., soccer), particularly pre-
dispose the improperly conditioned child to injury.23,37,169,273,
319,338,364
Children frequently try to return to these athletic
programs as quickly as possible after any injury, often before
complete healing. The additional stress from a parent or
coach to return the child to the playing field often makes
2. Injury to the Immature Skeleton
continuing medical care of these children difficult. Further-
more, sports for young children rarely emphasize the need
for conditioning, sports-related training, and warm-ups.
Children are invariably perceived as injury-resistant.
Zaricznyj et al. studied 25,000 school children in sports-
related (organized) activities.405 The injury rates of total
participants were 3% (elementary school), 7% (junior high
school), and 11% (high school). Nonorganized sporting
activities may have an injury rate twice that of organized
sports. The overall percentage of fractures during sporting
events is 18–20% of all injuries.405
Children may sustain fewer injuries in organized sports
(4%) than in routine physical education classes (18%).65,94
This difference reflects the mandatory nature of physical
education classes for all students of all physical ability, in con-
trast to organized sports, which tend to attract the more phys-
ically capable and coordinated youngsters.
A more detailed discussion of the role of sports in children
injuries is presented in Chapter 12.
Hockey
Ice hockey is gaining in popularity and, accordingly, indi-
vidual participation. Over the past decade an increasing
assessment of injuries at various competitive levels has led
to the mandatory use of safety equipment. Much of this has
been directed at the use of masks and guards to prevent sig-
nificant facial injuries.264 Extremity fractures may be rela-
tively infrequent, as the feet are rarely rigidly fixed to the
playing surface.
Soccer
Hoff and Martin studied injury patterns for indoor and
outdoor soccer.185 The number of fractures and injuries was
greater for indoor soccer. This may be related to the smaller
playing field and the impact against the walls (not unlike
hockey).
Skateboarding/Rollerblading
Skateboarding has had variable popularity. Its recent resur-
gence seems coattailed to the increasing popularity of roller-
blading. Most reported injury mechanisms are in
children.53,63,67,103,105,282 Head injuries are frequent but tend
to be mild because of requisites for helmet use. Upper
limb fractures are much more frequent than lower limb
injuries.180,194,239,292 The peak incidence for injury is in the 11-
to 15-year-olds, which certainly correlates with the increas-
ing willingness to take risks. One study noted more-serious
injuries in children less than 10 years.105 Another did not find
such a difference.190
A study of in-line skating evaluated 78 fractures in 61 chil-
dren.255 Distal radial and ulnar fractures comprised more
than 75% of the injuries. Almost half the patients were
novices, with less than 4 weeks of experience.
Equestrian Sports
Horseback riding is experiencing increasing popularity and,
accordingly, more exposure to injury (especially among
Common Injury Mechanisms
girls). Compared to other childhood sports, the sustained
injuries tend to be more severe, with head and facial injuries
being frequent.71,84,85,88,160,268 Upper extremity fractures are
frequent, due to falls and the impact against barriers and
jumps. In one series there were 152 injuries in 136 patients.71
Ten patients sustained spinal fractures. Five other children
sustained pelvic fractures, which occurred when the horse
fell on the rider.71
Head injuries caused 57% of the deaths.85 The upper
extremity was most commonly injured. Girls were injured
more often than boys. A previous horse-related injury had
occurred in 25% of those significantly injured.
Skiing
Winter sports enjoy increasing popularity but expose partic-
ipating children to the risk of injury. Interestingly, whereas
upper extremity and spine injuries are common in adults,
children tend to have more lower extremity injuries.83,183,367
The thumb of children appears particularly susceptible to
injury, especially in the physes at the metacarpophalangeal
junction.185 Lower limb injuries usually involve the knee and
tibia/fibula in children and are most likely when the binding
fails to release. Improvement in equipment is leading to a
decreasing incidence.
Snowboarding injuries were evenly distributed between
upper and lower extremities, and 41% were fractures.153 The
wrist was the most common injury site.
Playground
Both school and neighborhood playgrounds are frequent
areas of childhood activity. Safety factors are not always
evident in the design of activities. Even when a great deal of
thought has gone into the design of certain structures, it may
only predispose to a different injury pattern.165,382
The increasing utilization of preschool facilities places
young children in accident-suceptible situations.111,210,211,
219,327,377
These children, whose motor skills and attention
spans are incompletely developed, are often encouraged to
engage in play activities that may be beyond their physical
ability. Proper scrutiny of potentially hazardous environ-
ments should be undertaken by parents before enrolling
their child in a given center.
Mott et al. reviewed injury patterns in public play-
grounds.260 A total of 105 children fell from equipment
(usually the climbing frame); 125 children had surface-
related injuries (85 on bark, 30 on concrete). Fractures and
sprains, interestingly, were more common on the bark
surface; and lacerations and abrasions were more prevalent
on concrete. Children may take more risks on bark surfaces.
The play equipment is often more interesting and usually
entails climbing. However, the depth and firm underlying
(dirt) surface essentially fix the extremity as the fracture-
producing forces continue. On a concrete or hard surface
more slipping/sliding may occur, lessening the longitudinal
loading associated with children’s fractures.
Trampolines
Trampolines have become a significant risk to chil-
dren.54,93,227,275,345,398 A 6-year study (1990–1995) showed an
45
injury increase from 29,600 in 1990 to 58,400 in 1995.345
The median age of injured children was 10 years. The
male/female ratio was 1 : 1. Injuries to the extremities pre-
dominated among children of all ages and accounted for
more than 70% of the injuries. There was an inverse relation
between age and the relative frequency of upper extremity
injuries, fractures, and dislocations. There was a direct rela-
tion between age versus lower extremity and soft tissue
injuries. There was also an inverse relation between age
versus facial injuries, head and neck injuries, and lacerations.
Annually 1400 children required hospitalization, which
represented 3.3% of all children with a trampoline-related
injury. Fractures or dislocations accounted for 83%
of injuries among admitted children. A disproportionate
number of these injuries occurred on backyard, rather than
commercial, trampolines.
Olsen reported injuries in children on trampoline air
cushions and found that 70% of children explained that they
had either been pushed or had lost their balance because
of constantly changing rhythm on the “bouyant” surface.275
Olsen strongly recommended some type of control over the
apparatus.
Common Injury Mechanisms
The constant exploration of intriguing aspects of everyday
activity may lead to interesting ways of potential injury.
Misuse of common “vehicles,” such as a shopping cart, may
cause significant injury.347 Fads such as break-dancing may
cause acute and unusual chronic injuries.158,273,338
Automobiles
At all ages the automobile is the principal crippler of chil-
dren, causing severe skeletal abnormalities.323,341,370,375,389
However, other powered vehicles are assuming increasing
importance as causal mechanisms. They include off-road
vehicles, bicycles (especially off-road or downhill), skate-
boards, in-line skates, and jet-skis. Traffic accidents account
for 10–12% of the cases.
The serious hazards of snowmobiles, power lawn mowers,
trail bikes, and other small powered vehicles are becoming
increasingly evident.229,349,387 Even nonpowered vehicles, such
as skateboards and in-line skates, are becoming a significant
cause of fractures during childhood and adolescence.
Trauma secondary to all-terrain vehicle use (and abuse) has
become a significant health problem in the pediatric popu-
lation and has led to a variable prohibition of the use of such
vehicles.125,286,356,388
In the Vehicle
Most severe and fatal childhood accidents occur to young-
sters or adolescents who are in cars.38–47,208 The array of skele-
tal injury varies with the scope of the study. Many studies
describe only mortality and morbidity statistics and various
trauma score indices. Specific or likely fracture patterns are
infrequently documented in detail.
Agran et al. studied 191 seat-belted children41; 33 (17%)
children were injury-free. Among the 191 children, 6 had
46
extremity fractures (3 femur, 1 clavicle, 1 humerus,
1 forearm). There were no spine fractures. In a similar study
of pickup trucks, 14 of 89 children sitting in the back and 10
of 201 sitting in the cab sustained fractures.46 Most injuries
involved the head or soft tissues.
By the Vehicle
Children do not rationally comprehend the potential for
vehicles to harm them, nor do they adequately grasp con-
cepts such as velocity even when they take the time to look
both ways.130,170,186,289,322,323,329,360,394,400,401 Vehicles have become
the most frequent cause of death for children aged 5–9 years.
Extremity and head injuries are much less likely when the
child is properly seat-belted in a car.41,215 Soft tissue injury to
the arms or legs may be more frequent than fractures (38
of 60 extremity injuries versus 22 fractures.130 Bell et al.
described fractures in children run over by slowly moving
vehicles.76 They tended to be young children (all but one
under 6 years). The thorax, cranium, pelvis, and femur were
common injuries.39
Bicycle
Wheeled vehicles are common to childhood activity and are
frequently associated with injuries.89,137,146,151,191,266,270,330 Of all
bicycle accidents, 70% result from falls rather than impact
injuries. Tricycles tend to be kept within property bound-
aries, but that does not preclude injury. Small children may
dart or ride behind vehicles while they are backing up. Bicy-
cles provide “freedom” to the child. Because they are often
associated with fun or play, the child’s attention to potential
hazards such as traffic tends to decrease.
Head and neck injuries comprise approximately 20–30%
of the injuries.38 Head injuries are the most important etio-
logic factor in death, which has led to increased emphasis
on the mandatory use of helmets.126,267,279,315,316,333,335,363,379,380
Sosin et al. studied bicycle injuries and deaths (0–18
years).350 They found an annual average of 247 brain injury
deaths and 140,000 head injuries. They thought that as many
as 184 deaths and 116,000 head injuries could have been pre-
vented with the proper use of helmets while on the bicycle.
Statistics vary on finding more upper than lower extrem-
ity injuries and vice versa. In most series soft tissue injuries
were most prevalent, with upper and lower extremity frac-
tures being only about 14% 13%, respectively.
Seats on bicycles (front or back) expose small children to
adult-level injurious forces.331,361
Off the Road
Recreational vehicles have received increasing attention
because of the rate of accidents and the lack of licensure
to operate.52,125,132,163,229,283,348,356,386,388 Three-wheel all-terrain
vehicles caused enough serous injuries such that further sale
was banned in 1988.132 A variety of vehicles are available
(minibikes, dirt bikes, mountain bikes, snowmobiles), as are
water vehicles (ski-doos). Pyper and Black reviewed 233 chil-
dren (injured by these vehicles) who sustained 352 fractures
(60 physeal, 34 open).286 All-terrain vehicles were often asso-
ciated with pelvic and spine fractures.
2. Injury to the Immature Skeleton
Infant Walkers
Infant walkers have been the cause of multiple childhood
injuries.114,142,203,280,294,381 Mechanisms include falls from the
walker, falls down stairs, and burns. Sheehan et al. showed
that infant walkers are a significant cause of trauma.339 In this
case they reported a 10-month-old girl who sustained bilat-
eral fibular diaphyseal fractures.
Falls
Gratz reported that most pediatric injuries are caused
by simple falls, either from a level surface or a variable
height, accounting for 46% of injuries overall.167 The most
common falls come from playground equipment. Falls by
children are frequent and account for almost 50% of all
childhood deaths due to trauma.70,106,138,174,228,251,265,320,344,351
Musemeche et al. reported a fatality rate of 23%.265 One of
the highest national death rates due to falls occurs among
nonwhite children less than 5 years of age.340 Despite this sta-
tistic, falls are only the seventh leading cause of death in chil-
dren from all causes. Chadwick et al. reported seven deaths
in 100 children who fell 4 feet or less.106 One death occurred
among 117 children who fell 10–45 feet. The seven children
who died in the short falls all had other factors that suggested
fabricated histories.
Falls are of increasing importance in young children,
being the third leading cause of mortality in children
aged 1–4 years. Even simple falls by the infant or young
child can be significant.48 According to these investigators,
falls contributed to 41% of the deaths in this age group.
Musemeche and associates showed that falls occur pre-
dominantly in the younger population, with a mean age of
5 years and a 68% male preponderance.265 Seventy-
eight percent of the falls occurred from a height of
two stories or less and occurred at or near the home.
Most of the patients sustained a single major injury that
usually involved the head or skeletal system. Fortunately, chil-
dren can survive falls from significant heights, though
serious injuries do occur.296 As would be expected, morbid-
ity and mortality increase with the height of the fall, the
latter usually being related to falls of a distance exceeding
10 feet.
Falls may occur from a height (building, ski lifts), on a
level surface, or from a moving vehicle (e.g., bicycle, skate-
board). Falls from a height are an urban hazard, with fatali-
ties being as high as 23%.265 Rural children have similar
hazards (e.g., water towers, multistory barns) and so are not
immune to this etiology. Falls are probably the most frequent
cause of childhood fracture.154,156,347 Injuries to the pelvis and
spine are less common in children.
Falls from heights constitute a significant portion of urban
trauma.265 In one study 70 children (1985–1988) sustained a
fall of 10 feet or more. The patients’ ages were usually 5 years
or younger, and 68% were boys. About 78% of the falls
occurred from two stories (20 feet) or less and usually took
place at or near home. Most patients had a single injury, and
all survived. Injuries usually were head or skeletal. Falls are
the leading cause of nonfatal injury in the United States and
are second to motor vehicle accidents as a cause of acciden-
tal death.
Biologic Differences Between Child and Adult Skeletal Trauma
Falls down a set of stairs are also common.115 Joffe and
Ludwig studied 363 such injuries195: 50% were in children 5
years of age or younger. The severity of injury did not cor-
relate with the height of the top stair of the fall. Head injuries
predominated, but only 6 of 363 sustained an extremity frac-
ture. Most of the patients sustained superficial extremity
injuries. Osseous injuries occurred in only 7% of the patients
(six fractures). Children younger than 4 years of age were
more likely to sustain head and neck injury trauma than chil-
dren older than 4 years of age. In fact, almost three-fourths
of the injuries involved the head and neck. An injury to more
than one body part occurred in only 2.7% of patients. Chil-
dren who fell down more than four steps had no greater number, or
severity, of injuries than those who fell down fewer than four steps.
Therefore be suspicious of any extremity fracture if “stairway”
is mentioned as the cause.
This injury pattern was common in young children
learning to master the stairs.195 It also was a source of
injury as they gained more confidence and increased the
rate of ascent or descent. Joffe and Ludwig concluded that
when multiple, severe truncal, or proximal extremity injuries
were noted in a patient who “reportedly” fell downstairs a
different mechanism of injury (e.g., abuse) should always
be suspected and the child carefully assessed as to its
likelihood.195
Chiaviello et al. studied stairway-related falls in 69
children less than 5 years old.115 Head and neck injuries
occurred in 90%, extremity injuries in 6%, and truncal
injuries in 4%. Injury to more than one body region did not
occur. Fifteen patients (22%) sustained significant injuries:
concussion (m = 11), skull fracture (m = 5), cerebral contu-
sion (m = 2), subdural hematoma (m = 1), and a C-2 fracture
(m = 1).
Nimityongskul and Anderson studied 76 children from
birth to 16 years who were reported to have fallen out of a
bed, crib, or chair while in the hospital.269 About 75% of the
injuries were in children 5 years of age or younger. The
height of the falls ranged from 1 to 3 feet. Most injuries
were minor (hematoma, laceration). The only fracture
involved a child with osteogenesis imperfecta. Severe
head, neck, spine, and extremity injuries are rare when
children fall out of hospital beds.181,230 Child abuse must
be suspected in any child with a severe head or extrem-
ity injury following an alleged “fall from a bed at
home.”212,238,249,269,349,391
The exception might be the “bunk bed” fracture of the
first metatarsal when the child falls or jumps from the top
bed.336 However, this is a relatively innocuous fracture com-
pared to those usually associated with child abuse. This frac-
ture usually occurs as the child jumps (voluntarily) to the
floor from the top bed. It is a torus or impaction fracture in
the proximal metaphysis of the first metatarsal. It is not the
typical shearing fracture of abuse. This injury pattern is dis-
cussed in more detail in Chapter 24.
Helfer et al. studied 246 children aged 5 years or less who
fell out of bed (219 at home, 95 in hospital).181 The data
revealed no occurrence of a serious injury.
Interestingly, in various series70,265,348 the fractures common
with adult falls from a height (calcaneus, spine, pelvis) are
infrequent. The upper extremity is more likely to be
involved, and head injuries are common.
47
Vending Machines
Cosio and Taylor studied 64 patients with injuries sec-
ondary to being crushed by a vending machine.124 All
victims were male, except one. The average age was 19.8
years. Thirteen patients sustained multiple injuries. Fifteen
were killed.
Biologic Differences Between Child
and Adult Skeletal Trauma
Many if not all of the differences between the traumatized
skeletons of an adult and a child relate to the fact that
the child’s skeletal elements are in more dynamic, constantly
changing growth and remodeling modes. In contrast,
the adult skeleton essentially has ceased the processes of
elongation and apposition and is principally (and much
more slowly) remodeling the established elements in accord
with stress responses (i.e., forming increasing patterns of
primary, secondary, and tertiary osteons). The major prac-
tical differences between childhood and adult skeletal
trauma fall into three categories: anatomy, physiology, and
biomechanics.
Anatomy
Because of the endochondral ossification process, the
chondro-osseous epiphyses of children are variably radiolu-
cent, making roentgenographic evaluation difficult, if not
impossible, unless specific invasive (e.g., arthrography) or
noninvasive (e.g., MRI) procedures are used. Specific skele-
tal injury is sometimes inferred on the basis of clinical judg-
ment, as routine roentgenographic substantiation may not
be possible, although subsequently trauma-reactive subperi-
osteal new bone formation may verify the diagnosis. In con-
trast, MRI may delineate the injury. The physis is constantly
changing, with active longitudinal and diametric growth and
in its mechanical relation to other contiguous components.
Modes of failure thus vary with the extent of the chondro-
osseous maturation. The involvement of the physeal and
articular cartilages in angular deformities is important to
certain concepts of fracture treatment, both acutely and long
term.
The periosteum also differs in a child, being thicker
and more readily elevated from the diaphyseal and metaph-
yseal bone due to a subperiosteal fracture hematoma
or stripping during fragment displacement. It is less readily
completely disrupted and exhibits greater osteogenic
potential.
There is a pronounced reaction of periosteum and
endosteum that is significant in the correction of longitudi-
nal deformities. The vascular pattern of cortical bone and
its microscopic structure, as well as the vascular supply
of the physis, assume great importance with specific
fractures.
At birth developing cortical bone (primary bone) begins
with minimal lamellar components and a relatively greater
porosity than does mature bone. Intrauterine demands
start some biomechanically reactive processes. Within any
48
given anatomic region of a bone, cortical changes progres-
sively occur with increasing age, with the natural sequence
being increased formation of lamellar and osteon bone
within the diaphysis. This is a biomechanically sensitive
(responsive), reactive process. There are also relative dif-
ferences in the various regions within a given bone that
predispose certain regions to fracture over others. These
differences in microscopic and macroscopic architec-
ture also affect the process of fracture healing, which is dif-
ferent in the more dense, lamellar bone of the diaphysis
compared with the spongy, trabecular bone of the metaph-
ysis or epiphysis.
Physiology
The developing skeleton is continuously undergoing active,
frequently rapid growth and remodeling in response to bio-
mechanical demands. Accordingly, most fractures usually
heal rapidly, nonunion is rare, overgrowth may occur, and
certain angular deformities may correct totally. However,
damage to the capacity of the bone and cartilage to accom-
plish these reparative and physiologic functions may impair
subsequent growth and development in several significant
ways. Various portions of the longitudinal bones respond dif-
ferently to hormones, growth factors, mechanical factors,
vascular changes, and trauma.
The child responds differently from the adult to the meta-
bolic and physiologic stresses of trauma. Because the total
blood volume is smaller, depending on the size of the child,
less blood loss may be tolerated before signs of hypovolemic
shock develop. This is because the smaller volumes lost rep-
resent a larger percentage of the total. The higher surface
area/volume ratio also makes the child more vulnerable to
hypothermia. There is a significant difference in the meta-
bolic response between the adult and the child. Whereas the
adult has a significant increase in metabolic rate resulting
from the stresses of trauma, the child has minimal or no
change. This is believed to be caused by the child’s signifi-
cantly higher metabolic rate, which needs to be increased
only a small amount to accommodate the increased meta-
bolic demands. The accelerated metabolic rate response,
together with the ability to metabolize lipid stores, provides
a possible explanation for the increased survival rates in chil-
dren after severe trauma.
Biomechanics
The major changes undergone by developing bone are
increases in the density and thickness of the cortical com-
ponent, particularly in the diaphysis but also in the metaph-
ysis. There are also alterations in the proportions of
trabecular (endosteal) and cortical bone within the diaph-
ysis, metaphysis, and epiphysis (especially the subchondral
periphery). The porosity, which in the cross section of a
child’s bone is much greater than that of an adult, plays a
significant role in affecting or even stopping fracture prop-
agation in a trauma situation. This factor is undoubtedly
important, as obviously comminuted fractures (discerned by
routine radiographs) are distinctly uncommon in children.
The increasing amount of bone in the expanding epiphyseal
ossification center undoubtedly alters the stress and strain
2. Injury to the Immature Skeleton
response pattern throughout the epiphysis. Furthermore, it
is likely that the progressive establishment of the subchon-
dral plate of the epiphyseal ossification center adjacent to
the physis alters its response to fracture-induced stress and
strain.5 Adult bone usually fails initially in tension, whereas
a child’s bone may fail in either tension, compression, or
both. Shear failure obviously compounds any such reaction
to injury.
Patterns of Injury
Satisfactory treatment necessitates an understanding of what
constitutes each anatomically specific fracture. In essence, a
fracture may be defined as disruption of the normal conti-
nuity of the bone, cartilage, and contiguous soft tissues. Such
disruptions may or may not cause a radiologically evident dis-
ruption of the continuity of the cortical bone. The latter
situation may occur in children when the cortical bone,
because of a greater capacity for elastic and plastic defor-
mation prior to failure, buckles (plastically deforms), rather
than “breaks.” This often represents compression failure,
rather than tension failure, of bone. This structural failure
pattern essentially occurs only in children. Tension failure,
which certainly occurs in children and is the prevailing mode
of failure in adults, leads to disruption in the structural con-
tinuity of the bone. However, tensile failure may be in-
complete in children, leading to the greenstick pattern of
incomplete failure.
Any fracture pattern in the child or adolescent needs to
be described adequately.21,22 Such a description should in-
clude (1) the anatomic location of the fracture, (2) the type
of fracture, and (3) the physical changes caused by and asso-
ciated with the fracture. Although a verbal description of any
fracture is the usual response, the use of digital images
transmitted over E-mail and other evolving technologies
will probably be increasingly utilized and are capable of
more accurate visual description of the actual fracture and
patient.
Anatomic Location
Descriptive fracture terminology should accurately indicate
the location of the injury; it becomes especially important
for comparative treatment studies. As is seen in the subse-
quent clinical sections of this text, subtle differences in the
particular anatomic site of the fracture in children may have
a major impact on any acute treatment and potential long-
term problems. The anatomic definitions are illustrated in
Figures 2-1 and 2-2 and described below.
Diaphyseal: Indicates involvement of the central shaft of
any longitudinal bone, which is composed of progressively
mature (i.e., remodeling) lamellar bone. The thickness
and extent of osteon bone formation (which characterizes
this anatomic region) relates to both age and imposed
physical demands.
Metaphyseal: Denotes involvement of the flaring ends of
the central shaft of a longitudinal bone. The metaphyses
are usually composed of a composite of endosteal trabec-
ular bone and cortical immature fiber bone, both of which
Patterns of Injury
FIGURE 2-1. Humerus (left) and femur (right) from a 10-year-old
child showing the various anatomic locations and definitions. See
text for details.
predispose the metaphyses to the torus fracture pattern.
The cortical bone of the metaphysis is more porous than
diaphyseal cortical bone (Fig. 2-3). Osteon bone within
the metaphyseal cortex is variable, being present in the
region of progressive blending into the diaphysis, and
FIGURE 2-2. Radiographs of humeri from a neonate (A)
and a 10-year-old child (B) showing changes that occur
during progressive proximal and distal secondary ossifica-
tion. The radiologic technique visualizes the cartilaginous
portions of the epiphysis. These cartilaginous regions nor-
mally appear radiolucent in clinical radiographs.
49
absent near the physis (zone of Ranvier). Many torus frac-
tures occur near the transition between the metaphyseal
and diaphyseal cortices (Fig. 2-4).
Physeal: Involves the endochondral longitudinal-latitudinal
growth mechanism. Variable fractures involve this region
(see Chapter 6).
Epiphyseal: The chondro-osseous end of a long bone
is involved in basic growth. Fractures may selectively
involve the expanding ossification center. It is important
to realize that the epiphysis may be injured only in the
cartilaginous portion, which makes diagnosis extremely
difficult (see Chapter 6). As is shown subsequently and in
ensuing chapters, such fractures are referred to as “shell”
fractures, reflecting this chondro-osseous separation.
Fractures may occur within the trabecular bone or the
subchondral plate, creating an area of edema and hem-
orrhage. This injury pattern, which is generally invisible
radiographically, is referred to as a bone bruise on an MRI
scan.
Articular: Indicates involvement of the epiphyseal joint
surface. Such injury may be part of an extensive epiphy-
seal injury, or it may be localized (Fig. 2-5). In the latter
case, the fragment may include only articular cartilage and
juxtaposed, undifferentiated hyaline cartilage or both sub-
chondral bone and cartilage (e.g., osteochondritis disse-
cans) (see Chapters 6, 22).
Epicondylar: Involves regions of the bone, especially
around the elbow, that serve as major muscle attachments
and have extensions of the physis and epiphysis.
50 2. Injury to the Immature Skeleton

A B
FIGURE 2-3. These osseous preparations of the distal radius (A) and distal femur (B) from an 11-year-old boy show the relatively porous,
fenestrated cortex of the metaphysis (M), in contrast to the smooth cortex of the diaphysis (D).

Supracondylar: Pertains to involvement above the level of

Subcapital: Denotes involvement just below the epiphyses
of certain bones such as the proximal femur or radius.
Cervical: Indicates involvement along the neck of a specific
bone, such as the proximal humerus or femur.
the condyles and epicondyles (e.g., distal humerus or
femur).
Transcondylar: Indicates a location transversely across the
condyles (e.g., distal humerus or femur). These lesions
usually are complete physeal disruptions.
Intercondylar (intraepiphyseal): Involvement within and
through the epiphysis, with any fracture separating the
normal condylar anatomic relationships.

FIGURE 2-4. Fracture of the transition of the relatively thin metaph-
yseal cortex to the thicker, biomechanically remodeling diaphyseal
cortex. The microvascular injection shows vascular proliferation
within the anterior callus. In contrast, the posterior callus and vas-
cular reaction is minimal.
FIGURE 2-5. Articular fracture of the second metatarsal of an 8-
year-old girl sustained when the foot and leg were run over by an
automobile tire. She required a below-knee amputation to control
ischemia and infection. This particular injury, with minimal osseous
involvement, was not evident on clinical films.
Patterns of Injury
FIGURE 2-6. Tibia in a 3-year-old child showing
the various types of fractures: (A) longitudinal;
(B) transverse; (C) oblique; (D) spiral; (E)
impacted; (F) comminuted; (G) bowing (plastic
deformation); (H) greenstick; and (I) torus. See
text for details.
Malleolar: Indicates that distal regions of the fibula and
tibia are involved. Because of anatomic differences, there
are significant differences in the fracture patterns of the
medial and lateral malleoli.
Type of Fracture
Any method of description should also be based on an
appropriate roentgenogram of the injury pattern of disrup-
tion. The basic types, shown in Figure 2-6, are as follows.
Longitudinal: Fracture plane follows the longitudinal axis
of the diaphysis (Figs. 2-7 to 2-9).
Transverse: Fracture plane is essentially at a right angle to
the longitudinal axis of the bone (Fig. 2-10).
Oblique: Fracture plane is variably angled relative to the lon-
gitudinal axis, usually about 30°–45° (Fig. 2-11).
Spiral: Fracture plane encircles, in a twisting manner, a
portion of the shaft.
FIGURE 2-7. Combination of a longitudinal fracture (solid arrows)
and a spiral fracture (open arrows). This pattern of “comminution”
is relatively typical in the more resilient immature skeleton.
51
Impacted: Compression injury in which the cortical and tra-
becular bone of each side of the fracture are crushed
together (Fig. 2-12).
Comminuted: The fracture planes propagate in several
directions, creating variable-sized fragments (Fig. 2-13).
This type of fracture is uncommon in infants and young
children but becomes more common in adolescents, par-
ticularly involving the tibia as the cortical bone matures.
Bowing: The bone is deformed beyond its capacity for full
elastic recoil (back to its normal anatomic shape) into
permanent plastic deformation (see Chapters 1, 5). The
younger the child, the more likely it is that this type of
skeletal injury can occur. It is particularly common in the
fibula and the ulna, both of which may bow, whereas the
paired bone (i.e., tibia or radius) is more likely to fracture
(Figs. 2-14, 2-15). This permanent deformation of the
“nonfractured bone” may limit reducibility of the overall
injury. As primary osteons form and progressively remodel
into secondary and tertiary osteons, the diaphyseal bone
becomes more brittle and less likely to plastically deform.
Plastic deformation has been described even in adults (see
Chapter 5).
Greenstick: This is a common injury in children (Fig. 2-16).
The involved bone is fractured, but a portion of the
FIGURE 2-8. Incomplete, undisplaced longtitudinal diaphyseal frac-
ture. There is no plastic deformation of the intact portion of the
cortex.
52 2. Injury to the Immature Skeleton

FIGURE 2-9. Anteroposterior view shows a torus fracture (white

arrow) and a longitudinal fracture of the cortex (black arrows), sep-
arating it from the endosteal bone and terminating in the torus
injury. Also note the torus ulnar fracture (open arrow).

FIGURE 2-11. Oblique fracture of the tibia. The cortices appear rel-
atively intact. This is a twisting injury.

FIGURE 2-12. Impacted distal radial fracture.

FIGURE 2-10. Transverse fractures of the radius and ulna.

 FIGURE 2-15. Plastic deformation (bowing) of one cortex of the
distal femur, along with complete failure of the apposed cortex.

FIGURE 2-13. Comminuted radial fracture with a double fracture of

the ulna that included a transverse failure (open arrow) and a torus
failure (solid arrow).

FIGURE 2-16. Greenstick fractures of the radius.

FIGURE 2-14. Oblique view of radial and ulnar fractures in a 6-year-
old boy. The fracture of the radius shows an intact but plastically
deformed dorsal cortex (white arrowhead) and a partially fractured
palmar cortex (black arrowhead), a characteristic greenstick injury.
The fracture is angulated because of plastic deformation (bowing)
of the dorsal cortex. A significant ulnar injury is not evident in this
projection.

53
54 2. Injury to the Immature Skeleton

cortex and periosteum remains relatively intact on the

compression side. Because this intact cortical bone is
usually plastically deformed (bowed), angular deformity is
common; reversal of the deformity may necessitate con-
version to a complete fracture. Furthermore, as swelling
dissipates after an initial reduction, the angular deforma-
tion may insidiously occur even when the extremity is
casted.
Torus: This impacted injury occurs during childhood.
Because of the differing response of the metaphyseal bone
to a compression load, the bone buckles (Figs. 2-17, 2-18),
rather than fracturing completely, and a relatively stable
injury is created. This type of fracture primarily affects
developing metaphyseal bone. It is important to realize
that cortical disruption (fracture) occurs, but that such
disruption does not entail the entire cortex.
Shell (sleeve): This fracture pattern involves traumatic sep-
aration of articular or epiphyseal cartilage from the con-
tiguous bone. There may be no bone attached to the
cartilage, or there may be a thin (lamellar) piece (Figs.
2-19 to 2-21). The anterior tibial spine fracture, which is
usually composed of a small fragment of bone and a much
larger fragment of cartilage, is a typical example of this
failure pattern. The Legg-Perthes subchondral fracture
also represents this type of failure.
Bone bruising: This pattern of microtrauma occurs within
the trabecular or subchondral bone of the metaphysis or
epiphyseal ossification center (Fig. 2-22). Such focal hem-
orrhage may be detectable by alterations of signal inten-
sity in the MRI but is not usually detectable by routine
radiography.

FIGURE 2-17. (A) Anteroposterior view of a metaphyseal torus frac-

ture. Note that it does not extend completely across the diameter
of the shaft. (B), Oblique view shows longitudinal (striated) disrup-
tion (white arrow) paralleling the longitudinal axis and a longer lon-
gitudinal disruption (black arrow) of the opposite cortex.

FIGURE 2-18. (A) Apparent

torus fracture (solid arrow)
of the proximal humerus.
The open arrow indicates a
fracture of the opposite
cortex. (B) Histology shows
the fractures (open arrow)
and an intact periosteum
A B (solid arrow).
Joint Disruption 55

Physical Change
Whereas the aforementioned terms have been primarily
descriptive, the following terms indicate conditions that are
of practical importance clinically. These terms denote not
only the nature of the clinical problem but also the general
type of treatment that is probably required.
Extent: The fracture may be incomplete, in which case some
of the cortex is intact, or it may be complete, in which case
the fracture line crosses the entire circumference. Fur-
thermore, the fracture line may be simple (a single fracture
line), segmental (separate fracture lines isolating a segment
of bone), or comminuted (multiple fracture lines with mul-
tiple fragments).
Relationship of fracture fragments to each other (Fig.
2-23): These relationships define a deformity as it exists
during roentgenographic evaluation. However, because of
elastic recoil, especially in children, these relationships
may not represent the full extent of deformity or angula-
FIGURE 2-19. Shell or sleeve fracture of the distal fibula (arrow). tion maximally present at the time of injury, especially in
a greenstick injury. The fracture may appear undisplaced
or displaced, in which case the distal fragment is shifted
away from its usual relationship to the proximal fragment.
This shift may assume several types of deformation, which
may be present singly or in any combination: (1) sideways

B C

FIGURE 2-20. Shell fracture of the talus in an 11-year-old boy. (A) Radiograph. (B) Slab section. (C) Similar shell fracture of the talus
from a 12-year-old boy.

FIGURE 2-21. Shell fracture (undisplaced) of the distal femur
(arrow).
FIGURE 2-22. Bone bruising in the lateral metaphysis (arrow) due
to microtrauma and intratrabecular hemorrhage. This child sus-
tained an incomplete lateral condylar fracture and a traumatic
amputation.
shift, (2) angulation, (3) overriding, (4) distraction, (5)
impaction, and (6) rotation. The most important to
correct are angular and rotational deformities. Whereas
the former often corrects spontaneously, though unpre-
dictably, the latter usually does not correct and must be
adequately treated initially. So long as the reduction
emphasizes restoration of longitudinal and rotational
56
FIGURE 2-23. Tibia in a 6-year-old child showing the relations of
fracture fragments to each other: (A) translocation; (B) angulation;
(C) overriding; (D) distraction; and (E) rotation in a distal epiphy-
seal fracture.
alignment, sideways shifts and overriding are acceptable in
many children’s injuries.
Relationship of the fracture to the external environ-
ment: Basically, a fracture is either closed (skin covering
intact) or open (compound, a break in the skin). An open
fracture, in which a break in the skin allows communica-
tion between the fracture and the external environment,
may be caused when a fracture fragment penetrates the
skin from within or when an external object penetrates or
ruptures the skin from without. Such fractures carry the
risk of infection. The basics of treatment of open fractures
are covered in Chapter 9.
Periosteum
Throughout most of childhood the periosteum is thicker
and more resistant to disruption than in the adult. Because
of its increased contiguity with the underlying
bone, however, it may be injured whenever the bone
fractures. Because the periosteum separates more easily
from the bone in children, it is less likely to rupture
completely, and a significant portion of the periosteum often
remains intact, usually on the concave (compression) side
of the fracture (Fig. 2-24). This intact periosteal hinge
may lessen the degree of displacement and may be used
to assist in the reduction, as it imparts a certain degree
of intrinsic stability (Fig. 2-25). As is detailed in Chapter 6,
the periosteum blends imperceptibly into the perichon-
drium of the epiphysis and attaches densely into the zone of
Ranvier.
It is important to realize that the extent of separation
(elevation) of the periosteum from the metaphyseal and
diaphyseal cortices is rarely easily appreciated on the initial
radiograph (Fig. 2-26). However, as the subperiosteal
hematoma organizes and subperiosteal new bone begins
to form, any extent of soft tissue disruption becomes
progressively more easily appreciated. In the neonate,
periosteal stripping may extend from proximal physis to
distal physis.
Because the periosteum creates some soft tissue continu-
ity at the injury site, the subperiosteal new bone bridges the
Remodeling
FIGURE 2-24. Fracture of the distal femur from a 3-year-old
child fatally injured in an automobile accident. Histologic
section showing cortical damage (arrow) associated with an intact
periosteum.
fracture gap, leading to increasing stability. With severe
trauma, especially open injury with segmental loss of bone,
the periosteal sleeve may even make enough new bone to
negate any need for bone grafting to bridge the fracture gap
(Fig. 2-27). The role of the periosteum in basic bone devel-
opment, maturation, and replacement was discussed in
detail in Chapter 1.
Joint Disruption
Even though the soft tissues of the joint exhibit a greater
degree of laxity in the child than they do in an adult, the
capsule and ligaments are relatively more resistant to stress
than are the contiguous bone and cartilage, especially the
physeal cartilage.134 Consequently, discrete ligament rupture
and joint dislocations are much less frequent in children.112
When major ligaments attach directly into an epiphysis,
physeal fractures are the more common failure mode. Joint
dislocations in the child commonly affect the elbow and hip.
Shoulder and knee dislocations are less common. Other
joints only rarely are dislocated prior to skeletal maturity
(i.e., physeal closure).
The most common “dislocation” in young children is the
pulled elbow. Usually, no obvious roentgenologic findings
are evident, and the condition is often relieved during radi-
ography of the elbow when the radiology technician inad-
vertently supinates the elbow and relocates the subluxated
annular ligament (see Chapter 14).
Injury to the joint cartilage may involve only superficial
portions of the specific articular cartilage, or it may
also involve the ossification center of the epiphysis. If
only the cartilage is involved, traumatic lesions may not be
visualized initially without arthrography (i.e., the “shell” or
“sleeve” chondro-osseous separation fracture described in
Chapters 5 and 6). Osteochondritis dissecans is, in many
57
FIGURE 2-25. Dorsally displaced (A) and reduced (B) distal radial
metaphyseal fracture. The periosteum is connected with the prox-
imal fragment by an intact dorsal periosteal hinge. When the frag-
ment is reduced, this periosteal hinge prevents overreduction.
Fracture hematoma accumulates underneath the elevated perios-
teum and contributes to extensive callus formation.
cases, posttraumatic (a transchondral fracture), rather
than some type of underlying, more generalized disease (i.e.,
an osteochondrosis). Complications of articular trauma
are often not recognized until long after the injury, when
interference with joint function or growth disturbances
become evident. The use of continuous passive motion
may be an important factor in lessening intraarticular
consequences.171
Remodeling
Most children’s fractures are relatively easy to treat, but
they do not always remodel, and the results are some-
times unsatisfactory. The remodeling capacity of a deformity
caused by a fracture or epiphyseal injury is determined
by three basic factors: (1) the age of the child, (2) the
distance of the fracture from the end of the bone, and (3)
the amount of angulation.22,147–150,159,256,357 Physiologic re-
modeling of a bone depends on periosteal appositional
bone formation, resorption of some bone, and physeal
growth.82,376
The criteria for an acceptable position of a fracture
are based on the predictability of remodeling. For an axial
deformity, remodeling capacity is better in the young
patient (Fig. 2-28) and for deformities near the physis
(Fig. 2-29). For lateral displacement and shortening, re-
modeling capacity is good; but for rotational deformity,
essentially no remodeling capacity exists. Additional
factors that must be taken into account include (1) the
skeletal age of the patient, which may differ from the
chronologic age; (2) the relative contributions by different
physes to the longitudinal growth of a given bone; and
(3) in some bones, stimulation of the longitudinal
growth due to the fracture (reactive hyperemia with physeal
stimulation).
58
FIGURE 2-26. Sequence of subperiosteal new bone formation. (A) Original fracture (arrow). (B) Six days later. (C) Twenty-one days later.
The longitudinal extent of the subperiosteal elevation (arrows) was certainly not suggested by the minimally evident fracture.
Remodeling cannot be predictably relied on (Fig. 2-30).
Every effort should be expended to attain as adequate an anatomic
reduction as possible. Remodeling, in general, may be counted
on in children with 2 years or more of growth ahead, in those
with fractures near the ends of the bones, and in those with
FIGURE 2-27. (A) Periosteal new bone (arrowheads) in the poste-
riorly displaced periosteal sleeve 11 weeks after multiple trauma
and head injury to a 14-year-old boy. Following manipulation, the
fragments were placed in better alignment. (B) Film taken a year
later shows extensive remodeling and incorporation of the sub-
periosteal new bone.
2. Injury to the Immature Skeleton
deformities that are in the plane of movement of the joint.
Remodeling does not help with displaced intraarticular frac-
tures, fractures toward the middle of the shaft of a bone (par-
ticularly when shortened, angulated, or rotated), displaced
fractures in which the axis of displacement is out of the
normal plane of movement, and displaced fractures crossing
the physis. Remodeling in the diaphysis is largely a process
of smoothing the bone and surrounding callus; it is not a true
correction of longitudinal malalignment. With fractures of
the shaft, the intact but displaced periosteum produces
abundant callus on one side of the fracture, whereas the
other side is stripped of normal periosteum and resorbs. This
process eventually makes the fracture look less obvious when,
in reality, there is minimal improvement in the alignment.
Near an epiphysis, however, the physis may realign and
assume a more normal growth pattern, by means of which
metaphyseal remodeling improves the overall appearance.
With a supracondylar fracture that has healed with some pos-
terior displacement, the shaft acts as an anterior bone block
and restricts movement until growth moves the epiphysis
farther away from the bone block. As the child grows, move-
ment increases. The wrist, one of the areas most commonly
left to remodel, is a place in which altered longitudinal align-
ment corrects relatively readily, although not necessarily
rapidly.
Complications
The difference between complications in children and those
in adults is mainly due to the state of growth of the skeleton.
Delayed union and nonunion are rare in children because
the healing capacity is better.365 In Beekman and Sullivan’s
series of more than 2000 fractures in children, there was not
a single case of nonunion.75 Posttraumatic joint stiffness is
uncommon if the joint is not directly damaged. Mechanical
FIGURE 2-28. (A) Fracture of the mid-shaft of the femur in a 7-
month-old girl. (B) Callus formation (arrows) 2 months after the
injury. It is limited by the relatively intact periosteal sleeve. (C)
FIGURE 2-29. Extensive remodeling and longitudinal overgrowth
in a metaphyseal/epiphyseal fracture. (A) Displaced fracture
fragments in a 3-year-old girl who was thrown two stories (child
abuse). She also sustained ipsilateral distal humeral and distal
radial injuries. Repeated attempts at reduction with the patient
under general anesthesia were unsuccessful. (B) Four months
after the injury extensive subperiosteal new bone is evident,
59
Beginning remodeling (arrows) 7 months after the original fracture.
The angular malalignment, however, is still present.
although it is still partially separated from the original cortex
(arrow). (C) Beginning realignment and correction of angular defor-
mity 9 months after the injury. The patient has full use of her gleno-
humeral joint. Extensive subperiosteal new bone has formed and
is making a new medial cortex (arrows). (D) Appearance of the
remodeled fracture 2 years later.
60
(functional) hindrance resulting from malunion of the frac-
ture rarely exists. Refractures and myositis ossificans are less
common in children than in adults. Generalized complica-
tions are discussed in detail in Chapters 6, 9, and 10; and
specific complications unique to certain injuries are dis-
cussed in Chapters 12–24.
Disability Evaluation
Young, Wright, and colleagues developed scales measuring
physical function levels in children.402,403 They also reviewed
a large number of tabulated assessments applicable to
normal children, injured children, and children with impair-
ments (e.g., cerebral palsy) who might sustain an injury.
Anyone interested in developing outcome scales for pedi-
atric injury should review this article and the array of mea-
sures and scales in the appendix of their paper.
References
General Textbooks
1. Benson MKD, Fixsen JA, Macnicol MF (eds) Children’s
Orthopaedics and Fractures. London: Churchill Livingstone,
1994.
2. Injury to the Immature Skeleton
FIGURE 2-30. (A) Fracture of the left femur in
a 7-month-old girl with arthrogryposis multiplex
congenita. Bilateral hip dislocations are also
evident. (B) Postmortem roentgenogram at
15 months of age showing some remodeling
and minimal remaining callus. The angular
malalignment has not corrected at all.
2. Blount W. Fractures in Children. Baltimore: Williams &
Wilkins, 1955.
3. Calvert JM, Métaizeau JP. Les Fractures des membres chez
l’enfant. Monographie du CEOP. Montpelier: Sauramps,
1990.
4. Chapchal G (ed) Fractures in Children. New York: Georg
Thieme, 1981.
5. Devas M. Stress Fractures. London: Churchill Livingstone, 1975.
6. Dimeglio A, Hérisson C, Simon P. Les Traumatismes de
l’enfant et leurs séquelles. Paris: Masson, 1993.
7. Ehalt W. Verletzungen bei Kindern und Jugendlichen.
Stuttgart: Enke, 1961.
8. Emneus H, Gerner-Smidt M. Fracturer Hos Born. Aalborg,
Denmark: Vejle, 1979.
9. Havránek P. Deteské Zlomeniny. Prague: Nakladatelstri
Corvus, 1991.
10. Greene NE, Swiontkowski MF (eds) Skeletal Trauma in
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11. Judet R, Judet J, LaGrange J. Les Fractures des membres chez
l’enfant. Paris: Libraire Maloine, 1958.
12. Letts RM (ed) Management of Pediatric Fractures. New York:
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13. MacEwen HF, Kasser JR, Heinrich SD (eds) Pediatric Frac-
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14. Maroteaux P. Maladie osseuse de l’enfant. Paris: Flammarion
Médecine-Sciences, 1982.
15. Marcus RE (ed) Trauma in Children. Rockville, MD: Aspen,
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16. Métaizeau JP. Osteosynthèse Chez L’enfant. Montpelier:
Sauramps Ed, 1988.
17. Morrissy RM and Weinstein S (eds) Pediatric Orthopaedics
(4th ed). Philadelphia: Lippincott, 1996.
18. Ogden JA. Skeletal Injury in the Child. Philadelphia: Lea &
Febiger, 1982.
19. Ogden JA. Skeletal Injury in the Child. Beijing: Peoples
Hygiene Press, 1984.
20. Ogden JA. Traumatismos del Esqueleto en el Niño. Madrid:
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21. Ogden JA. Pocket Guide to Pediatric Fractures. Baltimore:
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22. Ogden JA. Skeletal Injury in the Child, 2nd ed. Philadelphia:
Saunders, 1990.
23. Ogden JA. Injury to the immature skeleton. In: Touloukian R
(ed) Pediatric Trauma. St. Louis: Mosby Yearbook, 1990:
399–439.
24. Ogden JA. Skeletal trauma. In: Grossman M, Dieckmann RA
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cott, 1991.
25. Poland J. Traumatic Separation of the Epiphyses. London:
Smith, Elder, 1898.
26. Pollen A. Fractures and Dislocations in Children. Baltimore:
Williams & Wilkins, 1973.
27. Rang M. The Growth Plate and Its Disorders. Baltimore:
Williams & Wilkins, 1969.
28. Rang M. Children’s Fractures, 2nd ed. Philadelphia: Lippin-
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29. Rettig H. Frakturen im Kindesalter. Munich: Verlag-
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30. Rockwood CA Jr, Wilkins KA, Beaty KH (eds) Fractures in Chil-
dren, 4th ed. Philadelphia: Lippincott-Raven, 1996.
31. Sharrard WJW. Paediatric Orthopaedics and Fractures.
Oxford: Blackwell, 1971.
32. Tachdjian M. Pediatric Orthopaedics, 2nd ed. Philadelphia:
Saunders, 1990.
33. Touloukian RJ (ed) Pediatric Trauma. St. Louis: Mosby
Yearbook, 1990.
34. Truesdell E. Birth Fractures and Epiphyseal Dislocations. New
York: Paul Hoeber, 1917.
35. Von Laer L. Frakturen und Luxationen im Wachstumsalter.
New York: Georg Thieme Verlag, 1991.
36. Weber BG, Brunner C, Freuler F. Die Frakturenbehandlung
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Other References
37. Adams JG. Bone injuries in very young athletes. Clin Orthop
1968;58:129–140.
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3
The Child with Multiple Injuries
Engraving of an epiphyseal avulsion fracture of the greater
trochanter. (From Poland J. Traumatic Separation of the Epiphysis.
London: Smith Elder, 1898)
hildren may be involved in severe injuries, often
C involving contact with or being a passenger in a motor-
ized vehicle or as a consequence of a fall from a height
of a building, playground equipment, or some type of
motorized or self-propelled vehicle. Such vehicular accidents
and falls are significant causal factors in childhood multiple-
system injury.44,45,108,125,135,196,224,226 Vehicular accidents may
occur to a pedestrian or when the victim is a passenger in a
vehicle or on some type of locomotive device such as a
bicycle, roller blades, or a scooter. These mechanisms
(vehicles, accidents, and falls) account for most traumatic
injuries and deaths of children. Proper management of chil-
dren with serious injuries obviously enhances the likelihood
that they will survive major trauma, even when there is
serious head injury.50
Skeletal trauma is often associated with damage to ex-
tremity soft tissues and intraabdominal, intrathoracic,
and intracranial structures.143,176,177 Involvement of these
nonskeletal structures may be severe or life-threatening, with
acute treatment usually taking priority over any fractures or
dislocations. In contrast to adults, children have a remark-
able resilience and are more likely to recover from major
injuries that might be lethal in an adult.146 Despite the
increased likelihood of survival, there is a significant inci-
dence of long-term disability following multiple trauma, a
factor that has been underemphasized in the past. Disability
usually relates to chronic problems in the musculoskeletal
and central nervous systems.
Children usually respond to trauma much differently from
adults. They often require variable, often specialized treat-
ment contingent on their age.11–13,39,58,76,101,183 They may have
smaller respiratory and circulatory volumes, proportionately
greater surface area, and often unique responses to drugs,
surgery, and stress; they frequently have difficulty localizing
symptoms and communicating about them. The margin for
diagnostic and treatment error in the pediatric age group
may appear greater because the response of the injured child
is different quantitatively and qualitatively, physiologically,
and psychologically from that of an adult. Although the
responses to injury may be “delayed” compared to those in
the adult, once such physiologic alterations commence they
may be precipitous, requiring rapid responses on the part of
any treating personnel. For example, abdominal distension
and diaphragmatic elevation from posttraumatic ileus or air
swallowing by a distressed child may significantly compro-
mise the child’s chest (respiratory) volume and ventilation
(Fig. 3-1).133 The loss of a seemingly small amount of blood
is important because of the child’s overall quantitative blood
volume. The relatively large skin surface area (compared
with body weight) causes rapid heat and water losses, which
increases the susceptibility to hypothermia and dehydration.
The problems requiring immediate attention in the man-
agement of the injured child are not different from those of
the adult. Establishment and maintenance of an adequate
airway, ventilation, control of hemorrhage, detection and
evaluation of head injury, replacement of blood and fluid
volume loss, treatment of shock, recognition of serious
nonskeletal and skeletal injuries, and the prevention of
69
70
FIGURE 3-1. Five-year-old boy who sustained multiple trauma.
Upon arrival at the emergency room he was experiencing consid-
erable respiratory distress. Breathing dramatically improved after
a nasogastric tube was inserted (after clearing the cervical spine)
to relieve the large volume of gastric air that had rapidly accumu-
lated by air-swallowing during the immediate posttraumatic period
of stress.
further injury through judicious and expeditious han-
dling of obvious and probable injuries are all of primary
importance.
In general, the tendency is to extrapolate data from inves-
tigations of the adult’s response to injury to more specifically
understand and interact with the child’s situation. However,
such comparisons are not always reasonable or accurate.
Adult patients usually have a marked increase in metabolic
activity following trauma. In contrast, pediatric patients often
demonstrate little change from preinjury enzyme or colla-
gen breakdown activity. The normal metabolic rate in chil-
dren is high because of the relatively increased activity
during growth. A slight increase in the biochemical response
may be all that is required in the injured child, even after
multiple trauma, to achieve the hypermetabolic condition
necessary for tissue survival acutely and during the days
immediately after trauma.
Almost 50% of deaths that occur during childhood, from
ages 1 through 14 years in the United States, are the result
of major trauma.109 This compares to approximately one
death in 12 persons (from injury) in the total population. A
similar situation for children exists in most industrialized
nations. In contrast, childhood death in underdeveloped
countries is more likely to be due to malnutrition or infec-
tion than trauma.
Traumatic death, hopefully, may be avoided by astute
observation, diagnosis, and care in the areas that are most
3. The Child with Multiple Injuries
likely to cause dire consequences: acute respiratory failure,
airway obstruction, tension pneumothorax, misdiagnosed or
inadequately treated intraabdominal or intrathoracic bleed-
ing, and changing brain injury due to epidural or subdural
hematoma.5,220,244 Hypoxia and shock are also potential
causes of death and are equally avoidable with proper care.
Sepsis may supervene in the traumatically immunocompro-
mised child.83 Garcia et al. found 14 deaths among 33 chil-
dren with rib fractures. The mortality rate for 18 children
with both head injury and rib fractures was 71%.97 Scholer
et al. showed that death from injury was more likely if the
child was born to a mother who had less than a high school
education and was multiparous.220
The death of an otherwise normal child is always a
great tragedy.191 However, crippling injuries (extremity and
head) and the resulting need for rehabilitation may have an
even greater economic and labor-intensive effect on our
health care system than a child’s death. More than 100,000
children are permanently impaired annually in the United
States by various accidental injuries.47,116,127,212,243 Another
200,000 are temporarily impaired. The ability to cope
with these individuals and to institute changes directed at
avoiding the injurious mechanisms becomes increasingly
important.47,68,72–74,85,95,102,126,165,170,216,234,239
The adjustments (often changing because of growth) to
severe disability and the child’s conceptualization of himself
or herself as an incomplete individual may overwhelm the
child or adolescent.16 To counteract this, appropriately
trained individuals must participate in the process of reha-
bilitation back into the previous social milieu.
The expenditure of resources and personnel, along
with the economic loss from work potential of the child
and any caretaker (parent) who must alter his or her life style
to care for the child acutely or chronically, especially
when the injured child is seriously handicapped, may be
enormous when compared to the cost from similar adult
injuries.129,164
The most common injuries to the child involve blunt
(nonpenetrating) versus open (penetrating) injuries. At
least 90% of significant (i.e., life-threatening) injuries are
blunt. These blunt injuries particularly involve head injuries.
The evaluation of such a patient, who is often comatose
during the acute hospitalization phase, presents a distinct
problem of communication, especially the absence of
response to pertinent questions.
Children often sustain injuries without external evidence
of trauma. The flexibility of the pediatric skeleton (cranium,
rib cage, pelvis) permits significant inward distortion and
energy transmission to internal organs. A common clinical
scenario is a child presenting with physical findings of a pul-
monary contusion, but without overt rib fracture.
The approach to any child with multiple injuries necessi-
tates a detailed approach that evaluates all organ systems
actually or potentially injured as problematic areas. It is
equally important to institute prompt specific therapy, often
as rapidly as possible.
In addition to the care of life-threatening problems, the
treating physician or physicians must also be careful not to
worsen injuries that are stable at the time of arrival in the
emergency room. In particular, great care must be taken to
avoid changing a child who is neurologically intact with a
Initial Response
potentially unstable spine injury into one who is paraplegic
or quadriplegic for the rest of his or her life.
Initial Response
Initial care at the accident scene may be critical to sur-
vival.82,96,114,151,194,203,222,236 The first steps are to establish an
airway, maintain oxygenation and immobilize the cervical
spine. Children under 6 years usually require a special immo-
bilization board to avoid relative flexion of the head (see
Chapter 18). External or possible internal bleeding should
be assessed and replaced with intravenous crystalloid
(Ringer’s lactate) while the child is being transported.
Because intravenous access can be difficult in a child, alter-
native methods such as intraosseous fluid infusion may be
effective.86 No adverse effects on the immature skeleton have
been found in animal models,124 although complications
that include growth arrest, compartment syndrome, and
osteomyelitis have been reported.38,217 The intraosseous
catheter should be removed within 24 hours to decrease the
risk of sepsis.
Maintenance of blood pressure is extremely important.
Because children usually sustain blunt rather than lacerating
trauma, any extensive blood loss is likely to be internal. Vis-
ceral injury and pelvic and femoral fractures (Fig. 3-2) are
the most likely sources of such internal bleeding. Initial and
subsequent fluid management requires attention to several
important factors. First, fluid must be carefully restricted if
there is a serious head injury. Second, excessive fluid replace-
ment may cause fluid space shifts that can lead to decreased
FIGURE 3-2. Fracture of the distal femur in a skeletally immature
Nyala antelope. Extensive hemorrhage (arrows) is evident anterior
and posterior to the fracture.
71
arterial oxygenation from interstitial pulmonary edema.
This situation is likely if there is thoracic trauma or pul-
monary contusion. Third, excessive fluid may also contribute
to compartment syndrome, either specific or generalized.
Airway
The assessment and stabilization of the airway is the initial
priority in the injured child.159,185 A child with a partially
obstructed airway may appear anxious, agitated, confused,
or somnolent. The oropharynx should be quickly and care-
fully examined for vomitus, blood, or foreign material, which
should be removed with suction or forceps. The airway
obstruction may be anatomic, especially in a child with head
injury, obstructed by the tongue or excessive neck flexion.
The jaw thrust maneuver may be used, provided the cervical
spine is stabilized. Oral and nasopharyngeal airways are not
routinely used acutely in children. They may be counter-
productive by causing gagging and vomiting. If the child
cannot spontaneously maintain an airway, or the Glasgow
Coma Score is 8 or less, intubation is usually essential.
The child’s trachea is relatively short, so it is easy to
perform right mainstem bronchus intubation.52 Auscultate
the chest to avoid this complication. Tracheotomy or cori-
cothyroidotomy may be necessary, especially if significant
facial injuries are present or if prolonged intubation be-
comes apparent.29,140,190
Adran and Kemp studied serial lateral radiographs of 100
children 6 months to 5 years of age.2 The component parts
of the airway were situated at a higher level relative to the
cervical vertebra than they are in the adult. Adult positional
relationships seem to be reached at around 6 years of age.
More recently Auringer et al. showed that magnetic reso-
nance imaging (MRI) was an excellent method for assessing
the vagaries of pediatric airway and any significant congen-
ital variations or malformations.8
Significant anatomic differences exist in the child’s
airway.52,69 The tongue is relatively larger in proportion to
the overall oral cavity. The epiglottis is shorter and more
flexible, which may make visualization of the vocal cords and
intubation more difficult. The volume of lymphoid tissue in
the pharynx may be twice as much as an adult. Tonsils and
adenoids may contribute to airway obstruction. The trachea
is shorter and more anteriorly located. The larynx is located
higher in the neck, compared to the usual cervical reference
vertebra. This may affect the position of the head that is
necessary for endotracheal or nasotracheal intubation.115
The tracheal diameter, usually the size of the nailbed of the
child’s little finger or external nares, is easily obstructed by
mucosal edema, blood, vomitus, or a foreign body.
Circulation
Establishing an intravenous access line is not always easy in
a child. Excessive subcutaneous fat may make vein location
difficult. Do not waste time. Cutdowns or central access lines
are effective and often essential alternatives. Intraosseous
infusion through the medial proximal tibial or distal femoral
metaphyses are acceptable sites.38,86 However, anyone using
them should be reasonably familiar with epiphyseal anatomy
to avoid damage to the zone of Ranvier or other physeal
72
areas. After 3 years of age the metaphyses become more rigid
and are more difficult to penetrate.
Shock
Unlike in adult skeletal injuries, shock is an uncommon
accompaniment to most children’s fractures.167,247 It does
occur in some patients with multiple-system injuries, partic-
ularly those resulting from vehicular accidents. Varieties
of shock encountered in children include (1) hypovolemic
shock, (2) septic (endotoxic) shock, and (3) cardiogenic
shock.
Infants have cardiovascular physiologic differences from
those in adults.213 The small heart has restricted capacity to
increase stroke volume. Cardiac output in young children,
especially infants and toddlers, is virtually dependent on the
heart rate.
The normal blood volume in an infant is roughly
100 ml/kg. Accordingly, the loss of a small amount of blood
(e.g., as little as 50–100 ml) may cause a significant reduction
in total blood volume. Mean arterial and systolic blood pres-
sure may remain “normal” and seemingly unaffected by
major trauma until approximately 20–25% of the total blood
volume is lost. Intrinsic physiologic compensation then fails,
leading to decreased blood pressure. Initial clinical signs
of volume depletion include tachycardia, decreased capil-
lary refill, tachypnea, and altered sensorium. Shock (hypo-
volemic) becomes evident by a decrease in systolic blood
pressure (although this may be a late finding). Pain, anxiety,
and hypothermia may mask other physical findings and signs
of hypovolemic shock.
In children, shock following injury is nearly always due to
blood loss. In the pediatric age group, cardiogenic shock
occurs almost exclusively in patients with a congenital car-
diomyopathy. Trauma to the central nervous system practi-
cally never causes shock unless there is significant cranial
separation or vascular disruption of a major vessel leading to
extensive intracranial bleeding (which may be decompressed
through an open skull fracture). Circulatory collapse result-
ing from an autonomic response to fear or pain is usually of
such brief duration that it is no longer present when the
child arrives in the emergency room. Shock resulting from
infection is infrequent and usually is a delayed complication,
partly because of the low incidence of open injuries in chil-
dren (see Chapter 9).
When any type of shock is encountered, treatment must
be specific and prompt. Although children have a much
greater capacity for subsequent recovery, their initial “down-
ward” response to blood or fluid volume loss may be
unexpectedly rapid after a period of apparent stability.
Hemorrhagic shock is characterized by hypotension, tachy-
cardia, restlessness or obtunded sensorium, oliguria, and
cool, pale, or slightly cyanotic extremities. Hypotension is
caused directly by the decreased blood volume, with tachy-
cardia and peripheral vasoconstriction being the compen-
satory mechanisms. Hypotension may lead to inadequate
cerebral and renal perfusion.
Compared with adults, children tolerate a greater degree
of blood loss (as a percent of total fluid volume) and take a
longer time to manifest any overt response to blood loss. It
is rare, with the exception of injuries involving a major vas-
3. The Child with Multiple Injuries
cular or organ laceration, for a child to lose sufficient blood
from a skeletal injury alone to manifest a shock response.
Any child presenting with or developing shock should
undergo complete evaluation to rule out intrathoracic,
intraabdominal, or retroperitoneal injury that might be asso-
ciated with blood loss into an extravascular space or a major
arterial transection in an extremity (e.g., femoral artery lac-
eration with a femoral fracture). Shock decreases renal func-
tion by reduced blood flow. Excessively decreased flow to the
kidneys may lead to progressive renal ischemia and eventu-
ally to renal tubular necrosis, shutdown, and anuria. Proper
management and attention to fluid and electrolyte adminis-
tration early in the course of the shock state usually aids in
the prevention of such renal insufficiency. Again, children
have a better capacity than adults for complete recovery of
renal function, even if they are temporarily anuric from
renal shutdown.
The management of shock should be directed at general
supportive measures as well as at the causative mechanism,
which should be specifically rectified. Immediate steps
include (1) maintenance of an airway; (2) insertion of a suf-
ficiently large intravenous line to allow rapid transfusion of
fluids, blood, or both; (3) maintenance of arterial blood
pressure though early infusion of Ringer’s lactate followed
by properly matched blood or blood substitute; (4) insertion
of a nasogastric tube because of the possibility for air swal-
lowing; and (5) cardiac monitoring. The use of adequate
monitoring equipment (e.g., central venous pressure or arte-
rial pressure lines) and pulse oximetry are also helpful for
following these problems through their acute phases. Large
amounts of blood transfused may be followed by altered
platelet counts.56
Familiarity with normal values is fundamental to the ratio-
nal management of shock. A child’s blood volume relates
directly to body weight and is approximately 40 ml/lb regard-
less of age or size. Pulse rates gradually decrease with age,
the upper limits of normal being 160/min in infants,
140/min in preschool children, and 120/min for older chil-
dren. The normal systolic blood pressure is 80 mmHg plus
twice the age (in years), and the normal diastolic pressure is
two-thirds the systolic pressure. Normal urine output aver-
ages 1 ml/lb/hr in small children, 0.5 ml/lb/hr in older
children, and 0.25 ml/lb/hr in adolescents.
Pain Management
One of the more difficult problems during initial manage-
ment of the multiply traumatized child is to deal with an indi-
vidual who may be confused, distressed, and in considerable
pain. The use of narcotic drugs should be minimized until
head injury and circulatory status are assessed and stabi-
lized.218 Children perceive acute traumatic pain in different
ways from adults, often because it is a new experience.119
Small children may not be able to effectively communicate
the sensation of pain at all.154 Aspects of pain management
and anesthesia, especially as they relate to the management
of musculoskeletal trauma, are discussed in Chapter 4.
Physical Evaluation
Upon arrival at the emergency room or trauma center the
basic ABC (airway, breathing, circulation) approach initiated
Metabolism
at the accident scene should be immediately repeated.77,166,233
Protocols for sequential diagnosis and treatment should be
in place.149,192,214,233,235
Intrathoracic, intraabdominal, intracranial, and intra-
pelvic injuries must be carefully evaluated, as they carry
immense risks for eventual morbidity and mortality. These
evaluations should be part of the trauma team evaluation.
The orthopaedist should ensure that they have been accom-
plished when he or she subsequently evaluates the patient
for appendicular, axial, and pelvic fractures. Open wounds
should be assessed carefully initially and addressed with com-
pression dressings until the child is taken to the operating
room for a more thorough wound evaluation.
Spinal cord function and spinal injury must be carefully
assessed, and more than once, as progressive neurologic wors-
ening may be an indication for the immediate inception of
treatment.28,105,199,208 Neurovascular function out to the hands
and arms must be carefully evaluated. Aberrations require
more detailed studies to rule out vascular or neurologic
injury. To avoid missed injuries the orthopaedist should per-
sonally examine any arm or leg splinted by the primary
responders or emergency room personnel.
Chest Trauma
Blunt trauma to the chest is the most common cause of chest
injury in the pediatric age group.22,75,186,228 Stabbing and
gunshot wounds are becoming more common in the pedi-
atric age group, especially in the urban environment. Chest
injury may be recognized by external evidence of the pene-
trating injury or a history of impact to the chest associated
with splinting or pain during respiration.
A flail chest is the paradoxical motion of the chest wall
after multiple rib fractures. This injury is potentially fatal and
should be treated with positive-pressure ventilation before
hypoxia supervenes or complications such as pneumonia or
atelectasis develop.66
If positive-pressure ventilation is necessary following a
penetrating injury, a small lung laceration may lead to a
tension pneumothorax. Judicious use of a chest tube and
reexpansion of the lung may be necessary.
Hemothorax is usually relatively benign in the child. Vir-
tually all patients can be treated conservatively with chest
tube drainage. Most bleeding is due to chest wall vessels.
Significant or continuing bleeding from the tubes should
arouse suspicion of injury to a major vessel. Fractures of the
first and second ribs increase the risk for major vascular
injury. Look for widening of the mediastinum on the
chest film.
Cardiac injury may result in cardiac tamponade. Disten-
sion of neck veins is highly indicative of the problem. Imme-
diate pericardiocentesis is done, followed by thoracotomy.
Injury of the upper six ribs is usually associated with res-
piratory problems and complications. Injuries of the lower
six ribs are more likely to be associated with abdominal
injuries. Penetrating injuries below the nipples may involve
the diaphragm and intraperitoneal contents.
Intrathoracic and rib cage injuries are discussed in more
detail in Chapter 13.
73
Abdominal Trauma
Abdominal injuries are most often due to shear forces, such
as being run over by the wheels of a tractor, bus, or auto-
mobile.182 Blunt abdominal injury in the child is especially
difficult to evaluate.25,46,54,65,67,88,131,132,200,215 Poorly fitting seat
belts are another mechanism of abdominal injury, especially
in conjunction with spinal injury.125,208 Shear forces often
cause devitalizing injury to the subcutaneous tissue and skin.
Major defects may require myocutaneous flaps for closure.
Seventy percent of liver injuries are innocous enough not
to require drainage.54,142 Hepatic vein injuries frequently
bleed massively.14
Until recently splenectomy had been the accepted treat-
ment for severely traumatized spleens, but splenectomy may
impair immunocompetence. This especially affects the clear-
ance of particulate antigens, production of opsonins, and
the elicitation of antibody response to blood-bone antigens.
This may lead to overwhelming septicemia when children
are exposed to encapsulated microorganisms (e.g., Pneumo-
coccus).91 Current teaching is to salvage the spleen whenever
possible.54,64,78,128 If splenectomy is necessary, the patient
should be immunized with pneumococcal vaccine.
A compression injury to the pancreas may cause leakage
of activated pancreatic materials into the retroperitoneal
space, beginning an autodigestive process. This deep area is
difficult to assess by physical examination. Documentation of
solid organ injury is probably best achieved by computed
tomography augmented by appropriate contrast media.
Abdominal and intrapelvic injuries are discussed in more
detail in Chapters 13, 18, and 19.
Metabolism
The importance of the severity of a child’s orthopaedic
trauma relative to metabolic alterations is evident when con-
sidering that, in terms of tissue injury, a fractured femur
(which invariably includes extensive, concomitant soft tissue
injury, hemorrhage, and third-space fluid loss) may be com-
parable to a third-degree burn. Metabolic management of
the child with any pattern of severe skeletal trauma must
encompass the complexities of immobilization, surgery,
management of other injuries (nonskeletal), and infection.
The management must be directed at providing metabolic
components sufficient to prevent end-organ failure and
enhance tissue healing. The child’s response to injury is
through protein catabolism to produce glucose, with the
brain being the major terminal oxidation site for glucose.
Protein catabolism is activated primarily to continue and
protect central nervous system function. This catabolic state
and the concomitant negative nitrogen balance may con-
tinue for weeks after the acute injuries. The length and sever-
ity of the catabolic state appear to be intimately related to
the severity of the injury. The catabolic state may adversely
affect the rate of callus formation and fracture healing.
To provide the optimal metabolic environment for healing
multiple fractures, adequate protein and caloric intake must
be maintained. Most pediatric trauma patients can be fed
orally. Occasionally, however, a temporary feeding or gas-
74
trostomy tube or total parenteral alimentation is indicated
in children with multiple posttraumatic complications or sec-
ondary anorexia.84 The use of parenteral nutrition through
central venous lines in severely traumatized children may be
helpful for providing essential additional metabolites for
healing. The requirements for protein and caloric intake
vary greatly with the age of the child, previous nutritional
status, and extent of trauma. Therefore monitoring elec-
trolytes and liver functions becomes appropriate.
Major trauma primes and activates polymorphonuclear
neutrophils (PMNs) within 3–6 hours of injury.26,81,179 This
priming by the generation of extracellular, cytotoxic super-
oxide anions (O2-) contributes to an excessive inflammatory
response that may precipitate multiple organ failure when
there is a subsequent stressful event (e.g., an operation or
delayed hemorrhage).
The response to trauma begins in the immune system at
the moment of injury. There is activation of macrophages
and production of proinflammatory mediators in the
wound. In the microcirculation activation of endotheial cells
and blood elements is evident and capillary leakage. These
processes are potentiated by ischemia, impaired oxygen
delivery, and the presence of necrotic tissue, each of which
exacerbates the inflammatory response. These stimuli acti-
vate the cytokine system as a final common pathway to
develop the systemic inflammatory response syndrome.113
Respiratory Distress Syndrome
Posttraumatic pulmonary insufficiency, a major cause of
death in adults, is less frequent in pediatric patients. Prompt
diagnosis on the basis of clinical and laboratory data is nec-
essary to prevent the complications of pulmonary failure.
Such problems may be managed with endotracheal intuba-
tion and aggressive positive-pressure ventilation on a volume
respirator.
Constant awareness and anticipation of pulmonary insuf-
ficiency following musculoskeletal injury may be critical to
the care of these children. Alberts and colleagues studied res-
piratory distress after major trauma and particularly exam-
ined the predictive value of blood coagulation tests.4 These
studies were done only in adults. As such, their applicability
to children is uncertain. They found that the most sensitive
indicator of adult respiratory distress syndrome (ARDS) after
injury was a decreased platelet count, although such a
parameter would obviously be affected by blood loss and the
volume of any blood transfusion. Such evaluations should be
assessed carefully in children.
Steroid use (usually for head trauma) may be associated
with a higher risk of pneumonia when there is concomitant
blunt chest trauma.245 Chest and intrathoracic injuries are
covered in more detail in Chapter 13.
Compartment Syndrome
Arm or leg compartment syndromes and their complications
may be a major cause of long-term disability. When a com-
partment syndrome is suspected, appropriate decompres-
3. The Child with Multiple Injuries
sion of the involved compartment or compartments should
be undertaken to prevent long-term complications. This
complication, with its diagnosis and management, is dis-
cussed in more detail in Chapters 10, 14, 16, 23, and 24. The
complication may be missed in obtunded children who
cannot respond appropriately to pain. Overhydration may
also predispose to compartment fluid overload even with
minimal or no skeletal injury. Burke and Kehl described
compartment syndrome following intraosseous infusion in a
4-month-old infant.38
Associated Soft Tissue and
Vascular Injuries
The determination of possible vascular injury to the extrem-
ity is another critical step in the initial evaluation of the
patient.53,188,223,227 Injury with profuse bleeding and fractures
or dislocations that have a high risk of vascular injury should
be assessed appropriately, regardless of the presence of
peripheral pulses. An arteriogram or Doppler study becomes
especially important in children with suspected popliteal
artery damage following displaced epiphyseal fractures or
dislocation about the knee.134,178
Severe soft tissue injuries associated with open fractures
are usually the result of high-energy trauma. The external
fixator is especially helpful for stabilizing the fracture while
concomitantly allowing access to the soft tissue injury (see
Chapters 4, 9). In the case of vascular injury needing surgi-
cal repair, bone stabilization is often needed, particularly in
children with associated trauma. Children tolerate these
devices well, as they also do with leg-lengthening procedures.
The external fixator also permits early mobilization of the
multiply injured patient with otherwise unstable fractures,
thereby reducing possible metabolic and pulmonary
morbidity.238,240
Rhabdomyolysis should be sought in the presence of any
soft tissue crush injury.198 Early recognition and treatment
may deter subsequent renal consequences. As many as one-
third of patients sustain acute renal failure.
Treatment of fractures or dislocations in children rarely
must be done acutely unless there is a disruptive effect on
blood flow (e.g., knee dislocation with loss of peripheral
pulses). Accordingly, fractures and locations usually can be
treated in a normal manner, as soon as the child’s overall
condition allows one to do so.
Imaging Studies
Once the child is stabilized diagnostic imaging is instituted.
An obvious head injury should lead to subsequent cervical
spine evaluation. Because many car restraints are not dif-
ferentially sized for specific-aged children, whiplash-type
injuries may adversely affect even the restrained, resilient
child.3 A lateral cervical spine film can reveal most fractures
and dislocations. Be certain that C7-T1 is readily evident.
Missing an unstable injury at this level may affect a neuro-
logic injury. The evaluating physician must be aware of
Orthopaedic Injuries
variations, such as cervical subluxation, that are normal vari-
ations in children (see Chapter 18). Another area to assess
carefully is the thoracolumbar junction, as this area may
exhibit subtle disruption.125,208
Computed tomography (CT) scans have evolved into an
important adjunct for the evaluation of head, intraabdomi-
nal, and intrapelvic trauma.18,141 These studies allow evalua-
tion of bleeding and an estimate of blood loss. With the
emphasis on nonoperative approaches to spleen and liver
injuries, the CT scan allows appropriate serial evaluation and
assessment of change.
The MRI scan has a particular role in evaluating spinal
cord injury and the search for occult injury. When an area
of probable fracture is initially evaluated by routine radiog-
raphy and found to have “no evidence of injury,” despite
physical findings (e.g., hemorrhage, effusion) highly sug-
gestive of injury, an MRI may reveal an occult fracture of a
physis or intraosseous bone bruising (i.e., trabecular bone
fracture with hemorrhage).
Ultrasonography has evolved into a useful method for
detecting intraabdominal bleeding. It may also be used to
evaluate joint injuries. The technique requires significant
familiarity with the methods and interpretation of the
results.
Radionuclide scans are most useful to detect occult injury
in the abused child. They may be beneficial in the comatose
child as well to detect fractures that are stable (e.g., torus
fracture) but should be diagnosed and treated (see Missed
Fractures, below).
The usefulness of various diagnostic imaging studies to
study specific musculoskeletal injury is discussed in detail in
Chapter 5.
Orthopaedic Injuries
Initial management must address any life-threatening,
nonorthopaedic injuries first. The orthopaedist’s initial role
often is to splint any probable orthopaedic injuries while
other appropriate resuscitative and diagnostic tests are
undertaken.
Buckley and coworkers studied 3472 children hospitalized
for acute traumatic injuries.36,37 Of this group, 805 patients
had a total of 953 fractures and dislocations. Pedestrian
accidents and falls each accounted for 34% of the muscu-
loskeletal injuries, and motor vehicle accidents comprised
13%. The fractured bones were the femur (32%), humerus
(16%), tibia/fibula (12%), ankle/foot (13%), and radius/
ulna (8%). Open fractures comprised 9% of the fractures.
The mortality rate was 3% overall. However, when specifically
broken down, the mortality rates for patients with clavi-
cle/scapula fractures was 11%, spine fractures 16%, and
pelvic fractures 11%. Other authors have also described
the significance of a first rib fracture to suboptimal
outcome.97,117,210
Loder reviewed 78 children with multiple trauma. There
were 137 musculoskeletal injuries,160 with 47 complications
(of overall treatment) in 27 children. Rapid stabilization of
the fractures was associated with fewer complications than
when the stabilization was done after 72 hours.
75
Initial Treatment
Initial fracture treatment should be based on the child’s
overall condition. Stabilization of obviously injured arms,
legs, or spine should be done rapidly with molded splints or
other devices.59,238 Any dislocation with apparent neurologic
or, particularly, vascular compromise should be reduced and
splinted. If the child is likely to be comatose, external fixa-
tors may be applied using regional blocks or local anesthe-
sia if the child is not a suitable candidate for general
anesthesia.92,100,168,169,197,237 This decreases the possibility of
subsequent deformities and complications such as fat
embolism.93,211,237 Open fractures should be judiciously
treated for potential risks such as infection.43,62 This latter
risk is addressed in more detail in Chapter 9. As conditions
stabilize, children with temporarily splinted fractures may be
taken to the operating room for more definitive fracture
treatment.197,207
Missed Fractures
A constant concern during the initial evaluation and hospi-
talization of any injured child is a missed soft tissue or skele-
tal injury.46,79,80,149,156–158,163,180,195 These occult injuries rarely
contribute to any life-threatening situation. However, lack of
diagnosis and, if necessary, the institution of proper treat-
ment may lead to deformity, embarrassment, or frustration.
Furnival et al. reviewed 1175 pediatric trauma admis-
sions.94 Altogether 50 patients had 53 injuries with a delayed
diagnosis; 38 were missed fractures. The delay in injury diag-
nosis ranged from 1 to 55 days. Altered treatment was nec-
essary in 68%.
Ward and Nunley reviewed 111 multiple-trauma
patients.240 There were 401 orthopaedic injuries, of which
24 injuries (6%) were not initially diagnosed in 20 patients;
70% of these occult injuries were eventually diagnosed by
physical examination and plain radiographs. Only 30% of
the fractures required sophisticated imaging techniques
for diagnosis.
Heinrich et al. undertook whole-body technetium scans to
search for undetected fractures in 48 patients with multiple
trauma or head injury.120 Radiographs had already been
made in all areas of clinically suspected or obvious trauma.
Follow-up films were subsequently obtained for all suspicious
areas with increased radionuclide activity. Among these
areas, 42 were detected in 18 skeletally immature patients
and 52 in 12 skeletally mature patients (<22 years). A total
of 19 previously unrecognized fractures were diagnosed
definitively with subsequent radiographs. Only six of the
patients required a subsequent cast or splint for the occult
injury.
Juhl and coworkers described a study assessing 15,806
patients treated in an emergency department; 783 of
these patients were admitted with orthopaedic injuries.139
Altogether 84 injuries in 83 of these admitted patients were
missed in the emergency department, for a missed injury rate
of 0.5%; in the orthopaedic department 23 injuries were
missed in 17 patients, for a missed injury rate of 2.2%. Juhl
et al. found that reexamination of all patients and matching
radiographs reduced the number of missed injuries signifi-
76
cantly. Almost one-third of the patients had missed finger or
hand injuries. They found that it was important to reexam-
ine all multiply injured patients carefully the day following
admission, especially with regard to the possibility of more
than one injury in an extremity, and that it was more diffi-
cult to diagnose less obvious (occult) injuries in children.
Assessment Rating
Improvements in the care of multiply traumatized patients
requires a means of assessing outcome on a reasonably com-
parative basis, whether the study is intra- or interinstitu-
tional.6,9,10,27,174 To this end a number of trauma scoring
systems have evolved, many of which have been readily mod-
ified for use in children.7,15,70,71,89,144,145,175,184,189,205,231,232,241
Beattie found that there were significant deficiencies when
coding ICD-9 of childhood injuries.17 They included inaccu-
rate codes for diagnosis and an insufficient number of diag-
nostic codes for multiply injured children. These factors
adversely affected the generation of meaningful statistics for
efforts directed at accident prevention and treatment–
outcome comparisons.
Christoffel et al. excerpted the results of a conference on
standard definitions for childhood injury research.50 Their
appendix is an excellent summary of parameters necessary
to undertake detailed research on childhood injury.
Pediatric Trauma Score
The appropriate triage of the multiply injured child man-
dates not only accurate initial assessment but also an appre-
ciation of those differences in pediatric physiology affecting
potential morbidity. Evaluation is based on several parame-
ters to create the Pediatric Trauma Score (PTS), which is out-
lined in Table 3-1.
The first obvious differentiating feature in the pediatric
trauma patient is size. The primary purpose of size catego-
rization is to center attention on the very small child (-1)
who, by nature of an increased body surface/volume ratio
and potentially limited physiologic reserve, is at greater risk
of morbidity and mortality for a given injury than older,
larger children (+1) and adolescents (+2).
Airway status is another vital factor, primarily because of
its central importance to survival. The adequate and correct
TABLE 3-1. Pediatric Trauma Score
Assessment factor +2
Weight (kg) >20
Airway Normal
Systolic blood pressure (mmHg) >90
Neurologic Awake
Open wound None
Skeletal injury None
Derived from Tepas et al.231,232
See text for detailed explanation.
3. The Child with Multiple Injuries
initial treatment of airway problems is also important to the
management of other organ injuries. This assessment system
considers not so much the status of the airway on the first
evaluation as much as a composite of the airway status and
the initial management required to protect it. Specifically,
the child whose airway is completely within normal limits
and who requires no additional supportive measures is cate-
gorized as a +2. Any child whose airway is partially obstructed
and who requires simple measures for protection, such as
head positioning, oral airway, or an oxygen delivery mask, is
classified as a +1. The child whose airway requires a more
definitive management that demands degrees of expertise
such as intubation, cricothyroidotomy, or other invasive pro-
cedures, is placed in a -1 category.
The child’s systolic blood pressure provides an initial indi-
cation of cardiovascular status. A systolic blood pressure of
90 mmHg or more suggests that the circulating volume is
usually adequate. However, a child whose systolic blood pres-
sure is 50 mmHg or less, regardless of size, is considered to
be progressing to hemorrhagic shock. A child whose blood
pressure falls between 90 and 50 mmHg may be in the early
stages of hypotension or hemorrhage or, in some circum-
stances, has a blood pressure appropriate for age. Such a
high-risk group is scored as +1. In the absence of adequately
sized blood pressure cuffs, the blood pressure assessment
may be replaced by being able to palpate the pulse at the
wrist (score +2), finding a pulse in the neck or groin (+1),
or finding no palpable “major” pulse (-1).
The evaluation of a child’s central nervous system is based
specifically on the level of consciousness. Although the
Glasgow Coma Scale (Table 3-2) is an effective initial neuro-
logic assessment tool, the specific level of consciousness is the
most important factor for determining the initial neurologic
status. The child who has sustained no loss of consciousness
and is fully awake is graded as +2. Any child who is obtunded
or who has sustained a previous loss of consciousness (no
matter how transient) is graded +1, indicating potential risk.
A child who is totally nonresponsive is graded -1.
Because of the frequent association of skeletal injuries
with blunt trauma in pediatric patients and their additive
effect on overall morbidity, an assessment of both the skele-
tal and cutaneous systems should be included in any scoring
scheme. The child who has no evidence of a fracture is
graded +2. A child with a single closed fracture is graded +1.
A child who has multiple closed fractures or any open frac-
ture is categorized -1.
Rating for factors
+1 -1
10–20 <10
Maintained Cannot be maintained
50–90 <50
Obtunded Comatose
Minor Major
Closed Open/multiple
Head Injury
TABLE 3-2. Glasgow Coma Scale
Parameter
Eyelid opening (E)
Spontaneous
To verbal stimulation only
To pain stimulation only
None
Motor response (M)
Responds (obeys) appropriately
Localizes to stimulus (nonverbal)
Withdraws reflexively
Abnormal flexion
Extensor posturing
None
Verbal response (V)
Oriented
Confused
Inappropriate
Incomprehensible
None
GCS = E + M + V (range 3–15).
The child who presents with no evidence of external
trauma is graded +2, and the child who presents with abra-
sions or minor cutaneous injuries is graded +1. The child
who presents with any penetrating injury, regardless of loca-
tion, or with a major avulsion or laceration is graded -1.
The Pediatric Trauma Score (PTS) thus becomes the arith-
metic sum of the specific scores assigned to the aforemen-
tioned categories. It may range between -6 and +12; and it
provides a comprehensive assessment protocol, especially
for the comparative assessment of outcomes after treating
trauma in pediatric patients.
Pediatric Intensive Care
Once the severely injured child is appropriately assessed,
the child should be referred to an internal unit (e.g.,
pediatric intensive care unit) or transferred to an ex-
ternal center that has the capacity to handle the special
requirements of pediatric intensive or comprehensive
care.30,55,110,111,115,137,138,187,193,202,204,219,242 Although each individ-
ual pediatric injury may not cause significant increase in the
risk of mortality, the combination of injuries, especially if less
than adequately or even incorrectly handled, may signifi-
cantly increase the morbidity, length of hospitalization, and
long-term rehabilitative needs. Effective triage of the injured
child thus requires consideration of both morbidity and
mortality.
The admission of children to non-pediatric-oriented facil-
ities may contribute to the failure to diagnose fractures and
dislocations. The organization of regional trauma units with
sophisticated laboratory and monitoring facilities has greatly
enhanced the care of the multiply injured pediatric patient.
Problems during the postinjury period, specifically with
monitoring pulmonary function and extremity vascular per-
fusion, play a critical role in morbidity and mortality.
77
Critical care of the multiply injured child should be an
effective extension of aggressive resuscitaton, stabilization,
Score and definitive care. During the hours and days following an
acute injury, initially unnoticed lesions (e.g., occult frac-
4 tures) may emerge, secondary organ dysfunction may
3 develop, and complications of primary injury or initial man-
2 agement may supervene.233
1 Criteria for a defined pediatric trauma center have
been defined by the American College of Surgeons.74,112
6 Essentially, a pediatric general surgeon must be in the
5 hospital at all times. He or she heads the trauma team
4 and is first to evaluate the child. Because these centers
3
are few the alternative of treating children in adult level I
2
1 trauma centers has been assessed.147 The results seem
comparable.60,90,155,162,184,193,209,225
5
4
3 Head Injury
2
1 Head injury is one of the leading causes of death in children
older than 1 year of age and is the primary cause of long-
term neurodevelopmental morbidity in this patient popula-
tion.51,122,123,161,224,230 In infants less than 1 year of age it is the
third leading cause of death.40,107,229 Many studies suggest that
traumatic injury to the developing brain has basic mecha-
nisms of response and recovery that differ, often profoundly,
from those of the mature brain.148 Similarly, the ability of the
developing brain to recover from significant injury differs
from the mature brain.
Almost two-thirds of head injuries in children are caused
by non-motor-vehicle accidents, with about 50% due to
falls.246 Approximately two-thirds of head-injured children
experience an episode of transient loss of consciousness, and
one-third have a period of coma at or shortly after the acute
injury.42
It has been estimated that 195 of 100,000 children (aged
0–14 years) and 295 of 100,000 adolescents and young adults
(aged 15–24 years) are hospitalized annually for traumatic
brain injury.136 Increasing attention to advanced techniques
for intensive care has significantly increased survival for
these patients compared to 10–15 years ago. Generally, chil-
dren and adolescents have a better outcome from severe
traumatic brain injury. However, children under 7 years of
age may fare worse than older children despite similar types
and severity of injury. Head injuries may have a more global
effect on the younger brain.
There are significant differences in the diploic and dural
vasculature of the infant compared to a child of 8–10 years.49
These differences may make extradural bleeding more likely
in nonaccidental head trauma. This pattern of bleeding has
a high mortality rate, despite decompression.
Hypovolemic shock is widely believed not to be the result
of head injury; therefore other sources of bleeding should
be sought. The very young are a notable exception, as an
infant may have a significant intracranial or subgaleal
hemorrhage.
Glasgow Coma Scale
Head injury may be evaluated with the Glasgow Coma Scale
(GTS) (Table 3-2). The use of the GTS is restricted in young
78
children with limited or no verbal development.171 Children
with a GTS score of less than 8 have a significantly compro-
mised chance of survival. The GTS should be repeated,
usually within an hour of the initial evaluation, which may
help assess progressive intracranial change.
Diagnostic Imaging
In general, skull films in children correlate poorly with the
presence or absence of intracranial pathology.118,173 In several
large studies fewer than 10% of patients having skull films
had obvious fractures. Furthermore, most of the patients
who had fractures did not have posttraumatic cranial lesions.
In contrast, many with serious intracranial pathology did not
have evidence of skull fracture. Thus management of head
injury should not be based on the presence or absence of a
skull fracture. CT scans with bone windows may demonstrate
clinically significant osseous cranial injury more effectively
and may also show concomitant soft tissue injury (e.g.,
subdural hematoma, cerebral contusion). Nonetheless,
concepts of management based on appropriate neurologic
assessment appear to be the most reliable approach.
The developing skull, especially in an infant, may be
deformed substantially without sustaining an obvious fracture
when struck or compressed. The elasticity of individual
cranial bones, the sutures, and chondro-osseous interfaces in
the basilar region (vestiges of the occipital somites) allow
injury without radiographic evidence of fracture. Typical
linear skull fractures do not occur until after 3 years of age.
Bell and Loop evaluated the “utility and futility” of
radiographic skull examinations after trauma.19 They cate-
gorized patients as high-yield (92 fractures, 1065 radi-
ographic studies) or low-yield (1 fracture, 435 radiographic
studies) groups. Significant factors in the high-yield group
included more than 5 minutes of unconsciusness, more than
5 minutes of retrograde amnesia, vomiting, palpable bony
malaligment, bilateral black eyes, eardrum dislocation, irreg-
ular breathing or apnea, anisocoria, and presence of a Babin-
ski reflex. They thought that the low-yield group, by not
undergoing immediate skull radiography, could potentially
save millions of dollars. Leonidas et al. duplicated the study
of Bell and Loop in children.153 They found that the high-
yield criteria for adults are poor predictors of skull trauma
in children. Important criteria additional to those of Bell
and Loop included cephalohematoma, drowsiness, and age
less than 1 year. Bleeding from the ear (Battle’s sign) was also
important.
Brown and Minns reviewed nonaccidental head injury
(whiplash shaking injury).32 They noted that skull fractures
may indent, causing a depressed “Ping-Pong ball” fracture.
The contiguous brain tissue may be easily depressed, causing
severe local bruising and hemorrhage.48,57 Skull fractures do
not heal by exuberant callus, which makes dating an injury
difficult. A skull fracture normally heals in 2–3 months and
disappears on a skull film by 6 months. In small infants,
however, the fracture site may not heal, instead forming a
growing skull fracture. In a small infant the compressibility
of the skull may cause a bursting fracture with failure at the
normal suture lines, similar to a physeal injury in a long
bone. Such an injury pattern is difficult to diagnose radi-
ographically. Most true accidental skull fractures are linear.
3. The Child with Multiple Injuries
A nonaccidental fracture mechanism is more likely if the
fracture line branches, is stellate, crosses suture lines, is bilat-
eral, is multiple with separate fractures, is more than 5 mm
wide at presentation, or expands as a growing fracture.
Growing skull fractures, or cephalohydroceles, are typically
nonaccidental.152 They are usually caused by a dural tear,
entrapment of dura between the fracture sides, pulsation of
the dura, or formation of a pseudarthrosis (i.e., a neosu-
ture). A phenomenon unique to children is the enlarging
leptomeningeal cyst.121 Separation of fractured bone edges
is wider in children than in older individuals. It results in a
dural tear with arachnoidal/cerebrospinal fluid herniation.
Hydrocephalus is also more likely in young patients because
of their limited resorptive capacities.
Diastatic fractures with wide lines are more common in
infants because of the membranous bone. Concomitant tears
in the dura or arachnoid (or both) may lead to a subsequent
leptomeningeal cyst, with enlargement of the bony defect at
the original fracture site. Basal skull fractures are considered
open injuries because of the frequent involvement of adja-
cent sinuses, mastoid chambers, and the ear. The use of
prophylactic antibiotics is still controversial regarding their
statistical efficacy.
Any patient whose head is struck with sufficient force
should be considered to have sustained a severe enough
mechanism of injury to also result in a cervical fracture,
subluxation, or dislocation. Accordingly, the neck must be
immobilized until an adequate assessment has been carried
out. In an alert patient, questioning and a responsive physi-
cal examination are possible. With altered levels of con-
sciousness or signs or symptoms suggestive of spine or spinal
cord injury, anteroposterior and lateral cervical films usually
constitute minimum screening. C7-T1 must be evident on
the lateral view. CT or MRI scans may be necessary to resolve
the issue.
Laham et al. studied isolated head injuries versus multiple
trauma in pediatric patients to determine the incidence of
cervical spine injury.150 They divided the patients into low-
risk and high-risk groups. The low-risk patients were capable
of verbal communication and did not describe neck pain. No
patient in this group had a neck injury. High-risk patients
were incapable of verbal communication or reported neck
pain (all patients under 2 years of age were considered high
risk). The latter group had a 7.5% incidence of cervical spine
trauma. Laham et al. thought that children with isolated
head trauma carried the same risk of cervical injury as the
multiply injured child.
When the head and neck are immobilized, care must be
taken to not inadvertently flex the neck because of the rela-
tively large size of the head. If necessary, the head can extend
beyond the mattress, or the immobilization board can have
a circular cutout to accommodate the head (see Chapter
18).
The commonest initial CT finding in head-injured chil-
dren is bilateral diffuse cerebral swelling.33,34,206 Studies
suggest that this swelling is due to cerebral hyperemia and
increased blood volume, rather than interstitial edema.206,248
MRI also offers an excellent method initially to diagnose and
then sequentially follow cranial and intracranial injuries.
Indications for obtaining CT or MRI studies of the skull and
brain are summarized in Table 3-3.
Head Injury
TABLE 3-3. Pediatric Head Injury: Indications for CT/MRI
Depressed level of consciousness upon initial presentation
Focal neurologic physical findings
Penetrating injury; palpable skull deformity
Progressive or increasingly severe headache
Confused or absent memory of injury
Basic difficulty of neurologically evaluating children under 2 years
of age
Obvious indications of basilar skull fracture such as
hemotympanum, nasal cerebrospinal fluid, raccoon eyes,
Battle’s sign
Multiple trauma, variable responsiveness and definite physical
evidence of head injury
Whenever child abuse is suspected (high risk of shaken baby
syndrome)
Treatment
The treating orthopaedic physician must be aware of some
of the basic principles of treating head injuries in chil-
dren.1,130 Fracture of the skull is generally less frequent than
the similar injury in an adult. The prime consideration is not
the presence or absence of a skull fracture but direct or con-
trecoup damage to the brain. In the young infant with an
elastic skull, much of the blow is absorbed by the usually pro-
tective osseous plates and sutures. This elasticity also allows
significant temporary indentation of the skull toward
the brain, with restoration of the contour after “release” of
the deforming force. Despite considerable depression of the
bone, there may be little brain injury. Even the skull of a
child with closing sutures absorbs a good deal of any blow,
transmitting a less injurious force to the brain itself. Fur-
thermore, despite the seeming absence of specific osseous
injury, severe injury to the brain may occur, followed by reac-
tive interstitial swelling. Injuries to the tips of the frontal
or temporal lobes may cause prolonged unconsciousness,
extending to weeks or even months, but usually with complete
recovery in the child. This makes these young patients differ-
ent prognostically from an adult with head injury, a factor
that has significant ramifications relative to the treatment of
any chondro-osseous injuries.
Restlessness, agitation, and confusion may imply lacera-
tion and hemorrhage of the frontal and temporal lobes,
whereas paralysis and deep shock suggest injury to deeper
portions of the brain. Extensor rigidity may be due to com-
pression of portions of the temporal lobes, the cerebellum,
or the brain stem. A child may have momentary uncon-
sciousness, followed by lucid intervals and then a second
period of unconsciousness. This change in responsiveness
suggests subdural or extradural hemorrhage.106,181,226 If the
pupils are fixed, dilated, oval, or contracted or if the child
cannot be aroused, serious brain damage should be sus-
pected.104,172 Intracranial pressure monitoring allows rapid
assessment of significant changes.41
A child with head injury and multiple skeletal injuries is
permitted to assume a comfortable position in bed unless
there is a fracture of the spine. Fractures of the extremities
are splinted initially for comfort and then treated more
definitively as the sensorium clears. Skeletal traction or fixa-
tion may be applied for major fractures (e.g., femoral shaft).
79
Opiates, except codeine, should be avoided; and restlessness
can be controlled by rectally administered aspirin or small
doses of phenobarbital. Lumbar puncture must be under-
taken only after careful evaluation of the child because ele-
vation of pressure as a result of hemorrhage or soft tissue
swelling may cause brain stem herniation.
The major problem with head injury is to control intracra-
nial pressure fluctuations. Movement of a fractured extrem-
ity, especially a femur, usually increases the intracranial
pressure. Accordingly, immobilization is essential (e.g., cast,
splint, skeletal traction). If the condition prevents use of a
general anesthetic, an external fixator may be applied with
local anesthesia. Stabilization also assists in transport for
diagnostic studies.
Blancafort et al. utilized brain stem auditory evolved
potentials (BAEPs) in children with posttraumatic coma.23
They found three groups: The first group had bilateral,
normal BAEPs; and all of the patients had a good to excel-
lent recovery. In the second group, who had asymmetric
BAEPs, 42% had a good recovery, and 29% were moderately
disabled. The third group had loss of BAEPs or responses
only of the seventh cranial nerve and cochlear nucleus; all
patients in this group died.
Depressed skull fragments, even with open fractures or
dural tears, may be replaced in their normal position with
no significant risk of wound infection or osteomyelitis.24 This
measure avoids a second operation for cranioplasty.
Extradural hematomas in children are often peculiar and
unpredictable compared to those in adults. Epileptic
seizures may occur, often within a few hours of injury, a con-
dition referred to as postcontusion epilepsy. Evacuation of
an acute subdural hematoma is a critical factor and should
be done within 4 hours of injury.221
A review of 104 extradural hematomas in children showed
that 57% of the patients had no disturbances in conscious-
ness at the time of injury, and 7% had no disturbances at any
time. In 19% there was no skull fracture. The hematoma was
distinctly localized in 59 children and widespread in 45. With
the exception of the coronal sutures, the sutures did not
limit spread of the hematoma. Altogether 18 patients died,
and in 21 altered motor sequelae were significant.221
Fracture Care
Head trauma adds to the difficulties of acute and prolonged
skeletal traction and casts. Children with altered states of
consciousness following central nervous system injury may
have spastic muscular posturing that requires rigid stabiliza-
tion of fractures. Fractures in children with head injury may
be difficult to control, even in traction.20,21 The child’s ability
to survive and recover from severe head injury makes main-
taining adequate alignment of any fracture critical, regard-
less of the severity of the initial injury. When alignment
cannot be readily or easily maintained by traction, stabiliza-
tion with internal or external fixation is indicated.98 Several
types of external fixator can be applied with relative ease,
even with the patient under local anesthesia; and they are
helpful for preserving the alignment of long-bone fractures
in children. Such external fixation usually allows mobiliza-
tion of the patient out of traction while maintaining osseous
alignment, even in cases involving spastic patients. Internal
80
fixation is rarely necessary in these patients. The risk of infec-
tion at the fracture site complicates open fracture manage-
ment. External fixation allows the continuing treatment of
such soft tissue injury.
Intramedullary nailing of some femoral fractures in chil-
dren has successfully prevented alignment complications
in the brain-injured child. The significant chance of injury
to the vascular supply of the femoral head or to the
trochanteric apophysis markedly increases the risk associated
with this procedure. Closed intramedullary nailing of
femoral fractures in children aged 12–15 years usually pro-
duces excellent results. When the procedure is properly per-
formed, operative trauma and complications are minimal,
and early mobilization is possible.
The postinjury physical problems of a head-injured
patient are similar to those of the child with cerebral palsy,
with some distinct differences. An aggressive surgical
approach to the prevention and treatment of fixed deformity
in these children is much superior to the use of physiother-
apy, phenol blocks, or simple orthoses. Such surgery is rec-
ommended at an early stage of appearance of the problem,
with appropriate postoperative orthotic management and
stable seating.
When subjecting the head-injured child to anesthesia
for fracture management, agents and drugs that increase
intracranial pressure or reduce cerebral oxygen supply
should be avoided. Intracranial pressure (ICP) is increased
by increasing the cerebral blood inflow. Hypercarbia, in par-
ticular, may increase cerebral blood flow. The combination
of nitrous oxide and thiopental sodium reduces cerebral
blood flow and probably decreases cerebral oxygen require-
ments. Elevated ICP is probably the main contraindication
for anesthesia to fix or stabilize orthopaedic injuries.
For indeterminate reasons the child with head injury,
especially if decerebrate, may have enhanced callus forma-
tion and may go on to heterotopic bone formation. It may
relate to elevated serum calcitonin levels.61
Spasticity may be present initially or may develop during
recovery. An inadequately immobilized fracture may severely
angulate. A fracture in a splint or cast may develop skin pres-
sure contact or even necrosis. Untreated contractures may
become permanent deformities.
Orthopaedic care in the child with a head injury should
be predicated on the concept that full neurologic recovery
is likely to occur. Thus failure to treat the orthopaedic
problem is inappropriate.
Posttrauma Care
Although reasonably good to excellent return of motion
function may be associated with head injury, more than
half of children who sustain a head injury have a “health
problem” at the 1-year follow-up.31,35,63,87,103 Fortunately, most
of the problems are minor. In previous studies, headaches
were present in 32% and extremity complaints in 13%.
Cognitive and behavioral sequelae are the most serious
and pervasive long-term impairments. The chance of a com-
plete cognitive recovery diminishes with lengthening coma
and posttraumatic amnesia.201 As many as 40% of children
who are comatose longer than 2 weeks require special edu-
cation. Survivors of severe head injury have a 10–15% risk of
3. The Child with Multiple Injuries
later epilepsy. Children with an open head injury have an
even higher risk (25%). Patients in a coma for more than 6
hours have an incidence of subsequent seizure activity
approaching 50%.
Gofin et al. developed disability scales for childhood and
adolescent injuries.99 Three dimensions of disability were
covered: (1) personal care and daily activities, (2) motor
activities, and (3) communication and sensory activities.
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4
Treatment Concepts
Engraving of a type 1 distal femoral physeal fracture. (From Poland
J. Traumatic Separation of the Epiphysis. London: Smith Elder,
1898)
istorically, the approach to children’s fractures has
H relied heavily on conservatism, with the implication
that the best opportunity for an optimal result is
simply afforded by putting the fragments of the bone in the
same room, avoiding any superimposed surgical trauma, and
allowing natural healing and remodeling to progress unim-
peded.18,140 Although this “philosophical approach” suffices
most of the time, it is an oversimplification in the treatment of
children’s fractures, especially those accompanied by extensive
soft tissue injury.
In particular, in the multiply injured child with life-
threatening injuries, less than optimal alignment may
have to be accepted temporarily until the child’s overall
condition stabilizes.74 Increasing emphasis on the use of
external and internal fixation in affected children should
lead to better initial and subsequent management of the
86
fractures, as well as better overall management of the
patients.20,63,100–102,124,143,164,171,176,196,209,210,216
Until the past 30 years most of the concepts offered to
explain healing of fractures in children were based on infer-
ence rather than demonstrated scientific fact. Among the
accepted premises have been the rapid healing of children’s
bone, remodeling of angular residuals, and overgrowth
to accommodate longitudinal overriding. In too many
instances this has led to a cavalier acceptance of less than
anatomic reduction and the frustration of parents (if not the
child) at the subsequent cosmetic or functional deformity.
We now recognize that there are limitations to these con-
cepts. Although they may be used as the basis for closed treat-
ment of many fractures in children, there must be a more
pragmatic approach to attaining as much anatomic restora-
tion as possible, as is done for adult fractures. A greater
emphasis has evolved utilizing both internal and external fix-
ation in children, a phenomenon that has been accompa-
nied by design changes and modifications that reflect the
differences between the growing and the mature skeleton.
When a fracture overrides, especially if too much overrid-
ing is accepted (e.g., in a casted femoral fracture), periosteal
and endosteal callus play a lessened or compromised role in
fracture healing. The osteogenic potential of these tissues
may be wasted. Union becomes more dependent on the
organization and maturation of the fracture hematoma.
Basics of Fracture Treatment
Fractures in children are more likely to be managed with
closed techniques than are similar injuries in adults.
However, adhering rigidly to the nonsurgical treatment of
children’s fractures may be counterproductive in the severely
injured child and with many specific single injury fractures.
By considering proper indications and utilizing good tech-
nique, percutaneous, internal, and external fixation are
each extremely helpful in attaining and maintaining reduc-
tion, preventing both early and late complications, and
allowing more rapid functional recovery. There may be situ-
ations in which closed reduction, external fixation, and
internal fixation may all be used, simultaneously or sequen-
tially, in a single pediatric patient.
Basics of Fracture Treatment
Because different treatment techniques may achieve
similar outcomes, making the appropriate decision becomes
an important step. An adequate approach should include (1)
a definition of the problem, particularly the complexity of
the fracture and the extent of cartilaginous (i.e., radiologi-
cally invisible) involvement; (2) consideration of options for
treatment; (3) choice of the best alternative for the given cir-
cumstances; and (4) when to change from one treatment
method to another commensurate with either positive or
negative healing responses.
Fractures in children usually result from relatively simple
(low energy) injuries, rather than the complex mechanical
(high energy) forces that frequently cause adult skeletal
injury. Accordingly, methods of treatment are generally
simple, with an appropriate emphasis on closed reduction.*
The basic principle of most fracture reductions, particu-
larly in children, is reversal of the mechanism of injury. It is
axiomatic that if a fracture is produced by an external force,
it should be reduced by making the distal fragment retrace its
steps back to normal. Reduction by this method, however,
depends on the presence of sufficient soft tissue linkages.
Another axiom of fracture treatment is to align the fragment
that can be controlled most easily. Usually the distal fragment
can be controlled, and it should be aligned longitudinally
with the displacing proximal fragment.204 The proximal frag-
ment adopts a position dictated by the variable pulls of the
muscles attached to it. These principles apply whether closed
or open reduction or internal or external fixation is used.
Closed reduction is adequate to maintain normal align-
ment of many fractures in children, in part because the
plastic remodeling of their bones renders good final
anatomic and functional results, even if absolutely accurate
reduction is not attained or maintained. Other fractures,
especially those near the elbow or involving a joint, may
require prompt operative reduction. Much unnecessary
surgery has been performed, sometimes resulting in per-
manent disability, because the treating physician failed to
appreciate the recuperative powers of the child.
Rotational deformities must be corrected. Except in frac-
tures involving joints and epiphyses, absolute anatomic
reduction of the bone fragments is not always necessary and
sometimes should be purposely avoided. Angulation in the
middle third of long bones may be unacceptable and should
be corrected as close to normal as possible. Particularly, in
girls under 10 and boys under 12 years of age, angulation of
fragments near the joints is more acceptable if the angula-
tion is less than 20° and axial within the plane of motion of
the joint. The younger the child, the greater is the amount
of anticipated remodeling. Direct apposition of bone ends is
less important. For example, bayonet or side-to-side apposi-
tion, especially in the mid-femur, may be acceptable (within
anatomic limits) and usually leads to strong osseous union.
After injury the bones of children may grow at an acceler-
ated rate for 6–12 months. Overgrowth is a concomitant
event of many childhood fractures, but it averages only
1 cm or less, depending on the bone involved. Accordingly,
shortening or stressed shortening (telescoping) of more
than 1.5 cm should be carefully addressed. This factor
* Refs. 1,18,27,29,34,39,41,46,48,57,58,71,72,75,85,88,89,92,97,126,138,
140,142,145,156,162,168,169,172,173,175,183,185,194,212,224–226.
87
must be discussed and emphasized with the child’s
parents.
Several biologic factors are the reason internal and exter-
nal fixation has not been utilized as frequently in children
prior to skeletal maturity as it has been in adults. Because
fractures in children usually result from relatively simple
injuries, rather than the complex mechanical forces that fre-
quently cause adult skeletal injury, there is less comminution
of a fracture involving the diaphysis or metaphysis. Many of
the problematic fractures in adults, such as hip fractures and
multiple, comminuted injuries, occur much less frequently
in children. Accordingly, the methods of treatment are gen-
erally simpler when dealing with the disrupted immature
skeleton. The appropriate emphasis is on closed reduction
for a large percentage of fracture patterns when compared
to similar, although not necessarily comparable, anatomic
injuries in the mature skeleton. About 20% of skeletal
injuries prior to skeletal maturity involve the physis, a struc-
ture obviously not found in the normal adult. Most growth
plate fractures, which principally involve type 1 and 2
patterns, are usually treated effectively by nonoperative
methods.
At any age, complicating factors such as burns, spasticity
(developmental or due to head injury), or multiple osseous
injuries, may significantly affect treatment decision-making.
For instance, fractures of the femoral shaft may be treated
more satisfactorily by fixation in cases involving severe hyper-
tonicity resulting from head trauma.157,158 The potential
calamities of nonunion and infection should be reasonably
avoidable through good surgical technique along with
appropriate prophylactic antibiotic treatment. Growth
abnormalities should not occur if the vulnerability of the
physes, both peripherally and centrally, is respected.
Advances in radiographic imaging have also greatly facili-
tated the specific anatomic diagnosis and, accordingly, treat-
ment of pediatric fractures (see Chapter 5). Fluoroscopy
may be used preoperatively to assess potential instability
(e.g., lateral condylar fracture of the distal humerus). Intra-
operative imaging may allow closed reduction with percuta-
neous fixation to minimize the use of hardware (e.g., the
relatively undisplaced lateral condylar fracture). Such tech-
nology also allows reasonably accurate external fixator pin
placement and closed reduction with appropriate fixator
adjustment. Magnetic resonance imaging (MRI) has an
increasing role in both acute diagnosis and treatment, as well
as follow-up for altered healing. MRI defines the fracture
anatomy (providing a better treatment basis) and the more
diffuse extent of an injury (e.g., the metaphyseal or epiphy-
seal bone bruise). Unfortunately, most metallic implants pre-
clude postoperative MRI evaluations (e.g., to evaluate the
possibility of ischemic necrosis following a femoral head or
neck fracture or a hip dislocation). Evolving MRI sequenc-
ing patterns may eventually allow reasonable acquisition of
desired information without distortion artifact.
Changing economic factors have also become important.
They have arisen in many sectors, especially from the insur-
ance industry, the availability of health insurance, and the
(sometimes negative) drive of health maintenance organi-
zations (HMOs). The use of fixation allows the child to leave
the hospital much sooner. Six to eight weeks of traction for
a femoral fracture leads to considerable inpatient costs.
88
Young parents have variable degrees of medical insurance
(or none at all). Insurance companies and HMOs exert pres-
sure to decrease hospitalization. In many families both
parents work, or there may be a single parent (separated,
divorced) who is working. The cost of closed reduction
under anesthesia or fixation under anesthesia may be com-
parable to 2–3 weeks of traction.
Changing concepts of rehabilitation, especially in children
with other problems (e.g., neuromuscular disorders) have
been applied to these children when they have fractures, as
well as to normal children. Fixation obviously allows more
rapid, appropriately paced and protected resumption of
motion than any fracture allowed to heal without hardware.
Associated Soft Tissue and
Vascular Injuries
Determination of possible vascular injury to the extremity is
a critical step during the initial evaluation of the patient.
Injury with profuse bleeding and fractures or dislocations
that have a high risk of vascular injury should be assessed
appropriately, regardless of the presence of peripheral
pulses. An arteriogram is especially important in children
with suspected popliteal artery damage following displaced
epiphyseal fractures or dislocation above the knee. By the
time clinical signs of vascular impairment become obvious,
the extremity may not be salvageable. Similar consideration
should be given to brachial arterial injury in supracondylar
fractures and elbow dislocations.
Severe soft tissue injuries associated with open fractures
are usually the result of high-energy trauma. The external
fixator is especially helpful for providing stabilization of the
fracture while concomitantly allowing access to the soft tissue
injury. In the case of vascular injury requiring surgical repair,
bone fixation decreases the risk of postoperative damage to
the vascular repair, particularly in children with associated
head trauma. The external fixator is ideal for this situation.
Children tolerate these devices well, as they do during leg-
lengthening procedures. The external fixator also permits
early mobilization of the multiply injured patient with unsta-
ble fractures, thereby reducing possible metabolic and pul-
monary morbidity.
Compartment Syndrome
Arm or leg compartment syndromes and their complications
may follow closed or open reduction as well as external or
internal fixation; and they may be a major cause of long-term
disability. Elbow and knee injuries are particularly associated
with this complication. Neither open reduction nor closed
reduction with an external fixator negates the risk of com-
partment syndrome.
A period of ischemia followed by resurgent blood flow may
cause increased intramuscular swelling. Similarly, an im-
paired venous overflow may increase interstitial edema.
Bleeding (extraosseous) may also cause compartment syn-
drome. The classic signs of compartment syndrome include
4. Treatment Concepts
pain not relieved by sedation, tenseness of affected com-
partments, hypesthesia, weakness, and significant pain on
passive stretch of the involved muscles. The presence of a
peripheral pulse (palpable or Doppler) does not rule out the
diagnosis of compartment syndrome.
In the young child or any child with central nervous system
injury, diagnosis of compartment syndrome may be quite dif-
ficult. Therefore careful palpation of soft tissue tautness or
compartmental monitoring is recommended. When com-
partment syndrome is suspected, appropriate decompres-
sion of the involved compartment should be performed to
prevent long-term complications. Such decompression may
be done electively (prophylactically) at the time of open
reduction.
Compartment syndrome is discussed in more detail in
Chapters 10, 14, 16, 22, and 23.
Head Injury
The orthopaedist should be aware of some of the basic
principles of treating head injuries in children, although
fracture of the skull is generally less significant than the com-
parable injury in an adult. The prime consideration is not
the skull fracture but, rather, the damage to the brain and
the subsequent intracranial fluid accumulation (blood,
edema). In the young child with an elastic skull, much of the
impact is absorbed by the relatively resilient osseous plates
and sutures. Despite considerable depression of the bone,
there may be little brain injury. Even the skull of an older
child with closing sutures absorbs a good deal of the impact,
transmitting less force to the brain itself. However, injuries
to the tips of the frontal or temporal lobes may cause pro-
longed unconsciousness, extending for weeks or even
months but usually with complete recovery ultimately.
Head trauma adds to the difficulties of skeletal traction
and casts. Patients with altered states of consciousness fol-
lowing central nervous system injury may have spastic muscle
posturing that often requires rigid stabilization of fractures.
Femoral fractures in children with head injury may be diffi-
cult to control in traction.157,158 Spastic activity may create soft
tissue pressure points within a cast, which can lead to pres-
sure sores.
The drawbacks of closed treatment may be a relatively long
period of immobilization, prolonged hospitalization, mus-
cular atrophy, and joint stiffness, all of which may be less-
ened if not eliminated by active, aggressive treatment.
Restoration of function in muscles and joints is not as
problematic in children. Even if perfect alignment cannot
be achieved and maintained by external immobilization,
remodeling and longitudinal growth often correct certain
degrees of angular malalignment.
There are substantial risks to early casting. For instance,
treatment of tibial fractures eliminates the ability to monitor
the child for signs of possible compartment syndrome. Mon-
itoring is essential because these children are unable to
describe pain and discomfort because of the comatose state.
In fact, direct compartment pressure monitoring is indicated
whenever there is a closed proximal mid-shaft fracture con-
comitant with a head injury. Shortening and angulation may
subsequently arise because of progressive spasticity and invol-
Closed Reduction
untary patient movements, particularly when the child
begins to recover from the head injury.
The child’s ability to survive severe head injury makes
maintaining adequate alignment of any fracture critical,
regardless of the severity of the initial injury. When align-
ment cannot be readily and easily maintained by traction, sta-
bilization with internal or external fixation is indicated. The
external fixator may be applied with relative ease, even
under local anesthesia, and is helpful for preserving the
alignment of long bone fractures in children. External fixa-
tion allows mobilization of the patient out of traction while
maintaining osseous alignment, even in cases involving
spastic patients. Internal fixation is less offen indicated in
these patients and is frequently contraindicated because of
the physiologic alterations of brain function and cerebral
edema, which could adversely affect anesthetic risk. The risk
of infection at the fracture site complicates open fracture
management. External fixation allows the treatment of such
soft tissue injury.
Intramedullary nailing of femoral fractures in children
has been successful in preventing alignment complications
in the brain-injured child. The significant danger of injury
to the vascular supply of the femoral head or to the tro-
chanteric epiphysis, with growth arrest in either instance,
markedly increases the risks of this procedure. Closed
intramedullary nailing of femoral fractures in children aged
10–15 years has produced excellent results. When the pro-
cedure is properly performed, operative trauma and com-
plications are minimal, and early mobilization is possible.
Young children may be treated with external fixators.
Fracture healing is often enhanced in the head-injured
child, so attention to problems of shortening and angulation
must be addressed early. External fixators may be applied
with local anesthesia if there is a problem of, and concern
for, the use of a general anesthetic. More than 90% of chil-
dren in a coma for more than 48 hours have excellent neu-
rologic recovery. Therefore it is important to be aggressive
early and treat all orthopaedic injuries on the assumption
that full neurologic recovery will eventually occur.
Head trauma and the associated problems of fracture
management are also discussed in Chapter 3.
Closed Reduction
Closed methods are usually successful in children because
of (1) rapid fracture healing; (2) minimal problems with
postimmobilization stiffness; and (3) progressive fracture
remodeling. Subsequent growth may allow acceptance of less
than complete anatomic alignment. However, such physio-
logic changes generally require at least 2 years of remaining
growth, a fracture near the end of the bone, and angulation
in the plane of motion of the contiguous joint. Remodeling
does not “correct” intraarticular fractures, displaced
physeal/epiphyseal fractures, angulated or rotated diaphy-
seal fractures, or certain displaced fractures, each of which
often requires a more aggressive (i.e., operative) approach
for effective reduction.
Except in those chondro-osseous fractures involving joints,
physes, and epiphyses, absolute anatomic reduction of the
metaphyseal and diaphyseal bone fragments is not always
89
necessary and sometimes should be avoided. Angulation in
the middle third of long bones is not ideal and should be
corrected to as close to normal as possible. In girls under 10
and boys under 12 years of age, however, some angulation
(preferably 15° or less) of fragments near the joints is more
acceptable.
Remodeling usually occurs only if the deformity is in the
plane of motion of the contiguous joint. Proximity to a joint
is also essential. A mid-diaphyseal angulation of 15°–20° may
not remodel at all, whereas a 45°–50° metaphyseal angulation
adjacent to the physis in a young child may remodel com-
pletely. The patient’s age is extremely important. There must be
enough growth remaining to allow such remodeling. Con-
comitant with the age concept is the fact that the physeal
regions contributing most to elongation are most likely to
correct progressively (e.g., proximal humerus, distal radius,
distal femur, and proximal tibia in older children; and the
proximal femur and distal humerus in the younger child).
These physeal growth rate factors change with time. For
example, considerable longitudinal growth occurs in the
proximal femur during the first 8–10 years. In contrast, the
distal femur becomes the more dominant growth region
after 10 years of age.
After injury, the bones of children may grow at an accel-
erated rate for several months.19 Accordingly, overgrowth is
a concomitant of many childhood fractures, especially those
involving the femur or tibia, although any longitudinal bone
may be involved. Furthermore, even a seemingly noninjured
bone in the same leg may undergo some overgrowth, prob-
ably because of the temporarily increased blood flow to the
leg following a major injury.
Children are not initially as stiff following immobilization,
nor do they remain so, compared to an adult who has one
or more joints immobilized for a similar period of time. The
rapidity of healing in children obviously decreases the time
of immobilization and may also allow progressive mobiliza-
tion of joints while the fracture itself is still specifically immo-
bilized (e.g., the progression from a long leg/arm cast to a
short leg/arm cast during the early stages of fracture
healing). Children are much more eager to resume daily
activities, which is a form of natural physical or occupational
therapy. They usually have a positive desire to resume their
normal preinjury life style. Adults, in comparison, usually
come out of a cast stiffer, require programmed therapy, and
often have other factors such as workmen’s compensation or
an unsettled lawsuit that may significantly or even adversely
affect the rate of rehabilitation and recovery.
The porosity of the metaphysis changes with time. The
metaphysis is rapidly formed bone (modeling) that is even-
tually replaced by mechanically responsive bone formation
(remodeling). The changing corticalization of the diaphysis
also affects fracture failure patterns and responsiveness. The
initial cortex is a combination of endochondral bone for-
mation and subperiosteal membranous bone formation.
This combination is in a constant state of biologic flux,
remodeling in response to applied biologic/biomechanical
demands of the individual child.84,163 This constant remod-
eling affects healing and any recovery from deformity. It also
affects the choice of a fixation device, whether internal or
external, and the need for its removal at an appropriate time
during the fracture healing process.
90
Rapid healing rates are characteristic of young children,
reflecting the osteogenic capacity of the developing perios-
teum. As the child gets older, especially into adolescence,
this periosteal reactive capacity for making a circumferential
stabilizing callus becomes progressively less.
Cast Application
For most simple fractures with minimal angular change or
displacement, a cast may be applied immediately. This is pos-
sible because significant manipulation and three-point pres-
sure are usually unnecessary. Furthermore, the extent of
concomitant soft tissue injury and lower energy fracture
mechanism make excessive swelling that could lead to com-
plications such as cast syndrome unlikely. If the fracture is
metaphyseal (e.g., distal radius) only the contiguous joint
may need to be included in the cast.
If cast padding is to be used, I usually first apply a stock-
inette liner directly over the skin. It can be folded over the
initial layers of casting material to make the proximal and
distal ends of the cast neat. This liner discourages pulling
out the cast padding, which children have a habit of doing
(although not necessarily any more frequently than adults).
The liner is particularly effective (and necessary) for men-
tally impaired children. An alternative padding is Gortex cast
liner, which may be used to allow bathing or swimming. The
material is considerably more expensive than regular cast
padding. We give parents the option of an extra charge if
they want it used. A stockinette should not be used with the
Gore-Tex cast liner, as it would retain moisture when the cast
is immersed in water. Commercial hair dryers may be used
for any residual moisture when Gore-Tex is used.
Adequate cast padding is applied, especially over promi-
nences such as the malleoli or the ulnar styloid. Extra
padding is also suggested around and just below the proxi-
mal fibula in short leg casts to prevent undue pressure on
the peroneal nerve.
Extra (excessive) cast padding should be used for certain
children. For example, children with spastic cerebral palsy
are likely to have continuing muscle spasms underneath the
cast, which can increase pressure between subcutaneous
skeletal prominences and the cast. Children with sensory
deficits (e.g., myelomeningocele, congenital insensitivity to
pain, spinal cord injury) cannot feel “pressure points” and
so need extra cast padding to prevent the development of
pressure sores.
Another method of localized pressure point protection is
to selectively apply pieces of felt (usually 3/8 to 1/2 inch
thick). This material is particularly useful during application
of a hip spica cast for a femoral fracture, where the felt
should be placed over the iliac crests, coccygeal area, and
symphysis pubis. An additional trick when applying a hip
spica, especially on an infant or toddler, is to place a small
folded towel over the abdomen, over which padding is
wrapped. The towel and padding are pulled out after the cast
material hardens, and the space that is left allows abdominal
expansion with meals.
Any abrasions or lacerations that have been repaired
should be covered by Xeroform, Adaptic, or other protective
dressing prior to the above steps. Any deeper wounds should
be similarly covered, with the cast being subsequently win-
4. Treatment Concepts
dowed over any involved region to allow wound observation
and, as necessary, continued care and dressing changes.
When working with casting materials, gloves are usually
used. Fiberglass sticks to skin for an extended period.
Contact dermatitis may also develop. Remember to consider
the possibility of latex allergy in any patient.129
The next step is application of the cast. The plaster or
fiberglass material is carefully rolled around the involved
extremity. An assistant is helpful for maintaining the position
of the hand or foot, which is particularly important for the
foot if the child is to be encouraged to bear weight. Alter-
natively, devices are available that allow the patient to main-
tain the right angular position. They are sized principally for
the adult, however, and require patient cooperation. Obvi-
ously there are age and size limits in the utilization of such
devices in children. After two or three layers of cast material
are rolled, the stockinette edges are brought over onto the
cast, and further rolling is continued.
If the fragments are significantly displaced or angulated,
manipulation is first undertaken. It usually is done before
applying any underlayers (stockinette, padding), with the
reduction being verified by fluoroscopy or portable x-ray
machine. Fractures requiring manipulation are best treated
with an assistant who can maintain the position of reduction
while the cast materials are progressively applied.
If there is significant swelling, or it is anticipated after a
manipulation, an alternative is temporary splint application.
The most common splint is probably the sugar tong, which
is applied along the dorsum of the hand and wrist, wrapped
around the elbow posteriorly, and then continued out to the
palmar surface of the forearm and hand. Alternatively, a cast
is applied and then bivalved after hardening. Be sure to use
the cast spreader to “pop” the bivalve cuts; it ensures that the
cuts are complete. Several days later the child can be reeval-
uated. A sugar tong splint may be converted to a circumfer-
ential cast. A bivalved cast may be reinforced with additional
casting material.
Marson and Keenan assessed skin surface pressures under
short leg casts.125 Fiberglass casts had significantly higher
pressure than plaster casts. Beneficial effects of bivalving and
cast spreading were confirmed by significant pressure drops.
They suggested that plaster is safer than fiberglass when
significant extremity swelling is likely or when a patient’s
skin is vulnerable to breakdown.
If manipulation is undertaken, it is imperative that a
postreduction x-ray study be obtained. This may be fluo-
roscopy or portable radiography. Because the fracture is sta-
bilized by the cast the child may also be sent to the imaging
department for a standard radiograph. Be certain to observe
the result personally. It is difficult to defend an unreduced frac-
ture later if such a study was not obtained initially.
The postreduction film may show that the initially accept-
able fracture reduction was lost during application and
molding of the cast. One method of addressing this problem
is to remove the first cast, repeat the reduction, and recast
the limb. If the principal problem is residual longitudinal
malalignment, the initial cast may be wedged.93 This is done
by a circumferential cut in the cast at the level of fracture
angulation. The cast is then wedged open, preferably under
fluoroscopy, until the desired alignment is attained. Addi-
tional casting material is then applied to maintain this cor-
Concepts of Skeletal Fixation
rection. Be careful not to kink the plaster at the wedging
apex, as it could lead to focal cutaneous ischemia or a deep
pressure sore.
Adequate counseling about cast care should be given by
ancillary personnel. If available, a personalized or commer-
cially prepared brochure or a leaflet on cast care, reporting
concerns and so on, should be given to the parents, the
child, or both.
Because children may devise ingenious methods for
destroying immobilizing devices, any casts or splints must be
applied securely. As a general rule, the joints on either side
of the fracture should be immobilized, especially if manipu-
lative reduction was necessary. Follow-up radiographs should
be obtained within 5–10 days after reduction. During this
time the reactive swelling and pain are subsiding and the
child’s activity level is increasing, so the cast may become rel-
atively loose and the reduction lost. This is also the period
during which loss of reduction or less acceptable reangula-
tion is easiest to correct.
Cast Removal
Most casts remain in place for several weeks. However,
certain fractures with a likelihood of displacement in a cast
must be checked within a few days to a week after the cast
has been applied. This is especially necessary if major
swelling was present. As the swelling dissipates, the pressure
points of the cast become less effective; such an eventuality
may be addressed by cast removal and application of a
new cast.
If I have used a long leg or long arm cast for a specific
fracture, I often evaluate the fracture radiographically at 3–4
weeks. If some callus is evident it is easy to convert to a
shorter cast simply by removing the upper portion of the
cast; hence a short arm or short leg cast is now in place
without having to completely reapply a cast. The additional
advantage is that the child can mobilize the previously
enclosed joint, usually attaining full range of motion prior
to complete cast removal.
Whenever I remove a cast or consider removing it, a con-
firmatory radiograph is obtained. This allows evaluation of
the extent of fracture healing, how much subperiosteal callus
is present, and how evident the fracture line still is. Never
remove a cast and release the child without verification of
adequate fracture healing. A refracture shortly thereafter is
difficult to defend if precautions were not adequate.
Cast Complications
Probably the two biggest problems with children in casts are
insertion of foreign objects and immersion of the cast in
water. Puddles are attractive to a child, who may step in one
and not inform his or her parents. It may lead to maceration
of the skin and even infection, especially fungal. Foreign
objects may cause pressure indentation of skin and subcuta-
neous tissue and even an open sore. Any malodorous com-
plaint from child or parent should be checked carefully.
A major complication may result if an object such as a
rubber band slips under the cast. A well-meaning parent may
put a plastic bag over the child’s cast for bath or shower,
making it snug by placing a rubber band over the proximal
91
end of the bag to keep out water. This can easily slip under
the cast when the bag is removed, especially if the child is
left alone to remove the bag.
Children may also contract a contagious disease just
before or while in a cast, which may lead to problems when
the skin is involved. Particularly, measles may severely involve
a casted extremity. The warm, often moist environment
under the cast can be an incubator and may lead to severe
involvement of the casted skin region, with many more
lesions than on other parts of the body. Cast removal may be
necessary. If so, a removable splint may be fashioned to allow
daily skin care while still protecting the healing fracture.
Pressure points under a cast are a significant potential
problem. The need to apply three-point pressure to effect
reduction may cause focal points that, if not adequately
padded, may lead to tissue necrosis and pressure sores. This
is a serious potential complication in children with either
sensory deficits or those with increased spasm that may con-
centrate pressure on certain areas of the cast.
It is equally important to remember that closed treatment
is not without hazard. Cast sores may develop when there is
insufficient padding, when swelling creates pressure, or
when there is an indentation in the cast. Compartment syn-
dromes may develop even with closed injuries. A compres-
sive cast may increase the extent of such damage. Loss of
position may occur when soft tissue swelling progressively dis-
sipates, allowing looseness to develop within the cast. Trac-
tion tape allergy may develop, especially in myelodysplastic
children with latex allergies.26
Functional fracture bracing has been shown to be effica-
cious in children 16 years of age or younger.128 The method
probably should be restricted to fractures in the distal third
of the femur or the entire tibia. Mid-shaft femoral fractures
should not be treated by this method. For children, the only
significant advantage of fracture bracing is the greater
freedom afforded to both the child and the parents,
although this advantage is difficult to evaluate quantitatively.
This methodology also has merit in conjunction with limited
internal fixation. In fact, the combination of a cast or a cast-
brace with limited or temporary internal or percutaneous
fixation may be highly effective in the child to minimize hos-
pitalization and maximize the rapidity of rehabilitation.
Concepts of Skeletal Fixation
Some physicians emphatically condemn operative fixation of
almost all fractures in children, suggesting that conse-
quences such as nonunion, delayed union, altered growth,
infection, and ugly scars may arise. Blount, in particular, was
a staunch advocate of closed reduction for virtually all pedi-
atric fractures.18 His philosophy has been championed by
many as a reason not to undertake operative fixation of frac-
tures in children.
It is certainly correct that the thoughtless use of internal
or external fixation should be strongly discouraged when
treating fractures in children, but it is also incorrect to deny its
judicious application. When adhering to reasonable indica-
tions and good technique, percutaneous, internal, and exter-
nal fixation methods are extremely helpful for preventing
both early and late complications of fracture treatment and
92
effectively treating specific fractures. A useful guide is that
operative treatment for a child’s fracture is indicated when
conservative treatment does not or probably cannot achieve
an acceptable result (Table 4-1).
Unnecessary surgery certainly has been undertaken,
sometimes resulting in permanent disability, because a treat-
ing physican has failed to appreciate the recuperative and
remodeling powers of the child. Such circumstances do not
enhance the acceptance of the role of internal or external skeletal
fixation in children.
There has been an increasing emphasis on the use of
open reduction in children and adolescents, especially in
the European literature.* Certainly, the trend in the treat-
ment of skeletal injuries in adults is toward operative inter-
vention, resulting in part from advances in the techniques of
fixation, the specific implants available, and increases in the
understanding and control of soft tissue dissection and peri-
operative wound infection.19,56
Adult fracture treatment during the 1960s and 1970s was
based on a concept of rigid, anatomic internal fixation. This
concept is not realistic in the biologically developing,
growing skeleton. Instead, the newer concepts for fractures
in adults (i.e., direct/indirect fracture reduction that is
stable and biologically benign) is more appropriate.19 This
methodology utilizes minimum soft tissue dissection and
retraction, thereby avoiding additional surgical soft tissue
trauma and devascularization of osseous and chondro-
osseous fragments. Such techniques require detailed preop-
erative planning. The trauma of bone fracture often
overshadows the concomitant contiguous soft tissue injuries.
It is important to realize that this soft tissue envelope pro-
vides vascularity and viability to cartilage, bone, and any iso-
lated fracture fragments. Because the amount of soft tissue
TABLE 4-1. Indications for Reduction and Fixation Prior to
Skeletal Maturation
Displaced epiphyseal or physeal fracture; realignment of the
physis
Displaced intraarticular fracture; realignment of the joint surface
Unstable fracture (e.g., hip, spine, lateral condyle of distal
humerus); fractures with a “bad reputation” for displacement
(both bones of adolescent forearm, medial malleolus)
Multiply injured patient, especially one with neurologic or head
injury
Open injury, especially with extensive muscle or soft tissue loss
Delayed union after closed treatment
Nonunion after closed treatment
“Floating” joints; challenging combinations of injury in the same
limb
Economics of hospitalization
Pathologic fractures
Segmental bone loss
Avulsion (traction) injuries
Neglected fractures
Unstable fractures with associated neurologic or vascular injury
Irreducible fractures with soft tissue interposition
Unstable or irreducible fractures in the older child or adolescent
* Refs. 6–11,28,30,32–34,37,40,42,44,45,47,49,59,61,66,70,73,81,82,
87,94,95,98,103–105,111,141,148,149,155,160,165,168–170,182,186–
188,190–192,193,197,202,203,207–210,217–227,230,231.
4. Treatment Concepts
wounding relates to the energy put into creating the frac-
ture, knowledge of the mechanism of injury is important for
anticipating the extent of soft tissue trauma.
The mechanical goal of fracture management is to attain
axial, longitudinal, and rotational alignment with stable fix-
ation of the fracture. The biologic goal is to maintain viabil-
ity of the bone by preserving its soft tissue attachments and
blood supply. Anatomic reduction of each fracture surface is
not critical, especially in children, except for involvement of
the articular surfaces and physes.
Open reduction and internal fixation (ORIF) are com-
monly indicated as an appropriate method of treating frac-
ture-separations of the capitellum, trochlea, and medial
epicondylar regions. In certain situations it may be more
appropriate to accept a less than ideal closed reduction and
undertake elective operative correction a few days later when
local conditions at the fracture site (e.g., excessive swelling)
or general conditions of the patient are relatively normal
(i.e., the child has recovered from other injuries). It should
also be remembered that surgeons have little reservation
about using internal fixation to stabilize an osteotomy (i.e.,
a controlled surgical “fracture”) yet often appear reluctant
to use comparable fixation for a spontaneous fracture in the
same anatomic region.
Thompson et al. reviewed 4411 pediatric fractures.208 Only
3.8% (m = 170) of these patients underwent skeletal fixation.
Group 1 included 90 skeletally immature children, and
group 2 involved 66 skeletally mature adolescents. Upper
extremity fractures (especially those involving the distal
humerus) were the major indication for ORIF in group 1,
whereas intraarticular fractures predominated in group 2.
Minor complications were found in 18% of group 1 and 12%
of group 2. The authors believed that these complications
were fewer than the number that would have occurred had
operative intervention not been undertaken. Most external
fixation devices were used for the lower extremity fractures.
In a similar study Slongo and Jakob reviewed 3037 fractures
in children treated over a 3-year period.194 Of these, only 245
were treated operatively, with 30% of 75 diaphyseal fractures
being treated with an external fixator.
Changes in technology may be both beneficial and detri-
mental to children’s bones.2 For example, titanium pins in a
slipped capital femoral epiphysis (SCFE) may be extremely
difficult to remove and may even break during such an
attempt. However, they are mechanically stronger and have
the advantage of potentially allowing some degree of MRI.127
Another reason to undertake fixation of fractures in chil-
dren is to avoid “fracture illness” in which a long period of
casting leads to osteoporosis and muscular atrophy. These
phenomena are more likely in children with a neuromuscu-
lar disease or injury who would probably benefit from more
aggressive fracture management, so they may be mobilized
to decrease the rapidity of onset of osteoporosis.
Finally, better medical care, especially in pediatric inten-
sive care units, has led to increased survival of multiply
injured young patients. Comatose children wake up with
greater regularity than head-injured adults. However, while
comatose they may have severe decerebrate rigidity that
makes fracture control difficult. External fixators may be
placed under local anesthesia if the neurologic situation pre-
cludes general anesthetic techniques. This practice avoids an
Specific Methods of Fixation
iatrogenic deformity and the subsequent need for recon-
structive surgery after recovery from the head injury.
Several concepts regarding the utilization of percuta-
neous, internal, or external skeletal fixation prior to skeletal
maturity may be considered. It is better to undertake gentle,
controlled open reduction of a physeal fracture than resort
to multiple, closed reductions. Operative fixation should be
considered from the same standpoint as casting, that is, tem-
porary stabilization of the fracture fragments in an anatom-
ically acceptable reduction until adequate healing occurs.
Whenever possible, the fixation should be easy to remove
(pins, K-wires, screws) or biodegradable. Internal stabiliza-
tion should always be supplemented initially with a splint or
cast. Absolutely rigid fixation is rarely necessary, as the initial
(primary) union disappears progressively with subsquent
growth and remodeling. Furthermore, such rigidity may
decrease the prolific subperiosteal callus formation that is
typical (and important) to fracture stability in a child.
Anatomic reduction and maintenance of physeal (especially
types 3 and 4) and articular injuries are usually necessary and
appropriate.
Fixation should be used for challenging combinations
of fractures, such as both bones of the forearm combined
with a distal humeral fracture or fractures of both sides
of the knee to create a floating elbow or knee. Fixation
should also be considered for potentially unstable fracture
cases, such as a Chance injury of the spine. Open reduction
is also indicated when there is loss of bone substance, such
as in the tibia, to allow subsequent bone transport later
without loss of length due to soft tissue contractures. Con-
traindications to internal fixation include contaminated
wounds or whenever such fixation is unnecessary or
inappropriate.
Internal fixation of nonarticular fractures in children does
not have to be absolutely anatomically perfect. However,
articular fractures in children require as much diligence in
reduction as in the adult.
Because of the variability allowed in the extent of anatomic
reductions, flexible rods and flexible plates may be used as
temporary expedients. They should be coupled, however,
with some external splinting or casting to allow controlled
healing and rapid rehabilitation.
Many fractures of the physis and epiphysis are best treated
by open reduction and internal fixation. However, open
reduction may be dangerous if performed several days or
weeks after an epiphyseal injury, because the chance of
damage to the physis may increase. If displacement is still
severe and open reduction is necessary, the surgeon may
lessen, if not altogether avoid, these risks by handling the
region around the physis with extreme care.
The physis is not particularly forgiving to transphyseal
hardware. Therefore any fixation device crossing the physis
invariably should be smooth and of a small diameter. Large-
diameter devices increase the risk of bridge formation
through the residual defect left after hardware removal.
Threaded devices are contraindicated, presumably because
of compression restraint whether the threads continually tra-
verse the physis or are placed beyond in the metaphyseal
bone, as a malleolar screw. However, even smooth pins, par-
ticularly if left for an extended time may be associated with
physeal bridging.
93
Perhaps one of the most important goals in the treatment
application of any fixation in children is to minimize the
amount of hardware. One should rely on cast augmentation
and soft tissues that are intact. For instance, the periosteum
is often incompletely disrupted and may be used as an effec-
tive internal splint that allows less hardware than might be
necessary in an adult.
Because children devise ingenious methods for destroying
immobilization devices, casts or splints that supplement fix-
ation methods must be applied securely. As a general rule,
one or more joints on either side of the fracture should be
immobilized initially. Follow-up radiographs are obtained
about 5–10 days after reduction. During this time, the reac-
tive swelling and pain are subsiding and the child’s activity
level is increasing, so the cast may become loose and put
increased stress on the implant. In contrast to closed reduc-
tion, the use of fixation minimizes loss of reduction when
the cast loosens. However, small fixation devices are subject
to bending, and small intramedullary rods may not rigidly
control rotation.
The selected indications for internal and external fixation,
with open or closed reduction techniques, in skeletally
immature children and adolescents include: (1) displaced
epiphyseal fractures; (2) displaced intraarticular fractures;
(3) unstable fractures; (4) fractures in the multiply injured
child or adolescent, especially those with concomitant neu-
rologic injuries: and (5) open fractures with extensive loss
of muscle and soft tissue. Detailed examples of the use of
skeletal fixation for both closed and open fractures are pre-
sented in subsequent chapters, particularly as they relate to
the specific regional anatomy and nuances of the fracture
anatomy.
Specific Methods of Fixation
Pins and Cast
External fixation pins may be inserted through proximal and
distal fragments and then incorporated into a cast. This
simple technique requires adequate reduction of the bone
fragments prior to application of the cast. It is relatively
lacking in flexibility and adjustability. It also carries a risk of
pin tract infection, as the pins are covered and not readily
available for local pin care.
Percutaneous Fixation
A fracture may be reduced by closed methods and then
stabilized by the percutaneous insertion of one or more
fixation pins (usually smooth). The pins should be inserted
under fluoroscopic control to ensure proper reduction as
well as proper pin placement.
If percutaneous pins are used, they must be used appro-
priately. Pins should be placed utilizing fluoroscopy so place-
ment is accurate. Blind pinning with presumed stabilization is
unacceptable.
One may decide whether the pins should be kept subcu-
taneous. If left penetrating the skin, there may be some reac-
tivity around the skin penetration sites that can lead to
94
hypertrophic granulation tissue as well as local infection. Per-
cutaneous pins associated with pin-site problems may be
readily removed in the office setting.
When the growth plate must be traversed it is important
to use smooth pins and to place them as close as possible to
the anatomic center of the physis (Fig. 4-1). Damage to
peripheral tissue such as the zone of Ranvier is more likely
to lead to angular growth deformity.39 Threaded pins are
more likely to be associated with growth plate damage if they
must cross the physis. With type 2 or 4 growth mechanism
injuries, efforts are made to fix the metaphyseal fragment
transversely to the rest of the metaphysis, and in the case of
type 4 epiphyseal ossification center to epiphyseal ossifica-
tion center, thereby avoiding any angularly directed pin fix-
ation across the physis.
K-wire fixation usually is supplemented with a cast or
splint. With more complex physeal fractures an external
fixator may also be used to increase stability (Fig. 4-1). A
smooth K-wire is less likely to disrupt growth if the physis
must be crossed. Pins may be placed percutaneously and, if
put in the proper position, usually do not interfere with neu-
rovascular function. The drawbacks are that they are not
rigid, especially the smaller diameter wires, and they some-
times lack stability. They do not compress, and they may pre-
clude early motion. The goal should be to use the smallest
diameter that allows anatomic reduction to be obtained and
maintained and to then use cast supplementation for stabil-
ity until there is sufficient healing in the fracture.
FIGURE 4-1. Open growth mechanism fractures of the distal
femoral and proximal tibial epiphyses were treated by débridement
and limited K-wire stabilization. The fractures were further stabi-
lized by an external fixator spanning the knee joint.
4. Treatment Concepts
External Fixators
The development and improvement of external fixation
devices in the adult with polytrauma has been expanded to
comparable situations in the child. These devices, whether
uniaxial or ring (polyaxial) fixators, are increasingly sophis-
ticated in design and usually easily applicable to traumatic
situations involving the immature skeleton.3,6,32,62,64,76,159,167,210
However, the nuances of the child’s bone, especially the
physeal anatomy and metaphyseal porosity, must be
respected during application, particularly in the choice of
pins and screws and the insertion sites.
There has been increased enthusiasm for the use of exter-
nal fixation in the care of the traumatized child, especially
the child sustaining multiple injuries (Fig. 4-2). The devices
allow appropriate soft tissue management and earlier mobi-
lization of the patient, with a decrease in complications
caused in part by prolonged bed rest.210 Although several
weeks of bed rest may not be as detrimental to young chil-
dren as they may be to adults, the subsequent care and mobi-
lization of many children sustaining multiple trauma is
facilitated using these techniques. Furthermore, many of
these children have head injuries, and appropriate manage-
ment of any fracture (maintenance of reduction and align-
ment) is extremely important. Children have a much higher
likelihood of recovering from head trauma than adults, such
that they eventually need to use limbs that are in normal
anatomic configuration, not deformed by less than optimal
care or decerebrate rigidity.
In multiple trauma patients, with or without head injury,
stabilizing the fractures enables earlier mobilization, often
facilitating recovery of nonorthopaedic injuries. However,
fewer than 5% of children admitted with polytrauma proba-
bly require operative fracture therapy or some type of skele-
tal fixation, especially application of external fixation.
Comatose children often have markedly elevated intracra-
nial pressure, the monitoring of which is readily done with
devices placed in the ventricles. In such children it is best to
have the head of the bed elevated about 30°. Fracture manip-
ulation must be minimized, as such manipulation may lead
to a further increase in intracranial pressure because of pain.
External fixation is recommended for children with an
open fracture associated with skin loss or burns and in poly-
trauma patients to facilitate care, transport to diagnostic
modalities, and therapeutic procedures. Children with skin
loss and deep soft tissue and bone loss are also excellent can-
didates for external fixation.31 The fixator facilitates dressing
changes and provides stabilization while further débride-
ment, grafting, and reconstruction procedures are carried
out (Fig. 4-3). Fixation also has the capacity to stabilize adja-
cent joints to prevent excessive soft tissue movement and
prevent contractures. If free vascularized tissue transfers are
used, direct observation is enhanced. Once skin coverage
has been obtained, consideration should be given to fixator
removal and subsequent application of a cast or orthosis.
The external fixator should also be considered when a
patient requires major fasciotomies.
External fixators allow maintenance of limb length during
initial treatment, particularly when there is extensive bone
loss. Meticulous pin care is necessary to avoid necrosis due
to the heat of insertion or infection (ring sequestrum).
Specific Methods of Fixation
FIGURE 4-2. (A) Stress film showing a type 1
growth mechanism fracture of the proximal
tibial epiphysis. The leg was also partially
degloved. (B) Treatment with a circular frame
to reduce and stabilize the fracture allowed
access to the soft tissues for adequate wound
skin care.
A B
Unstable pelvic fractures may also be stabilized by the use
of the external fixator, thereby aligning fracture compo-
nents, stabilizing blood loss, and permitting earlier mobi-
lization of the child or adolescent. The pins generally are
placed in the anterolateral iliac crest. The device is more
applicable for anterior fractures and separations, whereas
posterior pelvic fractures may not be as readily treated or
reduced by this technique. A diastasis or chondro-osseous
separation of the pubic symphysis may be closed by an ante-
rior frame (see Chapter 19).
Unilateral frames are relatively simple to apply and lead to
stable fixation. Half pins may be placed with minimal soft
tissue damage or neurovascular entrapment. There is an
adjustable aspect to these pins. Nonunion rates may be
higher, but some of the newer methods utilizing dynamic
compression on a progressive basis may avoid this problem,
particularly because nonunion is so rare in children. The cir-
cular external fixation frame is extremely stable. It allows
bone transport when there is bone loss, as well as angular
adjustment. However, the frame may be relatively compli-
cated to apply and may be restrictive to soft tissue recon-
structions. Reconstruction may preclude many of these
issues.
There are two stages when treating fractures with an exter-
nal fixator. Attention is initially focused on the soft tissue
injury and the general status of the patient. For this stage a
rigid or semirigid external fixator may be used. Next, atten-
tion is directed to the fracture. A subsequent, less rigid
device may be appropriate for continued fracture healing,
especially in children and adolescents. In children the
fixator is used during the acute stage, but when the soft tissue
95
heals the fixator may be dynamized or removed; other, more
commonly used forms of immobilization, such as a cast or
orthosis, may then be employed until healing is complete.
This practice is appropropriate in children because of their
more rapid rates of healing.
Many external fixation frames with varying degrees of
rigidity are available. In general, it is not necessary to apply
excessively rigid frames in children (compared to adults)
because they are in place for shorter periods and the repar-
ative biology of the child’s skeleton does not usually require
the same type of rigidity. The major factors to be considered
are the length of time for usage, the rigidity, the areas avail-
able for insertion of pins, the ease of application, and the
degrees of freedom allowed for fracture manipulation
before, during, and after application of the device. Rigidity
is obviously important if a segmental bone loss is present and
is contingent on the long-term plans for either allograft,
autograft, or transportation of a segment.181 If the bone is
basically “intact,” with no loss of any substance, and the frac-
ture is partially stable, a flexible frame may be easier to apply.
The more flexible the frame, the better the stress transfer
across the fracture site to facilitate healing and, more impor-
tantly, remodeling.86,124,130,141,144 Certain external fixation
components allow progressive dynamization of the fracture
site, thereby enhancing the remodeling of callus and
strengthening of the fracture union.
Several factors potentially affect the placement of fixator
pins. Obviously, the growth plate should be avoided. In
general, pins should be placed at least 1–2 cm from the
physis. Sometimes pins are placed in the epiphyseal ossifica-
tion center (transversely). Pins also should not be so close to
96
A tibial or distal femur. In the ankle region, half pin placement
B
FIGURE 4-3. (A) This multiply injured 14-year-old boy underwent
variable fracture stabilization. The femoral diaphyseal fracture was
reduced and fixed by closed intramedullary rodding. The open
proximal tibial fracture was treated by application of a ring fixator
that allowed repeated soft tissue débridement and eventual closure
(flaps, grafts). (B) Magnified view shows the proximal tibial physeal
fracture and a type 4 proximal fibular fracture (arrow). Antibiotic-
impregnated methylmethacrylate beads are evident.
the physis that a pin tract infection could extend to the
physis. Because of the potential thermal injury to the physis,
some have recommended leaving at least 2 cm between the
physis and the closest pin.3 Thompson and colleagues have
4. Treatment Concepts
shown moderate temperature changes due to automated
drilling bone 2.5–5.0 mm from the drill.208 Tapping the pins
in, rather than drilling, has been recommended to decrease
generated heat.229 A pin tract adjacent to the physis may
potentially adversely affect growth. Whenever possible, a pin
is inserted into bone in areas where the bone is most
superficial.
Cortical bone porosity in the metaphysis may affect the
purchase of pins and may allow pin migration. Meticulous
pin care is a requisite. Half pins may also be used with a cast
or orthosis. Pin placement should be monitored fluoro-
scopically to ensure proper placement.
Skin injury, both skin loss and extensive skin bruising,
affects pin placement. It is preferable to insert pins, when-
ever possible, through intact or uninjured skin.
Various external fixation devices may be used for short
periods to bridge joints in children. In cases in which the
fracture is metaphyseal, pin placement into the epiphysis is
generally avoided if the growth plate is still open. Instead,
the joint and epiphysis may be bridged temporarily. Children
with a fracture tend to recover rather rapidly with joint
immobilization, and the fracture generally heals rapidly
enough to allow placement in a different device and removal
of the external fixation device before absolute healing is
complete. To accomplish bridging of the joint, one set of
pins is placed in the metaphysis of the adjacent bone and the
other set in the metaphysis or diaphysis of the involved
(injured) bone. This technique is most commonly employed
in the knee area for metaphyseal fractures of the proximal
into the calcaneus, the metatarsals, or both allows placement
of an external fixation device that bridges the ankle joint and
allows foot control to prevent an equinus deformity of the
ankle during fracture treatment.
A relatively inexpensive external fixator may be fabricated.
Pins are first inserted, and the fracture is reduced or at least
positioned. A flexible tube (e.g., disposable corrugated
anesthesia tubing) is filled with freshly mixed methyl-
methacrylate. This filled tube is then inserted over the pin
ends, the final fracture reduction is made and fluoroscop-
ically verified, and the methylmethacrylate is allowed to
harden.36
As a precautionary measure to prevent the fixator from
becoming a distracting device at the fracture site, a com-
pression technique is used during the healing process. When
radiographic evidence of healing is present and pain at the
fracture site is minimal, the frame may be loaded by pro-
gressive weight-bearing. Use of these devices allows loading
and maintains fixation through axial load-bearing.
The complications of external fixation include pin tract
infection, pin loosening, and failure of union (Fig. 4-4).
These complications tend to be less of a problem in a child.
Strict adherence to asepsis, reasonable skin incisions around
pin entry sites, and meticulous postoperative pin care should
minimize them.
Jupiter et al. described the role of external skeletal fixa-
tion in the reconstruction of limbs involved in posttraumatic
osteomyelitis.90 The patients were skeletally mature. The use
of the external fixation device allowed approaches to dealing
with the chronic osteomyelitis with resection of damaged or
diseased bone, progressive soft tissue coverage procedures,
Specific Methods of Fixation
FIGURE 4-4. Effect of pin tract infection on the K-wire penetration
sites. Meticulous pin care is probably the best way to try to avoid
this problem, although even that may not completely prevent it.
and autogenous bone graft. Obviously, this technology is
applicable to children, especially in the adolescent range;
but with the application of the device, care must be taken to
avoid the areas of active growth.
External fixators should be removed as soon as possible
after some initial fracture stability is evident radiographically
or to manipulation. However, a cast or orthosis should then
be used to protect the child while further healing, remodel-
ing, and rehabilitation occur.
When significant soft tissue injury is present, removal of
the frame is delayed until the soft tissue is sufficiently healed
and close attention to wound care is no longer needed. This
means that in some patients the bone injuries may have
healed sufficiently to allow removal of the device.
Internal Fixation
When internal fixation is used in the immature skeleton, it
is not always necessary to observe the same principles of rigid
fixation generally applied to fractures in adults. The more
porous, elastic bone of the child requires fixation for align-
ment purposes, rather than to enhance the process of healing
through firm coaptation of fracture surfaces to attain
primary bone healing. The concept of primary bone healing
97
was developed for the mature, remodeled osteon bone of the
diaphysis.
Open reduction may be indicated after a failed attempt at
closed reduction. If the fracture can be reasonably reduced
in a closed manner but it remains unstable and cannot be
maintained with external immobilization, percutaneous or
internal fixation should be considered. Upper extremity
fractures, especially those of the distal humerus, and dis-
placed epiphyseal or physeal fractures are the major indica-
tion for internal fixation in the skeletally immature child,
whereas in the adolescent lower extremity diaphyseal and
intraarticular fractures predominate.
Screw Fixation
Screw fixation usually allows secure fixation, even of small
fragments. It is of particular benefit in periarticular, epiphy-
seal, and physeal fractures (Figs. 4-5, 4-6), leading to stable
interfragmentary fixation. There is a potential for growth
arrest if the threads cross the physis. Screw fixation may be
done with fluoroscopy, utilizing cannulated screws after
initial pin fixation of the fracture. The smooth pin may thus
function as the guidewire for the subsequent screw. It may
be subject to breakage from shear stress and, accordingly,
when used in the lower extremities should be coupled with
FIGURE 4-5. Polytrauma in a 14-year-old boy. The closed femoral
fracture was treated with an intramedullary rod. The type 2 physeal
fracture of the proximal tibia was stabilized with screws in the large
Thurstan-Holland fragment. The fracture still did not close com-
pletely because the fracture extended laterally between the
Thurstan-Holland fragment and the physis, creating a free me-
taphyseal fragment. It probably occurred during manipulations for
placing the femoral rod. The epiphysis was subsequently stabilized
with K-wires.
98
A B
FIGURE 4-6. (A) Multiple trauma in a 7-year-old girl (bicycle versus
car). Bilateral femoral shaft fractures and an intertrochanteric right
femoral neck fracture are evident. She also had a right tibial frac-
adequate protection with either a cast or brace and gradu-
ated weight-bearing.
Interfragmentary screws may also be effective in a child.
The decreased rate of comminution (compared to adult frac-
tures) lessens their necessity.
Plate Fixation
Plate fixation produces relatively rigid to completely rigid
internal fixation (Fig. 4-6), depending on the type of device
used.4 Again, it often should be supplemented with a cast in
a child. Such augmentation allows the use of smaller plates.
Rigid compression is not usually necessary because of the
remodeling potential of the developing skeleton. Plates do
give stable, definitive skeletal fixation. A drawback is that one
often must strip the periosteum and periosteal blood supply,
which may lead to a decrease in bone mass underneath the
plate for increased cortical porosity or increased endosteal
resorption. Periosteal stripping may also encourage new
bone formation that envelops the plate, making removal dif-
ficult, especially depending on the time between insertion
and removal. Overgrowth is a particular problem in the child
because of appositional expansion and periosteal reactivity.
The Arbeitsgemeinschaft für Osteosyntheseficagen (AO)
technique relies heavily on dynamic compression to enhance
primary bone healing with osteon remodeling.198 This is not
as important in children, as it is desirable to encourage for-
mation of the reactive callus in the subperiosteal region and
allow remodeling. In many children in whom a plate is used,
that particular cortex may no longer be “existent” in 2–3
years as the child grows the bone latitudinally (in width or
diameter) as well as length.
Foux et al. studied whole-bone flexural rigidity during
healing of plated osteotomized beagle femurs.51 They
thought that plated femurs may never reach the rigidity of
4. Treatment Concepts
C
ture and chest and head injuries. (B) Femoral neck fracture was
reduced and treated with a cannulated screw. (C) Both femoral
diaphyseal fractures were treated by plate fixation.
the “preinjury” state. Plating, especially rigid plating, sup-
presses external callus formation and essentially restricts
healing to direct growth of haversian systems across the frac-
ture gap (primary bone healing). Another consequence is
the development of osteopenia underneath the plate, which
is probably caused by stress shielding of the underlying bone
or by interference with vascular dynamics. Less rigid fixation,
which allows limited interfragmentary motion, results in
callus formation and more rapid healing.
Kregor et al. reviewed 12 children (15 fractures) with mul-
tiple injuries or head injury whose femoral shaft fracture was
treated with plating.102 The 15 fractures had clinically and
radiographically healed at an average of 8 weeks. The plates
were removed at an average of 10 months after the index
operation. Some overgrowth (average 0.9 cm) still occurred.
No child had a refracture after plate removal.
Metal plates certainly have a stress-protecting effect and
lead to a reduction in elastic stiffness and decreased mineral
content in the bone segment covered by the plate. The
extent of stress protection varies according to the species
studied, the extent of skeletal maturation, the duration of
the plate application, the dimensions of the plate relative to
the bone, and the rigidity of the plate itself.99 There is recov-
ery of diaphyseal bone strength after removal of rigid inter-
nal plate fixation.
Internal fixation may also be used in complex open frac-
tures during the reconstruction phase. Figure 4-7 illustrates
the case of a 14-year-old girl who had sustained an open
tibiofibular injury with removal of a segment of tibia during
her initial treatment. Following transfer, the fibular fractures
were plated and a long blade plate was used to restore and
maintain tibial length. As a precaution, the soft tissues were
again débrided and packed with antibiotic-impregnated
beads. When the wound cultures became negative, a vascu-
larized fibular graft was used to restore tibial integrity.
Specific Methods of Fixation 99

FIGURE 4-7. (A) Multiple trauma in a 14-

year-old girl. A large segment of tibia had
been extruded from the leg. She was
originally placed in an external fixator to
allow wound care and maintain length.
Subsequently she underwent plating and
implantation of antibiotic-impregnated
PMMA beads. (B) A vascular fibular
graft was transferred from the opposite
leg, and a synostosis spontaneously
developed.

A B

Intramedullary Techniques
Intramedullary rods allow axial alignment to be maintained
without undue stress to the surrounding bone. This stable
axial alignment allows progressive load-sharing and weight-
bearing, as most children’s fractures treated with these
devices tend to be simple rather than comminuted fractures.
They generally do not disrupt the periosteal blood supply.
Extensive reaming, however, may affect endosteal circulation
and is much less necessary in the child. The problems relate
to using care with the insertion when you are near the
growth plate.16,69,189 Flexible rods may still allow mild angular
deformation, which may be addressed by temporary appli-
cation of a cast or brace (orthosis).
Intramedullary techniques should not violate an active
growth plate.16,67 The increasing utilization of medullary rods
in femoral shaft fractures in children has led to a lower sug-
gested age for application. However, the growth plate of
the greater trochanter and any residual epiphysis and physis
along the superior and posterior femoral neck may be
damaged by inserting such a rod and can lead to
trochanteric growth arrest with a valgus deformity (see
Chapter 21).
Flexible intramedullary devices such as Nancy or Enders
nails or rods (Fig. 4-8) are more appropriate, as they can be
inserted through metaphyseal windows and kept away from
the growth plate.43,50,55,108,113–116,118,123,131–135,153,204,213 Ligier et al. FIGURE 4-8. Elastic stacked rods for femoral shaft fracture (large
assessed elastic stable intramedullary nailing of the femoral arrowhead). Small arrowheads indicate the entry points in the
shaft in children.113–116 Flexible rods were introduced metaphysis.
through the distal metaphyseal region. Complications were
minimal, the most common being minor skin ulceration
caused by the ends of the rods. There was no significant over-
growth when end-to-end apposition was attained. Early
100
weight-bearing was recommended, obviating the need for
prolonged bed rest.
The most extensive utilization of elastic nailing has been
reported by Metaizeau and colleagues.131–135 They developed
a wide array of these nails and have used them for virtually
every longitudinal bone in the growing skeleton. These
techniques and uses are well illustrated in Metaizeau’s
monographs.132,133
Biodegradable Materials
As discussed elsewhere in this chapter, a perennial concern
and argument in orthopaedics is the benefit of or need
to remove implanted hardware, especially when used for
fracture treatment or reconstructive surgery. The potential
for implantation of biomechanically acceptable plates
and screws that are eventually resorbed is an attractive
concept.79,136,147,149,154,199
Smooth pins, screws, and plates are being constructed of
various biodegradable materials. Several products are now
available for clinical use. They maintain clinically useful
mechanical strength for weeks to months after implantation.
The review article by Blasier et al. summarized much of the
basic biochemistry, resorption characteristics, and biome-
chanics of these bioresorbable implants.17
There are a number of reported osteolytic reactions to
these implants, often many months after the fracture has
been fixed and has healed.53,54,120 The appearance is compara-
ble to osteomyelitic changes. Friden and Rydholm reported a
severe case of aseptic synovitis of the knee after fixation for
osteochondritis dissecans.53 Fraser and Cole also reported
significant inflammatory resections.52 These changes have
lessened with alteration of implant composition.
Benz et al. showed that bioresorbable implants can be used
effectively to treat intraarticular and shaft fractures in chil-
dren.13 Their study was confined to the use of pins similar to
smooth K-wires. However, the smooth pins do not allow com-
pression of a fragment to the intact portion of the skeleton.
In a concomitant postmortem study they produced torsional
fractures in the femurs of infants aged 5–15 months. The
fractures were then fixed with one resorbable screw and put
under torsional loading until the bone (actually the screw)
refractured. The postfixation torsional force amounted to
77% of the original fracture force. They thought that the
mechanical stability of implanted biodegradable screws was
clinically acceptable.
These screws should be used as an adjunct to maintain
anatomic reduction while a child is also treated by other
means, such as a well-fitting cast.149 The biodegradable
devices may also encourage sufficient healing and remodel-
ing to allow the child to undergo more rapid rehabilitation.
Lehmann et al. studied the use of biodegradable plates
and screws in dogs followed up to 4 years after implanta-
tion.110 They found that polylactic acid materials were bio-
compatible, were of adequate strength, and had a suitable
absorption pattern. There was no interference with bone
healing, and there was complete resorption of the implant
after 4 years.
Böstman et al. studied the process of degradation and
tissue replacement of polyglycolide screws after experimen-
tal femoral osteotomy fixations.21–26 At 3 weeks the screw was
4. Treatment Concepts
intact. At 6 weeks the onset of degradation became appar-
ent. This process was associated with a foreign body reaction
(nonspecific). The reaction appeared to be an osteolytic
expansion of the implant cavity during screw degradation.
Occasionally a sclerotic rim of reactive bone formed around
the osteolytic cavity. By 12 weeks 74% of the periphery and
28% of the central core had been resorbed. At 36 weeks
there was no evidence of the implant material.21–26
Yamamuro et al. evaluated biodegradable screws, pins, and
nails in 143 patients.228 Only one patient failed to achieve
osseous union. In 12 cases, all done early in the study, screw
breakage occurred and was thought to be due to an inap-
propriate size of the bone tap. There were no instances of
foreign body reaction. Svensson et al. reported the use of
biodegradable osteosynthetic materials in 50 children with
transphyseal or osteochondral fractures.201 Two patients had
nonunion of articular radial head fractures, thought to be
related to a foreign body reaction.
Manninan et al. assessed polylactide screws in the fixation
of olecranon osteotomies.122 They found that after 6 weeks
the polylactide and metallic fixation groups were similar, but
after 12 weeks the polylactide osteotomy strength was signif-
icantly greater. They thought that the stress shielding asso-
ciated with metallic fixation could be avoided by the use of
bioresorbable screws, but they also emphasized the con-
comitant use of external support in places of high mechan-
ical strain.
Hope et al. used biodegradable pin fixation for children’s
elbow fractures.80 They compared patients treated with K-
wires. The K-wires were associated with pin tract infection
and soft tissue ossification, and they required removal under
anesthesia in 9 of 11 cases. Only one complication occurred
in the polyglycolic acid group; this patient developed
ischemic necrosis and premature fusion following stabiliza-
tion of a medial epicondylar fracture.
Ostuka et al. placed small-diameter pins (1.3 mm) across
the physis of skeletally immature rabbits.146 Although no
growth disturbances were evident 16 weeks after implanta-
tion, 7 of 10 rabbits had histologic evidence of osseous bridge
formation across the physis. In the more slowly evolving
human physis, this risk may be significant. Mäkela et al.
showed a similar growth disturbance.120 Donigian et al. found
that absorbable polylactic acid screws stabilized experimen-
tal type 4 growth mechanism fractures (goat distal femur)
effectively.38 Absorbable materials may also be a vehicle for
delivery of antibiotics, encourage bone regeneration, and be
an alternative to bone wax.109,139,200
Tissue glue is another type of biodegradable fixation
undergoing studies of clinical efficacy. Angermann and
Riegels-Nielsen used fibrin sealant for osteochondral frac-
tures of the talar bone.5 This technique has also been
described for other areas (e.g., knee). Currently this mater-
ial is not readily available in the United States but is under
Food and Drug Administration (FDA) study.
Complications of Fixation
During and following reduction and either external or inter-
nal fixation, it is imperative that radiographs be obtained to
document the position of the fragments. This may involve a
Complications of Fixation 101

portable radiograph or a “hard copy” from the image inten-

sifier. It is difficult to justify a film 1–2 weeks later that shows
malposition when none was obtained intraoperatively to
show the acceptability of the reduction.
Reliance on the implanted hardware is often a problem.
Children have an occupation known as play, and they try to
get back to it as soon as possible. The child, through his or
her parents, must be discouraged from resuming activity
when the fracture pain dissipates. The initial concern of
parents as to what the posttreatment limitations are quickly
changes to: “Should my child be doing . . . ?” As such, if one
follows the dictum of minimizing the amount of hardware,
one must supplement it with external restraint or constraint
devices such as a cast, braces, or splints. Otherwise, interest-
ing problems may occur (Fig. 4-9).
The other problems with internal fixation include osseous
overgrowth of the hardware (Fig. 4-10), soft tissue stripping
that may lead to dysvascular fragments, fixation devices that
are too rigid leading to bone atrophy and growth arrest, or
growth stimulation from the surgical approach and possibly
from the presence of the device.66,67,150 Placement of metal in
structurally weak or osteoporotic bone may also lead to
failure of fixation. FIGURE 4-10. Buried plate 21 years after application.
Inappropriate utilization of fixation devices may lead to
delayed union or nonunion. Large, rigid fixation devices are
generally unnecessary, as is extensive reaming of the
medullary cavity to fit a large rod. The use of such plates in stripping may increase the risk. If either develops after ORIF,
children may actually deter healing and contribute to removal of the device and more conservative methods (i.e.,
delayed union if not nonunion. Children’s fractures rely casting, orthotic bracing) are indicated.
extensively on subperiosteal new bone formation, which is Growth damage may occur from inappropriate applica-
deterred by both the rigidity of fixation and the stripping of tion of hardware. A malleolar screw or any other threaded
the periosteum to apply such a device. Small, thin plates are device that crosses the physis substantially increases the risk
less likely to cause such a problem. of causing or worsening growth plate damage. When inter-
Delayed union and nonunion are rare complications of nal fixation is used with an intramedullary rod, the physis
children’s fractures. Rigid fixation and excessive periosteal must not be damaged. Bjerkreim and Langard showed that
placement of a medullary nail through the growth plate in
rats led to damage of the central portion of the growth plate
and premature arrest.16
Infection is a serious complication of any operative pro-
cedure.78 The use of prophylactic antibiotics is appropriate,
even for a closed fracture treated with external fixation or
percutaneous pinning. The child’s skeleton is at greater risk
for hematogenous infection than is that of the adult. Pin
track infection may be significant.61 One study reported an
overall rate of 6% (10.3% for femoral pins, 2.1% for tibial
pins).61 The average time to pin removal was 11.7 weeks for
the femur and 10.0 weeks for the tibia. Infections tend to
occur late: 6–12 weeks after placement (average 9 weeks).
Pin migration may occur, often to a distant site,14 and is
more likely with a smooth pin. Vascular damage may occur
when fixation pins are near a major blood vessel.68 Similarly,
protruding screws or plates may damage vessels.

FIGURE 4-9. Treatment of a femoral fracture with a plate. The
patient fell from a trampoline (he was supposed to be exercising
minimal weight-bearing). The plate bent, but no screw pullout
occurred. He was taken back to the operating room, the plate was
removed, and a new plate was applied.
Hardware Removal
Once the fractured bone has healed, the treating
orthopaedist is presented with a dilemma: Should the plate
or rod be removed or left in the patient? The pain associ-
ated with the implant usually justifies reoperation and the
potential for refracture. The difficult decision comes in the
asymptomatic patient.
102
It is important to realize that when internal fixation is used
in children it may be removed as soon as sufficient healing
of the fracture permits more traditional methods of treat-
ment. Bone tends to overgrow plates and implanted screws
in children. Second, and more important, when noncircular
cross sections are constrained, the resulting shear stress dis-
tribution is different from what Saint-Venant torsion (with
warping) would predict.12 In children it is important to avoid
stress shielding because the bone is in a constant state of
remodeling and redistribution of osteon patterns within the
developing diaphyseal bone.163,198 It is important that the
child make any remodeling forces as natural as possible.
Removal of fixation devices as soon as possible is an appro-
priate approach that increases the ability of bone to remodel
spontaneously.
A number of authors recommend removal of currently
used fixation devices,106 whereas others oppose routine
removal.91,174 The AO group particularly recommends
removal of all plates after healing (except hip fractures in
elderly patients or non-weight-bearing bones such as the
humerus). DeLuca et al. reported high refracture rates,
especially with plates removed less than a year following
initial placement.35 Others have also reported refrac-
ture.77,91,107,161,180
Obviously any external fixation device pin or percuta-
neous (protruding) pin should be removed. The use of per-
cutaneous pinning to stabilize fractures, such as a
supracondylar distal humerus or a lateral condylar distal
humerus, allows rapid removal of the extraneous or subcu-
taneous fixation device. However, it is also important, with
the use of internal fixation, to consider removing the
implanted device as soon as healing and remodeling of the
fracture permits. Fixation devices effectively function as
FIGURE 4-11. Failure of bone remodeling around a fixation device.
It led to a pathologic fracture just below the plate. Reactive bone
is evident.
4. Treatment Concepts
stress risers and may affect the normal remodeling of the
enlarging skeleton. There are instances of device-related
fracture (Fig. 4-11). If there are deformities that require
subsequent reconstruction, the overgrowth of bone may
make removal of the devices difficult and may add to the
morbidity of the subsequent operative procedure. The
stress shielding the devices indubitably cause may inhibit
normal bone remodeling. They do not generally interfere
with appositional growth in a young child. In fact, this
process may continue to the point of complete envelopment
(incorporation) of the plate. The device may also be a focus
of late infection.
DeLuca et al. described 37 patients who had 62 diaphyseal
plates removed.35 Seven of these patients had a subsequent
refracture. The interval from the time of plate removal to
refracture ranged from 42 to 121 days. Radiolucency at
the site of the original fracture was seen in most patients
when the plate was removed. After removal protection was
minimal.
Spalding et al. assessed the removal of plates and screws
used for corrective femoral osteotomies in children.195 The
plates had been in place for 1–32 years and were either com-
pletely buried in bone or endosteal (in 24%). Approximately
one of five screw heads sheared or required excision, rather
than simple reversed screwing. The screw shanks had to be
cored from the bone. The procedure is far from benign.
Spalding et al. believed that plate removal should always
precede joint replacement, allowing the bone to “recover”
from the procedure before undertaking any major joint
reconstruction.
In a hospital setting where implanted hardware in pedi-
atric patients was routinely removed, 38% of the patients had
their hardware removed for indications other than uncom-
plicated healing.184 Almost 20% of the patients had painful
or subcutaneous hardware. Other indications were infection
(7%), fixation failure (7%), migration (4%), and malunion
(2%). Complications included incomplete removal of the
hardware (7%) and two postoperative fractures.
Residual screw holes may be a considerably more impor-
tant cause of bone weakness after plate removal than any cor-
tical atrophy or demineralization.179 In another study using
bone density measurements, significant cortical atrophy was
found in only 1 of 14 patients after plate removal.177,178
The process of screw removal may produce microfractures
within the screw hole. These microfractures create fresh
stress concentrations that temporarily weaken the bone.121
The result may be a complete fracture.
Rai et al. described a screw that loosened from a femoral
plate (for treatment of a fracture) and migrated to the knee
joint. The plate had been in place for 22 years.166
Leaving the plate in may not be a totally benign alter-
native. Once the plate has promoted fracture healing,
its presence becomes superfluous to the function of the
skeletal component. The length of time it takes to ac-
complish this may be short.152 An implant absorbs some of
the normal loads. Thus the bone loses strength owing to
cortical thinning and osteoporosis. Loss of strength may
predispose to fracture near the end of the implant,
where stresses tend to be concentrated. Some designs to
increase plate (implant) strength actually increase stress
shielding.12,15,51,137,205,206,211,214,215
Complications of Fixation
Labosky et al. removed plates and screws from 51 of 98
adults.106 One refracture occurred through an unhealed
fracture site (plate removed 6 months after surgery), and
one occurred through the proximal screw hole of a still
implanted ulnar plate inserted 3 years before. Leaving a
plate in for the remaining life of a young patient cannot be
thought of as a benign decision, considering the chance for
refracture and the potential complications from prolonged
exposure to metal corrosion complexes and metallic ions.
In addition to problems of altered biomechanics, other
considerations must be kept in mind when contemplating
permanent placement of a metal implant in a child or
adolescent. The most commonly used alloy employed in
implants is 316 L stainless steel, which is composed of iron,
nickel, chromium, and molybdenum. It is considered rela-
tively corrosion-resistant. However, any metal implant in the
saline environment of the human body has a finite corrosion
rate. The implant area is bathed with a protein-rich elec-
trolyte solution that contains a low concentration of chemi-
cal complexes and ions of the materials comprising the
implant. Thus the plate interface (surface) is consistently
going into solution, with local and systemic release of
constituent ions and corrosion complexes. The loss of the
implant’s protective external layer is termed depassivation.
This process increases with any minor mechanical damage
during insertion (e.g., a surface scratch or nick). Abrasion
between screw and plate may occur during insertion or sub-
sequently if there is micro- or macromotion.
Fretting corrosion is a degradation process in which fric-
tion between the screw head and plate creates small pieces
of metal at the abrasion site. Generation of these particles
increases the surface area of metal exposed to the saline envi-
ronment. Fretting particles may be small enough to be trans-
ported by bulk lymphatic flow or within phagocytic cells.
Galvanic or bimetallic corrosion occurs between two dis-
similar metals sharing the same electrolyte environment. It
is most evident when the plate and screws are composed of
different metals. However, even the use of implant tools of
different metals may set up an insidious local process where
contact is made (acute fretting leaving particles of the tool).
No one has ever considered the remote potential of other
implants, such as orthodontic devices, which are common in
children. The effect of such galvanic reaction may be black-
ened reactive tissue around the device, which is evident
during its removal. Try to ensure that all device components
are from the same fixation set (e.g., plates and screws). Using
different fixation methods such as internal and external fix-
ation or different types of internal fixation (pin in hip, plate
on femur) introduces a galvanic risk.
The most common physiologic response is inflammation
with creation of fibrous tissue and reactive fluid. Late infec-
tion may also occur. Concentrations of stainless steel con-
stituents adjacent to the implant inhibit macrophage
chemotaxis and phagocytosis, making the implant area more
susceptible to infection.
Implanted metal may become surrounded by proliferative
inflammation to form a granuloma, which may become
fibrotic over time. In rare instances benign and malignant
tumors may develop.117
When an external fixation device is removed, the child
needs to be protected for a variable period of time. My pref-
103
erence is either a cast or a full contact orthosis coupled with
progressive mobilization to minimize the risk of refracture.
Tourniquet Use
During open fracture reductions an extremity tourniquet is
often applied. Tourniquets must be used carefully in chil-
dren, as neuromuscular damage may occur.151 If not prop-
erly used, tourniquets can cause paralysis, sensory loss,
excessive edema, skin problems, or muscle damage. Less
pressure may be necessary in the child to obtain the desired
effect.83,112
Levy et al. recommended inflating a tourniquet initially to
300 mmHg and then decreasing it to a calculated value.112
The equation they used was:
Tourniquet pressure = 1.68 ¥ mean BP + 50
where BP is blood pressure. Using this formula the average
tourniquet pressures were 202 ± 34 mmHg compared to the
routinely used pressures of 250–300 mmHg.
The tourniquet may be applied to the forearm for hand
injuries.96 Khuri et al. assessed the efficacy of the forearm
tourniquet.96 No patient had neurologic complications.
Minimal intraoperative bleeding occurred when the pres-
sure was higher than 75 mmHg above systolic blood pressure.
Tourniquet time is also important and is directly related
to the extent of metabolic changes due to the temporary
ischemia. Tourniquet-induced hyperthermia has been
demonstrated in young children and is related to the dura-
tion of usage.244 Breathing periods are recommended,
although the recommendations vary from 60 to 120 minutes
of sustained ischemia.287
Postprocedure release, especially in a multiply trauma-
tized child, may have an adverse physiologic effect.60,119
Goodarzi et al. assessed the hemodynamic and metabolic
effects of tourniquet use.266 Maximum changes in tempera-
ture and pulse rate occurred in patients who had tourniquet
application lasting more than 75 minutes. Lactate and end-
tidal CO2 levels were also significantly increased in these
patients.
Venous blood from an extremity made ischemic by a
tourniquet shows a progressive decrease in pH and PaO2 and
an increase in PaCO2 and lactate as the ischemic time
increases. In children in whom O2 consumption and meta-
bolic rate may be two to three times higher than in adults,
tourniquet hemostasis may result in an even greater accu-
mulation of ischemic metabolites. When these ischemic
metabolites enter the general circulation after tourniquet
release, systemic acidosis may cause sympathomimetic activ-
ity and an increase in temperature and pulse rate. These
metabolites may also seep into the systemic circulation
through the nonoccluded intraosseous/intramedullary cir-
culation even while the tourniquet is inflated. This slow
leakage into the systemic circulation through the “skeletal
bypass” is responsible for increases in temperature, lactic
acid, and end-tidal CO2.
The vascular bed of bone has x-adrenoreceptors, mus-
carinic receptors, and prostaglandin H2/thromboxane A2
receptors.248 Such receptors may be affected, both
intraosseously and extraosseously, when ischemic metabo-
lites progressively accumulate in the extremity while the
104
tourniquet is inflated, leading to alterations in the tone of
the medullary vessels and affecting intramedullary hemody-
namics to “bypass” the tourniquet
Rehabilitation
Single Fractures
Physical therapy in the otherwise normal child has a negli-
gible role in the postinjury management of most childhood
fractures. Active use of the part by the child is almost always
superior to the use of massage, manipulation, and exercise
by a therapist. Exaggerated limps gradually disappear, and
stiff elbows loosen, even if little attention is paid to this phase
of treatment. Resumption of normal use and activity usually
permits a progressive return of motion. Residual loss of
motion in the child probably is caused in part by anatomic
malunion, which can rarely be corrected by aggressive phys-
ical therapy, usually perceived by the child as an unnecessary,
painful procedure.
The therapist does, however, play a major role in the reha-
bilitation of the child with a functional disability. Children
with neuromuscular disorders, such as cerebral palsy and
myelomeningocele, sometimes require extensive physical
therapy to attain preinjury activity levels, as trauma may
cause significant regression.
Regaining range of motion after specific joint (intraartic-
ular) injury is sometimes a problem with pediatric patients.
Guidera et al. showed that continued passive motion
machines may be applied effectively to decrease such
problems.65
Multiple Injury
Formal physical therapy and rehabilitation are generally not
necessary for most injured children. In the multiply injured
child, however, this is usually not the case. Because of the
severity and complexity of the injuries, long hospitalization
and multiple surgeries are often required. Although it has
been shown that a child can tolerate prolonged immobiliza-
tion without the usual complications seen in an adult (e.g.,
joint stiffness, severe muscular atrophy, disuse osteoporosis),
complications can and do occur, and a good result cannot
always be assumed or ensured. Significant long-term disabil-
ity, most often related to injuries to the central nervous
system (CNS) and musculoskeletal system, can occur in chil-
dren. Aggressive rehabilitation has been shown to decrease
these complications and improve the overall results.
Once any soft tissue and internal injuries have healed and
bone union has been obtained, rehabilitation of the multiply
injured child is important. It typically consists of range-of-
motion exercises followed by strengthening the musculature.
It is important that these children undergo long-term follow-
up to determine ultimate outcome with respect to function
and growth of the injured extremities. Follow-up to monitor
growth development of the injured extremities should con-
tinue until there is skeletal maturity.
Physical therapy should be initiated as soon as the child’s
medical condition permits. Early physical therapy consists of
gentle range-of-motion exercises of the noninjured or stabi-
4. Treatment Concepts
lized extremities to avoid soft tissue contractures and joint
stiffness. This is especially important in the head-injured or
spine-injured patient. Additional physical therapy can be
instituted as the child’s condition allows, including transfer
training, resistive strengthening, and eventually ambulation.
Each child must be dealt with individually, as the spectrum
and severity of injuries dictate the type and level of therapy.
Close communication and cooperation between physicians
and therapists is extremely important. Most physical therapy
can be initiated while the child is still in the trauma center.
Once the child’s condition no longer requires that level
of specialization, transfer to a different facility can be con-
sidered. It might be to another acute care facility that is not
a trauma center but is more accessible to the family or to a
long-term rehabilitation facility if acute care is no longer nec-
essary. Children are often transferred long distances to be
treated at trauma centers, and these distances can become a
burden for families. Therefore when the child’s condition
improves, every effort shold be made to transfer the child to
a facility closer to home. Some trauma centers are equipped
with facilities for both acute care and long-term rehabilita-
tion services. This enables transfer from acute care to long-
term care status while maintaining continuity of treatment
by many of the same physicians and therapists. This situation
is desirable because children develop important relation-
ships with, and dependencies on, the treating physicians and
therapists; severing these relationships can be traumatic to
the patient.
Children with severe head, spinal, and musculoskeletal
injuries are most often in need of prolonged rehabilitation
and are more likely to have permanent disabilities. Severe
head injuries account for most long-term rehabilitation and
long-term disabilities. Children with head injuries require
specialized facilities equipped for long-term rehabilitation—
both physical and cognitive capacity rehabilitation, includ-
ing speech and learning. Multiple fractures in the absence
of CNS injury can also result in long-term disability requir-
ing prolonged rehabilitation. In addition to the usual modal-
ities, specialized treatment with orthoses, prostheses, and
appliances is often necessary for rehabilitation to optimal
function. The fitting and use of orthoses and prostheses in
children are specialized because the child continues to grow,
and close monitoring and frequent modifications are neces-
sary. The appropriate use of physical therapy can signifi-
cantly improve the outcome of these children.
Psychological Rehabilitation
Psychological rehabilitation of the injured child is often as
important as physical rehabilitation.135 The physical trauma
often creates severe psychological trauma that is overlooked
in many cases. Following the initial traumatic event, the
patient is faced with continued pain from the injury and
often multiple, painful surgical procedures, disfigurement
and loss of body image, and prolonged separation from
parents, siblings, family, friends, school, and home. This psy-
chological trauma is not limited to the child; it also affects
the parents and family and often the person who feels
responsible for the injury. Dysfunctional behavior is fre-
quently seen in children after trauma, including phobias,
scholastic difficulties, depression, and rage attacks. It is man-
Sedation and Anesthesia
ifested not only by children with head injuries but also by
those with severe injuries without CNS involvment. Delays in
the normal developmental processes are common; and in
many cases the child is noted to regress. Such reactions are
considered normal, although they can become extreme.
Psychological problems cannot be avoided completely, but
they certainly can be lessened by appropriate early inter-
vention with the patient and the family. The physicians and
staff must be aware of these problems and try to be as sup-
portive as possible. It is important to spend time with the
patient and family, informing them of the injuries sustained,
what is to be expected, the procedures to be performed, and
the prognosis. Painful procedures should be explained in
detail and their importance stressed. Children should be
allowed to express their fears and concerns and be made to
feel a part of the process. They must be given assurances that
they have not lost total control over their environment. The
family should be allowed to be with the child as much as is
physically possible. It is often desirable to allow one family
member to remain in the patient’s room. Many rooms are
equipped with extra beds so parents can sleep in the room
with the child. Social and psychological counseling is often
necessary, especially when the child or family appears to have
problems coping with the situation.
Sedation and Anesthesia
Before satisfactory closed or operative treatment can be
undertaken, the fears and apprehensions of the child (and
often the parents) must be dispelled, and pain should be
alleviated.290,291,297 If reduction is necessary, proper levels of
sedation, anesthesia, or both are essential.251–253,293,296,298,299
Generally parents may be present when sedation, analgesia,
or anesthesia is started in the office or emergency room but
should be excused if any significant manipulation is
required.237
The need for reduction of a fracture or dislocation can be
a terrifying experience not only for the child but also for the
parents, who are often relatively young and may have a pre-
vious remembrance of a similar experience in their own
youth. The conception that a child, especially a young one,
cannot perceive pain is erroneous. Children over 18 months
of age can and do anticipate pain. Any fears or anxieties
they have are only heightened by similarly fearful and
anxious parents. Accordingly, before satisfactory treatment
of a fracture can be provided, the fears and apprehensions
of the child must be dispelled, and pain should be
alleviated.120,135,258,287
There is a tendency to undertreat pain in chil-
dren,262,273,274,283,288 often based on a concept that infants, tod-
dlers, and young children perceive pain differently.241,268 This
generalization is inappropriate. Any child feels and reacts
physiologically and neurologically to pain. The difference
lies in the psychological reaction to the pain. Some children
are stoic, and others are highly emotional. The presence of
the parents may additionally affect the child’s basic
responses.237 The CHEOPS scale is a reasonable method for
assessing pediatric pain.277 A survey of pain management pat-
terns found that emergency department analgesia was used
less frequently in the pediatric population than in adults.282
105
Inadequate dosing of discharge analgesic medication in chil-
dren was also a significant problem.
The proper choice of sedation, anesthesia, or both for
pediatric patients, particularly those who must undergo
emergency or relatively elective diagnostic procedures
related to injury, is controversial.232–234,257,263,281,294 Strain et al.
found that intravenous sodium pentobarbital (Nembutal)
was the most efficient, with only two failures among the 419
patients sedated this way.294
Children present unique sedation and anesthetic consid-
erations related not only to their small size but also to phys-
iologic differences.238,239,246 An inverse relationship exists
between age and anesthetic requirements. The changes in
anesthetic requirements with age parallel changes in cere-
bral oxygen consumption, cerebral blood flow, and neuronal
density.279,284
With any fracture requiring muscle relaxation for reduc-
tion, a general anesthetic is more useful, particularly for
supracondylar humeral and dorsally displaced distal radial
fractures. If general anesthesia is used, the child may be
admitted to the hospital for observation. Not only must they
be monitored for recovery from anesthesia but also for their
peripheral neurovascular response to the injury, as displace-
ment and manipulative reduction, which may be difficult,
certainly constitute further trauma to the already injured
tissues.
Children with multiple fractures or injuries usually have
significant pain and blood loss. There may also be cranial or
spinal nerve injury. These children are exposed to promi-
nent anesthetic risks that include decreased or delayed
gastric emptying (which increases the risk of aspiration
pneumonitis), hemodynamic instability, and positioning dif-
ficulty. Awake intubation, which can be extremely stressful,
may be necessary, especially if spinal cord function must be
assessed immediately after insertion of the nasotracheal
tube.
Respiratory disease, especially upper respiratory infection,
is common in children. There is a reasonable chance that
any child sustaining a fracture has recently recovered from
or is acutely suffering from an upper respiratory infection.
A viral etiology is most likely, but bacterial infections (e.g.,
suppurative tonsillitis or strep throat) may be present. These
infections may be introduced to other areas by the intuba-
tion process. Many of the medications exacerbate preexis-
tent airway disease by drying the airway, interfering with
ciliary function, enhancing atelectasis, and triggering croup.
Asthma, another common problem in children, may be con-
verted to status asthmaticus by anesthetic agents or the
mechanical obstruction of the airway by the endotracheal
tube. If acute or chronic lung disease is present, regional
anesthesia is preferable.
Children at risk for hemoglobinopathies (e.g., sickle cell
trait or disease, thalassemia) should be appropriately
screened. The syndromes may be triggered or worsened by
anesthesia, tourniquet use, or both.
Neurologic factors or diseases must be considered. Many
children, particularly those with cerebral palsy, may be on
antiseizure medications. The drugs used to control seizures
may interfere with preoperative sedation or neuromuscular
blocking agents. Monitoring neuromuscular blockade when
paralysis may be desired for reduction is not effective if the
106
limb is paralyzed consequent to central or peripheral neu-
rologic injury.
If extensive soft tissue injury has occurred, especially that
associated with denervated or crushed muscle, the use of
paralyzing agents must be reconsidered. Succinylcholine
administration may cause rapid release of massive amounts
of potassium, which creates a potential for cardiac arrhyth-
mia or asystole.
An ideal drug for fracture reduction in the emergency
room setting should have a rapid setup time and rapid onset
of action. Intravenous medications offer advantages over a
regional block or access to the operating room and general
anesthesia. The need to establish an intravenous access is a
minor disadvantage. However, the use of EMLA cream (lido-
caine/prilocaine) minimizes even this stressful portion of
the anesthesia/reduction sequence.
General anesthesia for emergency fracture treatment
carries with it special risks, the one of most concern being
aspiration pneumonitis. Consider that any child has a full
stomach. Normal times of “NPO” may be affected by delayed
gastric emptying due to traumatic stress and air swallowing,
causing gastric dilatation (which elevates the diaphragm and
reduces lung volume for a general anesthetic). A nasogastric
tube may be necessary to decompress both gaseous and solid
gastric contents.
A full discussion of general anesthesia is beyond the scope
of this chapter. Furthermore, this treatment for fractures is
not usually undertaken by the orthopaedist. Perhaps the
one exception is the use of self-administered nitrous oxide
(discussed below).
Hematoma Block
In older, more cooperative children, the fracture hematoma
may be infiltrated with a local anesthetic.235,272,302 Two points
must be stressed in relation to this technique. First, unless
the tip of the needle is in the fracture hematoma, as evi-
denced by aspiration of blood, anesthesia is often inade-
quate. Second, this procedure must be done with rigidly sterile
technique, after thorough preparation of the skin with a bac-
tericidal agent. Local infiltration may increase the risk of
infection, with all its disastrous sequelae, because theoreti-
cally local infiltration converts a closed fracture to an open
fracture.
Bier Block
Intravenous regional anesthesia may give sufficient relax-
ation for fracture reduction in a child that is superior to
a local hematoma block.236,242,245,247,249,251,259,261,265,269,273,275,295
Injuries that require quick manipulation with which the
trauma of repeated injections of local anesthesia may be
greater than the transient pain of the procedure include
greenstick fractures of the forearm, radial head subluxation
(nursemaid’s elbow), and some interphalangeal dislocations
at the fingers. Completing the greenstick fracture, as is
evident in other chapters in this book, is controversial.
However, if carried out rapidly, the pain is gone by the time
the cast or splint is being applied. Displaced epiphyseal
fractures may result from considerable compressive and
4. Treatment Concepts
translated force and often require strong manipulation for
reduction.
Olney et al. reported on the use of intravenous regional
anesthesia (Bier block) in the outpatient treatment of 400
upper extremity fractures and dislocations in children
ranging from 3 to 16 years of age.280 The procedures were
done in a hospital emergency department. Good analgesia
was achieved in 90% of the patients; only nine children
(2.3%) had unacceptable reductions that required further
treatment under general anesthesia. Olney et al. did not rou-
tinely use this method of regional anesthesia for a fracture
about the elbow, such as supracondylar Monteggia and radial
neck fractures. Similarly, children with bilateral upper
extremity fractures were not suitable for intravenous regional
anesthesia because of the increased combined lidocaine
dose that would be required.
The technique they described commenced with sedating
the patient. One parent is encouraged to remain with the
child to provide support and to ensure the child’s continued
cooperation. The pneumatic tourniquet is placed above the
elbow of the injured arm. A 23 gauge needle is inserted into
a vein on the dorsum of the hand, and the limb is elevated
for 30–60 seconds before cuff inflation between 100 and
250 mmHg. A solution of 0.5% lidocaine (5 mg/ml) is used
in a dose of 3 mg/kg body weight. The calculated volume is
injected over 30–60 seconds. Anesthesia is usually satisfactory
within 5–10 minutes. The fracture is reduced and a cast or
splint applied. Radiographs are obtained to verify the reduc-
tion. The cuff is kept inflated for at least 20 additional
minutes to allow time for the lidocaine to become fixed to
the tissues and to provide time for remanipulation under the
same block if the reduction is not acceptable. After the cuff
is deflated and removed, the cast may be extended above the
elbow if necessary, and the child is observed for at least an
hour in the emergency department before discharge to
home.
There was only one anesthetic complication in their
series.280 It occurred in a 9-year-old girl who had to be
admitted for observation after myoclonic muscle twitching
occurred approximately 30 minutes after the cuff was
released. In their study, a poor anesthetic rating occurred in
25 children (6.3%), although an acceptable reduction was
still obtained in 21 of them. An Esmarch bandage is not used
to exsanguinate the limb completely because it may be too
painful in the presence of an acute injury. Incomplete exsan-
guination may result in hemodilution of the anesthetic
agent, which might have accounted for some of the poor
results. Furthermore, the dose of lidocaine used in their
study (3 mg/kg) is below the recommended upper limit of
5 mg/kg.
Several conclusions may be drawn relative to the lidocaine
blood levels that may be obtained. First, lidocaine may leak
into the general circulation at the time of injection, as
demonstrated by the presence of lidocaine in the blood of
some patients before cuff release. Because cuff pressure is
more easily overcome if lidocaine is injected rapidly, the
injection should be given slowly over 30 to 60 seconds. Injec-
tion into the antecubital veins, rather than the more distal
veins of the hand, also increases the risk that the lidocaine
will enter the system by “overcoming” the cuff pressure.
However, it seems more appropriate, in view of studies by
Sedation and Anesthesia
Goodarzi et al., that there can be retrograde flow of blood
through the intraosseous (marrow) circulation, thereby
bypassing the cuff and entering the general circulation.266
Second, blood levels differ after cuff release because of vari-
ation in release, in the binding of lidocaine to tissues, and
the rate of release into the general circulation.
Resuscitation equipment must always be available. Chil-
dren should be observed in the emergency department for
at least 1 hour after the procedure before they return home.
Regional Block Anesthesia
Regional blocks, such as axillary or ankle blocks, may be
more difficult in children because of their intrinsic fear.
However, with adequate preparation and sedation these
blocks may be quite effective for both fracture reduction
and prolonged analgesia for a fracture that must be observed
or placed in traction for a finite period after reduc-
tion.250,259,278,300 The method is particularly helpful when
using a femoral block to control pain after a diaphyseal frac-
ture awaiting surgical stabilization.256,267,285
Cramer et al. found axillary block anesthesia to be effec-
tive in l05 of 111 children with elbow and forearm injuries
that required manipulation.254 The technique is well
detailed.
Spinal/Epidural Anesthesia
The use of spinal or epidural anesthesia or analgesia is prob-
ably best reserved for the multiply injured child.258 This
method allows titrated pain management over a relatively
short time while allowing continuing assessment of other
problems, such as intracranial, intrathoracic, or intraab-
dominal injury. Once a decision is reached to proceed with
specific fracture treatment, the anesthesia route is already in
place.
Skin Anesthesia
Many of the aforementioned techniques require needle
insertion for delivery of the anesthetic agent. Children are
fearful of needles and pain. An increasingly utilized method
of topical anesthesia is the application of EMLA cream to the
injection site. EMLA stands for eutetic mixture of local anes-
thetics. EMLA is a topical cream (2.5% lidocaine and 2.5%
prilocaine) that stimulates transdermal spread of the active
ingredients and achieves local anesthesia of underlying
tissues within 30–60 minutes. Another combination cur-
rently under study is a cream comprised of lidocaine,
epinephrine, and tetracaine, termed LAT.301
Sedation
Several analgesic/sedative combinations have been
described for treating children. One of the most commonly
utilized in the past is DPT: Demerol (2 mg/kg) plus Phen-
ergan (1 mg/kg) plus Thorazine (1 mg/kg) given intramus-
cularly 30 mintues before the manipulation. The reliability
of this combination has been questioned.233,293 Newer drugs
allow more predictable results. Guidelines for monitoring
children under the influence of sedating drugs have been
107
developed by the American Academy of Pediatrics
(AAP).232–234
Slovis et al. evaluated a number of drugs as short-term
sedation regimens for diagnostic imaging procedures.292 The
drugs were chloral hydrate, pentobarbital, midazolam, and
diazepam. On occasion fentanyl was used for enhancement
of these drugs. All were found to be safe and efficacious. The
long-term effects were that 84% of the children slept less
than 8 hours after the examination; 90% were drowsy,
unsteady, or both for less than 8 hours after they awoke; and
97% were normally active within 24 hours. Only pentobar-
bital was associated with any hyperactivity, and that usually
was evident in children over 8 years of age. They found that
midazolam was effective in 9 of 10 children who had failed
prior sedation with other drugs. The described drug regi-
mens may also be applicable to closed reduction of fractures.
Varela et al. studied a combination of meperidine
(1.47 mg/kg body weight; range 0.63–3.1 mg/kg) and mida-
zolam (0.11 mg/kg; range 0.020–0.625 mg/kg) for acute
fracture reduction in 104 children.296 One-half of the calcu-
lated dose for each patient was injected (intravenously) over
1–3 minutes. The patient was then observed for 5 minutes
to assess any adverse affects of the medications. Following
this interval the remainder of the dosage mixture was slowly
given until the patient was thought to be adequately sedated
(5–15 minutes), at which point fracture manipulation was
attempted. Of the 104 reductions, 96 were successful. Only
four patients required general anesthesia for a repeat
attempt at reduction. The authors thought that it was a safe
and effective method for closed reduction.
Midazolam (Versed) is a water-soluble rapid-onset benzo-
diazepine that has a short duration of action. Children
appear to have more resistance to the initial effects of
midazolam and systemically clear it faster than adults.286
The child’s emotional state (i.e., anxiety) may also affect
the effectiveness of the drug.276 The half-life of midazolam
ranges from 1 to 4 hours, in contrast to more than 24 hours
for diazepam (Valium).
When midazolam is combined with an opioid such as
meperidine, a narcotic agonist, or morphine, the two
drugs may act synergistically to potentiate those effects that
allow effective fracture reduction (i.e., analgesia, sedation,
amnesia, anxiolysis). Resuscitation equipment must be avail-
able because there are also negative cardiorespiratory effects
that may be potentiated by combining these two drugs.240 If
reversal is necessary, the opioid, which is the more likely
respiratory depressant, should be reversed first with nalox-
one (Narcan). If such reversal is not effective within 1–2
minutes, the effects of the benzodiazepine should be
reversed with flumazenil (Romazicon). Recommended
doses are for naloxone 0.005–0.01 mg/kg IV and 0.5 mg IV
of flumazenil.
Increasing sedation, by repetitive doses or the use of
potentiating agents, may result in prolongation of the recov-
ery period or in other more serious side effects (especially
cardiorespiratory depression).243,255 It is therefore appropri-
ate and advisable to use the most effective drug regimen with
the least side effects.
To minimize drug interactions, only a single sedating drug
may be used, with dosage limits defined and never exceeded.
Because of its therapeutic index and low toxicity, chloral
108
hydrate has long been considered a popular sedative-
hypnotic drug. Midazolam may be used when both amnesia
and anxiolysis are desired.
The use of intravenous diazepam, which has been popular
in the emergency room setting, must be undertaken with
extreme caution. Furthermore, one must remember that this
sedative functions as an amnesic, not an analgesic, agent. The
child feels and reacts to pain but usually does not remember
doing so. Furthermore, the onset of the sedative response
may be delayed, and if the child must be sent to another area
for postreduction films he or she must be appropriately alert
or a respiratory arrest may occur in an area where observa-
tion is minimal and resuscitation may be difficult. Appro-
priate anesthetic equipment must always be available (mask,
oxygen source, and so forth).
Nitrous Oxide
The use of nitrous oxide, especially self-administered, has
been increasingly described in the pediatric population.264
The clinical effects of nitrous oxide are due to low solubility
in blood, its transport in physical solution without protein
binding, rapid diffusion across the alveolar–arteriolar inter-
face, lack of metabolism, and being excreted essentially
unchanged by the lungs. The primary effect on the central
nervous system is an alteration of recent memory, cognitive
function, and sensory perception. The usual dose is a 50 : 50
mixture with oxygen. Complications may occur. About 15%
of patients experience nausea and vomiting.
Wattenmaker et al. described self-administered nitrous
oxide for fracture reduction in an emergency room setting
in a study of 22 children.298 They used a combination of 50%
nitrous oxide and 50% oxygen. The fractures they chose for
reduction under nitrous oxide were those in which a single
maneuver without need for fluoroscopy was judged likely to
be successful. There were two failures in which patients
required further manipulation or an open reduction. The
average time needed to achieve a satisfactory anesthetic level
for the manipulation was 2.6 minutes (range 1–5 minutes).
The average duration of the nitrous oxide administration to
allow reduction and casting was 16 minutes (range 10–30
minutes). When 20 patients were asked to recall their pain,
12 recalled no pain, 7 had minimal pain, and 1 had moder-
ate pain. No patient recalled severe pain.
Evans et al. used nitrous oxide combined with intramus-
cular sedation (meperidine and promethazine) for reduc-
tion of fractures.260 The combination regimen had a rapid
onset and short recovery period. The authors recommended
the use of nitrous oxide as an analgesic and amnesic.
Hennrikus et al. evaluated self-administered nitrous oxide
for fracture reduction in 54 children.270,271 Although 91%
of the children obtained an analgesic effect, 46% had a
CHEOPS score that indicated significant pain at the time of
manipulation. The least acceptable results were in children
with completely displaced distal radioulnar fractures. In
a subsequent study Hennrikus et al. combined self-
administered nitrous oxide with a hematoma block. This
combination proved satisfactory for fracture reduction in 97
of 100 children. The addition of the hematoma block caused
a significant reduction in the CHEOPS pain score compared
to their previous study.
4. Treatment Concepts
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5
Diagnostic Imaging
Engraving of a transphyseal fracture of the distal humerus. This
particular fracture is often found in child abuse. (From Poland J.
Traumatic Separation of the Epiphysis. London: Smith Elder,
1898)
he diagnosis of any injury to the developing muscu-
T loskeletal system relies principally on the appropriate
diagnostic imaging of the specific site of injury and
defining the unique anatomic pattern of the fracture or dis-
location. One of the first injuries depicted utilizing the newly
developed skiagrams of Röentgen was a distal radial physeal
injury in a child.131 Jones and Lodge, less than 2 months after
Röentgen’s announcement of x-rays, built an x-ray apparatus
and began its clinical application.131 Their first patient was a
12-year-old boy who had been shot in the wrist.
The evaluation of chondro-osseous injury by any diagnos-
tic imaging method is based on thorough knowledge of the
changing anatomy and injury response patterns in the devel-
oping skeleton as well as knowledge of the varying imaging
appearances.6,7,14,26,101,104,183,187,230,231,249 Any orthopaedist must
also become familiar with progressively evolving techniques,
such as magnetic resonance imaging (MRI), for diagnosing
obscure injuries of the child’s chondro-osseous skeleton and
the contiguous soft tissues.
Children, being notoriously poor historians regarding a
specific injury occurrence or if they have pain, may or may
not have discernible lesions. Oudjhane et al. found a frac-
ture in 20% of 500 consecutive children being radiographed
for limping or failure to bear weight on a leg.190 However,
children may still have an “occult” fracture even when radi-
ographs are of adequate technical quality and the fracture
cannot be readily determined by routine radiographic
techniques.
Since the previous edition of this book there has been a
technical revolution in the methods for imaging children.
Refinements have occurred in nuclear imaging, ultrasonog-
raphy (US), Doppler imaging, colorized Doppler imaging,
and computed tomography (especially three-dimensional
imaging and reconstruction). MRI, in particular, has evolved
into an important adjunct for the evaluation of otherwise
radiolucent injuries.
Selecting the appropriate imaging methodology consti-
tutes a significant part of the diagnostic strategy for each
patient. The differential diagnosis should initially direct the
choice, with modification as necessary, based on information
gained from any modality or from changes in the patient’s
status.
General Guidelines
Radiography and other diagnostic imaging modalities are
extremely important for concise evaluation of chondro-
osseous trauma involving the developing skele-
ton.113,133,134,169,179,185,191,192,202,214,223,229,260,264 Because of the
varying amounts of bone, differences in bone density (e.g.,
metaphyseal versus diaphyseal cortices), and radiolucent
physeal, epiphyseal, and articular cartilage, fractures in chil-
115
116
dren are not always easy to document radiographi-
cally.16,35,70,190,203,205,252 Interestingly, an article in the radi-
ographic literature was partially entitled, “What have we
been missing?”21
Diagnostic imaging studies must be of sufficient technical
quality to elucidate adequately not only obvious and
not so obvious skeletal trauma but also any distorted soft
tissue contours, extraosseous hemorrhage, fascial planes,
intracapsular fat-fluid levels, and other nonskeletal injuries
(e.g., muscle, tendon, or ligament damage) that may be of
significant import for the complete diagnosis and prognosis
of injured children.64,82,120 Technically poor images should
not be accepted. Standard positional radiographs (antero-
posterior and lateral) should be supplemented, as indicated,
with appropriate oblique views and special diagnostic pro-
cedures such as fluoroscopy, tomography, xerography stress
films, radionuclide scans, computed tomography (CT),
MRI, and US. Some fractures cannot be visualized
roentgenographically when the radiolucent cartilage is
involved (e.g., the distal humerus in an infant). Alternative
procedures such as MRI, sonography or arthrography may
be necessary to delineate specifically the fracture-induced
anatomic changes and displacements of these radiolucent
tissues.19,20,42,49,60,64,74,109,123,133,140,145,147,152,159,196,235,259
During the process of skeletal maturation, there are pit-
falls to avoid when evaluating radiographs. Fractures may
be missed if proper views are not requested. It is imperative
to get as many views as necessary to rule out a fracture
absolutely and to define any differences in the developing
radiographic anatomy. It may require active participation by
the orthopaedist using fluoroscopy to rotate the injured
areas through multiple views to attain the one that best visu-
alizes the injury.
Efforts should be made to appreciate the wide variety of
fractures that may occur in children as a result of the various
biologic responses to trauma at different ages. Small osseous
fragments may be difficult to visualize at the metaphy-
seal–physeal interface if the rest of the metaphysis overlies
them, yet they are essential for accurately diagnosing an
undisplaced physeal fracture in the child with symptoms
compatible with skeletal injury. Stress, torus, and toddler’s
fractures may cause minimal bone disruption. Plastic defor-
mation (bowing), with rare exception, is unique to the
immature skeleton and may be missed if the radiograph is
not carefully assessed.
The importance of an orderly approach to the differential
diagnosis of childhood skeletal trauma cannot be
overemphasized. Even in the case of a seemingly simple
fracture, care must be taken to evaluate other areas
thoroughly, such as the joints above and below the
injury, the contiguous soft tissues, and the extent of
the injury to the opposite of two paired bones or their
articular interrelationships when only one is obviously frac-
tured. Care also must be taken not to overlook plastic defor-
mation of the ulna or fibula or dislocation of the radial or
fibular head (i.e., Monteggia and Maissoneuve injury pat-
terns), as any of these injuries has the potential to add con-
siderable difficulty to the anatomic reduction, affect healing
and subsequent rehabilitation, and lead to significant
growth, cosmetic deformity, or dysfunction. Later recon-
structive surgery is often avoidable by proper astute
5. Diagnostic Imaging
diagnosis in the acute setting to obviate the likelihood of
deformity.
Unfortunately, when the skeletal elements are incom-
pletely visualized (as when the epiphysis is still partially or
completely cartilaginous), when a specific injury is seen
infrequently (as is the case with the less common types of
fractures of the developing skeleton such as sleeve or shell
fractures), or when there is chondro-osseous injury in an
atypical region (e.g., the interface of cartilage and bone in
the patella), an individual physician may have limited diag-
nostic experience. Thus a systematic, correlative examina-
tion with a review of clinical and imaging findings is essential.
Appropriate consultations should be requested.
Benign and malignant tumors may be found when evalu-
ating a child for an acute injury. Some may be evident,
whereas others are subtle. Further studies are often required
but should be based on both the treatment needs for the
fracture and the potential for malignancy that is best
approached by a “rapid” workup and staging while treating
the acute fracture.
Frush et al. evaluated the need for sedation during
imaging procedures in children.84 Sedation is often difficult
and always demanding. They detailed a number of agents
and discussed the relative merits of each. One agent with a
long record of safety is chloral hydrate, which is particularly
useful in the infant up to 2 years of age. The reader should
consult this article for a detailed discussion of presedation
and postsedation care and the effective use of various agents.
Because the radiologist is undertaking this phase of the
child’s diagnosis, it is appropriate that he or she assume
responsibility for the selection and administration of the
sedative drugs and not abrogate it to the referring physician.
Equally, complications of the medication, injected material,
or diagnostic procedure should be followed by the radiolo-
gist, not the referring physician.
Schrieber reviewed the radiologist’s responsibility for com-
municating with the referring physician.225 He presented
the standards set by the American College of Radiology. Any
urgent or unexpected findings should generate direct com-
munication with the referring physician, rather than a typed,
signed report delivered at a later date. Thus the presence of
a fracture (an urgent finding) should be communicated in
an appropriate and timely fashion (e.g., telephone, E-mail)
to the referring physician.
Predictive Value of Clinical Findings Versus
Radiographic Findings
Radiographic films of the extremities have become a routine
part of the initial evaluation of musculoskeletal trauma in
children. However, like many other radiologic examinations,
the efficacy of extremity films has been minimally subjected
to systematic scrutiny (i.e., outcome analysis).58,132,226 There
is a “high-yield criteria list” of physical findings in patients of
all ages who sustain head trauma in which a radiograph
shows a skull fracture.18 The number of extremity films done
annually in the United States, however, far exceeds that of
skull films. Despite this fact, only one study in adults exam-
ined high-yield criteria for such extremity injuries.33 The rel-
evance of these criteria for the pediatric population is
unknown, as this study did not assess patients younger than
General Guidelines
16 years. Furthermore, children with certain predictors, such
as pain and swelling, may not have a radiologically defined
fracture. In contrast, an MRI scan may show a distinct area
of hemorrhage and edema (bone bruising) within the tra-
becular bone.
There are definite physical findings in children, as there
are in adults, that correlate closely with the likelihood of
detecting a fracture with an extremity radiograph.209 The two
most powerful discriminators for upper extremity fracture
(gross deformity and point tenderness) are identical with
those found in adults. However, clinical predictors of lower
extremity fracture appear to be somewhat different in chil-
dren than in adults. The lack of any pain or minimal pain
on weight-bearing as a predictor in children may be the
result of the inability of children willingly to report differ-
ences in pain intensity between pain experienced when they
are lying down and pain felt when bearing weight on the
injured part. This is particularly true with toddler’s fractures
of the tibia, fibula, or calcaneus.
Ecchymosis, a significant discriminator for upper extrem-
ity injuries in adults, is not statistically significant in the pedi-
atric patient.209 The reason children have less subcutaneous
bleeding than adults is unclear, but it probably relates to less
disruptive fracture patterns, less severe injury mechanisms,
a thicker periosteum, and more confinement of bleeding to
the subperiosteal and intrafascial spaces, any or all of which
may limit bleeding into the more superficial (subcutaneous)
soft tissues.
With the present litigious climate in the United States,
many clinicians are hesitant to use a screening protocol for
fear of missing a fracture and increasing their risk of
liability. Unfortunately, this litigious attitude is becoming
more prevalent in other areas of the civilized world as
well. Medicolegal concern, however, should not be the prin-
cipal basis for obtaining or not obtaining a specific diagnos-
tic imaging study. Any clinical decision should be based first and
foremost on medical considerations. If the decision to omit a
roentgenogram is based on prudent, recognized evaluation
criteria carefully and thoughtfully applied to the individual
patient, the physician is acting with as much “reasonable
care and skill” as the physician who always uses multiple
roentgenograms to diagnose or exclude fractures for
all extremity injuries (often to the exclusion of an adequate
physical examination). As with “routine” skull films for
head trauma, routine roentgenographic examination of
all suspected injured bones of all trauma patients is not
necessarily the standard of care. Adequate physical examination,
however, is the appropriate standard. Even careful examina-
tion of a patient with multiple, often life-threatening injuries
may initially miss a minimal, incomplete, or undisplaced
fracture. The use of scintigraphy in the multiple trauma
patient may be effective at any age to find occult injury
(difficult to diagnose), just as it is recommended for
evaluating a case of potential child abuse. Severe pain
from a contiguous or even relatively distant fracture may
mask pain from a more “benign” fracture. The delayed diag-
nosis of such fractures may not significantly affect the long-
term prognosis. Thus although possibly of concern to the
parents, so long as the eventual outcome is not significantly
affected or altered no harm has been done by the delayed
diagnosis.
117
McConnochie et al., in a review of 1218 injuries in
children, showed that upper extremity injuries were more
likely than lower extremity injuries to have fractures (42%
versus 18%).167 The predictability of a fracture was based on
gross signs, point tenderness, injury during a nonroutine
activity, moderate to severe swelling less than 6 hours after
injury, and pain with motion. The potential for adverse
outcome was the first consideration when assessing the
actual and emotional cost of fractures not detected during
the initial assessment. The potential for adverse outcome
from minor fractures in children was minimal, even without
optimal compliance with follow-up instructions. The authors
thought that the risk of adverse functional outcome
from missed fractures appeared small. Their study suggested
that implementation of the clinical prediction rules
could save $100 million to $140 million in radiographic costs
annually.167
When considering the radiographic evaluation of any
injured child, especially the child who has multiple injuries
that may require “nonorthopaedic” imaging studies, the
orthopaedist should consider the overall radiation exposure.
One must carefully choose the specific study or studies based
on what is necessary to reach a treatment decision and to
determine the efficacy of such treatment. Guidelines to the
amount of radiation a child may receive from a given diag-
nostic study are available.34,218
Adequate Films
Planar radiographs are two-dimensional, time-restricted
depictions of a three-dimensional, constantly moving child.
One view does not always provide adequate conceptualiza-
tion of the discrete traumatized area. If only one view is
obtained, a fracture may be missed completely.
In general, any bone should be visualized in at least
two views. Ideally, they are true anteroposterior and lateral
projections 90° apart. Nonstandard projections, although
sometimes unavoidable because of pain, displacement,
or limitation of motion, may be misleading because the
variable radiographic appearances of normal structures,
especially the epiphyseal ossification patterns and physeal
contours of a child, may confuse an inexperienced physician.
Films of an improperly positioned patient may place the
physis in an unusual projection, making it appear to be
fractured.254 Large or long (14 ¥ 17, 14 ¥ 36) films in which
the x-ray beam is centered mid-diaphysis or mid-limb may
“distort” an epiphysis or any increasingly distant region by
foreshortening. Proper evaluation of an epiphysis should
always have the x-ray beam centered directly over the specific
area of interest.
Not all injuries to the developing skeleton are readily
evident in standard views. Minimally displaced areas of the
lateral or medial condyles of the distal humerus and the
tibial and fibular malleoli may be obscured by overlapping
bone and thus are not easily visualized by routine radi-
ographs. Oblique radiographs may show fractures not readily
evident on standard views. They are particularly helpful for
interpreting degrees of displacement in phalangeal fractures
of the finger or small Tillaux fractures in the distal tibia.
Lateral condyle fractures of the distal humerus may become
evident only in oblique views.
118
It is imperative that the joints above and below a fracture
be radiographed so the complete chondro-osseous unit is
visualized. Dislocations, especially those of the hip or radial
head, are not uncommon in association with diaphyseal and
metaphyseal fractures. An obvious metaphyseal fracture may
have a subtle extension into the physis, changing the prog-
nosis of the injury (see Chapter 6 for type 7 growth mecha-
nism injuries).
The extremity must be adequately splinted and protected
prior to sending the child for imaging. Although it may seem
axiomatic, the physician should request that the entire limb
be rotated to assess the fracture. Otherwise, the radiologic
technologist may simply turn the unprotected fracture and
distal region 90°, inadvertantly rotating the distal limb through
the fracture site, while leaving the rest of the limb (proximal
to the fracture) in the same position as the other film. This
problem is especially encountered with supracondylar and
condylar humeral and femoral fractures.232
Naimark et al. described a simple radiologic sign.178 When-
ever the diameter of a long bone changes abruptly across a
fracture line (the disparate diameter), a rotational deformity
must be present.
If a patient has radiopaque external devices (e.g., electro-
cardiographic monitor leads or metal splints) over a
fracture, the fracture may be missed. Similarly, the technol-
ogist may inadvertently place identification labels and
other markers over the injury, rendering it indistinct for
evaluation.
Comparison Views
Radiographs may demonstrate the injury adequately,
but because the appearance of displaced epiphyses may
be subtle an inexperienced observer may not recognize
the injury initially and usually resorts to a comparison
view.140,166,168,250 It has become common practice to obtain
comparison views of the contralateral extremity as a way of
potentially differentiating fractures from growth variants. It
generally is unnecessary, particularly when the films are inter-
preted by someone with sufficient experience. In most cases
this practice only exposes the child to unnecessary additional
radiation. Furthermore, there may be asymmetric epiphyseal
ossification (especially at the elbow), which might confuse,
rather than clarify. When an inexperienced observer must
immediately interpret the film, or when sufficient doubt
exists, comparison films may be justified if only to avoid
excessive confusion, multiple re-examinations, and inappro-
priate treatment. However, consultation with a more experi-
enced physician is usually more appropriate than
comparison films.
Merten noted that “some physicians consider comparison
views mandatory in the radiological evaluation of injuries in
childhood, while others support a more selective approach.
The medical controversy is now joined by mounting pres-
sure to limit radiographic examinations that contribute to
increasing medical costs and increased radiation exposure.
Medicolegal concerns encourage additional diagnostic radi-
ographic studies, especially in trauma cases. Socioeconomic
considerations exert increasing influence on medical prac-
tice, and require that established diagnostic routines be con-
tinually reappraised.”168 Routine radiographic comparison
5. Diagnostic Imaging
examinations were clearly not the predominant current prac-
tice among pediatric radiologists. The results suggested a rel-
atively low diagnostic yield from routine comparison views
insofar as affecting a specific diagnosis or treatment. Even
among those who routinely obtained these views, almost one-
third confirmed a low rate of positive return from such
studies.168 Because pediatric radiologists, who are well versed
in reading films of the immature skeleton, ascribe such a
“low yield” to comparison views, it is unlikely that the “inse-
cure” orthopaedist can attain much clinical benefit or clini-
cal assurance from comparison views. The inability to read
the film of the injured extremity confidently is probably
related to an equal inability to interpret the comparison
views.
Skull Films
Several studies have underscored the low incidence of
treatable conditions found by routine roentgenography
of the skull and emphasized the inability to use skull
roentgenograms intelligently to evaluate and treat chil-
dren with minor head trauma.77,118,149,210 Other studies,
such as CT, are much more beneficial for evaluating those
intracranial injuries (e.g., subdural or epidural bleeding)
that might require intervention. A review of 354 injured chil-
dren found that 4.2% had skull fractures, but no patients had
serious intracranial complications; in only one patient
was the treatment changed because a skull fracture was
detected.149
Thus for the mild head trauma usually sustained by chil-
dren, routine skull roentgenography is relatively ineffective
for either diagnosis or treatment. Furthermore, the high-
yield criteria established for skull films of adults were poor
predictors of skull fracture when applied to children whose
craniofacial bones are more resilient to applied forces.54
Obviously, medicolegal pressures and confusion regarding
indications for skull films in children with head trauma cause
overutilization of radiographic examinations. Significant
skull fractures are more likely among children who develop
recognizable neurologic complications after sustaining head
trauma. However, many severely neurologically impaired
children have no evidence of skull fracture because of the
aforementioned resilience of the cranial bones.
Soft Tissues
The normal soft tissues of the extremities, except adipose
tissue, absorb x-rays to a similar degree and cast shadows of
approximately equal radiodensity.82 The nonfatty soft tissues,
including epiphyseal cartilage, thus appear roentgeno-
graphically as a uniform, composite shadow with a
density intermediate between the heavier density of the
underlying bone and the lighter density of the overlying
subcutaneous fat. When there is introduced air, as with an
open joint injury, epiphyseal cartilage may be outlined.
Many of the anatomic specimen radiographs used through-
out this book exemplify this difference, allowing adequate
radiographic visualization of epiphyseal cartilage when
there is air rather than soft tissue contiguity. Adipose
tissue, with a specific gravity of 0.92, is slightly more radi-
olucent than the other soft tissues.37 The shadows of fatty
General Guidelines
FIGURE 5-1. Subcutaneous gas shadows throughout the clavicular
and subscapular tissues (arrows) secondary to a severe open
injury with concomitant fracture of the clavicle. The thoracic cavity
was not injured.
tissues thus may serve as a contrast density, partially outlin-
ing the margins of other, denser soft tissues. The external
margins of muscular masses are often clearly delineated by
the overlying and intervening envelopes of the more radi-
olucent fat. The large fat pads near the elbows, knees, and
ankles may outline contiguous epiphyses, tendons, bursae,
and muscular bundles.
Injury to surrounding soft tissues is a concomitant of any
fracture. The extent of such injuries should be assessed as
accurately as possible as part of the roentgenographic eval-
uation.67,230 MRI is most productive for demonstrating exten-
sive soft tissue edema or bleeding.
FIGURE 5-2. (A) Elevation of the patella from a
hemarthrosis and joint effusion. Cartilage from the
medial femoral condyle (chondral fracture) was
floating in the joint. Because the subchondral plate
was intact, no significant fat or marrow elements
from the secondary ossification center were
present in the reactive fluid. (B) Fat and marrow
elements (large arrow) create a more lucent
appearance than the reactive effusion in this boy,
who had a relatively undisplaced type 1 fracture of
the distal femoral physis. Similar radiolucencies
are present in the posterior joint space (small
arrows).
119
Many tissues surrounding a fracture are involved in the
overall injury, including soft tissue disruption and bleeding
and fluid accumulation. In some instances, because of either
a nondisplaced fracture or a spontaneously reduced fracture,
contiguous soft tissue swelling may be the only indicator of
musculoskeletal injury. The combination of subperiosteal
and extraperiosteal bleeding and edema may lead to pro-
gressive development of a compartment syndrome (see
Chapter 10).
Interstitial and Intraarticular Gas Shadows
Gas within the soft tissues casts shadows of variable radiolu-
cency. Air may be introduced through a wound (Fig. 5-1), or
gas may be generated subsequently by various types of oppor-
tunistic bacteria (see Chapter 9). After traumatic lacerations,
the presence of gas in the contiguous soft tissues should
always raise the additional suspicion of gas gangrene. Gas
shadows may be present in the subcutaneous planes of many
traumatized patients without clinical or bacteriologic evi-
dence of infection. The gas that enters the soft tissues from
local lacerations is primarily subcutaneous, whereas the gas
generated in clostridial infections tends to be within the mus-
cular masses and is usually accompanied by considerable
edema of the skin and superficial soft tissues. Wounds pen-
etrating a joint may introduce air, a factor that confirms the
diagnosis of an open joint injury, especially when the over-
lying skin lesion appears innocuous.
Intracapsular Fat-Fluid Level
A fat-fluid level (lipohemarthrosis) sometimes occurs in the
knee when a fracture involves the articular surface of the
femur, tibia, or patella, thus allowing the passage of fat and
blood from the epiphyseal or metaphyseal bone marrow into
the joint.221,222 Although the fracture itself may be difficult to
demonstrate radiographically, a diagnosis of fracture is
highly probable because of the presence of a fat-fluid inter-
face in the suprapatellar region (Fig. 5-2).
120
A B
FIGURE 5-3. Specimens of a distal humerus from a 6-year-old boy showing anterior (A) and posterior (B) fat pads.
Fat Pads
Minimally displaced fractures of the supracondylar region,
condyles, epicondyles, radial head, and proximal ulna may
be difficult to detect by routine radiographic studies of the
elbow. However, periarticular soft tissues may show swelling
or displacement that allow a probable diagnosis of fracture,
although such swelling is not pathognomonic of a specific
fracture.16,27,175,201
Extracapsular fat pads are present in the olecranon
fossa, coronoid fossa, and radial fossa (Fig. 5-3). The
dorsal (posterior) fat pad normally is not visualized on a
roentgenogram. It is lodged in the olecranon fossa and is
overshadowed by bone in the lateral view. This normal pos-
terior fat pad is almost never visible, in part because it is
pressed into the deep olecranon fascia by the triceps tendon
and anconeus muscle; it is also bound down by a fibrous
septum. The fat pads in the coronoid (anterior) and radial
fossae are more shallow. Owing to the differences in the radi-
ologic absorption of fat, muscular tissue, and bone, some of
this fat is readily recognizable on routine radiographs. The
anterior fat pads, which fit into the coronoid and radial
fossae, may be visualized as a triangular area of radiolucency
in the lateral flexion view of the normal elbow.
Norell erroneously described the dorsal fat as extracapsu-
lar.181 Bledsoe and Izenstark showed that the pads of fat are
extrasynovial but intracapsular.24
5. Diagnostic Imaging
Abnormal anterior fat pad signs result from an intra-
capsular collection of fluid that expands the intracapsular
space, displacing the fat pads. Displacement of these fat pads
appears to be related to the extent of bleeding and
fluid accumulation (the musculoskeletal equivalent of
third-space fluid), both intracapsular and subperiosteal. Sub-
periosteal bleeding may also push the dorsal fat pad further
posteriorly, so it becomes more easily recognizable radi-
ographically. Norell studied more than 300 normal children
with and without elbow trauma and found that invariably the
posterior roentgenographic fat pad of the humerus was diag-
nostic of injury, whereas a thin, elongated layer of anterior
fat was consistently observed in both injured and uninjured
children.181
When displaced, the posterior fat pad may be seen as
a radiolucent area posterior to the humerus at the
upper border of the olecranon fossa (Fig. 5-4). Traumatic
rupture of the synovial membrane and articular capsule may
permit intracapsular fluid to escape into the surrounding
soft tissues, so there is no synovial distension and conse-
quently no roentgenographically evident displacement of
the posterior fat pad. A fracture involving portions of the
bone outside the limits of the synovial membrane does not
necessarily produce synovial effusions, as the fracture may
not communicate with the joint. Displacement of the fat pad
is not a necessary concomitant to all fractures in the elbow
region.
FIGURE 5-4. Fat pads in the elbow. (A) Ele-
vation of the anterior and posterior fat pads
by fluid within the capsule. (B) Elevation of
the posterior fat pad by periosteal elevation
(B: Adapted from Murphy and Siegel175)
General Guidelines
Other areas may exhibit fat pads. A radiologic fat plane
located anterior to the distal ends of the radius and ulna
often undergoes alteration owing to trauma. Sometimes it is
easier to appreciate the changes in this fat plane than in the
bones themselves.155,215 This fat pad has a convex curve ante-
rior to the radius and ulna and is seen in true lateral pro-
jections of the wrist in almost all normal subjects, from
premature infants to teenagers who have attained skeletal
maturity. A fracture in this area may cause bleeding into the
pronator quadratus muscle. This bleeding displaces the over-
lying fat. Often this muscle is damaged by the bone ends,
which adds to the swelling.
Foreign Bodies
Opaque foreign bodies are frequently found after seemingly
insignificant trauma in children (Fig. 5-5).11,36,39 In
many cases these organic and inorganic foreign bodies are
not found until a significant time has elapsed since the
original injury. Fragments of lead-containing glass may be
visible in the more radiolucent areas of skin, muscle,
and joints.76,251 Small, minimally radiopaque foreign bodies
may be invisible in the standard, heavily penetrated film
made for demonstrating bone detail; but they may become
visible with special soft tissue exposures made with lower
voltage. Many biologic foreign bodies are invisible because
they have water density similar to that of the surrounding
tissues. Biologic materials may cause surrounding inflam-
mation or infection, which may enhance the likelihood of
radiologic detection.
Metallic foreign bodies in the soft tissues, whether intro-
duced accidentally or surgically, may remain at the original
site of introduction or may move considerable distances away
with little or no disability to the patient.10 It is likely that the
localized resorption of bone around the foreign body allows
the movement to start, and then muscular forces probably
FIGURE 5-5. Fragment of glass (arrow) within the joint. It should
not be misinterpreted as an osteochondral fragment (e.g., tibial
spine avulsion).
121
propagate additional migration. Migrating foreign bodies
that are sharp should be removed as soon as their movement
is detected, although it is not always imperative to remove
them at the time of injury, especially if extensive dissection
of already traumatized tissue is necessary. Migration may
place an object where it damages tissue. Solid objects, such
as glass fragments, may injure joint structures. Intraarticular
glass, because of sharp, irregular edges, may be particularly
destructive. Sharp objects such as nails may penetrate artic-
ular and epiphyseal cartilage, leave particulate debris, and
subsequently be extruded spontaneously or surgically
removed. The remaining minute particles are capable of
eliciting biologic responses (e.g., inflammation or regional
osteolysis).
Localization Problems
Two views may not be adequate for foreign object localiza-
tion.46 Two planar views, preferably at 90° to each other, are
usually needed to localize foreign objects by roentgeno-
graphic means. However, this holds true only for parts of the
body that are relatively rectangular in shape. Additional
views may be necessary to localize such objects when they are
lodged in nonrectangular, particularly oval, body parts. This
need has been demonstrated with the problem of recogniz-
ing whether a pin used for slipped capital femoral epiphysis
has penetrated the articular surface or subchondral bone
(see Chapter 21). The relationship of the foreign object to
the x-ray tube in the film changes because of differences in
anatomic contour. This phenomenon is a variant of parallax:
the difference in apparent position of an object when
observed from two different points, especially within a spher-
ical, rather than a cubic, object.
The need for various nonstandard views must be consid-
ered when evaluating the localization of foreign bodies, espe-
cially in the hand and the foot, when an attempt is being
made to remove them. Fluoroscopy is also useful when
attempting to remove these objects. Triangulation tech-
niques, as in arthroscopy, allow direction of needles or
probes to localize the site of the foreign body.
Roentgenographic Response to Trauma
The initial fracture line in a child’s bone is sometimes diffi-
cult to demonstrate radiographically. Because the immature
bones are relatively pliable, they do not sustain the same
fracture patterns, especially comminution, as is commonly
evident later in life with a more brittle skeleton. However,
the presence of comminution may not be radiologically
evident on the initial fracture evaluation films. Incomplete
comminution (additional fracture propagation) may not
result in sufficient fragment separation to be radiographi-
cally detectable.
Incomplete cortical disruptions, which are probably more
common than appreciated, may not be visualized well on the
initial roentgenograms. The first roentgenographic evidence
of a fracture in a child may be callus formation during reeval-
uation. The original fracture line may never be discerned,
even when the original films are reviewed retrospectively.
Stress (“toddler’s” or “march”) fractures, in particular, may
122
be manifested by limping and pain, with or without a sub-
periosteal reaction.
Whether the inciting injury is localized to the metaph-
yseal, diaphyseal, or even juxtaphyseal regions, the
new bone that forms at the cortical periphery in response
to fracture assumes two basic patterns151 that may be
described radiographically as solid or interrupted. Bone
exhibiting a solid periosteal reaction is of uniform density,
with the old periosteal and new subperiosteal bone
appearing to be similar on routine radiologic examination.
The newly formed bone is deposited as the result of
periosteal reaction to trauma and usually has an even,
uniform appearance. After several weeks the subperi-
osteal new bone gradually becomes indistinguishable from,
and an integral part of, the antecedent (pretrauma) cortical
bone. The thickness of the new, reactive bone seems to be
related to the degree of trauma, the amount of periosteal
stripping due to displacement of the bone relative to
the periosteum, and the extent of contained subperiosteal
hemorrhage.
In contrast, interrupted periosteal reactions have varying
roentgenographic patterns. Lamellar (onionskin) and per-
pendicular (sunburst) periosteal reactions are classic exam-
ples, and are often encountered in neoplastic or infectious
disorders, from which they must be diagnostically differenti-
ated (see pathologic fractures in Chapter 11 and posttrau-
matic infection in Chapter 9). Irregular subperiosteal
reactive bone may occur consequent to fracture-induced
hemorrhage, particularly in the neonate or in the metaphy-
seal regions of older children, in whom normal and trauma-
responsive bone formation in the thin metaphyseal cortex
tends to be more irregular than that seen in response to
diaphyseal fracture. This interrupted response pattern is also
caused by continuing hemorrhage, which may easily occur
with the repetitive trauma of child abuse or sensory neu-
ropathy (e.g., myelodysplasia or congenital insensitivity
to pain).
Postreduction Evaluation
Following any closed or open reduction, it is appropriate to verify
that an acceptable reduction has been attained. When a splint or
cast is applied, whether composed of fiberglass or plaster,
osseous landmarks may be obscured. However, changing
radiographic techniques may allow better visualization of
anatomic detail. Fiberglass casts do not obscure osseous
detail as much as plaster casts. In some cases tomographic
CT techniques are necessary to detail the reduction. Addi-
tional studies may be warranted (e.g., a CT scan following
reduction of a traumatically dislocated hip to rule out
intraarticular fragments).
Subsequent postreduction films should be taken at inter-
vals appropriate to the nuances of the particular fracture.
Some fractures, such as a minimally displaced lateral condyle
of the distal humerus, must be observed closely, as further
displacement or delayed union may occur when the trau-
matically induced swelling dissipates. If a cast is revised or
wedged within 4–6 weeks of injury, confirmation of the con-
tinued acceptable reduction is essential. Fractures that need
particularly close early reevaluation are detailed throughout
Chapters 13 to 24.
5. Diagnostic Imaging
Angulation
Evaluation of the true angulation of a long bone fracture
after reduction may yield variable findings. Geometric analy-
sis shows that the maximal angulation may occur in a plane
other than the standard anteroposterior or lateral
roentgenographic planes.207 The maximal angulation may be
obtained by rotating the limb during fluoroscopy, rather
than relying on two-dimensional graphic analysis (i.e., two
views that are 90° apart). Obviously, knowledge of the true
extent of any postreduction deformity may influence subse-
quent treatment, even in children in whom spontaneous cor-
rection of angulation is expected.
Correction of inappropriate angulation is an essential part
of fracture treatment. If the limb is manipulated to correct
the angular change, postprocedure documentation of
improvement is essential. Incomplete restoration of pre-
traumatic anatomic configuration may require additional
manipulation, rather than reliance on subsequent posttrau-
matic remodeling.
Fracture Healing
At a certain point, usually about 4–6 weeks after injury, a radi-
ograph is obtained to determine whether sufficient healing
has taken place to warrant removal of the cast and the incep-
tion of progressive utilization of the injured part. Callus is
usually readily evident in most children at this stage,
although the presence of callus per se does not mean that
the fracture is capable of being subjected to normal child-
hood activity. Gradually applied biomechanical forces
induce remodeling in the naive bone of the callus. This
process slowly integrates the bone with the pretraumatic
bone. In the child, the normal growth process hastens
this integrative process (see Chapter 8). However, even in
the adolescent, what appears to be a well-healed process
radiographically may not be, as shown with other studies
(Fig. 5-6). Accordingly, caution must be used regarding how
rapidly a child or adolescent is allowed to return to full activ-
ity after an injury.
Radiology of the
Developing Skeleton
The ossified portions of a growing, maturing bone have
radiopaque shadows of variable density, whereas the nonos-
sified skeletal components (i.e., chondroepiphyses) are vir-
tually impossible to distinguish from contiguous soft tissues
of comparable water density.37,68,95,136,186,224 Depending on the
extent of skeletal maturation, cortical bone varies consider-
ably in thickness, especially at the metaphyseal/diaphyseal
gradation. The central diaphyseal spongiosa and the primary
and secondary metaphyseal spongiosa appear as tightly
meshed networks of linear shadows that are always partially
obscured by the heavier, superimposed shadows of cortical
bone. The peripheral spongiosa and the cortices of the me-
taphyses fuse with the central spongiosa at the ends of the
bones. Along the borders of the medullary canal, the periph-
eral spongiosa may give rise to roughening of the endosteal
surface of the cortex.
Radiology of the Developing Skeleton
FIGURE 5-6. This adolescent had had a proximal tibial injury 10
months earlier. She had been extremely active on the leg for the
past 8 months. Only a sclerotic vestige of the fracture was evident
in the lateral film. As part of a study concerning posttraumatic
remodeling in the developing skeleton MRI was undertaken 10
months after the injury. It showed that despite apparent radi-
ographic healing the original fracture line was still evident. This
indicates that some remodeling, especially within the medullary
cavity, requires lengthy periods of time.
The unossified portions of the growing bone (epiphyses
and physes) are radiologically similar to the surrounding soft
tissues and thus are usually difficult to visualize, except when
there is a fluid or gas of different density adjacent to the car-
tilage (e.g., blood, fatty marrow, or air in a joint consequent
to trauma). Infrequently, the epiphyseal or articular cartilage
may be outlined on a routine film.
Epiphyseal Cartilage
Part of the diagnostic enigma of a fracture in a child is our
present inability to obtain routine radiographs of the carti-
laginous portions of the skeleton. There have been numer-
ous experimental methods to delineate cartilage that have
taken advantage of the potential contrast between cartilage,
bone, and joint fluid,91,182 but, they have usually proved to be
neither technically feasible nor clinically applicable.
Placing the joint under stress may cause a “vacuum” phe-
nomenon, with a radiolucent line (air arthrogram) that
follows the cartilage contours. Such a radiolucent line is due
to cavitation of normally dissolved gases within the joint
fluid. Arthrography (discussed later in this chapter) is not
always feasible for the acute injury, as hemarthrosis may
interfere and a disrupted capsule may allow extravasation of
dye, minimizing the efficacy of such a procedure.
Magnetic resonance imaging allows visualization of epiph-
yseal and physeal cartilage. However, it is not a practical tech-
nique for routine use because of both the expense and the
123
potential need for sedation or anesthesia in the young
child.
Growth Plate (Physis)
As previously emphasized, the radiographic evaluation of
any skeletal injury requires, at a minimum, two views that are
90° apart. Epiphyseal injuries, however, may be seen in
only one, not necessarily standard, projection. Rogers
reported that 15–20% of such injuries were evident only in
an oblique view, rather than the standard anteroposterior
and lateral views.213 Most epiphyseal injuries are manifested
by displacement of the shaft relative to the secondary ossifi-
cation center and by widening of the growth plate. However,
widening or narrowing of the physis may be difficult to inter-
pret, depending on the size of the secondary ossification
center relative to the entire epiphysis (i.e., the secondary
ossification center has not yet formed a definitive subchon-
dral plate). The greater the displacement, the more evident
is the injury. However, at times both displacement and widen-
ing of the plate are minimal, especially as spontaneous
reduction may occur after deforming forces dissipate. A
detailed discussion of the diagnosis of injuries to the growth
regions, especially the concept of undisplaced or incomplete
failure at the chondro-osseous interface, is presented in
Chapter 6.
Teates described an 18-year-old in whom a remnant of the
growth plate was misinterpreted as an acute fracture.254
Oblique views may show the physeal remnant appearing
much closer to the joint than it actually is. The growth plate
tends to persist laterally (peripherally) in the major epiphy-
ses during the last stages of physiologic epiphysiodesis. If the
position of the physis is unusual or the physis persists an
unusually long time after closure, fracture may be erro-
neously diagnosed.
With type 2 injury, a triangular fragment of the metaph-
ysis (Thurstan Holland sign) accompanies a displaced
epiphysis and aids in demonstrating the injury.100,121
Werenskiöld emphasized the presence of a thin flake or
lamella of bone accompanying the epiphyseal fragment.262
This lamellar sign differs from the corner sign of Thurstan
Holland in its size and position. The corner sign (triangular
metaphyseal fragment) is created by a compressive failure
on the side of the fulcrum. In contrast, the lamellar sign,
formed by an avulsive force, is found on the tension failure
side (Fig. 5-7). If the metaphyseal fragment is small, the dis-
placement tends to be less than that associated with a large
fragment. If the only evidence is widening of the physis, a
transverse lamella of metaphyseal bone (primary spongiosa)
may be evident.
Radiopaque markers have been used to delineate patterns
of physeal growth, especially after resection of bony
bridges.12 These markers are biologically inert.
Nutrient Canals
Nutrient canals enter the bones in reasonably predictable
anatomic regions. Usually there is one canal per diaphysis.
Nutrient canals may appear as roentgenographic “defects”
in the cortical bone. When a nutrient canal is projected
in profile, its oblique channel through the cortex may be
124 5. Diagnostic Imaging

forces within the range of elastic deformation appeared

FIGURE 5-7. Fracture of the distal phalanx of a finger in a 12-year-
old child showing the avulsion fragment (open arrow) on the
tension failure side and the triangular fragment (solid arrow) on the
compression failure side. This linear fragment (open arrow) was
described by Werenskiöld262 and contrasts with the more frequent
triangular metaphyseal fragment (solid arrow) known as the
Thurstan Holland sign.100,121
to be histologically normal. With progressively increased
stresses, microscopic fatigue lines (microfractures) were
detected. These prefracture lines were observed only in areas
of maximal compression of cortical and trabecular bone and
were oriented approximately 30° to the longitudinal axis of
the bone. They were found to parallel zones of fragmenta-
tion within the bone and represented areas of incomplete
bone shearing. Broad plastic curvatures of 15°–30° were pro-
duced routinely. In those bones with plastic curvatures,
microscopic sections showed prefracture lines in the concave
cortex and hemorrhaging in the periosteum and subperi-
osteal space. However, no periosteal reaction was found up
to 2 months following such experimental plastic deforma-
tion. The extent of osteon formation within the bone was
not discussed. This would be a significant factor, as such
formation (modeling) and reformation (remodeling) is a
mechanical reaction of the maturing skeleton. The less the
amount of osteon formation (i.e., the younger the patient
presenting with injury, pain, or limping) the more likely it is
that plastic deformation will occur.
Traumatic bowing of the forearm bones (Fig. 5-8) or the
fibula in children, which is being increasingly recognized as

demonstrated clearly. However, in other projections, the

nutrient canals are partially or completely obscured by
the radiodense cortex surrounding them. The canals may
be highly suggestive of incomplete fracture, particularly if
visualized in nonstandard views or by an inexperienced
observer.

Cortical Irregularities
Metaphyseal cortical irregularities occur in children
and adolescents in many bones. This strongly suggests
that there is a commonality of these entities as a variation
of normal growth and remodeling, rather than a traumatic
by-product.135 Cortical irregularities in children that simul-
ate bone destruction or periosteal reaction always elicit
great interest, as they immediately raise the possibilities of
neoplasia, infection, or trauma. The medial distal femur
is probably the most common site of these cortical
irregularities.

Failure of Immature Bone

If a longitudinal compression force is applied to each end of
a tubular bone, the distance between the ends of the bone
is approximated. Up to a certain point, the bone responds
(deforms or bends) in an elastic manner, losing all such
deformation once the evocative force is removed (see
Chapter 1). However, beyond a certain yield point, the bone
remains deformed (plastic deformation), even though it is
not macroscopically fractured sufficiently to be detected by FIGURE 5-8. Plastic deformation is not unique to the slowly matur-
routine radiography. ing human. This immature spider monkey fell from a tree in a
Investigations have confirmed these elastic and plastic primate exhibit, sustaining an undisplaced ulnar fracture and a sig-
responses.17 Skeletally immature canine bones stressed at nificant plastic deformation of the radius.
Radiology of the Developing Skeleton 125

a significant clinical problem, is a manifestation of trauma

that may occur because of this elastic and plastic defor-
mation capacity of developing bones.3,22,32,38,45,48,50,81,90,92,-
143,154,161,164,188,216,220,242,257,267,269
Borden described eight children
with traumatic bowing of the forearm.28,29 None of these
patients had evidence of subsequent responsive subperi-
osteal new bone formation. In my experience, however, reac-
tive subperiosteal bone may occur. Traumatic bowing may
involve the fibula when the tibia fractures.161 Plastic defor-
mation of the ulna may be associated with incomplete dis-
ruption of the radiocapitellar joint (see Monteggia injuries
in Chapter 16).
Roentgenologic investigation usually demonstrates bow-
ing, although the change is often subtle and may be detected
only when compared with the opposite extremity. No dis-
crete fracture line may be visible. Increased radioisotope
uptake on nuclear imaging may be noted shortly after the
osseous injury. Periosteal reaction may not appear during a
follow-up period, but remodeling may involve thickening of
the concave cortex.
Bowing injuries are relatively uncommon because the
stress must be applied relatively longitudinally. It must be suf-
ficient to exceed the maximal strength of the bone but must
last a shorter time than is necessary to achieve complete dis-
ruption. The main differential diagnosis of a bowing fracture
is that of the normal bowing of a bone; a comparison view
of the opposite side may be necessary to exclude this possi-
bility. However, extremity rotation must be strictly controlled
(i.e., duplication) for such a comparison. Owing to the
increased elasticity of bone, impaired osteon formation, and
micro- and macrofractures, bowing is common in osteogen- FIGURE 5-9. (A) Radiograph of a greenstick fracture. (B) Stress
esis imperfecta. makes the deformity more obvious. Note the bowing of the seem-
For the evaluation of bowing, one may need to determine ingly nonfractured cortex (arrows).
whether it represents a chronic or acute injury. Scintigraphy
is useful for such a differential diagnosis.171 In particular,
demonstration of a marked osteoblastic response by radionu- and trabecular bone has occurred (remember, bone is most
clide skeletal examination may be useful for substantiating likely to resist failure in compressive loading).
the recent nature of an injury. Greenstick fractures involve failure of a portion of the
Bowing or plastic deformation of the diaphysis is not the cortex in tension, with additional propagation toward the
only pattern of such failure in the child. Incomplete frac- diametrically opposite cortical surface (Fig. 5-9). The non-
tures, which do not extend across the cortical circumference fractured opposite cortex is usually plastically deformed
of the bone, may occur. It happens because the relative plas- (bowed) to a highly variable extent (see Chapters 16 and 23
ticity of a child’s bone enables it to bend or fracture incom- for additional examples). This is a compression response
pletely in a situation in which a complete fracture would area that may exhibit microscopic tensile failure. This
occur in the adult skeleton. The main types of such in- common fracture term, which admittedly is more descriptive
complete failure in children are torus, greenstick, and stress than scientific, should not be used synonymously with torus
fractures. or incomplete fracture.
A torus or buckle fracture involves part of the cortex of
the bone, with a resultant localized deformity. This buckled
area usually involves the cortex in a localized region, rather
Transverse Lines of Park (Harris Lines)
than completely circumferentially. The fracture is composed Radiopaque transverse lines across the metaphysis in
of the plastic deformation (curvilinear) of a segment of the growing long bones may be found in both healthy and sick
bone, with a small contiguous compressive cortical disrup- individuals.37,86,112,184,193,194 These lines form during childhood
tion, which may not be readily evident on routine films. and may persist into adult life, but, they do not arise de novo
There is also tensile failure of the opposite cortex, but not in adult bone. Usually, these transverse lines are distributed
necessarily at the same level (in fact, the diametric physeal relatively symmetrically through the skeleton and occupy
margin may be the site of chondro-osseous disruption). reasonably comparable sites in the contralateral bones on
Although this buckling often seems to be localized initially, either side of the body. The lines are thickest in the regions
follow-up examination may show a transverse band of that grow most rapidly, such as the distal femur and proxi-
increased density across the entire bone diameter, revealing mal tibia (Fig. 5-10). In regions of slow growth (e.g., pha-
that a more extensive transverse impaction injury of cortical langes) these lines either may not form or are exceedingly
126
FIGURE 5-10. Radiograph of the knees of a 12-year-old boy 14
months after a left femoral diaphyseal fracture. The Harris lines in
the proximal tibias are a similar distance from the physis. In con-
trast, the left femoral Harris line reflects greater growth than the
right in response to the fracture.
thin. Normally these transverse lines are parallel to the con-
tours of the physis. When several transverse lines are present
at the end of a shaft, they tend to parallel one another, each
duplicating the contours of the others. The lines nearest the
physis are ordinarily the thickest and widest. Lines farther
away from the physis tend to be less distinct, broken, and
irregular. This occurs because of continued longitudinal
growth of the physis and epiphysis away from the static
growth slowdown line. The line gradually disappears
through endosteal trabecular remodeling in the diaphysis.
Such lines may be evident on an MRI scan for a longer time
than they are evident on a radiograph. Comparable lines
may form within the enlarging secondary ossification center
(Fig. 5-11) or vertebral body, creating the bone-within-a-bone
phenomenon.
Transverse lines develop whenever the growing skeleton is
subjected to a biologic stress of sufficient severity over a
period of time, especially such stresses as injury, starvation,
and infection.2 Harris and Harris113 produced transverse
lines experimentally in growing animals by starvation, and
Park induced transverse lines in rats by feeding them diets
deficient in protein and fat but high in carbohydrate.194 Chil-
dren frequently form them in response to generalized illness
or focal injury. Even a seemingly innocuous, undisplaced
fracture (e.g., distal radius) may subsequently be associated
with these lines.
The lines represent a systemic physiologic response by the
child to some nonphysiologic event, such as a viral or bacte-
rial infection, nonskeletal injury, periods of chemotherapy
for neoplasia, metabolic abnormalities, or trauma. A local-
ized long-bone injury, such as a unilateral femoral fracture,
may be followed by the formation of such a line not only in
the contiguous distal femoral metaphysis but also the ipsi-
lateral proximal and tibial metaphyses. Similar lines may
develop in the same regions of the contralateral, uninjured
leg. When these lines form they may be used to assess dif-
fering rates of growth (e.g., overgrowth) of the injured limb
in response to the fracture.
5. Diagnostic Imaging
These transverse lines have been called “growth arrest”
lines in the belief that they develop during periods of absent
or halted growth.37 During the initial phase of growth cessa-
tion or slowdown, formation of the primary spongiosa
contiguous to the zone of proliferative cartilage becomes
thick and transversely oriented, similar to the normal pattern
of primary spongiosa bone formation in a slow-growing
bone such as the metacarpal, metatarsal, or phalanx. When
rapid longitudinal trabecular orientation resumes (recovery
phase), the transverse line “separates” from the radiolucent
physis and thus becomes visible radiographically (Fig.
5-12).193,194
If one observes the normal, constantly changing
morphology of various bones, the more rapidly growing
ones are generally associated with longitudinally oriented
trabeculae in the juxtaphyseal region, whereas the slower
growing bones, particularly the proximal radius,
metacarpals, metatarsals, and phalanges, normally have a
greater amount of transversely oriented juxtaphyseal
primary spongiosa (see Chapter 1). Because this pattern of
orientation is standard in many small bones, transverse septa
and slow rates of growth are normal. In response to injury,
the orientation of trabeculae in these particular bones do
not become sufficiently different to be radiographically
evident.
However, if growth slows down in those areas that grow
rapidly and are normally characterized by longitudinal ori-
entation of trabeculae, the primary spongiosa is formed with
a greater transverse, rather than longitudinal, orientation.
This bone may be thick, a factor related to the duration of
the biologic stress. Once normal rates of longitudinal growth
and trabecular orientation are subsequently reestablished,
the transversely oriented septal plate contrasts with the
injury and postinjury longitudinally oriented trabeculae and
thus appears as a specific transverse line radiographically. As
growth and remodeling continue, the epiphysis migrates
away from this region, the primary spongiosa is converted to
the secondary spongiosa, the secondary spongiosa is con-
FIGURE 5-11. Harris lines within the distal femoral and proximal
tibial epiphyseal ossification centers.
Radiology of the Developing Skeleton 127

A B

C D

FIGURE 5-12. Progressive development of a Harris line following a twisting ankle injury
treated for 4 weeks in a cast. (A) Two weeks after the injury a thin juxtaphyseal layer
of bone is evident. Some disease osteopenia is evident immediately proximal to the
sclerotic line. (B) Eight weeks after injury. (C) Twelve weeks after injury. (B, C) Bone
is formed but not resorbed or remodeled because of a relative lack of metaphyseal
vascularity across the sclerotic zone of the Harris line (in reality a plate or disc). (D,
E) Six months and seventeen months after the injury. E

verted to medullary bone, and the transverse trabecular ori-
entation is gradually disrupted.
When a growth slowdown line parallels the physis follow-
ing trauma to a growth mechanism, the likelihood of physeal
damage is minimal. The distance should be compared with
a similar line on the contralateral side (if present). It may
show a different distance, reflecting different rates of post-
traumatic longitudinal growth of the two physes. Such a dif-
ference may be overgrowth or undergrowth of the injured
side relative to the uninjured side. If there is an eccentric
physeal injury, the physis and growth arrest line usually con-
verge. Subtle “nonparallel” changes thus may be an early sign
of physeal damage that may eventually lead to growth arrest
and bridge formation and may indicate a patient who is a
candidate for bridge resection (see Chapter 7). Such a
patient should be evaluated with MRI to detect the bridge
early. Early resection before extensive sclerosis may increase
the likelihood of recovery of any residual growth potential.
Similar changes may occur in the carpal and tarsal bones
and the secondary ossification centers. They arise from the
128
same phenomenon of formation of thick trabecular bone in
the subchondral plate on a temporary basis, followed by
thinner, more “longitudinal” bone after recovery.
Evaluation of Development
and Growth
Development of Ossification Centers
The development of the primary ossification centers of
major longitudinal bones occurs prenatally.41,189 In contrast,
the only long bone with a radiologically evident secondary
ossification center consistently present at birth is the distal
femur. This particular center is a reliable radiographic indi-
cator of a full-term pregnancy. The carpal and tarsal bones
develop primary ossification centers to some degree prena-
tally but extensively postnatally, a factor of consequence
when estimating skeletal age. However, of all human carpal
and tarsal bones, only the calcaneus regularly develops a sec-
ondary ossification center.
Roentgenologic studies of skeletal development consist
essentially of determining the rate and time of appearance
of the ossification centers of the epiphyses and the small
FIGURE 5-13. Ages of onset of secondary (epiphyseal) ossification
of the major long bones in the arm (A) and leg (B). Specific pat-
terns in the hand and foot may be seen in Caffey.37
5. Diagnostic Imaging
bones (Fig. 5-13). The age at which physiologic epiphy-
siodesis occurs is also important (Fig. 5-14).
Skeletal maturation is affected variably in the multitude of
skeletal dysplasias. A complete description of these disorders
is beyond the scope of this chapter. Caffey37 and Edeiken and
Hodes68 have adequately presented the highly variable radi-
ologic appearances of bones affected by these disorders. The
ossification patterns may be affected in any region—diaphy-
seal, metaphyseal, physeal, or epiphyseal—and major distor-
tion of the bones may result. The orthopaedist should have
some familiarity with these disorders, as the milder forms
may not be diagnosed until observed fortuitously during the
evaluation of trauma (e.g., osteogenesis imperfecta, osteope-
trosis, Englemann’s dysplasia, endochondromatosis).
Postnatal Growth of Arms and Legs
An understanding of the growth of the individual human
long bones is of primary importance to any physician
concerned with the potential problem of unequal limb
length consequent to trauma. Whether this problem is the
result of shortening, overgrowth, incomplete or complete
premature epiphysiodesis, or traumatic amputation, the
FIGURE 5-14. Ages of physeal closure (physiologic epiphysiodesis)
in the major long bones of the arm (A) and leg (B).
Evaluation of Development and Growth
correct estimation of anticipated growth enhances the
results of any elective corrective surgery. Unfortunately,
appropriate decisions are frequently impossible owing to the
lack of practical information and the difficulty of adapting
findings of academic interest to the immediate needs of the
patient.
Figure 5-15 shows the contributions of the various growth
plates of the upper and lower extremities to the growth
of individual bones and the overall length of each extremity.
The contributions of the various physes to the linear growth
of the long bones were studied using the nutrient canal as
a point of reference.59 These studies must be considered
estimates because the two major bones, the humerus and
femur, sometimes may have more than one nutrient canal.
When dealing with these particular figures, it must be
emphasized that they represent the percentage of relative
growth derived from each physis (the ratio of growth
expected from a given physis relative to the overall length of
the respective bone).248 Specific charts should be used for
anticipated actual length of growth. It must be remembered
that these figures are based on selective population samples
and are not necessarily accurate for a given individual,
although the ratios appear to be relatively constant in boys
or girls, whether dealing with short or tall but otherwise
normal children.
Equally, the application of skeletal maturation parameters,
growth remaining charts, and so on may not be possible in
other ethnic groups. For example, bone sizes, lengths, and
so on in the Chinese differ from those in the North Ameri-
can such that implants must be customized to the averages
for each group.
When graphs are used to predict growth and the proper
timing for surgery, the role of relative maturity and
various other clinical factors must be taken into account.
FIGURE 5-15. Relative contributions of individual growth regions to
the overall length of an individual bone and the composite extrem-
ity in the arm (A) and leg (B).
129
Maximum length of the long bones in girls is attained at
earlier skeletal and chronologic ages than it is in boys.107,111
The relative physical maturity, which includes skeletal matu-
rity, of a child is of primary importance for predicting the
growth patterns of the long bones. The growth potential fol-
lowing an injury in two 10-year-old boys obviously differs if
one has a skeletal age of 8 years and the other of 12 years.
Because the 10-year-old boy with the greater skeletal age has
fewer years remaining before normal closure of the epiphy-
seal growth plates, the long bones will grow less than those
of a more skeletally immature 10-year-old. The more mature
child has less time during which deformity due to growth
arrest may occur and during which angular malunion can
spontaneously correct.
It is widely accepted that skeletal age is a more appropri-
ate criterion than chronologic age for the study of growth.
However, assessment of skeletal maturity by the method of
Greulich and Pyle is difficult in cases in which the ossifica-
tion centers appear in a different order and enlarge at dif-
ferent relative rates from those described by these two
authors as “normal.”99 There is also an unavoidable error of
technique, as the standards of comparisions may be as much
as 14 months apart at some ages. The question of accuracy
has been approached by others who have developed more
rigorous techniques for the knee, hand, and wrist.94,96
However, these methods have not been correlated with leg
length data; therefore the applicability to leg length prob-
lems cannot be fully assessed.
Estimation of Skeletal Age
The skeleton does not develop at a constant rate from the
fetal stage to adulthood.40,78,137 There is a relative accelera-
tion during early childhood, followed by another accelera-
tion during the adolescent growth spurt. Few individuals
exactly follow the idealized developmental curve, but most
stay within the boundaries of the normal range throughout
growth. Some entirely healthy children show sufficient
variations to be judged at least temporarily advanced or
delayed.111
Skeletal development is divisible into two components:
an increase in the longtiudinal and latitudinal size of each
bone and an increase in the maturation of the osseous
tissues within each bone. Although closely integrated in a
healthy child, each component basically follows its own
pattern and rate. The increase in size is relatively easy to
assess. Skeletal maturation, however, is more elusive of
precise measurement and difficult to define, especially
radiographically.69,75,85,93,107,111,150,200,228
The hand, including the wrist, has received most attention
because it may be easily evaluated radiographically and
includes a wide range of bone development, enlargement,
and maturation suitable for comparative study.5,17,51,80,99,212,258
The most popular method for assessing maturity therefore
has been to base comparison on a series of films typical of
the various age groups.71,80,99,156,212,258,261 However, these
methods involve considerable subjective error. To lessen or
eliminate such error, efforts have been made to assess
osseous maturity by measuring the size of various bones on
radiographs.93 Such techniques have seldom been used
outside the centers in which they were derived, because they
130
were often cumbersome, inaccurate, and had a prolonged
learning curve.
Another method entails radiographing all the joints on
one side of the body and counting the number of centers
that have fused.237,238 This system involves many radiographic
films and ignores the structural changes that occur in the
epiphyses between initial ossification and fusion. Acheson
presented the “Oxford Method,” in which each bone is
awarded a unit designation, depending on its stage of devel-
opment.1 This system is similar to the Tanner-Whitehouse
technique for the hand and wrist.253 Both are relatively
time-consuming and are not routinely utilized in clinical
situations.
There may be some mild asymmetry within the body. In a
radiographic study of the hands of 450 children, bilateral
symmetry of bone maturation was evident in only 117 (37%),
a factor that must be considered when relying on compari-
son films to evaluate either injury or skeletal age.66 The same
side should always be radiographed on subsequent exami-
nations. According to others, significant asymmetry of skele-
tal development, with the exception of a few specific
abnormal conditions (e.g., dysplasia, epiphysiolysis, hemime-
lia), for all practical purposes, does not occur.93 The left side
of the skeleton is sampled by convention.
There is a great variation in the time and order of
appearance of the primary ossification centers in the small
bones of the wrist and ankle. In the same individual, the
appearance of secondary centers in the epiphyses of the
tubular bones of the hands and feet may show wide discrep-
ancies compared to the appearance of the primary
center in the tarsals and carpals.211 These discrepancies
between round bones and epiphyseal centers sometimes
make it difficult to appraise the skeletal age according to
the standards of Vogt and Vickers,261 Todd,258 or Flory.80
Robinow suggested that two categories of skeletal age should
be established: “round bone skeletal age” and “epiphyseal
skeletal age.”211
Errors in the determination of skeletal age by the Greulich
and Pyle methods have been particularly well elucidated by
Roche, et al.212 Even experienced radiologists show a mean
replicability of 3–4 months, with the standard deviation in
most cases being approximately the same on repeated eval-
uations of sample radiographs. This replicability may be
improved by averaged dual reading in only about 30% of
cases. The accuracy obtained when assessing interval
changes in serial studies was even less encouraging.188 Exclu-
sion of the carpal centers has no real effect on replicability.83
In fact, evaluation of the carpals may decrease the overall
accuracy of the hand and wrist assessments.
Limb Length Evaluation
Radiographic Measurement
Orthoroentgenographic methods have been employed
increasingly for accurate measurement of normal and abnor-
mal upper and lower extremity osseous length.8,162,163,234 The
term “anisomelia” is often used to indicate inequality of leg
length. Green et al. were the first to use roentgenographic
measurement extensively.95 Goldstein and Dreisinger
described a spot orthoroentgenographic method in which
5. Diagnostic Imaging
each joint was exposed separately.89 The maximum error due
to distortion was 1.3%.244 Nordentoft’s studies showed that
movements of the legs between single exposures and inac-
curacy of positioning at separate examinations were the
major sources of error.180 He thought that orthoroentgeno-
graphic measurement was sufficiently exact for clinical use,
but that the errors might influence the accuracy of scientific
results.180
The technique I currently use is to take spot
roentgenograms centered directly over the hips, knees,
and ankles using a movable 14 ¥ 17 inch cassette. A ruler
with radiopaque measurements is placed between the legs or
adjacent to each arm. Direct measurements may be made
from the films and recorded on growth charts, such as the
Moseley graph, which is also available as a computer
program.
Assessing Longitudinal Inequality
The surgical improvement or correction of longitudinal
arm or leg discrepancies prior to chondro-osseous maturity
must rely on a reasonably accurate prediction of the remain-
ing growth in both involved and uninvolved bones and
an understanding of the pathologic mechanism of the
discrepancy. Furthermore, one must ascertain whether the
difference is static or changing. Treatment of any limb
length discrepancy depends on a repeatedly accurate assess-
ment of the limb over an adequate period of time, knowl-
edge of the cosmetic and functional deficits anticipated, and
a proper perspective of the various treatment modalities.
The patterns of growth must be determined. For most con-
genitally short limbs, the growth of the two extremities tends
to remain proportional, although an increasing difference
develops over time.
Traumatic or postosteomyelitic shortening is more vari-
able and may increase significantly during the adolescent
growth spurt. For instance, there may be a period of slow
growth due to a damaged growth plate, followed by com-
plete, premature cessation when a large bridge subsequently
forms. For growth prediction and treatment, the pattern of
growth is just as important as the absolute difference
between the two extremities at any point in time.
Serial measurements at yearly intervals usually determine
whether the growth is proportional or variable. During rapid
growth periods, 6-month intervals may give more accurate
data. Roentgenographic mensuration258 of limb lengths is
more reproducible than are clinical measurements. Full-
length scanograms provide the most accurate sequential
data.
The bases for growth prediction were introduced by Todd,
who formalized the concept of skeletal maturation,258 and by
Gill and Abbott, who emphasized that growth, aging, and
maturation are different but related processes.88 Concepts
were further refined by the skeletal aging methods of
Greulich and Pyle and the growth studies of Anderson and
Green, who correlated the lengths (growth rates) of the
femur and tibia of boys and girls with their skeletal ages and
introduced a graph showing anticipated remaining distal
femoral and proximal tibial growth. Fries determined a
method for straight-line equations derived from the standard
charts of growth remaining at normal epiphyses.83
Evaluation of Development and Growth
Using a similar sequential radiographic database of the
upper extremity, Pritchett has developed tables for growth
of the bones.31,197–199 These studies have more accurately
defined percentages of contributions of the various physis to
longitudinal growth of the forearm and arm. However, a
chart similar to the Green-Anderson or Moseley charts has
not been developed.
Moseley introduced a straight-line graphic analysis
method for evaluating leg length discrepancies (Fig.
5-16).173,174 This method is based on two important concepts.
The first is a simple mathematical manipulation comparable
to plotting exponential growth data against a logarithmic
scale. Accordingly, the growth of the short leg is represented
by a line that lies below that of the normal leg, which
may have a different slope. The leg length discrepancy at
any given skeletal age is represented by the distance between
the two parallel, converging or diverging lines. The percent
inhibition of growth in the shorter leg is represented by
the difference in slope of the two lines (the slope of the
normal leg is arbitrarily defined as 100%). The second
concept is that a nomogram relating leg lengths to skeletal
age may provide a mechanism for considering the child’s
growth percentile and the relationship to overall leg length
discrepancy.
The growth of the normal leg is arbitrarily represented
by a straight line. This method also depends on the implicit
assumption that the growth line of the short leg is
also straight. With leg length deformity consequent to
FIGURE 5-16. Moseley graph for depicting leg growth parameters
and predicting the timing of various surgical procedures.
131
femoral shaft fractures in children, there may be consider-
able variations for the first year or two after injury that
must also be considered, although rarely are there sufficient
differences in leg length to warrant any surgical procedures.
Similarly, growth slowdown, rather than growth cessation,
after physeal injuries is not as predictable and may not follow
a straight line. Finally, the late appearance of a peripheral
osseous block may affect both the length and angulation
of an extremity. This bridge may not appear until the
child enters the adolescent growth spurt, at which point a
rapid change in the slope of the line may result. The final
problem is the presence of any angulation of the bone, which
is not adequately factored into any method and may con-
tribute further to length inequality. Furthermore, resection
of an osseous bridge and possible resumption of the growth
rate are not predictable, nor is the “premature” closure of
the injured growth plate even after some resumption of
growth occurs. Even if the physis resumes some pattern of
growth, it usually closes prior to the contralateral physis. All
of these factors diminish the likelihood of simple linear
growth that is readily amenable to plotting on the Moseley
graph.
Figure 5-17 shows the initial steps when using the Moseley
graph for depiction of growth. At the time of each assess-
ment, three parameters must be obtained: (1) the length of
the leg, measured by scanogram; (2) the comparable length
of the shorter leg; and (3) the radiologic estimation of the
FIGURE 5-17. Steps for plotting lengths of normal and involved legs
and skeletal age on successive visits. See text for details.
132 5. Diagnostic Imaging

skeletal age. When one is dealing with fracture overgrowth, 7. The leg length discrepancy at any given time is repre-
the long leg (i.e., the usual reference leg) may be the abnor- sented by the vertical distance between the two growth lines,
mal one and should be plotted in a manner comparable and growth inhibition is represented by the difference in
to the short leg, but above the normal line rather than slope between the two lines.
below it.
Figure 5-18 depicts the steps in predicting future growth
Several steps should be followed:
to skeletal maturity.
1. A point for the normal leg is plotted.
1. The growth line of the short leg is extended to the right
2. A vertical line is drawn through this point extending to
side of the graph.
the skeletal age area for either girl or boy.
2. The examiner draws the horizontal line that best fits
3. A point for the short leg is placed on this vertical line
the points plotted in the skeletal (bone) age area. Because
at the appropriate length.
of the inaccuracy inherent in estimating skeletal age, these
4. The point for skeletal age is placed on the vertical line
points may not approximate a straight line. The horizontal
where it crosses the appropriate line in the skeletal age
line should be drawn so the total of the distance of points
area. Interpolating between two skeletal age lines is often
lying above the line is equal to the total for points lying below
necessary. For example, the vertical line crosses the skeletal
the line. This information may also be computerized to plot
ages at 4, 5, and 6 for both boys and girls. Examples are
the most probable slope with accuracy.
depicted for a girl of 4.5 years and a boy of 6 years (skeletal
3. At the point at which the horizontal line (normal leg)
ages).
meets the sloping line, the examiner draws a vertical straight
5. Successive sets of data points should be plotted in the
line that intersects the growth line of the normal and short
same manner.
leg.
6. Each of the child’s radiographic assessments are then
4. These points of intersection predict the anticipated leg
represented by a vertical line on which the three points
lengths and discrepancy at skeletal maturity.
(normal limb length, short limb length, bone age) for that
particular visit are plotted. The examiner then draws the Figure 5-19 considers the steps for the timing of surgery
straight line that best fits the points previously plotted for and the effects of leg lengthening. The new growth line for
successive lengths of the short leg. This is the growth line of the lengthened leg (1) should be drawn parallel to the pre-
the short leg.

FIGURE 5-19. Steps for planning leg lengthening prior to chondro-

FIGURE 5-18. Steps for plotting anticipated leg lengths and overall osseous maturity. Note that the leg is overlengthened and then
discrepancy at chondro-osseous maturity. See text for details. equilibrates. See text for details.
Evaluation of Development and Growth
vious line of the short leg but (2) should be displaced
upward by an amount exactly equal to the increase in
length achieved. The short leg should be lengthened by an
amount equal to the anticipated discrepancy at maturity,
not by the amount of the present discrepancy. If there is
significant growth inhibition in the short leg, one must make
the short leg longer than the long leg, anticipating
that because of the difference in growth rates this overcor-
rection will be equalized by maturity. The growth of a
leg that has undergone surgical lengthening usually still
follows a straight line of the same slope, as before; but it is
displaced upward by an amount equal to the lengthening
achieved.
After surgical lengthening, any projection of the growth
line as a line of unchanged slope essentially ignores the pos-
sibility that a surgical procedure on the diaphysis or me-
taphysis might stimulate the physis (or physes) of that bone,
thereby changing rates of growth (i.e., slope). There does
not appear to be any way of confidently predicting whether
such an effect will occur, how long the effect will be main-
tained, or the amount of additional length it might con-
tribute. Stimulation is probably temporary and, when
present, is usually beneficial to the clinical situation, as it
adds length to a leg that needs it.
Figure 5-20 plots the timing of surgical epiphysiodesis.
1. At the point representing cessation of growth of the
short leg, having taken into account the effect of a lengthen-
FIGURE 5-20. Steps for planning surgical arrest of physeal growth
to equalize leg lengths. (A) Surgical epiphysiodesis of the distal
femur (solid line) or both proximal tibia and distal femur (dotted
133
ing procedure, if necessary, the examiner should draw a line
parallel to the particular reference slope for the proposed
surgery until it intersects the growth line of the long leg.
2. The point at which this line meets the growth line of
the long leg indicates the point at which surgery should be
done. Note that this point is defined not in terms of the cal-
endar or skeletal age but in terms of the length of the long
leg.
3. The time it will take for the child to reach that point
cannot be stated exactly, but it may be estimated by drawing
a vertical line from that point to meet the horizontal line for
the skeletal age.
After surgical epiphysiodesis the slope for the longer leg
is altered, so it should intersect the line of the shorter leg at
skeletal maturity. The straight line of decreased slope fol-
lowing epiphysiodesis equals the percentage of contribution
the fused growth plate would otherwise have made to the
total growth of the extremity. Because the contributions
of the proximal tibial and distal femoral epiphyseal plates
are approximately 30% and 40%, respectively, of the total
growth of the leg, one can reasonably predict the amount of
inhibition introduced by epiphysiodesis. The growth line of
the leg, which has undergone tibial, femoral, or combined
epiphysiodesis, will thereafter have a slope of 72%, 63%, or
35%, respectively. Doing an epiphysiodesis on only one side
of the knee (i.e., distal femur) may be followed by an over-
growth in the remaining knee physis (i.e., proximal tibia),
line). (B) Surgical epiphysiodesis of the distal femur and proximal
tibia after leg lengthening (L). See text for details.
134
probably due to a hyperemic effect. This effect cannot be
predictably measured.
Another assumption has been made based on Moseley’s
data: that the individual child remains in the same growth
percentile with respect to each determined skeletal age.
This assumption is open to question, even for normal
children, but the inaccuracy of individual skeletal age
estimate makes it difficult to test. Neither the straight-line
graph nor other methods provide an accurate quantitative
means to account for such factors as varying nutrition
and levels of activity, which may influence the rate of leg
growth from year to year. The skeletal age nomogram is
based on the assumption that the lengths of the lower
extremities of all children of a certain skeletal age are the
same proportion of the leg lengths of those individuals when
they reach adulthood, regardless of the growth percentiles
or chronologic ages. It is unlikely that this assumption is
true for children of different races or for those with
markedly dissimilar habits. There appear to be no satisfac-
tory data describing the patterns of growth in children of
other than the select group used in Green and Anderson’s
studies. The surgeon must recognize this as a potential
source of error when applying the straight-line graph or the
growth-remaining method to children of different racial and
ethnic backgrounds.
Treatment
Minor limb length discrepancies of 1–3 cm usually can be
treated without surgery. Discrepancies of 1.0–1.5 cm often
require no treatment at all. Gross reported that only 50% of
patients with more than 2 cm of shortening thought that they
were unbalanced.102 Only 10% of his patients felt a need to
wear a lift if the discrepancy was 1.5 cm, increasing to 35% if
the discrepancy was 2 cm and 45% if the discrepancy was
3 cm. Generally, when using a shoe lift, the entire discrep-
ancy does not need to be corrected. Usually a residual dis-
crepancy of 0.5–1.0 cm does not cause functional problems
and makes the orthosis more attractive. Furthermore,
patients with footdrop and weakness of hip flexion and knee
extension are often improved functionally with 1–2 cm of
shortening, which facilitates clearance of the lower extrem-
ity during the swing phase of gait.
Discrepancies of 3–6 cm seem to produce more significant
cosmetic deformity and functional disturbance. If the esti-
mated final discrepancy is 3–6 cm, shortening the long
extremity by epiphysiodesis is a surgical method of achieving
limb length equality. Epiphysiodesis has good reliability
when carefully planned. The procedure may be done per-
cutaneously using fluoroscopy and causes minimal soft tissue
morbidity. Absolute equality of the limbs may not be a real-
istic goal because of scatter in the growth prediction table.
Therefore if an error is made, it is usually better to under-
correct than to overcorrect the normal extremity. Reducing
the discrepancy to 1 cm or less, rather than absolute equal-
ity, is an appropriate goal for most patients.
When considering surgical epiphysiodesis, the principle is
to stop the growth of the contralateral bone to allow the
shorter, traumatized bone to equilibrate. Relative accuracy
rests on the ability to predict not only the amount the long
leg will be slowed but also the ability of the short leg to catch
5. Diagnostic Imaging
up by the time of skeletal maturity. Is the physeal growth
arrest secondary to trauma incomplete or complete? If
incomplete, is this a longitudinal slowdown or an angulation
abnormality? If the growth arrest is complete one can rea-
sonably predict the loss; but if the growth arrest is incom-
plete it is sometimes difficult to predict accurately how much
growth may still occur in the involved side, especially when
the child begins the preadolescent or adolescent growth
spurt.
Controversy regarding the most efficacious treatment
method arises with leg length discrepancies of more than
6 cm. Patients with more significant losses of length due to
trauma also have a high likelihood of accompanying angular
deformity. Leg lengthening should be considered, primarily
for the extremity that has good motor and sensory function,
good stability, and functional range of motion of the involved
joints. Limb lengthening may cause some loss of function or
stability of the adjacent joints and some decrease in motor
strength. If they are already compromised preoperatively, it
may not be advisable to lengthen the extremity. Age also
appears to be a factor, as the results are best when lengthen-
ing is delayed until the adolescent period. With any length-
ening procedure, the aim is to increase the length of the leg
by the amount that will result in equal (or relatively equal)
lengths at maturity, rather than by the current discrepancy
when the patient is initially evaluated, as that may change.
Multiple methods of leg lengthening have been
described.243,245 The choice of a technique often must also
address correction of the angular deformity. These methods
are discussed in more detail in Chapter 7.
End of Skeletal Growth
When establishing skeletal criteria for the onset of adoles-
cence, it appears that ossification is usually present in the
iliac crest within 6 months of menarche (12.9 years).208 The
age of inception of iliac crest ossification in boys probably
represents a maturational level analogous to the female mat-
urational level at the menarcheal date. In boys, iliac ossifi-
cation appears on the average, at 14.5 years, or 1.6 years later
than in girls. In the proximal phalanx of the second digit of
the hand, fusion of the epiphysis with the shaft begins near
the menarcheal date. Completion of ossification along the
iliac crest generally coincides with the cessation of longitu-
dinal growth in the arms and legs. However, overall body
height may still be added by continued longitudinal devel-
opment of the thoracolumbar vertebral bodies, which may
not stop growing until the third decade.
Special Techniques
Because of the difficulty visualizing epiphyseal contours and
microscopic fractures, an absolute diagnosis of skeletal
injury in children sometimes requires the use of techniques
other than routine planar roentgenography.235
Fluoroscopy
Planar radiographs are static evaluations. Sometimes frac-
tures may be evaluated more effectively by introducing
Special Techniques
motion. A common example would be maximum
flexion–maximum extension lateral views of the cervical
spine to assess stability versus instability, especially of C1 rel-
ative to C2. This same range of motion could be assessed
fluoroscopically in a dynamic manner under the supervision
of the treating physician, rather than the ancillary physician
(radiologist). Examination of any joint for acute or chronic
instability by this method often shows significant positional
changes when the joint is ranged. Fluoroscopy may be used
to evaluate excessive motion in children with ligamentous
laxity syndromes (see Chapter 11). The technique may be
used to detect fracture motion or stability after reduction.
This is an underutilized technique that deserves more
emphasis in children because of the often benign appear-
ance of planar films in the presence of significant physical
findings.
Stress Films
Owing to the elastic and plastic capacities of developing
bone and contiguous soft tissues, the injured region often
“springs” back partially to completely into the pretraumatic
anatomic position once the deforming force is dissipated.
This occurrence is particularly common with epiphyseal frac-
tures around the knee. These fractures are the childhood
and adolescent analogue of ligamentous injuries in the
adult, and one can test for them using similar diagnostic
methods. Stress application, utilizing fluoroscopy or planar
radiography, may “open” a fracture sufficiently to document
the injury adequately. This technique is particularly useful
for evaluating an injury to the knee or elbow. Its applicabil-
ity for use in the diagnosis of specific fractures is addressed
in the sections dealing with each given injury.
Arthrography
Arthrography is probably more useful for diagnosing
chronic problems than for acute injury, although it certainly
may be used in the latter circumstance. In infants and young
children with a suspected epiphyseal fracture of a radiolu-
cent distal humerus or proximal femur, arthrographic eval-
uation often allows a correct diagnosis followed by proper
treatment.23,106,266 In the case of chronic problems, arthro-
graphic techniques may make unusual injuries or cartilage
deformation more evident (Fig. 5-21).10,56
The value of arthrography in the diagnosis of elbow
injuries was emphasized by Yates and Sullivan.266 They
pointed out that correct management of elbow injuries in
children depends on the ability to obtain an accurate diag-
nosis, which is frequently explicitly difficult because of mul-
tiple and variable patterns of ossification. Cartilaginous loose
bodies may be diagnosed by arthrography (especially double-
contrast using air and Hypaque). Dynamic films with fluo-
roscopy following contrast injection may detect instability
of joint motion, mobility of a fragment, or capsular tears.
Computed Tomography
Computed tomography (CT) is particularly useful in the
evaluation and better anatomic definition of spinal trauma
(see Chapter 14), pelvic trauma (see Chapter 19), and
135
FIGURE 5-21. Normal views of the wrist in a boy who had
complained of chronic pain following a fall but whose hand demon-
strated no radiologic abnormalities. An arthrogram of the
wrist, however, showed comminution with the tendon sheath
(arrows). Closure of the capsular tear produced complete relief of
symptoms.
complex knee and ankle injuries (see Chapters 21, 23).109,177
It allows a more accurate assessment of narrowing (stenosis)
of the spinal canal due to fracture of the posterior or ante-
rior elements or to translation of vertebrae.130,182 It is also the
most useful method for evaluating fractures of C-l, a difficult
area to assess with routine radiography or standard antero-
posterior and lateral tomographic techniques, especially in
children. In the pelvis, distortion or winging of a hemipelvis
and sacroiliac involvement are much more apparent. With
an ankle injury, disruption of the articular plafond may
be assessed more accurately and a triplane injury better
defined.177 Talocalcaneal injuries may also be anatomically
depicted more effectively with a CT scan.
Blickman et al. thought it was not cost-effective to
evaluate children’s elbows by CT scans, and that such
scans do not change the therapy dictated by the clinical
findings and conventional radiography.25 This generalization
is inappropriate. Although most elbow injuries are relatively
straightforward, less common injuries, such as a T-shaped
intercondylar fracture, may be specifically delineated.
To obtain the maximum benefit of a CT study it is
important that the requesting physician communicate with
the radiologist supervising the study, as the radiologist
should have control over accurately visualizing the anatomic
structures that are most apparent in a given image. The radi-
ologist may treat the basic information in different ways by
changing software processing to accentuate bone density
and structure or to enhance soft tissues. In the future, col-
orization of gray gradients as well as black and white may
further enhance diagnostic ability, as it may allow CT delin-
eation of cartilage, especially epiphyseal and physeal.
Accurate definition of fracture anatomy, especially in com-
minuted fractures around the pelvis, knee, or ankle may
be further augmented by computer-generated three-dimen-
136
sional reconstruction of the CT scan.73 Magid et al. showed
the efficacy of two- and three-dimensional imaging of acetab-
ular fractures.157 Such reconstruction may also be useful for
spinal injuries.240 These techniques must be preplanned with
the radiologist, as they require a slightly different technique
of interval thickness and overlap.
Kuszyk et al. showed that surface rendering (using pixels)
demonstrated gross three-dimensional relationships most
effectively but suffered from more stairstep artifacts and
failed to display lesions hidden behind overlying bone or
located underneath the bone cortex.146 In contrast, volume-
rendering (using voxels) effectively showed subcortical
lesions, minimally displaced fractures, and hidden areas
with few artifacts. Surface rendering creates more three-
dimensionally realistic images of the external bone mor-
phology. In contrast, volume-rendering is more flexible and
displays skeletal pathology and intracortical lesions (e.g.,
bone bridges across the physis) more effectively.
Magnetic Resonance Imaging
Magnetic resonance imaging is becoming increasingly effec-
tive for evaluating acute skeletal trauma in children.19,42,49,74,
172,233,263,265
Two areas that are readily visualized by MRI are
spinal injuries and occult physeal/epiphyseal trauma.13 It
may also be used to visualize soft tissue, tendons, and muscle
(e.g., early myositis ossificans).20,42,49,55,123,239,255,256 As technol-
ogy is refined, it should prove useful for assessing vascularity
in possible ischemic situations (e.g., following hip dis-
location or proximal-femoral fracture).126,129,259 It is also
extremely useful for evaluating the complications of epiphy-
seal, physeal, and articular injuries.30,60,62,64,127,128,142
Clinical MRI involves study of the hydrogen nucleus (a
proton) as found in water that is not bound to macromole-
cules.141 These hydrogen nuclei are often referred to as
either free water or mobile protons. When the patient is in
the bore of the magnet the static magnetic field elicits a
macroscopic net magnetization. This alignment occurs over
a period of time defined as the T1 relaxation time. Kneeland
has excellently described the basics of MRI.141
To interpret routine MRI studies properly, let alone the
increasing array of other techniques [e.g., Fast Imaging
with Steady State Precesion (FISP), Fast Low Angle Shot
(FLASH), Gradient Recalled Acquisition in the Steady State
(GRASS)], the treating physician must be familiar with some
basic terms.110 The T1 sequence depicts how fast the tissue
gives magnetization (i.e., the signal). The T2 sequence
depicts the loss of magnetization after the excitation pulse.
A fluid (e.g., water) or tissue (e.g., red marrow) with a long
T2 interval maintains the signal and is bright on a T2-
weighted image. TR is the repetition time between succes-
sive excitation pulses. NEX is the number of excitations or
the number of times a sequence is repeated and averaged.
A high NEX results in decreased noise and less grainy image
but a longer scan time. Spin echo refers to a standard scan
sequence in which a series of one or more echoes are formed
after an “initial excitation pulse.” FSE refers to fast spin echo,
a new technique in which spin echo images are generated in
much shorter times than usually used. GRE is a gradient
recalled echo, which is a scan sequence that uses changes in
adjacent tissue gradient units, rather than refocusing pulses
5. Diagnostic Imaging
to general echoes. The latter techniques (FSE, GRE) are
being applied increasingly to studies of cartilage, including
the physis. They are referred to by different acronyms
(GRASS, SPGR, FLASH, FISP). In addition to shorter scan
times they have improved signal-to-noise ratios compared to
conventional spin echo.
Meyers and Wiener showed that short tan inversion recov-
ery (STIR) sequence MRI could detect subtle injuries that
were not evident on routine MRI or radiography.170
Detection of a subfracture insult may be possible with MRI.
It indicates injury that may lead to subsequent damage to the
joint. Rubenstein et al. showed that routine clinical MRI does
not accurately reveal early changes in articular cartilage219; it
is useful only for large defects.
Disler et al. compared standard MRI with fat-suppressed
three-dimensional spoiled gradient-echo (SPGR) imaging.62
One-fourth of their patients at arthroscopy had isolated
hyaline cartilage lesions that were missed by standard MRI.
SPGR had a greater chance of detecting such injuries than
standard MRI (85% versus 38%). Disler et al. also found
that in-phase and out-of-phase gradient-echo MRI of bone
marrow helped distinguish between early neoplastic and
nonneoplastic lesions (e.g., cyst, stress fracture).63
Disler also described the efficacy of fat-suppressed
three-dimensional SPGR for evaluating lesions involving
the hyaline cartilage of the articular surface and physis.61,62
The technique may identify lesions not readily evident on
routine T1 and T2 scans and may allow better assessment
of lesion size. Utilizing this technique, hyaline cartilage has
a high signal intensity and high contrast-to-noise ratios
when compared to contiguous soft tissues or joint fluid. The
images are acquired by three-dimensional Fourier-transform
reconstruction, which allows high resolution and multiple
reformations. The technique is available on most MRI
systems.
We are currently exploring the colorization of MRI. This
technique has been used to more accurately distinguish
tumor tissue from reactive surrounding edema in brain
and pelvic lesions. Its efficacy with injuries to the physis,
epiphysis, metaphysis, and articular cartilage has yet to be
determined.
A well-recognized pattern of childhood spinal injury is
“spinal cord injury without obvious radiologic abnormality.”
It is often referred to by the acronym SCIWORA. The use of
MRI in these situations may detect edema or hemorrhage
within a fractured but nondisplaced vertebra, intrathecal
bleeding, and the level of a contused or disrupted spinal
cord. This injury pattern is diagnosed in detail in Chapter 18.
Sebag et al. assessed progressive changes in spinal bone
marrow as the child grew.227 There was a consistent change
from hematopoietic to fatty marrow, which may affect MRI
signal intensity during the evaluation of acute trauma.
Nonradiographically evident epiphyseal or physeal
injury may also become evident with MRI.124,125 These
injuries are often referred to as occult injuries.172,265 Appar-
ent type 1 injuries may be reclassified as type 2 when
MRI reveals the occult Thurstan Holland fragment. Fracture
propagation within the epiphyseal ossification center is
more detectable (Fig. 5-22). However, the fracture pattern
that is best visualized by this technique is bone bruising (Fig.
5-23). A direct impact to the epiphysis causes trabecular frac-
Special Techniques 137

A B

FIGURE 5-22. (A) Radiograph of the distal femur following a football injury.
The radiologist read it as a normal film. Because of severe pain and swelling
when he was referred for orthopaedic evaluation by the emergency room
physician (who based minimal treatment on the radiologist’s verbal report),
MRI was undertaken. (B) The T1-weighted image showed an apparent type
4 growth mechanism fracture of the medial condyle. (C) The T2-weighted
image showed fluid surrounding a fracture fragment that was more properly
classified as a type 3 growth mechanism injury. There is some microcom-
minution of the medial metaphysis. After the appropriate diagnosis was made
4 days after the injury, the boy was treated with open reduction and internal
fixation. The upset parents engaged the services of a lawyer who was advised
that the 4-day delay, although frustrating to the parents, did not substantially
affect their son. They were told that he had received appropriate care, albeit
delayed a few days. They did not pursue the matter any further. C

ture within the ossification center or an incomplete sep-
aration (fracture) at the interface of the ossification center
and the still unossified surrounding epiphyseal cartilage.
The latter is referred to as a “sleeve” or “shell” fracture. Fat-
suppressed three-dimensional SPGR is useful for detecting
early growth plate closure in patients after physeal trauma
(Fig. 5-24).61
Lynch et al. categorized intraosseous lesions in the knee.153
A type 1 lesion was a diffuse, often reticulated signal intensity
loss in the metaphyseal and epiphyseal regions. A type 2 loss
involved an interruption in the smooth black cortical line. A
type 3 finding was a profound signal intensity loss primarily
restricted to the immediate subcortical region. They found
that type 1 or 2 loss was most compatible with acute bone
injuries and was usually associated with cruciate or collateral
ligament injury. They thought that type 1 injury represented
a region of bone at increased risk for the subsequent devel-
opment of insufficiency fractures if the bone was not ade-
quately protected during trabecular healing.
Lee and Yao tried to assess the age of injury of bone
bruises.148 They found the high signal findings varied signif-
icantly with the age of injury. However, indirect evidence
suggested that the findings on T2-weighted images resolved
earlier than the corresponding findings on T1-weighted
images.
The MRI views may also be augmented with gadolinium.196
This material may be injected intravenously for evaluation of
the spinal cord, dura, and nerve roots. It may also be used
for joint evaluation (MRI arthrography). However, the best
results of such a technique are obtained by injecting gadolin-
ium directly into the joint, rather than intravenously.
Barnewolt et al. used gadolinium-enhanced MRI to differ-
entiate between physeal and epiphyseal cartilage.15 This
method also visualized cartilage canals. The canal distribu-
tion pattern changed with age.
Greenberg et al. thought that MRI was efficacious for eval-
uating pediatric elbow trauma, especially the soft tissues.97 In
particular, they showed a radial head dislocation (nonossi-
fied) with the annular ligament displaced between the radial
head and capitellum.
Although muscle tears are probably less common in chil-
dren than adults, they certainly do occur. More importantly
 138 5. Diagnostic Imaging

A B

C D

FIGURE 5-23. Bone bruising. This occult injury pattern has become a definite
diagnosis with the increased utilization of MRI for evaluation of acute trauma
in children and adolescents. (A) Central lesion. (B) Subchondral lesion. (C)
Juxtaphyseal lesion (which led to subsequent growth arrest—is it the
elusive type 5 Salter-Harris fracture?). There are also areas of bone bruising
in the distal femoral metaphysis and proximal tibial epiphysis. (D) Peripheral
lesion combined with metaphyseal lesion that subsequently developed
peripheral growth arrest and a bony bridge. (E) Specimen of a distal tibia fol-
lowing a traumatic amputation. The black areas were foci of intratrabecular
disruption and bleeding. These form the anatomic basis of the occult lesion of
E bone bruising.
Special Techniques
FIGURE 5-24. MRI of growth arrest following closed treatment of a
type 4 growth mechanism injury of the medial malleolus. A dense
sclerotic bone bridge has formed. The original fracture lines are
also still evident in the epiphysis and metaphysis. This MRI scan
was obtained 17 months after the original injury.
they may be associated with an avulsion of a cartilaginous
region such as an iliac, ischial, or tibial spine. These con-
comitant skeletal injuries may not be evident with radiogra-
phy but would be seen with MRI. The visualization allows
measurement of displacement.
The MRI may visualize muscle tears (acute, chronic)
because of changes in muscle configuration and a residual
abnormal signal within the muscle (atrophy, focal mass
effect).52,53,55 Abnormal signals in chronic cases undoubtedly
represent previous intramuscular hemorrhage. A predomi-
nantly linear pattern would be compatible with the presence
of blood that has dissected between muscle bundles.
The MRI scans may clearly delineate the severity of muscle
injury.53 The major finding is the extent of hemorrhage or
edema within the muscle. With acute tears, methemoglobin
within the extravascular blood causes high-signal areas on
both T1- and T2-weighted images. A residual abnormal
signal several months after the original injury probably rep-
resents recurrent injury.
When a soft tissue tear is suspected, initially imaging
is done with large field-of-view axial sections so the two
sides can be compared, and selective views taken. Selective
coronal or sagittal views along the axis of the torn muscle
are then useful for determining the overall extent of injury.
Muscle configuration changes may consist of atrophy or a
focal mass effect. Abnormal signal areas indicate intra-
muscular hemorrhage. The linear pattern is consistent
with dissection of hemorrhage between muscle bundles.
The MRI appearance of soft tissue blood has been studied
in animals247 and clinical series.4,65,79,195 Differences in
signal intensity probably represent different patterns of
blood breakdown. High signals may persist 1–3 years
after injury.53 The appearance of low-intensity signals
probably indicates fibrous reactive changes within the
hematoma and injured soft tissues. Repeated small hemor-
139
rhages are the most likely cause of a continued high-
intensity signal.
Ligament injuries are purportedly rare in children, the
basic concept being that the physis fails first. E1-Khoury
et al. showed in adolescents that the weakest link in the
muscle–tendon–bone (cartilage) complex is the apophysis.72
The use of MRI has certainly demonstrated that discrete lig-
ament injuries may occur and, more importantly, that partial
to complete tears may accompany avulsion fractures (see sec-
tions on ligament injuries in Chapter 22 and tibial spine
injuries in Chapter 23).
Scintigraphy (Radionuclide Imaging)
Systematic application of nuclear medicine procedures has
probably been underutilized in the detailed evaluation of
children’s trauma.114–116,138,139,158,165,204,217,246,268 The relatively
noninvasive nature of isotope studies makes them attractive
as a screening procedure (e.g., for multiple sites of injury
after child abuse). The reduced radiation dosage permits
repetitive studies to be done with relative safety. The appli-
cations of bone scans currently in clinical use include (1)
evaluation of fractures; (2) determination of osteomyelitis or
a tumor as the cause of acute bone pain following an injury;
(3) evaluation of ischemic necrosis of the capital femoral
ossification center after hip dislocation or fracture of the
femoral neck; (4) evaluation of radiographically normal
appearing bone to detect stress fractures, allowing early diag-
nosis of these lesions (see Chapter 12); and (5) screening
the entire skeleton in cases of suspected child abuse (see
Chapter 11).87,98,103,117,122,160,236 This method is particularly
useful for evaluating the toddler’s fracture in the limping
child (see Chapters 23, 24).
Heinrich et al. used whole-body scanning to detect undi-
agnosed fractures in severely injured children and adults.119
They studied 48 patients under 20 years of age who had mul-
tiple injuries or a head injury. Nineteen previously unrecog-
nized fractures were identified. In six patients the treatment
was modified on this basis.
Three-phase bone scintigraphy allows dynamic acquisition
of angiographic and early and delayed static images fol-
lowing injection of a radiopharmaceutical. The first, or
angiographic, phase records the vascular transit of the
radionuclide through the primary arterial vessels. Each
image is of only a few seconds duration. This image provides
an estimate of the regional vascularity but is insufficient for
individual bone vascularity. The second phase acquires
images immediately after the angiographic phase. It is
termed the blood pool phase. During this phase the radionu-
clide moves from the vascular space into the extracellular
spaces of soft tissues and bone. This phase begins to delin-
eate highly vascular, metabolically active regions such as the
physeal–metaphyseal interface. The third phase is usually
obtained 1.5–3.0 hours after injection. This static phase
depicts the distribution of the radionuclide within the entire
bone and specifically delineates regional bone perfusion and
metabolism with a minimum of soft tissue background inter-
ference. The procedure is useful for studying elastic de-
formation disorders (osteochondroses), which probably
represent microfailure in the spherical ossification center
of an epiphysis or nonlongitudinal carpal or tarsal bone. The
140
procedure is also useful for detecting toddler’s fractures
(usually of the tibia or calcaneus). The total skeletal scan
generated is an excellent initial screen for the multiple, asyn-
chronous fractures seen with child abuse. Overuse injuries
(e.g., stress fractures) also may be depicted.
SPECT Scanning
Murray and Dixon thought that single positron emission
computed tomography (SPECT) had a maximum advantage
for evaluating pain (often associated with acute trauma) in
the spine and knee.176 By removing the superimposition of
structures and unwanted surrounding radioactivity, SPECT
increases diagnostic accuracy.9
Conway has shown it to be particularly useful for evaluat-
ing chronic pain due to stress fractures of the back in
adolescents.43,44
Vascular Radioloqy
Trauma to blood vessels is an infrequent accompaniment of
children’s fractures, but it represents a potential catastrophe
when present. Arteriography is especially helpful for ade-
quately delineating a specific vascular injury (Fig. 5-25).
Fortunately, increasing awareness of soft tissue injury and
vascular compromise has led to a significant decrease in
Volkmann’s contracture, whether involving the upper or
lower extremity. A more detailed description of concomitant
vascular injuries, along with their diagnosis and treatment,
may be found in Chapters 10, 14, and 22. Venography has
less use during childhood and adolescence because phlebitis
and thrombosis are unusual complications of chondro-
osseous injury prior to skeletal maturation (see Chapter 10).
FIGURE 5-25. Arteriogram in a patient with fracture-displacement
of the proximal tibial epiphysis shows complete block of the
popliteal artery.
5. Diagnostic Imaging
An area unexplored in children’s trauma is the use of
angiographic MRI, potentially with three-dimensional
reconstruction, to evaluate vascular injury at the knee or
elbow.
Sonography
Sonography has been used to diagnose clinical entities such
as a displaced epiphysis of the proximal or distal humerus in
the newborn.105,108,221,241 This techique may be equally appli-
cable to patients in whom any ossification center has not yet
appeared.
Dias et al. used ultrasonic examination to delineate an
injury to the distal humerus.57 It defined the direction and
magnitude of the displacement and allowed monitoring of
reduction and early stages of reduction.
Davidson et al. studied the use of ultrasonography
(US) in the evaluation of elbow trauma.47 They studied
seven infants and a 10-year-old child. They found US was a
readily available, noninvasive technique that could be
useful for detecting nondisplaced or minimally displaced
fractures.
Koudsi et al. showed that color Doppler sonogrphy
could be used to assess patency and blood flow reliably
in small vessels.144 Color Doppler imaging combines
real-time US imaging with semiquantitative color encoding
of the Doppler information. Color assignment depends
on the mean velocity and direction of flow. Whenever
flow is detected it is color-encoded and superimposed on
the gray-scale, real-time image. Color saturation reflects
the relative velocity. Quantitative velocity information may
be derived from the spectral analysis of the arterial
waveform.
Ricciardi et al. used US to monitor fracture healing.206
They did not find it to be a reliable indication of healing.
The MRI findings of a dense black line at the fracture site,
in the presence of peripheral callus, may explain the lack of
reliability of this technique (see Chapter 8).
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Injury to the Growth Mechanisms
Engraving of an incomplete type 2 growth plate injury of the distal
femur. The metaphyseal propagation did not extend across the cor-
tical bone. (From Poland J. Traumatic Separation of the Epiphyses.
London: Smith Elder, 1898)
pproximately 15% of all fractures in children involve
A a physis.* Table 6-1 gives the relative incidence of spe-
cific physeal injuries from several patient series. The
series by Neer and Horwitz covered almost 2400 consecutive
physeal injuries,238 but certain fractures, particularly the fre-
quent metacarpal, metatarsal, and phalangeal injuries, were
not included. The first series by Peterson covered both local
and referral patients.281 The study by Ogden covered a 5-year
period at an urban university teaching hospital and referrals
for complex physeal injuries. The latter two studies thus did
not reflect true incidence patterns.
The latest study by Peterson et al. is probably the most sta-
tistically reliable because of the unique population dynamics
and selected hospital utilization.286 The referral base for
virtually all injuries in this specific county was relatively
* Refs. 1,2,10,23,24,26,27,35,38,43,45–47,49,52,59,66,67,72,74,77,78,80,
81,91,98,99,102,109,110,112,115,123,147,151,169,170,175,198,202,203,
207,208,214,216,219–222,228,235,240,241,248,249,252,258,264–266,
271,275,278,279,286,292,298–307,312–316,320,328,339,340,346,349,
356–358,361,373,375,376,379,384,387,388.
controlled because of finite medical resources. This study
showed that the most common site of physeal injury involved
the hand (specifically the phalanges). Most other studies
have minimized or neglected physeal mechanical injuries to
both the hands and the feet. Another series revealed more
phalangeal physeal injuries than did all the previous series
combined.286 This susceptibility might be expected because
of the tendency to break falls with the outstretched hand and
the high rate of exposure of the hand to injury in organized
childhood sports.
The distal physes are injured more commonly than the
proximal physes. The frequent occurrence of injury to
certain physes, such as the distal radius, distal tibia, and pha-
langes, results from the increased exposure of these more
distal regions to trauma, rather than from any unique phys-
iologic susceptibility of these particular physes.
Boys sustain physeal injuries more frequently than girls,
probably because of the greater exposure of boys to signifi-
cant etiologic factors, especially uncontrolled and controlled
trauma from athletic activities,137 and because the physes
of boys stay open longer than those of girls, extending the
duration of possible exposure to injurious trauma. Some
research studies have suggested that estrogenic compounds
strengthen intrinsic physeal properties, whereas androgenic
compounds cause a relative weakening during this rapid
growth period.233,234 The greater emphasis today on, and
exposure to, competitive sports involving girls will undoubt-
edly increase the incidence of physeal injuries in young
female athletes. Gymnastics, in particular, is associated with
a risk of not only spondylolysis but also other repetitive
physeal and nonphyseal injury patterns that may involve
radiographic “widening” of the physeal line and carry an
increased risk of premature closure (e.g., gymnast’s wrist,
swimmer’s shoulder). As more competitive sports involv-
ing the skeletally immature athlete are carefully and sys-
tematically analyzed, other patterns of injury, especially
those that are relatively sport-specific, are certain to become
recognized.
There are intrinsic biomechanical response differences in
the physis at different ages, especially during the adolescent
growth spurt.255,259,260 Morscher et al. also showed that there
are hormone-mediated (i.e., sex-related) differences in the
physeal response to experimentally applied stresses.233,234
147
148 6. Injury to the Growth Mechanisms

TABLE 6-1. Relative Incidence of Physeal Injuries

Site of injury Neer238 Peterson279 Ogden Peterson286

Proximal clavicle — — 8 4
Distal clavicle — — 5 2
Proximal humerus 72 22 41 18
Distal humerus (including epicondyles) 332 20 108 37
Proximal radius 124 1 12 6
Proximal ulna — 21 9 4
Distal ulna (not styloid) 136 12 13 27
Distal radius 1096 98 197 170
Metacarpals — 10 9 61
Phalanges (fingers) — 39 55 356
Pelvis — — 28 3
Proximal femur — 7 11 1
Trochanters — — 19 —
Distal femur 28 18 36 13
Proximal tibia 17 6 14 8
Proximal fibula 2 — 4 1
Tibial tuberosity — — 22 —
Distal tibia 238 59 83 104
Distal fibula 302 21 18 68
Metatarsals — 6 7 13
Phalanges (toes) — 11 22 55
Total 2347 351 721 951

Furthermore, as discussed in Chapter 1, anatomic changes “Little League elbow,” and the “gymnastic wrist,” do occur
in the metaphyseal cortex, primarily occurring during the frequently in specific competitive situations.1 Further
growth spurt, may also affect the injury response patterns.1,205 discussions of athletic injuries are presented in Chapter 12
These metaphyseal changes, coupled with physeal contour and in anatomic Chapters 13–24.
alterations unique to each physis (i.e., undulations, mam- Naturally occurring growth mechanism injuries are being
millary processes), the increasing size of the epiphyseal ossi- increasingly recognized in immature animals (Fig. 6-1). They
fication center, and contour changes in the ossification may potentially serve as natural models of physical trauma
center to conform to the shape of the epiphysis (i.e., the because they occur under spontaneous, rather than experi-
eventual adult contour) all change the likelihood of certain mental, conditions.70,79,88,165,215,245,246,257,267,273,354,372 In a collabo-
fracture patterns and particularly increase the incidence rative study with a major zoologic park, a large number of
of type 2 physeal fractures, compared to those of type 1. physeal injuries in large mammals with epiphyses of sizes
Secondary ossification of discrete anatomic structures (e.g.,
the malleoli and epicondyles) also undoubtedly affect
fracture patterns.
The ages at which most physeal fractures occur are 9–12
years in girls and 12–15 years in boys, suggesting that from
the standpoint of physiologic chronobiology the physes are
comparably vulnerable to injury in the two sexes. Relative
rates of maturation obviously affect such statistics. In partic-
ular, the tendency to delayed onset of menses (particularly
evident in anorectic ballet dancers and gymnasts) obviously
affects rates of skeletal maturation and, accordingly, suscep-
tibility to physeal and metaphyseal injury.
Athletics play an especially important role in the lives of
children and adolescents. An increasing number of children
of both sexes are participating in organized contact and non-
contact sports. Interestingly, a review of 2137 cases of athletic
injuries in children found only 58 epiphyseal and physeal
injuries, most of which were acutely symptomatic cases of
Osgood-Schlatter lesions.77 There does not appear to be a sig-
nificantly greater risk of sustaining an epiphyseal-physeal
injury during competitive athletics than during other “non- FIGURE 6-1. Type 2 physeal injury of the distal femur in a puppy
sport” activities.199 However, certain types of chronic (repet- struck by a car. It was percutaneously pinned and casted, with sub-
itive) epiphyseal injury, such as the Osgood-Schlatter lesion, sequent normal leg growth.
Classification
comparable to human skeletal components have been ana-
lyzed. These specimens are presented throughout this
chapter and in other chapters in this book. They further
our understanding of failure of the immature mammalian
skeleton.
Classification
Poland’s treatise on epiphyseal fractures particularly
recounts the history of physeal injuries.289 He stated that
the earliest references were apochryphal, attributing to the
Amazons the stunting of the growth of tribal males by sepa-
rating or damaging the physes and epiphyses at or shortly
after birth.289 Studies concerning birth and neonatal injuries
certainly corroborate a high incidence of physeal damage
when the physes are separated during a difficult delivery or
physical mishandling during infancy.157,252,258 These concepts
are detailed in Chapters 11, 14, and 22 in particular. Modern
observations of the consequences of child abuse (see
Chapter 11) attest to the relative ease with which trauma may
be inflicted on the growing parts of bones in neonates and
infants under 1 year of age. Did these descriptions of Homer
and others refer to the first documentation or recognition
of the worldwide phenomenon of child abuse?
Hippocrates appears to be given credit for the first medical
documentation of a physeal injury. It involved the thumb but
was erroneously considered a dislocation.289
Little specific documentation appeared until late during
the European Renaissance when Severin described anatomic
specimens of physeal fractures of the proximal and distal
tibia in 1632.289 In 1759 Reichel published a dissertation on
separations of the epiphyses.289 He recognized both sponta-
neous (probably rachitic) and traumatic separations. In 1837
Gueretin published cadaver research on separations that
were correlated with clinical observations.289 Foucher also
performed cadaver research and developed a system of
injury failure.119,120 He emphasized the role of tearing of the
periosteum and tried to address the likely pathomechanics
that create these fractures.
Basically, these early references alluded to the rarity of epi-
physeal/physeal injuries and suggested they were the equiv-
alent of the Salter-Harris type 1 pattern. In 1855 Malgaigne
noted that the injury was invariably accompanied by a me-
taphyseal fracture that adhered to the epiphysis (i.e., the
Salter-Harris type 2 injury).
The first specific classification scheme was suggested in
1863 by the French surgeon Foucher,119,120 who described the
following categories: (1) pure separation of the epiphysis
from the diaphysis, with no osseous tissue adhering to it
(divulsion épiphysaire); (2) separation of the epiphysis with a
thin, finely granular layer of osseous material attached to it
(fracture épiphysaire); and (3) solution of continuity of the di-
aphysis in the osseous spongy tissue near the epiphysis at a
time when the epiphyseal growth plate is closing (fracture
preépiphysaire).
In 1896, on the basis of a comprehensive review of mate-
rial that included specimens from various anatomic
museums and experimental work on cadavers of children
collected from throughout Europe, Poland showed that
these injuries were relatively frequent. He advanced a classi-
149
fication scheme dividing epiphyseal fractures into four basic
types.289 Types I, II, and III were comparable, respectively, to
Salter-Harris types I, II, and III. His type IV essentially was
one of bicondylar type III injuries (paired Salter-Harris type
III) and thus was really a variant, rather than an anatomically
distinct pattern. His work is a classic treatise on the historic
aspects of physeal injuries, and it is profusely illustrated with
engravings of these injuries (Fig. 6-2), a large number of
which were studied anatomically because of the high inci-
dence of fatality among children during that era. Many of
these engravings are used at the beginning of each of the
chapters in this book. Poland introduced the use of skia-
grams, the term for the x-ray studies discovered only 3 years
earlier (1895) by Roentgen, whose techniques rapidly spread
through western Europe (see Chapter 5). A colleague,
C. Thurstan Holland, pioneered the use of these x-rays in
England.161
Poland’s book was essentially limited to the experience of
western Europe. It would be interesting to know if historical
studies of other early and contemporaneous civilizations
(e.g., Egyptian, Chinese, pre-Columbian meso-American)
reveal any reference to these injury patterns.
Bergenfeldt, in 1933, studied 295 patients (310 fractures)
and devised a classification of six types.26 His type I corre-
sponded to Salter-Harris type I. His type II (small metaphy-
seal fragment) and type III (large metaphyseal fragment)
were variations of the Salter-Harris type II. His types IV and
V corresponded, respectively, to Salter-Harris types III and
IV. The last type (VI) incuded a thin, linear layer of me-
taphyseal bone across the entire metaphyseal width. This was
not included in the Salter-Harris scheme but was described
subsequently by Ogden (type 1B). It probably is an early
description of the corner fracture frequently described in
child abuse.
Aitken subsequently presented a classification scheme des-
ignating three fundamental types of epiphyseal fracture. He
emphasized that deformity consequent to initial malunion
or potential growth disturbance was probably rare, even
FIGURE 6-2. Retouched engraving of a distal radial injury (type 1
pattern) from Poland’s classic treatise on physeal injuries.289
Arrows indicate the dorsally displaced periosteal sleeve and epiph-
ysis. The asterisk (*) indicates the pressure in the carpal tunnel
from the palmar displacement of the metaphysis.
150
though displacement was often significant.2 Aitken empha-
sized that the third type of fracture, compression injury, was
extremely difficult to diagnose, was frequently thought to be
of little clinical significance, and could easily lead to major
growth deformities. Such “contention” still occurs in the
“acceptance” of the Salter 5 injury pattern.
Salter and Harris presented a scheme based on a combi-
nation of (1) the mechanism of injury; (2) the probable rela-
tionship of the fracture line to the various cellular layers of
the physis; and (3) the prognosis concerning subsequent dis-
turbance of normal growth patterns.58,149,314 It is important to
realize that this classification scheme was principally based
on radiographic analyses, rather than on any detailed
anatomic/histologic studies. The classification recognized
five types of injury. Type I was a complete transverse separa-
tion of the epiphysis and physis from the metaphysis, with
the fracture occurring, through the zone of the hypertrophic
cells. In type II, a similar transverse physeal fracture
occurred, but angulated such that a metaphyseal fragment
was included on the compression side of the fracture. Types
I and II were supposedly free of long-term complications
such as premature growth arrest, a concept that has unfor-
tunately led to a certain amount of complacency in advising
parents of the risk of growth impairment. Type III involved
a transverse fracture across part of the growth plate, with sub-
sequent propagation through the epiphysis and epiphyseal
ossification center into the joint (articular cartilage). Type
IV involved a fracture through the epiphyseal ossification
center, the physis, and a portion of the metaphysis; this
pattern also disrupts the articular surface. Type V was a
crushing (compression) injury to the growth plate. These
last three types of injury were associated with an increased
potential risk of premature growth arrest, whereas the first
two purportedly were not at such risk.314 There was minimal
histologic corroboration of the injury patterns. The authors
artificially created a physeal fracture in a single distal radius
specimen obtained during an autopsy following a nontrau-
matic death (Fig. 6-3). This served as the basis for their state-
ment that the fracture occurs through the hypertrophic zone
of the physis.
FIGURE 6-3. Experimental distal radial fracture created by Salter
and Harris for their publication on physeal injuries.314 The child had
died from nonskeletal problems.
6. Injury to the Growth Mechanisms
Shapiro classified physeal injuries based on pathophysiol-
ogy.327 The two factors he considered important were the
integrity of the blood flow (arterial) to the epiphysis and
the separation of epiphyseal and metaphyseal arterial blood
flows. He proposed three basic types of physeal fracture. In
type A the epiphyseal circulation is undamaged, and there is
no epiphyseal-metaphyseal vascular communication. This
type coincides with Salter-Harris type I and II injuries and has
a good prognosis. In type B the epiphyseal circulation is
undamaged, but a communication is established with the
metaphyseal circulation that allows formation of an osseous
bridge. His type B1 is the equivalent of a displaced type IV
Salter-Harris injury, and type B2 is the equivalent of either a
type III Salter-Harris injury or a type II Salter-Harris injury
with internal disruption of the physis. Type C, associated with
disruption of the epiphyseal circulation, leads to ischemic
necrosis of the epiphysis and germinal zone of the physis.
This type has no analogue in the original Salter-Harris
classification, although it would fit into the type V pattern
mechanism suggested by Ogden and Peterson, both of whom
thought there was vascular damage rather than cellular
crushing as the underlying mechanism.248,249,285 Realistically
this system would require diagnosis by magnetic resonance
imaging (MRI), MRI angiography, or possibly color Doppler
studies to ascertain vascularity. It is thus a clinically impracti-
cal scheme (although physiologically credible).
Peterson et al. studied all physeal fractures over a 10-year
period in Olmsted County, Minnesota.286 A series of 850 chil-
dren sustained 951 physeal fractures: 561 boys with 637 frac-
tures and 289 girls with 314 fractures. The highest fracture
rates were in 11- to 12-year-old girls and 14-year-old boys. The
most common site involved the finger phalanges (37% of all
the physeal fractures). Type 2 Salter-Harris fracture was most
frequent (54%), although 16% (149 fractures) of the physeal
fractures were not readily classified by the Salter-Harris
system. Of the 951 physeal fractures, 37 (3.9%) developed
premature complete physeal closure. In addition, premature
partial physeal closure occurred in another 24 fractures
(2.5%). Thus 6.4% of all the physeal fractures had docu-
mented obvious growth damage.
Peterson reported two new physeal fracture patterns.282 In
the first the principle fracture is transversely through the
metaphysis, but there are one or more longitudinal exten-
sions toward the physis. In the aforementioned study
(Olmsted County) this pattern was most common, occurring
in 147 of 951 injuries. In the second pattern a part or all of
the physis was anatomically missing due to the injury mech-
anism. The latter pattern was often associated with pene-
trating or open injury (e.g., lawn mower, gunshot).
Based on these detailed aforementioned studies, Peterson
proposed a physeal fracture classification that included six
patterns.281,284
Type I: Transverse fracture of the metaphysis with one or
more longitudinal extensions to the physis. The peripheral
metaphyseal fragment is different from the Thurstan
Holland fragment of the Salter-Harris type II. Physeal dis-
ruption was thought to be minimal (and probably focal),
without extension into the epiphyseal ossification center.
Follow-up films showed metaphyseal sclerosis, as described
by the Ogden type 8 fracture when there is a temporary
Basic Patterns of Failure 151

disruption of the metaphyseal circulation. This fracture

pattern comprised 15.5% of the fractures in the Olmsted
County study.
Type II: There is a metaphyseal fragment, and the type
corresponds to Salter-Harris type II. Peterson subclassified
type II as A, B, or C according to the location and size of the
metaphyseal fragment. He thought that the smaller the
metaphyseal fragment the more likely was the risk of physeal
damage that would disrupt normal growth. This fracture
pattern was most common (53.6%). The most frequent site
of the pattern was in the finger phalanges (47.6% of all type
II injuries). Growth arrest was noted in 6.5% of the involved
patients, in contrast to the “benign” nature of this injury
pattern according to the Salter-Harris system.
Type III: Separation of the epiphysis (and physis) from the
diaphysis (more properly the metaphysis); it corresponds to
Salter-Harris type I. This fracture occurred in 13.2% of the
fractures in the Olmsted study. The distal fibula appeared to
be the most common site, although Peterson thought this
particular injury was often overdiagnosed.
Type IV: The equivalent of Salter-Harris type III. This frac-
ture comprised 10.9% of the injuries in the Olmsted study
and was most common in the finger phalanges and the distal
tibia (medial malleolus and lateral plafond).
Type V: The equivalent to Salter-Harris type IV. It incuded
triplane injuries. This fracture pattern comprised 6.5% of
the fractures in the Olmsted study. The most common sites FIGURE 6-4. Not every fracture is easy to classify by the Salter-
were the distal humerus (lateral condyle), finger phalanges, Harris system. In this slab section from a traumatic below-knee
and distal tibia. amputation, the fibula exhibits a fracture through the cartilage of
the malleolar tip and a fracture at the chondro-osseous interface
Type VI: A portion of the physis is missing, usually accom-
of the fibula (sleeve or shell fracture) with extension across the
panied by missing fragments of the epiphyseal ossification physis longitudinally and subsequent angular propagation across
center and metaphysis. Peterson thought this pattern was the germinal zone to the opposite side. The tibia shows an articu-
associated only with open injuries (I disagree) and usually lar/epiphyseal fracture up to the ossification center. A nearby frac-
due to high velocity trauma (power lawn mower, farm ture extends toward the physis, takes two 90° turns, crosses
machine, boat propellor, snowmobile, gunshot). The injury the physis, and then variably propagates into the metaphysis.
occurred infrequently in the Olmsted study (0.2%). It Intraosseous hemorrhage is evident within the tibial metaphysis
should be seriously considered in any of the aforementioned and the distal tibial and fibular physes. These are “bone bruises”
mechanisms. As is shown subsequently, focal closed physeal on an MRI examination.
disruption may also produce this injury pattern.
mized in the original Salter-Harris classification. For obvious
Other authors have proposed classification systems, par-
medicolegal reasons it is important to realize that type I
ticularly as related to the distal tibial epiphysis, that do
and II patterns are not as innocuous as originally described
not readily fit the Salter-Harris system.38,73,102,152 One author
by Salter and Harris. Other growth mechanisms of bone
even questioned whether any fracture classification system is
and cartilage, detailed in Chapter 1, may also be affected by
needed.60
trauma and are included in this system, which is detailed in
Although the classification scheme of Salter and Harris,
this chapter. For continuity of classification, types I–V of the
which is certainly the most widely used, is relatively concise
Salter-Harris system are maintained but are broadened in
and has surely proved to be of diagnostic and clinical impor-
scope. Other patterns are added to this clinically accepted
tance, growth disruption is deemphasized, certain types of
scheme. Hopefully, the additional typing and subtyping of
epiphyseal and physeal injury are not readily classified, and
injury patterns will increase understanding of epiphyseal
complicated combinations of injuries obviously occur (Fig.
and other growth mechanism fracture mechanics, allow
6-4). Furthermore, injuries to other important growth mech-
better outcome studies, and improve the selection of specific
anisms, such as the metaphysis, diaphysis, periosteum, zone
treatments.
of Ranvier, and epiphyseal perichondrium, are not included
in this scheme.
Accordingly, an enlarged, more inclusive, physiologically
and histologically based scheme has been devised.248–253,256
Basic Patterns of Failure
Salter-Harris types I and II are given subtypes in this system
Histology
to explain the probable cause of premature, localized growth
plate closure and osseous bridging, a complication that is being Histologic evaluation of growth plate failure has been limited
recognized more frequently with these patterns even though mini- in the human. Smith et al. analyzed a distal tibial physeal
152
FIGURE 6-5. (A) Usual region of fracture propagation (F, arrows) at
the histologic level. This same pattern exists in types 2 and 3 when
the fracture propagates transversely across the physis. Note the
fracture in a 12-year-old boy who sustained a traumatic below-
knee amputation.338 The plane of separation was within the
hypertrophic zone, as suggested by Salter and Harris based
on the one autopsy specimen in which they attempted to
duplicate a physeal fracture experimentally.
Studies done in our laboratory over the past 20 years have
looked at more than 200 specimens of spontaneously occurring
physeal fractures in children (usually from traumatic ampu-
tations) and skeletally immature zoo animals. Typically, the
fracture propagates within the hypertrophic zone. The most
common level was the junction of calcified and uncalcified
hypertrophic cells (Fig. 6-5). The calcification of the extra-
cellular matrix undoubtedly changes the local microme-
chanics and the summated macromechanics of the entire
area/volume of the physis.210 The fracture usually propagates
in the typical region, but variation may occur. Particu-
larly, the fracture often shifts to the physeal–metaphyseal
chondro-osseous interface (Fig. 6-6). In the neonate and
infant fracture propagation may extend to involve the E-
vessels (Fig. 6-7). This is particularly problematic, as it devas-
cularizes segments of the germinal zone, which may explain
the examples of central growth arrest subsequently compli-
cating these fractures (see Chapter 7).
As is shown in subsequent sections of this chapter, subtle
variations in fracture propagation can and do occur. The
fracture may separate the germinal zone from the secondary
ossification center or propagate across segments of the ger-
minal zone. Such fracture redirection increases the risk of
permanent growth damage. These fractures are referred to
as “wrong-side” physeal fractures, as they do not anatomically
6. Injury to the Growth Mechanisms
B
perichondrium (PC), periosteum (PO), mesenchymal cells (M), and
ossification ring of Lacroix (ORL). (B) Typical pattern of a fracture
within the hypertrophic zone.
conform to the “textbook description” of physeal fracture
propagation (Fig. 6-4).
Diagnostic Imaging
The basic diagnostic method remains two radiographs taken
90° apart in standard anteroposterior (AP) and lateral
planes. The radiographs should be centered over the physis
in question. Entire bone radiographs, in which the epiphy-
ses are near the edge of the film, may present a distorted
view of the physis due to parallax. Subtle epiphyseal dis-
placement may be missed. Standard views should be added,
as indicated, to rule in or out the presence of a Thurstan
Holland fragment or epiphyseal displacement.
Scintigraphy, which is recommended for complete skele-
tal evaluation in child abuse cases (see Chapter 11), may also
be used to delineate unusual fractures.377 As with stress frac-
tures, a bone scan may be useful for evaluating a painful
bone region (in addition to the physical examination) in
which the basic radiographs appear normal. A positive bone
scan is strongly suggestive of such injury. Clinical situations
that are likely to need such evaluation include chronic,
repetitive use (e.g., gymnast’s wrist) or the asynchronous
fractures of child abuse. The distal fibula that has no evi-
dence of fracture but is swollen and painful around the
lateral malleolus may also be studied by nuclear imaging.
Sonography has been utilized to detect occult injury.133
Computed tomography (CT) methodology improvements
allow better visualization of physeal disruption, especially
with three-dimensional reconstruction.236
Fracture Patterns
FIGURE 6-6. Variable propagation of a type 1 injury
pattern at multiple levels. The segment separated from its
subchondral epiphyseal bone and blood supply (arrows)
is at risk for subsequent ischemic necrosis. This may be
a factor in growth damage and physeal bridging.
The introduction of MRI has allowed much better under-
standing of the responses to injurious trauma involving the
immature skeleton. Selective use of MRI in trauma victims
has led to the diagnosis of specific injuries that are not
readily evident by routine radiography. MRI has also better
defined the specificity of growth plate fractures.172,174,337
Imaging techniques have allowed elucidation of focal
intraosseous and chondro-osseous interface injuries (i.e.,
bone bruises and shell/shear/sleeve fractures). As MRI
techniques improve (see Chapter 5), we are better able
to enhance (i.e., visualize) the physis specifically, subtle
disruptions of it, and the early onset of damage.15,105,173
Fracture Patterns
Type 1
The epiphysis and most of the contiguous physis separate
from the metaphysis without roentgenographically evident
FIGURE 6-7. Penetrating epiphyseal vessels (arrow) repre-
sent potential weak spots to tensile failure. As the fracture
separates, they may pull out with the displaced metaphy-
seal fragment, which potentially could lead to germinal zone
ischemia and subsequent growth alteration.
153
osseous fragments from the metaphysis (type 1A). The trans-
verse plane of cleavage may undulate through the zone of
hypertrophic cartilage cell columns, usually leaving the
resting and dividing cell layers of the germinal region of the
physis undamaged and still connected with the epiphysis and
the E-vessel circulation (Figs. 6-8, 6-9). More precisely, the
region of failure appears to be the junction between calci-
fied and uncalcified portions of the hypertrophic zone. This
transition, necessary as a prelude to ossification, introduces
changes in tissue micromechanisms. Although the basic
failure pattern is a separation through the hypertrophic
zone, the propagation plane is not always a smooth, trans-
verse plane (Fig. 6-10). This fracture pattern is more
common in infants and young children in whom the
physeal–metaphyseal interface tends to be a relatively
smooth (flat) plane.
Progressive undulation of the normal physis and of the
fracture line may cause propagation into regions of the ger-
minal or resting zones of the physis or into the metaphysis,
154 6. Injury to the Growth Mechanisms

B C
FIGURE 6-9. (A) Type 1 physeal fracture of the distal femur in a
stillborn infant created by a mild valgus force. (B, C) Slab section
and radiograph of a type 1 injury of the distal metatarsal in a 15-
year-old who sustained a crush injury to the foot. He eventually
required a Chopart-level amputation. The physis is part of the
B epiphyseal fragment.

FIGURE 6-8. (A) Usual type 1A growth plate injury. The germinal
and resting zones of the physis remain atached to the epiphyseal
fragment, and the calcifying and hypertrophic regions remain with
the metaphysis. (B) Computerized fracture simulation of a type 1
injury of the distal tibia and fibula.

FIGURE 6-10. Experimental fracture in a skeletally imma-

ture rabbit proximal femur. Note the variable fracture prop-
agation through the different levels of the hypertrophic
zone. The shift occurs primarily at the central angular
change of the physeal contour.
Fracture Patterns 155

such that microscopic pieces of primary spongiosa may

be included on the “epiphyseal” side of the fracture. This
variable failure pattern occurs more frequently in those
physes that are beginning to develop contour changes in
response to dynamic, changing biomechanical forces. The
changes in contour may include small mammillary processes
extending into the metaphysis or larger curves, such as the
quadrinodal contour of the distal femoral physis in the ado-
lescent. In infants and young children this extensive remod-
eling and contouring (undulation) of the physis, with
formation of mammillary processes, has not usually com-
menced, so the fracture line tends to be relatively smooth
and transverse.
Displacement of the epiphyseal fragment from the me-
taphysis is generally much less in type 1 than in other types
of physeal injuries. It occurs because much of the thick
peripheral periosteal attachment into the zone of Ranvier
remains intact and so mechanically prevents significant dis-

FIGURE 6-12. Extent of periosteal stripping is evident in this distal

femoral physeal fracture (birth injury). Stripping is limited distally
by the attachments to the physeal periphery (zone of Ranvier).

placement (Figs. 6-11 to 6-14). Such a lack of displacement

of the involved fragments frequently makes radiologic diag-
nosis difficult if not impossible. Slight widening of the physis
may be the only sign; but if the secondary ossification center
is small, any widening may be difficult to assess. The exam-
ples shown in Figures 6-15 to 6-17 were microscopically
incomplete, with failure confined to the central region of the
physis; the strong peripheral soft tissue attachments remain
intact.

B
FIGURE 6-11. (A) Incomplete type 1 physeal fracture in a proximal
humerus of a 3-year-old child fatally injured in an automobile-
pedestrian accident. (B) Undisplaced type 1 proximal tibial physeal
fracture. The physeal periphery and periosteum are grossly intact. FIGURE 6-13. Incomplete type 1 physeal injury of the fibula accom-
This boy underwent a traumatic above-knee amputation. There panying a complex type 4 tibial physeal injury. This 11-year-old boy
also were tibial spine and tibial tuberosity fractures. sustained a traumatic below-knee amputation.
156 6. Injury to the Growth Mechanisms

FIGURE 6-16. Incomplete type 1 fracture with an intact physeal

periphery.

FIGURE 6-14. The periosteum is often partially intact (arrow),

limiting epiphyseal displacement. This intact periosteal sleeve
also prevents overreduction. The loose periosteum, on the tensile
failure side, may herniate into the fracture gap during reduction.

Minimal type 1 injuries often are not readily easily

detectable radiographically (Figs. 6-18, 6-19) but may be
deduced on the basis of an adequate history and physical
signs of pain and localized tenderness. In such a situation
the clinical diagnosis assumes particular import, rather than
reliance on the radiograph, as the patient should be treated
as having an occult fracture to prevent further injury. Other
confirmatory imaging modalities may be necessary.
These occult injuries may be termed skeletal injury
without obvious radiologic abnormality (SKIWORA). This
situation is analogous to spinal cord injury without obvious
radiologic abnormality (SCIWORA), a phenomenon dis-

FIGURE 6-15. Clinically undetectable, incomplete type 1 physeal

fracture in distal radius from a 9-year-old child. The arm had been FIGURE 6-17. (A) Anteroposterior (AP) view of a type 1A distal tibial
traumatically avulsed in a machinery accident. How often this injury injury with mild widening of the physis (arrow) compared to the
might occur in other clinical situations is unknown. The physeal uninvolved side. (B) AP view (left) and lateral view (right) of a type
periphery and zone of Ranvier were intact. 1A injury of the distal tibia with 90° rotation of the fragment (arrow).
Fracture Patterns
FIGURE 6-18. Type 1A injury with complete displacement of the
distal ulnar epiphysis. A small segment of the epiphyseal ossifi-
cation center remains (arrow). This represents tension failure
through the ossification center just above the subchondral plate
and has an ominous prognosis, as the E-vessel supply is
damaged.
cussed in detail in Chapter 18. In fact, in most instances of
such spinal cord injury the fracture is an occult, sponta-
neously reduced type 1 injury involving separation of the ver-
tebral end-plate (an epiphyseal analogue in the human)
from the vertebral body ossification center (the metaphyseal
analogue).
Complete displacement of the epiphysis and physis may
occur (Fig. 6-18), usually as a result of a significant shearing
or tensile (avulsion) force. Any displacement obviously
facilitates the anatomically correct diagnosis. Birth trauma
and child abuse are common etiologic factors associated with
displacement.
Type 1 injuries may be encountered in neonates and
infants with limited development (if any) of the secondary
ossification center (Figs. 6-12, 6-14). They are often misdiag-
nosed as dislocations, usually because of the nuances of
roentgenographic anatomy in this age group. However, true
traumatic dislocations are rare (if they even occur at all) at
this early age. Invariably, the clinical examination can eluci-
date or strongly suggest a fracture (usually by pain, abnor-
mal motion, crepitation). Definitive diagnosis may require
arthrography, ultrasonography, or MRI because of the lack
of secondary ossification.
The size (volume) of the secondary ossification center,
relative to the overall size of the epiphysis, probably plays
a major role in the dissipation of fracture forces during
propagation of the acute injury across the physis, particularly
on the compression side of the fracture. The larger the ossi-
fication center, the greater is the tendency of a fracture to
change direction and propagate into the metaphysis to
create the type 2 injury.
Type 1 injuries may also occur as pathologic fractures
complicating underlying diseases or disorders such as
rickets, juxtaphyseal cysts, osteomyelitis, and myelomeningo-
cele (Fig. 6-19).79 These various aforementioned conditions
affect the biomechanical susceptibility of the physis and con-
157
tiguous metaphysis (primary spongiosa) to shear stresses.
They are discussed in more detail in Chapters 9 and 11.
A subclassification of this fracture pattern, type 1B, may
occur in children with certain systemic disorders affecting
the ossification patterns of the metaphysis (Fig. 6-20). These
particular injuries may occur in children with myeloprolif-
erative disorders such as thalassemia and leukemia (in which
a fracture may be the initial presentation of the disease) or
neuromuscular sensory disorders such as congenital insensi-
tivity to pain and myelomeningocele, in which fibrofatty
replacement of the trabecular bone in the primary and
secondary spongiosa adversely affects mechanical suscepti-
bility to injury.
In contrast to type 1A fractures, which propagate pri-
marily through the zone of hypertrophic cartilage, the type
1B fracture pattern tends to occur in the zone involving car-
tilage replacement and primary spongiosa (bone) forma-
tion. If the fracture complicates a cellular proliferative
disorder such as leukemia, the initial fracture tends to be a
microscopic trabecular injury consequent to cellular hyper-
plasia, cystic expansion, and disruption of the spongiosa. If
the primary disease is stabilized, the microfractures may
improve or be less likely to recur. Major epiphyseal dis-
placements and long-term growth complications are uncom-
mon in these situations.
The type 1B injury pattern may appear as a displaced
epiphysis with an associated thin layer (line) of bone. A
radiograph 90° to this line of bone may show it as a small
peripheral fragment 1–2 mm in size. This is sometimes
referred to as a “corner fracture.” It may be seen with child
abuse. Two factors seem to play a role in this pattern. Abused
children may also suffer from mild metabolic bone disease
due to malnourishment. The physeal periphery may be asso-
ciated with a curvilinear change due to the shape of the artic-
ular surface. This overlap, or lappet formation, is discussed
in more detail in Chapter 1.
The morbidity of any underlying disease and the detri-
mental effects of chemotherapy on bone formation and
remodeling may also be factors in growth alterations.
However, with other cellular proliferative disorders, such as
thalassemia, the microscopic fractures and intertrabecular
hyperplasia may lead to the destruction of portions of the
physis, the eventual formation of transphyseal osseous
bridges, and subsequent premature physeal closure affecting
length and epiphyseal angulation. When these fractures
occur with myelodysplasia, they are often unrecognized
because of the absence of pain or the misdiagnosis of
osteomyelitis; accordingly, they are subjected to continued
motion as the child is moved in and out of bed, in and out
of orthoses, and ambulates or stands in assistive devices (e.g.,
prone stander). Considerable amounts of new bone may
form in the subperiosteal metaphyseal region. A more
detailed presentation of many of these disorders is given in
Chapter 11.
Another variation of type 1B injury is widening of the
physis from repetitive use. This particularly involves the
wrist in young gymnasts and the proximal humerus in
young pitchers, tennis players, and swimmers. The repeti-
tive microinjury of the physeal–metaphyseal interface
prevents metaphyseal vascular penetration into the
hypertrophic zone. This zone continues to widen because
158
FIGURE 6-19. (A) Pathologic type 1A injury occurring as a result of
rickets. The hypertrophic zone widens and fails through this region.
Gross (B) and histologic (C) sections from a juvenile arctic fox.
Note the massive widening of the distal ulnar physis (U). Clefts with
of constant growth in the germinal and dividing zones
coupled with compromised metaphyseal vascular ingrowth.
Tensile-induced fibrous hyperplasia may form. In essence,
this creates a situation similar to the physeal widening char-
acteristically found in rickets. However, in contrast to rickets,
the hypertrophic zone is adequately calcified.
Subsequent growth is usually normal with type 1A and 1B
fractures, as the essential germinal elements, the resting and
dividing cellular layers of the growth plate, and the attendant
epiphyseal and peripheral metaphyseal blood supplies are
essentially undisturbed. There may be a temporary cutoff of
the central metaphyseal circulation, so the invasive arcades of
the metaphyseal vessels cannot reach the hypertrophic carti-
lage. This condition causes temporary widening of the
6. Injury to the Growth Mechanisms
D
fluid developed between cell columns (closed arrows) and between
the cartilage and metaphyseal bone (open arrows). (D) Epiphy-
siolysis of the proximal humerus in a 3-year-old boy with renal
rickets.
growth plate within the hypertrophic zone. Once central
metaphyseal revascularization occurs, this thickened cellular
layer is rapidly invaded and restored to its normal thickness.
In some situations, such as injury to the proximal (capital)
femur, the major blood supply to the epiphysis may be
damaged. The ischemic condition may lead to osseous necro-
sis and deformity within the developing ossification center
and to growth irregularities in the physis. These changes may
be localized and cause asymmetric growth, or they may
involve the complete physis and result in an overall slowdown
of the rate of growth or even complete cessation of growth of
the capital femoral physis. In either instance, premature
closure of some or all of the physis may occur. Depending on
the remaining growth potential, partial closure is a significant
Fracture Patterns
FIGURE 6-20. (A) Type 1B injury. The fracture is in
the primary spongiosa rather than the hypertrophic
cartilage. (B) At 1 year after chemotherapy for
leukemia, residuals of the fracture are visible as
metaphyseal lucencies (closed arrows), with
subsequent normal metaphyseal bone and a
Harris growth slowdown line (open arrows). (C)
Myelodysplastic patient with chronic type 1B epi-
physiolysis of the proximal tibia. The metaphysis
is widened and new metaphyseal bone is forming.
This child’s presenting symptoms were fever and
a swollen knee. (D) Long-term consequences are
destruction of the overall growth potential and pre-
mature epiphysiodesis.
complication, leading to severe angular growth deformities
and decreased longitudinal growth.
Because the peripheral zone of Ranvier has a separate
blood supply new physeal cells may form around the pe-
riphery, allowing latitudinal growth. These new cells are also
incorporated into longitudinal growth that is compromised
by the central growth slowdown or arrest, which leads to a
conical shape of the physis and epiphyseal ossification
center. A bone bridge may not form initially, allowing altered
longitudinal growth (shortening) without angular deforma-
tion. When a bone bridge eventually forms, longitudinal
growth is further impaired.
Although type 1 injuries seem relatively straightforward, as
indicated by types 1A and 1B, another subclassification, type
1C, defines those infrequent fractures in which an associated
injury occurs to a germinal portion of the physis (Fig. 6-21).
Birth or early infancy is one of the most likely times for such
injuries to occur. A traumatic delivery or child abuse may
lead to fractures of the proximal or distal humerus, proxi-
mal or distal femur, or proximal tibia (Fig. 6-21). Each of
159
these injuries is detailed in subsequent chapters. Because of
the lack of (or minimal) secondary ossification, these epiph-
yseal injuries may be readily confused with or misdiag-
nosed as a joint dislocation. Most of the germinal region of
the physis is uninvolved. However, a localized region is sub-
jected to disruption of all layers of the physis or to localized
vascular (epiphyseal vessel) impairment. An osseous bridge
eventually forms but not until the secondary ossification
center has expanded sufficiently to reach the originally
damaged region, which may be many years after the evoca-
tive injury.
Attempted duplication of the possible mechanism of
injury using stillborn cadavers resulted in disruption of the
epiphysis from the metaphyseal shaft and localized frag-
mentation in the medial portion of the epiphysis and
metaphysis. In these type 1C cases, the initial injury occurred
either before the secondary ossification center had formed
or just after it had appeared. Yet once the secondary ossifi-
cation center had grown sufficiently to reach the originally
damaged area, an osseous bridge eventually formed across
160 6. Injury to the Growth Mechanisms

occurred. Furthermore, as more detailed studies of osseous

growth after type 1 and 2 injuries to regions such as the prox-
imal humerus and distal femur are undertaken, it is becom-
ing increasingly evident that decreased longitudinal growth
rates may occur without any specific roentgenographic evi-
dence of premature epiphysiodesis or angular deformation.
Such decreased growth may range from only a few millime-

FIGURE 6-21. (A) Type 1C injury. On the compression side there is

a disruptive injury to a localized segment of the physis. Eventually,
an osseous bridge will form. (B) Humerus varus in an 11-year-old
boy who had sustained a “birth injury to his shoulder.” An osseous
bridge has impeded the growth of the medial physis (arrow),
causing progressive angular deformity by differential growth.

the physis, a complication comparable to that of a type 3 or

4 injury. The type 1C injury is less likely to occur in children
older than 2–3 years of age, after which time the failure
pattern is more likely to create a concomitant metaphyseal
fragment (type 2 injury). The corner fracture seen with child
abuse is likely to exhibit such a focal injury with delayed
growth arrest.
Another etiology of the type 1C pattern may be referred
to as the “wrong-side fracture,” which can occur in areas such
as the distal fibula (Fig. 6-22). The fracture line propagates
at the interface of the epiphyseal ossification center and the
germinal zone of the physis. This effectively isolates the
physis from its blood supply, leading to ischemic necrosis of
the physis.
Because of the immense growth potential of the longitu-
dinal bones in these young children and the possible
multiple-year delay between an injury and the eventual clin-
ical or roentgenologic evidence of any complications, ade- B
quate long-term follow-up becomes essential to ascertain FIGURE 6-22. “Wrong-side” type 1 fracture of the distal fibula. (A)
whether such physeal injury and complications may have Slab section. (B) Histologic section.
Fracture Patterns
ters to several centimeters, but it does represent subtle, per-
manent impairment of growth potential of the physis.
Small focal areas of physeal damage may occur with a type
1 injury. If the ensuing bone bridge is small (i.e., 1–2 mm),
the immense hydrostatic forces generated in the hyper-
trophic zone may continually break the bridge (much like
lengthening by biologic chondrodiastasis). The effect is a
long linear sclerotic streak in line with the longitudinal axis
of the bone. Similarly, small longitudinal ossifications in the
distal radial or ulnar physes may represent a comparable
phenomenon following occult partial injury. The bone
bridging that complicates physeal fractures is discussed in
detail in Chapter 7.
Type 2
Type 2A injury is the most common physeal injury pattern
(Figs. 6-23 to 6-25). Similar to type 1, it is usually caused by
a shearing or avulsion force. Some twisting (rotational shear)
may also be part of the causal mechanism. This pattern
occurs frequently in young children who have undergone
their first major growth spurt (at 3–7 years). It is certainly
FIGURE 6-23. (A) Usual type 2A injury. The fracture propagates
across the physis, as in type 1A injuries, but then turns to enter the
metaphysis, creating a piece of metaphyseal bone still attached to,
and being displaced with, the physis and epiphysis. This fragment,
which is diagnostic of the injury, is termed the Thurstan Holland
161
the most common type of physeal separation in children
over the age of 8 years.
Like the type 1 pattern, some of these injuries are difficult
to diagnose, although the presence of even a small fragment
of metaphyseal bone makes the anatomic diagnosis certain.
Any child who has a history of trauma and swelling around
a joint or epiphysis should be suspected of having this type
of injury and should be treated as though he or she has a
physeal fracture, even if the diagnosis cannot be absolutely
confirmed by routine radiography. Oblique views may be
necessary to show a small peripheral metaphyseal fragment.
MRI may be useful for elucidating such a fracture pattern,
showing the metaphyseal propagation that may not have
been evident on the initial radiograph (although changes
along fracture edges may make the radiographic diagnosis
evident 7–10 days after the original injury).
As with the type 1 injury, the failure line of a typical type
2A fracture propagates through the hypertrophic and provi-
sionally calcified zones of the physis. However, in contrast to
the type 1 injury, propagation across the physeal–metaphy-
seal interface is more variable, with a point being reached at
which the fracture line changes direction and continues
sign. (B, C) Variable type 2 injuries created experimentally in
the proximal femora of skeletally immature rabbits. (B) Fracture
partially propagated between the physis and the metaphyseal
fragment (arrows). (C) There is a completely free metaphyseal
fragment.
162
A
B
FIGURE 6-24. (A) Computer simulation of a type 2 injury of the
distal tibia. (B) Type 2 injury in a 9-year-old girl with a traumatic
below-knee amputation. There is hypertrophic physeal cartilage on
the medial side. A bone bruise is evident in the medial tibial ossi-
fication center (arrow).
propagation through a variably sized portion of the metaph-
ysis. The metaphyseal fragment, which generally appears tri-
angular and may be extremely small, is diagnostic of this
pattern of injury. This radiologically evident metaphyseal
fragment is usually referred to as the “Thurstan Holland
sign.”138,161,322 It represents compression phase redirection of
the propagating fracture (principally a tensile failure) into
the metaphysis, which is structurally (biomechanically) less
able to withstand these propagating fracture-failure forces
than are the adjacent portions of the physis and epiphysis.
The final disruption of the metaphyseal cortex is probably a
combination of tensile and compression failure. In fact, this
segment of the fracture may be an incomplete or greenstick
injury. This plastic deformation may present anatomic reduc-
tion and may cause redisplacement after an attempted
closed reduction.
6. Injury to the Growth Mechanisms
A
B
FIGURE 6-25. (A) Type 2 growth mechanism injury. (B) Type 2
growth mechanism injury with a large metaphyseal fragment.
The size of the metaphyseal fragment may vary signifi-
cantly. Although there are no detailed studies that relate the
size of the Thurstan Holland fragment to prognosis, it has
been observed that the smaller the fragment the greater the
risk of subsequent growth arrest.246,249,256,281 Small corner frag-
ments are associated with child abuse fractures and are asso-
ciated with a recognized risk of altered growth. These small
fracture fragments may also be associated with additional
fracture propagation that affects the peripheral zone of
Ranvier.
Although it may be separated from the metaphyseal cortex
on the tensile failure side, the periosteum usually remains
intact on the “compression” side and still is attached to the
triangular metaphyseal fragment (Fig. 6-26). The periosteum
also strips away from the remaining metaphysis and diaphy-
sis beyond the triangular metaphyseal fragment, especially if
Fracture Patterns
FIGURE 6-26. (A) With most physeal injuries the periosteum strips
away from the metaphysis while remaining attached to the
epiphysis and physis. Portions of the periosteum may invaginate
into the fracture defect, especially during reduction, impeding
normal repair processes or preventing reduction. (B) Specimen
from an immature narwhal showing how the metaphysis and
diaphysis are displaced from the periosteal sleeve. (C)
Roentgenogram showing how the periosteal sleeve (open arrows)
remains attached to the epiphysis (solid arrow).
the cortical fracture is complete and allows displacement of
the epiphyseal–physeal–metaphyseal unit. In contrast, on the
opposite side, where initial separation occurs under tension,
the periosteum is usually stripped from the metaphyseal–
diaphyseal section while remaining attached to the epiphysis
and peripheral physis. In fact, this avulsed periosteum may
invaginate into the gap between the epiphysis and metaph-
ysis when the deforming forces are dissipated or when closed
reduction is undertaken.
The tendency for segments of the periosteum to remain
attached to the epiphysis, physis, and metaphyseal fragment,
while shearing away from the diaphysis, is due to the inter-
calated attachment of the periosteum into the physeal
periphery at the zone of Ranvier and the blending of the
more superficial fibers of the periosteum into the contig-
uous perichondrium of the epiphysis. In sharp contrast, the
periosteum is attached relatively loosely to the metaphysis
and diaphysis, particularly in children in the age range sus-
ceptible to physeal injuries (see Chapter 1).
163
Displacement of the fracture fragments is quite variable
and may be extreme—to the point of total displacement of
the epiphysis from the metaphysis. These injuries should be
reduced as closely as possible to their original anatomic posi-
tion. However, when attempting reduction, great care must
be taken to have the musculature as relaxed as possible
(which may require general anesthesia), so the physis is not
grated over the intact metaphyseal segments (Fig. 6-27), a
potential cause of further microscopic physeal damage and
an event more likely to occur if the child is experiencing pain
and involuntarily resisting the reduction. In general, closed
reduction is relatively easy (with adequate analgesia or anes-
thesia) and may be maintained without difficulty. As previ-
ously mentioned, the periosteum is usually attached on the
compression side and may be used as a “hinge” to help attain
and maintain the reduction. Furthermore, the triangular
metaphyseal bone fragment, especially if it is large and
stable, may additionally prevent overreduction by acting as a
mechanical block.
As with type 1 injuries, subsequent physeal growth is
thought, conceptually in the Salter-Harris scheme, to be
infrequently disrupted to any significant extent, as the ger-
minal layers of the physis remain attached to the epiphysis.
Furthermore, the epiphyseal circulation is usually uninter-
rupted. Normal undulations of the physis, however, espe-
cially in the distal femur, may cause selective regions of more
severe injury. In fact, type 2 injury involving any of the major
epiphyseal–physeal units of the lower extremity has a signif-
icant risk of some type of growth disruption, in contrast to
similar physeal fractures in the upper extremity. The
increased severity of fracture-producing forces in the lower
extremity, in comparison to the upper extremtity, also plays
a significant role in the risk of growth deformity.
The subclassification type 2B involves further propagation
of the fracture forces on the tensile side to create an addi-
FIGURE 6-27. Type 2 injury of the distal femur. There is consider-
able pressure (arrows) at any point of contact, which may lead to
secondary injury and microdamage. The latter may result from
micromotion of an unsplinted injury or from manipulation without
adequate analgesia, anesthesia, or muscular relaxation.
164 6. Injury to the Growth Mechanisms

(primary spongiosa). This fragment was described by

Werenskiöld.383
Again, as with the type 1 patterns, these injuries may not
be “pure” type 2. When the fracture force turns to propagate
into the metaphysis, an angular moment change is produced
at this site. Because of the forces of injury, this angulated
area of the metaphysis may be driven into a segment of the

FIGURE 6-28. (A) Type 2B injury with a free metaphyseal fragment.

(B) Type 2B injury in a 12-year-old boy. Open reduction was nec-
essary to stabilize the fracture.

tional, free metaphyseal fragment or fragments (Fig. 6-28).

The free metaphyseal fragment makes reduction more diffi-
cult (i.e., unstable) and may necessitate open reduction to
stabilize the comminuted fragments.
The fracture line may propagate bidirectionally, but this
additional propagation may not be readily evident radi-
ographically (Fig. 6-29). Such transverse fracture propaga-
tion transversely beyond the redirection propagation may
render a small segment of the physis ischemic by disruption
of the vascularity to the germinal zone, affecting the stabil-
ity of the Thurstan Holland fragment. This is also considered B
a type 2B variation.
Another subclassification, type 2C, is the inclusion of a FIGURE 6-29. Thurstan Holland fragment may sustain additional
juxtaphyseal fracture propagation that is not readily evident on the
thin layer of metaphysis along with, or instead of, the usual
radiograph. (A) Main fracture propagation with the metaphysis is
larger triangular fragment. Such an osseous layer may tra- indicated by the open arrow. The solid arrows show the micro-
verse most of the metaphysis (Fig. 6-30). This subtype is more scopic, incomplete propagation continuing along the physis. (B)
common in slowly growing regions, such as the phalanges, Bidirectional propagation (arrow), with physeal extension to the
which normally have increased transverse, rather than lon- periosteum, which was not disrupted. Not every Thurstan Holland
gitudinal, trabeculation in the juxtaphyseal metaphysis fragment is mechanically stable.
Fracture Patterns 165

FIGURE 6-30. (A) Type 2C injury, in which the more transversely

oriented primary spongiosa remains on the physeal side of the frac-
ture. (B) Type 2C injury (arrows) in the distal phalanx of the thumb.
This injury pattern is fairly typical of phalangeal physeal injuries.
(C) Type 2C injury of the proximal phalanx of the digit with
concomitant metaphyseal Thurstan Holland (open arrow) and
Werenskiöld (closed arrow) fragments.

growth plate, causing microscopic disruption (“type 5
injury”) in a localized area (Fig. 6-31). This complication
may occur in the distal femur and distal tibia and is of suffi-
cient potential risk to warrant follow-up care for many years
after the injury. This type 2D injury may occur even before
an ossification center is present. If a physis has significant
normal contour variations, rather than being a relatively
smooth, transverse structure, there is an increased risk of
type 2D localized damage consequent to the shearing forces
causing fracture propagation between the various regions of
the growth plate and the metaphysis. Focal cutoff of epiph-
yseal vessels to the germinal zone may occur. This kind of
damage may be the mechanism of growth slowdown, com-
plete premature closure, or localized angular deformity in
epiphyseal fractures of the distal femur.
D
FIGURE 6-31. (A) Type 2D injury in which there is compression
of the metaphysis into the physis, leading to permanent arrested
growth and formation of an osseous bridge. (B) At the age of 8
years this patient sustained a typical type 2 distal radial injury with
a metaphyseal fragment (open arrow). The angulation of the ossi-
fication center on the edge of the metaphysis (closed arrow) should
make one suspicious of a type 2D rather than a 2A injury. (C) Four
years later growth arrest and osseous bridging (arrow) have
occurred, confirming a type 2D injury. (D) MRI shows the extent of
compression at the site of fracture redirection. Note the extensive
bone bruising. This is a significant intraepiphyseal compression
injury within the trabecular bone, not a compression injury to the
physis.
166
FIGURE 6-32. Effect of physeal undulation on fracture propagation.
The binodal contour in the central regions of the distal femur pre-
disposes it to type 2D injuries with growth slowdown or arrest.
The anatomy of the distal femoral epiphysis and physis
shown in Figure 6-32 is one of progressive development of
binodal curves in both coronal and sagittal planes. A central
region extends further into the metaphysis than it does into
the mid-regions associated with either condyle. This central
region is probably particularly susceptible to more extensive
(but subtle) damage when the fracture propagates across it
during varus or valgus displacement. Such anatomic con-
touring is not unique to the distal femur but may explain its
greater predisposition to growth injuries, particularly pre-
FIGURE 6-33. (A) Type 3A injury. (B) Variation of type 3A, with
production of at least two epiphyseal fragments. (C) Histologic
diagram showing how involvement of the growth plate in this
fracture is bidirectional. Large arrows show transverse propaga-
6. Injury to the Growth Mechanisms
mature epiphysiodesis, than exists in most other physeal
regions. Physeal contour variations in other regions, such as
the proximal humerus or proximal tibia, may also predispose
to more severe cellular damage.
Type 3
Type 3 injury is an intraarticular fracture involving the
epiphysis (Figs. 6-33 to 6-37), with the plane of the fracture
extending from the articular surface through the epiphysis,
epiphyseal ossification center (if present), and physis to the
aforementioned zone of hypertrophic, columnar cells and
then extending along this layer of the physis toward the
peripheral margin (type 3A). The physis may fail first, with
the propagation then turning into the epiphysis and termi-
nating at the articular surface. In some cases, however, the
epiphyseal extent may be incomplete, with the articular
surface remaining intact.
Occasionally, transverse fracture propagation may be
through the primary spongiosa, leaving a thin layer of me-
taphyseal bone with the epiphyseal fragment (type 3B). This
finding is common in fractures of the lateral humeral
condyle (Fig. 6-38). Type 3 fragments may undergo signifi-
cant rotational deformation when the separation is com-
plete. This fracture pattern may occur as the physis is
undergoing the final phases of physiologic epiphysiodesis.
Such an injury pattern is common in the distal tibial epiph-
tion, and the small arrows show longitudinal propagation across
epiphyseal components. See Figure 6-5 for explanation of
abbreviations.
Fracture Patterns
FIGURE 6-34. Computer simulation of a type 3 injury involving the
medial malleolus.
ysis (Tillaux fracture) while the physis is closing during
adolescence (see Chapter 23).
Restoration of the congruency of both the articular
surface and the physis is essential, particularly in the young
child. Open reduction is usually necessary to obtain accurate
anatomic restoration. The prognosis for future growth is rea-
sonably good, provided circulation to the separated frag-
ment of the epiphysis and physis is not impaired and that
A B
FIGURE 6-35. MRI of radiologically occult type 3 injuries. (A) Distal femur. (B) Proximal tibia. Neither injury was readily evident on the
standard radiograph.
167
microdisruption of the physis at the turning point of frac-
ture propagation has not occurred. Because many of these
fractures occur when skeletal maturity is approaching, the
chances for eventual growth disturbance may be minimized
by the decreased or minimal amount of anticipated post-
traumatic longitudinal growth.
The type 3C subclassification includes injuries involving
epiphyses that have developed major contour changes, such
as the ischial tuberosity, in which epiphyseal fracture propa-
gation may not necessarily involve a joint surface (Fig. 6-39).
These seemingly isolated epiphyses have radiolucent carti-
laginous and fibrocartilaginous attachments to contiguous
regions, such as the symphysis pubis. The epiphysis is avulsed
from the metaphysis and attentuates or fractures the carti-
laginous or fibrocartilaginous growth region intervening
between the injured portion of the epiphysis and the remain-
ing, functionally separate portion of the originally contigu-
ous epiphysis. In some instances this connecting region is
injured, which may lead to growth disturbance.
A type 3D pattern involves a fracture propagating through
the germinal zone, separating it from its vascular supply
(Fig. 6-40). Wherever the fracture turns, a “comminuted”
fragment may occur. Such a region is deprived of its vascu-
larity, and growth arrest is likely. This pattern must be sur-
mised, as roentgenographic corroboration is difficult if not
impossible. MRI may be able to ascertain such fracture
propagation.
Type 4
The basic type 4 fracture (4A) involves the articular surface,
extending through the epiphysis (and ossification center
when present), across the full thickness of the physis, and
subsequently through a segment of the metaphysis, causing
 168 6. Injury to the Growth Mechanisms

FIGURE 6-36. (A) Type 3 fracture of the lateral condyle. Observe
how the fracture extends into the trochlear region, and note that
the fracture has not completely propagated through the articular
surface. (B) Slab section shows how the fracture “hinges apart” at
the cartilaginous continuity. Note also, as in Figure 6-26, that sec-
tions of the physis remain on the metaphyseal side. (C) Radiology
of the specimen showing the thin subchondral fracture line typical
of these injuries. (D) Histologic specimen. The physeal fragments
were separated through the germinal zone.

FIGURE 6-37. Type 3 variations. (A) Type 3 fracture of the medial malleolus is associ-
ated with complete fracture propagation along the rest of the physis as a seeming type
1 injury. (B) Bidirectional fracture propagation with splitting of the physis into the meta- B
physis (arrow).
Fracture Patterns
FIGURE 6-38. (A, B) Type 3B injury. The ex-
tensive lappet formation tends to propagate
the fracture across the primary spongiosa
centrally. This thin segment of bone is not
the same as either the Werenskiöld sign or
the Thurstan Holland sign. (C) Type 3B injury
involving the distal humerus (capitellum). The
arrows show the thin layer of metaphyseal
bone.
FIGURE 6-39. (A) Type 3C injury involving nonarticular epiphyseal
cartilage. These injuries particularly involve the pelvis. (B) Type 3C
injury of avulsion of the ischial tuberosity.
169
a complete longitudinal split of all zones of the physis,
including the germinal layer (Figs. 6-41 to 6-43).
Propagation of the fracture through the epiphyseal ossifi-
cation center is the typical pattern and usually is readily
evident on the radiograph. A variation may occur when the
fracture line splits the epiphyseal cartilage away from the
ossification center (a shell or sleeve fracture), a pattern not
readily evident on routine radiography (Fig. 6-44).
This type 4A injury pattern commonly involves the medial
and lateral condyles and epicondyles of the distal humerus
and the medial malleolar region of the distal tibia. The
fracture fragments may be displaced as a result of the
original injury mechanism and the subsequent pull of spe-
cific attached muscles (e.g., the extensor mass of the
forearm).
The amount of ossification on the epiphyseal side of the
type 4 fragment may make diagnosis difficult. If the sec-
ondary ossification center is small, the type 4 pattern may
not be easily recognized (Fig. 6-44). However, the presence
of a small metaphyseal fragment without evidence of other
physeal separation (clinical or radiographic) should make
one suspect a type 4 injury, rather than a type 2 injury.
Anatomic reduction is usually imperative for the restora-
tion of both a smooth articular surface and normal cytoarchi-
tectural relationships of the physis to minimize the risk of
subsequent osseous bridging and localized premature growth
arrest. Usually smooth Kirschner pins are utilized for internal
fixation when pins must cross the physis. If possible, however,
fixation pins or screws should be oriented transversely
through the epiphyseal ossification center fragments and
through the metaphyseal components, rather than obliquely
across the physis. If fixation devices must be directed across
the physis, they should be smooth and removed as soon as suf-
ficient fracture healing is evident to stabilize the fragments
170
(usually 2–3 weeks). They should also be placed as centrally as
possible to avoid the more active peripheral physeal regions.
If the metaphyseal portion of the fragment is small, it may be
excised, leaving the epiphyseal and physeal segments. Fat may
be interposed in the defect. This procedure may lessen the
risk of developing an osseous bridge.
Despite accurate reduction, growth damage and prema-
ture, localized epiphysiodesis may occur, most likely as a
FIGURE 6-41. (A, B) Type 4A injury, in which the fracture propa-
gates across both the epiphysis and the metaphysis. The arrows
show the direction of fracture propagation through the metaphysis,
6. Injury to the Growth Mechanisms
FIGURE 6-40. Wrong-side fracture, with involvement of
segments of the germinal zone.
result of microscopic injury (Fig. 6-45). When attempting
open reduction, care must be taken not to strip the intact
periosteum excessively to visualize the fracture adequately, as
it may damage the peripheral cellular activity of the zone of
Ranvier and thereby additionally contribute to the possibil-
ity of premature growth disruption.
A subclassification, type 4B, involves the aforementioned
epiphyseal–metaphyseal unit, with further additional propa-
gation of the fracture through the remaining portions of the
physis, and epiphysis. See Figure 6-5 for explanation of abbrevia-
tions. (C) Histology of an experimental type 4 fracture.
Fracture Patterns
FIGURE 6-42. Computer simulation of a type 4A injury pattern.
FIGURE 6-43. Histology of a type 4 fracture of the medial
malleolus.
171
FIGURE 6-44. (A) Type 4A variation in which the epiphyseal frac-
ture propagates through radiolucent cartilage. (B) Fracture of the
medial portion of the distal humeral metaphysis. It resembles the
Thurstan Holland sign. However, the capitellum is obviously unin-
jured, indicating a diagnosis of a type 4, not a type 2, injury.
(C) Computer simulation of the type 4A variation.
 172
physis to create an additional free fragment or fragments
comparable to an accompanying type 3 injury (Figs. 6-46,
6-47). This tendency for multiple fragmentation (comminu-
tion) is again more common in patients approaching skele-
tal maturity, a time when the physis is susceptible to fracture
propagation modes different from those that usually occur
in younger children. These commonly affect the ankle (e.g.,
triplane fractures) (see Chapter 23).
As with type 3C fractures, the type 4C fracture may prop-
agate through radiolucent cartilaginous regions. Figure 6-48
shows a proximal femur, with the fracture propagation from
the metaphysis through the contiguous physis and into the
epiphyseal region between the trochanter and the capital
femur. Such a type 4C injury involves the metaphysis, physis,
and epiphysis.
Accidents involving rotary lawn mowers or boat propellors
may result in multiple metaphyseal–physeal–epiphyseal
fragments (type 4D). Such fragmentation (comminution)
increases the risk of traumatically induced, localized epiph-
ysiodesis (Figs. 6-49, 6-50). The etiology is probably ischemia
caused by cutoff of the transversely directed circulatory pat-
terns in the various (especially more internal) comminuted
segments. Sometimes those fragments are “lost” at the scene
of the accident or prove to be nonviable at the time of sur-
gical exploration and débridement.
6. Injury to the Growth Mechanisms
FIGURE 6-45. Effect of a lack of accurate anatomic
reduction and fixation of a type 4A injury of the radial
head. (A) Resected radial head showing disruption of the
articular surface. (B) Histologic section. Despite the
absence of an osseous bridge, considerable deformity of
the physis is readily evident.
Type 5
The type 5 injury pattern occurs infrequently, is difficult
if not impossible to diagnose acutely, and often involves
weight-bearing epiphyses around the knee or ankle—those
articulations that normally move significantly in only one
plane (Figs. 6-51 to 6-53). The application of a significant
abduction or adduction (valgus or varus, respectively) strain
to such regions causes transmission of compression, tension,
and shear forces through certain segments of the epiphysis
and physis, which may disrupt germinal regions of the chon-
drocytes and adjacent hypertrophic, columnar regions. Such
forces are rarely direct compression. More realistically, there is
always a significant shear component. Some believe, as I do,
that this “pure compression” injury pattern (mechanism)
does not exist.283–285
The prognosis in patients with type 5 injury is poor, as pre-
mature growth arrest invariably occurs. However, such arrest
may not occur or at least not be evident for several months
to years after the initial injury, at which time the child may
present with an angular deformity and minimal memory of
the original injury.
An aspect of physeal physiology making compression
damage unlikely is that the hypertrophic zone exerts signif-
icant hydrostatic forces that create bone elongation. The
amount of this force was computed by Safran et al. in an
adolescent with a prosthesis after tumor resection.311 The
hydrostatic forces were sufficiently high to break the methyl-
Fracture Patterns
C poliomyelitis.89
FIGURE 6-46. (A) Type 4B injury, in which the type 4 fragment is
accompanied by a type 3 fragment. This pattern is particularly
encountered in the distal tibia as a triplane injury. (B) Type 4B injury
of the proximal humerus. The epiphyseal–metaphyseal fragment
involves the capital humerus, whereas the epiphyseal fragment
involves the tuberosity. (C) Computer simulation of a type 4B injury.
methacrylate–bone interface and allow continued proximal
tibial growth despite the central penetration of prosthetic
stem and surrounding methylmethacrylate. It is unlikely that
most fracture forces significantly exceed these pressures.
Epiphyseal and metaphyseal bone fail long before these pres-
sures are approached, let alone exceeded.
173
Attempts to crush intact physes (human and animal)
directly and machined portions of epiphyseal–physeal–
metaphyseal composites never resulted in a direct crushing
injury to the germinal zone of the physis.229 Bonnel et al. put
compression clamps across the distal femur in rabbits.40
Lesions varied in severity from a diminution in the height of
the cellular columns to development of bony bridges.
Release of compression showed a significant capacity for
restoration of normal growth. This experiment suggests that
traumatic compression as an etiology of the type 5 injury is
unlikely. Mendez et al. also tried unsuccessfully to create the
type 5 compression injury in rats,225 and Boullay et al. were
unable to do so in rabbits.44
Children with congenital sensory neuropathy often
have Charcot arthropathy with significant destruction of
articular surfaces.140 Premature growth arrest may occur in
these patients. Is it due to abnormal compression of the
physis? Probably not, as illustrated in Figure 6-54. This
boy had severe swelling and skin breakdown/ulceration. The
talus had been ground into small pieces. However, as
seen in the histologic sections, the articular surface of
the distal tibia was damaged with evidence of clone for-
mation, which typifies a subarticular cartilage response to
increased pathologic pressure. The distal tibial physis,
which was only 1 cm away, appeared to be histologically
normal in the presence of these pathologically increased
joint reaction forces. In contrast, the distal fibula had
growth arrest, but it was due to a previous shearing fracture
(type 4 injury).
Children with myelomeningocele often have occult
physeal disruption. They may walk on the disrupted physis,
causing chronic epiphysiolysis.226 This repetitive motion
may cause premature epiphysiodesis (see Chapter 11),
probably due to microshearing of the physis, rather than
compression.187
Infrequently, some or all of the metaphysis is driven com-
pletely through the physis into the epiphysis (Fig. 6-55). This
mechanically disrupts all layers of physeal tissue, which seri-
ously damages the vascular supply to the involved segment
of the physis.
Growth arrest may occur in physes distant from a metaph-
yseal or diaphyseal fracture.6,20,48,156,163,181,193,211 It has often
been attributed to an occult type 5 physeal fracture. Tibia
vara (Blount’s disease) repeatedly is said to be due to patho-
logically increased pressure on the medial side of the proxi-
mal tibial physis.182 Premature closure may also complicate
Displacement of the epiphysis is minimal and unrecog-
nizable by standard diagnostic techniques. Often the serious
nature of the condition is not suspected, with the injury
being misdiagnosed simply as a sprain (Fig. 6-56). Proper
diagnosis frequently must be empirical, with treatment
directed at an avoidance of weight-bearing (lower extremity)
and appropriate immobilization for 3–4 weeks.
Although Aitken2 and Salter and Harris314 suggested that
direct compression (crushing) of the germinal zone was
the mechanism of the type 5 injury, other pathomechanisms
are much more likely. The “type 5” closure may occur on the
tensile, not the compression, side of the injury. Figure 6-47
particularly shows that microcomminution, not germinal cell
crushing, may occur.
173
 174 6. Injury to the Growth Mechanisms

FIGURE 6-48. (A) Type 4C injury involving nonarticular epiphyseal

cartilage. (B) Clinical roentgenogram of such an injury does not
show the cartilaginous involvement along the superior femoral
B neck.

Two significant factors probably play an etiologic role in

the elusive type 5 injury pattern. First, increasing undulation
of the plane of the physis puts focal regions at risk. The frac-
ture may propagate in a relatively straight line that does not
follow the physeal contour. A central peak, as present in the
distal femur, may result in virtually all of the fracture fol-
lowing “textbook rules” while being in “violation” of these
rules at the peak, which separates at the epiphyseal ossifica-

䉳
FIGURE 6-47. Traumatic below-knee amputation. Type 4B injury of
the distal tibia. This patient also had a “wrong-side” type 2 fracture
of the distal fibula. (A) AP radiograph of the specimen. (B) Mor-
phologic section showing the lateral type 3 fragment. Note,
however, that an occult fracture has propagated medially at the
physeal–metaphyseal interface. In addition, there is some propa-
gation medially on the “wrong side,” effectively isolating a segment
of physis. (C) Histology. Multidirectional propagation and com-
minution are evident. Note that most of the distal fibular physis is
C missing. It was still attached to the fibular metaphysis. This com-
minution may be one of the real causes of the elusive type 5
physeal injury.
Fracture Patterns
FIGURE 6-49. (A) Type 4D injury with multiple
fragments of one condyle. (B) Film taken of a 6-
year-old boy several years after he fell under a
lawn mower, sustaining multiple type 4D injuries
of the distal femur and proximal tibia. (C) Sagit-
tal section showing severe long-term damage to
the articular surface and the epiphysis conse-
quent to this injury. (D) Type 4D injury involving
the entire epiphysis, with splitting of the frag-
ments. (E) Type 4D injury of the distal femur.
Arrows indicate the directions of fracture
propagation.
FIGURE 6-50. Histologic macrosection of a type 4D injury of the
distal tibia.
175
tion center–physeal interface. This devascularizes a segment of
the physis. Second, in a situation such as a distal femoral frac-
ture, the fracture surfaces may be apposed under relatively
high compressive forces (e.g., from the quadriceps). If
reduction is attempted, as by the emergency medical tech-
nician, coach or trainer on the playing field, or in the emer-
gency room without adequate muscular relaxation, portions
of the physis may be grated over the edges of the metaphy-
seal fracture surface, disrupting normal physeal morphology
as microscopic type 3 or 4 injures, rather than squeezing or
compacting the physeal zones as conceptualized by Salter
and Harris.
Peterson advocated a vascular etiology for this injury
pattern, rather than the originally postulated mechanical cel-
lular compression injury.279–281 This concept is realistic, espe-
cially in the older child, and is one with which I completely
agree (Fig. 6-57). Disruption of the subchondral plate of the
secondary ossification center or hemorrhage within this
structure would obviously affect circulation to the E-vessels
and could result in focal or more generalized patterns
of ischemia, not unlike the variable patterns of epiphyseal
and physeal growth damage in the Legg-Perthes lesion.
Decreased arterial supply to the physis, whether due to
extraosseous or intraepiphyseal disruption, certainly may
lead to irregular growth (Fig. 6-58).21,51,68,104,146,183,244,317,360,380,389
The physis and epiphysis may assume a characteristic conical
176 6. Injury to the Growth Mechanisms

type 5 injury etiologies are discussed in detail in the ensuing

sections.

Electrical Injuries
One such mechanism is electrical injury due to high voltage
wires or to being struck by lightning.2,56,96,108,188,263,366 The
unique properties of propagation of electrical forces
through the extremities cause highly variable, localized
injury to the growth plates and articular cartilage that results
in premature slowdown of growth and eventual arrest in
focal areas of the physis.
Brinn and Moseley observed that many factors determine
the ultimate effects of electric current on chondro-osseous
tissues: (1) the type of current, with alternating current
being three to four times more deleterious than direct
current; (2) the voltage and amperage; (3) the duration of

FIGURE 6-51. (A) Type 5 injury according to the concept of Salter

and Harris.314 This applied force eventually leads to growth arrest.
Unfortunately, it is difficult, if not impossible, to diagnose at the time
of the initial injury. The type of damage is probably microscopic dis-
ruption and splitting, not crushing, of the physis, as well as vascu-
lar disruption. (B) Although the torus fracture (open arrow) was
most evident in the clinical film of a 2-year-old child who died
several days after injury, this tissue preparation showed trabecu-
lar disruption and hemorrhage juxtaposed to the physis (solid
arrow), suggesting that some of the fracture energy was absorbed
in this region. The focal area of physeal displacement suggests
impaction of a section of the physis into the epiphyseal ossifica-
tion center. This is likely to disrupt the vascular supply, rather than
“crush” the cartilage cells.

shape in such circumstances.50,63,130,189,232,386 Histologic studies

in acute and chronic meningococcemia/disseminated
intravascular coagulopathy specimens have definitely shown
the deleterious effects of microvascular thrombi.139 Trueta
and Trias showed that chronically applied compression
across a physis could lead to ischemic changes in the
physis.369 This suggests the compression cause proposed by
Salter and Harris may be plausible, but that this mechanism
causes vascular compromise rather than discrete physeal cel-
lular disruption.
Intraosseous effusions have also been associated with
growth arrest.29,141 Presumably it is also due to pressure
FIGURE 6-52. (A) This adolescent football player sustained a type
disruption of normal circulatory physiology. 3 proximal tibial physeal fracture. The injury was treated by per-
Although physeal microinjury and focal ischemia proba- cutaneous reduction and pinning. (B) Seven months later there
bly are the major causes of this pattern of physeal injury was obvious tibial growth arrest. However, growth of the distal
(rather than compressive crushing), additional mechanisms femur was also arrested (arrow), probably due to tensile disruption
may lead to the same type of localized growth arrest. These of the physeal periphery.
Fracture Patterns 177

B
FIGURE 6-53. (A) Nine-year-old girl with a seemingly innocuous
injury to the distal radial metaphysis. (B) Four years later there has
been a type 5 injury to the distal ulna and secondary impairment
of distal radial growth.

contact with the electric current; (4) the propagation path

taken through the body; (5) the relative resistance at the
points of contact and exit; and (6) the patient’s general state
of health.56
During these electrical accidents tissue temperatures may
instantaneously reach several thousand degrees (celsius or
centigrade) and may cause heat-induced liquefaction and
necrosis of bone, cartilage, or both (as well as the marrow
tissues). The changes within any bone that is liquefied and
transformed into a gel may be attributed to the pathway of C
the electricity (Figs. 6-59, 6-60). Tissues offering the greatest
resistance to current flow suffer the greatest damage. Elec- FIGURE 6-54. This patient has a congenital sensory neuropathy.
trical injury may result in cell death or may alter cellular He has been walking on a completely crushed talus for several
activity temporarily or permanently.108 After electrical acci- months and eventually underwent a below-knee amputation for
dents, tissue repair, including callus formation, may be chonic ulceration in the foot. (A) The histologic macrosection
shows an old fibular fracture and an intact tibial physis. (B)
restricted. Additional basic research is needed before the
Because of chronic alterations due to weight-bearing, the subar-
modifications of developing chondro-osseous structure and ticular tibial cartilage had formed cellular clones and the articular
physiology as a result of electrical trauma are sufficiently surface was fibrillated and fissured. These changes are compara-
understood. ble to those seen in experimental animals whose joints are sub-
Granberry and Janes attempted to influence bone growth jected to increased pressure. (C) Despite the reactive changes
by stimulating the epiphyseal plates of bones in dogs with evident in (B), the physis, approximately 1 cm more proximal,
implanted electrodes.134 Their study revealed that growth was appeared histologically normal.
 178
not accelerated by such electrical stimulation. However, the
doses were deliberately kept small, so the experiment did not
allow observation of the potential detrimental effects of
high-voltage electricity.
Children may show osseous changes similar to those
evident in adults, but they also may have additional abnor-
malities secondary to the effect of the applied current on
the epiphyseal and physeal cartilage.260 The epiphyseal
ossification center and the epiphyseal cartilage may be
adversely affected by the applied current, and the me-
taphyseal region undergoes little remodeling. Kolar and
Vrabec reported three cases in which electrical accidents
resulted in extensive tissue burns requiring amputation of
several phalanges188; the remaining phalanges showed abnor-
mal elongation. Such overgrowth could be secondary to
chronic hyperemia resulting from the extensive soft tissue
injuries, with secondary infection contributing to the hyper-
emia as well. None of these studies described the histologic
changes.
Frostbite
Frostbite may lead to growth retardation because of ischemia
rather than a direct thermal effect on the physeal carti-
lage.23,86,87,107,116,127,136,144,206,321,359,362,382 Heat thermal injury (a
burned extremity or joint) may also compromise growth
potential (see type 6 injuries).
6. Injury to the Growth Mechanisms
FIGURE 6-55. This juvenile antelope was observed to be
limping for several days. (A) Radiograph shows a distal
femoral fracture. Note that the fracture does not follow
the exact contour of this highly undulated physis. A frag-
ment of metaphyseal cortex has been penetrating the
physis (white arrow), leaving an obvious channel (black
arrows). (B) Histology of the area of physeal damage.
The chronic pistoning of the metaphyseal cortical frag-
ment has led to bony bridging and growth arrest.
Cold thermal injury to the physes, with vascular ischemia,
has been detailed.33,107,116,144,200,206,209,237,324,359 Bennett and
Blount reported an 8-year-old girl who had frozen her left
hand 3 years before and as a result “lost” the epiphyses of
the middle phalanges of the index, middle, and ring fingers
and all the distal phalangeal epiphyses.23 Thelander
described a 9-year-old boy who had sustained a severe frost-
bite injury of the hand 2 years previously.362 The phalanges
were shortened, and it was presumed that the epiphyses had
been destroyed and growth arrested. Thiemann reported an
unusual case in which the epiphyseal ossification centers of
the phalanges disappeared during puberty, only to reappear
a few years later.363 Bigelow and Ritchie reported 13 patients
who experienced frostbite of the hands during childhood,
all of whom had “lost” one or more physes when evaluated
4–50 years after exposure.30 In Bigelow and Ritchie’s study,
the index and little fingers were involved in every frostbitten
hand and the ring finger slightly less; the middle finger was
involved least often. In each digit the distal phalanx and
distal interphalangeal joint were involved most often. The
proximal phalanx and proximal interphalangeal joint were
not affected if the distal phalanx of that same digit was not
also affected.30 Physes were not “lost” in these cases. Rather,
there was premature closure of the growth plates and loss of
the longitudinal growth potential.
In children, frostbite causes a characteristic radiographic
appearance, particularly at the articular ends of the bones
Fracture Patterns
on both sides of the joint (Fig. 6-61). The affected phalanges
are shorter and smaller than normal, and the juxtaarticular
bone is expanded and irregular, with the spongiosa altered
to show a coarse cancellous pattern. The same expanded
and irregular appearance is seen on the contiguous surface
of the more proximal phalanx, where there is no epiphysis
evident. The joint surfaces are irregular and uneven, but
the width of the joint space does not appear to be altered.
FIGURE 6-56. (A) Malleolar fracture questionably extends to the
physis. (B) Three months later a small bridge is forming (arrow).
(C) Eight months later, the physis and a Harris line converge
(arrow). The mechanism in this case was probably disruption of
the blood supply to the physis through the subchondral plate of the
secondary ossification center.
179
Usually, the physis disappears completely, but there may be
only partial destruction, with the undestroyed portion taking
part in subsequent joint disfiguration. Not uncommonly, the
base of an involved phalanx may have a pronounced V
shape, presumably resulting from central ischemic damage
and subsequent addition to the peripheral growth plate,
which attempts to grow latitudinally and longitudinally.232
There may be no obvious acute destruction of the epiphysis,
but eventually premature fusion of a part of the epiphyseal
line may lead to varus or valgus angulation.
Shumacker and Lempke confirmed that vascular channels
were constricted when an extremity was frozen and that
the capillaries contracted just before freezing.329 Within a
few minutes of the return of blood flow during thawing,
there was perivascular edema of the subcutaneous tissues
and swelling and engorgement of the capillary endothe-
lium.36,288 The edema resulted from increased permeability
of the capillary walls. The edema continued and extra-
capillary pressure increased, further augmenting capillary
stasis.85 Agglutination of blood cells in the small vessels
obstructed the circulation.22,329 After a few hours there
was dissolution of the endothelium of the small arterioles,
with further vascular occlusion, tissue edema, transudation
of fluid, and perivascular hemorrhage. Tissue necrosis
resulted because the returning demands of metabolism
could not be met. Angiography showed that the vascular
supply in the surviving tissue was abundant because of
the opening of side branches and the development of new
capillary outgrowths in both the arterial and venous sides of
the vascular tree.168
The freezing of articular cartilage produces changes
immediately after thawing. The articular surface becomes
darker, and the nuclei of the cartilage cells lose their normal
staining properties. Cartilage degeneration commences.
Eventually the cartilage may be completely absorbed. Lohr
said that epiphyseal and physeal cartilage also goes through
a series of similar degenerative stages, and the destruction
may be such that the cartilage is replaced by connective
scar tissue.209 Scow showed that growth arrest was evident as
early as 3–4 days after freezing the tail vertebrae of newborn
rats.321
Late changes may take the form of partial or complete
loss of the epiphyseal centers. When the patient is evaluated
after an interval of several years, the epiphyseal ossifica-
tion center may not be present. Whether it has been com-
pletely resorbed or has fused prematurely with the pha-
langeal shaft is not known (the latter is physiologically
more likely). Epiphyseal irregularity and fragmentation
may also occur, after which premature fusion is sometimes
noted. The metaphyses are often widened, and the length
of the phalanges is usually reduced. Contour irregularity
and the loss of the normal size of the joint space may be
seen during childhood, and linear synostosis may also
develop.
Irradiation
Another cause of generalized or localized growth slowdown
or arrest is irradiation. Innumerable reports document the
deleterious effects of radiation delivered for “therapeutic”
180
reasons and the experimentally produced effects of roent-
gen rays on the physis.*
Chemotherapy for malignant tumors may also affect
physeal growth.17 The use of adjuvant chemotherapy for chil-
dren’s bone, soft tissue, and systemic malignancies has
become well established. However, there is clinical and lab-
oratory evidence that some of these agents have significant
deleterious effects on the histologic and biomechanical
properties of bone and may specifically affect the physis,
especially in the germinal zone.14,277
Therapeutic irradiation has been used for many neoplas-
tic problems involving the developing skeleton and contigu-
ous soft tissues. Unfortunately, although necessary for the
FIGURE 6-58. Severe type 5 central defect resulting from neonatal
ischemia. There is some recovery of peripheral growth through the
less affected, latitudinally expanding zone of Ranvier.
* Refs. 7,16,18,19,32,57,61,90,101,121,126,159,160,176,178,180,191,
293,323,345,351.
6. Injury to the Growth Mechanisms
FIGURE 6-57. Traumatic below-knee amputation. Revas-
cularization (replantation) had failed. The physeal
changes centrally represent ischemic changes.
primary cancer, treatment may result in physeal growth
impairment or disruption (Fig. 6-62).195,290,378 Desjardins
reported a 9-year-old girl irradiated for a tumor of the upper
humerus; 5 years later there was marked shortening of the
humerus with atrophy of the shoulder musculature.101 Lan-
genskiöld described a child who had received irradiation
therapy for telangiectasias; the physis had a slowdown of
growth that created a varus deformity affecting both the
distal femoral and the proximal tibial growth plates.191 Judy
described changes affecting growth regions in three children
submitted to irradiation to correct asymmetry in the length
of lower extremities.176 Spangler used irradiation to cause
epiphysiodesis in children with leg length inequality.345
The effects of radiation on growth have been demon-
strated in humans and experimental animals.19 Nevertheless,
some aspects of the effect on the growth plate have not been
shown clearly, such as whether the apparent histologic
lesions in the growth plate and the consequent retardation
of growth are caused by the direct effect of radiation on the
chondrocytes or are secondary to the damage to contiguous
tissues such as blood cells, osteoblasts, and marrow cells. It
appears that a number of factors influence the histologic
changes found in the growth plate after irradiation. The
changes are proportional to the radiation delivered and
inversely proportional to the age of the animal at the time
of irradiation.
The dosage and type of rays are important factors. Exper-
imentally up to 800 rad produced retardation of bone
growth that was temporary and reversible. With the admin-
istration of 800–1800 rad, cellular survival was less, bone
growth was deterred, and if the germinal cells were damaged
growth ceased prematurely. With doses of more than 1800
rad, growth was completely arrested, although evidence of
later regeneration has been reported.7
There is less bone absorption with megavoltage tissue radi-
ation, but it is not known whether there is less chondroblast
damage than that observed with orthovoltage irradiation. A
low absorbed dose is sufficient to cause damage in young
children but not in older children; those less than 6 years of
age or those in puberty when treatment is instituted are
more seriously at risk.
Fracture Patterns
FIGURE 6-59. (A) This 12-year-old boy sustained a high voltage
electrical injury and required a below-knee amputation. Premature
epiphysiodesis occurred in the lateral tibial physis (arrow), along
the probable line of electrical impulse propagation. (B) Sagittal
section showing severe involvement of the proximal tibia in a
FIGURE 6-60. This girl was struck by lightning 3 years earlier. The
anterior distal femoral growth plate was damaged (arrow), leading
to patellofemoral irregularity.
181
patient who sustained a high-voltage electrical injury. Liquefaction
of trabecular bone is evident. The articular surface was destroyed
(open arrow) and had undergone fibrous ankylosis to the femur.
The physis (solid arrow) was destroyed except for the region under
the tibial tuberosity.
Type 6
The type 6 pattern of injury involves the peripheral region
of the physis, particularly the zone of Ranvier (Figs. 6-63,
6-64). Such an injury may not be associated with a major
fracture; rather, it may result from a localized contusion or
avulsion of the portion of the physis concerned specifically
with latitudinal (appositional) cartilaginous growth (see
Chapter 1). The injury may even result from a glancing type
of trauma primarily involving avulsion of overlying skin and
subcutaneous tissues, such as might occur from a bicycle or
lawn mower injury or from deep extension of a traumatically
induced infection or severe thermal injury (burn).171
Because of the highly selective and localized nature of
these particular lesions, peripheral osseous bridge forma-
tion frequently occurs and may lead to peripherally lo-
calized epiphysiodesis and subsequent progressive angular
deformity.
Involvement of the zone of Ranvier undoubtedly occurs
with type 3 and 4 physeal injuries, as the fracture propagates
to the periphery of the bone in two regions. At such points
localized type 6 damage may occur, leading to osseous bridge
formation. When a type 3, 4, or 6 injury is treated with open
reduction, care must be taken not to strip the zone of Ranvier
away from the underlying epiphysis when elevating the
periosteum. Such stripping may disrupt the blood supply
and directly traumatize these important peripheral germinal
cells, leading to more extensive physeal damage and growth
deformity.
182
Burns
Bone and joint changes due to severe burns are of clinical
interest from the standpoint of pathogenesis and because of
the significance for the rehabilitation phase.350 Burns may
extend directly down to the zone of Ranvier and the periph-
eral growth plate (Fig. 6-65) and may cause peripheral
impairment of growth and subsequent angular deformity, if
not complete disruption.13,348 Central or vascular disruption,
as with frostbite, is less likely to occur than is peripheral
damage.
Multiple osseous changes consequent to burns may
include osteoporosis, ectopic (heterotopic) bone, periosteal
new bone formation, pericapsular calcification and ossifica-
tion, osteophyte formation, and progressive joint destruction
with ankylosis. Many of these changes have been reported in
young children and adults. Evans and Smith thought that
such skeletal alterations fall into three groups: (1) alterations
limited to bone, which include osteoporosis and periosteal
new bone formation; (2) alterations involving periarticular
FIGURE 6-62. Growth arrest of the lateral postion (arrow) of the
distal femur secondary to irradiation of a vascular malformation
during the first year of life.
6. Injury to the Growth Mechanisms
FIGURE 6-61. Central growth arrest with peripheral
recovery following frostbite.
structures, including pericapsular calcification, osteophytes,
and heterotopic periarticular ossification; and (3) alterations
involving the joint proper, which include progressive articu-
lar destruction and ankylosis.111
If an area of bone is denuded by a deep burn, eventual
sequestration of the ischemic portion may occur. Such
necrotic bone may remain exposed until adequate granula-
tion tissue has developed. This condition represents damage
to the periosteal and physeal growth mechanisms in several
areas, potentially creating a type 5, 6, or 9 injury. Cartilage
desiccates and becomes necrotic. Direct involvement of the
joints may result in septic arthritis, articular destruction,
and ankylosis. The wrist and hand joints are frequently
involved.
Skeletal alterations after burns seem to occur more often
and to a greater degree in children than adults, a factor
that Evans and Smith ascribed to the exuberant granulation
tissue response characteristic of youth.111 Growth spurts
in children who have suffered severe burns have been
described, and it may be that skeletal growth is stimulated by
stasis, passive hyperemia, or chronic inflammatory processes.
The precise mechanisms causing growth retardation in
severely burned limbs are not well understood.122,154,224,318,319
Evans and Smith suggested that growth retardation could
result from the restrictive effect of thick scar about the
metaphyseal and joint areas with inhibition of epiphyseal
growth.111 Amputation specimens clearly demonstrated
the destructive processes existing in and around the
ankle joint. In addition to alterations in the bone and in
the periarticular and interarticular structures, there pro-
bably is initial thermal damage to the margins of the
epiphyseal plate, particularly the zone of Ranvier, as
demonstrated in Figure 6-65.179 This damage to the appo-
sitional chondro-osseous growth mechanisms may be
the most significant factor leading to eventual growth
deformity.
Osteochondroma Formation
Although the exact mechanism is not clear, trauma to the
peripheral region may also be the cause of solitary osteo-
chondroma formation. Rang suggested that particular types
of experimentally produced injury to the periphery of the
growth plate and periosteum could lead to osteochondroma
Fracture Patterns 183

FIGURE 6-63. (A) Type 6 injury, which involves the peripheral

region (especially the zone of Ranvier). Damage may lead to
osseous bridging. (B) Histologic diagram showing the area of
involvement in this injury. Arrows show the area of fracture involve-
ment. See Figure 6-5 for explanation of the abbreviations.

formation. Many children with solitary exostoses do have a
history of specific trauma to the area (Fig. 6-66).95,291
Ford and Key showed that an osteocartilaginous exostosis
might result when a patch of epiphyseal cartilage cells was
displaced outside the shaft of the bone.118 This was an inci-
dental finding during their efforts to traumatize the distal
femur experimentally in rabbits. Rang291 and D’Ambrosia
and Ferguson95 produced osteochondromas by damaging
and redirecting the peripheral periosteal zone of Ranvier
complex. Many cases of solitary osteochondromas possibly
result from such damage to the periphery of the growth
plate, although it is difficult to document this problem with
any degree of causal certainty.82
Type 7
The type 7 fracture patterns are completely intraepiphyseal
and represent propagation of the fracture from the articular
surface through the epiphyseal cartilage and into the sec-
ondary ossification center or preossification center, depend-

B C
A
FIGURE 6-64. (A) Computer-generated simulation of type 6 injury. (B) Type 6 injury with soft tissue damage down to the periosteum and
perichondrium, although there was no growth plate damage. (C) Peripheral bone bridge after a type 6 injury.
 FIGURE 6-65. (A) Peripheral burn injury (closed arrow)
with concomitant deeper involvement of the metaphysis
(open arrow). (B) Section of distal ulna from the patient
shown in (A). Thermal damage and secondary
osteomyelitis had caused an epiphysiolysis. The infec-
tion and burn have destroyed a portion of the physis
(solid arrow) and zone of Ranvier (open arrow), but then
the fracture line propagated in a more anticipated
manner through the zones of cellular hypertrophy and
calcification. (C) Severe bilateral burns of the feet and
lower legs. There was early closure of the distal tibial
and fibular physes.

B
FIGURE 6-66. (A) Formation of osteochondromas (arrows) of the mation complicating a combined type 4 and type 6 injury. The
posterior femur and tibia in a child who had sustained a severe physeal cartilage is extending proximally along the femoral me-
hyperextension injury 17 months earlier. (B) Osteochondroma for- taphysis (arrow).

184
Fracture Patterns
FIGURE 6-67. Type 7 intraepiphyseal injuries.
ing on the stage of maturation (Figs. 6-67, 6-68). They do not
involve the primary physis at all, although they affect the
spherical physis around the secondary center of ossification.
These types of injury are common at the malleoli and within
the distal humerus (capitellum) or distal femur as an osteo-
chondral fracture.
There are several basic subtypes. The first type (7A)
involves propagation of the fracture through the epiphyseal
and articular cartilage and the bone of the secondary ossifi-
cation center. The second type (7B) is more difficult to diag-
nose and represents a propagation of the fracture primarily
through the cartilaginous portions, with involvement of
some of the preossifying regions of the expanding secondary
ossification center, which are analogous to the hypertrophic,
fracture-susceptible zone of the main physis. This type of
fracture is likely to occur in the distal tibia and tibial spines
FIGURE 6-68. Computer simulation of a type 7 injury in an unossi-
fied medial malleolus.
185
FIGURE 6-69. Intraepiphyseal fracture at the medial malleolus.
(Figs. 6-82 to 6-84, later). The fracture pattern may also
involve nonarticular regions, such as the tibial tuberosity, the
greater trochanter, the tarsal navicular, and the proximal
fifth metatarsal. It commonly occurs in the ulnar styloid and
leads to an apparent radiologic nonunion when this area
subsequently ossifies (see Chapter 16). These are considered
sleeve fractures or chondro-osseous separations. Such sepa-
rations may be incomplete (Figs. 6-69 to 6-72).
Osgood-Schlatter injury, as well as other comparable
lesions usually classified as osteochondroses, represent stress-
type fractures (Fig. 6-73) involving regions of chondro-
osseous tissue that are beginning to undergo the normal
transition from cartilage to bone.227,257 These injuries have
been referred to as elastic deformations and may be com-
pressive or tensile failures. During the normal transition
phase, if subjected to high tensile forces (a phenomenon
FIGURE 6-70. Type 7 injury of the medial malleolus. The radiolu-
cency (arrow) was compatible with bone resorption from micro-
motion. See Chapter 23 for a detailed discussion of this injury
pattern.
186
FIGURE 6-71. Acute chondro-osseous fracture of the patella
(arrows).
particularly evident in the tibial tuberosity), the preossifica-
tion region may be partially avulsed away from the main
portion of the tuberosity. Such avulsion may occur prior to
the appearance of the ossification center, creating a type 7B
injury, or after the appearance of the center creating a type
7A lesion.
The fingers and toes may have small type 7 intraepiph-
yseal fractures (e.g., a variation of the mallet finger
injury). In the case of avulsion of portions of the phalangeal
physes and epiphyses concomitant with tendon “rupture,”
failure to reduce the injury adequately may result in
formation of a region of overgrown cartilage in the epiph-
FIGURE 6-72. Type 7 avulsion of the ulnar styloid (arrow). The
mechanism of this injury relates to the triangular fibrocartilaginous
complex (arrow).
6. Injury to the Growth Mechanisms
FIGURE 6-73. A classic area of type 7 injury is the ossifying tibial
tuberosity. The Osgood-Schlatter lesion is a stress fracture of a
portion of the anterior ossification center and nonossified cartilage
(avulsion). See Chapter 23 for a detailed discussion of this lesion.
ysis and the eventual creation of a structure similar to an
osteochondroma.
Osteochondral fractures (acute) and osteochondritis dis-
secans (chronic) involve a fragment that contains both bone
and cartilage. The cartilage is articular and may include
epiphyseal cartilage that has the potential eventually to ossify
(Fig. 6-74). The cartilage attached to the stabilized fragment
may retain some viability through nutritional diffusion from
the synovial fluid. However, if the bone fragment does not
heal promptly, the fragment may become unstable; and the
normal articular cartilage diffusion process is disturbed.
Thus both bone and cartilage may become necrotic, fre-
quently being extruded into the joint as a loose body. If the
fragment is replaced by closed or open reduction, the bone
may heal to the rest of the ossification center, permitting
the cartilage laceration to bridge with fibrocartilage. These
lesions are common in the knee and are discussed in more
detail in Chapter 22.
Olsson reviewed the problems of osteochondrosis (osteo-
chondritis) in growing animals.268,269 It appeared that the
common denominator was a disturbance of endochondral
ossification in animals exhibiting rapid musculoskeletal
maturation. The most important manifestation of the osteo-
chondrosis was osteochondritis dissecans, which began as
thickening of the articular and underlying epiphyseal carti-
lage, with necrosis of the deepest layer. Cracks and fissures
Fracture Patterns
A B
FIGURE 6-74. Type 7 injuries of the femoral condyle. (A) Radiographic appearance. (B) Defect found during arthrotomy.
then occurred, spontaneously dissecting a piece of cartilage
eventually to form a flap or loose body. The initial crack
occurred between the hypertrophic cartilage and the under-
lying bone, which appeared not to be forming a typical sub-
chondral plate. Subsequently, the cracks propagated toward
the articular surface. One study showed a high incidence of
osteochondrosis in the fetuses of sheep that received high
calcium diets.83
Osteochondritis dissecans is probably produced as a result
of an impact of one joint surface against another or chronic
repetitive injury that finally leads to separation.11,223,239,364
The cartilage, being resilient, may remain intact, whereas a
fragment of subchondral bone may fracture.190,192,268,269
FIGURE 6-75. Chondro-osseous interface fracture (arrow). This
patient was injured when struck by a car. There is some reactive
bone, as death did not occur until 15 days after the accident, when
he was taken off life support.
187
Figure 6-75 demonstrates such separation of cartilage from
the underlying bone but without any extension of the frac-
ture into the cartilage (type 7C). The more common
sites of this fracture type are the inner aspect of the medial
femoral condyle, the capitellum, and the talus. These
lesions are discussed in more detail in Chapters 15, 22, and
24.
The focal thickening of the epiphyseal cartilage is proba-
bly a consequence of segmental ischemia. Similar thickening
of the physis occurs when there is a metaphyseal fracture
with temporary disruption of the endosteal circulation.
Intraosseous damage may occur in the epiphysis subjected to
acute or chronic hyperphysiologic impacts. Such edema and
lack of normal vascularization would impair normal expan-
sion of the ossification center (chondro-osseous transfor-
mation). The phenomenon of bone bruising within the
epiphyseal ossification center should be considered a varia-
tion of intraepiphyseal injury (type 7D). As the process
continues in other surrounding areas, focal segments of car-
tilage would be “left behind.” This thickened cartilage,
similar to a widened physis, is not as mechanically adaptable
and therefore at greater risk for failure. Furthermore, the
subchondral bone is also “left behind” the rest of the epi-
physeal ossification center shell and therefore becomes bio-
mechanically susceptible to failure for acute or chronically
repetitive loads.
The nontubular bones of the hands and feet and most
epiphyseal ossification centers may be affected by alterations
of normal chondro-osseous transformation.332 Each has an
eponym attached (e.g., Sever, Kienbock, Legg-Perthes).
Trauma, especially repetitive trauma, probably plays an etio-
logic role.69,106,218,272 Acute trauma may also be a significant
factor (Fig. 6-76). The pathomechanism may also involve a
vascular disruption that affects either chondro-osseous trans-
formation, osseous remodeling, or both.113,114,185 This secon-
darily affects biomechanics, leading to collapse or distortion
of the ossification center.
Damage may occur completely within the trabecular bone
in any region (diaphysis, metaphysis, epiphysis). Such injury
has been difficult to detect in the past in patients who have
outward signs of injury. With the advent of MRI a new cate-
gory of injury, the bone bruise, has come into being. Such an
injury appears as an area of focal edema and hemorrhage
within the affected region of bone. Morphologic correlation
188
of such injury has been lacking in the literature. Figures
6-77 and 6-78 show the gross and histologic appearances
of these intraosseous injuries.
Realistically, type 7D injury (bone bruise in the epiphyseal
ossification center) is detectable only by MRI. The lesion may
be relatively small. Often it is a fortuitous finding during an
MRI evaluation for pain following an injury in which no frac-
ture was detected on routine radiography. More extensive
involvement may occur. The intensity of the signal changes
probably reflects the nature of the trauma and the extent of
intraosseous bleeding (Fig. 6-79).
FIGURE 6-77. Anatomic specimen showing areas of focal bleeding
in the epiphyses and metaphyses without obvious fractures. They
would appear as multiple bone bruises on MRI. A traumatic below-
knee amputation was associated with the main injury (upper di-
aphyseal fracture). A more obvious type 7A injury (arrow) at the tip
of the lateral malleolus is the analogue of lateral ligament injury in
the child and is comparable to a tibial spine fracture in the knee.
6. Injury to the Growth Mechanisms
FIGURE 6-76. Type 7 injury of the medial cuneiform
(arrow).
Type 8
Type 8A injuries affect the metaphyseal growth and remod-
eling mechanisms and represent transient phenomena
related to intrinsic vascularity (Fig. 6-80).205 The physis is sec-
ondarily affected by such fractures. If a significant fracture
occurs through the normal central or peripheral vascular
supply patterns (which may occur in normal bone and
pathologic situations), the metaphyseal circulation involved
in the formation of primary spongiosa from the cartilage
cell columns is temporarily disrupted, leading to failure of
normal osseous remodeling and subsequent, transiently
increased osseous density compared to the vascularized bone
on the other side of the fracture (Figs. 6-81 to 6-83).166,167 In
reality, the bone density is normal. The adjacent metaphy-
seal bone on the other side of the fracture line undergoes
the typical changes of disuse atrophy, becoming more radio-
lucent than the adjacent biologically quiescent bone in
the temporarily ischemic sector of the metaphysis. Osseous
density equilibration occurs after revascularization restores
the capacity for osseous trabecular remodeling.
Type 8 injury patterns may be the underlying cause of
angular overgrowth when a valgus deformity complicates a
proximal metaphyseal tibial fracture (see Chapter 23).
Experimentally, blood vessels (E-vessels) penetrate from
the epiphysis through the physis to substitute temporarily
for the M-vessels of the primary spongiosa.347 As the latter
circulation is restored, these transphyseal vessels regress.
Whether a similar phenomenon occurs in the skeletally
immature human is open to conjecture but is likely.
Following revascularization, the junction of the primary
spongiosa and hypertrophic cartilage may become biome-
chanically weaker, not unlike the revascularization phase of
Legg-Perthes disease. Epiphysiolysis may be a complication
of such temporary metaphyseal ischemia (Fig. 6-84). The
widened physis is mechanically susceptible, similar to the
widened physis in a patient with rickets. Children with seem-
ingly innocuous fractures (e.g., the distal radial metaphysis)
should be protected for 2–3 weeks after casting. I use a
removable splint, as it allows gradual remodeling in response
to progressively increased biomechanical demands.
Certain metaphyseal fractures are associated with anatom-
ically separate microscopic growth plate injury (Fig. 6-85).
Fracture Patterns
FIGURE 6-78. Histology of a type 7 injury of the medial
malleolus. The extensive hemorrhage would be
detected on MRI as a bone bruise. There is a
definite chondro-osseous separation.
A interface. There may be more than one longitudinal prop-
B
FIGURE 6-79. T1 (A) and T2 (B) images of bone bruising following
a direct-impact injury to the medial knee by a baseball bat.
189
This is a type 8B injury. Diagnosis is unlikely by routine
radiography.
Metaphyseal trabecular bone may also sustain microscopic
injury (bone bruising) that is difficult to detect radiograph-
ically but may be demonstrable by MRI. It may be adjacent
to the hypertrophic zone of the physis and may render the
focal area temporarily ischemic (see Fig. 6-95), which would
lead to thickening of the physis in this isolated area. Such
thickening, which may be radiologically evident, is usually
temporary, disappearing once focal revascularization occurs.
Peterson proposed a classification that included a com-
minuted metaphyseal fracture pattern extending to the
physis.281 In addition to the transverse metaphyseal fracture
line, there is longitudinal propagation from this fracture line
toward the physis. Longitudinal propagation may stop at the
physis or may be redirected along the physeal–metaphyseal
FIGURE 6-80. Type 8 metaphyseal injury. The decrease in blood
supply prevents replacement of the hypertrophic cartilage zone.
In contrast, the germinal zone, with intact circulation, continues to
grow, thickening the physis.
190 6. Injury to the Growth Mechanisms

FIGURE 6-81. (A) Undisplaced proximal

metaphyseal fracture (arrow). (B) Two
weeks later the metaphyseal bone is
sclerotic between the fracture and the
physis (arrows).

FIGURE 6-82. Avascular segment of metaphysis following a frac-

ture (arrows) in an antelope (greater kudu). The rest of the metaph-
ysis and the epiphyseal ossification center are well vascularized. FIGURE 6-83. MRI of distal femoral metaphyseal fracture. Note the
difference in signal intensity proximal and distal to the fracture. This
is a reflection of the altered vascular physiology.

FIGURE 6-84. (A) Metaphyseal fracture of

the distal radius (arrows). (B) Three weeks
later the cast was removed. Two days later
the patient reinjured the arm but suffered an
epiphyseal injury instead. The metaphyseal
fracture (arrow) is well healed. However,
temporary deprivation of the metaphyseal
blood supply to the hypertrophic cells of the
physis caused sufficient microscopic widen-
ing of this area to render it temporarily more
mechanically susceptible to injury.
Fracture Patterns
FIGURE 6-85. Torus fracture (arrow) is evident. There is extensive
juxtaphyseal bleeding (bone bruising), indicating that some of the
trauma energy was transmitted or absorbed in this area also. This
injury is type 8B.
agation. This is the type 8C injury pattern (Figs. 6-86 to
6-88).
Type 9
Type 9 injuries are selective injuries to the diaphyseal growth
mechanism of appositional, membranous bone formation
from the periosteum (Figs. 6-89, 6-90). Any direct injury
FIGURE 6-86. Type 8 metaphyseal fractures with extension to the
physis (arrow).
191
B
FIGURE 6-87. (A) Metaphyseal fracture with probable extension to
the physis. (B) MRI corroborated the extension to the physis and
suggested an undisplaced type 1 physeal fracture of the distal ulna.
causing permanent damage to the periosteum can adversely
affect the ability of the bone to replace endochondral corti-
cal bone, remodel the new membranous bone in response
to biomechanical demands, and increase cortical volume cir-
cumferentially.143 This type of injury may be associated with
severe fragmentation of portions of the diaphysis, which is a
significant problem if the damaged bone requires a thick di-
aphyseal cortex for normal biomechanical function, as the
tibia does. The periosteum may be damaged in a localized
area, which may lead to unusual patterns of extraperiosteal
bone formation (Figs. 6-91, 6-92).261 Wringer injuries may be
associated with significant avulsion (degloving) damage to
the periosteum.3,4 Damage to the interosseous tissue in
paired bones may also cause contiguity of damaged
periosteal elements between the tibia and fibula or the
 192
A
radius and ulna, leading to synostosis formation (Fig. 6-93).
Such patterns may also affect the adjacent metacarpals or
metatarsals.
Although these injuries may not be regarded as typical of
a growth mechanism, it must be remembered that one of the
major mechanisms for longitudinal and appositional bone
growth is the control imparted by the highly osteogenic
periosteal sleeve. Damage to this soft “skeletal” component
by open injury, burn, or infection must affect localized areas
of diaphyseal bone growth transiently or permanently. Fur-
thermore, significant loss of periosteal growth mechanisms
may affect intrinsic periosteal control of longitudinal physeal
growth (see Chapter 1).
Wringer injuries usually involve the upper limb, being sus-
tained by a child whose hand has been drawn into the power-
driven rollers of a washing machine, conveyor belt, or farm
machine.381 Comparable lesions that involve the lower
extremities usually occur when the child is run over by a car
or bus. In many instances the driver feels a “bump” and
FIGURE 6-89. Type 9 injury, which involves the periosteal growth
mechanism.
6. Injury to the Growth Mechanisms
FIGURE 6-88. (A) Slab section showing longitudinal
extension of a metaphyseal fracture and transphyseal
propagation. (B) Radiograph of the specimen.
B
reverses direction, adding additional injury. Maximum
damage to the soft tissues is generally sustained in the ante-
cubital fossa, although considerable trauma may occur in
the axilla if the elbow is extended and allows the arm to
go further into the machine. The extent of the injury is
increased by applying countertraction to the extremity or by
reversing the direction of the roller, thus subjecting the arm
to a second crushing. Other factors determining the sever-
ity of damage are the length of time during which the limb
is caught between the rollers, the size of the limb, the tension
between the degloving rollers, and the rapidity of the revo-
lutions. The crushing injury is primarily to soft tissues such
as skin, subcutaneous tissue, muscles, tendons, and nerves.
The bones are rarely fractured, although periosteal damage
(crushing, tearing, stripping) may be significant. This is pri-
marily a type 9 injury. These same above changes occur in
the leg trapped under a tire. The larger the vehicle the
greater is the risk of soft tissue injury and the likelihood of
compartment syndrome. Shearing damage consequent to a
limb being run over by an automobile tire produces an
injury similar to a wringer injury.
Akbarnia et al. reported a wringer injury in a 29-month-
old child on whom they did a 24-year follow-up study.3
Initially, there was extensive loss of the diaphysis and perios-
teum of both the radius and the ulna, limiting the capacity
for spontaneous restoration of the diaphyseal shaft. The
child was subjected to repeated onlay grafts to fill in the
defects and had rather dramatic restoration of a functional
radius and ulna. Akbarnia et al. thought that circulatory dis-
turbances were a major factor in the distal shortening of the
bone. With current technology, lengthening and bone trans-
port could have been alternative procedures.
Comparable compression and avulsion injuries may occur
when an ankle is caught in bicycle spokes. The ankle may
Physiology of Epiphyseal–Physeal Injury
FIGURE 6-90. Type 9 injury to the tibia of a young girl run over by
a school bus tire. (A) Initial appearance. (B, C) Progressive devel-
opment of apparent heterotopic bone (solid arrows). Open arrows
indicate pseudarthroses in the new bone. These were painful. (D)
Superimposed excised bone. (E) Cross section showing mature
bone with periosteum (P), Tidemarks (T), and longitudinally (LV)
and transversely (TV) oriented blood vessels. Typical haversian
bone, however, was not present owing to the lack of biomechan-
ical stimulation.
be severely twisted, and massive swelling of the soft tissues
may occur. Roentgenographic evidence of injury may be
subtle.
Physiology of Epiphyseal–
Physeal Injury
Biomechanics of the Physis
The specific three-dimensional configuration of the physes
in humans and other growing mammals is variable and devel-
ops in response to the principal stresses applied to each
specific epiphysis, although a genetically programmed, basic
developmental pattern (contour) also contributes to the
control of development.9,22,177 The overall complexity of the
large undulations of the growth plate and of the many
193
smaller mammillary processes cannot be fully appreciated in
standard two-dimensional radiographs. Because the devel-
oping, bipedal human is not as highly specialized for rapid,
twisting locomotion as a quadruped, the configurations of
the epiphyseal plates in humans are not as geometrically
complex as they are in many animals specialized for rapid
running, twisting, and leaping (e.g., the artiodactyls). In
such animals the attachments of ligaments to the epiphysis
and the patterns of gait are such that considerable rotatory
shear forces are applied, especially during abrupt directional
change (see Chapter 1). The distal femoral epiphysis in these
animals contains four or more cone-shaped projections from
the metaphyseal side that fit into appropriate, concave-
shaped areas of the epiphysis and physis (see Chapter 1).
These projections effectively prevent macrodisplacement in
anteroposterior, medial, and lateral directions and specifi-
cally prevent epiphyseal rotation. There is also a lappet
formation around the periphery of the epiphysis, so varus-
194 6. Injury to the Growth Mechanisms

FIGURE 6-91. Patterns of periosteal bone formation when the periosteum rolls into a tube during the posttraumatic healing period.

FIGURE 6-92. Views of bone formed in disrupted periosteum (lawn

mower injury).

FIGURE 6-93. Transverse fracture of the tibia and greenstick frac-

ture of the fibula apparently led to periosteal and interosseous dis-
ruption sufficient for the formation of a synostosis.
Physiology of Epiphyseal–Physeal Injury
valgus and anteroposterior shearing (displacement) forces
(strains) may be further anatomically resisted (constrained,
dissipated). This particular configuration of the epiphysis is
seen moderately in certain human physeal–epiphyseal
regions (Fig. 6-94). The major import is that the epiphysis
and growth plate are reasonably protected from major rota-
tory and shearing forces; but when the epiphysis is traumat-
ically translocated in any direction from its normal position,
the degree of potential deformity to the cone-shaped pro-
jections depends on their degree of development. In the
adolescent these cone-shaped projections are more signifi-
cantly developed, so a transverse fracture and displacement
may shear through the projections and induce fractures in
multiple regions of the growth plate, metaphysis, and epiph-
yseal ossification center, rather than shearing transversely
across only the hypertrophic cellular zone.
The strength of the physis is provided by both the cytoar-
chitectural types and arrangements and the intercellular car-
tilaginous matrix.39–42,71,76,92–94,113,135,145,153,255,257,259,260,262,274 In the
first two zones of the physis, the cartilaginous matrix is abun-
dant, and the physis is intrinsically strong. In the third zone,
in contrast, the hypertrophic chondrocytes enlarge, making
this zone potentially the weakest portion of the physis. This
weakness is to shearing, bending, and tension stresses but
not to compression. The fourth zone is reinforced by the
addition of matrix calcification, but it still is weaker than the
FIGURE 6-94. Lappet formation at the physeal periphery of the
distal fibula. It is more prominent on the medial side. This lappet
formation is a mechanical-cytologic adaptation to minimize shear
and tension stresses. Also note that a definite subchondral plate
has formed under the medial fibular articular surface (arrow), and
laterally the endochondral ossification is more irregular.
195
first and second zones. The process of calcification alters
the microscopic biomechanics of the matrix. Fractures gen-
erally involve the third and fourth zones, propagating a vari-
able distance into each one, rather than concisely cleaving
between the two zones.
The weakest part of the physis appears to be the third
layer, the zone of hypertrophic cartilage cells. If the perios-
teum around the periphery of an epiphyseal plate is incised,
the epiphysis may be more easily detached through this zone
than if the periosteal insertion were intact.26 The line of
cleavage is consistently through the layer of hypertrophic
cartilage.142 Harris and Hobson determined the shearing
strength of the upper tibial epiphysis in the rat and con-
firmed that when the epiphysis separated from the metaph-
ysis the plane of cleavage invariably passed through the third
layer.32,150 The clinical significance of these early experimen-
tal findings was that the germinal cartilage cells of the physis
remained with the epiphyseal fragment and intrinsic blood
supply. However, compared to humans, these studies were
undertaken in very small bones that attained relative matu-
rity in a short time (weeks to months) and slowly continued
to grow for an extended period. Physeal failure studies in
large animals with bone size equal to or greater than the
human are nonexistent.
The region of trabecular formation in the metaphysis also
contributes to the strength of the physis, although the thin-
ness and fenestration of the metaphyseal cortex make it
susceptible to certain injuries (e.g., compression or torus
failure) that are not seen in adults (see Chapters 1, 2).
The epiphysis renders a certain shock-absorptive effect,
especially when it is primarily cartilaginous. In this situation,
the fracture-producing forces are transmitted more directly
into the metaphysis, resulting in torus fractures. However,
as the epiphyseal ossification center enlarges, this resiliency
and the ability to absorb stress are probably changed, and
the deforming forces tend to be transmitted more directly
into the growth plate, which, as a potentially weaker region,
may be sheared through the third and fourth cellular zones.
The dense periosteal attachments around the physeal
periphery increase the resistance of the physis to shear and
tensile failure.92–94,97–100,204,247,385 The physeal periosteum also
blends into the epiphyseal perichondrium and joint capsule
ligament complex, further increasing its strength. In con-
trast, the periosteum is attached relatively loosely to the
underlying, fenestrated metaphysis, although there is conti-
nuity of fibrous tissue from the intertrabecular spaces. In
the child, the diaphyseal periosteum is attached even more
loosely than the continuous metaphyseal and physeal
periosteal regions. The diaphyseal periosteum does not
seem to contribute significantly to the strength of the bone
in adults, and because it is attached even more loosely in
children it is unlikely that it plays any major role in mechan-
ically protecting the developing diaphysis from fracture or
failure.164 However, it does add to the stability if incompletely
disrupted, and it is extremely osteogenic, leading to rapid
subperiosteal new bone formation and fracture stabilization
in the child (subperiosteal healing in contrast to endosteal
healing) (see Chapter 8).
The viscoelasticity of physeal cartilage is dependent on the
rate of loading.55 The total load before failure was substan-
tially higher when rapid loading rates were used. The load-
196
to-failure value of epiphyseal cartilage with intact periosteum
is almost twice that of epiphyseal cartilage with the perios-
teum removed.233,234 The fibrous periosteal membrane is
much softer than cartilage and has a lower elastic modulus.
Therefore it may play only a secondary role in load distri-
bution. The periosteum should be considered a check-rein
on the epiphysis once the physis has started to fail. It may
prevent marked displacement if the load is insufficient to
rupture its fibers, but its ultimate tensile properties are prob-
ably not tested until the physeal cartilage has failed first. This
concept is in keeping with the clinical finding that epiphy-
seal injury may occur without roentgenographic evidence of
significant epiphyseal displacement.
The quality of the physeal cartilage, in terms of its ultimate
tensile strength, was found to be physiologically reduced
during sexual maturation, particularly in male rats.148,233,234
Male and female rats differed with regard to the morphology
and strength of their epiphyseal cartilage during this phase
of sexual maturation (corresponding to the growth spurt of
human adolescence). The decrease in the quality of cartilage
during sexual maturation and the difference between the
sexes with regard to morphology and strength were due to
the influence of the various hormones, which generally
included sex hormones and somatotrophic hormone (STH).
These results suggested that both androgens and STH
reduced the overall (total) strength of the growth cartilage
or at least delayed its age-conditioned increase, whereas
female sex hormones increased the tensile strength of the
cartilage. Both STH and androgens had a positive effect on
nitrogen balance and promoted physeal and epiphyseal
cartilage cell proliferation. Estrogens had an insignificant or
no effect.
On the other hand, osseous maturation was not affected
by STH and reacted to androgens only if they were admin-
istered in high doses for a reasonably long time. Osseous
maturation was markedly accelerated by estrogens, which
may affect their function via several routes, one of which
is increasing the rigidity (decreasing the elasticity) of the
collagen and the tensile nature of the periosteal sleeve,
thereby secondarily controlling the rate of longitudinal (and
perhaps diametric) growth.
In essence, the effect of hormonal changes during adoles-
cence appears to be a slight physiologic decrease in the overall
tensile strength of the cartilage in boys, in response to STH
and androgens, and greater mechanical strength of the epi-
physeal plate in girls, in response to the estrogen compounds,
with the former hormones tending to increase physeal
column height (which is a reflection of growth rates) and the
latter tending to slow growth, decrease cell column height,
and precipitate physiologic epiphysiodesis. Bright et al.
showed a definite sex difference in failure responsemodes.53,55
Experimental Trauma to the Physis
Experimental investigations of the effects of injury to the
physis are numerous.* In 1867 Ollier made linear incisions
* Refs. 5,8,12,25,28,31,34,37,62,75,84,103,124,125,131,132,155,162,186,
194,196,197,200,212,217,229–331,242,243,250,270,276,287,294–297,
308–310,325,326,330,331,334–336,341–343,353,355,365,367,370,371,
390
6. Injury to the Growth Mechanisms
across the epiphyseal plate in skeletally immature rabbits and
cats; superficial cuts did not affect growth, but deep incisions
led to growth arrest.267 Vogt was unable to produce growth
disturbance in goats and sheep by separating the epiphysis
through the “natural line” of cleavage.374 Brashear produced
fractures through the distal femoral epiphysis of rats by a
varus angulation force50 that resulted in tensile disruption.
On the distraction side, the cleavage plane passed through
the aforementioned plane of hypertrophic cells, whereas the
compression side fracture line usually propagated into the
metaphyseal trabeculae, forming a type 2 injury pattern. A
combination of shearing and compression stresses pushed
the metaphyseal bone into the epiphyseal plate, damaging
all layers of cells, rather than just the hypertrophic layer.
Resection of portions of the epiphysis in rabbits often
resulted in premature growth arrest.124 Probably the major
factor preventing regenerating of cartilage was the fact that
the ossification ring of Lacroix and the zone of Ranvier,
which were regarded as the areas of greatest regenerative
capacity, were part of the resected segment.158,344 Friedenberg
found that he could not fully control the reactive osteogen-
esis secondary to the trauma with various interposition sub-
stances.124 The greater the degree of resection or the more
extensive the overall length of the growth plate damage, the
worse was the response to the interposition of various tissues.
On histologic examination, he noted small peripheral bone
bridges with minor deformities and thought that these
regions were capable of continued growth because they con-
stantly induced microfractures of the osseous bridge in the
experimental animals.
How significant this finding might be to human injury and
whether it is possible for the human to avoid arrest by simi-
larly breaking small osseous bridges is difficult to say. It seems
likely that with the lengthy period of bone growth a bridg-
ing structure of significant size might eventually form,
become radiologically evident, and lead to growth alteration.
Perforation of the epiphyseal cartilage of young rabbits
with a 1/8-inch drill did not cause any major shortening
despite osseous or fibrous bridging between the epiphysis
and metaphysis.117,118,128,184,213 When larger drills were used,
shortening became more marked. Resection of minor areas
of the peripheral growth cartilage and surrounding bone,
did not cause any major deformities, provided the fragments
were reduced immediately.64,65 However, if the fragments
were deprived of their blood supply, as is often done in
clinical situations by periosteal stripping to visualize more
precisely the edges of the fracture and accomplish anatomic
reduction, growth was permanently inhibited.
Harris and Hobson studied displaced proximal femoral
epiphyses in rabbits, finding a line of cleavage in the zone of
hypertrophic cartilage cells.150 In monkeys, Dale and Harris
described experimental fractures with a cleft through the
junction of the hypertrophic cartilage cells and the calcified
portion of the growth plate.91
In other experiments, short linear cracks developed within
the physis after partial failure.55 The repeated presence of
these cracks deep within the germinal physeal cartilage,
rather than just in the hypertrophic zone, before rupture of
the fibers in maximal tension, lends support to the concept
that these internal changes are the first evidence of cartilage
failure that result from subcritical loading. Many of these
Physiology of Epiphyseal–Physeal Injury 197

cracks were also observed to be within the planes of expected

high shear stress. Similar microfractures have been found in
human material from traumatic amputations.
The final failure of the physis occurred after the structure
that was being subjected to the increasing load had absorbed
about 50% of its expected failure energy, at which time shear
cracks began to occur within various levels of the growth
plate along those planes of high shear stress. If the load was
then released, the shear cracks remained. Their continued
presence presumably weakened the plate to further applica-
tions of similar transverse loads. If the deforming force
continued to increase, a secondary crack occurred, and the
outermost fibers that were in maximal tension ruptured. The
secondary crack then became the propagating crack and
passed through the plate to cause cartilage failure.24 This
may be the pattern of failure in entities such as gymnast’s
wrist (see Chapters 12, 16).
Such a failure crack may or may not coalesce with the
smaller, primary shear cracks in other levels of the physis. It
appeared to do so more frequently in the older animals than
FIGURE 6-95. Effect of a transphyseal pin. This patient underwent
in the young ones. Finally, no matter which species was
attempted reconstruction for pseudarthrosis of the tibia 7 months
studied, if the load application continued the periosteum prior to a below-knee amputation. The pin had been in place for
also reached its ultimate tensile strength and ruptured, 11 weeks. Note how the physeal cartilage extends along the fibrous
allowing epiphyseal displacement in the direction of the tissue, filling the pin tract into the metaphysis. The secondary ossi-
applied force.55 fication center has been split and has not replaced the fibrous
Multiple studies have shown considerable variability in tissue. Furthermore, a fibrous ankylosis is developing between the
fracture patterns that relate to the extent of skeletal tibia and the talus. Pins across the physis and articular surface
maturity, the amount of force applied, rates of loading, should be used with great caution in children, as similar changes
and particularly the direction of application of the may complicate subsequent growth and rehabilitation.
force.200,201,205,229,308 An important finding in all of these
studies were the highly variable undulation of the fracture
plane, with microdisruptions in the germinal zone that were
separate from the main cleavage plane. inserted so as to traverse the central regions of the epiphysis
and physis without contacting the physeal plate near its
peripheral margins.
Transphyseal Pins Thin, unthreaded wires across the central growth plate
When a drill hole traversed the central portion of the distal occupy such a small volume of the plate that even a local
femoral growth plate and a fibular graft was subsequently tether that occurs from metaphyseal to epiphyseal bone
inserted through this defect, the epiphysis and physis some- when the wires are removed or overgrown probably has little
times fused microscopically to the fibular graft. Despite or no clinical effect on the growth potential of the plate as
this, a microscopic cleft developed between the bone graft a whole. Threaded wires, which have a firmer hold in the
and the epiphysis–metaphysis, so physeal growth continued epiphysis and metaphysis and prevent longitudinal growth
in most cases. These bony defects or stretch factors were plate expansion, usually cause compression of the germinal
accompanied by an intense cellular reaction. Premature cells and produce subsequent epiphysiodesis. However, even
epiphysiodesis and permanent growth arrest were not smooth pins placed across the physis, epiphysis, or articular
necessary sequelae, at least in these central defects. However, surface may lead to significant histologic changes that may
the longer period of skeletal growth and maturation in predispose the physis to osseous bridge formation during
humans may decrease the likelihood for formation of these subsequent skeletal maturation (Fig. 6-95).
clefts and may increase the chances for osseous bridge
formation.
Hemiepiphyses
Surgeons operating for fusion in tuberculosis of the knee
have driven bone grafts across the center of the epiphyses of Barash and Siffert showed that a longitudinal bifurcation
both the distal femur and the proximal tibia without neces- osteotomy extending through the epiphysis, growth plate,
sarily causing deformity or clinical shortening. However, and metaphysis (type 4 injury analogue) of experimental
damage to the periphery of the growth plate at the metaph- animals subsequently produced variable deformities.14,333
yseal margin definitely causes prompt ossification at the site The degree of deformity produced was proportional to the
of injury, with resultant growth disturbance. volume of the epiphyseal ossification center present at the
Great care should be taken in the type and manner of time of surgery. If the secondary ossification center had a
insertion of any internal fixation devices in the region of the large volume, early epiphysiodesis and deformity occurred
physes. These devices should be smooth to minimize damage as a consequence of new bone formation, and a bridge
to the physeal plate and, whenever possible, should be quickly formed between the epiphysis and metaphysis.
198
If the epiphyseal ossification center was small at the time
of surgery and a larger portion of epiphyseal cartilage
separated the osteogenic sites (i.e., ossification center and
metaphysis), relatively normal growth continued until the
centrum came to rest against the growth plate, at which time
premature epiphysiodesis and deformity occurred. If the
bifurcation procedure was performed prior to the appear-
ance of the osseous centrum, relatively normal, undeformed
growth of the divided halves occurred. This latter observation
is in contradistinction to the situation in humans, in whom an
injury to a totally cartilaginous epiphysis appears to lead to
subsequent growth deformity, which often manifests at a later
time, such as during the adolescent growth spurt.
Intraepiphyseal Osteotomy
In the rabbit tibia (proximal end) transverse intraepiphyseal
osteotomy that was subsequently packed with fragments of
homogeneous iliac cortical bone, polyethylene plastic film,
or stainless steel showed no untoward effects on the intra-
epiphyseal vascularity; and normal endochondral ossifica-
tion continued at the growth plate and within the
epiphysis.333 This procedure represents a possible way to
correct growth plate angular deformities by making the
osteotomy within the epiphyseal ossification center rather
than within the metaphysis. Such an approach has been tried
in Blount’s disease but with variable, often unpredictable
results.352
Circulation and Ischemia
The effects of ischemia on the physis have been studied
extensively.368,369 Cutting off the epiphyseal circulation leads
to either temporary or permanent cessation of growth. The
central region seems more sensitive to ischemia than the
periphery, which may have the capacity to recover and con-
tinue growth.374 Furthermore, undifferentiated cells in the
zone of Ranvier may not be as sensitive to ischemia, and they
have a blood supply relatively independent of the cartilage
canal system. This allows latitudinal and subsequently longi-
tudinal expansion following central ischemia. These features
may lead to differential rates of growth and significant
changes in physeal contour. Immunosuppressive drugs may
affect growth in a similar fashion by differentially decreasing
the rate of cellular multiplication in the physis.54 Metaphy-
seal circulatory compromise appears less sensitive to perma-
nent change.
A cone-shaped epiphysis may develop after injury to the
distal tibia.232 This cone-shaped epiphysis apparently devel-
oped as a result of the temporary inhibition of growth of a
central, rather than a peripheral, portion of the physis. This
inhibition appeared to occur without formation of a signifi-
cant osseous bridge, at least in the early stage of develop-
ment, although it seemed possible that a bridge would occur
by the time the patient reached skeletal maturity. In addi-
tion, the cessation of growth appeared to involve the carti-
lage cells situated in the center of the growth cartilage, and
it appeared to be caused by interruption of the epiphyseal
circulation, possibly followed by revascularization. In con-
trast, the peripheral cells in the area of Ranvier’s ossification
6. Injury to the Growth Mechanisms
groove, which are supplied by the relatively separate
periosteal/perichondrial vascular system, continue to be
active and thus support further growth in the width and
length of the epiphyseal cartilage plate. The development of
these cone-shaped epiphyses is further proof that significant
growth of the epiphysis and physis may take place peripher-
ally following ischemic central damage.
Acute ischemia of the physis induces formation of actin
and myosin-like structures within the cartilage septa along
and between the cell columns. The role that such changes
might play in eventual bridge formation is not clear.
Based on rabbit experiments it was concluded that persis-
tent compression affected the growth plate by interference
with blood flow on one or both sides of the physis.368,369
Despite exerting the same pressure on both sides of the
growth plate, only the metaphyseal side was readily affected
in the early stages. So long as no damage was caused to the
epiphyseal side of the growth plate, the lesions appeared to
be fully reversible. Interference with growth was directly pro-
portional to the damage caused by compression of the
epiphyseal side of the growth plate. In general, the duration
and the severity of compression of the epiphyseal plate
affected its growth primarily by interrupting the microvas-
cular blood supply.
Healing Patterns
The physis heals primarily by temporarily increased cartilage
formation and gradual reinvasion by the disrupted metaph-
yseal vessels, which eventually replace the transiently
widened growth plate. Little experimental work has been
directed at posttraumatic normal cellular response patterns,
with most work being done in the rat. Contingent on the
level or levels of cellular injury within the physis, three basic
types of chondro-osseous healing have been observed.
1. If the fracture-separation occurs through the more
recently formed regions of cell columns (before significant
cellular hypertrophy has occurred), healing takes place pri-
marily by continued, relatively rapid increases in the number
of cells within the columns, which causes moderate widen-
ing of the physis. Because there are small epiphyseal vessels
in this region, some resorption of fracture debris may occur
early in the healing process. These vessels also exhibit a
hyperemic response, increasing the cellular proliferation
rates, especially peripherally in the zone of Ranvier.
The healing response of the metaphysis is continued
(perhaps rate-increased) replacement of the hypertrophic
cell columns by endochondral bone. Once the level of fibro-
sis and debris within the physis is encountered, the vessels
rapidly invade this damaged area to reach the maturing,
newer cell columns on the other side. These cellular
response patterns lead to restoration of the normal anatomy
and intrinsic strength within 3–4 weeks.
2. If the fracture-separation occurs through the transition
of hypertrophic cells to primary spongiosa (probably the
most commonly involved cellular level), there may be
marked separation, with the gap being filled by hemorrhage
and fibroblastic tissue. This region may then progressively
form disorganized cartilaginous tissue (Fig. 6-96), not unlike
Physiology of Epiphyseal–Physeal Injury
A B
FIGURE 6-96. (A) Type 2 injury in a lesser kudu. Radiograph
4 weeks later shows subperiosteal new bone on the side of
the Thurstan Holland fragment, where the periosteal frag-
ment was intact. The animal died of pneumonia sustained
while recovering from the fracture. (B) Histologic section. (C)
High power view showing widening of the physis and the
resolving hematoma along the fracture site.
the initial cartilaginous callus in a diaphyseal fracture (see
Chapter 8). Meanwhile, cellular proliferation, cell column
formation, hypertrophy, and calcification continue on the
“epiphyseal” side of the disorganized callus, leading to
widening of the physis. At the same time vascular invasion of
the remnants of hypertrophic, calcified cartilage rapidly
occurs on the “metaphyseal” side of the fracture.
However, once invading metaphyseal vessels reach the
disorganized cartilaginous callus, vascularly mediated bone
replacement is temporarily slowed, as there is no pattern of
cell columns to invade in an organized fashion. As the callus
cartilage matures, the metaphyseal vessels begin to invade
199
C
irregularly and replace the cartilage with bone. The thick-
ness of this callus varies depending on the degree of longi-
tudinal and lateral displacement and periosteal continuity
with the physeal periphery. The callus is replaced at differ-
ent rates; the invading metaphyseal vessels reach the normal
cell columns, which have been maturing in a normal
sequence, but osseous replacement does not take place. The
widened physis is rapidly invaded by the vessels, replaced by
primary spongiosa, and progressively restored to normal
physeal width.
The callus in the subperiosteal region contributes to early
stability. This region heals by vascular invasion of the callus,
200
through which process trabecular bone forms between the
original metaphyseal cortex and the subperiosteal membra-
nous bone that is forming continuously, external to the
metaphyseal cartilaginous callus. These three microscopic
bone regions progressively merge and remodel, making the
region biomechanically strong. With further growth and
remodeling this coalescent bone is completely replaced and
remodeled. These initial cellular replacement processes
in both metaphyseal and physeal regions probably take
4–6 weeks, but remodeling may continue for months to
years.129 In fact MRI evaluation even a year after osseous
injury exhibits significant retained signal alteration, even
though the bone appears radiographically healed (see
Chapter 5).
3. If the injury extends through all cell layers of the physis,
as it would with type 3, 4, and 7 injuries, the repair processes
differ slightly. Fibrous tissue initially fills the gap between
separated physeal components, and typical callus formation
occurs in the contiguous metaphyseal spongiosa, the epiph-
yseal ossification center, or both. If large surfaces of
nonossified epiphyseal cartilage are also involved, fibrous
tissue initially forms in the intervening region. The re-
parative response shows irregular healing of the epiphy-
seal and physeal cartilage, with loss of normal cellular
architecture.254
Within the central physeal regions diametric expansion of
the cell columns is minimal. Accordingly, closure of a large
defect by physeal cartilage is unlikely. The gap usually
remains fibrous but with the potential to ossify. Toward the
physeal periphery, diametric expansion is more likely but
still may not lead to closure of large cartilaginous gaps by
progressive replacement with fibrous tissue. This replace-
ment process consists essentially of diametric expansion of
the germinal and hypertrophic cell regions by cell division,
maturation, and matrix expansion. The intervening fibrous
tissue disappears through growth, but only if the cell gap
closes.
Because blood supply to this region is minimal, the fibrous
tissue similarly is not well vascularized. Hence significant cell
modulation, especially to osteoblastic tissue, may be less
likely over the short term.
The larger the gap filled with fibrous tissue and the longer
the time remaining from fracture to skeletal maturity, the
greater is the likelihood of developing sufficient neovascu-
larity to begin an osteoblastic response and form an osseous
bridge. Furthermore, in the young child with minimal
epiphyseal ossification, the blood supply to the physeal ger-
minal region is not as well defined. Once the ossification
center expands and forms a subchondral plate over the ger-
minal region, the microvascularity probably increases and
the chances for vascularization and ossification of the fibrous
region increase, explaining the delayed appearance of the
osseous bridge.
If accurate anatomic reduction is carried out, a thin gap
would be present, which should fill in with minimal fibrous
tissue and allow progressive replacement of the tissue by
diametric expansion of the physis. However, if the fragment
has been partially or completely devascularized by either the
initial trauma or subsequent surgical dissection to effect an
open reduction, cellular growth and diametric and longitu-
dinal expansion may not occur, increasing the chances of
6. Injury to the Growth Mechanisms
cellular disorganization, fibrosis, and an eventual osteoblas-
tic response. Failure to correct anatomic displacement, espe-
cially with type 4 injuries, increases the possibility of
apposition of the epiphyseal ossification center and metaph-
ysis, thereby enhancing the risk of formation of an osseous
bridge between the two regions.
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351. Stevens RH. Retardation of bone growth following roentgen
irradiation of an extensive nevocarcinoma of the skin in an
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352. Storen H. Operative elevation of the medial tibial joint surface
in Blount’s disease. Acta Orthop Scand 1969;40:788–796.
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353. Sudmann E, Busby OS, Bang G. Inhibition of partial closure
of epiphyseal plate in rabbits by indomethacin. Acta Orthop
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354. Sumner-Smith G, Dingwall JS. A technique for repair of frac-
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355. Sunden G. Some aspects of longitudinal growth. Acta Orthop
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356. Sussenbach F. Anatomie, Prognose und Behandlung von Epi-
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357. Tanner JM. Assessment of Skeletal Maturity and Prediction of
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358. Teates CD. Distal radial growth plate remnant simulating frac-
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359. Tempsky A. Gelenkschadigung durch Erfrierung. Zentralbl
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360. Teot L, Gilbert A, Amichot G, et al. Epiphyseal vascularization
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364. Tomatsu T, Lmai N, Takeuchi N, Takahaski K, Mimura N.
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6. Injury to the Growth Mechanisms
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7
Management of Growth Mechanism
Injuries and Arrest
Engraving of growth arrest and malunion following an anteriorly
displaced type 1 distal femoral physeal fracture. (From Poland J.
Traumatic Separation of the Epiphysis. London: Smith Elder, 1898)
arious clinical studies alluded to in Chapter 6 and
V
that are considered additionally in this chapter have
emphasized that significant growth plate injury
leading to growth impairment may occur more frequently
than the Salter-Harris classification scheme originally sug-
gested. This is particularly true in lower extremity physeal
injuries (Fig. 7-1), in which the mechanisms of injury are
often more mechanically severe than those causing upper
extremity physeal injuries.
The real incidence of growth impairment may prove
elusive to any accurate documentation. Long-term prospec-
tive studies are likely to fail because of the difficulty of
convincing families to continue regular visits and imaging
studies when their child outwardly or functionally appears
to have no obvious problem. This is compounded by
the array of health maintenance organizations (HMOs),
preferred provider organizations (PPOs), and others who
emphasize decreased costs and are thus reluctant, if not
adamantly opposed, to appropriate serial follow-up exami-
nations and imaging studies that are quintessential to long-
term outcome studies. Furthermore, occult injuries without
radiographic evidence of fracture, which are often minimally
treated (if at all), may lead to subsequent deformity. These
“benign” injuries are often treated by individuals who may
have never seen, in their training or practice, a child with
growth impairment or arrest after a physeal fracture. The
likelihood of statistically reliable follow-up in this patient
cohort is probably even less than in children with an obvious
fracture.
Finally, infants with a high potential risk for growth de-
formity (i.e., those sustaining repetitive injury from child
abuse) are difficult to follow for extended periods because
of such factors as parental flight and the risk of early death
when the infant or toddler is inadvertently returned to the
abusive environment by unsuspecting health care personnel
(see Chapter 11).
Many authors have recognized that acute injuries to the
growth mechanisms may lead to chronic, late-appearing
growth discrepancies.1,16,51,59,62,63,67,77,87,105,152,153,156,157,159,164,167
Reinforcing the concept of Salter and Harris, Ecke stipulated
that growth arrest could follow only type 3 and 4 injuries and
that type 1 and 2 injuries were without consequence.65,190
However, a contrasting study of 162 epiphyseal fractures indi-
cated that the type 2 injury, which has long been considered
a “safe” injury, may be responsible for significant discrepancy
and distortion in bone growth.169 Recognizing that type 2
injuries involving the distal femur have led to significant
problems, Oh et al. emphasized that more common sites of
injury, such as the ankle and wrist, may also lead to this par-
ticular problem.169 It is interesting that there were no type
5 injuries in their series. My experience with type 1 and 2
injuries is similar, and many examples are shown in this
209
210
FIGURE 7-1. Medial growth arrest of distal tibia with an eccentric
Harris line. A bony bridge is not evident, but there is a poorly
defined (radiologically) injury to the distal fibular physis.
chapter and in the chapters to follow. The increased recog-
nition of such permanent or partial growth arrest has led to
the development of more comprehensive descriptions of
growth mechanism injuries.152,153,160
Basic Approaches to Growth
Mechanism Fractures
General Management Principles
All reductions, whether closed or open, should be per-
formed with the utmost gentleness to prevent further
damage to the physis. Forceful, usually painful manipula-
tions are to be avoided. Direct pressure on the physis by
instruments must also be avoided during open reduction.
Gentle reduction, however, does not guarantee that a physeal
arrest will not occur. Intrinsic cellular damage more likely
affects such an outcome. Microvascular disruption also plays
a significant role.
Type 1, 2, 3, 4, and 7 injuries consolidate rapidly, usually
in about half the time required for a fracture through the
diaphysis of the same bone. However, if significant amounts
of cartilage are present in type 3, 4, and 7 injuries, as typi-
fies the preadolescent child, healing may be delayed. The
child should be immobilized for at least 3–4 weeks, as frac-
ture callus is biologically plastic and may deform if early
activity is allowed. Children usually become asymptomatic
and are willing to use the injured part vigorously long before
sufficient chondro-osseous healing and remodeling have
occurred.
7. Management of Growth Mechanism Injuries and Arrest
It is important to realize that healing essentially is com-
prised of bone-to-bone union and remodeling. Any cartilage
gaps probably heal initially by formation of fibrocartilage,
rather than new hyaline cartilage. As chondro-osseous trans-
formation continues, “healing” of the cartilaginous com-
ponent of the fracture essentially occurs by osseous
replacement of the fibrocartilage as the secondary ossifica-
tion center enlarges and remodels.
Owing to the rapidity of initial repair, epiphyseal separa-
tions should be reduced as soon as possible because each day
of delay makes reduction progressively more difficult. In fact,
after 10 days, type 1 and 2 physeal injuries probably cannot
be manipulated without exerting undue force, which may
damage the cartilaginous growth plate further and disrupt
early callus. When a type 1 or 2 injury is seen late (i.e., after
7–10 days), it probably is best to accept the malunion, rather
than potentiate growth arrest by forceful manipulation or
open surgery. Any residual malunion may be corrected sub-
sequently by appropriate osteotomy. With type 3 or 4 physeal
injuries, restoration of the articular surfaces is also essential.
Delayed reduction should be considered, if only to restore
joint congruity.
Type 3, 4, and 7 injuries require anatomic reduction.
For types 1 and 2, anatomically perfect reduction, although
desirable, is not absolutely essential, as chondro-osseous
remodeling usually corrects mild to moderate residual
angular deformities (but not rotational deformities, which
must be corrected accurately). In general, one can accept a
greater degree of deformity in multiplane joints, such as the
shoulder, than in single-plane joints, such as the knee and
ankle.
Reduction of type 1 and 2 fractures usually can be attained
and maintained readily by closed means, although even
some of these fractures require open reduction. With type 3
fractures, open reduction is ordinarily indicated to restore
both congruous articular surfaces and acceptable apposition
of the fractured surfaces of the physis. Open reduction is
required for almost all type 4 fractures of the epiphyseal plate.
Caution must always be exercised during open reductions
to prevent injury to the circulation entering the epiphysis.
Excessive stripping of the already damaged periosteum and
perichondrium must be avoided. Only smooth Kirschner
wires should be used for internal fixation if they must cross the
growth plate. Threaded screws or wires should not be inserted across
the physis. Internal fixation devices should be removed as soon
as the fracture is clinically stable. Smooth percutaneous
devices can probably be removed within 3–6 weeks and may be
done readily in the office setting.
Alternative fixation devices are evolving. The use of
biodegradable smooth pins, instead of metallic pins, is
becoming increasingly applicable.28 Similarly, biodegradable
screws are now available and may be selectively used for
certain physeal fracture patterns. These materials are dis-
cussed in more detail in Chapter 4. Another method is fi-
brin glue osteosynthesis for selected epiphyseal injuries.99
However, this material is still pending U.S. Food and Drug
Administration (FDA) approval for use in children in the
United States, although it is being used and clinically
assessed in many other countries.
Fractures involving the physis must be followed closely for
the possible development of growth disturbance during the
Basic Approaches to Growth Mechanism Fractures
first 12–18 months after the injury, and then they should be
examined annually or biannually until skeletal maturity is
reached because many growth disturbances do not manifest
until the adolescent growth spurt, not unlike the “rapid”
onset of scoliosis. Parents must be warned of potential com-
plications, and the importance of long-term follow-up must
be stressed.
Specific Physeal Injuries
Type 1
In general, type 1 injuries are treated by gentle closed reduc-
tion. Although the use of drugs such as diazepam (Valium)
or midazolam (Versed) is relatively common in the emer-
gency room setting, they are basically an amnesic to any pain
generated by the reduction. Any relaxation effect may be
transiently negated during the acute reduction maneuver,
even when analgesic agents are also used. Accordingly, for
displacements of areas at significant risk for further physeal
damage (e.g., an anteriorly displaced distal femoral epiph-
ysis), a short-acting general anesthetic and muscle relaxant
should be considered (see Chapter 4). Internal fixation is
rarely necessary for isolated injuries. However, if the reduc-
tion is unstable or if multiple injuries are present, temporary
percutaneous stabilization with smooth K-wires or an external
fixator may be appropriate.
Type 2
Type 2 injuries are treated, in most cases, the same as type
1. Closed reduction using the metaphyseal fragment as a but-
tress is usually sufficient. However, unstable metaphyseal
comminution may lead to overall fracture instability and
so should be addressed by some type of stabilization with K-
wires, percutaneous screws, or external fixation devices.
Open reduction/internal fixation has limited application. If
the metaphyseal fragment is large enough, pins or screws
may be directed across the metaphysis.
Type 3
Type 3 injuries almost always require stabilization by some
fixation method. If the fragment appears undisplaced or
slightly displaced, it may be appropriate to perform a stress
test to assess potential instability. Percutaneous pinning is
often sufficient to stabilize the fragment. If mild displace-
ment is evident, as with a lateral condylar fracture or a
Tillaux fracture, the percutaneous pin may be partially
inserted into the fragment and then used to toggle the dis-
placed fragment into place. A second pin may then be
inserted while reduction is maintained with the first, after
which the first pin may be advanced or redirected. If desired,
cancellous cannulated screws of appropriate size may then
be placed over the pins, using them as guidewires. Alterna-
tively, the pins may be left protruding through the skin. They
should be bent to prevent migration. Whenever possible
these fixation devices are directed transversely from the dis-
placed epiphyseal fragment into the unfractured portion of
the epiphyseal ossification center.
If the fragment is unstable or displaced more than 2 mm,
an open reduction should be considered. A computed
211
tomography (CT) scan may be helpful for defining the
amount of widening of the fracture, which may be hinged
such that only the smallest portion of the fracture gap is
evident on the radiograph. If open reduction is undertaken,
intact soft tissues should be left attached, whenever possible,
to the metaphyseal fragment, as they may contain important
epiphyseal arteries. Once reduced, the fixation method is
usually either pins or cancellous screws directed in a trans-
verse manner across the epiphysis. Cancellous screws are
recommended for any transepiphyseal fixation, as there is
no significant cortical bone to anchor the screw. The outer
portion of the epiphyseal ossification center is a relatively
thin shell. With lateral condyle fractures of the distal
humerus there may be no secondary bone in the uninvolved
trochlear epiphysis. A transversely directed pin within the
firm cartilage can maintain reduction. A postinsertion radio-
graph of such placement may not look “correct,” as the pin
is in radiolucent cartilage.
If there is physeal comminution along the fracture
propagation line or at the two exit points at the zone of
Ranvier, consider placing a small amount of fat in the
defect in an attempt to prevent posttraumatic bridging. I
have done it in a number of patients with distal femoral
and distal tibial injuries. None has “developed bridging
(maximum follow-up 11 years), but it is impossible to
say whether any of these patients would have otherwise
formed a focal growth arrest. The procedure is easy, adds
little operating time, and is unlikely to have any adverse
effect on fracture healing.
Type 4
Type 4 injuries are approached by the same basic guidelines
as type 3 injuries. Undisplaced fractures are fixed percuta-
neously with pins or cancellous screws directed transversely
across the epiphysis. If the metaphyseal fragment is large
enough, fixation is also directed transversely across the me-
taphysis. Although the ideal direction is from the metaphy-
seal fragment into the uninjured portion, alternative routes
are possible. Particularly with a triplane fracture with a pos-
terior metaphyseal component, the screw may be inserted
through the nonfractured anterior portion followed by inser-
tion into the displaced posterior fragment. In contrast to epi-
physeal fixation with cancellous screws, metaphyseal fixation
may utilize cortical screws if the cortex is sufficiently thick.
These screws allow, in appropriate circumstances, a lag-screw
insertion that helps reduce the fracture.
Displaced or rotated fragments require open reduction
and stabilization. Again, soft tissue attachments should be
left as undisturbed as possible.
For many medial malleolar fractures I routinely remove
any small metaphyseal fragment, leaving the adjacent physis
undisturbed, and insert a fat graft. There is no attempt to
repair the periosteum in this region.
Type 5
By definition, type 5 injuries cannot be diagnosed routinely
in the acute phase. Compression across a physis results in
reduction of the height of the proliferative and hypertrophic
zones and a decrease in the number of proliferating chon-
212 7. Management of Growth Mechanism Injuries and Arrest

drocytes.4 Any vascular disruption within the epiphysis

cannot, by current technology, be restored. Accordingly,
treatment is directed at symptoms (especially pain) or
physical findings (edema, swelling) using external immo-
bilization, based on a presumptive diagnosis of physeal
injury. Magnetic resonance imaging (MRI) may be useful for
delineating bone bruising within epiphyseal or metaphyseal
trabecular bone or diagnosing a type 1–4 occult injury
not readily discernible on the routine radiograph (see
Chapter 5).

Type 6
Type 6 injuries frequently comprise complete soft tissue loss
or an avulsed (undermined) flap extending down to the
zone of Ranvier. They require meticulous débridement. The
periosteum should not be reattached, as it may enhance
peripheral bridging.

Type 7
Type 7 injuries are located intraepiphyseally. They also are
usually intraarticular. Reduction is directed at restoring artic-
ular disruption. Smooth K-wires or biodegradable pins may
be used, especially when the fracture fragments have a large
amount of cartilage.
Altered Physeal Growth
Any growth mechanism injury carries with it the risk of alter-
ing the expected contributions to latitudinal and longitudi-
nal growth that would otherwise have been made by the
injured region. These alterations of growth are difficult to
predict acutely or during the first 2–3 months after the injury
because the normal response to childhood skeletal injury is
a slowdown or cessation of longitudinal growth (increased
period of status). It typically leads to the formation of trans-
versely thickened bone, the Harris line.154 Only when suffi-
cient longitudinal growth resumes does disruption become
evident. As time progresses, any adverse effects on growth
patterns, whether minimal or extremely obvious, become
increasingly evident.
Natural Bridging
In many animals the metacarpals or metatarsals have fused
to create a composite bone. Interestingly, the ontogenetically
fused physes retain a certain amount of anatomic indepen-
dence. Figure 7-2 shows a typical situation in which a central
region of the physis is replaced by an extension of the epiph-
yseal bone proximally into a region of centralized cortical
bone. This dense cortical bone extends to the germinal zone
of the physis but does not extend into the epiphyseal ossifi-
cation center. Histologically, this “composite” growth plate
shows no signs of impaired growth.
Growth Slowdown
When physeal damage is sufficient, the result may be per-
manent slowing of the normal rate of longitudinal growth.
FIGURE 7-2. Bone bridge formation is not necessarily detrimental
to growth. Central bone bridging is evident in this skeletally imma-
ture flamingo, but dynamic growth forces of the physes have
allowed continued growth. This bone embryologically is a “fusion”
of two metatarsals. Differences in the density of metaphyseal and
epiphyseal trabecular bone may be an integral factor in this lack
of disruptive transphyseal bridging.
This is not the complete arrest of growth that is usually asso-
ciated with premature epiphysiodesis but, rather, is impaired
cell formation in an “unhealthy” physis. Several studies of
distal femoral physeal injuries have demonstrated a relatively
high incidence of a decreased rate of growth without com-
plete growth arrest or angulation. It becomes evident as
increasing leg length inequality.
Growth Acceleration
Growth acceleration poses the opposite problem: elongation
of the injured extremity. The mechanisms are probably vas-
cular and periosteal. The response to a fracture is usually
hyperemia, and this increased flow to the injured tissues
may affect all the physes in the limb, not just those of the
fractured bone. The normal tension in the periosteal sleeve
has some control of the rate of longitudinal growth
(see Chapter 1). When it is circumferentially disrupted, the
associated physes may temporarily lose their biologic
restraining qualities.
The likelihood of overgrowth is used frequently as a
concept when treating femoral diaphyseal fractures by closed
reduction. The amount of anticipated “overgrowth” is about
1 cm, but this figure is not absolute. Every effort should
be made to minimize the extent of overriding in bayonet
fracture fragment apposition. Acute deformity of more
than 1 cm of shortening is unlikely to correct in the long
Altered Physeal Growth
FIGURE 7-3. Severe damage of the lateral side of the distal fibula
following a lawn mower injury. It is a type 6 growth mechanism
injury. Despite the apparent radiologic growth arrest (arrow), the
fibula has still continued to grow in pace with the tibia. Such equiv-
alent growth strongly suggests a bony block has not formed.
term and, accordingly, should be reduced acutely (see
Chapter 21).
Another area of anticipated overgrowth involves the prox-
imal tibial metaphysis.166 Fractures in this area, which often
are incomplete, appear clinically innocuous. Especially in 3-
to 10-year-olds, the probability of progressive posttraumatic
valgus is high. The parents must be warned. The change
occurs because of a selective overgrowth that involves the
medial side of the proximal tibial physis.163 This phenome-
non is discussed in more detail in Chapter 23.
FIGURE 7-4. (A) Apparent growth arrest of
the distal tibia. (B) The mortise view shows
a slowdown of growth in the area of the
medial malleolus but without a bony bridge. The
Harris line, interestingly, is divergent from the
underlying physis. A
213
Nonbridging
Some physeal injuries appear destined for growth arrest.
Routine follow-up films seemingly show that growth arrest
and bridging have indeed occurred. However, what appears
to be definite damage may be refrained from forming an
osseous bridge by intervening fibrous tissue (Fig. 7-3).
Oblique views or CT scans may demonstrate this lack of
osseous bridging (Fig. 7-4). However, as is discussed subse-
quently, the fibrous interface may not prevent subsequent
bridging as chondro-osseous maturation continues. These
patients still must be followed closely until growth has
ceased.
Nondisruptive Bridging
As discussed in Chapters 1 and 6, biologic growth forces
within the physis are significant. It is feasible that small
bridges may form and repetitively be pulled apart naturally,
similar to the surgical method of distraction epiphysiolysis to
pull a large bony bridge away from the more normal me-
taphyseal or epiphyseal trabecular bone.
The biological forces of growth within the physis, espe-
cially during the growth spurts (saltation) are immense.144 As
such, limited areas of physeal damage may become evident
as small transphyseal osseous bridges, but they do not
necessarily lead to significant overall growth disruption
(Fig. 7-5). In other instances growth may be slowed or may
not be disrupted until later.
The effect of such microbridging is to leave a trail in the
metaphysis (Fig. 7-6). As the microbridge is continuously
formed and broken in a repetitious cycle, a linear (longitu-
dinal) streak is left behind in the metaphysis. It shows up as
a dense line of longitudinally oriented sclerotic bone in the
radiograph or MRI scan. As with Harris lines, remodeling
and removal of such sclerotic bone is a slow process.
Such microbridging is commonly found in the distal
radius and ulna (Fig. 7-7). It most likely is the result of
minimal trauma sustained when a child breaks a fall with a
dorsiflexed hand. They have been referred to as longitudi-
B
 214
A B
FIGURE 7-5. (A) Acute fracture of the distal tibia and fibula in a 4-
year-old. Both injuries are type 2 growth mechanism fractures with
a posterior metaphyseal fragment (arrows). (B) Fourteen months
later the distal fibula appears to have complete growth arrest,
nal ossific striations in the radiologic literature.158 Histologi-
cally, these striations are comprised of extensions of metaph-
yseal bone into the growth plate. They are often associated
with finite areas of damaged microvascularity.
Bridge Formation
Although most physeal injuries are free of serious acute and
chronic complications, partial or total growth arrest may sub-
sequently occur. Partial physeal arrest is particularly apt to
produce progressive angular deformation when a discrete
bridge of sclerotic bone forms eccentrically between the
epiphyseal ossification center and the metaphyseal bone,
A B
7. Management of Growth Mechanism Injuries and Arrest
whereas the distal tibia appears intact but not normal. Two
“peaked” metaphyseal irregularities are evident (arrows). A Harris
line is parallel to the physis, indicating appropriate longitudinal
growth.
replacing a segment of the physis and zone of Ranvier. The
partial physeal arrest variably retards efforts at continued
normal physeal growth. So long as the remaining physis
grows, an angular, longitudinal, or latitudinal deformity may
occur, alone or in any combination. When growth arrest is
complete and rapid in development, the primary deformity
is longitudinal growth impairment, with minimal (if any)
angular deformity.
The type 3, 4, and 6 growth mechanism injuries, which
disrupt the metaphysis, physis, and epiphysis, have the great-
est potential to form an osseous bridge and may certainly do
so if anatomic, usually open reduction is not undertaken.
However, even with accurate anatomic reduction, a partial
FIGURE 7-6. (A) This boy had a defined
injury to the physis 5 years previously. A
small bone bridge has formed (white arrow)
but has been continually disrupted by
biologic growth forces, forming a linear
streak of sclerotic bone within the me-
taphysis (black arrows). (B) MRI of
a similar case (arrow). There is also a more
recent acute injury causing a bone bruise.
Altered Physeal Growth
A B
FIGURE 7-7. (A) Longitudinal ossific striations (arrow) in the physis
and metaphysis. The child had a history of previous wrist/forearm
trauma in addition to the recent trauma causing the torus injury. (B)
physeal arrest may still develop owing to microscopic physeal
fragmentation. I have stressed the risk of partial physeal
arrest even in types 1 and 2 physeal injuries (see Chapter 6),
in contrast to the belief of Salter and Harris that these two,
the most common physeal injury patterns, were essentially
free of such complications.
Anatomic differences between the various physes are
important risk factors increasing the likelihood that a
physeal bridge will occur. The size (area), rate of growth,
and contour of each physis change as the growing skeleton
progressively matures. Although the proximal radius is the
most frequently injured physis, it is usually described as
being an uncommon site for a partial physeal arrest.31,112,127
One study cited a 10% incidence of physeal growth damage
after a distal radial physeal fracture.169 In contrast, injuries
to the proximal tibia and distal femur represent only 3%
of physeal injuries, but these areas are among the most
frequent sites of partial or complete physeal damage. These
particular physes are large in area and irregular in contour,
and they account for at least 60–70% of the growth of
the lower limb and the specific bones. They are also fre-
quently the site of relatively violent injury mechanisms.
Accordingly, damage to one of these growth plates in a young
child may have a profound effect on subsequent longitudi-
nal development.
Although some osseous bridging is suggested within a few
weeks following the injury, it usually does not become
evident radiologically until months to years after the injury, a
factor that underscores the need for radiographic monitor-
ing of any physeal injury for an adequate period of time after
the injury, if not until skeletal maturity. If the damage occurs
when the epiphyseal ossification center is small, an osseous
bridge may not form until the epiphyseal center expands
sufficiently to juxtapose the damaged physeal area. For
example, there may be peripheral, step-like retardation of
metaphyseal cortical bone filled with relatively resilient scar
215
Slab section of a distal ulna shows these longitudinal ossification
patterns (arrow).
tissue (Fig. 7-4). After several years the epiphyseal ossifica-
tion center eventually expands to reach this peripheral
damaged area (Figs. 7-8, 7-9). Then a bridge may form, at
which time angular deformity may rapidly progress.
The size and location of the physeal bridge eventually
determine the extent of any clinical and radiologic defor-
mity. When the partial physeal arrest is located peripherally,
the remainder of the physis usually continues to grow, pro-
ducing a progressive angular deformity. Some longitudinal
deformity also usually occurs. When the partial physeal
arrest is central, the intact periphery continues to grow and
causes a conical “tenting” of the metaphysis, combined with
more extensive shortening of the bone and often with rela-
tively little angular deformity.
The appropriate length of follow-up is highly subjective.
For the lower extremity, 2 years of follow-up is likely to
detect even slowly developing problems. For the upper
extremity, where physeal deformity is less frequent, follow-up
of 1 year can probably detect most potentially significant lesions.
Ideally, the injured physis and patient should be followed
until physiologic epiphysiodesis commences in that physis
and the contralateral one. Premature onset of epiphysiode-
sis may also be a sequel of any physeal injury, as it commonly
occurs following limb lengthening by chondrodiastasis. Pre-
mature epiphysiodesis also typifies the resumption of physeal
growth after resection of an osseous bridge. Accordingly,
evaluation of the opposite side is essential to assess these pos-
sibilities, especially in the legs, where differential growth ces-
sation may create a functionally significant leg length
discrepancy.
Unless the patient has been followed sequentially after a
physeal injury, osseous bridging may not be evident until
there is a clinically obvious angular deformity or shortening
of the involved extremity. The earlier the diagnosis is made,
the sooner surgery (e.g., bridge resection) can be contem-
plated or attempted and the less likely it is that there will be
216
FIGURE 7-8. (A) Early fibrovascular (FV) response bridging the
region between metaphyseal bone and epiphyseal (E) cartilage.
This region is filled with small vessels that cross a region of the
physis normally not traversed by blood vessels. As the child grows,
this communication may gradually ossify and create an osseous
bridge between the epiphyseal ossification center and the me-
taphyseal bone. (B) Nine-year-old boy who had sustained a type
6 power lawn mower injury to the medial femur 2 years before this
a need for concomitant correction of angular deformity. The
younger the patient at the time of the physeal injury, the
more likely it is that a partial physeal arrest will lead to a sig-
nificant clinical problem.
FIGURE 7-9. This 5-year-old boy lost part of the distal femur in a
lawn mower accident. Extensive fibrous tissue has formed, but only
a minimum bone bridge formed (arrow). Most of the valgus defor-
mity was due to a lateral shift of the tibia. He probably will develop
a larger bridge and more deformity with time and growth.
7. Management of Growth Mechanism Injuries and Arrest
film. The epiphyseal ossification center is beginning to extend
toward the metaphysis (arrow), which is also deformed and sug-
gestive of early osteochondroma formation. (C) One year later a
distinct bridge has formed (arrow). Presumably, fibrovascular
tissue formed as the initial reparative response. Subsequently, it
ossified to finally lead to a solid bridge between the epiphysis and
the metaphysis.
Experimental Bridging
Drilling through the growth cartilage with small drills does
not result in permanent growth arrest.151 Similarly, curettage
of up to approximately 10% of the growth cartilage area
seldom leads to arrested growth. On the other hand, epiph-
ysiolysis and epiphysiolysis plus curettage of the cartilage
cause permanent osseous bridging in almost three-fourths of
the animals in which the procedure is combined with drilling
through the basement subchondral plate of the epiphyseal
ossification center. Excision of the periosteum and peri-
chondrium combined with epiphysiolysis and curetting did
not alter the course of growth significantly. Furthermore,
resection of minor bone bridges only worsened the growth
disturbance. Resection of the metaphysis experimentally
produced injuries to the growth plate that resulted in some-
what (but not significantly) improved growth compared to
that in the control leg, which was subjected to the same
injury but without subsequent metaphyseal resection. Nor-
dentoft thought that metaphyseal resection was unjustified
on the basis of experiments,151 in contradistinction to the
work of Langenskiöld.123
Experimental studies have explored the pathophysiology
of osseous bridge formation after growth plate injury.227
Others have demonstrated the effects of longitudinal,
transepiphyseal types of injury. Researchers have docu-
mented that more extensive injuries are more likely to
develop substantial bridging. Growth may occur after bridg-
ing of the epiphysis by bone graft if the osseous bridge is
central rather than peripheral.143 The tension of growth may
cause continuing microfracture of such osseous bridges and
thereby permit longitudinal advancement.
Altered Physeal Growth
The epiphyseal blood supply is probably the most impor-
tant determinant in the eventual development of the bone
bridges. Nordentoft showed experimentally that the ten-
dency for an epiphyseal bone bridge to develop is increased
if the blood supply from the metaphysis is also disrupted by
a partial, transverse section of the metaphysis.151
Aziz and Dhem produced acute physeal ischemia in the
skeletally immature dog.19 There was a loss of cellular pattern
and production of a myofibril-like material within the physis.
They thought it was a reflection of muscle and cartilage dif-
ferentiation from a homogeneous mesodermal cell popula-
tion, with the final expression of cell differentiation being
affected by several microenvironmental factors. Whether
such changes also occur in damaged human physes remains
to be seen. Once a physeal cell dedifferentiates, it may not
be capable of reverting to a normal physiologic state after
release of the partial physeal arrest.
Histopathology
Although the magnitude of the partial physeal arrest often
seems obvious on diagnostic imaging modalities, the true
extent of microscopic damage is not as easy to gauge.
However, knowledge of this additional cellular damage may
be important when assessing the potential for recovery of
growth after any attempt at surgical resection of the osseous
bridge. From observation of amputation and surgical speci-
mens, I have noted that abnormal physeal tissue has a
grayish, translucent appearance, whereas the normal physis
is usually opaque white. Microscopically, the nonwhite por-
tions of the physis may not exhibit normal columnar histol-
ogy. The extent of microscopic physeal damage in cases not
involving fracture, especially following infection, seems to
be much greater. Accordingly, one should not be optimistic
with parents that normal growth will resume, especially
in association with bridge resections involving cases with
nontraumatic causes. New MRI techniques (e.g., fat-
suppressed three-dimensional spoiled-gradient-recalled
MRI, or SPGR) may allow differentiation of such injury
extent (see Chapters 5, 6).
Obviously, the more severe the etiology, the greater the
potential for large areas of the physis to be involved in the
damage. A fracture is likely to limit physeal damage to
the actual cleavage plane. However, if the fracture also tran-
sects a significant intraepiphyseal vessel, more diffuse
damage may result. Partial physeal arrest after ischemia or
infection produces obvious bridging in areas of major physeal
damage but also less noticeable areas of microscopic damage
without bridge formation. Accordingly, recovery potential is
limited after resection of the obvious osseous bridge.
As discussed in Chapter 6, segments of the entire thick-
ness of the physis, including the germinal zone, may
be included with the metaphyseal side of the fracture
(the “wrong side” physeal fracture). This separates the
germinal region from its epiphyseal blood supply and thus
has a high risk of permanent ischemic damage and growth
arrest.
The histopathology of bridge formation has been des-
cribed only in animal experiments, with virtually no infor-
mation available concerning the changes in the more
slowly maturing human. The unique opportunity for me and
217
coworkers to assess spontaneously occurring bridging in
large zoo animals and human specimens during amputation
revision surgery has allowed a better understanding of the
process.162,163,165
The basic damage mechanism is probably a combination
of cellular disruption and vascular ischemia. This condition
leads to the damaged physeal segment or segments being
“left behind” while the rest of the physis continues to grow
longitudinally and latitudinally (Fig. 7-10).
The cartilage that is “left behind” may be quite elongated.
The cartilage within the metaphyseal extension loses cellu-
lar organization and gradually fragments as chondro-osseous
replacement slowly occurs. The extensions and fragmenta-
tions may be readily evident in MRI studies. Whether these
pathophysiologic physeal extensions usually form osseous
bridges is currently unknown but is certainly suggested in
Figure 7-11.
The initial changes that occur in a segment of disrupted
physis probably involve the formation of fibrous tissue that
may be relatively avascular. This fibrous bridging may
become permanent, adversely affecting subsequent overall
morphology but not forming a bony bridge (Fig. 7-12).
In other situations the fibrous tissue develops vasculariza-
tion (Fig. 7-13). The cartilage along these transphyseal
vessels undergoes calcification, which is a necessary prelude
to the eventual chondro-osseous transformation that leads to
early bony bridging (Fig. 7-14). Microscopically evident
osseous extensions then develop from both the epiphyseal
and metaphyseal sides (Fig. 7-15).
Small trabeculae form and begin to bridge the physis.
They may be present as extensions from either the secondary
ossification center (if present in the area) or the metaphysis.
In some cases, especially at the periphery, the cell columns
disappear, with the remaining cells forming random clumps
(Fig. 7-16). When the maturation process continues, the
bridge enlarges, becomes sclerotic, and causes angulation,
shortening, or both (Figs. 7-17 to 7-19).
Type of Bridge Formation
There are three basic patterns of partial physeal arrest:
peripheral, linear, and central. They affect normal growth
differently, create different patterns detectable by diagnos-
tic imaging, and are approached surgically by different
techniques.
Peripheral (Type 1)
The type 1 pattern involves a bridge of variable size along
the margin of the physis (Fig. 7-20). The bridge may extend
only a few millimeters in from the periphery. The zone of
Ranvier, a specialized group of cells necessary for progres-
sive latitudinal growth of the physis, is damaged and over-
grown with periosteum, rather than perichondrium. This
tissue (periosteum) extends farther toward the epiphysis
than normally, plays a role in latitudinal thickening of the
bone bridge, and must be completely excised rather than
replaced, during surgical removal of the area of partial
physeal arrest. This type of osseous bridge may create
angular deformation over a short period, especially in a
major growth contributor such as the proximal humerus or
218 7. Management of Growth Mechanism Injuries and Arrest

A B

C D
FIGURE 7-10. (A) Specimen of a proximal tibia showing elongated metaphyseal vessels to ossify. (B) Transverse section of the unos-
extension of physeal cartilage (arrow) into the metaphysis. It is sified cartilage surrounded by a ring of metaphyseal bone. (C, D)
probably due to ischemic change that altered cartilage maturation. Coronal and transverse MRI views of these physeal extensions
Lacking the ability to calcify, this tissue could not be invaded by (arrows).

distal femur (Fig. 7-21). These peripheral bridges may be
associated with an osteochondroma-like formation.
Linear (Type 2)
With the linear pattern the osseous bridge extends as a linear
structure across the physis, connecting and involving two
separate segments of the periphery of the physis (Figs. 7-22,
7-23). The most common site is the medial malleolus, where
the linear bone block extends anteriorly to posteriorly.
There is normal physeal tissue on either side of the defect,
including the periphery. This pattern is often associated with
significant angular deformity.
Central (Type 3)
The central injury tends to be the most severe type and the
most difficult to correct with surgery (Fig. 7-24). An osseous
bridge of variable size forms within the central portion of the
physis and is completely surrounded by normal physis. The
Epiphyseal Regeneration
FIGURE 7-11. Deformed proximal tibia (previous below-knee ampu-
tation converted to a knee disarticulation). A high power view
shows an eccentric extension of the epiphyseal ossification center
that is on the verge of fusing with the metaphyseal bone to form a
bridge. Note the thick sclerotic nature of this bone compared to the
epiphyseal and metaphyseal bone. This osseous density helps
delineate the abnormal bone that needs to be removed during a
bridge resection.
peripheral zone of Ranvier is usually not involved and con-
tinues to grow latitudinally, adding new growth plate capable
of central longitudinal growth (Figs. 7-25, 7-26). Accordingly,
the major effect is retardation of longitudinal growth,
while the uninvolved periphery continues to grow latitudi-
nally, creating new physeal cells that attempt to grow longi-
tudinally but are partially restrained by the bridge.
Radiographically, these lesions are characterized by a conical
extension of the epiphyseal ossification center into the
central metaphysis.
With all three types it is important to appreciate that the
osseous bridge is usually composed of dense, sclerotic bone
similar to cortical bone. This quality of the osseous bridge is
most evident at the time of surgery, when it obviously con-
trasts with the adjacent trabecular (spongy) bone of the
metaphysis and secondary ossification center. This qualita-
tive difference assists in determining whether adequate
abnormal bone has been removed.
Angular Deformity
Angular deformity of growing long bones, whether acquired
as a growth variation, a consequence of a pathologic process
(e.g., rickets), or a secondary result of trauma, has been long
recognized in clinical practice.1 However, the basic mecha-
219
nism of the process of correction and the factors influenc-
ing it are not completely known. It is generally accepted that
straightening of a deformity caused by a malunited fracture
is due mainly to variable apposition and resorption at the
fracture site (Wolff’s law), as well as progressive realignment
of the physis (Heuter-Volkmann’s law).
Normally, chondro-osseous tissues are exposed to the
action of the muscles that attach into the periosteum along
the diaphysis and metaphysis and may thereby affect the
intrinsic tension of the periosteal sleeve, which, in turn, may
affect the physes. In the growing child, these combined mus-
cular periosteal forces seem capable of modifying the growth
pattern. Furthermore, changes in the tension in different
regions of the periosteum may also contribute to increased
growth in one portion of the physis. Extremely mild forces
may inhibit or modify epiphyseal growth. Experimentally
increased pressure on the end of the bone modifies the
direction of growth of an epiphysis and physis. Pressure
acting obliquely on the epiphysis and physis deflects the
normal direction of growth.175
A number of factors contribute to the remodeling process
of a long bone. One major factor seems to be local remod-
eling by asymmetric latitudinal growth and changes in the
processes of resorption and apposition within the metaph-
ysis or diaphysis.
The growth plate responds eccentrically to changes in
pressure and through selective growth in different regions
attempts to reorient itself perpendicular to the major joint
reaction forces going across the physis (Fig. 7-27). This char-
acteristic of the growth plate explains the gradual correction
of some deformities, both those in the plane of motion of
the joint axis and those at right angles to it, such as varus or
valgus deformities. Certainly, with fractures around the knee
and particularly with those in the tibia, there is some mild
correction of varus and valgus deformation, which is not
seen in fractures around the elbow. In part, this variation
reflects the relative rates of growth and the relatively small
contribution to longitudinal growth made by the upper
extremities in the region of the elbow compared with the sig-
nificant portion of longitudinal growth of the lower extrem-
ity that occurs around the knee.
The distal and proximal fragments should be accurately
aligned, whether dealing with diaphyseal, metaphyseal, or
epiphyseal injuries. Although 30° is generally the defined
maximum angle for acute deformity, correction depends on
anticipated, and often unpredictable, subsequent growth
and distance of the angular deformity from the nearest
physis.175 From a pragmatic standpoint epiphyseal–physeal
fractures should be reduced as accurately as possible, including
correction of both angular and rotational malalignments.
Rotational malalignment, in contrast to angulation, does not
usually correct itself.
Epiphyseal Regeneration
Cellular epiphyseal components in small mammals (e.g.,
the rat) may partially regenerate following incomplete
and complete physeal–epiphyseal resection. However, the
extent of regeneration is unpredictable and never equal
to the amount of growth that takes place in the original
 220
epiphyseal–physeal unit. In large-boned, slow-maturing
animals, including humans, regeneration of the physis, for
practical purposes, is limited. The physeal cartilage adjacent
to an injury cleft tends to lose columnar orientation and
form rounded, clone-like structures, which introduce ran-
domness to growth. Fibrocartilage, undifferentiated hyaline
cartilage, and bone fill in the physeal defect.
7. Management of Growth Mechanism Injuries and Arrest
FIGURE 7-12. (A) Radiography of a resected proximal
radius 4 years after an injury in which “no fracture was
evident.” (B) Histologic section. Obviously a type 4 injury
had occurred, was not recognized at the time, and went
on to form a relative union in the displaced position. Ossi-
fication subsequently occurred in the epiphyseal frag-
ment. A bony bridge never formed, but significant
deformity developed. This may represent the tissue
pathology shown in Figure 7-4, where an osseous bridg-
ing growth arrest did not occur or had not yet developed.
Diagnostic Imaging
Planar films are useful initial imaging procedures for deter-
mining the probable or actual presence of an osseous bridge.
However, such conventional methods may not clearly define
the abnormality or its severity, as radiographs of irregular
FIGURE 7-13. Early fibrovascular bridging of a physeal
fracture gap.
Diagnostic Imaging
FIGURE 7-14. Histologic section showing a transphyseal vascular
communication after physeal injury. Darker staining cartilage along
the course of the vessels represents calcified cartilage capable of
undergoing chondro-osseous transformation that would lead to for-
mation of a bony bridge.
contours or views oblique to some or all of the physis may
be misleading.
Because the various causes of partial physeal damage,
including trauma, produce temporary slowdown of longitu-
dinal growth, followed by restoration of more rapid growth,
Harris lines are often evident. If the Harris growth slowdown
line is parallel to the physis, growth damage is unlikely.
However, if the physis and the Harris line converge, damage
is undoubtedly present.
Tomograms may be used to determine the configuration
and extent of the osseous bridge and the area of the remain-
ing normal physis. Tomography depends on the path the
x-ray beam takes relative to the imaged object. The farther
the beam moves, the more blurred the surrounding tissues
become and the more focused the beams are on the target
area. For evaluation of the variably contoured plane of the
physis, hypocycloidal tomograms are an accurate method for
“mapping” the bridge. This approach aids in determining
whether the bridge is resectable and in choosing the appro-
priate surgical approach. Hypocycloidal tomography is much
less available than linear tomography, which may lead to mis-
taken estimates of bridge size.
Scintigraphy has been proposed as an aid in evaluating the
physis after bridge formation. Hartke and colleagues have
successfully used quantitative scintigraphy to document
decreased activity in the region of a partial physeal arrest,
followed by a more normal uptake of radionuclide after
221
FIGURE 7-15. Sclerotic bone bridge transversing the physis.
The adjacent physeal cartilage is more deeply stained, indicating
calcification. Growth plate irregularity and clone formation are
evident.
bridge resection.98 Further investigation is necessary before
this method can become useful clinically. Howman-Giles et
al. particularly assessed the use of an apex view during the
bone scan.104 Neither special scanning system is readily avail-
able clinically. Single-photon emission computed tomogra-
phy (SPECT) has also been used to map the area of physeal
dysfunction accurately (i.e., the area arrested by a bony
bridge).224
Computed tomographic scanning may be useful for assess-
ing growth plate injuries, especially for defining the cross-
sectional representation of central physeal arrest,58,183,211,228
but it does not have a place in the routine screening evalua-
tion of partial growth plate arrest. CT may also define the
extent of coronal or sagittal arrest lines, which may prove dif-
ficult to visualize by conventional means. Physeal tethering
may be recognized on CT by obliteration of the low-density
physis by bone bridges.
Computed tomography is of limited use because the tomo-
graphic cut must be directly through the physis and bridge,
which may be difficult given the normal three-dimensional
contours of many physes (such as the distal femur) and the
further alteration of contours by linear or peripheral
bridges. The utilization of 1- to 2-mm cuts through the
involved area, with dimensional reformatting of sagittal and
coronal segments (at 5-mm intervals) may delineate the
bridge adequately. CT scans may be modified by off-coronal
imaging, positioning the patients in degrees of joint flexion
 222 7. Management of Growth Mechanism Injuries and Arrest

FIGURE 7-16. Resected specimen in a child with

osseous bridging after physeal fracture. The osseous
bridge is indicated by the black arrows. The cells have
lost their normal columnar orientation and have formed
clones surrounded by increased amounts of matrix. A
rudimentary cell column is evident at the left (open
arrow).

FIGURE 7-17. (A) Maturing bony bridge (arrow) with dis-

organized (dysfunctional) physis. (B) Dense sclerotic
bone bridge along with a fibrovascular gap extending into
the metaphysis. The physis of the right has lost cellular
B integrity.
Diagnostic Imaging
FIGURE 7-18. Anterior osseous bridge (black arrow) caused the
proximal tibia to rotate 90°. The open arrow shows damaged artic-
ular surface.
or rotation that maximimally place the angulated physeal
plane co-planar with the CT scanner.148
Osseous bridges may be assessed with magnetic resonance
imaging.100 This technique demarcates the dense, sclerotic
bone of the partial physeal arrest quite effectively.100 This
method awaits technologic refinements that allow thinner
cuts in both coronal and sagittal planes, as well as subsequent
three-dimensional, computer-assisted reconstruction and
definition of echo sequences that best define physeal tissue,
such as Gradient Recalled Acquisition in the Steady State
(GRASS) or fat-suppressed or short-T1 inversion recovery
(STIR).
Peterson et al. described a method of three-dimensional
MRI mapping and computerized enhancement to do a
FIGURE 7-20. Peripheral osseous bridging.
223
FIGURE 7-19. Result of a type 4 injury to the proximal tibia leading
to a varus deformity and formation of an osseous bridge between
the epiphyseal ossification center and the metaphysis. The physis
lateral to the bridge is relatively normal, whereas the epiphysis
medial to the bridge has failed to ossify or form normal physeal
cytoarchitecture.
detailed assessment of the physeal bridge, its specific mor-
phology, and the extent of area involvement.27,77 The tech-
nique relies on volume-rendering (voxels) rather than
area-rendering (pixels).
Jaramillo et al. studied formation of a transphyseal bony
bridge in rabbits with MRI.112 Gadolinium enhancement
indicated the development of vascularity across the physis,
which preceded the formation of a discrete bony bridge. They
thought that early bony bridging could be detected by MRI.
Whether this same process of rapid bridging occurs in the
more slowly maturing physis of the human is uncertain but
is well worth studying in selected physeal injuries, especially
with gadolinium enhancement.
Lengths of the involved and the uninvolved extremities
should be documented radiographically. Scanograms allow
the distance to be measured directly on the film and may be
compared in chronobiologic studies necessary to determine
the most appropriate method of limb length equalization.
Bone (skeletal) age indicates the remaining growth poten-
tial. At least 1 year (preferably 2 years) should exist between
 224 7. Management of Growth Mechanism Injuries and Arrest

FIGURE 7-21. (A) Medial growth arrest of the distal tibia. (B) Growth damage and a
Harris line of the right tibia. Note the Harris line and amount of growth on the left side
C since the trauma. (C) Lateral MRI of the growth arrest with eccentric Harris lines.

contemplated bridge resection surgery and anticipated Physeal Mapping

skeletal maturity. This rule is complicated by the observation
that, even after apparently successful resection and restora-
tion of growth, the damaged physis “closes” prior to the con-
tralateral, uninjured one. A roentgenogram of the hand is
most commonly used. However, because most significant
osseous bridges occur in the distal femur and proximal tibia,
an aging method using the knee (e.g., Tanner Whitehouse
methodology) may be more applicable.
Excision of osseous bridges constituting 50% or more of the
entire area of the physis usually gives poor results. However,
if the bridge does not increase in size during a period of
growth, resection may become feasible when coronal and
sagittal (peripheral) enlargement of the area of the normal
physis decreases the relative size (area) of the bridge.

FIGURE 7-22. Patterns of linear osseous bridging.

Physeal Mapping 225

A B
FIGURE 7-23. (A) MRI of a linear bone bridge of distal tibia. (B) Specimen showing linear bone bridge of the distal femur.

FIGURE 7-24. Patterns of central osseous bridging.

FIGURE 7-25. (A) Lateral view of anterior

tibial damage causing recurvatum deformity.
(B) MRI shows two areas of bridging
damage: a central bony bridge (curved
arrow) and an area of the tuberosity (straight
arrow). A B
226
FIGURE 7-26. Central bridging of the distal fibula and tibia.
Accordingly, mapping the physeal bridge becomes an
important part of preoperative planning.24,44 The two-
dimensional area of several physes may be roughly obtained
with the mapping method set forth by Carlson and Wenger.44
With use of the tomographic results, the bridge is “blocked
in” to this physeal contour outline. The bridge area/physeal
area ratio is then estimated. Only bridges occupying less than
50% of the estimated area should usually be considered for
resection.
Surgery
There have been numerous animal experiments in which
physeal bridging has been caused, prevented, or resected.
Although the results have varied, these data suggest that
bridge formation may be clinically alleviated when appropri-
ate cases are chosen for surgery.
Successful bridge resection in a human was first reported
in 1967 by Langenskiöld.123 It involved excision of an osseous
bridge in the proximal tibia. The resection space was filled
with autogenous fat. Over the next year and a half there was
a 10° improvement in the angle of the genu recurvatum, but
there was no documentation of significant longitudinal
growth. In contrast, Peterson has documented definite long-
term growth restoration.147 In one of his cases followed over
10 years, the tibia grew 16.7 cm after excision of a distal tibial
bridge in a 5-year-old child. Since the original work by
Langenskiöld in 1967, considerable progress has been made
in understanding the intricacies of bridge resection or re-
lease and the likelihood of significant resumption of longi-
tudinal growth.23,34,37,89,108,115,123–128,137,138,155,161,172,173,204,212–214,218
Interposition Materials
Multiple cases using several interposition materials, such as
Gelfoam, bone wax, beeswax, muscle, fat, methylmethacry-
late, silicone rubber, and cartilage, have now been
reported.130,131 Other than Peterson’s studies with cranio-
plast, there are not enough reported cases in most other
studies that have been followed to skeletal maturity to permit
7. Management of Growth Mechanism Injuries and Arrest
FIGURE 7-27. Concept for correction of angular malunion proposed
by Pauwels.175 He emphasized eccentric growth across the physis,
with minimal correction at the fracture site itself.
detailed, statistically significant assessment of the superiority
of one interposition material over the others.180,181 The
one common theme is that the properly selected patient
has an excellent chance of restoration of some, if not all,
growth potential, thereby lessening length and angular
deformities.
Fat, an autogenous implant, may be available in suf-
ficient quantity from the edges of the incision to fill the
defect. Sometimes additional fat must be obtained from
another site (e.g., buttock, lateral thigh, groin). Osseous cav-
ities of skeletally immature pigs, filled with autogenous fat,
were found to elongate during growth (Fig. 7-28).39,123,129,172
Histologic analysis showed living adipose cells.129 As the
cavity elongated, the fat expanded to fill the defect. The
revascularization and survival of transplanted free fat
grafts have been demonstrated by several others. Adipose
tissue has been shown to have an inhibitory effect on
osteogenesis. Fat, however, does not provide any hemostasis
within the resection cavity. When the tourniquet is re-
leased, blood may partially displace the fat away from the
physeal edges. I often coat the osseous and physeal edges
with bone wax before inserting the fat. Closing the
periosteum over the cavity to contain the fat may pre-
dispose to new bone formation peripherally, especially when
dealing with a type 1 or 2 bridge. The periosteum should not be
closed.
A large operative defect may predispose the bone to patho-
logic fracture, as the fat provides no intrinsic mechanical sta-
bility. Gradual ossification may occur within the cavity,
especially at the trabecular margins.
Methylmethacrylate (cranioplast) may be molded to fit
the contours of the resection cavity.148,149,179 This material,
widely used during skull surgery in children, has not caused
rejection or neoplastic change.38 Because a solid substance
fills the cavity and osseous interstices, there is better mar-
ginal hemostasis than that achieved with fat. Furthermore,
because it is a mechanically supportive substance, there is
less bone weakening and the necessary period of postopera-
tive immobilization of the extremity may be less. It may be
Surgery
A surgical defect to conform to the cavity. A significant draw-
B
FIGURE 7-28. (A) Histologic section of fat interposition in a resected
bridge. (B) Similar section showing reactive bone around the fat
but not at the physeal edges.
the material of choice to support the metaphysis and
epiphysis after creating a large exposure cavity. For implant
surgery, methylmethacrylate has barium added to it for radi-
ographic identification. Cranioplast, in contrast, has no
barium and is radiolucent. Postoperative bridge reformation
therefore may be more easily identified when using the latter
material.
227
Cranioplast may be poured into the cavity while still in a
semiliquid state, which allows it to fill and adapt to specific
contours. It may pull out with subsequent growth, so it
should be fixed into the epiphysis with a small K-wire.
Bueche et al. tested the effect of interposition materials
on the mechanical behavior of canine physes after partial
physeal resection. Polymethylmethacrylate (PMMA) inter-
position significantly moderated the likelihood of physeal
displacement with increasing areas of physeal resection.35
They recommended the use of this load-sharing interposi-
tion material following resection of large areas of physeal
arrest in weight-bearing areas.
Silicone rubber is allegedly a biologically inert substance
but is an excellent substratum to study cell locomotion.
How this substance might affect migration of fibrous,
osseous, and angioblastic cells that could predispose to early
stages of bridge reformation is unknown. Bright used Silas-
tic elastomer no. 382 from Dow Corning,32,33 but this mater-
ial was never approved by the FDA as a controlled substance,
unlike fat or methylmethacrylate. While in a semipolymer-
ized state, the vulcanizing material may be pressed into the
back is the need to sterilize both the monomer and the cat-
alyst before surgery. Cultures must be taken after mixing,
before insertion, and during the operation. Infection may
occur and usually necessitates removal of the implant mate-
rial. There is no indication to use this material in contemporary
bridge resection.
Hyaline cartilage may be superior to any other interposi-
tion material experimentally,22,132 but there are few reports
of the use of this procedure being used in humans. Autoge-
nous rib, sternal (e.g., xiphoid), and iliac crest cartilage are
potential interposition tissues.188 Segments of physeal carti-
lage have been implanted as blocks of tissue.21,121,225 The use
of iliac crest graft has had limited success.66
It must be remembered that such cartilage is capable of
ossification. Cultured chondrocytes may eventually prove
efficacious.94,191 Such growth of cartilage cells for use in
filling selected osteochondral defects of the femoral
condyles is currently under investigation in multiple centers.
Whether nonphyseal hyaline cartilage would effectively
prevent bridge formation is unknown.
Lee et al. studied various interposition materials.130,131
They found that a physeal graft from the iliac apophysis was
better than silicone rubber for preventing reformation of a
bony bridge. Fat yielded the poorest results in their particu-
lar experimental model.
Indomethacin
Animal experimentation suggests that recurrence of a bridge
may be inhibited by the use of oral indomethacin, even
when given without the use of interposition materials.185
Indomethacin causes nonspecific inhibiting of the osteoblas-
tic activity when triggered by fracture or postoperative
inflammation. Whether indomethacin may be given in suf-
ficient doses to children to prevent bone bridge reformation
without inhibiting normal bone growth remains to be seen.
Further “unknowns” are when it is best to administer the
drug and how long the administration should be continued.
228
FIGURE 7-29. Correction of a peripheral bridge. (A) Location of a
bridge at the margin of an epiphyseal ossification center. (B) A
block is removed that includes the epiphysis, metaphysis, and
osseous bridge. Bone is removed until the physeal margins are
well visualized. (C) The area on either side of the physis is under-
mined with a curette. (D) The area is packed with fat.
These same considerations must be analyzed if
indomethacin were to be used in conjunction with bridge
resection.
Resection Technique
The basic objective of surgical excision is complete removal
of the osseous bridge while preserving as much of the
A B
FIGURE 7-30. (A) Surgical exposure showing characteristic dense,
sclerotic bone, which differs from the soft spongiosa. (B) Surgical
exposure, with block removed. The normal physis (white line) is
7. Management of Growth Mechanism Injuries and Arrest
normal remaining physis as possible. This approach requires
careful preoperative evaluation and planning and may be
technically difficult when the bridge is irregular. Familiarity
with the surgical approaches to and the specific anatomy of
the various physes is necessary.
Any patient being considered for bridge resection should
have at least 2 years (or 2 cm) of remaining (anticipated)
growth. Lower limb length discrepancies of 2 cm or less are
usually well tolerated by patients. Bridges larger than 50%
of the physeal area are unlikely to respond to resection,
although Österman experimentally showed that physeal
defects of as much as 65% were associated with growth
resumption after removal.173
Magnification capacity (operating microscope, loupes) is
essential. A headlight is strongly recommended. The osseous
bridging may be removed using an osteotome, curette,
rongeur, or motorized burr. Radiography (fluoroscopy)
during resection is helpful for determining if the bridge has
been successfully removed. Dental mirrors and arthroscopic
equipment also may be used.
A tourniquet is used to minimize hemostasis in the oper-
ative field. However, remember that a tourniquet does not
completely occlude intraosseous flow.
To minimize damage to additional physeal tissue,
always try to reach the most sclerotic region and then
gradually work toward the uninvolved area. When ap-
proaching a peripheral or linear bridge, the perichondral
ring should be resected, rather than reflected and
reapproximated.
Peripheral Bridge
The peripheral bridge (type 1) is approached directly (Figs.
7-29 to 7-32). There is often a palpable prominence to help
locate the site. Any periosteum overlying the bridge should
be completely excised along with the bridge. With a saw
or osteotome, the bridge is “roughly” removed to create a
peripheral cavity. Then, under direct vision, the remaining
dense sclerotic bridge is carefully removed, working from the
C
evident across the surgical site. (C) Surgical exposure showing the
defect packed with fat (in this case, removed from the margins of
the surgical incision).
Resection Technique 229

nically easy procedure (Fig. 7-33). Fluoroscopy helps select

an appropriate area in which to begin tunneling.
If the linear bridge is close to the peripheral margin of the
malleolus, a peripheral approach similar to that described
for a type 1 bridge may be considered (Fig. 7-34). Preoper-
ative MRI is useful for determining the presence of physeal
tissue between the bridge and the periphery.
If more than a few millimeters of peripheral physeal tissue
is evident, the surgical approach is to make a metaphyseal
window, carefully use a curette to expose the hypertrophic
cell surface of the physis, and then proceed inward in the
metaphysis until the sclerotic bridge is encountered. The

B
FIGURE 7-31. (A) Peripheral growth arrest of the medial distal tibia.
(B) Large cavity left after resection of the bridge. This area is
mechanically weak and must be appropriately protected during
weight-bearing.

outside inward until the normal physis is visualized all along

the margins of the cavity. The exposed physis should be
evident out to the cortical edges of the metaphysis. The
resection cavity must include some of the epiphyseal ossifi-
cation center.

Linear Bridge
A linear bridge (type 2) extending completely across
the physis is common after type 3 or 4 malleolar fractures.
Such a pattern requires careful evaluation of the tomo-
graphic mapping to determine the most appropriate surgi-
cal approach to ensure complete removal of the bar while
leaving viable physis on either side. Creation of a “tunnel” FIGURE 7-32. (A) Peripheral growth arrest. (B) Four months after
through the bone is often the best approach but is not a tech- bridge resection. Note the Harris line displacement.
230
FIGURE 7-33. Tunnel resection of the linear bridge.
bridge is removed with a burr until normal metaphyseal
bone is encountered. Once the bar is maximally removed on
the metaphyseal side, the extension across the physis
becomes evident. Using an angled dental burr this may then
be removed until normal (i.e., nonsclerotic) epiphyseal bone
is encountered.
FIGURE 7-34. (A) Linear osseous bridge. (B) After resection. (C, D) Further growth. Note how the Harris line is progressively displaced
parallel to the physis.
7. Management of Growth Mechanism Injuries and Arrest
Central Bridge
A centrally located, conical bridge (type 3) that has sur-
rounding normal physis and an intact perichondrial zone of
Ranvier should not be approached from the physeal periph-
ery. Instead, such a conical bridge should be approached
through a surgical cavity within the metaphysis (Figs. 7-35 to
7-37). This transmetaphyseal approach requires removing a
window of metaphyseal cortical bone and internal cancellous
metaphyseal bone until the sclerotic physeal bridge is
reached. After removing the entire bridge, the normal physis
must be visualized circumferentially within the cavity. The
physis may then be assessed by the use of a small dental
mirror. An intracavitary light is helpful.
An alternative approach is to cut out a triangular
portion of metaphysis, which may be replaced or to perform
an osteotomy at the level of the bridge, hinging the epiphy-
seal unit open to directly expose the sclerotic bone.
This method also allows concomitant correction of angular
deformity.
General Concepts
The first step in preventing bridge recurrence is to
obtain good hemostasis at the time of resection. The
tourniquet is released. The cavity can be packed tightly with
thrombin-soaked Gelfoam. When stasis is obtained, the
Gelfoam is removed. A thin layer of bone wax can be applied
Resection Technique
FIGURE 7-35. Correction of the central osseous bridge. (A) A
window is made in the metaphyseal cortex. The physis, epecially
the zone of Ranvier, is left intact. (B) A metaphyseal “cyst” is care-
fully made, exposing the metaphyseal side of the physis and the
osseous bridge. (C) The bridge is selectively removed, and the
to the edges of the cavity. The interposition material is then
added.
The sides of any of these surgical cavities should be rela-
tively flat and smooth. Some undermining of the metaphy-
FIGURE 7-36. (A) Eighteen-month-old child sustained a seemingly
innocuous fracture (type 2) of the distal tibia. (B) Six months later
a central osseous bridge has formed (arrow); it was resected. (C)
Three years later the physis has grown normally without recur-
231
physis is undermined. (D) Defect is packed with fat, the fat being
impacted through the former site of the bridge. (E) The curette
shows the central bridge approach in a patient who had previously
undergone an osteotomy without bridge resection.
seal and epiphyseal bone away from the physeal edges may
be beneficial in reducing the likelihood of bridge reforma-
tion when fat is used as interposition material. However,
extensive removal of epiphyseal bone may damage the
rence of the bridge. The open arrow indicates the upper limit of the
metaphyseal surgical opening, and the solid arrow indicates the
level of the physis at the time of surgery.
232
A B
FIGURE 7-37. (A) Fracture of the distal femur fol-
lowing a traumatic delivery at home. (B) Two
years later the bridge is evident. (C) Radiograph
taken seven years after bridge resection. Growth
has resumed, as indicated by the length of the
central intramedullary channel, despite the
seeming reappearance of bridging. (D) MRI view
of the operative site 7 years after bridge resection
and fat interposition. C D
E-vessel supply to the exposed physeal margins, increasing
the risk of bridge recurrence. Bridge reformation is less
likely when the interposition material remains in the epiph-
ysis than when the epiphysis grows away from it.
The fat or methylmethacrylate should fill the epiphyseal
ossification center defect, abut the exposed physis as com-
pletely as possible, and fill some, but not necessarily all,
of the metaphyseal cavity. If a large metaphyseal cavity
was created, as during exposure for a type 3 central bridge,
portions of the metaphyseal cavity near the diaphysis may
be filled with the bone previously removed to create
the exposure cavity. A cortical metaphyseal window may be
replaced. However, any cortical bone that originally
traversed the growth plate should not be reinserted. Simi-
7. Management of Growth Mechanism Injuries and Arrest
larly, metaphyseal periosteum may be reapproximated, but
any periosteum crossing the physis (e.g., in type 1 and type
2 bridges) must be excised completely and not reattached.
A mild angular deformity secondary to peripheral bridg-
ing may be corrected spontaneously with postoperative
growth. Angular deformities larger than 15°–20° probably
will not correct spontaneously and usually will require
osteotomy, which may be performed at the same time as the
bridge excision (Fig. 7-38) or later. I sometimes prefer to wait
several months to see if the bridge resection is successful. If
there is evidence of reformation, the bridge may be removed
again during the osteotomy. An osteotomy sometimes facili-
tates direct exposure of the bridge, especially with central
type 3 bridges.
Resection Technique
FIGURE 7-38. (A) Growth arrest of the distal tibia
and fibula. (B) This condition was treated by a
combination of osteotomy and bridge resection.
Hamanishi et al. progressively corrected angular deformi-
ties with an intraepiphyseal opening wedge osteotomy.93 The
osteotomy was gradually opened similar to axial limb length-
ening. The bony bridge itself was not removed in any of
their cases.
Distraction Epiphysiolysis
Bollini et al. described a technique to remove a centrally
located bar of the distal tibia (Fig. 7-39).26 Ilizarov distraction
epiphysiolysis was used to separate the metaphysis from the
epiphysis. Eight days later the child underwent surgery. The
dense sclerotic bridge had separated from the epiphysis and
A B
FIGURE 7-39. (A) Central bone bridge of the distal tibia. (B) After distraction epiphyseolysis the bone bridge is evident (arrow), still
attached to the metaphysis. (C) Twenty months later considerable growth has resumed.
233
was still attached to the metaphysis. There was a cavity across
the physis with the epiphysis that was filled with methyl-
methacrylate. The sclerotic bridge was removed.
Cañadell and de Pablos have also recommended use of
distraction epiphysiolysis to break the osseous bridge, simul-
taneously addressing correction of the longitudinal and
angular deformities.40,41 They stressed that this technique
allowed some improvement but that it was experimental and
should be considered only for adolescents near skeletal
maturity. Premature complete epiphysiodesis usually follows dis-
traction epiphysiolysis.
Kershaw and Kenwright studied epiphyseal distraction
for bony bridges.119 They found a high potential for pro-
ducing premature physeal fusion, not unlike the phenome-
C
234
non after limb lengthening by chondrodiastasis. Selective
nonocompartment epiphyseal distraction has also been
described.187
Acute Fat Replacement
Although the current discussion focuses on resection of the
osseous bridge after it has formed, I have inserted far during
acute reduction of some comminuted type 4 malleolar
injuries, converting them to a “type 3” pattern, especially
when the medial malleolus is involved. None of the patients
so treated has subsequently formed an osseous bridge.
However, this procedure must be carefully assessed before its
routine use as part of the initial open reduction and fixation
can be recommended.
Postoperative Care
Joint motion can usually be started immediately when
methylmethacrylate is inserted. In the absence of con-
comitant osteotomy, a cast is unnecessary. Weight-bearing
is encouraged on the day of operation or as soon as
operative discomfort subsides. It is deferred 4–6 weeks,
however, when a fat implant is used. The length of time to
full weight-bearing must be individualized, based on the
location, the size of the resection defect, and the age of the
patient.
The patient should be observed clinically and radiologi-
cally until skeletal maturity.8 Physeal growth, even when re-
established, may cease at any time and usually does so prior
to anticipated physiologic epiphysiodesis (using the con-
tralateral epiphysis for comparison). The physis at the oppo-
site end of an operated bone sometimes “overgrows” to
compensate for damage at the other end.
Recurrent bridge formation has been successfully treated
by repeat excision. If a bridge recurs near maturity, or if the
entire physis ceases growing on the injured side earlier than
the contralateral regions (a fairly frequent finding), physeal
arrest of the contralateral side should be considered. Even
when bridge resection is successful, the leg length inequal-
ity may still be significant and may require appropriate equal-
ization treatment.
An analysis of radiographic patterns after bridge resection
emphasized that failure to recognize postoperative changes
in the size and appearance of the radiolucent surgical defect
may lead to a mistaken diagnosis of osteomyelitis.8 The
normal osseous response is that the margins of the surgical
defect become irregularly sclerotic and assume a slightly
fragmented appearance, especially near the physis. The
lucent area often elongates because there is no physis to
produce cartilage cell columns and only limited metaphyseal
vascularity to replace it with bone.
Peterson showed that the growth of the involved bone
varied from 0% to 200% when compared with the growth
on the contralateral side, with an average recovery of 94%.
In those cases followed to skeletal maturity, the mean value
decreased to 84%.180,181 Virtually all injured physes, although
they responded positively to resection by active growth,
closed earlier than the contralateral physis.
7. Management of Growth Mechanism Injuries and Arrest
Epiphyseal Transplantation
The only other reported procedure used to correct signifi-
cant physeal–epiphyseal injury is transplantation of an
epiphyseal late.20,29,74,91,96,101,135,170,198,205,208,216,217 This technique
has provided only limited success when autografts were used
and usually failed when allografts were attempted.31,74,103,220
Because an injured child essentially has no expendable
source of growth plate cartilage for transplantation, this
technique has minimal clinical application. Few indications
for transplanting an entire bone in a child are sufficiently
compelling to attempt the operation.
In 1966 Wilson reviewed the subject and reported 11 cases
in which an epiphysis had been transplanted. Early evidence
of longitudinal growth was present in only two patients and
full longitudinal growth in only one.220 Whitesides reported
a case in which transplantation was followed by normal
growth; the particular patient was first seen because of
osteomyelitis that had obviously destroyed the periosteum
(type 9 injury). The patient was followed to skeletal maturity
at the age of 15. The transplanted phalanx grew and func-
tioned. The transplanted phalanx was approximately the
same length as the corresponding phalanx in the normal
hand.217
Eades and Peacock transplanted the proximal inter-
phalangeal joint and epiphysis of the middle phalanx
from the long finger to the metacarpophalangeal areas of
the adjacent ring finger, reversing it 180° so the epiphysis
became a metacarpal.64 The functional result was reason-
ably good, but the transplanted epiphysis failed to remain
functional or to produce longitudinal growth in the
metacarpal area.
Microvascular transplantation of physeal allografts
requires immunosuppression. However, the pedicle–
physeal–epiphyseal unit as salvaged from an amputation
stump (autograft) may be a feasible microvascular
transplant.76,109
Allografting
Techniques for transplantation preclude large epiphyseal
transplants.232 However, microsurgical anastomosis may
increase the potential for survival of growth areas (see
Chapter 6).182,193 In a patient approaching or having attained
skeletal maturity, allografting with replacement of deformed
articular surfaces and correction of angular deformity offers
an additional means of dealing with major structural
changes consequent to physeal–epiphyseal and articular
damage.90
Limb Length Equalization
Growth Estimation
The difficulty of estimating the expected growth of a long
bone is highlighted by the increased interest in the problem
of equalizing the length of traumatically shortened lower
extremities, particularly when the shortening is due to epiph-
ysiodesis.80–84 Menelaus based calculations for leg length dis-
Limb Length Equalization
crepancy on chronologic age rather than skeletal age.139 The
calculations he used were based on the observation that the
lower femoral epiphysis provides 3/8 inch and the upper
tibial epiphysis 1/4 of an inch of growth per year. His origi-
nal calculations show that growth stops at the age of 17 in
boys and age 16 in girls, but this was later modified to ages
16 and 14, respectively.
Moseley discussed a method for recording and interpret-
ing data in cases of leg length discrepancy.145,146 This method
provides a mechanism for predicting future growth and auto-
matically takes into account the child’s growth percentile
and the degree of growth inhibition in the short leg. It may
be used to predict the effects of corrective surgical proce-
dures and to choose a surgical timetable. The computation
methods are presented in Chapter 5.
Whatever method of calculation is employed, good results
depend on accurate records. The records should be kept on
a standard chart included in the history of any child with a
leg length discrepancy. Measurements are recorded at
regular intervals, including those from the anterosuperior
iliac spine to the medial malleolus and to the heel, as dis-
crepancies may exist between the malleolus and the heel
owing to concomitant foot injury.
Epiphysiodesis
The most commonly employed procedure for equalizing
leg lengths is an appropriately timed surgical epiphysio-
desis of the contralateral, normal leg.203 Timing is based
on accurate computation of the anticipated discrepancy.75
The major drawback to this approach is that both legs
end up being shorter than they normally would have
been.
Several researchers have performed epiphysiodesis to
study the effect of the procedure on bone growth.127,172 One
of the significant findings was a greater growth contribution
from the remaining functional physis or physes of the
involved bone or limb. There may be a limit for the com-
bined rates of growth of the two physes of a long bone, and
either may increase the respective rate of growth if, because
of trauma or surgery, it becomes the only active growth
region. Whether such a phenomenon occurs in the skeletally
immature human is unknown, but it certainly is a factor to
be considered.
Open epiphysiodesis may be used. The epiphysis is
exposed through oblique incisions on the medial and lateral
aspects. A cortical rectangle is removed. The growth plate
may be isolated readily by raising a flap on the metaphysis
and extending it gradually down to the growth plate, where
it will be firmly adherent. This step allows adequate place-
ment of the transverse cuts so that one-third of the piece
removed consists of epiphysis and two-thirds of diaphysis.
This block, which should be at least 1 cm deep and 1 cm wide,
is removed, and the epiphyseal line is curretted as much as
possible. The rectangle of bone is then reversed and
replaced.
Alternatively, percutaneous curettage under fluoroscopy
may be undertaken.30,42,43,168 This technique is effective when
done carefully and causes much less surgical morbidity for
the patient.
235
Effect of Stapling
Another method of length equalization or angular defor-
mity correction is temporary slowdown by inserting staples
around some or all of the physis. When equal length or angu-
lation is attained, these staples theoretically can be removed.
However, the results are not dependable, and the stapled
physis may cease to function.
Christensen found that a significant number of animals did
not resume growth even if the staples were removed 3–4 weeks
after original placement.47 The growth plate could still be rec-
ognized but was functionless as far as longitudinal growth was
concerned. In a few cases, unilateral epiphysiodesis was seen
as a result of a massive bony union within half of the growth
region. Variable degrees of bridging across the growth plate
were observed even where growth was resumed. Christensen’s
study points out the significantly high probability that staples
cause permanent growth impairment, and it questions the
standard technique of using them to slow growth temporarily
with the intent of removing them at a later time.
Staples also may be used to modify angular deformity,
rather than addressing bridge resection. Staples are in-
serted peripherally around the physeal margins opposite the
growth arrest. Realistically, they prevent further deformity,
but they do not alter growth in any way that can correct the
deformity.
Bone Shortening
Segments of diaphyseal bone may be removed from the
femur or the tibia of the longer leg.223 This technique should
not be used until skeletal maturity is reached, and it is a more
difficult method than epiphysiodesis. It is also possible to
remove a section of femur from the longer leg and insert it
into the shorter femur.
Bone Lengthening
To maintain the length of the affected bone, efforts have
been made to lengthen it surgically (Fig. 7-40). Timing of
such a procedure is important, and it may be combined with
contralateral epiphysiodesis, depending on the anticipated
length of the inequality.
Bone lengthening by distraction osteogenesis (callotasis)
has become a widely accepted method of regaining longitu-
dinal bone growth loss due to a number of factors, includ-
ing trauma.* It is not without a number of complications,
which may in-clude delayed or incomplete osteogenesis,
infection, pin tract osteolysis, muscle weakness, muscle con-
tractures, joint contractures, altered articular cartilage phys-
iology, physeal damage, premature epiphysiodesis, and
neurologic dysfunction.†
Aronson and colleagues studied temporal and spatial
increases in blood flow during distraction osteogenesis,
using the nonoperated side as the control.12,14,15 At the
distraction site the flow increased to nearly 10 times the
opposite side, peaked at 2 weeks, and then decreased to
* Refs. 5,9,11–15,36,45,46,52–54,57,69,78,79,85,86,88,106,107,122,
174,192,221.
† Refs. 10,11,85,88,95,97,136,150,171,174,194,195,200,201,206,207,
222,229–231.
236
FIGURE 7-40. Selective lengthening of the fibula for growth arrest
and shortening after a lawn mower injury. Note the nondisruptive
small bone bridge (arrow) in the distal tibia that has led to a scle-
rotic metaphyseal line.
four to five times the control for the remainder of the
distraction period. During the consolidation period in-
creased flow persisted at two to three times the control.
Interestingly, the distal tibia away from the distraction site
showed similar amplitude and temporal patterns of in-
creased flow.
Physeal Stimulation
At present there is no applicable method for stimulating
physeal bone growth. Attempts to stimulate the physis to
increase the rate of growth, such as increasing the rate of
blood flow or periosteal release have been clinically unsuc-
cessful.102,116,120,134,137,209,219,226 Increased epiphyseal growth has
been observed experimentally in dogs with arteriovenous fis-
tulas and in association with venous stasis.
Porter inserted stainless steel distraction springs across
the upper tibial epiphyseal growth but did not find a suffi-
cient increase in longitudinal growth.184 Crilly using chick-
ens50 and Warrell and Taylor using rats215 showed that
reduction of pressure on the epiphyseal cartilage through
resection of the periosteum permitted increased longitudi-
nal growth. It has been recognized for some time that com-
pression retards epiphyseal growth.4
Sola and colleagues197 recorded experimental overgrowth
consequent to periosteal stripping, and Jenkins and associ-
ates113 applied this knowlege to reduce minor limb inequal-
ity in children with poliomyelitis. They suggested that the
enhanced epiphyseal activity after periosteal stripping was
7. Management of Growth Mechanism Injuries and Arrest
the result of a relative increase in blood to the epiphysis,
although it was never adequately substantiated.
Crilly postulated that the release of periosteal tension and
decompression of the growth plate might explain consider-
able overgrowth from complete transverse sectioning of the
periosteum in domestic fowl.50 This effect of circumferential
division of the periosteum was confirmed by Warrell and
Taylor in rats.215 They concluded that overgrowth could have
resulted from diminution of pressure on the growth plate or
from increased vascularity following trauma.
Any experiment to determine the effect of tension across
the growing epiphysis must recognize that surgical insult
alone may affect bone growth (possibly due to temporary
hyperemia), and the control limb must be subjected to an
identical operative procedure, excluding tension. Over-
growth did occur in Porter’s studies, but with angulation,
which was attributed to the design of the distraction spring.
Ring has shown that genetic factors and possibly neurologic
factors have a considerable effect on bone shape.189 It is not
known if an epiphysis stimulated by increased tension (as by
tension springs) can fuse permanently, nor is it known what
effect distraction of one epiphysis has on the other epiphy-
ses in the same limb. In fact, there are some indications that
premature physiologic epiphysiodesis may accompany this
type of distraction.
Distraction Epiphysiolysis
Lengthening may also be done through the growth plate.
Premature closure is a significant complication after length-
ening is completed prior to skeletal maturity.
Several authors have suggested that the epiphysis could
be detached and pulled away from the metaphysis, stimulat-
ing a greater rate of longitudinal growth.* Ray and associates
produced partial physeal closure in the distal femurs of dogs
and subsequently corrected the angular-length deformity by
controlled physeal distraction.186 This distraction method
produced a “pull-out fracture,” which occurred primarily at
the junction of the physis and the primary spongiosa. It is
interesting that the fracture line was not confined to a single
histologic layer, but in no area was the epiphyseal subchon-
dral plate involved. Resection of the osseous bridge was
essential prior to distraction. Elongation of cell columns, not
unlike that seen in rickets, occurred during the early dis-
traction phase. Up to 2.6 cm of lengthening was achieved.
Distraction epiphysiolysis has been used experimentally by
Connolly et al.48 and Monticelli and their coworkers140–143 in
large animals, with considerable success.130 Physeal closure
occurred shortly after transphyseal lengthening was accom-
plished.117,118 The procedure should not be used until the
final phases of the growth spurt. Monticelli has now per-
formed distraction epiphysiolysis on a large number of
patients. This procedure is still in the phase of clinical trials
and should not be used routinely without the patient
and family fully understanding the ramifications of the
procedure.
* Refs. 3,4,6,7,16–18,25,36,48,49,55,56,59–61,68,71–73,80,110,
111,133,140–144,147,149,176–178,196,199,202,210.
References
Alberty studied the effects of physeal distraction on
growth plate vascularity with microangiography.2 She
observed marked enlargement of the epiphyseal arteries and
defective metaphyseal capillary filling in association with
hyperplasia and physeal separation 3 days after distraction.
These changes persisted 21 days, when capillaries became
evident within the hyperplastic physes and separation gaps.
By 6 weeks vascular anastomoses were present across the
physes. Bone bridges were associated with these anastomoses
and led to premature epiphysiodesis in 75% of the experi-
mental animals.
Distraction epiphysiolysis, whether for lengthening or
for exposure of a central bridge, should be done close to
skeletal maturation for that particular physis. Premature
closure follows the procedure.92 The mechanism of such
has not been studied, but it is likely that the tension (stretch)
applied for several days before the “pop” that separates
metaphysis from epiphysis damages the periphery of the
growth plate when the encircling periochondral ring is
disrupted.
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8
Biology of Repair of the Immature Skeleton
Engraving of a healed malunion of a distal femoral epiphyseal
facture. (From Poland J. Traumatic Separation of the Epiphyses.
London: Smith, Elder, 1898)
he relatively static osseous skeleton of the adult has a
T limited number of healing patterns. In contrast, the
child’s skeleton is undergoing extensive growth, pro-
gressive chondro-osseous transformation, and continual
osseous rearrangement and remodeling that enhances not
only the capacity to recover from skeletal injury but to
remodel minor anatomic changes consequent to a specific
injury. The intrinsic cartilaginous and osseous vascularity is
much greater than any comparable region in an adult. The
periosteum is thicker and more osteogenic. Even articular
cartilage, which has an extremely limited capacity to recover
at any age, is more likely to do so in the child. Furthermore,
progressive modeling of nonarticular epiphyseal cartilage
may occur, contingent on the volume of the ossification
center relative to the volume of the nonossified cartilage
within an epiphysis.
Wound Healing
Any injured component of the developing musculoskeletal
system undergoes both basic or common steps of healing as
well as modifications and nuances specific to the tissue type.
The general phases of healing occur reasonably simultane-
ously, as few musculoskeletal injuries are limited to only one
tissue type. For example, a seemingly innocuous torus frac-
ture of the distal radius is associated with bone damage to
cortical and trabecular (marrow) bone, periosteum, and
contiguous soft tissues. Bleeding may be contained within
the periosteal sleeve, although it may also occur in disrupted
soft tissues external to the periosteum. Even skin and sub-
cutaneous tissues may be part of the overall injury. Each
injured area must undergo wound healing. In general, fibro-
protein elaboration overpowers cellular regeneration in
most wounded areas of the body, leading to scar formation
interposed between otherwise normal tissues.
Prequisites for proper wound healing include adequate
vascular perfusion (oxygenation) of the tissue, temporary
dysfunction in cellular mechanisms within the tissues and a
clean wound without bacterial contamination. If all optimal
conditions are present, primary wound healing with minimal
scarring occurs. Even if the wound is left open and closed
after a few days, secondary wound healing would have
already commenced, although such delayed primary closure
still usually results in late primary wound healing with
minimal scarring. When a wound becomes contaminated by
necrotic tissue or an infection occurs and leads to tissue dis-
ruption, heaing is delayed. A clean wound slowly fills in with
granulation tissue, and wound closure eventually takes place
by wound contraction.
In general, the chain of reactions that leads to wound
healing includes (1) a coagulation phase that occurs within
243
244
a few minutes of injury, (2) an inflammatory phase that lasts
several hours to days, (3) a granulation phase that occurs for
several days, and finally (4) a scar formation phase, which is
a remodeling process similar to the transformation of woven
bone to lamellar bone when a fracture heals.
During the coagulation phase the wounding of the tissues
opens up blood vessels, leading to bleeding within the
wounded tissue. The immediate physiologic reaction is to
reduce blood loss by the mechanisms of vasoconstriction and
hemostasis. Vasoconstriction, which occurs through vascular
smooth muscle, is a much more active process in the child
than in the adult; the child has more reactive blood vessels
and vascular lumens that are not “hardened” by arterioscle-
rotic processes. Hemostasis is also achieved through the
cascade clotting mechanism. Damaged tissues release a tissue
factor that initiates the cascade mechanism. This is an intrin-
sic pathway of coagulation.
Following the cessation of tissue bleeding there is rebound
vasodilation of local small vessels that leads to increased
blood flow to the injured area. Chemotaxis draws in cells,
particularly polymorphonuclear leukocytes (PMNs), which
begin to accumulate at the wound site. The PMNs produce
significant amounts of enzymes, mainly collagenases, to
digest and degrade particulate matter (damaged cells),
foreign bodies, and bacteria. The enzymes facilitate break-
down of necrotic debris. This process is associated with the
release of oxygen free radicals.65 The overall process affects
cell membranes and increases the transudation of fluid
across and out of the vessels, which is accompanied by
protein flux and lymphedema. The disruption of the con-
tiguous lymphatic system may adversely affect drainage of
fluid from the injured area. Monocytes are also attracted to
the wounded area. These cells are the circulating phagocytes
of the reticuloendothelial system. Within the wound they are
transformed into tissue macrophages and become important
in that they (1) comprise some of the main phagocytes of
debris and dead tissue, (2) form the first channels for blood
clot capillary reformation, and (3) produce angiogenesis-
and fibroblast-stimulating factors.50,51
The granulation phase, which occurs over several days, is
associated with fibroblast migration and aggregation leading
to the production of ground substance products such as pro-
teoglycans, structural proteins, collagens, fibronectin, and
laminin. Fibronectin is a multifunctional protein that acts as
a cell attachment protein, regulates the spreading of cells,
and has chemotactic properties for connective tissue cells.
Another multifunctional protein of the cellular matrix is
laminin, which is found only in basement membranes. Con-
comitantly, angiogenesis occurs through capillary budding.
The overall process leads to wound contraction.
The final phase is scar formation and maturation. In a
child this process may last not only months but years. The
balance of collagen formation and the orientation of the
collagen fibers affects wound strength and, under ideal
circumstances, leads to a progressive increase in wound
strength over time. Wound tissue rarely regains its full prein-
jury strength, and normal elasticity may be lost. Such obser-
vations, however, have been primarily in adults. Whether
a similar percentage of loss versus recovery of these factors
is present in children, particularly young children, is not
certain.
8. Biology of Repair of the Immature Skeleton
Osseous Fracture Repair
The progressive changes that make up the normal process
of osseous fracture healing, whether in the diaphysis, me-
taphysis, or epiphyseal ossification center, may be grouped
into sequential (chronologic) phases.46,81 Many factors that
influence bone healing may be identified from clinical
observation as well as from experimental work and should
be considered when treating childhood fractures. Experi-
mentation has been undertaken with animals (invariably
skeletally mature adults), which, because of species-specific
differences in macroscopic and microscopic bone structure
and skeletal homeostatic mechanisms, may respond differ-
ently from the skeletally immature human.3,4,17–19,27,47,52,96,140,
142,168
Because most experimental work has been done in
skeletally mature animals, the particular relevance of such
data to fracture healing in the developing skeleton of the
child is not always clear. Furthermore, as discussed in
antecedent chapters, certain areas of the developing skele-
ton, particularly the physis and epiphyseal cartilage, proba-
bly do not heal by typical callus formation. In fact, if osseous
callus repair occurs in cartilaginous regions (especially the
physis), it is likely to form an osseous bridge across the
physis, connecting epiphyseal and metaphyseal bone, which
most likely leads to significant longitudinal and angular
growth deformities. As in the adult skeleton, fracture healing
in the immature skeleton may be divided into three basic
integrated, sequential phases: (1) inflammatory phase, (2)
reparative phase, and (3) remodeling phase (Fig. 8-1). The
remodeling phase is more prolonged and physiologically
more active in a child (depending on the age of the child)
than the comparable phase in an adult. This phase is further
influenced by the responses to growth, changing body size
(mass), changing joint reaction forces, and biologic stresses
that alter growth dynamics within the physes.4,7,8,55,66,70,94,128,132–
135,149
These effects occur even when the fracture is mid-
diaphyseal and significantly distant from the active longitu-
dinal growth regions. Histologic descriptions and experi-
mental investigations are almost exclusively concerned with
compact, dense cortical bone of the diaphysis.120 However,
the mode of healing for such cortical fractures is distinctly
different from that of fractures involving principally trabec-
ular bone, as in the metaphysis.
Callus is the plastic exudate in tissue that develops around
the ends of a fractured bone and ultimately unites the
fracture fragments. It is the scar tissue of bone. The term
is derived from the Latin word callum, meaning “hard” or
“thickened.” Callus has been variously classified both tem-
porally (by its apparent age) and positionally (by its relation
to the portions of the fracture fragments). When callus is
only faintly calcified or visualized on the radiograph, it is
often referred to as fluffy or immature callus. Later, when it
becomes densely ossified and thick, it is referred to as mature
callus. The initial bone formed around the healing fracture
is woven (naive) bone that is formed randomly within the
fracture hematoma. Such bone is subsequently replaced by
lamellar bone characterized by successive and concentric
longitudinal and oriented layering (Fig. 8-2). This replace-
ment process represents a biomechanically responsive
restructuring of the woven bone to accommodate progres-
Osseous Fracture Repair
FIGURE 8-1. Three stages of healing of diaphyseal and metaphy-
seal bone: inflammatory, reparative, and remodeling. Subpe-
riosteal new bone dominates in diaphyseal fractures, whereas
endosteal healing tends to dominate in metaphyseal injuries. In the
child the periosteum tends to be intact on the compression side of
the fracture and disrupted on the tension side. The subperiosteal
callus is more extensive and mature on the compression side at
any given stage of fracture healing.
FIGURE 8-2. Cortical bone and reactive bone
from the periosteum.
245
sively to internal and external osseous stress patterns as the
fracture heals.
Inflammatory Phase
Immediately after a fracture through any of the osseous
portions of the developing skeleton (diaphysis, metaphysis,
or epiphyseal ossification center), a number of cellular
processes commence. The damaged periosteum, contiguous
bone, and soft tissues bleed. If the fracture is localized in the
maturing diaphysis, there is bleeding from the haversian
systems and from the multiple small blood vessels of the
microcirculatory systems of the endosteal and periosteal
surfaces and the contiguous soft tissue anastomoses. In the
metaphysis this bleeding may be extensive because of the
anastomotic ramifications of the peripheral and central
metaphyseal vascular systems.49,102 This hemorrhaging leads
to the accumulation of a hematoma within the medullary
canal at the fracture site, underneath the elevated perios-
teum, or extraperiosteally if the fracture has disrupted the
periosteum. With certain fractures, such as a femoral shaft
fracture, large amounts of blood may accumulate in the
extraperiosteal tissues. This extraosseous hematoma, along
with soft tissue (muscular) injury, may even contribute to
complications such as heterotopic (ectopic) ossification if it
is not subsequently resorbed.
In contrast to the adult, the thick periosteum strips away
easily from the underlying bone in the child, allowing the
contained fracture hematoma to dissect extensively along
the diaphysis and metaphysis, a factor evident in the amount
of subsequent new bone formation along the shaft (Figs.
8-3, 8-4). However, the dense attachments of the periosteum
at the zone of Ranvier limit formation of subperiosteal
hematoma to the metaphysis and diaphysis (Fig. 8-5).
Because the perichondrium is unlikely to be detached from
the epiphysis, a hemorrhagic response adjacent to the epiph-
ysis is absent, and formation of subperiochondrial callus
does not occur. Furthermore, because of the partially or
completely intracapsular nature of some epiphyses, propa-
246 8. Biology of Repair of the Immature Skeleton

FIGURE 8-3. Normal subperiosteal new bone formation. In this

torus (compression) fracture of the distal radial metaphysis the
periosteum is usually intact, limiting spread of the acute hemor-
rhage. Subperiosteal hematoma dissection of this specimen was
more extensive proximally (arrow) as the periosteum in this region
is attached more loosely and can be elevated by fluid (hematoma) FIGURE 8-4. Complete transverse fracture of the radius associated
under pressure more easily than in the adjacent region over the with plastic deformation of the ulna. Partial disruption of the perios-
metaphysis. teum of the radius has allowed extravasation of the hematoma and
extraperiosteal callus that is separated from the cortex of the
radius. In contrast, the intact ulnar periosteum was elevated by
contained hematoma and has formed callus that is integrated with
gation of the fracture to the joint surface causes decom-
the ulnar cortex.
pression of the hematoma into the joint. Such intracapsular
joint hematoma does not undergo the typical chondro-
osseous organization and callus information but, instead, is
liquefied and progressively absorbed.
The multiple small vessels of the haversian and Volkmann
intracortical systems are variably fractured and disrupted,
leading to intraosseous bleeding. The periosteal vessels and
the endosteal medullary vessels become involved, bleed, and
form a larger, more inclusive clot. This extravasation of
blood may lead to a temporary cessation of blood supply to
the osteocytes for a distance of a few millimeters on either
side of the fracture site, creating juxtaposed, relatively (and
temporarily) avascular trabecular and cortical bone. The
removal of this region of dead bone often makes the frac-
ture line more radiographically evident 10–14 days after the
fracture. Similarly, this phenomenon may make a stress frac-
ture that is not readily evident on initial radiographs to sub-
sequently be “obvious” on follow-up films.
Clot formation within the metaphyseal fracture may lead
to a complete, although temporary, cutoff of the central FIGURE 8-5. Pattern of subperiosteal callus response in a physeal
metaphyseal blood supply to a segment within the endosteal fracture (type 1 pattern). New bone is delimited by the dense
region between the fracture and the physis (Fig. 8-6). attachment of the periosteum into the periphery of the physis
Because of the nuances of the periosteal circulation, partic- (closed white arrow). The physis continues to widen and is irregu-
larly invaded to create random ossification patterns (black arrows).
ularly the peripheral metaphyseal circulation, there is some
The ulnar styloid process has also fractured and may heal by
blood flow to the more peripheral regions of the metaphysis, cartilaginous and fibrous tissue, leading to a radiographic, if not
especially the fenestrated cortex. The segments of ischemic actual, nonunion (open white arrow). This is a consequence of
bone eventually are replaced by viable bone through an fracture healing that is underemphasized in children in this parti-
integrated process of bone resorption and new bone depo- cular region, although it is rarely associated with posttraumatic
sition. The latter process leads to an initial appearance of symptoms.
Osseous Fracture Repair
FIGURE 8-6. Metaphyseal fracture temporarily renders the bone
segment between the fracture and the physis relatively avascular.
Once the fracture heals and remodels, the endosteal blood supply
across the injured region is progressively reestablished, allowing
resumption of the normal chondro-osseous transformation process
at the physis. Peripheral revascularization through the metaphy-
seal fenestrations also occurs, usually before the endosteal circu-
latory restoration. This MRI scan, obtained 5 months after a
metaphyseal fracture, shows that the marrow signal within the
metaphysis has not yet been restored to the equivalent intensity of
the marrow signal proximal to the fracture. Despite radiographically
evident healing, this scan still showed lack of bridging at the orig-
inal fracture site.
FIGURE 8-7. (A) Diffuse inflammation (INF) through the metaphysis of a neonate with
osteogenesis imperfecta. The fracture through the metaphysis has stimulated subpe-
riosteal new bone. (Arrow points to area shown in B.) (B) High-power view of metaphyseal
inflammation (MI), cortical bone (C), and new subperiosteal bone (SB).
247
sclerosis, and the former makes the fracture line more
obvious 2–3 weeks after an injury than it is immediately fol-
lowing injury.91,173
With a relatively undisplaced fracture much of the inter-
nal bleeding in and around the fracture site comes from the
disrupted nutrient and endosteal vessels. If the fracture is
more severely displaced, the periosteal sleeve may be variably
disrupted, leading to decompression of some of the bleed-
ing and subsequent hematoma into the contiguous soft
tissues. Whether this disruption of the periosteal sleeve has
a significant effect on the rate of the inflammatory and
reparative phases is unknown. The periosteal sleeve is more
likely to remain partially intact and able to effect a more
coordinated osteogenic response in children than in the
adult. It also decreases the amount of fracture hematoma in
the adjacent soft tissues.
Areas temporarily deprived of their vascular supply
develop microscopic areas of damage and necrosis in bone,
cartilage, and soft tissue. In this ischemic material and in the
fracture itself, the inflammatory response is a normal bio-
logic process. Children’s bones are much more vascular and
capable of a greater hyperemic response than are adult
bones. Accompanying any trauma-responsive vasodilatation
is a cellular response in which inflammatory cells, including
PMNs, macrophages, and mast cells, migrate into the region
of injury (Fig. 8-7).107,183 Macrophages appear to be a major
factor in any type of wound healing and may be a significant
producer of collagen, an important component for the even-
tual organization and maturation of the fracture callus.
Oxygen free radicals are released by PMNs during
the inflammatory phase of fracture healing. The experi-
mental administration of zymosan induces the release of
oxygen free radicals. Animals given zymosan had impaired
fracture healing, suggesting that oxygen free radicals were
responsible.65
248 8. Biology of Repair of the Immature Skeleton

Fracture healing is directed at reestablishing the specific

extracellular matrices that typify the injured musculoskeletal
region. Any extracellular matrix (not just those of the mus-
culoskeletal tissues) has a precise complement of collagens
that are necessary to achieve appropriate (often changing)
physical demands and to allow corrdinated differentiation
and development both prenatally and postnatally. Type III
collagen is the primary collagen of the fibrous matrix that
develops at the periosteal surface. Type I collagen is present
in the trabeculae of the membranous (fibrous) bone formed
by the periosteum. Type V collagen is found in bone and
fibrous tissue and is characteristically associated with blood
vessels. Type II collagen is the last of the major structural
collagens to be synthesized, as it is produced in response to
increased mechanical demands. Type II is also the last col-
lagen type to be sequentially produced in any fracture callus,
especially before the fracture callus stiffens. Type IX colla-
gen is present in various cartilaginous tissues. Type X colla-
gen is present only in calcified cartilage and is typically
associated with the hypertrophic zone of the physis. The syn-
thesis of type X collagen by fracture callus is further evidence
supporting its close association with the process of endo-
chondral ossification.67,169
The function of the various collagens, especially types I,
II, and III, is to give mechanical strength and support to
the tissues. Type I and III collagens also form a micro-
skeletal matrix for subsequent cell attachment and
migration, including the ingrowth of blood vessels. Fracture
healing differs from embryogenesis in that type I, rather
than type III, collagen is secreted and bone tissue is formed
prior to the appearance of any cartilage with type II
collagen.9
In healing fractures cartilage is produced only when the
cellular microenvironment precludes differentiation of
osteoblasts. The effects of mechanical stability on the extra-
cellular matrices and the cells themselves regulate the pro-
duction of these various collagens.105
Basic wound healing in fetal tissues consists of deposition
of extracellular matrix rich in hyaluronic acid but devoid of
collagen, suggesting that the fetal response to injury may be
a process more closely resembling regeneration or growth
than repair through scar deposition.40,55,73,74,116,165 This altered
response may be reflected in the reaction of skeletal tissue
to trauma during the perinatal period (e.g., the proliferation
of extensive callus following a clavicular fracture during a dif-
ficult delivery) (see Chapter 13).
The cellular inflammatory and proliferative responses
begin shortly after injury and usually reach a maximum
within 24 hours. Cellular reactivity occurs first in the subperi-
osteal region adjacent to the fracture but may extend the
entire length of the injured bone (Fig. 8-8).168 At this early
stage the ends of the broken bone, at least in the diaphysis,
are not participating in the proliferative activity of cellular
division. Instead, they undergo localized cellular necrosis, as
evidenced by the presence of empty osteocyte lacunae, which
extend for a variable distance away from the fracture. Cell
division occurs in the endosteal and subperiosteal regions. It
is best to conceptualize the ends of the broken “cortical”
bone as playing a passive role in bridging the macroscopic
fracture gap, particularly with incomplete fractures in chil-
dren, and as rendering a certain intrinsic stability to the
FIGURE 8-8. Localization of the hemorrhagic and inflammatory
response to the juxtaphyseal metaphysis (arrows) after an epiph-
yseal fracture of the proximal humerus in an 8-year-old child.
more complicated bridging process that occurs between the
separated regions of viable bone.
If one appreciates that the basic repair process of an
injured, immature skeletal element is the progressive cir-
cumvention of the localized, juxtaposed necrotic bone with
new peripheral connections between the separated regions
of viable bone, it is easier to understand why metaphyseal
fractures heal more readily than diaphyseal fractures and
why diaphyseal fractures in children heal more readily than
those in adults.42 In both situations the tissues normally
undergo extensive bone deposition and remodeling, par-
ticularly in the metaphysis. More importantly, latitudinal
(width) expansion of the diaphyseal and metaphyseal
peripheries is an ongoing process that is readily available to
make circumferential reactive bone to create a stabilizing
collar; the contained endosteal repair response occurs more
slowly. Osteon healing of cortical bone (i.e., primary bone
healing) is not of major consequence in the young child, as
the injured cortex is soon replaced by natural cortical expan-
sion subperiosteally and erosion endosteally. The normal,
extremely active processes of bone formation, replacement,
and remodeling participate concomitantly in the fracture
healing response. Because of this integration of normally
ongoing skeletal maturation with fracture healing, radio-
graphic evidence of the original fracture may disappear
within a year of injury, especially if the fracture was in the
metaphysis.
Osteoblasts are sensitive to the proliferative action of a
wide variety of growth factors.158 Many of these growth factors
have been isolated from fracture fragments and are thought
to be locally released in response to injury. Platelets stimu-
late proliferation and maintain the differentiated function
of human osteoblast-like cells. Platelets play an important
Osseous Fracture Repair
role in the early healing of fractures and are a continuous
source of multiple growth factors to enhance osteoblast
proliferation in vitro and in vivo. On degranulation at the
fracture site platelets release platelet-derived growth factor
(PDGF), insulin-like growth factor (IGF-I, IGF-II), and trans-
forming growth factor-b (TGF-b). IGF-II stimulates both the
proliferation and differentiated function of the osteoblast
and has a greater effect on osteogenic cell proliferation
when combined with fibroblast growth factor (FGF) or TGF-
b. TGF-b is a mitogen for cells and enhances formation of
the extracellular matrix. Recombinant human bone mor-
phogenetic protein (rhBMP-2) effectively induces the for-
mation of cartilage and bone in an orthotopic site.178 The
effect of growth factors on fractures of the immature skele-
ton is unknown.
Chemical messengers of fracture repair are classified as
autocrine (the secreting and target cells are the same),
paracrine (the producing cell diffuses to a different respond-
ing cell), and endocrine (cellular product transmits via of
the blood from source cell to target cell). Many of the
TGF-b superfamily are both autocrine and paracrine cell
modulators.
Sandberg et al. presented an excellent review delineat-
ing the consequences of genetic expression during bone
repair.151 They emphasized that the fracture healing process
repeats several stages of skeletal growth in a similar tempo-
ral order and thus represents an interesting model for devel-
opmental regulation of cellular types and specific genes.
They described the sequential expression of genes coded for
collagens, proteoglycans, and other matrix proteins during
callus formation. The temporal and spatial expressions are
closely linked to the sequential expression of genes coding
for their characteristic constituents.151
A number of factors influence the rates of fracture healing.
Factors promoting bone healing appear to be growth
hormone, the various thyroid hormones, calcitonin, insulin,
vitamins A and B, anabolic steroids, chondroitin sulfate, and
hyaluronidase, as well as certain types of electric current, low
dosages of hyperbaric oxygenation, and exercise.29,82–84,102
Factors that appear to retard bone healing are infection, cor-
ticosteroids, diabetes, endocrinopathies, high doses of
certain vitamins (e.g., A and D), anemia, unusual chemicals
such as aminoacetonitrile or b-aminoproprionitrile, dener-
vation, irradiation, high doses of hyperbaric oxygenation,
FIGURE 8-9. Subperiosteal new bone formation
(SB) and subperiosteal inflammation (SI) adja-
cent to the normal cortex. Trabecular inflamma-
tion (TI) is also present.
249
and some antibiotics and anticoagulants.70,82,87,146,148 Locally
administered dihydroxylated vitamin D metabolites into
experimental fractures enchanced endochondral bone for-
mation and strengthened the callus.106
Huo et al. studied the effect of ibuprofen, a widely used
drug that is an oxygenation inhibitor, on fracture healing.90
They did not find any significant difference in the rates of
healing of experimental fractures between animals adminis-
tered ibuprofen and those that were not.
A local factor affecting the rate of healing is the degree
of trauma. The more extensive the soft tissue damage, the
more delayed the normal reparative responses, especially if
the highly osteoblastic periosteum is involved. The degree
of bone loss is of import; but in view of the decreased
incidence of open injuries in children, significant bone loss
is infrequent.
The type of bone involved is also a factor. Cortical and can-
cellous bone, the major components of the metaphyses
and epiphyseal ossification centers, unite relatively rapidly;
remodeled osteon bone, the major component of the di-
aphyses, takes much longer. Compared with the osteon cor-
tical bone of adults, the haversian bone of children is more
porous and capable of greater, more rapid osteoblastic and
remodeling responses.
Periosteum
MacEwan stated that the periosteum was a limiting mem-
brane and that the cells responsible for production of new
appositional bone belong properly to the surface of the
bone.60,111 Ham pointed out that this is largely a matter of
definition and that the periosteum consists of at least two
layers: an outer fibrous layer and an inner cambial layer.75,76
The latter layer consists of cells termed osteoprogenitor cells,
to distinguish them from the osteoblasts, which have modu-
lated to become functional, rather than dividing, cells.38,39,101
If the periosteum is stripped away traumatically, the child’s
cortical bone is not completely deprived of its osteogenic
potential (Fig. 8-9). If a segment of bone is excised, the
remaining periosteal tube sometimes completely regenerates
new bone (see Chapter 1).102,123,184 Portions of stripped perios-
teum may form tube-like structures that make pieces of bone
extending from the diaphysis or metaphysis. However, if the
periosteum is significantly damaged or destroyed during the
250 8. Biology of Repair of the Immature Skeleton

showed a continuous increase of proximity between 1 and 6

weeks after fracture. These results suggested that there was
a temporal change in the balance of periosteal bone forma-
tion and absorption. The change was related to the restora-
tion of bone in continuity between the dense cortical bone
and the contiguous surrounding subperiostal new bone. It is
important to realize, however, that these studies were done
in the rat. The cortical bone in this species does not possess
a haversian system comparable to that in the human. Other
similar features occur in larger animals with bone formation
and responses that may be more typical. The primate model
needs to be assessed.

FIGURE 8-10. Loss of extensive amounts of periosteum severely
limits the reparative response capacity, even in the young child.
Hematoma
An early process is cellular organization within the fracture
hematoma (Fig. 8-11). Fibrovascular tissue generally replaces
the fracture hematoma with collagen fibers and matrix
elements, which eventually become mineralized and form
the woven bone of the enveloping provisional (primary)
callus.48,68,141,182 Initial invasion and cellular division occur
around the damaged bone ends and proceed centrifugally
away from the fracture site. The most mature tissues of the
repair process tend to be closest to the fracture site. In some
areas, particularly at the periphery of the callus, a type of car-
tilage forms that eventually is converted to bone through
endochondral ossification.
True endochondral ossification occurs only in the pres-
ence of a microvascular supply. If vascularity is insufficient
or deficient, this modulation of cartilaginous to osseous

fracture, the potential for extracortical repair may be irrevo-

cably lost, necessitating bone graft (Fig. 8-10), although this
is unusual in children’s fractures.14,184
Periosteal callus formation is often less evident in open
fractures. The fracture depth is also not usually evident in
these fractures because the injury is usually due to an
impaction and irregularity of the plane of fracture, rather
than shearing, with subsequent reduction after the deform-
ing forces dissipate. With fracture healing of primarily tra-
becular bone there is new bone formation on top of the
damaged trabeculae, resulting in an absolute increase of
bone mass on or within the space between the preexisting
trabeculae. This increased bone mass may be evident on
radiographs as an absolute increase in density, often in the
form of an ill-defined band. An alternative pattern is thick-
ened bands on the other side of the fracture that gradually
approach each other and fuse. Rarely this process leads to
nonunion. If one side of the fracture is relatively avascular,
the healing activity and radiologic signs are limited to the
vascular fragment. This happens for a certain time sequence
with a metaphyseal fracture (Fig. 8-6). The metaphysis and
the growth plate are rendered temporarily avascular, at least
in the central portions. The periostal contribution to the
peripheral portion of the trabecular bone and fenestrated
cortex remains intact and gradually can grow into the more
central regions until such point as the thickened cortical
bone at the fracture site has been broken down and remod-
eled and allows revascularization from the medullary canal.
Aro et al. studied remodeling of periosteal new bone FIGURE 8-11. Proximal tibial fracture (open arrow) with periosteal
during fracture healing.5,6 The adjacent cortical bone elevation and subperiosteal hematoma organization (solid arrow).
Osseous Fracture Repair 251

tissue does not readily occur.20 A lack of neovascular response

is unlikely in children and may be a significant reason for
the lower incidence of nonunion in children than in adults.
The amount of cartilage that forms is variable. It appears
to be a more prominent feature of fracture healing in non-
mammalian species and in cases in which excessive move-
ment is permitted. A common factor appears to be low
oxygen tension.11,23,24,62,75 Theoretically, cartilage provides a
suitable material with decreased oxygen demands that can
temporarily bridge the fracture gap until a microvascular
system is adequately established to commence the gradual
transformation to bone. Cellular and molecular morpho-
genetic factors may also play roles in progressive vascular
ingrowth into this enveloping tissue.85,161
The fracture hematoma is the medium in which the early
stages of healing take place. Osteogenic cells proliferate
from the internal layer of the periosteum to form the exter-
nal callus; and to a lesser extent they proliferate from the
endosteum to form an internal callus. When the periosteum
is severely disrupted, healing cells must differentiate from
the ingrowth of undifferentiated mesenchymal cells through
the hematoma. A few weeks after the fracture, the callus con-
sists of a thick, enveloping mass of osteogenic tissue around
the periphery. The callus itself does not contain any bone
and therefore is radiolucent and not apparent radiographi-
cally. The callus becomes progressively firmer and changes
from undifferentiated tissue into a cartilaginous state.176,181
The cartilage is progressively invaded by new blood vessels
and ossifies. This new bone is primarily woven bone. In chil-
dren this initial bone usually becomes radiologically evident
about 10 days after an injury.
The fracture hematoma is extremely important to effec-
tive mechanical healing of the fracture and may be an addi-
tional factor in the more rapid and effective rates of healing
in children than in adults. Removal of the hematoma may
impair fracture healing even more in children.
Miziuna et al. transplanted fracture hematomas to sub-
periostal and intramuscular sites separated from the original
injury.121 Two-day fracture hematomas produced new bone
by endochondral ossification at the subperiostal site but not
within the intramuscular site. In contrast, the 4-day fracture
hematoma produced new bone formation at both sites.
Their results suggested that fracture hematoma has an inher-
ent osteogenic potential, which may relate to factors within
the platelets that are a significant part of the hematoma
process.
Physiologic Response
Using nuclear magnetic resonance (NMR) spectroscopy,
local pH changes were assessed at the fracture site.124,125 The
fluid at the fracture site became more alkaline, and the depo-
sition of radiopaque callus occurred mainly during the alka-
line phase. When rats were treated with prednisolone, there
was a delay in the alkalinization and a resultant delay in even-
tual union.
Concomitantly, similar cellular activity begins within the
medullary region, although the vascular response is much
slower than it is in the subperiosteal tissues.66 Again, the
factor may be highly variable in children, inasmuch as their
trabecular bone is more vascular than that of adults. If the
FIGURE 8-12. Mature subperiosteal bone following a distal femoral
metaphyseal fracture. This bone has remained radiographically
separate from the cortex.
fracture involves the metaphysis, the vascular response is
usually rapid. The more mature the cortex and the greater
the amount of osteon bone involved, the more likely it is
that the vascular response will be slower. This observation
readily explains the rate-response differences between the
fenestrated, woven bone of the metaphyseal cortex and the
mature, lamellar bone of the diaphyseal cortex.104 The
amount of new endosteal bone is variable and depends on
the nature of the bone involved (Fig. 8-12). It is the method
of union of the cancellous (trabecular) bone of the me-
taphysis and epiphysis, but it can also form in predominantly
cortical bone, such as the immature diaphysis. Although
there is considerable cortical (lamellar) bone in the diaph-
ysis, the demands of growth and appositional increase in
diameter necessitate the presence of some trabecular bone
along the surface of the diaphyseal shaft (periosteal and
endosteal) in children.
The process of new bone formation may be enhanced
when the fracture surfaces are offset, in which case the
responsive, new endosteal bone from one side of the frac-
ture may unite with the responsive subperiosteal bone of
the opposite fragment (Figs. 8-13, 8-14). In situations such
as overriding fractures, this tends to be a dominant fracture
healing pattern and leads to fracture stability with relatively
rapid union. Remodeling eventually corrects the contour
changes and reestablishes medullary continuity and cortical
continuity.
The relative importance of these basic cellular processes
reflects a subjective effort to impute a simple, common
mechanism to the repair of all types of bone injury in all
animal species (including humans), no matter what the
degree of skeletal maturity. Many of the differences in
emphasis that appear in the various descriptions of fracture
252 8. Biology of Repair of the Immature Skeleton

healing are probably explained by differences between the

A B
FIGURE 8-13. (A) Early callus (arrow). (B) Maturing callus.
particular types of bone, the species studied, the pattern of
fracture, and even the experimental modes by which the
fracture was produced.117 Many of the animal specimens illus-
trated in this and other chapters are from relatively large
animals, with many sustaining spontaneous fractures and
healing patterns that more likely reflect the natural (non-
experimental) biologic response.
Ham questioned the role of the hematoma.75 He described
a zone of intense cellular activity in the subperiosteal region
that resulted in the formation of encircling collars of callus,
one on each side of the fracture gap, appearing as wedge-
shaped areas on a longitudinal section that gradually
approach each other until they meet and unite. This process
may take place external to the hematoma, which is thereby
bypassed and resorbed later. My review of radiographs of
thousands of pediatric fractures during the treatment
process does not uphold this concept of externalization.
Rather, new bone is usually formed directly against the orig-
inal outer cortex and thickens progressively, rather than
leaving a radiolucent region against the cortex that must sub-
sequently be obliterated.
Pritchard and Ruzicka, in contrast, drew a distinction
between the reparative tissue, or blastema, that arises from
the outer fibrous layer of the periosteum and the reparative
tissue that emanates from the cambial layer of the medullary
cavity, which they termed the osteogenic blastema.142 Nor-
mally, the osteogenic blastema, being more centrally placed,
invades the fracture hematoma, produces new bone, and
bridges the fragments, whereas the more peripheral zones,
which are fibrous, restore the continuity of the periosteum.

A B
FIGURE 8-14. Lack of contact does not prevent repair in a child. (A) Faint callus within the periosteal sleeve is evident. (B) Five weeks
later.
Osseous Fracture Repair
If the peripheral fibrous tissue invades the fracture gap
before the osteogenic blastema does, conditions are set up
for the development of delayed union or nonunion.
Because of the extreme activity of the osteogenic blastema
in the child, whether involving a metaphyseal or diaphyseal
osseous response, predominance of the fibrous response
is unlikely, an additional factor that may be important for
explaining the rarity of nonunion in children’s bone.8
However, in fractures within the epiphyseal or physeal carti-
lage, particularly if the secondary ossification center has not
developed or is small, the fibrous response is more apt to
develop.
A more fundamental argument concerning these cellular
processes is the source of the osteogenic tissue.137 There are
two basic, somewhat diametrically opposed, theories regard-
ing these cells. According to one theory, the repair tissue
arises from specialized cells with a predetermined commit-
ment to bone formation. These specialized cells are the
osteoprogenitor cells, which occur only in close association
with the surface of the periosteal bone or the endosteal bone
marrow.44 As the osseous cells proliferate, the fibrous perios-
teum is pushed away from the bone to produce the apposed
collars of callus that eventually fuse with each other.
The alternative view is that repair tissue does not arise
per se from these specialized cells but, rather, arises from
the activity of previously uncommitted fibroblasts that are
capable of developing osteogenic potential when given the
appropriate microenvironmental stimulus (which may be
biochemical, biomechanical, or both).7 Reparative tissue
arises not from the bone but from the surrounding soft
tissues. These two theories may not be totally opposed, as the
uncommitted fibroblasts may also be considered potential
osteoprogenitor cells.79 This phenomenon, by which unas-
sociated soft tissues are recruited into the osseous repair
response, is known as osteogenic induction.45,72,109,175
During the early stages of fracture healing in rats (skele-
tally mature), pluripotential cells consisting of fibroblast-like
mesenchymal cells and inflammatory cells develop.80,88,119
These pluripotential cells are proliferative on the muscular
side of the fracture. The cartilage of the callus then differ-
entiates from these cells. Direct bone formation in the
periosteal callus and in the marrow originates from a more
homogeneous cell mass of preosteoblasts, which does not
contain inflammatory cells. The function of the inflam-
matory cells in the differentiation process is not clear. The
presence of these cells during the formation of cartilage,
however, defines the endochondral pathway from direct
membranous (i.e., subperiosteal) bone formation. It seems
likely that cartilage does not develop as an alternative to
direct bone formation during fracture repair, but that both
tissues develop concomitantly, with each having its own ter-
ritory and origin. Furthermore, the formation of cartilage
from pluripotential cells is not necessarily due to an insuffi-
cient vascular supply and low oxygen pressure, as it is known
from other types of cartilage that the cells themselves may
regulate the optimal oxygen milieu.161 The occurrence of
mast cells in callus formation and their presence in relation
to small vessels suggest their role in angiogenesis.107
Rigid fixation, whether external or internal, may restrict
cartilaginous transformation to some extent but not com-
pletely. Any delay may be more significant in older patients
253
and contribute to delayed union. This phenomenon does
not appear restricted with “minimal” internal fixation (e.g.,
flexible rods).
Stafford et al. experimentally reamed and stabilized tibial
fractures and then excised 2 cm of periosteum on the side of
the osteotomy.162 They showed that the osteogenic cells par-
ticipating in callus formation were derived exclusively from
the remaining periosteum. Their study supports the impor-
tant role of periosteum in providing osteogenic cells and
suggests that the more destroyed or damaged or surgically
excised the periosteum is, the greater is the likelihood of
delayed union and nonunion. In another study limited
reaming appeared superior to extensive reaming in fracture
healing.69 Reaming induced a significant periosteal reaction
and a hypertrophic and immature callus.
Smith et al. showed that in a comparison of intermedullary
fixation versus an external fixator or a compression plate the
most significant impairment of cortical bone blood flow was
always associated with intermedullary fixation compared to
the other two fixation devices, and that this difference was
present even 90 days after the experimental injury.160 Despite
the initial differences in circulation, they thought there even-
tually was no significant difference in bone remodeling with
the various fixation devices. They believed that this long-
term similarity was due to the relative perfusion damage
being overcome by collateralization of the vessels to the
endosteal cortex.
The cortex is normally supplied through the medullary
vascular system, the flow of which is centrifugal. The perios-
teum makes an arterial contribution to the outer cortex.
In situations of trauma, however, this may become a more
dominant blood supply.26 After a fracture, an extensive,
extraosseous blood supply derived from the surrounding soft
tissue develops.144,145 Although it assists in revascularizing any
peripheral, necrotic tissue of the cortex, its main purpose
appears to be participation in the formation of the external
callus. Internal callus must rely on the medullary system,
which may be significantly disrupted on one side of the
fracture.
Reparative Phase
The next step within the enveloping hematoma is cellular
organization. During this stage the circumferential tissues
play only a small role in the mechanical stabilization of the
fracture. They serve primarily as a fibrous scaffold over
which subsequently appearing cells migrate and orient to
induce a more stable type of repair. The cells that migrate
are pluripotential mesenchymal cells theoretically capable of
becoming cartilaginous, osseous, or fibrous tissue. Common
stem cells migrate into the area and modulate, probably in
response to variations in the microenvironment (e.g.,
changes in the pH and the mechanical stresses of tension,
compression, or both on the developing extracellular matrix
and basement membranes).11
In the child, because of osteoblastic activity, the perios-
teum contributes immensely to new bone formation by
accentuating the normal process of membranous ossification
to supplement the increasing cellular organization within
the hematoma (Fig. 8-15). The region directly around the
fracture site thus undergoes a variation of the process of
254
FIGURE 8-15. (A) Massive proliferative new bone of the cartilagi-
nous callus (solid arrow) and more limited subperiosteal response
(open arrow). (B) This case shows a more extensive subperiosteal
response and less endochondral proliferation around the fracture
site. Note also the distal femoral and proximal tibial physeal frac-
ture. This child was a victim of repetitive abuse.
endochondral ossification, in juxtaposition to membranous
ossification from the tissues within the elevated periosteum.
Similar processes occur within the medullary cavity, where
endosteal new bone and cartilage are forming. An integral
part of the reparative process at this stage is microvascular
invasion, a process that occurs rapidly and readily in children
because of the extent of vascularity within and outside the
bone and the surrounding soft tissues. Vessels come from
the periosteal region as well as from the nutrient artery and
endosteal vessels.
The progressive organization of the hematoma by vascu-
lar invasion leads to the production of varying numbers of
fibrous, cartilaginous, and osseous cells that undergo cellu-
lar and extracellular maturational processes in the presence
of the invasive microvascular supply to create immature,
fibrous, and endochondral bone.98,115,123 As more and more
of this cartilage and bone (callus) forms, the stability of the
fragments progressively increases. Until this bone goes
through the final stages of maturation, it is still biologically
plastic and, if not protected, may plastically deform or
refracture.
The microenvironment plays a significant role in this
stress-responsive process.35,57,63,175 Compression, or at least the
absence of tension, discourages the formation of fibrous
tissue.45,177 Variations in oxygen tension probably modulate
cellular formation of bone or cartilage, with cartilage being
8. Biology of Repair of the Immature Skeleton
formed in the presence of lower oxygen tensions and bone
in higher oxygen tensions. Assuming that the initial fracture
region is “avascular,” cartilage becomes important in the for-
mation of a biomechanically responsive matrix that progres-
sively stiffens to immobilize the fracture sufficiently, and
vascularization proceeds into the callus and eventually leads
to ossification. Thus the true bridging and stiffening may
be cartilaginous, and ossification bridging is secondary. If
cartilage matrix does not stiffen sufficiently, osseous bridg-
ing may not be possible or may be delayed. The cartilage that
is formed is eventually replaced by bone through a process
that is essentially identical to prenatal and postnatal endo-
chondral bone formation, with two exceptions. The cell
columns are minimally formed, and there is nothing
remotely resembling the modified spherical growth plate in
the epiphyseal ossification center. Brighton et al. showed that
the mitochondria probably play an important role in the
initial matrix calcification of the cartilaginous fracture
callus.22 The initial ossification transformation process
appears randomly directed. However, force patterns may
direct neoangiogenesis and basement membrane formation,
thus preceding and, accordingly, giving direction to seem-
ingly random invasive ossification.
Therefore two types of healing are occurring: accelerated
membranous bone formation in the child and relatively
nondirected endochondral ossification taking place within
the fracture callus as cells modulate from fibroblasts to chon-
droblasts to osteoblasts. Clinical union is reached when the
fracture site no longer appears to move and attempts at
manipulation do not cause pain.
However, by no means is the bone restored to its original
strength at this point. As time progresses, the primary callus
is gradually replaced. This replacement is enhanced in the
child because appositional growth and increasing diameter
cause the original fracture region to be enveloped. When the
cartilage and woven bone have been replaced by mature,
lamellar bone, the fracture is consolidated and has returned
to biologic stress responsivity.2,37,64,77,78,94,122,127 The rate of
responsivity varies.143 Delay remodeling may lead to refrac-
ture, especially in the active child or adolescent.61,103,113
The cancellous bone of the metaphyses of long bones, the
epiphyseal ossification center, the short bones of the hands
and feet, and even flat bones such as the pelvis and ribs
have a much more delicate, interconnected trabecular net-
work with a much thinner cortex. Fracture healing in
this cancellous bone occurs through formation of an inter-
nal, endosteal callus and a periosteal (external) callus.172
Minimal “cortical” callus is formed. Because of the rich
blood supply to the trabecular region, much less necrosis of
bone occurs at the fracture surfaces, and there is a larger
area and volume of osseous contact to consolidate.
The radiologic and histologic healing patterns of tra-
becular bone following osteotomy or experimental fracture
differ markedly from those of compact bone.2,171 In particu-
lar, cancellous bone healing is characterized by endosteal
trabecular activity. There is an increase in the number and
thickness of trabeculae at the site closest to the lesion (Fig.
8-16). This localized activity is reflected by an increase in
bone density at the level of the fracture. Approximation
between the fragments with an anatomic reduction leads to
a radiodense band of contact healing. In the presence of
Osseous Fracture Repair
FIGURE 8-16. (A) Low-power view of a metaphyseal fracture in the
tibia of an arctic fox (Alopex lagopus). (B) Higher-power view of
(A) showing necrotic tissue and inflammation on the proximal side,
a gap, two bands develop and gradually approach each
other, narrow the gap, and finally fuse. Once union is
achieved, the fused band progressively decreases in density
with remodeling.
Union proceeds more rapidly in metaphyseal bone than
in the dense cortical bone of a diaphysis.152 The osteogenic
cells brought in by neovascularity and the existing vascular-
ity proliferate to form primary woven bone throughout the
hematoma and fracture area, resulting in a rapid, widely
formed internal callus that fills the open spaces of the
spongy, cancellous, frequently comminuted fracture sur-
faces. There is accompanying subperiosteal bleeding to
create the external, membranous callus. The periosteum
normally is more osteogenic in the metaphyseal region than
in the diaphyseal region and would be expected to generate
a greater fracture healing response (in terms of rate, not
necessarily volume). The denser attachments in this meta-
physeal region may mean less callus than in a more readily
stripped diaphysis. However, the response may be prolific in
a displaced metaphyseal fracture. Woven bone is gradually
replaced by more mature bone, although there is not a great
deal of conversion to osteon or lamellar bone, as such bone
is not characteristic of this region until skeletal maturation
approaches.
The initial stages of medullary callus formation in di-
aphyseal regions are probably not that much different from
those of periosteal callus formation, but it seems that a
second stage of intramedullary callus formation exists that is
different and occurs later in the healing process.134,179,180 The
obvious difference in this type of healing relates to mechan-
ical stability. Although motion appears to inhibit the devel-
opment of external callus, medullary callus seems to be
unaffected and may even be enhanced under “controlled”
motion. Medullary callus appears to form without an inter-
mediary stage of cartilage formation. One of its important
functions is to serve as a tissue that initially replaces the frac-
ture gap. New, immature woven bone (biomechanically inde-
pendent) is preparatory for the subsequent development of
255
with inflammation and trabecular thickening (small arrows) forming
the early callus. Subperiosteal callus is present in various stages
(large arrows).
lamellar, osteon bone (biomechanically dependent). This
type of fracture healing occurs in displaced (overriding)
fracture fragments uniting subperiosteal and medullary
callus. In the developing skeleton, there is often a significant
amount of trabecular, endosteal bone adjacent to more
dense cortical bone, thereby improving the rate of fracture
healing (bone modeling) in the child and the rate of
mechanically dependent remodeling.
During the reparative phase the ends of the bone gradu-
ally become enveloped in the confluent, fusiform mass
of callus containing fibrous and cartilaginous tissue with
increasing amounts of bone. The fragments become more
rigid because of internal (fracture site) and external
(periosteal) callus formation. Eventually clinical union
occurs. It must be stressed that “rigid” union, as a specific
endpoint, does not yet exist. At some point during the repar-
ative phase, the last phase of healing (remodeling) begins,
with resorption of mechanically and physiologically unnec-
essary, inefficient portions of the callus and the subsequent
orientation of the remaining trabecular bone along the lines
of stress. Thus the reparative phase is characterized by rela-
tively rapid formation of a randomly oriented bone collar
primarily composed of immature fibrous bone and able to
impart reasonable stability to the fracture site, although the
bone is still capable of some plastic deformation if inappro-
priate stress is applied.
Because the two (or more) fracture fragments usually
remain connected by the periosteum or related material
in a child, it is easy to see how reparative activity could be
conducted from one side to the other relatively easily and
rapidly. McKibben showed that well-developed callus formed
rapidly; but after 2 weeks, if the collars of the opposing frag-
ments did not make cellular contact, they began to undergo
involution. Even if interposed soft tissue was subsequently
removed, the periosteum rarely became reactivated.117 This
period within which the “collar” fragments must make
contact may be longer in the more osteogenic skeleton of
a child.
256 8. Biology of Repair of the Immature Skeleton

Initial Physeal Healing

When the fracture involves the growth plate through the
region of new endochondral bone formation, it becomes
necessary to unite the region of postfracture endochondral
bone formation with the fractured region of the metaph-
yseal bone. This union causes minimal disruption of the vas-
cular pattern and allows rapid reconstitution of solid,
structurally functional bone. The process comes about
because the hypertrophic zone of the cartilage through
which the fracture passes is not as dependent on blood
supply as is the adjacent bone. Therefore only one side of
the fracture is temporarily devascularized. With any
physeal/epiphyseal injury, fracture healing is necessary
between bone and cartilage (metaphysis to physis). Fibrous
tissue initially fills in the separation between bone and car-
tilage (fracture gap). The lack of a direct M-vessel supply and
invasive basement membrane, in the face of continued
physeal proliferation, causes the physis (zone of hypertro-
phy) to widen temporarily. The metaphyseal fragment main-
tains vascularity, which must begin proliferation across the
fibrous gap toward the widened physis. Once vasculature
reaches the physis it rapidly invades the widened area to
reach the usual level of hypertrophic cells. Ossification
rapidly follows. All of this brings the physis back to its normal
width.
Because there is temporary impedance of a normal
process that is rapidly reestablished, and because the normal
vascular systems on either side of the fracture remain intact
despite the fracture, this segment of any physeal fracture FIGURE 8-17. (A) Subperiosteal new bone separated from cortical
heals rapidly compared to the healing of diaphyseal bone. bone. (B) Progressive remodeling.
With the type 2 injury pattern there is also a need for
trabecular bone healing of the metaphyseal fragment
(Thurstan Holland fragment) to the rest of the metaphyseal imposed biologic stresses.167,177 However, as the bone grows
trabecular bone. The fractured metaphyseal cortex heals by and matures diametrically in the diaphyseal or metaphyseal
the aforementioned basic process of hematoma in the gap regions, the new bone is gradually and increasingly incor-
and subperiosteal new bone. porated into the already existent cortical bone, aligned in
With type 3 and 4 patterns there must be trabecular bone accord with predominant stress patterns, and to a great
to trabecular bone healing within the secondary ossification extent inexorably replaced by the normal physiologic re-
center and some type of intercartilaginous healing of the modeling processes (Fig. 8-17). The younger the child, the
fracture line through the versions types of cartilage: physeal, greater is the degree of remodeling and progressive replace-
epiphyseal, and articular. These particular healing patterns ment of the callus. Interestingly, although healing may be
have not been described particularly well. seemingly apparent on routine radiography, magnetic reso-
It has been suggested that indomethacin may be effective nance imaging (MRI) may show a surprising lack of remod-
in preventing early bone bridge formation with physeal eling at the fracture site (Fig. 8-18).
injuries, as there is inhibition of blood flow increase by The end result of fracture remodeling in the presence of
indomethacin during the early period following experimen- the continuing normal processes of growth of the immature
tal osteotomy, as well as retarded bone healing due to inhi- skeleton is that the bone almost invariably returns to its
bition of the inflammatory reaction.96 Fibrovascular bridging original form, or at least is altered in a way that enables it to
certainly is present prior to bone formation (see Chapters 6 perform the functions demanded of it during subsequent
and 7). growth and stress.
There is some suggestion that the control mechanism
modulating much of this cell behavior is bioelectric (piezo-
Remodeling Phase electric), so when a bone is subjected to compressive, tensile,
The remodeling phase is usually the longest of the three and shearing stresses, electropositivity occurs along the
phases. In the child it is theoretically possible for this phase more convex surfaces and electronegatively along the more
to continue unabated until skeletal maturation and even concave ones.4 Tissue culture methods have shown that
beyond in response to constantly changing stress patterns differentiation of the fibroblast may be influenced by
imposed by continued skeletal growth and maturation. The mechanical factors acting through such bioelectric
new bone initially formed by both the fracture callus and the phenomenona.10,11,25,56,58 The piezoelectric effect seems to be
more extensive, but confluent, subperiosteal tissue is ran- a function of collagen within the mineral crystals of bone. It
domly oriented and certainly not capable of withstanding all appears that electronegativity favors bone formation, and
Osseous Fracture Repair 257

FIGURE 8-18. Anteroposterior (A) and

lateral (B) MRI scans in a patient 9 months
after a fracture of the proximal tibial meta-
phyis that appeared well healed on the
clinical radiograph. In contrast, the frac-
ture line was still readily evident on the
MRI scan. The irregular grayish appear-
ance proximal to the fracture suggests
metaphyseal physiology, and blood flow
still has not returned to normal. The oppo-
site leg sustained a diaphyseal fracture
treated with an external fixator for 2
months. A screw hole is still evident dis-
tally 7 months after removal. Note the
grayish appearance of the proximal meta-
physis compared to the distal metaphysis.
It suggests that some of trauma energy
was dissipated into the proximal region
even though the fracture was at mid-shaft.

A B

electropositivity favors bone dissolution. Such an observation
suggests a hypothesis whereby Wolff’s law is explained as a
self-regulating feedback mechanism by which stresses and
strains in the bone modify the bioelectric environment of the
molecular biomatrix in such a way as to direct cellular behav-
ior. This is a complex field, and the reader is referred to
several references for further information.10,12,24,34,40,58,109,117
Studies of bioelectric phenomena in bone have shown that
potentials arise when the bone is stressed and are not com-
pletely dependent on cell viability.1,21–24 Areas of compression
where bone forms in the in vivo state are electronegative.
Live bone exhibits electronegativity over active areas of
growth and repair. Given the proper current and voltage
parameters, exogenous electricity applied to bone may
induce the formation of new bone. Although this concept
has been applied in clinical examples and has had satis-
factory results in many cases, its use in children is not well
defined; moreover, the effects such a bioelectric phenome-
non might have on other parameters such as physeal growth
are unknown. Brighton et al., in particular, showed that a
growth plate explant has accelerated growth when subjected
to an electric field of 1500 V/cm.22 Norton and coworkers
have demonstrated a change in cyclic adenosine monophos-
phate (cAMP) content of physeal plate cartilage subjected to
an oscillating electric field of 1500 V/cm.130
Fracture Motion
The degree of immobilization also affects the rate of heal-
ing. Whereas the emphasis in adult orthopaedics is in-
creasingly on absolutely rigid immobilization, often
coupled with internal fixation, this is less frequently
necessary in children. Nonunion is essentially nonexistent
in children, implying that a certain amount of biologic
(muscular) stress or motion, applied in a reasonably ap-
propriate and anatomic fashion, may enhance fracture
healing. Infections certainly delay healing but not ne-
cessarily prevent it. Pathologic conditions may retard or
preclude healing. However, the presence of even a large
benign lesion (e.g., bone cyst) may not affect eventual
healing in a child, although the process may be delayed (see
Chapter 11).
Terjesen and Svenningsen showed that experimental
animals with unilateral midshaft tibial osteotomies and fixa-
tion with plates were adversely affected if a cast was also
used.166 At 6 weeks none of the osteotomies had healed
with periosteal callus. Only endosteal callus was evident.
The strength of the bones without the cast was 107% of the
normal value, compared with 55% in the group with casts.
The authors thought that the immobilization led to reduced
function of the muscles, which led to decreased blood flow
to the fracture area. They did not address the lack of frac-
ture mobility.
In comparable experimental fractures in mature rabbits
there was a greater blood supply in the cast-treated
osteotomies after 5 weeks than in those treated with rigid
external fixation.43 Histologic examination showed that rigid
external fixation devices altered the proportions of
periosteal and meduallary ossification during the healing
process, decreasing the periosteal response but seemingly
258
enhancing both the endochondral ossification of callus and
the medullary ossification.
In contrast to the concept of fracture healing by method-
ology based on rigid fixation, controlled axial micromove-
ment applied for a short period daily significantly improved
the healing of experimental osteotomies.35
Fracture Bridge
The critical step between the reparative and remodeling
phases is discrete establishment of an intact bone bridge
between the fragments. Although this is the usual concept,
an antecedent cartilaginous or “soft” matrix continuity is
probably essential. Progressive stiffening of this material has
never been addressed experimentally. A process similar to
stiffening of skate and shark egg sacs may be occurring.100
Because it involves the joining of separated segments of
tissue, it follows that the whole system must become im-
mobile, at least momentarily.36 Again, absolute, momentary
rigidity for bone may not be the appropriate concept if suf-
ficient rigidity of the nonossified matrix is already attained.
Once the osseous bridge is established (which may not be
completely circumferential in a child) and provided ade-
quate continued biomechanical protection is given, subse-
quent biologic failure is unlikely.
There are two important points to stress. First, the
processes of replacement and repair are going on continu-
ously and concomitantly in the normal developing skeleton,
and the mechanisms involved in fracture healing are essen-
tially the same (again, these processes are more active in the
child than the adult and more active in the metaphysis than
the diaphysis). Second, there are differences in the process
depending on whether it is occurring in compact or cancel-
lous bone. The process in both types of bone essentially
involves simultaneous bone removal and replacement
through the osteoclast and osteoblast. In the cancellous
bone of the metaphysis or the endosteal surface of the di-
aphysis, the cells are never far away from blood vessels, and
the whole process of bone apposition and replacement takes
place on the surface of the trabeculae.
In compact bone, the more deeply placed cells require the
presence of an adequately functioning perfusion system that
must be restored after the injury-related disruption.89 This is
a much longer sequence of events and is not a common
method of bone repair in the child, except when the frac-
ture involves a densely cortical region, such as the femoral
shaft. The reader is referred to McKibben’s article for a more
extensive discussion of this process, which is sometimes
referred to as “primary bone union.”117,183 Even if primary
union were to occur in a child, further latitudinal expansion
of the diaphysis and metaphysis would erase this process over
time. Particularly in the metaphysis, the cortex is fenestrated
and contains immature osteons that are less biomechanically
determined than those in the diaphysis. These osteons are
extensions from the diaphysis into the transitional region
of corticalized metaphysis. Such osteons may enter into
“primary bone union,” but they are rapidly rearranged with
growth and progressive incorporation of the metaphyseal
cortex into diaphyseal cortex.
Once the fracture has been satisfactorily bridged by the
external callus, it is essential for this new bone to adapt pro-
8. Biology of Repair of the Immature Skeleton
gressively to normal function. Again, this circumstance is
easier in children, in whom the skeleton is actively and con-
tinually remodeling in response to stress, in contrast to the
more static skeleton of an adult. This bone does need a
protected period to respond, especially a weight-bearing
bone. Rapid return to childhood activity carries a risk of
refracture.
Mechanical Properties of Healing Fractures
Experimentally fractured femurs may regain the mechanical
properties of the contralateral intact bone after about 4
weeks in skeletally immature rats and about 12 weeks in adult
rats. For intact bones, both the ultimate torsional moment
or strength and the torsional stiffness increase with the age
of the animals, whereas the ultimate torsional angle remains
unchanged.122
Black et al. studied stiffness and strength of fracture callus
by uniaxial tensile testing and showed that there was a rapid
return of stiffness by 16 days, which correlated with callus
maturation.15 Kirkeby et al. showed that in bone ipsilateral
to an injury (e.g., the tibia in a femoral fracture or vice
versa), there was a significant reduction of mechanical strain
and stiffness both in bending and torsion compared to the
contralateral side.99 Failure through the healing fracture was
by delamination. No similar mechanical studies of fracture
healing strength in immature bone have been undertaken.
Bleman et al. studied the role of mechanical loading by
finite element analysis during progressive ossification of the
fracture callus.16 Their main variable factors were mechani-
cal stress and vascularity. The imposed shear and hydrostatic
stresses in some callus regions cause excessive tensile strains.
In some regions of the callus they may physically damage
the tissues and disrupt the newly formed vascular channels.
Therefore increasingly high tensile/shear loading began to
inhibit fracture healing. Mathematic analyses of wound
healing have also been developed.155 This particular theory
relates to a comparison between the concept of growing
versus sliding as new cells gradually decrease the size of a
wound during the granulation and scar formation or remod-
eling phase. Their application to the skeletal system has still
to be undertaken.
Carter et al. used models of the healing osteotomy.33 The
results suggested that intermittent hydrostatic (dilatational)
stresses played an important role in revascularization and
tissue differentiation when determining the morphologic
patterns of initial fracture healing. They thought that inter-
mittent stresses and the vascularity of the callus were the
major local factors to be considered for effective healing.
They proposed that with a fracture, if minimal stresses or
strains are created and there is a good blood supply, bone
effectively forms. High stress magnitudes encourage tissue
proliferation. High shear and tensile hydrostatic stresses
encourage fibrous tissue formation. High compressive
hydrostatic stresses encourage chondrogenesis. If cartilage
or fibrocartilage forms (tensile), shear predominates. Com-
pressive hydrostatic stresses inhibit endochondral ossifica-
tion. If a high intermittent shear or hydrostatic tensile stress
is maintained, it is unlikely that the fibrous tissue will ossify.
However, if fibrocartilage is formed, there is a possibility that
endochondral ossification will eventually occur.
Cartilage Repair
Noordeen et al. thought that cyclic micromovement
during the weight-bearing period of fracture healing was
detrimental and thus delayed fracture union.129 They
believed that the poor results of cyclical micromovement
versus simple axial compression or diminution by unlocking
the external fixator was due to disruption of the “delicate
developing vascular network.” They noted significant differ-
ences in the excursion between their work (2 mm) and that
of Kenwright et al.97 (0.7 mm) and noted the fact that this
cyclic micromovement was stopped at weight-bearing in
Kenwright’s study and continued in Noordeen’s study. It
seems that micromovement in the natural history of fracture
encourages healing, but late micromovement at a time when
the vascular network has been formed may be detrimental.
Long-Term Changes
Karlsson et al. studied bone mineral content in patients
15–38 years after fracture and found that posttraumatic
osteopenia was still evident in the injured bone decades after
the injury.93 All the patients were adults, and none had sus-
tained their injuries while skeletally immature. Whether the
same phenonmenon occurs in children is unknown.
Ulivien et al. showed significant loss of total bone mineral
(TBM) and bone mineral density (BMD) distal to a frac-
ture.174 This reached statistically significant levels by day 30,
with a maximum reduction by day 120 when TBM and BMD
were reduced to almost half their normal initial values.
Tuukkanen et al. demonstrated a significant reduction in
bone mass in the growing rat bone following mobilization.170
However, they were able to confirm that approximately half
of the lost bone mass was recovered in both tibia and femur
during the subsequent 6 weeks of remobilization. They
thought their results indicated that the loss of the bone mass
was reversible (to a certain extent) and that the recovery
depends on the duration of the immobilization period. This
study was the first to demonstrate that growing bone may
demonstrate bone mass loss and incomplete recovery similar
to that described in adults.
Sigholm et al. showed that the healing of perforated
demineralized bone graft was superior to unperforated
demineralized bone.157 Perforations in demineralized bone
became centers of osteoinduction. The areas within non-
perforated, undemineralized bone became partially seques-
trated in the more central regions because they are slowly
developing revascularization and incorporation of the bone.
Remodeling of Residual Angulation
It has been well recognized that children, in contrast to
adults, have a unique capacity for spontaneous correction of
residual deformities of the initial healing of a fracture. This
phenomenon has been particularly observed in forearm
fractures and most often in that of the distal radius. Certain
general conclusions may be drawn regarding the capacity for
remodeling. First, the younger the child, the greater is the
capacity for correction. Second, the closer the fracture is
located to the physis, the greater is the capacity for correc-
tion. Third, there seems to be a finite limit to angulation.
Certainly the smaller the remaining angulation, the more
complete the correction should be. Finally, the angulation is
259
more likely to correct if it is in the plane of movement of the
hinged joint. Unfortunately, many of these clinical observa-
tions have led to the concept that the biologic process
responsible for correction of angulations occurred at the site
of the fracture. This is incorrect. The angulation of the frac-
ture site per se remains. The correction occurs through
reorientation of the physis. The formation of subperiostal
new bone is on the concave side of the fracture angulation,
and dissolution of bone is on the convex side of the fracture.
Friberg studied the orientation of the growth plate of the
distal radius and ulna and found that for those in which
there was correction of the angular deformity there also was
change in the inclination of the growth plate to the longi-
tudinal axis of the distal fragment, rotating more toward the
longitudinal axis of the proximal fragment.55 In a significant
number of the patients there was an overcorrection of 1°–2°
in relation to the new long axis to the bone.
Friberg applied these same studies to the phenomenon of
valgus overgrowth following proximal tibial metaphyseal
fractures. He found that reorientation of both the proximal
and distal tibial growth plates was slow and that over a 2-year
period a change of only 3° was noted in each of these plates.
He thought this finding corroborated the clinical observa-
tion that fractures with the residual angulation that was not
in the normal plane of movement of the involved joint had
a much more limited potential for remodeling. (For further
discussion of this particular tibial fracture see Chapter 23.)
Friberg believed, then, that 20° of angulation was the most
that should be accepted in distal forearm fractures. This is
in contrast to that of Nonmemann, who observed that up to
30° degrees could be acceptable128 (see Chapter 10).
Cartilage Repair
Unlike bone, the differentiated hyaline cartilage composing
the joint surfaces and physes, and the relatively undifferen-
tiated hyaline cartilage within the epiphysis, appear to have
a limited ability to repair or regenerate.13,112,154,164 In fractures
involving the articular surface in skeletally mature indi-
viduals, the hyaline articular cartilage apparently cannot be
healed by the same tissue (e.g., proliferating articular chon-
drocytes) but is healed instead by fibrous granulation tissue
(Fig. 8-19) and fibrocartilage, which may be inferior as a
weight-bearing joint surface.59,108 The same cellular respon-
sive inability probably applies to epiphyseal and physeal
cartilage.
Cartilage tissue is resilient in response to compression
shearing. However, once damaged, cartilage has limited or
no ability to heal and often undergoes relatively rapid degen-
erative pathologic change.28 This probably occurs in the
child just as readily as the adult. In normal cartilage the pro-
teoglycan–hyaluronate aggregates attract water and become
responsible for the compressive resistance of articular joints.
In contrast, collagen fibrils are responsible mainly for the
properties of cartilage under tension.
There are three general responses to injury: (1) loss or
damage of the matrix macromolecules without visible tissue
disruption; (2) visible mechanical damage or disruption of
the cartilage; and (3) visible mechanical damage or disrup-
tion of the subchondral bone.28 The first type includes
260
FIGURE 8-19. Joint fracture showing inflammatory tissue (solid
arrow) and joint hematoma (open arrow).
injuries that are most capable of healing. The type of blunt
trauma is superphysiologic loading or repetitive high-energy
loading. There is an overall depletion of proteoglycan
matrix, which leads to alteration in the physical properties
of the cartilage, decreased stiffness, and increased perme-
ability. The second type is a partial-thickness injury. Because
articular cartilage is avascular the healing mechanism of
basic musculoskeletal tissue injury (i.e., hemorrhage, fibrin
formation, and inflammatory response) is completely
absent. The influx of cell growth factors normally present
during the healing response is missing. Therefore the chon-
drocytes and cells must elicit the entire healing response.
Chondrocytes near the defect are able to upregulate matrix
elements. However, the dense extracellular matrix keeps the
newly synthesized macromolecules secreted by chondrocytes
from reaching the defect area. The third type, osteochondral
injury with inclusion of the vascularized subchondral bone,
activates the inflammatory response. Nonetheless, complete
restoration of the defect with normal articular cartilage is
rare. Most often the osteochondral defect is healed by a
fibrocartilaginous tissue with properties dissimilar to those
of normal cartilage. The usual sequel of this imperfect
healing is deterioration of the tissue. The additional prob-
lem with this response is that there is restoration of the sub-
chondral plate within 6–8 weeks. The capillaries that at one
time entered the chondral portion of the defect recede, and
complete repair becomes unlikely.
If the fracture surfaces of the cartilage are reduced per-
fectly, the thin seam of fibrocartilage is probably of little
significance to normal joint function, even in a major weight-
8. Biology of Repair of the Immature Skeleton
bearing joint. However, if there is a gap, the reactive fibro-
cartilage may be unable to withstand normal repetitive joint
motion and may contribute to early degenerative changes.
Such degenerative changes may occur even before the end
of skeletal maturation. Articular cartilage, even in the skele-
tally immature subject, may live, grow, and calcify, but not
ossify, when completely detached from the subchondral
bone, provided it has access to the synovial fluid.163 Because
of this capacity and the absence, or minimal presence, of
blood vessels, articular cartilage nutrition is mainly synovial,
although there is evidence of some diffusion from underly-
ing subchondral bone. This allows joint “mice” to enlarge
while also changing shape, so they no longer fit the original
site of an osteochondral fracture.
With intraarticular fractures, an additional problem is
imposed. Synovial fluid apparently contains fibrinolysins.87
These fibrinolysins have the capacity to lyse initial clot for-
mation and retard the aforementioned first stage (inflam-
matory phase) of fracture healing. However, to consider this
as the cause of nonunion in fractures such as those involv-
ing the lateral condyle of the distal humerus is inappropri-
ate, as the real problem in many of these fractures is rotation
of the fragments and apposition of nonossifying articular
cartilage to the normal reparative osseous regions and, more
importantly, constant (excessive) micromotion of the vari-
ably coapted fracture surfaces.
Articular cartilage does not ossify under normal circum-
stances and therefore cannot participate effectively in the
normal biologic repair process of a fracture of the ossifica-
tion center. In one study a core of articular and underlying
epiphyseal cartilage was reversed 180° and replaced into
the defect. As the secondary ossification center enlarged, it
enveloped the core. The surrounded articular cartilage of
the reversed core failed to ossify, although the epiphyseal car-
tilage did, “creating” bone on the joint surfaces.118
The physical and chemical structure of normal hyaline
articular cartilage has been studied extensively, but little has
been published regarding reactions to injury and repair, par-
ticularly in the skeletally immature human.118 Observations
in animals have been described.31,41,114 The seemingly slow
metabolism and physiologic inactivity of joint cartilage were
established mainly from studies on animals and the general
view is that if cartilage has any reactions at all they are so
slow they may be neglected.30 Although this may be true for
articular cartilage in the skeletally mature individual, the
growing chondro-osseous skeleton is quite active biologically
and is capable of considerable change, even when injured.
Undoubtedly, this principle applies to cartilaginous as well
as osseous components.
Along with the rearrangement of cartilage cells and the
appearance of subchondral bone that take place with
increasing age, there are conspicuous changes in the carti-
lage matrix. There is less collagen and more proteoglycans
in the fetus and young child than in more mature matrix.
The developing matrix progresses through biochemical
changes characterized as metachromasia. From a histo-
chemical standpoint, this phenomenon consists of a strong
reaction with toluidine blue but a weak or absent periodic
acid-Schiff (PAS) reaction.147 With increasing skeletal
maturation, the PAS reaction becomes stronger and the
metachromasia less intense, although it is never completely
Cartilage Repair
lost. The collagen component becomes increasingly obvious
and prominent.
It is reasonable to suggest that during growth cartilage
cells first form an excessive amount of highly polymerized,
sulfated acid-glycosaminoglycans. The cartilage first loses its
metachromasia; then part but not all of the epiphysis or artic-
ular region becomes PAS-positive. The considerable varia-
tions in the shape of the cartilage cell and in the extent and
shape of the metachromasia around it are evidence of the
variable physiologic state of the cell, which is by no means
inert.
The repair of immature cartilage may originate from
several sources. Proliferation of cells from the intact cartilage
and perichondrium may play a significant role in the repair
of defects within the epiphyseal cartilage, particularly along
the nonarticular margins. However, such cellular responses
are not as dominant in the repair of defects in the articular
cartilage. Extension of tissue from the synovial margins may
result in fibrous ankylosis and surface necrosis and does not
contribute to healing (Fig. 8-20). The two principal methods
of repair of linear defects in articular and epiphyseal carti-
lage are by (1) extension of granulation tissue from the sub-
chondral tissue and ossification center and (2) origination
of granulation tissue in the transected cartilage canals.59,139
The articular and epiphyseal cartilages of the femoral
condyles of skeletally immature dogs were capable of prolif-
eration, regeneration, and even complete repair with hyaline
cartilage, although the conditions leading to this type of
repair were not well elucidated.31 The observed differences
in the repair of incomplete and complete defects suggested
that granulation tissue from the subchondral bone of the
epiphyseal ossification center inhibited cartilage formation.
It also suggested that if this initial cellular inflammatory
response could be prevented or minimized (i.e., by accurate
anatomic reduction), the full potential of cartilage repair
FIGURE 8-20. Much of the medial tibial plateau of this type 4 injury
(which occurred 2 years before this specimen was obtained) has
been replaced by fibrous tissue (F), which created a fibrous anky-
losis to the distal femur.
261
might, instead, be realized. Cartilage proliferation was indi-
cated by the presence of chondrons, which are cartilage
lacunae with multiple nuclei.31 However, chondron forma-
tion was a slow process and could occur only in the absence
of granulation tissue. Such granulation tissue is neither
primarily chondrogenic nor displaced to form cartilage sec-
ondarily, except perhaps by gradual fibrocartilaginous meta-
plasia. These researchers were the first to suggest a possible
role for the cartilage, and it has been corroborated in our
laboratory.
Cartilage repair in Holstein calves (distal femur) firmly
established the primary roles played by the subchondral
region and cartilage canals in the formation of reparative
granulation tissue.114 Whenever cartilage canal systems were
present at or near the fracture site, capillary proliferation
was evident.
Mechanical injury to articular cartilage has considerable
variation, depending on the nature of the injury (whether it
is deep, superficial, or impactive) and the extent of the
lesion created.112,126 Lacerations involving only the surface
and not extending to the underlying subchondral bone or
ossification center remain stationary for the most part,
neither healing nor progressing to degenerative osteoar-
thritis. When the injury extends to the subchondral bone, a
variable healing response occurs. If effective, it ultimately
produces a form of hyaline cartilage with some fibrocarti-
laginous elements. If the defect is not too large, the carti-
laginous material fills the defect and restores the surface
continuity, but it may undergo degeneration and lead to
localized, but probably nonprogressive, osteoarthritis.
Loading or impactive injuries to the cartilaginous sur-
face, whether single or repetitive, that exceed a critical
threshold cause injury not only to the chondrocytes but
also to the underlying bone; and at least in experimental
studies, such injuries progress rapidly to an osteoarthritic
lesion.
Katsaros et al. used costal cartilage with its accompanying
perichondrium to resurface injured articular joints.95 Two
patients were 15 years of age at the time of the procedure;
one had an excellent result, but the other had a poor func-
tional result.
Llinas et al. studied healing and remodeling of articular
incongruities in a rabbit fracture model.108 They created
step-off defects rather than full-thickness defects. Cartilage
and subchondral bone appeared to adapt to this surface
incongruity by modifying their structure. There appeared
to be a “flow” of cartilage to the articular surface, rounding
off the step-off defect. Presumably a similar response may
occur in the immature skeleton and joint. Thus mild step-
off defects do have some capacity for creating a reasonably,
but not anatomically, congruent joint and function.
Homminga et al. tested fibrin glue for chodrocyte trans-
plantation.86 They found that even when embedded within
the fibrin glue group chondrocytes multiplied and retained
their morphology and produced matrix.
Shapiro et al. showed that in full-thickness defects of artic-
ular cartilage the chondroblasts and chondrocytes were
derived through proliferation and differentiation of mes-
enchymal cells of the marrow.153 The residual adjacent artic-
ular cartilage did not participate in the repopulation of the
defect. These studies were done in mature rabbits. Whether
262
the immature cartilage, particularly the segments of epiphy-
seal cartilage destined eventually to transform into bone,
would respond in a similar or different matter was not
addressed in this report, but the question certainly needs to
be studied.
Healing of the osteochondral defects by fibrous tissue has
been described as potentially less than ideal, but in an inter-
esting anatomic study, Fuss showed that fibrous tissue or
fibrocartilage is a normal constituent of significant portions
of the tibial plateau in the kangaroo knee joints, and that
this tissue effectively damps and transmits joint reaction
forces to contiguous hyaline cartilage.59 They thought that
this fibrous cartilage covering the plateau was compliant and
readily served the function of deforming enough under high
joint loads (repetitive jumping) to allow surrounding regions
of the articular cartilage to share in carrying those loads,
thereby magnifying the articular contact surface and
decreasing the magnitude of the peak unit loads in the
regions of the fibrous tissue path. This pressure-absorbing
mechanism represents the evolutionary response to the
higher articular stress generated from normal kangaroo
locomotion. Accordingly, formation of fibrocartilage in
certain regions of the developing tibial plateau or femoral
condyle may not be totally detrimental to the subsequent
effective joint function.
The assessment of cartilage injury healing is often difficult
because methods of ensuring whether the initial injury even
occurs are limited.28 Obviously, damage that involves only
cartilage is not evident radiographically, and even MRI is of
limited potential for effectively elucidating focal areas of car-
tilage damage and alteration of water content (hydration).
However, some mechanical injuries must disrupt the articu-
lar cartilage sufficiently to lead to altered repair by mechan-
ical responsiveness and progressive degeneration of the joint
surface. Arthroscopic examination of injured joints certainly
corroborates visible articular surface disruption as a fre-
quent occurrence in association with other joint injuries and
significant injuries.
It is certainly well recognized that joint instability is asso-
ciated with progressive articular cartilage deterioration. Joint
instability probably causes focal increased loading in certain
regions of the articular surface. Focal changes in surround-
ing areas of more normal responsiveness may still lead to
decreased proteoglycan aggregation and concentration,
increased matrix permeability, and decreased matrix thick-
ness. Changes in the proteoglycans that cause these mechan-
ical changes secondarily increase the loading of the matrix
collagen fibrillar meshwork and cause it eventually to begin
to fail, which leads to fissuring of the cartilage. Injuries of
the third type involving both the cartilage and subchondral
bone elicit hemorrhage and inflammation from the con-
tiguous trabecular bone adjacent to the subchondral plate.
A repair eventually fills the bone defect and a variable
portion of the cartilage defect. The defect in the cartilage
rarely fills with completely reparative tissue. Furthermore,
reactive cartilage tissue differs significantly from the normal
surrounding cartilage. It also lacks blood vessels once the
subchondral bone re-creates the tide mark. The composition
and structure may be intermediate between hyaline cartilage
and fibrocartilage. This area, depending on size, is mechan-
ically ineffective and progressively breaks down to expose the
underlying subchondral bone.
8. Biology of Repair of the Immature Skeleton
Smith et al. using both adolescent and mature rabbits
showed that immobilization initially led to prominent sub-
chondral vascular interruptions and alterations within the
subchondral bone, and that these aspects of bone loss and
attempts at remodeling always preceded erosive cartilage
aggregation.159 Damage and disruption of the secondary
center of ossification accordingly could significantly affect,
over an extended period of time, the overlying articular
surface, its mechanics, and its ability to withstand normal
joint motion.
Experimental defects in cartilage may be filled in to some
extent by cartilage or matrix flow.27 The flow formations
exhibited bending of the collagen fibers centrally into the
defects, reduction of metachromasia, cell cluster formation,
and areas of reduced cell density. Flow seems to be a mechan-
ically induced phenomenon at the rims of cartilage lesions
that contributes little to reduction of the size of large osteo-
chondral defects. Flow is not associated with new cartilage
proliferation or production of cartilaginous matrix at the
rims of the lesions.
Calandruccio and Gilmer were the first to mention the car-
tilage or matrix flow phenomenon in studies with skeletally
immature puppies.31 Shear stress to cartilage is the most
important biomechanical stimulus for cartilage flow. Flow is
more evident in weight-bearing than in non-weight-bearing
areas. This is different from cluster formation.47 Flow is a
time-dependent mechanism that is evident within the first
few weeks of creation of a cartilage lesion.
Continuous Passive Motion
The use of continuous passive motion (CPM) immediately
after surgical repair of articular cartilage defects and injuries
seems to produce better results than when application of this
technique is delayed.71,150,156 The clinical ramifications are
that CPM machines have a great deal of potential for helping
to repair articular defects such as osteochondritis dissecans,
but that they must be utilized shortly after open reduction.
The same applies to intraarticular major fractures, such as
type 3 or 4 growth mechanism injuries, for which early
motion with reasonably rigid fixation should be considered.
An additional effect of CPM is the more rapid clearance of
a hemarthrosis from a synovial joint.131
Tendon and Ligament Repair
Traumatic injury within the substance of developing tendons
and ligaments is infrequent prior to complete skeletal mat-
uration. Biomechanically, immature chondro-osseous tissue
is usually the weakest component when compared to
attached musculotendinous or ligamentous units. Tendons
and ligaments do not always attach directly into the devel-
oping skeleton by Sharpey’s fibers, as they do in the mature
(adult) skeleton. Instead, the tendons attach to the cartilage
of modified growth regions (e.g., the lesser trochanter or the
tibial tuberosity) through a fibrocartilaginous intermediary
tissue or to regions of the perichondrium or periosteum
more densely associated with the underlying bone (i.e.,
near the physis and metaphysis).24,78 The molecular nature
of these attachments (e.g., the types of collagen, matrix
Nerve Regeneration and Repair
proteins) have not been detailed, nor have the temporal
changes of increasing biomechanical demands been
described.
Such methods of soft tissue/chondro-osseous continuity
allow the attachments to “grow” as the bone elongates. The
intrinsic capacity for elastic and plastic deformation without
failure is much greater in the ligaments and tendons than it
is in the bones; and only when the child is nearing the end
of the adolescent growth spurt do these structures exhibit
decreasing laxity and increasing tendency to intraligamen-
tous failure.
Experimental work has demonstrated that in an intact,
mature musculotendinous-osseous system the muscle belly
itself is the weakest point and ruptures under controlled
experimental circumstances.184 In children, muscle ruptures
are infrequent; and failure in these systems, at least in vivo,
appears to be through the nearest available bone, which
invariably fails in tension. The collagen orientation flows
smoothly from tendon into perichondrium and subse-
quently into the epiphyseal cartilage. Ossification introduces
“disruption” in a unit that is initially adapted to tensile
stress.136 This disruption certainly appears to be the basic
failure mode in the Osgood-Schlatter lesion (discussed in
Chapter 23).
The principal blood supply of a tendon is not from the
chondro-osseous insertion nor from the muscular origin;
rather, it is along the tendon from the mesotenon. The best
described examples are the vincula of the digital tendons.
Anastomoses are minimal between mesotenon supply areas
(a situation similar to the developing spinal cord-watershed
areas). A portion of the tendon deprived of its blood supply
may undergo localized degeneration.
The ends of a damaged tendon, compared with osseous
fracture surfaces, do not contribute significantly to the
initial healing process. Instead, the essential source of
reparative tissue is fibroblastic infiltration from the sur-
rounding soft tissues.32,92,138 If the tendon ends retract, they
are less likely to reapproximate each other, although
such spontaneous reattachment may occur in the child,
especially if the disruption is near either the cartilaginous
insertion or the musculotendinous insertion. The latter
region has a cellular structure not unlike that of the physis
and may facilitate repair without surgical intervention in a
child.136
The joint ligaments and capsules generally attach directly
and densely into the epiphyseal perichondrium. Under
polarized light, continuity of the collagen elements between
ligament and cartilage is readily evident. With time, the
epiphyseal ossification center expands and gradually reaches
the epiphyseal margins, forming a subchondral plate of bone
into which Sharpey’s fibers attach. Such expansion, depend-
ing on the child’s age at injury, may eventually encompass
the original injury, obviating any initial injury response. The
closer the ossification center is to the ligamentous attach-
ment, the more likely it will be avulsed. This osseous region
is certainly highly susceptible to failure. The laxity of the
developing ligaments allows a much greater degree of dis-
tortion without failure. However, this laxity decreases with
increasing age, which makes the ligament more susceptible
to disruption within its substance.
If the ligament fails at the osseous level (e.g., mid-
substance anterior cruciate ligament versus the anterior
263
tibial spine), healing is by fracture healing and is usually
rapid. However, if the ligament itself is damaged, it heals best
if reapproximated. Sutured ligaments subsequently tested
under tension are stronger than nonsutured ones, which fre-
quently fail through the area of scar tissue.41
Healing of both tendons and ligaments is based on
sufficient anatomic reapproximation to allow bridging with
collagen and fibroblastic tissue (analogous to callus forma-
tion) and subsequent reorientation of the collagen to
reestablish tensile strength. Again, because these tissues nor-
mally are growing and undergoing considerable remodeling,
the capacity for repair, even spontaneous repair, is much
greater in the musculoskeletally immature child than in the
adult.
Frank et al. compared ligament healing to injury loca-
tion.53,54 In experiments in which the medial collateral liga-
ment was sectioned adjacent to bone at either the fibula or
tibia and subsequently reopposed with sutures versus animals
that had no substance tears followed by repairs had signifi-
cant differences. The new insertion repairs were character-
ized by callus-like formation at the tibia insertion. Repair of
insertional injuries was slower than repair of mid-substance
injuries, although after 40 weeks no specific differences per-
sisted. All injured ligaments had ultimate strength and were
15–35% short of normal at 40 weeks. These results suggested
that rabbits healed more slowly than those injured in
the mid-substance and developed abnormal insertional
morphology.
The processes of healing of the ligament are similar to
wound healing. Owing to the intrinsic “poor” vascularity of
ligaments, however, the initial inflammatory phase takes
longer than wound healing. After approximately 1 week a
process of revascularization forms a diffuse vascular network
within the tissue that is predominantly fibroblastic in nature.
Collagen fibers are initially irregularly oriented. The
fibers gradually become arranged along the stress axis of the
ligament, and the scar tissue becomes less cellular. Over a
period of months the tissues become more structurally orga-
nized and remodeled to resemble ligament tissue micro-
scopically. However, the scar matrix always remains slightly
disorganized and hypercellular compared to normal undam-
aged ligamentous tissue. Early motion probably has a bene-
ficial effect on ligament function and particularly on
orientation of the reactive tissue during this scar formation
process.
Tendon healing is closely related to ligament healing. In
contrast to ligaments, tendons contain fewer fibrocytes
and have more collagen (almost exclusively type I), and they
have a different collagen-processing pattern. The overlying
paratenon and surrounding connective tissues play a do-
minant role in tissue reactions to injury. By the third or
fourth day the cells of the tendon sheet start to proliferate
and invade the initial blood clot. As in ligaments, the heal-
ing process is slow and is one of progressive structural
orientation of collagen and other extracellular matrix
components.
Nerve Regeneration and Repair
Injuries to peripheral nerves represent a challenging surgi-
cal problem. Healing of the injured nerve is a unique bio-
264
logic problem. Nerve cells do not multiply after injury.
Instead, each severed neuron extends new peripheral
processes to restore the axoplasmic volume lost with the
amputation of the original axon. This proximal cellular
repair contrasts with the intense proliferation of fibroblasts
and endothelial cells at the site of injury and Schwann cells
in the distal segment.110
Within the first few days or weeks after transection of a
nerve trunk, axons in the proximal stump produce a large
number of collateral and terminal sprouts that advance dis-
tally. At the distal part of each sprout, there is a growth cone
or swelling from which several filopodia arise. These filopo-
dia explore the local environment, displaying constant move-
ment. Contact guidance of these structures may be provided
by surfaces of cells or axons.110
The distal axon segments undergo wallerian degenera-
tion. The loss of axonal continuity is followed by prolifera-
tion of Schwann cells in the distal axonal segment. The
Schwann cells line up in columns. Sprouts growing from the
proximal nerve may approach these Schwann cell columns
and are thereby guided to the periphery. Misdirection of
these sprouts at the level of injury into the connective tissue
or external to the nerve can be a major problem. Animal
experiments have shown that the rate of growth in the
distal segments, once they reach the Schwann tubes, is
2.0–3.5 mm/day after transection (neurotmesis) and
3.0–4.5 mm/day after crush or stretch (axonotmesis).
Axonal growth in humans appears to be nonlinear, with a
gradually decreased regeneration rate in distal parts.110 In
humans, rates of 1–2 mm/day are realistic. The rate may be
faster in a child.
Because nerve repair may result in a great deal of axonal
misdirection at the suture site, the incorrect peripheral rein-
nervation patterns may lead to new patterns of sensory
impulses in the afferent fibers and a new cortical projection
of peripheral cutaneous areas. The brain must adapt to the
new language spoken by the peripheral part. Thus although
the complexity of peripheral factors influencing axonal
regeneration is striking, the central nervous component of
the problem is equally important. Sensory reeducation,
implying a detailed program for cerebral adaptation to
the new situation, represents an important component
of rehabilitation following peripheral nerve injuries. Obvi-
ously, these factors have more flexibility in a child than in an
adult.
Considerable neurologic injury may be incurred by rats
experimentally and still lead to full return of function.38
There is a direct correlation between the rate of return of
function and the extent of crushing, but even with signifi-
cant injury there was always some recovery. The only differ-
ence was the length of time to reach full recovery. That study
correlates well with the observation that with most nerve
injuries in children, particularly at the elbow, it is best to wait
for evidence of return of function rather than assume there
is complete transaction in the nerve. Pressure from direct
impact at the time of fracture, when bending is maximal,
may be much greater than at the time of presentation to the
hospital. The effects of stretch during reduction or direct
pressure from the nerve bent over the fracture, the nerve
being incorporated within a callus, or the nerve being
directly impinged on by soft tissue hematoma represent the
8. Biology of Repair of the Immature Skeleton
types of crushing from which the nerve can likely recover in
the child.
Skeletal Muscle Repair
Few data are available regarding structural and functional
recovery of lacerated skeletal muscle after repair in adults.
There are no such reports concerning children. Histologic
studies in skeletally mature rabbits have revealed that, after
the recovery period, the distal segment, which is initially iso-
lated from the nerve supply, showed histologic changes of
fiber atrophy varying in size, increased fibrosis, and nuclear
centralization suggestive of denervation.60 These data
demonstrate that skeletal muscle may recover useful, but
not normal, function after laceration and repair. The
distal segment of the muscle does not shorten and appears
denervated histologically. Tension production within the
whole muscle is diminished, but there is no reliable method
for determining whether the distal segment is adding any
force production to that from the proximal fragment.
It is also interesting that the distal fragment did not stretch
as the proximal muscle contracted. This was probably due
to the increased fibrosis within the distal segment. Essen-
tially, the distal segment then acts much like an elongated
tendon that connects the still innervated portion of the
muscle with the more distal true tendon. Connective tissue
present at the site of muscle repair must be adequate for
the transfer of tension through the distal muscle unit to the
tendon.
Healing of skeletal muscle often leads to extensive scar-
ring and may even exhibit calcification. Muscle necrosis may
cause fatty degeneration of the tissues, with the replacement
of muscular structure by collagenous connective tissue with
considerable or complete loss of function.
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9
Open Injuries and Traumatic Amputations
Engraving of an open distal femoral physeal fracture. (From Poland
J. Traumatic Separation of the Epiphysis. London: Smith, Elder,
1898)
pen injuries involving the musculoskeletal system of
O children have received limited but increasing atten-
tion. Although they represent a relatively small
portion of all musculoskeletal injuries in children, when
compared to adults, these injuries must be treated just as
carefully and usually just as aggressively as they are in adults
to avoid devastating, possibly unnecessary tissue loss and
growth deformities, as well as acute and chronic infec-
tions.13,28–31,38,52 Childhood and adolescent injuries are
increasingly being caused by actually or potentially violent
mechanisms, such as rotary lawn mowers, boat propellors,
trail bikes, go-carts, skateboards, rollerblades, and powered
recreational vehicles, especially as these devices become
more common in the developing individual’s milieu.8,15,38,
40,55,60,61,66
There has been a significant increase in the inci-
dence of penetrating injuries in children.34
Any open fracture in a child or adolescent involves a skele-
tal injury associated with disruption of the skin. The disrup-
tion may be a laceration, a puncture or even a deep abrasion.
The skeletal injury may involve, singly or in combination,
periosteal injury, cartilage fracture, osseous fracture, liga-
mentous injury, joint disruption, or penetration of any of the
aforementioned components by a blunt or sharp object (e.g.,
glass, nail, propeller screw). The opening may extend into
the underlying subcutaneous tissue, the muscle that envelops
the fracture site, the contiguous hematoma, or the fracture
and disrupted periosteum (Fig. 9-1). Although emphasis is
usually placed on direct continuity between the skeletal and
cutaneous injuries, a fracture in the vicinity of any cutaneous
disruption should be treated as an open injury, even if
a definite communication cannot be readily established
(Fig. 9-2).
Once the deforming, injurious force has dissipated, the
chondro-osseous fragments tend to snap back under the sur-
rounding soft tissues. Because of the resilience of a child
compared to an adult and differences in the mechanisms of
injury (e.g., elastic deformation), this is more likely to occur
in the child, so the acute original external wound leading to
deeper internal communication is not always evident or easy
to find. Conversely, a seemingly simple laceration or punc-
ture wound extending down to the periosteum, but not
resulting in or associated with a fracture, must still be con-
sidered an open skeletal injury and treated as such. Such
injuries frequently occur when children catch their ankle in
a spoked bicycle wheel, avulsing the skin and subcutaneous
tissues over a malleolus and exposing the periosteum and
perichondrium, but never sustaining a radiographically
evident fracture.
A frequent concern is whether a small, minor wound,
perhaps even an apparent puncture wound seemingly made
outward from within by temporarily protruding bone,
should be treated similarly to an obviously major open injury
269
270 9. Open Injuries and Traumatic Amputations

tibia, is associated with decreasing blood flow as the skeleton

matures (see Chapter 1).

Basic Open Wound Care

Wound Examination
After the general condition of any injured child has been
carefully evaluated and physiologically stabilized (see
Chapter 3), the specifically injured extremity may be
approached more deliberately. When assessing the severity
of damage to any extremity with an open wound, the func-
tional state of the neurologic and vascular supply distal to
the injury must be evaluated as carefully as possible. It is also
extremely important to assess the general condition of the
skin about the wound. Is there an associated abrasion or
burn? Is there contamination with dirt, clothing, or organic
FIGURE 9-1. Open fracture of the distal radius and ulna with pro- material, implying that they may have been dragged deeper
trusion of the radius (solid arrow) and dissection of air (open arrow) in the wound? What are the dimensions of the wound? Is the
in the subcutaneous tissues. surrounding tissue contused or flayed from the underlying
fascial bed? Is there bone or cartilage protruding from the
wound or muscle, or has it retracted within the muscles?
with a large laceration. No wound is minor when it is directly Detailed exploration of the depth of the wound is usually
associated with a fracture. The presence of any wound makes contraindicated during the initial evaluation in the office or
the fracture an open fracture because of the propensity to emergency room, as these wounds are better treated in a
both hematogenous and direct spread of infection. controlled environment (e.g., operating room), where
Clostridial species, in particular, may be introduced through careful débridement and inspection under analgesia or
even the smallest of wounds and lead to severe complications
(see subsequent section).
The variable stripping of soft tissues that takes place con-
sequent to the original injury renders both the soft tissues
and the skeletal components they cover more susceptible to
infection by creating deadspaces as well as less vascularized
regions and planes of damaged, potentially necrotic
tissue.39,46,67 The destruction or loss of soft tissue, especially
the highly vascular and osteogenic periosteum that normally
ensheathes developing bone, may affect the normal physio-
logic methods of bone healing.
For example, destructive stripping or damage to the
periosteum, particularly in the child, impairs the intrinsic
ability to unite the fracture rapidly and continue subsequent,
normal appositional bone growth in the involved portion of
the metaphysis or diaphysis. The consequences vary with the
extent of soft tissue (periosteal) damage. A severe open
injury may even indicate a need for immediate or delayed
amputation, although every attempt at partial to complete limb
salvage should be made.22,42
The primary problem of any open fracture is usually the
extent of the associated soft tissue injuries, particularly the
involvement of the neurovascular tissues. The degree to
which these aspects of the overall injury are effectively
managed ultimately determines the outcome of any con-
comitant bone or joint injuries and the likelihood of ensuing
complications.5,7,17,57,68,71 When skeletal and soft tissues are
not débrided and covered adequately, osteomyelitis or septic
arthritis may result, often involving the diaphysis, which is FIGURE 9-2. Open injury of the tibia. The laceration was posterior,
less common than the metaphysis as a site of infection in chil- at the level of the distal fracture (open arrow). However, because
dren and also more difficult to treat because of the increased of soft tissue stripping and fascial plane disruption, there was gas
amounts of dense cortical bone within the diaphysis.1 The superior and anterior to the fracture (solid arrow). This creates a
dense cortical bone of any diaphysis, especially that of the potential deadspace that can become infected.
Basic Open Wound Care 271

anethesia are possible. Furthermore, there may be clot for-

mation within the wound, and cursory exploration may
renew vigorous venous or arterial bleeding that has under-
gone spontaneous tamponade.63 If bleeding resumes, it may
be more effectively controlled in the operating room.
Be suspicious of any apparent “puncture” wound.54 Even a
small wound or one that does not seem to communicate with
the underlying bone should be adequately débrided, even if
it only goes down to the muscle overlying a fracture. It is pos-
sible for the bone to penetrate the muscle, be involved in
the laceration, and then retract, leaving no grossly obvious
muscle damage. In addition, devitalized soft tissue creates a
hazard of infection just as easily at the superficial surface as
farther down at the level of the skeleton, so it is still im-
perative to treat this situation as a potentially significant
complication.
Antibiotics are discussed later; but assuming they are to be
used, appropriate broad-spectrum coverage should be
started at the time of initial evaluation, before the patient is
taken to the operating room.3,59 Swabs for culture and sensi-
tivity should be taken from the wound in the emergency
room prior to the administration of any antibiotics. This
practice increases the probability of detecting unusual
microorganisms that may require additional antibiotic cov-
erage beyond the usually recommended protocols.

Débridement
The basic objective of treating open wounds, no matter what
their size may be, is conversion of a contaminated wound to
a clean, eventually closed wound (Fig. 9-3).47–50 Débridement
is undertaken to accomplish the removal of pieces of foreign
material, necrotic tissue, and wound debris. In a borderline
case, particularly one in which a decision must be made
whether to proceed with an amputation of a severely trau-
matized limb, adequate débridement allows an effective
means of evaluating the overall extent of the soft tissue
damage and if it is feasible to salvage some or all of the
extremity. Rarely does the specific chondro-osseous injury
itself determine the need for amputation. As discussed later
in this chapter, children require approaches to levels of
amputation and handling of soft tissue injuries different
from those used in skeletally mature adults with a similar
anatomic injury.
Any wound that breaks the continuity of the skin may allow
introduction of exogenous bacteria and cause soft tissue
infection in the subcutaneous region. Such infection can
proceed deeper into the muscle, where more serious damage
is eventually caused. The conservative approach to such a
wound is exploration and débridement; the radical
approach is simply to clean and dress the wound in the emer-
gency room. The size of a wound often belies the maximal
skin opening at the time of impact or injury. Because skin is
quite distensible, especially in children, the wound may have
been much larger than its apparent size, having retracted to
the smaller size once the deforming force was removed. FIGURE 9-3. Lawn mower injury. (A) Initial appearance of both
The basic objectives of adequate wound débridement legs. (B) Closure after multiple episodes of débridement followed
are as follows: (1) detection and removal of minimally vital by tissue flaps and skin graft. (C) Radiograph showing extensive
or nonvital marginal and deep tissues; (2) detection and irregular bone in the short diaphyseal injury stump that subse-
removal of foreign materials, especially organic foreign quently required revision. The distal tibia requires continuing
material; (3) reduction of bacterial contamination because follow-up to rule out physeal arrest prior to skeletal maturity.
272 9. Open Injuries and Traumatic Amputations

quantitative numbers of bacteria are necessary to start clini-

cal infections, microorganism populations lower than
certain levels are more adequately handled by the normal
cellular defense mechanisms, and the number of bacteria
that devitalized musculoskeletal tissue may effectively react
to is significantly different from that handled by healthy
tissue; and (4) creation of a wound whose viable tissue sur-
faces help cope with any residual bacterial contamination
and heal relatively normally.
Incisions play an important role. Small puncture wounds
may be elliptically excised and secondarily closed, but this
practice is not usually recommended, except as a delayed
closure procedure. Small wounds should be left to close
spontaneously; the scar may be revised later. It is always advis-
able to convert an irregular puncture wound to an elliptical
incision to make subsequent (secondary) closure easier and
to enhance the chances for a cosmetically acceptable thin,
linear scar.
Incisions for débridement should consider (1) the initial
amount of skin and subcutaneous tissue loss; (2) the extent
to which remaining, seemingly viable skin is separated from FIGURE 9-4. Antibiotic-impregnated PMMA beads were used in this
the underlying subcutaneous or muscular regions; (3) the open injury. The proximal fibular and tibial physes sustained type
1 injuries, and the femur had a mid-diaphyseal fracture treated by
need to extend existing wounds for adequate inspection of
an intramedullary rod for the floating knee.
deeper tissues and the best direction in which to do so; (4)
the usefulness of connecting adjacent, but separate, wounds;
(5) the survival prospect of any flaps created by the initial
injury or by any exploratory incision; (6) the amount of skin
that may be sacrificed (if any) to accomplish the most appro-
priate subsequent closure; (7) the usefulness of counterin- Cramer et al. reviewed 40 open diaphyseal fractures of the
cisions to facilitate adequate débridement and arrange lower extremity in 35 children.19 All wounds were treated
coverage of tissue or bone to provide adequate wound with immediate and repeat débridement and early soft
drainage; and (8) the likelihood that any planned incision tissue coverage. Twenty-two fractures healed primarily. There
might transect a major venous drainage system and further were three early amputations and one delayed amputation.
compromise distal tissue physiology. Twelve fractures had delayed healing (more than 6 months).
Débridement should proceed layer by layer from the skin Three fractures developed nonunion. Additional interven-
to the complete depths of the wound. Deep hemorrhage is tion was used in 8 of these 15 delayed union or nonunion
often controlled by packing or tourniquet, allowing an patients to achieve union. Of the 40 fractures, 10 had an
orderly, sequential approach. Any damaged or contaminated infection, but only one led to or was associated with
subcutaneous tissue must be excised. Clean, intact tissue osteomyelitis.
planes usually need not, and should not, be disrupted, as Bartlett et al. reviewed 23 open tibial fractures in children
the supporting circulation of the skin layers is often trans- aged 3–14 years.6 There were six type II, eight type IIIA, and
mitted across such planes. Undermining subcutaneous tissue nine type IIIB fractures. Treatment consisted in débride-
flaps while the wound is débrided is not usually indicated, ment of the soft tissues, closure of any deadspace, and sta-
as primary closure is not generally the goal in such bilization with external fixation. All fractures healed between
circumstances. 9 and 26 weeks. Wound coverage included two flaps, three
When an open fracture, despite débridement, subse- skin grafts, and two delayed primary closures. There were no
quently becomes infected, further treatment is indicated. deep infections. Cullen et al. reviewed 83 children with open
Such treatment may include external stabilization of the frac- tibial fractures.20 The average time to union was 15 weeks.
ture, appropriate débridement of additional damaged soft Eighteen patients (22%) had delayed union, and only one
tissue, pressure irrigation (pulsed lavage), and the use of had a nonunion. Two patients had wound infections. None
antibiotic-impregnated polymethylmethacrylate (PMMA) developed osteomyelitis.
beads, which may release therapeutically effective local doses Haasbeck and Cole described open fractures of the
of drug to the contiguous tissues (Fig. 9-4).15,36,186,187 humerus, radius, and ulna in 61 children.32 Among the
Bowyer and Cumberland compared antibiotic- humeral fractures there were arterial injuries in two and
impregnated PMMA beads with plaster of Paris (POP) nerve injuries in seven. All of the nerve injuries recovered
beads.11 They found a fourfold greater release of antibiotics spontaneously. Forty-six of the children had open forearm
from the POP beads then from the PMMA beads and injuries, with arterial injury in one, nerve injuries in five, and
thought that they were an adequate method of short-term compartment syndrome in five. Normal union occurred in
infection prophylaxis in open fractures. More than one only 36 of 46 children (78%). Delayed union, nonunion,
operative débridement may be indicated in severe, contam- malunion, and refracture frequently complicated type II and
inated wounds. III fractures of the radioulnar diaphyses.
Basic Open Wound Care
Puncture
Puncture wounds are common, but not necessarily trivial,
injuries in children because foreign material may be unsus-
pectingly retained in the wound and cause problems of
chronic inflammation and infection. Until proven otherwise,
it should always be considered that a child who has evidence
of chronic, intermittent inflammation or drainage after an
injury may have retained foreign material that may be radio-
lucent51 Glass and organic material are among the more
common objects. When organic foreign bodies penetrate
joints, it often leads to synovitis. In southern portions of the
United States and other, more tropical parts of the world,
palm thorn synovitis should be considered among the dif-
ferential diagnoses of apparent monoarticular arthritis or
continued soft tissue swelling.9
Use of a Tourniquet
During débridement and the evaluation of extremity
injuries, tourniquets are often used to control hemorrhage
temporarily. Exsanguination should be done by elevating the
injured extremity. Compression exsanguination should not be
used, especially over the areas of soft tissue damage, as it may
spread contamination.
The systemic responses to tourniquet release in multiply
injured children also must be considered.26 Acidosis from the
release of lactate and PaCO2 after tourniquet deflation do
not usually cause adverse effects in healthy children. The
longer any tourniquet is inflated (more than 75 minutes) or
if bilateral tourniquets are used, the greater is the increase
in lactate.53 The greatest decrease in pH occurs with simul-
taneous deflation of bilateral tourniquets. This situation
should be avoided. Multiply injured children are less able than
otherwise normal children to equilibrate acidosis.
Recommendations to minimize the systemic metabolic
effects after release of tourniquets in children under general
anesthesia include the following: (1) tourniquet inflation
times should be limited to less than 75 minutes; (2) con-
trolled ventilation should be used prior to and after tourni-
quet deflation to remove the respiratory component of
acidosis; and (3) blood gas tensions should be checked
within 5 minutes of tourniquet deflation in children with
tourniquet inflation times of more than 75 minutes or when
bilateral tourniquets are deflated within 15 minutes of each
other. The tourniquet is released after débridement and pul-
satile lavage to assess the vascularity of the surface tissues and
to be certain active arterial bleeding does not occur.
Obviously, in children who have experienced trauma and
acute changes in their metabolic pathways, these approaches
may need to be modified. Polytraumatized children are
under observation for central nervous system (CNS) prob-
lems. The effects of systemic acidosis include CNS depres-
sion, cardiac irritability, and decreased sympathomimetic
activity in altered peripheral perfusion. Minimizing an
increased susceptibility to these problems should be the
orthopaedist’s goal.
Muscle
Muscle tends to respond differently from skin to direct
trauma and, particularly, may develop localized areas of non-
273
vital tissue that are overlooked.58 Such devitalized areas may
be acute, due to direct injury or to selective vascular (small
vessel) damage, or chronic due to progressive pressure (com-
partment syndrome) or infection. Infection may be slow to
develop, especially with the unusual microorganisms such as
Serratia marcescens. Bacteria may take advantage of compro-
mised muscle or other soft tissues. Devitalized tissue offers
an excellent culture medium for subsequent bacterial
growth, especially infections caused by anaerobic and facul-
tatively anaerobic microorganisms. If there has been signifi-
cant damage to an arterial supply of the damaged muscle or
a segment of it, it may be necessary to resect some or all of
the devitalized muscular tissue. Complete ischemia may
produce muscle death in a few hours. Compartment syndrome,
in contrast, is slower to develop but is usually evident within 48
hours.
Several factors may be used to assess the viability of dis-
rupted muscle. Color may be misleading. What presents as
dark, seemingly abnormal tissue on the surface may be only
a thin layer of blood underneath the epimysium. When the
epimysium is incised and this seemingly necrotic material
(clot) removed, the underlying muscle may be normal.
Muscular tissue consistency is subjective and basically
relates to the firmness of the examined muscular tissue. The
less firm the muscle, the greater is the probability of damage
and the need for resection. Contractility best defines muscle
viability. Muscular tissue that readily retracts is probably alive
and sufficiently vascularized.
The capacity to bleed must be qualified. The presence of
an active arterial bleeder may mean that a vascular conduit
through the muscle has been transected. This bleeder may
be conveying blood to another area and not necessarily pro-
viding adequate capillary perfusion to the area of immedi-
ate concern. Persistent bleeding from capillaries suggests
that the muscle is likely viable.
Consistency and capacity to bleed are significant features
for judging viability of the muscle, with color being the least
useful indicator of potential viability.64 It is best to err on the
side of questionable viability during the initial débridement
and reassess the muscle tissue 24–48 hours later.
Periosteum
When débriding in the region of the fracture, care should
be taken not to remove any more periosteum than is
absolutely necessary. This tissue is essential to the ability
of the diaphysis and metaphysis to heal a fracture and to
“regenerate” any cortical fragments that may have been
missing (Fig. 9-5). Loss of both bone and overlying perios-
teum may cause a permanent defect, subsequently requiring
the use of a bone graft.56,69,72 As was discussed and illustrated
in Chapters 1, 6, and 8, the periosteum of the immature
skeleton is an osteogenic tissue that not only has a dominant
role in membranous, appositional bone formation along
the shaft but also significantly controls longitudinal growth
by providing tension to regions of the growth plate.
Extensive dissection and removal of portions of the perios-
teum, particularly in a circumferential manner, may
adversely affect longitudinal growth and localized osteogenic
responses.
274 9. Open Injuries and Traumatic Amputations

FIGURE 9-5. (A) Open radioulnar fracture treated with débridement and a sta-
bilizing medullary pin. (B) Several weeks later there is “regenerating” bone.
(C) One year later.

Soft Tissue Coverage
Few studies have been directed toward the specific problem
of extensive open fractures in children. Anderson, Arga-
maso, and colleagues1,2 approached the problem in adoles-
cents by using percutaneous, transosseous pin fixation stabi-
lization, skin grafts, and débridement to treat fractures with
complicating, posttraumatic osteomyelitis and those that
were difficult to close by routine methods. For many years
surgeons have suggested that large open defects of the lower
Basic Open Wound Care 275

extremity should be covered with pedicle flaps, yet most have

advised against using these flaps, especially cross-leg flaps, in
children. It has been thought that children cannot adjust to
the temporary postural restrictions necessary for the success
of such pedicle flaps.
In my experience, however, children are more resilient
and more likely to tolerate such pedicle flaps. Children adapt
amazingly well, so pedicle flaps may be used whenever
indicated.
The main indication for pedicle flaps, even in children, is
that they provide better-padded coverage to bone and
tendon than does the split-thickness skin graft and, in
general, are more resistant to infection.2 Furthermore, an
abundant blood supply, which is potentially beneficial to
fracture healing, is brought into the affected, devitalized
area. Evolving techniques of microvascular anastomosis raise
the possibility of using free grafts based on discrete arterial
distribution (angiosome) patterns (e.g., groin flap). These
repairs require longer surgical times and degrees of exper- A
tise that are not always readily available.
For lawn mower injuries in children, split-thickness skin
grafts (Fig. 9-6) are generally the first choice for early cover-
age.24,25 However, such grafts may not tolerate subsequent
weight-bearing, especially as the child grows and becomes
heavier, and may have to be revised later. Microvascular flaps
may be used for large, lower third leg defects. The medial
gastrocnemius may be used for the knee and upper third of
the leg.3 The soleus may provide coverage for the middle
third of the leg.10 Crossed-leg fasciocutaneous flaps are good
alternatives whenever microsurgical techniques are not fea-
sible. Whenever possible, the weight-bearing surface of the
foot should be covered with a local, vascularized, and most
importantly sensate flap. Larger defects may require free
flaps, cross-leg flaps, or gluteal-thigh flaps.2,12,16,27,35,37,39,41,45,53,
65,70
The small caliber of blood vessels in children less than 2
years of age may make microvascular surgery more difficult
though not insurmountable. Older children with larger
vessels are often better candidates for microvascular flaps
than their adult counterparts because of the lack of damage
to the vessels by acquired diseases, such as diabetes, hyper-
tension, and atherosclerosis. Pediatric patients also usually B
resist recurrent ulceration of foot skin grafts, tolerate pro-
longed immobilization, and are rehabilitated more readily FIGURE 9-6. (A) Lawn mower injury to the foot and ankle. Several
than adults. episodes of débridement were necessary. (B) Subsequent heel flap
The first choice of initial wound coverage is usually a split- coverage. A small area of ulceration is evident in an area of insen-
sate skin. It required further revision surgery.
thickness skin graft; exceptions include exposed bone or
neurovascular structures and the weight-bearing surface of
the foot. See Chapter 24 for a more detailed description
of specific soft tissue defect coverage methods when the foot
is involved. DiStasio et al. used multiple small relaxing skin
incisions to allow wound closure when extensive soft tissue tures with quantitative bacterial counts higher than 105 devel-
swelling is present.23 oped late infection, whereas only 2 of 44 (5%) fractures with
New technology allows a different approach to soft tissue quantitative bacterial counts of less than 105 or negative
defects that ordinarily would require grafting. The progres- quantitative counts became infected.14,153,163
sive enlargement of a volume of skin and subcutaneous tissue
encourages these overlying tissues to grow, effectively
Skeletal Stabilization
increasing the amount (area) of tissue available for subse-
quent flap formation and redirection.18 Concepts of effective internal or external fixation are specifi-
Quantitative bacterial counts have been used, primarily by cally covered in Chapter 4. Basically, when effectively and
plastic surgeons, to assess the ability of primary versus appropriately used, these devices allow much better wound
delayed wound closures and grafting. Fifty percent of frac- care and graft management (Fig. 9-7).
276
A B
FIGURE 9-7. External fixators allow fracture control while treating the soft tissue injuries. (A) Severely mangled hand from being caught
in a farm machine. (B) Stabilization allowed aggressive débridement. A functional hand (although not completely normal) was achieved.
Bone Loss
Complete extrusion of developing skeletal elements from an
open wound is infrequent in childhood injuries, primarily
because comminution of the fracture (i.e., a loose segment)
is infrequent. Those cases in which significant bone loss
occurs present major problems in management (Fig. 9-8).
Khalil reported a closed femoral fracture in which the inter-
calated fragment (lost bone) was displaced into the anterior
abdominal wall.44
Most open fractures are associated with violent injury,
especially power lawn mower or farm machine accidents.
As such, there is usually extensive, concomitant soft tissue
injury. Primary management must be directed at adequate
débridement of devitalized tissue, with an attempt to save as
much of the periosteum and the contained skeletal compo-
nents as possible.62 As indicated, débridement should be
repeated (continued) until the tissue components, both soft
and skeletal, are unquestionably viable and there is no
further risk of infection. Foreign material is often embedded
in tissue interstices and must be completely removed. All
wounds should be left widely open and never closed pri-
marily. Specimens for culture should be taken initially to
assess contaminants. Quantitative bacteriology is an effective
means of monitoring the potential for subsequent infection
and may be used to assess the optimal timing for indicated
wound closure and reconstruction of the skeleton. If a
segment of bone has been extruded, the remaining skeletal
elements must be stabilized, preferably with some type of fix-
9. Open Injuries and Traumatic Amputations
ation. An intact fibula renders some intrinsic stability and
may be augmented by an external fixation device, with the
skeletal fixation pins placed in the normal tissue above and
below the injured area. This practice allows repetitive wound
care without jeopardizing the overall stability. Metallic stabi-
lization should not be placed within the area of acute injury,
if possible, as the presence of a foreign body mass increases
the risk of infection. Replacement of any devitalized, con-
taminated chondro-osseous fragments is usually contraindi-
cated, although Kao and Comstock autoclaved and replaced
a fragment.43
In a report of segmental loss of the femur with open injury,
it was feasible to maintain soft tissue length through the use
of external fixation devices.56 This practice allows subsequent
bone grafting or vascular autograft if subperiosteal mediated
new bone formation does not occur within any remnants of
the periosteal sleeve. Callus formation within 3–6 weeks is
a good indicator of sufficient remaining periosteal sleeve
support healing without the need for bone grafting or inter-
nal fixation. The basic criteria for treatment of open
fractures associated with segmental bone loss include preser-
vation of limb length, maintenance of useful function to
adjacent joints and muscle groups, and union of the bone
within 6–12 months.
If segments of the periosteal tube can be salvaged, every
attempt should be made to do so. As shown in Chapter 1,
the periosteum is extremely osteogenic and capable of con-
siderable new bone formation (Fig. 9-5). However, damage
to this structure, a type 9 growth mechanism injury, may
Basic Open Wound Care
FIGURE 9-8. (A) Open injury of the proximal humerus. (B) Initial
treatment, prior to referral, included internal fixation and inappro-
priate primary closure of the wound. The proximal humerus
became purulent and was “discarded.” (C) Following transfer, an
necessitate placement of a bone graft, which should not be
attempted until there is no evidence of infection and the
wound is well granulated. Quantitative bacteriology, again, is
helpful for timing such bone grafting and skin grafting. If
the remaining skeleton has been stabilized (e.g., with an
external fixator), several weeks may lapse before bone graft-
ing. The graft may be placed through a separate incision
traversing nontraumatized tissue, if appropriate.
Although acute management takes precedence, the long-
term consequences of open injury with loss of chondro-
277
external fixator was applied to maintain length and allow soft tissue
care. (D) Vascularized fibular transplant. (E) Appearance 3 years
later. The fibular physis still appears functional.
osseous elements or damage to the growth potential must be
considered. Significant skeletal tissue loss affects stability.
Growth damage may be considerable and may affect leg
length and gait.
Vascular Bone Transplant
When soft tissue and osseous damage have been extensive,
external fixation and aggressive primary wound manage-
ment allow time to devise a more appropriate long-term
 278 9. Open Injuries and Traumatic Amputations

scheme of treatment. The amount of débridement necessary
to control deep infection may require removal of nonviable
bone segments and damaged periosteum. This limits any
child’s ability to regenerate bone and restore the defect.
After adequately controlling the tissue infection and stabi-
lizing the remaining skeletal components, it is then possible
to use allografts and vascularized bone grafts, as necessary
and appropriate, to attain an intact unit (Fig. 9-9).
Aronson et al. described the use of local bone transporta-
tion for treating intercalary defects.4 Bone transportation

A B C

FIGURE 9-9. (A) This patient was referred 2 weeks after an open injury. She had been placed
in an external fixator. (B) She was then treated by resection of the necrotic bone, internal sta-
bilization, and antibioptic-impregnated PMMA beads. (C) Vascularized fibular transplant was
D carried out 7 weeks later. (D) Two years later she has a stable, weight-bearing leg.
Foreign Bodies
involves moving a free segment of living bone to fill the inter-
calary defects with vascularized bone. The trailing end of the
transported segments maintains continuity with the distract-
ing bone surface by distraction osteogenesis. The leading
end of the transported bone segment eventually fuses to the
target bone surface by transformational osteogenesis.
However, it is sometimes necessary, because of the length of
this process, to subsequently expose the leading end seg-
ments to open the medullary cavity, which may be covered
by sclerotic bone. It also may be appropriate to make trans-
verse fresh osteotomies when getting close to apposition to
encourage a healing response as the final 2–3 mm are closed.
This is particularly necessary when spikes or other angula-
tions are present.
One of the important techniques is that the segment being
transported should be pulled rather than pushed. This
method usually decreases the likelihood of angulation as the
fragments approach each other. Accordingly, the transfixa-
tion wires need to be placed near the leading end of the
transported segment, rather than near the trailing end.
There is also a tendency for the two ends of the leading end
to begin to diverge. The placement of additional wires with
olives and outriggers may be used to control the translation
of the “transport” segment.
Complications from bone transportation include bone
necrosis from excessive local pin stress, wire pull-out from
the transport fragment, and damage to neurovascular struc-
tures that may cross the path of the transport wires due to
anatomic variation, redirection due to scarring from exten-
sive trauma, and so on. Pho et al. used a free vascularized
transfer of the proximal fibular epiphysis and diaphysis to
replace a proximal humeral epiphysis (see a similar case in
Fig. 9-8).349
Bite and Sting Wounds
Bites may occur on any part of the body and be caused by
an array of creatures.73,74,78,89,91,98 The bites are rarely deep
enough to involve the skeletal components, with the excep-
tion of the hand.96 The specific approaches to hand injuries
are covered in Chapter 17. Any animal bite injury carries the
risk of introducing common and rarely encountered bacte-
ria that may cause soft tissue and osseous infection.80–82,85
Phair and Quinton studied 29 human bite injuries.94 More
than one-third of their patients (especially the younger ones)
initially offered an alternative explanation for the injury. A
laceration over the dorsum of the metacarpopholangeal
(MCP) or proximal interphalangeal (PIP) joint should raise
suspicion. All were treated by surgical exploration. In 62%
the wound entered the underlying joint, and in 58% the
bone or cartilage was injured. Significantly less morbidity was
evident in the cases without extension into the joint. Human
bite injuries may be associated with severe complications,
such as septic arthritis, osteomyelitis, and persistent infec-
tion. The term “chondral divot fracture” has been applied.
Brogan et al. reviewed 40 cases of dog bites in children
under 16 years of age that resulted in hospitalization or
death.79 Most were boys (60%). The median age was 50
months. There were three deaths. Most dogs were familiar
to the victim. Injuries to the face, head, and neck were most
279
common. Most bites are unrecorded. The range is probably
500,000 to 2 million dog bites per year. They account for 1%
of emergency department visits and represent a common
childhood health pattern.
Dog bite injuries to the hand carry a serious risk of infec-
tion.76,78,79,83,95,97,99 Antibiotics and proper wound manage-
ment are essential. Injury to the hand is more likely to lead
to infection (36%) than any other extremity wound (17%)
from a dog.101 A wide variety of microoganisms may cause
infection. Pasteurella multocida has been stressed but is 10
times more likely in a cat bite. Staphylococcus aureus is also
common. The wide variety of potential organisms should
encourage proper culturing for identification. Penicillin or
a first-generation cephalosporin is reasonable for “initial”
treatment. Ampicillin-sulfbactam (Unasyn) and amoxicillin-
clavulanic acid (Augmentin) offer excellent broad-spectrum
coverage. Cat bite injuries require similar treatment.
Janda et al. reported that serious bacterial and viral infec-
tions may occur in nonhuman primate bites, particularly the
herpes B virus, which is enzootic in macaques.88 Herpes B
virus may be fatal. Accordingly, children bit by rhesus and
other Asiatic monkeys of the genus Macaque must be treated
appropriate to the high risk of this infection. Such bites may
occur at zoos or a circus where these animals are often
brought in the open by handlers.
Guidera et al. related that the incidence of shark attacks
is probably underreported.86 There are at least 20–25 docu-
mented attacks per year in Florida. Most are not fatal. The
infecting organism is usually of the Vibrio species.87 The teeth
often produce jagged, ripping lacerations and soft tissue
deficits with extensive blood loss (Fig. 9-10).92
The stinging apparatus of catfish are the bony dorsal and
pectoral fins, each of which contains a barbed spine attached
to venom glands.84 The injury is usually a puncture wound.
The toxins produce a severe localized inflammation that may
predispose the wound to subsequent infection, especially to
organisms normally present in the water inhabited by the
fish.75,77 Many species of nontuberculous mycobacteria
are free-living in both fresh and salt water.100 Radiographs
should be obtained to rule out the possibility of a retained
spine. Treatment includes hot water immersion and
cephalosporins.
Venomous snake bites may occur, especially in the south-
eastern and southwestern parts of the United States. The
venom has a number of serious effects. A significant problem
is the development of compartment syndrome in the entire
limb, even if only a distal part (e.g., toe or finger) is bitten.
Compartment releases are essential.
Foreign Bodies
A foreign body is any substance that is not natural to the body
passage or tissue where it is found. Clinical signs usually are
related to obstruction, irritation, or perforation. The symp-
tomatology caused by any foreign body depends largely on
the size, composition, and location and the length of time it
has been present. Organic substances produce more intense
tissue response than inorganic substances.102,103,107
An unsuccessful attempt to remove a foreign body usually
makes the situation worse. The properly formatted approach,
280
FIGURE 9-10. (A) Open injury with a femoral fracture caused by a
shark attack. There was extensive soft tissue damage (arrow) and
loss over the entire leg and gluteal region. (B) Internal fixation to
stabilize the femur. Unfortunately, all the wounds were initially
closed primarily within a few hours of the injury, which is inappro-
with appropriate instruments, fluoroscopy, and sedation or
anesthesia, enhances the likelihood of success.
Ramanathan and Luiz106 and Doig and Cole105 both
reported problems with penetration of plant thorns into
joints, particularly knee joints. Arthrotomy and synovectomy
were often necessary, in contrast to joint washouts and partial
synovectomy. Careful review of the entire joint is necessary,
as fragments of the thorns may be retained within the joint,
even when the major portion (seemingly all) of the thorn is
removed. Palm thorns may cause reactive synovitis.104 Specific
toxins in the thorns are probable etiologic agents. In most
patients, there is an average delay of almost 10 weeks
between penetration of the thorn and the eventual presen-
tation for treatment.
Palm thorn synovitis is usually mild, with the initial symp-
toms being tolerated, delaying presentation for treatment.
The differential diagnosis is usually septic arthritis. Cahill
and King recommended arthrotomy and extensive synovec-
tomy.104 In Ramanathan’s group, four patients were cured by
irrigation of the joint, apparently removing whatever stimu-
lation was present, with synovectomy being reserved for cases
that failed to respond to profuse irrigation.
Fine fragments may also be shed from the palm thorn and
become incorporated in the synovium, where they can
produce a hypertrophic synovitis through granulomatous
formation containing foreign body giant cells. The small
particulate matter is what necessitates more complete syn-
ovectomy and is probably retained in patients who do not
respond to irrigation.
A number of marine organisms can cause similar problems
when a sharp piece of organic material penetrates the
tissues. A barb from a stingray may cause not only a reaction
to the retained foreign material but also an intense reaction
to the venom.90,93
9. Open Injuries and Traumatic Amputations
priate for any contaminated or potentially contaminated wounds.
The mouth and teeth of sharks may harbor Vibrio species, which
are endemic to the marine environment. (C) Retained shark tooth
in the fibula.
Infection
The specific consequence of any open injury is the potential
for chondro-osseous infection with bacteria from the skin or
the external environment. Traumatized tissue has a greater
propensity for developing infection (Fig. 9-11) and may be
infected by a much lower quantity of bacteria than usually
would be required for a clinically significant infection to be
established through hematogenous spread in otherwise
normal tissue.21,121,137,142,151,152,156,182,188 Morrissy and Haynes
demonstrated a significant role of trauma in the etiology of
hematogenous osteomyelitis.164 Selective characteristics of
bacteria also affect pathogenicity.152,162,165
Cordero et al. showed that susceptibility to infection was
not only material-dependent but also bacteria-dependent.122
Kingella kingae is becoming a significant musculoskeletal
pathogen.194 Edna and Bjerkheset showed a distinct associa-
tion between blood transfusion and infection in injured
patients.129
General principles for the treatment of infected or poten-
tially infected fractures include (1) appropriate débridement
of necrotic or infected tissues; (2) effective prophylactic
antibiotic therapy; (3) secure fracture stability; (4) open
wound; (5) cancellous bone grafting over earlier, fully devel-
oped granulation tissue; and (6) appropriate wound closure.
Webb et al. showed that the surface-adherent mode of
bacterial growth played a pivotal role in the persistence of
infection involving foreign bodies or dead bones.191 This type
of bacterial growth seems to promote enhanced antibiotic
resistance.
Late infection may occur months to years after a fracture.
Stone et al. described a case of histoplasmosis in a multiply
injured child. They thought the trauma had reactivated a
latent infection.182
Infection 281

A B

FIGURE 9-11. (A) Open physeal injury of the distal tibia. This occurred when a
large, heavy, iron beam from a junkyard fell on this boy’s ankle. (B) The wounds
were débrided and minimally stabilized. (C) Infection ensued, leading to pin
removal. C

Role of Antibiotics development of localized infection; and it decreased the inci-

One of the most important aspects of an open fracture is
whether to treat prophylactically with a broad-spectrum
antibiotic.33,109,110,112,189 This situation is further complicated
by changing antibiotics and changing bacterial sensitivity.122
Patzakis and associates reviewed 310 patients with open
fractures, many of whom were children.172 The incidence of
infection was significantly higher in the untreated group.
The group receiving cephalothin had the most significant
decrease in infection rate. The data substantiate the value of
prophylactic antibiotic administration.
The fact that several days of bacteriologic culturing (at
least 48 hours) must elapse before a wound may be consid-
ered sterile supports the use of a regimen of antibiotic pro-
phylaxis that may be applied to all skeletally immature
patients with open fractures and then discontinued when
and if cultures are truly negative or if the microorganism is
more sensitive to a specific antibiotic or insensitive to the
administered antibiotic.
Clinical and experimental studies have shown that early
administration of a bactericidal or bacteriostatic antibiotic
prolonged the period between initial wounding and the
dence of systemic toxicity, bacteremia, and death, provided
the wounds were primarily contaminated with bacteria sen-
sitive, in vitro, to the specific antibiotic administered.109,193
The early administration of an antibiotic exerted little if any
beneficial effect if the wounds were contaminated with bac-
teria insensitive to the antibiotic.
The optimal period for the effective administration
of prophylactic antibiotics in contaminated wounds is
approximately 3–6 hours after wounding, which may be
after the time of presentation to the orthopaedist. The
ability of various antibiotics to penetrate normal and
damaged chondro-osseous tissue and joints varies signifi-
cantly.111,124,130,148,192 Nonperfused (nonvascularized) cartilage
or bone never gets adequate levels of parenteral antibiotics,
even by tissue perfusion.
The incidence of staphylococcal infection in open wounds
is significant. Many, though not all, of the currently used
cephalosporins have some degree of efficacy against the
Staphylococcus species, particularly when used prophylactically.
However, once a discrete staphylococcal infection is clinically
established, drug sensitivities are essential when selecting spe-
cific antibiotics for the infectious microorganism.
282
Gustilo found that cephalosporin alone was initially effec-
tive in reducing wound sepsis for type I and II open fractures
and that a combination of cephalosporin and aminoglyco-
side was effective for type III open fractures. Penicillin
should be added for soil-contaminated wounds, such as farm
injuries.140
Adequate débridement enhances neovascularization, even
within bone, and thereby increases perfusion of blood and
antibiotics. The use of antibiotics must not be misconstrued as a
substitute for the important principle of adequate surgical débride-
ment. Devitalized bone and cartilage do not have to be
removed arbitrarily, but if they become infected, adequate
débridement is necessary, just as it is for soft tissue damage.
Dellinger et al. described the risk of infection after open
fracture of the arm or the leg.126 Their series of 240 consec-
utive patients included only seven patients who were either
over 65 years or under 18 years of age. They found the risk
of fracture infection was increased in patients with grade IIIB
or IIIC fractures when internal or external fixation was used,
with a lower leg fracture, with any blood transfusion, and
with injuries resulting from motorcycle accidents or motor
vehicle/pedestrian accidents. These factors are less likely to
be associated with childhood injuries. The most significant
risk factors were (1) the greater the severity of the fracture,
(2) the use of internal or external fixation, and (3) fractures
involving the tibia. They concluded that the most important
intervention by the treating physician was to prevent infection
by adequate local wound care (i.e., débridement). They
found no relation between the timing of antibiotic adminis-
tration or the duration of antibiotic therapy and infection
risk. Presumably, these observations would be applicable to
older children who sustain comparable injuries, but they are
probably less likely in children under 10 years of age because
the severity of the trauma mechanism is usually not as sig-
nificant, fixation devices generally are not used, and open
injuries are relatively uncommon. Although their particular
study involved certain regimens of randomized antibiotics,
the choice of any antibiotic(s) should be left to the individ-
ual surgeon based on what drugs are available and which are
contemporaneously appropriate at the time of treatment.
For example, the drugs used by Dellinger et al.126 prior to
1988 may not necessarily be those in common usage or
appropriate, given varying drug resistance and the intro-
duction of newer generations and classes of antibiotics.
Although some might expect internal fixation to be asso-
ciated with an increased infection rate because of the intro-
duction of foreign material directly into the fracture wound,
this reasoning does not seem as relevant to the application
of external fixation devices that are usually separate from the
fracture wound. In fact, the infection rate was higher for
fractures treated with external fixation alone (27%) than for
all fractures with internal fixation (20%).126 Undoubtedly,
the choice of utilizing external fixation devices was probably
associated with more severe soft tissue damage than was
reflected in the statistics analyzed in the study. Their con-
clusion was most important.126
It is striking that local characteristics of the fracture wound pre-
dominate in predicting fracture associated infection risk. While
optimal management and the restoration of normal physiologic
characteristics are important for the prevention of nosocomial
9. Open Injuries and Traumatic Amputations
infections and other complications, local management of the open
fracture dominates the outcome of the fracture. These findings
support the general principles of fracture fixation without further
damage to vascularity and the surrounding soft tissues, and of metic-
ulous débridement of damaged tissues with a willingness to rein-
spect and redébride (with multiple operations, if necessary) the
damaged area.
The data of Dellinger et al. do not support the common
practice of administering antibiotics for 2–5 days following
an open extremity fracture.126 In fact, they found no relation
between either the time when the antibiotics were started or
the duration of their administration with the subsequent
incidence of fracture infection. A prudent course would be
to administer a brief course of antibiotics to discourage early
invasion and multiplication by contaminating bacteria.
Impairment of vascularity and inadequate soft tissue cover-
age of exposed skeletal elements enhance infection. Antibi-
otics may not prevent infection. A brief course of antibiotics
for 48 hours or less minimizes the risk of adverse reactions
and selective pressure for resistant organisms and nosoco-
mial infections.
A clear understanding of the significance of wound con-
tamination and knowledge of the microbial flora that could
be expected in the geographic area where the injury was sus-
tained is needed to administer a rational and effective antibi-
otic treatment for open fractures. Obviously, the area of the
world or even within a given geographic area is going to
affect the endemic (intrinsic) microbial flora. Interestingly,
in the study by Robinson et al. gram-negative rods, most com-
monly Pseudomonas, followed by Staphylococcus epidermidis and
Staphylococcus aureus, were the primary organisms, with about
equal representation.175 Despite the frequency of wound con-
tamination on arrival at the hospital, after thorough débride-
ment only 4 of 89 repeat cultures (less than 5%) 1 day after
débridement were positive for the same microorganism.
Toxic Shock Syndrome
Spearman and Barson described toxic shock syndrome
(TSS) in two children who developed focal cutaneous staphy-
lococcal infections underneath casts.181 TSS is an acute
illness characterized by high fever, diffuse macular erythro-
derma, hypotension, desquamation of skin, and multiorgan
dysfunction. In both cases the cast caused an abrasive injury
that became infected.
Mills and Swiontkowski described fatal TSS following
minor orthopaedic trauma in three patients.161 Other organ-
isms such as Vibrio may also cause toxic shock.176
Osteomyelitis
Direct osseous infection occurs infrequently in children
compared to that in adults, probably because of the lower
overall incidence of open wounds123 and the difference in
cortical vascularity. Because children most commonly get
osteomyelitis through the hematogenous route, such spread
in children with localized trauma from a source of infection
elsewhere must be considered even in the closed frac-
ture.119,131,167,170,183,190 One of the most common causes of
infected fracture in the child is an open injury from a lawn
Infection
mower, with high-velocity tissue injury being coupled with
the powerful introduction of organic debris.128,155
Direct inoculation with bacteria may cause osteomyelitis at
the fracture site. Adequate débridement, as discussed earlier,
is essential to the potential prevention of such infection.
Leaving the wound open to allow continued drainage and
observation can certainly lessen the risk of an undiagnosed
infection. Many open injuries occur on the street, in play-
grounds, and in other areas where the risk of bacteria other
than Staphylococcus (the most common cause of hematoge-
nous osteomyelitis) may be present. In such cases, broad-
spectrum antibiotic prophylaxis is essential. Left untreated
or inadequately treated, significant osteomyelitis may super-
vene, with loss of cortical bone, destruction of periosteum,
sequestration, and chronic disease.
Sorsdahl et al. showed that gallium imaging offered many
practical advantages over indium 111-labeled leukocyte
imaging to diagnose osteomyelitis.180 In particular, quantita-
tive ratios (gallium-to-bone, gallium-to-background, and
spatial incongruency of gallium and bone activity) could be
calculated to give a 93% sensitivity for osteomyelitis.
Peters et al. found polymorphonuclear neutrophil (PMN)
elastase could be detected in the blood at a level of diag-
nostic sensitivity comparable to the nonspecific erythrocyte
sedimentation rate (ESR).173 They found it useful to follow
patients after treatment. PMN elastase, one of the major pro-
teolytic enzymes released by activated granulocytes, degrades
a large number of proteins and the macromolecules of con-
nective tissue (elastin, proteoglycan, collagen).
Hematogenous Osteomyelitis
Hematogenous osteomyelitis secondary to musculoskeletal
tissue injury has been reported as an infrequent complica-
tion of closed fractures in children.108,119,134–136,144,167,169,177,185,195
In a study by Waldvogel and coworkers, one-third of the cases
of osteomyelitis had an association between the infection
and seemingly trivial, blunt trauma, although not necessar-
ily a fracture.188 Farr found no evidence of related trauma in
98 cases of hematogenous osteomyelitis.131
Canale et al. described children with posttraumatic
osteomyelitis.119 One had a wrist fracture and epiphyseal
injury that subsequently progressed to sequestration of a
considerable portion of the metaphysis and diaphysis but
without major evidence of growth deformity. The child,
however, had not completed skeletal growth, and a future
deformity could not be totally ruled out. The other children
had femoral fractures. The first developed osteomyelitis 7
weeks after the skeletal injury, following the onset of acute
tonsillitis. The other had a urinary tract infection with
pyelonephritis and developed the infection 10 days after the
injury. In both patients the microorganism causing the
primary infection also caused the secondary, distant
osteomyelitis at the fracture closed site.
Veranis et al. reported a closed fracture complicated by
osteomyelitis 2 weeks after the injury.185 Pain may have been
lacking or mild because the bone and periosteum were
already disrupted by the fracture.
Valerio and Harmsen described osteomyelitis in a 3-week-
old neonate who had sustained a fracture during delivery.184
A computed tomography (CT) scan showed an enlarged
283
clavicle due to involucrum formation, with sequestration
of the original clavicle. The sequestrum was removed.
Osteomyelitis of the clavicle in neonates is almost always due
to congenital syphilis, rather than Staphylococcus.
Hird and Byrne described a prevously healthy 17-year-old
boy who was injured in the thigh during a football game.146
He developed gangrenous streptococcal myositis after an
initial diagnosis of a thigh bruise. Delayed diagnosis is
common with this injury.
There may be a delay in recognizing the acute, compli-
cating osteomyelitis in these patients with more obvious
skeletal injury. It is not until fluctuance develops that infec-
tion of the fracture site is seriously considered as the cause.
Several clues should be noted. After the initial pain and
swelling have subsided, pain of a different character
becomes a complaint. The pain is constant, progressive, and
unrelieved by immobilization. A definite decrease in the
local signs of the skeletal injury should be present. Patients
usually have an obvious primary focus of infection and
exhibit a persistent febrile course much out of proportion to
that seen with an uncomplicated fracture or with an uncom-
plicated concomitant urinary or respiratory tract infection.
If hematogenous osteomyelitis complicates a fracture, par-
ticularly in a child, open débridement of the infected area is
indicated. At the time of initial injury, a deadspace is created
that is filled with hematoma. It may be transformed rapidly
into a cavity filled with purulent material. Many of the
enzymes released by bacteria and the reactive granulocytes
(white blood cells) are highly destructive to developing
chondro-osseous tissue.154 Penetration of an abscess by sys-
temic antibiotics is slow, if achieved at all.158,192 There is also
a variable amount of devitalized bone that may be seques-
trated. Such dead bone is inadequately perfused by antibi-
otics. Drainage should be through an incision of reasonable
size with adequate irrigation and débridement, and the
wound must be left open.
Late Infection
Late-appearing osteomyelitis may also complicate fractures
in children.118,127,145,149,166,168 Often these cases are due to low-
virulence microorganisms that are variably sensitive to com-
monly administered antibiotics (Figs. 9-12, 9-13). Figure 9-19
shows a boy who sustained an open distal radial fracture that
was successfully treated with no evidence of infection.
However, several years later, he presented with a swollen,
tender forearm and biopsy-proven osteomyelitis; Serratia
marcescens was the causative organism. It is likely that he had
harbored the infection from the time of the initial injury.
Such a delay in presentation is not uncommon with
osteomyelitis caused by Serratia microorganisms.128,138
Greene showed that an unrecognized foreign body may be
the focus for acute or chronic infection, often with unusual
organisms such as Serratia marcescens.138 Usually Serratia
occurs in patients in whom the immune system has been
compromised.128 In contrast, Green’s two patients were
essentially normal. Figure 9-13 shows a similar problem with
a delayed (indolent) infection. This boy cut himself in the
thumb web space. Purulent drainage persisted for several
days, but the boy was never treated with antibiotics. Three
years later, because of a fall on the wrist, a roentgenogram
284
A B
FIGURE 9-12. (A) Open fracture of the tibia. (B) Fourteen months
later the fracture had healed, but a lytic lesion was evident in the
proximal metaphysis. Decompression revealed serosangineous
fluid that cultured Aeromonas.
was obtained. During the subsequent operation, a membra-
nous cavity was found, and cultures grew Staphylococcus
aureus. This boy had been asymptomatic for almost 3 years
and symbiotic with a microorganism that is normally virulent
when invading the developing skeleton. Such cases are not
the usual presentation.
Such aforementioned cases, however, are unusual in the
traumatized pediatric population. Their eventual appearance
should not be miscontrued as initial fracture mismanagement.
Open Wounds and Osteomyelitis
Open wounds carry a reasonably high risk of infection.
When they involve a physeal region, the complication of
growth damage becomes increasingly significant (Fig. 9-14).
Aggressive débridement and parenteral antibiotics should be
essential treatment. Even with such treatment, however, per-
manent growth damage may occur (Figs. 9-15, 9-16).
Brand and Black demonstrated that seemingly innocuous
puncture wounds may also lead to osteomyelitis.113 Further-
more, infection with nonstaphylococcal microorganisms,
especially Pseudomonas species, is more prevalent. This par-
ticular problem is discussed in detail in Chapter 24.
Joint Involvement
Open joint injuries accompanying musculoskeletal trauma
are relatively infrequent in children. However, if intraarticu-
9. Open Injuries and Traumatic Amputations
FIGURE 9-13. Chronic osteomyelitis of the distal radial metaphysis.
This probably occurred 3 years before, following an infected soft
tissue hand injury. The physis has been damaged, leading to
retarded longitudinal growth (arrow). This proved to be chronic
osteomyelitis caused by coagulase-positive Staphylococcus.
lar (intracapsular) involvement is not recognized or inade-
quately treated, serious damage to the articular surfaces
(Fig. 9-17), loss of normal joint function, fibrous ankylosis,
or septic arthritis may occur.141,165 Because articular cartilage
may have some limited regenerative capacity in a child,
appropriate débridement and joint lavage may allow full
restoration of the articular surface.
Many open injuries in children affect the joints of the
lower extremity, with the knee and ankle being commonly
involved joints. Power lawn mowers are a common cause and
may introduce significant amounts of foreign (organic)
material into the joint (see section later in this chapter).
More frequently, the child falls on a sharp object. Many times
the only objective evidence of injury is air or an air-fluid level
within the joint. A less common cause is inflicted trauma, as
with a stab wound of the knee. When a sharp object pene-
trates a joint, the articular surface may be damaged directly.
Adequate inspection of the joint surface and removal of the
foreign body to prevent further damage are two major indi-
cations for immediate arthrotomy. In the event of an accom-
panying type 3, 4, or 7 fracture, arthrotomy also allows
anatomic reduction of the fracture.
The most important reason for arthrotomy or arthroscopy
is the prevention of subsequent septic arthritis. Curtiss has
demonstrated experimentally that articular infection with
various types of microorganisms, especially Staphylococcus,
causes enzymatic destruction of the joint cartilage.124 The
joint must be approached with an incision that includes
the penetration wound, the margins of which should be
adequately débrided. The joint should be irrigated profusely
with saline, antibiotic solutions, or both, and drains should be
left in place. The surgeon should not hesitate to repeat this
procedure 2–3 days later. An alternative is continuous lavage
for 2–3 days, although this technique is not easy and should be
used only if the support services are familar with it.
Clostridial Infections
Clostridial infections (such as gas gangrene) or similar infec-
tions due to other facultatively or completely anaerobic bac-
Infection 285

FIGURE 9-14. (A) Open physeal fractures of the tibia and fibula. (B) Five weeks later. (C) Four months later there is premature fusion
of the physes. Note the Hawkins’ sign of the talar dome (see Chapter 24).

teria may become significant, even in the more superficial
tissue planes. Although clostridial infections are usually
dismissed as insignificant problems in urban populations,
Brown and Kinman described the occurrence of this type
of infection in a large urban community during a major
disaster (an airplane crash in the Everglades).115
palmar aspect of the extremity (the impact surface). Severe
clostridial infection and myonecrosis, though not common,
may complicate these injuries.115,133,159,171,174 Fee et al.
described five cases, four of which were in children.132 Three
of these cases, all caused by Clostridium perfringens, eventually
required amputation, two at the elbow level and one at the

Gas Gangrene
Fractures of both bones of the forearm may be accompanied
by small lacerations or puncture wounds, particularly on the

FIGURE 9-15. Synostosis secondary to chronic osteomyelitis in an

insensate lower leg consequent to sciatic injury. The overall soft
tissue and osseous problems eventually were treated with a knee FIGURE 9-16. Chronic osteomyelitis, nonunion, and distal femoral
disarticulation. The original fracture is shown in Figure 9-2. growth arrest after an open distal femoral metaphyseal fracture.
286 9. Open Injuries and Traumatic Amputations

FIGURE 9-17. This patient with a congenital sensory

neuropathy had a small, penetrating knee wound
that was not initially detected. Several days later she
was evaluated for sepsis. Eventually the distal femur
and proximal tibia had to be resected. (A) Gross
appearance of the damage. (B, C) Histologic sec-
tions show the extent of the destruction and the
spread of the infection into the metaphyses.

junction of the proximal and middle thirds of the humerus.

In one case, subperiosteal resection of large segments of the
diaphysis of each bone was necessary. The ulna completely
regenerated, but the radius later required a bone graft. Such
regeneration may occur so long as reasonable longitudinal
and circumferential amounts of the periosteum remain
intact.
Common to these particular injuries is protrusion of the
fracture fragment through the skin into soil harboring the
clostridial microorganisms. The wounds may be relatively
small and deceptively innocuous in appearance. These cases
point out the need for aggressive initial management, with
adequate débridement of the skin and underlying tissues.
Under no circumstances should the wound be closed.
Débridement should be undertaken in the operating room,
where an adequate amount of irrigation and complete explo-
ration may be accomplished.
The symptoms and signs of these anerobic infections may
evolve insidiously and may not appear until 2–3 days after
the injury (Fig. 9-18). Once infection begins, however, the
ensuing course may be rapid. The earliest symptom is usually
pain in the affected area, followed by chills, tachycardia, con-
fusion, and other evidence of toxemia. In the early stages the
skin around the wound is cool and edematous, but it is
seldom crepitant. Later it becomes brawny, discolored, and FIGURE 9-18. Gas gangrene throughout the subcutaneous and
crepitant, with exudation of a serous, brownish fluid from intramuscular tissues following a deep laceration in a young child.
Infection
the wound. The Gram stain of the fluid usually shows gram-
positive rods, confirming the diagnosis.
Although local cleansing of a wound is advocated for
minimal openings, consideration must be given to a more
aggressive form of treatment when soil contamination is sus-
pected. Any injury occurring outdoors may be contaminated
by soil microorganisms, so treatment should include an
exploratory extension of the wound sufficient to provide
adequate visualization of the bone ends to ensure that all
foreign material has been removed. Meticulous débridement
and thorough irrigation should be part of the procedure,
and the wound should never be closed primarily. Removal of
damaged and necrotic tissue is essential to reduce the local
environment in which the bacteria proliferate.156
Once the diagnosis is suspected, treatment must be insti-
tuted immediately to avoid serious complications. The most
important aspects of treatment consist of immediately
opening the wound and adequately débriding it, even if
débridement was part of the initial treatment. Decompres-
sion must be wide and extensive to reach all areas that might
be involved. Usually the degree of involvement is much
greater than is first apparent. All involved muscle must be
excised. Early surgical treatment may avert the need for
amputation. General supportive measures are also essential.
Prophylaxis with antibiotics may be effective in avoiding
gas gangrene.195 The role of antibiotics in established cases
is to prevent opportunistic clostridial infection in trauma-
tized tissue and to prevent secondary infection with other
equally opportunistic microorganisms. Penicillin has demon-
strated superiority for both prophylaxis and treatment of
causative gas gangrene microorganisms. Certainly, any
patient with an open wound should already have been placed
on an appropriate antibiotic, but the addition of penicillin
in high doses may halt the establishment or progression
of gas gangrene. Other organisms may require additional
antibiotics.
The use of passive immunization with polyvalent gas gan-
grene serum for prophylaxis and treatment of gas gangrene
is controversial, with some investigators believing there is
considerable evidence that the serum is useful for both pre-
vention and treatment of gas gangrene, and that it should
be used in all cases. However, most investigators believe that
the value of the serum is uncertain, that it subjects the
patient to the risk of a hypersensitivity reaction, and that it
should not be in general use. In the series reported by Fee
et al. it was used in all cases without side effects, but no
beneficial effects on the disease process were evident.132
Hyperbaric oxygen therapy allows oxygen to gain access
to anaerobic areas and has been shown, experimentally,
to decrease the effect of clostridial endotoxins and to
affect the metabolic activity and release of additional
toxins.114,116,117,160,169,195 Hyperbaric oxygenation leads to a
higher arterial concentration of dissolved oxygen and allows
increased diffusion of oxygen through the tissues. A pressure
three times the atmospheric pressure is best for an optimal
effect. The PaO2 should be in the range of 1200–
1700 mmHg, with an exposure period of 60–90 minutes.
The treatment should be repeated for 3–5 minutes every
8–12 hours. However, aggressive early débridement
may obviate any need for hyperbaric oxygenation, which
should be reserved for those critical cases not adequately
287
controlled by standard means of surgical débridement and
antibiotics.
Clostridial Cellulitis
A less common and less severe clostridial infection is that of
anaerobic cellulitis (Fig. 9-19). It usually occurs in an inade-
quately débrided wound several days after injury. The onset
is gradual, and toxemia may be slight. It is easy to confuse
with gas gangrene because of the abundant formation of
foul-smelling gas and the comparable brown and seropuru-
lent exudate. Treatment consists in adequate débridement
and appropriate antibiotics.
Tetanus
Although tetanus is a rare complication in most urban,
immunized societies, it is still to be feared in seemingly
innocuous wounds (e.g., puncture wounds of the feet)
in areas of the world with limited immunization to this
organism. The organism, Clostridium tetani, produces
both tetanospasmin, a neurotoxin, and tetanolysin, a car-
diotoxin.114 Both of these exotoxins have severe effects on
human tissue, causing massive muscle spasm. It is important
to treat this disease prophylactically, as antitoxin is unable to
neutralize the toxin once it is tissue-bound in the nervous
system. Most children in urbanized countries have been
actively immunized and need only a booster. Any patient who
has not had normal prophylaxis should be treated with high
doses of penicillin and streptomycin, as well as tetanus
immunoglobulin. Tetanus prophylaxis is not universal at
present. Accordingly, those treating open fractures in certain
geographic areas must consider the possibility of this wound
complication and treat the patient accordingly.
Grossman addressed the question of the timing of tetanus
and immunoprophylaxis in wound management of chil-
dren.139 More than 80% of reported tetanus cases occur 3–14
days after the acute innoculation, and more than 90% occur
within an interval of 2–21 days. The peak time of onset is
day 7.
If tetanic spasm develops, anesthesia, muscle relaxants,
respiratory assistance, and tracheostomy should be part of
the treatment.178,179 Excessive spasticity during treatment may
cause vertebral compression fractures; extremity fractures
are mach less likely. Myositis ossificans and extension of
ossification along tendons are significant complications,
although rarely reported in pediatric patients.147 Luisto et al.
described hyperostosis, usually in areas of tendon insertion,
and osteoarthritis in adults.157 In the only child in their
series, a 12-year-old, the radiographic evaluation was normal.
Atypical Clostridial Infections
Some types of the Clostridium species may be part of the
normal anaerobic flora of the human colon.169,195 Following
blunt trauma to various portions of an extremity, local tissue
damage may create sufficient anaerobiasis to allow estab-
lishment of an opportunistic infection by the hematogenous
route. Figure 9-20 shows a case of a Clostridium sphenoides
osteomyelitis after a fall and direct blow to the lateral thigh.
The laminated subperiosteal layering in this and other cases
288
FIGURE 9-19. (A) Open dislocation of the index metacarpopha-
langeal joint. It was “débrided” in an emergency room and closed
primarily. The dislocation was neither recognized nor reduced. The
next day presenting symptoms were a fever of 105°F, intense pain,
and a frothy fluid exuding from the wound. The child had devel-
oped clostridial cellulitis, which responded to extensive débride-
ment. The dislocation also was reduced (open). (B) A few weeks
may lead to an erroneous diagnosis of a primary bone malig-
nancy, such as Ewing’s sarcoma.
Botulism
Botulism may be caused in open wounds infected by Clostrid-
ium botulinum.120,141,143,150 The microorganism may cause a
variable wound infection and release a neurotoxin. The
neural symptoms include a descending, progressive, sym-
metric cranial nerve paralysis with motor weakness but no
changes in sensory or mental status. Botulin affects cholin-
ergic nerve endings, blocking the release of acetylcholine
and producing pharmacologic denervation.125,150 Symptoms
may not begin for 4–14 days following injury.
9. Open Injuries and Traumatic Amputations
later some reactive bone is evident along the metacarpal (arrow),
and the metacarpal metaphysis and epiphysis are developing
some lucent areas. (C) A few months later the physis appears to
have closed, and the epiphyseal ossification center is damaged.
(D) When the patient appeared for follow-up examination 4 years
later, with 60° of motion, there was an unusual shape to the ossi-
fication center (arrow).
Treatment includes extensive débridement and support-
ive care, especially adequate ventilatory support. Death from
this disease usually results from respiratory failure. Neural
symptoms ordinarily resolve in time. High-dose parenteral
penicillin is essential. The effectiveness of botulinum anti-
toxin is not clear. Trivalent antitoxin effective against type A,
B, and E toxins is usually given.
Gunshot Injury
Most gunshot wounds in the pediatric population previ-
ously occurred in rural areas and usually were shotgun
injuries.201,202,205 With the rise of the drug subculture and
Gunshot Injury
FIGURE 9-20. Anteroposterior (A) and lateral (B) roentgenograms
of an 8-year-old boy who had been struck on the side of the femur
3 weeks before. The laminated appearance suggested Ewing’s
sarcoma as one diagnostic possibility. An open biopsy was done.
A small amount of fluid grew Clostridium sphenoides, and the boy
was treated effectively with penicillin.
gang violence, gunshot injuries to children have increased
significantly in the urban population.* More pediatric mor-
talities are being reported from gunshot wounds in Detroit
than from polio when it was epidemic.215 As many as 25% of
children who are shot have permanent physical sequlae.209
When children are shot, the incidence of extremity injury
(involvement) ranges from 21% to 48%.
Hoffer and Johnson noted that wounds caused by high-
velocity missiles are the focus of most “war reports.”203 In
contrast, children are not usually wounded directly by high
velocity missiles (except, obviously, as victims in war). They
are more often injured by fragments (shrapnel) from explo-
sive devices, such as land mines or bombs. Shrapnel wounds
tend to be equivalent to shotgun pellet injuries and rarely
cause fractures. Today more sophisticated weaponry than
what led to “shrapnel” has effectively approached the de-
structive effects of high-velocity missiles.
Between 1985 and 1989 Victoroff et al. reviewed 75
children and adolescents who had extremity gunshot
wounds.217 Only 30% of the shots caused fractures. More
than one-third of the patients had had previous treat-
ment for other gunshot wounds or trauma. No infections
occurred. Treatment consisted in local wound irrigation
with minimal débridement when there was no fracture.
Intravenous antibiotics were used (short-term prophylaxis)
for coverage of fractures. Large wounds required operative
intervention.
* Refs. 196,197,199,204,207,208,210–212,214,220.
289
Washington et al. reported that 16% of their patients
had physeal injuries directly related to the bullet.219 Five
of the six patients had either incomplete or complete
growth arrest. Despite the need for some type of reduc-
tion in 76% of the patients, only 25% required internal or
external fixation (most were fitted with casts). All patients
received antibiotic prophylaxis. Physeal injury was more
likely from direct impact rather than “close-passing”
projectiles.
Gunshot injuries vary significantly. The initial division is
between powder and nonpowder weapons.218 The powder
weapons can be classified as high- and low-velocity missile,
shotgun missile, and nonshotgun (low-caliber single-missile)
firearms.
The mechanism of injury is affected by the ballistics of the
weapon. Ballistics may be divided into interior (action within
weapon), exterior (weapon to point of impact), and termi-
nal (effect within the targeted object), but the most impor-
tant issue is the terminal phase when the interaction of the
missile relates to the wounding capacity or the extent of soft
tissue damage.
The terminal phase is affected by any factors that slow
or retard the rate of transition of the missile through the
targeted tissue. In addition to the direct energy of the
bullet, there are other energies to consider, such as heat
and mechanical and vacuum forces, all of which may cause
variable amounts of tissue damage.
Bone fractures from bullets vary depending on the
involved bone. The reaction in the metaphysis resembles
a drill hole, whereas a bullet in the diaphysis is more
likely to cause fragmentation and explosion, followed by
cavitation.
Assessment of the patient is important. Valentine and
coworkers have developed an algorithim for managing
the child with a gunshot wound.216 Perhaps the most im-
portant assessment, beyond the basic ABCs of any trauma
patient, is of vascular integrity. Obvious vascular deficiency
should be followed by wound exploration, without re-
sorting to arteriography. Neurologic damage must be as-
sessed. Ascertain where the entrance and exit (if present)
wounds are located, and assess the size and extent of tissue
damage.
In general low-velocity wounds do not require extensive
débridement unless neural vascular or osseous repair is
necessary. If a joint is involved, débridement and lavage are
indicated. Prophylactic antibiotics do not appear ne-
cessary unless there is an accompanying fracture or joint
involvement.
In contrast, treatment of shotgun and high-velocity injur-
ies should be more aggressive. Débridement and antibiotics
are indicated.
Removal of a bullet is controversial. Most studies advocate
removal if the missile is within a joint or readily accessible
during débridement. The long-term effects of a missile
embedded in bone are unknown, but reports of local alter-
ation of osseous physiology and systemic effects have been
described.200 Selbst et al. reported the only case of systemic
lead poisoning in a child.213 Dissolution of lead is more likely
if the missile is within a joint.206 Lead exposure certainly has
recognized long-term effects in children, especially on cog-
nitive function.198
290
Crushing and Avulsion Injuries
Crushing, avulsion, and degloving injuries are among the
most unpredictable and difficult to manage of all muscu-
loskeletal trauma, especially in the child. Any skin wound may
initially appear innocuous. During the ensuing 24–48 hours,
however, demarcation and skin slough may involve areas that
initially appeared viable. Furthermore, tissue necrosis may
extend progressively to the underlying skeletal components,
especially those that are relatively superficial (e.g., the malle-
oli). Common to all such wounds is a combined injury mech-
anism of crushing and avulsion. As the extremity is rolled
over by the deforming object, whether bicycle spokes,
washing machine wringer, or an automobile tire, interposed
tissue may be subjected to shearing, compression, burning,
and bursting forces. Primary wound healing without super-
vening infection is the goal of treatment, although it may not
always be easy to achieve. Adequate débridement and skin
grafting, as necessary, usually suffice. More extensive recon-
struction and pedicle grafts may be utilized on an elective
basis.
The simplest type of injury, and the one most likely if the
child catches a leg in bicycle spokes, is a crush-burn. It results
from a shearing, abrading mechanism; it may be patchy
in distribution and linear in orientation, with streaks of
dermal injury and more diffuse surrounding changes similar
to those of a second-degree burn. These wounds must be
treated as if they were burns, with daily observation for local-
ized, deep tissue necrosis. The wound should be washed
with sterile fluid and dressed with silver sulfadiazine cream
(Silvadene) and fine mesh gauze, with daily dressing changes
under sterile conditions. Epigard and similar dressings may
also be used temporarily.
Within 7–10 days, the wound should be reepithelializ-
ing unless there is a deep injury. If foreign material (e.g.,
macadam from a driveway surface) has been abraded into
the initial wound, it may become permanently embedded in
the dermis, resulting in a traumatic tattoo after the wound
heals and reepithelializes. Rigorous scrubbing during the
initial treatment may prevent this complication.
When more extensive trauma is involved, tissue loss may
be greater. A common pattern is a central zone of maximal
destruction (which may take a few days to demarcate) and a
larger, peripheral zone of progressively less severe injury
(which may take several more days to demarcate). These
central injuries are analogous to third-degree burns and
should be treated accordingly, with excision of the severely
involved tissue, daily dressing with sulfadiazine, and subse-
quent secondary closure or a split-thickness skin graft when
the condition of the wound permits.
Frictional abrasion of the soft tissue may extend down
to fascia, periosteum, and perichondrium, especially at the
ankle, where the malleoli are readily exposed to injury. Dis-
ruption of normal peripheral chondro-osseous develop-
ment (type 6 growth mechanism injury) may occur without
roentgenographic evidence of physeal injury. Long-term
follow-up is necessary to rule out subsequent peripheral
osseous bridge formation (see Chapter 4). Damage extend-
ing to and involving the peroneal tendons and sheaths may
also occur. Adequate coverage by fascial-fat flaps is neces-
9. Open Injuries and Traumatic Amputations
sary if either chondro-osseous or tendinous elements are
exposed. If tissue conditions do not permit flap rotation, free
split-thickness skin grafts are well accepted, especially by chil-
dren, and have a great survival capacity, even when placed
directly on the perichondrium or periosteum, both of which
are more vascular in children than in adults.
Avulsion of any soft tissue flap may occur without a major
crushing component, as the tissue response to shearing
force is usually failure through the subcutaneous–fascial
interface. Such flaps most often are viable structures. The
potential for flap survival is dictated by several factors:
(1) general vascular supply to the injured area along with
and specific supply to the flap (i.e., is there an arterial
supply that can maintain perfusion and sufficient venous
outflow sufficient not to impede capillary dynamics?); (2)
whether the flap is proximally or distally based; (3) dimen-
sions of the flap (length/base ratio); (4) depth of the
cleavage-separation planes; (5) condition of the skin edges;
and (6) extent of crush-contusion of the flap before cleav-
age failure.
If chances are good that the flap will survive, it should
be débrided along the tissue margins, irrigated, replaced,
and sutured primarily, unless there is significant chondro-
osseous injury. In the latter case, loose approximation of
the flap edges to prevent contracture allows observation for
infection and subsequent secondary closure. Occasionally,
flaps that seem to satisfy all criteria for viability subsequently
become necrotic. This necrosis is usually due to microscopic
crush injury that is not grossly evident during the acute
stage or insidious microvascular damage. Such a flap may be
excised and replaced with a (split-thickness) skin graft. Expo-
sure of significant neurovascular structures or larger areas
of avulsion are often better treated by local or distal pedicle
flaps. Consultation with a plastic surgeon may also be ap-
propriate, especially if a vascularized free graft becomes
necessary.
Degloving
Degloving injuries of the extremities in children are serious
and often associated with fractures (Fig. 9-21).224,226 Such
trauma most commonly results when a motor vehicle runs
over an extremity or when the extremity is caught in a piece
of moving machinery. The degloved skin may become gan-
grenous because of loss of the cutaneous blood supply from
the underlying tissue sources. These injuries are usually due
to sudden, severe shearing strains, particularly when the limb
is run over by a vehicular tire. The degloving may be obvious,
or it may be concealed, with no obvious break in the skin but
with complete disruption of all attachments between the skin
and subcutaneous fat from the underlying fascia. It may
disrupt the vascular supply to the dermis.
The plane of cleavage in the degloving injury typically lies
between the skin and the superficial fascia, except in areas
where the skin is densely attached to underlying fascia, such
as the palm or the sole, where both skin and fascia are gen-
erally involved as a degloved portion. When such skin is
noted, particularly with overt lesions, it is important to con-
sider defatting the avulsed skin before replacing it over the
degloved areas.
Crushing and Avulsion Injuries 291

A B C

FIGURE 9-21. Degloving of both lower legs after this child was run over by a school bus
(32 hours after the injury). The left limb had complete débridement of degloved skin and
fat with subsequent skin grafting. Because of muscle damage, extensive neurovascular
compromise, and several fractures, the right leg was amputated at the knee. (A, B)
Appearance of the left leg. (C) Appearance of both legs after initial débridement. (D)
Complete débridement. Note the degloved heel pad; it was salvaged. D
292
Wringer Injuries
Although progressively less frequent, wringer accidents,
which cause complex injuries, still occur. Such injuries
usually damage the soft tissue extensively but rarely cause
major fractures.150 However, they are extensive, often
comminuted, and frequently difficult to manage.223,225 Large
roller devices (e.g., presses) increase the extent of soft tissue
and chondro-osseous injury (Fig. 9-22). Occasionally, ampu-
tation occurs.
Osseous injuries tend to involve the more distal regions,
especially the distal radius, ulna, and hand. Because of the
direct crushing mechanism, greenstick and torus fractures
are common. Furthermore, the periosteal tube is usually rea-
sonably intact and may act as a relative internal splint.222 The
thumb may follow the rest of the hand through the rollers
in an abducted, hyperextended position, leading to separa-
tion of the first interosseous web space and the possibility of
significant soft tissue injury. The metacarpophalangeal joint
may be disrupted acutely but spontaneously reduced on
removal from the wringer. An epiphyseal Bennett’s fracture
equivalent may also occur (see Chapter 17).
Akbarnia and colleagues221 reported a case of wringer
injury in a 29-month-old child in whom a 24-year follow-up
study was done. Initially, there was extensive loss of the di-
aphysis and periosteum of both the radius and the ulna, lim-
iting the capacity to otherwise restore the diaphyseal shaft.
The child was subjected to repeated onlay grafts to fill in the
defects. The restoration of function to the radius and ulna
FIGURE 9-22. Wringer injury. Wrist disarticulation occurred in an
industrial machine. The hand was brought in along with the wringer
elements. Attempted replantation was unsuccessful.
9. Open Injuries and Traumatic Amputations
was excellent. The circulatory disturbances, however, were
thought to be a major factor in the shortening of the bone
by disturbing distal radioulnar physeal growth.
Maximal damage to the soft tissues is generally sustained
by the forearm and antecubital fossa, although if the elbow
is extended and allows the arm to go farther into the wringer,
maximum trauma may occur in the axilla. The extent of
injury may be increased if countertraction is applied to the
extremity by reversing the direction of the limb or increas-
ing the tension of the rollers or the rapidity of revolution.
Various degrees of superficial abrasion or burning occur
as well as an equally variable, and often changing, amount
of deep shearing of tissue planes and muscular damage. Both
types of injury may initially appear benign. The skin should
be treated as a burn: It is dressed (with a well-padded com-
pression dressing) and elevated accordingly. If an extensive
hematoma develops, it may be decompressed, evacuated, or
both by proximal and distal fascial incisions. If there is
an increase in compartment pressures, which may be mea-
sured with appropriate techniques, partial or complete fas-
ciotomies may also be indicated.
The most significant problems are edema and venous
congestion resulting from disruption of normal superficial
venous and lymphatic drainage patterns. A pedicle flap may
be of benefit in reducing this increased tissue perfusion
pressure, which may lead to additional tissue infarction. The
efficacy of sympathetic blocking agents, anticoagulants, and
antisludging parenteral therapy [e.g., dextran 40 (Rheo-
macrodex)] is unclear.
Lawn Mower Injury
Approximately 7 million lawn mowers are purchased annu-
ally and more than 30 million are now in frequent use in the
United States.231,243,249 Annually there are more than 100,000
injuries due to lawn mower accidents.227,229,231–233,235–237,239,244,248,
249,251
A large percentage of these injuries involve the lower
extremities of children less than 14 years of age.237,242 Accord-
ing to statistics from the Consumer Product Safety Commis-
sion, children under 14 years of age and adults over 44 years
of age are at the greatest risk of injury; children under 6 years
of age have the greatest risk of death.
Although a variety of injuries associated with power lawn
mowers have been described,229,230,234,244,246 extremities are the
most frequent site of injury, with the forepart of the foot pre-
dominating.234,238,241,248,249,251,253,254
The power lawn mower is capable of tremendous wound-
ing capacity. A 26-inch (66-cm) rotary power mower rotating
at 3000 rpm generates the kinetic energy of 2848 J, or
2100 ft 1b.228,231,234,247 This is three times the muzzle velocity
of a 0.357 magnum gun or equivalent to the energy of a
21-lb (9.45-kg) weight dropped from a height of 100 ft
(30 m).229,231,234
Power lawnmower accidents produce serious injuries to
the extremities of a growing child. These injuries are often
complex and may require prolonged treatment throughout
growth, potentially resulting in a permanent disability for the
child.250 Yet most of these accidents are the result of care-
lessness and are preventable.
Initailly, the lawn mower accident victim is treated with
general supportive care. Any open wounds and open frac-
Amputation
tures are irrigated and débrided. Assessment of associated
injuries, such as nerve or vascular involvement, is essential.
Tetanus immunization should be updated and cultures of
the wound should be obtained in both the emergency
room and at subsequent débridement sessions. Antibiotics
are begun immediately after aerobic and anaerobic cultures
are obtained.
At 24–72 hours after injury, most of these wounds should
again be examined in the operating room and débrided as
necessary. When the contaminated and necrotic tissue has
been adequately débrided, and early granulation tissue is
evident, soft tissue coverage can be considered, usually by
7–14 days A split-thickness skin graft (STSG) or Epigard
(a synthetic microporous material) may be used to cover
exposed muscle. Areas with exposed bone, tendons, vessels,
or nerves, or large soft tissue defects, should be considered
for free flap or rotation flap coverage. Modern micro-
vascular techniques have enabled improved coverage, with
demonstrated decreased early morbidity and improved func-
tion.237,243,252 The small blood vessels in children less than
2 years of age may make microvascular surgery in this
age group more difficult.237 The latissimus dorsi free flap is
widely used to cover large soft tissue defects in the lower
extremity and has yielded excellent results. When possible,
the weight-bearing surface of the foot should be covered with
local vascularized sensate flaps.237 The non-weight-bearing
surfaces of the foot, including the longitudinal arch, can
usually be adequately treated with an STSG.237
Skeletal fixation of the associated fractures must be
individualized. Most patients have either internal fixation,
usually with smooth K wires, or external fixation, particularly
of the tibial fractures. Anatomic joint congruity must be
maintained. In addition, restoration of the physeal anatomy
minimizes the chance of bony physeal bridge formation.
Stable fracture fixation enhances early range of motion.
Growth-plate injury may produce an array of defor-
mities.242 Limb-length discrepancy may result if the activity
of an entire growth plate is disrupted. Angular deformities
follow an injury to a peripheral portion of the physis. Re-
constructive procedures including epiphyseodesis, correc-
tive osteotomies, bony bridge resection, and revision
amputation may be necessary to improve both cosmesis and
function and are often repeated during growth. Children
involved in lawn mower accidents with injury to growing
chondro-osseous structures must be followed throughout
growth to skeletal maturity. Often problems develop or
become apparent only years after the acute injury. Their
effect can best be minimized with early recognition and
appropriate treatment.
Osteomyelitis is a potential problem whenever open
wounds are contaminated. Lawnmower injuries are most
often grossly contaminated with foreign material, including
grass and soil, which makes them prone to subsequent infec-
tion. For this reason, adequate and repeated débridements
are mandatory, along with prophylactic antibiotic coverage.
Most patients (15 of 27) were injured as innocent
bystanders. The current safety features protect the operator
of the mower but do little to protect a small child from slip-
ping or falling into the blades.240,241,244–246
Lowering the staggering incidence of injuries related to
the power mower is possible only through improved con-
sumer awareness and respect for the potential damage that
293
is possible with these machines.255 Education of the public
and encouragement to use the available safety features
and precautions are essential. Both the orthopaedist and the
pediatrician should stress to parents the need to keep small
children far away from power lawn mowers. Children should
never be allowed to ride as passengers on the riding type of
mower. Those accidents involving small children falling
under the blades of a power mower are not only the least jus-
tifiable of all, but they tend to be the most severe.235 Adoles-
cents should also have attained a reasonable amount of
maturity before they are allowed to operate these machines.
Anyone of any age who operates a power mower must
observe every safety precaution to minimize the chance of
being injured.
Amputation
Traumatic amputation during childhood has received
limited attention. Accordingly, specific management guide-
lines are limited.261,277,303 The extent to which optimal func-
tion may be provided, both initially and in the long term
until skeletal maturity is eventually attained is frequently
determined by appropriate or inappropriate initial manage-
ment. The major factors to consider must be infection,
vascular status, and the effect the amputation will have on
anticipated skeletal growth and development.
Trauma is not a frequent cause of childhood amputation.*
Only 17% of patients (21 of 120) at one juvenile amputee
clinic had sustained traumatic amputations.268 Another study
described 19 traumatic amputations among 39 acquired
amputations.320 The mechanisms of injury included thermal
and electrical burns, wringer injury, automobile accidents,
shotgun injury, and power mower and farm machinery acci-
dents. Unfortunately, relative to other forms of amputation,
children with traumatic amputations have a high incidence
of infections, wound healing complications, heterotopic ossi-
fication, and chronic prosthetic problems.
In the severely traumatized and contaminated wound,
avoidance of further infection and increased vascular com-
promise is essential. Constructive, long-term planning with
particular consideration of the effects of growth and of the
optimal stump condition throughout growth may dictate
the need for considerable staging in the treatment of the
child’s traumatic amputation and posttraumatic manage-
ment. Many of the problems encountered in the manage-
ment of traumatic childhood amputation may be attributed
to difficulties or complications during the primary manage-
ment, which may have precluded initial construction of an
optimal amputation stump. Accordingly, revision surgery for
such complications as reactive bone, scar adherence, and
inefficient stump length becomes likely.275,281,301,304,305,317,318
The most common patterns of trauma leading to ampu-
tation are those in which the limb is crushed or partially or
totally avulsed. Often both mechanisms occur concomitantly.
In some cases, major vascular injury occurs, independently
or additionally, in the presence of less severe musculoskele-
tal trauma, endangering the part of the limb distal to the
injury. Causes other than direct musculoskeletal trauma
* Refs. 257,263,264,267,268,270,273,279,280,295,302,316, 320,323,327.
294
that may eventuate in childhood amputation include burns,
gas gangrene, meningococcal septicemia, and electrical
injury.271,279,321,322
If a traumatic amputation is complete but the amputated
part is readily available (and adequately treated), one should
consider the possibility of limb replantation, although many
hospitals are not equipped to undertake such an extensive
procedure. If possible, the child should be referred to a unit
where a multidisciplinary team is available to attempt such a
procedure. If the amputation is incomplete, surgical care of
the residual tissue is the major problem, with control of the
vascular pedicle being a primary consideration.
Every effort should be made to save some or all of a
child’s limb, even if it means delaying an eventual amputation.*
One of the most difficult problems is that of a delayed ampu-
tation in which the surgeon finds he or she is tempted to
retain a limb that will serve only as an eventual burden to
the child. This problem occurs not only in cases of traumatic
injury but also with many types of congenital deformities in
children for whom function with a prosthesis is superior to
that of a braced, deformed, and often insensate extremity.
The use of parts that would otherwise be amputated should
also be considered. Hove and Gravem reported a 5-year-old
girl with traumatic amputation of both limbs.292 Tissue
was transplanted from the left leg (thigh amputation) to
the much less involved right leg. The transfer included
the posterior part of the pelvis, posterior tibial nerve, and
artery.
Hartford and others thought that the level of amputation
should be based on soft-tissue integrity rather than the frac-
ture level.284,285 Flaps of viable soft tissue distal to the fracture
may be devised. Similarly, some fracture fragments (stabi-
lized) may be incorporated. Both are directed at preserving
adequate length for improved prosthetic function. Weinberg
et al. emphasized the use of “spare part” flaps from a non-
replantable limb.326
Cole et al. reported the use of tissue expanders to
lengthen shortened amputation stumps.269 Persson and
Broomé used an endoprosthesis and tissue expander to elon-
gate a short femoral stump that was the result of a high
femoral amputation (at age 14).310
Scharli described 21 children in whom limb salvage
surgery following traumatic amputation was attempted.63 All
extremities with an injury score of 3 or more could be sal-
vaged. Among the nine incomplete salvages, complete ampu-
tation limb-saving procedures succeeded in three.
The basic principles of amputations in children differ
from those for adults in three major respects. Unfortunately,
adherence to these principles becomes more difficult in chil-
dren with variable, unpredictable, soft tissue disruption and
comminution.
1. Preservation of functional epiphyseal and physeal units
assumes a major priority, particularly when the distal femoral
epiphysis is involved. An above-knee stump in a baby even-
tually may become the equivalent of a high thigh ampu-
tation in the adult, as 70% of the growth of the femur is
eventually contributed by the distal femoral physis. Similarly,
an ankle disarticulation with preservation of the lower tibial
* Refs. 271,272,280,282,283,287,288,291,294,298,299,301,303,312,314.
9. Open Injuries and Traumatic Amputations
epiphysis leads to a much better stump than does a short
below-knee amputation.
2. The excellent healing potential of the young child
makes possible the use of flaps that might be questionable
in an adult.273 Skin grafts may be useful. It is sometimes
possible to preserve a knee joint with a below-knee stump
covered by a split-thickness skin graft, which with continued
growth, suitable modification, and eventual conversion to a
knee disarticulation can withstand the use of a prosthesis.
3. Stump overgrowth is the major problem with amputa-
tions in any child. In children, disarticulation through a joint
is usually preferable to metaphyseal or diaphyseal levels of
amputation.
When dealing with any child’s traumatic amputation, a
great deal of constructive planning is required to salvage the
best possible initial repair and long-term function. Planning
for optimal amputee function and prosthetic use obviously
must take a secondary role to the initial treatment of the
injury. The surgeon must keep in mind the potential types
of prosthetic device and the possible problems consequent
to continuing skeletal growth patterns, whether normal or
abnormal. Adequate amputee function requires an optimal
conversion site, pliable skin cover (preferably with some, if
not complete, sensation), uncomplicated healing, freedom
from infection, good vascular stump nutrition, and, if pos-
sible, a well muscled stump. Staging of any operative treat-
ment may be essential to provide these objectives safely and
with assurance of long-term efficacy. The use of tissue
expanders allows further staging for coverage or revision of
areas of adherent scar tissue from previous skin grafting.266,313
Guidelines for the management of traumatic wound
amputations, which may be a consequence of mutilating
forces due to lawn mowers, firecracker blasts, propellers, and
so forth, must take into consideration the extensive soft
tissue and chondro-osseous injury and the introduction of
significant amounts of contaminating material. For optimal
results, several basic guidelines should and must be recog-
nized and incorporated into the treatment algorithm.
1. The amputation should be at the most distal, viable
level. In the child, this principle must be modified, whenever
possible, to include ablation through the most distal, viable
joint whenever possible. Staged procedures may help. If
tissue viability is in question, err on the side of observation
and subsequent débridement of tissues that do not survive
over time.
2. Viable skin should be preserved whenever possible.
Flaps may be filleted from a portion of the segment being
amputated.
3. Primary closure of the wound should not be attempted.
4. Following débridement, skin traction may be effective
to prevent retraction of wound edges.
5. The proximal joint should be immobilized in a func-
tional position.
6. Immobilization should be comprised of longitudinal,
rather than circumferential, splints to avoid constriction
and possible further demarcation of tissue planes and
levels.
Any wound that can be closed at the time of initial débride-
ment may be repaired with equal facility and probably far
Amputation
greater safety a few days after the original injury, particularly
if considerable contaminating material was introduced
during the original injury. Increasing vascular embarrass-
ment due to closed space edema cannot occur in a com-
pletely débrided, fasciotomized, open wound. Because many
of these injuries are due to blunt, as well as sharp, trauma,
it is not always easy initially to estimate tissue viability and
wound contamination, necessitating secondary débridement
of residual necrotic tissue at the time of delayed closure or
some intervening time during the course of treatment prior
to closure. Certainly in any severely traumatized and poten-
tially contaminated limb wound with bone exposure, infec-
tion does not usually occur in the completely débrided, open
wound with viable tissue. This observation is particularly true
for the introduction of anaerobic bacteria, including Clostrid-
ium species.
Above-knee and below-knee amputations should be
avoided when possible in children, aiming instead for a knee
disarticulation, with the distal femoral epiphysis being left
intact. The presence of the distal femoral epiphysis with
prepatellar skin cover may effectively provide good end-
bearing control for a prosthesis. Knee disarticulation also
usually allows a good myodesis for a later (if necessary) mus-
cular above-knee stump revision.
Sometimes diaphyseal amputations are necessary; but in
young children, in whom a major cause of trauma is often
the power rotatory mower, a significant number of the result-
ing injuries involve the foot. The skin over the heel, although
traumatized, may be salvaged by adequate attention to metic-
ulous débridement. For severe foot injuries in the growing
child, the Syme level ankle disarticulation is the appropriate
site. The Chopart or Lisfranc level may be fitted and toler-
ated in the child, but each gives a less functional prosthetic
result by the time skeletal maturity is finally reached. The
Syme amputation is preferable in children for optimal func-
tion, so possible complications of the procedure should be
considered to see how they may best be avoided during
primary wound management.
When the tissues about the heel and plantar surface are
traumatized. a well-drained, débrided wound is essential.
Many of these injuries have contaminants such as dirt, grass,
and other organic materials. When the tissues are trauma-
tized but viable, as frequently occurs with severe foot injuries,
it seems unwise to subject the heel pad to the further trauma
of major surgical dissection. After open-flap treatment these
heel pads are often scarred, tender, and poorly adapted for
end-bearing function, even after subsequent delayed closure.
There is another reason for rejection of the open-flap Syme
technique in young children. The operation is not per-
formed, as in adults, with resection of the cartilage surfaces
of the ankle; rather, a true disarticulation is created that
leaves the distal epiphysis of tibia and fibula undisturbed.
Open disarticulations may be troublesome acutely and as
the patient matures. Articular cartilage deprived of nutrition
may undergo necrosis and desquamation, and the recesses
of the joint may allow persistent bacterial invasion. There-
fore, for a severe foot injury in a child in whom the heel pad
is thought to be viable, an open, more distal forefoot ampu-
tation may be undertaken initially. All surface cartilage and
bone are débrided. After the edema has resolved and nutri-
tion of tissues is established, a delayed, formal revision to a
295
Syme ankle disarticulation may be performed with relative
safety. In cases in which there is persistent wound edema or
surface infection or in which restoration of tissue nutrition
is delayed, the application of a split-thickness skin graft as a
temporary wound cover usually results in a clean, closed
wound that may subsequently be revised to a Syme ankle
disarticulation with safety.
There is virtually no indication for an immediate-fit pros-
thesis in a child with a traumatically amputated limb.250
Because of growth there may be frequent revisions and
replacements of any prosthesis. Children also recover faster
than adults and rarely have complications such as underly-
ing peripheral or diabetic vascular disease. Adaptability is
more likely in children and is particularly evident in pro-
prioception of the remaining limb in the prosthesis.274
Because of the flexibility of most (but not all) children to
recover physically and emotionally from trauma, even if it
causes partial limb loss, problems such as chronic disability
are much less likely than the same level of loss in an
adult.301,311 Energy expenditure in the child may be less but
obviously increases as the child grows.325
Overgrowth
In children in whom significant longitudinal growth
remains, any type of diaphyseal amputation often leaves
much to be desired in terms of the ultimate adult function
following skeletal maturation. Not only may there be a small,
poorly muscled stump, but the loss of one of the epiphyses
invariably results in progressive, further shortening of the
amputated extremity compared with the uninvolved ex-
tremity. Overgrowth stemming from terminal appositional,
endosteal proliferation (rather than physeal growth) is a
frequent complication, often requiring more than one
revision, each of which contributes to further shorten-
ing.257–259,276,307,308,315 This overgrowth results from a combined
process of periosteal and endosteal new bone formation and
from terminal remodeling (Figs. 9-23, 9-24). There is also a
phenomenon of traction, with the remaining periosteum
becoming fixed to the bone at the distal site and having no
remaining control over diametric or latitudinal expansion.
The end becomes progressively tapered because it fails to
grow adequately in a diametric fashion compared with the
more proximal portions, although longitudinal growth
(appositional: membranous, rather than endochondral)
does occur (Fig. 9-25).
Osseous overgrowth manifests clinically as an increasing
inequality in length between the stump skeleton and its soft
tissue covering. As this inequality increases, the end of the
stump becomes tented over the sharp bone and becomes
tender. Sometimes an adventitious bursa develops between
the skin and the bone, and it may or may not be acutely
tender. The tissues may also become densely adherent to the
bone end, not yielding or moving in the prosthetic socket.
In neglected cases, the sharp end of the bone may even
perforate the soft tissue covering, and ulceration develops
about the area of perforation. There is generally abundant
local production of granulation tissue, and the possibility of
osteomyelitis becomes significant.
This ability to produce bone in such an additive manner
is a characteristic of long bones in which the epiphyses are
296
open. Certainly the phenomenon does not occur in adult
amputees. Hellstadius demonstrated that if he resected long
bones at the midportion in rats with open epiphyses regen-
eration there would be a consistent result.290 It is possible
that juvenile amputees have the clinical counterpart of that
experiment.
The work by Speer showed that progressive orientation of
collagen fibers led to wound contraction in the healing
stump and provided tensile forces that promoted orientation
FIGURE 9-24. Multiple spicules from the fibula. There is also central
growth arrest in the proximal fibula.
9. Open Injuries and Traumatic Amputations
FIGURE 9-23. Distal tibia of a patient who had a below-knee ampu-
tation during childhood, showing overgrowth of the bone (solid
arrows) beyond the original amputation level (open arrows). There
is subperiosteal and endosteal new bone. (A) Radiologic section.
(B) Histologic section.
of scar collagen fibers and mediated traction on the perios-
teum of the osseous stump.319 This promoted axial growth of
the long bone in the absence of a growth plate. The mech-
anism of apical overgrowth is biomechanically identical with
that of normal longitudinal growth at the opposite end. This
type of apical membranous bone growth also characterizes
growth of certain horns in animals.278
Bone formation is of three types: (1) periosteal, (2)
endosteal, and (3) heterotopic. Ectopic bone is found at
areas of periosteal elevation or avulsion, whereas endosteal
bone, in combination with periosteum-derived bone, is
responsible for overgrowth at the apical stump skeleton.
Heterotopic bone may occur within the contiguous soft
tissues (Fig. 9-26).
Aitken demonstrated that conical bone formation at the
distal cortical site was associated with the osteogenic perios-
teum and accounted for the increase in length of the stump
skeleton.257–259 Speer extended the original studies of Aitken,
proposing that the amputation site was a wound contracture
undergoing periosteal and endosteal bone formation under
the influence of the local healing response.319 Although
these reports and others have detailed the pathogenesis and
general incidence of overgrowth, they have neglected to dif-
ferentiate between the metabolically distinct regions of a
given bone and the variable ability of each of these regions
to produce bone after amputation.
There appears to be a correlation between the ability of
each anatomic region to produce bone under physiologically
normal conditions and the potential for apical overgrowth
after amputation. Fifty percent of all amputation sites that
occurred at the level of the metaphysis required revision for
overgrowth. This compared with an incidence of 45% for
diaphyseal amputation sites and 0% for joint disarticulations.
The metaphysis of the growing bone is highly active and
contains major peripheral and central circulatory vessels
that contribute to considerable bone turnover during endo-
chondral and membranous bone formation. It seems likely
Amputation 297

capabilities of the adjacent orthotopic (skeletal) bones. The

FIGURE 9-25. Pathogenesis of amputation stump overgrowth,
showing mechanisms and evolution of stump shapes as seen by
polarized light microscopy. (A) Initial amputation and illustration of
the normal mechanism of longitudinal growth of cortical bone at
the growth plate. (B) Organization of collagen fiber groups of scar
and periosteum as a continuous mass. (C) Progressive longitudi-
nal orientation of collagen fiber groups about the apex by scar con-
traction, with deposition of new bone at the periosteal, endosteal,
and apical aspects of the original bone. (D) Conical shape of the
mature overgrown stump. (E) More extensive periosteal elevation
and hematoma than in (A). (F) Formation of a bulbous-shaped
stump. (Adapted from Speer.319)
ossicles are associated with all levels of amputation. Ossicles
at metaphyseal or diaphyseal amputations are usually en-
veloped by continued periosteal and endosteal osteogenesis.
These small bones likely form in response to the further dif-
ferentiation of periosteal or cartilaginous remnants left in
the soft tissue stump after injury or surgery. Ossicles located
at the site of an elective joint disarticulation remain non-
contiguous with the adjacent epiphysis.
Heterotopic ossicles may develop after skeletal matura-
tion, whereas true overgrowth of the stump skeleton remains
static and progresses minimally after skeletal maturation.
This observation supports the theory that amputation stump
overgrowth is a local, episodic phenomenon that progresses
for a time and then becomes quiescent. Furthermore, Pel-
licore et al. stated that children older than 12 years with an
amputation show no signs of overgrowth.309 In contrast, we
recognized several instances in which primary amputation
occurred after the age of 12 years, and overgrowth requiring
revision developed.308 There appears to be a renewed inci-
dence of overgrowth in amputation stump skeletons that are
surgically revised after the age of 12 years.309 Near the ado-
lescent growth spurt, there is a renewed incidence of over-
growth that ceases at the time of physiologic epiphysiodesis
or shortly thereafter.308 The occurrence of overgrowth after
maturation is minimal compared with that in amputees sus-
taining injury at an early age. It is not the chronologic age
of the amputee that is critical to overgrowth but, rather, the
skeletal maturation and overall growth potential.

that these factors would also produce a highly osteogenic

environment after amputation or injury. Although the
diaphysis is less active, overgrowth at both metaphyseal and
diaphyseal amputation stumps is due to an osteogenic
periosteum, endosteal remodeling, and the possible activa-
tion of osteogenic bone marrow precursor cells. These
factors contribute to progressive bone formation and subse-
quent tapering of the medullary cavity. A decrease in corti-
cal density of affected weight-bearing bones appears to be
coupled with an increase in the density of the contralateral
cortex.308
When an amputation involves the chondro-osseous epiph-
ysis, premature physiologic epiphysiodesis may occur at the
adjacent physis as a result of vascular compromise to the
epiphyseal circulation, and bony overgrowth may evolve
from the transected epiphyseal secondary ossification center.
In contrast, overgrowth never develops when the epiphysis is
left structurally intact, as there is no exposed bone or perios-
teum. Well-defined ossicles do occasionally occur within the FIGURE 9-26. Heterotopic bone formation along the posterior
soft tissue surrounding the distal stump and, once mature, portion of an above-knee amputation. It required revision for com-
contain marrow cavities that mirror the cell-producing fortable prosthetic fit.
 298
A B
Radiologically, osseous overgrowth has a characteristic
appearance. The distal end of the stump skeleton seems to
elongate; the medullary canal in the area of overgrowth is
diminished or absent, and the normal parallelism of the cor-
tical surfaces is lost. The involved bone becomes progres-
sively pointed, and the trabecular details of the area of
overgrowth are poorly differentiated. This type of bone for-
mation may occur rapidly following a traumatic amputation.
Some of the phenomenon may be due to the accompanying
soft tissue damage. In other children the process is much
slower. Age also seems to be a factor, with small children
elaborating more bone more rapidly than older children or
adolescents.
In cases in which the amount of overgrowth does not
require treatment and the new bone has an opportunity to
mature, the trabecular pattern becomes better defined.
Radiologically, one may liken early overgrowth to immature,
undirected callus formation. When Aitken revised these
stumps, he placed metal clips in the revised bone ends.257
Subsequent roentgenograms showed conclusively that the
overgrowing bone was added distal to the implanted metal
marker, presumably by the periosteal remnants (i.e., by
membranous ossification).
Treatment for the condition is revision of the overgrowing
stump. There does not appear to be any use for proximal
epiphysiodesis in the management of this complication, as it
is a distal additive process. Ablation of the next proximal
physis does not destroy distal additive bone formation. Appo-
sitional (distal additive) bone growth is probably an inher-
ent characteristic of growing bone. It does not appear in
patients whose epiphyses are physiologically closed and in
those who also have much less osteogenic periosteum.
Osseous overgrowth of the metaphyseal- or diaphyseal-
level amputation stump is a common problem for the skele-
tally immature amputee and may require surgical
revision.256,308 Pellicore et al. noted that children who sustain
9. Open Injuries and Traumatic Amputations
FIGURE 9-27. (A) A synostosis was created
between the tibia and fibula. Overgrowth of
both bones occurred despite this osseous
fusion (arrow). (B) Successful synostosis 3
years after the procedure. There is no irregu-
lar osseous overgrowth.
an initial amputation before the age of 12 years have a
greater incidence of revision for overgrowth, whereas
children older than 12 showed no signs of overgrowth.309
However, children of the latter group who had a revision of
their stump showed renewed incidence of overgrowth. Mul-
tiple surgical procedures are necessary in as many as 39% of
skeletally immature amputees.309 Overgrowth may be accom-
panied by a neuroma, bursa, cyst, or ulceration.256
There are notable differences in the incidence of over-
growth needing revision when the mode of amputation was
considered. Of all traumatic amputation sites, 43% required
revision for bony overgrowth, whereas 30% of congenital
amputations and 20% of elective amputations were revised.
The reason for the high incidence of overgrowth at sites of
traumatic amputation is likely due to the degree of damage
to a number of potentially osteogenic tissues (bone, carti-
lage, periosteum, and muscle). Revision of overgrowth at
congenital amputation stumps has been considered rare.
Such amputations are often the result of less violent
intrauterine trauma (e.g., amniotic band syndrome) and
seem to be much more likely to develop stump overgrowth
than previously believed. Partial limb deficiencies acquired
prenatally (e.g., incomplete paraxial hemimelia) as a result
of genetic defects also potentiate overgrowth. Those with
elective amputations performed under surgical conditions
likely had the least amount of tissue damage and subse-
quently were the least affected group of amputees. Speer
showed that 58% of elective diaphyseal amputations per-
formed on skeletally immature rabbits had overgrowth of
more than 1 mm.319 In comparison, our incidence of 42% for
overgrowth of more than 1 mm at sites of elective diaphyseal
amputations in children required revision.308
Recurrence of overgrowth is more likely than is the devel-
opment of it in the patient who has never had the problem.
Because this is a recognized clinical fact, efforts to prevent
recurrence have been made following the first revision.
Amputation
These efforts basically have been to develop a synostosis (Fig.
9-27) between the tibia and the fibula.262 The synostosis may
not develop. Aitken believed that continuing overgrowth of
the fibula produced tibia vara.260
Surgical or acute trauma to the healed stump creates a new
healing wound that may result in a further episode of
overgrowth. Multiple revisions were performed at 15% of
metaphyseal–diaphyseal amputation sites and 9% of all
amputation sites.308 Of those amputees who had an initial
revision for overgrowth, 20% required follow-up revisions for
recurrent overgrowth.308 Abraham et al. reported that more
than two revisions were performed in 25% of their cases.256
These figures are expected to increase because not all of the
children included had reached skeletal maturity at the end
of each study. Recurrence of overgrowth is more likely than
is the development of it in the patient who has never had the
problem. Thus the physician should closely follow up any
patient (symptomatic or asymptomatic) who has undergone
a stump revision, especially the young child in whom a poten-
tial for significant longitudinal growth remains.
Epiphyseal Grafting
As an alternative to tibiofibular synostosis, the possibility of
grafting epiphyseal–physeal composites onto the diaphyseal
end has been suggested on the basis of clinical human and
animal experiments.286–288,296,304,324 Although most of the
transplants may not survive unless microvascular anasto-
moses are undertaken, peripheral (appositional) physeal
growth may be sufficient to prevent the bone from tapering
(Figs. 9-28 to 9-30). It is important to realize and accept that
longitudinal growth potential is limited in such a procedure.
However, if latitudinal growth occurs, it may prevent or
lessen tapering and conical tension in the distal periosteum.
Benevenia et al. recommended the use of autogenous
epiphyseal transplants in traumatic amputations (spare-part
FIGURE 9-28. (A) Irregular stump overgrowth is evident. (B) A synostosis was made between the fibula and the tibia; and a graft of iliac
crest, including epiphyseal cartilage, was added to the distal tibia. (C) One year later there is no evidence of tibial overgrowth.
299
surgery).265 One must examine the potential part carefully
for any injury. Another method similar to epiphyseal graft-
ing may be used for the mangled foot. A portion of a viable
tarsal bone may be fused to the distal tibial ossification
center. Latimer et al. lengthened three below-knee amputa-
tion stumps.300
Complications
The various methods to create end-bearing stumps in chil-
dren may lead to altered anatomy and stress dissipation. This
factor, coupled with normal childhood exuberance, may
result in stress fractures. Treatment is usually protected
weight-bearing and prosthetic adjustment.
The extent of soft tissue damage often dictates the level of
amputation, although there are probably functional limits
even in a child. Leaving too short a stump to activate a pros-
thesis may only create difficulty for the prosthetist and rejec-
tion of the prosthesis by the child.
When the calcaneus is “shelled out” to create a Syme-level
amputation, remnants of the apophysis may be left behind.
These remnants may eventually ossify (Fig. 9-31) and
become painful.
Leaving too much tissue at the stump end may cause a
loose, bulbous end that shifts in the prosthetic socket,
causing poor socket fit and function. Reattachment of the
Achilles tendon through scar tissue may lead to posterior dis-
placement of the heel pad. This may be corrected by releas-
ing the tendon and revising the fat pad position.
Pressure from the prosthesis on the patella may cause
dislocation in the child with a below-knee amputation.306
Reactive overgrowth with skin ulceration may lead to
osteomyelitis. Chronic pressure from the prosthesis may
cause growth arrest. Growth damage may also occur because
of the primary trauma or local damage.
300
FIGURE 9-29. (A) This 2-year-old boy sustained a pathologic frac-
ture through a cystic expansion of the tibial midshaft. After repeated
grafts a below-knee amputation was done, with an attempt to
create a synostosis. Because of irregular distal bone formation 16
months later, the fibula was removed, reversed, and implanted into
the tibial endosteal cavity, with the periosteal sleeves being sutured
together. Two months after this procedure reactive subperiosteal
bone is forming (arrows). The boy was placed back in his pros-
thesis at this time. (B) Two years later the graft is fully incorporated
and shows no osseous overgrowth.
Jaeger et al. found that treatment with intravenous calci-
tonin led to a significant reduction or removal of phantom
pain.293 Davis used mexiletine in 18 patients with phantom
pain or reflex sympathetic dystrophy, having good to excel-
lent results.272 Another 11 patients responded to a combina-
tion of mexiletine and clonidine. Two patients had no
response.
Prostheses
Guidelines for the selection and use of orthotics and pros-
thetics are readily available.289,297 A stump should be fitted
with a prosthesis as soon as it can tolerate pressure. With
most traumatic amputations in a child a minimum period
of 3–4 weeks after the completion of surgical treatment is
required. Although immediate postoperative prosthetic
fitting has been advocated for some adults, such fitting is
usually after an elective, nontraumatic amputation. Wound
management, which is essential to the care of the traumatic
amputation, usually precludes the immediate fitting of a
9. Open Injuries and Traumatic Amputations
prosthesis. If a significant amount of time elapses before the
child is fitted with a prosthesis, however, he or she may reject
the substitute device.
Replantation
A major question concerning partial or complete traumatic
amputation in a child is whether to replant an arm, leg, or
any portion thereof (Fig. 9-32).320,329,330,333,335,336,339,341,348,350,
353,355,356,363
This decision is contingent on the availability and
technical ability of a team of orthopaedic, plastic, vascular,
and neurologic surgeons, as well as the overall extent of soft
tissue injury, the mechanism of injury, the time elapsed since
injury, the presence or absence of other serious injuries, the
condition of the severed limb, and a warm ischemic time of
less than 8 hours or a cold ischemic time of less than 18
hours. All aspects of the surgery must be adequately dis-
cussed with the parents, who must be informed that partial
or complete amputation may still be necessary during the
postoperative phase.
The injured part should be transported in a bag with
Ringer’s lactate or normal saline solution. Wrap the part in
moist gauze. The bag is then placed in an ice container with
an ice bath. Care is taken to avoid tissue contact with the ice
that might cause a frostburn. The stump end (proximal) is
thoroughly cleansed and a pressure dressing applied for
transport or in the emergency room. Care is taken not to
ligate or to use large instruments (even hemostats) to stop
bleeding to avoid causing further damage to the vessels.
In a child with contractile vessels the application of pres-
sure alone is usually enough to stop bleeding and induce
thrombosis.
For bulky parts the warm ischemia time is about 6 hours,
whereas digits may last up to 12 hours or more. This time
may be extended by cold ischemia. The length of acceptable
cold ischemia time does not seem to affect survival of the
implant but does alter the functional results.
Daigle and Kleinert reviewed 15 patients with a mean age
of 4.2 years (range 1.0–8.5 years).334 Average warm/total
ischemia times were 4.8/14.8 hours for failures and 1.1/7.5
hours for successful replantation. Overall limb survival was
87%.
Clean, sharp, “guillotine”-type injuries are those for which
replantation is most feasible. Long, linear stretch injuries
caused by avulsion are least suitable, as are crushing injuries.
Major soft tissue injury may seriously compromise attempted
replantation. Anastomosis of nerves has a better chance of
achieving reasonable recovery of function in a child than in
an adult. To facilitate vascular and neural anastomosis, it is
generally easier to shorten the major involved bone at the
site of the amputation by 1 cm or more. If possible, it should
be done in the diaphyseal or metaphyseal region. If the
involved bone is a femur or a humerus, the normal capacity
for overgrowth cannot be relied on, particularly as few long-
term studies have been done to show whether overgrowth
can occur with this particular type of trauma.
Specific operative techniques may be obtained from the
literature.340,342–344,347,351,358,360,362 At one time, major limb
replantation was not indicated in young children because of
the difficulties of shock due to fluid loss in the limb and the
Replantation 301

FIGURE 9-30. (A) Distal tibia was removed

from the extensively damaged soft tissues
and transplanted to the femur. (B) Seven
months later.

A B

technical problems of small-vessel anastomosis. The biggest

problem in children has been their small-diameter vessels.
Microsurgical techniques now can be applied to vessels less
than 0.5 mm in diameter.333,339,341,351,353,355 These concerns are
less real now that microvascular surgery and use of the
operating microscope have become more readily available,
allowing successful anastomosis of small vessels, and the
recognition of the need to repair enough veins to provide
adequate drainage of the part and reduce blood loss. Even
with reanastomosis of the circulation, the long-term viability
of the physis is not certain. It appears that premature growth
arrest may be frequent (Fig. 9-33). Upper limb replantation
is much more realistic than lower limb replantation.

FIGURE 9-32. (A) Mid-humeral amputation caused by an accident

FIGURE 9-31. Irregular bone formation from the cartilage of the
retained calcaneal apophysis.
with a farm machine. Note the radioulnar fractures and the torus
distal radial fracture. (B) Traumatic forequarter amputation in a 5-
year-old boy who caught his arm in a conveyor belt. Extensive soft
tissue damage and organic debris precluded replantation in both
patients.
302 9. Open Injuries and Traumatic Amputations

FIGURE 9-33. (A, B) Gross specimens of a

hand amputation in a 14-year-old boy. (C, D)
Roentgenograms of the two specimens. (E)
Roentgenogram of the reconstructed hand. Unfor-
tunately, the index finger did not survive the imme-
diate postoperative period. (F) Film obtained 3
months after surgery. Note the premature closure
of the third metacarpal physis. (G) Normal con-
tralateral hand, for comparison.
References
Sehayik presented the results of upper extremity re-
plantation in children.352 Results were good for the hand,
good to excellent for the digits, and best for the thumb.
Digits amputated distal to the flexor digitorum sublimis
usually had excellent recovery of neurovascular function.
However, the overall success rate was lower for the child than
for the adult, primarily because of microvascular problems.
The vessels are smaller in the child, and there is more
vasospasm. Because of the latter, Sehayik recommended
waiting 7–10 days for the first dressing change. No comment
was made regarding epiphyseal/physeal growth, although it
may be impaired.
The ability of the physis to withstand transplantation or
replantation is variable. Experimental studies certainly sug-
gest a reasonable chance of resumption of growth.331,337,
345,354
Clinical studies also support the possibility of retained
growth potential.346,357,361
Jaeger and colleagues found that with upper extremity
replantation, particularly digital replantation in children,
the reaction of the physis to replantation appeared to be an
all-or-none phenomenon.340 The patients either exhibited no
growth at all or had growth equal to or greater than that of
the opposite side.
Hou et al. replanted hind limbs in immature rats338 and
found a significant difference in length. This difference was
influenced by the ischemic interval (2 hours vs. 4 hours).
They thought that replantation of immature material should
be undertaken promptly because of the vulnerability of the
epiphysis to ischemic insult.
Carey et al. quantified growth within a period of 2 weeks.332
There was a linear inverse relation of growth with the length
of ischemic time. Long-term studies of replanted immature
extremities are infrequent.
Usui et al. reported a 4-year-old boy with distal-third leg
amputation.359 Results at 8 years showed no deformity, no
contracture, and healing of the plated fracture. More impor-
tant, the bone was shortened during replantation, resulting
in a 3.5-cm leg length discrepancy. At 4 years it had reduced
to 1.5 cm. The distal tibial and fibular physes were open.
Some believe there is no place for the replantation of
a severed lower limb, although recent success has been
described.352 I agree conceptually that lower extremity
replantation is usually unnecessary. Weight-bearing and loco-
motive functions in the leg are probably better served by a
properly devised prosthesis. Exceptions are severance of the
limb above the knee in a young child wherein successful
replantation may mean retention of the lower femoral
epiphysis, which contributes much to the lower limb length,
and replantation of a distal amputation (ankle or foot
levels), which is comparable to wrist-hand procedures. Even
if a true knee disarticulation is required later, a great service
will have been done to the patient in terms of function. In
the upper limb, however, sensation and manipulation are all-
important, and even a replanted hand that has little of either
may be superior to a prosthesis.
Costecalde et al.270 described subtotal avulsion of the lower
limb through the midshaft of the femur that was successfully
replanted. The long-term complications were partial paraly-
sis and development of a fracture through the distal tibia
and a distal tibial pseudarthrosis that had to be corrected
surgically.
303
Beris et al. reported 53 children with major limb (m = 18),
hand (m = 10), or digit (m = 25) amputations.328 They
thought that even with crush or avulsion injuries their results
justified an attempt at replantation considering the superior
recuperative ability of the child. Free tissue transfer was used
for reconstructive procedures in 26 children, including free
flaps, vascularized bone transfers, nerve grafts, and toe-to-
thumb transfers. The microsurgical success rate was 86.8%
for replantation procedures and 96% for reconstructive
procedures.
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338. Hou SM, Wang TG, Liu MRS. Longitudinal growth after
replantation of immature extremities on rats. J Hand Surg
[Am] 1993;18:828–832.
339. Ikeda K, Yamauchi S, Hashimoto F, et al. Digital replantation
in children: a long-term follow-up study. Microsurgery
1990;11:261–264.
340. Jaeger SH, Tsai TM, Kleinert HE. Upper extremity replanta-
tion in children. Orthop Clin North Am 1981;12:897–907.
341. Kobo T, Ikuta Y, Watari S, et al. The smallest digital transplant
yet? Br J Plast Surg 1976;29:313–314.
342. Malt RA, McKhann CF. Replantation of severed arms. JAMA
1964;189:114–117.
343. Malt RA, Remensnyder JP, Harris WH. Long-term utility of
replanted arms. Ann Surg 1972;176:334–342.
344. Nettlebland H, Randolph MA, Weiland AJ. Free microvascular
epiphyseal-plate transplantation. J Bone Joint Surg Am 1984;
66:1421–1430.
345. Nettlebland H, Randolph MA, Weiland AJ. Heterotopic
microvascular growth plate transplantation of the proximal
fibula: an experimental canine model. Plast Reconstr Surg
1986;77:814–820.
9. Open Injuries and Traumatic Amputations
346. Nunley JA, Spiegl PV, Goldner RD, Urbaniak JR. Longitudinal
epiphyseal growth after replantation and transplantation in
children. J Hand Surg [Am] 1987;12:274–279.
347. O’Brien BM. Replantation surgery. Clin Plast Surg 1974;1:
3–31.
348. O’Brien BM, Franklin JD, Morrison WA, MacLeod AM.
Replantation and revascularization surgery in children. Hand
1980;12:12–23.
349. Pho RWH, Patterson MH, Kour AK, Kumar VP. Free vascular-
ized epiphyseal transplantation in upper extremity recon-
struction. J Hand Surg [Br] 1988;13:440–447.
350. Rich HR, Knight PJ, Erikson DL, Broadhurst K, Leonard AS.
Replantation of the upper extremity in children. J Pediatr Surg
1977;12:1027–1032.
351. Rosenkrantz JG, Sullivan RD, Welch K, et al. Replantation of
an infant’s arm. N Engl J Med 1967;276:609–612.
352. Sehayik R. Reimplantation in children. Orthop Trans 1979;
3:84.
353. Sekijuchi J, Ohmori K. Youngest replantation with microsur-
gical anastomoses. Hand 1979;11:64–68.
354. Stark RH, Matloub HS, Sanger JR, et al. Warm ischemic
damage to the epiphyseal growth plate: a rabbit model. J Hand
Surg [Am] 1987;12:54–61.
355. Tamai S, Hori Y, Tatsumi Y, et al. Little finger replantation in
a 20-month-old child: a case report. Br J Plast Surg 1974;27:
1–4.
356. Taras JS, Nunley JA, Urbaniak JR, et al. Replantation in chil-
dren. Microsurgery 1991;12:216–220.
357. Tsai TM, Ludwig L, Tonkin M. Vascularized fibular eiphyseal
transfer. Clin Orthop 1986;210:228–234.
358. Usui M, Ishii K, Miura M, et al. Experience in replantation of
the totally severed lower limb in a child. Shujutsu 1974;28:
1349–1353.
359. Usui M, Minami M, Ishii S. Successful replantation of an ampu-
tated leg in a child. Plast Reconstr Surg 1979;63:613–617.
360. Varma BP, Srivastava TP. Successful regeneration of large
extruded diaphyseal segments of the radius. J Bone Joint Surg
Am 1979;61:290–292.
361. Volkow M, Bizer V. Homotransplantation of Bone Tissue in
Children. Moscow: Mir Publishers, 1972.
362. White SC. Nerve regeneration after replantation of severed
arm. Ann Surg 1969;170:715–718.
363. Zuker RM, Stevenson JH. Proximal upper limb replantation in
children. J Trauma 1988;28:544–547.
10
Complications
Engraving of nonunion and ankylosis of the knee following a distal
femoral fracture. (From Poland J. Traumatic Separation of the
Epiphyses. London: Smith, Elder, 1898)
raumatized children generally develop fewer general-
T ized or bone-specific complications than adults with
comparable musculoskeletal injuries.3 Even when chil-
dren do develop complications, the problems tend to be less
severe and more rapidly overcome than those in a similarly
involved adult. As discussed in Chapters 6, 7, and 9, certain
types of chondro-osseous injuries may result in short-term
and long-term problems that are relatively unique to the
developing skeleton. In this chapter, a variety of generalized
complications are discussed, with an emphasis on how they
may differ when a child is involved. Fortunately, most of
these complications are infrequent, if not rare, in children.
Unfortunately, this infrequent occurrence may minimize an
orthopaedist’s personal familiarity and experience with the
particular nuances the complication has in children, even
though he or she would usually be quite familiar with the
comparable problems in an adult.1 This situation decreases
the physician’s index of suspicion for such a complication.
Approaches to treatment that might be applied in an adult
must often be modified for use in a child, especially one
under 5 years of age.
A small child may respond differently from an adolescent
or an adult to minor injuries. Following blunt abdominal
trauma, air swallowing or paralytic ileus may be of greater
consequence in children because abdominal distension
may elevate the diaphragm and interfere with pulmonary
function (Fig. 10-1). Similarly, blood loss (either the con-
tained extravascular space or outside the body due to an
open injury) assumes greater significance in infants and
children because these patients have less circulating blood
volume than larger children or adults. A closed fracture of
the femur may be associated with a loss of several hundred
milliliters of blood into the contiguous soft tissues, no matter
what the age of the patient (Fig. 10-2). In a 6-year-old
child this may represent a significant percentage of the total
circulating blood volume and may contribute to hypo-
volemic shock. In contrast, the adolescent or adult may
suffer fewer consequences from a similar quantitative
volume depletion.
Major heat losses occur rapidly in children. A drop in core
temperature of only a few degrees may interfere with normal
metabolic processes and so affects the child’s response to
traumatic stress.2 The rapidity with which metabolic and car-
diovascular reactions occur emphasizes the importance of
good monitoring systems, especially in the polytraumatized
child (see Chapter 3). Minor changes in response to injury
or treatment must be detected early to prevent serious
sequelae.
Congenital abnormalities rarely complicate the manage-
ment of traumatized adults, whereas they may cause serious
complications in young children, particularly if previously
undetected. For example, seemingly minor trauma may pre-
cipitate cardiogenic shock in a child with a previously asymp-
tomatic ventricular septal defect.2 Fracture in a deformed
limb may interfere with subsequent function. Accordingly,
the ramifications of a fracture associated with any congeni-
tal deformity must be considered relative to modifications in
311
312
FIGURE 10-1. Gastric dilation from air swallowing in a 4-year-old
boy with femoral and tibial fractures after being hit by a car. It ele-
vated the diaphragm, leading to acute respiratory distress that was
rapidly relieved by passage of a nasogastric tube.
treatment and the potential effect on the deformity and pat-
terns of biologic healing.
Shock
Unlike with adult skeletal injuries, shock is an uncommon
accompaniment to most children’s fractures, although it
does occur in some patients with multiple-system injuries,
particularly those resulting from vehicular accidents.7 Vari-
eties of shock encountered in children include (1) hypo-
volemic shock, (2) septic (endotoxic) shock, and (3)
cardiogenic shock.
In children, shock following injury nearly always is due
to blood loss. In the pediatric age group, cardiogenic shock
occurs almost exclusively in patients with a congenital car-
diomyopathy. Trauma to the central nervous system practi-
cally never causes shock unless there is significant cranial
separation or vascular disruption of a major vessel. Circula-
tory collapse resulting from an autonomic response to fear
or pain is usually of such brief duration that it is no longer
present when the child arrives in the emergency room.
Shock resulting from infection is infrequent and usually is a
delayed complication, partly because of the low incidence of
open injuries in children (see Chapter 9).
When any type of shock is encountered, treatment must
be specific and prompt. Although children have a much
greater capacity for subsequent recovery, their initial “down-
10. Complications
ward” response to blood or fluid volume loss may be unex-
pectedly rapid after a period of apparent stability.4
Hemorrhagic shock is characterized by hypotension;
tachycardia; cool, pale, or slightly cyanotic extremities; rest-
lessness or obtunded sensorium; and oliguria. Hypotension
is caused directly by the decreased blood volume, with tachy-
cardia and peripheral vasoconstriction being the compen-
satory mechanisms.16 Hypotension may cause inadequate
cerebral and renal perfusion.
Compared with adults, children tolerate a greater degree
of blood loss, as a percentage of total fluid volume, and take
a longer time to manifest any overt response to blood loss.6
It is rare, with the exception of injuries involving a major vas-
cular or organ laceration, for a child to lose sufficient blood
from a skeletal injury alone to manifest a shock response.
Any child presenting with or developing shock should
undergo complete evaluation to rule out any intrathoracic,
intraabdominal, or retroperitoneal injury that might be asso-
ciated with blood loss into an extravascular space, or a major
arterial transection in an extremity (e.g., femoral artery lac-
eration with a femoral fracture). Shock decreases renal func-
tion by reduced blood flow. Excessively decreased flow to the
kidneys may lead to progressive renal ischemia and eventu-
ally to renal tubular necrosis, shutdown, and anuria. Proper
management and attention to fluid and electrolyte adminis-
tration early in the course of the shock state usually aids in
the prevention of such renal insufficiency. Again, children
have a better capacity than adults for complete recovery of
renal function, even if they are temporarily anuric from
renal shutdown.
The management of shock should be directed at general
supportive measures and at the actual causative mechanism,
which should be specifically rectified.5,8 Immediate steps
include: (1) maintenance of an airway; (2) insertion of a suf-
FIGURE 10-2. Large liquefied hematoma following a sub-
trochanteric femoral fracture 12 weeks earlier. Heterotopic ossifi-
cation is occurring at the margins.
Arterial Injury 313

ficiently large intravenous line to allow rapid transfusion of
fluids, blood, or both; (3) maintenance of arterial blood
pressure through early infusion of Ringer’s lactate followed
by properly matched blood or blood substitute; (4) insertion
of a nasogastric tube because of the possibility of air swal-
lowing; and (5) cardiac monitoring. The use of adequate
monitoring equipment (e.g., central venous pressure or arte-
rial pressure lines) and pulse oximetry are also helpful for
following these problems through their acute phases.
Familiarity with normal values is fundamental to the ratio-
nal management of shock. A child’s blood volume relates
directly to body weight and is approximately 40 ml/lb re-
gardless of age or size. Pulse rates gradually decrease with
age, the upper limits of normal being 160/min in infants,
140/min in preschool children, and 120/min for older chil-
dren. The normal systolic blood pressure is 80 mmHg plus
twice the age (in years), and the normal diastolic pressure is
two-thirds the systolic pressure. Normal urine output aver-
ages 1 ml/lb/hr in small children and 0.5 ml/lb/hr in older
children.
Arterial Injury
Blunt trauma severe enough to fracture a child’s long bone
may seriously damage adjacent arteries by direct or indirect
force.15,19,21–23,26,29,31–33,38–41,43 Disruption or thrombosis of the
traumatized artery may ensue, and the viability of some or
all of the extremity distal to the arterial injury may be jeop-
ardized.28,42 Delay in diagnosis lessens the opportunity to
salvage the extremity.15,20 Often temporizing measures are
utilized in the false hope that the vascular impairment does
not represent sufficient damage to require prompt operative
treatment. Guidelines for the management of this complex
problem in children are not readily available, as fracture with
concomitant arterial injury involving the immature skeleton
is uncommon (Fig. 10-3). However, it must always be sus-
pected with elbow and knee injuries.
There are several anatomic types of vascular injury: (1)
Lesions in discontinuity, in which the vessel is completely
transected. In children with contractile vessels the ends may
decrease the lumen size to limit or stop blood loss. Such dia-
metric change may also allow thrombosis and clot formation,
and it may further increase the likelihood of decreased
blood loss compared to a similar vascular injury in an
adult. (2) Lesions in continuity, including intimal lesions.
(Vasospasm in a child may convert an incomplete tear to a
complete occlusion.) (3) Contusions causing partial or com-
plete occlusion of the vessel. Spasm may also cause a lesion
in continuity. Traction on the affected vessel, particularly
that which occurs during the extremes of displacement
during the acute injury, is capable of producing such reac-
tive vasospasm. Compression, from the cast externally or a
fracture fragment internally, may cause variable occlusion of
a vessel. Soft tissue swelling and soft tissue structures (e.g.,
ligaments) may also compromise circulatory dynamics. Pro-
longed occlusion may lead to thrombosis and permanent
occlusion.

FIGURE 10-3. (A) Transection of the popliteal artery complicating a proximal tibial epiphy-
seal fracture in a 14-year-old boy tackled in a football game. The arteriogram shows com-
plete block of the popliteal artery (arrow) with some collateral flow. Retrograde filling did
not occur because of extensive thrombosis within the artery. Circulation through the col-
lateral vessels should not be relied on to sustain functional muscle demands as the indi-
vidual grows. (B) Subintimal damage (straight arrow) and complete block (curved arrow)
in a 15-year-old boy who eventually required a below-knee amputation for extensive soft
tissue damage in the distal leg and foot.
314
Various alterations in vascular pathophysiology may occur.
With complete arterial occlusion, the distal pulse is gener-
ally absent and the venous system relatively empty. The limb
gradually becomes white and cold. It may take time for anes-
thesia and paralysis to develop. Pain is usually severe until
functional nerve loss (from the ischemia) occurs. Arterial
occlusion of flow to bone results in severe hypoxic changes
in the osseous and cartilaginous circulations.27 In contrast,
moderate changes follow venous occlusion.
Incomplete occlusion, often a concomitant to compart-
ment ischemia, is compatible with an intact distal pulse and
seemingly adequate peripheral circulation (e.g., blanching
and recovery after nail compression and release). There may
be pain at rest in specific muscle groups and increased pain
on stretching the involved muscles. If the flow in the main
artery is reduced, the flow through collaterals (vascular
bypass) may be sufficient to maintain a pulse in the distal cir-
culation but insufficient to maintain perfusion into specific
muscle groups. These muscles become hypoxic and swell
within the closed fascial compartments. Arterial inflow, cap-
illary through flow, and venous outflow become variably
occluded, leading finally to ischemic necrosis of some or all
of the muscle with contraction. Decreased venous outflow
with variable arterial inflow is a significant cause in such
ischemic change.
In areas that are commonly problematic in children, such
as the forearm in supracondylar humeral fractures, selective
occlusion of a small vessel (e.g., anterior interosseous artery)
may also lead to this syndrome. Because the main aterial
vessel is intact, major signs of vascular problems, such as
decreased perfusion and compartment syndrome, are not
always readily obvious.
With compensated occlusion the extremity may be cool,
but there are no obvious signs of nerve or muscle ischemia.
The collaterals maintain adequate resting circulation.
Usually the distal pulse returns. In this situation, as well as
with incomplete occlusion, consultation with a vascular
surgeon should be sought if there is any concern over the
adequacy of the circulation. A feeble pulse that remains
feeble may subsequently create a painful subsequent defor-
mity as a result of the “demand” ischemia that occurs during
function, even though the child has no apparent symptoms
while resting.
In a review of 15 children with extremity fractures and
associated vascular injury, complete ischemia was present in
only two.49 In four partially ischemic patients the vascular
injury was not diagnosed until 12–14 days after the injury.
All limbs were preserved, but complications were frequent
and necessitated 28 operations (approximately two proce-
dures per patient). Short-term salvage depends on the
degree and duration of the deficient perfusion. Mid- to long-
term functional results depend on the severity of the skin,
muscle, bone, and nerve injury. The high salvage rate is
attributed to the short delay to arterial reconstruction for
complete ischemia and restoration of circulation for partially
ischemic cases.
Wolf et al. reviewed 30 children with upper extremity arte-
rial trauma.48 Trauma was penetrating in 87% and caused by
glass in 53%. Nerve repair was required in 53% and tendon
repair in 23%. Altogether 26 patients underwent vascular
repair. Postoperatively three children had no palpable pulse
distal to the repair; one required amputation due to exten-
10. Complications
sive soft tissue mutilation. Follow-up revealed no dysfunction
directly related to vascular injury (even in the three without
a palpable pulse). Neurologic deficit was evident in 33%, but
in only one patient was the limb completely dysfunctional.
Long-term outcome was largely dependent on the neuro-
logic injury, not the vascular injury.37,48
Friedman and Jupiter analyzed vascular injuries associated
with closed extremity fractures in children. They found that
most vascular injuries were not diagnosed initially, conse-
quently delaying repair23 and increasing the incidence of
complications such as wound infection, below-knee amputa-
tion, deep vein thrombosis, and motor and sensory deficits.
In suspected cases they thought arteriography should be per-
formed prior to any surgical repair of either the vascular
injury or the fracture. Because of potential problems with
growth disturbance, they recommended that all major vas-
cular injuries be repaired even if there appears to be ade-
quate collateral circulation to keep the limb viable. Another
factor, which they did not address, is demand ischemia as the
child grows. Increasing muscle mass and functional demands
years after a vascular repair that does not allow growth of the
lumen changes the hemodynamics and may not allow ade-
quate functional muscle tissue perfusion. This situation may
lead to a childhood or adolescent version of claudication.
Arterial injury should be suspected in any patient who has
been injured by direct or indirect trauma of sufficient mag-
nitude to fracture a long bone, particularly if the fracture is
displaced and distal physical findings are suspicious. The
appearance of the extremity must be scrutinized carefully,
and the presence or absence of pulses must be determined.
The color, temperature, adequacy of sensation, and diminu-
tion of the pulses in comparison to those of the contralat-
eral extremity may be significant. However, the presence of
a distal pulse does not positively exclude damage to a prox-
imal artery, as the collateral circulation may be adequate in
a child for resting tissue perfusion (although there may be
insufficient perfusion for childhood activity after recovery).
Capillary refill is a clinical sign popularized during the
past 15 years. Essentially, it measures peripheral perfusion,
which is likely to be a function of cardiac output and periph-
eral vascular resistance. It is a semiquantitative test, with
a value of less than 2 seconds generally considered normal.
However, capillary refill may not be a reliable clinical sign.9
Although 2 seconds is a reasonable value, the lowest capil-
lary refill time that included 95% of the study population
was substantially higher (2.9 seconds), and in the elderly it
was up to 4.5 seconds.9 Ambient temperature significantly
affects capillary refill.
Pulse oximetry is not a reliable means of detecting acute
arterial injury or a compartment syndrome complicating a
closed fracture or dislocation.14,17,24 The lack of reliability
relates to the extent of collateral circulation and the ability
to provide sufficient resting peripheral tissue flow.
If doubt remains regarding the intactness of the periph-
eral artery after physical evaluation of the circulatory status
of the involved limb, prompt angiographic studies should be
considered.40 As a diagnostic tool, arteriography is not always
necessary because in many cases the diagnosis may be made
based on the clinical findings alone. This is particularly true
in cases of open fracture. Arteriography is useful in ways
independent of diagnostic assistance, however, as it supplies
valuable details of confirmation about the exact anatomic
Arterial Injury 315

location, the extent of arterial damage, and the status of the

collateral circulation.
Digital subtraction angiography is a method with low mor-
bidity for evaluating the adequacy of vascular function.45 For
angiography the catheter is placed in the antecubital vein
after adequate sedation of the young patient to prevent
motion artifacts. Contrast material is injected, and subtrac-
tion imaging is conducted. Both arterial and venous phases
may be obtained. The technique is simple and minimally
invasive (venipuncture), with excellent visualization of the
vascular disruption in infants and children.
Whereas angiography presents a relatively static picture of
the vascular disruption, pulse volume and wave propagation
recording may provide a safe, noninvasive, reproducible,
dynamic evaluation of blood flow. Digital cuff impedance
plethysmography may be performed at the bedside, even if
the child is uncooperative. It may also demonstrate improve-
ment in arterial flow following fracture manipulation, reduc-
tion of joint dislocation, or vascular repair. Major vessel
disruption or luminal decrease affects pulse pressure wave
propagation distal to an injury. If noninvasive studies such as
pulse recording indicate decreased flow, arteriography
usually is performed to define the lesion more accurately. FIGURE 10-4. Knee of a 6-year-old child showing the conse-
The damaged arterial segment often must be excised, and quences of delayed diagnosis and repair (72 hours after injury) of
the remaining portions must be sufficiently mobilized and a femoral artery transection in a midshaft femoral fracture sus-
débrided to ensure normal arterial structures for recon- tained 3 years earlier. There is permanent damage to all of the
struction. The exact pattern of reconstruction varies accord- physes distal to the vascular injury, compromising longitudinal
growth.
ing to the extent of the injury to the vessel and surrounding
soft tissues. If the extent of injury requires so much sacrifice
of vascular tissue that primary reanastomosis is not possible,
the use of an autogenous vein graft is the next most desir-
able approach. Prosthetic vascular grafts should be avoided One study reported five boys with arteriovenous fistulas:
in children. four with factor VIII deficiency and one with hepatic-
If it is necessary to perform a primary anastomosis or induced coagulopathy.44 In each case the fistula was trauma-
excise a portion of the vessel and reanastomose it, it is appro- induced. All five developed a slowly progressive pulsatile
priate that the fracture be treated with adequate fixation mass over a period of several months. Surgical ligation is rec-
at the same time. An unstable fracture, particularly a supra- ommended for progressive enlargement.
condylar humeral fracture, may jeopardize the vascular
suture line. This is probably one of the few situations in
which open reduction should be carried out first, followed
Vasospasm
by the appropriate vascular repair. Firm stabilization of the Russo reported a tibial fracture in a 9-year-old boy who had
fracture site protects the vascular reconstruction. Either had diffuse arterial spasm and eventual gangrene.35 There
internal or external skeletal fixation may be used. The appli- was no evidence, during preamputation evaluation or at the
cation of skeletal fixation should not delay vascular repair subsequent below-knee amputation, of a specific arterial
beyond the 6- to 8-hour ischemic period. Temporary stabi- injury. Traumatic arterial spasm is an unusual cause of gan-
lization may be inserted quickly to allow vascular repair, fol- grene in vessels of medium or large diameter, especially the
lowed by the application of a different, more “permanent” resilient arteries of a child. Although recognized by micro-
skeletal fixation device. surgeons as a threat to successful replantation, it is generally
The importance of long-term follow-up of pediatric believed to be limited to vessels of small diameter and rela-
patients who require arterial reconstruction cannot be tively low flow. Some authors believe that children may be
overemphasized. Chronic arterial insufficiency (demand more susceptible to spasm and its effects, making recogni-
ischemia) may develop at any time owing to growth and tion and treatment extremely important for the pediatric
changing demands.34,47 Although vascular (arterial) injuries orthopaedist.15,18,19
are often associated with neuromuscular involvement, one Numerous theories have explained vascular spasm in the
also must not forget the potential long-term consequences absence of obvious injury to the vessel. Reflexes have both
of ischemia on longitudinal and latitudinal physeal growth autonomic and myogenic pathways. The autonomic re-
(Fig. 10-4). Circulatory compromise may cause central sponse results in constricted vessels when intraluminal
physeal growth arrest and the development of conical pressure decreases. This mechanism is mediated through
physes.10–13,30,46,47 The damage may be small (focal). Such adventitial sympathetic fibers. Of more importance for trau-
growth slowdown or arrest may not become evident clinically matic arterial spasm is the direct myogenic effect, which may
or radiographically for many years after the vascular injury be precipitated by a stretch or irritation of a vessel wall medi-
(see Chapters 1, 6, 7). ated by the muscle itself. Clinical examples of this form of
316
vascular spasm include the loss of pulses during limb length-
ening or after femoral or brachial arteriography. The inten-
sity of the myogenic reaction appears to be age-dependent,
because arterial spasm is more frequently encountered in
children and adolescents. The severity of ischemia resulting
from such spasm is related to the degree to which a young
vessel may contract. Because the degree of contraction is
inversely proportional to the amount of preexisting fibrosis
or atherosclerosis, obviously the minimally involved or unin-
volved vessels of children are more susceptible.
The basic treatment of vasospasm includes gentle fracture
realignment with stabilization and restoration of mean arte-
rial blood pressure. This treatment may include removal of
excessive traction or tight circumferential bandages, appli-
cation of warm compresses, and release of compartments
when indicated. Stellate or epidural blocks have limited
effects but may be helpful in conjunction with other mea-
sures. Another possible treatment is intraarterial injection of
vasodilating agents.25 The mechanism of action is directly
on the smooth muscle of the artery. Many agents, such as
papaverine, sodium nitroprusside, tolazoline, reserpine, and
prostaglandin E have proved useful. Surgical measures may
be applied, particularly following the failure of intravascular
injection of agents. Such measures may include external
irrigation with warm Ringer’s lactate, application of local
anesthetics or papaverine, and adventitial stripping as a last
resort. When all else fails, dilation of the involved vessel may
be accomplished by passing dilators or catheters. Resection
of the involved segment followed by an appropriate graft is
the final approach.36
Compartment Syndromes
Compartment syndrome occurs when increased tissue pres-
sure within a closed fascial space compromises the cir-
culation to the nerves and muscles within the involved
compartment. The syndrome may be caused by fracture,
severe contusion, limb compression (e.g., a leg bent at the
knee, pinned in flexion for an extended period), limb crush-
ing (a small foot being run over by an antomobile tire), drug
overdose (which is becoming an increasing problem in ado-
lescents), burns, or vigorous exercise.50–126
Intraosseous infusion may also lead to compartment syn-
drome. Vidal et al. reported compartment syndrome due to
extravasation of fluid in a 1-month-old infant who received
an intraosseous fluid infusion.121 It resulted in a below-knee
amputation.
Kline and Moore reported compartment syndrome in
neonates.87 Intrauterine conditions may initiate the syn-
drome so it is well advanced at delivery. An arm or leg may
become entrapped during the later stages of pregnancy and
descent. Examination for tenderness or painful range of
motion is not reliable. Infectious processes or large-vessel
thrombosis may be underlying causes. Massey and Garst
described compartment syndrome in a patient with osteo-
genesis imperfecta (femoral fracture).91
The initial insult causes hemorrhage, edema, or both in
the closed fascial compartments of the extremities. The
increase in intracompartmental fluid pressure causes
ischemia.81,93 The pressure changes particularly affect capil-
lary perfusion and venous outflow. Flow may not be signifi-
10. Complications
cantly compromised in the larger arterial vessels. Damage to
the contents of the compartment, if permanent, may result
in Volkmann’s contracture. To prevent such complications
the diagnosis must be prompt. The complication is just as
common in the child as in the adult.*
The most common source of compartment syndrome
in children is fracture; yet despite the high incidence of
forearm fractures in children, subsequent compartment syn-
drome is rare. In contrast, supracondylar fractures are more
likely to be followed by compartment syndrome.83 Compart-
ment syndromes have also been reported after radial neck
fractures and physeal injuries of the distal radius.79,99,119
Forearm compartment syndromes have also been reported
in cases of hemophilia and secondary to leukemic infiltrates,
in the avulsion of muscle origins, and with contusions, lac-
erated vessels, and the use of tourniquets.52,63,69,90,105,110,119
The common denominator of compartment syndromes is
elevated interstitial fluid pressure that causes vascular occlu-
sions within the muscle tissues enclosed in the involved
compartment. Although it may be high enough to produce
ischemia of muscle and nerve, elevation of intracompart-
mental pressure only rarely is sufficiently elevated to occlude
a major artery. In contrast, venous and capillary occlusion
may occur as the pressure increases. Failure to appreciate
that arterial circulation may be maintained in the face of
small-vessel and venous occlusion may lead to a false sense
of security. Several investigators have demonstrated the rela-
tion between increased tissue pressure and ischemia of
muscle.115,123 Analysis suggests that when tissue fluid pressure
exceeds 30 mmHg, the capillary pressure may not be suffi-
cient to maintain blood perfusional flow within the
muscle.71,72 Elevated compartment tissue pressure appears to
act synergistically with ischemia to produce more severe cel-
lular deterioration than does ischemia alone.77
Excessive participation in athletic activities may precipitate
muscle swelling or increased osmotic pressure,60,113 which
may lead to acute or chronic (more common) exertional
compartment syndrome. These patients typically describe
pain and swelling (usually in the lower leg). They may also
have sensory deficits, paresthesias, motor weakness, or motor
loss. Corroboration of the diagnosis may require compart-
ment pressure measurement before and after (or during)
exercise (the equivalent of a cardiac stress test). Hargens et
al. showed normal human resting intracompartmental pres-
sures of -3 to +5 mmHg, which may rise to 60–95 mmHg
during isometric contraction.73 The obvious treatment is
activity modification, but this may not be acceptable to some
individuals, in which case elective fasciotomies (and the
attendant risks) may be discussed and undertaken with the
patient and his or her family.
Despite a better understanding of the condition, the most
frequently encountered problem is making a timely diagno-
sis. Delay in doing so, particularly if in excess of 12 hours,
results in an increased risk of permanent functional deficit
or partial limb loss. The most important misconception
about diagnosing compartment syndrome has been the ten-
dency to delay treatment because a palpable distal pulse is
present at the wrist or ankle. This idea is based on the
* Refs. 50,54,57,73,75,79,80,85,87,88,90,91,96,101,109,111,119–121,
125.
Arterial Injury
assumption that there is not a significant elevation of pres-
sure until the pulse disappears. To minimize the failure of
appropriate diagnosis the use of tissue pressure recording
has been widely reported as an appropriate technique.
Recording methods vary and may include a simple
needle/manometer, wick cathether, slit catheter, or pressure
transducer.
Swelling and palpable tension over a muscle compartment
are the first signs of compartment syndrome and are
manifestations of increased pressure within the compart-
ment. A palpably soft compartment is a good prognostic
sign that pressures are not elevated, but it is a relatively
crude indication of compartment pressure. Other physical
findings should be sought. The earliest physical finding is
tenseness of the compartment, which is generally located
throughout the involved compartment, rather than being
limited to the area of the fracture. If there is any suspicion
of the complication, the cast or splint should be removed
for a thorough examination of the skin and palpable
soft tissues of the compartments. Fear of loss of reduction
should not preclude complete examination. Most compart-
ment syndromes may be highly suspected, if not diagnosed
clinically, and do not require sophisticated monitoring
techniques.
Pain with stretching of the muscles is a common finding,
but it is subjective and may be unreliable because the sign
may be enhanced by any chondro-osseous trauma, rather
than only by the ischemia and swelling. Furthermore, pain
on stretching may be absent later because of anesthesia
secondary to ischemia of neural receptors. Paresis is also a
difficult sign to interpret because it may arise secondary to
neural involvement or primary ischemia of muscle, and
there may be guarding secondary to the pain that stimulates
the paresis. Pain may be lacking if a central or peripheral
sensory nerve deficit is superimposed. It is important to
assess this possibility, especially with supracondylar fractures,
which have a reasonably high incidence of associated nerve
contusion or more severe damage.
Pain is the presenting complaint in a conscious patient
and is frequently but not always out of proportion to the
injury. Such distinction is not always easy to make in an
apprehensive child. Pain is usually aggravated by passive
stretch of the muscles in the involved compartment, but this
is less likely when sensory nerve deficit supervenes. Pain is
not relieved by splinting and tends to be progressive. It also
tends to be localized to the compartment area rather than a
specific nerve distribution. The absence of pain may be sec-
ondary to neurologic damage, particularly after 24–48 hours
of compartment pressure elevation or altered mental status
(as in a brain-injured child). Sensory examination usually
can be performed, even in relatively uncooperative children,
by careful two-point discrimination and light touch. This way
the use of needles for sharp sensory discrimination may be
avoided, as they may jeopardize cooperation in an already
apprehensive child.
Pulselessness is a late sign, and its presence should raise
concern about major vascular damage rather than tissue
fluid accumulation within a compartment. However, com-
partment syndrome is likely to occur after such major vas-
cular damage is corrected. Because compartment syndrome
is most often due to small-vessel occlusion, the presence of
317
a radial pulse or an ulnar pulse hardly precludes the pres-
ence of ischemia.
The three groups of patients particularly difficult to diag-
nosis on clinical grounds alone are uncooperative and unre-
liable patients such as very young children, unresponsive
patients such as those suffering head trauma and coma
(especially if they have decerebrate rigidity), children or ado-
lescents, and patients with peripheral nerve deficits or spinal
cord injuries.
Tenseness and swelling of a muscle compartment obvi-
ously are more evident in a superficial compartment than a
deep compartment. Other physical signs include pain out of
proportion to the clinical situation, loss of digital sensibility,
or paresthesias and pain when stretching the muscles of the
concerned compartment. Because not all signs are present
in each patient, the most reliable physical finding is a sensory
deficit. Such a deficit may appear early, but the only mani-
festation may be a paresthesia; after prolonged ischemia this
sensation may disappear. Reliance should be placed on a two-
point discrimination and light touch, for both are more sen-
sitive than the commonly used pinprick test.
Sullivan and Mubarek thought that compartment syn-
drome in the upper extremity could be diagnosed based
principally on clinical impressions and subsequently con-
firmed by intracompartmental pressure monitoring.117 The
infrequent occurrence of Volkmann’s ischemia in children
lessens suspicion. A high index of suspicion is important.
Intracompartmental pressure monitoring may be per-
formed in an awake, cooperative child using local anesthe-
sia. If the child is uncooperative, sedation or even general
anesthesia should be considered.
Intracompartmental pressures may be measured by the
wick catheter or a similar technique in patients suspected
of having acute compartment syndromes.95,109,123 By such
methods, a pressure of 30 mmHg or more sustained for 6–8
hours is a likely indication for decompressive fasciotomy.
Whitesides suggested that fasciotomy be performed when
the intracompartmental pressure approaches 20 mmHg less
than the patient’s mean diastolic blood pressure.123 Matsen
et al. suggested fasciotomy in the presence of any pressure
higher than 45 mmHg.93,95 Others have suggested fasciotomy
at a pressure of 30–40 mmHg over an 8-hour period. Seiler
et al. showed that in the uninjured volar (palmar) compart-
ment, clinically significant (5 mmHg) intracompartmental
pressure differences exist over distances as little as 4 cm.112
The pressure level at which surgical decompression (fas-
ciotomy) is appropriate probably depends on the rapidity of
tissue pressure increase and less on the measurement
method.
Triffitt et al. showed that patients with compartment
pressures elevated above 40 mmHg did not necessarily
develop compartment syndrome or long-term sequelae.118
More importantly, none required compartment release
(fasciotomy). Arbitrary reliance on specific values to define
treatment is to be avoided, especially if other factors are not
positive.
The time sequence of how long an elevated pressure can
be maintained is currently unknown in children. Mubarak
and associates suggested that any patient with an intracom-
partmental pressure higher than 30–34 mmHg should be
considered for fasciotomy if the elevated pressure is com-
318
bined with the aforementioned clinical and subjective find-
ings.104 Because of physiologic differences in children, exact
pressure parameters, and whether they significantly differ
from those in adults are unknown and need to be further
explored.
Given the vagaries of the syndrome, a questionably neces-
sary fasciotomy probably is reasonable to avoid the severe
permanent deformity that usually ensues from this
syndrome.
Heppenstall et al. studied muscle energy metabolism76–78
and found that the threshold for cellular metabolic derange-
ment in skeletal muscle subjected to increased tissue
pressure was more closely associated with the difference
between mean arterial blood pressure and compartment
pressure than with the absolute (elevated) compartment
pressure. The lowest difference at which normal metabolism
was maintained was 30 mmHg, whereas traumatized muscle
could accommodate 40 mmHg. They believed it was not
appropriate to specify any one absolute compartment
pressure measurement as the threshold for fasciotomy. The
perfusion pressure gradient is probably more important.
A good guideline is to consider fasciotomy if compart-
ment pressure approaches within 10–30 mm of diastolic
pressure.
Hackman et al. assessed muscle damage relative to
diastolic pressure.70 If compartment pressure approached
10–20 mmHg of the diastolic pressure (in normotensive
dogs) muscle ischemia was likely. They thought that these data
refuted the use of absolute tissue pressures for decision making.
Standard methods measure pressure in the dorsal and
superficial palmar compartments. The approach to deep
palmar compartment testing has not yet been described in
the literature. Deep palmar compartment syndrome of the
forearm may follow a minor crush injury.50 One of the first
descriptions of muscular hemorrhage or edema as a possible
cause of ischemic contracture involved an 11-year-old boy
who fell from a bicycle. There was no obvious fracture.
Because of pain, the patient had been placed in a cast. He
returned a few hours later with severe pain. Fasciotomy
showed that the superficial palmar compartment had
healthy muscles with no evidence of ischemia, whereas inci-
sion of the fascia of the deep palmar compartment revealed
bulging deep flexor muscles.50 Allen et al. described two
cases of crush injuries involving the deep palmar compart-
ment: one in a 25-year-old man and the other in a 15-year-
old boy.51
Fasciotomy in the arm or leg should be done by an open
method and not through percutaneous and subcutaneous
incisions. It is necessary, particularly with the lower leg, to
decompress all involved compartments through anterior and
posterior incisions, especially in cases of violent trauma or
major vascular injury. Fasciotomy-fibulectomy, which has
been described for adults, should not be used for children
because it may lead to major growth impairment, especially
at the ankle.61,84 If it must be used, a “locking” screw placed
from the distal fibula into the tibia, as often used for limb
lengthening, should be considered. Furthermore, the resec-
tion should be subperiosteal, allowing the potential for
regenerative membranous ossification.
Fasciotomy delayed even 24 hours in an experimental
animal model was associated with irreversible muscle
10. Complications
damage (necrosis), which did not become apparent histo-
logically for approximately 1–3 weeks after fasciotomy.110
Approximately 3–7 days after fasciotomy, skin closure is
usually possible.62 Tissue pressure measurement helps to
verify that pressure has not risen to ischemic levels during
secondary closure. With large wounds or too much swelling,
split-thickness skin grafting may be necessary. If there is
necrotic muscle, the tissues are débrided repeatedly until a
satisfactory granulation bed is present. If an infection is
present or suspected, quantitative bacterial counts help to
determine when to graft.
The insidious development of contractures should not be
overlooked, as they may develop during the subacute phase
owing to splinting secondary to pain, anterior compartment
weakness, or posterior compartment muscle involvement.
Posterior splinting of the unit or ankle in the neutral posi-
tion is essential.
Direct damage to the blood supply of the median nerve
may be a cause of some of the problems encountered in com-
partment syndrome. The median nerve is vulnerable to com-
pression, as it lies on the undersurface and within the
investing fascia of the flexor sublimis muscle. As the muscle
expands because of ischemic changes and edema, it may
compress the median nerve directly and cut off the arterial
supply of the nerve itself. Hemorrhage or swelling within the
nerve sheath may mimic compartment pain.
Volkmann’s Contracture
Volkmann’s contracture is a common term referring to the
end stage of ischemic muscle injury (i.e., the consequence
of unrecognized compartment syndrome). Decreased arte-
riolar and capillary perfusion appears to be the primary ini-
tiating factor of Volkmann’s ischemia, although other factors
may also be involved.122 Lesions caused by temporary arte-
rial occlusion are different from those caused by venous
occlusion. Venous obstruction does not appear to be signif-
icant in the pathogenesis of experimental or clinical
ischemic necrosis of skeletal muscle.122 However, the exten-
sion of ischemic muscle necrosis, once initiated by arterial
occlusion, may proceed by several pathways.
In a study of Volkmann’s contracture in children that
involved 58 limbs, there were 21 cases of femoral fractures
that led to compartment syndrome in the more distal
portion of the leg.104 Specific involvement of the forearm,
lower leg, and foot with these vascular complications is dis-
cussed in Chapters 14–16 and 21–24.
Mubarek and Carroll reported 55 cases of Volkmann’s
ischemic contracture over a 21-year period.101 They were
cases of established compartment syndrome at time of admis-
sion. Only 22% underwent fasciotomy, because of the fact
that the diagnosis was made more than 48 hours after injury
and referral. In the lower extremity, they noted that fractures
of the femur treated with skin traction, Bradford frame,
Dunlop traction, and fracture of the tibia were the most
frequent initiating causes of lower extremity Volkmann’s
ischemia.
The vulnerability of a muscle to vascular injury is deter-
mined by the specific pattern of intramuscular anastomoses
and the relation between volume of muscle and size of the
main nutrient vessels. For example, the only blood supply to
Arterial Injury
FIGURE 10-5. MRI scans of normal (left) and
ischemic (right) lower legs 17 months after an
untreated compartment syndrome. This undiag-
nosed compartment syndrome complicated a
femoral fracture.
the flexor digitorum profundus and flexor pollicis longus
muscles is the anterior interosseous artery. Because the cir-
culatory pathways are still developing in a child, some vessels
may subsequently enlarge to bring in sufficient collateral
flow. Ischemic muscle damage, once it has occurred, is
usually irreversible, even in a young child (Fig. 10-5).
Several types of intramuscular vascular patterns have
been demonstrated in adults. It is reasonable to assume
further variations in the developing muscle of skeletally
immature patients. There are features of the vascularity
peculiar to specific muscle groups, and anastomotic path-
ways are such that whole muscles, or segments thereof, may
be affected by vascular occlusion despite no signs of distal
ischemia.
It is important to realize that Volkmann’s ischemic con-
tracture is a staged process whereby secondary shortening
and contracture follow muscle ischemia and necrosis, with
the contracture and shortening worsening with growth.
When Volkmann’s ischemic contracture involves the
upper extremity, muscle necrosis, shortening, and tighten-
FIGURE 10-6. This 14-year-old boy avulsed both tibial tuberosities
while running. Four weeks after the injury he had acute onset of
shortness of breath. (A) Chest film showed opacification of the left
319
ing of the long digital flexors make good grip strength
difficult.126
Renwick et al. showed that cystic degeneration and calci-
fication may occur as late sequelae of compartment syn-
drome.108 Early et al. also demonstrated this phenomenon,
including compartment liquefaction.58
Landi et al. used computed tomography (CT) to establish
the diagnosis of Volkmann’s contracture of forearm
muscles.89 They found CT helpful for determining the sever-
ity and extent of muscle damage. Such evaluations are im-
portant, as there is considerable variation in the extent of
damage, which necessitates tailoring any subsequent thera-
peutic approach to the individual patient. Among the patients
reported by Landi et al., one was a 14-year-old boy who had
a humeral head fracture with Volkmann’s ischemia, and
another was a 14-year-old boy with a gunshot wound to the
upper arm who had forearm ischemia.89
Magnetic resonance imaging (MRI) may also better de-
fine the extent of muscle damage and may help when
planning the areas of resection (Fig. 10-6). The current
lower lung field. (B) Venogram of the right leg showed small vessel
thrombosis. The left leg was more severely involved, with throm-
bosis of much of the deep system (arrow).
320
limitations of MRI probably preclude using it effectively to
delineate the patency of the anterior interosseous artery or
the nerve.
The long flexor capability may be restored by muscle trans-
plantation, leading to improved hand function. Proper
patient selection and attention to detail during the operative
procedure are critical. For any transfer to function effec-
tively, particular attention must be directed to use of the
appropriate motor nerve and insertion of the muscle in the
correct position. Furthermore, placing the muscle under
tension should establish a functionally useful range of excur-
sion. It must also be considered that growth of the muscle
may or may not keep pace with that of the child’s skeleton,
and it may be necessary to modify the procedure, per-
form lengthening, and so on. Postoperative management
involves initial splinting followed by a coordinated rehabili-
tation program in which patient compliance is most im-
portant. A 6-month interval, at a minimum, should be
allowed for tissue conditions to optimize prior to muscle
transplantation.
The Zuker procedure harvests the gracilis muscle and
transplants it to the forearm with revascularization and rein-
nervation.126 The prerequisites for such muscle replantation
are the same as those for tendon transfer. They include (1)
adequate proximal joint stability and the potential for hand
positioning; (2) a virtually normal range of passive joint
mobility in the hand and fingers; (3) adequate hand sensi-
bility; and (4) the potential for tendon gliding. It certainly
is preferable that normal hand sensibility and intrinsic mus-
cular function be present. Furthermore, adequate skin flap
cover is required at the site of tendon and muscle trans-
plantation and repair to facilitate tendon gliding. If there is
extensive scarring from a previous skin graft (required
during treatment of Volkmann’s ischemic contracture or
compartment releases), preliminary procedures with tissue
expanders and cutaneous revision may be necessary before
undertaking a major muscle transplantation.
It is also important to assess the vascular supply to the
extremity, particularly the brachial artery and anterior
interosseous artery. If the anterior interosseous artery is
undamaged, it is likely that the anterior interosseous nerve
is also unaffected. If there is any concern about the status of
the circulation, digital subtraction angiography or arteriog-
raphy may be indicated.
Because both median and ulnar nerves are often com-
promised, a detailed evaluation that includes electromyog-
raphy and nerve conduction studies is necessary.
Accordingly, muscle transplantation is best deferred until
sensory recovery in the hand is optimal, because it can assist
in the rehabilitation and use of the hand after any forearm
reconstruction. The patient and family must be given a real-
istic appraisal of the problem and the potential for recovery.
Because both median and ulnar nerves may be encased in
scar, early decompression may be helpful in improving
motor and sensory recovery of the hand. If this is done as a
preliminary procedure, it is important not to expose the
naterior interosseous nerve, as subsequent exposure may be
more difficult. Nerve decompression or arterial reconstruc-
tion may be necessary with any of these procedures.
Goldie et al.68 described an 11-year-old patient with recur-
rent compartment syndrome and Volkmann contracture fol-
10. Complications
lowing a closed midshaft fracture of the left radius and ulna
that was complicated by hematogenous osteomyelitis. The
patient subsequently presented 8 years after the original
injury (age 19) with pain, swelling, and redness of the
forearm plus associated flexion posturing of the fingers.
Radiographs showed fragments of bone near the healed frac-
ture site and increased uptake on the bone scan. Eighteen
months later she again had episodic pain associated with
flexion posturing of the fingers that improved sponta-
neously. The patient was then referred, at age 20, because of
recurrent increased flexion contracture. Eventually, explo-
ration revealed an abscess cavity in the deep flexor muscle
compartment with pus and osseous sequestra. The deep
flexor muscles were contracted and scarred in the region of
the abscess. The patient subsequently was treated with
lengthening of the superficialis tendons.
Venous Disorders
Although thromboembolic disease is probably one of
the most common and feared complications in adult
orthopaedic patients, it is extremely unusual in children,
especially those who are otherwise normal.127–130,133–139,142–150,
152,153
Children appear relatively immune to venous throm-
bosis, possibly because of their continual, almost constant
movement in bed when ill or in skeletal traction. Certainly,
the risk rate is sufficiently low not to give prophylactic treat-
ment for the anticipated problem, as one might in an adult
patient.
Clyne and colleagues reported a 5-year-old boy who
required thrombectomy of the iliofemoral vein for occlu-
sion.129 Marks and Sussman described a case of superficial
thrombophlebitis in an 8-year-old girl and commented that
only one other case of phlebitis in a child had been reported
in the English literature during the previous 10 years.143
Dehydration may be important in vessel wall injury. There
are a number of reports on the deleterious effects of can-
nulation of the deeper limb veins.133,135,138
Horwitz and Shenker described 10 adolescent patients
who were admitted with diagnoses of primary or secondary
deep vein thrombosis.137 In three the venous thrombosis
occurred in the iliofemoral vein, and in five others the
politeal–deep saphenous venous system was involved. One
patient had a primary occlusion of the right axial and sub-
clavian veins after weight lifting. This condition, effort
thrombosis of the axillary vein (Paget-Schroetter syndrome),
may occur in healthy individuals after a forceful event
produces direct or (more likely in the child or adolescent)
indirect injury to a vein.140 In a study of 13 adolescents and
14 children, deep vein thrombosis in 8 of the 13 adolescent
patients occurred postoperatively or following trauma,
whereas this predisposing factor was present in only 3 of
14 younger children.152 In contrast, 7 of 14 children had a
predisposing infection, whereas only 3 of the 13 adolescents
did. Obesity is known to increase the risk of thrombosis
following surgery and immobilization but cannot be im-
plicated in spontaneous venous thrombosis in healthy,
nonobese youngsters.137 The patient shown in Figure 10-6
was an overweight 14-year-old boy who developed bilateral
Hemorrhagic Complications
thromboembolic disease after immobilization (including
4 days of bed rest) following bilateral tibial tuberosity
fractures.
McBride et al. reviewed 28,692 pediatric patients from the
National Pediatric Trauma Registry.144 The mean age was 9
years, and the mean severity score was 11. Deep venous
thrombosis was identified in only six patients. Two patients
had documented pulmonary embolism, and both patients
had spinal cord injury, paraplegia, pulmonary injury, and
high injury severity scores (25 and 27, respectively). The
overall incidence of pulmonary embolism was 0.000069%
and for spinal cord-injured pediatric patients 1.85%. The
authors recommended that pediatric patients with spinal
cord injury be treated expectantly by observation for pul-
monary embolism, not by prophylaxis.
In another study 61 children under 10 years of age suf-
fered a thrombotic event.145 A variant of prothrombotic
conditions (as in adults) were present in two-thirds of the
children. The family history was positive in seven. The
primary thrombotic focus was around a central vascular
access device (25%). Lung involvement occurred in 20%.
The primary thrombotic site for two-thirds of the children
was in the central nervous system. A high portion of these
children had a high incidence of lupus anticoagulants and
protein C and protein S deficiency.
Wise and Todd reviewed a 20-year period at a children’s
hospital.152 There were 28 cases of lower extremity venous
thrombosis unrelated to venous catheterization or venous
surgery. Local infection, trauma, and immobilization
were predisposing factors. Of the 28 patients, 7 had compli-
cations, including pulmonary embolus in 3; there was one
fatality.
Adults may develop venous thrombosis that cannot be
diagnosed by current clinical means, so it must be consid-
ered that thrombosis predisposing to embolic disease in chil-
dren may be more common than we fully appreciate.
Difficulty in diagnosis may be one reason it is not detected
frequently. The specific detection of deep vein thrombosis
is contingent upon several diagnostic tests. Venography, the
most specific test, shows the extent of thrombosis formation
and its adherence to the vein wall. Radioisotope-labeled
fibrinogen is a sensitive screening substance that becomes
concentrated in a forming clot; it is indicated by increased
radioactivity over the clot site, detected by a scintillation
counter.132 The technique may not be useful if the throm-
bosis is more than a week old, and it is unreliable in the pres-
ence of excessive edema. The Doppler technique is a simple
procedure that detects changes in the velocity of flow in
blood vessels.131 Extensive experience with these techniques
in children is not reported.
Treatment should be directed at compression of the
extremity, elevation, hydration, and appropriate anticoagu-
lant therapy. Plasminogen administration is a new treatment
method being used in children,141,146 but it is not always effec-
tive.147 Varicose veins represent a rare complication of deep
vein thrombosis.151
Pseudothrombophlebitis may be caused by the extrinsic
compression of the popliteal vessels by an enlarging Baker’s
cyst or by calf inflammation consequent to rupture of a
Baker’s cyst.134 Most reported patients under 18 years of age
have preexistent juvenile rheumatoid arthritis.
321
Hemorrhagic Complications
Hereditary Coagulopathies
Certain hereditary hemorrhagic disorders initially manifest
as excessive bleeding after skeletal trauma. This bleeding
may be the first indication of a disorder such as hemophilia,
especially if the child has not had a previous injury that
caused sufficient bleeding to make the diagnosis obvious or
if a mild clotting disorder is present.
A relatively common type of bleeding disorder is von Wille-
brand’s disease, which causes prolongation of the normal
bleeding time. It is probably the second most common inher-
ited hemorrhagic disorder. The most common is hemo-
philia, which is an X-linked disorder resulting in reduction
of factor VIII. Christmas disease, or hemophilia B (deficiency
of factor IX), may be differentiated from classic hemophilia.
Many factors have been identified as necessary for proper
coagulation. Interaction between these factors is described
by the vascular coagulation cascade theory.
The goal of appropriate hematologic management during
treatment of fractures is to maintain sufficient levels of clot-
ting factors for an adequate period to forestall complications
from intramuscular, periosteal, intracapsular, or subcuta-
neous bleeding. This practice allows microhemostasis to
occur. By this time adequate treatment should have been
rendered to minimize motion at the fracture site, which
might cause further hemorrhage. Fracture treatment and
specific problems in children with hemophilia are discussed
in Chapter 11.
Acquired Coagulopathies
Clotting factor deficiencies may be acquired. Neonates may
have excessive periosteal hemorrhage associated with trau-
matic delivery because of a relative deficiency of vitamin K.
Children with malabsorption syndromes, liver disease, biliary
atresia, and other similar conditions may also have insuffi-
cient absorption of vitamins, so they have an acute or chronic
vitamin K deficiency (see Chapter 11 for examples and
further discussion).
Disseminated Intravascular Coagulation
Disseminated intravascular coagulation (DIC) is a term given
to a group of bleeding states of diverse etiology that mani-
fest with accelerated, variable degrees of thrombosis and
bleeding. DIC may accompany fat embolism syndrome,
bacterial sepsis (especially from meningococcemia), mis-
matched blood, and the multiple-unit blood transfusions
that may be necessary in the polytraumatized child.154,155 The
central pathologic process appears to be a generalized acti-
vation or overactivation of the hemostatic mechanism
beyond that expected for the local vascular response around
a fracture. A notable feature of DIC is the reduced level of
plasma fibrinogen, although this parameter is variable
because of the complex interaction of the many factors
involved in DIC.
Disseminated intravascular coagulation usually causes
bleeding at multiple sites. Occasionally it produces throm-
bolic episodes or acrocyanosis. The diagnostic manifesta-
322
tions include a hemorrhagic-thrombotic diathesis, a specific
coagulation test profile, the presence of fibrin thrombi, and
a response to heparin therapy. Three abnormal screening
tests that tend to be diagnostic are the prothrombin time,
fibrinogen level, and platelet function. If only two of the
three are abnormal, a test for fibrinolysis (thrombin time,
euglobulin clot lysis time, or fibrinogen degradation prod-
ucts assay) should be abnormal to establish the diagnosis
definitively.
The treatment of choice is heparin, which usually results
in decreased bleeding.154 The prothrombin time, fibrinogen
level, and euglobulin lysis become normal within 1–3 days,
although platelet levels do not respond uniformly to heparin
therapy. Heparin should not be used if the risk of intracra-
nial bleeding is significant. e-Aminocaproic acid (EACA)
therapy aggravates DIC and may result in thrombosis. There
is no indication for its use in traumatized children.
Children who have this complication must be followed to
skeletal maturity, as microvascular thrombosis may perma-
nently and variably damage physeal growth capacity (see
Chapters 6, 7).155
Fat Embolism
The fat embolism syndrome is infrequent in normal children
following major trauma.156,162,163 Drummond and coworkers
reported an incidence of 0.5% in 1800 children with pelvic
and femoral fractures, compared with a 5.0% incidence in
adults with similar injuries.159 Carty found six cases of fat
embolism in children, but he found a 90% incidence of fat
embolism at autopsy in children dying as a consequence of
trauma, a statistic similar to that in the adult population.157
The greatest potential for developing fat embolism syn-
drome occurs in the presence of multiple fractures and
multiple-system injuries.164 Fat embolism occurs more fre-
quently in a closed fracture than an open fracture. Most cases
of fat embolism occur within the first 3 days after injury.
Weisz et al. reviewed 21 cases of fat embolism over a 20-
year span.165 Patients ranged in age from 3 to 16 years; 17
were younger than 9 years. Eight patients died (two with
severe head injury).
In adults the incidence of posttraumatic fat embolism syn-
drome ranges from 0.9% to 2.2%. The incidence in children
is lower and may relate to differences in the microanatomy
of the trabecular bone and intertrabecular tissues (e.g., less
fatty marrow in the long bones).
Children may sustain fat emboli relatively frequently but
do not develop the clinical syndrome as often as adults
because of a difference in the type of embolized fat or a
decreased susceptibility to the toxic effects of the fat emboli.
The fat content of the marrow in children, compared with
that in adults, is low, with relatively little of the more liquid
fat, olein, and higher proportion of other fats such as
palmitin and stearin.159
Limbird and Ruderman reported the complication in an
11-year-old boy with myelodysplasia who had been immobi-
lized for anterior spine fusion and sustained a fracture of the
proximal tibial metaphysis. Shortly after the fracture he
became tachypneic, febrile, mildly nauseated, and lethar-
gic.160 Children with myelodysplasia, juvenile rheumatoid
arthritis, collagen vascular disease, and various endocrine
10. Complications
and metabolic disorders associated with osteoporosis are
highly susceptible to the fat embolism syndrome.161 All those
involved in the care of these children should be aware of this
potentially fatal complication.
There is no completely accepted pathomechanism.161,165
Presumably, fat particles enter the venous bloodstream from
the fracture region and eventually come to rest in the pul-
monary capillary network. Triglycerides in the lung emboli
have the same proportions of fatty acids as does medullary
marrow tissue. The concomitant presence of hemorrhagic
shock from the extraosseous blood loss is also an important
factor. It causes alterations in rheology and especially pre-
disposes the pulmonary and cerebral capillary networks to
act as a sort of “sludge filter” for the blood in which sus-
pension has become unstable. Platelet adhesion is also
increased, which enhances aggregate formation in the pul-
monary capillary bed.
One possible source of embolic fat is the bone marrow.
Marrow and osseous fragments have been demonstrated in
lung sections frequently enough to indicate that mechanical
fat embolism probably does occur. However, more general-
ized blood lipid changes occur during stress, in combination
with changes in blood coagulation systems, which may result
in coalescence of chylomicrons into larger fat droplets. The
physicochemical explanation of fat embolism postulates that
changes occur in blood lipid stability after trauma, and the
altered microcirculatory flow patterns combine to result in
inadequate tissue perfusion, subsequent tissue hypoxia, and
the fat embolism syndrome. There may certainly be more
than one source of fat in this syndrome.
The biochemical effect of fat emboli in the lung is first to
cause hydrolysis of neutral fat by lung lipase. The released
free fatty acids diminish surfactant activity, disrupt the alve-
olar capillary membrane, and lead to leukocyte infiltration
and alveolar edema. Over time (which may be relatively
rapid in a child when the symptoms manifest) there is a
reduction in pulmonary compliance, functional residual
capacity, and oxygen diffusion along with increased pul-
monary shunting.
The major clinical features of fat embolism syndrome
include hypoxia (PaO2 < 60 mmHg), pulmonary edema,
central nervous system edema, and axillary or subconjuncti-
val petechiae. Other diagnostic criteria include tachycardia,
pyrexia, funduscopic evidence of retinal fat, fat in the urine,
a rapid drop in hematocrit or platelets, increased erythro-
cyte sedimentation rate and fat globules in the sputum.
The most significant laboratory finding that characterizes
the disease is decreased arterial oxygen tension. Arterial
blood gases usually reveal hypoxemia and mild alkalosis. A
sudden drop in hematocrit is also common. Urinary and
sputum fat and serum lipase levels are probably of little diag-
nostic value. The chest roentgenogram classically demon-
strates interstitial infiltrates and obliterated peripheral
vascular markings.
The onset may be immediate or 2–3 days after the injury.
Coma is the most severe presentation. There may be hemop-
tysis or pulmonary edema during the fulminant course. Early
symptoms include shortness of breath, restlessness, and con-
fusion. There may be progression to marked confusion,
stupor, or coma. Urinary incontinence may also occur.
Petechiae may develop 2–3 days after injury and are charac-
Neurologic Complications
teristically located across the chest, axilla, and base of the
neck. These lesions may be evanescent, and many milder
cases may be overlooked. The diagnosis of “fracture fever”
may be an unrecognized, mild variety of the fat embolism
syndrome.158
Treatment is directed at general respiratory support and
correction of respiratory acidosis, as well as at specific frac-
ture problems. The airway must be maintained, even if a
tracheostomy must be performed. Blood volume should be
restored and the fluid and electrolyte balance maintained.
The injured bones must be immobilized. Adequate oxy-
genation is the most important part of treatment, as respi-
ratory failure is the most common cause of death from this
syndrome. The use of steroids and heparin, although seem-
ingly beneficial, is still somewhat controversial. Because of
the obvious risks of heparinization in affected patients,
the indiscriminate use in all pediatric patients with fat
embolism should be avoided. It should be used only in those
who show alterations in the clotting and fibrinolytic systems,
as determined by careful sequential studies of coagulation
parameters.
Neurologic Complications
Head Injury
Head injuries as a result of blunt trauma occur much more
commonly in children than in adults; and if present, they
may complicate the overall evaluation of the child.172 Pos-
sible reasons for the higher incidence in children are that
the relatively larger head of a child may be more exposed
to trauma and the child’s head is less well supported on the
neck and shoulder girdle. It is important to realize that,
despite the greater incidence, children usually recover, even
from prolonged coma, such that adequate fracture care is
essential.168,170,173,175
In a study of 344 comatose children (82% following motor
vehicle accidents) followed for a minimum of 1 year, 73%
regained independence in ambulation and self-care, 10%
remained partially dependent in terms of self-care and
achieved limited ambulation, 9% regained consciousness but
were totally dependent, and 8% remained comatose.168
There was a favorable prognosis for recovery of motor func-
tion if the coma duration was 3 months or less.
Residual motor deficits 1 year after injury showed spastic-
ity (38%), ataxia (8%), spasticity and ataxia (39%) “soft”
signs (3%), spinal cord injury (1%), or peripheral nerve
injury (1%); and 10% were “normal.” However, in the group
tested as neurologically normal, many had cognitive or
behavioral problems.
Head injury, particularly in children, presents a major
problem during the treatment of fractures.170 Many times,
because of the severity of trauma necessary to cause a head
injury, there is a concomitant fracture of the postcranial
skeleton. Problems then arise out of conflicting demands for
treatment. The complications of one injury may interfere
with the treatment of the other. An unconscious patient is
frequently restless. Should such a patient also have a frac-
tured femur, this restlessness may prove problematic, as a
fractured femur requires immobilization. A head injury
323
requires cautious fluid replacement, whereas a femoral frac-
ture may require simple fluid replacement. In the presence
of a head injury, general anesthesia is better avoided, at least
acutely, whereas the presence of an open fracture may neces-
sitate adequate débridement of an open fracture with the
patient under anesthesia. The patient may remain in a coma.
Fat embolism from a femoral fracture may further compli-
cate assessment of the head injury. Deterioration in the level
of consciousness is usually due to causes other than the head
injury.
Fracture management is complicated by neurologic con-
sequences.188 Decorticate posturing involves upper extremity
flexion combined with lower extremity extension. Decere-
brate posturing involves severe hyperextension of upper and
lower extremities. Seizures, sustained hypertension, and
labile thermal regulation may also occur. All obviously have
an effect on maintenance of any fracture or dislocation
reduction.
The most serious orthopaedic problems in head-injured
children relate to residual deformity from fracture mal-
unions and persistent joint dislocations. Spasticity also may
interfere with the extent of functional recovery.
Fractures of the femur (Fig. 10-7) and humerus are often
difficult to manage in these restless, recumbent children.167
If the head injury is minor and expected to clear in a day or
two, the fracture should be immobilized by simple splinting
and subsequently treated as indicated. When decerebration
is likely to be prolonged beyond a few days, skeletal traction
or internal or external fixation is recommended, depending
on the degree of restlessness and the extent of other injuries.
However, if the patient is a young child, intramedullary fix-
ation could damage portions of the epiphysis and physis. If
necessary, external fixator pins may be inserted under local
anesthesia in the emergency room or intensive care unit.
Early osteosynthesis of fractures in multiply traumatized
patients has consistently been shown to decrease the inci-
dence and severity of fat embolism, acute respiratory distress
syndrome, and sepsis and to increase the chance of survival.
In children with severe brain injury, this approach is not
universally accepted. Instead, the goal is preservation of
residual brain function. Obvious concerns are the effects
of anesthesia and surgical procedures on the moribund
(comatose) patient. The monitoring, intubation, and
mechanical ventilation commonly used in these patients sim-
ulates general anesthesia.
Unfortunately, conservative management of traumatized
limbs may lead to difficulty in nursing care, a higher inci-
dence of thromboembolism and osteitis, and increased
requirements for sedatives and analgesia.
Significant heterotopic bone formation around joints
(Fig. 10-8) may complicate severe head injuries, even in chil-
dren.166,169,171,174 Mital et al. reviewed children and adoles-
cents who had head injury and formed ectopic bone.174 The
physiologic mechanism of heterotopic bone formation is
unknown. Fracture healing also appears to be accelerated.
Herold et al. reported accelerated fracture union, as deter-
mined radiographically, in fractured ulnae of brain-injured
guinea pigs.169
Heterotopic bone excision procedures, alone or in con-
junction with physical, pharmacologic, or both modes of
treatment, are usually followed by recurrence of ectopic
324
bone. However, when salicylates are added to the treatment
program, there appears to be either no recurrence or
minimal recurrence of ectopic bone, suggesting a useful role
for salicylates not only in preventing recurrence but also in
minimizing the occurrence of ectopic bone formation.174 A
successive rise in the serum alkaline phosphatase level in the
absence of other causes is a sensitive indicator of incipient
ectopic bone formation and generally precedes the radio-
logic appearance of ectopic bone. The indications and
optimal timing of surgery for removal of the ectopic bone,
when it interferes with joint function, appear to be when the
patient is no longer comatose and is showing progressive
neurologic and physical recovery. Corticalization of the
peripheral portion of the osseous mass is a good indicator
of maturation and decreased likelihood of recurrence.
A bone scan showing inactivity within heterotopic bone
indicates maturity rather than active bone formation and
thus less risk of recurrence following resection. However, this
study is not an absolute indicator of activity. Furthermore,
elevated alkaline phosphatase activity in adults is not a usable
parameter in children and adolescents, who normally have
FIGURE 10-7. Angulation of a femoral fracture in a 12-year-old boy
with a head injury (comatose for 11 weeks). The angulation
occurred despite initial external skeletal fixation of the fragments.
The fixation device had to be removed at 7 weeks because of pin
tract cutaneous infections. Progressive plastic deformation was
ensured while the patient slowly recovered from the head injury.
The massive posterior callus indicates the extent of stripping and
displacement of the periosteum that may have been accentuated
owing to the hyperactivity, restlessness, and decerebate rigidity
that characterized this boy until his sensorium became more
normal 14 weeks after injury.
10. Complications
FIGURE 10-8. Heterotopic bone around the shoulder in a 16-year-
old girl with severe head trauma.
a high level of enzyme activity because of skeletal growth and
remodeling.
The major residual motor problems in head-injured
patients are ataxia and spasticity. Ataxia may worsen over the
first 6 months after head injury but then gradually decreases
in severity over the ensuing years. Spasticity seems to become
maximal 2–3 months after surgery, and then years. Surgical
management of spasticity in a limb should be deferred for
1–2 years.
Although children usually “recover” from head injury,
they are likely to have limitations in physical health, have
behavioral problems, and to be enrolled in special education
programs. After controlling for head injury severity, poorer
outcomes were associated with poverty, preinjury chronic
health problems, and concomitant lower extremity injuries.
Any child sustaining a head injury should be provided with
appropriate rehabilitation and social services.
Peripheral Nerve Injuries
Nerve injuries associated with fracture or dislocation may be
acute or delayed.183,189,196,204 The physician may not discover
a nerve complication until several weeks after the injury, fol-
lowing removal of the splint or cast. The early recognition
of a primary nerve injury at the initial evaluation is impor-
tant. Nerve involvement does not always occur at the time of
trauma or during manipulation. Delayed nerve injuries may
develop secondary to inclusion by scar or callus, with pro-
gressive pressure causing eventual dysfunction of the nerve.
Such constriction of the nerve may cause neurometric
degeneration at the site of the lesion. The nerve may be
caught between fracture fragments, with healing bone devel-
oping progressively around it. Another type of nerve involve-
ment is the late (tardy) neuritis that may occur many months
to years after an injury because of progressive deformity
(e.g., progressive valgus deformity of the elbow associated
with tardy ulnar palsy).205
Neurologic Complications 325

Nerves tolerate stretch (strain) in the 8–10% range, developing. In these children, overlap and budding may
showing recovery to 50% of baseline within 2 hours.181 As bring about a normal or almost normal return of sensation
strain increases to 15%, nerve conduction ceases. Decreas- to the dermal plexuses. Even without repair of individual
ing motor action amplitude is thus associated with increas- nerves, the upper age limit at which sensation returns and
ing strain in nerves. When a nerve fails under tension, the whether the phenomenon is constant are unknown. This
perineurium within the nerve ruptures, even though the type of recovery of sensation appears to be most common in
exterior of the nerve may appear to be intact.194 This disrupts digital nerves.
the conduction capacity of the nerve. The outcome of an injured peripheral nerve is contingent
During an examination, one should remember that a on many factors, some of which are the age of the patient,
peripheral sensory nerve manifests in the skin in three the site of the lesion, the extent of the damage, the time
zones: autonomous, maximal, and intermediate.199,201 The interval before repair if the nerve has been severed, and the
autonomous zone is supplied exclusively by a specific nerve. accuracy of the repair.180,182,187,192,200 Children have a greater
After injury, whether contusion or transection, there is anes- potential for neural repair and regeneration than do
thesia in this isolated area. The maximal zone is the sensory adults.197 It has been estimated that for every 6 days of delay
area of a nerve that may be detected when function of adja- before suturing 1% of maximal performance is lost.212 There-
cent sensory nerves is interrupted. This area is larger than fore early repair, within 3 months after injury, should be
the gross anatomic field of the nerve. Between these zones encouraged. The time elapsed before repair does not seem
lies the intermediate zone, where painful stimuli to pinpricks to have as much effect on the recovery of sensory modali-
or extremes of hot and cold may be appreciated. This phe- ties. If repair has been delayed for more than a year, motor
nomenon is attributed to nerve overlap. It is more difficult function rarely returns. Sensation may return even if as
to determine concisely in a child, compared to an adult, much time as 2 years has elapsed.
because of natural apprehension to the testing method. Altered fracture healing has been reported in many
Leonard thought that sensation in the digital nerve could neurologic conditions, particularly peripheral nerve injury
return to skin “deprived” of its nerve supply by proximal
transection, even without nerve repair.195 Probable mecha-
nisms of this return of sensory function are fibers from adja-
cent nerves in the intermediate zone and budding from
these adjacent nerves into the dermal plexus of the
autonomous zone.190,191 Adeymo and Wyburn demonstrated
nerves running from the margins and from the bed into skin
grafts.176 This phenomenon seems to occur primarily in pure
peripheral sensory nerves. Local extension could replace
regeneration during nerve recovery in large sensory fields.198
An extensive study of nerve injury in children reviewed
37 surgically treated nerve lesions in the upper extremity
(33 children).178 Useful sensory function was restored in 31
patients (84%), but motor recovery was achieved in only 25
patients (67%). The median nerve showed the best ability
for recovery of motor and sensory function. The radial nerve
had the worst prognosis for recovery. Unfavorable prognosis
also related to a time interval of more than a year between
injury and surgical repair.
Recovery in children is sometimes surprisingly complete.
Furthermore, return of sensation in transplanted skin in
children is more complete than that in adults.209,210 Almquist
and Erg-Olofsson, on the basis of sensory nerve conduction
velocity studies, concluded that the better results of nerve
repair in children were due to the adaptability of the sensory
cortex, rather than to increased maturation of the nerves.177
Experimentally, growth of nerve fibers into denervated
areas has been demonstrated.208 Weddell and colleagues
suggest that the rapid recovery of sensation observed in baby
rabbits after nerve section was due to local extension in the
skin plexus of fibers from adjacent nerves.210 Fitzgerald and
associates demonstrated reinnervation of the dermal plexus
in young pigs.186
The parameters involved in the recovery of sensation
FIGURE 10-9. Complications of sciatic nerve injury in a 4-year-old
include the degree of neuronal regeneration and matura- girl who sustained sacroiliac and triradiate fixture-separations with
tion, the maintenance of function in the end-organs, the concomitant lumbosacral plexus injury. The healed femoral di-
adaptability of the sensory cortex (relearning), and nerve aphyseal fracture was complicated, 7 weeks after the original
overlap and budding. Nerve budding is probably more injury, by fractures of the proximal tibial and distal femoral meta-
intense in children, in whom the central nervous system is physes through the osteoporotic bone.
 326
A B
(Figs. 10-9, 10-10). Many clinicians have observed more rapid
union with exuberant callus in neurologically injured
patients, whereas others have noted decreased rates of
healing.80,90,95 Despite clinical observations, little experimen-
tal investigation has been directed at this phenomenon,
and most studies have been made on skeletally mature
animals.169,179,184,193,202,203 Herold and associates reported
accelerated fracture healing in fractured ulnae of neurolog-
ically impaired guinea pigs.169 Quilis and Gonzalez showed a
qualitative increase in callus formation in immature rats
in which the nerve roots of L3 through S1 had been
sectioned.202
Denervation may be associated with significant changes
that include (1) decreased bone length, (2) decreased
cross-sectional area but without cortical thinning, (3)
increased cartilage cross-sectional area, and (4) decreased
foot size.185
Magnetic resonance imaging may be useful for delineat-
ing posttraumatic or postamputation neuromas.206,207 On
MRI, neuromas appear as rounded masses and are usually
heterogeneous and intense compared with contiguous
muscle. MRI may also show additional causes of stump pain,
such as internal scar formation, fat in atrophied muscle, soft
tissue abscesses, osteomyelitis, and hematomas.
West et al. used short-term inversion recovery (STIR) MRI
to evaluate muscle signal characteristics.211 An increased
STIR signal was observed in muscles associated with severe
axonometric injury. These changes were noted as early as 4
days after injury. In cases of neuropraxic nerve injury (con-
duction block without axonal loss), the muscle STIR signal
was normal. MRI using STIR sequences may play an impor-
tant role in the prediction of clinical outcome and the for-
mulation of appropriate therapy early after peripheral nerve
10. Complications
FIGURE 10-10. (A) Tibial fracture. The patient also
had a complete sciatic injury. Three months after
the injury there is delayed healing. (B) Five months
later nonunion is evident.
injury associated with a fracture or in the evaluation of com-
partment syndrome.
Reflex Sympathetic Dystrophy
Reflex sympathetic dystrophy (RSD) syndrome has a
number of descriptive terms: Sudeck’s atrophy, causalgia,
posttraumatic painful osteoporosis, minor causalgia, post-
traumatic sympathetic dystrophy, shoulder-hand syndrome,
and chronic traumatic edema. Prior to the report by Fer-
maglich221 only six cases had been reported in children. RSD
is infrequent in children.* Fewer than 10% of the patients
in a large study of posttraumatic reflex dystrophies were less
than 19 years of age.237
The problem of childhood reflex neurovascular dystrophy
is complex. In only half of the children is trauma identified
as an initiating factor. Even in this situation many authors
have alluded to a possible psychological component, noting
common personality traits in the affected patients and
parents.213,244 Proper evaluation of the family and the child
must be an integral part of the treatment of this syndrome,
even after trauma.213,238 Sherry and Weisman reviewed psy-
chosocial factors.244 They thought that RSD frequently is a
stress-related disease, and that any therapeutic plan must
factor in these aspects.
The syndrome consists of continuous pain, hyperesthesia,
and autonomic symptoms in an extremity, often following
relatively minor trauma.227,229 The signs and symptoms
observed in the involved extremity are burning or aching
pain, discoloration (cyanosis, plethora, erythema), swelling,
joint stiffness, hyperhidrosis, and altered sensation (hyper-
* Refs. 215,216,219–225,228,231,234–236,239–241,244–246,248,249.
Neurologic Complications
esthesia, hypoesthesia, or paresthesia). These signs may
occur in a glove or stocking distribution or in a distinct
sensory distribution. Extreme hyperesthesia to light touch is
a common sign of RDS in children.
Characteristically, the patchy osteopenia evident on radio-
graphs may take 5–7 weeks to develop, but it is infrequently
seen in skeletally immature individuals (Fig. 10-11).
Although the progression of osteopenia may be reduced or
halted in many patients, bone mineral content does not
always improve.227 This failure to improve may reflect an
inability of bone to remineralize and remodel sufficiently
when osteopenia has been present for a critical period.
Goldsmith et al. reported the results of radionuclide bone
scans in a total of 19 children with RSD.223 In eight children
the bone scans demonstrated increased radionuclide uptake
FIGURE 10-11. (A) Ten-year-old child with reflex sympathetic dys-
trophy after an ankle sprain. Note the diffuse osteoporosis. The
subchondral plate of the navicular bone has a double contour.
(B) Reflex sympathetic dystrophy in a 12-year-old child following
a mid-diaphyseal tibial fracture.
327
in the affected extremity, whereas in eight other children
there was decreased uptake. In three additional patients the
bone scans appeared normal. Thus the finding of an abnor-
mal bone scan may be helpful in the diagnosis. A normal-
appearing scan, however, does not necessarily preclude
the diagnosis. RSD remains, in children, primarily a clinical
diagnosis.
Little is known about the pathophysiology of this syn-
drome, although increased local blood flow to the affected
limb has been demonstrated.232 One hypothesis is that a
reflex arc is established in the subcortical, internuncial neu-
ronal pool, producing chronic and excessive activity in the
autonomic nervous system. A series of reflexes dependent
on cross-stimulation between sympathetic afferent fibers and
damage to the myelin on which sensory fibers depend may
account for the underlying pathophysiology.
Another postulate is that chronic irritation of a peripheral
sensory nerve leads to abnormal activity in the internuncial
neuronal center, which leads, in turn, to a continuum
of increased stimulation of afferent motor sympathetic
neurons. As a consequence, normal vasoregulatory controls
are disrupted, and local blood flow is increased, producing
secondary changes in skin and subcutaneous tissue and de-
mineralization of bone.
Mild or early cases of RSD may recover spontaneously or
respond to conservative therapy, which includes immobi-
lization, analgesics, corticosteroids, and warmth. Prolonged
or severe RSD requires local block, sympathetic block, or
sympathectomy. Physical therapy and exercise must follow.
Psychotherapy or psychoactive medication (e.g., antidepres-
sants) may be useful as adjuvant therapy.
Many therapeutic modalities have been advocated, includ-
ing physical therapy, exercise, sympathectomy, and cortico-
steroids.214,217,218,226,233,242,243,247 Any or all of these measures
may be effective when employed early in the disease, but the
response rate progressively decreases the longer treatment is
delayed. Initial treatment should be conservative. Recent
studies have shown a predictable improvement in several
objective clinical parameters with systemic corticosteroid
therapy, even in patients who have had symptoms for several
months or longer. Success has also been reported in children
with transcutaneous nerve stimulation and sympathetic
blocks.226
Children, in general, respond more rapidly to physical
therapy and psychological counseling and to transcutaneous
nerve stimulation. Steroid use remains controversial in chil-
dren in terms of both efficacy and side effects. Narcotic anal-
gesics should be avoided in children.
Lagier and Linthoudt showed that immobilization, volun-
tary or involuntary, of an extremity affected by RSD could
lead to superficial pannus formation, deep erosion, fibrous
ankylosis, and, at times, bony ankylosis.230 They recom-
mended physiotherapeutic mobilization of joints as an
important part of the treatment.
Following the introduction of the gate control theory of
pain, there has been a great interest in the use of electrical
stimulation for the relief of pain. The gate theory basically
states that nonpainful stimulation of the peripheral nervous
system may interfere with the relay of pain sensation to the
central nervous system. This theory may explain why trans-
cutaneous electric nerve stimulation (TENS) appears to be
328
effective in pain reduction. It should be reemphasized that
the etiology and the pathophysiology of RSD remain
unknown. Thus all recommended treatments for RSD are
symptomatic, and none, including TENS, has been shown to
be of proven efficacy in controlled studies.
Kesler et al. described the treatment of RSD in children
with TENS.226 All children were treated as outpatients with a
transcutaneous electric nerve stimulator and home-based
physical therapy. Utilizing this regimen, seven patients had
complete remission within 2 months. Two others improved
but did not have complete remission. One patient had no
response.
Although Kozin et al. reported that the systemic use of
steroid therapy was effective in as many as 90% of adults with
RSD, such steroids have been used so infrequently to treat
RSD in children it is impossible to determine the benefits or
the liabilities from this form of therapy.227–229 Intensive phys-
ical therapy, often requiring prolonged hospitalization, has
been the mainstay of treatment for children with RSD.
Although most children treated in this fashion respond well
and ultimately recover, it is obviously a time-consuming and
costly therapeutic regimen.
Wilder et al. reported on 70 patients (59 girls, 11 boys).248
The average time from the initial injury to symptom onset
was 1 year. Treatment included physical therapy, TENS, psy-
chological therapies including cognitive-behavior manage-
ment and relaxation training, and tricyclic antidepressants.
Sympathetic blocks were helpful in 28 of 37 patients; 38% of
the patients continued to have some degree of residual pain
and dysfunction.
Dielissan et al. described amputation as a treatment for
intractable RSD.218 None of their patients was skeletally
immature. Only two patients were relieved of pain following
the amputation. In all of the other patients RDS recurred in
the stump. As a result of the recurrence, only two patients
wore a prosthesis satisfactorily. Nevertheless, despite contin-
uation of some pain of the RDS, 24 of 28 patients were sat-
isfied with the results.
Muscle
Chronic limb immobilization results in variable, often severe
muscle atrophy, especially in muscles immobilized in a short-
ened position.251 Although the phenomenon is well recog-
nized in adults, it probably also occurs after skeletal injury
in children. Atrophy is associated with a net loss of muscle
protein that is initiated by a decreased rate of protein syn-
thesis within hours of immobilization (even in muscles not
directly injured).250 Approximately one-half of the final
extent of atrophy may occur within the first week of
immobilization.251
Immobilization of the knee in extension may lead to
damage in the vastus musculature. Myofibrillar disorganiza-
tion becomes evident within 48 hours. These ultrastructural
changes are caused by temporary ischemia. This may be the
underlying cause of such complications as atrophy, rigidity,
and weakness. Acute changes and metabolic disturbance
occur within 48 hours, and atrophy ensues and fibrosis
becomes evident by 14 days. There is a significant increase
in serum creatinine kinase activity. Muscle mitochondria are
highly susceptible to hypoxia.
10. Complications
Chondro-osseous Complications
Hypercalcemia
As part of the normal repair process, calcium mobilizes from
the developing skeletal system. It is enhanced by decreased
use (disuse), limited or non-weight-bearing, and immobi-
lization.261,268 This activity may be reflected clinically as hyper-
calciuria. A significant elevation of serum calcium levels does
not usually occur in normal pediatric patients who are con-
fined to bed rest or immobilized in body casts for the treat-
ment of fractures. The metaphysis, with its normal high rate
of remodeling, is the likely “donor” site of much of the
calcium.
Short periods of immobilization of skeletally immature
rats were associated with loss of bone weight (mainly due to
mineral losses). Ca+2 incorporation was decreased and
showed strong dependence on the age of the rat. Much of
the bone loss was evident as trabecular bone loss, not corti-
cal (although the metaphysis is more trabecular than corti-
cal bone). The loss of bone mass was reversible—but not
back to the control (opposite) side. Recovery of bone mass
depended on the duration of the immobilization period.
Interestingly, physeal and periosteal bone formation is less-
ened but still occurs. Thus overall bone growth may continue
in the face of extensive trabecular bone loss (e.g., as occurs
in myelodysplasia, flaccid cerebral palsy, or muscular dystro-
phy). One week of immobilization required up to 8 weeks to
recover lost bone mass.
The classic description of hypercalcemia complicating the
immobilization of a patient without preexisting metabolic
disease was by Albright and associates, who named the con-
dition “acute bone atrophy” and emphasized that it must be
distinguished from hyperparathyroidism.252
Hypercalcemia complicating the treatment of pediatric
fractures is encountered occasionally in immobilized
patients with preexisting metabolic or bone disease;
and although seen less frequently, it may also accom-
pany immobilization in patients with no predisposing
factors.253–256,258,259,262,263,267
Most reported cases of immobilization hypercalcemia have
occurred in children between the ages of 9 and 14 years.269
This observation is attributed to the fact that the normal rate
of osseous metabolism and turnover prior to immobilization
is already high because of the growth rate. There is a balance
between bone formation and resorption in the active young
individual. The balance is influenced by age, nutritional and
hormonal factors, and degrees of activity. Bone formation
temporarily decreases when immobilization eliminates or
alters the normal stimuli to remodeling. The normal equi-
librium is upset, resulting in (1) bone demineralization that
is excessive compared with bone formation and (2) release
of calcium into the extracellular fluid. Ordinarily, this extra
calcium load is excreted by the kidney, with resultant hyper-
calciuria and maintenance of a normal serum calcium level.
Urinary excretion reaches a peak value approximately 4
weeks after immobilization begins. Rarely does the hyper-
calciurea lead to problems such as kidney stones.
Cristofaro and Brink reported that 7 of 20 patients demon-
strated hypercalcemia ranging from 10.7 to 13.2 mg/dl, with
their upper range of normal being 10.5 mg/dl.255,261 Return
Chondro-osseous Complications 329

to normocalcemia coincided with mobilization in five of

seven patients. Four patients developed heterotopic ossifica-
tion, with two of them having concurrent hypercalcemia.
Cristofaro and Brink concluded that hypercalcemia due to
immobilization occurred frequently.255 They also found that
elevated alkaline phosphatase levels were associated with het-
erotopic ossification. However, they thought that the role of
hypercalcemia in the development of heterotopic ossifica-
tion must remain speculative.
It is important to recognize this syndrome. The patient
may complain of nausea, vomiting, and abdominal pain
and tenderness. Anorexia and dehydration are common.
Lethargy, pain with movement, an apparent flaccid paralysis,
and muscle hypotonia appear. Vision may be blurred. Serum
calcium levels should be determined immediately. The sig-
nificance of this syndrome lies in the fact that it is readily
treated when recognized early.
An elevation of the serum calcium level above 15 mg/dl is
considered an acute crisis. Menke and colleagues reported a
13-year-old boy in whom failure to consider hypercalcemia
as the source of progressive anorexia, nausea, vomiting, and
irritability resulted in respiratory arrest and a nearly fatal FIGURE 10-12. Myositis ossificans is evident several months after
outcome after a femoral fracture.264 The mortality from elbow dislocation.
acute hypercalcemic crisis has been reported to be as high
as 50%.
Calcium levels of 10–15 mg/dl may be associated with calcium salts may be induced by degenerated myofilaments
milder symptoms. Usually the serum alkaline phosphatase of muscle calcification following trauma.276,280 Biophysical
level is normal, distinguishing the condition from hyper- studies of posttraumatic myositis bone have confirmed that
parathyroidism, in which this level is usually high. The dif- it represented otherwise normal young bone. In contrast,
ferential diagnosis of immobilization hypercalcemia, as most involved children have hereditary or nontraumatic
distinct from primary hyperparathyroidism, is probably best myositis ossificans.275 The latter situations probably have an
accomplished by parathormone assay. etiology different from that of traumatic heterotopic bone.
Treatment is relatively easy and effective. A low-calcium Certain muscles (e.g., quadriceps) and joints (e.g., elbow)
diet limits calcium ingestion. Mithramycin also effectively are affected preferentially; and the condition seems to follow
lowers serum calcium by either direct antagonism of bone an orderly, predictable course. The condition is seen most
resorption or interference in the metabolism of parathyroid frequently in teenagers, although it is occasionally observed
hormone.257 Dehydration is usually a factor, so fluid replace-
ment assumes primary importance. Saline diuresis, with
volumes of up to 10 liters per day, appears effective. Phos-
phate ion, administered orally or intravenously, binds with
calcium ion and is deposited in the bone. The most impor-
tant therapeutic measure is immediate institution of as much
movement and weight-bearing as is practical and safe. If the
condition is not treated, significant neurologic complica-
tions may occur, especially residual convulsions and loss of
hearing. Phosphate therapy, however, may be complicated by
acute renal failure.266
Calcitonin therapy may relieve the symptoms rapidly.260
Pezeshki and Brooker described two adolescents in whom
hypercalcemia was successfully treated by subcutaneous
injections of salmon calcitonin.265 The danger that an exces-
sive drop in the calcium level can lead to tetany must be
avoided. The use of calcitonin for hypercalcemia in children
has minimal documentation. Corticosteroid administration
has also been effective in treating hypercalcemia.

Myositis Ossificans (Heterotopic Ossification)

Traumatic myositis ossificans is a poorly understood condi- FIGURE 10-13. (A) Myositis ossificans after an ankle injury. The
tion in which heterotopic bone forms within injured muscle ankle was caught in bicycle spokes. (B) Four months later there is
or around a joint (Figs. 10-12, 10-13). Crystal formation of partial spontaneous dissolution.
330
in younger children.270,274,279,284 Wilkes reported a case in a 3-
year-old boy, with the lesion removed 7 months later.283 Dick-
erson described this condition in a 5-year-old child.273 The
early tissue changes may mimic osteomyelitis in chil-
dren.277,282 A meta-analysis of 195 reported cases of myositis
confirmed that it is most common in young (mean age 23.8
years), athletic men.272
Of 152 pediatric patients with spinal cord injury, 15 devel-
oped heterotopic ossification (HO) (19 lesions). The
average time to detection of the HO was 6.5 years.274 The hip
was involved in 15 of 19 sites. Progressively decreased range
of motion was the most evident sign. Three patients had
some spontaneous resorption, and one had nearly complete
resorption. The pediatric population appears to have lower
incidence and delayed onset compared to adults.
Triple-phase bone scans in pediatric brain-injured patients
found HO in 25 of 111 patients (22.5%). In 55 affected sites
the hip was the most commonly affected. Scans revealed HO
in multiple areas not clinically suspected. Treatment was with
physical therapy and indomethacin.271
The relatively common occurrence of myositis ossificans
after dislocation of the elbow is even greater when there is
an associated fracture. The incidence also appears to be high
if the elbow is treated by open reduction beyond the first
24–48 hours after injury. Even when ectopic calcification
forms, there is a greater propensity to resorb it before it
becomes mature bone.281
Patients in whom this complication develops generally
have roentgenographic evidence within 3–4 weeks after their
initial injury. Bone scans are active when the lesion is actively
forming and maturing. Ultrasonography may be useful in
the early diagnosis. The findings are a focal, elongated
10. Complications
hypoechoic mass located in the muscle. CT scans may allow
more definition of the anatomy of the mass.
The heterotopic bone may gradually resorb with the incep-
tion of joint motion (if periarticular). Resorption is less likely
if the bone is adjacent or attached to the diaphysis.
Attempts to excise the ectopic bone should be delayed
until the process has completely matured, usually about 9–12
months after injury. Technetium scanning is used to evalu-
ate the level of activity.
Moody et al. described three cases of posttraumatic myos-
titis ossificans in children who subsequently sustained a frac-
ture through the mature, quiescent ossification mass.278 In
no case did the fracture reactivate the original pathologic
process. Interestingly, all three patients failed to develop
callus and went on to painful nonunion. Treatment of the
complication should be temporary immobilization or exci-
sion if painful nonunion persists.
Synostosis
A complication due to type 9 growth mechanism (periosteal)
injury (see Chapter 6) is the formation of a synostosis
between the radius and ulna or the tibia and fibula (Fig.
10-14). An incomplete synostosis may develop (Fig. 10-15).
This complication is unusual in children because the sever-
ity of trauma is generally not enough to disrupt interosseous
tissues sufficiently to lead to any type of (potentially)
osteogenic tissue continuity between paired bones.286–288 This
complication may occur in the elbow region, although one
must be careful not to attribute proximal radioulnar synos-
tosis to trauma when the synostosis may be congenital (and
previously unrecognized).
FIGURE 10-14. (A) Seemingly innocuous frac-
ture of the tibia. (B) Four months later bone for-
mation is evident within the interosseous
space. (C) At 1 year a mature synostosis is
present.
Chondro-osseous Complications 331

Pseudarthrosis
Pseudarthrosis is a rare complication in the diaphysis of chil-
dren (Fig. 10-16), undoubtedly because the periosteal and
endosteal osteoblastic response in children is so rapid and
prolific, quickly bridging the fracture with primary callus.
Open injuries, which are often associated with pseudarthro-
sis in the adult, are infrequent in children. When they do
occur, the child may lose sufficient periosteal tissue (type 9
injury) to predispose the fracture to pseudarthrosis. Under-
lying bone disorders (e.g., fibrous dysplasia) may create a
predisposition to pseudarthrosis, which often occurs after
apparently minimal trauma.
Pseudarthrosis occurs in older children who show osseous
involvement similar to that in adults.289–291 The tibia is most
often involved. Forearm fractures in adolescents who are
nearing skeletal maturity may require operative treatment to
prevent nonunion of at least one of the bones.
The treatment of choice for pseudarthrosis in children, as
in adults, is operative, with utilization of bone grafts and, if
necessary, some type of skeletal fixation. Complete (circum-
ferential) subperiosteal stripping to expose the entire
FIGURE 10-15. Incomplete synostosis with a defect in the tibia pseudarthrosis is not always necessary. Leaving some of this
(pressure-related). tissue, which has mechanical integrity and the potential to
modulate into osteoblastic tissue, may minimize or negate
the need for metallic fixation. Once exposed sufficiently,
most of the interposed fibrous tissue is removed, although
Several factors are associated with radioulnar cross-union complete resection is generally not necessary in children.
in children: severe initial displacement, residual displace- The dense subchondral bone on either side of the
ment, periosteal interposition, open reduction with internal pseudarthrosis occludes the marrow space and essentially
fixation, delayed surgery, remanipulation, excision of the impedes the normal endosteal response. This bone should
radial head, and fracture at the same level of the radius and
ulna.287 The complication may occur even with a mild injury
(e.g., greenstick fracture) treated by closed reduction and
minimal, if any, manipulation.
With diaphyseal lesions, careful resection of the synostosis
may be successful, but only after the lesion has completely
matured (a bone examination is done to determine activity).
Such an injury is comparable to myositis ossificans, and as
such, early resection increases the possibility of recurrence.
Because fibular rotation is often necessary for normal ankle
function, resection of a synostosis may be advisable in a
young child if only to redirect chondro-osseous development
along a more normal pathway.
Vince and Miller believe that a 1-year hiatus between
injury and excision is appropriate in adults, but they gave
no similar guideline for children.287 A bone scan is positive
while there is active bone formation and remodeling. When
the process becomes stable (i.e., physiologically mature),
however, the bone scan should be negative; and resection
may then be considered (but it is not an absolute indicator).
When excising a synostosis it is important not to strip the
bridging bone subperiosteally. The periosteum should be
removed intact along with the bridging (osseous) segment.
Interposition of fat or Silastic has been recommended, but
reported experience in children is minimal. The parents
should be warned about the risk of recurrence.
A combination of radioulnar synostosis resection followed
by low-dose, limited-field irradiation in four patients led to
A B
improvement in motion and no recurrence of the synosto-
sis.285 However, such irradiation is deleterious to the imma- FIGURE 10-16. (A) Pseudarthrosis of the fibula. (B) Pseudarthro-
ture physis and thus of questionable use in children. sis of the fibula with overgrowth and flaring.
332
be removed and reamed so the marrow cavity on each side
is open and in communication with the surgically created
defect. Iliac crest (corticocancellous) bone may be obtained
and fashioned into inlay-onlay grafts. If fixation is used, the
remaining growth potential of the bone must be respected
when choosing the type of fixation.
Pseudarthrosis may also affect growth mechanism injuries.
The most common site of involvement is the lateral condyle
of the distal humerus. This specific problem is discussed in
detail in Chapter 14.
Fracture Recurrence
Recurrence of fractures in children is probably an under-
reported problem.292–299 Arunachalam and Griffiths de-
scribed 20 children with refractures, predominantly of the
forearm.292 They noted that a significant increase in defor-
mity occurred after refracture. Refracture probably takes
place either because the original fracture has not united
soundly or an identical mechanism of injury has occurred.
Cortical necrosis delays bridging of fracture gaps, with the
gaps then acting as stress risers, which, following resumption
of activity, may lead to refracture.296
There is sufficient confidence in the certainty of rapid and
effective union of injuries in children that delayed union is
never seriously contemplated. Therefore the tendency is to
remove children from immobilization devices earlier than
they probably should be, especially in view of their general
hyperactivity. It was noted in the study of fracture recurrence
that for many of the children roentgenograms were not
obtained at the time of discontinuation of immobilization,
the decision that they were sufficiently healed being based
on clinical examination. Because children often deny pain,
it is imperative that adequate fracture evaluation be done
before treatment is stopped.
Because of the unique physiology of the metaphysis, con-
siderable osteoporosis may occur with prolonged immobi-
lization and non-weight-bearing. This osteoporosis is evident
as a significant radiolucency of this region (Fig. 10-17) and
FIGURE 10-17. Relative osteoporosis of the proximal metaphysis
in a 14-year-old girl immobilized in a patellar tendon-bearing (PTB)
cast for a distal third tibia-fibula fracture. This minimally empha-
sized change temporarily weakens the metaphysis.
10. Complications
may occur throughout an entire bone, even an adjacent one
not involved in the fracture. The loss of bone weakens the
actively remodeling bone in an area that normally arranges
new cortical and trabecular bone in response to biome-
chanical demands. When the child is subsequently mobilized
after casting, the bone may not be mechanically strong
enough in such a region (even though the actual fracture is
strongly healed), and the exuberant return to activity,
despite warnings about progressive, partial weight-bearing,
may cause a new fracture.
In one study 28 refractures of the forearm occurred at a
mean of 14 weeks after cessation of conservative (casting)
treatment of the primary fracture(s).298 Interestingly, the
cause of refracture was incomplete healing of a primary
greenstick fracture in 21 cases. Two of the patients who were
treated for the refracture with a cast went on to a third
fracture.
Epiphysiolysis
As shown in Chapter 6, a temporary type 8 growth mecha-
nism impairment is caused by blockage of the nutrient arte-
rial circulation to the juxtaphyseal metaphysis. Because the
epiphyseal side of the physis is unaffected, the physis con-
tinues to grow by deposition to the cell columns. Without
concomitant replacement by the metaphyseal neovascularity,
the physis widens and becomes slightly less mechanically
stable. If a child treated for metaphyseal fracture inadver-
tently stresses the contiguous physis after removal of a cast,
an epiphyseal fracture (type 1 or 2) may occur (Fig. 10-18).
This fracture should be treated by reduction and further
immobilization.
Rees described fracture-separation of the distal femoral
epiphysis as a complication of the Sarmiento below-knee
functional cast.335 The fracture was middle-third tibia, with
no evidence of knee injury.
Postfracture Cyst
Asymptomatic cyst-like cortical defects may appear during
fracture consolidation (Fig. 10-19).300–313 They are usually
located within the reactive subperiosteal bone, proximal to
the fracture line; they do not enlarge and with growth and
remodeling gradually disappear. The pathogenesis of a
variety of cystic bone lesions in children remains in
doubt.300–313 Trauma has been implicated as the inciting
factor for some cystic lesions, although the occurrence
during fracture healing has not been well documented.
Levine and colleagues described a case of fracture of the
tibia and fibula with development of a cystic lesion in the
fibula during healing.308 There seemed little doubt that vas-
cular injury with hemorrhage into a closed space resulted in
an encapsulated hematoma that produced the lesion. Pre-
sumably, the periosteum was stripped on each side of the
fracture site. It is possible that this lesion represented a false
aneurysm. The lesion had an appearance similar to that of
a pseudotumor complicating hemophilia.
Malghem, Maldague, and colleagues reported transient
fatty cortical defects following fractures in children.309,310
They were self-regressing subperiosteal defects that appeared
during consolidation of fractures involving the tibia and
Chondro-osseous Complications 333

FIGURE 10-18. (A) Metaphyseal fracture in a 5-year-old child. (B) This fracture was casted for 4 weeks. (C) Three days after removal
of the cast the child fell and sustained a physeal fracture (type 2). The metaphyseal fracture has healed.

radius in two children ages 6 and 10 years. The defects
appeared several weeks after fracture and often distant from
the original fracture site. They involved the newly formed
subperiosteal bone, did not enlarge, and were progressively
replaced by normal-appearing bone. CT in one patient
showed a density consistent with fatty content. The authors
suggested that these transient posttraumatic defects resulted
from the inclusion of medullary fat in the subperiosteal
hematoma near the fracture site. These defects are totally
asymptomatic and do not disturb the healing of the fracture.
They rarely appear before 3–4 weeks after the fracture. They
may also be seen following greenstick fractures.
Phillips and Keats demonstrated the development of
cyst-like lesions in the radius and tibia in two children as a
postfracture event.313 Pfister-Goedeke and Braune reported
cyst-like cortical defects a few weeks after greenstick fractures
in the undamaged areas of the radii in nine children.312 The
normally extensive porosity undoubtedly predisposes the
metaphyseal region to the transient development of these
lesions (see Chapter 1).
Another possible explanation for these defects is that a
piece of periosteum, muscle, or fat is caught within the
fracture gap. As shown in Chapter 1, the periosteum may
herniate even into greenstick injuries as the fracture

A B
FIGURE 10-19. (A) Minimal torus injury to distal radius. (B) Lytic (cystic) lesion 4 weeks later.
334 10. Complications

FIGURE 10-20. (A) Overriding distal radial and

ulnar fractures in an 11-year-old boy. (B) The
radius healed smoothly, but a large exostosis
developed in the ulna. It did not impair function.

spontaneously reduces. This entrapped tissue may not
resorb quickly and may even elicit a fibrous reaction
around it.313
Moore et al. described two patients who developed post-
traumatic cysts and cyst-like lesions following fracture.311 The
first case was a 9-year-old girl who sustained a minor torus
fracture. The second was a 6-year-old boy with both bones of
the forearm fractured. Histologic examination in the second
case showed features of a unicameral bone cyst. The authors
thought that there were two principal clinical and radiologic
types of posttraumatic cyst: (1) asymptomatic, transient, cor-
tical lesions found only in children and (2) more central-
expanding lesions found in a wider age group and associated
with pain, swelling, and pathologic fractures.
although at one margin an osteochondroma formed. This
complication is also discussed in Chapters 6 and 7.
Angulation
Angular deviation from the longitudinal axis is often
encountered in pediatric fractures. In fact, it is usually
suggested that any angulation up to 30° beyond the normal
longitudinal alignment corrects spontaneously. Remodeling
and physeal growth may not always realign the bone (Fig.
10-23), and every effort should be made to obtain longitu-

Exostosis and Osteochondroma

The possible role of trauma in the formation of exostoses or
solitary osteochondromas is uncertain. Figure 10-20 shows a
fracture of the distal radius and ulna that was left in side-to-
side (bayonet) apposition after an unsuccessful closed reduc-
tion. Although the ulna remodeled considerably during the
ensuing 16 months, a small area of the proximal fragment
remained. Presumably, this was herniated through the
periosteal sleeve and was not subsequently surrounded by
any tissue capable of resorbing the protruding fragment.
Another possible explanation is that heterotopic bone
formed in the interosseous membrane.
If the peripheral growth plate (or epiphysis) is avulsed or
otherwise damaged (type 6 or 7 injury), the normal
restraints to appositional physeal cartilaginous growth may
be disrupted, and formation of an osteochondroma may be
allowed. Figure 10-21 shows a teenager with a large, solitary
fibular osteochondroma that developed progressively over a
5-year period after he was kicked in the popliteal fossa. Pro- FIGURE 10-21. Lateral view of a large proximal fibular osteochon-
gressive peroneal neuropathy necessitated removal. Figure droma. The boy had been kicked in the popliteal fossa, and a mass
10-22 shows a boy who sustained a type 3 distal femoral injury had developed within 2 years. Roentgeongrams were not obtained
that was complicated primarily by an osseous bridge, until 5 years after the injury.
Chondro-osseous Complications 335

FIGURE 10-22. (A) Type 3 physeal injury to the distal femur treated by open reduction and
pin fixation. (B) Premature osseous bridging and a peripheral osteochondroma developed.
(C) Pathologic specimen, showing a remnant of the physis and a larger portion of the physeal
cartilage along the metaphysis. The osseous bridge is adjacent to the physis.

dinal alignment of the fracture fragments in both sagittal
and coronal planes. Rotational malalignment may never
correct (although this is controversial), so it should be
restored during fracture treatment. Some degree of rota-
tional malunion (which often accompanies supracondylar
fractures) may be compensated for in the upper extremity,
primarily because of the nature of the scapulothoracic and
glenohumeral joints. In the lower extremity, however, rota-
tional malunion may cause significant changes in the gait
pattern.

FIGURE 10-23. (A) Malunion of the proxi-

mal humerus in a 7-year-old child. This
fracture was sustained 5 months prior to
death from leukemia. The lateral view
shows 40° of malunion from a proximal
metaphyseal fracture. The plane of
section used to create the “opened” frac-
ture shown in (B) is indicated by the
arrows. (B) New bone and fibrous tissue
have filled the subperiosteal space, and
extensive remodeling has taken place in
the 5 months, although the original cortex
(arrows) is still evident. Juxtaphyseal
metaphyseal changes (darkened trabecu-
lae) are also grossly evident, reflecting the
changes caused by decreased blood flow
when the nutrient artery was disrupted.
336
FIGURE 10-24. Tuberosity growth arrest from a traction pin.
Traction Complications
Proper traction pin placement is essential in children (Fig.
10-24). Because of the relative porosity of the metaphyseal
bone, placement too close to the surface may cause the pin
to pull out of the bone or may result in subperiosteal or
extraperiosteal movement of the pin, such that there is no
effective skeletal traction. The pin must not be placed near
or through a physis lest long-term growth complications
follow. The treating physician must be aware of the contours
of the physes of the proximal ulna, distal femur, and proxi-
mal tibia—the areas used most often for placement of skele-
tal traction pins. Although not often employed in children,
calcaneal traction must also be used carefully, as there is an
epiphyseal–physeal growth mechanism in this region.
Pin Migration
The use of small, smooth pins may be associated with subse-
quent migration resulting from the normal muscular activ-
ity of children (Fig. 10-25). Such migration of pins to the
spinal canal and thoracoabdominal organs has been
reported in adults.314–318 As is evident in Figure 10-26, pins
originally placed in the pelvis can migrate along anterior
abdominal muscle planes to enter the chest and peri-
cardium.
Hypertension
Children placed in skin or skeletal traction for fractures of
the femur may have transient acute hypertension.319,320,323–325
Children with orthopaedic immobilization have a fourfold
greater incidence of significantly elevated blood pressure
than other hospitalized children.327 Blood pressure should
be monitored carefully in children undergoing such
traction. If hypertension occurs, traction weights are
decreased.323–326
10. Complications
FIGURE 10-25. (A) Treatment of pseudarthrosis by K-wires. (B)
Posterior pin migration 7 weeks later.
Heij et al. found arterial hypertension in 31 of 50 children
(62%). In most cases it occurred within the first 3 weeks of
treatment. In seven it developed after 3 weeks or more of
traction. All children became normotensive within 1 week
after discontinuing traction. Hypercalcemia occurred in 11
children and was equally distributed between hypertensive
and normotensive children.321 Hamdan et al. found hyper-
tension in 39 of 57 patients (68%).320
Antihypertensive therapy may be necessary.320,327 Helal et
al. found increased serum renin in pediatric patients devel-
oping hypertension after orthopaedic procedures.322 Two
patients required the use of an angiotension-converting
enzyme (ACE) inhibitor to control the persistent hyperten-
sion while undergoing prolonged orthopaedic procedures
(i.e., bone/limb lengthening).
Miscellaneous Complications
Foreign Bodies
Children frequently insert a variety of objects underneath
a cast. Neff and coworkers reported a child in whom a
rubber band, placed around a plastic bag to protect the cast
during bathing had gotten under the cast and was constrict-
ing the common peroneal nerve, causing neurologic dys-
function.328 One of my small patients placed several pennies
into a short leg cast. He had an exposed K-wire from percu-
taneous fracture fixation. He also enjoyed walking through
puddles. The result of copper, steel, and moisture coated his
entire plantar surface with a blue-green layer of copper
oxide.
Miscellaneous Complications
FIGURE 10-26. (A) Early migration of a smooth pin used to “mini-
mally” fix a proximal femoral fracture. (B) Migration toward the
pelvis. (C) Pin is now in the epigastric muscles. (D) Pin penetra-
Fat Fractures
The most common cause of fat fracture is a sharp, nonlac-
erating force, such as a dog bite.330 The phenomenon is infre-
quent and usually late to appear, with an interval of several
months between injury and the initial observation of the
cutaneous defect. It is almost impossible to foresee this clin-
ical entity because of the swelling accompanying the under-
lying skeletal injury. Fat fractures are probably caused by a
shearing force through the subcutaneous fat, superficial
fascia, and on occasion the deep fascia. This force creates a
diathesis in the fat compartment. Fat necrosis is present as
a result of the original compression-contusion force. As it
resolves, the proximal edge is elevated and the distal edge
flattened. Attempts to restore normal planes by fat, fascial,
and muscle rotation flaps are difficult and sometimes asso-
ciated with major complications.
Fat Necrosis
Canteli et al. reported a 13-year-old with a painless soft tissue
mass over the medial side of the knee following trauma. His-
tologic analysis confirmed fat necrosis.329
337
tion of the pericardium caused myocardial irritability and heartbeat
irregularity, necessitating thoracotomy and removal of the pin.
Cast Syndrome
Although cast syndrome is an uncommon problem during
treatment of childhood fractures, the greater emphasis on
immediate reduction and application of the spica cast for hip
dislocations and femoral fractures, and the treatment of
childhood spinal fractures by casts, increases the potential
for its occurrence. The severity of the symptoms and the
need for prompt, effective treatment mandate recognition
during the early stages. The term “cast syndrome” has been
applied primarily to the association of arterial (mesenteric)
duodenal obstruction with immobilization. It has been
reported relatively frequently in adolescents and young
adults, with or without cast application, and particularly fol-
lowing spinal surgery.331,338
Signs and symptoms are typical of upper gastrointestinal
obstruction. They may develop acutely or insidiously. Initial
symptoms include “fullness,” nausea, vomiting, and progres-
sive abdominal distension. Vomiting may lead to dehydration
and metabolic alkalosis.
The pathogenesis appears to be localized to the junction
of the third and fourth parts of the duodenum, where the
duodenum is bound by the ligament of Treitz. This area is
338
juxtaposed to the origin of the superior mesenteric artery.
The duodenum may be compressed posteriorly by the
lumbar spine and aorta and anteriorly by the mesenteric
artery. Recumbency further contributes to the compression,
as does increased lumbar lordosis. These conditions lead to
gastric outflow obstruction, gastric dilation, and thus com-
pounding of the problem.
Treatment is contingent on the severity of the symptoms.
Although dietary restriction may be sufficient, nasogastric
intubation may be necessary to decompress the gastric dila-
tion. In severe cases intravenous hyperalimentation may be
required. Electrolyte balance should be monitored closely
and corrected as indicated. Positioning the patient on the
left side or prone may relieve the symptoms. Windowing the
cast over the abdomen is rarely successful. Surgery is infre-
quently necessary, with duodenojejunostomy being the relief
procedure.
Hutchinson and Bassett described superior mesenteric
artery (SMA) syndrome in 14 patients ranging in age from
14 to 19 years.333 They were all of a similar body build
(asthenic). Clinical presentation included nausea and inter-
mittent, voluminous bile-stained vomiting despite interven-
ing periods of normal appetite and bowel sounds. The
average delay in diagnosis was 5 days. Nasogastric drainage
and intravenous fluids were successful in every case. Fifty
percent of the patients had more than one episode requir-
ing treatment. Two of three patients with body casts required
cast removal. No patient required intravenous hyperalimen-
tation, removal of spinal instrumentation, or abdominal
surgery to relieve the obstruction. Three of the eight patients
had not had spinal surgery or cast immobilization. The
primary problem is due to extrinsic pressure on the third
part of the duodenum, causing small bowel obstruction. Of
the childhood cases reported by Hutchinson and Bassett,
two patients were posttraumatic: one with cerebral anoxia
secondary to a lightning injury and one with a closed head
injury.
Cast Complications
Immobilization may cause rapid and extensive trabecular
bone loss rather than cortical changes. This loss is reversible
to a certain extent, but the recovery depends on the dura-
tion of immobilization.
Spearman and Barson described two cases of toxic shock
syndrome with focal cutaneous staphylococcal infections
complicating abrasions underneath casts.336
Kaplan reported the occurrence of superficial burns fol-
lowing the application of plaster splints.334 Simonian and
Staheli described periarticular fractures complicating
manipulation of the knee after cast removal.299
Fracture Blisters
Blisters represent a cleavage injury at the dermoepidermal
junction. A “blood” blister is a slightly deeper injury than a
clear-fluid-filled blister and is associated with a slightly higher
risk of wound-healing problems. Blisters are common with
ankle injuries.
Giordano et al. found that the status of the blister did not
affect the timing of surgery (average time was 2.1 days after
10. Complications
injury).332 Blisters were intact at the time of surgery. Incisions
circumvented any blisters. No infections occurred.
Patients operated on within 24 hours of injury had the
lowest incidence of fracture blisters (compared with delayed
intervention).337 For patients whose fracture blisters were
present at the time of surgery, patient care was affected in
10 of 13 cases (71%), with two developing significant wound
infections. There were no adverse effects if the blister devel-
oped postoperatively.
Infection
Infections may certainly complicate fracture treatment in
children. The infection may be introduced directly, as in an
open fracture, or it may be caused by hematogenous seeding
of the traumatized tissue from an extraosseous, often distant
source. Infections complicating childhood fractures are dis-
cussed in detail in Chapter 9.
Cartilage
Alterations may ocur in chondrocytes and extracellular
matrix if cartilage is allowed to dry during an open proce-
dure or injury.340 The changes appear reversible but only
if no mechanical injury has been superimposed on the
cartilage.
Maffulli et al. described a high incidence of osteochon-
dritic lesions, intraarticular loose bodies, and precocious
signs of joint aging following joint trauma.339 The prognosis
for continued high-level activity is limited.
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11
Fractures in Pediatric Growth Disorders
Engraving of a birth injury to the distal humerus. (From Poland J.
Traumatic Separation of the Epiphyses. London: Smith, Elder,
1898)
n the chapters to follow an array of trauma is covered that
I affects specific anatomic areas of the developing skeleton.
Most of the material involves normal children who have sus-
tained variable degrees of musculoskeletal trauma as isolated
injuries or as part of multisystem trauma. Children with pre-
existent congenital or acquired deformities and diseases may
also injure their skeletons, often with seemingly innocu-
ous mechanisms. It may occur because of susceptibility to
346
chondro-osseous failure due to the antecedent disorder. The
underlying problem may introduce difficulty for both diag-
nosis and treatment of the acute skeletal injury and may raise
the question of intentional infliction.
Pain in the child’s back or extremity may be the initial pre-
sentation of systemic diseases or disorders such as leukemia
or Englemann’s disease. Pain may follow participation in
sports, with the child being evaluated for some type of mus-
culoskeletal injury. Expansile or destructive osseous lesions,
such as a bone cyst or osteogenic sarcoma, may come to
medical attention only when the child is injured during play
and the structurally weakened bone is fractured.
In this chapter various predisposing congenital (genetic)
and acquired diseases and deformities, their characteristic
acute fracture patterns, and their treatment problems are
addressed. The fracture itself may seem simple to diagnose
and treat, but the underlying condition may complicate
both, as well as the healing process.
General Injuries
Intrauterine Fractures
Fractures of the fetal skeleton are infrequent and may be dif-
ficult to identify with certainty.2,4,8,12,13 The criteria for a true
intrauterine fracture of normal bone are roentgenograms
showing an absence of generalized osseous disease and
normal callus appearance. Films should be obtained as
soon after birth as possible, as callus can form so quickly in
the newborn that roentgenograms obtained even 1 week
after delivery would not definitively rule out birth trauma.
Most intrauterine fractures, however, are due to underly-
ing, generalized diseases, such as osteogenesis imperfecta,
arthrogryposis, chondrodystrophies, congenital rubella, and
syphilis.10,11
Intrauterine fractures may occur consequent to abdomi-
nal or extrauterine trauma during pregnancy, with indirect
injury to the fetus (Fig. 11-1).1–3 The accident rate during
pregnancy may be as high as 7%.2 Pearsall et al. reported a
mother (29 weeks pregnant) who jumped from a balcony to
elude attackers, sustaining multiple rib and pelvic fractures.8
Abdominal films revealed a midshaft fracture of a fetal
femur. At 33 weeks abdominal ultrasonography suggested
General Injuries
FIGURE 11-1. Antenatal film following maternal abdominal trauma.
A fracture of the fetal femur is evident (arrow).
A B
FIGURE 11-2. This infant was born following abdominal trauma to
the mother 1 week earlier. (A) The radiograph shortly after birth
shows an apparent fracture through a region of sclerotic bone. Is
this a form fruste of proximal focal femoral deficiency (PFFD)?
347
healing and callus formation, but postnatally there was no
evidence of callus. Figure 11-2 shows the femur of a newborn
noted to have a thigh deformity during the newborn exam-
ination. This seemingly minimal, undisplaced fracture, sub-
sequently angulated but healed and remodeled. The mother
had been struck in the abdomen prior to delivery.
Experimentally produced fetal fractures have a less
active inflammatory phase and smaller amounts of
hematoma than experimental fractures in postnatal
animals.9 These characteristics typify other fetal tissue wound
responses as well.6 Proliferative activity in the periosteum
and endosteum is more intense and appears earlier than
does postnatal injury. Fetal callus is more abundant and
differentiates into cartilage more rapidly. Chondro-osseous
transformation is also rapid. Thus it appears that the second
phase of fracture healing predominates over the first phase
(see Chapter 8). The decreased inflammatory reaction
during the first phase permits more rapid cellular differen-
tiation in the callus. In general, these prenatal fractures heal
uneventfully.
Perhaps the most common single-bone prenatal fracture
is a tibial pseudarthrosis. These fractures cause angulation of
the lower limb. They are discussed later in the chapter (see
Pathologic Fractures). Some intrauterine fractures may be
misdiagnosed as a pseudarthrosis. Freedman et al. described
a neonate diagnosed at birth as having a clavicular
pseudoarthrosis,5 although significant callus was evident at 6
weeks of age.
Development of the hip, distal femur, and tibia/fibula appeared
smaller than the opposite side. The mother had been “abused” with
repetitive blows to the abdomen during the 3 weeks prior to deliv-
ery. (B) Appearance at 4 months of age. Healing is evident.
348
McCullagh et al. fractured chick embryonic radii (mid-
diaphysis) prior to primary ossification center formation.7
Most of the specimens healed the defect during subsequent
primary osteogenesis. Of the 33 specimens, however, 4 devel-
oped a typical pseudarthrosis with “hourglass” constriction.
Such embryonic disruption may be a factor in the develop-
ment of any congenital pseudarthrosis.
Birth Fractures
Through improved antenatal and perinatal care, birth
trauma and neonatal skeletal injuries are now encountered
less frequently.19,20,23,24,26,31,36,38,41,42,45,63–65,68,74,75,82,84,86 However,
trauma to long bones in the newborn may still be sustained
during a difficult delivery, particularly if the baby is large,
the mother has a small pelvic outlet, or the presentation is
breech or transverse.46,69,73,76,85,87 Fractures may occur even
during cesarean section, especially if the procedure is pre-
cipitous due to fetal distress.14,16,18,33,39,54,55,66,83 When more
than one fracture is present, one must suspect underlying
dysplastic, muscular, or metabolic bone disease.32,40,52,80 Mul-
tiple birth fractures may occur in fetuses with arthrogrypo-
sis, especially if there is rigid extension of a joint.29 Fetal
anoxia and urgent delivery may necessitate forceful extrac-
tion, increasing the likelihood of fractures and neurologic
injury.48
Rubin, over a 6-year period, found 116 injuries in 108
infants among 15,435 births (one injury per 143 births).75
Camus et al. found 291 cases of obstetric trauma in 20,409
deliveries, including 116 extremity fractures.31 Fractures not
detected at birth or neonatal hospital discharge should raise
the suspicion of child abuse when the neonate is brought
back to the hospital with an injury.35,51
Fractures of the diaphyses are usually easily recognized.
Diaphyseal skeletal injuries, in order of decreasing fre-
quency, usually involve the clavicle, humerus, and
femur.17,34,38,49,62,70,73,77,79,81,89 Fractures distal to the elbow and
the knee are unusual. Fracture of the tibia is often patho-
logic, and congenital pseudarthrosis of the tibia should be
considered. Pseudarthrosis of the radius and ulna may also
occur. Neonatal plastic deformation (bowing) also has been
described.88
In contrast, fractures of the epiphyseal regions are more
difficult to recognize and may require definitive diagnostic
techniques such as arthrography, ultrasonography, or mag-
netic resonance imaging (MRI).28,47 The most commonly
involved epiphyses are those of the proximal and distal
humerus and femur.43,72,78 Such epiphyseal separations are
frequently misdiagnosed as acute, traumatic dislocations.
Dislocation, though often discussed as part of a differential
diagnosis, is essentially nonexistent in the major joints of
children younger than 12 months and particularly in the
neonate.50 Invariably, the suspected “dislocations” are epiph-
yseal/physeal separations (type 1 injuries).
Traumatic displacement of the proximal humeral physis
may occur alone or, less frequently, in association with
brachial plexus paralysis.27,43 The shoulder is usually
markedly swollen and may be misdiagnosed as an acute dis-
location or as osteomyelitis or septic arthritis with secondary
dislocation.71,76 The clinical signs of traumatic epiphysiolysis
are pseudoparalysis and internal rotation posturing of the
11. Fractures in Pediatric Growth Disorders
arm. Initially, diagnosis is difficult because the cartilaginous
humeral head is ossified in only 20% of full-term new-
borns. Arthrography may be undertaken, but it is rarely
necessary. Sonography may also be useful. The diagnosis is
established by the subsequent appearance of callus of the
healing fracture. The arm should be held temporarily across
the chest. Although the prognosis generally is excellent,
these children must be followed to skeletal maturity, as
significant growth problems may occur (see Chapter 14,
Humerus Varus).
Fracture of the humeral diaphysis usually occurs in the
middle third. The diagnosis is generally made by the obste-
trician, who feels or hears the bone break. The infant then
refuses to use the arm (pseudoparalysis). Roentgenograms
disclose the fracture, although care should be taken not to
confuse the nutrient canal as a fracture line. Treatment con-
sists of immobilizing the arm with the elbow flexed over
the chest. The fracture heals quickly, usually within 2 weeks,
and angular deformities are spontaneously corrected by the
extensive growth that occurs. Transient radial nerve palsy
may be associated with these fractures, but it usually resolves
completely within 6–8 weeks.
Fracture-displacement of the proximal femoral epiphysis
is usually confused with or misinterpeted as developmental
dislocation of the hip.56,72 The term “pseudodislocation” of
the hip has sometimes been applied. The diagnosis is pri-
marily clinical, as radiological signs become evident only
after an interval of healing. Michail et al. noted that “so far
as we are aware, the existence of an obstetrical (traumatic)
dislocation of the hip has never been demonstrated,” a state-
ment with which I completely agree.67
The line of separation is distal to the combined proximal
femoral epiphysis. Acute injury is suggested by pseudoparal-
ysis. At birth the femoral head, neck, and greater trochanter
are entirely cartilaginous, making roentgenographic diag-
nosis of any separation (fracture) extremely difficult. The
proximal femoral metaphysis is displaced upward and later-
ally. Because the femoral epiphysis has been in its normal
position in utero, the acetabula are developed symmetri-
cally, which makes developmental hip dysplasia unlikely.
Treatment consists of immobilizing the hip in abduction,
partial flexion, and medial rotation for 3–4 weeks. However,
the diagnosis is frequently not made until the healing phase,
when coxa vara may have developed. Although there is
a high potential for remodeling and spontaneous correction
in infants, coxa vara may persist or even worsen (see
Chapter 21).
Traumatic separation of the distal femoral epiphysis pre-
sents less of a roentgenographic diagnostic problem because
the secondary ossification center of the distal femur is
usually present at birth in the full-term child. However, the
injury frequently is unsuspected until the subperiosteal
hematoma ossifies. The lower femoral epiphysis usually dis-
places posteriorly, with extensive stripping of the periosteum
from the posterior portion of the distal femoral shaft. The
fracture is a type 1 epiphyseal injury with an excellent prog-
nosis for subsequent normal growth. Manipulative reduction
must be undertaken carefully to minimize injury to popliteal
neurovascular structures. A single leg hip spica cast with the
knee in partial flexion should be applied for 3 weeks. A resid-
ual angular deformity usually corrects spontaneously during
General Injuries
FIGURE 11-3. (A) Rachitic-type fracture in a
1200-g premature infant. (B) Multiple rachitic
fractures in a 1000-g premature infant (one of
triplets).
A B
the rapid growth the child undergoes during the first
year of life, although growth plate injury may occur (see
Chapter 21).
Specific birth injuries are discussed in more detail in the
anatomic sections of other chapters.
Prematurity
Fractures in premature infants usually occur within a few
weeks after birth (Fig. 11-3; see also Fig. 11-6, below). They
are nearly always pathologic and in most cases are due to
metabolic bone disease through deficiencies of vitamin D,
calcium, phosphorus, and prolonged treatment with sodium
bicarbonate, furosemide, and parenteral nutrition.15,57–61 In
some infants multiple fractures may be the first presenting
signs of rickets.25,30,37,44 Immobilization of fractures in
preterm infants is not always easy, although minimal splint-
ing may be highly effective in these low-birth-weight indi-
viduals, especially for pain relief.53 Several risk factors may
be associated with mineralization problems in preterm
infants: cholestatic jaundice, prolonged total parenteral
nutrition, bronchopulmonary dysplasia, prolonged diuretic
therapy with furosemide, physical therapy with passive
motion, and chest percussion therapy. Treatment of frac-
tures in these situations usually requires appropriate sup-
plementation of calcium and phosphorus, which may be
accomplished through the use of new formulas with high
calcium and phosphorus contents.
Dabiezes and Warren reviewed 247 very low-birth-weight
(under 1500 g) premature infants.37 Rickets was diagnosed in
96 (40%), and fractures were diagnosed in 26 (10%), with
349
multiple fractures being common (98 fractures in 26
infants).
Demineralization is present because 80% of calcium and
phosphorus deposition and two-thirds of the birth weight are
gained during the exponential intrauterine growth of the
third trimester. Premature infants with these conditions
require daily doses of calcium (150 mg/kg), phosphorus
(80 mg/kg), and vitamin D (400–1200 IU). Postnatal bone
mineralization in preterm babies lags significantly behind
expected intrauterine bone mineralization.21,22 Further
osteopenia in preterm babies is caused by increased bone
resorption, not by decreased bone formation.22
The tendency is for many of these fractures to be found
fortuitously.59 Fractures may mimic child abuse secondary to
aggressive physical therapy in children with joint contrac-
tures.51 No infant exhibited skeletal deformity at the 1-year
follow-up.59
Fractures During Infancy
Fractures that occur during the first year of life must be dif-
ferentiated according to a number of predisposing factors,
such as syphilis, tuberculosis, scurvy, rickets, osteomyelitis,
tumors, and child abuse.91,92 A cause should be sought when-
ever epiphyseal or metaphyseal fractures are found. Treat-
ment is primarily symptomatic, as these fractures usually are
incomplete compression failures.
Most fractures of the diaphyses of long bones are readily
recognizable. However, the appearance of subperiosteal new
bone, in the absence of an obvious fracture, may cause some
concern, especially regarding the possibility of child abuse.
350 11. Fractures in Pediatric Growth Disorders

cell column integrity, cleavage disruption planes may

develop between the columnar clones, leading to further
instability and failure (see Chapter 6). Osteodystrophic
changes in the metaphysis may also increase susceptibility
to fracture at this level and may cause delay in the repair of
any fracture.
Treatment should be directed at the primary cause with
large doses of vitamin D (with or without diphosphonates),
and the deformed or painful regions should be splinted until
a drug response is seen. This process may take several weeks
to months. Permanent deformation may require subsequent
osteotomy.
Rickets may result from a variety of other causes. It is
becoming increasingly evident in premature infants who rely
on parenteral alimentation.96,98,100,103–105,116 (See Prematurity,
above.)
Vitamin D-resistant rickets is relatively frequent in the
United States. Renal tubular abnormalities associated with

FIGURE 11-4. One-month-old child with subperiosteal diaphyseal

bone (arrow). This is a relatively normal finding and may be due
to birth trauma to the lower leg. Rough handling of the neonate,
as with child abuse, may cause a similar roentgenographic
appearance.

During infancy the femur or the tibia may have a longitudi-

nal layer of subperiosteal bone, often extending the entire
length of the shaft (Fig. 11-4). Usually, this new bone is bilat-
erally symmetric, but it is less likely in an abused child, who
more often has evidence of asynchronous subperiosteal reac-
tive bone.90 Child abuse is discussed in detail later in the
chapter.

Rickets
Vitamin D deficiency rickets is rarely encountered in the
United States, but it remains a distinct problem for the mal-
nourished childhood populations in many areas of the
world. Florid cases may be associated with progressive me-
taphyseal–epiphyseal deformation (Fig. 11-5), especially at
the wrist or knee, which are areas of rapid growth during
infancy and early childhood.116 Because of excessive widen-
ing of the physeal cell columns and irregular metaphyseal
bone formation and remodeling, these areas become sus-
ceptible to gradual plastic deformation and failure. The
radio-graphic changes may be similar to those seen with
child abuse.111,116 Rachitic changes may be a consequence of
a type of child abuse (malnutrition), rather than classic phys-
FIGURE 11-5. (A) Rachitic epiphysiolysis (arrow) in a child suffer-
ical trauma. Many fractures initially are not radiographically ing from kwashiorkor and dietary deficiency rickets. (B) Four-year-
demonstrable. old child with dietary deficiency rickets. The distal tibial physis has
Rachitic changes in the physis result in excessive cells in widened. The fibular physis has widened similarly; and owing to
the uncalcified hypertrophic zone. The metaphyseal vascu- the valgus forces at the ankle it has developed a type 2 physeal
lar loops do not invade the cell columns unless they fracture that did not heal until adequate dietary modification and
are appropriately calcified. With distortion of normal supplementation was provided.
General Injuries
FIGURE 11-6. (A) Child with renal rickets in whom bilateral coxa
vara is beginning to improve (on the left) following renal trans-
plantation. The child died 1 year later. (B) Postmortem specimen
phosphaturia and hypophosphatemia account for a large
number of cases of rickets and may lead to proximal humeral
or femoral failure and coxa vara (Fig. 11-6).93,99,107,113,115 Sec-
ondary hyperparathyroidism in association with the florid
form of vitamin D deficiency, vitamin D resistance, or renal
tubular rickets may also occur.
Children under treatment for renal osteodystrophy, par-
ticularly those on dialysis, may show metaphyseal fractures or
even slipping of the proximal femoral epiphysis. This may
occur earlier than the classic slip and lead to coxa vara. Shea
and Mankin reported slipped capital femoral epiphysis in
patients with renal rickets.113 Slipping appears to be associ-
ated primarily with renal or glomerular rickets.107,112 Chil-
dren with renal or glomerular rickets have not only calcium
and phosphorus metabolism disorders, they also have
defects in protein synthesis. Unlike classic coxa vara, a
slipped epiphysis may not occur until adolescence. Only in
recent times have a significant number of children with these
disorders survived to this age to manifest problems.113 The
mechanics of coxa vara and a slipped epiphysis are probably
not significantly different. They occur because of different
degrees of chondro-osseous maturation along the develop-
ing femoral neck.
351
of the left hip showed healed coxa vara. (C) Coxa vara and severe
physeal involvement in a child who died in renal failure.
Other epiphyseal regions (e.g., proximal humerus,
distal radius, distal tibia) may also exhibit such epiphy-
siolysis. Swiersta et al. treated five distal femoral epiphy-
siolyses in three children with immobilization and medical
correction.115 All had renal osteodystrophy. They found
that displacement of the distal femoral epiphysis was more
common in preschool children than older children or
adolescents.
Many of these epiphysiolyses require surgical correction
of the skeletal structural deformity. However, optimizing
medical treatment, until transplanted, is integral to prevent-
ing further deformity. Equally important is the avoidance of
deforming forces through the judicious use of preventive or
corrective orthotics when appropriate.
Oppenheim et al. noted that aluminum-containing
phosphate binding agents have been given in the past to
control or prevent hyperphosphatemia in renal osteodystro-
phy.110 This may lead to bone demineralization and diaphy-
seal–metaphyseal fractures, rather than the typical
epiphysiolyses.114
The excessive intake of carbonated beverages instead of
milk may have an effect on bone density and fracture
susceptibility. Carbonated beverages affect the dietary
352 11. Fractures in Pediatric Growth Disorders

FIGURE 11-7. (A) Distal femoral epiphysiolysis associated with scurvy. (B) Variable subperiosteal bone (right versus left) several
weeks later.

calcium/phosphorus ratio and has been correlated with an Lead

increased incidence of diaphyseal and metaphyseal fractures
in girls but not boys.119 The high consumption of carbonated
beverages and declining consumption of milk have signifi-
cance for girls relative to susceptibility to osteoporosis in
later life.
Scurvy
Vitamin C deficiency (scurvy) is rare. It is associated with
epiphysiolysis and extensive stripping of the periosteal sleeve
(Fig. 11-7).95,109,112 This eventually causes massive subperi-
osteal new bone formation not unlike that seen with neona-
tal osteomyelitis.
Excessive absorption of lead may cause retardation of bone
growth.97 It may also cause a significant delay in fracture
healing in children.102
Gaucher’s Disease
Children with Gaucher’s disease have an increased incidence
of femoral neck fractures (Fig. 11-9) compared to that in
normal children.121,126,128–131,135 These fractures usually occur
prior to 10 years of age, often with minimal or no trauma. It
is postulated that expansion of the medullary space by the

Vitamin A
The use of vitamin A analogues for various inherited skin
disorders may cause problems similar to those seen with
hypervitaminosis A, namely premature physeal closure
(Fig. 11-8) and altered long bone remodeling.106,108 This does
not seem to predispose to fractures. However, if children
who are being treated with these drugs experience a frac-
ture, there may be alteration of normal healing and accel-
erated physeal closure. The effect on the growth plate may
be due to alteration of the expression of the genotype, par-
ticularly affecting the expression and synthesis of various
collagens.94,101
Hyena disease is an uncommon disorder in young dairy
cattle that causes dwarfism. The injection of high doses of
vitamins A and D to newborn calves caused a similar disor-
der.117,118 Assessment of the physes showed significant dis-
ruption of the normal cytoarchitecture. Whether a similar FIGURE 11-8. Sclerosis and early bridging of the distal tibial physis
syndrome (combined megavitamin disorder) exists in in a patient with hypervitaminosis A during treatment of congenital
humans is currently unknown. ichthyosis.
General Injuries 353

been seen on previous radiographs. However, 6–8 weeks later

a periosteal reaction was seen at the site of all 15 crises. Bone
scans showed decreased uptake. Horev et al., using MRI
during “bone crises” in patients with Gaucher’s disease,
identified subacute intramedullary hemorrhage and
microinjury.130
The issue of whether splenectomy has a direct effect on
skeletal involvement and fracture susceptibility in children
with Gaucher’s disease is still being studied Many of the frac-
tures described in the literature occurred after the child had
undergone splenectomy.121,126,129 The new genetically engi-
neered treatment methods of the metabolic abnormality will
obviously affect the incidence of these fractures.

Endocrinopathy
Children with specific or generalized endocrinopathy may
become increasingly susceptible to fractures owing to the
effect of hormonal alteration on chondro-osseous develop-
ment. Hypothyroidism may affect protein metabolism and
the production of normal chondroid and osteoid within the
extracellular matrix. Children with craniopharyngioma
may have slipped capital femoral epiphyses. Comparably, a
child with Schmidt syndrome (diabetes, hypothyroidism)
may develop a slipped epiphysis when placed on thyroid sup-
plementation.134 Rapid growth rates following the adminis-
tration of growth hormone may predispose the child to
epiphysiolysis, especially in the proximal femur.

FIGURE 11-9. Gaucher’s disease. (A) Femoral neck fracture. (B)

Subsequent deformities 5 years later.

lipid-laden cells leads to poor bone density and undermines

the medial supporting structures along the femoral neck.
Mid-cervical or basicervical femoral neck fractures may
occur with minor or no trauma.126 They usually appear
between 5 and 9 years of age. None of the reported children
has developed ischemic necrosis.
In a series of 23 pathologic fractures in nine children with
Gaucher’s disease, fracture healing was prolonged, taking as
long as 2 years for completion in some patients.131 Inade-
quate periods of immobilization and early weight-bearing led
to malunion.
Fifteen of the fractures in long bones occurred after a
“crisis” at the fracture site 2–12 months earlier.131 Character-
istic of these crises was marked pain, swelling, and tender-
ness with or without systemic fever. These cases, not unlike
those seen with sickle cell disease or myelomeningocele,
must be differentiated from osteomyelitis (Fig. 11-10).135
Radiographic examination at the time of the onset of pain FIGURE 11-10. Pseudoosteomyelitic appearance of Gaucher’s
showed either normal findings or osseous lesions that had disease in the distal femur.
354 11. Fractures in Pediatric Growth Disorders

others in their age group. In contrast, the epiphysis, physis,

and metaphysis are most likely to be involved in any dys-
plastic process and are the more likely regions to sustain
micro- or macroinjury. If a dysplastic child has a fracture, it
is sometimes possible to correct any angular epiphyseal
deformity by manipulating the fracture into a position com-
parable to that achieved by a corrective osteotomy.
The evaluation of pain, often due to stress fractures in
abnormally modeling and remodeling bone, may be the
initial presentation of a dysplasia (Fig. 11-12). Stenzler
et al. reported a case of diaphyseal dysplasia (Englemann’s
disease) that was causing micro (stress) fractures leading to
joint and extremity pain.142
Bagga et al. described a girl with Kozlowski’s spondy-
lometaphyseal dysplasia who also had hypocalciuric hyper-
calcemia.122 It was associated with femoral neck fractures
leading to coxa vara.
Nail patella syndrome is often associated with radial head
dislocations.138 A hypoplastic patella may cause subluxation
and chronic knee instability or pain.138,139
FIGURE 11-11. Pathologic fracture of the distal femur in a Som-
Two-thirds of children who have below-elbow deficiencies,
mering’s gazelle with hyperparathyroidism. Multiple fractures congenital or acquired, have concomitant radial head
were found in this skeletally immature animal during postmortem dislocations.140 The direction of the dislocation is often
examination. related to the length of the residual limb. Dislocation does
not usually require specific surgical treatment. Gorham’s
(disappearing) bone disease may predispose to extremity
and vertebral fractures.141
Metabolic Disorders
Some children with various chemical deficiency syndromes
have an increased risk of fracture (Fig. 11-11). They may
manifest extensive subperiosteal new bone formation that
must be distinguished from infection.120,123–125,127,128,132,136,137
Lysinuric protein intolerance is characterized by defective
transport of cationic amino acids.136 It leads to osteoporosis
and increased fracture susceptibility.
Hill et al. reviewed fractures in 117 children with end-stage
liver disease who underwent orthotopic liver transplanta-
tion,129 19 of whom sustained 69 fractures. There was no
documented trauma in 14 of the 19. Metabolic bone
disease (rickets, osteopenia, osteosclerosis) was present in 17
of the 19. Fractures were essentially a pretransplant problem.
Drug therapy and immobilization also were factors.
Blumenthal et al. studied a preterm infant with copper
deficiency that led to femoral fracture.124 Haddad et al.
reported carpal tunnel syndrome in children with
mucopolysaccharidoses and mucolipoidoses. They reviewed
48 children. Symptoms were rare, but signs such as decreased
sweating, pulp atrophy, thenar wasting, and manual clumsi-
ness were common. The flexor retinaculum, tenosynovium,
and epineurium were all thickened. They recommended
carpal tunnel release and tenosynovectomies.127

Dysplasias
There are more than 200 differently described dysplasias
that have variable effects on the development of the
chondro-osseous skeleton. Most cause alterations of longitu-
dinal and latitudinal growth that are part of the basic dys- FIGURE 11-12. Engelmann’s disease. This patient initially
plasia. Most dysplasias eventually lead to normal or relatively presented with thigh pain due to microstress fractures in the
normal osteon diaphyseal bone, with the children having no nonremodeled diaphyses (detected by focal lesions on a bone
increased susceptibility to diaphyseal fracture compared to scan).
General Injuries 355

Alman and Frasca used three-point bending to determine

the pattern of fracture.144 The OI bone consistently required
a lower load to fracture and had reduced collagen organi-
zation compared to normal controls. The fracture surface of
the OI bone was rough and exhibited a pull-out type of mor-
phology, in contrast to the smoother fracture surface of
control bone. The metaphysis and diaphysis exhibited
various patterns of involvement.145 The physeal–metaphyseal
interface may show considerable disruption of cartilage cell
columns and primary spongiosa.
Sillence has classified four main types and a number of
subtypes of OI based on clinical and radiographic features
and on modes of inheritance.169,170 However, the clinical

A
FIGURE 11-13. Pathologic fracture through a fibula centralized for
tibial hemimelia.

Fractures may occur in the deformed bones of reduction

disorders such as proximal focal femoral deficiency (PFFD)
and radial hemimelia. Corrective or reconstructive surgery
may also be associated with stress fractures or obvious
fractures. Figure 11-13 shows a fracture of a centralized,
hypertrophic fibula in a patient who was born with tibial
hemimelia.
Children with progeria have a susceptibility to fracture.
They also have an increased rate of delayed union and
nonunion relative to comparably aged children.133

Osteogenesis Imperfecta
Children with osteogenesis imperfecta (OI) have a basic
mesenchymal defect that manifests primarily as fragility of
osseous tissues.147,158,159,162,163,166,171 In the developing skeleton
this causes a generalized hyperosteocytosis, increased inter-
trabecular resorption, and immaturity of the bony micro-
and macroarchitecture (Fig. 11-14). Metabolism of some
amino acids, particularly hydroxyproline, also may be defec-
tive, which affects collagen development.149 Sanguinetti et al.
studied segments of physeal cartilage in four patients with
OI.165 In addition to the known molecular defects in colla-
gen, there were changes in matrix glycosaminoglycans and
noncollagenous proteins. These changes led to structural
B
changes in the hypertrophic zone and changes in calcifica-
tion and mineralization. Cohn and Menten described a FIGURE 11-14. (A) Postmortem radiograph of a neonate with type
potential animal analogue of OI.148 II osteogenesis imperfecta. (B) Proximal humeral specimen.
356 11. Fractures in Pediatric Growth Disorders

picture is by no means uniform within each group, and the
tendency to fracture may vary widely. The basic biochemical
defect appears to involve type I collagen, the main organic
component of bone. Aberrations in the structure or pro-
cessing of either pro 1(I) or pro 2(I) polypeptides have been
detected, and many defects at the gene level have been
demonstrated.
Shapiro has presented a classification of OI based on
the radiographic appearance of the skeleton, enabling clas-
sification during infancy or after the first fracture.168 This
may provide the physician with guidelines for treatment
during the difficult first few years in the severely affected
patient.
Vetter et al. studied 127 children with OI for the first 10
years of life.175 Using the Sillence classification there were 40
with type I, 39 with type III, and 48 with type IV disease.
During the first 10 years the number of fractures, extent of
deformities, and growth retardation were the same for types
III and IV, and fracture nonunion was more frequent for
types III and IV.
Infants with the severe form of the disease usually have
multiple fractures at birth (Fig. 11-15). Those with less severe
involvement (tarda) may not be diagnosed until later, when
they present with a fracture and short stature.
The diagnosis of OI is not always easy, particularly with
some of the milder versions.161 Differention from child abuse
is a constant problem.143,151 Although the primary concern is
often proving that a potentially abused child really has an
underlying predisposition such as OI, a patient with OI may
also be subjected to abuse, making the abuse diagnosis even
more difficult.154
Orthopaedic treatment of OI aims at not only acute
fracture treatment but, more importantly, at the prevention
of deformities occurring through repetitive fractures
and plastic deformation of the bones.150,160,174 The fracture
response may be relatively normal. Deformities come
about because of malalignment following fractures and by
progressive bowing due to excessive softness of the bone
and redirection of growth at the metaphyseal–physeal
junction (Figs. 11-16, 11-17). Unfortunately, immobilization

FIGURE 11-15. (A) Multiple fractures of the humeri, clavicles, and ribs in a
neonate with osteogenesis imperfecta. (B) Histologic appearance of the distal
femur and proximal tibia in a stillborn infant with severe osteogenesis imperfecta.
Normal metaphyseal trabeculation has been replaced by inflammatory (reactive)
tissue.
General Injuries
FIGURE 11-16. Ribbon-like femur and fibula in a never-ambulatory
child with osteogenesis imperfecta.
357
for treatment of these fractures may lead to further
osteoporosis and may render the patient more vulnerable
to subsequent fractures.152,173 Curvilinear deformation of
the bone also predisposes to tensile stress fractures at the
curve apex (Fig. 11-17). Cracks may slowly propagate to a
complete fracture. Attempts at daily weight-bearing with
orthotics and a standing A-frame become extremely impor-
tant to impart physiologic stimulation of osteon modeling
and remodeling.
The basic principles of fracture treatment are the same as
they are for normal children, except that angulation should
be corrected as much as possible because remodeling does
not appear to be normal. Callus formation may be massive.167
Mobilization and prevention of contractures assume major
importance to decrease stresses predisposing to subsequent
fracture.
Repeated fractures may lead to significant deformity and
often require subsequent osteotomy (Fig. 11-18) at multiple
levels.146,155,156,172 If possible, corrective surgery is deferred
until the bone has matured in strength and when the rate of
fracture decreases (later childhood and adolescence).
Intramedullary fixation of the long bones has become a
generally accepted method of treatment of selected patients,
although there is a tendency of these rods to grow out of
the bone with subsequent fracture (Fig. 11-19); bowing of
FIGURE 11-17. (A) Moderate bowing of the tibia and fibula with
anterior fracture and posterior bridging callus. (B) Severe
bowing resulting from osteogenesis imperfecta. (C) Nonunion
complicating severe bowing.
 358
the unsupported part of the bone may also occur. This
phenomenon has led to the development of extensible
intramedullary rods (Fig. 11-20), but this measure has not
completely corrected the problem.153,173
Ryöppy et al. recommended that early intramedullary sta-
bilization with rods, even soon after birth, was justified in
selected patients with severe OI, as it improved the possibil-
ities for motor development and later insertion of telescop-
ing nails.164 The material presented by Ryöppy et al. does
have some potential drawbacks in that these nails are often
placed percutaneously across joints such as the ankle.
Although claiming there have been no effects on growth, this
concept is difficult to monitor in the children, as many of
them already have altered physeal development because of
A B
11. Fractures in Pediatric Growth Disorders
FIGURE 11-18. (A) Corrective medullary rodding.
(B) The rod has gradually cut out the bone with
subsequent growth.
the underlying disorder. Furthermore, as shown in Chapter
6, even a smooth pin, across a growth plate, may have a dele-
terious effect on the physis and spongiosa, leading to a struc-
turally deformed endochondral model on which to lay down
periosteally mediated bone.
A patient with OI may develop compartment syndrome of
the thigh after a femoral fracture.157
Multiple Fractures of Unresolved Etiology
Fulkerson and Ozonoff reported a 10-year-old boy with mul-
tiple symmetric fractures.176 The findings did not indicate OI
or osteomalacia, despite apparent osseous fragility. Elevated
serum pyrophosphate and low urine phosphate contents
FIGURE 11-19. (A) Fracture at a stress riser at the end of
the rod. (B) Complete fracture.
General Injuries
FIGURE 11-20. Telescoping rods. Note the distal
femoral physeal damage, especially on the left. This
damage may be due to the dysplasia, rod insertion, or
continued presence of the rod.
suggested that abnormalities in phosphate metabolism con-
tributed to the formation of bone that was biochemically and
structurally deficient.
Osteosclerotic Disorders
Osteopetrosis and pyknodysostosis are the result of a failure
of bone remodeling processes.178,185 The common cause of
these diseases is impaired function of the osteoclasts, which
leads to excessive accumulation of bone due to insufficient
bone resorption and remodeling. Gell et al. showed that
pyknodysostosis is due to cathepsin K deficiency.181 This
enzyme is a major protease contributing to bone resorption.
Meyerson et al. analyzed fibroblasts and found that impair-
ment of the c-src gene was unlikely.188 Isozymic changes in
liver acid phosphatase and comparable changes in the bone
may explain the physiologic dysfunction.
The congenital form or malignant type of osteopetrosis
is severe and often fatal during early childhood. The benign
form is often not detected until later childhood or adoles-
cence, when the child presents with a pathologic fracture.
The benign form of osteopetrosis has varying severity
(types I and II). In the worst cases the marrow space is com-
pletely obliterated by medullary bone formation. The brittle
bone then develops microfractures and reactive subperi-
osteal bone. Marrow obliteration may lead to anemia and
decreased white blood cell counts, with increased suscepti-
bility to infection.
El-Tawil and Stoker reviewed 42 patients.180 Using the clas-
sification of Bollerslev and Andersen,177 29 patients had type
II disease (banding of metaphyses, rugger jersey spine) and
sustained 18 fractures. Thirteen patients had type I disease,
one of whom sustained a single fracture. Banding is found
only in type II (but not all cases) and does not correlate with
the liability to fracture.
Lack of remodeling in these diseases leads to thickened
trabeculae and cortical bone and to osseous obliteration of
the medullary cavity, creating bone that is termed “brittle”
(Figs. 11-21 to 11-23).189 Fractures are relatively common
(Fig. 11-24) and must be protected for an adequate period
of healing, which may be considerably longer than normal because
of differences in remodeling of callus and patterns of bone
359
formation.177,179,183,187,190,192 Stress fractures are common and
often fortuitous findings during evaluation with a skeletal
survey. There is “resistance to drilling” because of the dense
sclerotic bone.182
Animal models demonstrated delayed fracture callus
remodeling and healing in osteopetrosis.191 This finding has
been corroborated in the clinical situation.182,184,186
Joint Laxity/Dislocation
Multiple joint dislocations are unusual (Fig. 11-25). Bartso-
cas described familial multiple joint dislocation in a mother
and child.193 Larson syndrome manifests as multiple con-
genital dislocations associated with osseous abnormalities
and a characteristic flat facial pattern, with a depressed
nasal bridge and prominent forehead. Other causes
of hypermobility include Ehlers-Danlos syndrome and
homocysteinuria.194–196
Joint “noise,” often described as “popping” or “cracking,”
is a common phenomenon in children, who have greater
range of motion in the joints.197,198 Translocation of the knee
and hip tendons over chondro-osseous prominences may
cause palpable or audible clicking. The tensor fascia lata is
particularly prone to snap over the greater trochanter.
Studies of cracking in the metacarpophalangeal joints sug-
gested that bubbles of previously dissolved gases formed in
the joints. Unsworth et al. showed that the bubble was the
effect, rather than the cause, of the crack, and that fluid cav-
itation was responsible for the cracking sound.198
Studies of the geometry of the metacarpophalangeal joints
demonstrated that the joint surfaces were essentially spheri-
cal; and hydrodynamic equations for such configuration
show that when the joint surfaces are usually closely apposed,
separation may produce large subatmospheric pressures.
Under such pressures the synovial fluid vaporizes, and dis-
solved gas is released from the solution. The collapse of the
vapor cavity gives rise to the noise.
Joint Stiffness
Children with congenital or acquired stiffness of the joints
may be predisposed to fractures. Inability to move a joint
360 11. Fractures in Pediatric Growth Disorders

attaining progressive increase in motion. However, because

the child has usually been non-weight-bearing or only partial-
weight-bearing, the bone becomes porotic, predisposing to
fracture (Fig. 11-26).
The child with arthrogryposis (rigid joints) may sustain
perinatal fractures consequent to a normal delivery.199

FIGURE 11-21. Osteopetrosis. (A) Distal tibia shows dense, scle-

rotic bone in the metaphysis, diaphysis, and epiphysis. A Harris
growth slow-down line (arrow) shows new distal tibial growth occur-
ring after an ipsilateral femoral fracture and prolonged immobiliza-
tion in a cast (with relative osteoporosis of this newly formed bone).
(B) Distal femur with healing stress fracture (white arrow) and
osteoporotic bone in the epiphysis (black arrow).

adequately means the bones are not subjected to model-

ing/remodeling stresses. The bone becomes weak and
porotic. Additionally, aggressive physical therapy is often
employed to diminish the severity of the contractures. Either
event may lead to fracture.200
Arthrogryposis is the most common congenital disorder
predisposing to joint contractures. Manipulation of such
joints is directed first at obtaining lost range and then
B
FIGURE 11-22. (A) Lower extremities of a neonate with the malig-
nant form of osteopetrosis. (B) Traumatic delivery resulted in an
epiphysiolysis of either the proximal or distal humerus with exten-
sive subperiosteal hemorrhage and new bone formation.
General Injuries 361

Another type of “congenital” contracture is the clubfoot,

which may have a genetic or an intrauterine posturing cause.
Rarely, vigorous manipulation during the neonatal period
causes a distal tibial fracture. This is more likely if there are
predisposing problems such as spina bifida.
Nonneurogenic acquired contractures in children are
uncommon. Burns are associated with contractures and
extensive osteoporosis. Manipulation of the tight joints may
cause fracture. Juvenile rheumatoid arthritis may cause joint
stiffening or even ankylosis. Osteoporosis ensues, creating
bone that may be fractured by efforts at physical therapy or
weight-bearing.

Pathologic Fractures
Because of the infrequent occurrence of benign and
malignant tumors, the child’s skeleton is not a common
site of pathologic fracture (Figs. 11-27, 11-28) compared
to the adult skeleton.203,205,206,213,214,217,218,221,222,224,226,229,233,234,238
However, fracture may be the initial presentation of many
primary osseous malignancies,227,237 especially osteogenic
sarcoma of the lower extremity in an active adolescent (Fig.
11-29). The first presenting symptom of a metastatic malig-
nancy (e.g., neuroblastoma) may also be acute skeletal
injury. Treatment must include primary fracture care as well
as further diagnosis and treatment directed at the specific

FIGURE 11-23. (A) Transverse section shows bone in the medullary

cavity, “normal” cortex, and reactive subperiosteal bone. (B)
Physeal damage may occur from microtrauma.

Aggressive physical therapy and splinting may also cause frac-

tures in these children. If angulation occurs, it is sometimes
wise to use it as a means of overcoming severe soft tissue FIGURE 11-24. Stress fracture (asymptomatic) of the tibia in a
contracture. patient with pyknodysostosis.
 362
A sis is a distinct risk.235
B
FIGURE 11-25. Patient in Figure 11-24 also had excessive joint
laxity of the hip. (A) Dislocated. (B) Reduced.
pathologic lesions. Fracture healing may be impaired by radi-
ation therapy, chemotherapy, or other methods of treatment.
Particularly, resection followed by allograft replacement may
be associated with subsequent fracture of the incorporating
graft.204,236
Simple bone cysts are common in the proximal humerus,
distal tibia, proximal tibia, and femoral neck.201,219,239
FIGURE 11-26. Arthrogryposis. (A, B) Manipulation of knee contracture caused proximal tibial injury. (C) Several months later a defor-
mity of the tibial tuberosity is evident.
11. Fractures in Pediatric Growth Disorders
They are usually asymptomatic until an acute, pathologic
fracture develops (Fig. 11-30). Such fractures may be
complete or, more commonly, stress fractures in the thinned
cortical bone. Cysts that are fractured infrequently
heal spontaneously. Enlargement of the cyst and recurrent
fracture are much more likely. These cysts may disappear
slowly following skeletal maturation. So long as they
remain, they represent an actual or potential mechanical
weakness in the bone. The fallen fragment sign is typical of
the cyst.231
Cyst fractures usually are minimally displaced and often
exhibit only small, incomplete cortical fractures. In certain
areas, such as the femoral head, subsequent ischemic necro-
The initial fracture involves the thin cortical bone associ-
ated with the cyst, with subsequent propagation into the
uninvolved cortical bone, which is often incompletely frac-
tured. In some instances the insidious pain that leads to diag-
nosis is due to hairline fractures in the thin bone. At surgery
these incomplete fractures and the thin, compressible (elas-
tically deformable) cortex become evident.
Although infrequent, these cystic defects, which probably
begin adjacent to the physis, can erode the physis and
expand into the epiphysis. This increases the risk of local-
ized growth arrest. Other lesions may cause more profuse
involvement of the juxtaphyseal tissues.
The presence of a cyst does not interfere with the normal
healing of the fracture; and certainly, if one is considering
definitive treatment of a cyst with grafting and curettage, a
sufficient period should elapse to allow adequate fracture
healing. It is not necessary, however, to wait for a second
pathologic fracture through the cyst before attempting
curettage and grafting, particularly if a weight-bearing area
is involved.
Neer et al. found that 80% of all children had one to three
refractures through a cyst (even after surgery), and 10% had
some residual deformities; only 1 of 42 patients did
not undergo surgery eventually.225 Up to 30% required
General Injuries
FIGURE 11-27. Pathologic fracture in a distal femur due to
angiosarcoma. (A) Fracture (curved arrow) with physeal extension
(straight arrow). (B) Slab section radiograph showing pathologic
fracture (curved arrows) with extension to physis (straight arrows).
reoperation because of failure to incorporate the graft totally
or because of resorption of the graft.
Cystic fractures occur more often in weight-bearing bones,
such as the femur or tibia. Deformity is likely to occur, and
curettage and bone grafting are indicated once the diagno-
sis is made and the initial fracture has healed. Internal fixa-
tion may be necessary, especially if the femoral neck is
involved. Primary fracture treatment should be considered
(with internal fixation) for femoral neck and sub-
trochanteric fractures.
A B
FIGURE 11-28. (A) Lytic lesion of distal femur in a patient with chronic leg pain. (B) He tripped and sustained this fracture. (C) Eventual
focal growth arrest.
363
(C) Fracture (solid arrow) with cortical buckling (open arrow).
Cortical erosion (small curved arrows) is also evident. M =
metaphysis; D = diaphysis.
Steroid injection may be beneficial,209 but it should not be
done until a pathologic fracture has healed, as steroids may
adversely affect the callus response necessary for fracture
healing. Others believe the benefits of steroid injection are
limited.215
Nonossifying fibromas commonly involve the tibia and
distal femur.202,207,208,211,212,216,220,228,230,232 They are usually
located eccentrically in the cortex of the metaphysis,
although they may involve the diaphysis. They are generally
not large enough to cause a significant problem, but they
C
364 11. Fractures in Pediatric Growth Disorders

osteoporosis and impaired growth in the region distal to the

pseudarthrosis. Even after successful repair, stress fractures
and complete fractures may occur.

Osteochondroses
Several authors believe that most lesions of the immature
skeleton that are called ischemic (avascular) necrosis and

FIGURE 11-29. Pathologic type 1 physeal fracture (arrow).

may be quite painful if a small cortical fracture occurs.

Nonosteogenic fibromas of the bone seldom present prob-
lems for diagnosis or treatment; but some lesions, by virtue
of their size, predispose the bone to fracture and lead to
confusion in diagnosis. The lesions may take 2–6 years
to become obliterated and may not disappear until skeletal
maturity has occurred. Complete reossification occurs more
rapidly in large lesions treated by bone graft.
McBroom et al. showed that with a drill hole/bone diam-
eter ratio of 0.2, cortical bone retained only 62% of its
expected strength.223 This measurement, in canine femoral
cortical bone, was done to determine if metastatic lesions
that radiologically penetrated the cortex significantly
affected the risk of fracture or—potentially in children with
damage from fibrous cortical defects—infection or tumor. A
lesion that thins the cortex must involve 40–50% before it
becomes radiologically evident.
One of the most common chondro-osseous growths is an
osteochondroma, which may be solitary or multiple. One
pattern of growth is the pedunculated osteochondroma,
which elongates away from the underlying metaphysis. These
lesions are common around the knee and may sustain a frac-
ture (Fig. 11-31A).210 Reactive changes (e.g., cortical defor-
mation) to an apposed osteochondroma may also lead to a
stress fracture (Fig. 11-31B).

Congenital Pseudarthroses
Pseudarthrosis of the tibia (Figs. 11-32, 11-33) has a variable
presentation, ranging from a fracture present at birth or
shortly thereafter to an angular (often cystic) deformity that
eventually fractures.242,243,245,247,256,259,262,264,266 Some patients
have relatively sclerotic tibias that do not fracture until mid-
childhood or even adolescence. Angular and sclerotic defor-
mities of the involved tibia carry the risk of pathologic
fracture. Treatment involves a protective orthosis. Despite
such treatment, however, a fracture may occur in the
abnormally modeled/remodeled bone.261 Other bones (e.g.,
radius or ulna) may be involved.248,254,255,265
Treatment continues to be unpredictable,240,241,252 FIGURE 11-30. Pathologic fracture in a benign cyst. The distance
although, vascularized fibular transplants seem to offer a rea- from the physis is important when considering curettage. (A)
sonable chance for success.244,246,249,250,251,253,257,258,260,263 Surgery Humerus. (B) Tibia. Spiral fracture followed by opacification of the
should be done as early as possible to defray the risk of severe cyst.
Neurologic Disorders
A whole bone but merely affect its chondro-osseous maturation
B to be educated about the susceptibility of osteoporotic bones
FIGURE 11-31. (A) Fracture of the stalk of a pedunculated osteo-
chondroma. (B) Stress fracture in a thinned fibula due to an
adjacent tibial osteochondroma.
osteochondrosis are focal stress fractures and deformities of
the epiphyseal ossification centers.269 Conway (see Chapter
5) has referred to them as elastic deformations of bone.
These lesions are characterized radiographically by focal
compression and repetitive stress of zones of ossification
(chondro-osseous transformation). Many of them pass
through a series of progressive radiographic changes that
include sclerosis, flattening, fibrous replacement of the scle-
rotic bone, and reossification of the fibrous tissue with com-
365
plete healing—but sometimes with severe crippling defor-
mity (as in Legg-Perthes disease).270 These cyclic changes
may recur. The deformity and disability depend on the dura-
tion and degree of continued stress(es) to which the soft
fibrous and cartilaginous parts of the bone were subjected.
The exact cause and mechanisms are not known, although
excessive, repetitive mechanical stress appears to play an
important etiologic role.
The traditional causal hypothesis suggests impairment of
the local arterial blood supply as the primary cause, because
it reduces the flow of essential nutrients and oxygen to the
developing bone. Caffey believes that with coxa plana and
Blount’s disease the deformity and sclerosis follow a frac-
ture.268 Boznan proposed that the primary injury and causal
mechanism might be direct mechanical compression of the
convex edges of the epiphyseal ossification centers and
the round bones.267 This would not immediately damage the
processes. The necrosis that follows is secondary to the orig-
inal compression fractures in cancellous trabeculae.
Neurologic Disorders
The number of children with significant neurologic deficits
is increasing because of the improved survival of those
with myelodysplasia, the increased incidence of spinal cord
injury, and the higher survival rate for patients with
spinal tumors. Fractures due to such disorders involve not
only diaphyseal and metaphyseal bone but also physes.
Failure to recognize the latter may lead to significant growth
deformity. Charcot-like fragmentation and destructive
changes in the physis and metaphysis may lead to diagnostic
errors and unnecessary diagnostic procedures (e.g.,
biopsy).303 Roentgenographically, many of these injuries
resemble osteomyelitis, metabolic bone disease, or
malignancy.273–276,278
Part of the management of fractures in children with
various neuromuscular disorders is their prevention.271,272
Everything possible should be done to encourage periods of
daily standing such as the use of an A-frame, even in those
with no hope of functional walking, early in the treatment
program to try to stimulate some bone remodeling and
strengthening. Parents, patients, and health personnel need
to fracture. They should also be taught to recognize the
signs of fractures in children with sensory deficits, as these
more often mimic an infection than injury (e.g., swelling,
erythema, localized warmth, fever).
These children often undergo reconstructive surgery,
especially at the hip. They must be temporarily immobilized,
which increases the risk of both further disuse osteoporosis
and joint stiffness, factors that increase the risk of subse-
quent fracture (Fig. 11-34).277 Accordingly, postoperative
immobilization should be minimized as much as possible,
and again the children should be placed early in suitable
casts or orthoses to increase stimulation. A hip spica does not
preclude modified standing in an A-frame. If joints are stiff
postoperatively, extra caution should be used by parents and
therapists to prevent inadvertently fracturing through a
porotic metaphysis.
366 11. Fractures in Pediatric Growth Disorders

FIGURE 11-32. Pseudarthrosis of tibia. (A) Initial presentation at 5 months. (B) Fracture while wearing an orthotic device. (C) Progres-
sive deformation. (D) It was eventually treated by a vascularized fibular transposition and allograft of the fibular donor site.

FIGURE 11-33. Posteromedial bowing. (A) Presentation at 7 months. (B) Two years. Treatment with orthosis. (C) Six years. Contoured
orthotic protection. (D, E) At 11 years a stress fracture developed in the abnormal bone.
Neurologic Disorders 367

FIGURE 11-35. (A) Seven-year-old child with myelomeningocele

whose presenting symptoms were fever and a hot, swollen proxi-
mal tibia. A chronic fracture of the proximal tibia and tuberosity is
evident. (B) Such an injury may lead to premature epiphysiodesis.
Charcot-type fractures of the posterior femoral physis and epiph-
ysis are evident.

FIGURE 11-34. Pathologic fracture after cast removal (for hip

surgery).

Susceptibility to fracture also occurs in children with para-

plegia resulting from such causes such as subdural
hematoma, spinal cord injury, avulsion of lumbosacral roots,
transverse myelitis, and cord tumors.279 In children with
atrophic limbs due to poliomyelitis, in whom sensation is
intact, spontaneous fractures are much less frequent.
Absence of active movements in the limbs due to paralysis
enhances the likelihood of bone atrophy, and the prevention
of passive movements caused by brace treatments may
enhance atrophy even further. Fractures occur in atrophic
bone much more frequently when the limbs are also
deprived of sensation, probably because strains applied to
legs are not protectively restricted when normal sensation is
absent.

Myelodysplasia
The increased emphasis on mobility for children with
myelodysplasia produces a greater incidence of injury to
their poorly innervated lower extremities. Fractures in these
children follow no definite pattern, may occur in unusual
sites, and are difficult to diagnose.279–318 They may occur
during ambulation with protective orthoses. There is a pre-
disposition toward metaphyseal and physeal fractures, espe-
cially at the knee joint (Figs. 11-35, 11-36). FIGURE 11-36. (A) Manipulation of a clubfoot in a patient with
Norton and Foley described 43 fractures in 48 patients myelomeningocele caused disruption of the distal tibia. (B) Several
with spina bifida.306 Quilis reviewed 130 children with weeks later callus extends proximally. There is also a fracture of
myelodysplasia and found 15 children had sustained a total the proximal physis.
368
of 55 fractures.310 Only three of the children sustained one
fracture; the remaining sustained multiple fractures, includ-
ing one child who had 12. Of the injuries, 62% occurred
around the knee joint. Callus formation was described as
excessive in 19, moderate in 23, and minimal in 10. Inter-
estingly, although 50% of the fractures occurred in children
paralyzed below the L2 or L3 level, 16 of the 19 fractures that
healed with excessive callus formation were in this group.
Excessive callus formation may lead to significant complica-
tions such as further limitation of joint motion.115,123,126
Thirty of the fractures occurred during limb manipulation
during therapy, intraoperatively, or postoperatively following
removal of the immobilization casts.
Drennan and Freehafer reported that 25 of 84 patients
sustained at least one fracture of the lower extremity, for a
total of 58 fractures.284 These fractures occurred in patients
with levels of paralysis ranging from T8 to L3; four patients
with a T8 level incurred a total of 24 fractures. Handlesman
found that 11 of 77 children developed spontaneous frac-
tures of the lower limbs that were usually multiple and recur-
rent.294 In 17 additional patients, cast immobilization after
surgery, particularly around the hip, was followed by juxta-
epiphyseal fractures, usually at the level of the knee. Of the
34 fractures, 32 healed rapidly, usually with exuberant callus,
which was indicative of the excess motion allowed by the lack
of painful response. Fractures involving the neck of the
femur may require subtrochanteric osteotomy for increasing
coxa vara.
Pfeil et al. reviewed 947 children with myelodysplasia.290,309
In 82 of these children there were 224 osseous lesions. Me-
taphyseal and diaphyseal lesions were more numerous than
epiphyseal lesions. Most of the latter were epiphysiolyses
(type 1 injuries).
Boytim et al. reviewed six neonates with fractures.281 They
found that neonates with thoracic or high lumbar neurologic
levels had a 17% chance of sustaining fracture during
delivery.
Lock and Aronson reviewed 37 of 186 children (20%) with
myelomeningocele who had a total of 76 fractures.302 The fre-
quency of fractures was related to the neurologic level: 13
(45%) at the thoracic level, 15 (46%) at the upper lumbar
level, 8 (10%) at the lower lumbar level, and 1 (3%) at the
sacral level. Sixty-five (86%) of the fractures occurred before
the child was 9 years old. Altogether 58 (76%) occurred after
the limb was in a cast, and 74 (97%) involved the lower limbs.
Eleven patients (all thoracic or upper lumbar levels) sus-
tained multiple fractures. All fractures were distal to the level
of neurologic involvement. Femoral fractures prevailed in
the thoracic level, whereas tibial fractures were more
common in the lumbar level. All metaphyseal and diaphy-
seal fractures healed satisfactorily with cast or bulky dressing.
The seven physeal fractures had delayed union in three and
premature growth arrest in two.
Diagnosis is frequently delayed in these patients. The
sensory deficit with myelodysplasia makes the history of
injury of doubtful value to the diagnosis. Many patients or
parents cannot specify the incident that may have caused the
fracture. The symptoms, which are usually a fever and a
swollen, erythematous limb, are similar to those seen in
acute osteomyelitis. In the absence of pain, a fracture may
be overlooked unless a roentgenogram is obtained. Any
11. Fractures in Pediatric Growth Disorders
child with myelodysplasia who has a fever should be evalu-
ated for occult fracture as part of the diagnostic workup. The
white blood cell count and erythrocyte sedimentation rate
may be elevated, although the likelihood of concurrent
urinary tract infection may make these findings of limited
value.
Treatment of fractures in patients with sensory deficits
is difficult. Eichenholtz condemned circular casts, skeletal
and skin traction, and open reductions.288 Instead, he
recommended simple, well-padded plaster shells. This is
an oversimplification. Unfortunately, the immobilization
itself may predispose the myelodysplastic patient to further
spontaneous fractures elsewhere. Lack of adequate immo-
bilization may be associated with excessive callus (Fig.
11-37).
Treatment is aimed at keeping the child as active as pos-
sible. Overriding and displacement are rarely problems
because of the flaccid paralysis, although the child who has
contractures may accentuate angulation. Alignment and
rotation must be maintained as nearly normal as possible.
Because of the sensory neuropathy bulky cotton dressings
and splints are used to limit motion in these children. It
minimizes the problem of cast pressure points. Because
many of these children are in braces as part of the treatment
program, they can be taken out of a relatively rigid, padded
dressing early and placed in their orthotics for the duration
of fracture healing.
Fractures in children with myelodysplasia usually heal
rapidly when the metaphysis or diaphysis is involved.295
Physeal injuries may show delayed healing and excessive jux-
taphyseal widening, and they may proceed to nonunion or
premature closure (Fig. 11-38). The juxtaphyseal widening
may be due to a number of factors. The chronic, continued
micro/macro motion may cause formation of fibrous and
excessive inflammatory tissue. This delays or prevents
normal extension of the metaphyseal vessels toward the
hypertrophic zone of the physis. Concomitantly, the physis
continues to grow, leading to an increase in the thickness of
the hypertrophic zone, which is not invaded by the me-
taphyseal vessels. Stabilization allows gradual restitution of
the vascular supply to the radiolucent gap, and reformation
of the vascular loops of the hypertrophic zone. The widened
hypertrophic zone is appropriately calcified, such that rapid
chondro-osseous transformation occurs and restores a
normal physeal thickness. Microscopic longitudinal disrup-
tion toward the germinal zone may, however, cause focal
physeal damage and contribute to growth potential damage
and premature growth arrest.
Damage to the growth plates of the lower extremities may
result in a lesion characterized by “broadening and loosen-
ing” of the physis (Fig. 11-38). Edvardsen described these
epiphyseal lesions in 6 of 50 patients and advocated an
annual examination of weight-bearing physes until the
physes have fused.287 In one case this situation proceeded to
a well-established pseudarthrosis.
Prospective examination is of major importance, as both
the growth rate and the configuration of the involved bones
affect shortening and deformity. These physeal injuries, if
not properly recognized and treated, may exhibit delayed
healing. Treatment must include adequate immobilization
and avoidance of weight-bearing until there is clinical and
Neurologic Disorders
B
FIGURE 11-37. (A) Early excessive callus from continued motion
(no immobilization). (B) Exuberant callus due to motion.
roentgenographic evidence of healing. Immobilization in a
brace, as recommended for diaphyseal fractures, is not
appropriate for physeal separations until there is evidence of
sufficient healing and a normal radiolucent width.
369
Fractures occurring in patients with myelodysplasia may
lead to significant complications. Leg length discrepancy,
bowing, angulation, and rotational deformities have been
described; but nonunion is rare. Joint destruction due to a
Charcot orthopathy may occur by the end of skeletal growth.
Skin necrosis may also result from the use of skin traction.
Skeletal traction may be associated with a high incidence of
pin tract infection and poor fixation in atrophic bone. Pres-
sure sores may increase in frequency.
The prevention of conditions that predispose bones to
fractures assumes paramount importance. Vigorous passive
stretching of contractures is applicable in these children. As
dysfunctional as it may be, the continuous muscle activity of
B
FIGURE 11-38. (A) Widening (pseudarthrosis) of the physis in a boy
who presented with a fever and a red, swollen knee. Note the
physeal widening in the proximal tibia. (B) Further osteoporosis of
the physeal region despite treatment in a cast. Also note the exten-
sive subperiosteal new bone.
370
active exercise and ambulation may be the best protection
against disuse-related osteoporosis. Katz found that fractures
are less likely to occur in myelodysplastic patients if the
patients are actively ambulating in braces.297
Because of the preponderance of fractures around the
knee and ankle joints in young patients with impaired sen-
sation, a great potential exists for the development of
Charcot-type joints. As advances in the care of these children
allow more of them to live to adulthood, the development
of significant joint deformity and dysfunction becomes a sig-
nificant problem.
Spinal Cord Injury
Spinal cord injury may result from obstetric trauma. One
instance of spinal cord injury was recorded in a review of
15,000 infants delivered at the University of Pennsylvania
Hospital.325 However, such injuries often escape diagnosis.
There is evidence that some children with a diagnosis of
cerebral palsy may have actually sustained spinal cord injury
during birth.332,336,338
There was a high incidence of vertebral artery damage and
significant epidural hemorrhage in neonates in whom the
spinal cord was examined during autopsy.338 Most reported
cases of spinal injury have occurred during breech delivery,
when traction was applied to the trunk while the head was
manipulated. Cesarean section delivery has been suggested
for infants shown radiographically to be in a hyperextended
(“star-gazing”) breech position.
Lateral traction on the head increases tension on the cord
at its junction with the brachial plexus and may result in avul-
sion of the cervical roots. Hyperextension, with traction
applied to the legs and with the head held firmly by uterine
contraction, may result in rupture of the cords and
meninges. The cartilaginous spine of the infant may be
grossly distorted, but it does not usually disrupt completely
because of its relative elasticity. Generally, the damage
extends over several spinal segments. The infant is noted at
birth to be hyponotic with depressed respirations. Prompt
resuscitative measures are followed by the appearance of
reflex movement to stimulation, which may lead to the diag-
nosis of primary muscle disease (myotonia).
It should be noted that the spinal shock seen in adult
patients after severe cord trauma is not usually present in the
infant, and recovery of reflex function follows a time course
similar to that of recovery of movement after any resuscita-
tive procedure in the newborn. Continued flaccidity is prob-
ably due to destruction of the cord over many segments, as
a result of either intramedullary hemorrhage or infarction.
Minor degrees of cord damage may account for some of
the spastic conditions now grouped with cerebral palsies.
Secondary injuries to the cerebral cortex may result from
hypoxia caused by the transient respiratory depression that
is associated with reversible, undiagnosed neonatal cord
injury. The true contribution of neonatal traumatic myelopa-
thy to the broad group of neurologic diseases associated with
birth injuries remains to be defined.
Denervation through spinal cord injury affects the rate
of susceptibility to fracture healing and chronically
affects the skeleton so it is predisposed to other frac-
11. Fractures in Pediatric Growth Disorders
tures.319,321–326 Similarly, the joints may incur chronic neuro-
pathic damage.320
A comprehensive approach to the child and adolescent
with spinal cord and spinal injuries is found in Chapter 18.
Poliomyelitis
Although acute poliomyelitis may be disappearing in certain
areas, it is still reasonably prevalent in much of the world,
and many of these children come under an orthopaedist’s
care. Robin reported 62 fractures in children under the age
of 16 who had residual paralysis following polio.327 Two-
thirds of the fractures occurred while the children were inpa-
tients, and one-third happened while they were outpatients.
Only five fractures were in the contralateral, normal limbs.
The remaining 57 occurred in severely paralyzed limbs and
most commonly involved the femur (32 fractures, with 29 in
the supracondylar region), the tibia (18 fractures), and the
humerus (7 fractures). Most were impaction types with little
displacement. There were no physeal fracture types with
little displacement.
The most common causal pattern was antecedent cast
immobilization or some other corrective procedure, such as
osteotomy, with subsequent immobilization. Of the 29 supra-
condylar femoral fractures, 17 involved patients with preex-
isting limitation of movement of the knee joint or
contracture of the joint. Thirteen of the limbs had just been
removed from cast immobilization for 6 weeks or less before
the fracture occurred.
In view of the connection between joint stiffness and frac-
ture, it is important that remobilization of the stiff joint be
carried out as the first stage of rehabilitation following
surgery, especially in the lower limb.328 Until the knee joint
is freely mobile, the patient should not be allowed complete
freedom of activity.
Treatment of these fractures should be directed at rapid
functional restoration and at early use of protective braces
when they are already available. Manipulative reduction is
rarely needed because of the compressive nature of most of
the fractures. There is no significant delay in the rate of frac-
ture healing.
Cerebral Palsy
Fractures in children with spastic cerebral palsy are uncom-
mon.333 The constant stimulation of hyperactive muscle
results in relatively strong bone that has minimal evidence
of osteoporosis and intrinsic susceptibility to fracture,
unlike the previously discussed neuromuscular disorders.331
However, less common types of cerebral palsy, especially
flaccid palsy, may have an increased incidence of functional
osteoporosis and be predisposed to obvious or occult
fractures when ambulated.334,335 Furthermore, if patients
have been immobilized following surgery, particularly
after tendon-lengthening and transfer procedures, they
may develop immobilization osteoporosis. More severe forms
of cerebral palsy, particularly those associated with convul-
sions and severe spasticity, as well as severely involved patients
who are confined to bed and are relatively undernour-
ished, may sustain fractures. An overly aggressive therapy
Neurologic Disorders
program also may cause fractures when trying to overcome
joint contractures.
McIvor and Samilson reviewed fractures in 57 cerebral
palsy patients. Invariably the patients sustained closed frac-
tures, with the exception of one open fracture.333 There was
no definitive correlation between the type of cerebral palsy
and the incidence or location of the fracture.
The major causes of fractures appeared to be a fall or
direct blow (such as striking the side of the bed during a
seizure). Only five fractures followed orthopaedic proce-
dures. The more severe the disease involvement, the greater
was the number of fractures. A contracture or paralytic hip
dislocation predisposes to femoral fracture, and knee con-
tractures predispose to distal femoral and proximal tibial
fractures.
Brunner and Doderlein reviewed 37 patients with 54 frac-
tures without significant trauma.329 The major causes were
long and fragile lever arms and stiffness in major joints. An
additional factor was osteoporosis following a long period of
postoperative immobilization. Seventy-four percent of the
fractures involved the femoral shaft and supracondylar
region. Stress fractures were rare (7%) and involved only the
patella.
Henderson et al. reviewed 43 patients with spastic quadri-
plegia (mean age 7.9 years) who underwent bone mineral
density (BMD) studies.331 Baseline measurements showed
that the BMD fell further behind normal with increasing age
and was more than 1 SD below the age-matched normal
mean in 38 of 43 patients. The fracture rate did not differ
between those with low and very low spinal BMD. However,
the fracture rate was fourfold greater following spica casting
and more than threefold greater following an initial fracture.
Fracture rates in the study group were similar to those
reported for age- and sex-matched normal children, though
FIGURE 11-39. Nonunion of a fracture in a patient with
severe spastic quadriplegia. (A) Five months after
injury. (B) One year after injury. A B
371
generally the location of the fractures and mechanisms
of injury differed. Other factors in the susceptible quadri-
plegic include limited sunlight exposure, inadequate
caloric, protein, and calcium intake, and anticonvulsant
medications.
Most fractures in patients with cerebral palsy can be
treated with casts or splints. The type of cast immobilization
must be modified according to coexisting joint contractures.
Contiguous joints, wherever possible, should be included in
the cast, although severe contractures of these joints may
prevent more adequate immobilization.
Nonunion is rare (Fig. 11-39), except when the distal
patella is involved (see Chapter 22). Malunion is infrequent,
usually relating to a preexistent contracture and usually
occurring in severely spastic patients. Malunion is particu-
larly a problem with femoral fractures but may also occur in
the humerus. The malunions never compensate for the joint
contractures. Remodeling in children under 10 years of age
is usually comparable to that in neurologically normal chil-
dren. Significant growth disturbances are uncommon, and
physeal injuries are rare.
Refracture was encountered primarily in bedridden
patients with severe deformities, and osteoporosis (disuse)
was usually followed by malunion. Factors predisposing to
refracture appear to be contractures, inadequate mainte-
nance of reduction, and disuse-related osteopenia of bedrid-
den patients.
Progressive subluxation of the proximal femur or radius
may eventually result in complete dislocation, especially
during the adolescent growth spurt.337
The crouch-knee gait and chronic knee flexion cause sig-
nificant increases in joint reaction forces in the knee, which
in turn may cause tensile failure in both the patella and the
tibial tuberosity. The patella may incur slow plastic defor-
372
mation leading to an elongated patella; or a piece of the
chondro-osseous interface may pull away, leading to an
accessory patellar ossicle (Fig. 11-40). The increased patellar
tendon tension may cause tensile-induced modifications of
the tuberosity growth region (Fig. 11-41).
In a study of Rett syndrome there were no fractures in 9
patients. However, all were ambulatory.330
B because growth stimulation from normal muscular activity
FIGURE 11-40. (A) Patellar deformity due to an antecedent sleeve
fracture. (B) Patellar elongation consequent to long-term crouch-
knee gait. Partial avulsion of the patellar tendon attachment is
evident as an Osgood-Schlatter’s ossicle (arrow).
11. Fractures in Pediatric Growth Disorders
B
FIGURE 11-41. Chronic stress effect in the tibial tuberosity. (A)
Initial appearance during evaluation of tuberosity pain. (B) Six
months later.
Muscular Dystrophy
Many of the progressive muscular dystrophies that com-
mence during childhood lead to osteoporosis in the
metaphyseal and diaphyseal cortices and in the metaphyseal
and epiphyseal trabecular bone.345 This osteoporosis leads
to increased tubulation of the bone and occurs primarily
is deficient.339,349 Disease progression and weakness may
be severe enough to cause frequent falling and worsening
of contractures by the time the child is 9–10 years old
and to wheelchair confinement by adolescence.346 Fractures
Neurologic Disorders
occur readily in porotic bones that lack protective muscle
bulk.340,341 Fractures may be sustained by a fall even while
in braces.347 Usually fractures are minimally displaced and
less painful than they are for the nondystrophic patient
because little muscle spasm accompanies the break. Healing
appears to be unimpaired by muscular dystrophy. Because
these children lose strength rapidly when confined to bed,
ambulatory treatment of fractures is used whenever
possible.342–344,348
Patients with spinal muscular atrophy (Werdnig-Hoffman
disease) may have birth fractures resulting from osteoporo-
sis in utero. This condition could be erroneously diagnosed
as osteogenesis imperfecta.
Head Injury
Partial maintenance of the position of a reduced fracture by
the stabilizing action of the muscles with constant, normal
tone is well recognized. If muscle tone is increased abnor-
mally, a fracture may be easily displaced or angulated. Trac-
tion may increase muscle tone abnormally by overactivating
the stretch reflexes, with greater displacement and angula-
tion. These factors must be considered during conservative
treatment of fractures of long bones, as decerebrate postur-
ing results in full extension of the hips and knees and plantar
flexion of the ankles. The arms may be extended or flexed,
but they are held firmly in either position. The fluctuation
in the level of consciousness determines the severity of the
brain stem injury.
After a head injury, if consciousness is not lost or is
regained rapidly, a serious injury to the brain stem has prob-
ably not occurred. The importance of this observation is that
the original resistance present on testing joint movement in
the patient is not followed by permanent decerebrate rigid-
ity, and the fractures may be treated temporarily by conser-
vative methods, provided the increased muscle tone is not
displacing the fracture significantly.
Children with a head injury have a propensity to form
excessive callus around shaft fractures.354,356,358 There does
not appear to be any delay in fracture healing.357 Heterotopic
bone around joints may also occur.353
Several factors must be considered when managing these
patients: (1) The ultimate recovery potential of the head
injury victim cannot be predicted accurately, particularly in
the acute state and in children, who seem to have a remark-
able capacity for recovery.350 The orthopaedist must proceed
with effective treatment as if full neurologic recovery is going
to occur. If the fractures of a patient with head injury are
only minimally treated, the child may recover almost com-
pletely and exhibit severe deformities that should have been
prevented. (2) Anesthesia in head-injured patients poses spe-
cific problems and may be delayed for a few hours to days to
establish baseline neurologic levels before proceeding with
the surgical treatment of severe or open fractures. (3)
Nursing and respiratory management of unconscious or
uncooperative patients is often greatly improved by internal
or external fixation of the fractures.351,352,355,359 If the patient
falls into either category, appropriate fixation, using
methods that do not affect longitudinal bone growth, may
be indicated. A compression plate for a femoral fracture is
much preferred to a medullary rod that must be placed
373
through the proximal femoral growth plate (intraepiphyseal
region).
Epilepsy
Children with epilepsy are at risk for fractures for two major
reasons. First, during an intense seizure there is a possibility
of sufficient muscular spasm and jerking to cause frac-
ture.361,363 Such injuries may be obvious, but subtle injury
(e.g., plastic deformation, bone bruising) may also occur.
Second, the various medications necessary for chronic
control of seizure activity may alter calcium metabolism,
including a relative or actual osteoporosis/osteomalacia that
enhances the risk of fracture.360,362
Nilsson et al. reviewed 155 institutionalized epileptics.
Sixteen (10%) sustained fractures during a 1-year period.362
Serum and urinary calcium values were below the average
for the general population. Elevated levels of alkaline phos-
phatase and parathyroid hormone were also found. Bone
biopsies revealed a significantly increased amount of osteoid
and increased osteoclastic resorptive activity.
Nerve Root Injury
Brachial plexus injury is the most common injury affecting
spinal or peripheral nerves (see Chapter 13). However, spe-
cific peripheral injuries may involve individual nerves and
other areas, such as the lumbosacral plexus, owing to extrem-
ity or lower spinal fractures. The nerve injury predisposes
the bone to injury through a combination of sensory neu-
ropathy and osteoporosis (Fig. 11-42).
Congenital Sensory Neuropathy
Several syndromes are associated with congenital insensitiv-
ity to pain in patients with otherwise normal muscle
tone.364–387 These disorders may be classified on the basis
of genetic patterns and age of onset of the various disorders
of sensory deficit. They include the conditions denoted
as the hereditary or sensory neuropathies and familial
dysautonomia. In particular, children with congenital
sensory neuropathy have insensate joints.365–367,371–387 Pro-
gressive destruction of the articular surface is common (Fig.
11-43). Epiphyseal fractures are also relatively common and
may lead to chronic epiphysiolysis, physeal damage, and
premature physeal closure (Fig. 11-44). Severe, mutilating
deformity of the hands and feet, often accompanied by
osteomyelitis or neuropathic osteopathy, may occur in con-
ditions with impaired perception of pain.368
Evidence of previous injuries is often found in the form of
old fractures that are frequently malaligned. The osseous
shafts may be widened considerably as a result of remodel-
ing of large subperiosteal hematomas. Recent fractures are
often oriented transversely through the metaphyses. This
type of fracture seems to be more common than a fracture
through the adjacent growth plate, although the latter may
occur. Severe epiphyseal damage may lead to premature
fusion of the growth plate. The extensive periosteal tearing
may result in enlarged periosteal hematomas, which may be
visible in the acute state because of their contrast with the
374
FIGURE 11-42. (A) Multiple fractures following a sciatic nerve injury. (B) Later fracture of proximal tibia while in a protective orthotic
device. (C) Tibia valga following the fracture shown in (B).
fatty infiltration of the muscles; a few weeks later ossification
allows a definitive diagnosis.
Neuropathic joint changes take the form of fragmentation
of the articular surfaces (Fig. 11-45), often with synovial
hypertrophy and reactive sclerosis. These changes are similar
to those seen in adults, but a finding peculiar to children is
that of growth plate widening with metaphyseal fragmenta-
tion and sclerosis caused by repetitive growth plate disrup-
tion and reactive changes.
Derwin et al. found an absence of substance P in biopsies
of various tissues within the knee during open reduction with
internal fixation of a patellar fracture.369 They thought the
absence provided evidence that this neuropeptide is impor-
tant in nocioceptive innervation of dysarthroidal joints.
11. Fractures in Pediatric Growth Disorders
Hematologic Disorders
Coagulation Disorders
Hemophilia refers to deficiencies of factor VIII and IX.
Patients with a severe deficiency of factor VIII or IX (less
than 5% of the normal amount) have spontaneous bleeding
episodes and usually come to medical attention during
infancy. Patients with moderate deficiencies (10–20% of the
normal amount) may come to medical attention because of
unusual bleeding after relatively mild trauma. Mild defi-
ciencies (20–50% of the normal amount) or deficiencies of
another of the clotting factors are generally associated with
few significant bleeding problems in daily life but may cause
Hematologic Disorders
FIGURE 11-43. Loss of joint space and fragmentation of the distal
femoral ossification center in a 13-year-old with a sensory
neuropathy.
bleeding complications following dental extractions, trauma,
or surgery.
Fracture treatment of patients with congenital disorders of
blood coagulation has become easier for three fundamental
reasons: (1) ease and specificity of diagnosis, which have
been facilitated by an increased understanding of the coag-
ulation mechanism and improved laboratory methods for
making a specific diagnosis of the disorders; (2) greater avail-
ability of concentrated clotting materials and experience in
the medical management of patients with clotting disorders;
and (3) a longer life expectancy, which has led to an
increased probability of traumatic injuries in those having
bleeding disorders.391,394,397
Many hemophiliacs, because of the current intensive
replacement programs, do not suffer major problems of
musculoskeletal deformity. Children with moderate or
severe hemophilia may be more susceptible to fracture
because of limited joint movement, poor muscular function,
and associated osteoporosis. Every effort should be made to
maintain joint range of motion and promote isotonic and
isometric exercises.398,392 Those who develop inhibitors,
which lead to poorly controlled muscular and joint bleeds
and contractures, also may be predisposed to fracture.
Recurrent bleeding in a child who has an inhibitor increases
the immobilization necessary to treat acute bleeds, which
leads to osteoporosis. More significant in these children is
bleeding into the forearm or lower leg compartments to
create Volkmann’s contractures.393
Table 11-1 summarizes the requirements for the ongoing
treatment of fractures in patients with hematologic disor-
ders. Inhibitor screening tests are mandatory. The presence
of an inhibitor necessitates a modified approach to fracture
treatment. When treatment would be improved considerably
by the use of factor replacement and an inhibitor is present,
several therapeutic options are available, including the use
of high-dose factor concentrates, exchange transfusion, or
375
FIGURE 11-44. Severe hip disruption in a patient with sensory neu-
ropathy. A large pseudoacetabulum had developed (arrows).
experimental concentrates containing activated clotting
factors.388,390,395
Use of the antifibrinolytic agent e-aminocaproic acid
(EACA) has been recommended as an alternative in patients
undergoing active treatment for acute fractures. The use
of EACA is contraindicated in patients for whom adequate
replacement therapy is available.395 The clots formed
by EACA on the fibrinogen strands may not lyse for 6
months and thus can cause considerable fibrosis, particularly
during bleeds that complicate fractures around and within
joints.
The proper dosage of specific replacement products must
be based on a variety of factors, including the nature and
severity of the bleeding defect, the patient’s weight, and the
biologic half-life of the infused factor (Table 11-2). The
orthopaedic surgeon should work closely with the hematol-
ogist to see that appropriate replacement product and levels
are given. Careful monitoring of the patient is mandatory,
particularly to detect the gradual buildup of an inhibitor that
might affect the level of coagulation attained.
The goal of hematologic management of a fracture during
the initial 3- to 4-week period, until the child has reached
the remodeling phase, is to maintain sufficient clotting
factor levels for a sufficient time to forestall bleeding com-
plications. In general, the regimen outlined in Table 11-2 has
proved efficacious. The distinction between major and
minor fractures is fallacious in patients with a clotting
disease, as a seemingly minor fracture (e.g., one involving a
metacarpal) may lead to severe bleeding and, potentially, to
the loss of a hand or digit if too large a bleed occurs within
a closed space. Hemostatic factors must be maintained at
high levels for at least 5 days when the injured areas are
immobilized. The degree of replacement may be tapered
376
A B
C
FIGURE 11-45. (A) This teenager with sensory neuropathy essen-
tially ground the talus into multiple fragments. Because of severe
ulceration and chronic infection he underwent a below-knee ampu-
tation. (B) Radiograph of the distal tibia and fibula. The fibula had
an epiphysiodesis as a consequence of an untreated injury (prob-
ably a type 4 physeal fracture). (C) Histologic section of the distal
TABLE 11-1. Requirements for Fracture Treatment (Closed and
Open) in Hemophilia
Adequate, readily available replacement material (factors)
Survival studies of factor in patient
Inhibitor screening
Pretreatment evaluation of hemoglobin, hematocrit, reticulocyte
count, haptoglobins
Capacity to do assays
Blood bank facilities
Willingness to deal with acquired immunodeficiency syndrome
(AIDS) risk in these patients
11. Fractures in Pediatric Growth Disorders
D
tibia and fibula. (D) Fibrillated distal tibial articular surface. The car-
tilage cells, in response to the pathologically increased joint reac-
tion forces, have formed rounded cell clusters. Interestingly, the
tibial growth plate, approximately 1 cm away, showed no abnormal
histology.
TABLE 11-2. Therapeutic Guidelines
Raise the plasma clotting factor level to 100% at the time of
fracture for 48 hours.
Maintain plasma clotting factor level at more than 60% for 1 week.
Then maintain plasma clotting factor level at more than 40%
until subperiosteal new bone is evident (3–4 weeks).
Increase the level to 100% for 3 days during acute mobilization.
Decrease to 40% for 1 week.
Monitor plasma clotting factor levels with daily assays, when
feasible, during the first 7–10 days, when the fracture is most
unstable and most likely to bleed.
Hematologic Disorders
during subsequent healing until rehabilitation and mobi-
lization are started, at which time sufficiently high factor
levels must again be achieved.
When planning treatment it is important to consider the
lowest level to which the patient’s clotting factor can fall
between transfusions, because recurrence of bleeding is
determined by this level. Certain damaged tissues may
require higher clotting factor concentrations than others. In
general, the more extensive the injury, the higher is the con-
centration required. Second, transfusion should be contin-
ued at least for the shortest time necessary for the healing
of a particular injury because there is always considerable
risk of recurrent bleeding during this period.
Finally, the importance of immobilizing of the fracture
must be emphasized, as even slight movement in children
with clotting disorders may cause a recurrence of bleeding.
Even maneuvers such as changing a cast may have to be
accompanied by infusion of the appropriate replacement
factor. Soft tissues may bleed enough to produce compres-
sion of nerves and vessels with consequent neuropraxia or
ischemia. Peripheral gangrene and Volkmann’s ischemia
have been observed in these patients.
No fracture or soft tissue injury in the limb of the hemo-
philiac should be immobilized in a circumferential cast
unless hemostasis is absolute and swelling is subsiding. Any
cast applied during the first 24 hours should be adequately
padded and completely split after application. Fracture
healing in hemophiliacs is not delayed, even in patients who
have not received treatment with coagulation factors.
Because most patients in major hemophiliac programs are
on transfusion regimens, fracture treatment does not neces-
sarily require hospitalization. However, if bleeding is exces-
sive, it may be wise to hospitalize the child for observation.
This is particularly important if the patient has an inhibitor.
The patient must be kept in protected immobilization and
elevation and under close observation for evidence of neu-
rovascular compromise and the need to consider other
methods of hemostasis.
An important finding is the relative lack of subperiosteal
callus, which suggests that fracture healing in these cases is
largely endosteal. Because healing does follow this pattern,
FIGURE 11-46. Thalassemia. (A) Mild osseous bridging (arrow) in
the left distal radius. (B) More severe bridging (arrow) and relative
growth retardation in the right distal radius. (C) Posterior bridge for-
377
care should be taken during the postfracture mobilization
period. When fractures of certain bones, such as the femur,
are treated by rigid compression, which emphasizes
endosteal repair rather than periosteal repair, the incidence
of refracture after removal of the hardware increases, imply-
ing that a longer period of immobilization may be necessary
for remodeling adequate to support the weight and activity
of the child.
The orthopaedist must maintain awareness of the likeli-
hood that a hemophiliac has human immunodeficiency virus
(HIV) infection from antecedent blood and factor replace-
ment.396 As of January 1988 there were 463 cases of acquired
immunodeficiency syndrome (AIDS) in patients with hemo-
philia.396 These numbers have undoubtedly increased in a
population of 15,000–18,000 hemophiliacs.
Thalassemia
Thalassemia is a genetically determined hemoglobinopathy
characterized by an abnormal hemoglobin that leads to
severe hemolytic anemia. The anemia and the secondary
hemochromatosis affect most organ systems, including the
developing chondro-osseous skeleton. Many patients have
hypoparathyroidism and hypothyroidism with delayed sexual
maturation. This combination affects the developing skele-
ton and its biomechanical response to stress.412
The skeletal changes basically reflect compensatory hyper-
activity and hypertrophy of the bone marrow manifested
by osteoporosis, widened medullary spaces, thinning of the
intratrabecular cortices, and thinning of the diaphyseal and
metaphyseal cortices with coarse reticulations.399–401,403,410,411,
419,420
In a rapidly growing skeleton these alterations may be
particularly prominent in the metaphysis, especially in the
juxtaphyseal area, where they may lead to osseous bridging
that may not become evident until the adolescent growth
spurt (Fig. 11-46). These profound skeletal changes may also
be caused by impaired ossification, a result of faulty protein
metabolism.411
Another common roentgenographic finding is abnormal
modeling of the bones. The reported skeletal manifestations
include delayed skeletal maturation and premature fusion of
mation in the proximal tibia (arrow). None of these bridges was
associated with significant antecedent trauma.
378
the epiphyses of long bones. In one study, 11 of 79 patients,
all of whom were older than 10 years, showed premature
fusion, most often involving the proximal humerus and
distal femur.404 The presence of fusion did not relate to
either the severity of the disease or the number of transfu-
sions. Although the cause of the disturbance of growth is not
yet understood, antecedent trauma, infection, or pathologic
microfractures are obvious possibilities, with the last being
most likely. The incidence of these complications is decreas-
ing with improved medical therapy.
Major fractures rarely occur because of the inactivity that
characterizes many of these children. Some studies, however,
suggest the osteoporotic bones in patients with Cooley’s
anemia have a significant predisposition to pathologic frac-
tures or microscopic stress fractures.407,408 Although data on
healing times are lacking, healing may be slow in these
patients and permanent deformities are frequent.409
Michelson and Cohen found that over a 5-year period
there were eight fractures in 38 patients (with thalassemia),
which yields an incidence that is 70% higher than the
expected rate in the general population. The iron overload
common in thalassemia may deplete the body of vitamin C,
which may retard fracture healing.414
In an extensive study of fractures in 75 patients with
homozygous b-thalassemia, 25 had one or more fractures,
and 7 had evidence of premature fusion of an epiphysis of
one of the long bones.405 A total of 47 fractures were noted
in these 25 patients. Ten patients had more than one frac-
ture, and one patient had experienced nine separate frac-
tures. Most of the fractures occurred in the lower extremity.
A permanent deformity had occurred by the time of diag-
nosis in all but two patients. These results indicated that
these patients often sustain multiple fractures that frequently
heal with resulting deformities. These patients now live
longer because of the more adequate transfusion and other
medical therapies. These therapies, particularly when they
are started early, allow subtle growth plate damage to mani-
fest as shortening or angular deformity during adolescence.
Orzincolo et al. reviewed 12 patients with thalassemia who
had an intensive transfusion regimen with continuous iron
chelation therapy.416 Radiographic abnormalities resembled
those of rickets or scurvy and were associated with growth
retardation. The toxic effect of desferrioxamine was thought
to be a factor.
Refractures are common and often result from minimal
trauma. The high frequency of fracture undoubtedly is a
consequence of the severe osteoporosis that commonly
accompanies the marked erythroid hyperplasia of the
marrow. Normal bone metabolism is dependent on normal
endocrine function and protein metabolism, and
thalassemic patients often have demonstrated deficiencies in
these areas. Possible abnormal thyroid function, impaired
parathyroid and gonadotropic hormone function as a
result of pituitary dysfunction, and hemochromotasis of the
affected end-organs secondary to the thalassemia have
been reported as major causes of the concomitant skeletal
disorders. Protein hypermetabolism and increased catabo-
lism, as evidenced by the increase in urinary excretion of
hydroxyproline in these patients, interfere with normal
chondro-osseous protein metabolism.411 This interference
11. Fractures in Pediatric Growth Disorders
may well contribute to the deficient ossification seen in the
disease.
Treatment of pathologic fractures in these children is
not simple. Skeletal traction or external fixation may be
a problem in view of the extreme degrees of osteoporosis,
although as these children are now being treated more
effectively and from an earlier age, they do not have such
severe chondro-osseous changes and can probably be treated
safely and effectively. However, if skeletal traction is
chosen as therapy for a femoral fracture, the pin must be
checked carefully to make sure it does not migrate through
mildly osteoporotic bone into the distal femoral physis or
the proximal tibial tuberosity, if either is the site of pin
placement.
Similarly, open reduction has rarely been contemplated
because of the relatively short life expectancy of the children.
Again, because of improved medical treatment, these chil-
dren are reaching skeletal maturity and young adult life with
deformities that should be prevented. The changes causing
premature fusion, particularly in the proximal humerus,
seem to relate to small osseous bridges; and it is feasible that
they might be resected. However, the primary consequence
of the proximal humeral deformity is deficient length of
the humerus. Because deformity does not seem to cause a
major functional limitation, it seems unlikely that an effort
at bridge resection should be made in these cases. If the
patient exhibits some functional limitation, fusion of the
more lateral portions under the greater tuberosity (epiphy-
siodesis) should be considered to prevent worsening of the
humerus varus.
Scott et al. was one of the first to advocate the use of cor-
rective osteotomies in children with thalassemia who had sus-
tained malalignment of fractures or premature closure of the
epiphysis.418
Sickle Cell Anemia
Children with sickle cell hemoglobinopathy do not seem any
more susceptible to fractures than uninvolved children.406
However, the frequent clinical presentation of pain and
extremity swelling should prompt the consideration of
trauma in a differential diagnosis that also includes infection
or infarction (sickle cell crisis).402
Leukemia
Pathologic fractures in the spine (Fig. 11-47) and lower
extremities and pain in the metaphyseal regions due to
microscopic fractures or intertrabecular myeloid hyperplasia
often are the presenting signs and symptoms of leukemia.398
Multiple or even single vertebral compression fractures in an
otherwise healthy child, especially in the absence of signifi-
cant trauma, should make one suspicious.415,417 When pain in
the joint region is the complaint, roentgenography of the
metaphyses may show trabecular irregularities or collapse.
Pain is usually reduced if the child is placed on effective
chemotherapy, implying that many of the changes that occur
are a skeletal response to expansile marrow hyperplasia
caused by the disease.
Child Abuse
FIGURE 11-47. (A) Severe leukemic involvement in the distal tibia
and talus, with marrow hyperplasia and expansile destruction. The
Harris growth slow-down line demarcates the start of chemother-
apy for the leukemia, after which the formation of more normal tra-
becular patterns is seen. (B) Wedging of the vertebral bodies due
to leukemic involvement. Back pain was the initial presentation of
this child with leukemia.
Manson et al. found that patients with leukemia had dis-
abling distal metaphyseal transverse fractures, usually tibial
and bilateral.413 A number of these patients had a magne-
sium deficiency. Mechanical disruption of trabecular
marrow bone by cellular infiltration is a cause. Metabolic eti-
ology is also possible, as many patients are undergoing
chemotherapy.
379
Child Abuse
Confronting a case of actual or potential child abuse remains
a difficult one for any health care professional. In many
instances it is difficult to accept that the plausible, often
charming person being interviewed could be responsible in
any way for the devastating injuries to his or her child.
Although most of these children may be expected to make
a full, physical recovery from skeletal and extremity soft
tissue injury, psychological injury may remain. Concomitant
head injury has the most severe consequences for both fatal-
ity and long-term serious outcome.517,527 An abused child
returned to his or her home has a 50% chance of repeated
abuse and a 10% chance of death.
One study in the United States estimated that the number
of reported cases ranged from 60,000 to 400,000.470 For every
reported case of child abuse there are possibly at least four
unreported cases of child neglect. Nationally, there were
1.7 million cases of child abuse in 1984 and 2.2 million
in 1985.526 In Connecticut the documented number of
reported patients rose from 12,186 in 1980 to 16,804 in
1985.526
Statistics indicate that 10% of all injuries in children under
the age of 2 years and 25% of all fractures in children under
the age of 3 years may be due to assault and battery.423,524,565
Fractures in these age groups always should be approached
with a high index of suspicion.427,433,451,471,485,528,543 Skeletal
trauma is detected in fewer than one-third of abused patients
and is uncommon beyond 2 years of age.529 Fractures are
rarely present without other clinical evidence of physical
abuse. Regardless of whether the injury would normally
demand admission to the hospital, the child should be
admitted for protection and to provide sufficient time for
appropriate investigation.
The unexplained fracture in a young child may be the first
indication of nonaccidental injury.426,434,443,461,467,478,509,569
However, it is important to keep in mind other uncommon
bone disorders, including forms of osteogenesis imperfecta,
various patterns of rickets, scurvy, copper deficiency, infan-
tile cortical hyperostosis, fibrous dysplasia, infantile cortical
hyperostosis, and various congenital insensitivities to
pain.421,437,444,445,450,452,466,474,479,523,535,536,540,561,570 Another defi-
ciency syndrome is lysinuric protein intolerance.423 Multiple
fractures in the neonate with congenital syphilis can mimic
child abuse.514
One of the important heritable dysplasias that often must
be distinguished from child abuse is osteogenesis imperfecta
(OI). This is a particular problem with the milder forms of
OI, which may not have the classic features (e.g., blue sclera,
osteopenia). OI has at least four main types, with additional
subclassifications. Severe osseous fragility in types II and III
make it unlikely that the infant is considered an abuse victim.
Types I (common) and IV (rare) may, however, be misdiag-
nosed. Ablin et al. thought that difficulties arose with types
III and IV, and that type I should not be a diagnostic
problem.421
Biochemical studies of skin fibroblasts in children who
present with fractures suggestive of child abuse should be
undertaken if (1) there are no other signs of abuse such as
380
bruises or head injuries; (2) the fracture location and
pattern are consistent with the history; (3) the mechanism
of injury seems too minimal normally to cause a fracture; or
(4) the child has sustained multiple fractures in multiple
environments (e.g., home, preschool). Skin fibroblast cul-
tures are available (Dr. P.H. Byers, Department of Pathology,
University of Washington, Seattle, WA) that allow detailed
biochemical analysis of the collagens.
A battered or abused child is an unwitting victim of
deliberate physical trauma, usually inflicted by one or more
persons responsible for some or all of the child’s care.
The radiographic and orthopaedic aspects of this syndrome
were elucidated by Caffey, when he drew attention to
the association of multiple fractures of the long bones with
a subdural hematoma.439–442 Subdural hematoma is a
common problem in the battered child. Possible brain
damage due to repeated cranial trauma should receive
prime consideration. Initially, these fractures were thought
to be pathologic. Silverman reported on multiple long bone
fractures without subchondral hematoma and firmly estab-
lished their deliberate basis.550–552 The term “battered child
syndrome” was first used by Kempe and colleagues.488 Ini-
tially, little information appeared on this subject in the
orthopaedic literature, but the increasing awareness and
concern has led to multiple publications.*
Battered children tend to be young, with about two-thirds
under 3 years of age and one-third under 6 months. Their
general health is often poor. They tend to be underweight
and malnourished and often exhibit retarded physical and
mental development. Evaluation may reveal multiple frac-
tures with evidence of repeated trauma. The fractures are
usually in different stages of repair (asynchronous). There is
a predilection for the metaphysis to fracture because of the
poor nutrition. It is possible that these areas are more sus-
ceptible to injury because of such acquired “metabolic” bone
disease. There is marked subperiosteal reaction and a mul-
tiplicity of lesions in various stages of healing and repair. The
trauma is often inflicted by vigorous pulling on the limbs,
direct blows, or throwing the child.
It is impossible to say specifically that a given fracture, even
the characteristic ones of infancy, is due to battering and not
to other trauma, such as a fall or vehicular accident.428–462
Most parents of a battered child are evasive about the mech-
anism of injury. They often simply state that the child fell out
of the crib, during a diaper change, or down the stairs, often
a few days before. Such falls are unlikely to cause serious
skeletal injury.480,507 Most concerned parents bring a child for
medical attention immediately after an injury. They are rea-
sonably distraught about the circumstances. A caretaker
(nonfamily) may be responsible for the injury. Part of any
evaluation should consider other individuals (even family
members) who may have been with the infant or child. Lack
of emotional interest in the injury should again arouse
suspicion.
The likelihood of serious injury produced by falling
from a table or similar height is small. Akbarnia and col-
leagues showed that of approximately 100 infants who had
fallen (these were only the falls that alarmed the mother)
* Refs. 429–432,448,459,465,476,477,481,483,484,517,519,522,533,
544–546,555,563,568.
11. Fractures in Pediatric Growth Disorders
there was virtually no injury to the skeletal system.424 Nimi-
tyongskul and Anderson studied 76 children from birth to
16 years who were reported to have fallen out of a bed, crib,
or chair while in the hospital.531 Seventy-five percent involved
children 5 years of age or younger. The height of the fall
ranged from 1 to 3 feet. Most injuries were minor with soft
tissue damage. Severe head, neck, spine, and extremity
injuries would be highly unlikely in a comparable “fall at
home.”
Osseous trauma is the most common roentgenologic
finding of child abuse.543 More than one-half of patients have
demonstrable fractures; and of these, more than one-fourth
have multiple fractures. Analysis of one large series showed
that the mean number of fractures was just over three per
child.424 The most common site of fractures is the ribs, fol-
lowed in order of decreasing frequency by the humerus,
femur, tibia, and skull. Diaphyseal fractures are twice as
common as metaphyseal avulsion fractures, although the
latter are so characteristic they call attention to the probable
diagnosis more strikingly.505
Unusual injuries or small bone involvement may be the
only manifestation of intentional harm.481,532 Johnson et al.
reviewed two time periods and found the incidence of hand
injury due to child abuse to be 8.2% and 13.4% of the
patients.486 Of the 94 involved patients, 19 sustained injury
only to the hand. Eight of them were immersion burns. Only
2 of the 19 had fractures.
Dravaric et al. reviewed 793 abuse victims; 156 had con-
firmed skeletal injury.458 Review of roentgenograms in 136
infants revealed 234 fractures. Fifty-five percent were under
1 year of age. Common injuries were to the femur (20%),
humerus (18%), skull (18%), and tibia/fibula (18%).
Periosteal new bone formation (27%) and transverse
fractures (25%) were evident more frequently than
spiral/oblique fractures (14%) or metaphyseal corner frac-
tures (5%), which are usually considered typical of battering.
Thirty-eight patients had multiple fractures. Twenty-two
patients were referred more than once for fractures due to
suspected battering. These authors thought there was no
pathognomonic skeletal injury pattern.
Loder and Bookout reviewed 75 battered children
(average age 16 months) with 154 fractures (77% acute; 23%
healing or old).516 The most common long bone fracture was
of the tibia (16%) and the most common pattern was trans-
verse (41%). Corner fractures accounted for 28% of the long
bone fractures. Multiple fractures were present in only 10
(13%) of the children; an isolated acute fracture was present
in 65. Recent studies have identified single, fresh, long bone
diaphyseal fractures as the most common fracture pattern
seen with intentional injury.489,513,516
The fracture types that may arouse suspicion of child abuse
because of their location and nature involve the lateral end of
the clavicle, transverse fractures of the sternum, transverse
scapular or acromial fractures, and those affecting the
spine.472,528 Vertebral injuries include fracture-dislocation,
anterosuperior wedging, or compression of the vertebral
body and disc space (Fig. 11-48). Spinal cord injury without
radiographic abnormality (SCIWORA) may occur and lead to
long-term problems due to paralysis. Skeletal changes include
bones that have healed in malalignment, diaphyseal widening
caused by healed subperiosteal hematomas, and metaphyseal
Child Abuse 381

A B
FIGURE 11-48. Spine trauma due to abuse. This baby monkey was thrown from a tree by a fellow tribe member (not the mother). “Child”
abuse is common in primates. The fractures were through the neurocentral synchondroses. (A) Radiograph. (B) Sectioned spine.

cupping and other alterations of the epiphyseal–metaphyseal fractures) concluded that the likelihood of intentional
relation or late sequelae of growth plate injury. injury was low.436 However, there were no discriminating
Skull fractures are seen in about one-fifth of cases, and chinical parameters to help determine which injuries were
almost as many have sutural spreading.424,429,446,475,515 In such intentional.
a situation, complete neurologic evaluation and computed
tomography (CT) may be advisable.
In a review of 231 patients with battered child syndrome,
about one-third of the patients required orthopaedic treat-
ment.424 Among 74 children there were 265 fractures, with
an average of 3.6 fractures per child (range 1–15 fractures).
The distribution of the fractures was as follows: ribs 72;
humerus 42; femur 32; tibia 31; skull 25; hand 15; ulna 12;
radius 11; and others 24. It is interesting that only 1 of the
168 fractures of long bones in this particular study specifi-
cally involved the growth plate (Fig. 11-49). However, this is
a misconception. The corner fracture, although typically
metaphyseal bone, must involve some of the physis (see
Pathology, below).
Fractures of the midshaft of the clavicle are fairly
common, but it appears that fractures of the lateral
margin of the clavicle are more common in cases of battered
children or perinatal trauma. Sternal fractures are most
unusual at any time and result from severe, direct blows to
the chest. If such a fracture is present and there is no
substantiating history, such as an automobile accident or
crush injury, one should strongly consider the possibility of
child abuse. FIGURE 11-49. Distal femoral physeal fracture in an 8-month-old
A review of femoral fractures in children 1–5 years of age baby. This small corner fracture (arrow) is the equivalent of the
(excluding pathologic fractures and motor vehicle accident Thurstan Holland fragment typical of a type 2 physeal fracture.
382
Strait et al. found that most humeral fractures were acci-
dental, especially before the age of 15 months.556 However,
they found a higher incidence of supracondylar fractures in
child abuse patients than previously reported. In their study
group, abuse was diagnosed in 9 of 25 (36%) children under
15 months of age and in only 1 of 99 (1%) in children older
than 15 months.
Rib fractures are also rather uncommon, particularly
in the age range of the battered child.548 The normal
resilience of the young child’s thorax as well as the need for
a direct blow to have occurred probably account for this
fact.464 Healing rib fractures are sometimes seen shortly after
birth and may result from perinatal injury.464 If fractures are
encountered later than this and a legitimate history of
trauma is absent, the presence of rib fractures (Fig. 11-50)
should raise the possibility of intentional abuse.518,564 In the
battered child syndrome, rib fractures are usually multiple
and are seen mostly in the posterior or lateral region of the
ribs. A first rib fracture in an infant is highly suspicious of
abuse.557,558
Trauma to the spine and spinal cord in the battered child
syndrome has been reported but is not common.449,456,460,468,
469,525,541,560,567
It appears as: (1) anterior notching of the
vertebral body produced by hyperflexion injury, with
or without anterior herniation of the nucleus pulposus;
(2) compression of the vertebral body; and (3) fracture-
dislocation, which is certainly the most important, as it is
A B
FIGURE 11-50. (A) Multiple upper thoracic acute rib fractures in a
shaken-baby syndrome. The child was comatose due to intracra-
nial bleeding. (B) Multiple posterior rib fractures in a child kicked
repeatedly in the back. The child subsequently died of intraab-
11. Fractures in Pediatric Growth Disorders
unlikely that such injury could have been sustained, in the
absence of significant vehicular or crushing trauma, other
than from severe, purposefully directed blows, violence, or
shaking.
The orthopaedist can support the assertion that old as well
as recent injuries are present and that the changes are trau-
matic in nature, rather than attribute them to other causes
of periosteal new bone formation. A firm diagnosis leads to
the appropriate investigation of the home situation and, if
necessary, removal of the child from danger. When this step
has not been done, subsequent, repetitive traumatic insults
have caused permanent, crippling deformities, and death
has resulted from repeated brain, intrathoracic, and intraab-
dominal damage.
It is the responsibility of the involved physician to report
these cases of child abuse to the appropriate agency.512,520,
526,562
In most states it is now legally mandatory for a physi-
cian to report a suspected case of child battering to allow the
state the opportunity and responsibility to prove or disprove
the allegation. This type of legislation protects the physician
from being sued for misrepresentation. Large medical
centers have set up means of identifying suspicious cases,
and most pediatric emergency departments are attuned to
recognizing these children and usually notice the injuries
as part of their initial evaluation. Hence the orthopaedist is
rarely the first person involved or the one responsible for
reporting the situation.
dominal injuries when she was sent back to the hostile environ-
ment (A second-degree manslaughter conviction was eventually
obtained against the person who abused this child.)
Child Abuse
The amount of postfracture swelling at presentation of
long bone fractures was less with abuse-induced fractures
than with similar injuries sustained nonintentionally.457 The
difference probably indicated a delayed presentation such
that the history and time of injury are not reliable.
Nonosseous abnormalities must always be sought. The
subcutaneous fat and fat deposits within the thoracic cage
and abdomen in many of these deprived, malnourished
infants is often reduced. The force transmitted through ribs
that have not broken may lead to pulmonary or cardiac lac-
eration or contusion or to gastrointestinal hemorrhage; and
it may cause obstruction or mass formation, most often
affecting the duodenum, jejunum, spleen, or retroperitoneal
area. Traumatic pancreatitis and release of enzymes may lead
to distant osteolytic lesions. Muscle damage may result in
rhabdomyolysis.505
Radiology
Whenever child abuse is suspected, a total skeletal survey
should be done to rule out other fractures. The standard
approach is to obtain a roentgenographic survey of all the
long bones, pelvis, spine, ribs, and skull. Only one projection
of the long bones may be obtained at first, with additional
views as necessary.463,508,537–539,542,566 Radiologic skeletal surveys
for suspected abuse should include a minimum of two views
of the spine even if the infant or child has no symptoms or
signs referable to the axial skeleton.455
Roentgenographic findings in the battered child syn-
drome are well documented.506 The classic picture in infants
is multiple epiphyseal–metaphyseal fractures in various
stages of healing. Spiral and transverse fractures of the long
bones are also common, and one should not rely too heavily
on the “classic” epiphyseal or metaphyseal fractures (Fig.
11-51).482 Multiple chondro-osseous injuries, especially if
FIGURE 11-51. Battered child syndrome. (A) Metaphyseal lipping of
the distal femur (arrow). (B) Similar metaphyseal fractures involving
the distal tibia (arrows). (C) Anteroposterior view in the same patient
shows that this fracture extends across the entire metaphyseal
383
seen in various stages of healing, must be considered highly
suspicious but not absolutely diagnostic of the battered child
syndrome. Only 23% of the patients show this pattern of mul-
tiple, metachronous fractures.506 One should be suspicious
of even solitary fractures with an incongruous clinical
history.
Multiple fractures of the spinous processes of the thoracic
and lumbar vertebrae have been noted and are presumably
secondary to hyperflexion during shaking. Fraying and de-
mineralization of the acromion processes also occur, proba-
bly secondary to avulsion at the deltoid muscle attachments.
An unusual pattern of demineralization of sternal ossifica-
tion centers may be secondary to a fracture through sternal
synchondroses. In the extremities, radiolucent bands similar
to those seen with leukemia may be present without associ-
ated metaphyseal infraction. Torus fractures similar to those
seen with unintentional trauma have also been noted.
Unusual patterns of demineralization with bony disruption
have been seen in the calcaneus, but the etiology of this
finding is obscure. The subtlety of these findings further
points out the need for thorough, high-quality skeletal
surveys for any infant in whom abuse is suspected.490,502
The best method of searching for multiple injuries is
still subject to some debate. Nuclear scintigraphy is useful,
but cases have been reported in which obvious periosteal
reaction and other roentgenologically visible bone trauma
cannot be seen on the bone scan.454,549,554,559 In addition,
lesions near the metaphyseal–physeal complex may be
observed by the normally increased uptake, thus not
allowing sufficient differentiation from peripheral avulsion.
Sonography has also been used to screen for radiographi-
cally occult injuries.521,553
Arthrography or aspiration and bone aspiration do
not reveal any abnormality on bone scintigraphy.447 There-
fore detectable lesions on scintigraphy must be considered
significant injuries. Further bone scintigraphy can detect
width (arrows). (D) Chronic epiphyseal separation leads to avulsion
of the entire periosteal sleeve, with formation of subperiosteal new
bone along the entire shaft, not just the metaphysis. This bone must
be differentiated from normal diaphyseal new bone.
384 11. Fractures in Pediatric Growth Disorders

FIGURE 11-52. Pathology. (A) Radiograph of the distal tibia of a fatally

injured child showing a typical corner fracture (arrow). (B) Low-power
photomicrograph showing peripheral disruption (arrows). (C) Higher-
power view showing trabecular and physeal damage with reactive
bone formation (arrows).

subtle bone injuries not usually detected by radiography. Pathology

Examples are bowing, microtrabecular fractures, and stress
injuries. Older, healed fractures may not be evident on
bone scintigraphy. The younger the child the more difficult
is the interpretation of both the radiographs and bone
scintigraphy.
About 10–25% of subdural hematomas in infants are asso-
ciated with long bone fractures, and they are probably
induced by severe shaking and whiplash-type injuries.515 If
there is a suspicion of cerebrospinal injury, especially when
there is associated roentgenologic evidence in the form of
widened sutures or skull fracture, CT or magnetic resonance
imaging (MRI) may be helpful for elucidating the presence
and type of meningeal or cerebral trauma. A significant
factor in the infant whiplash-shake injury is not cranial
trauma but, rather, injury to the high cervical spinal cord
(cervicomedullary junction).438,473
Kleinman described a number of radiologic variants that
should not be confused with fractures (especially corner frac-
tures) caused by abuse.491
Perhaps the most important studies correlating histopathol-
ogy with radiographic changes in child abuse victims have
been undertaken by Kleinman and coworkers.490–504,534 Most
of the skeletal lesions in this syndrome result from traction
stresses, rather than from impact or compression stresses.511
They are produced by stretching and shearing forces in the
periosteum and in the tendinous and ligamentous attach-
ments to the growing bones, rather than by direct compres-
sion from the hit of a hand or from a kick. The high
frequency of these traction lesions indicates that the infant
is commonly grabbed and held by the extremities while
being shaken. In the extremities the soft tissue stretching
and squeezing are aggravated by the resistant counterforces
of the infant as he or she twists and squirms.
Knowledge of the anatomy and histology of bone and
periosteum in the young child gives some insight into the
radiologic response. In infants the periosteum is a thick, vas-
cular osteogenic layer, loosely bound to the shaft but tightly
Child Abuse 385

anchored into the perichondrium, zone of Ranvier, and the injury should alert the physician to the possibility of abuse.530
epiphysis. Sharp traction, twisting, or shaking stresses may In children 10 months to 3 years of age, multiple soft
easily separate the periosteum from the shaft of the bone.511 tissue injuries or a burn (especially of the head or face)
Many of these children are also malnourished. This factor should arouse suspicion. All such children should
increases the tendency of the metaphyseal area to come have whole-body skeletal radiographic or scintigraphic
apart. The vascularity of the region may allow large studies (or both). In children over 3 years of age, soft tissue
hematomas to accumulate under the periosteum, ballooning injuries were frequently the only sign of abuse. Radiographs
out the periosteum centrally but maintaining continuity are obtained as clinically indicated. A careful physical exam-
peripherally at the zone of Ranvier attachments. The
subperiosteal hemorrhage becomes evident when ossifica-
tion commences in the area.
The basic histologic alteration in the metaphyseal lesion is
a series of physeal–metaphyseal microfractures through the
primary spongiosa.496 This variable fracture pattern leaves a
zone of bone peripherally that is often radiologically
detectable. The radiologic manifestations may be described
as a corner fracture, a bucket handle fracture, or a metaphy-
seal lucency. The metaphyseal fractures result from avulsion
of fragments of the metaphyseal growth plate and epiphysis
by the strongly anchored periosteum. Small segments or com-
plete rims of bone may be avulsed (Figs. 11-52, 11-53).
Osier et al. examined 40 bones from 11 infants (under 1
year of age). Twenty-three bones had conspicious frac-
tures.534 A characteristic feature they described was the me-
taphyseal extension of hypertrophied chondrocytes (i.e.,
focal widening of the hypertrophic zone), which would be
compatible with a metaphyseal–physeal fracture-separation
followed by healing.
Increased density of the bone is often associated with
subperiosteal hemorrhage and metaphyseal avulsions.
Although it is theoretically possible that this sclerosis is
a manifestation of abnormal bone that is more fragile
than normal, it is much more likely that the sclerosis is an
expression of repeated microtrauma with reactive bone
change and is evidence of injury rather than a predisposing
situation.453
Some battered children do not demonstrate the classic
findings but do exhibit traumatic slipped epiphyses. They A
may be difficult to detect in initial studies, particularly if
limited views are obtained. This injury is potentially harmful
to the infant. If the injury is intracapsular, the periosteal
pattern is not demonstrable along the shaft. If the displaced
shaft is not realigned with its growth center, resorption of the
primary shaft occurs and a new shaft forms in line with ossi-
fication centers. Sequential radiographs are sometimes
strongly suggestive of osteomyelitis, and children have occa-
sionally undergone unnecessary antimicrobial therapy. The
prognosis in these injuries depends on the degree of carti-
laginous physeal injury. Reconstitution may be almost com-
plete; or if damage is severe, marked growth disturbances
may occur. Follow-up to assess long-term physeal damage
may be difficult because many of these families move to a
different area of the state or country to avoid further inves-
tigation.
B

Soft Tissue Injury FIGURE 11-53. (A) Metaphyseal hemorrhage in a corner fracture.
(B) Histologic section shows splitting of the periosteum and peri-
Abused children should be examined for soft tissue chondrium away from the metaphysis. Hemorrhage is evident in
injury. In infants under 9 months of age, any soft tissue the gap.
386
ination may not be sufficient, as old (stable) fractures may
be missed.
Bruising is the result of blood escaping from damaged cap-
illaries into the contiguous interstitial tissues. This noncir-
culating blood undergoes progressive degradation of the
hemoglobin. The thickness of the skin, ambient light, and
skin color all play roles in the visual expression of this degra-
dation process.
The assessment of soft tissue damage is an integral part
of the evaluation of a child with multiple, particularly
asynchronous skeletal injuries. Unfortunately, there is no
dependable way to clinically age bruising.547 A frequently
used technique compares the visible color of a bruise to
established charts.
Assignment of a color may be difficult because of the
presence of more than one color. Langlois and Gresham
use any amount of a particular color to assign that color
to a bruise.510 Another approach may be the predomi-
nance of a color. With modern technology and the avail-
ability of low-cost digital cameras, which probably should
become standard in pediatric emergency centers, allows
photodocumentation of the cutaneous lesions. Programs
could be readily developed for computerized color assess-
ment and determination of the percentage distribution of
multiple colors.
The only scientific study of visual aging of bruises appears
to be that of Langlois and Gresham.510 They assessed 369
bruises in 89 patients. Only bruises with known age were
photographed. They came to the following conclusions: (1)
The presence of yellow indicates the bruise must be at least
18 hours old. (2) Red, blue, purple, or black may be present
at any time from within 1 hour of bruising to resolution. (3)
Bruises of comparable age and cause on the same person
may not appear as the same color and may not change at the
same rate.
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503. Kleinman PK, Zito JL. Skeletal injury in the young battered
infant: an expanded radiologic spectrum. Pediatr Radiol
1984;14:185–191.
504. Kleinman PK, Zito JL. Avulsion of the spinous processes
caused by infant abuse. Radiology 1994;151:389–391.
505. Knottenbett JD. Traumatic rhabdomyolysis from severe
beating: experience of volume diuresis in two patients.
J Trauma 1994;37:214–219.
506. Kogutt MS, Swischuk LE, Fagan CJ. Patterns of injury and
significance of uncommon fractures in the battered child
syndrome. AJR 1974;121:143–149.
507. Kravitz H, Driessen G, Gomberg R, Korach A. Accidental falls
from elevated surfaces in infants from birth to one year of age.
Pediatrics 1969;44:869–876.
508. Krige HN. The abused child complex and its characteristic x-
ray findings. S Afr Med J 1966;40:490–493.
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509. Kurland RL, Bianco AJ Jr, Hick JF, et al. Child abuse. Minn
Med 1982;65:477–483.
510. Langlois NE, Gresham GA. The aging of bruises: a review and
study of the color changes with time. Forensic Sci Int
1991;50:227–238.
511. Laval-Jeantet M, Balmain N, Juster M, Bernard J. Les rapports
de la virole périchondrale et du cartilage en croissance normale
et pathologique. Ann Radiol (Paris) 1968;11:327–335.
512. Leake HC, Smith DJ. Preparing for and testifying in a child
abuse hearing. Clin Pediatr 1977;16:1057–1063.
513. Leonidas JC. Skeletal trauma in the child abuse syndrome.
Pediatr Ann 1983;12:875–881.
514. Lim HK, Smith WL, Sato Y, Choi J. Congenital syphilis mim-
icking child abuse. Pediatr Radiol 1995;25:560–561.
515. Lis EF, Frauenberger GS. Multiple fractures associated with
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516. Loder RT, Bookout C. Fracture patterns in battered children.
J Pediatr Orthop 1991;5:428–433.
517. Lynch MA. Child abuse before Kempe: an historical literature
review. Child Abuse Negl 1985;9:7–15.
518. Magid N, Glass T. A “hole in a rib” as a sign of child abuse.
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519. Mallet JF, Padovanni JP, Rigault P. Le syndrome de Silverman
ou syndrome des enfants battus. Ann Pediatr (Paris) 1984;
31:117–125.
520. Markham B. Child abuse intervention: conflicts in current
practice and legal theory. Pediatrics 1980;65:180–185.
521. Markowitz RT, Hubbard AM, Harty MP, et al. Sonography of
the knee in normal and abused infants. Pediatr Radiol
1993;23:264–267.
522. McClain PW, Sachs JJ, Froehlke RG, Ewigman BG. Estimates
of fetal child abuse and neglect, United States, 1979 through
1988. Pediatrics 1993;91:338–343.
523. McClelland CQ, Hejpel KG. Fractures in the first year of life:
a diagnostic dilemma? Am J Dis Child 1982;136:26–29.
524. McCurdy K, Daro D. Current Trends in Child Abuse Report-
ing and Fatalities: The Results of the 1992 Annual Fifty State
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Abuse, 1993.
525. McGrory BE, Fenichel GM. Hangman’s fracture subsequent to
shaking an infant. Ann Neurol 1977;2:82.
526. McRae KN, Cameron A, Ferguson CA, et al. The forensic pedi-
atrician as a child advocate. Dev Behav Pediatr 1984;5:259–262.
527. Ment L, Duncan CC, Rowe DS. Central nervous system mani-
festations of child abuse. CT 1982;46:315.
528. Merten DF, Kirks DR, Ruderman RJ. Occult humeral epiphy-
seal fracture in battered infants. Pediatr Radiol 1981;
3:341–343.
529. Merten DF, Radkowski MA, Leonides JC. The abused child: a
radiological reappraisal. Radiology 1983;146:377–381.
530. McMahon P, Grossman W, Gaffney M, Stanitski C. Soft tissue
injury as an indication of child abuse. J Bone Joint Surg Am
1995;77:1179–1183.
531. Nimityongskul P, Anderson LD. The likelihood of injuries
when children fall out of bed. J Pediatr Orthop 1987;
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532. Nimkin K, Spevak MR, Kleinman PK. Fractures of the hands
and feet in child abuse: imaging and pathologic features. Radi-
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533. O’Neill JA Jr, Meacham WF, Griffin PP, Sawyers JL. Patterns of
injury in the battered child syndrome. J Trauma 1973;
13:332–339.
534. Osier LK, Marks SC, Kleinman PK. Metaphyseal extensions
of hypertrophied chondrocytes, in abused infants indicate
healing fractures. J Pediatr Orthop 1993;13:249–254.
535. Paterson CR. Osteogenesis imperfecta in the differential diag-
nosis of child abuse. Child Abuse Negl 1977;1:449–452.
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536. Paterson CR, McAllion SJ. Osteogenesis imperfecta in the dif-
ferential diagnosis of child abuse. BMJ 1989;299;1451–1454.
537. Pavlov H, Murov K. Orthopedic aspects of child abuse. Part I.
Contemp Orthop 1990;21:21–23.
538. Pavlov H, Murov K. Orthopedic aspects of child abuse. Part II.
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539. Pavlov H, Murov K. Orthopaedic aspects of child abuse. Part
IV. Contemp Orthop 1991;22:21–23.
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neonatal fractures mimicking abuse secondary to physical
therapy. Skeletal Radiol 1982;8:85–86.
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542. Radkowski MA, Merten DF, Leonidas JC. The abused child:
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262–297.
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549. Sfakianakis GN, Haase GM, Ortiz VN, Morse TS. The value of
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556. Strait RT, Siegel RM, Shapiro RA. Humeral fractures without
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11. Fractures in Pediatric Growth Disorders
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12
Pediatric Athlete
Engraving of an avulsion of the apophysis of the lesser trochanter.
(From Poland J. Traumatic Separation of the Epiphyses. London:
Smith, Elder, 1898)
he term “sport” has continued to envelop increasing
T aspects of human activity, and the term “sports medi-
cine” has become almost a cultural phenomenon.
Sports-related injuries are hardly unique. The multitude of
injuries have always affected the developing and developed
musculoskeletal tissues. Specific sports certainly lead to
increased risk of selective injury patterns to the immature
skeleton. Concentrated efforts are needed to minimize or
prevent such repetitive injury patterns.52
The past two decades have witnessed a major proliferation
of organized sports and progressive levels of competitive
intensity for children.98,105,110 There are roughly 35 million
nonschool (but often still structured) sports participants
in the United States in the age range of 6–18 years. This
includes an estimated 20 million children and adolescents
who are involved in organized sports; 5 million adolescents
are involved in increasingly complex and regimented high
school sports.59 Thus, significant numbers of youngsters are
exposed to the risk of sports-related injuries.94 On a global
basis, as societies evolve toward increasing amounts of recre-
ational time for children, adolescents, and young adults, the
number of potential participants and injuries increases
dramatically.
A phenomenon surfacing over the past 15 years has been
the evolution of the young, single-sport athlete. These chil-
dren may start relatively intense training and competition
as young as 4–5 years of age. Training is often intense and
continual, rather than seasonal. Overuse syndromes are
not uncommon.22,44,99,117 The intensity of training may lead
to significant retardation of physiologic development, such
as the delayed onset of menses.57,58
More than 1.8 million children aged 5–14 years sought
medical attention as early as 1980 for sports-related injuries.8
The actual number of injuries was probably much higher, as
many children are not taken to medical facilities for formal
evaluation but, rather, are treated by coaches, peers, train-
ers, parents, or other well-meaning adults who may have
limited knowledge, if any, of the nuances of developmental
skeletal biology and the patterns of acute and chronic (repet-
itive) failure.
The periods of increased athletic activity, particularly
under the aegis of organized (i.e., structured and super-
vised) team sports, coincide with the times of relatively
rapid developmental maturation of the chondro-osseous
skeletal systems of boys and girls. Any physician dealing with
children who participate in these organized sports must con-
sider the variations in growth, maturation, and coordination
of the musculoskeletal system during both the prepar-
ticipation physical examination and the treatment of specific
injuries.7,53,111
Body type (somatotype) and physical maturity seem to be
important variables for determining susceptibility to injury.
Standard physical development charts indicate that in a
given age group it is not unusual for one child’s body weight
to be twice that of another child within 2 standard deviations
(SD). Children in a given participation age group may be at
completely opposite ends of the Tanner scale. Accordingly,
399
400
age-specific categorizations for participation must be app-
roached judiciously because of the immense variation in
height, weight, and maturity within a given age group.
The physician must also have an appreciation for the vari-
able development of the skeleton, particularly the response
to repetitive stress, the normal and abnormal responses to
injury, and how to rule out potential diagnostic problems
(e.g., a bone tumor or hematogenous osteomyelitis) that may
become symptomatic during or following a sports injury.40
Any abnormalities of skeletal development, whether local-
ized or generalized, and any chronic disorders must be
evaluated on an individual basis that considers the activities
that can be performed safely in view of the musculoskeletal
problem.74 Dysplastic conditions may affect the ability of
the bone to withstand the physical demands of a sport
(Fig. 12-1).
Certain injuries or medical conditions effectively preclude
participation in certain sports but not others, thereby allow-
ing the child an opportunity to participate in some degree
of physical activity without risking further injury. For
example, “little league elbow” is essentially a disorder affect-
ing preadolescent pitchers. By changing to a fielding posi-
tion or decreasing the amount of structured game and
A B
FIGURE 12-1. (A) Stress fracture in a child with congenital antero-
medial bowing of the tibia. (B) Three months later, while in a clam-
shell orthosis, she propagated the proximal stress fracture and
additionally developed a second stress fracture in the distal tibia.
Also note the reactive sclerosis in the proximal fibula. Congenital
pseudarthrosis in its various forms is discussed in detail in Chapter
11.
12. Pediatric Athlete
practice pitching, the youngster may continue to participate
in the chosen athletic activity. Adolescents with disorders
such as Klippel-Feil syndrome should be discouraged from
sports with recognized risks of head and neck trauma (see
Chapter 18). Children also must be made aware of their spe-
cific physical limitations.
Many athletic injuries can occur only in the developing
skeleton (i.e., injury to the growth mechanisms). The treat-
ment of any child or adolescent must factor in the ramifica-
tions of the specific injury on subsequent growth and realize
that other aspects (e.g., parental or personal drive, coaching,
peer pressure, and strength and body mass relative to that of
other competitors) may significantly contrapose individual
ability and reality.
Although acute trauma (sprain, strain, epiphyseal injury,
fracture) produces the most debilitating patterns of injury,
most sports injuries in children are overuse syndromes
caused by repetitive frictional, tractional, or cyclic loading
forces on the reactive chondro-osseous skeleton. Frictional
microtrauma may be responsible for chondromalacia. Trac-
tion or tension microtrauma leads to entities such as the
Sever or Osgood-Schlatter lesions. Cyclic overloading
produces stress fractures.85
Injuries seem to increase in frequency and severity as
the child ages, probably reflecting increasing dexterity and
familiarity with the skills of the sport, increasing height and
weight, and increasing intensity on the part of the partici-
pants who make each level of cut to proceed to the next level
of a sport.71 As children become teenagers, the likelihood of
injuries shifts from upper to lower extremities.2
Injuries to the musculoskeletal system involving the young
athlete, especially children under 10 years of age, appear to
be much less prevalent than those involving the adolescent
athlete, particularly when ligamentous injuries are consid-
ered.* This may be a result of accuracy of reporting injuries
in any structured manner when they involve elementary
school or recreational sports.
Larson reported a series of 4854 injuries sustained during
athletic activites. Only 933 occurred in children under 15
years of age, even though that group represented the great-
est number of participants in organized athletic programs.149
Selective examination of tackle football programs in this
study showed the injury rate for the junior high school age
population to be 11%, whereas the injury rate in the high
school population was 33%. Similar differences were seen for
other sporting activities, such as baseball, basketball, track,
gymnastics, wrestling, and cross-country running.18,52 In
these particular sports, junior high school students had an
injury rate of 12%.
In a 1-year study of all sports injuries at a large high school,
1283 student athletes were found to have 280 injuries, for an
overall injury rate of 22%.62 The sport with the highest injury
rate was football (61%), followed by girl’s and boy’s gym-
nastics, wrestling, and boy’s basketball. Five sports had no
reported injuries: boys’ tennis, golf, boys’ and girls’ swim-
ming, and girls’ water polo. They measured the severity of
injury by the number of days lost to athletic participation.
Girls’ track had the greatest number of days lost, followed by
* Refs. 8,19,20,23,25.29.34,38,47,48,59,60,74,75,80,120–122,140,
142,161.
Pediatric Athlete
girls’ basketball, girls’ cross country running, boys’ track,
and boys’ wrestling. Sprains and strains accounted for 57%
of all injuries. Only five athletes eventually required surgical
intervention.
DeLee and Farney reviewed the incidence of injury in 100
Texas high school football programs.21 A total of 4399
student athletes sustained 2228 injuries, for an injury inci-
dence of 0.506 injuries per student per year. Severe injuries
that required hospitalization were recorded in 137 students
(0.031 injury/athlete/year). The knee was the most com-
monly injured anatomic site, followed by the ankle.
Certain sports seem to have prevalent injury pat-
terns.12,15,32,36,37,41,45,49,55,66,67,90,93,95,101,112,116,118,119 For instance, ice
hockey is associated with a high incidence of cranial, facial,
and cervical trauma, a fact stressing the need to wear pro-
tective head gear, including not only a helmet but also a face
mask.9,10 In all sports, the fingers are constantly exposed.158
New “sports,” such as in-line skating or trampolining, often
introduce new risks.16,123
Lorish et al. evaluated 1742 male wrestlers in two tourna-
ments whose ages ranged from 6 to 16 years.51 The overall
injury rate was 12.7%. Injuries requiring withdrawal from the
tournament occurred in 4.6% of the adolescents.
Organized sports produce fewer significant injuries than
structured general physical educational activities or nonor-
ganized sports. Among the organized sports, the highest
frequency of injury occurs in those involving collision and
contact.113 The childrens’/adolescents’ sports at highest risk
for musculoskeletal injury are tackle (American) football,
basketball, gymnastics, soccer (football to the rest of the
world), and baseball. These statistics obviously reflect the
popularity of certain sports in the United States and do not
necessarily indicate overall incidence of injury by sport in
other parts of the world. No matter what the sport, most
musculoskeletal injuries are minor (sprains, strains) rather
than debilitating injuries such as fractures or tendon
disruptions.
Pasternack et al. devised a prospective, population-based
injury survey of injuries during a Little League baseball
season.82 The 2861 players ranged from 7 to 18 years, and
there were 140,932 player-hours. An injury was included in
the database if it was serious enough to require medical care.
There were 81 total injuries, of which 66 (81%) were acute
and 15 (18%) were due to overuse. The severe injuries were
ball-related in 46% and due to collisions in 27%. Two-thirds
of the ball-related injuries occurred to defensive players, who
do not wear the same face mask and helmet that offensive
players do.
Pritchett reviewed insurance claims for injuries sustained
in high school football in the 1965, 1975–1977, and 1983–
1985 seasons.88,89 The incidence of knee injuries remained
similar: approximately 13% of all injuries each season. In
1965 about 12% of the patients with knee injuries were
treated operatively, whereas in 1985 one-third (33%) of the
adolescents underwent knee surgery, undoubtedly a reflec-
tion of the evolution of arthroscopy. Among this group, 68%
responded to a follow-up survey (mean 10 years after injury)
with 25% having knee ligament injuries, 30% with internal
derangement of the knee, and 17% with patellofemoral pain
or dysfunction. Surgery was common during the post-high
school period, ranging from 52% for ligament injury to 95%
401
for internal derangement. All were at significant risk for rein-
jury during continued organized sport, recreational sport,
or work. Patients with residual patellar subluxation had the
highest risk of injury to the contralateral knee.
The main differences between organized athletic pro-
grams and unorganized play appear to be adult supervision
and participation. Without adult supervision, youngsters are
not bound by rigid rules. They create their own rules, which
usually conform to their physical abilities and enjoyment
(although not always without a modicum of dispute). Their
activities are more varied, changing frequently from one
game to another according to their moods. As a rule, they
do not force themselves beyond their physical tolerance or
ability, and they stop playing when tired or slightly injured.
Ifinjured, medical attention is not complicated by pressures
from parents and coaches, so healing usually progresses
normally.
In contrast, in organized sports the youngster’s activities
are completely dominated and regulated by adult supervi-
sion: by the coach and often by overaggressive and demand-
ing parents. This deprives the youngsters of much of the fun
and enjoyment they should derive from participation in
sports. Although many rules of organized sports have been
modified to conform to the age and size of the participants
and to specific recognized risks (e.g., the number of innings
a youngster is allowed to pitch), basically most games are
played the same no matter what the age level of the partici-
pants. The tendency is to treat the youngsters as miniature
adults. Instead of being varied, physical activity becomes rep-
etitious, increasing the risk of overuse injury. Such injury
is even more likely with persistent practice and the demand
for maximal effort, spurred on by the competitive pressures
of winning at any cost and a spartan attitute toward injury.
Murray and Duncan proposed that aggressive athletic activ-
ity during adolescence, particularly for boys, was a significant
etiologic factor in the eventual development of degenerative
hip disease during adulthood.69
Competitive sports sponsored by schools or other com-
munity agencies are now so universally played by boys and
girls 13 years old and younger there is a compelling need for
positive and realistic guidelines to govern participation.
Young children are not miniature adults. They are boys and
girls in the process of progressively maturing into adults at
their own individual rate. They seek and can profit from suit-
able play opportunities, but the benefits do not come
without appropriate planning, quality supervision, and a
broad range of physical educational activities adapted to the
realistic needs and capacities of growing children.65,66
Unless an obvious fracture, dislocation, or other muscu-
loskeletal injury occurs, treatment is often recommended or
instituted by coaches or parents. Their recommendations
may be based on a minimal understanding of musculoskele-
tal disease or injury and on the knowledge and experience
gained during their own playing days in high school or
college. Unfortunately, talented athletes, on whom the coach
and the team depend, often have their future and potential
as “star” athletes jeopardized by the lack of proper medical
attention or pressure to return to play before complete
recovery from the injury.
Preventive factors assume an important role. They relate
to preparticipation evaluation (including physical examina-
402
tion), education in preventive factors (e.g., avoidance of
heat-induced illness), review of local safety rules, appropri-
ate education of professional and voluntary athletic trainers
and assistants as well as team physicians (who may be not
only orthopaedists but also family practitioners and pedia-
tricians), and overall health education programs for all indi-
viduals involved in the sport, from coach to participant.33,78,114
Team Physician
The team physician is responsible for the care of children
and adolescents who are part of one or more organized
sports teams. Increasingly, competitive sports involving
subteen children utilize a defined team physician or “side-
line doc” (at least during competition). Such a physician pro-
vides care in the office and surgical settings (inpatient/
outpatient), as well as in places separate from the former,
such as the practice field or the sporting event itself. Team
physicians may be nonorthopaedists, but they must have a
reasonable knowledge of musculoskeletal pathology, as most
of the problems encountered by athletes involve this system.
The team physician should also have some familiarity
with cardiorespiratory problems, infectious diseases, and
psychology.27,56,63,75,108
The team physician should develop good relationships
with all people connected with the team (or teams) for which
he or she provides coverage. This particularly relates to ath-
letic trainers, who are becoming increasingly prevalent in
high school sports and who are ever present among elite
training locales (e.g., gymnastics schools). A good relation-
ship with the coaching staff facilitates professional interac-
tion, especially instilling a confidence in decisions regarding
a given athlete’s participation in practice or competition.
The team physician or sports medicine specialist (or
even the generalist or family practitioner) is in a unique
capacity to intervene in the treatment of microtrauma (i.e.,
overuse syndromes and to offer ways to prevent certain
injuries.79,87,104,109 Macrotrauma (acute anatomic disruption)
is probably not as easily prevented and must be dealt with in
the individual situation. However, even certain acute injury
patterns, when appropriately analyzed, may be lessened both
in occurrence and long-term impact by effective modifica-
tion of the equipment or the extent of participation in a
given sport or a specific aspect of that sport.
The role of the sports medicine practitioner is to prevent
long-term dysfunction, encourage fitness, and allow the
developing (physiologically and psychologically) young
athlete to enjoy himself or herself while pursuing individu-
ally motivated goals. Unfortunately, other factors intervene.
They usually include peer pressure on a capable individual
to overcome team deficiencies, parental pressure (especially
the frustrated parent using the child to attain the accom-
plishments they could not during their youth), and coach-
ing pressure. Unfortunately, the public perception of sports
medicine is to “intervene” (appropriately or not) to move
the athlete, no matter what his or her age, back to competi-
tive activity as soon as possible.
Team players should be treated just as you would interact
with an office or hospital patient. The only difference may
be the frequency of interaction. Always consider the appro-
12. Pediatric Athlete
priateness of adequate documentation of any interaction
and the needs for confidentiality and informed consent.
Sideline consultations are often like hospital hallway opin-
ions. Dictate a note, however brief, of the interchange, or it
may come back to haunt you.
Be prepared to treat nonorthopaedic emergencies. Train-
ing in basic life support (BLS) or advanced cardiac life
support (ACLS) should be strongly considered. Appropriate
emergency medical equipment should be rapidly accessible.
The team physician should set up such medications and
equipment at the beginning of a season, with certain equip-
ment relating to anticipated problems.83 Cutting devices to
remove a football or hockey helmet need not be part of a
gymnastics kit.
The team physician must often face conflicts among
athletes, coaches, fans, media, and team management,
especially relative to when an injured team member should
be removed from a game or when the player may resume
normal athletic demands of the sport. Resumption of a
sports activity is often based on “how soon,” rather than when
the injury is most likely to be healed.
Any individual who wants to be a team physician must
address ethical and legal issues. This includes the physician
being a well-rounded individual comfortable in areas beyond
his or her specialty that relate to overall team care.
Preparticipation Screening
Children and adolescents require evaluation for most team
sports. This evaluation may be rendered by the child’s
primary physician or as part of a complete team group eval-
uation. The latter must be adequately planned to avoid the
chaos that may rapidly supervene with a group of young
individuals.
Preparticipation evaluation is important to protect the
young athlete. Pediatricians should pay particular attention
to the history, physical examination (including blood pres-
sure), and urinalysis. If the pediatrician does not feel capa-
ble of a thorough musculoskeletal examination, including
fitness and conditioning, appropriate referral to other ex-
perienced personnel is recommended.35,39
Many children who are screened in the preparticipation
examination or who already have a known condition affect-
ing the musculoskeletal system want to participate in sports.
The most publicized condition in Down syndrome is whether
cervical stability is sufficient to allow safe participation in
certain sporting activities (see Chapter 18).
The efficacy of the preparticipation history and physical
examination during generalized screening has been ques-
tioned for both children and adults, even though the pro-
cess has become a culturally ingrained ritual. Although the
generalized or routine physical examination may not be a
productive prescreening tool, the sports-oriented physical
examination often is.35
Goldberg et al. showed that 15% of children being
assessed by such preparticipation examinations had medical
problems that merited further evaluation.35 Only 2 of the 701
students were eventually excluded for medical reasons, and
7 students were excluded for orthopaedic problems. An
important aspect of this study was the finding that routine
physical examination produced a low yield when screening
Exercise
for sports participation (less than 0.3%). One-third of the 35
musculoskeletal problems detected during the screening
were unknown to the primary care physician and required
further assessment prior to the child’s participation.
Causation
There is an assumed risk when participating in any sport,
some more so than others. It is imperative that the sports
physician and other adults eliminate or significantly dimin-
ish the risk of any injury, especially when an injury is fairly
predictable in a given sport, or when it is likely to cause
long-term disabilities. Equally important is the correct diag-
nosis of the specific injury and the inception of optimum
treatment.
Athletic trauma, whether incurred during participation in
organized or recreational sports, usually has a recognizable
cause. For example, dancers who experience prolonged
periods of hypoestrogenism through delayed menarche or
secondary amenorrhea may be at risk for scoliosis and frac-
tures.116,118 Moreover, even the bone-strengthening effects
of their rigorous physical training may be insufficient to
counter the adverse effects of estrogen loss and improper
diet. Among a group of 75 professional ballet dancers, the
incidence of scoliosis was 24%. In contrast, the rates of idio-
pathic scoliosis in adolescents in the general population and
among white girls are 1.8% and 3.9%, respectively.103 Scolio-
sis is more prevalent among dancers with secondary amen-
orrhea. In addition, dancers with scoliosis exhibit a greater
degree of abnormal eating habits. Altogether 61% of the
survey population had suffered fractures, and the incidence
increased with the dancers’ ages at menarche. Furthermore,
among a subgroup of 40 dancers, those who had had stress
fractures experienced secondary amenorrhea at a rate that
was double that of dancers who had not.118
The most important factors leading to injury during ath-
letic activity appear to be the following.66
Conditioning: The young athlete must learn the funda-
mentals of both a specific sport and a generalized physical
conditioning program conducive to his or her degree of
musculoskeletal development. Injury commonly occurs in
novice participants during the early part of the season or the
early part of a game.36 As a young athlete develops coordi-
nation, confidence, and experience, the risk of injury lessens.
Ligament strength may increase with conditioning. This
increased strength undoubtedly is important in the older
adolescent but may not be as crucial in the younger child,
in whom ligamentous laxity is a normal musculoskeletal phe-
nomenon. Unfortunately, the emphasis is usually placed on
the competition itself (the game, meet, or tournament, often
at the expense of adequate preparation (training).
Endurance: Continued physical conditioning and in-
creased familiarity with the specific demands of a sport make
an athlete less susceptible to injury. Fatigue is an important
predisposing factor but becomes less consequential as the
child learns to pace himself or herself. Obviously, the inter-
vention of adults (coach, parents) may affect the compliance
or reaction to fatigue.
Antecedent injury: Failure to diagnose and treat minor
trauma may culminate in serious injury. For example, repet-
403
itive, unprotected ankle “sprains” in a young gymnast may
lead to serious inversion injury with complete ligamentous
disruption and a need for subsequent surgical reconstruc-
tion. Failure to recognize “back sprain” as being caused by
traumatic spondylolysis, possibly in association with spondy-
lolisthesis, may lead to serious impairment of the activity
levels of a young gymnast.
Adherence to rules: Many injuries are incurred during rule
infractions. Such violation of rules includes failure to wear
required protective equipment. It is the responsibility of
team physicians to see that equipment rules are enforced
strictly and to discuss with officials any serious oversights
regarding enforcement of rules that may affect the incidence
of injury. It is extremely important that physicians on duty
at a game identify themselves to the coaches as well as to the
officials, and that they establish a role as final arbiter in any
decision-making process that affects the physical well-being
of the participants.
Altered Physiology
Warren et al. showed that delay in menarche and prolonged
intervals of amenorrhea that reflected prolonged hypo-
estrogenism predisposed ballet dancers to scoliosis and
stress fractures.118 The incidence of stress fractures rose with
increasing age of menarche. Gymnasts are probably at
similar risk, although former gymnasts develop a normal
bone mineral mass during early adulthood. This reflects
“catch-up” as a result of decreasing athlete activity, estab-
lishment of normal menstrual cycles, and the use of oral
contraceptives.
Olmos et al. studied 12 patients with anorexia nervosa.77
Serum concentrations of calcium, phosphate, albumin, alka-
line phosphatase, parathyroid hormone, calcitonin, and
osteocalcin and 24-hour calcium excretion were normal.
Serum 25-hydroxy vitamin D was normal, whereas 1,25-
dihydroxy vitamin D was significantly reduced. The concen-
tration of vitamin D-binding protein was normal, but serum
binding capacity was diminished. Olmos et al. thought that
these individuals had a qualitative (rather than quantitative)
defect in serum transport proteins.
Exercise
There is tremendous pressure on the child or adolescent by
coaches and parents to improve performance. Accordingly,
increasing emphasis has been placed on physical training,
especially for the single-sport child athlete who exhibits any
prowess at the specific sport. Exercise methods have basically
been extrapolated from the adult world, with little under-
standing or incorporation of the differences in developing
physiology.61,72
Children have decreased ability to utilize muscle glycogen
and to produce lactate. As a result they have lower anaero-
bic capabilities than adults, even when adjusted for body
weight. Anaerobic capacities increase with age. Children
are able to recover from an oxygen deficit quickly; they also
tend to have more oxygen utilization (O2/kg body weight),
increased heart rates, lower stroke volumes, and higher res-
piratory rates during exertion than adults. Children appear
404
to expend a higher metabolic cost than adults for endurance
activities.
Thermoregulation is a distinct problem in children. They
produce large amounts of metabolic heat but do not have
an efficient cooling system. They tend to sweat less often
despite a higher anatomic density of sweat glands; and they
have a higher threshold for sweating than adults.
Muscle strength tends to parallel growth. The largest gains
are most obvious during the adolescent period. Children’s
muscle strength increases in response to resistance exercises.
However, they do not respond to properly programmed
strength training with muscle hypertrophy and increased
lean body mass.106 Strength may increase through myogenic
and neurogenic adaptations. The latter (e.g., improved
recruitment of motor units) may be attained through the
judicious use of lighter weights and more repetitions,
thereby minimizing stress-related injury such as osteolysis of
the distal clavicle.89,91,102 Weight lifting may also be related to
an increased risk of Scheuerman’s disease or even herniated
discs68 in the immature skeleton.68
Fitness
An important goal of developmental and sports medicine is
to encourage physical and mental fitness. This requires three
essential elements: psychological well-being, nutritional
awareness, and physical performance.
Psychological Fitness
It is often difficult to be responsive to the psychological
implication of the child’s complaints. However, it is essential
to do so to prevent “burnout,” which may be more frequent
than realized in young athletes. The more common signs are
(1) an overly quiet or reserved youngster in the company of
an overly involved parent, (2) chronic or inappropriate
pain, and (3) the injury-prone child (see Chapter 2). These
signs commonly occur when the child loses interest in
the sport, or when there is gratification gained by the
attention the injury brings. A child should be made to realize
that it is important to accomplish his or her best, rather
than to be the best of all the participants. Mature adults
(parents, coaches) should realize that the child or adoles-
cent is socially and psychologically labile.13,84 These young-
sters experience enough stress simply by competing. They
do not need the additional stress of parental or coach
pressure.
Nutritional Fitness
American children are often overweight and unfit, factors
that affect the child’s ability to pursue sports activities.28,96,97
Unfortunately, “big” is often interpreted as “strong.” These
individuals are often placed in positions such as goaltender,
catcher, or lineman; or they are assigned to field events in
track and field. These positions or events often are associ-
ated with increased injury risk that may be caused by their
peers or their own body weight. Overweight children are
often the least conditioned on the team.
12. Pediatric Athlete
Exercise and dietary habits should be stressed to the
family. The child may readily accept and enjoy structured
exercise. Rarely, however, do they follow dieting concepts, a
factor made worse by one or both parents being overweight.
Nutritional supplements, which are increasingly available
and the subject of much nonmedical writing, probably have
limited if any significant effect in the growing child or ado-
lescent to increase body size, change body image, increase
performance level, or hasten healing of an injury.46 The only
exception is iron supplementation, which may be necessary
in endurance athletes (both male and female).73,100 Such a
condition is best determined by serum ferritin levels, not by
the hemoglobin level.
Any sports physician should be alert to the possibility of
eating disorders, which often result from attempts to control
body weight. Although female gymnasts and dancers are
often diagnosed with these conditions, young male athletes
may also have such a problem. It particularly affects wrestlers
who are trying to make or break weight to participate in a
certain weight class in which they believe they would have
the best chance to win.
Physical Fitness
Physical fitness means different things to different people.
A number of parameters should be considered: strength,
agility, speed, flexibility, jumping ability, muscle coordina-
tion (balance), aerobic capacity, endurance, and body fat.
However, being physically fit does not necessarily equate with
or guarantee superior sports-specific performance.
Head Injury
Each year approximately 300,000 head injuries occur in the
United States, with about 10% being sustained during recre-
ational sports. Many involve young athletes. For example,
approximately 20% of high school football players suffer a
closed head injury each season.17,31 Other high risk sports for
head injury include ice hockey, wrestling, horseback riding,
gymnastics, diving, and trampolining.
Genuardi and King reviewed 33 children and adolescents
with sports-related closed head injuries.30 Discharge instruc-
tions were appropriate in only 10 (30%).
Spinal Injury
Prior to skeletal maturation, injury to the lower back is rela-
tively uncommon, but it becomes more frequent in the older
(adolescent) age groups.14 Lower back injuries usually
involve soft tissue stress and inflammation, and they may
manifest as a loss of lumbar lordosis due to paravertebral
muscle spasm. Anatomic variations may place the child at
risk. An increased incidence of lower back injuries is appar-
ent in certain sports characterized by repetitive spinal stress.
For example, spondylolysis and spondylolisthesis are more
frequent in young gymnasts and figure skaters.35,107,115
Muschik et al. followed children involved in competitive
sports for an average of 4.8 years following a diagnosis of
Physeal Injury
spondylolytic spondylolisthesis.70 There was minimal pro-
gression of the initially present slip despite rigorous training.
They thought that there was no contraindication to taking
part in competitive sports. Olerud and Karlström reported a
cervical spine fracture in a 13-year-old high jumper who was
using the backward, or flop, technique.76
The “stinger’ or “burner” is probably caused by trauma
to the brachial plexus or nerve roots (or both).43,64 It is
common in collision sports such as tackle football. The
injury typically involves unilateral shoulder or arm pain with
burning dysesthesias. Muscle weakness most commonly
involves the biceps, deltoid, and spinatus muscles. Meyer et
al. found that cervical spinal stenosis increased the risk for
having stingers associated with a prolonged or complicated
clinical course.64 Rathbone et al. reported 12 children who
were treated for transient sensory or motor loss after a spinal
injury.92 They did not find a consistent interrelation between
risk and the Torg ratio.
Pizzutillo et al. assessed the spines of 111 patients with
Klippel-Feil syndrome.86 They found a significant difference
if there was increased motion per open interspaces in the
upper, but not the lower, cervical spine. They thought that
individuals with hypermobility of the upper cervical spine
were at risk for neurologic sequelae, whereas those with
altered motion of the lower cervical spine were predisposed
to degenerative osteoarthritis.
Muscle Injury
Injury to muscle may be the result of direct or indirect insult.
Direct injuries cause muscular contusions, hematomas,
strains, lacerations, myositis ossificans, or rhabdomyolysis.
These problems result in the destruction of all or part of an
individual muscle, with the extent of loss being directly pro-
portional to the severity of the insult. Warming up before
any musculoskeletal activity increases flexibility and
decreases some muscular damage.
Muscles have a limited capacity for regeneration and
repair in response to direct injury.5 Injured muscle fibers
initially degenerate for a short distance away from the spe-
cific area of injury. This necrotic tissue is removed by
macrophages and other phagocytic cells. Activation of
reserve myoblasts (probably more prevalent in a child) then
provides a period of rapid cellular proliferation within the
injured muscle. The proliferating myoblasts fuse to form
small myotubes that eventually fuse to reform the muscle.
This complicated repair process is capable of bridging only
small local injuries, whereas the repair process in larger
defects is primarily through the formation of scar tissue.
Indirect injuries occur as a result of either a neurologic or
vascular insult to the skeletal muscle. Neurologic compro-
mise is usually secondary to an upper or lower motor neuron
lesion causing paralysis and eventual muscle disuse. Vascular
insufficiency causes muscle tissue ischemia and usually cel-
lular death to some or all of the muscle.
Magnetic resonance imaging (MRI) is the primary
imaging modality for detecting muscle injury and for deter-
mining the type of injury and the degree of muscle involve-
ment. This technique is highly sensitive to muscle edema and
hemorrhage.
405
Exertional Compartment Syndrome
Acute or chronic exertional compartment syndrome may
occur. Patients typically experience pain and swelling and
may also have sensory deficits, paresthesias, motor weakness,
or motor loss. The diagnosis may be confirmed by intra-
compartmental pressure measurements before, during, and
after the evocative exercise. Modification of athletic activity
usually alleviates symptoms. Fasciotomy is rarely necessary.
Compartment syndromes caused by athletic activity are infre-
quent in children because of differences in muscle metabo-
lism and less strenuous athletic training programs compared
to older adolescents and young adults.24
Congenital/Acquired Limb
Deficiencies
The success of individuals such as Jim Abbott in attaining
major league status in baseball despite congenital absence of
the hand increases the desire of any otherwise physically
normal child who happens to have one or more limb defi-
ciencies to participate in a normal life style as much as pos-
sible. Such participation obviously must address sports.
The significant progress in prosthetic technology allows
limb-deficient children to increase their involvement in
athletics. Energy-saving prosthetic feet (Carbon Copy II,
Seattle Foot) permit the athlete to have better toe-off during
ambulation and a more natural gait pattern, no matter what
the speed. Lighter-weight prosthetics also enhance perfor-
mance.26 Special assistive devices may be attached to the
upper extremity prosthesis to allow the child to catch a ball.
Physeal Injury
Epiphyseal and physeal fractures, which are common in chil-
dren, do not appear to occur more frequently as athletic
injuries in organized or recreational sports during child-
hood.129,130,135,140,145,149,150 Such fractures usually heal within
3–4 weeks, contingent on the type of epiphyseal–physeal
injury. These areas are much stronger during the earlier
phases of repair than healing fractures in the metaphysis or
diaphysis. Return to athletic participation, however, must be
individualized and must include consideration of the
patient’s overall ability, assessment of any damage to joint
function (particularly when a type 3, 4, or 7 growth mecha-
nism injury is involved), and appreciation of the particular
musculoskeletal demands the sport may impose on the
injured area. When the epiphyseal fracture involves a joint,
it is recommended that the child not participate in contact
sports for at least 4–6 months and that sports such as swim-
ming, which allows joint exercise with lessened weight-
bearing stress, be encouraged.
Nyska et al. studied 8 boys (age 13–15 years) who incurred
a fracture of the medial epicondyle while arm wrestling.154
Three fractures occurred during formal competition and
five in friendly matches. The injuries occurred just as the
individual was about to win a match.
406
Specific acute physeal injuries, whether related to sports
injury or other mechanisms of injury, are covered in detail
in Chapters 13–24.
Repetitive Physeal Injuries
One of the more common problems affecting the adolescent
athlete has been termed “epiphysitis” or “apophysitis.” These
terms are used to describe presumed “inflammatory” reac-
tions involving the ligamentous or tendinous insertions into
an epiphysis affected primarily by tensile forces (e.g., ischial
tuberosity, tibial tuberosity, or medial epicondyle of the distal
humerus).153 In reality, many are chondro-osseous fractures,
albeit incomplete, that have not had an opportunity to heal
because of continued stress.157
Epiphyseal Injury
One of the most publicized epiphyseal injuries is “little
league elbow,” a term applied to the throwing (pitching)
mechanism that causes the clinical problem.1,3,4,11,42,50,81,124,125,
128,138,141,144,166,169,171
Excessive duration of throwing or attempts
to throw a curve ball force an immature elbow to change
rapidly from acute flexion to forced extension or to severe
hyperextension with a supinated forearm. This movement
causes an excessive increase in muscular strain within the
flexor-pronator muscle group, manifesting in increased
tensile force at the medial epicondyle of the distal humerus.
Similarly, compressive stresses may damage the proximal
radial epiphysis or capitellum, causing development of an
osteochondrosis in either region (Fig. 12-2).131,167,170 A similar
FIGURE 12-2. Panner’s lesion (arrow) of the capitellum. A congen-
ital angular deformity of the proximal radius probably predisposed
to further injury in this aspiring baseball player (dominant side).
Interestingly, a comparable radial head angulation was present in
the left arm but was not associated with a capitellar lesion. His
father had had similar radial head angulation (bilaterally) and a
deformed capitellar region that had foreshortened a baseball
career.
12. Pediatric Athlete
sort of problem is now being recognized in young children
playing intensely competitive tennis. The mechanism of the
serve is similar to that of overhand throwing of a baseball.
Torg and Moyer described the nonunion of a stress fracture
through the olecranon epiphyseal plate in an adolescent
baseball pitcher.236 It represented another type of injury to
the elbow that must be suspected in young adolescents who
complain of persistent pain around the elbow.
Because of the hypervascularity associated with the normal
repair response, these various areas may be the sites of exces-
sive growth, leading to localized overgrowth of the capitel-
lum and radial head and, possibly, to a cubitus varus or valgus
deformity. Furthermore, when the capitellum is involved the
articular surface may be fragmented, and loose bodies may
be created within the joint (see Chapter 15). Limiting the
amount of pitching to some degree probably affects the inci-
dence of this condition.
Carter and Aldridge reported 21 children with stress
injury to the distal radial growth plate;132 all of these injuries
were seen in elite class gymnasts. There were 17 boys and 4
girls with an age range of 9–17 years. The symptoms included
pain around the wrist aggravated by both active and passive
dorsiflexion. Often the pain was localized to the radial
styloid process. Symptoms were worsened after exercise rou-
tines involving weight-bearing on the hands (rotation and
compression). Retardation of skeletal age in boys and girls
increases the length of time during which the physis is at
risk for damage. Of these 21 patients, 11 had symptoms
of other osteochondritic conditions (Osgood-Schlatter,
Sever, Sinding-Larsen). Others have reported similar find-
ings.126,133,139,147,152,159,164,175 Any sports that stress the wrist
may cause similar problems.163 Vender and Watson de-
scribed bilateral Madelung-like deformities in a 17-year-old
gymnast.172
Roy et al. studied 21 gymnasts with chronic distal radial
injuries.162 Eleven had radiographic changes: physeal widen-
ing, fragmentation, cystic changes, and irregularity of the
metaphyseal margin (referred to as a “beaked effect”).
Recovery took at least 3 months. Ten other gymnasts with
symptoms but no roentgenographic changes recovered
within an average of 4 weeks.
Aubergé and colleagues reported that 87 (83%) of 105
adolescent gymnasts had stress changes of the distal radius
at the European Junior Gymnastics Championships in 1980.
They found a delay in bone age in 73% of boys and 78% of
girls.6 They thought it was probably due to unbalanced diet
and repeated microtrauma to the physes. Although most of
the changes affected the wrist (the only area radiographed),
some changes were also noted in the proximal carpal row.
They noted increased density in the metaphyseal bone
adjacent to the physis. The sclerosis appeared to be wider
and less well defined than the typical Harris line. The
ulna was also widened in a significant number of these
adolescents.
The magnitude of the forces generated across the distal
radius during gymnastic activities and the influence of these
forces on the growth plate are not well understood. Chang
and associates found similar changes in wrists of acrobats and
dancers who practiced routines comparable to gymnasts.134
They described small areas of focal growth arrest (metaphy-
seal clefts) often associated with an area of physeal widening.
Stress Fractures
It is probably compressive, twisting loading that leads to
these irregularities. They noted an increase in ulnar-plus
variance. Fourteen (8.2%) of 170 wrists in the fused physis
group had an exceedingly large ulnar-plus variance. Of
352 wrists, 61 (17.3%) had abnormal morphology of the
distal radius in the unfused physis group. Widening of the
physis was the most common finding. Significant ulnar--
plus variance may cause pain sufficient to warrant ulnar
shortening.
Tolat et al. described a clinical test in which pain was
elicited when the ulna was held down, the wrist deviated
ulnarward, and the forearm supinated.165 Significant pain
in two of five patients was treated by ulnar shortening, and
a third had shaving of a triangular fibrocartilage complex
perforation.
Some authors have described bilateral proximal humeral
physeal injuries in gymnasts that is similar to little league
shoulder.136,169 In one instance there was progression to a
slipped proximal humeral epiphysis.136
Atraumatic osteolysis of the distal clavicle (AODC) is a
painful stress overload syndrome that may occur in primary
(power) weight lifters and in throwing athletes or tennis
players who are adjunct weight lifters.89,91,102 The adolescent
athlete is at the early stage of symptom presentation and may
develop the lesion by chronic inflammation of the distal cla-
vicular physis. This creates widening similar to the gymnast’s
wrist.
Apophyseal Injury
Another pattern of chronic (repetitive loading) injury is that
of apophyseal failure. Although any apophysis may be acutely
avulsed, the chronic injury is associated with minimal (if any)
displacement and an ongoing reparative inflammatory
process. These injuries typically occur in the athletically
active child or adolescent between 8 and 15 years of age.
They usually present as periarticular pain associated with
muscle–tendon imbalance (e.g., the tight heel cord in the
Sever lesion). Conservative therapy includes rest, ice, com-
pression, nonsteroidal antiinflammatory agents, modi-
fication of the athlete’s participation intensity level, change
in position played, temporary discontinuation of the evoca-
tive activity, and increased flexibility and strengthening upon
resumption of sports. All of these measures are essential.
Mafulli et al. described overuse injuries in 12 elbows of
eight elite gymnasts aged 11–15 years.151 There was a spec-
trum of radiologic abnormalities that included widening of
the olecranon physis and fragmentation of the epiphyseal
ossification center. The authors thought that the injury
pattern was similar to the Osgood-Schlatter lesion. Two older
boys (18 and 19 years) had stress fractures through the olec-
ranon physis. One required screw fixation.
Nonunion of an olecranon physeal stress fracture was
described in 16-year-old wrestler.127 The opposite side was
closed. He was treated by bone grafting and tension band
wiring. A biopsy showed tissue compatible with a nonhealing
fracture. Others have also described isolated instances of this
lesion.146,156,160,174
In the lower extremity, insertion of the Achilles tendon
into the epiphysis of the calcaneus sometimes leads to an
entity known as Sever disease (calcaneal apophysitis). This
407
condition is best treated by rest and heel cord stretching; and
it sometimes benefits from the use of heel cups.
The most frequently affected area in the lower limb is the
tibial tuberosity, where the Osgood-Schlatter lesion mani-
fests. Anatomic and experimental studies suggest that this
lesion represents an avulsion of portions of the patellar
tendon and contiguous tibial tuberosity as the secondary
ossification center is forming.155 The condition leads to the
formation of displaced, excessive osteocartilaginous tissue
(callus) and a prominent deformity on the anterior tibia that
may elevate the patellar tendon and patella enough to affect
mechanical function along the patellofemoral axis. This
lesion is best treated by rest and may require immobilization
in a cylinder cast for 3–4 weeks. It is considered a type of
chondro-osseous stress fracture.
Around the pelvis, the attachments of the sartorius to the
anterosuperior iliac spine, the rectus femoris to the anteroin-
ferior iliac spine, the psoas to the lesser trochanter, an the
hamstrings to the ischial tuberosity are all areas of potential
apophysitis. They are also areas that can be completely
avulsed as a result of excessively severe muscle contrac-
tures.148,173 Repetitive avulsion of any of these regions may
lead to overgrowth of the region due to a biologic equiva-
lent of chondrodiastatic bone lengthening (see Chapter 19).
Osteochondroses
An additional type of chronic, stress-related injury is the
osteochrondrosis. The exact cause is unknown, but presum-
ably there is repetitive (trauma-induced) disruption of the
microvasculature of a developing ossification center leading
to focal osteonecrosis followed by resorption and reforma-
tion of some or all of the ossification center.137,143 The osteo-
clastic resorption of the original ossification center may be
focal or complete. The bone that replaces the original center
is like any fracture callus: randomly oriented primary bone
trabecula that must be gradually remodeled to respond
effectively to biomechanical demands. When the biome-
chanics of the ossification center are exceeded, microfrac-
tures occur that may cause early pain (which is when the
child presents for evaluation). The process may continue to
significant deformation (collapse) of the ossification center.
In a tarsal region (e.g., the Kohler lesion in the tarsal navic-
ular) complete restitution may occur. However, in a long
bone the contiguous growth plate may be adversely affected,
leading to impaired longitudinal growth while more periph-
eral latitudinal physeal growth continues—but under restric-
tions imposed by the impaired central physis. This
redirection of growth potential may lead to major structural
deformation, which is readily evident in the Legg-Perthes
lesion.
Mafulli and Bayter-Jones noted that young gymnasts were
found to have a high incidence of osteochondritic lesions,
intraarticular loose bodies, and signs of precocious joint
aging.54
Stress Fractures
Bone is a dynamic tissue. Its functional mass models and
remodels in predictable patterns in response to externally
408 12. Pediatric Athlete

and internally applied stresses. A stress fracture results from

application of a relatively acute abnormal stress or torque or
from excessive, highly repetitive “normal” stress to a bone
that has normal elastic resistance, a characteristic of most
children’s bone. Stress fractures may result from muscular
activity on bone, rather than from direct impact. Most stress
fractures share one or more of the following causal factors:
(1) the activity is new or different for the individual; (2) the
activity is strenuous; or (3) the activity is repeated frequently
enough to produce the symptoms. Fractures may also occur
when normal, or physiologic, stress is placed on a bone that
has deficient elastic resistance (e.g., osteogenesis imperfecta
or a sclerotic rather than pseudarthrotic tibia). The fatigue
stress fracture occurs in normal bone when abnormal mus-
cular tension or torsion is placed on it. The insufficiency
stress fracture results when normal muscular stress is placed
on a bone in which elastic resistance is deficient. Most stress
fractures are of the fatigue type (i.e., overuse or repetitive
use). Stress fractures usually occur at reasonably predict-
able sites, which relates to the activity that produces
them.168,182,187,188,197,204,214,225,229,233,237
The incidence of stress fractures increases with age. Orava
et al. found that 9% of these injuries occurred in children
less than 15 years old, 32% in the 15- to 19-year group, and
59% in patients older than 20 years.225 Such studies, however,
rarely include toddlers with their specific array of stress
fractures.
Youth is a risk factor for stress fracture. Milgrom et al.
studied 783 male military recruits for the 14 weeks of
basic training.217 The risk of developing a stress fracture
reduced by 28% for each year increase of age above 17 FIGURE 12-4. Distal fibular stress fracture (arrow).
years.

Yngve reviewed the published literature on stress fractures

FIGURE 12-3. Stress fracture of the posterior proximal tibia (white
arrow). Did the adjacent fibrous cortical defect (black arrow) affect
cortical remodeling at the metaphyseal–diaphyseal transition?
in children less than 14 years old.243 The tibia was most com-
monly involved (51%), followed by the fibula (20%), pars
interarticularis (15%), femur (3%), metatarsal (2%), and
tarsal navicular (2%). Interestingly, there was no mention of
the calcaneus, which has been reported relatively frequently
as a stress fracture site in limping toddlers.179,192
The most common sites of stress fractures in children are
the upper third of the tibia (Fig. 12-3), the lower half of the
fibula (Fig. 12-4), followed by the metatarsals, rib, pelvis,
femur, and humerus.* Meaney and Carty reviewed five stress
fractures of the femur in children aged 5–14 years.215 Stress
fracture of the metacarpal has been reported in an adoles-
cent tournament tennis player.222 These stress fractures
become more common when children increase their level of
activity after a period of relative inactivity (e.g., spring activ-
ity after a relatively dormant winter).203
Most stress fractures of the tibia occur in the upper or
lower third, are posterior, are associated with running, and
usually heal with rest. Diaphyseal stress fractures may occur
to the posterolateral cortex (Fig. 12-5). In contrast, stress
fractures of the anterior tibial diaphysis (Fig. 12-6) are less
frequent and occur mostly in leaping athletes. Beals and
Cook stated there is a high risk of complete fracture if the
* Refs. 167,178,180,185,189,194,196,200,206,211,213,215,218,226,239,
241,242,246.
Stress Fractures 409

was obtained). The fibular stress fracture healed following

resection of the synostosis.
Stress fractures have an especially high incidence in amen-
orrheic athletes, especially runners. Stress fractures occur
much more often in female athletes than in their male coun-
terparts.210,212,240 The incidence may be as much as 12 times
higher in female athletes. Gait differences, more slender
bones, different biomechanics caused by the wider pelvis,
and amenorrhea may be factors. Amenorrhea may be
primary (has never begun) or secondary (menstruation has
started but then stops for longer than 3 months). The inci-
dence of secondary amenorrhea may be as high as 40%,
whereas the incidence in the general population is less than
1%. Amenorrheic athletes also should be evaluated for
anorexia nervosa or having an eating disorder. The clinical
implications of amenorrhea center on the loss of bone mass
that results when estrogen levels are low for a prolonged
period.212,224
Bone bruises may be another manifestation of a stress
reaction. They are generally transient, and most disappear
within 6 months. Pathologically, they are associated with
marrow hemorrhage and edema. Arendt and Griffiths did
not believe they were related to trabecular or cortical frac-
tures.176 However, recent histologic studies support a role for
trabecular injury (microtrauma) in bone bruising (see
Chapter 6).

FIGURE 12-5. Diaphyseal tibial stress fracture (arrow).

affected patients are allowed full activity.177 They believed

that rest alone allowed only a 40% return to full activity.
Instead, they recommended excision of the fissure, trans-
verse drilling at the fissure site, and cancellous bone
grafting.
Haasbeek and Green described stress fractures of the
ala of the sacrum in two adolescent female athletes being
evaluated for low back pain.201 Rajah et al. also reported
a sacral stress fracture.228 An example is shown in Chapter
18.
Singer et al. reported multiple identical stress fractures in
monozygotic twins sustained while undergoing basic military
training.234 The stress injuries were within the femurs (bilat-
eral, but with differing scintigraphic activity) and the right
talus. The identical patterns suggested a genetic role in addi-
tion to other recognized factors.
Zlatkin et al. described five patients who developed stress
fractures of the distal tibia or calcaneus while under treat-
ment for acute fractures of the tibia and fibula.244 Three
patients were under 10 years of age (youngest was 5 years).
The other two were 17 years (open physes) and 38 years.
These authors thought that the children may have been
unable to discern new pain (stress fracture) from the exis-
tent fracture pain.
A 19-year-old developed a fibular stress fracture associated
with a distal tibiofibular synostosis.205 He had injured his
ankle at age 11 years and reinjured it at 16 years. Apparently
there was no radiographic evidence of a synostosis (or none FIGURE 12-6. Stress fracture of the anterior cortex.
410
Pathomechanics
When a bone–muscle system is stressed, changes take place
that generally result in increased tone or strength of all com-
ponents of the system. Bone usually hypertrophies or remod-
els as a response to directed exercise, but the rate of this
response is much slower than it is for muscle. If an individ-
ual uses increased muscle strength to perform an activity
more vigorously, a stress fracture may result in bone that has
not yet completely compensated (remodeled) for the spe-
cific demands of the new activity.183,223
Stress fractures usually begin as small cortical cracks that
progress as the osseous strain increases or continues.186,191,235
Crack propagation is initiated by subcortical infractions
ahead of the main crack. With increasing age, the elasticity
of bone decreases and its predisposition to fracture
increases. This predisposition may be particularly true of the
adolescent going through major physiologic changes during
maturation of bones during rapid longitudinal growth. In
many instances the patient is unaware of the developing
crack until it extends to a complete fracture. This finding is
common among young children and adolescents who often
perform “with pain,” attributing it to pulled muscles or
“pointers.”
Experimental tibial diaphyseal stress fractures may be
induced by repetitive application of nontraumatic impulsive
loads.181 No definite fractures were seen on the radiographs,
although microdamage (multiple intracortical microcracks)
were readily evident at these sites on a positive bone scan.
Description of the histologic appearance of stress fractures
are limited. The initial pathologic change appears to be
increased cortical resorption.197 Such resorption results
from formation of hollow channels through the cortex. This
process of osteoclastic tunneling normally takes place grad-
ually throughout childhood, adolescence, and early adult
life. The resorption spaces are normally filled with mature
haversian systems. In this fashion, the circumferential lamel-
lar bone of childhood is gradually converted to osteon bone,
which is structurally more compatible with weight-bearing
stresses.
The most important stimulus to this conversion process is
use. However, with excessive use, cortical resorption may be
stimulated to an accelerated rate as susceptibility to localized
injury is increased. Relatively immature trabecular bone can
be formed more rapidly than mature osteon bone, as it is the
normal healing response. If the temporary buttressing bone
is not formed rapidly and if continued excessive stress is
applied to the bone, microfracture or gross fracture may
occur.
Resorption of cortical bone is a normal process that takes
place during childhood and adolescence. Osteoclastic activ-
ity results in many microscopic channels through the cortex,
especially in the metaphyseal region. Eventually, these
resorption cavities are filled by mature haversian systems.
The lamellar bone is gradually replaced by more structurally
adapted osteon bone.
The usual sites of stress fractures in children are areas of
junction between the metaphyseal and diaphyseal cortices in
regions in which fenestration is less prominent, compared
with the juxtaepiphyseal region, and in which biomechani-
cal stresses change between lamellar bone and osteon bone.
12. Pediatric Athlete
Bone responds to excessive stress and strain by accelerating
the normal process of cortical resorption and remodeling of
the haversian systems. The cortex may be weakened by for-
mation of numerous resorption channels, but usually such
structural changes are the consequence of normal anatomic
variations.
In the child subjected to undue stress, particularly after a
period of relative inactivity, the buttressing process that nor-
mally strengthens the bone at the metaphyseal–diaphyseal
junction has not occurred, and excessive stress continuously
applied to the bone may result in a subclinical fracture. With
a stress fracture, cortical resorption is increased, periosteal
and endosteal new bone forms, the resorption cavity in the
cortex is filled in, and the periosteal and endosteal new bone
matures. All this represents excessive modification of the
normal chondro-osseous developmental patterns.
Historically, stress fractures have been described to be the
result of a healing process in bone, as this is the response
pattern usually evident on the standard radiograph. The
stress fracture may not be recognized until it has progressed
to an intracortical fracture with extension to and elevation
of the periosteum.238 It is more appropriate to consider a
stress fracture as the end result of a continuum of biologic
reaction of a region of the bone to repetitive external stress.
This biologic response alters the balance between normal
tissue repair and the remodeling process. It results in tem-
porary disturbance in the equilibrium between bone resorp-
tion and bone regeneration.
Mori and Burr proposed that fatigue damage and micro-
cracks initiated the remodeling events.220 Bone remodeling
occurs preferentially in fatigue-damaged regions and sup-
ports a direct cause-and-effect relation between the initiation
of microdamage in bone and its repair. Any suppression of
this repair mechanism would potentially allow microdamage
to accumulate and cause eventual failure of the bone.
Carter and Caler suggested that tension damage in bone
from high-stress, low-cycle repeated loading may be creep
damage rather than tension failure.184 Such creep damage
consists of failure along cement lines and cement bands.
Such a pattern is compatible with changes shown in torus
greenstick fractures (see Chapters 1, 2) and occult physeal
fractures (see Chapter 6).
Diagnosis
Clinical and radiographic findings in children may differ
from those in adults, in part because of the greater tendency
of the young bone to undergo normal elastic and plastic
deformation and remodeling and in part because of the rich
blood supply of the growing bone. Stress fractures in chil-
dren present diagnostic problems because the child may
exhibit listlessness, slight fever, swelling, and tenderness that
must be distinguished from the clinical features of tumors
and osteomyelitis.207 A biopsy should be considered if any
uncertainty exists.
Radiology
Routine radiography of suspected stress fractures should
include repeat examinations in 1–2 weeks (Fig. 12-7). Mag-
nification studies with fine focal spot technique and tomog-
Stress Fractures
FIGURE 12-7. Radiograph of the tibia 2 weeks after the onset of
pain. Subperiosteal reactive bone is evident. The fracture line
(arrow) is barely evident.
FIGURE 12-8. (A) Scan of 10-year-old child with shin splints. (B) CT scan of the stress fracture callus (arrow). (C) More extensive reac-
tive change in a 12-year-old jogger.
411
raphy may prove helpful for making the diagnosis. Radio-
logic studies of stress fractures reveal a range of relatively late
skeletal responses from periosteal reactions and endosteal
sclerosis to obvious fractures.
The roentgenographic changes of stress fractures, as typi-
fied by the tibia, may be divided into three phases.208 Initially,
there is a small area of radiolucency in the cortex of the tibia,
associated with some metaphyseal/endosteal increase in
bone density and a fine haze of periosteal reaction. These
findings are usually present 2–3 weeks after the onset of
symptoms. This phase is often missed in children. Follow-up films
reveal a gradual increase in the periosteal and endosteal new
bone. The second phase is sometimes associated with the
appearance of a definite, incomplete, radiologically evident
defect. If a fracture does occur (phase 3), this periosteal and
endosteal new bone matures and is partially resorbed.
The possibility of other causes of bone pain and signal
changes should be considered. Several conditions should
receive consideration in the differential diagnosis of stress
fractures in the adolescent232: osteoid osteoma, chronic scle-
rosing osteomyelitis, and Ewing’s or osteogenic sarcoma.
Early infection or marrow tumors (lymphoma, leukemia)
may cause similar signal changes on MRI scans. Most solid
tumors (Ewing’s, osteosarcoma) would show up as a “mass”
on T1 and T2 sequences. Periosteal changes may indicate an
osteomyelitis.
Radioisotope scanning with technetium 99m is useful for
evaluating stress fractures.199,216,221,230,245 This technique allows
early diagnosis of suspected lesions, as the bone scan is
usually positive before there are any radiographic findings
(Fig. 12-8). Scintigraphy allows a much earlier diagnosis
and, accordingly, earlier inception of treatment. However,
the technique is not specific for stress fracture. Early
osteomyelitis, which often has similar clinical signs and
symptoms, may produce the same scintigraphic appearance.
412
TABLE 12-1. Grading of Stress Fractures
Grade Radiograph
1 Normal Poorly defined areas of increased activity
2 Normal More intense, but still poorly defined
3 ? Fracture line Sharply marginated areas of increased fusiform
? Periosteal reaction
4 Fracture or subperiosteal reactive bone More intense focal uptake
Modified from Arendt and Griffiths.176
STIR = short tan inversion recovery; T1, T2 = MRI images.
Prather and associates reported the use of bone scanning for
evaluating stress fractures.227 The roentgenograms of 15
patients were normal, whereas the bone scan was positive.
The need to obtain total body scans, rather than focal spot
films, should be emphasized, because four of the patients
had other fractures.227
Rosen et al. studied 26 patients with stress-related abnor-
mal scintigraphy.230 Twelve (46%) had a multifocal pattern
of abnormalities; only eleven (28%) had abnormal
roentgenograms. The multiple abnormalities were fre-
quently unsuspected clinically, and studies limited to the
symptomatic areas would have failed to detect them. Of 19
patients with a tibial abnormality, 11 had a contralateral
clinically silent lesion.
Miller and Osterkamp described increased radionuclide
uptake in an 8-year-old with ulnar bowing.219 This corrobo-
rated the traumatic nature of the bowing.
Single-photon emission computed tomography (SPECT)
is especially useful for delineating early pars interarticularis
weakening, sometimes before a fracture finally occurs. Roub
et al.231 and Floyd et al.198 proposed a gradation of radionu-
clide findings ranging from early symptoms (occult injury)
to evident fracture. These scintigraphic gradations were cor-
related clinically by others.186,245 However, these gradation
schemes are not widely accepted in either the orthopaedic
or radiologic communities,231 undoubtedly due to the vague-
ness of the demarcation between each of the grades. Perhaps
quantitative scintigraphy could be applied to allow numeric
intensity gradation staging.
Magnetic resonance imaging may be more sensitive than
bone scans for demonstrating early stress changes in
bone.202,209 Arendt and Griffiths proposed an MRI grading
system (Table 12-1).176 They augmented the usual T1 and T2
images with MR sequences that demonstrate subtle marrow
changes, most of which rely on fat suppression. They include
FLASH (fast low-angle shot), FISP (fast imaging steady-state
precession), and STIR (short tan inversion recovery). They
used the STIR sequencing to detect early stress-related
changes. STIR sequences suppress normal bone marrow
fat signal, allowing better visualization of intramedullary
abnormalities. They also noted an infrequent finding of
periosseous edema surrounding a long bone. This undoubt-
edly reflects subperiosteal hemorrhage, especially in the
12. Pediatric Athlete
Bone scan MRI
Positive STIR
Positive STIR
Positive T2
Positive T1
Positive T2
No cortical beak
Positive T1
Positive T2
Fracture line
child or adolescent in whom this tissue separates readily in
response to fluid such as blood or pus that seeps through
microcracks or normal fenestrations in the diaphysis or
metaphysis. It is seen most often in the fibula and ulna.
These authors have thought it useful to group grades 1 and
2 as “low-grade” stress fractures or “stress phenomena.”
Grades 3 and 4 are “high-grade” stress fractures. They
thought that grade 3 was the most variable in their MRI pre-
sentation and the most difficult to define.
Burr et al. described an occult proximal tibial metaphyseal
fracture not seen on regular film but evident on MRI.181 It
was probably an undisplaced type 2 growth mechanism
injury. Interestingly, the youngster had been complaining of
pain for several days and was being evaluated for the possi-
bility of a proximal tibial stress fracture.
Treatment
Treatment of low-grade stress fractures comprises 3–6 weeks
of rest and discontinuation of athletic activity. High-grade
stress fractures may require 3–4 months of the same regimen.
At the end of this period the patient may still have discom-
fort but should not have the same pain level that was present
at the inception of diagnosis and treatment.
As the patient resumes activity, ice and physical therapy are
used to control inflammation. If normal walking causes pain,
crutches are used until pain-free walking is present. Activi-
ties that minimize weight-bearing, such as swimming, flota-
tion running, and low resistance cycling, may be used. Upper
body training may continue.
Once the patient has pain-free walking, he or she may ini-
tiate light-weight exercises and nonimpact loading activities
(e.g., Stair-Stepper, gliding machine). The final phase is
resumption of the evocative sports activity. Activity should be
undertaken initially on alternative days.
Toddler’s Fracture
A characteristic stress injury of children 9 months to 4 years
of age is the toddler’s fracture (Figs. 12-9, 12-10).190,195 It is
found in a child who suddenly refuses to bear weight and is
irritable, often with no observable trauma. There is localized
Stress Fractures 413

FIGURE 12-10. Minimally evident stress fracture in a toddler who

had been limping for 9 days. A radiograph after 2 days of limping
was read as “negative for fracture” by the radiologist.

FIGURE 12-9. (A) This 14-month-old girl sustained a “toddler’s frac-

ture” of the fibular diaphysis. (B) One year later she was limping
again. The roentgenogram showed residual bowing of the fibula
but no acute injury. The area over the proximal tibia was tender.
She was placed in a non-weight-bearing cast. Three weeks later
reactive subperiosteal bone compatible with a tibial stress fracture
was evident.
hematoma formation; and as it calcifies this callus may
become evident on the radiograph.
The fibula may also sustain a stress fracture at a younger
age than most other bones (Fig. 12-11). The youngest child
in Devas’ series was 2 years.193

warmth and tenderness but no clinically observable swelling.

Roentgenologic investigation discloses soft tissue edema as
the earliest sign. Sometime later an undisplaced fracture line
that runs in a spiral or oblique manner inferiorly and medi-
ally may be noted (Fig. 12-10). Detection of this line may
require an oblique projection. The fracture often extends
proximally into the upper tibia. The only suggestion of the
antecedent injury may be subperiosteal new bone.
In the tibia of a slightly older child (3–5 years), the stress
fracture is nearly always in the upper third of the bone (trans-
verse fracture). The child has a painful limp that is usually
of gradual onset but occasionally manifests suddenly. Young
children, especially toddlers just beginning to walk or still
mastering the mechanics of walking, often refuse to bear
weight on the affected leg. Sleep is usually unaffected. The
pain improves with rest but may not go away entirely until
the process resolves. Tenderness may extend along the shaft,
depending on the size of the subperiosteal reaction. Radio-
graphically, there is a (haze) of internal callus across the
shaft, subperiosteal new bone formation, and sometimes
slight disruption of the cortex. No linear fracture is radio-
graphically evident because it is usually a compression FIGURE 12-11. Distal fibular stress fracture with subperiosteal new
stress fracture. The periosteum is elevated, presumably by bone.
414
Stress fractures of the fibula are much more common in
toddlers and young children than in adults.193 It has been
noted that fractures of the fibula accompanying the toddler’s
fracture of the tibia are uncommon. Stress fractures of the
calcaneus, although uncommon in children, should be con-
sidered in the differential diagnosis of the limping child (see
Chapter 24).
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13
Chest and Shoulder Girdle
Engraving of a scapula and clavicle showing separation of the
entire cartilaginous glenoid from the scapula. (From Poland J.
Traumatic Separation of the Epiphysis. London: Smith, Elder,
1898)
lthough the clavicle is one of the most frequently
A injured bones in the developing skeleton, especially
before 5 years of age, the remainder of the pectoral
girdle components are infrequently injured in infants and
children. Prior to 10 years of age the ribs and sternum are
extremely pliable and capable of much more elastic and
plastic deformation than comparably skeletally aged longi-
tudinal bones of the appendicular skeleton. The scapula is
resilient, mobile, and well padded with muscles, all of which
are qualities that afford it a great deal of protection from
externally applied forces. In contrast, the clavicle is not as
flexible as the other elements of the pectoral girdle and is
extensively subcutaneous. The clavicle develops a thick
cortex and multiple curves and is relatively rigid at the ster-
noclavicular and acromioclavicular joints, characteristics that
increase its susceptibility to fracture and to sustaining prox-
imal or distal physeal disruptions.1,18,21
Anatomy
Ribs
The ribs develop elongated cartilage segments anteriorly
that are analogous to an epiphyseal–metaphyseal junction
and a vertebral end, with two epiphyses, physes, and sec-
ondary ossification centers. The sternal ends have a growth
plate that contributes to elongation of the ribs. Although no
parameters of growth contribution have been derived for the
rib, it is likely that more rib elongation occurs at the sternal
end than from the growth plates at the spinal (posterior)
end. The cartilage of the 2nd to 6th ribs forms an articula-
tion within the sternum, with each joint being located
“between” successive sternebrae. The remaining ribs have
longer cartilaginous ends that generally articulate with the
cartilage of the superior rib.
The sternal junction of the first rib differs from that of the
other ribs. It is usually a rigid cartilaginous interposition
between the manubrium and rib that subsequently ossifies
to create another nonresilient “joint” compared to the lower
ribs (2nd to 10th).28 This factor probably predisposes the first
rib to stress fractures.
The “chondral” (chondro-osseous) portions of the ribs
are epiphyseal analogues. Eventually the proximal tissue may
form multifocal calcifications or even secondary ossification
centers, although this occurrence is most often present in
adults. Damage to the chondro-osseous junction could hypo-
thetically affect rib growth, although the absence of an anal-
ogous secondary ossification center makes growth arrest
unlikely.
Sternum
The sternum is comprised of three anatomic regions:
manubrium, sternebra, and xiphoid. The manubrium
usually ossifies as a single center. In contrast, the sternal
segment develops multiple, paired ossification centers that
reflect both embryonic metamerism and the two lon-
gitudinal components that migrate toward the midline (Fig.
13-1). These ossific sternebra progressively arise owing
to biomechanical modification within the cartilaginous
anlagen.5,15,25,27,31 The sternebra appear separate on the
419
420
lateral roentgenogram and may also show right/left seg-
mentation in the anteroposterior view.11,16 Such right/left
ossification may be asymmetric or oblique, although the
latter may be due to congenital variation. The intervening
normal cartilaginous regions between sternebrae should not
be misinterpreted as fractures. Pain or tenderness at such a
chondro-osseous junction may indicate an undisplaced
occult fracture through the juxtaposition of cartilage and
bone. The xiphoid is the last segment of the composite
sternum to ossify. Ossification is usually unifocal.
The sternum articulates with the upper ribs (2nd to 6th,
sometimes the 7th) through nonsynovial joints. There is
limited motion in each junction, with the resilient cartilage
of the developing ribs allowing the increased chest excursion
characteristic of a young child. In contrast, the 1st rib never
forms a comparable “joint” with the manubrium. The carti-
lage of the 1st rib is anatomically continuous with the carti-
lage of the manubrium. This anatomic difference is a
significant biomechanical factor in the development of stress
fractures and nonunion of 1st rib fractures in children and
adolescents.
The 8th through 10th ribs have elongated cartilage that
extends cranial toward the next rib, rather than the sternum.
There is no discrete articulation between rib cartilage (Fig.
13-1). Anterior cartilage is minimal on the 11th and 12th
ribs.
Clavicle
The clavicle is the first fetal bone to undergo ossification,
doing so initially by membranous ossification with minimal
or no prior endochondral staging.2,12,23,29 Cartilaginous
growth areas subsequently develop at both ends. Normal
primary ossification of clavicle begins within two mesenchy-
mal anlagen, each with a center of ossification.9 They appear
at 6 gestational weeks and fuse approximately 1 week later.
This bipartite ossification pattern may be a factor in the
13. Chest and Shoulder Girdle
FIGURE 13-1. (A) Development showing bifid
sternal ossification (3 years). (B) Fusion of the
sternal units in an adolescent. The manu-
briosternal junction has not comparably fused.
development of congenital pseudarthrosis (although there
is still the conceptual problem of why this entity almost
invariably affects the right side). The junction of the two
embryonic centers of ossification are situated between the
lateral and middle third of the clavicle and consequently
does not correspond to the usual site of the congenital
pseudarthrosis.
The clavicle extends from the manubrium to the acromial
process of the scapula, serving as the only normal osseous
articulation between the arm and the chest. It is constantly
subjected to medially directed forces from the arm. The
bone has a double curve, being convex along the medial two-
thirds and concave along the lateral third (Fig. 13-2). The
pattern of the curve changes during postnatal development
and growth as the medial (sternal) segment elongates more
rapidly than the lateral (acromial) segment (Fig. 13-3).13,21,26
The double curve of the clavicle is a potential point of weak-
ness in the active child. Furthermore, this double curve imi-
tates an undisplaced clavicular fracture in some radiographic
projections, especially if the nutrient artery is visualized in
an unusual position.6
The medial end of the clavicle is concave and larger than
the clavicular notch of the sternum, with which it forms an
articulation. The two articulating surfaces are thus incon-
gruent, and the joint is potentially unstable. An intraarticu-
lar meniscus partially contributes to joint stability and acts as
a shock absorber. Strong ligamentous support anteriorly and
posteriorly also stabilizes the joint. Virtually every motion of
the upper extremity involves some motion within this joint.
The lateral third of the clavicle provides attachment for
the trapezius and deltoid muscles. In the medial two-thirds,
the sternocleidomastoid muscle inserts above, and the pec-
toralis major muscle inserts below. The subclavius muscle
originates along the inferior clavicular groove. Awareness of
these various muscular insertions and origins is important
for understanding the directions of displacement in clavicu-
lar fractures. There are strong costoclavicular ligaments
Anatomy
FIGURE 13-2. Series of clavicles from subjects
ranging in age from 3 months (postnatal) to 14
years. Note the medial (sternal) ends (M), lateral
(acromial) ends (L), and the usual location of
fractures (F).
proximally, and the conoid and trapezoid ligaments connect
the clavicle with the coracoid process distally. In the child
these two ligaments primarily attach into the thick
periosteum. As skeletal maturity is reached, Sharpey’s fibers
attach these ligaments more densely into the clavicular
cortex.
The superior surface of the clavicle is subcutaneous
throughout its entire length. This subcutaneous location
potentially increases the risk of penetration of the skin in an
angulated fracture, but such open fractures are rare in chil-
dren and adolescents, although “tenting” of the skin often
occurs. It also makes the reactive callus after a fracture quite
prominent, a fact that should be emphasized to the parents
FIGURE 13-3. Clavicular growth patterns between the ages of 3
and 16 years (relative sizes derived from specimen radiographs).
The endochondral cones show relative increases in length and
width from the proximal (sternal) and distal (acromial) ends, with
the nutrient artery used as the base reference point. Note the nutri-
ent foramen (N) and canal, the proximal endochondral cone (PEC),
and the distal endochondral cone (DEC).
421
at the beginning of diagnosis and treatment, not after the
mass appears and the parents voice concern.
Between the ages of 15 and 18 years a secondary ossifica-
tion center develops in the sternal end of the clavicle (Fig.
13-4). It is normally the last secondary center to appear. It is
often difficult to visualize, even in special sternoclavicular
views.6,7 The secondary center usually fuses with the shaft by
25 years of age14,16,26 and is the last epiphysis to fuse with the
adjacent metaphysis. This area usually sustains a physeal frac-
ture, rather than a sternoclavicular joint disruption, because
of this unique anatomic configuration.17
The medial end of the clavicle is attached to the sternum
and first rib by dense fibrous tissue that is difficult to disrupt
in a child.3 This joint also has a meniscus that further con-
tributes to sternoclavicular stability (Fig. 13-5).
The distal clavicular epiphysis is relatively thin and resem-
bles the distal epiphyses of the phalanges. Developmentally,
much of the epiphyseal cartilage is replaced directly by me-
FIGURE 13-4. Sternoclavicular ends from two adolescents (15 and
17 years) show early development of proximal epiphyseal os-
sification centers (open arrows) and satellite ossification (small
arrows). The usual location of a fracture of the medial clavicular
epiphysis is shown (F, curved arrows).
422 13. Chest and Shoulder Girdle

FIGURE 13-5. (A) Intact left (l) sternoclavicular joint and exploded right (r) joint
show actual anatomy. Note the manubrium (ma), meniscus (m), and proximal
clavicular epiphysis (e). (B) Slab section showing the meniscal articulation of the
sternoclavicular joint. On the opposite side the nonarticulated synchondrosis of
the first rib to the sternum (manubrium) is evident (arrow).

taphyseal bone. This small epiphysis and physis contribute
only about 20–30% of the overall longitudinal growth of the
clavicle.24 Caffey did not describe secondary ossification in
the distal clavicle.4 Similarly, in an anatomic and roentgeno-
graphic study of postnatal clavicular development, no distal
secondary ossification was observed.24 In an extensive review
of hundreds of specimens and radiographs, there was only
one example of secondary ossification in the acromial end.30
This may have been a pseudoepiphysis, which certainly forms
in those ends of the phalanges and metatarsals that do not
form a true secondary ossification center. Hence this bone
resembles the longitudinal bones of the hands and feet with
a secondary ossification process in one end and direct
osseous expansion from the metaphysis at the other end.
The acromioclavicular joint appears to be a relatively fixed
joint with minimal motion. Shoulder motion is such that the
clavicle rotates in continuity with the scapula, with little
motion between the clavicle and scapula.10
Scapula
There usually are seven scapular ossification centers.25 One
primary center occurs in the body prenatally. In contrast, six
occur postnatally: two in the acromion, two (sometimes
three) in the coracoid process, one along the vertebral
border, and one in the inferior angle (Fig. 13-6). These post-
natal ossification centers first develop in the middle of
the coracoid process between 15 and 18 months of age (Fig.
13-7). A separate coracoid ossification center, sometimes
called the subcoracoid bone, forms in the base between 7
and 10 years of age. This bone rapidly fuses with the scapula,
but it does not fuse with the earlier-appearing midcoracoid
ossification center until 14–16 years of age. A third coracoid
ossification center at the tip may appear around 14 years and
fuses by 18 years of age.17,25
Ossification of the acromial process originates from at
least two (if not three) centers, one at the base and the other
at the apex (at 14–16 years of age).8 The centers form one
epiphysis at about 19 years, finally fusing with the scapular
spine at 22–25 years. Osseous union sometimes fails to take
place between the acromion and the scapula, leaving a
fibrous union that should not be misconstrued for a frac-
ture.19,20 The acromial metaphyseal ossification process may
appear irregular.
Yazici et al. studied the morphology of the acromion in
neonatal cadavers.32 They found that the hooked-type
acromion allegedly responsible for rotator cuff lesions in
adults was virtually nonexistent in the neonate. Hence there
does not appear to be a congenital morphologic variation
that predisposes to soft tissue pathology, especially rotator
cuff injuries and subacromial impingement.22
A secondary ossification center of the inferior scapula
appears at the age of 15 years and fuses by 20 years. That of
the vertebral margin appears by 17 years and fuses by 25
years.
Trauma to the Thorax and Ribs
Rib fractures in children are often associated with blunt chest
trauma. Vehicular trauma and child abuse are the leading
causes of chest (rib) injury (Fig. 13-8).97,101 Rib fractures are
approximately 11 times more frequent among older children
and adolescents than young children, although injury to the
ribs is frequent in children. Fractures are rare. The resilience
of the individual ribs and the composite rib cage and sternum
allow significant elastic deformation without progression to
plastic deformation or fracture.34 One needs only to observe
an infant or young child with respiratory distress to appre-
ciate the degree of elastic sternocostal deformation that
is possible even without direct external pressure. Unfor-
tunately, this elastic deformability also predisponses to severe
rib cage deformation and internal injury during child abuse.
Considerably more energy is required to fracture ribs in a
child than in an adult.63
The intrinsic resilience of the ribs often results in sponta-
neous reduction of greenstick or complete fractures along
the course of a rib after the deforming force is dissipated.
Furthermore, the thick periosteum remains partially intact
and contributes to the spontaneity of reduction and stabil-
ity. Many of these fractures are greenstick injuries. All of
these aforementioned factors make roentgenographic diag-
Trauma to the Thorax and Ribs
nosis extremely difficult. Often the rib injury is not diag-
nosed until fracture callus is evident.
Another major difference is the free movement of the
mediastinum. In contrast to the relatively fixed mediastinum
of the adult, that of a child is capable of wide shifts, with dis-
placement of the heart, angulation of the great vessels, com-
pression of the lungs, and angulation of the trachea. The
cardiopulmonary consequences of such anatomic displace-
ments following severe thoracic trauma may become life-
threatening.
Most fractures involve several ribs and result from major
trauma, especially as a consequence of child abuse or vehic-
ular accidents. Fracture of a single rib from minimal trauma
is less frequent. Because of the presence of a physis at the
anterior (anterolateral) end of the rib, a growth plate frac-
ture may occur. This injury may be undisplaced or sponta-
neously reduced once the evocative force is dissipated.
Similar physeal trauma might affect the costovertebral
region with major spinal or chest trauma. However, such an
FIGURE 13-6. (A) Multiple areas of primary
and secondary ossification in the scapula. 1,
3 = secondary coracoid centers; 2 = primary
coracoid center; 4 = secondary infraglenoid
center; 5 = secondary center at the tip of the
scapula; 6 = secondary center of vertebral
border; 7, 8 = secondary centers of the
acromion. (B) Secondary ossification in the
superior cartilage of the glenoid labrum.
This is analogous to acetabular ossification
(see Chapters 19, 20). (C) CT scan showing
the glenoid secondary center (arrow). B C
423
injury pattern has not been well described in the literature.
Kleinman et al. studied the histopathology and radiologic
correlations of rib fractures in abused infants.67–69 Fifty-one
percent of osseous injuries in such circumstances involved
the ribs, although only 30 of 84 rib fractures (36%) were
evident on a skeletal survey. The anterior rib cartilage was
highly deformable, leading to 10 injuries at the costochon-
dral junction. Greenstick fractures within the bone were
evident in 19. Most of the rib injuries were posterior, in the
costotransverse region.58
The diagnosis of thoracic trauma is difficult, especially in
the child under 2 years of age. Cardiopulmonary symptoms
may not be present during the first 24 hours after injury, and
there is often no correlation between evident external
chest wall injury (e.g., abrasions) and underlying abnormal-
ities. Chest radiography remains the primary evaluation
of chest injuries, although it may not adequately or con-
cisely demonstrate or may even underestimate specific
abnormalities.104
424
A B
FIGURE 13-7. (A) Specimen radiograph duplicating the Y view. It shows the ossification of the coracoid process. (B) Morphologic
specimen.
Healing of rib fractures is rapid and usually requires little
more than symptomatic treatment. Evaluating the possibility of
internal organ injury is extremely important, as treatment of these
injuries generally supersedes concern about the rib fractures.
In the unusual circumstance in which the child sustains
multiple rib fractures, the chest wall may be unstable, result-
ing in a flail chest with paradoxical movement of the thorax
and progressive respiratory insufficiency. Lung contusion
from blunt trauma contributes to the respiratory insuffi-
ciency and is a more serious component of the injury than
are the rib fractures. Examination may reveal subcutaneous
emphysema, palpable rib fractures, and paradoxical motion.
13. Chest and Shoulder Girdle
Arterial blood gas values may indicate actual or impend-
ing respiratory failure. Treatment usually consists of stabi-
lization using endotracheal intubation and volume-cycled
respiration.
Simultaneously, assessment of thoracic and upper abdom-
inal viscera for serious injury is mandatory.49,70,96 Because the
chest wall of a child is resilient and inwardly deformable, the
intrathoracic or upper abdominal contents may be severely
injured, even if the ribs are not obviously fractured. The mor-
tality for closed-chest injuries may be higher in children
without obvious rib fractures than in those with fractures.
Closed-chest injuries vary significantly in severity and may be
FIGURE 13-8. (A) Chest trauma in a 6-year-
old boy. The open arrow indicates a con-
cavity suggestive of a rib cage deformity; the
solid arrow points to an apparently minimally
displaced rib fracture. (B) Healing multiple
rib fractures in a case of child abuse (the
child subsequently died).
Trauma to the Thorax and Ribs
FIGURE 13-9. Aerophagia. There is massive distension of the
stomach in this 2-year-old child injured in a motor vehicle accident.
Decompression with a nasogastric tube relieved the acute respi-
ratory distress.
missed in the multiply-injured child with more obvious severe
trauma to the extremities or head. Closed injury to the chest
wall produces few outward signs, but palpable crepitation
from a rib fracture, changing level of consciousness due to
hypoxia, and alteration of blood gases may be evident.
Children sustaining major trauma often experience
aerophagia (Fig. 13-9). The resulting gastric dilation may
compromise diaphragmatic excursion. This process is aug-
mented by the reflex ileus often seen with pediatric trauma.
Nasogastric decompression of the stomach may be necessary
to protect the diaphragm and to allow the lungs to be ade-
quately aerated.
Pediatric chest trauma is not as well documented as in
adults.51,53,66,74,103,105 Among 230 children sustaining blunt
chest trauma, intrathoracic injury was observed in 29%.52
Chest injuries are associated with the second highest mor-
tality rate for children younger than 15 years.52,53 The mor-
tality associated with pediatric thoracic trauma ranges from
7% to 14%.74,99,105
Garcia et al. analyzed 2080 children up to 14 years of age.62
There were 14 deaths among 33 children with multiple rib
fractures (42% mortality rate). During one phase of the
study, child abuse accounted for 63% of the rib injuries in
children less than 3 years old. Pedestrian injuries predomi-
nated among children older than 3 years. Children with rib
fractures were more severely injured and had a higher mor-
tality rate, but no difference in morbidity, than children with
blunt or penetrating trauma but without rib fractures. The
mortality rate for 18 children with both rib fractures and
head injury was 71%, with the risk of mortality increasing
with the number of ribs fractured. They found that the pres-
ence of four or more fractured ribs identified a unique
425
group of children who were likely to benefit from computed
tomography (CT) evaluation of the head, chest, and
abdomen, given the high probability of multisystem injury
and the mortality associated with severe head injuries. Garcia
et al.62 undertook their study because considerable ambigu-
ity existed owing to the fact that prevailing assumptions con-
cerning rib fractures in children were based principally on
adult experience; moreover, there was no consensus in the
literature as to the frequency, significance, or severity of rib
fractures sustained in pediatric trauma.54,76,83,84,95,99,102
First Rib Fracture
Some first rib fractures occur as a result of a large amount
of energy transference to the thoracic skeleton. The force
required to break the first rib often results in other serious
injuries.33 One study showed that traumatically acquired 1st
rib fractures were associated with a high incidence of tho-
racic, vascular, abdominal, and central nervous system
(CNS) injuries.63 They described six pediatric patients with
traumatic 1st rib fracture. Five patients required operative
intervention. Two sustained major vascular injuries detected
on physical examination (distal signs of proximal vascular
injury: pulse deficit, blood pressure discordance) and con-
firmed by arch aortography. In view of the high percentage
of patients with vascular injury, 1st rib fracture in a pediatric
patient, when associated with acute, severe trauma, should
prompt a search for a major vascular injury.72 In contrast,
stress fractures are not usually associated with such vascular
or intrathoracic injury.37,39,71,78–80 Begley et al. reported such
fractures due to spasmodic coughing.41,92
Children have been included in several series of patients
with traumatic 1st rib fractures,64,85,86,91,106 and many others
have been described in case reports.60,65,89,93,95 Because a
child’s thorax is more compliant than that of an adult, the
injury required to fracture the 1st rib acutely may also result
in deep vascular or organ damage. Congenital variation of
the first rib may simulate a fracture.45
Vascular complications may be present with 1st rib frac-
tures.58,60,91 Pseudoaneurysm formation is circumstantial evi-
dence that injuries of the subclavian artery and brachial
plexus may occur later, rather than concomitantly with the
initial trauma.
Long-term sequelae associated with 1st rib fractures
include brachioplexus injury, upper extremity arterial insuf-
ficiency, Horner syndrome, and thoracic outlet syndrome
secondary to healing fractures. In Harris and Soper’s
study there was only one long-term complication (Horner
syndrome); none of the six patients had thoracic outlet
syndrome.63 Borrelli et al. described compression of the bra-
chioplexus consequent to a chronic pseudarthrosis.44
When the 1st rib is fractured in the absence of major
trauma, it is usually a stress injury (Fig. 13-10).90 In adoles-
cents this occurs particularly during vigorous weight-training
programs. Hoekstra and Binnendijk described a 1st rib frac-
ture from a poorly fitting motocycle helmet.64 Stress fractures
of the rib have been reported in increasing numbers in ado-
lescents who were participating in evocative sports or condi-
tioning activities, included weight lifting, body building,
repetitive throwing, and gymnastics. Proffer et al. described
a 12-year-old highly competitive gymnast who had a history
of shoulder pain for 2 years.88 Conservative treatment was
426
FIGURE 13-10. (A) Stress fracture (arrow) of the first rib in a 14-
year-old. (B) Six months later a characteristic pseudarthrosis
is present, with hypertrophy of the ends (arrow). The roentgeno-
graphic appearance changed little after this time, and the fracture
was still unhealed several years later. Nineteen years later the
patient, now an orthopaedist, still has a nonunion that is minimally
symptomatic and a radiograph that is no different from that in
13-10B.
unsuccessful. She underwent 1st rib resection, which allowed
complete return to competitive gymnastics.
Repetitive stress to the 1st rib causes stress fracture because
the junction of the 1st rib and manubrium is rigid. In the
young child it is a cartilaginous continuity (Fig. 13-5), and as
the child grows this area increasingly ossifies. This pattern is
analogous to the asymptomatic-to-symptomatic (painful) flat
foot of an individual with a calcaneonavicular (tarsal) coali-
tion. The rigidity is also a factor in failure to heal, leading to
pseudarthrosis.
Gamble et al. pointed out that magnetic resonance
imaging (MRI) may lead to overestimation of the seriousness
and extent of the nonunion. This in turn could lead to con-
fusion regarding the diagnosis (i.e., evaluation for tumor).61
Initial treatment is symptomatic immobilization of the arm
and discontinuation of the evocative sports activity, especially
if it is weight training. Nonunion or delayed union are
common complications.59 If pain or neurologic symptoms
13. Chest and Shoulder Girdle
continue, bone grafting can be considered but may not be
successful because of the intrinsic biomechanics.
Thoracic Outlet Syndrome
During the evaluation of pain over the upper anterior chest
wall, stress injuries of the 1st rib assume a diagnostic prior-
ity. Yang and Letts showed that thoracic outlet syndrome may
be present, especially during the rapid growth of adoles-
cence.107 The symptoms include aching, limb tiredness or
discomfort, and occasional paresthesias.
Shoulder strengthening exercises should be tried first,
although resection of a cervical rib, if demonstrable, may be
necessary. The cervical rib may have a delayed appearance,
similar to a calcaneonavicular coalition.
Pulmonary Contusion
Lung contusion is the most common major complication of
rib fracture in the child, but it usually presents insidiously
in this age group. Because of greater pulmonary reserve, a
child may be completely asymptomatic, and the contusion
may go unrecognized until there is blood-tinged sputum or
hemoptysis or until a routine chest radiograph demonstrates
parenchymal hemorrhage. Most lung contusions resolve
within a week or two. Basic respiratory supportive care is
usually sufficient.
Manson et al. evaluated CT for assessing blunt chest
trauma.73 They noted a propensity for pulmonary contusions
to be located posteriorly or posteromedially and for them to
be anatomically nonsegmental and crescentic in shape. They
thought it was probably due to the relatively compliant chest
in children. They also noted that for clinically significant
chest trauma in children a single supine chest radiographic
examination was insufficient to identify the extent of
endothoracic injury.
Pulmonary contusion should be anticipated in any child
with a chest injury.43,99 Children with pulmonary contusion
show a diminution in the PaO2 and an increased intrapul-
monary shunt. Swelling of the endothelial cells is followed
by edema of the alveolar epithelium. Because the integrity
of the capillary vessels is affected, the movement of excess
fluid into the interstitial and alveolar spaces causes progres-
sive hypoxia and increasing opacification of the lung field
on the chest radiograph. Serial evaluation of the blood gases
documents the increasing shunt and progressive respiratory
insufficiency.
Fluid resuscitation should be performed judiciously. A
Swan-Ganz catheter is useful for monitoring the pulmonary
capillary wedge pressure to prevent fluid overload of the
compromised lung. When pulmonary contusion is recog-
nized clinically, fluid administration must be restricted to
maintain the serum osmolarity between 290 and 300 mOsm.
Diuretics may reduce excessive pulmonary interstitial fluid.
Pulmonary contusion may require endotracheal intuba-
tion and mechanical ventilation with positive end-expiratory
pressure (PEEP) to improve the ventilation/perfusion ratio.
Neuromuscular blockade may be effective for maximizing
the benefits of the ventilator. Antibiotics lessen the chance
of infection. As continuing improvement becomes evident,
the patient is progressively weaned from the respirator. If
Trauma to the Thorax and Ribs
continued mechanical assistance is required beyond 2 weeks,
a tracheostomy may be necessary.
Pneumothorax
Pneumothorax is an uncommon pediatric thoracic injury
but must be considered during evaluation of the multiply-
injured child.42 Blunt or penetrating trauma may lead to
collapse of the lung and increased intrathoracic pressure.
Pneumothorax may result from air leaking into the pleural
space due to disruption of the lung parenchyma, a tear in
the tracheobronchial tree, esophageal perforation, or pene-
tration of the chest wall. The elasticity of the thorax in chil-
dren accounts for the presence of pneumothorax in the
absence of rib fractures.
Pneumothorax in a child may vary from being asympto-
matic to producing severe respiratory distress. Physical exam-
ination usually shows decreased breath sounds on the
involved side and a shift of the trachea to the contralateral
side. Chest roentgenography confirms the diagnosis.
A pneumothorax of less than 15% in an asymptomatic
child may be managed by close observation, as this amount
of air usually resorbs. If a pneumothorax is suspected in a
child with respiratory distress, a needle may be initially
inserted to aspirate the air from the pleural space. However,
proper treatment of the pneumothorax consists of subse-
quent insertion of a chest tube. A convenient place in the
child’s small chest is the anterior axillary line lateral to the
pectoralis major muscle in the fourth interspace. Open
wounds of the chest wall are closed to establish the integrity
of the thorax so “negative” intrathoracic pressure may be
maintained by thoracostomy suction. A child with chest
trauma who requires general anesthesia (e.g., for fracture
management) is best treated by insertion of a thoracostomy
tube to prevent tension pneumothorax during the operative
procedure.
Tension pneumothorax occurs because of progressive (con-
tinued) entry of air into the pleural space. The intrapleural
pressure rises with collapse of the ipsilateral lung, shift of the
mediastinum, and gradual compression of the contralateral
lung. The ipsilateral diaphragm may be markedly depressed,
further compromising respiratory function. Because the
mediastinum in children is not fixed, wide shifts of the
intrathoracic viscera may occur. Such a shift may cause angu-
lation of the vena cava, which may incrementally decrease
blood return to the right side of the heart, reduce cardiac
output, and lead to cardiovascular collapse. If a thoracos-
tomy tube is not available, an 18-gauge needle may tem-
porarily equilibrate the intrapleural and atmospheric
pressures. Thoracostomy tube drainage to water seal is
usually therapeutic.
Subcutaneous Emphysema
Subcutaneous emphysema occurs when air is forced into the
tissue planes of the chest and may reflect underlying injury
to pleura, intercostal muscles, bronchus, trachea, or lung
parenchyma. Treatment of children with subcutaneous
emphysema is directed toward the primary injury, as the sub-
cutaneous air has no physiologic effect and eventually is
spontaneously absorbed.
427
Injuries to the Tracheobronchial Tree
Injuries to the trachea and main bronchial system are rare
in the pediatric patient.105 Disruptive injury to the airway is
a consequence of blunt or penetrating trauma. The diagno-
sis is considered when the patient manifests a persistent air
leak through a thoracostomy tube following pneumothorax,
mediastinal and subcutaneous emphysema, hemoptysis,
tension pneumothorax, or massive atelectasis. The side
of the injury may be readily apparent from the clinical signs.
The patient should undergo bronchoscopy, so laceration of
the bronchial tree can be demonstrated. Once the injury
is recognized, a thoracotomy with selected ventilation of
the opposite lung may be lifesaving. A high tracheal
injury requires repair and tracheostomy. A low tracheal
or bronchial injury is usually approached directly with
thoracotomy.
Hemothorax
Blood in the intrapleural space may result from vascular
injury (e.g., disruption of an intercostal artery). Trauma to
the major vessels is unusual in children. Parenchymal
pulmonary injuries rarely bleed profusely because of the low
perfusion pressure to the lung. Occult bleeding within
the chest may gradually produce significant hypotension. An
upright chest roentgenogram usually demonstrates an
air–fluid interface.
In addition to identification and treatment of the source
of bleeding, ancillary treatment requires blood and volume
restoration and evacuation of blood from the intrapleural
space. Thoracostomy in the posterior axillary line (seventh
or eighth interspace) drains the hemothorax, reexpands the
lung, and provides a means of monitoring ongoing bleed-
ing. Autotransfusion of the aspirated blood may be possible
if an appropriate collection system is available.
Cardiac Tamponade
Injury to the heart or the major intrathoracic vessels is
uncommon in children. Any penetrating injury may permit
blood to enter the pericardial space. The fibrous, relatively
nondistensible pericardium compromises the dynamics of
cardiac function by progressive pericardial tamponade. Air
may dissect into the pericardium following initiation of
ventilatory support with high inflation pressure and PEEP.
A small volume of blood or air can severely compromise
cardiac function in the child by decreasing venous return
and restricting cardiac output.
Cardiac tamponade is diagnosed by recognizing specific
clinical features. The child who is hypotensive despite fluid
resuscitation is suspect. The association of neck vein disten-
sion with elevated central venous pressure, paradoxical
pulse, and peripheral vasoconstriction in a patient in shock
suggests the diagnosis.57 Elevation of the central venous pres-
sure is the most reliable clinical sign of tamponade.
Injuries to the Diaphragm and Abdomen
Injury to the lower rib cage may produce a ruptured
diaphragm or intraabdominal damage to the liver, pancreas,
428
kidney, or spleen.40,48,81,94,100 Each of these potential injuries
must be sought, as the consequences of a missed diagnosis
may be significant.
The diaphragm may rupture from forceful blunt trauma
to the lower chest or upper abdomen.36,105 A diaphragmatic
disruption, which most often involves the left side, may allow
the intraabdominal contents to enter the thoracic cavity,
with consequent respiratory embarrassment by lung com-
pression. An upright chest film shows a distorted, indistinct
diaphragmatic contour, with abdominal viscera in the
thorax. Insertion of a nasogastric tube may facilitate the diag-
nosis by showing translocation of the stomach.
Brandt et al. described 13 children with diaphragmatic
injury ranging in age from 1 to 15 years (average 7.5 years).46
Eight of the patients sustained penetrating trauma, and five
sustained blunt trauma; nine had associated injuries, most
commonly involving the liver. All 13 patients underwent
exploratory laparotomy with repair of the diaphragm. There
were two deaths, both unrelated to the diaphragmatic
trauma. All surviving patients recovered without sequelae.
Brandt et al. believed that diaphragmatic injuries should be
considered in any child suffering blunt or penetrating tho-
racoabdominal trauma.
Melzig et al. reported two patients: a 2-week-old infant and
a 10-year-old boy.77 They pointed out the problem of con-
comitant injuries masking diaphragmatic rupture. Such
injuries usually involved rib fractures, splenic tears, femoral
lacerations, and bowel injury.
Because of the increased compliance of the thoracic cage
in children, the diaphragm may rupture without obvious
signs of external injury. Morbidity and mortality may be min-
imized by a high index of suspicion, prompt recognition,
and surgical repair of even a small diaphragmatic injury.
Diaphragmatic injury occurs in 3–5% of adults with blunt
trauma to the abdomen and in as many as 10–15% of
patients with penetrating wounds to the lower chest.
Diaphragmatic injury in children is more difficult to assess
than in adults because of anatomic and physiologic differ-
ences. The child’s chest wall is more compliant than that in
adults. Major compression with resultant internal injury may
occur without fractures or other external signs of trauma.
The mediastinum of a child is more mobile than that of an
adult; and venous return is more likely to be compromised
by hemothorax, pneumothorax, or herniation of abdominal
contents into the chest.
Virtually all children respond to trauma by swallowing air,
leading to gastric distension. This may cause respiratory
decompensation, particularly if the stomach is herniated
into the chest through the diaphragmatic tear.
The pathophysiology of blunt diaphragmatic injury is
not clearly understood. The timing of the impact within the
respiratory cycle may be especially important and may
explain the lack of correlation between the severity of the
trauma and the occurrence of diaphragmatic rupture. In
adults, pain referred to the ipsilateral shoulder is virtually
always present. Unfortunately, children seldom describe this
symptom.
Physical examination is rarely specific for diaphragmatic
injury. Signs of abnormal tissue fluid in the chest, such as
dullness to percussion, diminished fremitus, or decreased
breath sounds, may be present. Respiratory distress is more
often present in children than in adults because of the
stressed child’s tendency to swallow air. The presence of
bowel sounds in the chest is not a reliable physical finding,
13. Chest and Shoulder Girdle
as they may be transmitted from the abdomen. Furthermore,
with true herniation bowel sounds may be absent because of
an associated ileus.
The chest roentgenogram is the most important diagnos-
tic study if diaphragmatic injury is suspected. However, it
should be noted that in some series as many as 30–50%
of the initial chest roentgenograms appeared normal.
The injury became evident only subsequently with serial
roentgenograms.77
Splenic Injury
The spleen is frequently injured when the left side of the
chest is traumatized. The overlying rib cage is resilient and
rarely fractures, but it allows sufficient temporary inward
osseous deformation to contuse, displace, or rupture the
spleen. Blood loss may be immediate or delayed if the splenic
bleeding is intracapsular.
Immediate splenectomy has been advocated, but more
recent clinical trials suggest that complete removal may not
be necessary.35,47,50,55,56,82 Smith et al. corroborated that splen-
orrhaphy in children is a significant and safe alternative to
splenectomy in patients without other major injuries who
appear to be hemodynamically stable.98 Furthermore, fol-
lowing splenectomy many children exhibit regeneration of
some splenic elements (the “born-again spleen”).73,108
Splenectomy is not without long-term complications, the
most severe being inappropriate function of the immune
system, often leading to sepsis.38
Pancreas
Pancreatic injury may lead to pancreatitis or pseudocyst
formation. Osteolytic lesions have been observed in patients
with traumatic pancreatitis.81,94 These lesions are presumably
due to metastatic fat necrosis.
Slipping Rib Syndrome
The eighth, ninth, and tenth costal cartilages do not attach
directly to the sternum; rather, they are attached to each
other by cartilage, fibrocartilage, or fibrous tissue (Fig. 13-
11). This type of attachment allows greater mobility than the
more rigidly attached upper ribs and makes the lower rib
region susceptible to trauma. Disruption of the fibrous con-
nections between the ribs makes the costochondral junction
potentially unstable, loosening this area so there may be
micromotion or macromotion.
The slipping rib syndrome is a sprain disorder in children
produced by trauma to the costal cartilages of the 8th, 9th,
and 10th ribs.75,87 The symptoms are neuritic pain, auto-
nomic symptoms, and a perception of movement of the ribs.
This syndrome may be confused with intraabdominal disor-
ders. Direct trauma from a fall or blow and indirect trauma
from lifting or athletic activities are probable inciting causes.
Most patients with slipping rib syndrome have pain in an
upper abdominal quadrant, the epigastrium, or the inferior
costal regions. Many complain of pain under the ribs.
Another common presenting symptom is the perception of
a “slipping” movement of the ribs.
A study of the pathology and anatomy of resected costal
cartilages showed minimal changes in two patients. Exami-
nation of specimens of the 8th, 9th, and 10th ribs of cadav-
Trauma to the Sternum 429

Trauma to the Sternum

The sternum, like the ribs, is resilient in a child, and
fractures are rare (Fig. 13-12). There are few reports of
sternal fractures in chidlren.109–111,114–122 The manubrium
and sternum have a cartilaginous junction, allowing some
motion. This manubriosternal joint may be displaced and is
the most frequent region of sternal fracture in children.
The cartilage between individual sternebra also represents
a potential site of chondro-osseous separation, if not
dislocation.
The sternum is anatomically protected from fracture by
the surrounding ligaments and cartilaginous attachments
A from the ribs. In children these structures are even more
elastic, and the ribs are more flexible. Furthermore, inter-
cartilaginous connections between the sternebra add addi-
tional resilience to the sternum. Most injuries occur in the
older child, in whom the capacity for elastic deformation,
especially through the synchondroses, has lessened consid-
erably. The primary mechanism of injury is direct violence,
particularly chest compression, which may occur in sports
such as wrestling in which encircling holds are a common
part of the maneuvers. These injuries may occur when chest
seat belt restraints are used.110
Bizzle reported that sternal fractures are potentially fatal
injuries and stressed the need for close monitoring of cardiac
B
FIGURE 13-11. Rib cage to show the mechanism of slipping ribs.
(A) Normal appearance in a 7-year-old child. (B) Displacement with
a “slipped rib.”

ers (age range 3–72 years) showed that the intercostal muscle
mass was sparse at the rib tips.75 Most often found in young,
highly competitive athletes, it may follow an acute blow to
the lower rib cage, although repetitive strain may also cause
the symptoms.
The cartilage of these ribs was not mobile enough to allow
them to come in contact with the cartilage of the ribs above
or to become locked behind them. However, when the
fibrous connecting tissue was incised, the cartilaginous rib
tip could be subluxated, becoming trapped posterior to the
rib above it.
Diagnosis is made by demonstrating tenderness of the
affected cartilage. The pathognomonic finding, although
not present in all cases, is a positive hooking maneuver.
The examiner should place fingers under and along the
inferior rib margins and pull anteriorly. Characteristically,
the symptomatic child recognizes the reproduced pain or
sensation of instability. Because the condition usually
involves only one side of the chest, the other side may
serve as the control. Diagnostic, particularly radiographic,
studies are inconclusive. The use of cross-sectional tomog-
raphy to evaluate patients with this disorder has not been
reported.
The principal methods of treatment are reassurance, injec-
tion of the affected area with local anesthetic, and in patients
with severe pain, surgical excision of the subluxating carti- FIGURE 13-12. (A) Sternebral (S) and xiphoid (X) sternal fractures
laginous rib tip. Resection of the cartilage involves little mor- in a 15-year-old boy, sustained from a “bear hug” during a wrestling
bidity if care is taken not to enter the thoracic or abdominal match. (B) Magnification of the sternebral fracture (arrow). (C)
cavity. It may be undertaken with the adolescent patient Magnification of the xiphoid fracture (arrow). Both injuries are
under local anesthesia.99 incomplete (greenstick) fractures.
430 13. Chest and Shoulder Girdle

and respiratory status.109 Scudamore and Ashmore noted

that dislocation of a segment of the unfused sternum could
occur secondary to direct or indirect trauma, osteora-
dionecrosis, and sickle cell anemia.121
Patients with isolated sternal fracture usually do not
require cardiac monitoring, and patients under 4 years of
age generally require short-stay observation. Only four
patients out of 272 developed cardiac arrhythmias, and three
of them had associated injuries.110 There is a small associa-
tion with concomitant thoracic spine fractures.
Treatment is generally symptomatic.109,118 Most sternal
fractures are symptomatically painful for a period of 2–3
weeks. Bizzle treated teenagers with a sternal brace that was
similar to a clavicular brace.109 One 16-year-old boy sustained
a crushing injury to the chest and required surgical reduc-
tion and internal fixation.120 The xiphoid may be depressed
inward and may require removal or elevation if pain persists.
Haje and Bowen have shown that damage to the cartilage
of the sternum may produce pectus carinatum or excavatum
deformities.112,113 Similar injuries can hypothetically or actu-
ally occur in the injured child to produce similar deforma-
tion, although most of these deformities are undoubtedly
congenital failures of the embryonic midline and sternebral
fusion processes.

Trauma to the Clavicle

Fractures of the clavicle occur most frequently in children
during the first 10 years of life and are certainly the most
prevalent skeletal injury under 5 years of age.123–179 Fractures
may occur throughout the diaphyseal region, the medial
epiphyseal end, and the distal metaphyseal end (Fig. 13-13).
Fractures of the midshaft, however, are most common and
range from greenstick to complete. True dislocation or sub-
luxation of proximal (sternoclavicular) or distal (acromio-
clavicular) joints is rare prior to skeletal maturity, which does
not occur until the mid-twenties in this particular bone.
Wilkes and Hoffer found that 7% of children with a head
injury had concomitant clavicular fractures; 16 of 28 chil-
dren sustained mid-clavicular fractures.178 Accordingly, the
clavicle should be carefully assessed in the multiply-injured
child.
The most common birth injury is a fracture of the clavicle
(Fig. 13-14), occurring in approximately 5 of 1000 vertex
deliveries and 160 of 1000 breech deliveries.134,150 Oppen-
heim and coworkers found 58 clavicular fractures among
21,632 live births (2.7 clavicle fractures per 1000 live
births).165 Balata and associates noted an increasing inci-
dence of perinatal fractures of the clavicle.126 In 1977 there
were 2.2 clavicular fractures per 1000 live births, and in 1980
there were 4.8 per 100 live births.126
Clavicular fractures in breech deliveries frequently occur
when the obstetrician has difficulty delivering the extended
FIGURE 13-13. Usual areas and likelihood of clavicular injury.
FIGURE 13-14. (A) Undisplaced fracture of the clavicle with hyper-
trophic callus. It was not diagnosed until 3 weeks after the injury.
(B) Massive callus 3 weeks following a birth fracture.
arms and shoulders. Clavicular fractures have also been
reported during cesarean section.143,165
Cohen and Otto analyzed the factors related to birth frac-
tures, finding that they seemed to correlate best with birth
weights over 3800 g, the level of obstetric experience of the
delivering physician, and mid-forceps deliveries.133 Oppen-
heim et al. found that increased birth weight and shoulder
dystocia were the most predictable predisposing factors.165
Baskett and Allen reviewed the perinatal implications of
shoulder dystocia over a 10-year period.127 They found 254
cases of shoulder dystocia among 40,518 vaginal cephalic
deliveries, with 33 cases of brachial plexus palsy and 13 cla-
vicular fractures. They found that the incidence of dystocia
was increased in the presence of a prolonged pregnancy
(threefold), prolonged second stage of labor (threefold),
mid-forceps delivery (tenfold), and increased birth weight.
Downward traction correlated significantly with brachial
plexus injury. There was only one case of recurrent shoulder
dystocia among 80 women having 93 subsequent vaginal
deliveries.
Chez et al. reviewed multiple factors in 3880 deliveries (34
fractured clavicles) and concluded that the fractured clavi-
cle is an “unavoidable” event.132 Roberts et al. reviewed 215
fractured clavicles among 65,091 vaginal deliveries.168 They
also concluded that obstetric clavicular fracture was an unavoid-
able, unpredictable complication of an otherwise normal birth.
Clavicular fractures in the newborn may produce little dis-
comfort, so the fracture may not be recognized until healing
callus is palpated after the neonate has been taken home.
In one survey of 300 consecutive living newborns, 5 had
fractured clavicles, of which none was suspected during
the routine neonatal evaluation.140 Conversely, neonates may
Trauma to the Sternum
present with pseudoparalysis, in which case the physician
must distinguish between a fractured clavicle, birth injury to
the brachial plexus, traumatic separation of the proximal
humeral epiphysis (see Chapter 14), or acute osteomyelitis
of the shoulder.156,169,170 Valerio and Harmsen described
osteomyelitis as a complication of perinatal clavicle frac-
ture.176 This infant required curettage and sequestrectomy.
The infant recovered completely.
It is important to realize that brachial plexus injuries and
clavicular fractures can coexist. However, temporary pseudo-
paralysis consequent to clavicular fracture is more likely.
Mechanism of Injury
The clavicle may be fractured neonatally during a difficult
delivery.131,135,140,154,160 Fracture of the clavicle positioned
anteriorly during delivery predominates over the more
posteriorly positioned clavicle. The anterior shoulder is
compressed by the maternal symphysis during cephalic pre-
sentation and passage through the pelvic outlet. Another
mechanism is incidental torsion, traction, and digital pressure
applied to the clavicle by the obstetrician. Finally, the obste-
trician may choose to fracture the clavicle deliberately to facil-
itate a difficult delivery, particularly if there is fetal distress.
FIGURE 13-15. (A) Questionable fracture (arrow) in
a child who fell on the shoulder. It is really the nutri-
ent foramen. (B) Greenstick fracture. (C) Complete
fracture with moderate displacement.
431
Meghdari et al. performed an image analysis of shoulder
dystocia utilizing the finite element method.157 These studies
showed that the clavicle almost always fractured under appli-
cation of compressive stresses at the midshaft. It showed that
a stretch of about 15–20% was necessary to damage the
brachial plexus nerves. The most damaging force appeared
to be shear forces. Other engineering studies have con-
firmed this concept.171,172
Once the child is ambulatory, the most common mecha-
nism of injury is a fall. The patient may land on an out-
stretched arm, hand, or elbow or directly on the shoulder,
directing the forces into the clavicle, which is relatively fixed
and immobile at the manubrium.
Pathologic Anatomy
The most common fracture site is the junction of the middle
and distal thirds of the bone. In the infant and young child
the break is usually incomplete (greenstick), whereas older
children and adolescents tend to have complete or com-
minuted fractures (Fig. 13-15), even though the fragments
may not be displaced significantly. Some periosteal continu-
ity is usually retained. Angulated, sharp fragments may pen-
432
etrate the subcutaneous or cutaneous tissues and may also
lacerate subclavian vessels or the brachial plexus, although
these complications are infrequent in children. The clavicle
does not exhibit a great capacity for plastic deformation,
especially in the toddler or older child.
When the fracture is complete, muscle forces affect and
maintain the subsequent deformation. The glenohumeral
joint pulls the lateral fragment downward and inward. This
displacement is a combination of the overall weight of the
limb and the pull of the pectoralis muscles anteriorly and
part of the trapezius posteriorly, with their summated forces
being directed inferiorly. In contrast, the medial half is
pulled upward and posteriorly by the sternocleidomastoid
muscle (Fig. 13-16). The costoclavicular and sternoclavicular
ligaments may act as check reins.
Diagnosis
Birth fractures are not always easy to diagnose, as they are
often asymptomatic. In a roentgenographic survey of 300
consecutive live newborns, 5 had fractured clavicles (1.7%).160
In none of these cases was the fracture suspected following
the routine pediatric examination in the delivery room and
the nursery. However, after each positive roentgenogram,
reexamination demonstrated crepitation of the fracture
site. Even in the newborn this fracture may be complete, with
an overriding fragment. This should not be confused with
congenital pseudarthrosis of the clavicle. Rounded ends
typify the pseudarthrosis, in contrast to the sharp edges of a
fracture.
13. Chest and Shoulder Girdle
FIGURE 13-16. (A) Typical overriding of a complete
clavicular fracture. (B) Muscle forces creating and
maintaining this displacement pattern.
Clavicular fractures may result in an apparent Erb’s palsy
(pseudoparalysis) because of the neonate’s reluctance to
move the arm. This pseudoparalysis clears readily and
rapidly (usually within days), with no residual neurologic
defect, as the fracture heals. Some patients, however, sustain
both injuries, in which case the paralysis may be reduced, but
slowly and not always completely.
Muscle function in the upper limb should be assessed by
reflex stimulation to rule out associated brachial plexus
injury. Sensation to pinprick should also be tested. This is
likely to be present with pseudoparalysis but less so with true
brachial plexopathy.
Infants and young children tend to be asymptomatic, and
there may be no clinical evidence of the injury until the child
develops callus. The callus causes marked swelling, disturbs
the parents, and finally brings the antecedent injury to
medical attention.
Radiography
Undisplaced fractures of the shaft and especially fractures of
the medial end of the clavicle in young children may be
missed on routine radiographs. The overlying second rib
may obscure incomplete fractures. Normally, a soft tissue
shadow parallels the superior border of the clavicle. When
this shadow is absent unilaterally, more careful evaluation
is recommended. Fractures in the middle third are usually
depicted on routine anteroposterior roentgenograms.
Demonstration of fractures of the medial and lateral ends of
the clavicle often requires special oblique, lateral, or pos-
Trauma to the Sternum 433

teroanterior views. In the adolescent the diaphyseal fracture

has a greater tendency to be comminuted.
The apical oblique view may be helpful for detecting a
fracture of the clavicle. This particular view is obtained with
the injured side of the patient angled 45° toward the x-ray
tube and a 20° cephalad angulation of the x-ray beam. This
view is effective for detecting nondisplaced fractures of the
middle third of the clavicle in neonates and young children.
Because of the normal clavicular curvature, routine radio-
graphic views may foreshorten the central section, where
most of the fractures occur. The apical oblique view has
proved sensitive in cases in which the routine projection was
nondiagnostic or negative.152,177
Occasionally, fracture of the clavicle at birth is accompa-
nied by a physeal fracture of the proximal humeral epiph-
ysis. Although it may not be seen on initial roentgenograms,
subperiosteal new bone formation around the proximal
humeral metaphysis makes it evident. Such osteoblastic reac-
tion may be confused with osteomyelitis. Goddard et al.
reported the association of clavicular fracture with atlantoax-
ial rotatory fixation in five patients.145

Treatment
Birth fractures, which are often unrecognized, do not always
require treatment; they form callus rapidly and often
become evident only when the mother notices the palpable
callus of the healed fracture. Union usually occurs without
external immobilization; and any malalignment is corrected
rapidly with growth and remodeling. The infant should be
handled gently, with no direct pressure over the clavicle. If

FIGURE 13-18. (A) Overriding and separated clavicular fracture.

(B) Partial reduction just after application of a figure-of-eight strap.
(C) Callus formation, at 3 weeks, within the intact inferior periosteal
sleeve.

the fracture is painful or there is pseudoparalysis, it is best

FIGURE 13-17. Figure-of-eight orthosis should pull the shoulders
backward (large curved arrows) and be tightened regularly (small
arrows). It should not be so tight that it impairs neurologic function
of the brachial plexus.
to protect the arm with a splint for 2–3 weeks. Within a week,
or at most 10–14 days, the pain subsides, and the fracture
begins to unite.
Children under 6 years of age with a fractured clavicle do
not usually require formal, manipulative reduction. Callus
formation remodels and disappears, generally within 6–9
months, a fact that should be impressed on the parents so
they are not disturbed by the clinical appearance or the
length of time necessary for remodeling. The child should
be made comfortable by application of a figure-of-eight
splint (Figs. 13-17, 13-18). The splint may be tightened
434
slightly by the parents each evening. Immobilization should
be continued for 3–4 weeks. Neuromuscular and vascular
function in the arm should be checked frequently by the
parents. Professional reevaluation at reasonable intervals is
advisable to rule out problems.
In the older patient the figure-of-eight splint does not
always adequately immobilize the fracture. Its main purpose
is to remind the patient to hold the shoulders back. Accord-
ingly, within a week it may be removed daily for hygienic
purposes.
As the child gets older, the capacity for remodeling, par-
ticularly of any significant angular deformity, lessens. This
factor increases the desirability of reasonable anatomic
reduction. If the fracture is complete, markedly displaced,
or overriding, closed reduction may be necessary. Reduction
may be done after local injection of procaine or lidocaine,
with great care being taken to avoid introduction of skin bac-
teria. The patient should sit, and the physician should be
positioned behind to pull the shoulders backward while
applying leverage between the scapulae. The patient may
also be placed in a recumbent position, with the back over a
midline sandbag and the arm over the side, which generally
effects gradual reduction. In older children who require
closed reduction, plaster may be added to the figure-of-eight
splint to reinforce its rigidity.141
Even if there is significant angulation of the fracture in an
adolescent, it is usually better to let the fracture heal without
operative procedures and deal with the osseous prominence
of the healed fracture, if clinically necessary, at a later date.
Such prominences are usually remodeled, even in the ado-
lescent patient.
Fracture of the clavicle in a child who is forced to rest in
bed because of other major trauma may be managed more
easily in the supine position with a small sandbag or pillow
placed between the scapulae so the weight of the upper limbs
gradually falls backward and reduces the fracture. For
comfort, a figure-of-eight splint may be applied. If significant
cosmetic deformity is present, and one does not wish to
undertake an open reduction, modified lateral arm skin trac-
tion may be used, with the shoulder at 90° of abduction and
90° of external rotation.
It is unwise to complete a greenstick fracture, as is often
taught with regard to other bones, inasmuch as the subcla-
vian vessels and brachial plexus lie directly underneath the
clavicle. Rupture of the subclavian vessels has been described
as a cause of death.136,138 Despite the proximity of pleura,
skin, brachial plexus, and brachial vessels, complications of
this fracture are rare in children. Most often the deforma-
tion in anterior and away from major neuromuscular struc-
tures. Furthermore, the injury mechanism is often a fall,
rather than the more violent trauma that usually causes this
bone to fracture in the adult.
Open reduction of a fractured clavicle is not generally
indicated in children but may become appropriate in the
adolescent.124,149,151 If open reduction is done, a small plate is
used. Alternatively, malleable plates (e.g., reconstruction
plates) may be contoured to the variable anatomy of the
clavicle. Small K-wires can migrate and should be avoided.
If used they should be left protruding to allow removal
3–4 weeks after the injury. The fractured clavicle, like
the fractured rib, heals despite almost continuous motion
13. Chest and Shoulder Girdle
of the upper extremity. Nonunion is rare with closed
treatment.
Remodeling
Clavicular fractures unite quickly, almost invariably with
some degree of accentuated angulation. Remodeling is gen-
erally complete within a year, especially in young children.
This bone remodels adequately and quickly and may be left
in a reasonable degree of angular deformity. Anatomic
realignment assumes more importance in adolescents, as
remodeling is less active and may not correct significant loss
of axial alignment.
Complications
The primary justification for exploratory surgery is to repair
damaged subclavian vessels or brachial plexus. A vascular
complication is suggested by a large, rapidly increasing
hematoma. Surgical intervention in this case must be imme-
diate, as the patient may die owing to extravasation of blood
into the chest and shock.124,138,148
Subclavian vascular compression may occur owing to
greenstick fracture and inferior bowing.158,166 This complica-
tion is recognizable by venous congestion and edema of the
ipsilateral arm. A chronic arteriovenous fistula has also been
reported.148
The incidence of nonunion of clavicular fractures in
patients of all ages ranges from 0.8% to 3.7%.142,179 Nonunion
of clavicular fractures in skeletally immature individuals,
however, is rare. In fact, the main differential diagnoses of
discontinuity of the clavicle in children and adolescents
should include congenital pseudarthrosis, cleidocranial
dysostosis, and neurofibromatosis, rather than nonunion fol-
lowing fracture.
A review of 33 patients with nonunion of a clavicular frac-
ture included a 12-year-old and a 13-year-old, neither of
whom underwent treatment of the nonunion.179 Each had
unlimited activity and hypertrophic nonunion, in contrast to
the more characteristic atrophic nonunion of older patients.
A third patient, 7 years of age when injured, still had a hyper-
trophic nonunion 6 years after the injury and underwent fix-
ation and bone graft, which established union and restored
unlimited activity. Nogi reported nonunion of the clavicle in
a 12-year-old child.162
The treatment of discontinuity of the clavicle in children
seems to be well defined. In most cases there is little func-
tional impairment. Thus surgery may be for cosmetic pur-
poses to eliminate the enlarged mid-clavicular mass. In
patients whose presenting symptoms include pain and
limited function, surgery may return the patient to full, pain-
less activity.
Nonunion and shortening of mid-clavicle fractures, espe-
cially in young patients, does not usually occur.139 Plate fixa-
tion for mid-clavicular fractures with gross displacement and
shortening of more than 15 mm may be necessary. A one-
third tubular plate is placed under the platysma to cover the
plate and prevent skin discomfort. Bone grafting is rarely
necessary. Mullaji and Jupiter used a low-contact dynamic
compression plate that could be readily bent to contour to
the specific demands of the individual clavicle.159
 Congenital Pseudarthrosis
A
B embryonic ossification centers to fuse. This is in contrast to
FIGURE 13-19. Complex fracture-dislocation. (A) Fracture in the
junction of the proximal-middle third. The sternoclavicular region is
not well visualized. (B) CT scan shows the anterior sternoclavicu-
lar disruption and the fracture.
Complex Clavicular Injury
Concomitant ipsilateral medial epiphyseal injury with frac-
ture of the clavicular diaphysis (Fig. 13-19) during childhood
is rare.146,174 Thomas and Friedman thought that such
injuries were the result of sequential trauma rather than the
same traumatic incident.174 Hardy particularly reported a 7-
year-old girl who was knocked off her horse when she struck
a stable door against her right shoulder as she rode past; she
landed on the same shoulder. The obvious mid-clavicular
fracture was treated conservatively. The sternoclavicular dis-
ruption (i.e., physeal fracture) was not noted until 12 days
later, at which time the clavicular diaphyseal fracture had
healed to an extent that they were able to apply external
pressure to the medial end of the anteriorly displaced medial
clavicle and attain full reduction.146
FIGURE 13-20. Congenital pseudarthrosis in a 2-month-
old baby. It must be distinguished from an acute fracture.
435
Congenital Pseudarthrosis
Congenital pseudarthrosis invariably affects the right clavi-
cle.180–194,197–208 It is often misinterpreted as an acute fracture.
The lesion is present at birth and most likely results from
failure of normal ossification patterns.184,186,195,197 Swelling or
prominence may be found at or soon after birth, although
the diagnosis may be delayed for months to years. The chil-
dren do not have obvious histories of birth injury, and the
limb is usually painless. However, the child may be reluctant
to move the arm or be unable to push it when crawling.
Minor trauma often brings the deformity to medical atten-
tion. The relation of the two fragments is always the same,
with the sternal fragment being larger and lying in front of
and above the shorter, inferiorly directed acromial fragment
(Fig. 13-20). The bone ends at the pseudarthrosis are smooth
and usually overriding.
Histologic examination of the resected ends of congenital
pseudarthroses of the clavicle showed cartilaginous caps
and pathologic changes that were equivalent to those in
epiphyses that were adding new bone.193 This finding was
confirmed by preoperative tetracyline labeling. The authors
believed that the pseudarthrosis was caused by failure of the
the material discussed earlier in the anatomy section, which
pointed out that the point of fusion of the two anlagen was
different from the area of pseudarthrosis usually seen clini-
cally. The difference, however, could be justified by differ-
ential growth of the two segments.24,186 Differential growth
certainly is compatible with observations that the lateral
segment seems to be relatively underdeveloped when com-
pared to the opposite clavicle.190 This would affect the rela-
tive position of the pseudarthrosis. These studies also have
shown a predominance of longitudinal growth from the
proximal (sternal) end compared to the lateral (acromial)
end (approximately 70–30%).190
Congenital pseudarthrosis should be treated as a
nonunion, with careful resection and removal of the smooth
cortical bone ends to expose the medullary cavity.196,202,205
The posteroinferior periosteal continuity should be main-
tained. The ends may be approximated with “bone” sutures.
Bone graft may not be necessary, especially in younger chil-
dren. In nine cases, all done in children under 4 years of age,
nonunion has not recurred.190 All had osseous bridging
within 6–8 weeks postoperatively, and all were solidly healed
by 14 weeks after surgery. Interestingly, there was delayed
remodeling of the callus bone that formed, and the distal
436 13. Chest and Shoulder Girdle

end of the clavicle was not as well developed as that on the

contralateral side.

Trauma to the Proximal

(Sternal) Clavicle
Traumatic separation of the epiphysis of the sternal end of
the clavicle (Fig. 13-21) occurs infrequently.209–222,224–261
Because of the late closure of this physis, proximal physeal
separation may occur even in young adults in their early
twenties. The injury usually occurs with either a fall on the
outstretched arm or posteriorly directed impact to the shoul-
der. Disruption of this region may occur during traumatic
delivery (Fig. 13-22).258
This injury mimics sternoclavicular dislocation, which
does not usually occur until the clavicle is completely
mature. Any injury to this end of the clavicle in a neonate,
child, adolescent, or even young adult should be considered
an epiphyseal injury, not sternoclavicular joint dislocation.
Infrequently, fracture of the diaphysis and sternal end
may occur concomitantly, creating an unstable proximal
fragment.237
The stability of the sternoclavicular joint is contingent on
the joint capsule, the fibrocartilaginous meniscus, and the
interclavicular and costoclavicular ligaments. Sternoclavicu- FIGURE 13-22. (A) Sternoclavicular injury (arrow) in a newborn
lar injury is commonly caused by indirect violence, such as sustained during a difficult delivery. (B) Subperiosteal new bone
a fall on or blow to the shoulder, which drives the clavicle (arrow) filling the intact periosteal sleeve.
posteriorly or anteriorly. The injury is occasionally produced
by direct impact to the sternoclavicular region.
Pain and swelling are usually obvious if a sternoclavicular
injury is present. Posterior displacement may be associated Radiology
with respiratory difficulty or dysphagia.235 Most of the
Anteroposterior roentgenograms may appear normal even if
injuries are anterior, with a mass evident over the sterno-
sternoclavicular injury is present. Special oblique views may
clavicular region. The sternal end of the clavicle (i.e.,
show the displacement of the sternal end of the clavicle.
metaphysis) may be sharply prominent and palpable
Brooks and Henning212 recommended a 30° tangential
immediately underneath the skin. The clavicular part of
radiograph instead of the lordotic projection, with the x-ray
the sternocleidomastoid muscle is pulled anteriorly with the
tube directed at a 40°–50° cephalad tilt. The Hobbs view is
bone and is often in spasm, causing the patient’s head to tilt
a superoinferior projection.233 The Heinig view is taken with
toward the affected side. Posterior displacements, accom-
the patient recumbent and the x-ray tube parallel to the table
panied by an indentation next to the sternum, may cause
top, approximately 30 inches away from the involved joint.232
intrathoracic problems, such as tracheal compression and
The grid cassette is placed perpendicular to the beam against
dyspnea.228,229,241,259
the opposite shoulder, and the shoulder closest to the tube
is abducted. If the injury occurs before ossification in the
medial epiphysis, the condition is easily and often mistaken
for dislocation of the sternoclavicular joint.
Cope et al. reported several radiographic projections
which have been recorded as being diagnostically
helpful.217,218 These include the Rockwood or “serendipity”
projection, which employs a 50° tube tilt toward the head.
Computed tomography, the optimal method for demon-
strating disruption of the sternoclavicular joints, may be used
not only to define the displacement (Figs. 13-23, 13-24) but
also to reveal the relations of the great vessels, esophagus,
and trachea to the sternoclavicular joint, the disrupted pos-
teriorly displaced clavicular metaphysis, and any impinge-
ment on these structures.223,224,239,240,249 CT is the best study
for evaluating the extent and severity of the posterior dis-
FIGURE 13-21. Epiphyseal displacement of the proximal clavicle: placement. It is also useful for follow-up studies of healing
injury pattern. and remodeling.
Trauma to the Proximal (Sternal) Clavicle
A B
FIGURE 13-23. (A) Anterior sternoclavicular disruption (solid arrow), leaving behind an intact Thurstan Holland fragment (open arrow).
(B) Healing callus (arrow) connects the displaced fragments.
Treatment
Treatment initially consists of closed, manipulative reduction
and immobilization.212,236 This approach is more effective for
anterior than posterior displacement. Because a portion of
the periosteal sleeve is intact, whether the displacement is
anterior or posterior, complete closed reduction is not
necessary in the young child. Significant amounts of sub-
periosteal bone fill in the “displacement defect” and pro-
gressively remodel, although the process may take several
months to years.
FIGURE 13-24. (A) Posterior sternoclavicular dislocation. (B) CT
scan shows the dislocation (arrow).
437
When the proximal metaphysis is displaced anteriorly,
direct pressure is placed on the osseous prominence,
pushing it back into the sternoclavicular region. The perios-
teum should be intact posteriorly, effectively preventing
overreduction into the thoracic cavity.
Posterior displacement is more difficult to reduce by
closed methods. A bolster may be placed under the spine to
elevate the shoulders. Direct pressure is then applied to both
shoulders, forcing them backward. Application of the same
force to both shoulders is more likely to move the proximal
metaphysis out from behind the manubrium, where it often
lies. This retrosternal location is much more difficult to
reduce than one displaced directly posteriorly. If the reduc-
tion cannot be accomplished, a towel clip may be used to
grasp the clavicle percutaneously to pull it forward (again
with a bolster under the spine).
Open reduction may be indicated when closed, manipu-
lative reduction fails. A threaded Kirschner wire may be drilled
obliquely through the anterior cortex, across the epiphysis,
and into the sternum to stabilize the fragments. Operative
treatment with smooth pins across the fracture site or across
the sternoclavicular joint is contraindicated because of the
potential hazard of pin breakage or migration of the pin into
the vital structures in the mediastinum (see Chapter 10).
The arm must be immobilized to minimize joint motion and
stress, which enhances the risk of pin breakage. The wires
are removed in about 4–6 weeks. The location of the pins
must be monitored closely.
Alternatively, Dacron mesh or heavy sutures using bone
anchors may be used. Tricoire et al. use the tendon of the
subclavian muscle to stabilize the disrupted joint.255 All cases
were posteriorly dislocated. They also found meniscal
damage in three of six patients. Extensive capsular repairs
may be unnecessary.
With anterior displacement, the periosteal sleeve may be
pulled into the displaced region, effectively creating a mem-
brane between the epiphysis, which is still in the joint, and
the metaphysis. This situation increases the instability of the
joint after closed reduction.
Eskola reviewed 12 adults and noted that primary open
reduction was preferred for acute cases of proximal clavicu-
lar displacement, whether anterior or posterior.227 Barth and
Hagen also advocated surgical repair, but only for those in
438 13. Chest and Shoulder Girdle

whom an acute displacement could not be reduced by

manipulation, as is the case in most children and for those
in whom frequent recurrent subluxation or dislocation has
occurred.209

Complications
Posterior displacement of the medial portion of the clavicle
is potentially dangerous owing to the proximity of major
anatomic structures within the chest and mediastinum.
Levinsohn et al. demonstrated the proximity of the joint to
vital structures in an autopsy/imaging study.239 Death re-
sulting from erosion of the trachea and major vessels,
perforation of the esophagus, mediastinitis, thoracic outlet
syndromes, syncope secondary to carotid artery compres-
sion, and arteriovenous fistula may occur.221,229,230,252,257,259
Recurrent displacement (partial to complete) is a significant
complication.
Southworth and Merritt reported complete obstruction of
the innominate vein with retrograde flow up the anterior
jugular vein and across the inferior thyroid vein, establishing
collateral venous return.252 A repeat venogram after closed
reduction demonstrated patency of the innominate vein and
normal drainage into the superior vena cava. Other compli-
cations have included tracheoesophageal fistula,257 brachial
plexus injury,229 and intrathoracic great vessel tamponade230
or laceration.259 Great vessel damage is usually associated
with venous distension in the neck and ipsilateral arm,
hemothorax, and hemomediastinum.
Smolle-Juettner et al. described intracardiac malposition-
ing of a fixation wire used for sternoclavicular disruption.251
It was in a 17-year-old boy who had a posterior subluxation.
The immediate postoperative films show that the fixation FIGURE 13-25. (A) Lateral clavicular fracture, showing the intact
wires were probably in the area of the right atrium and obvi- inferior periosteal sleeve and coracoclavicular ligaments. (B) Simi-
lar injury with concomitant fracture of the coracoid process.
ously were too deep into the chest. Unfortunately, the wires
were not pulled back. Two hours later the patient went into
hypovolemic shock. Emergency aortography showed bleed-
ing into the chest and pericardium, with a tear in the ante- each had a disruption of the distal clavicle and, in some
rior wall of the right atrium. The outcome was fatal. cases, an associated fracture of the coracoid.267 Concomitant
Howard and Shafer reported that neurovascular compres- fracture may also involve the acromion (Figs. 13-28).
sion fell into two groups: (1) obstruction of the carotid artery These injuries, especially in the older child and adoles-
by the displaced medial end, causing syncopal symptoms; cent, mimic acromioclavicular separation, although they are
and (2) compression of the subclavian vessels or brachial really physeal injuries in which the thin epiphysis and physis
plexus.148 Another complication may be damage to the apical maintain their normal anatomic relation to the acromio-
pleura, with subsequent pneumothorax, hemothorax, or clavicular joint, and the distal metaphysis is displaced supe-
both.234 riorly. The periosteal sleeve is generally intact inferiorly, and
the ligamentous structures connecting the clavicle with the
coracoid remain attached to the periosteal sleeve. This allows
rapid “reattachment” of these ligaments to the subperiosteal
Trauma to the Distal callus that is formed by this sleeve of tissue.
(Acromial) Clavicle
Pathology
Children may sustain an injury to the distal clavicle that is
analogous to a metaphyseal–epiphyseal fracture (Figs. 13-25 The acromioclavicular ligaments attach densely into the peri-
to 13-27) but is easily misinterpreted as an acromioclavicular chondrium of the distal clavicular epiphysis and then subse-
separation.262–284 The coracoclavicular ligaments usually quently blend into the periosteum. As in other regions of the
remain intact and attached to the periosteal sleeve. Falstie- developing chondro-osseous skeleton, the weakest region
Jensen and Mikkelsen used the term “pseudodislocation” biomechanically is the physeal–metaphyseal interface, ren-
because some or all of the cartilage displaced with the dering acromioclavicular ligament disruption much less
periosteal sleeve.268 Eidman et al. reported 25 children likely in the infant, child, or adolescent. Instead, the deform-
thought to have acromioclavicular joint separation; instead, ing forces that would cause such a separation in an adult
Trauma to the Distal (Acromial) Clavicle 439

invariably result in a clavicular fracture at either end or the

midshaft in a child.
The pathomechanism is variable stripping of the perios-
teum. In severe cases, the proximal end of the clavicle is
displaced superiorly, whereas the periosteal sleeve, with
attached distal epiphysis, acromion, acromioclavicular joint,
and coracoclavicular ligaments, remains anatomically intact
(Fig. 13-29). Variations in the fracture pattern and the
degree of displacement occur (Fig. 13-30). Inferior dis-
placement also may occur. The most infrequent pattern is
subcoracoid displacement.
Because the distal epiphysis retains a cartilaginous cap into
the mid-twenties if not longer (similar to the delayed matu-
ration and physiologic epiphysiodesis characterizing the
proximal clavicular epiphysis), this injury pattern may occur
even in the young adult. It must be distinguished from true
acromioclavicular joint disruption.279
A

Diagnosis
The severity of the injury determines the clinical presenta-
tion.282,295 There is discrete tenderness over the joint, and this
pain is accentuated by motion. If fragment separation is com-
plete, the end of the proximal segment may be prominent,
tenting the skin as the weight of the arm pulls the scapula
downward.

B Radiology
FIGURE 13-26. (A) Thin distal clavicular fracture (arrow). (B) Four When there is minimal disruption of the periosteal sleeve,
weeks later. the acromial process is in its normal position relative to the
lateral end of the clavicle, whereas disruption of the sleeve
leads to increasing discontinuity between the acromion and
clavicle. Because the ends of the clavicle and acromion are
incompletely ossified, a normal cartilage space width may be
misinterpreted as widening of the acromioclavicular joint

B C
FIGURE 13-27. (A) Distal clavicular fracture. Note the separation of the coracoid from the proximal fragment compared to the opposite
side. (B) Appearance after closed reduction. (C) Appearance 1 month later.
440 13. Chest and Shoulder Girdle

A B
FIGURE 13-28. (A) Lateral clavicular fracture (straight arrow) with acromial fracture (curved arrow). (B) Thin avulsion of acromion (arrow)
in a 10-year-old child with an acromioclavicular injury.

B
FIGURE 13-30. (A) Inferior displacement of the distal clavicle. (B)
B Maturation of bone formation in the intact sleeve.

FIGURE 13-29. (A) Disruption of coracoid and trapezoid ligament

bony attachments (arrow). (B) Irregular bone formation 9 years
after a clavicular/coracoid injury.
Trauma to the Distal (Acromial) Clavicle
instead of a fracture of the lateral end of the clavicle. Dis-
placement is variable, so stress films with the patient holding
weights may accentuate the injury and help ascertain the
diagnosis, as with acromioclavicular separation in the skele-
tally mature patient.
Associated Fractures
Avulsion fractures may be associated with distal clavicular
separation.263,267,276,280,282 These fractures undoubtedly occur
because of the ligamentous attachments, with the zone of
failure pulling the coracoid from its bipolar growth plate
with the main body of the scapula. The bone may avulse from
the clavicle or may involve some or all of the coracoid
process.
Distal acromioclavicular disruption is often associated with
an epiphyseal separation of the base of the coracoid
process.264 Such a fracture of the base of the coracoid is often
overlooked on routine radiographs. The Stryker notch view
offers the clearest profile of the entire coracoid and is the
same view used to demonstrate the Hill-Sach compression
fracture of the posterolateral aspect of the humeral head.
This fracture is a separation of the common physis of the
base of the coracoid and the upper portion of the glenoid
fossa.
Scavenius and Iverson studied weight lifters and found
“nontraumatic” clavicular osteolysis in these individuals.281
The chronic repetitiveness of this injury and the changes are
compatible with minimal disruption of the distal clavicular
epiphysis with metaphyseal remodeling, not unlike similar
instances of “widening” of the growth plate in the distal
radius and proximal humerus in competitive young gym-
nasts and pitchers due to chronic repetitive “nontrauma” to
the aforementioned regions.
Treatment
Treatment is contingent on the degree of injury, although
the general principle in children and adolescents is closed
reduction.26,279 Sprains require symptomatic treatment with
a sling. Undisplaced lateral clavicular fractures require symp-
tomatic treatment with a sling, a figure-of-eight clavicle strap,
or both; but they must be watched closely for subsequent
displacement. Subluxation of the distal fragment may be
treated with an adjustable strap going across the acromio-
clavicular joint. With complete displacement, the same
immobilization should be employed initially; but if the
reduction cannot be maintained easily, internal stabilization
can be considered. The injury may be reduced by direct pres-
sure over the distal end and then may be fixed by percuta-
neous pins.
Alternatively, the fracture may be opened and reduced
under direct visualization. Falstie-Jensen and Mikkelsen
strongly advocated open reduction.268 When open reduction
is necessary, especially for the displaced pattern, the bone
should be reduced into the periosteal sleeve, which is then
repaired. If the periosteal repair is not stable, threaded fixa-
tion pins may be used. The fixation wires should be removed
in 4–6 weeks. The patient must be monitored closely for pin
breakage. An alternative to pin fixation is the use of heavy
nonabsorbable sutures with bone anchors.
441
If the lesion is left displaced, new bone may form within
the periosteal tube, and the distal clavicle may become bifid
or Y-shaped. This may lead to a deformity sufficiently
uncomfortable for the patient to require subsequent recon-
structive surgery (i.e., resection of the nonremodeled origi-
nal distal clavicle).
Furthermore, the distal fragment may be displaced and
may override, comparable to a dorsally displaced distal radial
metaphyseal fracture. Such displacement may be difficult
to treat by closed reduction and may be corrected more
effectively by open reduction. Leaving the distal fragment
overriding, especially in an older child, may result in a per-
manent deformity because there is a decreased tendency for
metaphyseal remodeling in this region. The periosteal sleeve
is usually extremely osteogenic and readily fills in any gap
between the periosteum and metaphysis.
Results
Good to excellent results are seen in most cases. No children
have been reported to develop growth disturbances.
Acromioclavicular joint arthritis is rare, although long-term
follow-up of injured children and adolescents into adult
years is not available in the literature.
Clavicular “Duplication”
Partial duplication of the distal clavicle, without other abnor-
malities, has been termed “developmental, without clinical
significance, and of purely anatomic interest.”278 Similar
cases were termed “os subclaviculare” or “os acromiale.”270,274
These authors were unable to explain adequately the dupli-
cation on an embryologic basis. Oestreich suggested that at
least one entity, the lateral clavicular hook, could be an
acquired lesion or occur congenitally.278 Twigg and Rosen-
baum reported a case of duplication of the clavicle.283 Mont-
gomery and Lloyd described a similar case involving fracture
of the distal epiphysis of the coracoid process and separation
of the acromioclavicular joint.276 Rather than being congen-
ital abnormalities, it is likely that these cases represent
varying degrees of unrecognized antecedent trauma in the
acromioclavicular region.265
Following initial separation of the distal epiphysis from
the metaphysis (with the acromioclavicular joint intact), the
metaphysis may be displaced through a longitudinal tear of
the periosteum. The patterns of healing and subsequent
growth after the injury allow a partial duplication (Figs.
13-31, 13-32), limited by the extent of periosteal stripping,
that may or may not remodel prior to skeletal maturation.
Subcoracoid Displacement
Gerber and Rockwood reported three cases of subcoracoid
dislocation of the lateral end of the clavicle, one of which
involved a 14-month-old baby.269 There were only two previ-
ous reports of the particular injury pattern, both involving
adults. The mechanism of dislocation appeared to involve
forceful abduction and external rotation of the arm. The two
adults reported by Derter and Rockwood had multiple
injuries, including rib fractures; the infant had no other con-
comitant injury, although forceful abduction was a probable
 442
FIGURE 13-31. (A) Distal clavicular fracture in a patient with a head injury. The distal end is superiorly displaced. Bone is beginning to
form in the intact, inferior periosteal sleeve. (B) Six months later, a clavicular “duplication” is evident.
mechanism. The infant underwent an open reduction and
was found to have had the lateral end of the clavicle stripped
from the periosteal tube in a manner somewhat similar to
that of the more usual superior displacement.
A clavicle, whereas in dislocation there is complete disconti-
B
FIGURE 13-32. (A) Progressive clavicular “duplication.” (B) Three-
dimensional CT scan.
13. Chest and Shoulder Girdle
Acromioclavicular Dislocation
True dislocations of the acromioclavicular joint are unusual
in children, primarily because the deforming forces that
would cause such a separation in an adult result in a metaph-
yseal fracture in children. Contact sports during adoles-
cence, however, may cause acromioclavicular dislocation.
Several acromioclavicular injuries may occur: (1) ligamen-
tous strain; (2) rupture of the acromioclavicular ligaments
only; or (3) rupture of the entire ligament complex
(acromioclavicular, conoid, and trapezoid).
The severity of the injury determines the clinical presen-
tation. There is discrete tenderness over the joint that is
accentuated by motion. If separation is complete, the end
of the clavicle may be prominent. The patient usually com-
plains of pain upon all movement of the shoulder, particu-
larly forward rotation. There is specific tenderness over the
acromioclavicular joint. If the joint is dislocated, the upright,
prominent lateral end of the clavicle is easily palpated.
Roentgenograms are attained with the patient standing,
holding weights in each hand, and a central beam passing
anteroposteriorly through the joint. In subluxation the acro-
mial process is depressed relative to the lateral end of the
nuity of the articular end. Because the ends of the clavicle
and acromion may be incompletely ossified, a normal carti-
lage space width may be misinterpreted as widening of the
acromioclavicular joint. An associated fracture of the lateral
end of the clavicle should be ruled out.
This dislocation is primarily an “adult” injury. Therefore
the reader should consult the literature on adult trauma for
specific details of diagnosis and treatment.
Trauma to the Scapula
During childhood fractures of the scapula, which is highly
mobile and well protected by bulky muscles, are rare.294,299,312
Like the ribs, this thin bone is much more resilient in the
child than in the adult. Until late adolescence the entire
vertebral border is pliable hyaline cartilage that is equivalent
to an epiphysis. Fractures usually occur along the lateral
margin, including the glenoid, coracoid, and acromion.
Trauma to the Scapula
Many of these regions have secondary ossification centers
that should not be confused with fractures.287,305,306,311
Wilber and Evans reported 40 cases of fractured scapu-
lae.312 The patients ranged in age from 3 to 80 years. Most
of the fractures were through nonarticular regions and did
not lead to significant problems. The authors thought that
open reduction was indicated only when the glenohumeral
joint was involved, an unlikely event in a child. Brachial
plexus and other neural injuries may accompany the frac-
ture, and a pseudopalsy may also occur. Ada and Miller
described 148 fractures involving 116 scapulae.285
Fractures of the body of the scapula result from direct vio-
lence, such as a crushing injury, an automobile accident, a
fall, or child abuse. The blade of the scapula is often com-
minuted, with the fracture lines running in various direc-
tions. At times there is a small fracture along the scapular
margins. The spine of the scapula may be fractured along
with the body of the scapula. The infraspinous portion is
more frequently fractured than the supraspinous area (Fig.
13-33). Usually the fracture fragments are minimally dis-
placed, if at all, as they are held together by the surround-
ing muscles and thick periosteum of the child. Because
the mechanism of injury generally involves major trauma,
accompanying extensive crush injuries of the soft tissue of
the thorax may be present, as well as fractures of the ribs and
spinal column, pneumothorax, and subcutaneous emphy-
sema. Rarely, the inferior tip may be dislocated between the
ribs. Nettrour and associates reported a locked dislocation
of the scapula when it displaced between ribs.308
A stress fracture may involve the scapular body in a child.
Hart et al. described a 7-year-old who sustained a “minor” fall
and continued to use the extremity, despite discomfort.
Complete healing, after an initial 2-week period of rest, led
to resolution of pain and radiologic healing 3 months
later.298
Fractures of the scapular neck are usually caused by a
direct blow to the front or back of the shoulder. The frac-
ture line begins at the suprascapular notch and runs down-
ward and laterally to the axillary border of the scapular neck,
FIGURE 13-33. Scapular fractures. (A) Greenstick fracture of
the margin (arrow). (B) More extensive fracture of the subglenoid
region (arrow).
443
inferior to the glenoid, with the capsular attachments of the
glenohumeral joint remaining intact. Displacement varies
but is usually insignificant. Congenital deformities may
mimic fracture lines.
To demonstrate these fractures adequately it is often nec-
essary to obtain oblique or tangential views, in addition to
the routine anteroposterior roentgenograms. CT scans may
more effectively delineate the extent of a glenoid injury.309
The primary objective of treatment is to make the patient
comfortable. Usually reduction of the fracture is unneces-
sary. Simple immobilization of the entire arm and shoulder
is generally sufficient. Alternatively, the scapula may be
immobilized with a sling-and-swathe dressing.
Treatment consists of support of the shoulder and arm in
a sling-and-swathe dressing, with the onset of pendulum
exercises about 14 days later when the patient is comfortable.
Markedly displaced fractures, which are rare in children,
may be treated with skeletal traction comparable to Dunlop’s
traction for a supracondylar fracture.
Fractures of the glenoid region are rare in children (Figs.
13-34, 13-35). They are produced by direct violence and may
be associated with child abuse. They should be managed con-
servatively unless a large displaced fragment is present; open
reduction is used as a last resort. The results of surgery are
not good, although the data are derived from treatment of
this injury in adults.
The acromion occasionally fractures as a result of direct
violence or of indirect force transmitted vertically by the
humeral head. Care must be taken when making the diag-
nosis, because the tip of the acromion may form a separate
ossification center that is confused with a fracture line in an
acutely traumatized patient. A chondro-osseous separation
may occur.
Beim and Warner described a symptomatic adolescent
swimmer. MRI showed an os acromiale,287 which was treated
by bone grafting and internal fixation. The pain subsided,
and the patient returned to competitive swimming. Cur-
rarino and Prescott reported six similar children. A fracture
was evident in four, and two were diagnosed as having
an anatomic variant.290 Morisawa et al. described acromial
apophysitis in three adolescent athletes.306 Sclerosis and
osseous irregularity was evident. Conservative treatment was
used. This lesion should be considered analogous to the
symptomatic accessory navicular in the foot.
Edelson et al. studied the os acrominale, believing that in
some cases symptomatic patients could benefit from opera-
tion.293 Their patients were probably similar to what we have
previously reported for accessory ossification of the navicu-
lar of the foot. The acrominal apophysis is a continuous car-
tilage, also covering the scapular spine. It may develop one
or more ossification centers.
Kalideen and Satyapal described bilateral acrominal
fractures in 10 of 171 neonates admitted for tetanus
neonatorum.300 The long-term results of the injury were
not described. Nakae and Endo described fracture of the
acromion complicating a shoulder dislocation.307
Fractures of the coracoid process are infrequent and may
be caused by sudden muscular action of the short end of
the biceps and the coracobrachialis muscles or by direct
violence.288,291,295,310 Coracoid fractures more often are asso-
ciated with acromioclavicular injury or shoulder disloca-
444
FIGURE 13-34. Glenoid growth mechanism fracture. (A) Specimen
radiograph showing the fracture (arrow). (B) Morphologic view
showing the injury. The glenoid cartilage is intact superiorly
tion.313 Closed reduction and conservative treatment are
indicated. Again, great care must be exercised during the
roentgenographic diagnosis because of the variable ossifica-
tion patterns.
Prior to epiphyseal closure, the coracoclavicular ligaments
are often stronger than the epiphyseal plate, and an injury
that would result in ligamentous disruption in an adult may
injure only the physis of the coracoid process in a child. In
addition, an accessory ossification center often develops as a
shell-like, rounded ossification at the tip of the coracoid
process. This area is the site of insertion of the coracocla-
vicular ligament. The conjoined tendon of the short head
of the biceps and coracobrachialis, as well as the pectoralis
minor, insert into the coracoid process anterior to the
accessory physis. During adolescence, acromioclavicular
separation may be accompanied by avulsion of a fragment
of the coracoid epiphysis, rather than by disruption of the
ligaments.
13. Chest and Shoulder Girdle
(analogue of greenstick fracture). (C) Radiograph of the specimen
showing fracture (arrow). (D) Histology showed that a microfrac-
ture (arrow) extended into the cartilage.
Glenoid Hypoplasia
Infrequently, children present with pain in the shoulder or
apparent displacement. The possibility of glenoid dysplasia,
similar to acetabular dysplasia, should be considered.
Borenstein et al. reported a 12-year-old boy with symptomatic
restriction of shoulder motion.289 Lintner et al. presented
a similar adolescent with sports-elicited pain.303 Both were
treated symptomatically with therapy and medication.
Scapulothoracic Dissociation
Scapulothoracic dissociation (Fig. 13-36) is a rare injury in
children.286,292 Repair of the clavicle requires internal fixa-
tion because of the extensive soft tissue disruption. The
severity of brachial plexus and vascular disruptions deter-
mine the ultimate outcome. Severe scapulothoracic dissoci-
ation, in which minimal soft tissue continuity within the
Trauma to the Brachial Plexus
FIGURE 13-35. Glenoid fracture following child abuse.
axilla is the only bridging tissue, is not suitable for attempted
replantation. Forequarter amputation is more realistic.
Lange and Noel presented several patients with traumatic
lateral displacement with variable neurologic injury includ-
ing neurologic compromise.302 They proposed the term
traumatic lateral scapular displacement rather than scapu-
lothoracic dissociation, to emphasize this spectrum of possi-
ble presentations.
Scapular Winging
Mah and Otsuka reported that traumatic winging of the
scapula is uncommon in children.304 They described three
cases of athletic injuries, each resolving within 6 months after
conservative management. Winging probably resulted from
an isolated injury of the serratus anterior muscle.297 This
muscle is innervated by the long thoracic nerve. The trauma
FIGURE 13-36. (A) Open clavicular fracture and scapulothoracic
dissociation. This was associated with avulsion of the entire
brachial plexus at the root level. Several large veins required liga-
445
may be acute or chronic. Trauma is probably responsible for
more than 50% of scapular winging injuries. Traction played
a role in the etiology in the first case, but the second case
was probably due to compression of the long thoracic nerve.
Usually when the traction mechanism is involved in athletic
injuries, there is full return of function. No documented
cases of posttraumatic scapular winging in children have
required surgical intervention or muscle transfer.296
Kauppilä studied the anatomy and blood supply along the
thoracic nerve and found that the nerve and its blood supply
were vulnerable to both compression and stretching injury
along the lower part of the scapula.301 The nerve could be
injured in compression rather than previously described
through angulation of the nerve trunk across the second rib,
subjecting it to traction during shoulder movements. Infe-
rior movement of the scapula could result in compression of
the nerve, whereas winging of the scapula might cause trac-
tion on the nerve.
Trauma to the Brachial Plexus
The incidence and long-term problems of injury to the
brachial plexus have dramatically decreased since the recog-
nition of cephalopelvic disproportion (shoulder dystocia)
and improved means of managing the sequelae of neonatal
Erb’s palsy.320,322,326,333,334,342,344,345,353,355,369,370 Most babies with
brachial plexus injuries are products of prolonged or diffi-
cult deliveries; 10% are born in the breech position.317
Brachial plexus injury has also been reported in babies
delivered by cesarean section.318,319 The pattern is different
from vaginal delivery, with 81% having avulsion of the upper
nerve roots.337 This type of injury cannot be treated satisfac-
torily by microsurgical grafting and carries a worse long-term
prognosis than the more typical lower plexus injury.
Drew et al. reported a 9-year-old boy who sustained a prox-
imal humeral fracture and experienced a slowly evolving
brachial plexus injury.332 There was no deficit noted on the
initial clinical examination. Forty-eight hours later he devel-
oped progressive pain and numbness. He was explored and
the nerve ends were found to be contused and under trac-
tion from the distal fragment. Variable recovery occurred
tion, but the artery was intact. (B) After extensive débridement, the
clavicle was reduced and fixed with a medullary pin. The patient
has a flail extremity 6 years later.
446
after the nerves were freed from the end of the humerus.
Peterson and Peterson described brachial plexus injury in
an infant due to a car safety seat. The child recovered com-
pletely after 8 weeks.362
Brachial plexus injuries may involve root avulsions com-
bined with postganglionic nerve trunk ruptures. The site,
level, and extent vary considerably. Common factors are
evident. The roots most commonly injured are C5 and C6.
Postganglionic nerve rupture is common in the C5 nerve
root. Root avulsions are most common in the C7 and C8
nerves. Complete (global) plexus involvement is the second
most common injury pattern. Kawai and coworkers, explor-
ing experimental disruption of the brachial plexus in rabbits,
found that the direction of the traction force was the deter-
mining factor.351 Stretch injuries without nerve or root dis-
ruption (transection) may also occur.
Oppenheim et al. showed that brachial plexus injuries
were associated with large neonates, shoulder dystocia, the
use of forceps, and abnormal presentations, each of which
results in wide separation of the head and shoulder.165 Trac-
tion on the plexus may be lessened if the clavicle fractures.
Although birth weight and general size are usually signifi-
cantly greater, the complication has been reported even in
normal-size neonates.
Al-Qattan et al. reviewed the prognostic value of clavicular
fractures in newborns with obstetric brachial plexus palsy.317
They found that of 13 newborn babies with palsy and con-
current clavicular fractures 2 required primary brachial
plexus surgery. On the other hand, surgery was undertaken
in 43 of the remaining 170 infants with palsy associated with
intact clavicles. They found no prognostic value in the asso-
ciation of the two injuries.
Brachial plexus injury is usually diagnosed in the newborn
infant when one upper extremity is not moving actively and
the passive range of motion is equal on both sides.326,369 If
the active and passive motions are equally restrictive, injury
to the proximal humeral epiphysis is suspected and con-
firmed by roentgenographic examination, although it may
be difficult to interpret these roentgenograms.356 All infants
with suspected or proven Erb’s palsy should be radiographed
routinely to rule out concomitant osseous injury. Newborns
with clavicular fractures often have a pseudoparalysis that
mimics brachial plexus injury.
In newborns it is often difficult to localize the exact
anatomic extent accurately. Overlap of innervation, result-
ing in partial loss of motor power in the muscles innervated
by the various trunks of the brachial plexus, may make dis-
crete anatomic diagnosis difficult. However, an absolutely
accurate anatomic diagnosis probably has no real advantage,
for either management or prognosis, in the neonate. Classi-
fication into upper (Erb), lower (Klumpke), or whole (Erb-
Duchenne-Klumpke) types is useful only insofar as it conveys
a general picture of the probable pattern and extent of
involvement.318,328
During the neonatal period the degree of severity and the
time at which spontaneous recovery may be expected are dif-
ficult to estimate. Complete, spontaneous recovery of func-
tion is hoped for in all patients, but it is impossible to predict
which patients will recovery fully. Some severely involved
extremities recover spontaneously after many months. The
maximal time of recovery ranges from 1 to 18 months.314,343
13. Chest and Shoulder Girdle
Hardy reviewed more than 41,000 live births, found 36
brachial plexus injuries, and showed that 80% had a com-
plete recovery within 13 months.346 A wide difference in
the incidence of complete recovery has been reported;
Wickstrom and colleagues found an incidence of 13%,
whereas Adler and Patterson reported only 7%.314,343,374
Because specific muscle testing is difficult in the neonate,
gross movement of the shoulder, elbow, hand, and wrist
should be recorded. Precise testing is not of significance,
especially if a traction injury is present, as it changes over
time. More precise diagnosis becomes important only if sur-
gical intervention is being considered. Complete (global)
plexus involvement is evident by a totally limp arm; scapular
winging; absence of the deep tendon reflexes in the biceps,
triceps, and brachioradialis; absence of the grasp reflex;
torticollis; facial palsy; Horner syndrome from injury to the
cervical sympathetic nerves; and diaphragmatic paralysis
from phrenic nerve injury. Injury to only the C7 and C8
roots (Klumpke’s paralysis) results in weakness of the wrist
and finger flexors and the intrinsic muscles of the hand. The
Moro reflex may be present, except for terminal fanning of
the digits and flexion of the thumb and index finger. The
grasp reflex is absent. Extensive sensory deficit implies a
poor prognosis, but usually sensation is surprisingly intact.
Al-Qattan et al. reviewed Klumpke’s palsy, finding it to
occur in only 0.6% of 235 cases of obstetric plexus injury.318
They noted that obstetric brachial plexus palsy was classified
into upper (C5 or C6, ± C7 root), lower (C8–T1), and total
(C5, C6, C7, or C8, ± T1) palsies. A fourth type of birth palsy,
named the intermediate type, predominantly involves the
C7 root.324 The lower palsy is referred to as Klumpke’s, and
the paralysis is usually confined to the hand. Phrenic nerve
paralysis and Horner syndrome may also be present.
Of far greater prognostic use is a clinical description, joint
by joint, of the extent of involvement, particularly for
patients whose care may not remain the responsibility of a
single physician from year to year. Such information allows
an overall plan of management to be followed.
An infant with a brachial plexus injury should be exam-
ined at 4- to 8-week intervals to further evaluate the extent
of the injury and the degree of recovery. A record should
be made of the range of active and passive motion of the
extremities and the gross reaction to pain. Neurologic
examination of the upper and lower extremities should
be repeated, as brain and spinal cord injury may also occur
in these children. Edema, skin changes, and trophic ulcers
should be noted; and two-point discrimination and proprio-
ception should be tested in cooperative, older children.
Hentz and Meyer reviewed brachial plexus injury in chil-
dren.347 They documented 61 cases of brachial plexus palsy
in 3451 live births. Thirty-eight of these patients were fol-
lowed from age 1 to 11 years; 35 patients had upper root
involvement, and 3 had total palsy. The prognosis was excel-
lent with full recovery by 1 week in 25 (66%) and by 3
months in 35 (92%); 96% of patients recovered completely.
In contrast, Clarke and Curtis studied 25 patients and found
that only 8 had normal upper limbs when examined 2.5–10.0
years after birth. Of the 25 patients, 10 showed abnormal
abduction of the shoulder, and 7 of 25 had excessively poor
upper limb function.327 The differences probably reflect the
lack of a uniform system of evaluation. They reevaluated and
Trauma to the Brachial Plexus
assessed another 44 children in whom complete recovery was
possible only if the biceps and deltoid reached the M1 state
(contraction without nerve) by the second month.
Marshall and DeSilva applied CT scanning to the evalua-
tion of brachial plexus injuries in the adult.358 It is not known
whether this technology or MRI would be efficacious in a
newborn for evaluating the level of the lesion—whether it is
at the root from the spinal cord itself or further out periph-
erally. However, with current technology, and with MRI par-
ticularly, heavy sedation or an anesthetic may be necessary
in the infant, which may be a contraindication to effective
clinical utilization of such an evaluation.
Urabe et al. studied a 2-month-old baby with brachial
plexus palsy by MRI.373 They demonstrated traumatic
pseudoparalysis involving an avulsion injury. They noted that
MRI provided accurate information for evaluating the type
and level of the brachial plexus injury, thereby improving
the choice of subsequent treatment. They also noted that it
was superior to myelography or CT. In view of the newer
approaches to brachial plexus surgery, Francel et al. evalu-
ated the efficacy of fast spin-echo MRI.335 The method is
highly effective for delineating pathologic anatomy.
Boome and Kaye showed that if beginning recovery is not
evident by 3 months, a significant residual (permanent)
functional deficit is likely.323 They also thought that infants
without evidence of recovery at 3 months were candidates
for root grafting. Jackson et al. studied two brachial plexus
injuries.349 There was full recovery at an average of 3 months
(range 2 weeks to 12 months). A small number had residual
paralysis at more than 26 months. They concluded that the
newborn usually has a favorable prognosis for recovery.
Others have supported this conclusion.331,360
Regardless of the incidence of spontaneous recovery and
the transient quality of the paralysis in some patients, con-
tractures and deformities may occur rapidly. Therefore every
child in whom birth palsy is diagnosed or suspected should
receive early therapy. One should not await spontaneous
recovery, as limitation of motion and deformity may persist,
despite complete return of muscle power, if therapy is
delayed.
Frequent, diligent, gentle exercises that put all the joints
of the involved extremity through a full range of passive
motion are the cornerstone of early management of the
patient with obstetric palsy. It is hoped that such therapy can
prevent or decrease contractures. If some degree of paraly-
sis persists, prevention of contracture allows more latitude
in the choice of subsequent reconstructive procedures.
As for deformities complicating poliomyelitis, it is a basic
axiom of treatment that fixed deformity must be overcome
before tendon or muscle transfers are performed in order
to produce more normal function.
Braces, strapping, splints, and pinning the arm to the head
of the crib have been recommended. These procedures are
attractive because they supposedly prevent the most obvious
deformity of an internally rotated and adducted shoulder.
It is more important, however, that the parents be taught
how to apply gentle motion to the shoulder, elbow, and wrist
joints with each diaper change. The parents should hold the
top of the shoulder and lift the patient’s arm gently for effec-
tive, passive exercises at the glenohumeral joint. If there are
supination contractures of the forearm or adduction con-
447
tractures of the thumb, the parents should stretch them care-
fully. Occasionally, posterior plaster splints at the elbow and
wrist can prevent palmar flexion contractures. The physician
should review the performance at each follow-up visit.
Kennedy reported early suture of brachial plexus injuries
in 1903, but virtually nothing further was done in the way
of surgical intervention until a recent resurgence of inter-
est.316,352,354,364 Advances such as refined electroneuromyo-
graphic methods for early assessment of brachial plexus
lesions and encouraging results from microsurgical re-
construction of peripheral nerves and brachial plexus in
adults have led to application of this technology to the
newborn.339,357,368,371 Solonen and associates operated on
three patients with brachial plexus palsy from birth injury
within 3 months of birth.368 Reconstruction of part of the
torn brachial plexus was accomplished with free nerve grafts.
They noted that the improvement found an average of 2
years or more after surgery was much better than that which
could have been achieved without surgery. Many patients
end up with permanent incapacity; and if surgical interven-
tion can diminish the disability without undue risk, it is jus-
tified. The primary improvement in the cases reported by
Solonen and associates was in the function of the deltoid and
biceps, which are important to overall shoulder and elbow
function, especially to position the hand for adequate func-
tion. Repair may involve direct neurorrhaphy or, if it is not
possible, reconstruction with free nerve grafts.
The patient with global palsy and no return of neurologic
function after 3–4 months of age is probably the best candi-
date for nerve transfer (neurotization).336 This procedure
attempts to restore partial function through nerve transpo-
sitions, such as using branches of the intercostal nerves.
Gilbert et al. reviewed 21 cases of brachial (Erb’s) palsy
explored between 7 weeks and 9 years of age.340,341 They
found that ruptures of the upper root junction of C5–6 were
frequent and could be repaired by nerve graft. Avulsion from
the spinal cord was more frequent in the lower roots. They
concluded that exploration and attempted repair should
be done early, preferably at the age of 2–3 months, in the
absence of spontaneous recovery.
Sloof reviewed repairs followed for at least 2 years and
noted that good results were achieved with an upper plexus
lesion. On the other hand, in those with root avulsion and
subtotal lesions the final result was less positive, particularly
when those children had been breech deliveries.367
Kawabata et al. described neurotization of the accessory
nerve with transfer to multiple brachial plexus injuries
(mean age at surgery 5.9 months).350 Altogether 67% of the
patients regained deltoid function, 88% in the infraspinatus
and 100% in the biceps. Wrist dorsiflexion and triceps was
the least (25%) successful. There was no functional com-
promise in the trapezius. Chuang et al. have reported similar
good results in 99 patients.325
The problems of later management and consequences of
operative procedures to restore function are well described
in articles by Adler and Patterson,314 Wickstrom and col-
leagues,374 Marshall et al.,359 and others.329,375 Phipps and
Hofer used latissimus dorsi and teres major transfer to
the rotator cuff.363 They found that the procedure pro-
vided active external rotation and, less frequently, shoulder
abduction.
448
It is important to follow these children through to skele-
tal maturity, as their abnormally innervated muscle may lead
to differences in the growth of the bones, particularly the
shoulder and elbow.315,321,330,359,361,365 Undoubtedly, these dif-
ferences are due to abnormal growth stimulation from
muscle imbalance. Attitudinal posturing of the shoulder may
lead to a posterior dislocation.372 The overall shape of the
humeral head may be different from that of the opposite
side. Posteromedial dislocation or subluxation at the elbow
is common.
These children are subject to fractures. In children with
severe muscular insufficiency there usually is concomitant
osteopenia and osteoporosis, increasing the susceptibility
to pathologic fractures. Because of the lack of appropriate
sensory perception, they may not be aware of either bone or
joint injury. Delayed union and nonunion may occur
because of the sensory neuropathy. Charcot arthropathy may
develop. In instances of flail shoulder or breakdown from
a Charcot arthropathy, a glenohumeral fusion may be
appropriate.
Hernandez and Dias emphasized the use of CT to evalu-
ate the shoulder in children with brachial plexopathy.348
They found a significant number of patients with subluxa-
tion and glenoid or humeral head deformity.
Trophic ulceration may lead to loss of portions of the
digits. Rossitch et al. presented a 1-year-old who began to
self-mutilate digits following brachial plexus injury.366 They
thought that this process was probably motivated by subjec-
tive pain in an effort to relieve the pain, a concept that has
relevance to deafferentation animal models.
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14
Humerus
Engraving of a type 1 physeal injury of the proximal humerus.
(From Poland J. Transmatic Separation of the Epiphyses. London:
Smith, Elder, 1898)
t birth the initial contour of the proximal humeral
A physis has a transverse orientation, similar to the prox-
imal femur. However, during subsequent postnatal
development, this physeal contour is progressively modified
into the conical (pyramidal) shape that characterizes the
adolescent.19 A medial growth zone under the humeral head
usually is subjected to compression stresses, and the lateral
region is subjected to both compression and tension forces,
depending on the position and functional activity of the
various shoulder muscles (Figs. 14-1 to 14-3). Variations in
glenoid development may also affect the morphology of the
proximal humerus.6,15
As the proximal humerus matures, the anatomic struc-
tures of the physis and contiguous metaphysis play a major
456
role in the overall resistive strength and patterns of fracture.
The progressively conical apex has a posteromedial position
that resists forces directed posteriorly and axially. The apex
of the cone is medial to a plane drawn from the anterior to
the posterior insertions of the rotator cuff musculature. This
plane includes a small portion of the medial metaphysis ante-
riorly but more of it posteriorly, and it is probably a signifi-
cant anatomic factor predisposing the proximal humerus to
the common type 2 growth mechanism fracture in the older
child.
The epiphyseal (secondary) ossification center of the
proximal humerus may not be present at birth, except in
its formative (preosseous) stage. Approximately 20% of
neonates have a radiologically evident epiphyseal ossification
center at birth. By 4 months this ossification center becomes
radiologically evident. The ossification center in the greater
tuberosity appears between 6 and 18 months, and an ossifi-
cation center for the lesser tuberosity occurs later, although
this structure is highly variable and frequently does not
appear as an independent ossification center. The ossifica-
tion centers of the greater tuberosity and humeral head form
osseous connections at the microscopic level as early as
10–14 months, although it depends on individual rates of
development. Coalescence of these two osseous centers
usually becomes radiologically evident at 4–7 years. The
physis undergoes histologic closure at approximately 12–14
years in girls and 15–17 years in boys (Fig. 14-4).
The periosteum plays a significant role in the strength of
the proximal humeral growth plate and its susceptibility to
injury. The periosteum is thicker posteriorly than anteriorly.
This anatomic variation plays a significant role in preventing
posterior displacment of the metaphysis. In contrast, dis-
placement of the metaphysis is relatively easily produced
through the thinner anterior portion of the periosteum. This
anatomic variation in thickness remains throughout skeletal
maturation. When the periosteum gives way, it tends to
disrupt lateral to the intertubercular groove under the long
head of the biceps. The bicipital tendon and osseous groove
appear to be predisposing factors to the development of the
medial metaphyseal fragment in type 2 growth mechanism
injuries.
The proximal humeral physis is significant to both
humeral and overall arm length, contributing approximately
Humerus
FIGURE 14-1. Development of the proximal humerus. (A) Neonatal
humerus showing a vascular cartilage canal penetrating from the
greater tuberosity (open arrow). The solid arrows indicate the plane
of separation in a birth injury or child abuse. Such an injury invari-
ably involves a fracture, rather than a shoulder dislocation. (B) At
A B
FIGURE 14-2. (A) Osseous specimen from a 7-year-old showing
the conical contour. Note the vascular foramina in the capital
humeral region and the increased fenestration of the metaphysis
in the conical region, which may predispose the proximal humerus
457
7 months, secondary ossification centers are present in the capital
humerus, A, and greater tuberosity, B. A vascular channel, C,
enters the capital humeral center. The medial physis curves dis-
tally at D, creating a contour similar to that of the early proximal
femur.
to certain failure patterns. (B) Serial sections of proximal humerus
from a 12-year-old show the variable contour of the physis depend-
ing on the anteroposterior depth. This varied contour affects frac-
ture patterns.
458 14. Humerus

FIGURE 14-3. Air/cartilage roentgenograms demonstrating cartilage and bone. (A) Two months. (B) Seven months. (C) Three years.
Note also the acute metaphyseal fracture (arrow).

80% of the longitudinal growth of the humerus. Impairment

of this normal growth process may have a major effect on
the overall length of the involved limb.
The metaphysis is initially flat at its interface with the
physis. With growth, the central area extends upward, creat-
ing a pyramidal shape. Several large muscles attach to this
area; such attachment may affect metaphyseal cortical devel-
opment, creating irregularities (Fig. 14-5). This situation is
similar to the cortical variants described for the medial distal
femoral metaphysis (see Chapter 21).

FIGURE 14-5. Medial cortical irregularity in a 14-year-old boy being

FIGURE 14-4. (A) Roentgenogram from a 13-year-old boy, showing evaluated for shoulder pain. This is a normal radiologic variant,
subchondral sclerosis preceding final physeal closure. (B) Slab similar to the medial irregularity often seen in the distal femur.
section from a 15-year-old showing almost complete physeal
closure with coalescence of subchondral plates.
Humerus 459

FIGURE 14-6. Distal humeral development in a 6-month-old baby. cartilaginous epiphyseal contours. Note the medial epicondyle (M),
(A) Intact elbow joint with air outlining the radiohumeral portions of trochlea (T), and capitellum (C).
the joint. Note the capitellum (C). (B) Air/cartilage contrast showing

As a rough definition, the diaphysis extends from the upper the instability of a fracture in this region. The two-column
border of the insertion of the pectoralis major to the sup- structure also affects surgical fixation.
racondylar ridge. This area has multiple muscular attach- Diagnosis of distal humeral injuries is rendered particu-
ments, which, depending on the level of the fracture, larly difficult because of the variable extent of secondary ossi-
significantly affect the displacement of the fragments. The fication (Figs. 14-6 to 14-12).8,9,11,12,17,20,21,23 Significant injury
humeral shaft is roughly cylindrical in its upper half but may occur with deceptively little roentgenographic evi-
becomes gradually broadened and flattened distally. dence.5 The overall joint contours and separation of capitel-
The major nerves variably traverse along the humeral lar and trochlear surfaces are present at birth and do not
shaft. The most serious likelihood of potential injury is to change significantly with subsequent development. Disrup-
the radial nerve, which lies adjacent to the posterolateral tion of these relations with medial or lateral condylar frac-
surface of the shaft. It traverses obliquely and laterally as it tures may alter joint contours, mechanics, and circulatory
passes from the axilla to the anterolateral epicondylar dynamics.10 The ossification centers appear in the following
region. It may be injured acutely or be subsequently sequence: capitellum (at 3–4 months), medial epicondyle (at
entrapped in fracture callus. Nerve entrapment may occur 4–6 years), medial condyle (at 8–9 years), and lateral epi-
even with greenstick diaphyseal fractures. condyle (at 9–11 years). The trochlear center consistently
The supracondylar process is a normal variation in develops from multiple foci (Fig. 14-9). A small, medial
approximately 1% of patients.3 It is usually located 5–7 cm accessory ossification center of the trochlea may appear after
above the medial epicondyle at skeletal maturity. Obviously, the major foci have fused. These variations may simulate a
this distance may be less in the younger child, as growth fracture fragment.23–25 There may be considerable variation
increases the position (distance) of the process from the
physis. It may be connected distally with a tendinous band
extending to the medial epicondyle and may provide an
anomalous insertion for the pronator teres. When this
tendinous band is calcified or ossified, it may outline a
foramen. When the median nerve and artery pass through
this structure, increased traction from growth or com-
pression or swelling following trauma may cause arterial or
nerve dysfunction. On rare occasions, this supracondylar
process is fractured.7,13,16
In the supracondylar region of the distal humerus, the
osseous septum separating the olecranon fossa from the
coronoid fossa varies in thickness (see Fig. 14-8, below).
Roentgenographically, it has variable radiodensity. Occa-
sionally, there is complete osseous perforation, although
fibrous tissue still separate the anterior and posterior por-
tions of the fossa. The variability of the radiographic appear-
ance must be considered when evaluating a patient.7,25 The
foramen (fossa) essentially divides the supracondylar me-
taphysis into two columns.1,14 This is an important feature in FIGURE 14-7. Distal humeral development in a 2-year-old.
460 14. Humerus

FIGURE 14-9. Distal humeral development in an 8-year-old. (A)

Roentgenogram shows that trochlear ossification is beginning
(arrow). (B) Histologic section. Note the multifocal ossification of
the trochlea (solid arrows) and the satellite ossification of the
capitellum (open arrow).

FIGURE 14-8. Distal humeral development in a 6-year-old. (A) Air

outlines the joint and epiphyseal contours. (B) Sagittal (S) section
of chondro-osseous epiphysis and transverse (T) section of shaft
at the level of “T”. Above the olecranon fossa (O), the anatomic
configuration of the shaft is more stable than the transverse
contour at the fossa.

FIGURE 14-10. Distal humeral development in a 10-year-old. The trochlear

ossification center is beginning to coalesce with the multiple ossific foci
and the capitellar ossification center (arrow). Note the trochlea (t) and
capitellum (c).
Humerus 461

The ulnar nerve runs in a groove along the posterior aspect

of this epicondyle, an anatomic relation responsible for the
frequency of ulnar nerve injury, especially contusion, with a
medial epicondylar fracture, The medial epicondyle is often
considered an epiphysis that does not contribute to the lon-
gitudinal growth of the humerus. This is a misconception.
This particular region initially develops as an integral part of
the medial condyle. With growth it becomes a functionally,
though not anatomically, separate entity; and it appears to
be unassociated with the major histologic changes charac-
teristic of a traction-responsive physis, such as the tibial
tuberosity. Injury to the medial epicondyle, if it occurs in a
young child, may lead to growth alteration because it causes
disruption of the physis as it curves around the main portion
of the condyle. The older the child at the time of a distal
humeral injury, the less likely it is that any significant growth
disturbance will follow.
A supratrochlear dorsale accessory ossicle may develop
behind the supracondylar fossa.18,27 It may be excised if the
patient is symptomatic.

FIGURE 14-11. (A) Distal humeral development in a 12-year-old.

Both epicondyles have developed secondary centers (L = lateral
epicondyle; M = medial epicondyle). (B) Distal humerus of a 14-
year-old. The lateral epicondyle has fused with the capitellum (solid
arrow) but not with the metaphysis (open arrow).

of secondary ossification from right to left. Comparison views

are not totally reliable for symmetry to rule out injury.
The lateral epicondyle serves as the origin of the radial
collateral ligament, the supinator muscle, and the common
extensor muscle tendon. Irregular or multifocal ossification
is typical in the immature lateral epicondyle of the humerus
and may be misdiagnosed as an avulsion.11
Comparison to the opposite side is not always helpful, as
asymmetric epiphyseal ossification is relatively common,
most likely due to differing muscular activity and strength in
dominant versus nondominant arms. The ossification center
of the lateral epicondyle appears at about 12 years of age and
fuses with the lateral condyle at age 14 years. The lateral epi-
condyle does not fuse directly with the humeral metaphysis
as does the medial epicondyle. Instead, it fuses first with the
contiguous epiphyseal ossification center of the capitellum
at 14–16 years (Fig. 14-12); then the combined ossific mass
fuses with the distal humeral metaphysis.
The ossification center of the medial epicondyle appears FIGURE 14-12. Serial transverse sections of the distal humerus.
about 5 years of age and unites with the metaphysis between Because of the anterior tilt of the distal epiphysis (see Figure 14-
14 and 16 years.19 The common tendon of the flexor muscles 13) portions of the epiphysis and metaphysis are evident in the
of the forearm originates from the medial epicondyle, which same transection. The capitellar ossification center is readily
also attaches to the ulnar collateral ligament of the elbow. evident (arrow). The bicolumnar morphology is also evident.
462
FIGURE 14-13. Normal lateral view showing anterior angulation of
the capitellum (arrow). This angulation must be restored in fracture
reductions.
The carrying angle of the elbow does not have a signifi-
cant gender difference, but it does have an age difference in
that there is a gradual increase in the carrying angle with
progressive skeletal maturation.4 The mean carrying angle is
15° in the 0- to 4-year age group and increases to 17.8° by
the time of skeletal maturity.4 This contrasts with a reported
slight gender difference of the mean carrying angle of 13°
in women and 11° in men.2,26
The distal humerus has a normal forward angulation that
is most evident when supracondylar or capitellar (lateral
condylar) fractures are being evaluated (Fig. 14-13). Realign-
ment of this anatomic configuration should be attempted
during any fracture reduction, as misalignment (usually a rel-
ative hyperextension) may affect elbow mechanics, especially
the ability to flex or extend completely.22 Capitellar mis-
alignment may also significantly affect the ability to supinate
or pronate.
Glenohumeral Joint Dislocation
Subluxation and dislocation of the shoulder are rare in an
infant or young child but become more common during
adolescence.30,33,34,35,44 Instability may occur as a complication
of various types of neurologic abnormalities, particularly
brachial plexus injuries (see Chapter 13). Developmental
anterior capsular redundancy predisposes certain individu-
als to progressively unstable shoulders.42 Subluxation and dis-
location may develop slowly.46–50
Congenital morphologic differences may predispose to
shoulder instability. Glenoid dysplasia, although much less
common than acetabular dysplasia, certainly may be associ-
ated with a chronically painful shoulder.15 The patient shown
in Figure 14-14 was referred for bilateral “chronically dislo-
cated” shoulders, but evaluation revealed intact gleno-
humeral joints and redirection of the scapulae almost 90°,
14. Humerus
such that they were rotated onto the sides of the rib cage.
The underlying deficit appeared to be hypoplasia of the
clavicles.32
The anatomic structure and extent of functional motion
predispose the proximal humerus to epiphyseal separation
in the child and adolescent in response to forces that, in con-
trast, may lead to glenohumeral dislocation in an adolescent
or young adult.36,39,43 Rowe and Sakellarides reviewed 500
cases of shoulder dislocation and found that only 8 involved
patients between the ages of 6 months and 10 years.40 Almost
20% of the cases occurred during the second decade of life,
usually in those ages 17–20 years (generally after skeletal
maturity had been attained). The highest recurrence rates
were in patients under 20 years of age, rather than adults.
They also showed that many young adults with habitual vol-
untary dislocation of the shoulder probably commenced the
process during early adolescence, at a time when the growth
plate was undergoing physiologic closure and the laxity of
the ligamentous structures around the shoulder was nor-
mally decreasing.
Huber and Gerber reviewed 25 children with voluntary
(habitual) subluxation (36 shoulders).35 Eighteen children
were managed by “skillful neglect.” Only two required shoul-
der surgery as adults; the others were satisified with the
function of the shoulder. Seven children (10 shoulders)
underwent stabilizing procedures, but only three patients
were satisfied with the results. None of the patients had emo-
tional or psychiatric problems. Huber and Gerber thought
there was no indication for prophylactic surgical interven-
tion. None of the patients developed osteoarthritis during
the follow-up ranging from 6 to 26 years.
The capsule of the shoulder joint has an intrinsic laxity
that allows some displacement during stress. This may be
documented arthrographically in a child with chronic shoul-
der discomfort or pain (Fig. 14-15). It may also be seen in
pseudosubluxation of the proximal humerus when there is
a fracture with hemarthrosis or reactive joint effusion (Fig.
14-16). The intrinsic capsular elasticity and joint volume con-
tribute little to anterior shoulder instability.41 Rather, insta-
bility probably relates to damage to the surrounding
muscular stabilizing structures.
In an assessment of 75 children (150 joints), signs of insta-
bility were found in 57% of the boys and 48% of the girls.30
The most frequent sign was a positive posterior drawer test
(63 shoulders). Seventeen patients had multidirectional
instability. Generalized joint laxity was not a feature of these
subjects.
Dislocation in the skeletally immature patient is usually
anteroinferior (Fig. 14-17), probably due to an intrinsic area
of laxity and the common mechanism of hyperabduction
and extension. The affected child’s appearance is compara-
ble to that of the adult. The arm is usually in slight abduc-
tion and external rotation. An anterior bulge may be seen
from the side. In the case of subluxation or persistent pain
after reduction, translation should be tested in the anterior
and posterior directions. The “apprehension test” should
also be used, wherein external rotation and abduction elicits
concern that the shoulder is about to displace.
The radiologic diagnosis of displacement of the develop-
ing shoulder is usually readily evident. Any patient should be
radiographed prior to reduction to be certain that the more
Glenohumeral Joint Dislocation 463

FIGURE 14-14. (A) This boy was referred for evaluation of

“bilateral congenital shoulder dislocations.” His mother had
the same “problem.” (B) CT scan shows redirection of the
scapula into lateral positions, rather than glenohumeral
dislocations.

FIGURE 14-15. (A) Laxity was present in a 7-year-old, demonstrated in a specimen from a forequarter amputation. (B) Motion evident
in an arthrogram. This patient had chronic shoulder pain due to pitching in the Little League.
 464
FIGURE 14-16. Traction creates a vacuum arthrogram that outlines
the extent of subluxation and thickness of the humeral head
cartilage.
common injury, proximal humeral physeal fracture, has not
occurred. Other diagnostic imaging modalities may be
helpful. A computed tomography (CT) scan can corroborate
chronic residual subluxation after a documented dislocation
that has been acutely reduced. Magnetic resonance imaging
(MRI) may delineate areas of internal trabecular damage
that are part of the progressive biologic changes leading to
a Hill-Sachs lesion (Fig. 14-18).31 A classic Hill-Sachs lesion
is evident in Figure 14-19.
Treatment of this injury is similar in adults and children.
Longitudinal traction is applied to the arm, concomitant
with countertraction. The arm initially is held in an inter-
A B
14. Humerus
nally rotated position. External rotation is applied gradually.
Adequate muscle relaxation facilitates the maneuvers. Many
children have generalized joint laxity, which makes reduc-
tion relatively easy. Great care must be taken not to use exces-
sive force (particularly rotatory), as it could theoretically
cause a complicating traumatic epiphysiolysis, similar to a
slipped capital femoral epiphysis associated with reduction
of a hip dislocation. However, I am unaware of any reported
patient with this potential complication.
The arm should be immobilized in a sling-and-swathe
dressing. Pendulum exercises may be started at 10–14 days.
If the patient develops pain during the postinjury period,
MRI may be useful to delineate soft tissue (i.e., labrum,
capsule) damage that may contribute to chronic instability
or subluxation. Rotator cuff injury does not commonly occur
in this age group.85,86
Redislocation may occur. Wagner and Lyne reported that
traumatic shoulder dislocations were rare in adolescents
when the epiphyses were open. In 8 of 10 of their affected
patients, however, the dislocation recurred and ultimately
required operative intervention and capsular repair.43
The Bankart lesion is an avulsion of the glenohumeral
ligament–labral complex.45 These ligaments may be dis-
rupted from the cartilaginous humeral head as well. Children
may sustain a chondro-osseous glenoid rim fracture as a com-
parable injury (see section on scapular injury in Chapter 13).
Operative approaches are comparable to those used in the
adult. Because capsular redundancy is common, soft tissue
procedures should be emphasized. No child or adolescent
should have surgery, though, without an intense period of
rehabilitation.37,38
Coracoid transfer may be used for recurrent anterior insta-
bility of the shoulder in adolescents. Placement of the screw
through the coracoid process does not appear to affect
subsequent development of that region adversely.28 The
youngest patient was 14 years,28 and the procedure is not rec-
ommended for boys younger than that; it should not be con-
sidered in boys or girls under 12 years of age.
FIGURE 14-17. (A) Dislocation (anterior) in
a 5-year-old. (B) Dislocation in a 12-year-
old girl.
 Glenohumeral Joint Dislocation
FIGURE 14-18. Bone bruising in the humeral head after a disloca-
tion that required reduction in the emergency room. Would this
create the preconditions necessary to lead to an area of collapse
(Hill-Sachs lesion)?
Brachial Plexus Injury
A chronic subluxation or dislocation of the shoulder may be
associated with a childhood brachial plexus injury.46,47,49,50
Several years may elapse before such instability becomes a
clinical problem. Acquired disorders such as a septic shoul-
der during infancy may cause a similar problem.48
FIGURE 14-20. (A) Luxatio erecta in a neonate following traumatic delivery. It must
be distinguished from a physeal fracture. (B) Luxatio erecta in a 5-year-old boy.
465
FIGURE 14-19. Severe chondro-osseous deformity in a 15-year-old
boy with multiple dislocations.
Luxatio Erecta
Luxatio erecta is an infrequent condition that may occur
during a difficult delivery (Fig. 14-20A).23,29 The arm is held
in an overhead position and is externally rotated and
abducted. The humeral head becomes locked below the infe-
rior glenoid margin. Capsular laxity due to the effect of
maternal hormones may be a predisposing factor, similar to
developmental hip dysplasia.
The same infrequent pattern of inferior dislocation with
the arm overhead may occur in older children (Fig. 20B).
The tendency for children to hang from heights (e.g.,
monkey bars, tree limbs) may play a role in the causation.
B
466
Closed reduction should be attempted for luxatio erecta.
Adequate anesthesia and muscle relaxation should be under-
taken to avoid complications such as a proximal humeral
physeal disruption. The need for open reduction is rare.
Obstetric Injury
Congential “dislocation” of the shoulder has been described
as a birth injury.51–64 It is usually associated with difficult deliv-
ery and must be differentiated from a proximal humeral
physeal fracture. Many cases are not diagnosed until several
months after birth. When diagnosed acutely, closed reduc-
tion should be undertaken. If the infant presents several
weeks to months after delivery, soft tissue contractures may
necessitate open reduction.
Great caution should be taken before rendering such a
diagnosis of dislocation. The proximal humerus is more
likely to be fractured as a transphyseal injury (Fig. 14-21), an
injury that usually leads to anteromedial displacement of the
shaft and an apparent dislocation roentgenographically.65–85
During the perinatal period the usual mechanism of
injury is a difficult delivery consequent to shoulder-pelvic
disproportion (dystocia).66,74,77,80 The injury has been
reported following cesarean section.72 In actuality, the prox-
imal humerus is still contained within the joint, and the
proximal metaphysis is laterally displaced.
Clinical diagnosis may be difficult. A neonate with a frac-
ture consequent to the birth injury may have a relative
“paralysis” (pseudoparalysis) of the arm, so the injury may
be misinterpreted as a brachial plexus palsy.49,65 It is usually
possible to stimulate the child to move the major part of the
arm and forearm musculature. Crepitation and discomfort
(crying, irritability) contrast a fracture from a brachial
plexus palsy. The type of trauma that causes a brachial plexus
injury also may cause chondro-osseous injury.
About 20% of newborns have an ossification center that is
radiologically evident. This assists in making a definite diag-
nosis. A shoulder arthrogram may be used to make the diag-
nosis (Fig. 14 -21), or ultrasonography can be useful.41,67,71,83
The arm should be splinted to the body with some type of
wrap. Confirmation of a fracture is possible by repeat films
7–10 days after birth, when metaphyseal callus usually
becomes evident.
Although often alluded to as an injury that heals quickly
without problems, these fractures are not inconsequential.
Children sustaining these fractures should be followed
closely throughout skeletal maturation so growth abnormal-
ities, particularly humerus varus (Fig. 14-22), may be
detected.73,75,79 These growth discrepancies may lead to
altered anatomy and significant arm length inequality.
Unusual deformities of the shoulder may predispose to
neonatal fracture. In the patient illustrated in Figure 14-23
a “snap” was felt during birth. The child subsequently
became asymptomatic. Follow-up showed a glenohumeral
fusion with an established nonunion at the site of a proba-
ble transphyseal fracture. This went on to create a
pseudarthrosis as a substitute for the absence of gleno-
humeral motion.
14. Humerus
Proximal Humeral Physeal Fracture
Epiphyseal fractures constitute the major injury pattern to
the shoulder and proximal humerus prior to skeletal matu-
rity.87–168 Neer and Horwitz reported a 3% incidence of
proximal humeral epiphyseal injuries in their series of all
epiphyseal fractures.141 If metaphyseal fractures are also con-
sidered (including the commonly encountered unicameral
or aneurysmal bone cyst with pathologic fracture), the inci-
dence of proximal humeral injuries in children and adoles-
cents is probably reasonably comparable to the incidence in
adults.
Injuries to the proximal humerus occur infrequently
during the neonatal period, more frequently during the first
decade, and relatively frequently between 11 and 16 years of
age. Any such injury in a child under 18 months of age
should raise the possibility of child abuse in the differential
diagnosis. The oldest reported patient with a proximal
humeral epiphyseal injury was a 23-year-old with pituitary
dysfunction, although Poland mentioned the injury in a 26-
year-old.149,163 In most involved age groups boys outnumber
girls 3 : 1 or 4 : 1. Participation in structured athletics is a sig-
nificant predisposing factor.93,103,156 As with neonatal frac-
tures, these injuries may be associated with a slowly evolving
brachial plexus palsy.
Mechanism of Injury
During infancy a child may be injured by a fall. However, the
battered child syndrome always must be considered, as injury
to the proximal humerus is unusual in an infant. The injury
during later childhood and adolescence is associated with
two major causal mechanisms. First, a falling child throws the
arm into an abducted, extended, and externally rotated posi-
tion to break a fall. This transmits the force toward the shoul-
der joint, at which point the most structurally weak anatomic
area fails: the metaphysis in the young child and the physis
in the older child. Second, the child or adolescent may fall
directly on the lateral side of the shoulder, in which case the
major deforming force is imparted directly into the epiph-
ysis, growth plate, and metaphysis. After the initial deform-
ing forces cease, maintenance or worsening of the deformity
is contingent on the interplay of the muscular forces and the
extent of osseous and periosteal disruption.
Pathologic Anatomy
Several types of fracture may be encountered. A type 1
physeal injury is characteristic of neonates, infants, and
young children up to the age of 4–5 years (Fig. 14-24). In
older children and adolescents the characteristic growth
mechanism injury shifts to type 2, with a posteromedial me-
taphyseal fragment remaining attached to the physis (Figs.
14-25, 14-26). Other types of physeal injury are encountered
infrequently because of the mobility of the glenohumeral
joint and the anatomy of the proximal humerus. In particu-
lar, because the humeral head is much larger than the
associated glenoid and less anatomically restricted, the
mechanical forces that may be applied usually are not
Proximal Humeral Physeal Fracture 467

FIGURE 14-21. (A) Apparent dislocation of the shoulder following shaft. (C) Reactive metaphyseal bone 8 days after the birth injury.
traumatic delivery. Instead, it was a physeal fracture. A small me- (D) Six months later. (E) Nine years later there is medial growth
taphyseal fragment (arrow) remained with the humeral head. (B) arrest. MRI shows the bone bridge (arrow).
Arthrography confirms the located humeral head and the displaced
 A B
FIGURE 14-22. (A) Humerus varus at age 8 years. A “snap” was felt at birth. (B) CT shows the bone bridge.

A B
FIGURE 14-23. This child was being evaluated for abnormal shoul- through this space, which was a pseudarthrosis that developed
der motion. (A) Anteroposterior view shows an abnormally wide because of congenital fusion of the glenoid to the proximal humeral
space between the humeral ossification center and the metaph- epiphysis.
ysis. The glenoid is hypoplastic. (B) Abduction showed motion

FIGURE 14-24. Type 1 injury in a 6-year-old.

(A) Displaced epiphysis. (B) Reduced.

468
Proximal Humeral Physeal Fracture
FIGURE 14-25. Type 2 injuries. (A) Small medial metaphyseal fragment (arrow). (B) Large metaphyseal fragment (arrow), more char-
acteristic of the injury during adolescence.
capable of introducing shear forces comparable to those that
cause type 3 and 4 injuries in other epiphyseal regions.
However, type 5 microinjuries or bone bruises may accom-
pany type 1 or 2 injuries as a result of the adduction nature
of the injury mechanism. This explains some of the growth
abnormalities (e.g., humerus varus) and limb length
inequalities. Type 3 injuries may occur in the older adoles-
cent undergoing closure of the physis.37,101,158
With these aforementioned fracture types, partial dis-
placement is much more common than complete dis-
placement. The fracture-producing mechanism and the
deforming muscle forces usually cause an adduction defor-
mity of the proximal fragment relative to the distal fragment,
although abduction (valgus) angulation may occur.136
During the neonatal and early childhood periods, when
children are more susceptible to type 1 than type 2 injury,
the contour of the growth plate tends to be more transverse
FIGURE 14-26. Mechanism of a medial fragment
caused by the path of the biceps tendon (long head).
(A) Normal anatomic relations of the long head
(arrow). (B) The tendon may be displaced behind the
distal fragment (arrow), which may prevent anatomic
reduction.
469
than conical. As the child grows, the underlying metaphyseal
region assumes an increasingly asymmetric configuration,
with the apex tending to be posteromedial. As this pyrami-
dal pattern becomes more prominent, the child becomes
more susceptible to a type 2 rather than a type 1 growth
mechanism injury.
With type 2 growth mechanism injuries the fracture begins
in the lateral portion of the physis (tension failure), propa-
gates medially, and turns distally to continue into the me-
taphysis, leaving a variable-sized metaphyseal fragment. The
periosteum tends to be stripped from the more lateral por-
tions of the humeral metaphysis while remaining intact
medially in the area of the metaphyseal fragment.112 The
distal (metaphyseal) portion of the fracture may displace
through a rent (buttonhole) in the periosteum (Fig. 14-27).
The portion of intact periosteum extending from the me-
taphyseal fragment to the more distal portions of the diaph-
470 14. Humerus

FIGURE 14-27. (A) Distal fragment has probably displaced through a periosteal rent. (B) The injury.

ysis tends to contract, making reduction difficult after a few is aggressive, accurate correction of the displacement.
days.106 Periosteal continuity also allows some control over However, as the child approaches adolescence, significant
the formation of membranous new bone (callus). displacements become much less acceptable and must be
As previously discussed, the degree of displacement of the reduced to being as anatomically correct as possible.
fragments is contingent on three factors: the deforming The main neurovascular bundle is anteromedial to the
forces that cause the initial displacement, the morphologic joint. The axillary nerve courses inferior to the gleno-
extent of the fracture, and the muscle pulls that maintain humeral joint, wrapping around it to supply the deltoid
angulation and displacement or worsen them. Displacement muscle. It is adjacent to the fragment of the metaphysis with
may be graded into three types: (1) displacement less than a type 2 injury and near the apex of the injury with a type 1
one-half the diameter of the metaphyseal shaft; (2) dis- injury. Complete paralysis of the deltoid may accompany
placement more than one-half the metaphyseal diameter; injury. Because the mechanism of injury is often a direct fall
and (3) complete displacement. With grades 2 and 3 there on the shoulder, a contusion to the nerve may occur as it
usually is an accompanying varus angular deformity. When tranverses between the deltoid and the proximal humerus.
there is angular displacement, the epiphysis tends to be
adducted and posteriorly displaced, while the remaining
metaphysis and shaft are comparably adducted but anteri-
orly displaced. Although some displacement relates to the
primary mechanism of the injury, the epiphysis tends to be
rotated into mild adduction and external rotation by the pull
of attached muscles, and the shaft is drawn forward by the
combined pulls of the pectoralis major, latissimus dorsi, and
teres major muscles. Lateralization and cephalad displace-
ment of the distal fragment tend to be accentuated by the
pull of the deltoid muscle (Fig. 14-28). When the fracture
initially is minimally displaced, an inherent stability is
imparted by the contour of the epiphyseal plate and the sur-
rounding periosteum. This tends to negate any effect from
muscular attachments and the directions of pull. However,
when the separation is grade 2 or 3, the fracture becomes
less stable, and muscular deforming forces tend to play a
more dominant role, often converting partial displacement
to complete displacement.
Displacement is a highly variable factor in injuries to the
proximal humerus and, along with a patient’s age and antic-
ipated growth (Fig. 14-29), is taken into account when decid-
ing on therapy. The younger the child, the less important FIGURE 14-28. Muscle pull.
Proximal Humeral Physeal Fracture
FIGURE 14-29. (A) Initial injury in a 3-year-old, with medial dis-
placement of the proximal fragment and overriding. Multiple
attempts at closed reduction under general anesthesia were
unsuccessful. (B) Four weeks later new bone formation is evident
Most of these neural injuries are transient and recover
spontaneously.
Proximal humeral epiphyseal fractures may be associated
with glenohumeral dislocation.109,144 The dislocation may be
missed.
Diagnosis
Swelling and localized tenderness around the shoulder joint
enhance the likelihood of a shoulder fracture. Ecchymosis
may appear 2–3 days after the injury. Because displacement
is often not a major part of these injuries, relative shorten-
ing of the arm is infrequent, although the presence of such
a physical sign certainly helps in the diagnosis. False motion
and crepitus between the fracture fragments may be
detected, but searching for such findings should be kept to
a minimum to avoid risking injury to the axillary or any other
471
in the periosteal sleeve (arrow). (C) Eight weeks later the medially
displaced sleeve is filling. (D) Four months after injury longitudinal
growth and remodeling have taken place. (E) Four years after the
injury.
nerve. Diagnosis is best made on the basis of roentgeno-
graphic, rather than physical, findings.
Roentgenographic Findings
The evidence for a proximal humeral fracture depends
on the age of the child, the extent of the ossification of the
humeral head and greater tuberosity, and the presence of
any pathologic conditions. Pathologic changes are reason-
ably obvious in the adolescent, the age at which they are most
likely to be encountered. Similarly, fractures of either the
metaphysis or growth plate tend to be reasonably obvious
because of their characteristic anatomic changes, particu-
larly the displacement and the contiguous metaphyseal frag-
ment. In the infant or young child, diagnosis may be difficult
because of the small amount of epiphyseal cartilage that has
undergone ossification.
472
Areas such as the acromion may be injured concomitantly.
Adequate radiologic evaluation should include the entire
pectoral girdle.
Treatment
In general, treatment of injuries to the proximal humerus
utilize closed methods, with open reduction saved for diffi-
cult cases and for older patients in whom the initial nonop-
erative methods are unsatisfactory.99,105,106,115,122,134,167 The
fracture usually heals satisfactorily and has a high propensity
to remodel, despite displacement (Fig. 14-29). The extent of
remaining growth potential must always be kept in mind.
The arm is brought out to length by gentle longitudinal
traction and then placed in a comfortable position. The use
of a general anesthetic may not be necessary, as perfect
anatomic reduction usually is not required. Most series have
shown that young children treated in a conservative fashion,
with minimal efforts at reduction and with significant dis-
placement of the proximal humerus relative to the shaft,
have virtually no significant long-term functional disabilities
or abnormal morphology. Even in adolescents sufficient lon-
gitudinal growth and remodeling capacity remain to justify
leaving the fragments overriding or in mild varus.
In older children and adolescents the fracture is usually a
type 2 injury, generally accompanied by a grade 1 (mild) dis-
placement. This fracture is stable, and manipulation is not
usually necessary. With grade 2 and 3 injuries, in which angu-
lation and displacement are greater, it is recommended that
the humeral fragments be manipulated into a more accept-
able position, although absolute anatomic reduction is still
unnecessary.
The use of various anesthetic agents should be based on
the experience of the surgeon and the cooperativeness of the
patient. It may be better to perform such a reduction under
a general anesthetic, as the use of an analgesic/amnesic
agent (e.g., diazepam) may not allow enough muscle relax-
ation to gain adequate reduction. As the time interval from
onset of injury to attempted reduction increases, so do the
amount of soft tissue swelling, the degree of contracture
(especially in the damaged periosteum), and the involuntary
muscle activity, which makes reduction increasingly difficult.
It is difficult to control the proximal epiphyseal fragment, as
it is a relatively mobile structure and almost impossible to
stabilize completely during manipulation.
The arm is brought into approximately 90° of abduction,
flexion, and mild external rotation to accomplish the reduc-
tion. The arm is then brought back into a position adjacent
to the body. This maneuver gives an idea of the degree of
stability of the reduction and if it is possible to treat the
patient with shoulder immobilization. Whenever possible,
the physician should avoid treatment in a forced abduction
position, as it would increase the deforming forces applied
through the pectoralis major and may affect the stability
of the fracture. If there is any angular deformity, even with
a grade 1 fracture, a gentle closed reduction may be
attempted. Absolute anatomic reduction is usually unneces-
sary, as gradual growth and remodeling correct most mild to
moderate displacements.
The shoulder and arm should be immobilized by whatever
method the physician prefers to use.123 My preference is a
shoulder immobilizer.
14. Humerus
Should the fracture prove unstable, Nilsson and Svartholm
have reported successful use of a hanging cast, with gradual
spontaneous reduction of the displaced, angulated proximal
fragment.143 The shoulder also may be placed in a spica cast
with the arm in abduction, forward flexion, and neutral rota-
tion. The exact position may be determined using image
intensification. The arm should be abducted only as far as
necessary to ensure stability of reduction. Placement in the
extreme positions (e.g., “Statue of Liberty”) may cause prob-
lems, such as incomplete brachial plexus palsy, and are to be
avoided. If that is the only stable position, percutaneous pin
fixation should be used. When casting, splinting, or a sling
is used, reduction should be confirmed.
The patient may be placed in traction using skin traction
or, if necessary, skeletal traction with an olecranon pin. This
method of treatment, however, may stretch the capsule and
subluxate the humeral head, rather than disengaging the
fragments. Increasing emphasis on reduced hospitalization
(costs) makes this treatment one to reserve for children
needing a few days of observation. This applies particularly
to the polytraumatized patient.
Whether a sling, cast, or traction is chosen as the primary
method of nonoperative treatment, it is imperative that peri-
odic roentgenograms be obtained because the reduction
may be lost anytime within the first 2–3 weeks. By the end of
3 weeks, however, there usually is sufficient cartilaginous and
ossifying callus to impart intrinsic stability. Solid union
should be present by 3–4 weeks, and the child may then be
progressively allowed out of immobilization. Early motion,
the mainstay of therapy in adults, is relatively unnecessary in
children because of their intrinsic ability to restore function
rapidly after an injury.
Open reduction or closed reduction with percutaneous
fixation (Fig. 14-30) should be reserved for the older or dif-
ficult to treat patient in whom there is concern over persis-
tent deformity and shortening. The inability to control
fracture fragments because of severe multisystem injury, par-
ticularly head injury, is also an indication for open reduction
or closed reduction with percutaneous pinning. The long
head of the biceps may be caught between the fragments and
impede adequate reduction.106 This condition is difficult to
diagnose and should not be used as the primary indication
for open reduction. A child whose presenting problem,
many days after injury, is a prominent segment of bone (the
lateral metaphysis) is not necessarily a candidate for an oper-
ation either, as remodeling usually leads to gradual disap-
pearance of such a protuberance and improved shoulder
abduction.
Other than children with a head injury and uncontrolled
rigidity, I have encountered few patients who seemed to fit
the criteria for open reduction. One such patient had mul-
tiple injuries, including a Monteggia fracture-dislocation of
the ipsilateral elbow. Following reduction of the elbow,
he was placed in traction. What appeared to be a type 2
epiphyseal injury of the proximal humerus did not respond
effectively. Because of inability to control the additional
metaphyseal fragment, the injury was explored. The segment
was a large portion of the anterolateral metaphysis that had
fractured completely free from the remainder of the shaft
and from the adjacent metaphyseal fragment, which was still
attached to the epiphysis. In contrast, the free fragment had
been denuded of all soft tissue attachments during the acute
Proximal Humeral Physeal Fracture
A B
FIGURE 14-30. (A) Percutaneous pins through a large metaphyseal fragment. (B) Percutaneous fixation, which is inappropriate because
the pin penetrates too far and the fracture has not been reduced. This solution should not have been accepted.
injury. The fragment was placed back in an anatomic posi-
tion underneath the biceps tendon, which was preventing its
reduction. It was stabilized with tension-band wire fixation.
Results
Most believe that proximal humeral injuries heal well, even
in instances of serious displacement, and that a normal
shoulder may be expected at the completion of skeletal
growth.88,89 However, Neer and Horwitz showed that the
long-term results are not as benign as most authors have
described, with a high incidence of subtle to overt longitu-
dinal growth impairment being the main complication.141
Complications
The usual problems encountered with adult shoulder
injuries, such as joint stiffness, malunion, avascular
(ischemic) necrosis, nonunion, myositis ossificans, and
extraarticular calcification, are rare in children. The major
complications in children are (1) limb length inequalities
and (2) varus deformity. Mild angular growth deformities are
more readily tolerated in this joint than any other because
of the degrees of freedom of motion and scapular mobility.
Neer and Horwitz found a large number of patients who
had shortening whether associated with displacement of less
than one-third the shaft diameter or total displacement.141
This shortening appeared to affect mainly patients who sus-
tained their injury after the age of 11 years. Patients younger
than 11 years did not have major growth abnormalities
and, in fact, appeared to make up for the initial shortening
through a process comparable to femoral overgrowth fol-
lowing fracture. The same criteria appeared to apply to
angular deformity: Children over age 11 had less correction
and maintained some varus deformity. The major factor to
consider in any decision for treatment thus appears to be the
anticipated remaining longitudinal growth in the physis.
Baxter and Wiley reviewed 57 patients with proximal
humeral epiphyseal fractures. They found that, regardless of
treatment, the maximum shortening of the humerus aver-
aged 2 cm and residual varus angulation was insignificant.94
473
Varus deformity complicating proximal humeral fractures
in adults is a well acknowledged clinical occurrence, but it is
virtually ignored as a significant complication during child-
hood.69 Most authors state that such an angular deformity
corrects spontaneously with subsequent growth. Similarly,
varus deformity sustained during the neonatal period, when
diagnosis of a fracture is difficult, is also considered to have
minimal long-term consequences.
Posttraumatic humerus varus may develop gradually and
not as a result of immediate angulation of the humeral head.
It most likely occurs as a result of undetectable microtrauma
to the medial side of the proximal humeral growth plate,
eventually resulting in the formation of a small osseous
bridge followed by a significant radiologic deformity. If a
patient presents early with such a beginning deformity, he or
she should be followed at least annually, as physeal fusion
may eventually occur, and the apparent radiolucent defect
(in reality filled with articular and epiphyseal cartilage) does
not appear to represent a major risk to fracture. If the abnor-
mality is encountered at a relatively early age (before 6–7
years of age), it may be possible to resect the osseous bridge.
If any significant functional limitations occur during the late
adolescent period, acromionectomy may be more beneficial
than a valgus osteotomy of the surgical neck.
An infrequent complication is injury to the circumflex or
axillary nerve adjacent to the region of the fracture. This
usually results in transient paralysis of the deltoid and
resolves within a few weeks or months.
Stress Injury
Barnett described “Little League shoulder syndrome” as a
chronic proximal humeral epiphysiolysis in adolescent
baseball pitchers.93 Characteristic of this chronic lesion is
widening of the growth plate with metaphyseal cystic
changes.93
These abnormalities may be encountered in a number of
increasingly popular childhood and adolescent highly com-
petitive sports, including swimming, tennis, and gymnastics.
As described in Chapters 4 and 12, repetitive force to a
474
FIGURE 14-31. Apophysitis in an adolescent tennis player. Note the
widening of the lateral physeal region.
growth plate may cause microfailure and a degree of osteol-
ysis in the juxtaphyseal metaphysis, which causes widening of
the physeal region (Fig. 14-31).
Lesser Tuberosity Avulsion
Lesser tuberosity avulsions are rare.129 Unrecognized acute
avulsion of the attachment of the pectoralis may result in the
subsequent formation of an exostosis (Fig. 14-32).
Shoulder Fusion
Pruitt et al. described shoulder arthrodesis in 17 patients.
All were undertaken for neuromuscular deficiencies (polio,
posttraumatic).146 The position of fusion was not important,
although excessive abduction or forward flexion should be
avoided.
FIGURE 14-33. (A) Metaphyseal fracture in a 5-month-old. Strong
periosteal attachments maintain the alignment. (B) Proximal me-
taphyseal fracture in a 12-year-old. It is anatomically comparable
14. Humerus
FIGURE 14-32. Old fracture of the lesser tuberosity.
Proximal Metaphysis
The proximal metaphysis is highly susceptible to fracture
in the 5- through 11-year range, during which period such
injuries may be more frequent than proximal epiphyseal
fractures. The susceptibility of the metaphysis to these frac-
tures probably relates to the rapid elongation and the struc-
tural changes and remodeling that take place in the cortex
and spongiosa. Pathologic fractures through cystic lesions
are also quite common in this age group.170 Two basic frac-
ture patterns occur: (1) a transverse fracture with or without
loss of cortical continuity; and (2) a torus fracture with main-
tenance of much of the cortical integrity despite the buck-
ling (Figs. 14-33, 14-34).
to a physeal fracture. The shaft is displaced laterally and the prox-
imal fragment rotated 90°. It must be corrected.
Diaphyseal Fractures
FIGURE 14-34. (A) Metaphyseal fracture in a 3-year-old who had
been fatally injured in an auto accident. The fracture crosses the
metaphysis transversely; the periosteum (P, white arrow) remained
intact and prevented significant displacement. This fracture is pri-
marily a compression failure, a mechanism that is more likely in a
young child. (B) Undisplaced transverse metaphyseal fracture with
minimal medial torus injury.
Greenstick fractures are common but seldom occur with
significant angular deformity. They are usually torus frac-
tures. Completely displaced metaphyseal fractures may be
much more difficult to manage than type 2 physeal injuries.
The shaft may penetrate the deltoid muscle and lie subcu-
taneously, making reduction difficult because of the inter-
posed muscle.
475
The use of a hanging cast may align the fragments effec-
tively over a few days. Roentgenograms must be attained to
assess any displacement, as it may result in delayed union or
malunion (Fig. 14-35).
Fracture of the proximal metaphysis may lead to tempo-
rary ischemia of the juxtaphyseal bone (Fig. 14-35), the
mechanism of which is described in Chapters 1 and 6.
The area is well vascularized, and quickly reestablishes the
normal peripheral and central metaphyseal circulatory pat-
terns. Because of the rapid rate of growth of the proximal
humeral physis, the cartilage may become relatively thick
until the invasive metaphyseal circulation is re-established.
Pathologic fractures may be treated as metaphyseal frac-
tures are, with immobilization in a sling for several weeks
until the acute fracture healing is completed, after which
time primary treatment of the cyst can be undertaken, if indi-
cated.170 However, treatment of the cyst with bone graft at
the time of fracture is not absolutely contraindicated. The
fracture region often has collapsed into a varus position,
and while an attempt should be made to correct this, it is
often difficult (see Chapter 11). Steroids should not be
injected at the time of an acute pathologic fracture, as they
may adversely affect the normal inflammatory component of
the healing response. Allow any pathologic fracture to heal
spontaneously before attempting steroid eradication of a
bone cyst.
Diaphyseal Fractures
Diaphyseal injuries are relatively uncommon in chil-
dren.171–205 The proximal and distal humeral chondro-
osseous structures are more likely to fail. Significant
segments of the periosteum remain intact, lessening de-
grees of displacement and facilitating treatment (Fig. 14-36).
Transverse humeral shaft fractures generally result from a
direct blow (tapping fracture), whereas spiral fractures are
produced by twisting injuries, although muscular violence
without an associated fall may also do this. In children under
18 months child abuse must be considered in the differen-
tial diagnosis. The incidence of child abuse is approximately
20% in children under 3 years, and even higher in infants
under eighteen months.
Mechanism of Injury
Most fractures of the shaft of the humerus are caused by
indirect violence, such as a twisting or fall, rather than direct
impact. This mechanism tends to cause oblique or commi-
nuted fractures (Fig. 14-37). When the child lands on the
elbow or hand with a twisting motion to the remainder of
the body, the incidence of spiral or oblique fractures is
greater. Less commonly, athletic activities such as throwing
may cause a spiral injury. However, if a child sustains an
injury in such situations, the possibility of a pathologic frac-
ture must be closely assessed. Transverse fractures tend to be
associated more frequently with obstetric injury or direct
blows, often by landing on the upper arm or shoulder. In
contrast to adults, segmental (comminuted) diaphyseal frac-
tures are infrequent in children.
476
FIGURE 14-35. Malunion of a proximal humeral fracture in a 14-year-old. (A) Anterior view. (B) Specimen
was sectioned to produce the slabs. Little remodeling has taken place between the proximal and distal
cortices. The darker metaphysis reflects temporary ischemia and physiologic slowdown of growth and
remodeling.
FIGURE 14-36. Diaphyseal fracture. (A) Three weeks after reduc-
tion early bone formation is evident along the periosteal tube, which
remained intact along one side of the fracture (arrow). (B) By six
weeks, extensive callus formation is evident along the side with
intact periosteum; the side with periosteal rupture shows much less
formation of new bone.
14. Humerus
Pathologic Anatomy
The direction of displacement of fracture fragments is con-
tingent on the level of the fracture relative to the levels of
muscular insertion, especially the deltoid muscle. Fractures
involving the lower third of the shaft below the level of
deltoid insertion generally exhibit anterolateral displace-
ment of the proximal fragment due to the combined pull
of the supraspinatus, deltoid, and coracobrachialis muscles.
The distal fragment usually is displaced proximally and
medially by the spasm and contraction of the biceps and
brachialis muscles (Fig. 14-38). If the fracture involves the
diaphysis or metaphysis proximal to the insertion of the
deltoid, but distal to the insertion of the pectoralis major,
the deltoid muscle displaces the distal fragment laterally and
upward. At the same time, the pectoralis major, latissimus
dorsi, and teres major muscles and the rotator cuff muscu-
lature of the shoulder joint adduct and internally rotate the
proximal fragment (Fig. 14-38).
The proximal humerus is usually retroverted relative to
the supracondylar region. Therefore when treating these
injuries in children, particularly those with significant dis-
placement, an attempt should be made to restore this
normal anatomic configuration. Rotation of the fragments
does not usually correct itself following fracture. Therefore
it must be assumed that treatment of the arm with signifi-
cant internal rotation of the lower fragment may, if the
upper fragment is at all displaced or externally rotated,
Diaphyseal Fractures
FIGURE 14-37. Diaphyseal fracture patterns. (A) Trans-
verse, with some of periosteum intact. (B) Transverse,
with complete periosteal rupture. (C) Oblique. (D)
Spiral.
cause decreased retroversion and predisposes the shoulder
to subsequent subluxation anteriorly. Because, the more
powerful forces deforming the proximal fragment tend to
be those that represent the rotator cuff and internal rotators
of the shoulder, it usually cannot be sufficiently internally
rotated to have a major effect on the normal degree of retro-
version.
Diagnosis
The clinical diagnosis is usually obvious because of defor-
mity, local swelling, and pain. Roentgenographic studies can
establish the fracture pattern.
The close relation of the radial nerve to the humeral shaft
along the musculospiral groove makes it particularly vulner-
able to injury (contusion, neurotmesis, axonotmesis). Fur-
thermore, injury to the nerves may occur consequent to
their deformation by the fracture fragments, either during
the original injury or with subsequent manipulation. Careful
assessment of nerve function, both sensory and motor, is
FIGURE 14-38. (A) Effects of muscle pulls on displacing fracture
fragments when the fracture is above the deltoid insertion. (B)
Effects of muscle pulls on displacing fracture fragments when the
fracture is below the deltoid insertion.
477
absolutely essential before and after any manipulation. If
the radial nerve is paralyzed, the dorsum of the hand
between the first and second metacarpals is commonly anes-
thetic, and a variable amount of motor power is lost in the
extensors of the wrist, fingers and thumb, and the forearm
supinators.
Treatment
Treatment of children requires an appreciation that their
normal state of activity is greater than that of adults and that
once pain subsides they are less willing to be quiet and prop-
erly utilize such methods of treatment as hanging casts. If
there is marked displacement of the fragments, the initial
step must be reduction of the fracture, which should be
accomplished by closed means unless there is an open injury.
Priority should be given to nonoperative treatment.169,190
The initial reduction maneuver is application of down-
ward traction to correct overriding, disengage the fracture
fragments, and displace them from muscular interpositions.
The proximal fragment must be put in continuity with the
distal fragment. Roentgenograms following reduction must
be obtained in both anteroposterior and lateral views.
Overriding of 1 cm may be accepted because the humerus
exhibits overgrowth, similar to the femur. Angulation of
15°–20° is the most that should be accepted. This is particu-
larly true if the angulation is at the middle or lower third
because the bulk of the corrective growth occurs proximally;
hence there is not the same amount of remodeling in this
area as with an angularly displaced fracture involving the
more proximal regions (Fig. 14-39). In the more proximal
regions, a 20°–25° angular deformation is likely to be cor-
rected by growth and remodeling. The only exception might
be in the neonate, in whom fractures that seem innocuous
initially may rapidly deform to significant malunion during
treatment but remodel with equal rapidity.
In infants and young children, the fracture requires immo-
bilization for 4–6 weeks, usually by the use of a modified
Velpeau bandage or sling-and-swathe.172 If the fracture is
unstable, traction may be indicated. In small children this
probably can be accomplished with skin traction. In the
older child it may be necessary to use skeletal traction with
478 14. Humerus

an olecranon pin, especially if the fracture is extremely

unstable or if there is any suggestion of neurovascular com-
promise. A shoulder spica also may be used in the older child
with a relatively unstable fracture that can be reduced only
in abduction.
It is possible that older children will cooperate enough
to allow utilization of a device such as the hanging cast (Fig.
14-40) or cast-brace.198 The supinating force of the biceps is
lost by a fracture at this level, and the elbow joint is held in
pronation by the unopposed action of the pronators.
Because the joint is relatively fixed in pronation, attempts to
place the forearm in supination may result in varus defor-
mity at the fracture site. A collar and cuff are attached to a
plaster loop at the wrist and passed around the patient’s
neck. The cast should be light, so distraction of the fracture
fragments does not occur, although continuity of at least
some of the thick periosteum tends to prevent this problem.
The forearm should be transverse to the longitudinal axis of
the body when the patient is standing. The length of the sus-
pension collar is adjusted to allow the arm to be in this posi-
tion. The patient should sleep in a semirecumbent position,
rather than totally supine. As soon as pain subsides, the
patient may be treated with range of motion exercises (cir-
cumduction and pendulum).
The use of internal or external fixation should be consid-
ered for unstable fractures or children with multiple man-
agement problems (e.g., head injury, polytrauma). Internal
fixation with flexible intramedullary nails has been recom-
mended.200 Plating may also be considered. The use of exter-
nal fixation must be approached cautiously, as the distal pins
FIGURE 14-39. Retention of angulation.
may be near the radial nerve.

FIGURE 14-40. (A) Angulated diaphyseal fracture. (B) Initial cast treatment without reduction. (C) After closed reduction and molded cast.
Diaphyseal Fractures 479

thermore, the nerve may become entrapped at the time

of fracture between reduced fracture fragments or subse-
quently in the developing callus (Fig. 14-41).191,205
Permanent radial nerve paralysis is infrequent in chil-
dren.185 Complete transection of the nerve is unlikely with
a closed fracture. Nerve function is usually recovered com-
pletely. If the damage appears to be a major contusion of the
nerve that will take a long time to recover, the hand and wrist
are splinted in positions of function as part of the treatment.
Follow-up includes electromyographic evaluation to deter-
mine the level and extent of injury and the chances for
recovery. So long as continued improvement occurs, there is
no indication for exploration. However, if, after the fracture
has satisfactorily healed without evidence of neurologic
improvement, exploration of the nerve and appropriate
surgery are indicated. In some instances the nerve is trapped
in scar tissue or even in callus; if so, it must be carefully
removed and transposed to prevent recurrence of the injury.

FIGURE 14-41. This patient had a radial nerve injury accompany-
ing the fracture. It was elected to see if spontaneous recovery
would occur, rather than explore the region. Three months after the
injury a “Matev” sign is evident. Exploration revealed an entrapped
radial nerve, which was carefully extricated by unroofing the tunnel.
Radial nerve function returned completely within 4 months.
Supracondylar Process
The supracondylar process (Fig. 14-42) usually is connected
to the medial epicondyle by a fibrous band referred to as the
ligament of Struthers.206,209 The pronator teres muscle may
partially originate from the ligament. The median nerve
and brachial artery may pass between this ligament and the
underlying humerus. A compressive neuropathy may occur
either chronically or acutely following distal humeral frac-
tures.207,208,211 The process may be fractured.210,212,213 If neu-
ropathy occurs in a patient with a combined distal humeral

MacFarlane and Mushayt reported a 5-year-old girl who

had a proximal physeal fracture and a mid-shaft fracture.191
Closed manipulation was not successful. The proximal frac-
ture was opened, reduced from herniated muscle, and
pinned. The diaphyseal fracture was plated. This injury
might be termed a floating shoulder.

Complications
Malunion may result if too much angulation is accepted or
if pathologic circumstances (e.g., cerebral palsy) are present.
Cerebral palsy may also lead to exuberant callus because
of muscle. Because the humerus exhibits preferential prox-
imal growth (80% of overall humeral length), angulation in
the middle and distal thirds of the diaphyseal/metaphyseal
shaft has little likelihood of correction. Furthermore, if the
malunion is at the level of the deltoid tuberosity, normal
muscular forces may help maintain the deformity.
Torode described a humeral fracture in a newborn
(cesarean section)202 that had not healed at 3 years. The
patient underwent internal fixation and bone grafting. The
bone and arm appeared normal at 15 months.
Nerve injury is particularly likely to occur with fractures of FIGURE 14-42. Supracondylar process. It was found incidental to
the junction of the middle and lower thirds of the shaft. Fur- a healing olecranon fracture.
480
injury and an evident supracondylar process, prophylactic
resection of the process and ligament is recommended.208
Al-Nail described a 10-year-old boy who fell and presented
with compression of the median nerve and brachial artery.206
Radiography revealed a fracture of the supracondylar
process. He was treated by excision of the process and liga-
ment. Full recovery followed.
Distal Metaphysis
(Supracondylar) Injuries
Supracondylar humeral fracture is the most common elbow
injury in the developing skeleton, accounting for approxi-
mately 50–60% of injuries to this area.214–576 It is also a rela-
tively common fracture in immature animals (Fig. 14-43). It
occurs most frequently in children between the ages of 3 and
10 years. It is associated with a high incidence of compli-
cations consequent to both (1) malunion resulting from
inadequate reduction and maintenance and (2) growth
mechanism injuries. Angular malunion has minimal chance
of correcting spontaneously in the varus/valgus plane and
should be corrected during the initial reduction. In contrast,
anterior or posterior angulation usually improves, if it does
not correct completely. The potential for neurovascular
FIGURE 14-43. Supracondylar fracture in a skeletally immature
giraffe.
14. Humerus
FIGURE 14-44. Specimen of distal humerus showing the charac-
teristic region of fracture (dotted line) relative to the epiphyseal
region and articular surface. Note how the fracture traverses the
supracondylar foraminal region.
compromise, both acute and chronic, may also lead to
serious dysfunction in the forearm and hand.
Classification
Supracondylar fractures may be classified into four types,
all basically involving the foraminal region (Fig. 14-44): (1)
flexion type (which probably accounts for 1–2% of these
fractures) and the extension types (each representing
about one-third of the fractures); (2) pure extension type;
(3) extension-abduction, which is usually easy to treat, espe-
cially in traction, because the osseous instability lies on the
lateral side where soft tissue stability is available and where
traction tends to reduce the fracture; and (4) extension-
adduction, which constitutes the source of most posttreat-
ment varus deformities, especially when the fracture line lies
in the oblique plane and is comminuted on the medial side.
Pathologic Anatomy
Extension Type
Viewed from the sagittal plane, the fracture line traverses
obliquely upward and backward. Viewed from the coronal
(frontal) plane it usually appears relatively transverse. The
more transverse the fracture is in both planes, the more
stable is the injury. Although the fracture is usually complete,
greenstick injuries do occur (Fig. 14-45). The latter may be
deceptive. Impaction or widening may lead to acute, often
unrecognized, cubitus varus (Fig. 14-46) or valgus deforma-
tion at the time of acute injury. The distal fragment may
be displaced proximally and posteriorly by transmission of
the fracture force upward through the bones of the forearm.
Rotation of the fragments is usually evident on the radio-
graph (Fig. 14-47).
The distal end of the proximal fragment projects anteri-
orly and may pierce the periosteum as it is stripped from
Distal Metaphysis (Supracondylar) Injuries
FIGURE 14-45. Greenstick supracondylar fracture.
FIGURE 14-46. (A) Greenstick fracture causing medial trabecu-
lar/cortical compression leading to cubitus varus. It must be cor-
rected with manipulation. (B) Acute cubitus varus in a 5-year-old.
This was not corrected.
481
FIGURE 14-47. (A) Rotation. (B) Roentgenogram of acute injury
showing an anteroposterior view of the proximal fragment and a
lateral view of the distal fragment forearm.
both the anterior surface of the lower fragment and the
posterior surface of the upper fragment (Fig. 14-48). With
severe displacement, the proximal fragment may penetrate
the skin, creating an open injury. The displacement of
fracture fragments is somewhat limited by the extent of
periosteal stripping, as this structure is rarely disrupted
completely.236
There may be considerable extravasation of blood from
the open marrow cavity and disrupted periosteum, causing
associated swelling and accumulation of fluid in the elbow
region. Because this compartment is fairly tight, it is essen-
tial to observe closely the extent of swelling and decide if sur-
gical release is indicated. The nerves and blood vessels may
be contused or lacerated by the osseous fragments or by the
dissecting hematoma that infiltrates the antecubital region.
Flexion Type
The fracture line in the sagittal plane generally courses
upward and forward, with the proximal fragment being dis-
placed posteriorly and the distal fragment anteriorly and
upward. Again, the degrees of varus, valgus, tilting, and
rotation vary. The periosteum is disrupted on the posterior
482 14. Humerus

A B

C D
FIGURE 14-48. (A) Posterior displacement and overriding when growth gradually corrects the deformity. Note the extensive poste-
first placed in traction. The proximal fragment is subcutaneous due rior callus, complete lack of anterior callus, and porotic change in
to posterior displacement of muscle. (B) Distal fragment settled into the anterior fragment. (D) There is minimal evidence of the injury
a better anatomic position. (C) Similar case showing how further 4 years later.
Distal Metaphysis (Supracondylar) Injuries
surface of the distal fragment and stripped from the anterior
surface of the proximal fragment. Soft tissue swelling and
damage are usually less than with the extension type, and
neurovascular complications are rare.
Displacement
In general, three main types of displacement occur with a
supracondylar fracture. The first type is loss of the normal
anterior tilt of the distal end of the humerus. This is usually
a greenstick fracture and probably requires no reduction.
With the second type, the distal fragment is displaced and
tilted posteriorly. In addition, there may be a medial or
lateral shift. With the third type, the distal fragment is com-
pletely displaced in a posterior direction, with medial or
lateral shift and usually some medial or lateral angulation.
The displacement may be such that the distal end of the
shaft projects through the skin or deep fascia. If it projects
through the deep fascia, ecchymosis may be evident in
the antecubital fossa in addition to the gross deformity and
marked swelling. Antecubital ecchymosis means that the
deep fascia has been punctured and signifies that reduction
of the fracture may be difficult owing to the interposition
and redirection of soft tissues.
Because the muscles around the elbow are ensheathed in
dense fascia and reinforced by the lacertus fibrosis, these
vessels are held down tightly as they traverse the antecubital
fossa. If there is marked posterior displacement of the distal
fragment, the neurovascular bundle may be stretched over
the distal end of the shaft fragment. This may occlude the
venous or arterial blood supply (or both) by causing attenu-
ation, direct compression, or irritation of the adventitia
and sympathetic nerve fibers, causing spasm at the level of
or distal to the injury and even in the collateral circulatory
branches.
Graham studied adult cadavers to better comprehend the
problems encountered with a supracondylar fracture and
found that soft tissue stability was provided on the lateral side
of the fracture by expansion of the triceps, the brachioradi-
alis, and the extensor carpi radialis longus.346 Similar tissue
stability was not evident on the medial side. The expansion
of the triceps provided some posterior soft tissue stability, but
the muscle mass spanning the fracture site anteriorly was
insufficient to provide such stability. Except for a few
clinically insignificant fibers arising from the medial supra-
condylar ridge, the pronator teres arises only from the
medial epicondyle and therefore is part of the forearm. This
muscle did not reliably influence rotation of the distal frag-
ment.347 Experimental work in primates suggests muscular
soft tissue and periosteal hinging have little effect on frac-
ture stability.217
When the fracture is forcibly rotated, the sharp corner of
the proximal fragment may tear the periosteum, permitting
gross displacement. The rent in the periosteum leaves some
of the periosteum around the fracture intact to form a useful
hinge that may aid the attempted reduction. The periosteum
may be stripped from the shaft for several inches proximally,
depending on the degree of displacement at the time of
injury. The extent of stripping becomes evident 2–3 weeks
later by observing the length of the posterior callus.
483
The anatomic cause of fracture instability relates not only
to the obliquity of the fracture surfaces but to the bicolum-
nar nature of this region (Fig. 14-49). The supracondylar
foramen effectively creates two divergent columns, each of
which must be anatomically reduced. However, the pattern
of fracture obliquity in each column often differs.
Diagnosis
Supracondylar fractures may be diagnosed by history, clini-
cal findings, and roentgenographic studies. Swelling may be
minimal if the injury is seen shortly after occurrence or
when displacement has been minimal. The more the dis-
placement, the more swelling and deformity are likely to be
evident. The forearm is usually held in pronation during
examination. Note the degree of pronation or supination, as
it may help to determine the varus/valgus instability.
Whereas examination of the fracture site is important,
careful assessment of the distal neurovascular function in
the injured limb is mandatory (Fig. 14-50). Radial and ulnar
nerve injuries are recognized relatively easily. Median nerve
involvement is generally incomplete and often overlooked.
It may result in loss of flexion of the distal interphalangeal
joint of the index finger, loss of flexion of the interpha-
langeal joint of the thumb, or numbness of the tip of the
index finger. Any neurovascular deficit must be assessed
completely and followed carefully.
Failure to detect vascular injuries may be disastrous and
lead to permanent deformity and disability of the forearm
musculature.101 Signs of vascular compartment syndrome
may include pain, pallor, cyanosis, absence of pulse, cold-
ness, paresthesia or paralysis, any of which may indicate
the possibility of impending Volkmann’s ischemia. The arm
should be checked also for possible concomitant fractures
of the proximal or distal radius (Fig. 14-51) or proximal
humerus.
Roentgenographic Evaluation
Roentgenographic examination confirms the diagnosis. The
limb must be splinted adequately (well above the elbow) and
comfortably before the patient is sent for radiographic
evaluation. The elbow should be in some flexion, although
excessive flexion of the elbow must be avoided to minimize
possible neurovascular compromise by edematous tissue and
displaced fragments.
Instructions to the technician must indicate that true
anteroposterior and lateral projections of the distal humerus
and elbow joint be obtained without simply rotating the
forearm. If instructions are not given to move the entire
upper extremity as a unit, the technician may simply rotate
the forearm through the fracture site and give two views
of the distal fragment rotated 90°, with the proximal frag-
ment remaining the same. An anteroposterior view of the
elbow can reveal whether the fracture line is transverse or
oblique and whether the distal fragment is medially or
laterally angulated. A lateral view of the elbow shows whether
the distal fragment is displaced posteriorly or anteriorly and
the extent to which normal anteroposterior angulation is
lost.
 A B

C,D
FIGURE 14-49. (A) Radiograph of foramen dividing the distal
humerus into columns. (B) If a cut is made through the supra-
condylar foramen, the “bicolumnar” nature of this region becomes
evident, as seen in (C) looking proximally, and (D) looking distally.
E
(E) Lateral slab emphasizes the “precarious” nature of the central
region, which cannot be counted on for any stability. (E) is from our
genetically closest relative, the chimpanzee.

FIGURE 14-50. Sensory and motor functions of the radial nerve (A, B, G), median nerve (C, D, H, I), and ulnar nerve (E, F, J).

484
Distal Metaphysis (Supracondylar) Injuries
FIGURE 14-51. Concomitant fractures of supracondylar and wrist
regions.
Treatment
Millis et al. presented an algorithm for management of
supracondylar fracture; it is an excellent review for anyone
treating these particular injuries.450 Of 108 consecutive chil-
dren with supracondylar fracture in this study, an initial
attempt at closed reduction was undertaken in 101 cases.
The attempt was successful in only 61. Any fracture with per-
sistent vascular defects should be explored, reduced, and
pinned without delay. Traction is never considered a substi-
tute for reduction, though it may be useful to allow swelling
to subside over a short period of time (e.g., 24–48 hours),
after which reduction is attempted. Finally, open reduction
should be considered whenever closed reduction cannot be
achieved gently.
FIGURE 14-52. Reduction utilizing flexion
methods.
485
The direction of the fracture line is a major factor in the
success or failure of closed reduction treatment. Generally,
fracture fragments separated by a long, oblique line are
more difficult to reduce and more likely to slip after closed
reduction than those separated by a relatively transverse frac-
ture line.
Treatment of undisplaced or minimally displaced
extension-type fractures consists of fixing the arm with the
elbow flexed to 90° (less if possible) and the forearm in a
neutral or pronated position. This positioning is continued
for 3–4 weeks. Follow-up roentgenograms are obtained after
a few days to be certain the fracture has not displaced or
angulated (especially into varus).
Cubitus varus may occur even following minimally dis-
placed fractures. One always must be cautious that a minimally
displaced fracture is not of more magnitude than seems evident. A
belief that no reduction is necessary may be inappropriate
(Fig. 14-46). If there has been compression on the medial
side or widening laterally with an incompletely broken
medial cortex, the fracture may be carefully manipulated
and the medial or lateral tilting of the distal fragment cor-
rected. The carrying angle of the elbow is matched to the
normal side whenever feasible. However, a stable impacted
fracture should not be converted to a grossly unstable one
merely to correct varus.
Compression forces from normal muscle tone and elas-
ticity of soft tissues surrounding the fracture fragments also
may tilt the distal fragment, even during immobilization. In
the presence of mild medial or lateral displacement, these
factors may further a deformity that is already present or has
been unrecognized.
The moderately displaced extension-type supracondylar
fracture with some residual bone continuity should be
treated by closed reduction under general anesthesia, pro-
vided there is no neurovascular compromise. The tech-
niques are as follows (Figs. 14-52, 14-53). Length is restored
by traction and countertraction with the elbow in exten-
sion, not hyperextension, to prevent excessive traction on
the brachial vessels and nerves. Next, while maintaining trac-
tion with the forearm pronated and the elbow in slight
flexion, the posterior displacement of the distal fragment is
reduced. This is done by lifting it anteriorly while pushing
the proximal fragment posteriorly. Then the lateral dis-
placement is reduced by pushing the distal fragment medi-
ally. Any rotational deformity is corrected at this time. The
elbow is then flexed to 90° to tighten the posterior perios-
teum and to maintain the reduction. With supracondylar
fractures the biceps temporarily loses its supinating action.
486 14. Humerus

FIGURE 14-53. Reduction utilizing extension

methods.

Because of the discontinuity of the humerus, the unopposed The displaced fracture is reduced under general anesthe-
action of the strong pronator teres muscle may swing the sia because of the difficulty of reduction and the importance
proximal radioulnar joint into pronation. Because the joint of trying to obtain reduction on the first attempt. Repetitive
is fixed by the pronators, varus deformity of the fracture site manipulations should be minimized because of the possibil-
may gradually result from unopposed muscular force, even ity of injury to vessels and nerves during each manipulative
with a properly applied cast.315 attempt. Once the fracture has been reduced satisfactorily,
The direction of the original displacement of the distal the peripheral circulation must be assessed again. If it is
fragment is also considered when deciding on the position normal, a long arm cast or splint may be applied. The cast
in which the forearm is to be immobilized in a cast (Fig.
14-54). If the distal fragment is displaced medially, the
forearm is pronated to tighten the medial hinge, close the
fracture line on the lateral side, and decrease the tendency
to cubitus varus deformity. If the distal fragment is displaced
laterally, supination of the forearm tightens the lateral
periostal hinge, closes the fracture line on the medial side,
and prevents cubitus valgus. With a posteriorly displaced
fracture a posterior hinge of the periosteum is present. The
use of intact periosteal hinges to aid in and maintain reduc-
tion is part of successful closed reductions.
The effect of various types of displacement of the distal
fragment on the carrying angle was studied by simulating
transverse supracondylar fractures by osteotomy.517 Medial
and lateral displacement of the distal fragment without con-
comitant angular deformity did not change the carrying
angle. Internal rotation of the distal fragment also had no
effect on the degree of the carrying angle.517
The osseous relations of the medial and lateral epi-
condyles and the olecranon process may be assessed through
the Lyman Smith triangle or Bauman’s angle. With the elbow
flexed to a right angle, three osseous points make a fairly
symmetric equilateral triangle and tend to lie in a plane par-
allel with the plane of the posterior surface of the upper arm.
In some children the capitellum becomes quite prominent
in 90° of flexion and disturbs the symmetry of the lateral
segment of the triangle. When the elbow is in complete
extension, the three osseous points are almost in a straight
line.
Circulation must be assessed frequently within the first 48
hours after injury. The family should be made aware of the
signs of circulatory compromise so they can watch the child
carefully at home. If there is a mildly displaced fracture but FIGURE 14-54. Pronation and supination positions relate to fracture
a moderate amount of swelling with a suggestion of vascular obliquity and which soft tissues are intact. This may be assessed
compromise, overnight hospitalization should be considered by stress testing under fluoroscopy while attempting closed
for close observation and elevation of the extremity. reduction.
Distal Metaphysis (Supracondylar) Injuries
should not constrict the soft tissues of the antecubital area.
A window cut in the wrist region of the radial artery allows
the distal circulation to be checked.
About 120° of flexion may be necessary to ensure stability.
The radial pulse may disappear for a few minutes after initial
reduction. If the fingers are pink, this may be satisfactory;
but if the fingers become white, the degree of flexion is
reduced. If flexion to a right angle is not possible without
circulatory impairment, check to see if the posterior dis-
placement is corrected. If the moderately displaced fracture
is anatomically reduced but the vascular status remains
questionable, several options are available: (1) fixation with
percutaneous K-wires; (2) casting in this position, then
increasing the flexion when the swelling is less, usually in
3–7 days; (3) placement in traction; (4) open reduction
and internal fixation, with or without direct exploration
of the vessels. When in doubt, obtain a vascular surgical
consultation.
Roentgenograms in the anteroposterior and lateral pro-
jections determine the adequacy of reduction (Fig. 14-55).
Any lateral or medial tilting must be corrected completely.
Appositional alignments are less significant, as they usually
correct spontaneously through remodeling and have little or
no effect on the carrying angle or the final range of motion
of the elbow. Posterior angulation and flexion deformities
are in the plane of motion of the elbow and usually correct
themselves. Rotation of the distal fragment is not corrected
by remodeling and may appear unusual on the roent-
genograms. Although this rotation is well compensated clin-
ically by the degree of rotation at the shoulder, this should
not be an excuse to fail to observe and attempt to correct
rotational malalignment as much as possible.
In the presence of marked swelling, closed reduction is
carried out just as outlined, but the patient is placed in
FIGURE 14-55. Attempted reduction. It has been incompletely cor-
rected for rotation and so the “reduction” is unacceptable.
487
Dunlop’s skin or skeletal traction for several days until the
swelling subsides. If it is difficult or impossible to maintain
adequate skin traction, it may be necessary to apply skeletal
traction with a pin inserted through the proximal ulna. In
general, however, skeletal traction is reserved for a severely
displaced fracture, one that cannot be reduced satisfactorily,
or one that proves unstable. Prolonged traction is used
decreasingly because of hospital costs, although its use in
other parts of the world may be necessary and effective.
After swelling subsides, the arm may be removed from
traction and immobilized. The overall degree of stability
is checked before and after application of a cast.
Roentgenograms are obtained at short intervals following
the injury to verify maintenance of the reduction. These
films are best obtained 5–10 days following the injury and
2–4 weeks later. These roentgenograms are important
because muscular forces may reintroduce deformity during
the first 10–14 days after injury, particularly if a crushing
injury has occurred to the medial or lateral side with loss of
cortical integrity.
Flexion Injury
The flexion injury usually is relatively simple to treat. Closed
reduction is carried out by traction and flexion, followed by
correction of the lateral tilting and displacement by manual
pressure. The elbow then is immobilized in “extension,”
although 20°–30° of flexion may be more comfortable for
the patient.
Unstable Fractures
A completely displaced supracondylar fracture is treated best
by closed manipulative reduction, followed by skeletal trac-
tion or some type of internal fixation (e.g., percutaneous
pins). Because of increasing emphasis on the cost of hospi-
talization, traction is often bypassed in favor of skeletal fixa-
tion. However, for the severely swollen elbow with a variable
pulse or a question of compartment syndrome, 24–48 hours
may make a big difference in the ease and safety of a closed
or open reduction. Extended placement in traction (2–3
weeks) is probably best avoided for most children.
The basic traction technique is as follows. Under general
anesthesia a Kirschner wire is inserted through the proximal
ulna about 2–3 cm distal to the tip of the olecranon process
and beyond the physis. Osseous landmarks about the elbow are
carefully identified, and the wire is drilled from the medial
to the lateral side to avoid tethering of the ulnar nerve.
Because considerable swelling is often present, great
care must be taken to ensure insertion of the pin into the
metaphyseal bone. A threaded Kirschner wire has less
chance of becoming loose and causing skin tract infection
but is more uncomfortable during removal.276,373 As an alter-
native, screws are available for placement directly into the
olecranon.
Once the pin is in place the surgeon must decide on
the most efficacious method of traction. Traction may
be directed to the side (Fig. 14-56) or overhead (Fig. 14-
57).308,313 If used properly and diligently, neither method is
superior to the other. When setting up the traction, medial
488 14. Humerus

FIGURE 14-56. (A) Side-directed (Dunlop’s) traction. Control of pronation and supina-
tion is not easy. (B) Additional traction may be applied to the proximal fragment.

FIGURE 14-57. (A) Placement of a patient in bed

relative to overhead traction. (B) Angulation of
the traction may control rotation.
Distal Metaphysis (Supracondylar) Injuries
A B
FIGURE 14-58. Bicolumnar nature of the distal humerus in a 7-year-old boy. The supracondylar fossa may be large. (A) Slab section.
(B) Radiograph.
and lateral tilting of the distal fragment must be assessed and
carefully corrected. Roentgenograms are made to determine
the accuracy of reduction.
Lateral traction may be applied with the shoulder
abducted 60° and the arm elevated 20° from the horizontal,
a position that improves venous drainage of the upper
limb and limits patient movement. Overhead traction does
not always provide optimum control of the proximal
fragment as the patient moves about in bed. However, if
the child is placed in overhead traction with his head
against the headboard, he can only move downward
and rotate externally, thereby minimizing rotational
abnormality. It is possible for the child to force the elbow
into acute flexion and cause circulatory embarrassment.527
A 3- to 5-pound weight is applied to the lateral traction
bow, and the forearm is suspended. For fractures in
which the proximal fragment is anteriorly displaced, a
sling with a 1-pound weight is applied to the upper
FIGURE 14-59. Techniques of pin fixation.
(A) Reduction allows anatomic restoration
and accurate pin placement. (B) Proper pin
placement: one in each osseous column
medial and lateral to the supracondylar
foramen.
489
arm, pulling it posteriorly to try to reduce this angular
displacement.356
The maintenance of reduction is determined by serial
roentgenograms. The fracture is removed from traction
when it proves stable enough to be casted (usually 10–14
days).
Rotation and varus or valgus deformities do not always
correct spontaneously in traction and may require re-
manipulation. If deformity exists after 3–4 weeks, corrective
osteotomy may have to be considered; but it should be post-
poned until maximum improvement of function has been
obtained. The functional result may be such that late
osteotomy may be unnecessary.
When considering any fixation, whether inserted percuta-
neously or under direct vision, the unique bicolumnar
nature of the distal humerus must be considered (Fig. 14-
58). The pins should be either driven obliquely along the
anatomic curve of each column (Fig. 14-59) or directed
490 14. Humerus

more transversely across the cortical bone of the supra-

condylar forearm. The latter method may give three or four
cortex fixations per pin.
Closed reduction may be performed and percutaneous K-
wires introduced (Fig. 14-60) to prevent redisplacement,
particularly when the elbow cannot be flexed beyond a right
angle.354,531 After the fracture has been reduced by closed
methods, one K-wire is inserted through the medial epi-
condyle and another through the lateral epicondyle. This is
best done using the image intensifier. Alternatively, two pins
may be introduced from the lateral side (Fig. 14-61). Trans-
fixing the ulna and condylar fragment by traversing the
elbow joint is unnecessary and may lead to stiffness. Any pin
must adequately cross the fracture and stabilize it.
Open reduction is indicated if the fracture is markedly
unstable or if there is significant neurovascular compromise.
In the latter case, it may be necessary to explore the artery
or increase the amount of space through which the vessels
traverse at the level of the lacertus fibrosus.328,352,374,485,511,558,
559,567
Open reduction and internal fixation have been con-
demned because of elbow stiffness. However, a careful open
reduction with minimal soft tissue dissection should not
FIGURE 14-61. Closed reduction with percutaneous pin fixation.
Two pins have been placed in the lateral epicondyle to maintain
reduction and control rotation.

create any more problems than multiple attempts at closed

reduction. Certainly for older adolescents, especially those
with T-shaped intercondylar fractures, open reduction is
indicated.
A posterior approach may be used for open reduction.339
The triceps aponeurosis is incised as an inverted V and
turned distally. The ulnar nerve is isolated and protected.
Kirschner wires then may be introduced retrogradely
through the fracture site into the medial and lateral epi-
condyles, emerging through the skin, but avoiding the ulnar
nerve. Under direct vision the fracture is reduced, and
A the Kirschner wires are passed into the proximal fragment.
Rotational correction is checked before passing a second
Kirschner wire.

B especially if the child is followed for more than a year after
FIGURE 14-60. Reduction may be verified by flexing the forearm.
(A) With the arm still on the fluoroscope. (B) Pins may be inserted
percutaneously under direct fluoroscopic vision.
Results
Most minimally to moderately displaced fractures heal
without significant problems (Fig. 14-62), and function is
fully returned within 3 months after the injury. If displace-
ment is severe, the recovery time is longer, but return of
function is usually complete. However, complete return of
flexion may take from several months to several years
because of prominence of the anteriorly directed metaph-
ysis. Remodeling generally corrects this problem.
The child is allowed to set his or her own pace of reha-
bilitation and to determine any physical limitations. In most
instances, there are minimal or no residual contractures,
the fracture. Weights and aggressive physical therapy are
never used to stretch the elbow into full extension. In fact,
it may be impossible depending on the direction of the distal
Distal Metaphysis (Supracondylar) Injuries
FIGURE 14-62. Displaced distal fragment usu-
ally has posteromedial attachment of the perio-
steum, but the periosteum strips away from the
proximal fragment. Anteroposterior (A) and
lateral (B) views show the extensive subperio-
steal new bone that forms if the fragment is
not reduced.
A B
fragment. Growth and redirection of the distal humerus may
be necessary to restore some range of motion.
Complications
Varus-Valgus
The “carrying angle” is the lateral angle made by the longi-
tudinal axis of the fully supinated forearm and the longitu-
dinal axis of the upper arm when the elbow is completely
extended but not hyperextended. If the forearm is pronated
or the elbow is flexed, this carrying angle cannot be evalu-
ated adequately. However, if the flexed elbow is examined
posteriorly and compared with the opposite uninjured
elbow, changes in the carrying angle become more
apparent.
It is important to remember that the carrying angle is
subject to considerable normal individual variation. In 150
normal children it averaged 6.1° in girls (range 0°–12°) and
5.4° in boys (range 0°–11°).518 Some children (9%) have no
carrying angle (cubitus rectus), and 48% have a carrying
angle of 5° or less.518
The complication of reversed carrying angle (gunstock
deformity; cubitus varus) has several causes: (1) incomplete
correction of displacement of the distal fragment at the time
of original reduction (Figs. 14-63, 14-64); (2) growth distur-
bance of the trochlear portion of the physis; and (3) vascu-
lar-mediated stimulation of the capitellar physis, creating
eccentric overgrowth (similar to tibia valgum following a
proximal metaphyseal fracture). This reversed carrying
angle rarely causes significant loss of elbow joint function but
may create an unappealing cosmetic deformity.245,323,331,396,412
Ippolito et al. presented a long-term follow-up into young
adult years, finding that the carrying angle remained the
same in 18 patients, decreased in 22 patients, and increased
in 13 compared to the value present at the time of initial
491
fracture healing several weeks after the injury.377 They
thought that this indicated there was a potential for growth
imbalance of the physis of the distal humerus and that it
might be comparable to the phenomenon occurring in the
proximal tibia due to vascular variation.
The mediolateral variability of blood supply to the proxi-
mal tibia is described in Chapter 23. Particularly, it seems to
stimulate medial physeal growth in the proximal tibial physis
preferentially, causing postinjury angulation (tibia valga).
The advanced maturation of the capitellum versus the
trochlea is associated with a greater circulation laterally than
medially. Temporary asymmetric hyperemia as part of the
generalized fracture healing response could certainly occur
and contribute to varus angulation.
The varus angulation may be mild, moderate, or severe.
Depending on the age at the time of injury, it may lead to
deformation of the forearm as a secondary response.
Although uncommon, physeal damage may occur, leading to
progressive deformity.
If treated properly, there should be minimal varus as an
immediate complication.129 However, this type of injury is
deceptive, particularly if there is minimal displacement.
Malunion or angular deformity noted after acute treatment
(i.e., 4–6 weeks) is most likely due to malunion, not to a
growth disturbance.
If the varus or valgus deformity of the elbow is severe and
stable (i.e., not related to growth injury but to static defor-
mity from the original injury), correction may be indicated
by supracondylar osteotomy of the humerus.226,316,387,449 If
there has been injury to the nerve or perhaps involvement
with the fracture callus, it can be corrected at the same time.
Corrective supracondylar osteotomy is not always an easy
operation. It is best to use a closing wedge osteotomy. Care
must be taken during the placement of internal fixation, as
false aneurysm formation, nerve injury, and bone infection
may occur.
492 14. Humerus

FIGURE 14-63. (A) Acute fracture with primary varus impaction. (B) has not corrected at all. (D) Clinical appearance of the cubitus
Reduction failed to correct the varus angle, although the position varus. (E) Appearance after corrective osteotomy.
appeared good from the lateral view. (C) One year later the varus
Distal Metaphysis (Supracondylar) Injuries
A B
FIGURE 14-64. (A) Varus deformity was not corrected when the patient was placed in a cast. (B) After-casting the deformity.
Oppenheim et al. reviewed 45 corrective supracondylar
osteotomies performed for posttraumatic cubitus varus in
43 children.468 Excellent results were obtained in only 33
patients, with unsatisfactory results in 12. The operation,
though seemingly simple, had a significant complication rate
of almost 25%; the complications included neuropraxia,
sepsis, and cosmetically unacceptable scarring. The authors
believed that a comprehensive preoperative plan and a
lateral closing wedge osteotomy, leaving the medial cortex
intact and ignoring the rotational deformity in the correc-
tion, were the best ways to avoid complications.
Lateral condylar or transcondylar fractures may occur in
patients who have a cubitus varus following supracondylar
fracture. I have seen this in five patients (Fig. 14-65). The
varus configuration should not be arbitrarily termed a “cos-
metic” deformity. The mechanics of the elbow are variably
disrupted. When patients attempt to protect themselves
during a fall by using the arm, the varus position excessively
loads the lateral side, enhancing the varus forces and causing
lateral condylar fracture.
Volkmann’s Ischemia (Compartment Syndrome)
As awareness of compartment syndrome has increased, the
incidence of the complication has decreased.322,423,500,506,571
The five classic warning signs of Volkmann’s ischemia are
pain, pallor (cyanosis), pulselessness, paresthesia, and paral-
ysis. The most important is pain. Ischemia should always be sus-
pected when increasing pain develops in the forearm
following injury to the elbow and forearm or following treat-
ment for such injury. A characteristic physical finding is
493
exaggeration of the pain upon passive extension of the
fingers, followed by taut, progressive swelling and firmness
of the lower compartment of the forearm. The radial pulse
may be absent or present. The presence of a normal radial
pulse does not absolutely rule out Volkmann’s ischemia.
There may be a varying degree of sensory loss, with the
median nerve almost always involved and the ulnar nerve
involved in many cases.
The pathophysiology is as follows. The ischemia initially
produces anoxia in the muscles. The increasing intramus-
cular edema causes a progressive increase in the intrinsic
pressure within the muscles. Circular, relatively unyielding
dressings of the limb and limited expansion of the taut fascia
around the muscles of the forearm increase the venous com-
pression and intramuscular compression, further increasing
the intrinsic compartmental pressure. Pressor receptors
within the forearm compartment and within the muscle
itself stimulate reflex vasospasm, which subsequently affects
the vessels. This vasospasm further aggravates and worsens
the initial vascular compromise, setting up a destructive
ischemia–edema cycle.
If the process persists, the next stage is necrosis of muscle,
with eventual secondary fibrosis and possible development
of heterotopic calcification. The time frame necessary to go
from pressure increase to necrosis is not firmly established.
The infarct is ellipsoid shaped and is along the axis of the
distribution of the anterior interosseous artery. The flexor
digitorum profundus and pollicus brevis muscles and the
median nerve are most commonly and severely affected. If
during the acute stage the palmar compartment of the
forearm is surgically exposed, the deep fascia is taut and
494
A treatment should be urgent. If the various signs and symp-
B crease of the wrist. Proximally, the incision may be extended
FIGURE 14-65. This boy had a cubitus varus following a supra-
condylar fracture. He fell, reinjuring the elbow. (A) Radiograph was
interpreted as a lateral condylar fracture. (B) However, the MRI
showed it to be a transphyseal injury. During the open reduction a
corrective wedge was taken from the metaphysis.
spread widely when split. The muscles may be pale or blue-
black due to extravasation of blood resulting from the
altered hemodynamics.
This circulatory embarrassment may occur if the brachial
artery is (1) caught and kinked at the fracture site (Fig. 14-
61), (2) the artery is contused and in spasm at the moment
of fracture, (3) a tight encircling cast is compressing the
brachial vessels, (4) there is rapidly progressive swelling in
the taut fascial compartment, or (5) a subintimal hematoma
is present.291,455,522,528 Distal to the lacertus fibrosus, the
brachial artery branches into the radial and ulnar arteries.
The radial artery is superficially located, whereas the ulnar
artery is situated more deeply, traversing deep to the prona-
14. Humerus
tor teres. The ulnar artery gives origin to the common
interosseous artery, which divides into anterior and posterior
interosseous branches. The flexor digitorum profundus and
flexor pollicis longus receive their blood supply from the
anterior interosseous artery. The median nerve is particu-
larly vulnerable to damage because of its course deep to the
lacertus fibrosus and through the substance of the pronator
teres muscle.
The acute destructive processes of Volkmann’s ischemia
are progressive and generally reach a peak (i.e., irreversibil-
ity) within 8–12 hours after the injury. If untreated, the
swelling and sensitivity gradually subside, even if ischemia
has been present, and the muscles of the flexor compart-
ment undergo progressive fibrosis leading to contractural
deformity. The elbow becomes fixed, the forearm pronated,
the wrist flexed, the metacarpophalangeal joint hyperex-
tended, and the interphalangeal joint flexed.
A decision must be made whether to continue observation
or consider surgical decompression. The situation can be
assessed by measuring compartment pressures at appropri-
ate intervals to see if the pressure in the palmar (volar) com-
partment is increased. During the acute ischemic stage,
toms cannot be relieved within a few hours after pressure
measurement by extending the elbow, removing tight encir-
cling bandages, or reducing the fracture, arteriography
should be considered. If the brachial artery is only in spasm,
a stellate ganglion block may lead to relief. If this does not
improve the situation, fasciotomy of the forearm and explo-
ration of the brachial artery are indicated. The major vessels
are often intact with compartment syndrome.
Surgical Release
A longitudinal incision is made at the flexor crease of the
elbow, medial to the biceps tendon. It is extended along the
middle of the palmar surface of the forearm to the flexor
to expose the brachial artery without crossing the flexor
crease. The subcutaneous tissues are divided and the ante-
brachial fascia sectioned longitudinally throughout the
entire length. The fascial sheath of each muscle (the epimy-
sium or perimysium) is carefully divided from its lower to
upper margin. Muscle fibers should not be sectioned.
Usually circulation returns immediately. If these measures
do not lead to improvement, the brachial artery should be
explored or arteriography performed. The fascia must be
left open. Muscle edema may prevent approximation of the
skin edges, in which case the wound is left open and closed
several days later after the edema has subsided. A skin graft
may be necessary. Postoperatively, the wrist and hand must
be splinted to prevent deformation.
Treatment of established Volkmann’s ischemia is contin-
gent on the severity of the deformity and the length of time
since the original injury. The contracted flexor muscles in
the forearm may be lengthened at their muscle junction,
along with neurolysis of the median and ulnar nerves. In
severe cases it is possible to shorten both bones of the
forearm to gain relative length of the contracted muscles.
Myocutaneous transplants may be considered.
Intercondylar Injuries
Osseous Vascular Changes
Graham et al. reported avascular necrosis of the trochlea in
one child with supracondylar injury.345
Neurologic Complications
At any given time the radial, ulnar, or median nerve may be
injured at the time of fracture, during attempted reduction,
by compression from Volkmann’s ischemia, or by entrap-
ment in the fracture callus.244,370,371,428,479,523,532,544 Entrapment
may be evident as the Matev sign (Fig. 14-66). The radial
nerve is most commonly injured because of its position rel-
ative to the fracture line. Siris reported 11 nerve injuries in
330 supracondylar fractures (7 radial, 4 ulnar).514 Brown et
al. found a nerve injury incidence of 7% (16 of 207) with 7
ulnar, 4 radial, 4 median, and 1 combined ulnar-median.271
In another review of 162 supracondylar fractures, there were
23 neural injuries: 12 radial, 6 ulnar, 5 median, 4 ulnar, 1
radial, and 1 iatrogenic from percutaneous pins. All deficits
resolved within 2–6 months.
Lipscomb and Burleson described selective anterior
interosseous nerve compression.423 It is of major importance
to assess the arm carefully for the possibility of damage to
this particular nerve, although the findings are often subtle.
A significant number of nerve injuries are isolated to the
anterior interosseous branch. The physical finding is an
inability to flex the distal phalanges of the thumb and index
finger without associated sensory deficits. This problem
usually resolves within a few weeks of the injury. A review of
101 supracondylar fractures found 6 cases of isolated ante-
rior interosseous nerve palsy.290
With a few exceptions most nerve injuries accompanying
supracondylar fractures recover full activity within 6–10
weeks, although a time lapse of as much as 5–6 months has
been reported. Observation and supportive therapy com-
FIGURE 14-66. Matev sign due to entrapment of the ulnar nerve.
495
prise the preferred initial approach to neural injury.293 If
there is no evidence of recovery by 5–6 months, evaluation
by electromyography, exploration, and neurolysis may be
necessary.
Elbow Dislocation
Failure to correct the normal anterior angulation of the
entire distal epiphysis after hyperextension injuries based
on the assumption that this type of malunion will correct
with time may alter elbow mechanics. Recurrent posterior
dislocation following supracondylar fracture has been
reported.419
Myositis
Spinner et al. described an 18-year-old man who sustained
blunt elbow trauma.524 He had developed decreased elbow
motion over the next year, followed by acute onset of pain
after another fall. Radiography revealed a fracture of the
base of a myositis ossificans lesion.
Intercondylar Injuries
Intercondylar (T) fractures of the distal humeral condyles
are unusual during childhood, tending to occur more fre-
quently in older children and adolescents.577–584 They repre-
sent type 4 growth mechanism injuries involving each of the
distal columns (Figs. 14-67 to 14-69). It is possible even to
have an undisplaced intercondylar fracture (Fig. 14-70).628
Most of these injuries are unstable.
Diagnosis is often difficult with standard views. Lateral
condylar fractures commonly remain undiagnosed until
FIGURE 14-67. Intercondylar T fracture, creating a type 4 growth
mechanism injury of each column.
496 14. Humerus

FIGURE 14-68. Anteroposterior (A) and lateral (B) views of a severely comminuted intercondylar fracture. (C) Appearance after 6 weeks
in traction. The fracture is anatomically reduced. Note the subperiosteal new bone laterally.

FIGURE 14-69. (A) Comminuted intercondylar fracture in an adolescent. It was treated by open reduction and multiple pin fixation. (B)
Appearance 3 months later, with all pins removed.
Transcondylar Injuries
FIGURE 14-70. Undisplaced intercondylar fracture in a 15-year-old
boy.
oblique films reveal the medial condylar fragment. An
MRI scan may better delineate the fracture components
(Fig. 14-71).
Treatment depends on the extent of soft tissue and
osseous injury. If swelling or comminution is severe, olecra-
non traction is appropriate. If unstable fragments are
present, some type of internal fixation may be necessary
A B
FIGURE 14-71. (A) Intercondylar fracture with two type 4 condylar fractures. (B) MRI shows the displacement.
497
(Fig. 14-72). The recommended surgical approach is a
posterior (triceps splitting) method.632 Factors affecting the
outcome include accuracy of reduction, development of
ischemic necrosis of the trochlea or capitellum, and the
degree of initial displacement.
A growth plate fracture pattern of a metaphyseal frac-
ture (e.g., supracondylar) may have additional linear longi-
tudinal propagation toward the physis. This pattern may
propagate along the physeal–metaphyseal interface or
into the epiphysis, creating a variation of intercondylar
injury.
Transcondylar Injuries
Transcondylar injury of the entire distal humeral physis and
epiphysis (Fig. 14-73) may be a much more common injury
than is fully appreciated.583–634 Smith is credited with the first
description, in 1850.628 It is often misdiagnosed as a dislo-
cated elbow because of the difficulty interpreting the
roentgenogram, particularly in neonates, infants, and young
children.588,601,605,610 The entire distal epiphysis of the
humerus is displaced posteriorly, laterally, or forward,
depending on the mechanism of the injury (Figs. 14-74, 14-
75). The violence may be direct or indirect. Separation of
the entire distal humeral epiphysis is a relatively common
injury during difficult deliveries and the battered child syn-
drome (Fig. 14-76).
DeLee et al. described three categories of transcondylar
distal humeral fracture.596 Group A (0–9 months of age) had
no capitellar ossification center visible and generally no or a
minimal metaphyseal fragment. Group B (ages 7 months to
3 years) had a capitellar ossification center and usually a
small metaphyseal fragment. Group C (ages 3–7 years) had
a well developed capitellar ossification center and generally
498 14. Humerus

A B
FIGURE 14-72. (A) Intercondylar fracture in a 9-year-old-boy. (B) It was reduced and pinned.

a large metaphyseal fragment.319 Thus there was an age-
related shift from a type 1 to a type 2 growth mechanism
injury.
These fractures may be difficult to diagnose. The most
important distinguishing feature is the normal relation of
the ossification center of the capitellum to the proximal
radius, although in the small infant child it may not be
readily evident. A longitudinal line drawn through the shaft
of the radius normally passes through the capitellum, but
with dislocation of the elbow or radial head, it does not. The
latter indicates some type of disruption of the radiohumeral
joint.
A type 2 physeal injury of the entire epiphysis must be dif-
ferentiated from a fracture of the lateral condyle of the

FIGURE 14-74. Apparent elbow dislocation. The medial dis-

FIGURE 14-73. Transcondylar fracture, an injury of the entire distal placement should make one consider a complete distal humeral
humeral physis. fracture.
Transcondylar Injuries 499

FIGURE 14-75. Transcondylar fractures. Note the thin plate of metaphyseal bone
(arrow). Another clue was the lateral view of the radius and ulna versus the antero-
posterior view of the humerus.

FIGURE 14-76. Child abuse. (A) Appearance of

transcondylar fracture 3 weeks after injury.
Note the thin metaphyseal bone (arrow). It was
treated by closed reduction. (B) Six weeks.
(C) Five months. (D) Two years.
500 14. Humerus

humerus, which is a type 3 or 4 physeal injury. With type 3

or 4 physeal injuries the fracture fragment is often displaced
by the pull of the common extensor muscles of the forearm,
with subsequent loss of the normal relation of the radial
head. Transcondylar epiphyseal separations usually displace
medially, whereas elbow dislocations are usually lateral.
Other fractures (e.g., olecranon) may also occur (Fig. 14-77).
Stricker et al. described a 3-year-old child with an unusual
variation of a transcondylar fracture.629 The fracture was a
coronal fracture, as described for the lateral condyle (see
Lateral Condyle Injuries, below) but also including the
trochlea. An anterior portion of the metaphysis had led to a
diagnosis of lateral condyle fracture. The olecranon was also
fractured.
If the diagnosis cannot be made accurately, the child
should be treated empirically. However, if there is any ques-
tion, particularly regarding the possibility of deformity, it is
feasible to use arthrography to help diagnose the injury (Fig. FIGURE 14-77. Combined transcondylar and olecranon fractures.
14-78). Sonography also may be used.589,623
Closed reduction is the initial treatment of choice. Reduc-
tion is performed by traction on the forearm and, most
importantly, gentle correction of the medial displacement
and varus tilt of the epiphyseal fragment. Because the cross- When there is a delay between the time of injury and the
sectional area at the physis (level of the fracture) is greater institution of medical care, there may be massive swelling
than that in the supracondylar area, the tendency to tilt and about the elbow. It may necessitate traction following reduc-
displace is less. Malrotation should be corrected. The elbow tion to reduce the swelling.
is flexed to 90° and the forearm pronated. Open reduction may be indicated, although closed reduc-
The distal epiphysis is usually displaced medially, and the tion with percutaneous pinning is also an acceptable
medial portion of the periosteal hinge remains intact. There- approach (Fig. 14-80). If the patient is not seen until several
fore by pronating the forearm, the intact periosteal sleeve weeks have elapsed since the initial injury, reduction is not
may be used as a hinge to maintain the reduction. attempted. Any residual deformity may be corrected by
Corroborative roentgenograms should be obtained to osteotomy. In the case shown in Figure 14-81, no acute reduc-
ensure the adequacy of reduction (Fig. 14-79). A posterior tion was done. Several months later the altered anatomy was
splint is applied for 3–4 weeks. Admission to the hospital fol- still impossible to define accurately. The entire condylar unit
lowing reduction allows monitoring of the circulation. apparently has shifted medially, forming a large area of new

FIGURE 14-78. (A) Medial shift of radius and ulna. This is not a dislocation. (B) Arthrography outlines the displaced distal epiphysis.
Transcondylar Injuries 501

FIGURE 14-79. Closed reduction. Rotation, however, has not been

corrected.

FIGURE 14-80. (A) Transcondylar fracture in a

2-year-old showing the complete metaphyseal
plate. (B) This fracture was treated with open
reduction and pin fixation (note air outlining the
capitellum).

FIGURE 14-81. Unusual transcondylar fracture in an infant. Note ment. (A) Appearance early during initial treatment. (B, C) Large
the massive subperiosteal new bone formation. Apparently, the subperiosteal new bone segment medially, with irregular bone in
fracture left the lateral epicondyle attached to the proximal frag- the region of the presumptive lateral epicondyle.
502
bone subperiosteally. Some of the lateral epicondyle was
probably left behind and has subsequently ossified.
Cubitus varus occurs less frequently with transcondylar
fractures than with supracondylar fractures, but growth
deformity due to focal premature epiphysiodesis is a signifi-
cant complication. Abe et al. found that 15 of 21 children
with transcondylar fracture developed varus deformity fol-
lowing treatment.585 One was progressive owing to a definite
physeal injury. Neurovascular complications also appear
infrequently.
Medial Condyle Injuries
Medial condyle injuries have been reported infrequntly.635–665
The fracture is comparable to the lateral condyle fracture,
with a type 4 growth mechanism injury being the most
common pattern (Fig. 14-82). Type 3 growth mechanism
injuries also may occur. Epiphyseal propagation of the
FIGURE 14-83. (A) Apparent displaced medial epicondylar injury. (B) Arthrogram shows the medial condylar component.
14. Humerus
FIGURE 14-82. Type 4 injury of medial
condyle. (A) The injury. (B) Typical fracture
pattern (dotted line) on the specimen
roentgenogram.
fracture probably remains within the trochlea. This injury
may be confused with displacement of the medial epi-
condyle (Fig. 14-83), particularly if it occurs at a time when
there is minimal ossification within the trochlear portion
of the epiphysis.638,642,651 Differentiation between condylar
versus epicondylar is essential because treatment is quite
different.
As part of the differential diagnosis, one must consider
congenital abnormalities. Tanabu et al. described two cases
of the hypoplasia of the trochlea that resulted in a progres-
sive cubitus varus and ulnar nerve palsy.663 Sato and Miura
described several cases of hypoplasia of the trochlea.661
Several other abnormalities were also present (hypoplastic
capitellum, hypoplastic radial head). None of the patients
had well-documented childhood injury.
In a review of fractures of the medial condyle, children less
than 5 years of age tended to have undisplaced fractures that
could be treated with closed methods and generally gave
good results, whereas older children tended to have more
Medial Epicondyle Injuries
severely displaced fractures that required open reduction.635
Good results were obtained when the patients were seen
early after injury and when there was adequate reduction of
their fractures.
Medial condylar fractures are usually unstable, with both
physeal and articular surface disruption. In general, they
should be treated with open reduction and accurate restora-
tion of the joint congruency (Fig. 14-84). A posterior
approach through or around the triceps is effective. Release
of the ulnar nerve may be necessary to mobilize the
fragment.
Significant complications have not been reported. Exten-
sive dissection of the fragment should be avoided because it
might predispose the patient to ischemic necrosis of the
trochlea. A neglected medial condyle fracture may develop
a nonunion (Fig. 14-85). Growth injury also may occur,
leading to cubitus varus deformation.
Eighteen years after an original injury, Hanspal reviewed
the case originally reported by Cothay.638,649 This patient had
FIGURE 14-84. (A) Anteroposterior view of a type 4 injury with
90° of rotation of the fragment. (B) Appearance following open
reduction.
503
FIGURE 14-85. Untreated medial condyle fracture with established
nonunion.
a loss of 15° of full flexion, 15° of full extension, and a 10°
decrease in the carrying angle compared to the opposite
side. She was not complaining of any significant problems.
Repetitive stress injuries may involve the trochlea. They
may lead to ischemic changes (Fig. 14-86) or fragmentation
with a loose body (Fig. 14-87). Ferretti and Papandres
described a trochlear stress fracture in a 14-year-old male
gymnast.644
Medial Epicondyle Injuries
Fractures of the medial epicondyle usually occur between 7
and 15 years of age and constitute about 10% of all fractures
of the elbow region in children.666–714 This injury is unusual
in young children. The mechanism is generally a valgus
strain of the elbow joint that produces traction on the medial
epicondyle through the flexor muscles (Fig. 14-88). The epi-
condyle may be variably displaced or even dislocated into the
elbow joint owing to the opening up of the joint by a marked
valgus stress.666,697 There may be displacement in association
with posterolateral dislocation of the elbow. Many of the
cases are associated with partial or complete dislocation of
the elbow (see Chapter 15).
Several patterns of epicondylar fracture are possible (Figs.
14-89 to 14-92). Epicondylar fractures represent type 3 or 4
growth mechanism injuries: Part of the fracture propagates
through the epiphyseal cartilage between the epicondyle
and condyle, disrupting the normally continuous distal
humeral growth plate. Articular cartilage is not normally dis-
rupted in this injury.
Physical findings often depend on the degree of displace-
ment. The elbow usually is partially flexed for comfort.
504 14. Humerus

A B

C
FIGURE 14-86. (A) Trochlear osteochondritis in a competitive gymnast. The patient had intermittent elbow pain. (B) MRI shows irregu-
larity of the metaphysis and epiphysis. (C) Result 2 years later.
Medial Epicondyle Injuries 505

FIGURE 14-87. Chronic medial condylar injury due to pitching.

There is sclerosis in some of the trochlear ossification and an
osteochondritic fragment.

FIGURE 14-88. Medial epicondylar injury. (A) Normal. (B) Type 3.

(C) Type 4. (D) Typical pattern of fracture (dotted line) depicted on
a specimen.

A B C
FIGURE 14-89. (A) Fragmented, undisplaced fracture of the medial condylar physis (arrow). This was an undisplaced “greenstick”
epicondyle. (B) Displaced fracture showing a small metaphyseal injury. (D) Transversely directed fracture (arrow). (E) Sleeve frac-
fragment (arrow). (C) Propagation of a fracture into the medial ture of the medial epicondyle.
 D E
FIGURE 14-89. (Continued)

FIGURE 14-90. (A) Superior displacement. (B) Inferior displacement.

FIGURE 14-91. Intraarticular displacement.

FIGURE 14-92. Intraarticular entrapment of the medial epicondyle.

It was removed by arthrotomy.

506
Medial Epicondyle Injuries 507

Motion is painful, particularly to a valgus stress or pronation

of the forearm. The medial joint line is tender. There are
some diagnostic problems. The unossified region in a child
less than 5 years of age is not easily diagnosed radiographi-
cally. Separation of the medial condyle may seem to be an
epicondylar separation (Fig. 14-83).
The clinical signs of medial hematoma and pain may be
more obvious than any radiographically evident separation
of the epicondyle. The degree of displacement must be
assessed as accurately as possible and the presence of con-
comitant injury noted. Concomitant fracture of the radial
neck may occur as a result of the injury mechanism (see
Chapter 16). The ulnar nerve frequently is traumatized by
the force and direction of displacement.
Roentgenograms may disclose the absence of the medial
epicondyle from its normal position or widening of its physis
compared to the physis of the opposite side. The displaced
fragment may be seen in the lateral and posterior-oblique
projections. If the diagnosis is in doubt, roentgenograms of
the opposite elbow are obtained in the same degree of rota-
tion (remember, asymmetry may be normal). When the
medial epicondyle is displaced into the joint space the
articular cartilage space may be widened, although in a
young child with a large mass of unossified cartilage in the
trochlear region this is often not readily evident. When the
elbow is dislocated posterolaterally, the medial epicondyle is
usually located posterior to the trochlea. Stress views may be
necessary to establish the true stability or instability of the
lesion (Fig. 14-93).
If the medial epicondyle is displaced, the joint should be
immobilized for 3 weeks in a long arm cast with the elbow
in moderate flexion and the forearm in pronation. If the epi-
condyle is moderately displaced but the elbow is stable on
valgus strain, treatment again consists of immobilization in
a long arm cast for 3 weeks. According to some authors, the
functional result may be excellent, even if the fracture heals
by fibrous union.667 Occasionally, the fragment fails to heal,
and symptoms of ulnar nerve damage and irritation occur.
If such symptoms supervene, the fragment should be
excised. If closed treatment is chosen for treatment, the
elbow is radiographed again in 4–5 days to see if the pull of
the attached flexor musculature has caused subsequent or
further displacement.
In a review of a large number of patients treated opera-
tively, it was noted that if the fracture was displaced more
than 2 mm consistently good results were obtained with
closed reduction and percutaneous pinning.687 If the medial
epicondyle is markedly displaced (i.e., more than 5 mm) and
rotated 90° or if the elbow joint is unstable on application of
valgus strain, open reduction and internal fixation are indi-
FIGURE 14-93. (A) Positioning for stress radiography. (B) Three-
cated (Fig. 14-94).
year-old child with pain over the medial epicondyle and apparent
A longitudinal incision placed slightly posteriorly allows separation. (C) Application of valgus stress (arrow) pulled the epi-
visualization of the ulnar nerve. There often is significant condyle inferiorly.
hematoma throughout the subcutaneous tissue, and dissec-
tion must be carried out carefully down to the level of frac-
ture. Any joint hematoma is evacuated. Some physicians erative ulnar compression symptomatology. This procedure
recommend ignoring the ulnar nerve by not dissecting it. My also allows evaluation of the nerve, and in virtually every case
impression has been that significant swelling and contusion some degree of contusion of the nerve has been evident.
are present, and neurolysis and decompression of the tunnel This explains some of the problems that develop as part of
in which the ulnar nerve traverses usually results in alleviat- the normal healing phenomenon following closed reduc-
ing symptoms in patients who had mild to moderate preop- tion. To attribute all postoperative nerve injuries to surgical
508
FIGURE 14-94. Open reduction with pin fixation of an unstable
elbow.
trauma is probably inaccurate, inasmuch as these children
are frequently operated on immediately after arrival at the
hospital, sometimes without an adequate neurologic exami-
nation to ascertain the damage preoperatively. Further-
more, it might take a few days, or at least a few more hours,
for the signs of neurologic damage from a contusion to
develop. If the ulnar nerve has been displaced into the
joint with the fragment, it must be extricated during open
reduction.
The elbow is flexed and held in neutral rotation to
minimize traction in the flexor muscles. Rotation may be
checked by lining up the flexor muscle fibers. The fragment
is secured by Kirschner wires: Two wires lessen the chance
for rotation. The arm should be in a cast for 4–6 weeks,
at which time the pins are removed and early motion is
started. A small compression screw may also be used. Pre-
mature epiphysiodesis is unlikely to cause any long-term
problems.
Skak et al. reviewed 24 displaced medial epicondylar
fractures,703 all but one of which had been treated by an open
procedure. They were reviewed 2–13 years later. Five types of
deformity were found: pseudarthrosis, ulnar sulcus, double-
contoured epicondyle, hypoplasia, or hyperplasia. None of
the deformities interfered seriously with daily activities, but
there were symptoms and signs that made a difference
between a good and an excellent result. The patients
thought that their athletic ability was compromised. Skak et
al. noted that some deformities occurred through the use of
rigid internal fixation in the young child.
There are few reports of long-term follow-up of medial
epicondylar fractures.667 Treatment of medial epicondyle
fractures purportedly produces good results. Flexion con-
tractures of 40°–45° may occur if the patient is immobilized
more than 3–4 weeks. Early immobilization of the elbow fol-
lowing medial epicondyle fractures within 3 weeks or less
should be encouraged, although it may lead to delayed
union or fibrous nonunion if the fracture has been treated
nonoperatively.
14. Humerus
Ulnar nerve paresis is a common complication of this
injury but may not occur until several months or years after
the initial injury.714 It is probably more common with mod-
erately displaced fractures that are allowed to heal by fibrous
union and then develop an irritative pseudarthrosis. Exci-
sion of the fragment and neurolysis are usually sufficient
treatment in such cases. Translocation of the nerve anterior
to the epicondyle may also be necessary.
This injury is not usually associated with any major growth
problems, primarily because it tends to occur at a time when
physiologic physeal closure is commencing. Therefore pre-
mature epiphysiodesis generally does not result in any major
growth deformity. Full extension may be slow to return and
incomplete when it does, although this occurs in only a few
cases.
Nonunion of medial epicondylar fractures may lead to pain
(see Fig. 14-116, below). Josefsson and Danielsson followed
56 nonoperatively treated medial epicondylar fractures in
children ranging in age from 7 to 17 years.689 These patients
and displacement ranging from 1 to 15 mm. They were
examined an average of 35 years (range 21–48 years) after
their injuries. Pseudarthrosis had developed in 31 patients,
but only 3 had mild ulnar nerve symptoms. The function
and range of motion of the elbow was good in all cases. The
authors did not describe any significant radiologic changes of
degenerative arthritis. If the epicondyle is painful, however,
excision of the fragment may be undertaken.
Degenerative arthritis is an underemphasized, but real,
long-term consequence of nonunion of the epicondyle with
chronic elbow instability (Figs. 14-95, 14-96).
Woods and Tullos showed that the tendency of forward
rotation of the medial epicondyle could interfere with col-
lateral ligament function in certain positions, particularly
if this is the dominant arm in a young athlete.713 Chronic
microdisruption of the medial epicondyle from repetitive
stress may lead to radiographic changes (Fig. 14-97).
FIGURE 14-95. Displacement of fragments 2 years after a “normal”
radiograph. This elbow was painful.
Lateral Condyle Injuries 509

A B
FIGURE 14-96. (A) Displaced medial epicondylar fracture and radial head fracture. Both were treated conservatively. (B) Similar combi-
nation of injuries. This patient is 27 years old and has incapacitating elbow pain.

Zaltz et al. found a high incidence of subluxation or dis-
location of the ulnar nerve in patients.714 Inoue described a
13-year-old boy who underwent closed reduction for an
elbow dislocation. Six months later he presented because
of restricted elbow motion. At arthrotomy the entrapped
medial epicondylar fragment was removed.688
Lateral Condyle Injuries
Fractures of the lateral condyle are relatively common, con-
stituting approximately 10–15% of all fractures in the region
of the elbow.715–807 These injuries occur in children between
the ages of 3 and 14 years but seem to be most common
between 6 and 10 years of age.
Classification
The injury is usually a type 4 physeal injury, although it also
may be a type 3 injury if there is minimal or no extension
of the fracture into the metaphysis (Fig. 14-98). In most
instances however, there is a thin plate metaphysis where the
fracture has propagated; therefore, by definition, a type 4
injury exists. The thin metaphyseal bone plate may be cen-

FIGURE 14-97. This Little League pitcher complained of a painful elbow. (A) Presenting film shows reactive bone (open arrow) and mild
separation (solid arrow). (B) Healing 7 weeks later.
510
FIGURE 14-98. Type 3 (A) and type 4 (B) lateral condyle fractures.
Note how the fracture does not involve just the capitellum but
extends through part of the trochlear cartilage. (C, D) Specimen
roentgenograms depicting these two patterns.
14. Humerus
trally located because of the lappet contour of the physis.
This fracture is both an intraarticular injury, and a disrup-
tion of a major portion of the physeal growth mechanism of
the distal humerus (Figs. 14-99, 14-100). Propagation of the
fracture through the epiphysis rarely occurs exactly at the
junction between the trochlea and the capitellum. Most
often the fracture extends into the trochlea to disrupt the
trochlear articular surface. The capitellar articular surface is
usually intact.
The condylar fragment usually includes the physis and sec-
ondary ossification center of the capitellum, cartilaginous
portions of the trochlea (including physis), the lateral epi-
condyle, and part of the lateral metaphysis with the radial
collateral ligament and the common tendon of the extensor
muscles attached to it. The fracture fragment may be undis-
placed or variably displaced and rotated by the pull of the
extensors of the wrist and fingers (Figs. 14-101, 14-102).
The degree of the rotation of the fragment varies. It may
be turned 90° so the articular surface faces inward (toward
the remaining trochlea) and the fracture surface laterally
(Fig. 14-103). In its extreme form, it is rotated 180° around
both horizontal and vertical axes, with the distal articular
surface facing outward and the lateral surface inward. If left
in these malrotated positions, the apposition of joint surface
cartilage to the remaining fracture surfaces of the metaph-
ysis and trochlea invariably results in a nonunion and sub-
sequent deformity, as the articular tissue is not associated
with a normal process of ossification (see Chapter 1).
Less frequently there is a fracture through part of the
capitellar ossification center (Fig. 14-104) (sleeve or shell
fracture concept).382 With such fractures only the capitellum
and extreme lateral portions of the physis (especially the epi-
condyle) are involved.
Fractures of the lateral condyle of the humerus may also
be associated with partial or complete medial dislocation of
the elbow or with olecranon fractures (Fig. 14-105).
Lateral humeral condyle fractures have been classified
into three types: (1) Incomplete fracture in which a hinge of
articular cartilage is present, allowing some lateral angula-
tion at the elbow, with no other displacement evident. (2)
Complete fracture of the condyle in which the initial lateral
displacement may be slight. The fracture fragment is free to
move, and the displacement may be proximal, lateral, rota-
tory, or a combination.779 (3) Complete fracture in which the
fragment is displaced and rotated. Type 1 fractures are
stable. Type 2 fractures are prone to progressive displace-
ment, delayed union, or nonunion. Type 3 fractures do not
unite unless they are reduced and fixed, which usually
requires open reduction.779
Pathomechanics
The fracture usually results from indirect violence, such as a
fall on the outstretched hand with the forearm abducted and
the elbow extended. The force is transmitted through the
radius. The lesion also may be produced by a traction force
that thrusts the elbow into a varus position (Fig. 14-106). In
such instances the fracture may begin at different points.
When there is indirect force, as from a fall on the hand, the
fracture may start as an intraarticular fracture propagating
toward the physis. In contrast, a varus stress to the region
Lateral Condyle Injuries 511

FIGURE 14-99. Lateral condyle fracture in a child sustaining a traumatic forequarter amputation. (A) Disruption of the articular surface
of the trochlea. Note that the fracture is incomplete. (B, C, D) Variable displacements of the lateral condylar fracture.

A B
FIGURE 14-100. (A) Radiograph of a lateral condylar fracture in a child suffering a traumatic amputation. (B) Slab section showing a
section of the capitellar physis on the “wrong” side of the fracture and additional longitudinal propagation into the supracondylar foramen.
 FIGURE 14-101. Undisplaced fractures through the lateral. (A) condylar injury. (C) Thin metaphyseal plate with propagation into
Metaphyseal disruption should alert one to condylar injury. (B) Thin the trochlear ossification center.
metaphyseal (juxtaphyseal) remnant indicates the presence of a

FIGURE 14-102. (A) Seemingly

minimally displaced lateral con-
dylar fracture. (B) Two weeks later
A B separation is evident.

FIGURE 14-103. (A) Rotated lateral condylar fracture in a specimen. (B) Fragment rotation. (C) Clinical example.

512
Lateral Condyle Injuries 513

FIGURE 14-104. (A, B) Patterns of fractures through the capitellar ossification center. (C) Undisplaced (arrow). (D) Displaced. (E) Oblique
view shows a metaphyseal fragment. (F) Stress view shows extension into the capitellum.
514
FIGURE 14-105. Combined lateral condyle and olecranon frac-
tures. Is this medial epicondyle or olecranon?
may be associated with disruption of the peripheral zone of
Ranvier and propagation across the physis to the junction
of the capitellum and trochlea. The biomechanics of the
cartilage probably change because of the variable appear-
ance and size of the capitellar and trochlear ossification
centers.
Jakob et al. produced this fracture experimentally by
applying a varus strain to the extended elbow.765 In this
anatomic study, the only deforming force that produced a
fracture of the lateral condyle was forced varus angulation
14. Humerus
with the elbow extended and the forearm supinated. This
caused a fracture in four of seven elbows. The children, all
of whom had died from injury, were between 2.5 and 10 years
of age at the time of death. In one case there was an associ-
ated transverse adduction fracture of the olecranon, as seen
in the clinical situation. In three of the four elbows the
lateral condylar fragment was attached to the trochlea by a
substantial bridge of cartilage. When the arm was reposi-
tioned, this bridge acted as a hinge, guiding the fragment
back into position, preventing significant displacement, and
maintaining an intact articular surface enclosing the fracture
line. Whether this occurs in the clinical situation is difficult
to say. However, the case shown in Figure 14-99 shows that
an incomplete (hinged) fracture may occur clinically.
Arthrography may help delineate this situation, particularly
if there is any question about whether to go ahead with an
open reduction. The trochlear ridge on the ulna behaves as
a fulcrum for avulsion of the lateral condyle by the lateral
fragment. The bone separates, but some epiphyseal and
articular cartilage may remain intact as a hinge. As soon as
this hinge is divided, the fracture becomes highly unstable,
and the condyle can be easily displaced and rotated. The
hinged fracture reduces when the varus angulation is cor-
rected. If deforming angulation is increased, the cartilage
hinge may tear, which may lead to fracture displacement and
dislocation of the elbow (type 4 injury). The incomplete and
complete injury patterns have been encountered in trau-
matically amputated arms.
Some of the blood supply to the lateral condyle enters by
its soft tissue attachments, particularly posteriorly at the
origin of the long extensor muscles.754 However, the impor-
tant intracartilaginous vessels traverse between trochlea and
capitellum and are disrupted by the transepiphyseal nature
of the fracture. Extensive dissection during open reduction
may affect the remaining vascularity beyond the initial trau-
matic disruption.
FIGURE 14-106. (A) Formation of a fracture by
“locking” of the olecranon and concomitant fracture
of the olecranon. (B) Example of the injury pattern
with concomitant olecranon and lateral condylar
fractures.
Lateral Condyle Injuries 515

Diagnosis miss. When there is clinical evidence of a fracture but no

These patients generally have severe pain following injury,
with marked swelling, ecchymosis, and local tenderness over
the lateral portion of the elbow. Rotation of the forearm is
often unrestricted, especially with undisplaced fractures, but
it may be quite painful. In most cases the diagnosis can be
made easily by the roentgenographic findings. Sometimes
only the oblique view discloses either displacement or evi-
dence of the undisplaced fracture line. A true lateral view,
particularly when compared to the opposite side, may show
loss of the normal anterior tilt of the capitellum, suggesting
the diagnosis.
Lateral condylar fractures are serious injuries. The frac-
ture is often diagnosed merely as a chip fracture on the outer
margin of the elbow (i.e., the metaphysis) and is not recog-
nized as being half of the distal humerus. This leads to
undertreatment, allowing fracture motion and increasing
the likelihood of delayed union or nonunion.
Grossly displaced fractures are usually obvious on radio-
graphs, but undisplaced (“hairline”) fractures are easy to
radiographic signs, further views should be obtained, partic-
ularly oblique views, until the fracture is evident or ruled out
as unlikely. Stress films may be used to show this fracture
(Fig. 14-107). In the particularly young child, the ossification
center may not be present, and the true nature of the injury
may not be completely comprehended. An arthrogram may
help (Fig. 14-108). The younger the child and the less well
developed the ossification centers, the greater is the likeli-
hood that this injury will be overlooked. MRI may better
define the fracture morphology (Fig. 14-109).
Treatment
With lateral condyle fractures, it is recognized that displace-
ment is almost always underestimated on routine radio-
graphic studies. At surgery one is often surprised by the
instability of these fractures. Surgical techniques must be
minimally aggressive to preserve the soft tissues essential to
condylar vascularization. One should not hesitate to incise

A B

C D
FIGURE 14-107. (A) Seemingly undisplaced lateral condylar fracture. (B) Stress film opens the fracture, emphasizing its latent instabil-
ity. (C, D) Reduced and stress opening of fracture.
516 14. Humerus

ensured. Repeat roentgenograms should be obtained within

the first 5–10 days to detect any subsequent displacement
that may require open reduction (Fig. 14-110).
Even these undisplaced fractures must be considered
unstable, as they tend to become displaced, even with immo-
bilization, because of the pull of the common extensors.
Because the fracture line crosses the physis, accurate
anatomic respositioning is imperative to decrease the likeli-
hood of growth damage. Furthermore, the congruity of the
joint must be restored.
Badelon et al. noted that during surgery slight pronation
or supination movements of the forearm mobilized the
condylar fragment, despite the use of pins or sutures. They
thought that slight movement of the hand could affect the
fracture despite open reduction and internal fixation.720
They also thought that this explained the delayed union of
the lateral condyle when closed treatment and casting were
used and moted that a minimum of 6 weeks of immobiliza-
tion in a cast was necessary. Wiggling the fingers, which is
usually encouraged in children, causes some fracture site
motion in the child treated by closed methods and a long
arm cast.
Flynn et al. emphasized that all minimally displaced frac-
tures of the lateral condylar epiphysis should be watched
closely for increasing displacement and delayed healing.741
When there is a small area of osseous fracture compared to
a large surface area of cartilaginous fracture (physis), the
amount of bone/bone healing ratio is small, and the healing
of the cartilaginous areas may take significantly longer. If
an undisplaced fracture is unstable, as seen by stress film or
arthrography, percutaneous fixation or open reduction is
appropriate. The undisplaced or minimally displaced lateral
condyle is more likely to have displacement, delayed union,
or nonunion because of closed reduction and an assumption
that it will readily heal.
Any evidence of acute or delayed displacement is an indi-
cation for open reduction and internal fixation (Figs. 14-111,
14-112). It should be done by fixation across the entire

FIGURE 14-108. (A) Diagnosis is impossible on standard films in

the young infant without capitellar ossification. (B) Arthrography
helps with the diagnosis. The dye has surrounded the capitellar
fragment.

small remnants of capsule and synovium to control the

intraarticular reduction. The vasculature is usually not enter-
ing through this region; and if the fracture is not being oper-
ated on until several days after the original injury, this tissue
may contract significantly.
The undisplaced fracture may be treated by immobiliza-
tion in a long arm cast with the elbow in 90° of flexion and
the forearm in full supination to minimize the pull of the
extensor muscles. Even undisplaced fractures of the lateral condyle
are potentially unstable and may become displaced while immobi-
lized. With an undisplaced lateral condylar fracture, if the
adjacent soft parts are intact, a satisfactory outcome is usually FIGURE 14-109. MRI of a lateral condylar fracture.
FIGURE 14-110. (A) Presenting radiograph. The
patient was treated with a long arm cast. (B)
Three weeks later a widened fracture gap is
evident. It was treated by removing the fibrous
tissue down to the physis, bone grafting, and
percutaneous pins.

FIGURE 14-111. (A) Moderately displaced

lateral condylar fracture. (B) Open reduction
with internal fixation.

FIGURE 14-112. (A) Completely displaced and rotated capitellar fragment. (B) Open reduction and pin fixation. (C) Three years later.

517
518
FIGURE 14-113. (A) Inappropriate reduction. Air outlines the disrupted radiohumeral joint. No attempt was made to reduce this further.
(B) Healing 5 months later. (C) Three years later. The elbow is painful.
epiphysis and fixation of the fragments of the metaphysis if
they are sufficiently large. If possible, pins crossing the physis
are avoided. Image intensification may be used, but it is prob-
ably wise to treat these injuries with an open reduction, as
part of the concept of reduction is adequate restoration of
the various articular surfaces. Any intraarticular fragments of
cartilage or bone are removed and the joint thoroughly
irrigated.
Open reduction and internal fixation is done under
tourniquet, with an incision made directly over the lateral
condyle. The joint is irrigated to obtain a clear view of the
articular surfaces. the fragment is minimally dissected free
of soft tissue attachments but should be visualized sufficiently
to see if it is rotated in different planes. The periosteum may
be herniated into the region between the fragments and
should be removed. The fracture must be reduced anatom-
ically, at the fracture line in the metaphysis and at the
joint surface. Failure to do so may create an abnormal elbow
joint (Fig. 14-113). Kirschner wires, which should be smooth,
are placed across the region. Fluoroscopy, image intensi-
fication, or biplane radiographs are obtained to ensure
reduction.
When opening and reducing the fracture one must not
detach all the muscles from the lateral epicondyle, because
these carry some of the blood supply to the condylar
fragment. If detachment is undertaken, the condyle may
undergo partial to complete aseptic necrosis and premature
epiphysiodesis.
The Late Case
A patient with a relatively undisplaced fracture and no clin-
ical or roentgenographic union may not seek treatment until
several weeks or months after injury (Figs. 14-114, 14-115).
14. Humerus
Flynn et al. reported a series of nonunited minimally dis-
placed fractures.740,741 They noted that with unrecognized
fractures the results of the nonunion were the symptoms that
brought the child to the attention of the surgeon. Jeffrey
pointed out that: (1) nonunion may originate in a fracture
with relatively minor displacement and little or no rotation;
(2) the orthopaedist may be unaware that union has failed;
and (3) the nonunion may not be discovered until some later
date.766
Flynn et al. believed that early roentgenographic evidence
of nonunion was seen best in the anteroposterior view as
a “high collar-like projection” of the posterolateral metaph-
yseal fragment attached to the epiphysis.741 There was
lateral shifting and blunting of the fracture edges of the
metaphyseal fragment, little or no callus formation, and a
still distinct fracture gap. If this phenomenon is observed
after the fifth week, it should be recognized as a delayed
union. If it persists after the third month, nonunion is defi-
nite, and appropriate surgical treatment should be carried
out.
This delayed union pattern may respond effectively to pin
stabilization, even several months after the injury. Minimal
resection of fibrous callus is needed. Bone grafting may be
unnecessary if the metaphyseal subchondral plate adjacent
to the nonunion is fenestrated with two or three drill holes;
the fragment is immobilized by pin or screw fixation. The
epiphyseal segment of the fracture should not be débrided
of fibrous tissue.
Jakob et al. found that the results of open reduction per-
formed more than 3 weeks after the fracture are no better
than the results of no treatment at all.765 Reduction may
infarct the lateral condylar fragment by damaging the blood
supply. The degree of displacement seems to be significant.
The greater the displacement, the more likely it is that
surgery will lead to complications.
Lateral Condyle Injuries 519

FIGURE 14-114. Delayed union. (A) Appearance 5 months after an “undisplaced” fracture. (B, C) The child was subsequently treated by
excision of the fibrous nonunion and internal fixation. Healing was rapid.

Occasionally, a parent seeks treatment several weeks
after the original injury for a significantly displaced fracture
of the lateral condyle. Should it be accepted or corrected?
Late surgery often causes stiffness and osteonecrosis. Some
authors recommend a “hands-off” policy for any displaced
fracture that has gone untreated for more than 4 weeks.769
However, if it is still reasonably early (within a few weeks
of the injury), open reduction, careful dissection, and
anatomic reduction may still be recommended. It may be
necessary to carefully currette some healing callus to obtain
accurate anatomic reduction. Ununited fractures beyond a
few weeks of age, in which nonunion is established, proba-
bly are difficult to treat by any method. However, an effort
should be made to create bone-to-bone apposition of me-
taphyseal fragments in the displaced position. Once solid
union is established and there is no evidence of growth
arrest, a corrective osteotomy may be done.
The child who presents with a several-month delay and
established nonunion still should be treated. An anatomic
reduction is not the goal. Instead, the osseous metaphyseal
portion of the fracture is exposed, carefully curretted, and if
necessary packed with bone graft. Pin or screw stabilization
is also used. The epiphyseal and articular portions are not
exposed.
Results
Flynn and Richards studied the healing responses of frac-
tures with less than 4 mm displacement, most of which were
treated with closed reduction. They recognized three pat-
terns of healing.740 The first, which comprised almost half of
the lesions, healed rapidly in 6 weeks with reasonably abun-
dant callus and subperiosteal new bone. The second group
(38%) healed slowly over 8–12 weeks, mostly by endosteal

FIGURE 14-115. (A) Nonunion 6 months after injury. (B) Three weeks after pin fixation and bone graft. There was no attempt to take
down the fibrous union completely. (C) Four months after surgery. Union is complete.
520
union with little peripheral callus. The remaining 13% dis-
played progressive displacement of the fragment in the cast
and required subsequent surgery to prevent nonunion.
These elbows were salvaged with fixation or bone grafting,
sparing the physis of the condylar fragment. Flynn and
Richards740 also noted that if the fracture was displaced less
than 2 mm the union was usually adequate. If the displace-
ment was 3 mm or more, however, the incidence of delayed
union, malunion, and nonunion was much higher.
Jakob et al. reviewed 48 children: 20 with minimally dis-
placed fractures and 28 with displaced fractures requiring
open reduction and internal fixation.765 Four patients had a
fracture line crossing the capitellar epiphysis and entering
the joint lateral to the trochlea. The rest had injuries in
which the fracture fragment included the capitellum and
lateral part of the trochlea. Three of the patients developed
avascular necrosis, and in two the lateral part of the distal
humeral growth plate closed prematurely.
Complications
Nonunion
Severe, unrecognized injuries may progress to nonunion
and marked elbow deformity (Fig. 14-116).766 Smith recently
reported an 84-year follow-up of a patient with nonunion.792
The functional disability was minimal, but complete ulnar
nerve palsy was present.
Nonunion and growth arrests result from minimally dis-
placed fractures more commonly than from markedly dis-
placed and rotated fractures, probably because the severe
fractures are treated more adequately with surgery.740,741 Min-
imally displaced fractures may displace more (in millime-
ters) by continued motion but rarely rotate to the degree
significantly displaced injuries do. The continual motion
creates a bridge of fibrocartilage between the osseous and
cartilaginous fragments.
FIGURE 14-116. (A) Condylar nonunion. (B, C) Development of a nonunion from 4 to 17 years of age in an untreated patient.
14. Humerus
Nonunion subsequently results in progressive cubitus
valgus due to retardation and growth arrest of the lateral
condylar physis and continued normal growth of the medial
condylar region of the physis. Eventually, degenerative
changes supervene.
Suggested causes for delayed union and nonunion have
included lack of immobilization, synovial fluid bathing the
fracture, and soft tissue interposition. Continued micromo-
tion is probably the most significant factor. In many cases the
fracture has rotated 90° in at least one, if not two, planes,
causing articular cartilage to appose epiphyseal cartilage or
metaphyseal bone. It is unlikely that this articular cartilage
surface will heal to the remaining osseous portions of the
distal humerus.
Flynn and Richards argued that nonunion in a good posi-
tion was acceptable but that it may become symptomatic,
especially in athletic children.740 Furthermore, careful dis-
tinction must be made between what is considered nonunion
in good position and nonunion in poor position. Early
surgery is recommended for established nonunion when the
condylar fragment is in good position. If the united fragment
is in poor position, unless the surgeon is skilled and familiar
with the area, particularly the contours of the growth plate,
it is advisable to refer the patient to another surgeon or leave
the fracture fragment as is. An attempt to replace it anatom-
ically may traumatize the physis of the fragment; and
although the remainder of the elbow continues to grow, the
physeal plate of the fragment may close and growth poten-
tial is lost. This in turn leads to valgus deformity, and little
benefit is derived from the semiacute surgery.
Extensive bone grafting to obtain union before comple-
tion of growth is not recommended because functional dis-
ability is not usually significant in the presence of nonunion.
If the fracture has been treated by closed reduction, the pres-
ence of nonunion is a strong indication that the fragments
have not been adequately stabilized or that they may have
rotated 90° or 180° and only seem to be reduced. In such a
B,C
Lateral Condyle Injuries 521

situation, open reduction and exploration are indicated,

despite the fact that the fracture may be several weeks old.
Surgery may reveal that there is a rotation or that there is
unopposed tissue that can be removed with firm reduction
and Kirschner wire fixation. Bone graft from the metaphy-
seal fragment to the remainder of metaphysis may be
helpful.
A patient with established nonunion in which the epiphy-
seal cartilage plate of the lateral condylar fragment is already
closed is not a good candidate for surgery. Surgery may
achieve union, but the condyle is unable to grow with the
remainder of the elbow. Thus surgery may not prevent recur-
rent valgus deformity and may not yield a satisfactory elbow.
Such a patient may be better left untreated until growth is
complete, with later transfer of the ulnar nerve if tardy ulnar
palsy occurs. In the adult, when the site of nonunion is
painful, the fragment can be fixed (with or without bone
graft) or excised, but only after careful consideration of the
effect it may have on elbow function. The fragment should
never be excised in the immature elbow because the same FIGURE 14-117. Histology of physeal damage in a lateral condylar
fracture. Arrows indicate segments of physis that are completely
sequelae that follow excision of the radial head would ensue.
separated from the epiphysis. They included germinal cells devoid
Osteotomy of the distal part of the humerus at maturity may of physeal blood supply.
be necessary to correct the deformity.

Growth Damage ossification center fused to the metaphysis; with the second
Lateral condylar fractures generally are type 4 injuries, with type the capitellum and trochlea ossifications fused together
most passing through the cartilaginous trochlear epiphysis. and then fused subsequently to the metaphysis at the apex
They are thus likely to affect subsequent growth, although to of the original fracture. Delayed union results in prolonged
a highly variable and unpredictable degree. Because they do go hyperemia and possible stimulation of growth on the lateral
through an area that subsequently ossifies, there may be pre- side of the elbow producing a cubitus varus. If there is
mature fusion between the trochlea and capitellar ossifica- damage to the growth plate, an osseous bridge inevitably
tion centers, limiting latitudinal development and osseous forms across the plate. In addition to the obvious premature
bridging across the physis. If the fracture involves the growth arrest and fusion, an additional 11 of the remaining
margins of the secondary ossification of the capitellum, the 22 patients had narrowing of the distal humeral epiphyseal
likelihood of subsequent growth arrest increases. Should plate, implying some loss of appositional growth.424
there be growth arrest, it increases the cubitus valgus defor-
mity. As shown in Figure 14-117, microscopic physeal dis-
ruption may occur and predispose to physeal arrest, even
with excellent closed or open reduction techniques.
Figures 14-99, 14-100, 14-101, and 14-117 show anatomic
specimens of lateral condylar fractures that had significant
damage to the physis. Particularly, segments of physis were
on the wrong side of the fracture, attached to the metaph-
ysis instead of remaining with the epiphysis, rendering the
segment ischemic. Presumably, this fragmentation occurs in
a number of children and may be the real reason for pre-
mature bridging. Accordingly, the treating physician must
warn the parents of the risk regardless of whether closed or
open treatment is used.
Malunion and premature growth arrest (Fig. 14-118) to
the lateral condyle also may cause progressive cubitus valgus.
This deformity of the elbow may be corrected by osteotomy
of the distal humerus; but if it is corrected in the face of pre-
mature growth arrest, the deformity may recur because of
the localized growth injury. If a specific localized defect can
be observed, it may be possible to treat it with resection and
fat interposition.
Wadsworth studied 28 children with fractures of the
capitellum.799,800 He distinguished two types of premature FIGURE 14-118. Abnormal growth after lateral condylar fracture
epiphyseal fusion. With the first type the capitellar secondary (treated closed).
522 14. Humerus

Another complication is poor articulation of the ulna with

the trochlea, which impairs elbow movement.778 Because the
fracture usually extends through a significant portion of the
trochlea, it is easy to understand how inadequate apposition
of the joint surfaces creates this complication.
An infrequent radiologic finding is the “fishtail” deformity
of the distal end of the humerus. This deformity is probably
due to damage of the growth plate immediately adjacent to
the fracture line (Fig. 14-119). The abnormality may
produce cubitus valgus with limitation of movement, or it
may even progress to degenerative arthritis.799,803 None of the
three patients with this abnormality reported by Jakob et al.
had a deviation of the carrying angle, nor did they lose any
mobility of the elbow.765
This phenomenon may occur in well reduced as well as
poorly reduced fractures, and it may be due to deficient
development of part of the trochlea or to fibrous union not
unlike that shown in Chapter 6, in which there is fibrocarti-
lage rather than true hyaline cartilage. This deformity is
always most marked when the capitellum united in a rota-
tional deformity and in cases with overgrowth of the lateral
condyle.
Another infrequent complication of lateral condyle frac-
tures is radioulnar synostosis, although great care must be
taken when ascribing this particular deformity to the frac- FIGURE 14-120. Split capitellar fracture.
ture. The possibility of preexistent synostosis must be
considered. condyle should be removed and the nerve allowed to move
One of the more important complications of injury to the over the remaining area. Use of the latter approach is con-
capitellar epiphysis is ulnar neuritis, which is usually due to tingent on the degree of deformity and the age of the child;
progressive cubitus valgus.749,756,761,781 Neuritis may be due to it should not be used prior to skeletal maturity.
simple compression by the band bridging the two heads of
the flexor carpi ulnaris when the capacity of the cubital Split Capitellar Fracture
tunnel is less than normal.
The ulnar nerve is repeatedly stretched by motion of the As previously alluded to, a variant of the lateral condylar frac-
elbow at the apex of the deformity and by the increasing ture goes through the capitellar ossification center735,736,783
valgus deformation; and it may become progressively irri- rather than extending to the trochlear region. These frac-
tated in its course behind the medial epicondyle.715 At the tures may be undisplaced (Fig. 14-120) or variably disrupted
earliest signs of neuritis, either the ulnar nerve should be (Figs. 14-121, 14-122). In some instances the separation is at
transferred anterior to the medial epicondyle or the epi-

FIGURE 14-121. Type 4 displaced split capitellar fracture treated

FIGURE 14-119. Fishtail deformity. with open reduction with internal fixation.
Floating Elbow
FIGURE 14-122. Split fracture.
or near the maturing chondro-osseous interface. This
pattern may leave only a thin shell of subchondral bone
attached to the displaced fragment (Fig. 14-123).
As with more typical lateral condylar fracture patterns, the
injury may appear to be stable. Such a fracture must be
observed closely for displacement as hydrostatic pressures
dissipate. Most of these fractures require careful open reduc-
tion and internal fixation.
Lateral Epicondyle Injuries
The lateral epicondylar ossification center often is irregular
and easily confused with a fracture. Injury to this particular
epicondyle, compared to the medial epicondyle, is infre-
quent (Figs. 14-124 to 14-127).808,809 Most often the injury
FIGURE 14-123. Sleeve fracture of the capitellum. It was reposi-
tioned and held with polyglycolic pins.
523
FIGURE 14-124. (A) Fracture of the lateral epicondyle. (B) Roent-
genographic depiction of a specimen.
accompanies elbow dislocation. Chronic avulsion may occur
as a repetitive athletic injury.
In most cases there is relatively little displacement of the
fragment. Immobilization of the elbow for 3–4 weeks may be
sufficient. If the fragment is displaced more than 2–3 mm,
open reduction should be considered. Because these injuries
tend to occur in children approaching skeletal maturity, the
risk of associated growth arrest is minimal.
Floating Elbow
A distal humeral fracture and an ipsilateral forearm fracture
or fractures (Fig. 14-128) create a difficult combination of
injuries.810–814 Closed treatment of both usually leads to unac-
ceptable reduction of at least one of the injuries.
The distal humeral injury should be stabilized by closed
reduction and percutaneous pinning or open reduction and
internal fixation. The forearm fractures are then treated by
closed reduction and casting.
The distal humeral injury may be a supracondylar,
transcondylar, lateral condylar, or medial condylar fracture.
Similarly, a variety of forearm injuries may be present, such
as an olecranon fracture, a radial neck fracture, a Monteggia
equivalent, or diaphyseal radioulnar fractures.
As many as 10–15% of all supracondylar fracture patients
also have a second injury involving the ipsilateral radius and
 FIGURE 14-125. (A) Acute fracture of the
lateral epicondyle. (B) Appearance of the frac-
ture 5 years later, following skeletal matura-
tion. Fibrous nonunion had occurred.

FIGURE 14-126. Lateral epicondylar avulsion injury (arrow) in a 14-

year-old boy who fell directly on his elbow. There was mild varus
instability. The fracture was treated by closed reduction and immo-
bilization at 90° of elbow flexion.

FIGURE 14-128. (A) Floating elbow with fractures of the humeral

diaphysis and ulnar metaphysis. (B) The cast has not effectively
treated the fractures.

FIGURE 14-127. Medial and lateral epicondylar fractures following

elbow dislocation.

524
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ulna. The distal radius/ulna is the most likely site of radioul-
nar injury.
Elbow swelling is a significant problem. The potential for
the development of compartment syndrome or ischemia
may be higher with combined injuries than with either injury
alone.
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the humerus in children. Acta Orthop Scand 1974;45:518–523.
763. Inoue G, Horii E. Combined shear fractures of the trochlea
and capitellum associated with anterior fracture-dislocation of
the elbow. J Orthop Trauma 1992;6:373–375.
764. Ippolito E, Tudisco C, Farsetti P, Caterini R. Fracture of the
humeral condyles in children: 49 cases evaluated after 18–45
years. Acta Orthop Scand 1996;67:173–178.
765. Jakob R, Fowles J, Rang M, Kassab M. Observations concern-
ing fractures of the lateral humeral condyle in children. J Bone
Joint Surg Br 1975;57:430–436.
766. Jeffrey CC. Non-union of the epiphysis of the lateral condyle
of the humerus. J Bone Joint Surg Br 1958;40:396–405.
767. Johansson J, Rosman M. Fracture of the capitulum humeri in
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768. Kalenak A. Ununited fracture of the lateral condyle of the
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181–185.
769. Kini MG. Fractures of the lateral condyle of the lower end
of the humerus with complications: a simple technique for
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15
Elbow
Engraving of dislocation of the elbow and concomitant medial
epicondylar fracture. (From Poland J. Traumatic Separation of the
Epiphyses. London: Smith, Elder, 1898)
uch of the chondro-osseous anatomy of the elbow,
M particularly the variable development of the epiphy-
seal ossification centers, is dealt with in Chapter 14
(humerus) and Chapter 16 (radius and ulna). The develop-
ment and chondro-osseous transformation of each of
these ossification centers may be irregular and often asym-
metric (which must be remembered when assessing com-
parison films). The changes should not be confused with
acute fracture, osteochondritis, or any other elbow lesions
frequently encountered in childhood and adolescent
athletes.1,5,7,10,11
The elbow has a complex geometry with three integrated
joints (radiocapitellar, trochleoulnar, proximal radioulnar).
It is a hinge joint tightly constrained by the contiguous
ligamentous and capsular tissues.3,4 These soft tissues attach
proximally to various points around the distal humeral me-
taphysis and epiphysis, including the epicondyles. The distal
attachments are primarily to the ulnar metaphysis, both
medially and laterally (Fig. 15-1). The ligamentous attach-
542
ments of the proximal radius do not add appreciably to sta-
bility laterally. In the child these ligaments often exhibit suf-
ficient laxity prior to skeletal maturity that subluxation,
dislocation, spontaneous reduction, and manipulative
reduction are relatively easy compared to that in the adult.
Such laxity also predisposes to nursemaid’s elbow. The high
incidence of concomitant medial epicondylar fracture when
the child’s elbow dislocates suggests that the medial collat-
eral ligament is a significant constraining factor compared
to other ligaments. Both the ulnar and radial ligaments prin-
cipally attach to the ulna. No major collateral arm-to-forearm
stabilizing structures attach directly to the proximal radius.
The soft tissues stabilizing the medial side of the elbow
consist of the anterior and posterior fibrous groupings of the
medial collateral ligament and the medial capsule located
between these bands. The anterior portion of the medial col-
lateral ligament is a primary stabilizer of the elbow, both in
extension and when subjected to valgus stress.2 The relative
contribution of the posterior ligament to elbow stability is
minimal. The lateral ligament complex consists of the lateral
collateral ligament, the annular ligament, and the accessory
posterior annular ligament.9
Compromise of the anterior portion of the medial collat-
eral ligament renders the elbow grossly unstable except in
full extension. The anterior capsule provides primary stabil-
ity, augmented by the lateral and medial ligaments.6 In the
skeletally mature patient posterior dislocation of the elbow
invariably disrupts the anterior portion of the medial collat-
eral ligament.8 However, the rarity of redislocation or chronic
instability following posterior elbow dislocation in children
attests to the ultimate functional integrity of the medial col-
lateral ligament and suggests that the ligament may not be
significantly disrupted in elbow dislocations. In children the
frequent concomitant fracture of the medial epicondyle
allows chondro-osseous failure and extensive subperiosteal
stripping, rather than discrete medial ligament failure. So
long as the fracture heals, elbow stability is usually main-
tained. However, if the epicondyle undergoes nonunion or
displaced fibrous malunion, variable elbow instability may
occur, similar to the residual functional weakness in the ante-
rior cruciate ligament seen with tibial spine injuries in chil-
dren (see Chapter 23). This may predispose to degenerative
osteoarthritis at an early age. There are no studies in chil-
dren or adolescents with epicondylar injury to ascertain
Dislocation
FIGURE 15-1. Elbow capsular and ligamentous attachments in
an 8-year-old. These attachments may change with progressive
chondro-osseous development. The medial and lateral capsules
and ligaments are relatively taut in extension but become relaxed
in flexion. The anterior and posterior ligaments have more redun-
dancy to allow flexion and extension. The ulna is outlined by the
narrow dashed line in the lateral view.
whether concomitant ligament damage also occurs (similar
to the concomitance of cruciate injury associated with tibial
spine avulsion).
In an experimental study of ligamentous injuries
using cadaver elbows from adults, posterior dislocation of
the elbow could be produced only when combined valgus
and external rotatory torque was applied.9 These investi-
gators were unable to dislocate elbows with varus and
internal rotatory torque forces or in extreme positions. In
the elbow specimens that had an experimentally pro-
duced posterior dislocation, there usually was simultaneous
rupture of the anterior part of the medial collateral liga-
ment along with the annular ligament. In contrast, a
lateral collateral ligament tear was evident in only 2 of 10
specimens.
Dislocation
Elbow dislocation, which constitutes about 5% of elbow
injuries in children, appears to be the most common joint
dislocation in children.12–111 It is increasingly frequent after
8 years of age, reaching a peak during adolescence. This
injury usually follows a fall on the outstretched hand with
the elbow incompletely flexed, but dislocation also may
occur as a hyperextension injury. Deforming forces,
however, tend to be transmitted away from the joint to the
proximal third of the radial and ulnar shafts or to the distal
humerus; and they usually cause radioulnar shaft, supra-
condylar metaphyseal, or transcondylar physeal fractures,
rather than elbow joint dislocations, much like the injury
pattern at the knee.
The direction of displacement varies with the direction of
the applied deforming force. Posterior displacement, which
543
is usually accompanied by lateral displacement, is most
common. Medial displacement should arouse suspicion of a
transcondylar (physeal) fracture, rather than an elbow dis-
location. Rotatory luxation with total displacement of one
forearm bone and part of the other may occur with the pos-
terior type when only one collateral ligament is torn. Diver-
gent dislocation of the radius and ulna is rare in the child,
as is anterior dislocation.
The complex association of axial and rotatory forces
may cause not only capsular and ligamentous disruptions
but a wide variety of concomitant chondro-osseous
injuries.13,42,61,82,86,94,95,99,100 Pure dislocation, unaccompanied
by fracture, is relatively uncommon in children. Always look
for an associated fracture, many of which are subtle (e.g., occult
type 1 physeal injury or a chondro-osseous sleeve fracture),
and be cognizant of cartilaginous epicondylar injuries that
may not be evident radiographically. Multiple injuries may
occur in the same arm, with distal radioulnar fractures
being relatively common (Fig. 15-2). Complete examination
of the injured extremity and sufficiently detailed pre- and
postreduction films are essential to the diagnosis of these
associated injuries. In the young child (under 5 years)
evidence of condylar displacement may not be obvious until
an extended period of time has elapsed following the acute
injury.
Dislocation of the elbow is unusual in children under 2
years of age. Instead, they usually sustain a fracture of the
entire distal humeral physis (transcondylar). This usually
leads to a posteromedial shift of the radiolucent distal
humeral epiphysis that is often misinterpreted as an elbow
dislocation. The diagnosis must be accurate, as the treatment
for elbow region fractures and an elbow dislocation differ
significantly (see Chapters 14, 16).
Because of the hazard of concomitant neurovascular
injuries, reduction frequently may have to be urgent.32,71,
74,87,97,108
The complete neurovascular status at and distal to
the injured elbow must be ascertained before reduction, par-
ticularly in view of the potential for entrapping the median
nerve or stretching the ulnar nerve. The same, careful neu-
rovascular evaluation must also be carried out after reduc-
FIGURE 15-2. Dislocated elbow in a 10-year-old boy. This roent-
genogram focused on the open injury. The solid curved arrow indi-
cates the intraarticular air present because of the open wound.
Note how the air–cartilage interface has outlined the cartilaginous
components of the capitellum and trochlea (*arrows). A concomi-
tant fracture of the distal radius was also present (open arrow) but
was barely visible on the roentgenogram, which had been centered
specifically on the supracondylar region.
 544
A B
FIGURE 15-3. Lateral (A) and anterior (B) views of a posterolateral
dislocation (black arrow) in a 7-year-old. The medial epicondyle is
fractured but undisplaced (white arrow). (C, D) Posterior disloca-
tion, as a potential complication of closed reduction is nerve
entrapment within the joint.
Classification
Several patterns of elbow dislocation occur in children.
1. Posterior dislocation of the radius and ulna without
other obvious osseous injury (Fig. 15-3).
2. Posterior dislocation with a fracture of the coronoid
process (Fig. 15-4). There may be a shell separation of
the unossified portion.
3. Posterior dislocation with a separation of part or all
of the medial epicondyle (Fig. 15-5). This epicondylar
fragment may be completely displaced into the elbow
joint.
4. Posterior displacement with a fracture of the radial head
or neck (Figs. 15-6, 15-7).
5. Posterior dislocation with a fracture of the olecranon
(Fig. 15-8).
6. Lateral dislocation with a fracture of the lateral epi-
condyle of the humerus (Fig. 15-9).
A B
FIGURE 15-4. (A) Posterior elbow dislocation with an osseous fragment (arrow). The point of origin of the fragment cannot be readily
determined. (B) Reduced dislocation shows that this fragment was a concomitant fracture of the coronoid process (arrow) of the ulna.
15. Elbow
C
D
tion in flexion (C) and hyperextension (D), which has a higher risk
of capsular disruption.
7. Dislocation with a medial or lateral condylar fracture
(Fig. 15-10).
8. Anterior dislocation, which is rare in children.
9. Divergent dislocation of the proximal radius and ulna
(Fig. 15-11).
10. Convergent dislocation with translocation of the radius
and ulna (Fig. 15-12).
11. Anterior or anterolateral displacement of the radius
with a fracture of the ulna, the Monteggia fracture-
dislocation, or a variant of it (see Chapter 16 for a com-
plete discussion of this pattern).
Pathomechanics
Posterior dislocation usually results from a fall on the out-
stretched hand with the forearm supinated and the elbow
extended or partially flexed. The force of the fall is trans-
mitted along the forearm to the coronoid process. The coro-
noid process, which resists posterior displacement of the
ulna, is more readily temporarily deformed in children
because it is incompletely ossified. The laterally sloping
surface of the inner two-thirds of the trochlea converts the
Classification 545

A B
FIGURE 15-5. (A) Posterolateral dislocation with a displacement of
the medial epicondyle. Such mild displacement may be missed on
the initial evaluation. The additional fragments are multifocal
trochlear ossification. (B) Posterior displacement of the medial epi-
C
condyle. Posteromedial soft tissue attachments are intact and may
allow a satisfactory closed reduction without the need for fixation
of the epicondyle. (C) Posterior dislocation with concomitant avul-
sion of the medial epicondyle, which may be pulled into the joint.

B
A
C

FIGURE 15-6. (A, B) Mechanism of displacing the radial epiphysis during injury or reduction. The radial head may impact posteriorly
against the capitellum during attempted reduction. (C) Elbow dislocation with a displaced and rotated radial head fracture.

A B

FIGURE 15-7. (A) Radial head displacement with a dislocation of the elbow. (B) Following reduction the radial head is displaced (arrow).
546
FIGURE 15-8. Posterior dislocation in a 14-year-old with concomi-
tant olecranon fractures (arrows). One fracture line initially involved
the closing physis but then extended into the joint. The medial
epicondyle (M) has been displaced posteriorly.
A stripped superiorly. The posterolateral capsule is torn, and
B to varying degrees, depending on the extent of injury to the
FIGURE 15-9. (A) Lateral displacement (arrow) with concomitant
fracture of the lateral epicondyle. (B) Dislocation and lateral epi-
condylar fracture (arrow) in a 15-year-old girl.
applied vertical thrust to a lateral rotation and partial valgus
strain. The anterior capsule of the elbow joint is stretched by
the force of the impact. The upper end of the ulna is dis-
placed backward and then laterally. Collateral ligaments are
stretched or ruptured (Fig. 15-13). On the outer side of the
15. Elbow
B
FIGURE 15-10. (A, B) Elbow dislocation complicated by displaced
medial epicondylar and lateral condylar fractures that required
open reduction and internal fixation.
joint, the lateral ligament and capsule are attenuated or
the posterior periosteum is often stripped in a distal to prox-
imal direction. The biceps tendon is the rotational valgus
fulcrum. This muscle, along with the triceps, then contracts,
effectively “locking” the posterior dislocation.
With posterolateral dislocations, damage also occurs to the
medial side of the joint, with considerable bruising and
swelling often evident. Most often the medial epicondyle is
detached in children; it is unlikely that the medial ligament
is stretched or ruptured. After reduction, especially pin fix-
ation of the medial epicondyle, it is not usually possible to
stress the joint into valgus. The ligaments retain relative con-
tinuity with the periosteum, even though the attachment
may have been stripped from the underlying bone.
The forearm bones may be laterally or medially displaced
radial and ulnar collateral ligaments and contiguous
musculotendinous tissues. Without damage to the ulnar
collateral ligament, continued valgus stress may avulse
the medial epicondyle, displacing this fragment along
with the forearm bones. The lateral ligament may be torn
at its upper attachment; frequently there is accompa-
nying detachment of a fragment of the lateral epicondyle.
The posterior part of the capsule, particularly the part
behind the lateral ligament, may be torn from its superior
attachment.
Classification 547

A B

FIGURE 15-11. (A) Divergent dislocation. There is dislocation not require open reduction and repair or reduction of the ligament. This
only of the elbow joint but also of the proximal radioulnar joint (up injury is analogous to a Monteggia injury. (B) Demonstrative case
arrow), leading to separation of the radius and ulna. This may of divergent dislocation (arrows).
disrupt or displace the annular ligament significantly and may

A B
C

FIGURE 15-12. Translocation (convergent dislocation) of radius and ulna following dislocation. (A) Initial posterolateral displacement.
(B) Translocation of the radius to “articulate” with the trochlea. (C) Convergent dislocation in a five-year-old girl.

FIGURE 15-13. Mechanics of an elbow dislocation. See text for details.

548
The radius and ulna, being firmly bound together by the
annular ligament and interosseous membrane, are usually
displaced posteriorly in unison. Infrequently, however, the
two bones may be separated when the annular ligament is
displaced over the radial head or disrupted (divergent dis-
location). The coronoid process of the ulna may become
locked in the olecranon fossa of the posterior distal
humerus.
Diagnosis
The differential diagnosis of an elbow dislocation basically
consists of distinguishing a dislocation from the various frac-
tures that may involve the variably radiolucent elbow region,
especially supracondylar fracture, lateral condylar fracture,
or transcondylar fracture, all of which may superficially or
clinically appear to be a dislocation. It is important to realize
that a dislocated elbow may spontaneously reduce when the
evocative forces dissipate, further complicating the diagno-
sis. A careful history helps diagnose this injury.
The child usually presents with a painful, swollen,
deformed elbow that is held in partial flexion and often sup-
ported by the opposite hand because of extreme discomfort.
Attempted motion of the elbow may be painful, restricted,
and associated with marked muscle spasm. The forearm
appears shortened. Many physical findings are obscured by
the marked soft tissue swelling. It is imperative that the neu-
rovascular function of the forelimb be closely assessed to
determine variable damage to the brachial artery and the
major nerves.
Because the child is often apprehensive, noncontact obser-
vation or simply encouraging the child to move the fingers
are ways to initiate the examination until cooperation can be
gained. Sensation must be gently tested in the three major
nerve distributions, including the anterior and posterior
interosseous divisions. The child should be encouraged to
make the O sign with the index finger and thumb. If it
cannot be done, injury to the anterior interosseous nerve has
probably occurred, causing paralysis of the flexor pollicis
longus. This is usually a traction-type injury, with recovery
likely.
Dislocation is diagnosed most easily roentgenographically.
Except when there is a serious vascular injury requiring
“immediate” reduction, roentgenograms are obtained prior
to treatment to rule out the presence of associated fractures
of the epicondyles, coronoid process, proximal radius and
ulna, or lateral condyle. Furthermore, an apparent disloca-
tion may be a transcondylar fracture of the distal humerus
(especially in children under 2 years of age). A child should
never be sent for diagnostic imaging without adequate splin-
tage, both for comfort and to prevent further soft tissue
injury and osseous displacement. Insist that the entire arm
be rotated as a unit for the radiographic views; otherwise the
technologist may inadvertently rotate only the forearm
through the dislocation.
A significant problem in the young child is determination
of avulsion of a nonossified medial or lateral epicondyle. If
palpation evinces significant tenderness or there is a palpa-
ble mass, avulsion has probably occurred. Stress radiography
that opens the medial joint is also most likely to be accom-
panied by epicondylar damage. Arthrography may be helpful
15. Elbow
in the small child with an unossified medial epicondyle.
Diagnosis is important because this fracture, and others,
may require reduction and skeletal fixation. Furthermore,
an apparent medial epicondylar fracture, may instead be a
larger, medial condylar injury of the nonossified trochlear
epiphysis (remember, this is radiolucent for most of the first
decade of life). Medial epicondylar injury is more likely than
lateral epicondylar injury.
Spontaneous reduction of a dislocated elbow is common.
Often the child presents with a history of a fall and the phys-
ical finding of a swollen, edematous elbow but without
obvious radiographic evidence of injury. However, if one
looks carefully at the radiograph, signs of antecedent dislo-
cation may be present: avulsion of the coronoid process,
avulsion of the medial epicondyle, or fracture of the radial
epiphysis. The avulsion indicates that the elbow most likely
has been transiently out of the joint, with the brachialis
muscle often avulsing the coronoid process. On spontaneous
reduction or with reduction in the emergency room, the
capitellum may cause a fracture of the radial epiphysis,
resulting in posterior or anterior displacement of the epi-
physis upon reduction (Figs. 15-9, 15-10). With posterior dis-
locations the radial head is usually displaced posteriorly and
dorsally, whereas with an anterior dislocation the radial head
is displaced onto the palmar surface of the radius.
Treatment
An acute posterior dislocation can often be reduced without
general anesthesia. Reduction in children under age 12,
however, is probably best done with relaxation and an anal-
gesic to prevent complications such as an iatrogenic fracture
of the radial head. Prior knowledge of lateral rotation and
displacement is useful for the reduction, as initial hyper-
supination may be necessary to free the head of the radius
and the coronoid process.
A gentle, effective reduction method is as follows. Place
the patient in the prone position with the injured limb
hanging over the edge of the table. The weight of the arm
usually provides sufficient distal traction. Encircle the arm to
give countertraction and push the olecranon downward and
forward (Fig. 15-14). Following reduction, the elbow should
be acutely flexed as much as swelling permits without
causing neurocirculatory impairment. An alternative
method of reduction comprises extension to slight hyperex-
tension, subsequent downward traction, and finally flexion
(Fig. 15-15). The hyperextension should be as little as possi-
ble because it increases reduction forces and may lead to
anterior muscular injury. Open reduction is indicated if
closed reduction is unsuccessful to anatomically reduce or
stabilize a chondro-osseous fragment or in a chronic dislo-
cation that is several days to weeks old. Always assess neu-
rovascular function after the manipulative reduction.
In most cases the presence of the epicondyle in the joint
is an indication for open reduction to reduce the epicondyle
satisfactorily and fix it with pins. The fragment is removed
from the joint, as it may impede reduction and subsequent
function. More importantly, the ulnar nerve may and should
be explored, as it also may have been displaced, stretched,
or otherwise compromised. Valgus stress and closed manip-
ulation occasionally succeed in displacing the epicondyle
Classification
FIGURE 15-14. Reduction utilizing mild elbow flexion. Posterior
pressure has been applied directly to the olecranon.
from the joint. If the medial epicondyle remains displaced
more than 2–3 mm, it should be fixed in place to add to the
stability of the elbow.
Once the elbow is reduced, the integrity of the medial and
lateral collateral ligaments is tested and the elbow moved
through a full range of motion to ensure that no fragment,
particularly the medial epicondyle, is caught within the joint
where it may impinge on joint surfaces. Roentgenographic
confirmation of reduction is essential, as swelling may lead
to a false impression that complete reduction has been
attained (Fig. 15-16). This also allows further assessment of
the associated fractures. An adequate preoperative assess-
ment should have revealed any accompanying fractures that
must be reevaluated after closed reduction or that necessi-
tate open reduction as the primary treatment (e.g., a com-
pletely displaced radial head).
Fowles et al. reported on 28 children with combined elbow
dislocation and avulsion of the medial epicondyle.43 Nine-
teen underwent a successful closed reduction. Eleven had a
normal elbow at follow-up, but eight had lost an average of
15° of flexion. Nine children required open reduction and
internal fixation of the epicondylar fragment (one for an
open injury, three for displacement of the epicondyle, and
six for intraarticular entrapment of the fragment). Five of
these children had ulnar nerve contusion, and four required
anterior transposition of the nerve. Of these nine patients,
only three had normal elbows; six had lost an average of 37°
of flexion. Fowles et al. thought that surgery was indicated
only for those children in whom the epicondyle was trapped
within the joint or significantly displaced after closed
reduction.
FIGURE 15-15. Reduction utilizing mild elbow hyperextension.
549
FIGURE 15-16. Postreduction film showing failure to obtain ade-
quate reduction. The distal humerus is locked on the coronoid
process of the ulna (arrowheads). Subsequent closed reduction
was successful.
Greiss and Massias reported a patient in whom a postero-
lateral elbow dislocation proved irreducible because the
radial head was caught in a buttonhole tear of the lateral
collateral ligament and capsule. It necessitated open
reduction.46
Divergent Dislocation
During elbow dislocation the annular ligament may be
damaged or displaced over the radial head. This causes addi-
tional dislocation of the proximal radioulnar joint, creating
complex joint disruption referred to as divergent elbow dis-
location (Fig. 15-11). Clinical descriptions of divergent dis-
location were reported as early as 1854 by Warmont107 and
1893 by Wright.110 There have been several radiographically
verified cases.16,26,34,57,96 With one exception all cases of trans-
verse divergent dislocation of the elbow have occurred in
children, undoubtedly because of the ligamentous laxity nor-
mally present. This pattern could be considered a variant of
the Monteggia injury (see Chapter 16).
Closed reduction has been possible in most reported
cases, either by traction alone or in combination with direct
pressure to the upper ends of the radius and ulna.96 Reduc-
tion requires reducing the ulna in routine fashion and at the
same time applying medial pressure over the radial head. If
left untreated (Fig. 15-17), the radial head remains dis-
placed, creating a situation analogous to a chronic Mon-
teggia injury.
Reduction is accomplished under sedation with longitu-
dinal traction to reduce the ulna, followed by lateral elbow
compression and flexion to partially reduce the radial head,
and finally continued supination to completely reduce the
radial head. The elbow should allow immediate full range of
motion. If not, suspect interposed tissue. Surgery may be
necessary to reduce and stabilize the proximal radioulnar
joint, as the annular ligament must be torn or completely
displaced (similar to the Monteggia injury).
550
FIGURE 15-17. Chronic divergent elbow dislocation 11 years after
the original injury.
Translocation (Convergent Dislocation)
An unusual elbow dislocation is proximal radioulnar translo-
cation (Fig. 15-18; also see Fig. 15-12). During dislocation,
the proximal radioulnar soft tissue interrelations (especially
the annular ligament) are dislocated, disrupted, or both
to the extent that the two bones become “unlinked” and
then cross (hyperpronation mechanism).68 In a case of con-
vergent dislocation, the upper radius and ulna were dislo-
cated posteriorly in a reversed relation due to extreme
pronation.26 This dislocation is usually irreducible by closed
means because of the interposition of the annular ligament.
The reversed anatomic relation may remain after reduc-
tion. The radial head then articulates with the trochlea and
the ulna with the capitellum. In one reported case of this
complication, open reduction and restoration of the
anatomic relations were undertaken. It required ulnar
osteotomy. Ischemic necrosis of the proximal radial epiphy-
seal ossification complicated the reduction.49
FIGURE 15-18. Translocation mechanism. *Annular ligament dis-
ruption. The arrow in (B) indicates the lateral shift. The arrows in
(C) show the subsequent anteromedial displacement and “reduc-
tion” of the radial head in the trochlear joint.
15. Elbow
Complications
Vascular Complications
Vascular injury is rare if a simple dislocation occurs, but
becomes more likely if a fracture is also present.52,53,56,62,63,67
Hemorrhage into the closed antecubital space may produce
sufficient tension to cause forearm ischemia. Volkmann’s
ischemic contracture also may complicate posterior disloca-
tion of the elbow when the brachial artery has been injured.
Following closed reduction, depending on the severity of the
trauma, the extent of soft tissue swelling, and the diminished
pulse (e.g., found by examination, Doppler study), it may be
wise to admit the child to the hospital overnight to allow
close observation.
When assessing vascular integrity in a child’s arm, caution
must be advised against placing too much reliance on “cap-
illary filling.” Collateral circulation may be sufficient to
provide excellent superficial and digital capillary filling but
insufficient to ensure adequate muscle physiology, especially
as the young child grows into a mature adolescent. Doppler
flow evaluation studies along the course of the vessel are
more reliable noninvasive indicators of vascular integrity.
Arteriography may also be considered.
Wheeler and Linscheid reported vascular complications in
8 of 110 elbow dislocations.109 They are generally associated
with the more violent injuries, particularly open ones. The
severity of injury to the brachial artery may vary from simple
contusion or spasm to laceration, rupture, or subintimal
hemorrhage. Any discrete vascular injuries should be
repaired, as indicated, following diagnosis by direct obser-
vation (if the wound is open) or arteriography (see Chapter
7 for generalities of the vascular injury).
Neurologic Complications
Neural injury appears to be more frequent than vascular
injury.32,40,45,48,70,71,75,87,88,90,97,98,108 Wheeler and Linscheid
reported neurologic complications in 24 of 110 elbow dislo-
cations (three times more neurologic complications than
vascular complications).109 The ulnar nerve was involved in
16 of 24 patients, the median nerve in 3, and both ulnar and
median nerves in 4; the remaining patient sustained a
brachial plexus injury. Most injuries are contusions or stretch-
ing injuries, without gross disruption of nerve continuity.
The ulnar nerve appears to be the most frequently injured
nerve. The common posterolateral dislocation of the elbow
results in a stretch injury to the medially based ulnar nerve.
The tight constraints on the nerve at the medial epicondy-
lar level affect the risk of injury (e.g., contusion, interstitial
hemorrhage).
Hallet described three types of ulnar nerve injury. In type
I the nerve is caught between the humerus and ulna. In type
II the nerve runs through a healed fracture in the medial
epicondyle. In type III the nerve is looped into the humeral-
ulnar joint anteriorly.48 Types I and III are the most common.
Early removal of the entrapped nerve is the treatment of
choice. A type II injury often escapes notice. If a palsy or any
type of neuropathy exists, entrapment should be considered,
with a diagnosis by type undertaken. A fracture of the medial
epicondyle with an otherwise normal radiograph and a full
Complications
range of joint motion should alert the examiner to the pos-
sibility of type II entrapment.
Because most capsular damage, even when medial and
lateral ligaments are involved, is anterior to the epicondyles,
and the medial epicondyle stays attached to the postero-
superior periosteal/perichondrial tissue (which may be
stripped extensively from the distal humeral metaphysis), the
ulnar nerve rarely is mobile enough to be displaced into the
joint. Even when the epicondyle is displaced into the joint,
the ulnar nerve usually stays attached to the less-displaced
soft tissues.
Close observation of radiographs may document the frac-
ture callus-forming Matev’s sign, which is the sclerosis-
rimmed osseous tunnel caused by passage of the median
nerve through the maturing callus.74
The median nerve may be injured, displaced into the
joint, and associated with delayed diagnosis. Interestingly,
intraarticular entrapment of the median nerve has been
reported only in children. Persistent pain or increasing
median nerve dysfunction should alert one to the possibility
of such entrapment. Median nerve exploration must be
undertaken once such entrapment has been diagnosed. If
the nerve is functionally intact, which may be demonstrated
by nerve stimulation, its removal from the joint is sufficient
treatment. If, however, the nerve is severely damaged,
crushed, or scarred and is seemingly nonfunctional, resec-
tion of the damaged section with end-to-end reanastomosis
or interposition graft may be necessary or appropriate.
Intraarticular entrapment of the median nerve may occur
during dislocation or reduction.88,90,97 Because the medial
epicondylar attachments are usually intact, it is assumed that
the median nerve loops into the trochleoulnar joint through
the torn medial capsule as the forearm is forced into valgus
and extension during acute dislocation.65 It is then trapped
in this location, during reduction, by the flare of the medial
condyle of the trochlea. To avoid such a rare neurologic com-
plication, Watson-Jones suggested gentle traction on the
forearm while it is in the flexed position, with no hyperex-
tension of the joint preliminary to reduction.108 Hyperex-
tension is a potentially dangerous reduction procedure,
predisposing the median nerve to intraarticular displace-
ment. However, all nerves displaced into the elbow joint had
good return of function after open reduction and removal
of the nerve from the joint.71
The treatment of neurologic complications should be con-
servative because most are stretch injuries that recover spon-
taneously. Persistent ulnar nerve paralysis should be treated
by neurolysis and, if necessary, anterior transposition. Any
intraarticular entrapment should be treated by open release
of the nerve from the joint whenever the diagnosis is made.
Surprising recovery of nerve function may occur even many
months after entrapment.
Contractures
As in adults, joint stiffness is often encountered following dis-
location and reduction of the elbow in children. Both the
child and the parents should be informed that the major dif-
ficulty is regaining full motion in the joint. Complete exten-
sion may never be recovered in older children, although the
loss of the last 5°–10° of extension usually is not associated
with a significant functional deficit. To prevent contractures,
551
elbow immobilization usually is no longer than 4 weeks in
the child over 10 years of age. Younger children can proba-
bly tolerate longer immobilization.
Capsular tearing is responsible for the prolonged stiffness
that often follows dislocation of the elbow. The capsular
attachment to the ulna is frequently torn. The posterior
capsule may also be torn at its attachment to the humerus,
although it is more likely that it is stripped away because of
the contiguity of the capsule with the posterior periosteum.
Manipulation or passive physiotherapy is seldom required
for joint stiffness.35 In fact, this approach may be detrimen-
tal because it may be accompanied by further joint irritation,
capsular tearing, and hematoma formation. A year may be
required to regain full motion in the child’s elbow. The child
is usually his or her own best physiotherapist.
Correction of posttraumatic flexion contracture of the
elbow by limited anterior capsulotomy may effectively
decrease the posttraumatic flexion contracture in properly
selected patients.103 However, whether such procedures are
necessary or appropriate in young children is still open to
discussion. Similarly, lack of flexion may be treated by V-Y
advancement of the triceps aponeurosis.
Heterotopic Bone
Myositis ossificans is uncommon with a simple dislocation,
but when it occurs it usually restricts motion (Figs. 15-19,
15-20). Reactive bone around chondro-osseous disruptions
and capsular tears may also restrict motion.
Although heterotopic bone formation occurs less fre-
quently in children than in adults, it is frequent enough to
be of concern in children who dislocate an elbow. If such
ossification occurs, it may restrict elbow motion. In one
series, this complication occurred in 32 of 110 disloca-
tions.101 Formation of heterotopic bone usually occurs below
the medial or lateral epicondyle along the course of the col-
lateral ligaments (Fig. 15-21) or the posterior capsule (Fig.
15-22). It is often evident within 3–4 weeks after the initial
injury. Bone also may form in damaged muscle as myositis
FIGURE 15-19. Ossification around the radial head allowed a range
of motion of only 40°–90°. Over a 6-month period, however, this
increased to 15°–160°, with diminution of the ossification.
552 15. Elbow

FIGURE 15-20. Excessive anterior heterotopic bone following dislocation. It moved with the
radius and ulna and blocked flexion beyond 105°. The proximal radius also shows evidence
of reactive bone where the capsule and periosteum were stripped.

A B

FIGURE 15-21. (A) Heterotopic bone (arrow) in the “medial collat- a true ligamentous injury. The radial head is still subluxated and
eral ligament.” It was probably due to chondro-osseous failure of exhibits some altered physeal growth. (B) Five years later the
a portion of the medial epicondyle as a sleeve fracture, rather than avulsed bone (arrow) is still evident.

A B C
FIGURE 15-22. (A) Anterior heterotopic bone formation. (B) Extensive heterotopic ossification in the posterior capsular, subperiosteal,
and muscular regions following dislocation. (C) Massive heterotopic bone following elbow dislocation.
Complications
FIGURE 15-23. Complete lateral dislocation of the elbow in an 8-
year-old. Note the extensive myositis ossificans in the biceps of
this child 5 months later.
ossificans (Fig. 15-23). Large deposits of bone may impair
normal joint function. Children show a tendency to resorb
ectopic calcification and ossification before it becomes
mature bone, although it may not occur until 6–8 months
after the injury (see Chapter 10). If surgical excision is nec-
essary, the best results occur in skeletally immature patients.
Excision should be done only after 6–9 months have elapsed
since the injury and only when the ectopic ossification
appears mature, with well defined peripheral sclerosis. A
“cold” bone scan, reasonably indicative of cessation of bone-
forming activity, is a favorable prognostic study for the timing
of resection but cannot be absolutely correlated with a less-
ened risk of recurrence.
Recurrent Dislocation
Recurrent elbow dislocation is rare in children.* Linscheid
and Wheeler found only two recurrent cases in 110 children
with elbow dislocations.66 The pathologic defect is usually
a laxity of the posterolateral ligamentous capsular struc-
tures consequent to the failure of any spontaneous repair or
reattachment.84 The medial or lateral epicondyle may
also develop nonunion, contributing to micro- or macro-
instability. Lateral nonunion allows displacement of the
radius from its normal articulation with the capitellum (Fig.
15-24). The intact lateral ligament normally prevents this
displacement; but if its superior attachments have been
stripped or if it is more lax than normal, the head of
the radius no longer closely apposes the contour of the
capitellum, and at some point in extension backward
slipping of the radial head may occur.
Ejsted et al. described two cases of habitual recurrent dis-
location of the elbow.37 Both patients had a mental disorder,
which presumably was a contributory factor, just as for recur-
rent shoulder dislocation. The elbows in both patients were
stabilized surgically.
Not all patients with recurrent dislocation have complete
dislocation. Instead, the radial head may subluxate into a
capitellar defect or capsular pocket and be reduced easily by
the child, who may complain only of a sensation of locking.
Progressive damage to the osteochondral surfaces is often
* Refs. 36,37,47, 50,55,58,73,75,84,102,111.
553
FIGURE 15-24. Recurrent dislocation. (A) The ligaments are atten-
uated (small arrow), and the lateral epicondyle did not heal (large
arrow). (B) This allows chronic posterior displacement (arrows) and
may lead to progressive deformation of the capitellum and radial
head.
significant. As the head of the radius displaces backward, it
may abrade the posterolateral margin of the capitellum. An
osteochondral fracture may occur. A permanent defect in
the posterolateral margin of the capitellum may result, and
the edge of the radial head may be damaged. The ulna, espe-
cially the coronoid process, may be deformed; and the ole-
cranon process may be deficient. Anterior capsular instability
may also contribute to chronic dislocation. Arthrography
may be useful for diagnosing these lesions and delineating
the pathoanatomy.38,59 In the older child or adolescent three
dimensional computed tomography (CT) reconstruction
may help define morphology and assist in preoperative
planning.
Trias and Comean strongly advocated the concept that
chondro-osseous changes, such as congenital hypoplasia of
the olecranon, were secondary to ligamentous instability,
which was the primary cause of chronic dislocation.102
The normal hyperlaxity of the ligaments of children may
also be a significant causal factor. Certainly, subtle, if not
overt, subluxation due to ligament instability may affect
acetabular development, so there is no reason comparable
cartilaginous changes could not occur in the unossified elbow
components.
Because recurrent dislocation is infrequent, one should try
to refrain from any operative ligament reconstruction during
childhood. The normal process of growth is associated with a
gradual tightening of ligaments and may lead to improved
overall stability. Operative treatment is indicated if the dislo-
cation recurs following minimal injury in the older child or
adolescent. Reattachment of the capsule and ligaments to the
lateral epicondyle (Fig. 15-25) is the most important step in
repairing this complication.18 Other available methods
include transfer of the bicipital tendon to the coronoid
process by an intraarticular bone graft (which cannot be used
effectively in the skeletally immature child in whom this area
is still cartilaginous), and repair or reinforcement of soft
tissues around the elbow joint using fascial or tendon strips
to reinforce the collateral ligaments. Zeier repaired both the
medial and lateral ligaments using fascia lata slings.111
554
FIGURE 15-25. Described repair for recurrent elbow dislocation.
Unreduced Dislocations
Allende and Freytes reported a series of chronic, untreated
dislocations of the elbow.14 They thought that any acute
elbow dislocation that had not been reduced by 3 weeks
could not be reduced satisfactorily by closed, manipulative
reduction. They described 31 cases of chronic dislocations
of the elbow in children and reported various operative
methods for reduction. The major impediment to reduction
is soft tissue contracture, particularly in the triceps, as the
elbow has usually been held in extension.93 Often it is impos-
sible to reduce these dislocations adequately and maintain
the full length in the triceps. The tendinous portion usually
must be lengthened. There often is fibrous pannus within
the joint, which must be removed from the olecranon region
to permit adequate reduction.
If the dislocation remains for several months to years, the
distal humerus may progressively deform, as may the proxi-
A B
FIGURE 15-26. (A) Appearance of the elbow in a 23-year-old man
who had had an elbow dislocation at 9 years of age. The radius
was never reduced. Morphologic change is evident. (B) Severe
15. Elbow
mal radius and the ulna (Figs. 15-26 to 15-29). Undoubtedly,
such deformations result from the lack of normal joint reac-
tion forces, as with hip dysplasia. The younger the child, the
more likely it is that an alteration of morphology will occur.
The longer the elbow remains dislocated, the greater is the
likelihood that reduction will be unstable or impossible
owing to both altered morphology and soft tissue contrac-
tures.21 Even if reduction can be attained, normal mobility
(function) may not be possible, and instability subluxation
and dislocation become more likely.
Volkov and Oganesian used the Ilizarov device to mobilize
chronic elbow joint contractures progressively and to reduce
old dislocations.106 The basic concept for correcting the con-
tracture is first to distract the joint surfaces and maintain a
space between them to prevent excessive pressure and then
to produce gradual, controlled passive flexion and extension
of the joint until adequate (not necessarily normal) function
is restored.
Fowles et al. studied 15 children with untreated posterior
dislocations of the elbow.41 Three had a useful range of pain-
less flexion and were not treated by surgery. Twelve had a
stiff elbow and underwent open reductions between 3 weeks
and 3 years after the original injury. The triceps was length-
ened whenever it prevented reduction. Kirschner wires were
sometimes necessary to stabilize the elbow temporarily. Com-
plications included transient paralysis of the hand in one
patient and myositis ossificans with a rigid elbow in another.
These authors followed the patients for 1–6 years after
surgery. In 11 of the patients the average range of flexion
was increased fourfold; and in all children who underwent
surgery the elbow had a useful range through 90° of flexion.
Eleven of the children thought that the function of the arm
was improved. Four had been operated on within 6 weeks of
the original accident and probably were in a better position
to do well. Fowles et al. noted that open reduction was always
worth trying, at least in children.
heterotopic bone in a 20-year-old woman who dislocated her elbow
at 10 years of age.
Pulled Elbow
FIGURE 15-27. Incompletely reduced old elbow dislocation (16
years previously at 8 years of age). The radial head remains
subluxated. Osteoarthritic changes are evident.
Pulled Elbow
One of the most common elbow injuries encountered in
infants and young children is the “pulled” elbow.112–154,156–172
This term is used to identify an entity in which the radial
head is traumatically “locked” because of sudden traction on
the hand or forearm when the elbow is extended and the
forearm hyperpronated. This entity has various eponyms,
such as nursemaid’s elbow and temper tantrum elbow. It may
occur when pulling a child as he or she stumbles, when
swinging the child, or when forcefully pulling the child away
from something enticing. It is one of the most common
injuries to the elbow in children under 4 years of age; it
rarely occurs after age 5, with a peak incidence between 1
and 3 years.
High incidences of this injury have been reported.132,160,172
Quan and Marcuse showed that 0.5% (4.6/1000) of the total
visits to one hospital’s emergency department were attribut-
able to pulled elbow.157 These patients constituted 22% of all
young children presenting for evaluation of an elbow injury.
Most studies show that radial head subluxation occurs
predominantly in the left elbow. This observation is logical,
as most parents or caretakers are right-handed and when
walking naturally hold the child by their left hand. The con-
dition is rarely bilateral.
Pathomechanics
The suspected pathophysiology and clinical presentation
have not changed from the early description by Lindeman142
in 1885. Radial head subluxation occurs when there is
sudden traction on the wrist or hand while the elbow is
extended and the forearm is hyperpronated. It cannot occur
when the elbow is flexed or when the forearm is supinated.
One of the early theories reported that the head of the
radius was not fully developed and that the periphery of the
cartilaginous end was smaller than or equal to the neck, such
that the head was not firmly held in place by the annular lig-
555
ament. This is a misinterpretation of a statement attributed to
Piersol.155 Ryan examined the upper end of the radius in 15
fetal specimens and found that the radial head, even at birth,
was definitely larger than the neck and that the ratio of the
two (head/neck) does not differ greatly from that of an
adult.158 Salter and Zaltz found that the diameter of the
radial head was larger than the neck by 30–60%.160 Similar
studies (unpublished) in our skeletal developmental labora-
tory of 29 prenatal and 54 postnatal specimens support this
observation that the radial head, from before birth through
adolescence, is always larger than the metaphysis.115 Thus the
concept that the radial head is easily pulled through the
annular ligament because it is smaller than or equal in width
to the radial neck is erroneous.
Stone studied the mechanism of injury in 12 anatomic
specimens and was able to produce the lesion in 6 of the
elbows.167 He observed that the annular ligament slipped
partially over the radial head only when the forearm was
pronated. He also observed that the radial head was slightly
oval, rather than circular, and that when the forearm was
supinated the anterior aspect of the radial head was relatively
elevated from the neck. Conversely, in pronation the ante-
rior aspect of the radial head is tilted slightly downward.
Salter and Zaltz also observed that the superior surface of
the radial head, viewed from above, was slightly more oval
than circular and, with forearm supination, the sagittal diam-
eter of the radial head is consistently greater than the
coronal diameter.160
My studies have shown that the plane of the articular
surface is not completely perpendicular to the longitudinal
axis of the radius (similar to the proximal tibia). Laterally
and posteriorly the radial head “rises” gradually, so when
traction is applied with the forearm in pronation the annular
FIGURE 15-28. Chronic elbow dislocation in a 9-year-old boy who
had sustained an “injury” to the elbow 4 years earlier. It had never
been treated. The lateral view shows posterior displacement of
radius and ulna. Ossification is evident in the capitellum, trochlea,
and medial epicondyle.
556
A
B
FIGURE 15-29. (A, B) Chronic anterior dislocation.
ligament must lie over the less prominent (i.e., “lower”)
portion, which also has a straighter side angle relative to the
longitudinal axis. The annular ligament may stretch and slip
over a portion of the radial head (Figs. 15-30 to 15-33). In
full supination the radius, at the site of the annular ligament,
is outflared, so it is difficult for the annular ligament to
displace onto the edge of the epiphysis or further onto a
portion of the articular surface. However, when the arm is
fully pronated, this portion of the metaphysis and epiphysis
assumes a much straighter position that more easily allows
the annular ligament to be displaced in a proximal (upward)
direction, allowing the ligament to cover a portion of the
radial head. This effectively “locks” the radial head, pre-
venting rotation.
McRae and Freeman studied 25 elbows from stillborns and
concluded that a pulled elbow was caused by the annular
ligament slipping partially over the radial head.145 Salter and
Zaltz anatomically duplicated the mechanism of displace-
15. Elbow
A
B
FIGURE 15-30. (A) Normal radial head showing slightly eccentric
central depression. (B) Effect of hyperpronation prior to tissue fix-
ation. The annular ligament partially displaced over the anterior
margin and indented the biologically plastic cartilage (arrows).
ment with sudden, firm, steady traction on the extended
elbow, first in supination and then in pronation.160 They were
not able to subluxate the radial head in any of the specimens
when the traction was applied with the forearm in supination,
but when traction was applied in pronation, a transverse tear
was produced in the thin distal attachment of the annular lig-
ament, allowing it to displace over the radial head.
Our studies show that displacement may occur without
tearing the annular attachments of the annular ligament
(Figs. 15-32, 15-33). When the proximal edge of the annular
ligament did not extend beyond the diametric (midportion)
of the radial head, the interposed ligament could be reposi-
tioned to its normal anatomic position by simple supination
of the forearm. In specimens from older children, a compa-
rable tear or displacement could not be produced because
of the thicker, stronger attachments. In operative cases and
one traumatic amputation with a Monteggia injury, we found
that the annular ligament may remain intact and yet slip
Pulled Elbow
A B
FIGURE 15-31. Proximal radius from a 17-month-old toddler. (A)
Morphological specimen. (B) Radiograph of specimen. There are
subtle contour differences in the metaphyseal-epiphyseal flaring.
completely over and off the radial head. This ligament is
highly mobile in the infant and young child.
Diagnosis
The diagnosis of a pulled elbow is usually based on both
the history and clinical findings. The parent, caretaker, or
child describes an activity in which the forearm was sub-
jected to significant traction while extended and pronated
(Fig. 15-34). Occasionally a click is felt or heard. The child
A B
FIGURE 15-32. Mechanism of a pulled elbow. (A) In pronation the
radial head subluxates slightly away from the ulna, and the annular
ligament displaces onto the radial head. (B) With supination,
557
In pronation the more gradual flare is presented to the annular lig-
ament. In contrast, supination presents the more angulated contour
to the annular ligament.
is usually in discomfort or pain and refuses to use the
affected arm. The pain is generally at the elbow, mainly over
the radial head, although a few children complain of pain in
the wrist or the shoulder. The arm remains in pronation and
either hangs limp in slight flexion or is cradled on the chest
by the other hand and guarded from manipulation by appro-
priately concerned adults. Bobrow stated that fewer than
50% of physicians in one family practice residency program
were able clinically to recognize a typical case of nursemaid’s
elbow.115
however, the radial head relocates into the radioulnar joint, and the
annular ligament relocates below the radial head.
558 15. Elbow

A B
FIGURE 15-33. Anatomy of the pulled elbow. (A) In pronation the annular ligament slips over the anterolateral radial margin. (B) With
supination the higher, more flared side of the radial head forces the annular ligament back into anatomic position.

Radiographs are usually reported as normal.123,128,136,165
One textbook noted that “although we have examined the
elbows radiographically in scores of such cases, we have not
been able to demonstrate the dislocation. The radiography
technicians probably reduce the dislocation consistently
before the film is exposed to their manipulations of the
elbow by positioning the patient. In an attempt to obtain an
adequate anteroposterior film of the joint, the technician
routinely supinates the forearm, much to the child’s momen-
tary opposition. The arm then no longer hurts and is usually
mobile after the radiograph.
Salter and Zaltz identified Stone’s 1916 report as the only
existing radiographic demonstration of displacement of the
proximal end of the radius in relation to the capitellum in
this entity, but they believed the evidence to be unconvinc-
ing as a reliable radiographic demonstration of nursemaid’s
elbow.160,167 Frumkin believed that nursemaid’s elbow could
be demonstrated radiographically by a line drawn through
the longitudinal axis of the radius that fails to bisect the
capitellar ossification center (Fig. 15-35).128 Many authors
do not advocate obtaining radiographs if the clinical pre-
sentation and response to reduction are typical.160 A
roentgenogram may be useful for ruling out actual or asso-
ciated fractures, which are rare. Ultrasonography has been
used for the diagnosis but has not been found overly
useful.140

FIGURE 15-34. Hyperpronation mechanism of a pulled elbow sustained as the child forces the elbow into a direction opposite to the
person holding him, causing the annular ligament to subluxate (arrow).
Little League Elbow
FIGURE 15-35. Nineteen-month-old girl with a pulled
elbow. The metaphysis appears laterally (A) and pos-
teriorly (B) subluxated relative to the capitellar ossifi-
cation center. The radial longitudinal axis does not
bisect the capitellum.
A B
Treatment
Reduction, in virtually all patients, is easily accomplished by
rapid supination. The preferred method of reduction is to
flex the elbow to 90° and place the thumb over the radial
head while exerting mild pressure to the radial head (Fig.
15-36). Using the other hand, the child’s forearm is then
rapidly and firmly rotated into full supination. As reduction
is achieved, a palpable, sometimes audible, click may be felt
in the region of the radial head. The child generally evinces
instantaneous relief of pain, stops crying, and begins, almost
immediately, to use the arm in a normal fashion. Some chil-
dren take a longer time, sometimes 2–3 days, to recover.
Immobilization, other than the use of a sling for comfort,
is not usually necessary unless the displacement is a repeat
occurrence. Immobilization with a sling for several days to a
week or more has been suggested to protect the ligament
from further stress and to allow it to heal. The efficacy of this
treatment has never been evaluated statistically.
FIGURE 15-36. Mechanism for reducing a pulled elbow. The thumb
is placed directly over the radial head (a) while the forearm is
supinated (b).
559
Treatment failures are rare and are usually associated with
not feeling or hearing a click. Occasionally, several attempts
at reduction are necessary before a full range of motion is
restored.
If the subluxation is irreducible (a rare situation), open
reduction is indicated.170 Although it may require dividing
the annular ligament, usually small nerve hooks are used to
grasp and pull the ligament over the radial head and allow
appropriate reduction to the neck (metaphysis) without
transection of the annular ligament. I have never encoun-
tered a case that required open reduction.
Results
Restoration of motion and function is usually instantaneous
following pronation to supination manipulation. Recur-
rence of the injury, however, is relatively common (my
daughter experienced four episodes within a 10-month
period). Salter and Zaltz,160 Snellman,165 and Quan and
Marcuse157 each noted an almost 40% incidence of recurrent
injury. However, there are no long-term studies of the con-
sequences. A long-term effect may be chronic mild subluxa-
tion. No documented cases of subsequent complete radial
head dislocation have been reported.
Little League Elbow
The overhead throwing of a baseball or other object is a rel-
atively abnormal activity for the developing arm and puts
an unusual, repetitious strain on the wrist, shoulder, and
elbow.173 The overhead serve in tennis creates a similar
motion. The elbow joint is whipped forcefully from acute
flexion into complete extension with either pronation or
supination of the forearm and ulnar flexion of the wrist.174
Throwing a curve ball puts additional traction strain on the
medial epicondyle, which is the point of attachment of the
pronator and flexor muscles of the forearm. The epiphyses
are still open in boys of the age groups involved in most
560
FIGURE 15-37. Small Panner’s lesion (arrow) of the capitellum.
organized baseball, so the epicondyle is often subjected to
the repetitive forceful pull of these muscles.182 Little league
elbow reaches its peak in boys at the age of 13–14
years.175,178,185,188,189,198,199 Other sports, such as tennis, are also
capable of causing these lesions in skeletally immature
athletes.191
This condition classically has been restricted to boys
playing organized baseball and involves the dominant elbow
almost exclusively. Girls are being diagnosed with increasing
frequency, however, with tennis and gymnastics being the
more likely evocative sports. Most of the patients are first eval-
uated between 9 and 15 years of age, when they usually com-
plain of a dull ache, effusion, and restricted elbow extension.
Singer and Roy reported seven cases of osteochondrosis of
the capitellum in five high-performance female gymnasts
between the ages of 11 and 13 years.196 They thought that
this injury was potentially an increasing problem in girls put
through exercise regimens that placed major stress on the
elbow. In gymnasts the arm often functions as a weight-
bearing extremity under considerable stress. In contrast to
the comparable lesion in young baseball players who are just
FIGURE 15-38. Panner’s lesion. MRI shows a large defect in the
capitellum.
15. Elbow
potentially beginning their careers, young female gymnasts
are basically reaching the peak of their sport when they
acquire this injury. They are also likely to be approaching
skeletal maturity. Others have reported this problem.191
Adams studied both elbows of 162 boys 9–14 years of age,
dividing them into three categories: pitchers, nonpitchers,
and a control group who had never played organized base-
ball.173 Changes involving the medial epicondylar epiphysis
and opposing articular surfaces of the capitellum and the
head of the radius in the throwing arm appeared to be
directly proportional to the amount and type of throwing.
The most striking changes were in the arms of pitchers.
Some degree of accelerated growth, separation, and frag-
mentation of the medial epicondylar epiphysis was noted in
the throwing arm of all eight pitchers in the study. Five cases
of traumatic osteochondritis of the capitellum and the head
of the radius were also found among the pitchers. Because
these conditions invariably develop only in the pitching
(throwing) arms, the major cause undoubtedly is the exces-
sive, repetitious microtrauma.
Studies of the mechanics of the pitching motion using
accelerometers showed there was no difference in the pat-
terns of muscle activity during acceleration with different
delivery styles, even when trying to throw breaking pitches.
The main factors causing an elbow injury were not the
method of delivery but, rather, the amount of throwing and
the force with which the ball was thrown.174,184 The same
applies to repetitive use in the overhand tennis serve and
various impact and swinging routines in gymnastics.
Many coaches and managers argue that most sore arms
are due to incorrect throwing motions or failure to warm
up properly, which is often true in adults. In youngsters,
however, regardless of the throwing motion, the physes are
continually subjected to the pull of the attached muscles.
Structurally and histologically the epicondylar physes do not
seem to be as specifically adapted to excessive, forceful, trac-
tion stress as is the tibial tuberosity. The opposing articular
surfaces of the joint are also subjected to repetitive trauma
from excessive throwing. Trauma of this kind may eventually
cause osteochondritic changes and chronic widening of the
physes (similar to that reported in the wrist and shoulder in
response to repetitive athletic activity).
In a survey of 120 pitchers aged 11 and 12 years, 20% were
found to have elbow symptoms, 10% had flexion contrac-
tures, and 23% had radiographic changes related to traction
stresses on the medial side of the elbow.188 Five percent had
more serious lateral compression findings related to either
the radial head or the capitellum. However, none of the boys
with lateral joint compartment problems had significant
symptoms. Radiographic changes in the medial epicondyle
include fragmentation, irregularity, mild separation,
enlargement or beaking, and sclerosis (Figs. 15-37, 15-38).
These are all various stages of the same reactive process.
Capitellum
The pathogenesis of osteochondral lesions of the elbow still
is not completely understood. The sex and age of the patient
and the location and laterality of the lesion suggest repeti-
tive trauma as the most probable cause. Underlying this
rationale are the possibilities of epiphyseal cartilage failing
Little League Elbow
FIGURE 15-39. Capitellar defect in a 12-year-old baseball pitcher.
to ossify, chronic vascular deficiencies, or defective repair
mechanisms.175–177,179–181,185–187,190,192–197,200 This involvement of
the capitellum is usually referred to as Panner’s disease. In
some cases congenital deformities predispose to the devel-
opment of these lesions.
The capitellum of the humerus is most frequently involved
(Fig. 15-39), and the radial head less frequently. The earliest
radiologically evident lesion is usually a minimal radiolu-
cency of the convexity of the capitellar epiphyseal ossifica-
tion center adjacent to the radial articulation. Tomography
may show the defect, which eventually becomes apparent
on plain radiographs. Magnetic resonance imaging (MRI) is
also useful for demonstrating the lesion, often before it
becomes radiologically evident. Arthrography may show the
articular cartilage to be normal or irregular, and it is helpful
for determining the mobility of a fragment and the indica-
tions for surgery. The edges of the fossa may be ragged and
are sometimes sclerotic. If the chondro-osseous fragment is
significantly displaced, it may become free within the joint,
leading to chronic damage (Fig. 15-40).
Mitsunaga et al. divided the lesions into type I (in which
the fragments were still attached) and type II (in which the
loosened fragments were lying free and floating within the
joint).190 Residual limitations were highest in the type II
lesions that had been treated nonsurgically or surgically after
a long delay. The best surgical results occurred with excision
of the osteochondral defect or loose body or bodies along
with drilling or curettage of the subchondral bone.
The prognosis for healing and recovery is good once any
loose fragments have been removed. If all loose bodies are
not removed, overgrowth, secondary reactive sclerosis, and
cystic changes may be evident in the condyle, and normal
motion may be compromised (Fig. 15-41). Long-term follow-
up (averaging 23 years) showed impaired motion and pain
on effort. More than half of the patients had degenerative
osteoarthritis in the elbow.
Epicondyle
Epicondylar trauma often occurs without roentgenographi-
cally apparent separation. Chronic traction may lead to
561
increased underlying bone formation, effectively enlarging
the medial epicondyle. It is essentially the self-induced focal
equivalent of chondrodiatasis limb lengthening. Accord-
ingly, the diagnosis must be made on clinical grounds. Radi-
ographic evidence may occur later (Fig. 15-42).
Demonstrable epicondylar separation may be associated
with capitellar fragmentation of the ossification center or, in
cases of violent motion, dislocation of the elbow joint. Soft
tissue injury may be evident. Roentgenograms of the con-
tralateral elbow may be helpful for diagnosing minimal sep-
aration, but beware of asymmetry due to the excessive use of
the involved arm. Such minimal epicondylar separation may
heal by fibrous union. Consequently, roentgenographically
demonstrable callus is not always encountered. Sclerosis of
the epicondylar center may also occur (Fig. 15-43). Clinical
pain (on examination) may indicate a need to intervene.
Initial treatment should be cessation of the evocative activ-
ity. Closed (percutaneous) or open fixation is indicated in
rare cases.
Treatment
Treatment for these various conditions is primarily preventive.
The following steps are recommended: (1) Alert parents,
coaches, administrators, and family physicians that these
conditions exist and that the presenting symptoms of sore-
ness or pain in this age group indicate “epiphysitis.” More-
over, it should not be treated as muscle soreness or “pointer.”
(2) Encourage youngsters to report elbow pain or soreness
immediately and reassure them that doing so does not always
mean they can no longer participate in the sport. (3)
Discourage youngsters from excessive practice, as such
excessive activity invites trouble rather than perfection. (4)
Abolish evocative activities, such as curve ball throwing
for the younger age groups, as it not only places additional
strain on the elbow but encourages excessive practice to
perfect it.
FIGURE 15-40. Loose body in the elbow joint of a teenage high-
performance throwing athlete.
562 15. Elbow

A B
FIGURE 15-41. (A) Some fragmentation may remain “separate” but reasonably in place, yet cause pain by micromotion. (B) Postoperative
appearance following fragment removal.

FIGURE 15-42. Chronic medial epicondylitis in a young gymnast. FIGURE 15-43. Sclerotic appearance of a portion the medial epi-
Subperiosteal new bone formation (arrow) has occurred owing to condyle in an adolescent baseball pitcher. An irregularity is also
the repetitive application of stress, loosening the chondro-osseous present in the trochlear ossification center.
interface.
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112. Amir D, Frankl U, Pogrund H. Pulled elbow and hypermobil-
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114. Beagel PM. “Slipped elbow” in children. Maine Med Assoc
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115. Bobrow RS. Childhood radial head subluxation: physician
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116. Bourquet J. Memoire sur les luxations dites incompletes de
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117. Boyette BP, Ahoskie NC, London AH Jr. Subluxation of the
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119. Broadhurst RW, Buhr AJ. The pulled elbow. BMJ 1959;1:1018.
120. Caldwell CE. Subluxation of the radial head by elongation.
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122. Corrigan A. The pulled elbow. Med J Aust 1965;2:187–189.
123. Costigan PG. Subluxation of the annular ligament at the prox-
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124. Cushing HW. Subluxation of the radial head in children.
Boston Med Surg J 1886;114:77–78.
125. David ML. Radial head subluxation. Am Fam Physician
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126. Davis JH. Subluxation of the radial head in children (nurse-
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130. Gatrell CB. Radiologic findings in radial head subluxation. Am
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132. Griffin ME. Subluxation of the head of the radius in young
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141. Lamont AC, Dias JJ. Ultrasonic diagnosis of dislocation of
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144. Matles AL, Eliopoulous K. Internal derangement of the elbow
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146. McVeagh TC. The slipped elbow in young children. Calif Med
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148. Mehta L. Subluxation of radial head in children with reference
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149. Meyer RJ, Roelofs HA, Bluestone J. Accidental injury to the
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the normal elbow. Injury 1989;20:365–367.
152. Miller TO, Insall J. Radial head subluxation in adolescence.
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153. Moore EM. Subluxation of the radius from extension in young
children. Trans NY Med Assoc 1886;3:18–19.
154. Newman J. “Nursemaid’s elbow” in infants six months and
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155. Piersol GA. Human Anatomy, 9th ed. Philadelphia: Lippincott,
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156. Piroth P, Gharib M. Die traumatische subluxation des radius-
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158. Ryan JR. The relationship of the radial head to radial neck
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159. Sachetti A, Ramoska EE, Glascow C. Non-classic history in chil-
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160. Salter R, Zaltz C. Anatomic investigations of the mechanism of
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16
Radius and Ulna
Engraving of a complication of a distal radial physeal fracture
leading to premature growth arrest and radial shortening. (From
Poland J. Traumatic Separation of the Epiphysis. London: Smith,
Elder, 1898)
he development of secondary ossification of the prox-
T imal ulna may make interpretation of injury difficult,
as variations of normal radiographic findings are fre-
quently misinterpreted as a fracture (especially an avulsion
fracture).2 Consequently, the characteristics and variations of
secondary ossification of the olecranon process must be
learned so false-positive diagnoses are avoided.17
There are two functional ulnar prominences, the olecra-
non and the coronoid, with epiphyseal and articular carti-
lage connecting them (Fig. 16-1). It is important to realize
that an epiphysis and physis are present under the articular
cartilage, even if some of the epiphyseal region extending
toward the coronoid process does not develop a distinct sec-
ondary ossification center. The secondary ossification
process is essentially confined to the olecranon segment,
although a small anatomically separate ossification center,
may develop infrequently in the coronoid. The distal portion
of the proximal ulna and the coronoid process are formed
by the ulnar metaphysis, and the proximal portion is formed
by the olecranon epiphysis (Fig. 16-1). The secondary ossifi-
cation center does not usually appear in the olecranon until
the ninth to tenth year (Figs. 16-1 to 16-3). This secondary
ossification center is usually unifocal, although it is bipartite
or multipartite in some children (Fig. 16-4). When bipartite,
the accessory center is usually located near the tip of the
olecranon.10,17 A variation, the patella cubitus, is defined
radiographically as a sesamoid bone in the triceps tendon.
The accessory bones, however, are not anatomically separate
from the rest of the olecranon. It is likely that a patella
cubitus represents partial avulsion of the epiphysis as it is
ossifying, not unlike the Osgood-Schlatter lesion in the prox-
imal tibia. Pain may indicate an occult chondro-osseous
injury, similar to the painful accessory navicular (see
Chapters 6, 24). These osseous variations often must be dis-
tinguished from fractures. A bone scan may be useful for
such differentiation, with a positive scan strongly indicative
of acute injury.
Closure of the ulnar physis occurs from the juxtaarticular
side outward, so when a boy is about 13 years old the inner
portion of the olecranon physis is closed, and the outer
(most external) portion may still be evident as a radiolucent
line. The normal open or fusing physis of the olecranon has
a well-defined sclerotic margin, which is not present with an
acute fracture. Girls experience similar closure patterns, but
earlier than boys, usually between 11 and 12 years.
An olecranon bursa is not usually present in children
younger than 6–7 years of age. With increasing use of the
arm and progressive ossification, this gliding structure pro-
gressively develops.4 Formation of the bursa during late
childhood explains the relatively low incidence of olecranon
bursitis consequent to trauma in children. An older child
may injure the bursa by a direct blow, leading to acute
swelling or, less likely, to chronic inflammation.
The anatomy of the proximal radius also affects injury pat-
terns.10,22 The discoid-shaped head of the radius is always of
greater diameter than the neck (even during fetal develop-
ment). The head and neck of the radius are well defined,
the head is larger than the neck, and a radial notch appears
in the ulna. Although not as distinct during the fetal stage,
the radial head, even during the first year, shows the same
eccentric concavity and defined anterolateral rim as in the
adult.10
The plane of the articular surface is tilted relative to the
longitudinal axis of the radius. This tilt varies depending on
the rotation. The exact degree of tilting and shifting may be
measured only on films obtained at proper angles to the
plane of angulation (Fig. 16-5). The changing tilt affects
the up-and-down sliding motion of the annular ligament.
Because one of the problems of proximal radial fractures is
increased angulation, during reduction one should remem-
ber that there is normally a mild tilt. The concavity within
the proximal radius that articulates with the capitellum may
567
568 16. Radius and Ulna

B
FIGURE 16-1. (A) Section of the proximal ulna from a 2-year-old
girl. Epiphyseal cartilage is present from the olecranon to the coro-
noid process. (B) Histologic section. There is a continuous growth
plate all along this cartilage.

B
FIGURE 16-2. (A) Sagittal section of the proximal ulna from a 5-
year-old child. The olecranon ossification center is well estab-
lished. (B) Radiograph of the specimen.
be eccentric (Fig. 16-5), which affects rotational dynamics
and the tautness within the annular ligament.
The epiphysis of the radial head is covered extensively by
articular cartilage. It is present not only over the end of the
radius but circumferentially around the sides to allow
radioulnar movement. There is no perichondrium on this
particular epiphysis. The epiphyseal blood supply has a short
intraarticular course along the metaphysis, which is sur-
rounded by the annular ligament. This situation creates a
susceptible intracapsular epiphyseal blood supply similar to
that of the capital femoral epiphysis (Fig. 16-6). The blood
supply may be damaged by epiphyseal or metaphyseal
separation. Because the usual level of injury through the
metaphysis is near the entry of the vessels, ischemic necro-
sis must be considered a potential complication. However,
there is often hyperemia of the fracture site, causing
overgrowth of the radial head, rather than significant growth
limitation.
The proximal radial epiphysis may not ossify until a child
is 5–7 years old and usually unites between 12 and 15 years
of age. It generally ossifies symmetrically. Because of the epi-
physeal tilt, however, ossification may be asymmetric and may
resemble a triangle rather than an ellipse in certain posi-
tions.10,11,16 An angular shape may also indicate a problem of FIGURE 16-3. Slab sections of the ulna and radius of a 13-year-old
abnormal radiohumeral joint stress, such as a radioulnar syn- boy. The olecranon ossification center is well developed. Note the
ostosis or Panner’s disease. Because these conditions are not coronoid process (solid arrow) is part of the proximal radioulnar
diagnosed in many children until an episode of trauma, the joint (open arrow).
Radius and Ulna
FIGURE 16-4. Normal variations of the formation of
the olecranon secondary ossification center. They
could easily be interpreted as a fracture during the
evaluation of acute trauma.
physician should be aware of these potential problems of dif-
ferential diagnosis as related to normal anatomic develop-
ment and maturation.
The upper end of the ulna articulates with the trochlea of
the distal humerus and provides primary flexion-extension
of the elbow. It also articulates with the head of the radius
through an extension of the joint proximally on both the
radius and the ulna (Fig. 16-7). The proximal and distal
radioulnar joints tend to be clinically ignored articulations,
although they are especially important in the Monteggia
injury, pulled elbow, and the Galeazzi injury.
FIGURE 16-5. Sagittal section through the radial head and bicipital
tuberosity. The radial head concavity is eccentric and slightly tilted
relative to the longitudinal axis of the radial shaft.
569
The radial head is tightly constrained by the capitellar and
ulnar articular surfaces. This anatomic construction permits
rotation and flexion-extension while creating intrinsic sta-
bility. Both articular relations are disrupted during a Mon-
teggia injury. The annular ligament holds the radial
metaphysis against the shaft of the ulna and the ulnar artic-
ular extension. The annular ligament further restrains the
radioulnar joint. This ligament has some laxity, which allows
displacement in radial head subluxation and may permit dis-
placement of the radial head without significant tearing,
especially in younger children. The ligament may be torn or
displaced in Monteggia injuries. A synovial recess usually
extends under the ligament.
FIGURE 16-6. Intraarticular blood supply of the proximal radius.
Several small vessels (arrow) extend transversely and longitudi-
nally under the annular ligament, which has been pulled down.
570 16. Radius and Ulna

ficiently to allow adequate roentgenographic evaluation.3 By

the time a child is 5 years of age, the tuberosity begins to
have enough prominence to be visible roentgenographically
(Fig. 16-8). Prior to this age, forearm fractures are infre-
quent and are generally greenstick, with the intact cortex
and the thick periosteal sleeve maintaining longitudinal con-
tinuity and minimizing any rotational misalignment.
The sagittal and coronal cross-sectional diameters of the
radius and ulna change with age and anatomic level. Proxi-
mally, both have a circular appearance, although for much
of the diaphysis the two bones have a cam (pear) shape. As
such, rotational deformities often are detected by the dif-
ferences in the widths of the apposed fragments.
The radius and ulna are bound together firmly by the
interosseous membrane, which provides a hinge mechanism
A for integrated rotatory movements.5,8,9 This interosseous lig-
ament attaches along the tip of the “cam” of both the radius
and the ulna. Correction of the rotational deformity is
directed at restoring the interosseous ligament mechanics,
which are important in pronation and supination. Special-
ized ligaments are present at each end. The annular liga-
ment holds the proximal radioulnar joint together. The
distal radioulnar and radiocarpal joints are connected by the

B
FIGURE 16-7. (A) Proximal and distal ulna showing the articular
surfaces (*) for the radius. These joints are important and must be
considered during the evaluation and treatment of wrist and elbow
trauma. These joints remain throughout skeletal maturation, and
the correct structural relationships are necessary for forearm rota-
tion. (B) Histology of the proximal radioulnar relations.

The proximal radioulnar joint is stable in supination

because (1) the radial head is not circular but slightly oval,
and with the forearm in supination the greatest diameter of
the head comes in contact with the proximal radioulnar
joint; (2) the margin of the radial head is not the same width
around the head, so in full supination the broadest portion
of the margin of the radial head comes in contact with the
proximal notch of the ulna and gives the broadest articular
contact; (3) in full supination the interosseous membrane is
most taut; (4) the annular ligament is reinforced by the ante-
rior and posterior components of the radial collateral liga-
ments; and (5) in full supination the anterior, thicker fibers
of the quadrate ligament of Denuce stabilize the radial head
FIGURE 16-8. Appearance of a specimen from a 6-year-old in
more strongly into the proximal radioulnar joint.18,19
supination (A), neutral position (B), and pronation (C). In supina-
The biceps tendon inserts onto the radial tuberosity. This tion the bicipital tuberosity (probe) faces anteriorly, whereas in
osseous prominence becomes progressively larger as the pronation it rotates posteriorly. Again, note that in supination the
child grows. Evans stressed its potential use for assessing the radial “flare” is prominent but that it decreases in pronation. This
relative rotation of the proximal fragments in forearm frac- lessens the mechanical block to proximal migration of the annular
tures.7 Its usefulness is contingent on its being developed suf- ligament.
Radius and Ulna
dorsal and palmar radiocarpal ligaments and by a meniscus
(triangular fibrocartilaginous complex, or TFCC) bridging
the distal radius to the ulnar styloid. The TFCC effectively
separates portions of the interarticulations. The TFCC
should be intact in the normal child, although anatomic vari-
ations may occur.
Throughout the diaphyses, the radius and ulna exhibit
gentle curves (Fig. 16-8). The radiologist and orthopaedist
should be familiar with these patterns, as they allow detec-
tion of mild to excessive bowing (plastic deformation)
without evident fracture. Such a pattern of deformation,
rather than a complete fracture, is characteristic of these
bones in infants and young children and should alert the
physician to be aware of other problems, such as the Mon-
teggia injury.
When these gentle curve patterns are present along the
shafts of both the radius and the ulna, basic forearm rota-
tion (supination-pronation) follows a relatively simple
conical pattern when analyzed mathematically.3 The essen-
tial feature is paired joint motion at both the proximal and
distal radioulnar joints. The mechanical axis of the forearm
is a line connecting the rotational center of the proximal
radius and the similar rotational center of the distal ulna.
This line is the stable side of a right triangle, of which the
hypotenuse is the radial longitudinal axis and the rotating
leg is the transverse axis of the distal radius and triangular
ligament. Rotation of the radius about the ulna thus nor-
mally generates a half-cone (Fig. 16-9).
If the effective mechanical rotational axis is disrupted, as
with angulation of the radius, ulna, or both following injury,
paired joint motion is variably disrupted, and a simple rota-
tional cone becomes mechanically or geometrically impossi-
ble. Radial angular deformity is more significant, as this bone
essentially generates the rotational half-cone. Angular defor-
FIGURE 16-9. Rotation of the radius on the ulna. The mechanical
triangle of rotation (ABC) has an axis from the center of the radial
head (A) to the ulnar styloid (C). The radial styloid (B) rotates
around to a pronated position (B¢), subtending a semicircular
conical base (stippling).
571
mity introduces nonaxial torsion of the segment distal to the
fracture.
When there is a fracture of one or both of the forearm
bones, the direction and extension of displacement of the
fragments are contingent on the initial deforming force, the
level of fracture, and the degree of muscle action. During
reduction and immobilization of these fractures, the origin,
insertion, and action of the various forearm muscles must be
considered. The biceps and supinator muscles insert into the
proximal third of the radius and are powerful supinators of
the forearm. The pronator teres inserts into the middle third
of the radius, and the pronator quadratus is located on the
anterior aspect of the lower forearm and inserts into the
distal third of the radius. The brachioradialis originates from
the lower end of the humerus and inserts on the lateral
surface of the distal radius immediately above the styloid
process. Depending on the position of the arm, this muscle
assists in pronation or supination, bringing it from either
position to neutral. The extensors of the wrist and digits have
a less deforming influence on forearm fractures than does
the brachioradialis. The extensors may also act as a dynamic
posterior splint when under tension. The extensor and
abductors of the thumb are synergistic with the brachiora-
dialis and tend to pull the distal fragment of the radius prox-
imally. The flexor muscles of the forearm usually pull the
distal fragments anteriorly and produce dorsal bowing of the
radius and ulna.
With fractures involving the upper third of the forearm
above the insertion of the pronator teres, the proximal frag-
ment is often supinated and flexed because of the relatively
unopposed action of the biceps and supinator. The distal
fragment is pronated by the action of the pronator teres and
quadratus muscles. Therefore to align the fracture properly,
during reduction and treatment the distal fragment usually
should be supinated.
For fractures of the middle third (i.e., below the insertion
of the pronator teres), the proximal fragment of the radius
is held in neutral rotation by the action of the biceps. The
distal fragment is pronated and drawn toward the ulna by
the pronator quadratus. When achieving anatomic reduc-
tion, the distal fragment is brought into neutral rotation.
Failure to correct excessive angular deformities of childhood
fractures may limit normal rotational mechanics during
adulthood.
The distal radioulnar joint is a double-pivot joint that
unites the distal ulnar epiphysis, ulnar notch of the radius,
and distal radial epiphysis by the TFCC.6,15,21 The distal radius
develops a biconcave contour to accommodate the scaphoid
and lunate (Fig. 16-10). However, as the secondary ossifica-
tion center enlarges, it rarely duplicates the undulating artic-
ular contour. The distal ulnar articular cartilage surface is
completely covered by this disc, so normally the ulna never
articulates directly with the proximal carpal row.20 The distal
ulnar surface glides against the articular disc of triangular
cartilage.1 This triangular cartilage is attached by a thick apex
to the base of the ulnar styloid (Fig. 16-11). The thinner base
of the triangular ligament is attached to the leading edge of
the radius just proximal to the carpal articular surface.
The dorsal portion of the triangular fibrocartilage and the
dorsal radiocarpal ligament tend to be taut in pronation.
The slight dorsal displacement in pronation, with the ulnar
572 16. Radius and Ulna

B
FIGURE 16-10. Histologic specimen (A) and radiograph (B) showing the biconcave shape of the distal radius to accommodate the
scaphoid and lunate.

FIGURE 16-11. Slab sections showing sequential development of the distal radius and ulna. (A) Neonate. (B) One year. (C) Eight years.
(D) Twelve years.
Radius and Ulna 573

styloid relatively fixed, explains the tendency of the fracture
to propogate through the ulnar styloid, even in children in
whom the entity may not be recognized because the area is
completely cartilaginous. As this area ossifies, radiologic
nonunion often becomes evident. Permanent radiologic
“nonunion” is much less frequent.
The distal radial ossification center appears at 6–12
months. In contrast, the distal ulna does not initially ossify
until 5 years (Figs. 16-11, 16-12). The radial and ulnar
centers then progressively expand. The radial center is ini-
tially spherical but becomes triangular.13 The distal radial
and ulnar physes are the major contributors to elongation of
these two bones.13,14 Physiologic epiphysiodesis occurs at 14
years in girls and 16 years in boys. The metaphyseal cortex
changes significantly during development, as does the thick-
ness of the hypertrophic zone of the physis. Both factors
undoubtedly play a role in the age-related changing patterns
of distal radial injury.
The radial styloid is one of the last areas to ossify and does
so by the extension of the secondary center. Accessory bones

FIGURE 16-12. Sequential histologic development of the distal radius and ulna. (A) One year. (B) Seven years. (C) Ulna minus variant.
(D) Thirteen years. (E) Fourteen years. The biconcave radial articular contour is readily evident.
574
FIGURE 16-13. Radiologic variant of the distal radioulnar joint.
have not been reported in this styloid. A fracture is more
likely if a lucency is seen in this area. The ulnar styloid is the
last region to ossify. A cartilaginous fracture of the ulnar
styloid may accompany a distal radial fracture and may not
become evident until a radiographically separate secondary
center eventually appears in the styloid. This is not a varia-
tion of ossification. A truly separate (accessory) ossification
center for the ulnar styloid is rare.
Variations of the ulnar side of the distal radial metaphysis
may occur and have the appearance of a peripheral cystic
“defect” (Fig. 16-13). They should be considered a normal
radiologic variant. Irregular development of the physis in
this area may lead to a Madelung’s deformity, which should
be considered comparable to Blount’s disease in young
children.
Before and during adolescence many children show lon-
gitudinal osseous striations in the physis between the me-
taphysis and the distal epiphyseal ossification centers, both
FIGURE 16-14. (A) Transphyseal longitudinal ossification pattern (arrow) in a 10-year-old child detected during evaluation of a me-
taphyseal fracture. (B) Longitudinal striation accompanied by linear striation within the endosteal metaphyseal bone.
16. Radius and Ulna
radial and ulnar (Fig. 16-14).12 These striations are normal
calcifications or ossifications in the portions of cartilage con-
tiguous to the channels of the transepiphyseal arteries. They
probably represent areas of microtrauma that lead to
minimal or incomplete physeal bridge formation but do not
lead to restriction of growth. The hydraulic pressures gen-
erated by continued growth probably constantly microfrac-
ture these bridges. In some instances a sclerotic line is
evident in the marrow following the orientation of the lon-
gitudinal axis. This may be considered, conceptually, as
microcallatosis.
Fracture Incidence
Forearm fractures are common in children. Problems of
treatment vary considerably with the age of the patient and
the level and displacement of the fracture. Generally, there
is less comminution, union is more rapid, and residual defor-
mities tend to be corrected by subsequent growth, compared
with similar injuries in an adult.23–39
From the standpoint of the age relation to injury, the
average ages of children with radioulnar fractures are 6.1
years for upper third fractures, 6.7 years for middle third, 6.9
years for lower third, 8.5 years for lower sixth, and 9.8 years
for distal epiphyseal fractures.32 Gandhi and colleagues
reported that only 20% of distal fractures were in children
under 5 years of age.32 The susceptibility of the lower radial
epiphysis to injury in children older than 10 years may be
related to the increased growth rate that occurs about that
time and the consequent microscopic changes at the level of
the physis.23 Data from our skeletal development laboratory
suggest there are changes in physeal thickness, the zone of
Ranvier, and metaphyseal cortical density during these
various age-susceptibility periods.13
One series of 375 forearm fractures included 23 fractures
of the radial head and neck, 8 fractures of the upper third,
28 fractures of the middle third, 54 fractures of the lowest
third, 195 fractures of the distal metaphysis, and 67 jux-
taepiphyseal injuries.37 Gandhi and colleagues studied more
than 1700 fractures of the forearm in children under 12
years of age.32 The incidence of the fractures (excluding
Olecranon Fractures
those of the olecranon and the head and neck of the radius)
was as follows: 0.4% Monteggia’s fracture dislocation; 1.0%
fracture of the upper third; 2.6% complete fracture in the
middle third involving both bones; 0.9% complete fracture
of the middle third of both bones; 42.0% greenstick fracture
in the lower third of one bone; 24.6% greenstick fracture of
the lower third of both bones, 5.2% complete fracture of the
lower third of the radius with or without complete or green-
stick fracture of the lower third of the ulna, and 14% involv-
ing a fracture separation of the lower radial epiphysis.
Most fractures of the radius and ulna in children are either
distal compression fractures or undisplaced, angulated
greenstick fractures. They present few treatment problems.
However, there tends to be complacency about reducing
some deformities. Significant problems may occur if any
bowing (plastic deformation) remains, even in the undis-
placed greenstick fracture. The goal of treatment of any
radial or ulnar fracture should be restoration of full function
as soon as possible, with prevention of loss of supination and
pronation.
Rotational deformities should not exist at any forearm
fracture site after manipulative reduction. Loss of pronation
of up to 30° may be hidden by abduction of the shoulder. In
contrast, loss of supination is not as easy to conceal.
Some authors have stated that angular deformity of up to
35° remodels in fractures of the distal third, but that more
than 15° of residual angulation for more proximal fractures
probably leads to diminished function. Because the extent
of correction of malunion depends on further longitudinal
bone growth, it is influenced also by the distance of the frac-
ture from the metaphysis. The closer the fracture is to the
metaphysis (especially the distal one), the greater the poten-
tial for spontaneous correction. The nearer the fracture is
to the midshaft, the more likely there will be a residual problem.
Therefore angulation in the midshaft of the bone should be accepted
with caution.
The usual outcome of forearm fractures in children
appears to be complete functional recovery in most patients
when manipulative closed anatomic reduction and immobi-
lization are used. However, in one series, fractures of the
upper third showed unsatisfactory results in 50% of the
patients, with the major problem being loss of supination and
pronation, although the children did not complain of any sig-
nificant functional disability.37 By the end of 4 years, only nine
children had any problems when judged by the same stan-
dards. Thomas and associates stressed that the patients with
a poorer outcome were usually treated by open reduction
and fixation.37 Among 67 patients with juxtaphyseal fractures,
5 developed a Madelung-type deformity that was probably
due to an unsuspected or undetected physeal injury.
Some authors believe that open reduction of radioulnar
fractures is unnecessary.24–26 Although open reduction and
internal fixation are not usually indicated, they should not
be discounted totally as treatment modalities when deemed nec-
essary. With the improved methods of internal fixation and
anesthesia, there is an increasing tendency to use closed and
open reduction for young children and adolescents—treat-
ments that are extremely successful for forearm fractures in
adults.
Refracture at the same site after an apparently solid union
may occur with forearm fractures in children.25 Bosworth
encountered six cases in a study of 54 fractures.27 In another
575
series, refractures occurred in only nine patients, represent-
ing 0.5%, at intervals varying from 2 to 6 months from the
time of presumed radiologic union.32
Olecranon Fractures
Fractures involving the olecranon physis are infrequent in
children.41–47,51,53,55–62,64,65 Mahlahn and Fahey reported only
19 such patients in a series of 300 elbow fractures in chil-
dren.58 Newell reviewed 40 cases in children ranging in age
from 15 months to 11 years and found that olecranon physeal
fractures usually occurred around the age of 5 years.59
Mahlahn and Fahey found the average age was 8.5 years.58
Papavasiliou et al. reviewed 58 fractures of the olecranon
in children; 43 were associated with other injuries to the
elbow, and 15 were isolated fractures of the olecranon.60
They particularly studied the latter 15 and described a clas-
sification that basically subdivided them into group A (iso-
lated intraarticular fractures of the olecranon) and group B
(isolated extraarticular fractures of the olecranon, or a
greenstick fracture). The latter injuries were generally me-
taphyseal and distal to the coronoid process. The authors did
note a case of pseudarthrosis developing approximately 1
year after injury. Recommended open reduction had been
refused by the parents in this case.
Suprock and Lubahn reported a case of olecranon frac-
ture through the physis accompanying a radial shaft fracture,
essentially a reverse of a Monteggia lesion.62 It required open
reduction of the olecranon fracture for stability.
Classification
The olecranon physeal fracture is often undisplaced or
incomplete. Usually the fracture is approximately perpen-
dicular to the longitudinal axis of the ulna, probably because
of a locking into the olecranon fossa. The longitudinal split
fracture, which appears in approximately 10% of adult cases,
is atypical in children.
These fractures usually occur through the metaphyseal
bone adjacent to the olecranon physis (Fig. 16-15). Occa-
sionally, there is a fracture through the chondro-osseous
FIGURE 16-15. Fracture patterns in the proximal ulna. (A) Fracture
through the entire metaphysis. (B) Fracture into the joint. (C) Coro-
noid fracture.
576
FIGURE 16-16. Patterns of fracture within the metaphysis, most likely due to valgus force rather than avulsion. (A) Mild displacement
with comminution (arrows). (B) Greenstick injury (solid arrows) with comminution of cortex (open arrow).
junction in a child (under the age of 10 years) before the
olecranon secondary ossification center appears. Often the
fracture is incomplete and does not encroach on the joint
surface, as the fracture has not propagated through the
cartilage (Fig. 16-16). There may be minimal widening
of the space between the olecranon ossification center and
the metaphysis. Follow-up radiographs may reveal the true
nature of the injury as an undisplaced physeal fracture
(Fig. 16-17).
A sleeve fracture may occur, separating the unossified (car-
tilaginous) proximal ulnar epiphysis from the ossification
center. A fracture may also occur through the ossification
center. These patterns are rare.
FIGURE 16-17. Minimally displaced olecranon fracture. Periosteal
continuity probably prevented further displacement and is making
new bone (arrow).
16. Radius and Ulna
Pathomechanics
The structure of the olecranon in a child differs significantly
from that in an adult. The bone is more trabecular, and
fractures may be difficult to identify. Articular cartilage and
epiphyseal cartilage layers are thick and permit osteo-
chondral fractures. The transversely oriented subchondral
bone of the metaphysis tends to direct fractures into the
metaphysis rather than the physis. In one series, 20 of 33 chil-
dren in whom the olecranon fracture was the only injury
had a direct blow to the elbow from a fall, rather than a fall
on the hand while the elbow was hyperextended.59
If the elbow is extended, the olecranon is locked in the
olecranon fossa of the distal humerus. When a varus or
valgus force is then applied (Fig. 16-18), the olecranon levers
against the fossa margins, and the deforming strain is
absorbed by the metaphyseal region located at the level of
the joint. With a valgus force, the radial head or medial epi-
condyle may also fracture. Always look for these potential
associated injuries.
Once the fracture occurs through the metaphysis, the con-
tractile force of the triceps may further displace the frag-
ment, pulling it proximally (Fig. 16-19). A simple evocative
test of stability is to obtain lateral films in extension and
flexion (Fig. 16-20). Widening of any gap mandates open
reduction and fixation.
The metaphyseal fragment may be small and the equiva-
lent of a patellar sleeve fracture. The displaced fragment may
become locked within the elbow joint (Fig. 16-21).
Diagnosis
In most cases the diagnosis is readily evident on the lateral
film. However, if the fragments are undisplaced or the frac-
ture is through the physeal-metaphyseal interface of an
epiphysis with no secondary ossification center, the diagno-
sis is sometimes empirical or based on careful examination.
Palpation of the fracture gap may not be easy because of
soft tissue swelling.
Ossification variations may also affect the interpretation of
fractures.40,42,48,49,52,54,66 Burge and Benson reported a case of
Olecranon Fractures
FIGURE 16-18. (A) Common fracture mechanism. (B, C) Roentgenograms showing how the olecranon pivots (arrows) in the humeral
fossa in varus (B) and valgus (C) deformations.
bilateral congenital pseudarthrosis of the olecranon, which
must be distinguished from fracture of the olecranon and
patella cubiti.42 Habbe reported a fracture through a patella
cubiti.49 Whether such lesions are a congenital anomaly, an
ununited epiphysis of the olecranon, or a posttraumatic
process is still subject to debate.66 Most of the patients
described in the literature are male. Because boys are more
apt to be involved in injuries and are more likely to have radi-
ologic studies of the elbow, the apparent difference in sex
predisposition may not be significant.
The absence of soft tissue swelling and joint effusion is
usually incompatible with the presence of a fracture of
the olecranon, especially one extending directly into the
joint space. Occasionally, however, difficulty arises when
a patient has a positive fat pad sign and the physeal
line extends into the joint space. A comparison radiograph
may be indicated in these patients. Occasionally fractures
of the proximal tip of the olecranon are not associated with
FIGURE 16-19. (A) Fracture of proximal ulna. The fragment is a portion of the metaphysis, not the secondary ossification center. (B)
Displaced fracture pattern.
577
a joint effusion, as the joint capsule and synovial tissue do
not always extend to the tip. The proximal part of the olec-
ranon and the radial neck are the two areas of the elbow in
which a fracture may occur without displacement of the fat
pads.
There may be a normally wide space between the early
ossification of the epiphysis and the adjacent metaphysis.
This separation is larger than 5 mm in some patients and
should not be mistaken for an epiphyseal separation. Figures
16-19 and 16-20 show metaphyseal avulsion fractures of the
olecranon. One can assume that the olecranon epiphysis,
although not yet ossified, is displaced proximally along with
the avulsed metaphysis. This type of injury, although often
referred to as a chip fracture, is far more serious and a great
deal more complicated. This fracture really represents sepa-
ration of a nonossified (radiolucent) epiphysis of the olec-
ranon with an associated metaphyseal avulsion. With such
fractures, the separation occurs because of the pull of the
578
A B
FIGURE 16-20. (A) Seemingly minimally displaced olecranon fracture. (B) Flexion (a simple stress test) shows the fracture to be at risk
for further displacement. This fracture needs to be treated with tension band wiring.
attached triceps muscle (as when the elbow is suddenly
flexed against the opposing triceps muscle).
Treatment
Closed reduction should be the initial method of treatment,
as many olecranon fractures are greenstick fractures with
some cortical and epiphyseal integrity (especially if the frac-
ture is acquired by locking the olecranon during a varus or
valgus stress). The fracture usually occurs in extension with
this pathomechanism. The greenstick deformity may be
hyperextended relative to the rest of the ulna and should
be pushed back with the elbow flexed. The elbow should
be splinted and a repeat roentgenogram obtained to be sure
the fracture fragments are still in continuity.
Although immobilization in a cast with the elbow at
approximately 90° for 3–4 weeks is recommended, the results
indicate that in the usual undisplaced, incomplete fracture
a period of 3 weeks in a sling may be the only treatment
necessary.
FIGURE 16-21. Intraarticular displacement (arrow) of the olecranon
epiphysis.
16. Radius and Ulna
The displaced olecranon fracture during childhood is best
treated by open reduction with internal fixation of the frac-
ture, repair of any triceps aponeurotic tear, and external
immobilization (Figs. 16-22 to 16-24). Methods of fixation
include transfixing the epiphysis to the metaphysis with
smooth pins and annular wire or suture fixation. Pins should
be small and are removed when healing is evident (at least
4–6 weeks, as this is a slowly growing physeal unit, and new
formation of metaphyseal bone on the proximal side of
the fracture is limited). Annular fixation has the advantage
of avoiding the physis. The wire should loop through the
triceps aponeurosis as it attaches to the olecranon and a
transverse tunnel in the metaphysis just distal to the joint to
avoid physeal damage. Minimum soft tisse stripping (i.e.,
periosteum) should lessen the risk of peripheral physeal
damage. A transfixation screw should not be used, as it may
permanently damage the physis. Pins should not be removed
prematurely, or the injury may recur. Small diameter pins are
unlikely to cause any physeal arrest, especially in a slow-
growing physis.
An and Loder reported intraarticular entrapment of a dis-
placed olecranon fracture in a 4-year-old.41 It required open
reduction and internal fixation.
Results
Olecranon fractures usually heal without any limitation of
function or growth deformity, especially when a greenstick
injury is involved. With displaced injuries, healing may be
delayed, especially if a thin layer of metaphyseal bone must
fuse to the rest of the metaphysis.
Complications
Growth arrest is unusual after an olecranon fracture, pri-
marily because this region does not contribute significantly
to the overall longitudinal growth of the ulna. In the young
child, growth arrest could lead to disparate development of
Olecranon Fractures 579

FIGURE 16-22. (A) Fracture of the proximal ulna of a 9-year-old 6 weeks later. (D) Three days after removal of the wires the frag-
child. The triceps has displaced the fragment. (B) Closed reduc- ment redisplaced during normal activity. (E) This was fixed by cer-
tion in extension failed to reduce the fragment. (C) This fragment clage wiring.
was fixed with crossed Kirschner (K) wires, which were removed

FIGURE 16-23. (A) Displaced sleeve fracture of the olecranon. (B) Result of longitudinal pin and cerclage wire fixation. No secondary
ossification is present in the olecranon.
580
FIGURE 16-24. Combined injury of the olecranon and medial epi-
condyle. Both were treated with open reduction and pin fixation. A
tension band suture also was used on the olecranon.
the proximal ulna relative to the proximal radius and
thereby affect varus or valgus position and limit elbow
function.
Matthews observed a patient who sustained nonunion fol-
lowing an olecranon fracture that was fixed with a suture.57
Pavlov et al. reported two cases of nonunion of the olecra-
non epiphysis in adolescent baseball pitchers.61 Figure 16-25
shows a patient treated conservatively (with a cast in 90° of
flexion) who developed a fibrous union.
Figure 16-26 shows the elbow of a 10-year-old girl who had
sustained an “elbow injury” 6 years earlier but was told there
A B
FIGURE 16-25. (A) Displaced olecranon fracture. This was splinted. (B) Ten weeks later nonunion was evident.
16. Radius and Ulna
was no fracture evident on the radiograph. She had pro-
gressive loss of elbow motion. In retrospect, she had avulsed
the unossified region of the olecranon away from the ossifi-
cation center (shell fracture). Repetitive motion continued
to pull the area proximally, and it subsequently ossified.
It was removed, and the triceps aponeurosis was repaired.
Function improved but did not equal that on the other
side.
Heterotopic bone may complicate this injury pattern.
Because of the hinge mechanism of the injury (see previous
section), delayed healing of the olecranon and radial head
abnormalities may occur.
Gymnastic Injury
Avulsions of the olecranon through the physis may occur
in competitive gymnasts. The spectrum of abnormalities
ranged from widening of the olecranon physis to fragmen-
tation of the epiphyseal ossification center. The appearances
are similar to that of the Osgood-Schlatter lesion.
Typical of gymnastics is a sudden extension of the elbow
through the action of the triceps that results in traction and
shearing forces on the olecranon. It can act at two sites: (1)
the insertion of the triceps tendon into the olecranon, cre-
ating a situation on the developing ossification center similar
to the patellar tendon on the tibial tuberosity, and (2) the
olecranon physis itself.
Coronoid Process
Coronoid process fractures may be classified as follows: type
I, avulsion of the tip of the coronoid process; type II, a single
or comminuted fragment involving 50% of the process or
less; and type III, a single or comminuted fragment involv-
ing more than 50% of the process. They may be subclassi-
fied with regard to the absence (a) or presence (b) of an
associated dislocation of the elbow. There is an increased
incidence of complications associated with elbow dislocation
and fewer optimal results than with type III.
Olecranon Fractures 581

A B

FIGURE 16-26. (A, B) This 10-year-old girl had an “elbow injury” at age 4 years that went untreated. It probably was an olecranon frac-
ture coupled with dislocation of the radial head. An attenuated olecranon is evident, along with a deformed proximal radius.

Coronoid process fractures certainly occur in children
(Figs. 16-27, 16-28). Fractures of the coronoid region may be
missed in children during routine lateral radiographs of the
elbow, as the radial head may overlie the coronoid process.
Accordingly, an oblique radiograph may be necessary to visu-
alize the fracture if suspected.
The anterior portion of the epiphysis, including the coro-
noid process and its subchondral bone, may flip 180° and
displace into the joint. This injury is treated by arthrotomy
and replacement of the fragment.
Hanks and Kottmeier reported a fracture involving the
entire coronoid process of the ulna50 that was treated with
open reduction and internal fixation. The patient also had
a fracture of the distal radius. The authors noted that most
fractures of the coronoid process are small, they are often
associated with dislocation of the elbow, and the suggested
treatment is to “ignore them,” as they usually have no effect
on the final outcome. Open reduction and internal fixation
is recommended for fractures that interfere with joint
motion. The stability of the elbow is dependent on the sta-
bility of the collateral ligaments and on the coronoid
process. The natural history of a large, displaced coronoid
process fracture is not well known, but data suggest that
these patients are at risk for developing chronic instability of
the elbow.
Tanzman and Kaufman described a similar coronoid
injury in a 12-year-old girl who also sustained a right wrist
fracture.63 When the arm was immobilized in a cast at 90°,
the fracture was further displaced. The arm was taken out of
the cast and the limb immobilized in full extension, with the
concept that the tension induced in the brachialis tendon
would reduce the fracture. It led to accurate and complete
reduction of the fracture. Immobilization was maintained for
4 weeks, after which active mobilization was begun. The
authors thought that this injury occurred because of hyper-
extension or as a result of abutment of the coronoid against

A B
FIGURE 16-27. Anteroposterior view of a coronoid fracture. (B) Oblique view. The “intraarticular fragment” is rarely the early trochlear
ossification center (according to the radiology report).
582
FIGURE 16-28. Intraarticular displacement of a sleeve fracture of
the coronoid process.
the trochlea during forceful posterior displacement of the
ulna. In this particular patient they believed that a disloca-
tion had not occurred. This method of reduction was in
contrast to the usual suggestion of maximum flexion.
The surgical approach to the ulnar coronoid process is
usually medial, involving sharp dissection of the flexor carpi
ulnaris and flexor digitorum profundus muscles from the
medial side of the ulna. These muscles are reflected superi-
orly to protect the ulnar nerve and its motor branches. By
continued dissection, the coronoid process and distal
tendon of the brachialis muscle are exposed.
Proximal Radial Fractures
Proximal radial fractures are common in the developing
elbow.67–154 Radial head and neck fractures account for
5–10% of injuries to the elbow region.101 Newman described
48 displaced radial neck fractures in children 4–13 years
old.121 In two children, the fracture occurred before ossifi-
cation appeared and was recognized only by a thin, displaced
piece of metaphysis (Thurstan Holland sign). In 38 cases the
pattern of injury was lateral or valgus angulation. In all cases,
the angulation of the radial head was at least 30° from the
normal axis. Henrikson found 55 fractures of the proximal
radius, which included 50 fractures of the neck (metaphy-
seal injury) and 5 fractures through the epiphysis and
apophysis.94
O’Brien reviewed 125 cases.122 He found only four that clas-
sified as a type 1 or 2 growth mechanism injury, believing that
most proximal radial injuries were fractures through the
juxtaphyseal metaphysis. There were 40 patients (almost
one-third of his patients) who had early closure of the epiph-
ysis and increased carrying angles up to 25°, although none
was severe enough to require osteotomy. A complicating
proximal radiohumeral synostosis developed in six patients.
Fractures commonly occur when children are 10–13 years
of age, with the range beginning at about 5 years, when
the ossification center first appears. Whether these injuries
16. Radius and Ulna
occur before that time is difficult to ascertain because of the
absence of the ossification center. Approximately 75% of the
cases occur in children 9 years of age or older.
Multiple injuries may occur.79,112,121 In one series, 11 of 38
patients had associated avulsion injuries of the medial side
of the elbow, 5 had olecranon fractures, 4 had avulsed medial
epicondyles, and 2 had ruptured medial collateral ligaments.
Other injury patterns include the following: (1) radial head
dislocation and fracture; (2) rupture of the annular liga-
ment; (3) elbow dislocation; (4) capitellar fracture; (5) dis-
located radial head; (6) navicular fracture; and (7) radial
nerve palsy. The wrist also must be assessed carefully. Chil-
dren may get Essex Lopresti injuries or their equivalents. As
in adults they may be difficult to diagnose and may be
present as variants because of the presence of physeal frac-
tures instead of cortical fractures.
Classification
Fractures vary from growth mechanism involvement to
injuries through the metaphysis with angular deformity. The
fracture line may appear to be through the epiphysis, but it
usually is a compression of the epiphyseal head into the
metaphyseal expansion of the narrow neck. Thus these frac-
tures tend to be impaction or greenstick injury patterns.
With either injury pattern the fragment may be completely
displaced.
A fracture of the metaphyseal neck of the radius should
be differentiated from a true physeal or epiphyseal fracture
of the head of the radius, which occurs less frequently during
childhood. McBride and Monnet believe that a true slipped
epiphysis is unusual.113 However, in one report of 34 cases,
50% were in the radial neck proper and 50% were type
2 fractures involving the proximal radial physis and
metaphysis.139
Growth mechanism injuries range from type 1 to 4 (Figs.
16-29 to 16-31). The type l and 2 pattern injuries are often
difficult to differentiate from adjacent metaphyseal injuries,
although treatment and prognosis are virtually the same.
Type 3 and 4 injuries require accurate diagnosis and open
reduction. Because of the limited vascularity to the radial
head, these small fragments carry a high risk of ischemic
necrosis and physeal bridging (premature closure). Type 7
injuries (intraepiphyseal) are infrequent.
The most common injury pattern involves a fracture
through the metaphyseal neck (Figs. 16-32 to 16-34). These
fractures are often greenstick angulations (compactions)
with some intrinsic stability. Fractures may be defined as (1)
mild: less than 30° of angular deformity; (2) moderate:
30°–60° of angulation; or (3) severe: greater than 60° of
FIGURE 16-29. Growth mechanism injuries of the proximal radius.
(A) Type l. (B) Type 2. (C) Type 3. (D) Type 4 transphyseal injuries.
Proximal Radial Fractures 583

FIGURE 16-30. (A) Type 3 fracture of the

proximal radius in a 13-year-old girl during
the final stages of epiphysiodesis (similar
to a Tillaux fracture). (B) Type 4 fracture
(arrow). Both of these fractures should be
anatomically reduced.

FIGURE 16-31. (A) Type 4 fracture of

the radial head. (B) Seven months later.
Further ossification led to physeal
bridging.

FIGURE 16-32. (A–C) Metaphyseal injuries, showing patterns of FIGURE 16-33. Mildly crushed metaphyseal fracture of the proxi-
angular deformation. (D–F) Presentation of injury relative to the mal radius (arrow).
annular ligament.
584
FIGURE 16-34. Severely angulated proximal radial fracture. Note
the deformed metaphyseal cortex (arrow).
FIGURE 16-35. (A) Completely displaced metaphyseal fracture in a 9-year-old child. (B) Similar injury in a 6-year-old child. (C) Two
months after open reduction. (D) Four months later. Note the bipartite medial epicondylar ossification, indicating injury to that area also.
16. Radius and Ulna
angulation. The fracture may also be completely displaced
(Figs. 16-35 to 16-37).
Pathomechanics
The normal carrying angle of the elbow makes valgus injury
more likely in a fall on the outstretched arm. The position
of the elbow at impact determines whether the ulna is also
fractured. In full extension, the tight ligaments around the
elbow direct the olecranon into the fossa of the distal
humerus, so varus and valgus movements are minimized. In
this position, continued valgus strain fractures the radial
neck. The olecranon frequently sustains a concomitant
oblique fracture. If there is some flexion, the olecranon is
not held as firmly within the olecranon fossa and may rotate,
so a solitary fracture of the radial neck results from the force.
If a child sustains a dislocation of the elbow, a displaced frac-
ture of the radial neck may also occur.
The mechanism of injury, a fall on the outstretched hand,
drives the capitellum against the outer side of the head of
the radius, tilting and displacing it outward. Such a mecha-
nism applies a valgus strain to the elbow at the moment of
Proximal Radial Fractures
FIGURE 16-36. Mechanistically many of these fractures occur
with an elbow dislocation or Monteggia injury in which the posteri-
orly/inferiorly displaced radial head is subsequently knocked off by
spontaneous or attempted reduction. Probably some failure of the
physis has occurred in the original injury that makes completion of
the fracture likely during reduction.
injury. Accordingly, one may find an associated traction
lesion of the inner side of the joint, which may take the form
of a medial epicondyle avulsion or, much less likely in a child,
rupture of the medial collateral ligament.
The direction of tilting of the displaced head of the radius
relative to the shaft of the radius varies with the rotational
position of the radius at the time of injury. Thus, if the
forearm is supinated at the moment of impact, the dis-
placement of the capital epiphysis is outward (lateral). This
displacement is shown in the usual anteroposterior radio-
graph taken in supination. If the forearm is in midposition,
the adjacent posterior quadrant of the radial head is sub-
jected to the greatest violence; and when the forearm is
returned to a position of full supination, the head may be
tilted backward relative to the radial shaft.
According to Jeffrey, another mechanism of injury is when
the patient first falls on the hand and sustains a temporary
posterior dislocation or subluxation of the elbow joint.96,97
The resulting upward force of the flexed elbow displaces the
radial head posteriorly almost 90° by the impact against the
inferior aspect of the capitellum. Spontaneous reduction of
the elbow dislocation leaves the separated radial head under-
neath the capitellum.96,122,153 This particular form of injury is
discussed further in Chapter 11.
Diagnosis
The injured elbow is usually held in moderate flexion, with
the forearm in neutral rotation. There may be local swelling
and ecchymosis over the lateral aspect of the elbow. Palpa-
tion of the radial head and neck may elicit tenderness. There
may be occasional crepitation of the fragments when motion
585
is attempted. Pain may be referred distally to the wrist.
Flexion and extension are restricted; pronation and supina-
tion are painful and restricted.
Roentgenograms initially are obtained in anterior and
lateral views (Figs. 16-34, 16-35). When clinical findings are
suggestive, but the standard roentgenograms are inconclu-
sive, it is advisable to examine several views of the proximal
radius in various degrees of rotation or evaluate the proxi-
mal radius under fluoroscopy. Sometimes small metaphyseal
fragments are visible. A dislocated proximal fragment may
be projected into the shadow of the ulna. As a result, the
structural changes may be missed on routine films. In such
cases, oblique or tangential projections may be useful. The
maximal degree of the tilting of the radial head should be
determined, which, again, may require nonstandard views or
fluoroscopy. Fat pad signs may be the only indication of an
undisplaced injury.
A child with a fracture of the radial head may present with
more distally referred pain, even in the wrist.67 As with any
injury in which there is rather diffuse or even selective pain
in a child, it is important to radiograph the entire involved
bone. As many as 50% of patients with a fracture of the radial
head or neck have an associated injury, such as fracture of
the olecranon, avulsion of the medial epicondyle, or dislo-
cation of the elbow.
The degree of angulation may be accurately determined
only by an anteroposterior radiograph obtained with the
forearm in the position of rotation at the moment of
impact.152 Jeffrey has advocated obtaining radiographs in
various degrees of forearm rotation.97 A more practical
method is to assess the child with fluoroscopy by pronating
and supinating the forearm to find the maximal extent of
angulation. Alternatively, if a well-formed secondary ossifi-
cation center is present, it appears as a rectangle when the
bone is in the maximal degree of angulation. Comparison
views are less appropriate, as there are normal variations in
the radiographic appearance of the proximal radius.
Treatment
For the undisplaced or minimally displaced fracture of the
radial head or neck, treatment consists of immobilizing the
FIGURE 16-37. This radial head flipped 180° during spontaneous
reduction. The articular surface faces the metaphysis.
586
elbow with a posterior splint in 90° of flexion and neutral
rotation of the forearm for approximately 10–14 days. Move-
ment should be started when the injury is no longer
painful.90 Early mobilization is recommended but is not used
if there is residual pain at the fracture site on either motion
or direct palpation. Initial movements include flexion-
extension and pronation-supination exercises; the arm
should be protected in a sling because of the normal state
of activity of a child.
The basic aim of treatment is to restore the normal range
of forearm supination and pronation. Tilting of the radial
head 20°–30° may be compatible with this aim in a young
child with remodeling potential. However, this observation
is not an excuse to leave this degree of angular deformity
because it may not improve with time. Every attempt should
be made to achieve an optimal degree of angular correction.
Lateral tilting of up to 30° is probably acceptable, as there is
usually spontaneous correction through remodeling. This
correction is less likely with the older child (over 10 years)
because the proximal radius has much less growth potential
than does the distal physis. Furthermore, with a crushing
metaphyseal injury one cannot be certain there is no con-
comitant physeal injury that may lead to growth slowdown
or arrest and that may cause further angular deformity and
tilting of the radial head. Permanent malunion may result.
Closed reduction is usually accomplished by partial to
complete extension of the elbow to provide some fixation of
the ulna relative to the humerus, followed by adduction of
the forearm to correct or overcorrect the carrying angle and
widen the radiohumeral articulation, a maneuver designed
to create a space into which the displaced radial head may
be reduced.90 This position is held, and the forearm is
rotated to bring the radial head into a position from which
it may be pushed by direct pressure into correct alignment
(Fig. 16-38). As a prelude to manipulation it is important to
FIGURE 16-38. Mechanism of reduction of radial head angulation.
The thumb is pressed against the radial head (black arrow) while
the forearm is directed into a varus position (open arrow).
16. Radius and Ulna
determine the direction of displacement of the radial head.
Manipulative reduction is carried out with the forearm in the
degree of rotation that brings the most prominent part of
the displaced head farthest laterally. If it is done under image
intensification, it is often possible to determine the position
of supination or pronation that best emphasizes the fracture
in such a way that the thumb may be applied to produce
a correction force. Firm digital pressure is applied in an
upward and inward direction to complete the reduction. If
roentgenography proves that the reduction is satisfactory,
the arm is immobilized in a posterior splint.
When there is angulation of 30°–60°, closed reduction
under anesthesia is appropriate and usually successful. Some
accept an initial angulation of less than 30°, but even this
should be treated with an attempted reduction. If the an-
gulation is more than 60°, closed reduction is usually un-
successful and open reduction or the toggle maneuver is
indicated. The proximal humerus of the affected limb is
stabilized by an assistant. The elbow is flexed to 90°. The
forearm is held by the surgeon’s ipsilateral hand (i.e., the
left hand for the left forearm and vice versa) in maximum
possible supination. No varus strain is applied. Pressure is
then applied by the thumb of the surgeon’s other hand over
the anterolateral aspect of the head of the radius, just distal
and lateral to the cubital fossa. At the same time the affected
forearm is gradually but steadily rotated to a neutral position
and then into a position of full pronation. This maneuver
rotates the displaced and tilted radial head under the exter-
nal pressure; and with the elbow flexion providing a lax
capsule, the radial head is usually reduced. Reduction and
stability may be confirmed fluoroscopically.
For moderately displaced fractures (i.e., 30°–60° of
angular deformity), closed reduction with the patient under
general anesthesia is attempted first.124 If satisfactory reduc-
tion is achieved, a long arm cast is applied with the elbow
held at 70°–90° of flexion, neutral rotation, and three-point
fixation with the medial elbow as the fulcrum; a slight varus
stress is then applied to the cast to lessen pressure at the
radiohumeral joint. Usually, a period of 3–4 weeks is suffi-
cient to achieve healing. It should be remembered that this
area does not normally have a dense cortex and is not accus-
tomed to assuming significant joint reaction forces, so it
might collapse if the arm is used and pronation-supination
movement is started. Repeat roentgenograms during the
first 2 weeks ensure that reduction is maintained.
Open reduction may be undertaken when the radial
epiphysis is displaced completely from the shaft or when
manipulative reduction has been unsuccessful. It should be
done as soon as possible after the injury, as extended periods
are sometimes associated with a higher incidence of myosi-
tis ossificans and ischemic necrosis.124,146
Even if it is completely separated, the radial head should
be replaced anatomically, as revascularization may occur
(but is unlikely after 24 hours). The head and neck of
the radius normally are relatively poorly vascularized (i.e.,
dependent on only a few vessels), so ischemic change is a
likely complication. In cases with major dislocation of the
fragments, the periosteum may be completely severed.
Extensive stripping of the periosteum should not be under-
taken. Removal may result in significant relative differences
of growth rates between the radius and ulna.108 Silastic
Proximal Radial Fractures
FIGURE 16-39. (A) Completely displaced proximal radial head fracture. (B) Open reduction with pin fixation. (C) Seven months later.
spacers should be avoided in children. The annular ligament
is not sectioned unless it is absolutely necessary to achieve
reduction. Every effort should be made to protect the
annular ligament; if it is damaged, it should be repaired.
The forearm should be fully pronated and supinated to test
the stability of the reduction.
When necessary, fixation may be accomplished by angular
placement of wires through the margin of the radial head
into the metaphysis (Fig. 16-39). Placing the wire through
the capitellum into the center of the radial head and along
the radial shaft with the elbow flexed at 90° and the forearm
in midrotation is less desirable and rarely necessary if it is
possible to achieve fixation without involving the articular
surfaces.
Fowles and Kassab described the breaking of two trans-
articular K-wires from the humerus to the radius.86 This
method should be avoided. Oblique placement of K-wires
through the radial head is the best approach.
I recommend peripheral placement of the fixation wires.
The ends of the wires are left subcutaneously or penetrating
the skin so they can be easily removed. The ends are bent
90° to prevent migration. A well-padded dressing is applied,
followed by a posterior shell that can be converted after 3–4
days to a formal long arm cast when swelling subsides.
Other authors have recommended various methods of
fixation. Key used sutures in the periosteum of the neck
and sutured the annular ligament about it.102,103 Reidy and
Van Gorder did not use any internal fixation, except for an
occasional suture.131 O’Brien occasionally used a Kirschner
wire.122 Jones and Esah used K-wires introduced behind and
lateral to the lateral condyle of the humerus, crossing the
radial head obliquely into the shaft.98
Merchan thought that displacement of more than 2 mm,
rather than 5 mm, was an indication for open reduction.114
He also recommended K-wires for transfixing the joint, but
the risk of breakage is significant. He reported 36 children:
18 with a good result, 8 a fair result, and 10 a poor result.
He believed that the risk of poor results was associated with
severe displacement and that use of open reduction per se
587
was not the causal factor. In six cases the K-wire bent, and in
two cases it broke. In one instance it could not be removed,
remaining permanently in the medullary cavity.
Carl and Ain described a complex fracture of the radial
neck in a child that involved fractures of the radial neck, the
olecranon, and the medial epicondyle.75 Medial and lateral
fixation were necessary to control the three planes of insta-
bility. They thought that the combination of the two injuries
(olecranon or medial epicondyle), which often singularly
accompany the radial head fracture, created the unstable
situation.
Care must be taken to protect the posterior interosseous
nerve. This nerve may be exposed by separating the fibers
of the supinator muscle. Wide exposure may prevent neu-
ropraxia of the posterior interosseous nerve and facilitates
positioning of the radial head on its neck.
Metaizeau and colleagues described an interesting tech-
nique in which a K-wire was passed from the distal end of
the radius through the medullary canal.115,116 By toggling it
under fluoroscopy, they manipulated the radial head into
place without having to undertake open reduction of the
radial head. The K-wire was then left in place until healing
occurred. They thought that inadequate reduction of radial
head fractures led to long-term limitation of elbow and
forearm movements. They also believed that these compli-
cations could be alleviated by distal-to-proximal placement
of a Kirschner wire with a toggle maneuver to flip the radial
head into place if closed reduction with the thumb did not
work.115,116
Metaizeau et al. used their technique of intramedullary
reduction and pinning in 31 fractures with a tilt between 30°
and 80° and 16 fractures with a tilt of more than 80°.115,116
Altogether 30 of 31 in the first group and 11 of 16 in the
second group had excellent or good functional results. Their
technique is to bend a Kirschner wire 1.2–2.0 mm in diame-
ter, depending on the patient’s age; the last 3 mm are bent
more sharply. Four of the lesions that were more than 80°
could not be reduced satisfactorily with this technique and
were subsequently treated with open reduction. The authors
588
thought that a residual angulation of more than 10°–15°
in the 10- to 12-year range or an angulation of more than
20°–30° in a younger child would not be remodeled by sub-
sequent growth and would therefore lead to variable sub-
luxation of the joint, depending on the position of the
forearm.
Bernstein et al. used a technique of percutaneous reduc-
tion under image intensification,71 generally for significantly
displaced radial neck fractures. Eighteen patients were so
treated. Steele and Graham described use of the same
technique.143
With type 3 or 4 growth mechanism injuries, closed reduc-
tion should be attempted first, although open reduction is
frequently necessary. Most of these injuries result in prema-
ture closure of the epiphysis and may accentuate valgus
angulation, depending on the amount of remaining growth.
The type 4 physeal injury produces a dilemma. The dis-
placed fragment is often too small to be fixed effectively. In
some cases it can be excised. The result may not be good,
but the loss of motion after this fracture may be due to other
factors because the injury is usually produced by consider-
able violence.
When treating markedly displaced and fragmented frac-
tures, many authors believe that only two methods are likely
to give satisfactory results: excision of the capital fragment
or open reduction. However, the radial head usually should
not be excised in a child because marked growth disturbance
can occur. A Madelung-type deformity may also develop at
the wrist, with radial deviation of the hand, depending on
the amount of growth remaining. In a patient close to skele-
tal maturity, with a severely comminuted injury of the prox-
imal radius, it is probably best to treat the adolescent as an
adult and excise the radial head.
If the fracture is diagnosed late, radial head tilting may
be corrected by an osteotomy and, if necessary, bone graft.
If the patient is skeletally mature, the radial head may be
excised.
Immobilization following open reduction is as described
for closed treatment and should be continued for 2–4 weeks.
If K-wires have been used, they should be removed before
active rehabilitation.
Results
Full return of supination and pronation may take several
months, although there is little permanent disability. Restric-
tion of motion of the elbow may also occur. Rotation of the
forearm is most often affected. Pronation was limited in 21
elbows, supination in 14, and both motions in 13.37 Flexion
and extension, in contrast, were infrequently limited. When
the upper radial epiphysis has been completely displaced
from the shaft, some permanent loss of movement is antici-
pated, even when accurate reduction has been secured by
open operation.96
McBride and Monnet reported nine patients with a follow-
up that ranged from 3 to 15 years.113 In general, the results
were good. They were negative about the results of open
reduction in these injuries but did recommend that after dis-
ruption or transection of the annular ligament, reduction
could be maintained by a small K-wire through the center of
16. Radius and Ulna
the head and into the neck and by a good repair of the
annular ligament. Nonunion developed in two patients
treated by open reduction, and eventually resection of the
radial head was undertaken because of persistent pain.113
In another study the carrying angle was increased 5°–10°
in six cases and 15°–20° in three; 17 patients had no change
in the carrying angle.126 Only two patients showed an
increased valgus angle of more than 10° in the injured arm,
compared with the unaffected arm. The carrying angle
increased in about 30% of the children owing to premature
closure of the growth plate of the radius.
Steinberg and associates, in a long-term review (more than
4 years) of fractures of the neck of the radius in children,
showed that 31% had a poor result.144 Primary angulation
appeared to be the most important factor affecting the
results. Periarticular ossification, ischemic necrosis, and
enlargement of the radial head were the most important
causes of poor results. They thought that more accurate
reduction was mandatory to improve the final outcome. The
prognosis is good, with the fractures often giving a usable,
but seldom normal, elbow.86,144 In the Steinberg et al. series,
a good reduction at surgery did not always guarantee a good
result at follow-up examination.144
D’Souza et al. studied 100 patients with radial neck frac-
tures.80 Excellent and good results were obtained consis-
tently after closed manipulation. Open reduction was often
followed by a fair or poor result. They thought that opera-
tive correction should not be attempted unless the radial
head is displaced 45°.
Complications
The complications of radial neck fracture include synostosis,
avascular or ischemic necrosis (Fig. 16-40), premature fusion
of the physis (Fig. 16-41), enlargement of the radial head or
neck, deformed epiphysis (Fig. 16-42), ectopic calcification,
nonunion (Fig. 16-43), vascular or peripheral nerve injury,
and impaction injury to the articular surface, with loss of
motion and abnormal wear of the cartilage.
There is a slightly higher incidence of complications fol-
lowing open reduction than after closed reduction. Synosto-
sis, though rare, is a hazard even of closed reduction and
may result in cubitus varus. Heterotopic ossification may
also occur and reduce rotation; it is more likely after open
reduction.
Key described an elbow dislocation with posterior dis-
placement of the radius.102 Roentgenograms showed an
irregularity of the epiphyseal plate a year later. There was
also an indentation of the capitellum, suggestive of irregular
joint reaction forces across the radiohumeral joint. Wood
reported two similar cases of posterior displacement of the
epiphysis.153 One patient was treated with open reduction
and 6 years later had good function and a normal radio-
graph. The second patient was also treated with open reduc-
tion; and when the patient was seen 2 years after injury,
radiographs showed distortion of the growth of the prox-
imal end of the radius and limitation of pronation and
supination.
Synostosis between the proximal radius and ulna has
been reported.79,84,122 In three patients in Henrikson’s study,
Dislocation of the Head of the Radius
FIGURE 16-40. (A) Complete displacement of the radial head
(arrow). It was placed back on the shaft by open reduction. Antero-
posterior (B) and oblique (C) views showing ischemic necrosis and
a synostosis developed between the radius and the ulna.94
In one, a radioulnar synostosis developed consequent to
osteotomy.113 Fielding reported radioulnar cross-union fol-
lowing displacement of the proximal radial epiphysis in an
11-year-old boy who was treated with closed reduction.84
Fibrous adhesions between the radius and ulna were also
noted.98 Such adhesions block rotation of the forearm com-
parable to synostosis.
Nonunion is infrequent. It results from failure to achieve
adequate reduction and maintain it (Fig. 16-43).
Premature fusion of the upper radial epiphysis occurs
often with moderately and markedly displaced fractures and
may cause shortening of the radius and increased cubitus
valgus, contingent on the age of the child at the time of the
FIGURE 16-41. Premature fusion of the physis (arrow).
589
premature epiphysiodesis 18 months later. (B) Ectopic bone is also
evident (solid arrow).
injury and the severity of the cartilaginous damage. Prema-
ture fusion occurred in about one-third of O’Brien’s
patients, but in none of them was the ensuing cubitus valgus
severe enough to require osteotomy.122
Ischemic necrosis of the radial head may occur. It does not
appear to be related to the degree of initial displacement
or to the age at the time of injury. The results are poor.98
Ischemic necrosis of the whole head is rare, even when the
head is completely reduced. Partial ischemic necrosis is seen
more frequently. Irregularity of the radial head and prema-
ture closure of the proximal radial physis are common. In
one series premature fusion occurred in 11 of 30 cases.131
Other complications have been noted. New bone forma-
tion (heterotopic bone) and deformity of the radial head
with enlargement occur in some cases and may restrict elbow
motion. O’Brien reported a notch in the radial neck in 6 of
125 cases, and believed it due to scarring and damage to
the annular ligament.122 Colton showed a patient with a 180°
flip of the radial head during closed reduction (Fig. 16-37).
Follow-up showed significant growth arrest and irregular
overgrowth with decreased function. Failure to correct dis-
placement or angulation may affect the rotation of the radial
head in the ulnar notch, producing a cam effect, rather than
a rotation.
Dislocation of the Head of
the Radius
Isolated dislocation of the head of the radius (Figs. 16-44,
16-45) with no other congenital abnormality in the elbow
is infrequent.155–203 White suggested that some of the cases
reported as congenital dislocations of the radial head may
have been caused by trauma during delivery or early
 590 16. Radius and Ulna

C
FIGURE 16-42. (A) Nonunion of type 4 injury of the radial head. The parents opted for radial head excision because of severe pain.
(B) Radiograph of the specimen. (C) Histology shows loss of central articular cartilage and nonunion of the fragment.

A B
FIGURE 16-43. (A) Fracture treated by closed reduction. Delayed union is evident at 6 weeks. (B) Nonunion and ischemic necrosis at
14 weeks.
Dislocation of the Head of the Radius
FIGURE 16-44. Progressive, nontraumatic subluxation of the radial
head in cadaver specimens. The child had severe cerebral palsy
with elbow contractures that undoubtedly led to progressive dis-
placement of the proximal radius, similar to the progressive
appearance of subluxation and dislocation of the hip in these
severely spastic children. (A) Roentgenogram of the right side. This
infancy.199 For distinguishing between congenital and trau-
matic dislocations, one of the most reliable signs is the con-
dition of the capitellum. If it is significantly underdeveloped,
a congenital dislocation is likely, although early postnatal
subluxation or dislocation (i.e., infantile “nursemaid’s”
elbow) might lead to secondary joint deformation on both
sides of the joint, as with developmental hip disease. Confu-
sion may arise when a child with a congenital or pathologic
dislocation falls on his or her elbow. The ensuing radio-
graphs may mimic an acute injury.
591
side could be reduced in some positions. (B) More severe involve-
ment of the left side. This could not be reduced because of severe
capsular distortion. (C) Annular ligament over the radial head
of the specimen shown in (A). After dissection freed this from
the capsule, it could be reduced. (D) Intact, back around the
metaphysis.
With congenital dislocation of the radial head, there is no
capsular inclusion and a poorly developed radial head with
a convex shape (Fig. 16-46). Vesely explored radial heads in
cases of congenital dislocation and described capsular dis-
tortion and displacement of the annular ligament.198 These
findings were similar to those of the case shown in Figure
16-44.
The annular ligament is quite mobile in infants. Accord-
ingly, it may completely displace over and off the radial head
and not be recognized because of the limited ossification in
592
A
FIGURE 16-45. (A) This child had an elbow injury 3 years earlier.
No fracture was seen on the radiograph according to the dictated
radiology report. The child, now 9 years old, had painful, restricted
the infant’s elbow epiphyses. It is the equivalent of nurse-
maid’s elbow in toddlers.
Isolated traumatic dislocation of the radial head has been
regarded as a “pseudo-Monteggia” lesion (Fig. 16-45). The
absence of the concomitant ulnar fracture is due in part
to the plasticity of the ulna in infants and young children,
which permits transient bowing of the bone without pro-
gression to fracture. However, the “weakness of the annular
ligament” that predisposes certain children to nursemaid’s
elbow may allow a rare individual to develop complete dis-
location of the radial head.
Caravias reported acute radial head dislocation that
resembled classic “congenital” dislocation of the head of
A B
FIGURE 16-46. Anteroposterior (A) and lateral (B) views of a congenitally dislocated proximal radius.
16. Radius and Ulna
motion made worse by pitching a baseball. (B) Although the antero-
posterior view seemed unremarkable (according to the radiologist),
the lateral view readily shows the posterior displacement.
the radius. The first case was treated with closed reduction,
but anatomic restoration was not attained. During follow-up,
after skeletal maturation had been obtained the head of the
radius was completely displaced from its radiohumeral artic-
ulation. Caravias’ second case was a 36-year-old woman who
had injured her elbow at the age of 5 years. The head of the
radius was lateral to the capitellum but not as high-riding as
some cases of congenital dislocation. His third case was a girl
of 18 years who apparently had a lesion that was first recog-
nized when she was approximately 2 weeks old, although it
had not been associated with any known birth trauma.159
For distinguishing isolated radial head dislocation due to
trauma from a congenital deformity, Mardam-Bey and Ger
Dislocation of the Head of the Radius
found that congenital radial head dislocation never occurred
as an isolated anomaly.182 It was ordinarily associated with
a misshapen metaphysis and epiphyseal ossification center
(when the latter finally appeared). With true acute isolated
dislocation of the radial head, the radial head is usually
shaped normally. Unfortunately, because these cases are
often in infants the radiolucent anatomic shape may be
ascertained only by arthrography or arthroscopy.
Schubert described a case of a dislocated radial head in
a newborn who was treated with the arm in supination;
the infant had an uneventful recovery.190 Cockshott and
Omololu described a 6-day-old baby with bilateral disloca-
tions that seemed to reduce easily in full supination and
dislocate in pronation.161 Some radial head dislocations in
the presence of Erb’s palsy may be due to unrecognized
accidental subluxation or dislocation in the newborn (i.e.,
neonatal “nursemaid’s” elbow) or progressive postnatal dis-
placement resulting from muscle imbalance.
Vesely described isolated traumatic dislocations of the
radial head in children.198 He reviewed 17 cases and found
2 with concomitant fractures of the radial head; 13 of the dis-
locations were anterior, 3 were lateral, and 1 was posterior;
4 were treated with open reduction. Chronic dislocation
FIGURE 16-47. (A) Appearance of the elbow in a 4-year-old boy
with “congenital” dislocation of the proximal radius. (B) Arthrogram
showing maximal displacement. (C) Arthrogram of “reduction,”
which was incomplete because of soft tissue interposition. The
patient subsequently underwent exploratory surgery. The annular
593
developed in two cases, including one case that was not
reduced until 8 months after the injury. A synostosis devel-
oped in one case.
Neviaser and LeFevre reported an isolated dislocation of
the radius in a 7-year-old child.185 They treated the child with
open reduction because of irreducibility and found a trans-
verse tear in the anterior capsule, exactly where one might
expect it if this were a mechanism somewhat similar to that
of nursemaid’s elbow. The proximal portion of the capsule
was lying in the normal anatomic bed of the radial head, pre-
cluding reduction. The constricting buttonhole effect of the
tear was relieved by a capsular incision; and when the capsule
was withdrawn from the joint, the radial head was easily
reduced.
Lloyd-Roberts and Bucknill believed that many of these
cases represented perinatal or infantile radial head subluxa-
tion that progressively deformed.266 They believed that open
reduction and reconstruction of the annular ligament were
indicated to reestablish radiohumeral and radioulnar rota-
tional mechanics. I have treated a similar case in a boy with
generalized joint laxity. He was found to have sternoclavicu-
lar and radial head “dislocations” at birth, but no treatment
was given. Figure 16-47 shows the roentgenographic appear-
ligament was displaced completely over the radius, sitting in the
space between the radius and the ulna. It was dissected free of
the capsule, divided, and reattached in anatomic position. (D)
Appearance 6 months later. (E) Eight years later.
594 16. Radius and Ulna

ance when he was examined at 4 years of age. He lacked full

rotation and was having elbow pain localized to the radial
head. The annular ligament was displaced over the radial
head (between the radius and ulna), similar to the case
shown in Figure 16-44. The ligament segments were dis-
sected free anterior and posterior to the ulnar attachments.
The ligament was then divided, the ends were replaced in
their encircling anatomic position around the neck, and the
ligament was repaired. The capitellum was mildly deformed
and permitted some continued subluxation. The reduction
was maintained with a pin for 6 weeks. He has complete
flexion and extension 10 years postoperatively, but a mild
subluxation is present in full pronation.
Whether the management should be conservative or sur-
gical depends on the ease of reduction, maintenance of the
reduction, and the delay in diagnosis. An acute reduction
may be possible through traction and full supination, with
application of direct pressure over the radial head. The
elbow should be flexed to 90° and the forearm held in full
supination. This position diminishes the pull of the biceps
and tenses both the interosseous membrane and the
quadrate ligament. In the series of Hudson and Beer, five
FIGURE 16-48. (A) Be wary of the seemingly normal-appearing
of the six cases were easily reduced by closed means.175 The
anteroposterior view. (B) In the lateral view of this 8-year-old girl,
duration of immobilization following a closed reduction is the Monteggia injury is evident. The ulna had only a plastic defor-
3–6 weeks. mation (bowing).
Armstrong and McLaren reported a case in which the
biceps tendon wrapped around the displaced radial head
and prevented closed reduction.157

injuries often accompany Monteggia fracture-dislocations in

Monteggia Lesions
Classically, the Monteggia injury involves a fracture of the
proximal third of the ulna in association with dislocation of
the radial head. However, the injury must be suspected
whenever there is any pattern of injury (bowing, greenstick
injury, fracture) anywhere along the ulna without an obvious
associated fracture of the radius204–321; and, in fact, the radial
head may not be completely dislocated. It may be subluxated
such that normal function is subsequently compromised if
left untreated.
The level of the fracture of the ulna varies. In approxi-
mately two-thirds of patients it is located at the junction of the
proximal and middle thirds of the shaft, in 15% it is located
in the middle third, and in the remainder it is equally dis-
tributed between the distal third of the shaft and the olecra-
non region. The ulnar fracture may be greenstick (Figs.
16-48, 16-49) or subtle bowing, and the apparent mildness of
the ulnar injury may deter accurate appreciation of the entire
injury. It is important to remember that the appearance of
the latter two ulnar injury patterns does not reveal the extent
of angular deformation at the movement of maximal injury;
spontaneous, incomplete reduction is common. Fractures of
both bones combined with dislocation of the radial head may
also occur, although this pattern is infrequent. Such varia-
tions of injury have led to classic patterns of injury and
variants, which are more likely in children.
Theodorou described three patients in whom the radial
head dislocation was associated with fracture of the distal
radius and ulna, a combination not usually found in
adults.308 Because of the mechanism of a falling injury, wrist
children. It is imperative that the wrist be accurately assessed
at the same time the elbow and midforearm are being
roentgenographically examined.
The age of incidence has been reported as 2 months to
adulthood, but the injury occurs most frequently in children
between 7 and 10 years.
Classification
There are three basic types of Monteggia fracture-
dislocations: type 1 (extension type), in which the head of
the radius is dislocated anteriorly, with palmar (volar) angu-
lation of the fractured shaft of the ulna (Figs. 16-50, 16-51);
type 2 (flexion type), in which the radial head is dislocated
posteriorly, with dorsal angulation of the fractured shaft of
the ulna (Fig. 16-52); and type 3, in which the radial head is
dislocated laterally along with the fractured shaft of the ulna
(Fig. 16-53). A type 4 injury essentially has a type 1 pattern
with an additional fracture through the radius in its proxi-
mal third (Fig. 16-54). It is a physeal injury in some children,
a Monteggia variant.
In one series, type 1 was the most common (85%), fol-
lowed by type 2 (10%) and type three (5%).236 Bado de-
scribed an incidence of 1.7% in 3200 forearm fractures, with
57% being type 1, 15% type 2, 19% type 3, and the others
scattered through the various equivalents of type 4 and
subtle variations of the previous types.208
There are equivalents to these basic types, such as dislo-
cation of the head of the radius without evident fracture of
the ulna, which may occur because of the capacity of the ulna
to deform elastically or plastically and to return, variably,
Monteggia Lesions 595

A B
FIGURE 16-49. In this 6-year-old boy with an ulnar diaphyseal angulated greenstick fracture, the anteroposterior view (A) looked “normal,”
whereas the lateral view (B) showed the medial head dislocation.

FIGURE 16-50. (A) Anterolateral Monteggia injury.

(B) Roentgenographic appearance.

FIGURE 16-51. Angulated ulnar diaphyseal frac-

ture associated with anterior dislocation of the
radial head.
596 16. Radius and Ulna

FIGURE 16-52. (A) Posterior Monteggia injury. (B) Roentgenographic appearance. The arrow shows the radius pointing away from
the capitellum (c).

almost to the original shape (Fig. 16-55). Other variants
include fracture of the ulna associated with (1) a located
radial epiphysis but a displaced radial shaft or (2) a dislo-
cated radial epiphysis associated with a radial shaft in its
normal anatomic alignment with the capitellum.
The type 3 Monteggia lesion with lateral dislocation, which
occurs in both children and adults, has a higher incidence
of associated radial nerve injury. Lateral dislocation of the
head of the radius associated with incomplete fracture of
the olecranon producing varus deformity is considered an
unusual Monteggia fracture.210,317,319
Pathomechanics
When a child falls forward on an outstretched hand, the
forearm is usually pronated; and at the moment of impact
the hand becomes relatively fixed to the ground. Because of
the downward momentum of the falling body, a rotational

FIGURE 16-53. (A) Lateral Monteggia injury. (B) Roentgenographic appearance. (C) Lateral subluxation associated with fracture of both
bones. Note the widening of the proximal radioulnar joint, which should be a warning sign of disruption of this joint.
Monteggia Lesions
FIGURE 16-54. Anterolateral dislocation of the
radial head associated with diaphyseal fractures of
both radius and ulna. It is considered a Monteggia
variant or equivalent.
force is added when twisting of the trunk causes external
rotation of the humerus and ulna. If this force continues
until the normal limit of pronation at the proximal radioul-
nar joint is reached, something must give. The ulna is liable
to deform or fracture. At the same time, the radius is forced
into extreme pronation and lies across the ulna at the junc-
tion of the upper and middle thirds. Evans believes that as
the ulna fractures the two bones come in contact, and at that
point a fulcrum is formed over which the upper end of the
radius is forced forward.236 As the pronation force continues,
the radius is either levered forward out of the superior
radioulnar joint (probably after disruption of the annular
ligament) or is fractured in its upper third. Contact is
not necessary, as hyperpronation places the radial head
and radiocapitellar morphologic relationships in a position
whereby the relatively lax annular ligament may be dis-
placed but stays intact, allowing dislocation (Figs. 16-56,
16-57).
Speed and Boyd reported that a direct blow over the
posterior aspect of the proximal ulna could produce this
injury.302 This hypothesis was accepted until evidence gained
from 18 cadavers and clinical observations suggested hyper-
pronation as a mechanism of injury. Speed and Boyd stated
that the bicipital tuberosity was most posterior in hyper-
pronation and that this position made the radius subject to
the greatest force from the biceps tendon during violent
contraction of the muscle. Evans236 and Penrose282 produced
Monteggia’s lesions by pronation in cadavers.
Both hypotheses were challenged by Tompkins, who pre-
sented evidence that hyperextension with the forearm in a
neutral position was also an acceptable pathomechanism for
type l injuries.310 He based this assertion on clinical and
radiologic examinations of acutely injured patients that
showed type 1 Monteggia’s lesions with the forearm in a
neutral or slightly supinated position. With open type l frac-
tures, the proximal ulnar fragment usually penetrates the
FIGURE 16-55. Greenstick fracture of the ulna with
anterior dislocation of the radial head.
597
palmar skin on the ulnar side of the forearm. Biomechani-
cal investigations of the moments and components of force
suggest, theoretically at least, that with the hand fixed in
pronation and the elbow in full extension or hyperextension,
contraction of the biceps pulls the head of the radius into
the lesser sigmoid notch. A neutral position of the forearm
tends to lift the radius slightly out of the confines of the
annulus.
Hume described three cases of anterior dislocation of the
head of the radius associated with an undisplaced fracture
of the olecranon in children.251 Hume appears to have been
the first to describe this particular mechanism, although
Speed and Boyd suggested that a hyperextension injury to
the elbow may cause displacement of the olecranon epiphy-
sis associated with anterior dislocation of the radial head.302
Evans showed that with the anterior Monteggia injury,
forced hyperpronation first ruptures the capsular and
annular ligaments, then fractures the shaft of the ulna, and
finally rotates the head of the radius so it lies in front of the
capsule.7 Having prevented reduction of the radial head, the
interposed capsule then acts as a mechanical block to full
flexion.
Because of the ease with which the radial head is often
reduced in children, especially if treated early, and the excel-
lent long-term results, it is possible that the annular ligament
is not disrupted longitudinally. Rather, it may tear trans-
versely along its more distal insertion and incompletely her-
niate into the radiocapitellar joint, similar to the mechanism
for a nursemaid’s elbow in a young child (see Chapter 11).
With a greenstick ulnar injury, the most probable mecha-
nism is a fall on the outstretched hand during which the
forearm is supinated, as it might be if the child were falling
backward. The direction of the angulation of the ulna is
determined by the exact direction of the fall, which may
produce a varus, valgus, or hyperextension strain in the
forearm.
598
Figures 16-56 and 16-57 show the mechanism in a boy who
sustained a traumatic forequarter amputation. There was a
greenstick ulnar injury. By accentuating the deformity, it was
possible to duplicate the radial head dislocation (Fig. 16-56).
An important observation was that the annular ligament had
not been torn but, instead, had been displaced over the
radial head and lodged between the proximal radius and
ulna. Such displacement of the ligament may certainly occur
in the clinical situation and may be more common than a
ligament tear (Fig. 16-58), which is less likely in any joint
injury in a skeletally immature individual.
Diagnosis
For practical purposes, there is never an isolated fracture
of the ulna (Fig. 16-59). The radius must be closely
examined clinically and roentgenographically for injury to
the proximal radiohumeral joint. Some fractures in Evans’
series were greenstick, and the mildness of this injury
may have prevented accurate interpretation and appre-
ciation of the actual severity.236 Wright also reported the
combination of greenstick ulnar fracture with Monteggia
injury.319 A fracture of the ulna with angulation or overriding
and without an accompanying fracture of the radius makes
dislocation of the radial head suspect until proved otherwise.
Proof may be obtained by including the elbow in all
radiographs of suspected fractures of the ulna. In children
it is significant that with a Monteggia lesion a high
percentage of ulnar fractures are greenstick or even exces-
sive bowing, lulling one into a false sense of security regard-
ing the possible subluxation or dislocation of the proximal
radius. Furthermore, it is often difficult to distinguish
the exact location of the radial head, as it may not be
ossified. Great care must be taken not to miss this particular
diagnosis.
16. Radius and Ulna
FIGURE 16-56. Monteggia injury in a child suffer-
ing a traumatic forequarter amputation. (A)
Radiograph showing a greenstick ulnar fracture.
(B) Duplication of the probable fracture force dis-
places the radial head.
A patient with a Monteggia injury usually holds the elbow
partially flexed, with the forearm in pronation (not unlike a
young child with “nursemaid’s elbow”). Any rotation of the
forearm or flexion-extension of the elbow is painful and
restricted. The dislocated radial head may be palpable.
In the presence of soft tissue swelling or deformity of the
forearm or elbow, a dislocated radial head may be difficult
to demonstrate clinically.
The arm should be splinted in a position of comfort. The
dislocated radial head may severely limit flexion or exten-
sion. Accordingly, anteroposterior views of the humerus,
radius, and ulna and a lateral view of the elbow should be
obtained.
Roentgenograms of the forearm must include the elbow
and the wrist to rule out injuries at both the proximal and
the distal ends of the radial head. Normally, the longitudi-
nal axis of the radius passes through the ossification center
of the capitellum of the humerus (in the lateral view). If it
does not, the radial head may be subluxated or dislocated.
A line drawn through the long axis of the radius should pass
through the capitellum in all lateral views, from full exten-
sion to full flexion. Because of extension of ossification from
capitellum into the trochlea, the location of the longitudinal
axis in the anteroposterior view is not as reliable as it is in
the lateral view. The radial head may be displaced anteriorly,
laterally, or occasionally posteriorly.
If the roentgenographic beam is centered over the mid-
forearm, as it often is, the elbow is included toward the edge
of the radiograph, especially if the ulna is fractured at the
mid- or distal shaft. Distortion may make the radiohumeral
relation seem normal. The fractured ulna may be the pre-
dominant clinical and radiographic finding that focuses
attention on the ulnar lesion. Accurate anteroposterior and
lateral views must center on the elbow to give the best chance
to delineate subtle injuries.
Monteggia Lesions
FIGURE 16-57. Specimen of the ulna and radial head shown radio-
graphically in Figure 16-56. (A) Dislocated radial head. The annular
ligament is between the radius and ulna. (B, C) The ligament is
Treatment
To reduce the anterior Monteggia dislocation the forearm
is placed in full supination, and longitudinal traction is
applied. The elbow is gently flexed 90°–120° to relax the
biceps. The radial head is repositioned by direct manual
pressure. The angulated ulnar shaft is then reduced, which
may not be difficult once the radial head has been reposi-
tioned. Following reduction, the radial head is usually stable,
so long as the elbow is kept in acute flexion and the annular
ligament is in its normal position (Fig. 16-60). Radiographic
proof of reduction is essential (Fig. 16-61).
Tompkins pointed out that the ulnar fracture tends to
develop an increased radial bow during immobilization.310
This bowing is caused by the normal slight bowing of the
599
pulled onto the radial head. (D) Annular ligament back in its
anatomic position. (Also see Figure 16-73.)
ulna and the isometric contraction of the flexor muscles in
the forearm. The forearm should be immobilized in neutral
rotation or only slight supination, with the cast carefully
molded over the lateral side of the ulna at the level of the
fracture. So long as the elbow is in acute flexion of 110° or
more, the biceps is relaxed and it is unnecessary to keep the
forearm in full supination to maintain the reduction.
A posterior Monteggia fracture is usually reduced by apply-
ing traction to the forearm with the elbow in full extension.
The radial head is reduced manually, and the posterior angu-
lation of the ulnar fracture is anatomically aligned. The arm
should be positioned in almost full extension, with a cast or
splint then applied.
Once the radial head is reduced completely, the elbow
should be flexed, extended, and then flexed again. If there
600 16. Radius and Ulna

Late Case
In instances in which the diagnosis is delayed or missed,
open surgery may be necessary to reduce the radial head.
Bell Tawse reported six children with undiagnosed Mon-
teggia fractures.211 Malunited fractures of the ulna with per-
sistent dislocation of the radial head, restricted flexion, and
increased cubitus valgus developed in all of these patients.
These children originally had greenstick fractures of the
ulna. Five were treated successfully by open reduction and
reconstruction of the annular ligament. One patient experi-
enced recurrence of the dislocated radial head.
Bell-Tawse constructed a new ulnar ligament by dissecting
a slip of the triceps tendon, leaving it attached to the ulna,

FIGURE 16-58. Specimen from an 11-year-old boy showing dis-

placement of the radius after transection of the annular ligament.

is no interposition of the annulus, the radial head should

remain reduced, especially if the reduced ulnar fragments
are also reasonably stable. In children it is more important
to reduce the radiocapitellar dislocation accurately than to
gain absolute anatomic reduction of the ulnar fracture,
as remodeling corrects minor ulnar angulations of 5°–10°.
Residual angulation beyond 10° may enhance the risk of
recurrent subluxation or dislocation. Confirming roent-
genograms should be obtained at intervals to be certain that
the radial head has not redislocated during the postreduc-
tion period.
Open reduction may be necessary, particularly when the
radial head cannot be returned to its normal position by
closed manipulation. Interposition of the annular ligament
may prevent reduction of the radial head. Interposition is
of three types: partial, in which portions of the ligament are
interposed between the radial head and the ulna; complete,
in which the radial head pulls out of the ligament, leaving it
intact, an injury that accounts for most failures of reduction;
or fragmentary, in which small cartilaginous or osteocarti-
laginous fragments may be present, most frequently associ-
ated with type 2 lesions. If open reduction is undertaken,
great care must be taken during the postoperative assess-
ment to avoid inadequate reduction (Fig. 16-62).
Open reduction of the radial head and repair of the
annular ligament always carry the risk of subsequent ectopic
ossification. Although closed reduction of the radial head
displacement may be successful, open reduction may still be
necessary for the accompanying ulnar injury.
Immobilization is maintained until there is union of the FIGURE 16-59. (A) Lateral view of an olecranon fracture associated
ulna, which ordinarily requires 3–8 weeks, depending on the with radial head dislocation. It was “reduced,” casted, and allowed
patient’s age. The patient’s elbow is then progressively mobi- to heal. (B) Seven weeks later the olecranon fracture has healed,
lized. Emphasis should be on flexion-extension exercises, but the radial head is still dislocated. Such a divergent fracture-
followed by supination-pronation exercises. dislocation is a variation of the Monteggia injury.
Monteggia Lesions
FIGURE 16-60. (A) Mid-shaft ulnar fracture
associated with proximal radial dislocation. As
the distal radius and ulna are displaced dorsally
(open arrow), the radial head levers out anteri-
orly (solid arrow). (B) Closed reduction of the
dislocated radial head allowed closed reduction
of the ulnar fracture.
passing it around the neck of the radius, and securing it
through a hole in the ulna.211 Accurate dissection of the
damaged or displaced annular ligament allows direct repair
instead (Fig. 16-63). The radioulnar joint and the radio-
humeral joint must be accurately reduced. The arm should
be held in extension and supination probably for at least 6
weeks after open repair.
The triceps fascia may not grow or elongate as the child
grows. Accordingly, the still enlarging (widening) radial neck
may have to grow around the tissue, which can lead to a con-
strictive deformity of the radial neck (Fig. 16-64).
If reduction of the radial head is difficult because of ulnar
shortening or angulation, it is better to lengthen the proxi-
mal ulna with an oblique (overlapping) osteotomy, rather
A B
FIGURE 16-61. Neither of these patients (A, B) shows postreduction evidence of successful reduction of the radial head dislocation.
Unfortunately, both were accepted as being adequately “reduced.”
601
than shortening the radial neck. It is not always necessary to
fix the ulnar osteotomy internally.
There is no absolute time interval between injury and
open reduction. If more than a year has elapsed since the
injury, however, the chances of a good result decrease. I have
performed the procedure on several children 19–26 months
after injury (Fig. 16-63) and 4 years later for a “congenital”
injury (Fig. 16-47), all with acceptable functional results,
although none had anatomically normal radiographs.
A major factor influencing the possibility of reduction and
the risk of recurrence of subluxation or dislocation postop-
eratively is the extent of biologic deformation of the radial
head and the capitellum. I recommend an arthrogram with
videotaped range of motion. A computed tomography (CT)
602
FIGURE 16-62. (A) Anterior Monteggia injury accompanying a proximal ulnar fracture. (B) The ulna was reduced and stabilized with a
tension band wire; the radius was reduced without opening the radiohumeral joint.
or magnetic resonance imaging (MRI) scan with three-
dimensional reconstruction also may provide essential infor-
mation. A bullet-shaped radial head or a major indentation
of the capitellum may presage a poor result. If a period of
more than 3 months has elapsed, the possibility of postop-
erative heterotopic ossification causing ankylosis or fibrosis
of the elbow following surgery must be considered.
In a child, a dislocated radial head is resected only if no
other treatment is possible, as it may lead to cubitus valgus,
prominence of the distal end of the ulna, and radial devia-
tion of the head. Removing the radial head should be
deferred until the completion of skeletal growth and then
done only if decreased function or symptoms, especially
pain, make it necessary. Individual circumstances, however,
may necessitate removal of the radial head prior to skeletal
maturation.
Results
In most reported series, children have fewer sequelae from
a reduced Monteggia lesion than do adults. The major com-
plications generally occur in adult patients, with usually no
significant healing problems of the ulnar fracture in children
and full return of elbow function. Redislocation of the radial
head is rare. The incidence of residual subluxation has not
been well documented.
Complications
Complications, although infrequent in children, may
include the following: (1) Chronic dislocation and malposi-
tion as a result of misdiagnosis (Fig. 16-65), which is prob-
ably the most frequent complication. (2) Recurrent
subluxation or dislocation of the radial head after initial
closed reduction. (3) Posterior interosseous nerve neuropa-
thy, which is most common in the type 3 injury pattern,
although it has also been reported in type l and 2 patterns.
Because spontaneous recovery usually occurs, exploration
16. Radius and Ulna
should not be attempted prior to 6 weeks after the injury.
(4) Fracture of the radial head may occur with type 2 lesions
and may lead to premature epiphysiodesis of the proximal
radial physis. If the fractured radial head is displaced in the
child, it should be reduced and kept in place, as removing
the radial head in a child usually is not indicated. (5) Distal
radioulnar joint disturbance may occur but is not believed
to be significant. (6) Open wounds may cause infection. (7)
Myositis ossificans (Fig. 16-66). (8) Radiohumeral ankylosis.
(9) Radioulnar synostosis (Fig. 16-67). (10) Radioulnar
dysfunction.
According to Thompson and Hamilton, the develop-
ment of myositis ossificans is usually associated with dis-
location of the entire elbow, rather than just the radial
head.309 The time lapse between injury and operation has
been implicated as a predisposing factor in the formation of
myositis.
Spinner and coworkers described posterior interosseous
nerve palsy as a complication of Monteggia injuries in chil-
dren.303 The posterior interosseous nerve is the motor
branch of the radial nerve. In 25% of all individuals the
nerve lies in direct contact with the radius during its passage
to the supinator, and in 30% a fibrous band (arch) is formed
by the muscle insertion, by which the nerve is held close to
the bone. This area may easily be injured during dislocation
of the radial head. The area where the nerve passes around
the proximal radius is most susceptible to a traction- or com-
pression-type injury. With radial head dislocation, a lesion in
continuity (stretching) is created at this level. Two of Spinner
et al.’s cases were transitory, with neuropraxia-type lesions.303
Stein and colleagues also described posterior interosseous
nerve compression at the proximal edge of the supinator
muscle through the fibrous arch of Frohse.304
Morris reported a case in which the radial head disloca-
tion was irreducible because of entrapment of the radial
nerve between the radial head and the ulna.271 Jessing
described nerve injuries in 6 of 14 patients.255 Of the three
children in his series, one had a type 1 lesion with complete
Monteggia Lesions 603

FIGURE 16-63. (A) Original injury. Treatment was directed to the greenstick
ulnar fracture (white arrow). The dislocated radial head was missed at the
time of injury and in several postreduction films (black arrow). (B, C) Two
years later a secondary ossification center has developed in the proximal
radius but not in the normal side. It may be due to injury-induced hyperemia.
Open reduction and internal fixation were performed. The annular ligament,
which was torn, displaced, and scarred, was dissected sharply from the ante-
rior and posterior capsules. It was anatomically intact on the ulna. The
damaged ends were repaired, restoring it to an annular configuration. (D, E)
Appearance 6 months after operation. The radius is stable, and there is full
return of motion. (F) Seven years after open reduction.
 FIGURE 16-64. Bell-Tawse repair 3 years previously. The graft did not grow
or elongate, causing indentation of the neck. There is also heterotopic bone
formation.

FIGURE 16-65. (A) Acute Monteggia injury. Unfortunately, the “reading” of this radiograph was “ulnar greenstick fracture.” (B) Appear-
ance 3 years later. The parents chose not to attempt reduction.

FIGURE 16-66. Ectopic bone around a redislocated radial head that

had been treated by open reduction. FIGURE 16-67. Synostosis after a Monteggia injury. This patient
had a transarticular temporary fixation. The K-wire broke.
Diaphyseal Injuries
FIGURE 16-68. (A) Delayed healing of a Monteggia
injury in a girl with an Erb’s palsy. The radial head
readily dislocated when the nonunion was angu-
lated. (B) As healing slowly occurred, the radial
head subluxated.
paralysis of the deep branch of the radial nerve. Beginning
functional improvement was evident 8 weeks after the injury.
Bado’s 55 cases included 4 with radial nerve injuries, 2 with
ulnar nerve injuries, and 1 with both ulnar and median
nerve injuries.207
Preexistent neurologic deficits may create problems. The
presence of neuromuscular imbalance from an Erb’s palsy
may allow chronic motion at the fracture site. In the case
shown in Figure 16-68, the ulnar fracture was readily diag-
nosed, but disruption of the lateral and annular ligaments
was not originally appreciated. The delayed union of the
fracture eventually healed after surgical intervention, but the
radiocapitellar joint remained unstable.
Chronic dislocation is sometimes compatible with normal
use of the elbow. Many patients have no symptoms and are
able to use the arm in sports and daily activities.
FIGURE 16-69. Ischemic necrosis of the radial head. Capitellar
change is evident.
605
A rare complication of the Monteggia injury is ischemic
necrosis (Fig. 16-69). The infrequent occurrence of this com-
plication is probably related to the variability of the circula-
tion to the radial head.
Another infrequent complication arises with transarticular
temporary stabilization. If the patient decides to “mobilize”
the joint, a K-wire may be bent. If repetitive motion is
attempted, it may lead to pin failure (Fig. 16-67).
Diaphyseal Injuries
Diaphyseal injuries of the radius, ulna, or both are common
in children.24–38,322–437 The severity may vary from pure
bowing to greenstick to complete fracture with displace-
ment. The diaphyseal level of the fracture varies. In chil-
dren there is a greater tendency for the radius and ulna
to deform or fracture (whether greenstick or complete) at
the same level, rather than at significantly different
levels. There is also a likelihood of complete fracture of
one bone, with plastic deformation or greenstick injury or
the other. The thick periosteum allows maintenance of
some skeletal tissue continuity, even when both bones are
displaced. This highly osteogenic tissue also allows excel-
lent healing of both fractures by closed means. When the
adolescent is approaching skeletal maturity, the periosteum
loses some of this capacity, increasing the risk of delayed
union or nonunion.
Classification
Radioulnar fractures follow many patterns. There may be
simple plastic deformation (bowing), greenstick injury, or
complete fracture. The bones may be angulated or dis-
606
placed, with or without significant overriding. The bones
may be fractured at different levels, or only one bone may
be fractured. However, one must look carefully for bowing
or greenstick failure of the seemingly noninjured bone or a
Monteggia or Galeazzi injury. Greenstick fractures are often
evident only in one projection, whereas a view at 90° may
slow a seemingly intact, uninjured bone. Oblique views
may even be necessary to delineate the injury pattern
specifically.
Plastic deformation is a failure pattern affecting tubular
bones such as the fibula, radius, and ulna (see Chapters 2,
5, 6). The deformation is often difficult to diagnose. Because
of microstructural failure, permanent deformation may be
introduced (Figs. 16-70). Stress fracture may also occur (Fig.
16-71). More often there is definite evidence of a greenstick
injury (Figs. 16-72, 16-73). Cortical failure may be minimal.
The radius often sustains a greenstick failure, whereas the
ulna, instead, undergoes plastic deformation (Fig. 16-74).
The ulna may also sustain a greenstick fracture without
apparent radial injury. Both bones may sustain greenstick
injuries (Fig. 16-75).
Angular deformation varies. The radius may deform
30°–40° without concomitant ulnar injury. The periosteum
is disrupted on the tensile failure side in such angulation but
is usually intact along the compression side, a factor that
should be considered during any reduction manipulation.
Even when both bones are fractured, only one may be angu-
lated. Angulation varies from mild to severe. The true degree
of angulation may require oblique views. Mid-shaft angula-
tion should be defined as accurately as possible and subse-
quently corrected, as osseous remodeling is least likely in the
mid-shaft. Similarly, overriding varies significantly.
Diagnosis
Roentgenograms should include both the wrist and elbow
joints to be certain there is no dislocation of either the prox-
imal (Monteggia injury) or the distal (Galeazzi injury)
radioulnar joint. It is possible to have a Monteggia injury
with a fracture of the radius or plastic deformation of the
ulna, as well as the typical pattern of a fracture of the ulna.
Initial roentgenograms should be true anteroposterior and
lateral views. Nonstandard angles and degrees of rotation
may complicate interpretation but may eventually be neces-
sary to better define fracture patterns and the extent of trau-
matic deformation.
The radius is a curved bone that is cam-shaped in cross
section at several levels. Malrotation of the radius may be rec-
ognized by a break in the smooth curve of the bone or a dif-
ference in the width of the cortices of the apposed fracture
fragments. In fractures of the forearm, palmar or flexor
bowing (i.e., of the apex) is usually a sign of pronation defor-
mity, whereas dorsal or extensor bowing (at the apex) usually
signifies a supination deformity.
Evans drew attention to the bicipital tuberosity roentgeno-
graphic sign.7 The problem in the younger child is that this
region of the tuberosity may be minimally developed and
may not suffice as an accurate indicator, as it does in older
children, adolescents, and adults. The tuberosity normally
lies medially when the forearm is fully supinated (i.e., it faces
the ulna). It lies posteriorly in midposition and laterally in
full pronation. If there is any question about this position-
16. Radius and Ulna
ing, a similarly rotated view of the normal, uninvolved arm
may be obtained. The estimated degree of proximal rotation
may be used as a guideline to determine the best treatment
position in which to place the distal fragments relative to the
proximal fragments.
In infants and young children under 3 years of age (espe-
cially under 18 months), child abuse must be considered as
part of the differential diagnosis, especially when the frac-
ture already has callus or when metachronous, multiple frac-
tures are present (see Chapter 11).
Neurovascular Injury
Because nerves and blood vessels are infrequently injured in
children’s forearm fractures, there is a tendency to overlook
the possibility of such damage. Detailed, well documented
examination is essential. The median nerve is protected from
the radius by intervening layers of muscle. The ulnar nerve is
close to bone and is occasionally damaged, especially with
open fractures near the lower end. Warren described two
cases of anterior interosseous nerve palsy.432 In both cases
there was complete, but temporary, paralysis of the flexor pol-
licis longus and index finger segment of the flexor digitorum
profundus. Both patients made a full, spontaneous recovery
without exploration of the nerve. The anterior interosseous
nerve branches from the median nerve distal to the neck of
the radius and passes along with the anterior interosseous
vessels extending along the interosseous membrane. Because
of the proximity of the nerve to the radius, it is subject to
injury in a displaced forearm fracture.
Davis and Green reported six nerve injuries: four median,
one ulnar, and one posterior interosseous.31 All cleared spon-
taneously within 3 weeks, suggesting that each was a neuro-
praxia. The possibility of nerve injury is particularly
important in distal third fractures; adequate assessment of
the median nerve must be done. Although it happens infre-
quently, the medial nerve may be traumatized when the distal
fragment is dorsally displaced and the forearm is shortened.
Compartment Syndrome
Despite the presence of closed fascial spaces in the forearm,
the frequency of compartment syndrome followed by
ischemic (Volkmann’s) contracture is low in children, espe-
cially when compared to the risk in supracondylar fractures.
The fractures, particularly when complete, tend to allow dis-
sipation of intracompartmental pressure into the more
superficial area and throughout other compartments. Care
must be taken to watch for increased pressure in the ante-
rior compartment. Clinical monitoring of pressure is appro-
priate. If signs warrant such a diagnosis, the child should be
admitted, the cast bivalved, and the arm elevated. If symp-
toms of excessive pain and pain with finger motion do not
rapidly dissipate, increased pressure is likely and should be
addressed with fasciotomies or, better yet, direct measure-
ment of compartment pressures. This complication is dis-
cussed in detail in Chapter 10.
Rotation
Before discussing treatment, it is essential to consider rota-
tion (supination-pronation), as restoration of this function
Diaphyseal Injuries 607

FIGURE 16-71. (A) Nondisplaced stress injury (arrows) of the

radius and ulna. (B) Eight weeks later.

D
FIGURE 16-70. (A) Plastic deformation of the ulna (arrow). (B) Con-
tralateral side. This girl lacks full supination and pronation. (C)
Plastic deformation of the radius with ulnar fracture. (D) Greenstick A,B
bowing of both bones (arrows) in a 4-year-old.
FIGURE 16-72. (A) Greenstick fracture of the ulna. (B) Four months
later.
608
is an important aspect of treatment. Forearm rotation nor-
mally has a range of 180°.15,398,405 The vertically paired prox-
imal and distal radioulnar joints move synchronously.
Normal radial bowing is essential to the rotational axis of the
radius about the ulna and should be maintained in any
reduction. Failure to do so potentially disrupts the rotational
cone (Fig. 16-76).
Although a child may adapt functionally to a decrease in
rotational motion up to 50%, forearm fractures should be
treated in a manner that avoids, as much as possible, any sig-
FIGURE 16-74. (A) Radial greenstick and ulnar plastic failure
pattern. Ulnar failure is proximal (arrow) to the radial fracture. (B)
Ulnar greenstick fracture with barely discernible radial injury
(arrow). It was a hyperpronation injury.
16. Radius and Ulna
FIGURE 16-73. Greenstick injury shown
radiographically in Figures 16-56 and 16-57.
(A) Histologic view showing entrapped
muscle (arrows). (B) Duplication of bending
to fracture one cortex.
nificant loss of normal supination and pronation.424 Rota-
tion is lost with loss of longitudinal alignment of one or
both bones. This causes variable widening and narrowing
of the interosseous membrane during attempted rotatory
movements.
Loss of rotation is a common problem after forearm frac-
tures, no matter what the level of fracture.348 Knight and
Purvis found a residual rotational deformity between 20°
and 60° in 60% of their patients.373 Evans found a malrota-
tion deformity of more than 30° in 56% of the cases.7,349 The
FIGURE 16-75. (A) Greenstick injury of both radius and ulna. The
lateral cortex is intact on both (arrows). (B) Greenstick fractures of
both bones. The radius is angulated, and the ulna is spontaneously
reduced.
Diaphyseal Injuries
FIGURE 16-76. (A) Angular malunion introduces a frustrum (D) into
the normal cone of rotation, thereby limiting the area (stippling) of
the cone base. In this example, residual pronation of the distal
radius restricts full supination. (B) Type of angulation that may seri-
ously impair forearm rotation. See Figure 16-9 for normal rotational
axis cone.
distal fragment is usually pronated, so supination is primar-
ily affected.
Fractures have been produced in skeletally mature cadav-
ers to determine the effects of various degrees of angular
malunion.349 Malrotation of 10° limited rotation by 10°, but
10° of angular malunion limited rotation by 20°. Bayonet
609
apposition did not limit rotation. Pure narrowing of the
interosseous space was important in proximal fractures. Nar-
rowing impeded rotation by causing the bicipital tuberosity
to impinge on the ulna. Malalignment of the fractures of the
ulnar metaphysis increased articular tension so the head of
the radius was not free to rotate. These observations proba-
bly are readily applicable to children.
Matthews and colleagues tested specimens for the effect
of residual angulation from simulated fractures of both
bones of the forearm.386 Ten- and twenty-degree angulations
were selected for testing. With 10° of malunion there was
little significant functional loss of forearm rotation, but
with 20° of angulation, in any direction, there was statisti-
cally significant and functionally important loss of forearm
rotation.386
Christensen and colleagues tried to ascertain why there is
a difference of opinion in the literature concerning the
proper positions of immobilizing the forearm that would
ensure separation of the radius and ulna and prevent cross-
union.5 They studied 36 adult cadaver forearms. The small-
est interosseous distance was in pronation. The greatest
distance was in midposition. The widest base was on the
middle-third of the forearm. They further showed that the
interosseous membrane was tense in 30° of supination but
became increasingly relaxed with further supination or
pronation.
It is usually possible to recognize these rotational defor-
mities and correct them when treating the fracture. The vari-
ability of supination and pronation of the proximal and
distal fragments may be demonstrated radiographically. If
the upper part of the arm lies in supination and the distal
part looks as if it is pronated, supination should be the major
reduction direction to move the fracture back to anatomic
position. Infrequently, the fracture reduction is sufficiently
stable to allow testing of the range of movement. Of course,
a full range of movement indicates an accurate reduction.
Determination of the correct rotational position in which to
immobilize fractures of both bones of the forearm is impor-
tant to prevent a corresponding limitation of rotational
movement.
Significant rotational deformity may be created at the time
of reduction of complete fractures if they are manipulated
improperly. The concept of pronating all distal third frac-
tures, supinating all proximal third fractures, and leaving
middle third fractures in neutral has been repeatedly rec-
ommended as the proper method of reduction since Evans’
original article on the rotatory nature of forearm fractures.349
The “rule of the thirds,” however, should not be applied rigidly to
these fractures. Reduction of the complete distal third fracture
by forcible pronation may in fact result in malrotation of the
fracture site, a deformity that usually does not completely
correct with growth, regardless of the age of the child.
Accurate reduction of the bone ends is best accomplished
when the rotational deformity is corrected and fluoroscopi-
cally assessed. Even a small inaccuracy can prevent the inter-
locking of the bone ends, on which stability depends. The
orthodox position in which to immobilize these fractures is
that of full supination for the upper third and of midposi-
tion (neutral rotation) for fractures of the middle and lower
thirds. These positions are based on the anatomic arrange-
ment and function of the pronator and supinator muscles in
610
the forearm. It is unreasonable to suppose that all fractures
at a given level present the same degree of rotational defor-
mity. Other factors may also be involved, such as variations
in the direction and leverage of muscle pull with varying
degrees of angulation of the fragments, differences in the
tension of the biceps with flexion and extension of the elbow,
and the effect of the interosseous membrane. The position,
with respect to rotation, in which such fractures should be
immobilized is governed by the degree of rotation of the
upper radial fragment, the upper fragment of the ulna being
stable because of the type of elbow articulation.
It has been standard teaching that fractures of the upper
third of the radius and ulna be immobilized in full supina-
tion because the proximal fragment may be pulled into
supination by the biceps and supinator muscles.339,346,348
Some suggest that this arbitrary concept is a mistake because
cases in which the fully supinated position is used may have
a significant incidence of malunion. In full pronation the
brachioradialis muscle may act as a bowstring to increase the
dorsal tilt of the distal fragment and cause angulation or
redisplacement. However, flexing the wrist may counteract
this deformity. An accurate study of the radiograph is
required to decide whether these lesions are pronation or
supination injuries, and the degree of rotation should be
assessed to determine the position of greatest stability.
Gainor and Hardy recommended immobilizing these frac-
tures in full extension to control rotation.358 Manipulation
under fluoroscopy is often helpful to determine the
optimum position of stability.
Although remodeling often corrects 30°–40° of angular
displacement of a distal metaphysis in a child with sufficient
remaining growth, remodeling usually does not do anything
more than round off the ends of malunited fractures of
the diaphysis, and it never corrects rotational deformity
accompanying the malunion. It must always be remem-
bered that angular fractures of the forearm are asso-
ciated with some degree of rotational deformity. Any loss of
motion due to mid-shaft or proximal fractures tends to be
permanent.
Treatment
When treating fractures of the radius and ulna in children,
longitudinal (axial) and rotational alignments are the most
important goals of reduction. Reduction may be more diffi-
cult when the radial fracture is proximal to the ulnar frac-
ture. Reduction of these fractures may be more difficult
to maintain with the elbow in flexion. Sometimes they are
more stable in extension. Overriding is acceptable so long
16. Radius and Ulna
FIGURE 16-77. Completion of the fracture in greenstick injuries of
the radius and ulna.
as longitudinal alignment and the interosseous spacing
are maintained.
The completion of greenstick fractures may be necessary.
Failure to do so may predispose to recurrent displacement
or angular deformation. Reangulation may be prevented
by placing the arm in the correct degree of pronation or
supination and holding this position in the cast. In general,
greenstick fractures should be slightly overcorrected by slow
manipulation to take the plastic deformation out of the frac-
ture (Fig. 16-77). Overcorrection may complete the fracture
and may be accompanied by an audible or palpable crack. If
this is not done, the plastic deformation may reappear, even
in a cast (Fig. 16-78). This observation applies primarily to
mid-shaft fractures.
Sanders and Heckman reported 14 cases of plastic defor-
mation of the radius and ulna and suggested a method of
pressure application over a period of several minutes to
lessen the plastic deformation.414 They thought this reduced
the clinical deformity, allowed treatment of any accompany-
ing fractures, and led to earlier return of full supination and
pronation in the forearm. Certainly, their method of pro-
longed pressure should be attempted prior to considering
open reduction or osteoclasis.
Complete fractures of the radius and ulna may be trou-
blesome. The following guidelines should be used: (1) Good
reductions must be attained and held with a well-molded
cast. (2) Cortical apposition, even if bayonet, is adequate so
long as rotation is correct, the interosseous space is pre-
served, and there is no longitudinal axial angulation. (3)
Immobilize the fracture in the position—any position—in
which the alignment is correct and the reduction feels (and
FIGURE 16-78. Residual angular malunion
complicating greenstick fractures in which the
injury was not “completed.”
Diaphyseal Injuries
fluoroscopically appears) stable. (4) Minor improvements
can and should be made through remanipulation up to 3–4
weeks after injury, at which time the fracture becomes
mechanically firm. Do not be afraid to remanipulate. (5) Be pre-
pared to carry out either closed reduction with percutaneous
intramedullary rodding or open reduction and internal fix-
ation, even in children under the age of 10 years, rather than
accept a poor position. Skin traction is a method that may
be used to try to attain a reduction during the first few days
after significant injury, subsequently attempting another
closed reduction. (6) Always warn the parents about the pos-
sibilities of remanipulation of short-term recurrent defor-
mity to prevent long-term deformity and loss of function.
The method of reduction advocated for complete frac-
tures of the radius alone or the radius and ulna together pre-
cludes the possibility of a rotational deformity. After enough
analgesia, anesthesia, or both have been administered
to provide adequate muscle relaxation, the arm may be
suspended by finger traps and a counterweight of 10–15
pounds applied across the upper arm. Enough time should
elapse to allow the fracture to be brought out to length
and to correct the overriding of the distal fragment,
although a toggle maneuver is often necessary to connect
the cortices. After length has been restored in this fashion,
the fracture is allowed to seek its own level of rotation, rather
than manipulating the distal fragment into any preconceived
position of theoretically correct rotation. With the forearm
suspended in fingertip traction, the two fragments usually
FIGURE 16-79. Satisfactory closed reduction
of both bones. (A) The anteroposterior view
shows longitudinal alignment and good main-
tenance of the interosseous space. (B) The
lateral view shows mild overriding but with
adequate longitudinal alignment. (C) Subperi-
osteal new bone.
611
spontaneously assume correct rotational alignment.
Such fractures usually attain a neutral or slightly pronated
position.
No rotatory manipulation of the fracture should be done
once the overriding has been corrected and the cortices
engaged. The examiner should check to see if there is ade-
quate rotational correction by assessing the width of the cor-
tices of the two fragments, which is usually easily recognized
by the disparity of width between the two fracture fragments.
Remodeling may correct the cortical width difference, but it
does not correct the rotational (or angular) deformity.
The width of the interosseous space often can be restored
by manual pressure to the soft tissue between the bones, pro-
vided swelling is not excessive. If swelling is present, attempts
to reduce the fracture may be deferred several days and over-
head traction or splinting used until the soft tissue swelling
subsides. When traction is maintained, a long arm cast is
applied with the elbow in 90° of flexion and the forearm fully
supinated. The cast must be molded well over the palmar
aspect of the radius. Again, pressure is applied to maintain the
interosseous space while the cast material is consolidating.
Failure to restore normal alignment, with regard to both
longitudinal and rotational deformation, may cause restric-
tion of pronation and supination of the forearm after frac-
ture healing. Bayonet or side-to-side apposition with some
overriding is acceptable, provided the ulna and radius do
not deviate toward one another and that the interosseous
space is maintained (Figs. 16-79, 16-80). Reduction of
612
FIGURE 16-80. (A, B) Appearance 4 months after injury of displaced, overriding fractures in a child with multiple injuries. (C, D) Appear-
ance 16 months later. Extensive remodeling has occurred.
one bone with continued overriding of the other is not
usually an acceptable reduction. To determine if this
condition exists, it is best to obtain true anteroposterior and
lateral films. Any obliquity in the film may be deceptive in
terms of the degree of angular deformation (longitudinal
malalignment).
These fractures must be maintained in an immobilized
position in a well-molded cast with three-point fixation
(Fig. 16-81) for longer than most children’s fractures (about
6–8 weeks), to allow satisfactory callus formation. The cast
should be changed as necessary to compensate for decreased
swelling.
Because deformation and angular malalignment may
occur at a much later time after the initial injury, it is imper-
ative that serial roentgenograms be examined to detect any
loss of position. If closed manipulation is unsuccessful, open
surgical reduction may be indicated, especially in the older
child (over 10 years) or the patient who is close to skeletal
maturity. A well-padded cast that acts as a compression dress-
16. Radius and Ulna
ing may be applied and combined with elevation. The
fracture should be remanipulated 5–7 days later. Skeletal
traction may also be applied.
Open reduction of both bone fractures in young children
may be necessary. There is a belief that open reduction is
forbidden in children, but not all fractures of both bones
can be successfully managed by closed reduction (Figs.
16-82 to 16-84). Internal fixation is preferable to malunion.
High oblique fractures in teenagers are likely to require
open reduction.
There is an increasing acceptance of percutaneous
pinning of one or both bones. With this technique flexible
rods (of which several varieties are available: Rush rods) and
the Nancy nail are inserted through small metaphyseal fen-
estrations. The radius is best approached in a distal to prox-
imal method. The ulna is easier to approach in a proximal
to distal direction. Because of relatively early maturation and
growth of the proximal end of the ulna, a rod or nail may
be inserted through an epiphyseal drill hole. However,
FIGURE 16-81. Principle of three-point fixation
(arrows) of the greenstick fracture to prevent rean-
gulation while the arm is in the cast.
Diaphyseal Injuries 613

FIGURE 16-83. (A) Radial fracture combined with torus injury to the
ulna in an 11-year-old child. Closed reduction was impossible. (B)
Tubular plate was applied.

During the first decade of life there is usually complete

correction of angular (longitudinal axis) deformity up to
20°–25°, but beyond this age or this degree of malposition
the likelihood of spontaneous correction decreases.367 The
correction occurs principally at the distal physis and less so
at the proximal physis and by cortical drift and remodeling
FIGURE 16-82. (A) Displaced fractures. They were not stable after at the fracture site. The longitudinal angulation may remain.
closed reduction. (B) Similar fractures of the radius and ulna in an
adolescent. These fractures were treated with intramedullary rods.
If this technique is used, it is recommended that the ulnar rod be
placed through the proximal metaphysis if the adjacent physis
is still functional. In this patient the proximal radius and ulna had
undergone physiologic epiphysiodesis. The distal ends were still
functional, and rod placement in the radial metaphysis did not inter-
fere with growth.

my preference is a fenestration just distal to the proximal

epiphysis.

Results
In a series of 88 greenstick fractures, the only complication
was recurrent palmar angulation of the fracture. When
encountered during the first 3 weeks after injury, they were
remanipulated.31 Beyond this time, remanipulation is
decreasingly successful. Of greenstick fractures of the distal
third of the radius and ulna, there were 8 complications in
62 patients; all developed recurrent palmar angulation of
15°–30°. This loss of position, which resulted in up to 30° of
palmar angulatipn, occurred witin the first week in five
patients, all of whom experienced improvement by rema-
nipulation. A gradual increase in angulation over 4–6 weeks
may occur in these patients but usually does not increase FIGURE 16-84. Bilateral plating. Use the smallest plates possible
beyond 15°. that can stabilize the fracture.
614 16. Radius and Ulna

recurrence, although recurrence is probable in the highly

osteogenic immature skeleton.
Allowing children out of immobilization too early may
result in a stress or complete fracture through the original
fracture and new callus (Fig. 16-90). One way to prevent this
is gradual remobilization. At 4–6 weeks the long arm cast is
converted to a short arm cast. This conversion allows elbow
movement and limited supination-pronation and begins to
stimulate some corrective remodeling of the trabecular and
cortical bone. A protective splint or orthosis for 2–3 months
in an active child is often appropriate, especially for fractures
that have healed slowly or in the child insistent on returning
rapidly to a structured sport.
In one series, 3 of the 547 fractures were open, and 1 was
subsequently complicated by gas gangrene, even though ade-
quate débridement had been carried out at the time of pre-
sentation.31 Osteomyelitis of closed forearm fractures has
also been reported (see Chapter 9).
Rayan and Hayes described a case of fracture of both
bones of the forearm in which the flexor digitorum profun-
dus was trapped within the ulnar fracture.406 The complica-
tion was not recognized until 2 years after the fracture, when
it healed with a lytic defect in the ulna. Release of the muscle
belly from its entrapment and release of the adhesions
allowed full restoration of function. As shown in Figure 16-
73 the greenstick fracture undoubtedly opened up enough
FIGURE 16-85. (A) Delayed union and malunion of the ulna with
delayed union of radius. The radius had healed by 4 months after
the injury. (B) One year later the patient still had a tender ulnar
malunion. She was treated with a compression plate. Four weeks
postoperatively, the fracture is healing. Note that the radius has
healed well.

Complications
Complications are infrequent but often difficult to manage.
Although delayed union or nonunion is rare in young chil-
dren because of the highly osteogenic periosteum, older
children and adolescents are increasingly susceptible to this
complication. One bone may unite, albeit delayed, and
delayed union or nonunion may develop in the other bone
(Figs. 16-85 to 16-87). This delayed union or nonunion
occurs because of rotational micromotion of the slower
healing fracture once the other fracture heals. These com-
plications should be treated with compression plating and
localized bone grafting. Extensive bone grafting is usually
unnecessary once the fracture is internally immobilized.
Angular union (malunion) is also infrequent (Fig. 16-88).
When present, it should be allowed to mature and then be
treated by appropriate corrective osteotomy. Fuller and
McCullough believed that in children with malunited frac-
tures of the forearm little useful correction of deformity
could be anticipated with diaphyseal fractures when the
child was older than 8 years.356
Synostosis may occur, especially when the fractures are at
the same level (Fig. 16-89). Removal of the synostosis is not
easy and should not be attempted until the process is mature
(at least 6 months). An important technical point is to
remove the synostosis segment by an extraperiosteal dissec-
tion. Otherwise, a possible periosteal continuity may remain
and enhance the likelihood of recurrence. Interposition of FIGURE 16-86. Less acceptable method of treating delayed union
soft tissue, fat, muscle, or Silastic membrane may prevent or nonunion using small percutaneous pins.
Distal Radial and Ulnar Metaphyseal Injuries
FIGURE 16-87. Delayed union following closed
reduction. (A) Delayed union of both bones. (B)
Delayed union of the ulna.
FIGURE 16-88. Angular malunion and delayed union with accom-
panying severe plastic deformation of the ulna. Correction required
osteotomy of both bones.
615
at maximum deformation to allow some muscle tissue to
become lodged in the open fracture gap of the damaged
cortex. As the fracture “closed” with the dissipation of the
deforming force, this muscle tissue became entrapped within
the fracture. This phenomenon may happen more fre-
quently than realized in these fractures. However, functional
problems do not seem to be common.
Distal Radial and Ulnar
Metaphyseal Injuries
The distal radius and ulna are among the most commonly
injured regions of the developing skeleton.438–527 One of the
most frequent types of fracture is the greenstick injury, which
may take several forms. A torus fracture (Fig. 16-91) is vari-
able buckling of the cortical bone of the radius, with minimal
evidence of trabecular disruption.479 This pattern is common
in young children. The diagnosis is often made in a film
taken weeks after the original injury because the original
roentgenogram did not disclose the injury. Careful attention
must be paid to both anteroposterior and lateral views to
look for subtle metaphyseal deformation. If the wrist is
tender and swollen, consider oblique views if a torus injury
is not evident on the standard views. It is a type 8 growth
mechanism injury that results in temporary ischemia of the
metaphysis distal to the fracture and subsequent sclerosis
during immobilizatior and normalization of bone density
with subsequent revascularization (see Chapter 6). The ulna
may be (seemingly) uninvolved or may sustain variably severe
injury (beware the ulnar styloid injury and late-appearing
“nonunion”). The other pattern is a classic greenstick injury
with buckling of the palmar cortex, angulation, and loss
of dorsal cortical integrity (Fig. 16-92), which may also
be associated with a crushing injury with some cortical
displacement.
 FIGURE 16-89. (A, B) Progressive develop-
ment of radioulnar synostosis complicating
proximal third fractures of both bones.

FIGURE 16-90. Refracture following injury to

the distal third. The ulna has fractured
through the callus at the level of the original
injury, and the radial callus has fractured
proximal to the original injury. (A) Antero-
posterior view. (B) Lateral view.

FIGURE 16-91. (A) Typical distal radial torus fracture (arrows). (B) The ulnar styloid is fractured, with the fracture still minimally
Similar injury in an older child. There is mild sclerosis in the distal evident (arrow).
metaphysis and subperiosteal new bone proximal to the fracture.

616
Distal Radial and Ulnar Metaphyseal Injuries
FIGURE 16-92. (A) Buckling of the entire radial cortex with a con-
comitant ulnar fracture. Cortical integrity and overlap are present
on the dorsal (compression) side. The ulna was intact in this
In a more severe greenstick injury, the fracture may be
dorsally angulated, with disruption of the palmar cortex and
an intact, but deformed, dorsal cortex (Fig. 16-93). The frac-
ture may also exhibit complete loss of cortical integrity. If the
fracture is undisplaced, the periosteal sleeve is usually intact
and imparts a significant degree of stability.
In the most severe injury pattern, the distal fragments are
displaced dorsally and radially with various degrees of over-
riding (Fig. 16-94). The fracture of the radius is usually com-
plete, although fractures of the ulna may be complete and
similarly displaced, greenstick, or minimally involved, with
injury to the styloid process, similar to a Colles’ fracture in
an adult.
There is an injury pattern with longitudinal propagation
toward the physis. This increases the risk that the physis has
absorbed some of the fracture energy and so is at risk for
FIGURE 16-93. (A) Angular deformity of
a distal radial metaphyseal fracture. (B)
Nine weeks later.
617
patient. (B) Greenstick distal radial fracture with intact cortex on
the “ulnar side” (arrow).
growth alteration. This pattern, a variant of a type 8 growth
mechanism injury, is discussed in detail in Chapter 6.
Pathomechanics
With a greenstick injury, the impact of indirect violence of a
fall on the outstretched hand coupled with a rotational strain
crumples the dorsal cortex, but the palmar cortex remains
intact. The distal fragment in a torus fracture may be angu-
lated dorsally or may be displaced minimally. Because the
greenstick injury absorbs a large amount of energy that is
not dissipated by a complete cortical fracture or displace-
ment of fragments, the compression force may be transmit-
ted into the physis as a type 5 injury, which is difficult to
diagnose at the time of original injury but must be sought at
the follow-up examinations.
618
FIGURE 16-94. Displaced distal metaphyseal fractures. (A) Lateral view of characteristic dorsal displacement. (B) Severe displacement
and angular deformity.
Even when there is no displacement of the radial fracture,
the ulnar styloid is often fractured, which occurs because
of the integrated relation of the distal radius and ulna
through the triangular fibrocartilage (Figs. 16-11, 16-12).
However, because the ulnar styloid is often unossified in
those who are in the usual age range for this fracture, the
diagnosis is not ordinarily evident until several weeks to
months after the injury, when the area finally ossifies and
appears radiographically as nonunion.
Diagnosis
The diagnosis is usually evident clinically. The child presents
with a painful, swollen wrist. If there is dorsal displace-
ment, the classic “silver fork” deformity may be evident.
Roentgenography confirms the injury in most instances,
although in some cases the initial roentgenograms may not
show any evidence of injury. In these cases the diagnosis
must be made empirically on the basis of clinical findings. It
is still wise to treat the patient, even in the absence of obvious
radiologic findings, because subsequent use of the unpro-
tected extremity may lead to an obvious, sometimes com-
pletely displaced fracture.
The neurovascular status should be assessed carefully.
With the dorsally displaced fracture, the median nerve is par-
ticularly susceptible to acute injury (especially stretching)
from the fracture fragment and more chronic injury from
the swelling and compromise of the tunnel by the displace-
ment of soft tissue and skeletal elements. Posttraumatic
carpal tunnel syndrome is rare in children.
Treatment
A torus fracture is an undisplaced injury that usually involves
only the distal metaphysis and does not necessitate reduc-
tion, merely immobilization in a well-fitting splint or cast
for 3–4 weeks. Hughston advocated using a cast that includes
16. Radius and Ulna
the wrist and elbow, believing that if this type of cast is
not used there may be angulation during the healing
process.367
Onne and Sandblom defined the angular deformity of the
distal third fracture but did not define an absolute number
of degrees to use as a guideline.395 If the angle exceeds
25°–30° in infants or 15°–20° in children beyond the second
year, closed reduction with completion of the fracture by
reversal of the deformity is usually indicated. Like greenstick
fractures of the mid-shaft, torus fractures may deform
because of powerful muscles acting across the wrist, coupled
with intrinsic deforming plasticity in the remaining intact
bone.
A greenstick fracture of the radius at the junction of
the metaphysis and diaphysis with some supination is
common and problematic because angulation tends to
recur, even after reduction. The forearm should be held
in full pronation in an above-elbow cast with three-point
fixation. If the deformity is severe, it may be necessary
to complete the fracture, as previously described for
fractures. However, casting in full pronation with an above-
elbow cast allows the intact periosteum to lock the fracture
in place and usually stops a supination deformity from
developing.
Complete fractures should be reduced with the patient
under an anesthetic, as relaxation is an essential part of the
reduction and is rarely obtained without complete muscular
relaxation.282,454,459 The technique of reduction is to re-create
and overexaggerate the deformity (Fig. 16-95). First, the
extremity is subjected to longitudinal traction in the line
of the deformity, with countertraction at the elbow. The
surgeon pushes the fragments into normal position, and
the distal radius and ulna are pressed to restore the width of
the interosseous space. It is desirable to achieve anatomic
alignment (Fig. 16-96) in the longitudinal and rotational
directions, but the cortices may overlap in the lateral
view. Bayonet apposition usually should not be accepted
Distal Radial and Ulnar Metaphyseal Injuries
FIGURE 16-95. Method for reducing a dorsally dis-
placed distal radial or radioulnar fracture. R = radius;
U = ulna. (A) Initial deformity. (B) Hyperextend the distal
unit. (C) Push or “walk” the fractured ends until they
lock. (D) Bring the wrist back to its neutral position.
Although complete anatomic reduction is not essential,
longitudinal and rotational alignments must be attained
and maintained.
(Fig. 16-97). Encroachment of the interosseous space by
the fragments should be corrected, as it may restrict
the rotation of the forearm, although with growth there
may be sufficient remodeling to overcome this problem.
Minimal overriding may be remodeled. Marked overrid-
ing occasionally requires skeletal traction through the
metacarpals to stretch soft tissues enough to allow manipu-
lative correction.
An above-elbow cast may be applied for immobilization
and should be maintained for 6 weeks. Again, it is impera-
tive to check the injury at adequate intervals to assess any
subsequent redisplacement. A splint should be used for
several additional weeks, especially in children with com-
plete fractures.
FIGURE 16-96. (A) Successful closed reduction. (B) It was not held well in the cast, however, and progressively angulated.
619
Open reduction is infrequently indicated in children (Fig.
16-98). In my experience, it has been necessary in only a
few cases among several hundred examples of this injury.
In these cases the pronator quadratus muscle had been
disrupted, with the proximal fragment of the radius button-
holed into or through the muscle; it was impossible, except
under direct vision, to free the fragments and replace them
on the palmar side of the forearm because some of the
muscle had been displaced onto the dorsal aspect of the
proximal fragment.
A totally unstable distal radial fracture in a child who is
approaching skeletal maturity can probably be treated more
like a fracture in an adult: Open reduction and internal fix-
ation with pins or plates is undertaken.
620 16. Radius and Ulna

Failure to Break the Cortex Completely in Angulated

Greenstick Fractures
Failure to break the cortex completely in angulated green-
stick fractures is one of the most common pitfalls. Merely to
straighten the bone is not sufficient. The intact cortex must
be completely broken. In some instances when there is no

FIGURE 16-97. (A) Dorsally displaced distal radial fracture (the

ulna is not displaced). This fracture does not always or adequately
remodel.

Treatment Problems
These fractures may appear simple to treat, but they are
often more difficult to take care of adequately than can be
appreciated initially and may be less than ideally managed
because of certain concepts. The following are areas that
lead to poor results.

Failure to Attain Adequate Initial Reduction

The more accurate the initial reduction, the less is the poten-
tial for loss of alignment. Reduction of displaced, overriding
fractures of the distal forearm is particularly difficult in the
presence of marked local swelling. Unless neurovascular
compromise is present, there is no emergency in treating
these fractures. Compression is applied with a splint and the
child treated by elevating the extremity (hospital or home);
adequate reduction is then undertaken once the swelling has
receded. Reduction with the patient under anesthesia is less
traumatic, as the fracture may be manipulated under optimal
conditions and with the use of an image intensifier.

Failure to Immobilize the Forearm in

a Position of Stability
The degree of rotation of the forearm in which fractures of
the radius and ulna should be immobilized has been the
subject of some controversy. The forearm should be immo-
bilized in that position of rotation (i.e., supination, prona-
tion, neutral) in which the reduction appears to be most
stable. This position may be determined best using an image
intensifier. A standard routine practice has been full prona-
tion in lower third fractures, but it should be approached
only as a relative guideline and not an absolute indication
for positioning the wrist and forearm. If the reduction is
stable, full supination is recommended to allow the radius
and ulna to parallel each other. If an adequately applied cast
is maintained during this period, the pull of the muscles
should not cause malalignment of the satisfactorily reduced
stable fracture. Stability of reduction may be determined FIGURE 16-98. (A) Open reduction of a distal metaphyseal fracture.
clinically and by a roentgenographic examination. (B) Open reduction and plate fixation.
Distal Radial and Ulnar Metaphyseal Injuries
apparent fracture of the ulna, there may be significant green-
stick bowing in association with the complete fracture or a
true greenstick fracture of the radius. These fractures are
deceptive. The fracture of the radius should be completed
in such an instance, as the intrinsic plastic deformation of
the ulna makes it bow the potentially unstable radius.
Loose Cast
To maintain reduction, external compression by the cast
must be secure. As swelling around the fracture site subsides
and muscles atrophy, the cast may become loose and the
fracture fragments are subsequently displaced or are in loose
alignment. A loss of position may occur as late as 3–4
weeks following reduction. A loose cast may be detected by
roentgenography, as can the possibility of angular deforma-
tion. It is important that the fracture be radiographed within
a week after initial reduction. If there is any evidence of loos-
ening of the cast or beginning angular deformity, particu-
larly toward the original deformity, the cast should be
removed and replaced with a snug, well-fitting, three-point
fixation cast. The type of cast is, of course, the preference of
the individual surgeon. One cannot overemphasize the
importance of a snug, but not constricting, cast or splint for
preventing loss of alignment and frequent cast changes, as
necessitated by the subsidence of swelling. Sugar tong
(incomplete) casts accommodate swelling during the early
stages but should usually be followed by a well-molded cir-
cumferential cast after the swelling dissipates.
Displaced fractures of the radius and ulna are immobilized
in a sturdy long arm cast that extends from the upper arm
to the metacarpal heads, with the elbow in 90° of flexion.
Stiffness of joints from prolonged immobilization is gener-
ally not a problem in children. For unstable fractures of the
distal third of the radius, the plaster should include the prox-
imal phalanges to immobilize the metacarpophalangeal
joints. Secure fixation of the proximal phalanx is particularly
important; otherwise children tend to use the thumb and
fingers and may cause redeformation in an anatomically
unstable fracture.
Failure to Detect and Correct Loss of Position
The fracture must be roentgenographed at appropriate
intervals. By 10–14 days some radiolucent callus may begin
to appear. This biologically plastic callus may enhance the
stability of a re-reduction, but it may also impede attempts
to improve angulation. Adequate roentgenograms are essen-
tial. In particular, anteroposterior and true lateral views must
be obtained, as oblique views may be misleading and may
make the fracture appear more or less deformed than it is.
Results
In general, the results of treating distal metaphyseal fractures
are good to excellent. Because many are undisplaced green-
stick injuries, there is minimal rotational or angular defor-
mity requiring extensive remodeling. Even with displaced
fractures, the results are good when a satisfactory reduction
has been attained. Problems arise when the fracture rean-
gulates or is left dorsally displaced.
621
Complications
A relatively high incidence of complications occur with com-
plete fracture of the distal third of the radius and ulna. Of
47 patients in one series, 22 had complications, including
angular deformity, rotational deformity, gas gangrene,
medial nerve injury, and refracture. In another series, recur-
rent dorsal angulation at the fracture site was the most
common complication, occurring in 43 of 547 patients.31
The incidence of the complication after greenstick fractures
of the distal third of the radius alone or after fractures of the
radius and ulna together was 10%, and after complete frac-
tures of the distal radius and ulna it was 25%.31 An intact ulna
apparently helps stabilize a complete fracture of the distal
radius alone, as the incidence of reangulation of this frac-
ture pattern was only 10%. This significant difference in the
incidence of reangulation between greenstick and complete
fractures of the distal third suggests that breaking the intact
cortex, thereby converting the greenstick distal fracture into
a complete fracture, may not be the best method of reduc-
tion. As seen radiographically, greenstick fractures appear
to be angulated. I agree with the concept and believe that
greenstick fractures may be satisfactorily managed by the
technique of converting the greenstick fracture into a com-
plete fracture when appropriate and indicated. However,
Evans pointed out that the apparent angulation deformity
seen with greenstick fractures in children is often a rota-
tional deformity.7 By rotating the forearm under an image
intensifier, one can observe that the apparent angulation dis-
appears or lessens as the forearm reaches the proper plane
of rotation. Rotational correction may be easier and more
efficacious than trying to convert the angulated greenstick
fracture into a complete fracture.493 Evans showed that distal-
third greenstick fractures reduce relatively easily by maximal
pronation of the forearm.7
Circulatory compromise and its major consequence, Volk-
mann’s ischemia, may occur with fractures of both bones of
the forearm when the forearm is swollen or when a displaced
fracture that requires repeated manipulation is present.
The more extensive the soft tissue trauma, particularly
from a direct blow or wringer injury, the more likely is the
possibility of enough swelling to create forearm compart-
ment problems. Compartment pressure monitoring should
be considered.
One of the “complications” of least concern is radio-
graphically delayed union, nonunion, or overgrowth of
the ulnar styloid, which represents a type 7 growth mecha-
nism injury (Fig. 16-99). This injury occurs because of the
anatomic relations, especially the triangular cartilage. The
injury often occurs through a completely cartilaginous
styloid, making diagnosis roentgenographically difficult.
Subsequently, as the styloid ossifies the nonunion becomes
evident. Nonunion probably occurs because of the difficulty
of epiphyseal cartilage healing and chronic tensile stresses.
Onne and Sandblom found two cases with follow-up prob-
lems relative to the ulnar styloid, with pain on maximal
supination caused by a pseudarthrosis of the styloid process
or by a fibrous union between the styloid and the remainder
of the ulnar secondary ossification center.395 My experience
has been similar. A radiographic nonunion is not necessar-
ily an anatomic nonunion, nor is it usually symptomatic.
622
FIGURE 16-99. (A) Ulnar styloid nonunion (arrow). It accompanied a torus radial injury. (B) Hypertrophic overgrowth (arrow) of the ulnar
styloid fracture. (C, D) Progressive ossification in the styloid nonunion.
These fractures usually heal rapidly with extensive callus for-
mation. However, severe periosteal injury or possible vascular
disruption may be associated with delayed healing. The child
must be protected until the fracture is completely healed.
Disrupted periosteum may not heal completely. A fragment
that is displaced beyond the confines of the periosteum may not
remodel completely and may lead to formation of an exostosis.
In the series described by Davis and Green, most of the 16
distal-third greenstick fractures that reangulated were
treated initially in neutral rotation; only two were reduced in
pronation.31 It appears that, although reduction of a green-
stick fracture of the distal third by pronation of the forearm
does not entirely eliminate the possibility of reangulation,
recurrent palmar angulation is less likely to occur if this
method of reduction is used. Palmar angulation is probably
not of significant consequence in a child under 10 years of
age, as the growing bone adequately remodels the deformity.
In the child over 12 years, angulation cannot be accepted
because of the limited amount of remodeling. The most dif-
ficult clinical problem then arises: How much angulation is
acceptable in the child between the ages of 10 and 12 years?
16. Radius and Ulna
There were 36 fractures with significant deformities in
the series of Gandhi and colleagues.32 They believed that
angulation as great as 35° in the distal third of the radius
would correct itself within 5 years; but they emphasized that
knowing that this bone has “correcting power” is not an
excuse for leaving the fracture unreduced or for not attempt-
ing to secure an adequate reduction (Fig. 16-100). At the
same time, these results suggest that there is no justification
for carrying out repeated manipulations or open reduction
of such fractures. Despite reassurance, parents naturally are
anxious if there is a clinical or radiographic deformity when
the cast is removed, and they require an answer to the ques-
tion of how long it will persist. In my experience, it appears
that most deformities of the distal third of the radius are cor-
rected fully in 2–3 years (Fig. 16-101). There should be a
reluctance to accept an angular deformity of more than 20°
in a child over 10 years old who has less capacity for full cor-
rection, particularly if the child is a girl who undergoes early
fusion at 12–14 years of age.
Open fractures that involve the distal radius are relatively
common, especially if the mechanism of injury is a fall on
FIGURE 16-100. Anteroposterior (A) and lateral (B) views of resid- left angulated, resulting in decreased rotational capacity and rela-
ual malunion in a 12-year-old girl. Insufficient growth was left in the tive ulnar lengthening. A corrective osteotomy is necessary.
distal radius after a fracture 8 months previously. The radius was

C D E
FIGURE 16-101. (A) Displaced fracture of the distal third of the radius. (B) Appearance of the fracture 3 weeks after reduction. (C) At
6 weeks there was further reangulation. (D) One year later remodeling is evident. (E) Three years later the malunion is fully corrected.
624
the wrist. If this fall occurs in dirt, the risk of contami-
nation with soil microorganisms is significant (and may
include Clostridium). These injuries must be treated aggres-
sively with débridement and left open to heal by secondary
granulation or subjected to delayed closure. Even with
appropriate treatment, osteomyelitis may supervene (Fig.
16-102). Failure to appreciate fully the severity of such open
injuries may lead to significant damage and loss of cartilage
and bone.
The possibility of growth arrest with distal radial me-
taphyseal or physeal fractures has been minimized in the
past. However, a study by Lee et al. showed that some type
of an important growth disturbance developed in 7% of the
children.476 Four of the seven patients had a significant com-
pression mechanism according to the history. Premature
closure of the growth plate of the distal ulna, leading to dis-
parity, did not occur in any of the children in the study of
Lee et al. The correction of the deformity is contingent on
FIGURE 16-103. Growth mechanism injuries. A. Type 1. B. Type 2. C. Type 3. D. Type 4. E. Type 8. F. Type 6. G. Type 7.
16. Radius and Ulna
FIGURE 16-102. (A) Malunion after an open fracture
complicated by infection. (B) Two years later the
angular malunion is markedly improved, and the scle-
rotic bone at the sites of the fracture and the
osteomyelitis is remodeling.
the specific anatomic changes. Growth arrest may compli-
cate even a torus fracture.440
Although the Madelung deformity is considered a con-
genital abnormality, Vender and Watson described a case of
bilateral closure of the ulnar side of the distal radius in a
patient with a history of high-level gymnastic training.500
They thought that cumulative microtrauma to the ulnar side
of the growth plate was responsible.
Distal Radial Epiphyseal and
Physeal Injuries
Classification
Every type of growth mechanism injury may affect the distal
radius (Fig.16-103).440–444,446,447,451,452,460,467,470,476,477,481,484,485,487,488,
Distal Radial Epiphyseal and Physeal Injuries 625

FIGURE 16-104. Type 2 injury. (A) Anteroposterior view shows minimal metaphyseal injury. (B) Lateral view shows more extensive cor-
tical disruption. The possibility that a type 4 injury is present, rather than the type 2 injury, must be considered.

495,498–500,505,506
The distal ulnar physis, however, is less fre-
quently involved. Because of the crushing, twisting nature of
many of these injuries, localized physeal damage (type 5)
may occur and is probably more frequent than realized.
Type 2 injuries are the most common, especially in older
children (more than 10 years of age) and are usually associ-
ated with posterior (dorsal) displacement of the metaphyseal
fragment. They are often accompanied by a fracture through
the ulnar styloid (Figs. 16-104 to 16-106).
Type l injury patterns are the next most common (Figs.
16-107, 16-108). The epiphysis may be significantly displaced
(Fig. 16-109). Type 3 and type 4 injuries also occur but are
infrequent (Fig. 16-110). Type 7 injuries usually involve the
radial styloid (Fig. 16-111).
The radial fracture may be associated with a greenstick
fracture of the ulnar metaphysis, separation of the distal
ulnar epiphysis, or fracture of the ulnar styloid process.465
The ulnar injury usually does not involve the ulnar physis.
A

FIGURE 16-105. Barton’s fracture. This volar displacement is rare B

in children, who usually have a dorsal displacement because of the
frequent mechanism of falling on the extended or hyperextended FIGURE 16-106. (A) Type 2 radial fracture with a type 2 ulnar frac-
hand. ture. (B) Type 2 radial fracture with a type 1 ulnar fracture.
626 16. Radius and Ulna

FIGURE 16-107. (A) Distal radial fracture (type 1). This fracture is returned complaining of pain over the ulnar styloid. The distal ulna
open on the “radial” side and compressed on the “ulnar” side. Such had overgrown, and the distal radius closed prematurely. An ulnar
a fracture must be watched closely for growth arrest. (B) Two years styloid nonunion is evident. There was no indication of the ulnar
later the patient, who did not have proper follow-up examinations, injury on the initial film.

Pathomechanics
Injuries to the distal radial epiphysis and physis usually result
from a fall on the outstretched hand. The forces are dorsally
and longitudinally displaced and produce a combination of
impaction and shearing at the level of the physis. Because of
the triangular fibrocartilaginous complex (TFCC), the ulnar
styloid frequently is fractured concomitantly (Fig. 16-112).
The shearing forces of hyperextension and supination dis-
place the distal radial epiphysis dorsally. The periosteum is
stripped from the dorsal metaphysis but remains attached to
the physis and epiphysis. If the transverse vector is greater
and more shearing is present, the likelihood of physeal
damage decreases. However, when the longitudinal vector
increases, the tendency for damage to the physis and the
potential rate of growth disturbance increase.

Diagnosis
The fracture is usually dorsally displaced, and the child may
present with pain and swelling. There are rarely signs of neu-
rologic or vascular deficiency, but they must be adequately

FIGURE 16-109. Dorsally displaced physeal injury. (A) Antero-

posterior view. (B) Lateral view.

FIGURE 16-108. Type 1 injury. Mild displacement with widening of

the physis.
Distal Radial Epiphyseal and Physeal Injuries
FIGURE 16-110. Undisplaced type 3 injury (arrow).
sought, as they do sometimes occur. Finger motion, though
painful, is ordinarily present and may appear normal. Some-
times only pain and swelling are present, with apparently
normal roentgenographic findings.
Roentgenograms establish the diagnosis, which is best visu-
alized in the lateral projection. Often the dorsal metaphyseal
fragment is small, but it is pathognomonic of the type 2
injury pattern, even if there is no epiphyseal displacement.
The lack of ossification in the ulnar styloid makes diag-
nosis of the usual accompanying fracture difficult. Pain over
the styloid is usually indicative of concomitant injury.
FIGURE 16-112. (A) Distal radial fracture. The periosteum (solid
arrows) strips away and may be used to stabilize the reduction.
The triangular cartilage (T) causes avulsion of the ulnar styloid
(open arrow). (B) Nonunion following combined fracture. Note the
627
FIGURE 16-111. Type 7 injury of the radial styloid (arrow).
Because of fibrous union, direct expansion of ossification
cannot occur across this tissue to unite with ossification
within the fragment.
Treatment
The injury usually is easily reduced by direct pressure (with
the patient under appropriate anesthesia and muscle relax-
ation). Wrist flexion does not help to hold the reduction,
because the wrist joint easily flexes to 80° before the capsule
tightens enough to exert any influence on the distal frag-
premature closure of the radial physis (type 1 injury) and open
ulnar physis. (C) Histologic specimen showing a type 1 fracture of
the distal radius. Note that the triangular fibrocartilage complex is
pulling on the ulnar styloid.
628
ment. This position is unacceptable. Therefore the wrist
should be left in a neutral position once an epiphyseal sep-
aration has been reduced, and one must rely on three-point
molding of the cast. After closed reduction, immobilization
is maintained for 3–4 weeks.
Repeated, forceful manipulations must be avoided
because of the potential for further damage to the
physis.444,474 Bragdon reported a case of premature closure
of the distal radius consequent to forceful, repetitive
manipulation.452
Malposition does not persist, as was well demonstrated by
Aitken.441,442 Within a maximal period of 2–3 years, but more
usually within 6–12 months, the distal radial epiphysis
FIGURE 16-113. (A) Extensive new subperiosteal bone formation after a type 2 injury. (B–D) Progressive formation and remodeling of a
type 2 physeal injury.
16. Radius and Ulna
assumes its normal relation to the radial metaphysis through
remodeling and longitudinal growth. New subperiosteal
bone forms on the dorsum and side of the distal radius (Fig.
16-113), and the palmar portion of the metaphysis is grad-
ually absorbed. If repeated attempts at closed reduction
fail, it is wise to leave the epiphysis partially displaced and
count on extensive metaphyseal remodeling, rather than risk
further physeal injury (Fig. 16-114).
Closed reduction is accomplished readily in most instances
owing to the type 1 and type 2 lesions with an intact dorsal
periosteum. Rarely are they totally displaced, as with com-
parable fractures of the distal metaphysis. Despite the usual
ease of reduction, it is not always possible to reduce the
Distal Radial Epiphyseal and Physeal Injuries
FIGURE 16-114. (A) Type 2 fracture. (B) Two years later. (C) Four years later. Note the nonunion of the ulnar styloid.
dorsal displacement fully. However, repeated, forceful
manipulations are not necessary, provided that approxi-
mately 50% apposition of the fragments has been attained.
Open reduction of the markedly displaced epiphysis is
usually not indicated, although type 3 or type 4 injuries
require open reduction (Fig. 16-115). Soft tissue interposi-
tion may also prevent closed reduction.472,477,481,505
Results
In general, results are good to excellent. These injuries tend
to occur in older children; and if growth arrest supervenes,
the amount of remaining growth may not be enough to
cause significant angular deformity or ulnar overgrowth.
Functional limitation is minimal within a few weeks.
Complications
Neurologic Problems
Sterling and Habermann reported a case of posttraumatic
median nerve compression in a 10-year-old boy who experi-
FIGURE 16-115. Type 3 injury of the distal radius with recom-
mended transverse pin or small screw placement.
629
enced immediate alleviation of many of his symptoms fol-
lowing initial reduction.497 The initial sensory decrease took
several more days to return to normal. The boy did not
require an open reduction or carpal tunnel release. The
association of median nerve compression with Colles’ frac-
tures in adults is well known, but there have been few reports
of this associated phenomenon in children.438,483 Sterling and
Habermann, were able to reduce the symptoms with the frac-
ture reduction. In one of my cases, traction and elevation
after reduction did not relieve the symptoms, and explo-
ration and carpal tunnel release were finally necessary. The
median nerve was contused. It appears that carpal tunnel
anatomic relations do not change significantly with age. Con-
sequently, compression of the median nerve in the carpal
tunnel may occur at any age. It is important to examine the
child carefully and recognize the condition of the medial
nerve prior to as well as after reduction.
Growth Disturbance
Of 53 patients with fractures of the distal radial epiphysis,
only one patient in the Davis and Green series had a growth
disturbance.31 However, I have encountered a significant
number of patients with distal radial growth deformities.
The distal end of the radius is an infrequent site for growth
disturbance due to injury (Figs. 16-116 to 16-120). Several
articles have emphasized the possibility of growth damage.467
The distal ulna may also be involved, which may be due to a
localized type 5 injury initially diagnosed as a sprain because
there is no significant fracture evident radiographically.
Occasionally, longitudinal forces of the impact damage
some of the germinal cells of the physis, producing a local-
ized type 5 physeal injury (Fig. 16-119). This microinjury
pattern cannot be detected immediately but is often evident
6–12 months following injury. If the injury is detected early,
the possibility of resecting the osseous bridge may be
considered.
A Madelung-type deformity may appear, although radio-
graphically it does not resemble the congenital deformity
630 16. Radius and Ulna

FIGURE 16-117. Premature growth arrest of the radius after type l

injury.

FIGURE 16-116. Partial physeal damage (arrow).

FIGURE 16-118. (A) Premature arrest of the entire distal radius fol- the “ulnar” side. (C) Complete growth arrest of the distal radius with
lowing type 2 injury. Note the styloid nonunion. (B) Growth arrest overgrowth of the distal ulna.
of the “radial” side of the distal radius, with continued growth on

A B
FIGURE 16-119. (A) Localized osseous bridge (arrow) following type 1 injury. (B) Computed tomography shows such bridging.
Distal Radial Epiphyseal and Physeal Injuries
A B
FIGURE 16-120. Radial growth arrest. (A) Slowdown of growth at 7 years. (B) Premature bridging at 10 years. (C) Premature growth
arrest at 14 years.
(Fig. 16-121). The Madelung-like deformity occurs because
of premature partial fusion of the distal radial epiphysis.37,491
Synostosis
Disruption of periosteum and soft tissues around the distal
radioulnar joint may lead to excessive bone formation in the
interosseous membrane region. The reactive process may
proceed to a discrete synostosis (Fig. 16-122). Resection of
this complication must await maturation of the reactive
process.
Exostosis
An exostosis may form (Fig. 16-123). It is probably due to
localized type 6 damage to the periphery of the physis.
Ulnar Styloid
Onne and Sandblom found that two patients had follow-up
problems relative to the ulnar styloid, having pain on
maximal supination because of a pseudarthrosis of the
FIGURE 16-121. Localized growth arrest with Madelung-like
deformity.
631
C
styloid process or at least a fibrous union between the
styloid and the remainder of the ulnar secondary ossification
center.395 This fracture was not evident roentgenographi-
cally at the time of the original injury because of the extent
of cartilage in that area. The physician must always be careful
to consider the possibility of an ulnar styloid cartilaginous
fracture, even when ossification does not extend out to
that region. The patient and parents should be warned
about it and follow-up roentgenograms obtained to deter-
mine if it is present as ossification progresses into the
region. The likelihood of long-term problems such as pain
are rare.
The anatomic interrelation of the ulna and the carpus is
important for understanding the high incidence of associ-
ated styloid fractures and the uncommon nature of ulnar
physeal injury. The distal ulnar epiphysis articulates with the
ulnar notch of the radius and, through the TFCC, with the
FIGURE 16-122. Synostosis with ulnar growth damage.
632
FIGURE 16-123. Ulnar exostosis following an injury that occurred 3
years previous to this film.
distal radial epiphysis. The thick base of this fibrocartilage
complex attaches to the ulnar styloid.
Distal Ulnar Physeal Injuries
Injuries to the distal ulnar physis are infrequent but may lead
to significant deformity (Figs. 16-124 to 16-128). Most of
these injuries accompany distal radial fractures. Most often
the distal ulnar injury is a type 7 (styloid) injury. However,
A B
FIGURE 16-124. (A) Widening of the distal ulnar physis indicates a type 1 injury. (B) Subperiosteal reactive bone 5 weeks later confirms
the injury.
16. Radius and Ulna
discrete ulnar physeal fractures may also occur, as solitary
lesions or accompanying a distal radial fracture.528–540
Fractures of the distal ulnar physis are an associated injury
in fewer than 4% of distal radial injuries. Specific ulnar
physeal injuries are clinically distinct and merit differentia-
tion from styloid injuries. Ulnar epiphyseal injuries may also
occur in the presence of an ulnar metaphyseal fracture or
fractures of both bones of the forearm. They are sometimes
listed as the childhood equivalent of the Galeazzi injury.
The low incidence of distal ulnar physeal fracture may be
explained in part by the cushioning effect imparted by the
interposition of the meniscus between the ulna and the prox-
imal carpal row and propagation of deforming forces through
the triangular cartilage directly into the styloid process. These
styloid fractures, classified as a type 7 growth mechanism
injury, do not usually extend to the primary ulnar physis.
Roentgenographic diagnosis of ulnar physeal and epiphy-
seal injuries may be difficult. The distal ulnar epiphysis
appears later than the radius, not usually ossifying until the
sixth year. A separate ossification center for the styloid
process has been described but generally occurs at the same
level as the main ossification center at its ulnarmost border,
rather than at the distal tip of the styloid. A true accessory
ossification center for the distal ulnar styloid is infrequent.
When present, antecedent trauma with a fibrous union
should be suspected. A fracture of the ulnar styloid prior to
ossification may not be evident until a radiographic, but not
necessarily anatomic, nonunion appears.
In our study, type 1 growth mechanism fractures were the
most common physeal pattern.533 There were six of type 3
growth mechanism injury and one each of types 2 and 4. The
specific ulnar physeal injury pattern was not recognized ini-
tially in two patients, both of whom developed premature
physeal closure. No obvious fracture was present radio-
graphically in either of the anatomic dissections of trau-
matically avulsed arms, although, microscopic type 1 injuries
Distal Ulnar Injuries 633

FIGURE 16-125. Completely displaced type 2 physeal

injury of the distal ulnar physis.

FIGURE 16-126. Growth deformity (arrow), probably due to type 4 ulnar injury (original films unavailable). (A) Six months. (B) Two years.
(C) Four years after the injury.

A B
FIGURE 16-127. Type 4 injury to the distal ulna 5 years earlier. (A) Radiograph. (B) Pathologic specimen after resection and release of
soft tissue tethering.
634
FIGURE 16-128. Angular deformity due to physeal damage.
were present in both ulnas. These two patients, who had sus-
tained traumatic amputations, had a greenstick ulnar di-
aphyseal fracture associated with a Monteggia dislocation
of the radial head and displaced radial and ulnar mid-
diaphyseal fractures in addition to a torus fracture of the
distal radial metaphysis. Eleven patients sustained distal
radial metaphyseal fractures, four of which were incomplete
torus injuries. The remaining seven patients sustained distal
radial physeal injuries.
Fractures of the distal ulnar physis have been most
commonly reported as a type 2 growth mechanism injury
pattern. The high incidence of type 1 growth mechanism
injuries in our series has not been described previously.533
The distal ulna that was resected in one case was examined
histologically (Fig. 16-127). The region underneath the
ulnar styloid had growth arrest of the physis. In contrast, the
region adjacent to the radius had continued to grow, albeit
in a deformed manner. A fibrovascular bridge separated the
two portions and was probably the remnant of the original
type 3 or type 4 injury.
FIGURE 16-129. (A) Type 1 injury of the distal ulna associated with
a radial metaphyseal fracture. (B) Fracture was treated with open
reduction and a transplanted fixation pin. (C) Patient came back 3
16. Radius and Ulna
Displacement may be minimal and difficult to diagnose,
with the injury being evident only as widening of the physis.
In five of our cases the ulnar injury was not apparent initially
and was diagnosed only retrospectively with the development
of distal ulnar growth impairment.533
Initial treatment for displaced ulnar physeal injuries
should be directed at anatomic reduction. Fourteen patients
were treated with closed reduction, although open reduction
was offered (and refused) in three of the fourteen.533 Oper-
ative reduction was necessary after failed attempts at closed
reduction in four of our patients (Fig. 16-129). As seen in
our cases even with anatomic (open) reduction, there was a
high incidence of physeal closure, which most likely reflects
the significant disruptive force, ischemia, and soft tissue
damage that accompanies these injuries.
Evans et al. described an irreducible type 2 injury of the
distal ulna without an accompanying radial fracture.532 At
surgery the extensor carpi ulnaris was trapped between the
epiphysis and metaphysis. Sumner and Khuri also described
tendon and nerve interposition that prevented closed
reduction.539
There has not been long-term follow-up of a sufficient
number of patients with distal ulnar physeal injuries to
outline accurately the prevalent natural history of the injury
pattern. Of 183 reported cases, adequate long-term follow-
up was documented in only 17 cases. Eleven of these patients
had premature growth arrest of the distal ulna.
Growth arrest with creation of an ulnar minus variant may
occur relatively frequently. Peinado showed that experimen-
tal impairment of distal ulna growth in the rabbit had a
major effect on deforming the distal radial growth patterns
and causing displacement to the ulnar side.485
Bell et al. reported on the phenomenon of ulnar impinge-
ment syndrome, in which a shortened ulna was impacted
against the distal radius and caused a painful, disabling
pseudarthrosis.448 Ten of the eleven cases resulted from exci-
sion of the distal ulna after injury to the wrist. However, one
was due to growth arrest after fracture of the distal ulna in
a child. The symptoms are a painful, clicking wrist and a
weak grip. Clinical examination reveals a narrow wrist with
pain on compression of the radius and ulna and on forced
supination. Radiographs may show scalloping of the distal
radius at the site of impingement. The best treatment for
symptoms of distal radial ulnar problems after injury in
young, active patients is reconstruction, not excision.
years later because of wrist pain. The ulnar physis had closed pre-
maturely, and the radial articular surface was deformed angularly.
Galeazzi Fracture-Dislocation
Long-term clinical and radiographic follow-up data were
obtained for 18 patients.533 Follow-up ranged from 1 to 14
years, with an average follow-up of 3.5 years. Premature
physeal closure occurred in 10 of these patients (55%). The
degree of ulnar minus variance ranged from 2 to 30 mm. For
comparing the ulnas we preferred this measurement to
additional x-ray exposure of routine contralateral films. Sec-
ondary changes of the distal radius and carpus were evident
on the radiographs of seven patients. No patient has devel-
oped Kienbock’s disease.
Despite the radiographic findings, patients with posttrau-
matic growth arrest have surprisingly few symptoms. In fact,
most are asymptomatic. Cosmetic appearance was the most
common complaint. Radial deviation was limited, but it was
generally not the patients’ concern.
Nelson et al. reported four cases of posttraumatic distal
ulnar growth arrest with ulnar shortening of 22–39 mm and
secondary changes in the radius and carpus.535 They noted
that the progression of deformity was greatest during ado-
lescence. No patient in their study had significant pain or
functional impairment, but the cosmetic appearance was
displeasing.
The ulna derives 70–80% of its longitudinal growth from
the distal epiphysis. Accordingly, longitudinal growth slow-
down or arrest could be expected to result in significant
deformity. Premature physeal closure is an uncommon com-
plication of forearm fractures, reported to occur in fewer
than 7% of distal radial epiphyseal injuries. The exact inci-
dence of premature closure of the ulnar physis is unknown,
but it occurred in 55% of our cases with long-term follow-up
and in a significant number of cases in the literature. This
high incidence of premature physeal closure undoubtedly
reflects the force required to overcome the protective
anatomy of the wrist before sustaining a distal ulnar physeal
injury. All distal ulnar physeal injuries should be followed
closely for possible premature physeal closure.
Follow-up radiographs of the skeletally immature wrist
may show multiple longitudinal osseous striations crossing
the physis of both the radius and ulna. These striations were
originally thought to be anatomic variants (i.e., calcification
surrounding transepiphyseal vessels). However, recent radio-
graphic and histologic analysis of these striations indicate
that they most likely represent a microscopic response to
antecedent minor wrist trauma.12
Premature closure of the distal ulnar physis may result in
several changes at the distal radioulnar joint. Shortening
results in the development of an ulnar minus wrist. Ulnar
shortening from posttraumatic or other causes, such as
hereditary multiple exostoses, may cause a tethering effect
on the radius, producing characteristic secondary changes
related to the degree of shortening. These changes include
lateral bowing of the radial diaphysis, ulnar angulation of the
distal radial epiphysis, and ulnar translation of the carpus.
There may be tethering and contracture of the soft tissues
on the ulnar side of the wrist. Radioulnar convergence also
causes loss of the radioulnar joint buttress. Laboratory
studies producing impairment of distal ulnar growth in
rabbits have demonstrated similar deforming forces on distal
radial growth patterns.
Treatment for the posttraumatic ulnar minus wrist is
similar to that for other causes of postaxial longitudinal defi-
ciencies and ulnar clubhands. Surgical intervention may be
indicated for cosmetic deformity, progressive ulnar subluxa-
635
tion of the carpus, pain, and restricted range of motion at
the wrist. Options include resection of the soft tissue tether-
ing, distal radial epiphysiodesis, lateral stapling of the physis
for selective partial epiphysiodesis, opening or closing wedge
osteotomies of the radius, and ulnar callotasis or chondro-
diatasis. Reconstructive procedures, rather than excision of
the distal ulna, are preferred whenever feasible.
Galeazzi Fracture-Dislocation
The Galeazzi injury was originally described by Sir Astley
Cooper in 1822 but did not receive its eponym until reported
by Galeazzi in 1934. The significance of recognizing the
Galeazzi-equivalent fracture is (1) appreciation of the pres-
ence of a physeal injury and the possible risk of growth plate
arrest, and (2) maintenance of stability of the distal radioul-
nar joint by accurate reduction of the distal ulna. The TFCC
usually remains intact. In adults the Galeazzi injury is more
common than the Monteggia combination. It is the reverse
in the pediatric group. The pediatric injury also has less soft
tissue injury or tearing of the interosseous membrane than
in the adult.
The Galeazzi injury is a fracture of the shaft of the radius
combined with dislocation of the distal radioulnar joint
(Figs. 16-130 to 16-133).541–563 This definition does not
include those rare injuries in which there is a fracture of the
radial neck and head associated with dislocation of the distal
radioulnar joint (Essex-Lopresti injuries).
Schneiderman et al. anatomically studied the interosseous
membrane of the forearm with a particular concern for
evaluating its structure in the Roland-Galeazzi fracture-
dislocation.561 They thought that the term “interosseous
membrane” was a misnomer, and because the structure was
a complex of multiple elements with a significant role in
force transmission across the forearm, they believed that
the term “interosseous ligamentous complex” would be
more descriptive. With the Galeazzi fracture-dislocation, this
complex may act as a constraint to radial shortening, but it
may also act as a stress riser for radial fracture. Anatomic
reduction and internal fixation of the radius with early mobi-
lization of the extremity are probably indicated for treatment
of most Galeazzi fracture-dislocations in adults and adoles-
cents, and they should be considered in children.
Mikic described 125 patients, including 14 children with
the classic lesion and 25 patients with a special type com-
prising fractures of both bones as well as dislocation of the
distal radioulnar joints.554 Of the children in Mikic’s series,
there was only 1 patient under 10 years of age and 13 patients
between 10 and 16 years.
Landfried et al. studied variants of Galeazzi fracture-
dislocation.549 They thought that a fracture of the radial shaft
or metaphysis associated with a fracture through the ulnar
growth plate with the epiphysis still attached to the TFCC
and accompanied by displacement of the shaft and metaph-
ysis created the equivalent. They described three cases, all of
which were treated by open reduction and internal fixation.
The distal ulnar epiphysis is more likely to avulse before
rupture of the triangular fibrocartilage complex.
Letts and Rowahani reviewed Galeazzi equivalent injuries
of the wrist in children and found that the variant—
separation of the distal ulnar growth plate with displacement
of the ulnar metaphysis—was much more common than the
 A B

FIGURE 16-130. (A, B) Galeazzi injuries accompany distal radial metaphyseal fractures.

A B
FIGURE 16-131. (A) Galeazzi injury with distal radial physeal fracture. (B) Computed tomography scan.

FIGURE 16-132. Re-creation of a Galeazzi injury in specimens, showing how the ulna rotates out from under the triangular cartilage. (A)
Beginning rotation. (B) More pronounced rotation.

636
Galeazzi Fracture-Dislocation
FIGURE 16-133. Isolated Galeazzi injury.
classic Galeazzi fracture-dislocation.551 They found that the
outcome of the equivalent fractures compared to classic
Galeazzi injuries was less favorable. One child sustained com-
plete growth plate arrest of the distal ulna.
Involved children frequently have greenstick-type frac-
tures with angular displacement. Most of the time the dislo-
cation of the distal radioulnar joint is evident clinically and
roentgenographically (Fig. 16-130). However, sometimes the
ulnar head is only subluxated, which is more evident clini-
cally than roentgenographically (Fig. 16-131).
The distal radioulnar joint is stabilized by various struc-
tures, such as the ulnar collateral ligament, the anterior and
posterior radioulnar ligaments, and the pronator quadratus.
The most important stabilizing force is the TFCC. There can
be no dislocation of the distal radioulnar joint without some
damage to this strong intraarticular fibrocartilaginous liga-
ment. The specific function of the TFCC is to limit the rota-
tional movements of the radius and ulna relative to one
another. However, in the skeletally immature patient, avul-
sion of the ulnar styloid process is the equivalent of rupture
of the TFCC and was noted in 30% of the patients in Mikic’s
series.554
There is disagreement over the exact mechanism produc-
ing the Galeazzi injury. Most likely, the mechanism is a fall
on the outstretched hand combined with extreme pronation
of the forearm. The forces cross the radiocarpal articulation,
FIGURE 16-134. (A) Premature growth arrest of the distal radius
1 year after bilateral type 1 injuries. The ulnar styloid exhibits
nonunion. This patient subsequently had her wrist “twisted” and
had chronic, unremitting pain for 3 months prior to this film. (B)
Arthrography was performed. Dye surrounds the styloid ossicle,
but the triangular cartilage is intact. (C) Extrusion of dye through
637
initially producing the dislocation and forced shortening of
the radial shaft as the displacement discontinues. Dislocation
of the distal ulna causes tearing of the TFCC, which then
loses its stabilizing influences on the wrist. Rotational stresses
on the forearm also seem essential for dislocation of the dis-
tal radioulnar joint. It has been demonstrated clinically and
experimentally that a tear or detachment of the triangular
articular disc is the first step to dislocation and occurs at the
extreme of pronation and extension of the wrist.
Although diagnosis of the Galeazzi fracture-dislocation
should not be difficult, it is often missed. The radial fracture
is always noted, but the disruption of the distal joint may be
easily overlooked, and the ulnar head may seem to protrude
and be slightly more mobile than usual. Every roentgeno-
graphic examination of an isolated fracture of the radius
must include the inferior radioulnar joint. Mikic advocated
the use of arthrography to ascertain the presence of the
Galeazzi lesion.554 An abnormal arthrogram showing passage
of contrast medium from the wrist into the inferior radioul-
nar joint cannot be specifically diagnostic of a triangular disc
rupture because there may be perforation of the normal
disc. However, this perforation is usually present in older
patients, not in children, so arthrography can probably be
used diagnostically when indicated in younger patients (Fig.
16-134). MRI offers a noninvasive technique for assessing the
distal radioulnar joint.
the capsular defect (arrow). Exploration showed that the triangular
cartilage was subluxated from the ulnar articular surface. There
was extensive synovitis. It was thought to be an incomplete
Galeazzi injury. Treatment consisted of excising the triangular car-
tilage and styloid fragment, with capsular repair. Eight months after
treatment the patient was asymptomatic.
638
Disruption of the distal radioulnar joint, particularly low
grade versions of a Galeazzi injury, can probably be analyzed
by CT through this joint (Fig. 16-131).
In Mikic’s group, 12 patients were treated nonopera-
tively.554 Adequate, stable reduction was easily achieved by
manipulation in all cases, probably because most of the frac-
tures were subperiosteal (greenstick). In nine patients the
results were excellent, and in only one 15-year-old boy was
there redisplacement of the radial fragments with palmar
angulation. Closed reduction failed in one patient, and he
was subsequently treated with internal fixation and had a fair
result. In one 16-year-old boy, percutaneous pinning yielded
an excellent result. The patient shown in Fig. 16-134 was
treated by resection of the triangular cartilage.
Once the radial fracture is anatomically reduced and the
forearm supinated, the subluxation or dislocation of the
distal radioulnar joint generally reduces spontaneously
and becomes stable. Open reduction is required in some
children.
Walsh et al. reviewed 41 children under 15 years of age
with a fracture of the radius and probable “disruption” of the
distal radioulnar joint.562 In 41% of the cases the second
injury to the radioulnar joint had not been recognized ini-
tially. The results of conservative management were gener-
ally good; the authors found that the more distal the radial
fracture, the greater were the problems encountered. They
were able to obtain an initial reduction in all except two
patients, both of whom required open reduction. None of
these patients had associated fractures of the ulna. They were
true disruptions along the joint. Thirty-six of the patients
had excellent or fair results after simple manipulation and
immobilization. Walsh et al. stressed the importance of
obtaining a true lateral radiograph during the evaluation of
these injuries, both before and after treatment.
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559. Reckling FW, Peltier LF. Riccardo Galeazzi and Galeazzi’s frac-
ture. Surgery 1965;58:453–459.
560. Rose-Innes AP. Anterior dislocation of the ulna at the inferior
radio-ulnar joint. J Bone Joint Surg Br 1960;42:515–521.
561. Schneiderman G, Meldrum RD, Bloebaum RD, Tarr R,
Sarmiento A. The interosseous membrane of the forearm:
structure and its role in Galeazzi fractures. J Trauma 1993;35:
879–885.
562. Walsh HPJ, McLaren CAN, Owen R. Galeazzi fractures in chil-
dren. J Bone Joint Surg Br 1987;69:730–733.
563. Wechsler RJ, Wehbe MA, Rifkin MD, Edeiken, Branch HM.
Computed tomography diagnosis of distal radioulnar sublux-
ation. Skeletal Radiol 1987;16:1–5.
17
Wrist and Hand
Engraving of a complex metacarpophalangeal dislocation. (From
Poland J. Traumatic Separation of the Epiphyses. London: Smith,
Elder, 1898)
he changing osseous anatomy of the hand and wrist
T is probably better known than the rest of the child’s
skeleton, as this region is evaluated so frequently for
skeletal injuries. However, virtually all studies are based on
roentgenographic data and have minimal if any substantia-
tion with specific chondro-osseous anatomic studies.4,18
Anatomy
Development
Prenatally, each carpal bone assumes a basic morphologic
shape as a cartilaginous anlage that is reasonably compara-
ble to the final ossified adult shape. During postnatal devel-
opment there are minimal changes in the general contours
of these cartilaginous components. Garn et al. studied 138
embryos and fetuses and showed that carpal metacarpal and
phalangeal fusions arose from incomplete separation of
these cartilaginous precursors.7
Carpal primary ossification is minimally present at birth.
Each primary ossification center gradually proceeds from a
650
relatively small focus out to the peripheral contours, which
are comprised of articular cartilage, perichondrium, or
periosteum (Fig. 17-1). The immature, enlarging osseous
contours are variable and changing, and they do not always
reflect the actual contour of the unossified cartilage prior
to adolescence. Longitudinal growth deformity in the distal
radius or ulna or abnormal muscle forces exerted across the
wrist may cause mild to moderate structural changes in the
cartilaginous portions of the carpal bones. Ossification basi-
cally follows any preexistent cartilaginous shape, whether
normal or a deformation.
The scaphoid is the largest bone in the proximal carpal
row. Ossification begins when the child is between the ages
of 4 and 6 years and is complete by 13–15 years of age.4,5
Ossification begins in the more distal portion and progres-
sively extends into the more proximal segment (Fig. 17-2).
This developmental pattern may be a factor predisposing
to delayed union and nonunion in the adolescent and
young adult. How this pattern is affected by intraosseous
blood flow is unknown. The retrograde blood supply of the
scaphoid is such that waist fractures endanger the vascular-
ity of the proximal pole, and ischemic necrosis may accom-
pany nonunion, although to a lesser extent in children than
in adults. Disruption of the venous system may be a signifi-
cant factor in the altered vascular physiology of the injured
scaphoid.10
Until ossification is complete, the scaphoid is almost
entirely cartilaginous circumferentially, which increases the
cushioning effect during trauma and thus lessens the sus-
ceptibility to fracture throughout skeletal maturation. The
susceptibility of the scaphoid to being fractured changes
commensurate with this increasing chondro-osseous trans-
formation and with the changing stiffness of the individual
bone and the entire carpal region.
Gelberman and Menonn studied the extraosseous and
intraosseous vascularity of the carpal scaphoid in adults.8
Most of the intraosseous vascularity and the entire proximal
pole come from branches of the radial artery entering
through the dorsal ridge, whereas the bone of the distal
tuberosity receives its blood supply from palmar radial artery
branches. There is collateral circulation to the scaphoid by
way of the dorsal and palmar branches of the anterior
interosseous artery. The palmar operative approach appears
Anatomy
A center forms in the proximal epiphysis of each phalanx. In
B doepiphyseal ossification centers are common in the distal
FIGURE 17-1. Anatomic sections. (A) Three-year-old. (B) Ossifica-
tion within the carpus at 6 years.
to be the least traumatic to the blood supply of the proximal
pole. In the child, because the ossification center develops
more distally and then proceeds into the proximal portion,
it appears that there may be selective dominance of the distal
supply initially and a progressive “takeover” from the proxi-
mal supply to reach the adult pattern. This would certainly
explain the pattern of ischemic damage. However, both
vessels may participate in the formation of the ossification
center.
The lunate may develop two ossification centers that sub-
sequently fuse, although rarely separation persists. Some-
times the lunate fuses incompletely with an adjacent carpal
bone, giving rise to a spurious “fracture line.” Kobayashi
et al. described complete congenital absence of the lunate
bilaterally in a young adult who presented for evaluation of
pain in the left forearm.12 Interestingly, there was shell-like
ossification of the left lunate but none of the right lunate.
Computed tomographic (CT) scans showed that there was
651
cartilaginous tissue present in the radiolucent areas. Bipar-
tite ossification has also been described for the trapezium
and trapezoid. The pisiform, the smallest carpal bone and
the last to ossify, often does so from multiple foci.
Irregular or multifocal ossification should not be misin-
terpreted as chondro-osseous trauma, although unrecog-
nized damage to carpal bones during progressive maturation
may be the cause of many radiologic variants about the wrist.
Furthermore, as shown with variations of the patella, foot,
and ankle, what appears to be a separation on radiologic
examination may actually have complete cartilaginous
continuity.
In the proximal phalanx of the thumb and the proximal
and middle phalanges of the fingers, small, sharply defined
linear “defects” are often visible on routine radiographs.1,4
They are the diaphyseal nutrient foramina, which are less
frequent in the distal phalanges (except the thumb). These
defects should not be confused with incomplete cortical
fractures.
Chondroepiphyses are initially located at the proximal
and distal ends of each phalanx (see Chapter 1), although
only one epiphysis in each phalanx and metacarpal eventu-
ally forms a secondary ossification center.9,15,16 In such areas
the associated physis is transversely oriented. The secondary
contrast, the secondary centers of the metacarpal epiphyses
are distal, except for the thumb in which it is proximal.
At the opposite end of each of these developing bones
the epiphyseal cartilage is rapidly replaced by endo-
chondral ossification until only a thin layer of cartilage exists.
This layer is composed of articular cartilage, germinal
epiphyseal cartilage, and a slow-growing physis that con-
tributes little to longitudinal growth but does allow contin-
ued hemispheric growth of the end of the bone as the joint
enlarges.
There may be an apparent epiphysis and physis at the
nonepiphyseal end of a metacarpal or phalanx. Such pseu-
first metacarpal (Fig. 17-3). Caffey believed that the term
pseudoepiphysis was a misnomer and that there is no such
anatomic entity. Histologically, there definitely is such a
structure that results when metaphyseal ossification mush-
rooms into the epiphyseal region (see Chapter 1).4,8,15
The developmental morphology of secondary ossification
in the “nonepiphyseal” ends of small longitudinal bones is
characterized by formation of the pseudoepiphysis.14–16 Both
direct ossification extension from the metaphysis into the
epiphysis and pseudoepiphysis formation proceed and con-
tinue to be more mature than formation and expansion of
the classic epiphyseal (secondary) ossification center at the
opposite end of each specific bone. Direct metaphyseal to
epiphyseal ossification usually starts centrally and expands
hemispherically, replacing physeal and epiphyseal cartilage
simultaneously. Three basic patterns of pseudoepiphysis for-
mation may occur. First, the aforementioned central osseous
bridge extends from the metaphysis across the physis into
the epiphysis and subsequently expands to create a mush-
room-like osseous structure. In the second pattern, a periph-
eral osseous bridge forms, creating an osseous ring or an
eccentric bridge between the metaphysis and the epiphysis.
In the third pattern, multiple bridging occurs. In each situ-
652
C D
FIGURE 17-2. Sequential development of the wrist and hand. Early
development in the neonate (A) and at 14 months (B). Note the
variable development of the secondary ossification centers of the
metacarpals in (B). The second metacarpal epiphysis ossifies first,
followed in order, by the third, fourth, and fifth metacarpals. The
ation the associated remnant physis lacks typical cell columns
and is incapable of contributing to the postnatal longitudi-
nal growth of the involved bone. Pseudoepiphyses are well
formed by 4–5 years of age and coalesce with the rest of the
bone months to years before skeletal maturation occurs at
the opposite epiphyseal end, which ossifies in the typical
pattern with formation of a secondary center completely
within the cartilaginous epiphysis.
Solitary pseudoepiphyseal involvement should not be mis-
interpreted as a fracture line or as indicative of systemic
disease. Multiple pseudoepiphyses may indicate an underly-
17. Wrist and Hand
E
last metacarpal epiphysis to ossify is the first (thumb). (C–E) Sub-
sequent developmental sequence into adolescence. The scaphoid
does not completely ossify until relatively late in skeletal matura-
tion, a factor that may minimize readily recognizable fractures
during childhood and adolescence.
ing illness or dysplasia. In particular, hypothyroidism may
be associated with such developmental chondro-osseous
variations.
The precise origin and insertion of collateral ligaments
into the metacarpals and phalanges prior to physeal closure
are not clearly described.3,11 Middle and distal phalangeal
attachments are into the epiphyses and metaphyses, not
unlike what is seen in the long bones. In contrast, attach-
ments at the metacarpophalangeal joint are only into the
epiphyses of the metacarpals and proximal phalanges. These
attachments affect fracture and displacement patterns.
Anatomy
FIGURE 17-3. Pseudoepiphysis of the distal end of the thumb
metacarpal in a 3-year-old. The lucency extends across most of
the transverse diameter of the shaft. Metaphyseal ossification
“mushrooms” into the cartilage and leaves peripheral cartilage rem-
nants that appear roentgenographically like peripheral physeal car-
tilage during physiologic epiphysiodesis. (See Chapter 1 for a more
detailed discussion of this process.)
Berger and Landsmeer studied the palmar radiocarpal
ligaments in 54 adult cadaver wrists and 23 fetuses.2 They
identified three palmar radiocarpal ligaments. The
radioscaphocapitate ligament originates from the radial
styloid process and inserts into the radial aspect of the waist
of the scaphoid. It spreads over the distal pole of the
scaphoid and interdigitates with fibers of the triangular
fibrocartilage. The long radiolunate ligament originates just
ulnar to the radioscaphocapitate ligament and is separated
from it by an interligamentous sulcus. A short radiolunate
ligament inserts as a flat sheet of fibers into the proximal
margin of the palmar surface of the lunate. Each ligament
is intracapsular and is enveloped within a continuous super-
ficial fibrous stratum and deep synovial stratum. Palmar
radiocarpal ligaments as a group are a major structural com-
FIGURE 17-4. (A) Classic position of
function for immobilization of the adult
hand. (B) More appropriate intrinsic-plus
position of function for immobilizing hand
injuries in children.
653
ponent of the palmar wrist from fetal development through
skeletal maturation. These ligaments are intracapsular.
Pulley positions are relatively constant throughout post-
natal development, with the gross anatomic characteristics
correlating closely to those of the adult hand.6 Flake et al.
particularly showed the relation of certain pulleys, such as
the “a” pulley of the thumb, to the growth plates and physes.
Interestingly, the physes appear to be relatively free of attach-
ments of pulleys, which is compatible with allowing contin-
ued growth of the pulley attached to areas that are “static”
compared to the region of growth.
Functional Anatomy
Proper hand splinting after an injury is extremely important,
even though complications from inappropriate positioning
are less likely to develop in a child than in an adult. Because
of the overall amount of ligamentous laxity usually present,
permanent joint contractures are not as common a residual
problem in children as they are in adults. Furthermore,
injuries to the hand produce bleeding and swelling in the
surrounding soft tissues. The inflammatory process, an
essential part of healing during the early stages, may create
adhesions between complex gliding tissue planes. Such
adhesions are often inevitable and necessary for complete
healing, and their formation cannot be prevented. Their
effect, however, may be minimized by appropriate position-
ing during treatment and controlled, progressive mobiliza-
tion. Even in the child, stiffness and swelling after injury may
last several months; but unlike that in the adult, it usually
dissipates.
The classic “position of function” for the hand is better
termed the “ready-to-grasp position” or the “position of rest”
(Fig. 17-4). Children’s fingers, particularly the fleshy hand
of an infant or toddler, may become temporarily stiff in this
position. In view of better concepts of hand anatomy and
rehabilitation, this is not the optimal position.
The metacarpophalangeal joint is a biaxial, ball-and-socket
joint. In acute flexion the collateral ligaments are at their
greatest length and tension because of the eccentric origin
of the ligament on the metacarpal and the flare of the
metacarpal epiphysis. If the metacarpophalangeal joint is in
extension, the collateral ligaments may become stiff in the
shortened position. Therefore the preferred functional posi-
tion of splinting for the metacarpophalangeal joint in the
injured hand appears to be full 90° flexion (Fig. 17-4).
654
The ligamentous morphology becomes different at the
proximal interphalangeal joint,13 a hinge joint without sig-
nificant lateral motion capacity. The palmar plate is less
mobile than that of the metacarpophalangeal joint. It is
attached firmly to the epiphysis of the middle phalanx. In
flexion the palmar plate folds like an accordion. If the
palmar plate is left in the flexed position, portions of it may
become adherent to each other, leading to a stiff joint. The
checkreins appear to be the primary pathologic structure
causing proximal interphalangeal joint contracture.19 The
collateral ligaments of the proximal interphalangeal joint
are under the greatest tension (length) in the lateral aspect
of the condyle of the proximal phalanx.13 Consequently,
proximal interphalangeal joints should be splinted in
15°–20° of flexion to prevent shortening of the collateral
ligaments and palmar plate.
Edema after surgery or trauma is a significant concomi-
tant and plays a role in stiffness of the hand.17 Local venous
return is a causal factor in edema formation and plays a role
in its management. There are three functional independent
venous systems: superficial palmar, deep palmar, and dorsal
veins. These systems act synergistically, producing the great-
est velocity increase when concurrently activated during
fist-clenching. There is a large perforator in the first
interosseous space and a relatively constant one in the fourth
interosseous space. They transmit significant volumes of
blood from deep palmar veins to the dorsal superficial
venous system, where variable cutaneous tension continues
the pumping mechanism. This pumping mechanism is just
as important in the child as it is in the adult.
Injury Incidence
Because of the activity level of children, the hand is one of
the most frequent areas of trauma, although not necessarily
specific chondro-osseous injury.20–75 Bhende et al. reviewed
364 patients (187 boys and 177 girls; median age 10 years)
with hand injuries.24 The most common types of injury were
lacerations (38%), soft tissue injuries (28%), fractures
(20%), and sprains (8%). About 60% of the injuries were
sustained in the home. The little finger was the most com-
monly fractured digit (37%) and the fifth metacarpal the
most commonly fractured bone.
17. Wrist and Hand
Beaton et al. studied 1003 patients with hand injuries; only
58 of these patients were less than 16 years of age.22 They
found that among both left- and right-handers injuries to the
right hand were more common than to the left hand. The
exception was accidents to right-handers at work, in which
group there were more injuries to the left hand.
Unfortunately, many trauma studies involving children
specifically preclude the incidence of hand or wrist injury.
Carpal injuries and multiple unstable fractures of the
metacarpals are certainly infrequent in children, whereas
other hand fractures, especially phalangeal fractures and
interphalangeal dislocations, are common. Probably the
most frequent fracture is a crush injury to the distal phalanx
and the fingertip. The spontaneous exploration of the
surrounding enviroment by any child predisposes to such
injuries. Various hand fractures in children, which often
seem like minor injuries, may have serious consequences
because of aberrant growth and occult infection. Unfortu-
nately, many of these fractures are treated according to
guidelines established for comparable adult injuries.
Hastings and Simmons reviewed 354 pediatric hand frac-
tures and found that the incidence of epiphyseal injury was
much higher than that reported elsewhere in the skeleton,41
but growth disturbances were rare. Fractures were most
common in the border digits, with displacement within a
given digit being most common in the metacarpal, next
most common in the proximal and distal phalanges, and
least common in the middle phalanx. Malunion most often
was associated with failure to obtain adequate lateral and
anteroposterior roentgenograms of the individual digits,
failure to evaluate postreduction alignment, and the
erroneous assumption that growth would correct deficient
reduction.
Children’s finger ligaments are strong and resilient.
Because they are stronger than the associated physes, the
sudden extension of a ligament generally results in chondro-
osseous, rather than ligamentous, damage (Figs. 17-5, 17-6).
To a lesser extent, this is also true of the fibrous joint
capsules.
Leonard and Dubravicik collected 276 fractures involving
a child’s hand; 41% were physeal fractures. However, these
children’s hand fractures constituted only 0.45% of their
overall practice. Of these fractures, 10% required open
reduction for adequate restoration of normal anatomy.49
FIGURE 17-5. Interphalangeal injuries caused by
osseous failure prior to ligament failure. (A) Normal
anatomy. (B) Unicondylar. (C) Partial condylar.
(D) Lateral avulsion. (E) Bicondylar. (F) Type 3
epiphyseal.
General Treatment Guidelines
FIGURE 17-6. Metacarpophalangeal injuries caused by osseous
failure prior to ligament failure. (A) Normal anatomy. (B) Type 2
physeal. (C) Type 3 physeal. (D) Type 2 physeal. (E) Type 3
physeal.
Bora and colleagues reviewed 100 patients with epiphyseal
fractures of the hand; 90 fractures were closed and 10 were
open.25 Of the 90 closed fractures, 80 were treated success-
fully with closed manipulation. Seven of the other ten were
treated with closed reduction and percutaneous pin fixation;
three were old fractures that had healed in an unacceptable
(malaligned) position.
Almost all metacarpal and phalangeal fractures heal suffi-
ciently by 3–4 weeks to allow active range of motion. In chil-
dren, radiologic union is not necessarily a prerequisite to
starting protected motion. Fractures should probably not be
immobilized in children longer than 6 weeks, unless there is
an obvious delay in healing. If such is evident, a change in
treatment (e.g., open reduction and internal fixation) may
have to be considered.
There is definite conservatism in the treatment of chil-
dren’s hand fractures. Greater degrees of displacement and
deformity seem to be tolerated on the assumption that the
patient’s young age and potential for further growth will
correct the deformity. Although remodeling usually occurs,
a deformity may not correct spontaneously unless the angu-
lation or displacement is within a plane of anatomically
permitted motion.
Diagnostic Imaging
Roentgenograms in at least two planes (anteroposterior and
lateral) are essential to assess any hand fracture adequately.
It is imperative that a true lateral view of the involved digit
be obtained. Superimposition of other fingers in the lateral
view may obscure significant details. The fourth and fifth
metacarpals may be brought into lateral view with 10° of
supination; and the second and third metacarpals may be
brought into lateral view with 10° of pronation. Alternatively,
lateral tomography of a specific digit may delineate the
anatomy of the injury. Perhaps the most common cause of
missed or improper diagnosis of fractures in children’s
fingers is failure to obtain a true lateral view of the involved
655
finger. Additional oblique views may also be necessary to
evaluate joint injuries properly, particularly to assess small,
juxtaarticular fractures.
Magnetic resonance imaging (MRI) of the hand and wrist
has lagged behind its use for larger joints. It is the procedure
of choice in children with chronic wrist pain. Intercarpal lig-
ament tears, although uncommon, may occur, along with
triangular fibrocartilage complex (TFCC) lesions. Ischemic
necrosis may also occur. Chondro-osseous separation is prob-
ably an underdiagnosed entity in the immature carpus. MRI
can help delineate tendon abnormalities.
General Treatment Guidelines
Initial evaluation and primary care of the injured hand are
critical. One of the greatest pitfalls in treating these injuries
is that the primary focus is the fracture, and the damage to
soft tissues is overlooked. Both open and closed injuries must
be examined meticulously for damage to tendons, nerves,
and blood vessels. Maximal functional recovery must be the
goal of treatment for every hand injury.
Immobilization of a child’s hand always presents a chal-
lenge. Well-fitting plaster casts and splints are notoriously
difficult to apply in the small child. Bulky, soft dressings may
be used for immobilizing the infant’s hand. In older children,
gutter splints incorporating at least one adjacent uninjured
digit may be used to help control rotational deformity.
The true “position of safety” is the intrinsic-plus position,
with 90° of flexion at the metacarpophalangeal joints and
almost complete extension in the proximal interphalangeal
joints (Fig. 17-4). The thumb is best held in an abducted,
opposed position.
Placing the fingers in a banjo splint, in which the fingers
are extended and divergent, is rarely acceptable. Wrapping
the hand around a gauze bandage over which all the fingers
may stiffen is also poor practice. Universal splints rarely fit
children. Because of the ease with which the small child’s
hand can slip backward, the universal splint may cause
fingers to assume a suboptimal position.
A solitary finger should rarely be immobilized in a child.
When a single finger is immobilized, there is an increased
possibility that angulation or malrotation will develop by the
time the cast or splint is removed.
For fractures of the metacarpals and phalanges, it is impor-
tant to recognize and correct rotational malalignment.
Remodeling never corrects rotational deformity of a digit.
Accordingly, it is imperative to reduce all fractures of the pha-
langes and metacarpals in proper rotational alignment. This
practice is not always easy, as subtle degrees of malrotation
that are not recognized during the period of immobilization
may result in significant functional impairment after full
range of motion has been regained. The best way to monitor
rotational alignment is to study the planes of the fingernails in
the splint carefully, comparing the injured digit with the adja-
cent normal fingers and the counterpart in the opposite hand
(Fig. 17-7). Assessing malrotation of the thumb is more diffi-
cult. True lateral radiographs are helpful. Normally, a true
lateral radiograph provides simultaneous lateral views of the
interphalangeal joints of a finger and the metacarpopha-
langeal and interphalangeal joints of the thumb.
656
Davis and Stothard reviewed 678 finger fractures seen in
an emergency department.31 They noted that of 624 initially
treated by nonhand surgeons, 169 (27%) had inappropriate
treatment. Many of the management errors were simple:
failure to prescribe antibiotics for open injuries, failure to
reduce displaced fractures accurately, and unsatisfactory
splintage. They strongly recommended that all finger frac-
tures be assessed and treated by surgeons with sufficient
training in the management of hand injuries. Although the
title of their article implied that all fractures should be
referred to a hand surgery service, their comment that such
fractures should be treated by surgeons with training in the
management of hand injuries suggests review and treatment
by an orthopaedic surgeon. Their recommendation that
treatment not be undertaken by emergency room physicians
with no or minimal training in the nuances of hand injuries
deserves support.
Johnson et al. surveyed two time periods during the early
and the late 1980s and found that 8.2% of child abuse
injuries involved the hands during the earlier time period
and that it increased to 13.4% during the late 1980s.44 Of 94
patients, 19 sustained injury only to the hand: 8 burns, 2
bruises, 2 human bites, 3 lacerations, and 4 fractures. Chil-
dren with burns to the hand alone were significantly younger
than those with other types of injuries. They thought that the
hand was frequently the primary or incidental target of child
abuse and must be considered for any child with such
injuries, particularly in the age range of high child abuse
incidence.
Rankin et al. described acquired rotational digital defor-
mity as a result of digital sucking.56 It was usually radial
rotation of the index finger. In most cases rotational defor-
mities spontaneously resolved once finger sucking ceased.
However, in a few cases, particularly when the habit is unduly
prolonged, deformities may persist and cause functional
impairment. Surgical intervention may be indicated in such
a patient, possibly rotational osteotomy of the metacarpal or
the proximal phalanx depending on where the deformity
seems to be most obvious.
Ryan and Turner also described hand complications in
children due to digital sucking.57 They noted that digital
sucking is common among children and often regarded
17. Wrist and Hand
FIGURE 17-7. Fingernails should be coplanar, and
all of the flexed fingers should be reasonably par-
allel. In malrotation, whether involving a metacarpal
or phalanx, the uniform plane of the fingernails is
disrupted, and the involved digit overlaps the
normal digits.
as a harmless habit. However, the effects of prolonged
or vigorous digital sucking on the development of ortho-
dontic abnormalities certainly have been described. Reports
of hand complications are much less frequent. Stone
and Mullins found that thumb sucking was the most
frequent predisposing factor for chronic paronychia in
children.68 They described five patients with significant
rotational abnormalities and were able to rectify all of
the problems with corrective splintage. None required
surgery. Four of the five patients had a history of digital
infection.
Carroll and associates reported a case of acute calcific
deposition adjacent to a metacarpal in an 11-year-old child.29
This patient participated actively in gymnastics but denied
any specific injury. The mass was injected with methyl-
prednisolone acetate and lidocaine, resulting in complete
relief. The deposition may have been caused by chronic
trauma.
Closed phalangeal fractures in children are usually treated
by simple methods, with a return to normal or almost
normal function expected. The exceptional case requires
open reduction. The most common exception is a fracture
through the distal end of the phalanx, with rotatory dis-
placement of the head of the phalanx in relation to the more
distal phalangeal base.
Fractures of the phalanges and metacarpals heal rapidly,
and remodeling of angulation often occurs in fractures
in the metaphyseal region. Little remodeling may be
expected for fractures distant from the epiphyseal end con-
taining the secondary ossification center. For example, in the
distal end of a phalanx, growth is primarily from a spherical
rather than a transverse physis, which is nonlongitudinal
growth. Accordingly, malunion usually requires operative
correction.
Greene et al. have described a simple technique of com-
posite wiring for various oblique and transverse fractures in
the phalanges and metacarpals.38 These methods are readily
applicable to children. Parsons et al. recommended the use
of micro external fixators for unstable fracture patterns in
the phalanges.55 These devices should be used carefully in
children, avoiding the growth plate and secondary ossifica-
tion centers whenever possible.
Wrist
Wrist
Carpal Subluxation and Dislocation
Injury to the wrist joint is unusual prior to skeletal matu-
rity.79,95,112 Except in children with significant ligamentous
laxity, such as those with Larsen or Ehler-Danlos syndrome
(see Chapter 11), subluxation or dislocation of the wrist is
almost nonexistent. Because of the density of ligamentous
and capsular attachments from the carpus into the distal
radial and ulnar epiphyses, injurious forces invariably cause
distal radiolunar epiphyseal and metaphyseal fractures.
The wrist joint capsule may be partially damaged during a
fall; and because of the proximity of extensor tendon
compartments, a communication may develop, leading to
progressive symptoms of chronic, painful tenosynovitis
(Fig. 17-8). These injuries may be accurately diagnosed by
wrist joint arthrography or MRI and subsequently treated
by operative closure of the capsular defect.
Gilula presented an excellent review of various geometric
principles of parallelism and overlapping articular surfaces
for the analysis of carpal injuries.98,99 These lines are princi-
pally described for skeletally mature individuals, and their
complete applicability to the skeletally immature child is
limited.
Cooney et al. described TFCC tears in 33 patients,85 includ-
ing 3 patients under 15 years of age. They found that open
repair of the peripheral tear produced excellent results, par-
ticularly in the younger patients. This certainly should be
considered in children, rather than resection of portions of
the TFCC.85 Arthroscopy also should be used as the initial
approach for analysis and repair.88
Dautel et al. studied 26 patients with arthroscopy who had
otherwise normal static or dynamic radiographs.88 They
found five patients with true scapholunate instability; none
was a child.
FIGURE 17-8. Ulnar pain in a gymnast. A capsular and intercarpal
defect is evident distal to the ulnar styloid.
657
Carpal Fractures
Nafie reviewed carpal fractures in children.127 The scaphoid
was involved in 71, the triquetrum in 5, the trapezium in 3,
the hamate in 2, and the trapezoid in 1.
Scaphoid Fractures
Fracture of the scaphoid (Figs. 17-9 to 17-11) is the most
common carpal injury in the child.* It has been reported in
children less than 7 years of age.110 Bloem reported a 4-year-
old patient with fractures of the capitate and the third,
fourth, and fifth metacarpals; a scaphoid fracture, however,
was not evident at the age of 4 years. Instead, nonunion of
the scaphoid fracture was diagnosed only when the patient
was 11 years old. This nonunited scaphoid fracture was pre-
sumed to have occurred when the patient was 4 years of
age.81 Greene et al. reported a patient, injured at 6 years
of age, whose subsequent radiographs usually showed a
nonunited fracture through the ossific nucleus of the
scaphoid.102
Horii et al. described scaphoid fractures following repeti-
tive punching.105 They found that the location of the frac-
ture was comparable to a scaphoid fracture caused by wrist
extension injuries.
Mussbichler reviewed more than 3000 hand and wrist
injuries in children and noted that injuries of the scaphoid
were relatively common, finding 107 with roentgenologically
evident damage to the carpal bones, 100 of which had a frac-
ture through the scaphoid.126 They included 15 injuries
through the waist, 33 in the distal aspect, and 52 avulsions
of the radiodorsal aspect. There were no fractures through
the proximal part of the bone. In another series of 108
scaphoid fractures, 49% of the patients had distal third frac-
tures and 38% had avulsion fractures, with all fractures
except one being on the dorsoradial surface of the distal
pole.150 Avulsion fractures really represent sleeve fractures,
similar to type 7 growth mechanism injuries in long bones
(see Chapter 6).
In one report of 64 patients with a mean age of 11 years,
only one patient had a concomitant injury (fracture of the
neck of the fifth metacarpal in the same hand), and the most
frequently fractured area was in the distal third (60%), pri-
marily involving the scaphoid tuberosity.83 The waist of the
scaphoid was fractured in 24 cases (33%). Displacement was
present in only five cases. In four patients the displacement
was visible on the initial radiograph, and in the fifth it
became apparent 6 weeks after injury during the course of
treatment with a cast (this was the only patient in whom the
bone eventually failed to unite).83
When evaluating the child with distal radial fracture, it is
important to rule out the potential complication of associ-
ated fracture of the carpal scaphoid.83,94,102,126,139,150 Lahoti et
al. described an associated fracture of the scaphoid accom-
panying the distal radial physeal fracture.109 Trumble et al.
described six patients with ipsilateral fractures of the
scaphoid and radius,148 including one skeletally immature
* Refs. 77–83,87,89,93,94,100–102,104–106,109,110,113–115,117,118,
120,121,123,125–129,133,137–139,141,142,144,145,147,148,150,154.
658
FIGURE 17-9. (A) Chondro-osseous avulsion fracture (arrow) of
the scaphoid in an 11-year-old child. (B) Arthrography showed a
diverticulum near this fracture (arrow). At surgery, the capsule
individual. Coexistence of the two injuries is infrequent
(Fig. 17-12) but must be assessed in any case involving a
distal radial fracture. Other carpal bones may be fractured
concomitantly.
Early, appropriate treatment obviously depends on an
accurate diagnosis. The diagnosis is difficult when the frac-
ture involves the primarily cartilaginous scaphoid. Arthrog-
raphy, CT, or MRI might delineate this fracture at an earlier
time.
Tiel-Van Buul et al. evaluated the role of radiography and
scintigraphy for diagnosing a suspected scaphoid fracture.147
They believed that the best diagnostic strategy and the man-
agement of clinically suspected scaphoid fractures consisted
of initial radiography followed by bone scintigraphy in
patients who had seemingly negative radiographs. The posi-
tive predictive value for initial radiographs was 0.76 and
FIGURE 17-10. Distal pole scaphoid fracture in a 14-year-old. This
pattern of injury is common prior to skeletal maturation.
17. Wrist and Hand
was damaged, and nonunion was evident. The small fragment
was removed and the capsule reattached to the scaphoid
perichondrium.
decreased to 0.15 for follow-up. The sensitivity of radio-
graphs decreased from 64% to 30%. In contrast, the speci-
ficity of the bone scan was 98%.
Finkenberg et al. studied the diagnosis of occult scaphoid
lesion in fractures by ultrasound vibration.93 Whether this
methodology is applicable to children is unknown because
cartilage may have different vibratory rates from the fully
ossified bone of an adult.
As discussed in Chapters 1 and 6, the carpal and tarsal
epiphyses may have a unique failure pattern in which there
FIGURE 17-11. Waist fracture. Delayed union with widening of the
fracture line due to repetitive motion in a child being initially eval-
uated 9 weeks after a wrist injury. The radiodensity of the two
sides is similar, suggesting that the vascularity to the proximal half
is intact.
Wrist 659

FIGURE 17-12. Concomitant scaphoid and distal radial epiphyseal

fractures. The “widening” of the scapholunate gap must be FIGURE 17-13. Sclerotic appearance of the carpal scaphoid, sug-
assessed carefully. It was normal in this child because of incom- gesting an ischemic complication.
plete chondro-osseous transformation.

portion of the scaphoid that is usually intact in the avulsed

fragment, thus supporting healing of the area.111
is separation of some of the unossified cartilage from the Cristiani et al. evaluated ischemic necrosis of carpal
expanding primary or secondary ossification center (sleeve bones by MRI and found that the MRI was more sensitive
or shell fracture pattern). Actual separation (displacement) than scintigraphy.87 It certainly should be considered in
may be minimal and not associated with fracture propaga- patients with unusual pain following injury to the wrist, par-
tion into the cartilage to create a loose fragment. The true ticularly to look for potential separations at a chondro-
extent of such an injury pattern in the scaphoid or any other osseous interface.
carpal bone is unknown. The increased application of MRI Because of the high incidence of avulsion and distal third
in children with wrist pain may help ascertain the specific fractures in children, rather than waist fractures, the
morphologic diagnosis. Eventual ossification of the carti- incidence of nonunion in scaphoid fractures (Figs. 17-14 to
laginous region, coupled with fibrous or fibrocartilaginous 17-16) is considerably lower in pediatric patients than
nonunion, is a likely cause of the eventual development of a
bipartite carpal bone.
As with the young adult, the child who presents with a
painful wrist following even low-energy trauma and with pain
in the anatomic snuffbox, but shows normal radiographs,
should be treated until a fracture is either confirmed or
refuted by follow-up clinical and radiographic examinations.
Scaphoid fractures in children usually heal with closed
treatment. A short arm-thumb spica cast is recommended for
avulsion and incomplete fractures in children. For transverse
fractures, 4–8 weeks of immobilization is recommended. In
cases in which the injury was neglected, the diagnosis was
delayed, or in which there is apparent bone resorption, a
longer period of immobilization, often 8–16 weeks, may be
necessary.
One of the major concerns with adult scaphoid fractures
is ischemic necrosis.146 It does not appear to be a frequent
complicating factor in children’s fractures (Fig. 17-13), but
children must still be followed closely for such a complica-
tion. Grundy reported irregularity of the margin of the
scaphoid at the site of the healed fracture in four cases.104
However, this irregularity might have been a change conse-
quent to micromotion of the injury and not necessarily
indicative of a vascular complication. Letts and Esser showed FIGURE 17-14. Well-established nonunion of a carpal scaphoid
that there is a separate small artery supplying the distal fracture in an 11-year-old child.
660
A B
FIGURE 17-15. (A) Appearance of a scaphoid fracture 5 weeks
after a wrist injury. The radiograph obtained at the time of the acute
injury was read as negative, and the youngster was not casted.
FIGURE 17-16. (A) Initial radiograph shows an obvious triquetral
fracture (arrow) but no evidence of a scaphoid fracture. (B) Several
weeks later the triquetral fracture is healing. Sclerosis and irregu-
larity are evident along the proximal edge of the navicular ossifi-
cation center (arrow). (C) Radiologic nonunion (arrow) several
months later. This was interpreted by the radiologist as a bipartite
17. Wrist and Hand
Open reduction and internal fixation were done. An allograft was
also used. (B) Appearance 8 months after surgery. The fracture is
healed, but there is altered carpal morphology.
scaphoid. Because the patient had no pain the family refused
surgery. A fibrous union was most likely present. (D–G) Drawings
depicting this case. (D) Preinjury. (E) Fracture at the chondro-
osseous junction. (F) Micromotion widens the fracture gap. (G)
Nonunion is evident as the proximal fragment ossifies.
Wrist
in adults.123,129,138 Mussbichler126 reported two cases of
scaphoid nonunion in children, Southcott and Rosman142
reported eight cases, Maxted and Owen120 reported two
cases, and Pick and Segal133 reported one case.120,127,133,142 All
nonunions were grafted with autogenous bone, which led to
good clinical and radiologic results. Nonunion in children is
best managed by bone grafting through the palmar
approach.142,154
In the case shown in Figure 17-16 radiologic nonunion was
most likely due to motion, rather than intrinsic damage to
the blood supply. It should be noted that Mazet and Hohl
referred to neglected scaphoid fractures; they stated that
vacuolation and pseudocyst formation appear earlier in
the proximal fragment, and sclerotic changes do not
usually appear for a year.121 In contrast, Kohler and Zimmer
suggested that posttraumatic cystic changes developed
mainly in the distal fragment because of the better blood
supply.108
DeBoeck et al. described nonunion of a carpal scaphoid
fracture in an 8.5-year-old.89 The original injury occurred 7
months prior to roentgenograms that showed nonunion of
the scaphoid with sclerosis of the distal portion and cyst for-
mation at the fracture site. The child healed with conserva-
tive treatment.
Kerlinke and McCabe analyzed the literature on scaphoid
fractures and union and concluded that the natural history
of nonunion of the scaphoid was not as severe as had
been reported.106 They noted, however, that there is much
variability in the studies, and absolute recommendations
could not be derived from this study. In contrast, Lingström
and Nyström reviewed 32 patients 2–37 years of age following
scaphoid trauma.113 They found a 100% incidence of
progressive radiocarpal osteoarthritis. They thought that an
effort to attain reduction should be attempted. The only
exception was the patient in whom the radiocarpal joint
was already severely deteriorated by advanced degenerative
arthritis.
The rationale for operative treatment of scaphoid
nonunion in the adult is well established. It has been shown
that the altered kinematics of the nonunited scaphoid pre-
dictably lead to late intercarpal and radiocarpal degenera-
tive arthritis. The validity of these conclusions has not been
proved in children. Although it is technically possible to fuse
scaphoid nonunions in skeletally immature patients,92,114,141
previous reports have generally dealt with adolescents
who have waist fractures. Furthermore, a radiographic
“nonunion” in a child (Fig. 17-16) may not be an anatomic
nonunion. The tarsal navicular/accessory navicular is an
excellent example of such disparity (see Chapter 24).
Mintzer and Waters described open reduction and inter-
nal fixation in a 9-year-old.125 It was undertaken because of
significant deformity and displacement of the child’s initial
presentation. Suzuki and Herbert also described a 10-year-
old boy treated with open reduction and internal fixation
with bone grafting.145 Nakamura et al. reviewed 10 patients
with symptomatic scaphoid malunion.128 All suffered from
pain, restricted range of motion, and decreased grip
strength. In another study seven patients underwent correc-
tive osteotomy, grafting, and internal fixation. Refracture of
a proximal pole scaphoid fracture may occur, as it did in two
skeletally immature patients.80
661
The existence of a “congenital” bipartite scaphoid
continues to be questioned.92,103,108,110,116,140 It is possible
that some children fracture the ossifying scaphoid, present
minimal or no symptoms, and eventually develop a scaphoid
that appears to be bipartite.101,133 If this is true, the assumption
supports the concept that bipartition is secondary to
trauma.116 This bipartite entity may result from an undiag-
nosed fracture of the scaphoid early in its distal to proximal
ossification sequence (see Fig. 17-16 above). Similar phenom-
ena are now recognized as potential etiologic factors in
cases of bipartite patella and accessory tarsal navicular bone
(see Chapters 22, 24). Morphologic and histologic studies
have definitely shown that epiphyseal cartilage bridges the
radiolucent gap between the ossification centers in these
two conditions and that this gap may continue into adult
years or gradually disappear when the ossification centers
coalesce.
Doman and Marcus studied a patient with congenital
bilateral bipartite scaphoid with MRI.92 They showed the
presence of contiguous cartilage between the seemingly
“separated” bones and no evidence of significant signal
changes in the adjacent bone that would indicate a previous
injury or reparative process. They thought this case sup-
ported the congenital nature of some of these bipartite
bones, although they did not preclude trauma as a factor in
other cases, particularly the unilateral one.
Injuries to Other Carpal Bones
Injuries of the other carpal bones are infrequent in chil-
dren.84,91,96,97,111,119,122,124,135,136,143,152,155 It has been suggested
that the cartilaginous covering of the juvenile bones imparts
a certain resilience that renders the enclosed osseous
centrum less susceptible to fracture than the comparable
mature bone.
The diagnosis may be missed because of a lack of suspi-
cion and the difficulty of assessing minimal radiographic
change in the acutely injured child. The diagnosis of a lunate
or capitate fracture in a young child may be supported by
findings of pain, swelling, and limited motion at the
wrist (Figs. 17-17, 17-18). Other bones are involved infre-
quently (Figs. 17-19). These fractures may not be easily
demonstrable on initial radiographs; and like adult fractures
they may not appear until weeks following the injury.122,143
Treatment with immobilization should begin when a sus-
pected diagnosis is rendered. They usually heal without
consequence.
The carpal tunnel view is helpful for unrecognized frac-
tures of the carpus, especially those involving the pisiform
and hamate.76,143 The hook of the hamate shows quite well
in this view (if it is ossified). The carpal tunnel view is
obtained by placing the pronated forearm against the film
cassette and having the patient manually dorsiflex the hand
by pulling the fingertips dorsally with the opposite hand. The
central x-ray beam is angled approximately 25°–35° and
directed at the palmar surface of the carpus. If the patient
is unable to dorsiflex the hand secondary to pain, the angu-
lation of the x-ray tube may be varied to achieve a good view
of the carpal tunnel.
Letts and Esser thought that fractures of the triquetrum
in children (Fig. 17-19) were more common than fully appre-
662
FIGURE 17-17. Lunate fracture. While the anteroposterior view
showed no evidence of injury, the lateral view readily revealed the
fracture.
ciated.111 The fractures were often subtle, often appearing as
a flake avulsion that required a good oblique radiograph to
diagnose. Fifteen patients were reviewed; all but three were
missed initially. Follow-up, averaging 4 years, showed only
two patients with complaints of wrist stiffness and discomfort.
Three fractures involved the body.
Light noted that Keinbock’s disease has been reported in
skeletally immature individuals in children as young as 7–8
17. Wrist and Hand
years of age112,136 A patient with a lunate fracture (11-year-old
boy) treated by open reduction and K-wire fixation, devel-
oped fragmentation and collapse (“genuine” Kienbock’s
disease) 1 year after the injury.91 Trumble and Irving showed
that MRI could be used for early evaluation of Keinbock’s
disease, especially in young patients.149 Viegas and Ampar
also emphasized the usefulness of MRI for early assessment
of revascularization of Keinbock’s disease.151
Peyton and Moore described a fracture through a trape-
zoid-capitate congenital coalition.132 Such fusions are infre-
quent, and fractures through them are rare.
Compson described associated transcarpal injuries with
distal radial physeal fractures in three children.84 Two cases
involved simultaneous fractures of both the scaphoid and the
capitate. The third case involved the scaphoid and the tri-
quetrum. Compson emphasized that the full extent of these
injuries is not always recognized on the initial radiographs.
He cited the study of Nafie of radiographs of proven carpal
fractures in 82 children127: 71 fractures were isolated to the
scaphoid, whereas all the other carpal bones accounted for
only 11 fractures. He noted that others had described iso-
lated fractures of the capitate.135,155 In each study he pointed
out the delay in diagnosis, noting that no radiograph
obtained before 3 weeks showed the fracture on the same
view. In fact, fractures of the capitate were seen only on
oblique views and did not show on the standard anteropos-
terior projections.
DeCoster et al. described an unusual pediatric carpal frac-
ture dislocation in a 10-year-old child who sustained a type 3
fracture of the distal radius associated with fractures across
the scaphoid, lunate, and triquetrum90 (Fig. 17-20). The frac-
tures were treated with open reduction and internal fixation
with ligamentous repair to combine dorsal and palmar
approaches. At follow-up there was good wrist function but
abnormal carpal development.
FIGURE 17-18. (A) Minimal evidence of cap-
itate injury (arrow). (B) Healing made the
capitate fracture more evident because of
reactive sclerosis.
Wrist 663

FIGURE 17-19. (A) Triquetral fracture (arrow). (B) Hamate fracture (arrow).

subluxation at the midcarpal joint. Gerard reported a 7-year-

Intercarpal Disruptions
Traumatic intercarpal instability (Figs. 17-21, 17-22) in the
young child presents problems of diagnosis and management
because of variable degrees of carpal ossification.86,107,131,153
The scaphoid and lunate do not ossify until a child is 4 years of
age. Peiro and associates documented transscaphoid, perilu-
nate dislocation in a 10-year-old boy.130 The mechanism of
injury undoubtedly is similar to that in the adult. Fluoroscopy
and arthrography may be useful.134
Children with ligamentous laxity may be predisposed to
perilunate instability. Prospective evaluation using stress
views and motion fluoroscopy can disclose the problem
much more easily than static radiographs.
Craigan described a 10-year-old-girl with a complaint of
thumb dislocation.86 Radiographs, however, revealed dorsal
old girl who had fallen from a table at 3 months of age.95 She
did not use her hand when crawling. Radiography revealed
osteopenia in the carpus. The capitate was displaced into the
proximal row, and the entire carpus was displaced with col-
lapse into a palmar flexion deformity.
Gidden and Shaw reported a combined physeal fracture
of the distal radius with lunate subluxation.97 The patient was
initially treated with closed methods for the radial fracture.
The lunate subluxation was not diagnosed until 4 weeks
later; because of continued clinical and radiologic evidence
of instability, he underwent surgery. The lunate subluxation
was corrected by longitudinal traction, following which the
dorsal ligaments were repaired.
Letts and Esser111 noted only two reports of scapholunate
dissociation in the skeletally immature patient secondary

A B
FIGURE 17-20. (A) Original injury. (B) Three months later. It is a complex fracture-dislocation of the wrist.
664
FIGURE 17-21. “Terry Thomas” sign. This patient had a painful wrist
7 weeks after acute injury without treatment. This is a scapholu-
nate dissociation. Such widening, in the absence of pain, may be
due to patterns of chondro-osseous maturation.
to ligamentous disruption. They were by Zimmerman and
Weiland156 and Gerard.95
Closed reduction should be attempted first. Even when
scapholunate dissociation is suspected and is treated by im-
mobilization, the outcome is based on the patient’s symp-
toms and skeletal maturity. Any operative treatment is
directed toward achieving a stable, painless wrist. In a young
child another important treatment goal must be to prevent
the development of structural deformities. For long-term
treatment a protective orthosis should be used. So long as
these bones have a significant amount of cartilage, remod-
eling may occur.
17. Wrist and Hand
FIGURE 17-22. Transscaphoid perilunate dislocation. The distal
radius was also fractured (type 1 physeal injury).
Carpometacarpal Joint Dislocation
Dislocation or subluxation of the carpometacarpal joints are
rare in children. Such an injury is usually associated with
crushing and fracture of one or more metacarpals. The
thumb carpometacarpal joint is the most likely to be involved.
Kleinman and Grantham described multiple car-
pometacarpal joint dislocations.107 This injury was associated
with physeal fractures of the middle and ring fingers. This
patient is similar to the case shown in Figure 17-23. The
FIGURE 17-23. Carpometacarpal (CMC)
fracture-dislocation and concomitant
metacarpophalangeal (MCP) dislocations.
(A) Anteroposterior view shows CMC dis-
ruption and MCP dislocations of the index
and long fingers. (B) Lateral view shows
dorsal CMC displacement and MCP
displacement.
Thumb
FIGURE 17-24. Dislocation of the thumb MCP joint in
a 5-year-old child that was reduced and stabilized.
There is a slight shift of the epiphysis of the proxi-
mal phalanx, suggesting an occult type 1 growth
mechanism injury.
patient was treated with open reductions. A 10-week follow-
up described good appearance and function. Unfortunately,
further follow-up was not available.
Whitson described a 10-year-old boy who fell and sustained
fracture-dislocations of the medial four metacarpal-carpal
joints.153 A 4-week follow-up showed partial recurrence of the
luxation and some sclerosis in the proximal end of the third
metacarpal. Further follow-up was not described.
Thumb
Dislocation
Dislocation of the thumb usually involves the metacar-
pophalangeal joint (Fig. 17-24). The metacarpal head is
pushed through the thumb musculature, especially the
flexor pollicis brevis, and may also buttonhole through
the joint capsule (Fig. 17-25). Such structures may partially
entrap the metacarpal head. In contrast to digital metacar-
FIGURE 17-25. Displacement of the metacarpal head through the
flexor pollicis brevis (A) or capsule (B).
665
pophalangeal dislocations, however, complete, constricting
encirclement of the metacarpal neck does not occur, thereby
increasing the likelihood of closed reduction. The intrinsic
muscles retain their insertion with the sesamoids and serve
to guide the plate palmarward, keeping it from being irre-
ducibly displaced into the joint. The sesamoids, which may
not be roentgenographically evident in younger children,
indicate the position of the palmar plate.
The initial treatment is closed reduction, which is usually
successful. Reduction may be simplified by first flexing
the metacarpal to reduce intrinsic muscle tightness while
concomitantly applying longitudinal traction. Flexion with
continued traction completes the reduction. If capsular or
muscular interposition is present, an open reduction may
be necessary (Fig. 17-26). Because the digital nerves of the
thumb may be displaced by the traumatic anatomy, care must
FIGURE 17-26. Dislocation of the thumb MCP joint that required
open reduction and stabilization.
666
be taken to visualize them adequately prior to, as well as fol-
lowing, any open reduction.
Interphalangeal Dislocation
Interphalangeal dislocation of the thumb is less frequent
than dislocation of the thumb metacarpophalangeal
joint. Closed reduction is usually successful. Small avul-
sion fractures (type 7 injuries) may accompany the disloca-
tion and may require internal fixation if joint stability is
compromised.
Rath and Kotwal described an unusual injury with a closed
dislocation of the interphalangeal joint of the thumb accom-
panied by dislocation of the secondary ossification center
of the proximal phalanx in an 8-year-old-boy.161 It became
infected and following débridement was thought to be totally
necrotic and ischemic. They maintained the length of the
thumb with an external fixator and incorporated a bone
FIGURE 17-28. (A) Displaced type 3 injury. (B) Seven weeks later there is malunion and joint deformity.
17. Wrist and Hand
FIGURE 17-27. Gamekeeper’s thumb in a 12-year-
old child. (A) Type 3 avulsion fracture with 90° of
rotation of the epiphyseal fragment. The articular
surface faces the epiphyseal fracture line. (B) It was
treated by multiple K-wires that fixed the fragment
and buttressed and immobilized both the fragment
and the phalanx.
graft from the ipsilateral ulna to maintain the length of the
thumb without significant loss of function.
Collateral Ligament Injury
Gamekeeper’s thumb of the metacarpophalangeal joint
results from partial or total disruption of the ulnar collateral
ligament in the adult. In a child, ulnar and radial collat-
eral ligament “tears” of the thumb are usually type 3 or 4
chondro-osseous injuries (Figs. 17-27, 17-28), although type
2 injuries may also occur (Fig. 17-29).157 These corner frac-
tures of the epiphysis are equivalent to collateral ligament
injuries in adults.164 If the articular surface is involved, these
fractures should be accurately corrected by open reduction
and pinning. Failure to treat them adequately may cause per-
manent deformity and instability.
Winslet et al. reported three adolescents with open physes
who sustained fractures of the ulnar side of the proximal
Thumb
FIGURE 17-29. Displaced, angulated type 2 injury.
phalanx while break-dancing.167 All had ligamentous laxity
and at least 90° rotation of the fragment, requiring open
reduction.
A pure ligamentous avulsion of the ulnar collateral liga-
ment of the thumb of a 12-year-old child with open epiphy-
ses has been described.159,165,166 There was no reported
evidence of cartilaginous injury in any of these patients.
A B
FIGURE 17-30. (A) Mildly displaced Bennett’s fracture leaving an ulnar metaphyseal fragment and adduction angulation of the rest of
the thumb. (B) Displaced Bennett’s fracture analogue. (C) It should be reduced and internally stabilized.
667
Bennett’s Fracture Analogue
Impacted fractures of the base of the thumb metatarsal
(Bennett’s fracture) usually occur in children as a physeal
injury, with the most frequent pattern being type 2
(Fig. 17-30).158,162 An analogous fracture may involve the
metaphyseal–diaphyseal junction. The anterior oblique liga-
ment that anchors the first metacarpal to the trapezium is
strong.
The two primary variables of childhood Bennett’s fracture
are the size of the metaphyseal fragment and the amount of
displacement of the shaft from the epiphysis. The base of the
metacarpal is pulled proximally and radially by the abductor
pollicis longus, which inserts at the base; and the insertion
of the adductor further distally levers the base radially
(abduction). The periosteal sleeve is usually partially intact
and may be used effectively for stabilization during closed
reduction.
Minimally displaced fractures require protection with a
cast. In a young child, up to 30° of angulation may be accept-
able at the base of the thumb, although reduction to a lesser
degree of malalignment should be attempted. Angulation of
more than 30° should be corrected by manipulation. Pres-
sure is applied to the base of the thumb, and counterpres-
sure is placed over the head of the metacarpal. A common
error is to hyperextend the metacarpal joint by applying
pressure too far distally, which does nothing to correct the
deformity.
Occasionally, complete displacement may buttonhole
through the periosteal sleeve. Although a closed reduction
may look easy and is worth attempting, many of these injuries
require open reduction to maneuver the metaphysis back
into position through the periosteal tear.
Radial displacement of the thumb may be corrected by
manipulation and cast immobilization. Ulnar displacement,
however, usually defies attempts at closed reduction and
frequently requires open reduction with internal (wire)
fixation. Even if an ulnar displacement is treated by closed
reduction, this type must be followed closely because redis-
placement may occur in the cast.
C
668
FIGURE 17-31. Type 2 fracture of the proximal phalanx. The
Thurstan Holland fragment is usually on the radial side. Radial
angulation of the rest of the thumb is common.
Fracture of the Phalanges
The proximal bases of the proximal phalanx and the thumb
metacarpal of the thumb are common sites of epiphyseal
injury. A closed injury at the thumb metacarpophalangeal
joint that results in ulnar or radial instability is probably an
epiphyseal fracture of the proximal phalanx, rather than the
ligamentous injury commonly seen in the adult. Stress views
may be necessary to delineate the undisplaced fracture or
the small fragment.
FIGURE 17-32. (A, B) Anteroposterior and lateral views of a frac-
ture of the distal end of the proximal phalanx of the thumb in a 7-
year-old child. This fracture was undisplaced, and healing was
uneventful. (C) A similar injury in a 4-year-old child had this appear-
17. Wrist and Hand
The proximal phalanx most often sustains a physeal frac-
ture compared to a diaphyseal or phalangeal neck (distal)
fracture (Fig. 17-31). This fracture may be a type 1, 2, 3, or
4 injury, depending on the mechanism and the degree of
skeletal maturity. There is usually an associated radial angu-
lation. Treatment for type 1 and 2 injuries is closed reduc-
tion with adduction to correct the radial angulation. Types
3 and 4 usually require open reduction and accurate restora-
tion of joint surface anatomy.
Posttraumatic angular deformity of the base of the proxi-
mal phalanx of the thumb may be corrected by epiphyseal
distraction using a minidistractor.160
The proximal phalanx may sustain a distal (condylar) frac-
ture (Fig. 17-32). This fracture may be acutely or pro-
gressively unstable, despite an initial innocuous appearance.
There may be complete rotation of 180°, directing the artic-
ular surface at the fracture. Delayed union may occur, espe-
cially if the original injury is not splinted, necessitating
closed or open reduction and pin fixation. Remodeling is
not extensive in this end of the bone, and malunion may
result in permanent deformity.
Fracture of the distal phalangeal epiphysis of the thumb is
relatively common (Figs. 17-33, 17-34). It is often a crushing
injury associated with an open fracture and must be handled
carefully so as not to lose soft tissue or cause complicating
osteomyelitis, which could result in premature epiphysiode-
sis in a young child. The flexor tendon attaches to the palmar
shaft surface, and the extensor slip primarily attaches into
the epiphysis. Accordingly, the epiphysis may retain a normal
relation to the proximal phalanx, whereas the remainder of
the distal phalanx is flexed. This angular deformity must be
corrected during closed reduction. Open reduction may be
necessary for a type 3 injury.
Shibu and Gault reported a 12-year-old girl with sequen-
tial crush injury to the tip of the thumb at 18 and 36
months.163 She had overgrowth of the tip of the phalanx.
ance 7 weeks after injury (splinted for 2 weeks, with no
roentgenogram at the time of splint removal). The child was sub-
sequently treated by open reduction. (D) Three weeks after open
reduction, the fracture shows osseous healing.
Metacarpals
FIGURE 17-33. (A) Type 2 fracture of the distal phalanx of the
thumb. Note the transverse remnant of the subchondral metaphy-
seal plate (Werenskiöld fragment) on the tension failure side (open
Metacarpals
Proximal Injury
The proximal area is likely to be injured when the hand is
crushed (Fig. 17-35). Closed reduction and attention to soft
tissue swelling and damage are essential.
Isolated fractures of the base of the metacarpals are
infrequent.171 The fourth and fifth metacarpals are most
FIGURE 17-34. Displaced type 2 injury of the thumb.
669
arrow) and the Thurstan Holland fragment on the compression
failure side (closed arrow). (B) Type 3 injury pattern. (C) Type 7
(intraepiphyseal) injury pattern.
often involved (Fig. l7-36). Fractures involving the second
metacarpal usually involve the radial side. That in the boy
shown in Figure 17-37 involved the ulnar side and dis-
placed the fragment into the palmar space in contrast to
the usual dorsal displacement. Open reduction may be
necessary.
Diaphyseal Fracture
Fractures of the metacarpal shaft (diaphysis) are less
common in children than in adults (Fig. 17-38).177 Trans-
verse fractures of the metacarpals are usually the result of
direct blows. They angulate dorsally because of the original
deformation and the palmar force subsequently exerted
by the interosseous muscles. Oblique fractures of the
metacarpal shafts result from a torque force, with the finger
acting as the long lever; and they tend to shorten and
rotate (Fig. 17-39), rather than angulate. Fractures of the
third and fourth metacarpals tend to shorten less because
of the tethering effect of the deep transverse metacarpal
ligament, whereas fractures of the second and fifth
metacarpals tend to have more pronounced shortening and
rotation.
A stress fracture of the index metacarpal has been
described in a highly competitive tennis player.179 Other
metacarpals may also sustain comparable stress fractures.
Royle reviewed 98 metacarpal fractures for rotational
deformity.175 Approximately 25% had minor malrotation of
less than 10°. Only five had more than 10° of malrotation.
In only 2 of 98 patients did such rotary malunion require
operative intervention.174
The same principles apply to these fractures in both chil-
dren and adults. Most fractures are correctly treated by
simple immobilization. Dorsal “bowing” may be corrected
by relaxing the wrist extensors, the long finger flexors,
and the interosseous muscles. If the hand is properly posi-
670 17. Wrist and Hand

tioned with a splint, these fractures usually heal with little

difficulty.
Nonunion may occur.169 It usually heals satisfactorily after
adequate fixation and does not require extensive grafting
(Figs. 17-40, 17-41). A synostosis may complicate a crushing
or blast injury (Fig. 17-42).

Distal Fractures (Epiphyseal)

With the exception of the fifth metacarpal, fractures involv-
ing the distal metacarpal heads (Figs. 17-43, 17-44) appear
to be relatively infrequent in children and adoles-
cents.170,172,177 They must be analyzed carefully to determine
the actual or potential extent of damage to the interrelated
mechanisms of longitudinal or latitudinal growth as well
as disruption of the articular surface. Shortening of the
metacarpal is the most significant complication and may
occur after a seemingly innocuous injury. Brown described
a boy who sustained a fracture through the neck and
epiphysis of the third metacarpal (a type 2 injury).168
Three years later roentgenograms showed a slowdown in
growth of the third metacarpal. Figure 17-45 shows a similar
fracture of the distal metacarpal of the index finger, with
accompanying diaphyseal injury. Three years later
roentgenograms showed a slowdown in growth of the third
metacarpal.
Type 3 growth mechanism injuries may occur (Fig.
17-46).173 Growth arrest is a potential complication of

FIGURE 17-35. (A) Minimally evident proximal metacarpal fracture

(arrow). This injury may be confused with a pseudoepiphysis
(which is painless). (B) It was not treated, and the patient subse-
quently presented for evaluation of carpal pain, undoubtedly due
to the pseudarthrosis that has developed.

FIGURE 17-36. Fracture of the proximal end of the fifth metacarpal.

Metacarpals 671

A B
FIGURE 17-37. (A) Fracture of the ulnar side of the second metacarpal (arrow). (B) Oblique view showing palmar displacement of the
fragment.

type 3 and 4 growth mechanism injuries. Schiund reported
a case of locked metacarpophalangeal joint due to an
intraarticular fracture of the metacarpal head that was not
readily evident on standard radiographs.176 It proved to be
an osteochondral fracture, splitting the head as a type 3
injury.
Open reduction and internal fixation of the fracture may
be necessary. As Hastings and Simmons have indicated,
however, open reduction does not guarantee a good result in
displaced, intraarticular hand fractures in children.41
The probability that vascular injury plays a role in growth
deformity must be considered. Because of the extensive

FIGURE 17-38. (A) Diaphyseal fracture of the fourth metacarpal. (B) Undisplaced transverse diaphyseal fractures of the third and fourth
metacarpals.
672
FIGURE 17-39. Fracture of the diaphysis of the fifth metacarpal.
articular surface and joint capsular attachments, there is a
limited intracapsular course of the epiphyseal and physeal
vessels, making these regions potentially as susceptible to
temporary ischemia as the radial and femoral heads. The
temporary vascular interruption could lead to decreased
longitudinal growth and premature closure. However, the
posttraumatic revascularization would allow enlargement
of the metacarpal head and peripheral growth through the
zone of Ranvier, a well-recognized phenomenon in Legg-
Calvé-Perthes disease. Wright and Dell described ischemic
necrosis and the vascular anatomy of the metacarpals.180
They noted that in 35% of specimens a main artery to
the distal epiphysis was absent, making these metacarpal
FIGURE 17-40. (A) Delayed union. (B) Progressive healing with continued immobilization. (C) Healed fracture.
17. Wrist and Hand
heads dependent on small circumferential pericapsular
arterioles.
Distal Fifth Fractures (Boxer’s Fracture)
Fractures of the distal fifth metacarpal are relatively
common, particularly during adolescence. These injuries
may be metaphyseal or physeal injuries (Fig. 17-47). Cor-
rection of the angular deformity may be necessary, as remod-
eling may not correct malunion, particularly in the patient
close to skeletal maturity. Infrequently, open reduction, pin
stabilization, or both are indicated. Premature epiphysiode-
sis may occur (Fig. 17-48).
Thurston described closed osteotomy for correction of
nonunion of metacarpal neck fractures in which there
was excessive flexion.178 It involved removing a small dorsal
wedge followed by tension band wire fixation.
Metacarpophalangeal Dislocation
Reports of complex dislocations of the metacarpophalangeal
joints (Fig. 17-49) have combined patients of all ages, but a
significant number of these patients are skeletally imma-
ture.181–198 Baldwin reported four patients, three of whom
were children.182 Five of the nine patients reported by Green
and Terry were 16 years old or younger.190 Similarly, 8 of 13
patients reported by Becton, 1 by Bohart, 1 by Milch, 8 of 10
by Murphy and Stark, and 11 by Gilbert were all skeletally
immature.185,186,189,196,197 The incidence of this injury in chil-
dren and adolescents has been underemphasized.
Forced hyperextension of the proximal phalanx of the
index finger, usually from a fall on the hand, results in the
metacarpal heads being pushed through the palmar capsule.
The fibrocartilaginous palmar plate is torn loose at its
weakest point of attachment, the membranous attachment
to the metacarpal. The metacarpal head is displaced toward
the palm, and the palmar plate remains attached to the
phalanx and is folded into the joint, where it becomes
FIGURE 17-41. (A) Nonunion of metacarpal fractures. The fracture of metacarpal 4, in contrast, has healed. (B) Pin fixation. (C) Healing.

FIGURE 17-43. Distal second, third, and fourth physeal metacarpal

fractures associated with fractures of the second and third
metacarpal at the diaphyseal/proximal metaphyseal transition.
FIGURE 17-42. Synostosis of the fourth and fifth metacarpals after
a blast injury to the hand.

A B
FIGURE 17-44. (A) Fracture of the second metacarpal 4 weeks after injury. (B) Remodeling 10 weeks after injury.
 674 17. Wrist and Hand

FIGURE 17-45. (A) Type 2 fracture of

the third metacarpal head. (B) Three
years later the head is large (probably
because of hypervascularity following
the injury), but the physis has closed;
it is leading to shortening.

FIGURE 17-46. (A) Type 3 fracture

after being hit by a baseball bat. (B)
A B Three months later.

FIGURE 17-47. (A) Metaphyseal fracture of the fifth

metacarpal. Angulation was not corrected and has
A B led to malunion. (B) Moderate angulation.
Metacarpals
FIGURE 17-48. Premature epiphysiodesis 4 months after a teenage
boxer’s fracture.
wedged between the metacarpal head and the base of the
proximal phalanx. The phalanx is dislocated dorsally on the
metacarpal head, which is forced through the transverse
metacarpal ligament to become fixed between the ligament
and the longitudinal portion of the superficial palmar fascia.
The flexor tendons are displaced ulnarward and the lum-
FIGURE 17-49. (A, B) Complex MCP dislocation in a 10-year-old
boy following a fall from a tree. It was an open injury but unfortu-
nately was “cleaned, closed, and reduced” (no postreduction
roentgenogram) in an emergency ward. When the boy returned to
the hospital 1 day later with acute sepsis from clostridial infection,
675
brical tendons radialward, with both lying dorsal to the dis-
placed metacarpal head (Fig. 17-50). Gilbert found that the
lumbrical and flexor tendons were displaced ulnarward
together in eight cases, whereas in two cases the lumbrical
was displaced separately to the radial side.189
When the fifth finger is involved, because of the more
distal course of the long flexor tendons to the little finger,
these tendons are displaced radially and trap the metacarpal
head on that side; the tendon of the abductor digiti quinti
is the lateral trapping element. The fibrocartilaginous plate
and superficial transverse ligament, as in the index finger,
respectively form the floor and roof of the trap.
Widening or lateralization of the joint space on the an-
teroposterior radiograph suggests complex dislocation
with interposition of the palmar plate within the joint.
However, the anteroposterior radiograph may be deceptive, not
readily showing complete joint disruption (Fig. 17-51).
Usually the metacarpal head is directed radially (relative to
the proximal phalanx). Lateral films of the hand clearly
demonstrate the dorsal dislocation of the proximal phalanx,
if care is taken to visualize each of the overlapping proximal
phalanges. Lateral tomography through the involved finger
removes superimposition of the other metacarpophalangeal
joints.
The term “complex metacarpophalangeal dislocation”
primarily acknowledges the difficulties of management. The
principal impediment to reduction is entrapment of the
palmar plate. The treating physician should not undertake
multiple attempts at closed reduction before concluding that
the dislocation is irreducible because definite clinical and
radiographic clues exist. First, displacement of the phalanx
on the metacarpal is not at 90° (as it generally is with a simple
interphalangeal dislocation) but is more nearly parallel,
roentgenograms showed that the dislocation was still present.
Open reduction was successful, and the infection was controlled
with débridement, with the wound kept open, and administration of
parenteral antibiotics. (C) Three years later there has been some
“regeneration” of the ulnar side of the epiphysis.
676
FIGURE 17-50. Structures involved in complex MCP dislocations of the index and little fingers.
often with only slight displacement and minimal angulation.
Second, there often is dimpling of the palmar skin (see the
engraving at the beginning of this chapter). In the index
finger (the most common site of complex dislocation) the
dimple may be difficult to visualize because it lies within the
proximal palmar crease. Finally, widening or lateralization of
the joint space on radiography suggests a complex disloca-
tion because of interposition of the palmar plate within
the joint.
Reduction usually can be attained through a palmar
approach once the fibrocartilaginous plate has been partially
incised, although an attempt should be made to reduce it
FIGURE 17-51. Subtle second MCP dislocation.
17. Wrist and Hand
prior to plate incision. Excessive transection of the palmar
plate is not usually necessary in the child because of normally
increased laxity of ligamentous structures.192,194 Only enough
fibrocartilaginous plate or ligament to effect a reduc-
tion should be incised. If the diagnosis has been delayed
longer than 3–4 weeks, the ulnar collateral ligament of the
metacarpophalangeal joint must sometimes be incised
through a separate dorsal incision before reduction can be
accomplished.183,188
Early, protected mobilization of the joint with a dorsal
splint preventing full extension is the postoperative prefer-
ence. The reduction is stable so long as hyperextension is
avoided the first few weeks after surgery. Internal fixation is
usually unnecessary. In fact, K-wires crossing the physis may
be harmful in skeletally immature patients; a 10-year-old boy
had a deformed metacarpal head and articular surface and
a distorted physis.182
Concomitant osteochondral fracture (Fig. 17-52) from the
ulnar side of the metacarpal epiphysis may occur.185,189 These
chondro-osseous injuries represent the analogue of liga-
mentous injury in the skeletally immature patient and may
involve peripheral physeal injury. It is also important that
this fragment not be confused with a sesamoid displaced into
the joint.199 The sesamoid usually remains unossified until
mid- to late adolescence.
Gilbert reported concomitant proximal phalangeal
physeal injury.189 This injury mechanism would be similar to
the physeal disruption of the radial head that occurs while
an elbow dislocation is being reduced (see Chapter 15).
The possibility of vascular damage must be considered
in the skeletally immature patient, as the epiphyseal and
physeal circulation may be compromised by the dislocation
or exposure for the reduction. Irregularity of the metacarpal
head has been described after injury and open reduc-
tion.186,198 However, these reports did not discuss vascular
compromise as a possible cause, nor did they address
any “significant” growth deformities following reduction.
Ischemic necrosis and growth damage involving the meta-
carpal physis and epiphysis have certainly not been recog-
nized in the literature as specific complications of index
finger metacarpophalangeal dislocations.
Phalanges
FIGURE 17-52. (A) Osteochondral fragment
(arrow) often found in a complex MCP
dislocation. (B) Type 3 epiphyseal fracture
is evident following reduction of an MCP
dislocation.
A B
Phalanges
Interphalangeal Dislocation
Dislocations involve the proximal interphalangeal joint
(PIP) more than the distal interphalangeal joint (DIP) (Figs.
17-53 to 17-55). These hinge joints allow only flexion and
extension. The accessory fibers of the palmar plate and the
paired quadrilateral collateral ligaments form three sides of
each joint. The thickest portion of the collateral ligament
reinforces the insertion of the palmar plate into the base
of the middle phalanx. With a dislocation, generally two of
the three sides are disrupted. Following relocation, a
collateral ligament in a child usually heals with little
difficulty.227 Even in children, however, a collateral ligament
may be avulsed and does not become reaffixed to the
FIGURE 17-53. (A, B) Anteroposterior and lateral views of disloca-
tion of the proximal interphalangeal (PIP) joint. (C) Seemingly
simple PIP dislocation. (D) Postreduction films of the fracture
677
chondro-osseous structures. Callus may create a mass on the
side of the finger. If it occurs, it may be necessary to remove
it surgically.
Ligaments and capsular structures around the joints in the
child are strong in comparison to the physis, and injuries
that would frequently cause a dislocation in an adult more
often result in an epiphyseal fracture in the finger of a child
or adolescent (Fig. 17-5).218,235,242 For this reason it is impor-
tant to obtain roentgenograms of any joint injury prior to
and after reduction (Figs. 17-53, 17-55). Concomitant frac-
tures may be more evident after reduction.
As with a slipped capital femoral epiphysis complicat-
ing reduction of an acute hip dislocation, a phalangeal
epiphyseal-physeal unit may be acutely fractured and left
displaced when the rest of the phalanx is “reduced”
(Fig. 17-55).218,235,242
shown in (C) demonstrated type 3 dorsal (3) and type 7 palmar (7)
epiphyseal ossification center fractures.
678
FIGURE 17-54. (A) “Dislocation” of the PIP joint. It is actually a dis-
placed unicondylar fracture-dislocation.
With most interphalangeal dislocations, reduction is easily
accomplished by closed manipulation. The correct tech-
nique for closed reduction is to hyperextend the joint and
then push the distal bone over into the reduced position in
a dorsal to palmar direction.228 One should not apply trac-
tion to a dislocated finger joint and attempt to pull the distal
bone back into position, as it may entrap soft tissue within
17. Wrist and Hand
the joint and prevent reduction.219,241 After reduction it is
imperative to check the stability of the collateral ligaments,
as they may be torn at the time of initial displacement.
However, it must be remembered that joint laxity is common
in children. The motion should be compared with that of
the contralateral digit. If the joint is stable after reduction,
which it usually is, immediate protected motion of the finger
should be allowed by taping it to an adjacent normal digit
(dynamic splinting). An acceptable alternative is to immo-
bilize the finger for 10–14 days in the aforementioned func-
tional position (position of safety).
Crick et al. described dislocation of the proximal inter-
phalangeal joint with an avulsion fracture of the phalangeal
head that was locked through a tear in the central slip that
required open reduction.205 Irreducibility of a dorsal dislo-
cation of the distal interphalangeal joint may also be due to
the interposition of the volar plate.217,227,234
Simultaneous dislocations of the distal and proximal inter-
phalangeal joints may occur.214,215 The mechanism of injury
appears to be a longitudinal compressive force along the
extended digit. These dislocations should be reduced by
closed manipulation. There may be small avulsion fractures
of the volar plates.
Fractures of the Phalanges
Leonard and Dubravicik described 263 phalangeal fractures
in children: 75% were treated by simple external immobi-
lization; 15% required manipulative reduction with the
patient under anesthesia; and 10% required open reduc-
tion.49 Epiphyseal separations or fractures through the
metaphysis formed the largest group (41%); seven open
reductions were necessary for these injuries. Only 26% were
shaft injuries. Eight diaphyseal fractures necessitated open
reduction and lateral fixation, the main indication being
marked displacement with comminution and instability.
When there was sufficient angulation to warrant surgical
FIGURE 17-55. (A) Apparent dislocation of the
distal interphalangeal joint. (B) Lateral view
shows a type 2 injury of the distal phalanx.
The displaced epiphyseal fragment is also
dislocated.
Phalanges
intervention, it was necessary to immobilize the fracture for
about 6 weeks, as the distal fragment was relatively avascular
and healing was slow. Using small K-wires for internal fixa-
tion did not interfere significantly with the ultimate function
of the interphalangeal joints or cause degenerative arthritis
or epiphyseal arrest in the transfixed joints.237 DeJonge et al.
found that in the 10- to 29-year age group sports injuries and
accidental falls were the most common cause of injury of the
phalanges.209 Shewring and Coleman described phalangeal
fractures as a complication of finger wrestling.231
Some displacement of phalangeal fractures in children
may be accepted so long as the fragments are aligned in axial
and rotatory planes. Even mild angulation of a fracture in
the plane of motion of a hinge joint often disappears, par-
ticularly if the apex is toward the flexor side.
Malrotation is the most frequent complication of
phalangeal fractures, and must be avoided by careful atten-
tion to anatomic detail.201,233 When the fingers are individu-
ally flexed, they do not remain parallel as they do in full
extension but, rather, point toward the region of the
scaphoid tubercle. However, they do not converge on a
single fixed point, as is sometimes depicted (Fig. 17-5).
When the finger is only semiflexed, it helps to use the planes
of the fingernails as an additional guide. Rotatory malalign-
ment is primarily due to three contributing factors: (1)
failure to recognize the rotational deformity; (2) failure to
reduce the fracture properly; and (3) failure to immobilize
the fracture properly. Malrotation in a finger is especially dis-
abling. The fingers overlap and become entangled when
flexed.
A true lateral roentgenogram of the phalanx should show
an image of a single condyle if the two are properly super-
imposed. However, when rotation exists, the shaft may be
seen in the lateral position and the head in an oblique posi-
FIGURE 17-56. (A) Angulated (ulnarward) type 2 fracture of the
proximal phalanx of the ring finger. As is typical of many of these
injuries, there is transverse failure across the entire metaphyseal
subchondral plate, rather than just across the physeal cartilage. (B)
679
tion. This arrangement is not easy to assess in children
because of the variable degrees of ossification.220
Correcting malrotation in an acute fracture is relatively
easy. Vandenberk et al. described the use of percutaneous
absorbable pins to control rotation of children’s finger frac-
tures.236 If the fracture heals with malrotation, an osteotomy
may become necessary to correct the position. Most malro-
tations occur in the proximal phalanx. If an osteotomy is
needed, a useful technique was described by Lewis and
Hartman.223
Kirner’s deformity is a condition of the little finger char-
acterized by palmar and radial curving of the terminal
phalanx. Trauma was originally considered a causal
factor, but Dykes showed that it probably is congenital
(nontraumatic).211
Fortens et al. described a fracture through an incomplete
preaxial fusion of the phalanges.212 This type of radiolucency
is not unusual when there is failure to form the joint, and
probably because of lack of motion it increases susceptibility
to injury.
Connelly and Leicester described a 7-year-old boy who
underwent pulley reconstruction at the A2 pulley.202 Two
years later he caught the finger in a fence and fractured
the proximal phalanx. At surgery it became evident that the
reconstructed A2 pulley had become caught between the
fracture fragments. Open reduction led to successful healing
and resumption of normal motion.
Fracture of the Proximal Portion of the
Proximal Phalanx
Fractures of the proximal phalangeal growth region are
among the most common finger fractures in children (Figs.
17-56, 17-57). The fracture-failure pattern frequently leaves
This fracture was reduced to a more appropriate alignment. (C)
Type 3 fracture of the proximal phalanx of the ring finger (arrow),
with a concomitant metacarpal fracture in the long finger.
680
FIGURE 17-57. Variant of a type 2 injury with two peripheral
Thurstan Holland fragments.
not only the classic Thurstan Holland metaphyseal fragment
but also a transverse plate of metaphyseal subchondral bone
(the Werenskiöld fragment). Types 3 and 4 growth mecha-
nism fractures may also occur (Fig. 17-56C).
Coonrad and Pohlman focused attention on the poor
results obtained in 41 children with impacted fractures of the
proximal third of the proximal phalanx of the finger.203 An
impacted fracture of the proximal phalanx in the finger
usually angulates toward the palm (Fig. 17-58); and if a
significant degree of deformity remains, digital flexion is
limited. The fracture angulates toward the palm because the
intrinsic muscles flex the proximal fragment, and the long
extensor tendon causes shortening by axial pull. If the dis-
placed or impacted fracture is allowed to heal at an angula-
tion of 20° or more, the extensor tendon and its expansion
over the proximal phalanx become shortened and exert a
tethering effect on the bone.
Closed reduction is usually successful. Open reduction
and internal fixation of these proximal phalangeal fractures
may be required in the following situations: (1) when closed
methods have failed to correct rotation; (2) when open frac-
tures must be reduced; (3) when the articular congruity of
small articular fractures must be restored221; and (4) when
widely displaced fractures are irreducible because of sec-
ondary soft tissue interposition. An unusual, irreducible jux-
taepiphyseal fracture of the little finger may result from
interposition of the flexor tendon.213,238 Cowen and Dranick
reported a badly angulated type 2 injury of the proximal
phalanx of the little finger that was irreducible by closed
methods because the distal fragment was trapped in a but-
tonhole rent in the periosteum of the fractured phalanx, and
the dorsal hood simulated a “Chinese finger trap.”204
The most common cause of angular malunion in this type
of fracture is immobilization of the digit in insufficient
flexion.202 Extension permits gradual loss of reduction. A
true lateral roentgenogram evaluates angulation in these
patients both before and after reduction. If the fracture heals
17. Wrist and Hand
FIGURE 17-58. Proximal phalangeal growth mechanism fracture.
in an abnormal position, an opening wedge osteotomy cor-
rects the deformity.
Dameron and Engber described a tension band technique
for replacement of adolescent type 3 physeal fractures.208
The technique is satisfactory if applied with careful surgical
technique.
Extra-Octave Fracture
A frequent fracture of the proximal phalanx involves the
fifth digit (Fig. 17-59) and is often referred to as the “extra-
octave” fracture because of the extreme ulnar angulation
(Fig. 17-60). The mechanism of injury and the age of
the patient may result in a greenstick fracture of the ulnar
cortex. Treatment should correct rotational and angular
malalignment.
As with most type 2 epiphyseal fractures, closed reduction
usually gives a satisfactory result, although it may be difficult
to gain adequate purchase of the proximal fragment while
manipulating the distal fragment into anatomic alignment.
A pencil placed in the web space may serve as an effective
fulcrum to bring the digit radialward (Fig. 17-61). Another
method is to flex the metacarpophalangeal joint to 90° (or
more), which tightens the collateral ligaments and provides
purchase on the proximal (epiphyseal) fragment. Reduction
is then accomplished by pushing the distal fragment across
the palm and toward the thumb.
If the ulnar cortex is incompletely fractured (greenstick),
overcorrection and completion of the cortical fracture may
be necessary. The intact periosteal sleeve on the ulnar side
of the bone generally prevents overreduction and provides
stability in the reduced position. If the ulnar cortex is not
completely fractured, the residual plastic deformation may
cause gradual recurrence of some, if not all, of the angular
deformity.
These fractures may be difficult to control; and once the
fracture is reduced, the little finger must be splinted to the
adjacent uninjured finger. Protection of the reduction for 3
weeks in an ulnar gutter splint incorporating the adjacent
ring finger is advisable. Because of the pull of the abductor
digiti quinti muscle, these fractures tend to drift and become
redisplaced. Rarely, open reduction with pin fixation is
required.
With a severe fracture the epiphysis may remain in place
while the remainder of the phalanx is totally dislocated pal-
marward. Open reduction may be necessary in this fracture
pattern.241
Phalanges 681

FIGURE 17-59. (A) Type 2 fracture of the fifth proxi-

mal phalanx, with concomitant ulnar deviation. Note
the transverse metaphyseal fragment, which is char-
acteristic of this type of injury when it occurs in the
small longitudinal bones. This greenstick injury is
often referred to as the “extra- octave” fracture.
Reduction must overcorrect and complete this frac-
ture, or recurrent angular deformity may occur even
while the fracture is immobilized. (B) The greenstick
component was not completed in this patient. Thus
the fracture drifted back and healed in a malunion.

Fractures of the diaphysis of the proximal phalanx
(Fig. 17-62) may angulate as well as rotate. Some degree
of overriding (shortening) may be accepted. However,
malrotation must be corrected. Percutaneous fixation may
be used to control rotation. Open reduction is usually
unnecessary.
Fractures of the Phalangeal Neck
Phalangeal neck fractures, whether involving the proximal
or middle phalanges (Fig. 17-63), are common.200,206,210,225
Such injuries may be treacherous. It is a classic “booby-trap”
fracture in the hand that is transverse through the neck of

A B
FIGURE 17-60. (A) Stress view showing the extent of angulation probably present at maximum acute deformity. (B) Postreduction film
showing a thin linear juxtaphyseal fragment (arrow).
682
FIGURE 17-61. (A) Extra-octave fracture. (B) Method of reduction
utilizing a pencil in the web space.
either the proximal or the middle phalanx, with dorsal dis-
placement of the distal fragment (Fig. 17-63D). In children
the palmar plate may roll on itself, causing 90° rotation of
the condylar fragment, which is then entrapped by the
capsule and collateral ligaments (Fig. 17-64).226
The problem of adequate visualization of the fracture in
the splint may be overcome by using a tomographic cut
(lateral view) coinciding with the long axis of the injured
finger. The 90° (or more) rotation of the supracondylar pha-
langeal fracture can easily be missed. It is essential that an
adequate lateral roentgenogram or tomogram be obtained
to delineate it thoroughly.
A B
FIGURE 17-62. (A) Transverse fracture that occurred when the finger was crushed in a door. (B) It healed in a malunion. (C) Remodel-
ing and correction of the deformity 7 months later.
17. Wrist and Hand
Reduction may be easy, but redisplacement after closed
reduction can readily occur. The problem in recognizing this
complication is that it is difficult to visualize the bone clearly
on the postreduction lateral views because of superimposi-
tion of the other fingers in the splint. The resulting loss of
reduction may cause an unacceptable deformity (Fig. 17-65),
and late treatment of the healed, displaced fracture (even
as early as 3 weeks after injury) is difficult. Early open
reduction or closed reduction and percutaneous pinning
(Fig. 17-66) of the fracture generally yield better results
than later attempts to correct the malunion.222,226
In the series reported by Leonard and Dubravicik, 9 of 38
phalangeal neck fractures necessitated surgery.49 Dixon
and Moon reported treating five cases of phalangeal fracture
through the neck of the proximal phalanx of the finger
or thumb with 90° of rotation of the condylar fragment
and entrapment by the capsule and collateral ligaments.210
These fractures could not be reduced by closed methods
because the condylar fragment had rotated 90° and
was restrained and trapped by the capsule and collateral
ligaments. They did not describe any associated injuries of
the epiphysis of the middle phalanx. Whipple et al. described
an irreducible proximal interphalangeal joint injury in
a 6-year-old child and found that the palmar one-half of
the articular cartilage of the middle phalanx blocked
reduction.241
To correct chronic (healed) malunion of fractures of the
distal end of the proximal phalanx in children, Simmons and
Peters recommended a palmar approach to remove the bony
block to flexion.232
Complete remodeling of a displaced phalangeal neck frac-
ture may occur.226 Although this fracture is “removed” from
the active proximally located physis, for a few years there is
a physis present distally. It ossifies by “pseudoepiphyseal”
ossification. The peripheral zone of Ranvier and the tempo-
rary presence of a physis explain the remodeling in such
cases.
C
Phalanges
FIGURE 17-63. (A) Distal end of a phalanx fracture.
(B) Lateral view shows that it is mildly displaced. (C)
Fracture of the distal end of the proximal phalanx. (D)
Lateral view reveals a major problem: dorsal dis-
placement of the epiphyseal end.
FIGURE 17-64. (A, B) Rotation of the fragment.
683
A variation of this injury may include both distal pha-
langeal fracture and adjacent epiphyseal injury.
Intercondylar Fractures
Intercondylar fractures in children should be treated as they
are in adults. Displaced T-fractures of the distal end of a
phalanx require open reduction and internal fixation with
K-wires.240 When 30% or more of a joint surface is involved
or if there is instability of the joint, it should be opened
(Figs. 17-67, 17-68).
When pin fixation becomes necessary, healing of the frac-
ture may be delayed. Therefore fixation wires should be left
in place for at least 6 weeks. Epiphyseal avascular necrosis
has not been described. Stiffness after injury is not as
common a problem in children, as they usually regain com-
684 17. Wrist and Hand

FIGURE 17-67. (A) Displacing unicondylar fracture 4 weeks after

FIGURE 17-65. This distal end fracture healed in malalignment,
leaving an ulnar-directed angulation. It will not spontaneously
correct.
injury. (B) Percutaneous fixation. The fragment was left displaced
because of concern that open reduction would jeopardize the blood
supply.

plete mobility. Stiffness may occur, however, especially in

older children; and an extended period (months to years)
may be required for motion to return to normal. Arthrode-
sis may also occur.

Fractures of the Middle Phalanx

Fractures of the epiphysis are common (Figs. 17-69, 17-70).
They are ligament injury analogues and are associated with

FIGURE 17-68. (A) Undisplaced unicondylar fracture in an adoles-

cent. (B) The patient removed the cast-splint to play basketball,
FIGURE 17-66. Open reduction of rotated distal condylar fractures losing the position. The obliquity of the fracture line enhances this
sustained when the fingers were caught in a door. complication.
Phalanges 685

FIGURE 17-69. (A, B) Physeal fracture of the proximal or middle of the middle phalanx. (E, F) Type 3 condylar fracture treated by
phalanx and method of pinning. Dashed lines represent potential open reduction.
courses for buttress pins. (C, D) Types 3 and 7 condylar fractures

articular surface displacement. They often require open

reduction and pin fixation to avoid malunion.
The middle phalangeal shaft injury has specific deform-
ing musculotendinous forces (Fig. 17-71). The important
forces are insertion of the central slip onto the dorsal
aspect of the proximal middle phalanx and insertion of the
flexor digitorum sublimis along the palmar shaft. The
central slip extends the proximal phalanx, particularly if it is
a more proximal or epiphyseal type of injury. If the fracture
is proximal to the sublimis, the distal fragment tends to be
flexed. If the fracture is distal to the sublimis tendon, the
proximal fragment is flexed and the distal fragment hyper-
extended.
Fractures of the middle phalanx may be undisplaced or
angulated. If the fracture site is distal to the insertion of
the flexor superficialis tendon, it can usually be treated by
manual traction and flexion of the distal fragment. The
extensor tendon pulls the distal fragment into extension,
and the flexor superficialis causes flexion of the fragment,
producing an overall palmar angulation. Fracture of
the middle phalanx proximal to the insertion of the flexor
superficialis tendon may also be treated in a closed
manner.
FIGURE 17-70. Malunion of a type 2 injury of the middle phalanx.
686 17. Wrist and Hand

FIGURE 17-71. (A, B) Variable effects of tendons on deformation of

fracture fragments in a middle phalangeal injury.

The central slip of the extensor tendon extends the prox-

imal phalanx. The flexor superficialis flexes the distal
fragment, producing dorsal angulation of the fragments.
Therefore these fractures should be reduced and held in
extension. These injuries are often due to the finger being
caught in a door. Such crushing injuries may cause severely
comminuted epiphyseal fractures (Fig. 17-72).
Fractures of the shaft of the middle phalanx heal correctly
so long as the position of immobilization is recognized and
maintained. Immobilization for up to 7 weeks may be
required, even in a child.
On rare occasions, the proximal epiphysis is displaced
(Fig. 17-73).219 Open reduction is often required in such a
situation.
Premature partial physeal growth arrest subsequent to a
fracture in the hand of a child appears to be unusual
FIGURE 17-72. Complex epiphyseal/physeal fracture due to a
crushing injury.
(Fig. 17-74). Culp and Osgood reported a child with a frac-
ture of the middle phalanx that went on to a physeal bar
formation.207 Malunion may fail to remodel (Fig. 17-75).
Mallet Finger
Mallet finger deformities in children are anatomically dif-
ferent from those in adults, but the treatment is similar. In
children it is an epiphyseal injury with avulsion of a portion
of the epiphysis.232 In the small child, the deformity is usually
a displaced type 1 or 2 epiphyseal fracture at the base of the

FIGURE 17-73. (A) Displaced type 2 injury of the middle phalanx. (B) Displaced type 3 injury. (C) Displaced type 1 injury (B) and (C) are
comparable to a mallet finger injury of the distal phalanx.
Phalanges
FIGURE 17-74. Lateral view of growth arrest. The physeal fracture
was caused by a crushing injury.
distal phalanx (Fig. 17-76). In the adolescent, however, the
injury is likely to be a type 3 or type 7 growth mechanism
injury, which splits the epiphysis. The deformity ordinarily
results from forcible flexion of the end of the finger while
the extensor tendon is taut, as when catching a ball or strik-
ing an object with the finger extended.
The epiphysis of the terminal phalanx may completely dis-
place, being pulled by the extensor tendon to a position
dorsal to the middle phalanx.224,239 Savage showed that when
the distal phalanx epiphysis is displaced it may detach com-
pletely from the extensor digitorum communis and flip onto
the volar side of the middle phalanx.229 These injuries
require open reduction.
The lateral radiograph is important because rupture of
the extensor tendon is uncommon during childhood. The
A B
FIGURE 17-75. (A) Crush injury to the metaphysis. Angulation was not sufficiently corrected. (B) The malunion did not remodel.
687
flexor digitorum profundus tendon flexes the metaphysis,
into which it is inserted; and the extensor tendon, which
inserts into the epiphysis, maintains the epiphysis in the
extended position. The proximal epiphysis may be rotated
significantly. Sometimes the proximal epiphysis is not ossi-
fied, a finding that may lead to diagnostic difficulties and
delay in treatment.
Methods of treatment should be directed at joint hyper-
extension, which may be accomplished with small splints
(aluminum) to provide three-point fixation (Fig. 17-77).
Commercially available plastic splints are also reasonable. If
anatomic reduction cannot be achieved with closed reduc-
tion, open reduction and internal fixation may be required.
In many children this condition is an intraarticular or
intraepiphyseal type 3 injury and warrants open reduction as
the initial treatment. Failure to reduce the fragments may
result in significant malunion with exostosis formation and
joint dysfunction (Fig. 17-78). Partial or complete growth
arrest may occur (Fig. 17-79).
Inoue et al. described 14 patients with mallet fingers with
a large displaced fracture.216 They were treated using an
extension block Kirschner wire technique.
Because mallet finger injuries are often due to crushing,
which causes extensive soft tissue damage, the possibility of
infection is high (Fig. 17-80). Any type of fixation should be
used judiciously.
Open mallet-type fractures of the distal phalanx pose a sig-
nificant treatment problem. They are frequently associated
with osteomyelitis and poor results. The major problem is
that the nail is not elevated sufficiently to expose the open
fracture site. This situation may leave the fracture unreduced
and inappropriately irrigated, as any open fracture should
be. Ideally, the nail is removed, the fracture site properly
irrigated and débrided, the fracture reduced, the nail
matrix meticulously repaired with 5-0 or 6-0 chromic suture,
and the nail replaced as a stent (splint) after having
been perforated to allow drainage of any subungual
hematoma. Internal fixation of the fracture with K-wires is
usually unnecessary.
 FIGURE 17-77. Mallet finger. (A) Displaced. (B) Acceptable but
incomplete reduction with hyperextension.

FIGURE 17-76. (A, B) Two types of mallet finger epiphyseal injury

in the child and adolescent. (C) Typical appearance of type 1 injury
in a 5-year-old. (D) Type 2 injury.

FIGURE 17-78. (A) Fragmented injury of the entire epiphysis in an FIGURE 17-79. Partial growth arrest after a mallet finger injury.
adolescent. (B) Exostosis formation following nonoperative treat-
ment. It has caused a flexion deformity and impaired joint function.

688
Phalanges
FIGURE 17-80. Mallet finger. (A) Open injury. (B) Widening of the
physis due to osteomyelitis in an open injury.
Dameron and Engber described a tension band technique
for replacement of adolescent type 3 physeal fractures.208
The technique is satisfactory if applied with careful surgical
technique.
Fractures of the Distal Phalanx
Fractures of the distal phalanx are common. Radiating
fibrous septa form a dense meshwork and probably stabilize
these fractures, effectively preventing significant displace-
ment (Fig. 17-81). Most of these injuries result from crush-
ing and therefore are usually accompanied by extensive soft
tissue damage and subungual hematoma.
The terminal periosteum may be separated from the end
of the phalanx, which may or may not be accompanied by a
thin sleeve of bone. If fibrous tissue intervenes during the
reparative process, nonunion may develop, creating a
U-shaped piece of bone (Fig. 17-81C).
FIGURE 17-81. (A) Closed tip injury. (B) Displaced tip injury. (C) Reactive bone.
689
Avulsion of the nail and frequently associated lacerations
of the nail bed are probably produced by protrusions of the
phalangeal fragment. The presence of fracture of the
epiphyseal plate in association with avulsion of the nail and
laceration of the nail bed has important therapeutic impli-
cations because it becomes an open fracture. Simple reduc-
tion must also be accompanied with a strong appreciation for
the open injury. Engber and Glancy described osteomyelitis
and premature closure of the distal phalangeal epiphysis.249
Banerjee described two patients with physeal fractures of
the distal phalanx in which reduction was prevented by a
bridge of nail fold that had herniated into the gap.244 They
noted that Seymour230 was the first to describe open distal
phalangeal epiphyseal injuries with this complication.
Nail Bed
Probably one of the most frequent injuries in children
involves the nail bed, usually a crushing injury. About 50%
of nail bed injuries have an associated fracture of the distal
phalanx. Nail growth occurs at the rate of 0.1 mm per day. If
the nail is removed entirely, a delay of 21 days occurs prior
to significant evidence of nail growth.
Traumatic avulsion of the fingernail in skeletally immature
patients should arouse the physician’s suspicion of associated
bone injury. Lateral roentgenograms frequently reveal frac-
ture of the distal phalangeal epiphyseal plate.
Inadequate initial treatment may result in permanent
residual deformity.243,250 Lacerations of the nail bed should
be sutured as carefully as lacerations of the skin. Although
not all late deformity is preventable owing to the crushing
nature of the injury, it probably can be minimized by metic-
ulous operative repair of the lacerated nail bed with fine
absorbable material.
Meticulous primary repair of the nail bed increases the
likelihood of normal growth.252,253,258,263 The nail plate is com-
pletely removed. Incisions are made at the lateral corners of
the eponychium to allow evaluation of the nail bed. Any inci-
sion required in the eponychium should be made at 90°
690
angles to minimize the risk of deformity. Copious irrigation
is undertaken. The bed is repaired using 7-0 chromic catgut.
The avulsed matrix is placed under the eponychial fold
with a suture tied over a bolster, and the nail plate may
be replaced as a stent. Accompanying fractures should be
reduced and stabilized.
Zook et al. found that 90% of repaired nail beds could be
graded good to excellent. The poor results generally were
due to crush or avulsion injuries to both nail bed and nail
fold, usually with an associated infection.264,265
In an attempt to determine the most likely contaminating
organisms in crushing fingertip injuries in children, Rayan
and Flournoy assessed nontraumatized human fingernails.
They found that 95% of the subjects had a moderate to heavy
growth of Staphylococcus epidermidis and that most of these iso-
lates were highly susceptible to antibiotics.259 It is interesting
that 13 of the 20 subjects also had fungi. These organisms,
however, do not routinely cause infection in children.
The following treatment protocol is recommended for
nailbed injuries. When the fingernail attachment is nearly
completely avulsed, the nail should be removed. If only the
proximal portion is avulsed, a small proximal portion should
be removed, leaving the remainder of the nail to act as a
splint. After meticulous débridement and irrigation, a small
drain is inserted through the lacerated nail bed, and the
epiphyseal separation is reduced and maintained by splint-
ing.245 Oral antibiotics are given for at least 2 weeks. Because
a high percentage of infections of the hand are due to
staphylococci resistant to penicillin, appropriate synthetic
penicillins (e.g., dicloxacillin) should be used. Cephalo-
sporins may also be given, as they have been shown to
decrease the infection rate after open fractures.257 Consulta-
tion with an infectious disease specialist and consideration
of other antibiotics are appropriate. The drain is removed
after several days, and splinting is maintained for 4–6 weeks.
Subungual Hematoma
Any blood in the nail fold indicates disruption of the nail
bed and an open fracture. Bleeding underneath the finger-
nail may be painful, and significant relief of pain may be
attained by draining the blood through the nail. A paper clip
may be heated until it glows red. A match does not ordinar-
ily get the tip hot enough to melt painlessly through the nail
without having to apply any pressure. Although this tech-
nique may be somewhat frightening to the small patient, it
is usually less painful than boring a hole in the nail with a
sharp instrument. The lunula must not be damaged by the
heat or hole. Otherwise, a permanent nail deformity may
ensue.
Fingertip
Fingertip injuries in children are generally easier to treat
than similar injuries in adults because the regenerative
capacity of local tissues in children is greater.246 Loss of skin
only, with intact underlying subcutaneous tissue, is usually
managed best by careful neglect (i.e., by allowing the wound
to heal by secondary intention). All that is usually required
is initial débridement and cleansing of the wound, applying
a bulky, compressive dressing for the first 24 hours to control
17. Wrist and Hand
bleeding and then small dressings to keep the wound clean
(a small adhesive strip with a gauze pad usually suffices after
the first few days). The finger may be soaked daily when the
child is bathed, and the wound may then be redressed. Good
results with maximal preservation of length and good sensi-
bility may be achieved using this technique, even for injuries
in which there is a rather sizable loss of skin. If the tip of
the distal phalanx is protruding slightly, the same plan
of management may be carried out if the bone is cut with
a rongeur at a level underneath the soft tissue at the time of
initial débridement. As much bone as possible should be
maintained.
The injuries cause exessive parental concern. When an
open fracture includes portions of skin and fat that are only
partially attached, the tissue should not be removed. Bits of
tissue that one suspects would not heal in an adult may com-
pletely heal in a child. The regenerative potential in the
child is remarkable. Even when the injury has caused com-
plete amputation and the pieces are missing, regeneration
occurs and the tip of the stump becomes covered with
surprisingly good tissue.251,255,260,261 In general, one should
save as much tissue as possible. However, even when soft
tissue healing occurs, the damaged bone ends may not
“regenerate.”
Duthie and Adams described the use of meshed adhesive
tape to treat crushed fingers in children.247 They believed
that this method was better than multiple suturing.
Mennen and Wiese used a semipermeable dressing to
cover the avulsed fingertip once a week.254 The dressing
provided a temporary skin, making the finger painless and
allowing an appropriate healing environment that actively
promoted granulation tissue formation and epithelializa-
tion. They found that within an average of 20 days more than
200 fingertip injuries were successfully treated by this
methodology. Certainly, it is one to consider in children.
Partial amputations of the fingertip in which the tip is dan-
gling from a narrow bridge of skin should not be removed
in the child. Even when the chances of survival of the tip are
poor, the tissues should be loosely approximated and given
an opportunity to heal. Little has been lost if the tip does not
survive. If the tip does become necrotic, it is best to allow it
to demarcate spontaneously, so long as it is clean and free of
drainage.
The completely amputated fingertip that is picked up at
the scene of the accident and brought in separately with the
child in some instances warrants replantation. Replacement
of the tip with skin sutures is often surprisingly successful.
Moiemen and Elliot found that 11 of 18 amputated digital
tips replaced within 5 hours survived completely.256 In con-
trast, none of 32 digital tips replaced more than 5 hours after
injury survived completely. The mean delay between injury
and replacement for the successful group was 3.9 hours. In
the unsuccessful group it was 7.2 hours.
Thompson and Sorokolit advocated using the cross-finger
flap for treating avulsions of the fingertip.262 Several authors
have recommended using the cross-finger flap in all finger-
tip injuries in children 7–8 years of age or older but do not
advise it in younger children because immobilization is
“more difficult in the younger age group.” Thompson and
Sorokolit arrived at the following conclusions based on 75
children who had undergone 79 operative procedures: (1)
Bite Injuries
Following cross-finger pedicle grafts the lack of tactile sense,
osteogenesis, and disability due to altered sensation is not as
common in children as in adults. (2) From the cosmetic
standpoint, the pedicle flap and its donor site were not
entirely satisfactory. (3) The contour and color of the graft
tip were less than ideal. (4) Neglect of the index finger was
encountered in 20% of the children, but the middle finger
was trained to compensate for this disability. (5) There was
no postoperative joint stiffness. (6) Spread scars and inter-
rupted suture scars were noted on the abdomen at the donor
site of full-thickness free grafts. (7) The accepted indications
for a cross-finger pedicle flap should be modified in children
to include all age groups. The procedure has been associ-
ated with better clinical results in children than in adults.
Thenar flaps are also useful for these injuries in children.
The finger is flexed toward the palm and a flap is elevated
from the thenar region to resurface the fingertip pulp
deficit. This type of flap often leads to proximal interpha-
langeal joint stiffness in adults because of the necessary posi-
tion of immobilization. In contrast, the position is well
tolerated by children. The donor site may be closed primar-
ily, so donor site morbidity becomes less than that experi-
enced with cross-finger flaps. This procedure works best for
the index and middle fingers, which naturally reach to the
thenar region. It may be possible to use it for the ring finger.
The little finger, however, cannot be easily brought across
and should not be treated with this type of flap.
Elliot and Jigjinni described a lateral pulp flap evolved
from the volar tissue.248 This method, though applicable in
the child, should be used as a secondary closure method.
The wound is dressed and cleaned with an attempt at cov-
ering it to allow primary tissue healing, which is more likely
for such a defect in a child.
Amputations at more proximal levels through the distal
phalanx or distal interphalangeal joint may require more
sophisticated treatment in the operating room, and many
techniques for closure and coverage of these amputations
have been described.
Partial amputations of the fingertip in which the tip is dan-
gling from a narrow bridge of skin should not be removed
in the child. Even when the chances of survival of the tip are
poor, the tissues should be loosely approximated and given
an opportunity to heal. Little has been lost if the tip does not
survive. If the tip becomes necrotic, it is best to allow it to
demarcate spontaneously, so long as it is clean and free of
drainage.
Bite Injuries
The child’s hand often sustains a bite injury or penetration
by a sharp organic object. Common household pets (dog,
cat) normally have Eikenella corrodens or Pasturella multocida
in their mouth.271 Wiggins et al. described severe hand infec-
tion in a 15-month-old infant bitten by a dog.273 The wound
was initially sutured and the child given oral antibiotics.
These lesions should be considered contaminated crush-
avulsion injuries requiring aggressive irrigation and débride-
ment; they should never be closed primarily.
Infection of a metacarpophalangeal (MCP) joint resulting
from a tooth wound sustained in a fist fight was described in
691
1911.268 The injury pattern has been referred to as a “fight
bite” and occurs when a clenched fist strikes the opponent’s
tooth.267,270 Given the natural tendency of some children to
fight, particularly during adolescence, this pattern of injury
is likely to occur in all age groups. Because of the flexion of
the MCP joint, the impact usually results in a subchondral
fracture of the articular and epiphyseal cartilage of the
metacarpal epiphysis. The injury also violates the soft tissue
dorsal to the joint, allowing bacteria to be implanted directly
in the joint, bone, cartilage, and overlying extensor tendons
and their sheaths. As the fingers extend after the impact,
the soft tissues retract proximally, often sealing the contam-
inated wound and impeding the search for implanted
organisms.
The significance of the fight-bite injury is often over-
looked in children. Anyone with a history of such a wound,
no matter what size, over a metacarpal head should be
treated with suspicion, particularly as children are often poor
historians and when involved in fights are reluctant to give
a history of the nature of the injury.
Eyres and Allen described a skyline view in which the MCP
joint is fully flexed as is the proximal interphalangeal
(PIP).266 The x-ray beam is then directed along the axis
of the proximal phalanx. This allows visualization of the
metacarpal head and may reveal intraarticular lesions. In the
child, with increasing amounts of cartilage involving the
epiphysis, such fight-bite lesions may still be difficult to
detect. However, it is important to look for these intraartic-
ular fractures, which represent type 3, 4, and 7 growth plate
injuries in any child who has a history of hitting an object or
person with a hand in a clenched fist position.
Characteristically, roentgenography shows a wedge-shaped
defect in the dorsal articular surface subchondral bone
of the metacarpal head. It represents a subchondral
fracture.
Phair and Quinton studied human bite injuries involving
the MCP and PIP joints.269 All were treated by surgical explo-
ration within 24 hours. In 62% the wound had entered the
joint, and in 58% the bone or cartilage was injured. The
authors emphasized the concept of “chondral divot frac-
tures,” which might increase the likelihood of septic com-
plications. They recommended a combination of surgery
and broad-spectrum antibiotics. Bacteriologic culture
showed mixed coliforms in eight, Staphylococcus aureus in
three, Staphylococcus albus in one, and anaerobes in 1. In 8
patients the injury was confined to the depths of the skin,
whereas in 21 patients the depth of the bite extended to
tendon, joint capsule, or chondro-osseous tissue. Seventeen
patients had injury to the bone, with eleven osteochondral
fragments, four metacarpal head indentations, and two
indentations of the metacarpal shaft.
The most important factor governing the final outcome of
human fight-bite injuries to the hand is the time elapsed
between injury and the commencement of treatment. If left
untreated for 24–48 hours, the injury may lead to serious
septic arthritis, osteomyelitis, and extension of the soft tissue
infection to the deeper spaces of the hand or proximally into
the forearm within days to weeks. The two most common
organisms usually described for fight-bite injuries include
Staphylococcus and Streptococcus species, although anaerobic
organisms may also be encountered.
692 17. Wrist and Hand

Seiler et al. reported that venomous snake bites are a rel-

atively common occurrence in the southeastern and south-
western United States.272 They most commonly involve the
pit viper family (Crotalidae). Almost 50% of bites occur
on the fingers, and 30% involve children under 13 years.
Because of their small size children exhibit the most severe
manifestations of envenomation, including coagulopathy,
renal failure, compartment syndrome, cardiopulmonary
arrest, and even death. There should be judicious use of
antibiotics, tetanus, immunization, and antivenom. The use
of the latter is preceded by skin testing because of anaphy-
lactic reactions. Compartment syndrome is common and
requires appropriate treatment (see Chapters 9, 10).

Open Injuries
The hand is often the site of multiple open injuries (Fig.
17-82). Power tools and machines (especially lawn mowers),
explosives (e.g., firecrackers), and firearms may cause not
only the obvious acute injuries (Fig. 17-83) but also long-
term growth problems (Fig. 17-84).274,275 The basic treatment
of such open wounds is discussed in Chapter 9.
The presence of foreign bodies in open wounds should be
FIGURE 17-82. Open crush injury and fracture from entrapment in
suspected in children. Roentgenograms cannot be relied on
a car door.
to visualize foreign bodies, as wood splinters, glass, and other
foreign materials, especially biologic ones, may not be
radiopaque. usually detected by MRI. Wooden foreign bodies, especially
Russell et al. assessed the detection of foreign bodies in when wet, were seen only by CT and MRI. Xeroradiography
the hand.279,282 Using fresh cadaver hands, they implanted exhibited no benefit over plain films in identifying foreign
glass, gravel, plastic, and wood in the soft tissues. The bodies and should be discarded in favor of CT or MRI when
methods of assessment were routine radiographs, xeroradi- plain films were unrevealing.
ography, CT, and MRI. All types of glass were usually seen by Fackler and Burkhalter emphasized the importance of
all imaging methods. Gravel was visible with all methods minimizing excision of uninjured or questionable tissue in
except MRI; usually ferromagnetic streak artifacts obscured the hand and going back to look for further tissue necrosis
visualization. Plastic was not readily seen by routine radiog- 24–48 hours later to try to save as much tissue as possible.277
raphy or xeroradiography, was faintly seen by CT, and was The intricate anatomy of the hand requires more careful

FIGURE 17-83. (A) BB gun injury apparently impinging on the physis. (B, C) Tomographic cuts. (D) Six months after removal.
Amputations
A B
FIGURE 17-84. (A) Lawn mower injury with multiple areas of growth damage. (B) One year later.
attention to tissue excision. Any penetrating projectile must
crush sufficient tissue to form a hole, referred to as the per-
manent cavity. Surrounding tissue is pushed aside by radial
stretching. This larger area is referred to as the temporary
cavity. The amount of damage caused to such tissue by dis-
placement is dependent on the tissue’s elasticity and the
extent of displacement.
Fackler and Burkhalter evaluated the ballistics of various
penetrating injuries involving bullets and shotgun buck-
shot.277 Wound profiles for even the highest velocity military
bullets might cause minimal disruption in the initial 12 cm
of tissue penetration. Thus when the hand is involved the
total tissue path is much less (<12 cm), and the projectile’s
potential for increased tissue disruption is unlikely to be
reached. Accordingly, wounds from high velocity bullets do
not differ much from wounds produced by bullets of much
lower velocity. However, a bullet striking bone increases the
likelihood of more severe tissue disruption. Only necrotic or
severely ischemic muscle is excised in the hand and even in
the forearm and wrist, as aggressive, potentially unnecessary,
excision of questionably viable tissue may increase the ulti-
mate disability by removing tissue that may prove functional
so long as it does not become infected. They recommended
additional débridement with a “second look” at 1–3 days.
Ada et al. described problems of machinery rolling belt
injuries in children in a rural agricultural population.274
They described 16 children, most of whom were under 4
years of age, whose hands had been caught in the rolling
belts of agricultural machinery. Injuries included friction
burns; injuries to flexor tendons, digital nerves and arteries,
and skin; and fractures. They also had a number of patients
who sustained amputations. Their study concentrated on
finger injuries. Ten fingers in four patients had total ampu-
tations; replantation was attempted in three, with only one
patient doing well.
The problems of closure in children who sustain major
explosive-type injuries or degloving is the availability of con-
693
tiguous healthy tissue. Dap et al. described a posterior
interosseous flap that they used successfully in 23 cases.276
The youngest patient was 15 years old.
Reconstruction of these mutilating hand injuries is chal-
lenging. Various rotation and free flaps are used for soft
tissue loss.224,226 Phalangeal and metacarpal shortening due
to bone loss or growth arrest may be treated by bone graft
interposition or gradual lengthening.278,280,281,283
Amputations
Amputations at more proximal levels through the distal
phalanx or distal interphalangeal joint usually require
sophisticated treatment in the operating room. Many tech-
niques for closure and coverage of these amputations have
been described.
Replantations and Transplantation
Basic principles of replantation are discussed in Chapter 9.
The specific problem of replanted or transplanted epiphyses
and their subsequent capacity for growth are discussed in
Chapters 6 and 7.
Yamano has recommended replantation of the amputated
distal part of the fingers in zones I and II.304 The normal tech-
niques of microsurgery sometimes have to be modified,
especially when there are no veins to anastomose. This mod-
ification may require leaving a fishmouth incision and using
heparin irrigation. The procedure was done in children as
young as 14 months of age.
Significant advances in microvascular surgical techniques
have made replantation of entire digits of the hand a clini-
cal reality (Figs. 17-85, 17-86).284–304 Not all amputations are
suitable for replantation. If the primary care physician sees a
patient with a completely amputated digit, referral should be
made as soon as possible to a surgeon experienced in micro-
 694 17. Wrist and Hand

FIGURE 17-85. Replantation of an amputated hand. (A) Radiograph shows the hand to be intact, but fragmentation of the distal radius
is present. (B) Four months later. (C) Eight months later.

FIGURE 17-86. (A) Centralization of

replanted hand on the ulna. (B) One
A B year later.
Amputations
surgical techniques. The digit should be wrapped in a sterile
gauze pad soaked in Ringer’s lactate, placed in a plastic bag,
and cooled in ice. It should not be frozen, nor should the
vessels be cannulated or irrigated.
To be considered thoroughly successful, digital replanta-
tion in children after trauma must allow for physeal growth
to skeletal maturity, continued finger joint motion, stability
of the digit, and viability of the digit. With new techniques
for microvascular anastomosis, the survival of replanted
digits is becoming more and more frequent. Digital replan-
tation in children has not generally attained the same success
achieved with adult replantation, with reported viability rates
being no more than 67% compared with 80% in adults. In
children undergoing digital replantation with microsurgical
repair of digital nerve and flexor tendon, the immediate
functional results have generally surpassed results attained
in adults. If there is to be normal function of the hand at
skeletal maturity, the physis must also continue to grow lon-
gitudinally. The hand in a normal child doubles in size
between 2 years of age and skeletal maturity.
Saies et al. described the results following 73 replantations
and 89 revascularizations of the upper extremity in 120 chil-
dren.299 The rate of survival of the amputated part was sig-
nificantly higher after revascularization (88%) than after
replantation (63%). They also found that there was a signif-
icantly higher rate of survival after replantation in children
who were less than 9 years old (77%) compared to those who
were 9–16 years (52%). The one significant factor was the
lack of radiographic follow-up to see what the effects were
on growth plates and whether compromise of growth plate
function similar to frostbite was evident in any of these
extremities.
Continuing longitudinal epiphyseal growth has always
been a major concern following surgical reconstruction for
congenitally defective or traumatically amputated digits in
children. Epiphyseal transfers with and without microvascu-
lar anastomosis have yielded varying and unpredictable
results.302,303 In general, epiphyses transferred without
microvascular anastomosis have rarely grown in a normal
manner postoperatively.
Kröpfl et al. stated that only three of their patients had
normal growth.294 Fifteen patients attained 88% of normal
growth, and one patient had overgrowth (118%). Four
patients developed deviation of the replanted finger in the
frontal plane. The cause of deviation in each case was
an incorrect primary reposition and not a disturbance of
growth of the replanted epiphysis. Demiri et al. reported that
the average longitudinal growth in the injured bone was
94.5% in the phalanges of the amputated distal part.289
Ninkovic et al. described development of an arteriovenous
fistula after free flap surgery in a replanted hand.296
Phalangeal Lengthening
The lengthening of metacarpals and phalanges after severe
hand injuries with loss of bone substance has been used
in adults. It has been reported more recently in chil-
dren.278,280,281,283 Microfixators should be considered as a
means of maintaining length in children who have lost a
segment of the phalanx and offer an opportunity for bone
grafting when the wound is clean.
695
Autoamputation
Children with sensory neuropathy syndromes often have
severe hand involvement because of self-mutilation. Lack of
sensation may result in injuries, especially thermal injuries,
which cause skin breakdown and exposure of the chondro-
osseous elements. Many of these children have mild mental
retardation and may chew their fingers, further exposing
bone.
Treatment must always be directed at obtaining soft tissue
healing without a complicating infection. Because of the
“chewing” mechanism, cellulitis from microorganisms such
as Streptococcus is just as significant a possibility as staphylo-
coccal osteomyelitis. These wounds should never be closed;
granulation and spontaneous epithelialization should be
allowed.
Repetitive infection of the bone (chronic osteomyelitis)
may require amputation. In a child, amputations are best
done at a joint, although this principle is applied less rigidly
to a child’s hand. Only as much bone as necessary to control
infection and assist in soft tissue coverage is removed.
Repetitive trauma may lead to chronic epiphysiolysis or
crushing injury to the physis. Either increases the functional
loss of the hand and wrist. Because these children cannot
perceive pain, the parents should be taught to look for signs
of swelling or erythema, especially about the wrist, so
roentgenograms may be taken to evaluate the presence of a
fracture. Treatment (immobilization) lessens the likelihood
of repetitive epiphysiolysis, which is associated with a much
higher incidence of premature growth arrest.
Thermal Injuries
The hand is often the site of major thermal injury, which
may involve either cold (frostbite) or heat (burn).305–316
Primary management is generally directed toward obvious
soft tissue damage, although long-term effects on the
chondro-osseous elements may occur and should be of suf-
ficient concern to warrant serial roentgenograms. The
middle phalangeal physes seem particularly susceptible to
premature growth arrest, whether the thermal injury is
excessive heat or cold.309,311
Burns
The appropriate management of a burn injury of the hand
is dictated largely by the depth of tissue damage. Superficial
epidermal burns are easily diagnosed, and they heal with-
out intervention.310 On the other hand, partial-thickness
(dermal) burns may be superficial or deep, requiring dif-
ferent courses of therapy. Superficial partial-thickness burns
also heal by themselves, generally within 3 weeks and without
scarring.
In contrast, deep partial-thickness burns, if left alone, heal
primarily by wound contracture aided by epidermal prolif-
eration from the few surviving skin appendages. The process
takes more than 3 weeks and, if it involves the hand, often
results in serious impairment of function.305,308 As a result,
nearly all burn surgeons now recommend early excision and
grafting of these wounds. Early wound closure allows early
mobilization and prevents joint stiffness and contractures,
696
particularly of the proximal interphalangeal joints. Early
wound closure avoids the need for continuous splinting and
elevation of the injured extremity. Early wound closure
lessens the possibility of wound infection with its attendant
risks of further damage to the hand. For all of these reasons,
early wound closure reduces the total length of hospitaliza-
tion of the patient. Finally, the ultimate cosmetic and func-
tional outcome is also improved.
Children with contact burns of the hand that result in
more than epidermal injury should be managed in a con-
servative manner. They should be hospitalized when first
seen and consultation arranged. Local wound care and phys-
ical therapy can be maximized while providing the opportu-
nity for intensive observation. Given 2–3 days for the burn
to declare its own ability to heal, more competent decisions
regarding appropriate therapy may be made.
For burns that demonstrate an ability to heal without sig-
nificant scarring or functional impairment, the brief hospi-
talization is a justifiable expense. During this time parents
may be instructed about the techniques of proper burn care,
simplifying outpatient management. An added advantage to
hospitalization is the opportunity to provide optimal pain
management during the acute stage.
Stern and colleagues reviewed 264 surgically treated prox-
imal interphalangeal joint flexion contractures following
burns in children.312 Contracture severity was determined
from preoperative radiographs and physical examination.
Eighty per cent of the digits were successfully treated when
the postoperative contractures were less than 20°. Unsatis-
factory results were present in 12% of the digits, and they
were directly proportional to the severity of the contracture
and tended to occur in older children with large total body
surface burns. The time interval between burn and con-
tracture release did not correlate with contracture severity or
therapeutic failure. The most common cause of an unsatis-
factory result was failure to release the contracture fully. Gen-
erally, simple releases with or without scar excision were
performed for type I contractures, with coverage being
achieved by skin grafting or Z-plasty. The type I contracture
has skin involvement only and does not require joint release.
Type II deformities often required a capsular release in addi-
tion to the dermal release. Coverage was achieved by skin
grafting, Z-plasty, or cross-finger flap. There were only 14
type III contractures; 8 were treated by release and autograft,
5 by arthrodesis, and 1 by cross-finger flap. All fusions were
performed through the dorsal approach. Bone shortening
was necessary to gain extension and to accommodate the
palmar soft tissue contracture.
Graham et al. reviewed 278 postburn MCP joint extension
contractures and devised a classification system.307 Type 1
(47%) had more than 30° of MCP flexion with the wrist fully
extended. Scarring was generally limited to the dorsal skin.
Type 2 (34%) showed less than 30° of MCP flexion with the
wrist maximally extended and scarring typically involved
skin, dorsal apparatus, and MCP capsule. Type 3 (19%)
exhibited more than 30° of MCP hyperextension and often
demonstrated incongruity or dorsal subluxation of the MCP.
Improvement after reconstruction was evident in 95% of
type 1, 73% of type 2, and 47% of type 3. Failure to improve
functionally was related to the adequacy of the scar release.
The ring and small fingers accounted for 65% of the digits
17. Wrist and Hand
in this study, 68% of the failures, and all 7 amputations. The
authors did not address whether there were areas of thermal
injury to the underlying distal metacarpal physes and
epiphyses. They did note that an “abnormal radiographic
appearance of the MCP joint” often precluded a satisfactory
result. They did not stipulate exactly what they meant by
“abnormal.” The ulnar side of the hand appears particularly
vulnerable to the development of extension contractures
and accounts for a disproportionally high percentage of
unsatisfactory results.
Frostbite
Long-term sequelae of frostbite include premature fusion
and abnormal growth of the physes,314–316 which lead to short-
ening and deformity of the affected metacarpals and proxi-
mal and middle phalanges. There may also be irregular
involvement of the physis. The articular surfaces may also
have premature degenerative arthritis. Frostbite in children
typically affects the forefingers while sparing the thumb,
probably because the thumb is protected by being clasped in
the palm when the child is outside. The pathologic theories
include extracellular ice crystal formation causing chondro-
cyte damage, ionic shock in chondrocytes owing to abnor-
mal movement of intracellular fluid, and microvascular
damage, with the latter being the most likely. A detailed
description of this injury pattern and its complications is
found in Chapter 6.
Tendon Injuries
Tendon injuries are relatively common in children. They
often result from grasping sharp objects. As such, the tendon
ends are likely to retract. Treatment of tendon injuries in
children is similar to that in adults.314–346
In one study glass was the most common cause of injury,
involving 30 of 38 patients.327 Five patients were cut by a
knife, and three sustained their injuries by other means. As
mentioned previously, the little finger was most commonly
injured, followed, in order, by the ring finger, middle finger,
and index finger. The most frequent accompanying injury
was injury to the digital nerve, which occurred in 20 patients
(almost half). There were three fractures of either a carpal
or a phalangeal bone.327
Levine and Leslie described the use of ultrasonography to
detect a radiolucent foreign body in the hand.279 It was a
small piece of glass from a laboratory instrument that was
not evident on radiographs. The authors were able to show
that the glass was embedded in the deep synovial surface of
the flexor pollicus longus, facilitating surgical exposure and
removal of a foreign body. They noted that ultrasonography
for the detection of small foreign bodies in the hand
required slow, meticulous scanning where there are many
complex echogenic structures. They also emphasized
the importance of studying the extremity from multiple
orientations.
Recognizing tendon lacerations is more difficult in the
small child than in the adult because of problems of accu-
rate physical examination. Precise testing of specific tendon
function in a small child requires considerable skill and
Tendon Injuries 697

patience. It may be virtually impossible to carry out in the

painful hand of a frightened, injured child. In such situa-
tions the best information is usually gleaned from careful,
almost surreptitious observations, specifically looking for a
digit that is held in an atypical position or one that does not
move in normal synchrony with the other digits. Sometimes
the absence of specific muscles is seen by the lack of normal
retraction response to gentle pinprick examination.
Passive observation is just as important as active testing of
function. Observe whether the child at rest holds all the
fingers in the same position. If one finger seems slightly out
of position with the rest of the fingers, a tendon injury is sus-
pected. If there is a flexor tendon injury, the involved finger
usually lies in more extension than the rest of the digits. In
contrast, if a finger lags in flexion when the child extends
the fingers, an injury of an extensor tendon should be sus-
pected. Squeezing the forearm may create some motion that
aids in diagnosis. Passive motion of the wrist may also be used
to look for disparate motion of one finger relative to the rest.
Both of the aforementioned tests are suggestive only and do
not help diagnose an incomplete injury. In children, nerve
injuries frequently occur in association with tendon injuries.
Interestingly, although all children are susceptible to
tendon injuries, the incidence appears to be slightly higher FIGURE 17-87. (A) Tendon injury followed by contracture of the
during the first 3 years of life. This obviously has a signifi- digit.
cant effect on the ability to make a diagnosis because of the
poor history and the variability of the child to cooperate
during a detailed if not complex physical examination.
Routine tests for sensation and function may create adverse mechanical forces resulting from tendon lacerations causes
responses. For instance, a child is more likely to withdraw the growth disturbance. Again, this complication of delayed
from pinprick than to be willing to allow repetitive stimula- repair may be potentially avoided by primary repair. Main-
tion to delineate a neurologic deficit. The concept of two- taining normal tension may be the most important factor in
point discrimination may not be part of the child’s thought longitudinal tendon growth.340
processes. There must be concern for whether the tendon will grow.
The suspicion of tendon laceration requires thorough Maintaining normal tension may be the most important
exploration with the patient under tourniquet control and factor in longitudinal tendon growth.340 A study by Hage and
adequate anesthesia because it is the only sure way to iden- Dupuis suggested that the graft elongates with growth of the
tify specific tendon injury. Exploration is done in an oper- child,328 but the elongation may have been growth at either
ating room, where proper equipment is available for tendon end of the original tendon rather than within the graft itself.
repair. Interestingly, they noted that the fingers requiring tendon
Although concepts regarding the repair of some tendon grafts were smaller and thinner than those of the contralat-
injuries are often controversial, the current thinking is that eral hand. There is virtually no published material on the
the best results in children are likely to be achieved with the behavior of grafted tendon tissue with growth.
primary repair of all lacerated tendons in clean wounds. This
includes lacerated flexor tendons in the region often
Flexor Tendons
referred to as a “no-man’s-land”—that portion of the flexor
apparatus between the proximal palmar crease and the prox- O’Connell et al. reviewed 78 patients younger than 16 years
imal interphalangeal joint. Aggressive postoperative therapy who had 95 flexor tendon lacerations and repairs in zone I
is essential to avoid loss of function (Fig. 17-87). or II.341 The average postrepair follow-up interval was 24
The absence of any part of the total mechanical force, months. They divided their patient groups into 0–5 years,
such as the flexor tendons, may be responsible for retarda- 6–10 years, and 11–15 years of age. All repairs in zone I
tion of bone growth during a child’s growth phase.322 A dis- returned to excellent function. The repairs in zone II
turbance in digital growth after an unrepaired tendon injury achieved comparable results when managed with an early
in the child is a phenomenon that has received little atten- passive motion program following immobilization for 3–4
tion. Gaisford and Fleegler reported unrepaired flexor weeks. Immobilization for longer than 4 weeks resulted in
tendon injuries in children that were associated with distur- appreciable deterioration of function. In many digits, notice-
bances of digital growth.326 No such findings were reported ably improved digital motion was found when the patients
in another study of flexor tendon injuries.319 returned after several years of continued growth.
Some studies have documented growth retardation of Lacerations of the flexor tendons in the carpal canal
the finger in which repairs of flexor tendon injuries were region (zone IV) should be repaired primarily. Some of the
significantly delayed.322,326 The actions of appropriate carpal ligaments are left intact to prevent bowstring dis-
698
placement. Primary repairs are indicated for all lacerations
in the palm of the hand (zone III). To minimize scarring,
the palmar fascia over the tendon juncture is excised. Results
of the primary repair of flexor tendons in the digital sheaths
(zone II) have been unpredictable. Repair of the profundus
tendon and excision of the subliminus tendon are recom-
mended with repair of the sheath when both are injured
in children under 4 years of age. If the sheath cannot
be repaired, the surgeon should consider a fascia graft,
although there is no evidence in children that this practice
improves the repair results.
Stahl et al. compared 17 partially lacerated flexor tendons
(less than 75% of the cross-sectional area) in children
treated by surgical repair to that of 19 tendons treated non-
operatively.344 The outcome of the two groups was compa-
rably favorable. There were no complications, such as
triggering or furthering of the tear in either group. The
authors advocated early mobilization for partial tear and
exploration for complete tear.
Bell et al. have advocated using tendon grafts for injuries
within the digital sheath in children.319 The proximal super-
ficialis flexor tendon is the preferred source of graft when
both tendons have been lacerated. Other sources of tendon
grafts include the palmaris longus, a toe extensor, or the
plantaris tendon. In children the superficial and deep
tendons tend to be the same size, in contrast to those in
adults.
Satisfactory results may be obtained by primary repair of
tendon lacerations in the distal portions (zone I). It is impor-
tant in children to repair the tendon laceration rather than
advancing the profundus, so suture lines do not cross the
epiphyseal plate of the distal phalanx. The flexor pollicis
longus may be repaired primarily at any level in children
with consistently good results.327 Two-stage tendon grafts
are rarely necessary in children. The advantages of primary
repair include a shortened period of disability, lack of stiff-
ness, and decreased incidence of joint contractures. Sec-
ondary procedures are not usually necessary.
Postoperatively, it is essential to protect the surgical repair,
which is made difficult by the inability or unwillingness of
the young child to cooperate or understand the importance
of total postoperative immobilization as part of the rehabil-
itation. Children under 5 years of age should be immobi-
lized, which may involve an enveloping cast that does not
allow any type of finger motion. Children over 5 years,
particularly over 7 years, are probably more mature and
better able to understand the concept of immobilization. It
is also important to immobilize the elbow in a cast because
the child will move the muscle masses of the extensor and
flexor tendons. Immobilization is maintained for 3–4 weeks.
Following cast removal use of the hand and wrist is encour-
aged. The parents are instructed in passive range of motion,
and the child is encouraged to play. Aggressive, defined
occupational therapy is probably unnecesary in most
children.
Tenolysis, the surgical release of nongliding adhesions
after tendon repair, may be used in children. The same
attention to detail necessary in an adult must be applied to
the child. Significant improvement in active flexion after
tenolysis is more likely to occur in children over 11 years
of age.320
17. Wrist and Hand
Grobbelaar and Hudson studied tendon injuries in 38 chil-
dren with a mean age of 6.7 years.327 All were treated by
primary suture and controlled remobilization. There were
53 tendon injuries with an average of 1.5 digits per patient;
most commonly the little finger was injured (23 of 38
patients). Sixty percent of the injuries occurred in zone II.
These authors found that repair of both the flexor digito-
rum superficialis (FDS) and the flexor digitorum profundus
(FDP) was better than repair of the FDP alone, even in zone
II. Eighty-two percent achieved excellent or good results.
There were three tendon ruptures, and all were classified as
poor results. Other poor results occurred with a zone II
injury with an associated ulnar nerve palsy. Grobbelaar and
Hudson believed that the outcome of flexor tendon repair
in children was much better than that in adults because
of rapid healing of the tendons. No child in their series
required subsequent tenolysis due to adhesions. They
strongly emphasized that both flexor tendons should be
repaired, irrespective of the zone of injury.
Woods and Sicilia reviewed congenital trigger digits,
emphasizing that they sometimes present following an
apparent injury with the parent having been unaware of the
lesion before.346 The tendency in the child is for involvement
with the thumb. Surgical treatment is simple and effective.
The diagnosing physician should be aware of the fact that
these injuries are more likely to be congenital than a conse-
quence of trauma.
Miura et al. showed that among 62 patients with campto-
dactyly of the little finger, only 5 failed to respond to con-
servative treatment.339 Ogino and Kato showed that in five of
six cases of camptodactyly, the FDS tendon was hypoplastic
and there was no continuity of the normal tendon between
the muscle belly and the osseous insertion.342
Extensor Tendons
Extensor tendon injuries are just as important as flexor
tendon injuries (Fig. 17-88) but do not usually receive the
same emphasis in the literature. Primary repair in the child
is currently the treatment of choice at all levels of injury.
Attention must be paid particularly to the various types of
mallet finger equivalents at the distal phalanx in which
some or all of the epiphysis is displaced, effectively shorten-
ing the extensor tendon and leaving the nonrepaired finger
with a permanent flexion deformity. Primary repair allows
adequate exploration of the wound in an otherwise ap-
prehensive individual. Unrecognized injuries may require
tendon grafts or transfers. In either case, postoperative
immobilization is paramount. The recommendation of 30°
of wrist extension and 15° of MCP flexion should not be
approached as rigidly in a child because of the rapidity with
which they overcome contractures. These tendons are much
thinner and more ribbon-like than the flexor tendon and
must be protected for a longer period of time, usually up to
6 weeks.
Posner and McMahon described congenital radial sublux-
ation of the extensor tendons in a boy who complained of
increasing pain and snapping at the MCP joints with active
finger flexion.343 It was surgically repaired with an excellent
result. They noted that the tightness of the radial, sagittal,
and transverse bands of the dorsal hood was the cause of the
Nerve Injuries
FIGURE 17-88. Deformity after an unrepaired extensor tendon
laceration.
radial shift. They also noted that there were at least two sim-
iliar cases in the literature that had resulted from trauma
involving a single finger.
Calcification
Acute calcific tendinitis has been described in a child.338 It
was found in a 10-year-old boy who had had a week of pro-
gressive pain and swelling. It was initially diagnosed as a
finger infection. The patient denied trauma. There was cal-
cification in the flexor tendon region adjacent to the proxi-
mal phalangeal metaphysis. The patient was splinted, and
within 1 month the calcification disappeared.
Nerve Injuries
Recognizing nerve injuries in children is even more difficult
than recognizing tendon injuries. A lacerated digital
nerve in the small child is almost impossible to diagnose by
physical examination alone, and even injury to the major
nerves in the forearm may be difficult to demonstrate
objectively.
Severance of a peripheral nerve includes sensory and
motor function and sympathetic intervention. Simply touch-
ing the fingertips may indicate a difference in moistness in
a child, which helps with the diagnosis. The diagnosis may
be ascertained with little patient cooperation. A smooth
piece of plastic, such as the barrel of a pen, may be drawn
699
across the surface of the fingertips. In the presence of
sweating, there is adhesion between the plastic and the
fingertip; in fact, a plastic device may squeak against dry
skin.353
Instead of using pinprick, scratch the fingertip with a fin-
gernail and then stroke it with the pulp of the examiner’s
finger.350 If the patient can feel the difference, the nerve is
probably intact. If the patient cannot discriminate, it is likely
that nerve function has been damaged. Furthermore, if the
child cannot discriminate between fingernail scratch
and simple touch, he probably cannot feel a pin stick. The
child may also respond to actual or anticipated poking in a
reactive way (i.e., anticipating pain from a sharp object)
rather than as a response to the invoked pain. Another trick
is to immerse the hand in water. Finger skin with intact sen-
sation wrinkles after being submerged in lukewarm water
after about 5 minutes, whereas denervated areas remain
smooth.
The size and location of the skin laceration aid little in
the diagnosis, as a penetrating wound may extend a great
distance from the point of injury, and a small, benign-
appearing skin laceration often masks rather extensive
underlying soft tissue injuries. A tiny puncture wound in the
palm is often overlooked as the point of injury that could
result in a digital nerve laceration.
Because primary repair of lacerated nerves in clean
wounds is likely to give the best results, recognizing these
injuries when the child is first seen is important. It is imper-
ative that all penetrating wounds with any possibility of nerve
laceration be examined under appropriate conditions,
including adequate anesthesia and tourniquet control. A
lacerated nerve should be repaired in the operating room
under appropriate magnification.
Primary nerve repair utilizes the operating microscope
and may or may not necessitate someone specifically skilled
in techniques of nerve repair. Because children in general
have better regeneration after repair of peripheral nerves,
most surgeons do an epineural suture for divided nerves in
the child’s hand. Fascicular nerve repairs and suturing are
probably not necessary in a child unless there are nontrans-
verse lacerations.
Most articles dealing with peripheral nerve suture con-
clude that children regenerate sensation better than adults
with similar injuries. However, the mechanism of improved
functional recovery is still in question. Almquist et al. studied
nerve conduction velocities and microscopically evaluated
median nerves in baby and adult monkeys.347 Three years
after laceration and repair, nerve conduction velocities were
essentially identical. The only difference was that the infants
had slightly more accidents than the adults. This study sug-
gested that there is no difference in axon regeneration at
any age; rather, the improved sensory recovery is most likely
related to the intrinsic elasticity of the central nervous system
in children.
Although some surgeons advocate sensory reeducation
after suture of peripheral nerves, children probably ex-
perience spontaneous postoperative sensory reeducation
with the activities of daily living. Children have an intrinsic
mechanism that encourages the use of an extremity or
a digit if it has sufficient sensation and motion to be of any
function.
700
Return of muscle function following nerve repair usually
lags behind return of sensibility. A minimum of a year is
required to assess return of motor function, especially in the
hand. When motor deficits persist after peripheral nerve
injury, standard tendon transfers that apply to adult radial,
medial, and ulnar nerve palsies may also be useful in children.
The few transfers that require bony insertions must be modi-
fied to ensure that open physes are not damaged.
Poilvache et al. described carpal tunnel syndrome (CTS)
during childhood.354 One of their cases was posttraumatic.
This boy had sustained a palmar wound in his right hand at
the age of 2 years. Surgical exploration had revealed a partial
laceration of the transverse carpal ligament. From age 2 to
9 he was asymptomatic, after which pain gradually devel-
oped. Surgical release at age 10 years led to complete subsi-
dence of symptoms. Most cases of CTS in children are usually
associated with space-occupying lesions (e.g., congenital
abnormalities such as neurofibroma or angioma).349,351,352
CTS may appear after fractures of the distal end of the radius
or burns.348
Hair Strangulation
Because of the propensity of small children to take hands
and fingers they have been sucking and to then twirl them
in their hair or to play with clothing that may be frayed may
lead to digital constriction.355–361 According to Abel and
McFarland, this was first reported in 1832 and involved a con-
stricting band around the penis.355 Since then, approxi-
mately 70 additional cases have been reported involving the
toes, fingers, and genitals. In the various reviews, the inci-
dence of involvement was the toes in 44%, the genitals in
32%, and the fingers in 24%. The mean age for patients with
involvement of the toes is 4 months. Finger involvement,
interestingly, tends to present within the first month of life,
averaging 3 weeks of age.
Abel and McFarland stated that the exact pathologic
sequence was not known.355 Infants have a tendency to twirl
objects such as hair, causing it to become encircled around
the involved region; and continued movements and growth
may result in tightening of the hairs with resultant initial
lymphatic obstruction. As swelling and growth continue, the
hairs may cut into the skin, causing more inflammation and
making a diagnosis more difficult.
These children may present a diagnostic dilemma to a
primary care physician or pediatrician who initially con-
fronts a swollen digit in a child, especially in the office or
emergency room. The constricting agents are often difficult
to see, particularly when it involves blond hair or a light
fabric. Successful treatment obviously depends on prompt
recognition of the problem and alleviation of the con-
striction, which usually involves isolating the constriction
material, which then may be cut to remove it. The use of
magnifying loupes enhances the ability to visualize the
material. In rare instances partial resection of some tissue
may be necessary. Of the reported cases, approximately 50%
were successfully managed with specific removal of the hairs
or threads in the emergency room. Operative exploration
with sharp dissection was done to release the constrictions in
all of the remaining patients, except two who required
amputation.356
17. Wrist and Hand
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326. Gaisford JD, Fleegler EJ. Alterations in finger growth follow-
ing flexor tendon injuries. Plast Reconstr Surg 1973;51:
164–168.
327. Grobbelaar AO, Hudson DA. Flexor tendon injuries in chil-
dren. J Hand Surg [Br] 1994;19:696–698.
328. Hage J, Dupuis CC. The intriguing fate of tendon grafts in
small children’s hands and their results. Br J Plast Surg
1965;18:341–349.
329. Herndon JH. Tendon injuries. In: Carter PR (ed) Recon-
struction of the Child’s Hand. Philadelphia: Lea & Febiger,
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330. Herndon JH. Treatment of tendon injuries in children.
Orthop Clin North Am 1976;7:717–731.
331. Herndon JH. Tendon injuries: extensor surface. Emerg Clin
North Am 1985;3:333–340.
332. Hunter JM, Salisbury RE. Use of gliding artificial implants to
produce tendon sheaths: techniques and results in children.
Plast Reconstr Surg 1970;45:564–572.
333. Joseph KN, Kalus AM, Sutherland AB. Glass injuries of the
hand in children. Hand 1981;13:113–119.
334. Jozsa L, Reffy A, Demel S, Balint JB. Foreign bodies in tendons.
J Hand Surg [Br] 1989;14:84–85.
335. Leddy JP, Packer JW. Avulsion of the profundus tendon inser-
tion in athletes. J Hand Surg 1977;2:66–69.
336. Masquelet AC, Gilbert A. Plaies récentes des tendons
fléchisseurs des doigts chez l’enfant. Rev Chir Orthop
1985;71:587–593.
337. McFarlane RM, Hampole MK. Treatment of extensor tendon
injuries of the hand. Can J Surg 1973;16:366–375.
338. Millon SJ, Bush DC, Harrington LP. Acute calcific tendinitis in
a child: a case report. J Hand Surg [Am] 1993;18:592–593.
339. Miura T, Nakamura R, Tamura Y. Long-standing extended
dynamic splintage and release of an abnormal restraining
structure in a camptodactyly. J Hand Surg [Br] 1992;
17:665–672.
340. Nishijima N, Fujio K, Hamamuro T. Growth of severed flexor
tendons in chickens. J Orthop Res 1995;13:138–142.
341. O’Connell SJ, Moore MM, Strickland JW, Frazier GT, Dell PD.
Results of zone I and zone II flexor tendon repairs in children.
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342. Ogino T, Kato H. Operative findings in camptodactyly of the
little finger. J Hand Surg [Br] 1992;17:661–664.
343. Posner MA, McMahon MS. Congenital radial subluxation of
the extensor tendons over the metacarpophalangeal joints: a
case report. J Hand Surg [Am] 1994;19:659–662.
344. Stahl S, Kaufman T, Bialik V. Partial lacerations of flexor
tendons in children: primary repair versus conservative treat-
ment. J Hand Surg [Br] 1997;22:377–380.
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345. Vahvanen V, Gripenberg L, Nuntinen P. Flexor tendon injury
of the hand in children: a long-term follow-up of 84 patients.
Scand J Plast Reconstr Surg 1981;15:43–48.
346. Woods VE, Sicilia M. Congenital trigger digit. Clin Orthop
1992;285:205–209.
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347. Almquist EE, Smith OA, Fry L. Nerve conduction velocity,
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[Am] 1983;8:406 –410.
348. Fissette J, Onkelinx A, Fandi N. Carpal and Guyon tunnel
syndrome in burns at the wrist. J Hand Surg [Am] 1981; 6:
13–15.
349. Gibson CT, Manske PR. Carpal tunnel syndrome in the ado-
lescent. J Hand Surg [Am] 1987;12:279–281.
350. Harrison SH. The tactile adherence test estimating loss of sen-
sation after nerve injury. Hand 1974;6:148–149.
351. Lettin AW. Carpal tunnel syndrome in childhood. J Bone Joint
Surg Br 1965;47:556–559.
352. Lettin AW. Carpal tunnel syndrome in childhood. Proc R Soc
Med 1966;59:40–43.
353. McCarroll HR Jr. Nerve injury. In: Carter PR (ed) Recon-
struction of the Child’s Hand. Philadelphia: Lea & Febiger,
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354. Poilvache P, Carher A, Rombouts JJ, Partoune E, Lejeune G.
Carpal tunnel syndrome in childhood: report of five new cases.
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Hair Constriction
355. Abel MF, McFarland R. Hair and thread constriction of the
digits in infants. J Bone Joint Surg Am 1993;75:915–916.
356. Alpert JJ, Filler R, Glaser HH. Strangulation of an appendage
by hair wrapping. N Engl J Med 1965;273:866–867.
357. Barton DJ, Sloan GM, Nichter LS, Reinisch JF. Hair-thread
tourniquet syndrome. Pediatrics 1988;82:925–928.
358. Beck AR, Wesser DR. Constrictive digital injuries in
infants caused by human hair. Plast Reconstr Surg 1972;49:
420–422.
359. Kerry RL, Chapman DD. Strangulation of appendages by hair
and thread. J Pediatr Surg 1973;8:23–27.
360. Mann TP. Finger-tip necrosis in the newly born: a hazard of
wearing mittens. BMJ 1961;2:1755–1796.
361. Miller PR, Levi JH. Hair strangulation. J Bone Joint Surg Am
1977;59:132.
18
Spine
Engraving of an adolescent lumbar vertebra showing the ring
apophyses and secondary centers of the transverse processes.
(From Poland J. Traumatic Separation of the Epiphyses. London:
Smith, Elder, 1898)
he morphologic and histologic patterns of spine and
T spinal cord injury in children and adolescents, espe-
cially in the cervical region, relate to the changing
anatomy and particularly to the various cartilaginous
growth regions of the neurocentral synchondroses, physeal
end-plates, and facet growth regions.3,28 The skull is relatively
large at birth when compared to the rest of the body. With
subsequent postnatal development, this ratio gradually
lessens, such that a decreasing mass (potential angular
momentum) is presented to the cervical spine during
any traumatic incident. The skull, through the occipital
condyles, articulates horizontally with the atlas. The occipi-
toatlantal joints are relatively tightly constrained, allowing
flexion and extension but minimal rotation. Rotation
principally occurs between C1 and C2, although some
rotation also occurs between each of the other cervical
vertebra.
Anatomy
The dens is attached to the anterior arch of the atlas by
several ligaments: (1) alar or check ligaments; (2) apical
dental ligament; (3) tectorial membrane; and (4) cruciate
708
ligament. The transverse portion of the cruciate ligament is
probably the most important mechanically, no matter what the
age of the patient. The atlantoaxial joints have a contiguous
synovial lining between the anterior arch of the atlas and
dens, between the transverse ligament and dens, and
between the lateral masses (Fig. 18-1).
The atlantoaxial relations permit mobility and rotation
combined with intrinsic stability.5,16,28,29 The possible move-
ments are extension, forward flexion, and rotation. Rotation
is limited to approximately 45°, although the usual range
is 20°–60°. The atlantoaxial joints may be disrupted in
children, in part because the normal ligamentous laxity
characteristic of this age group allows significant motion
in these joints during rotation. Such disruption, which is
most likely to occur at the facet joints rather than at the
dens–C1 joint, is likely to be a subluxation rather than a
dislocation.
Separate primary ossification centers are present in the
lateral masses of the atlas. A third primary center for the
anterior arch is ossified in only about 20% of neonates and
may not be seen until the child is 1 year of age (Figs. 18-2,
18-3). This particular ossification center may be bifid but is
not always symmetric.13,21,25 Posterior ossification may be
incomplete, resulting in a variable ossific spina bifida. (In
contrast, the cartilaginous ring may be complete.) These
ossification variations and synchondroses should not be con-
fused with traumatic disruption of the rings. The diameters
of the C1 canal reach “adult” size by the time a child is 4–5
years of age, at which point little further canal growth occurs
in C1, although the bone does continue to enlarge by appo-
sitional (periosteal) growth.
In the axis the usual primary ossification pattern pertains
in the centrum and neural arches. In addition, ossifica-
tion of the dens begins prenatally with two longitudinal
primary ossification centers, which are usually fused by
birth.8,13,26,28 In rare instances one may not form, creating a
thin dens.
The dens is separated from the body of the axis by a
region of growth cartilage termed the dentocentral syn-
chondrosis (Figs. 18-4, 18-5). This cartilage progressively
disappears when the child is 5–7 years old. It is important
to realize that this is a bipolar growth zone responsible for
longitudinal growth of the upper part of the C2 centrum
Anatomy 709

FIGURE 18-1. Relation of C1 and C2 in the immature spine. There are joints ante-
rior and posterior to the dens, as well as the horizontal joints (arrows). The aster-
isk marks the transverse ligament, a major stabilizer of this joint.

A B C

D E F

FIGURE 18-2. Early development of Cl. (A) At birth. (B) Three transverse ligament intact. Subsequent maturation of C1 is shown
months. (C) Seven months. (A) Solid arrow points to the posterior in three specimens from cadavers aged 7(D), 9(E), and 12 (F)
synchondrosis; the open arrow points to the unossified anterior years. All show comparable shapes and cervical canal size. The
arch. The asterisk (*) marks the locations of the dens, with the arrow in (D) shows the anterior closing synchondrosis.

FIGURE 18-3. Variations in the anterior development of C1 at 3 region and irregular ossification centers in the arch (arrows).
years. (A) Normal development with a posterior synchondrosis and Asterisks mark the location of the dens, with the transverse liga-
an anterior arch with two synchondroses. (B) Widened posterior ment intact.
710
FIGURE 18-4. Morphologic development of the second cervical ver-
tebra. (A) Neonate. The bifid ossification of the dens is evident
(solid arrow). There is considerable cartilaginous continuity
throughout the centrum, posterior elements, and dens (open
arrow). The asterisks indicate the neurocentral synchondroses
between the centrum and the posterolateral elements. (B) At 3
months the dens ossification centers have coalesced and the neu-
18. Spine
rocentral synchondroses separate the centrum from the postero-
lateral elements. (C) At 1 year. (D) At 3 years the dens has fused
to the lateral elements. (E) At 7 years the ossiculum terminale is
beginning to form (arrow). (F) At 9 years the ossiculum terminale
is more evident. (E, F) Note the remnant of the growth cartilage
between the dens and centrum (arrow in F). It creates a radiolu-
cent cleft that may be mistaken for a fracture.
Anatomy 711

FIGURE 18-6. Comparable C2 ossification in a skeletally immature

3-month-old seal. Secondary ossification is present in the dento-
central synchondrosis. This would be expected, as the area is a
developmental fusion of epiphyseal equivalents and thus is com-
parable to secondary ossification in the human triradiate cartilage
(see Chapter 19).

long bones. The circulation enters the dens from two areas.
At the upper end, near the ossiculum terminale, there are
B soft tissue attachments that allow penetration of vessels.
However, the distal end is supplied by vessels entering medial
FIGURE 18-5. (A) Chevron-shaped upper dens with early sec- to the facet joints. These go toward the dentocentral syn-
ondary ossification (arrow) at 8 years. (B) Well-formed terminal chondrosis and into the main portion of the dens, which is
ossification center at the tip of the dens at 10 years. Some of the almost totally free of soft tissue attachments. The latter cir-
dentocentral cartilage remains within the “body” of C2. culation is usually undamaged by childhood fractures but
may be cut off by adult fractures because of the aforemen-
tioned difference in the fracture patterns.
and lower part of the dens. In most animals a secondary The tip of the dens usually has a chevron shape in the
ossification center appears within the dentocentral syn- anteroposterior view (Fig. 18-5). This variation, sometimes
chondrosis, similar to ossification within the triradiate carti- termed a bicornuate dens, represents a normal pattern of
lage (Fig. 18-6).
The dentocentral cartilage is located below the level of the
articular facets, within the eventual C2 vertebral body (Fig.
18-4). It is histologically continuous with the neurocentral
synchondroses of the centrum and the posterior elements of
C2 in the infant and young child. A “ghost” of this structure
may remain for several years and should not be confused
with a fracture (Fig. 18-4). In children, dens fractures extend
along this growth mechanism and thus are partially within
the body of C2, a factor that significantly enhances healing.
In contrast, the fracture level in the adolescent and adult is
usually several millimeters higher, at the articular facet level
(Fig. 18-7).
The dentocentral synchondrosis effectively prevents vas-
cularization of the dens by direct extension of vessels from FIGURE 18-7. Dens fracture patterns in the mature (M) and imma-
the centrum.1,22,35 This separation of circulations probably ture (I) dens. Note the vascular entrance points (V) and how the
remains, to some degree, after closure of the synchondrosis, childhood fracture pattern (I) does not interfere with the dental
similar to the physiologic separation of the metaphyseal and blood supply, whereas the adult fracture pattern (M) does. The
epiphyseal circulations for years after growth plate closure in neurocentral and dentocentral synchondroses are stippled.
 712 18. Spine

fusion of the two lateral ossification centers that extend supe-
riorly to enclose the normal ossiculum terminale. It should
be considered normal. Within this chevron, a separate sec-
ondary ossification for the tip of the dens occurs, but not until
the child is about 6–7 years old. This ossiculum terminale
fuses with the rest of the dens around 12 years of age.26,28
Although these centers usually fuse completely in the adult,
the lines of fusion may be demarcated by clefts in different
stages of skeletal maturation. There may also be failure of
osseous union of a normal ossiculum terminale with the dens.
Injury theoretically could avulse the terminal epiphysis
from the rest of the odontoid. It may enlarge to contribute
to the formation of an os odontoideum. In the lateral view,
the posteriorly tilted slope of the anterior surface allows
normal flexion-extension between C1 and C2.
The lymphatic drainage of the cervical spine region is pri-
marily into the retropharyngeal glands and ultimately into
the deep cervical glands. Both sets of glands also drain the
nasopharynx. This fact is significant in cervical pseudosub-
luxation secondary to pharyngitis and lymphadenopathy
(Grisel syndrome).
The third through seventh cervical vertebrae and all of the
thoracic and lumbar vertebrae exhibit a common ossifica-
tion pattern.28,37 One ossification center develops in each
of the two neural arch cartilage centers, and one ossification
center generally forms in the vertebral centrum (Fig. 18-8).
The position of the two neural arches and single vertebral
centrum ossification center is such that the cartilage
separating them, the neurocentral synchondrosis, is slightly
anterior to the anatomic base of the pedicles. This synchon-
drosis disappears when the child is between the ages of 3
and 6 years. The ossified portions of each neural arch
fuse with each other posteriorly by 2–4 years of age. Prior to
this time, they produce radiolucent lines on the frontal pro-
jection of the spine (Fig. 18-8) and should not be confused
with congenital abnormalities (e.g., spina bifida) or
trauma.13 Thus, posterior cervical spinal canal diameters
reach maturity long before longitudinal growth (height)
of the anterior centrum ceases during mid- to late
adolescence.
The normal planes of the articular surfaces change angula-
tion with growth. The lower cervical spine facets change from
55° to 70°, whereas the upper cervical spine (i.e., C2–C4) may
have initial angles as low as 30°, which gradually increase to
approximately 60°–70° (Fig. 18-9).27 This angulation variation
is a major factor in the pseudosubluxation of the upper cervi-
cal spine of infants and young children.28
Similarly, development of the upward curve of the lateral
margins of the cervical vertebral centra varies considerably
with age. This region, referred to as the joint of Luschka or
uncinate process, does not exist as a rigid (osseous) struc-
ture in the infant and young child, although it is anatomi-
cally present as a cartilaginous structure.27 By 7–10 years of
age, the marginal ossification has progressed sufficiently into
the antecedent cartilage to begin radiologically detectable
formation of this structure. This is another developmental

FIGURE 18-8. (A) Representative cervical vertebrae (C4) at 7 months (left) and 15
months (right), showing the location of the three growth regions: the posterior one
at the spinous process and two anterior ones at the neurocentral synchondroses
(arrows). These growth regions allow diametric increase in spinal canal diameter.
(B) Oblique specimen radiograph of the cervical spine from a 7-month-old baby
B shows the radiolucent appearance of the neurocentral synchondroses.
Anatomy
FIGURE 18-9. Changes in angulation of the articular facet plane in
the cervical spine from birth to 10 years. The pins follow the artic-
ular plane. (A) C3 vertebra, which has a less acute angle than C7,
anatomic factor affecting mobility and fracture pattern sus-
ceptibility in the immature cervical spine.
Development of the thoracic vertebra is comparable to the
lower cervical spine,18,27,28 but this development is integrated
with the ribs (Fig. 18-10), which tend to protect the thoracic
vertebra from injury. These interrelations also explain some
of the patterns of costovertebral injury in child abuse (see
Chapter 11).
The neurocentral and posterior synchondroses are usually
evident in thoracic spines removed from neonates. Within
2–3 months of postnatal development the posterior
synchondroses close, except for an infrequent occurrence
in the upper thoracic region. In contrast, the neurocentral
synchondroses remain open until 5–6 years of age and
begin patterns of closure similar to those of the cervical
spine. Closure occurs in the upper region before closure
FIGURE 18-10. Juxtaposition of various growth regions of a tho-
racic vertebra and the ribs in an “adolescent” cape water buffalo.
Apposed secondary ossification centers are evident (arrows).
713
which is shown in (B). This progressive angular change may be a
major factor in allowing subluxation of the second, third, and fourth
cervical vertebrae in young children compared to adolescents.
in the middle region, which occurred before closure in
the lower region. There may be considerable variation in the
overall shape of the canal from spine to spine and among
individual thoracic vertebrae of a single spine.
The transverse process develops a progressive posterior
angulation during development. When viewed from the
anterior projection, there is progressive downward angula-
tion. A similar progressive angulation increase occurs in the
aforementioned directions when the upper, middle, and
lower thoracic spines are compared. Specifically, there is
much greater posterior angulation in the lower thoracic
spine than in the upper region.18,27
The facet joints maintain a relatively constant alignment
along a given spine and throughout development. Signifi-
cant changes in angulation comparable to those seen in
the cervical spine were not evident, but there was a mild
angulation of the facets from initially perpendicular to
the spinous processes during development. This was more
evident in the lower thoracic spine than in the upper tho-
racic spine.18,27 The ligaments of the facet joints are relatively
lax in the child, similar to joint laxity in the extremities. The
amount of longitudinal or angular displacement allowed by
such laxity, especially in the cervical spine, may exceed the
intrinsic elasticity of the cord.15
The relative contributions of the anterior versus the pos-
terior portions of the thoracic spine to the overall sagittal
dimensions vary at different levels and ages. The centrum
contributes the larger proportion of growth in the latter
stages, particularly after the synchondroses have closed. The
rate of growth of the vertebral body markedly increases in
the lower thoracic levels. The spinous process elongates
threefold to fourfold and shows a mild increase in its angu-
lation relative to the longitudinal axis when spines were com-
pared throughout development.18,27
Ossification with the vertebral body occurs in a systematic
way, beginning as a hemispheric type of expansion during
the prenatal stage and continuing with this type of expan-
sion pattern during the postnatal phase to create the bulk of
the vertebral body. Expansion occurs much more quickly
toward the superior and inferior surfaces than toward the
714
peripheral surfaces around the sides of the vertebra. Similar
expansion occurs relatively rapidly toward the posterior
portion of the vertebral body, where the junction with the
spinal canal is present. Once these factors are established, at
approximately 2 years of age, the bulk of expansion of the
vertebral body occurs in anterior and latitudinal directions
rather than posteriorly.18,27
Vascular foramina are evident thoughout the peripheral
margins and end-plates superiorly and inferiorly. Expansion
of the peripheral margins of the ossification center is
undulating. Within the indentations around the peripheral
margins, a layer of cartilage is evident. A ring-like secondary
ossification center, the ring apophysis, eventually develops
in this region. Radial or spoke-like interdigitation of the
physis (ring apophysis) with the expanding ossification
center is evident by 6–7 years. This pattern is variable and
often asymmetric (right half versus left half) within a single
vertebra.18,27
The first thoracic vertebra has an uncinate process, not
unlike the lower cervical vertebra. However, proceeding
in a distal direction, this upturned lateral portion shifts to a
more posterior position; and by the mid-thoracic region,
any vestige of an “uncinate-like” process is no longer
evident.18,27
The thoracic spinous processes elongate three to four
times, depending on the region, and show a mild increase
in angulation relative to the longitudinal axis when neona-
tal and mature spines are compared for any given level. The
rates of increase in angulation of the spinous processes of
the upper and lower regions are greater than the rate for the
middle region. The angulation changes appear necessary to
allow close overlap of spinous processes while the vertebral
body increases in height.
Lumbar spine development follows the same basic pattern
of three primary ossification centers. These vertebra have sig-
nificant height growth during adolescence through growth
plate analogues. This epiphyseal equivalency is more evident
in other mammals, including most primates. The posterior
synchondrosis of L5 often remains as a fibrous radiolucent
defect referred to as spina bifida occulta, which may be
present in as many as 20% of the population.13,36
A B
FIGURE 18-11. (A) Vertebra within a vertebra (arrow). This process is the spinal analogue of the Harris growth slowdown line. (B) Anatomic
specimen of a thoracic vertebra from a 2-year-old boy showing the vertebra within a vertebra.
18. Spine
The initial ossification centrum of all vertebra is spherical
in utero30 and progressively enlarges after birth to conform
to the cartilaginous contours of the vertebral anlage.
Because this expansion process is similar to that of the ossi-
fication center of a long bone, there may be similar reactions
to trauma or illness. Specifically, the chondro-osseous trans-
formation may stop temporarily and then resume, with a thin
shell of sclerotic bone the result. It appears as a vertebra
within a vertebra (Fig. 18-11).24 As the ossification center
approaches and conforms to the edges of the vertebra and
remodels to conform to biologic demands, the vertebral
body becomes increasingly responsive to trauma in a manner
similar to the adult spine.11
The spinal canal, at any level, enlarges so long as the two
neurocentral and single posterior synchondroses remain
open.17,20,28 They close first in the cervical region at about 6–7
years of age,28 followed by thoracic closure (7–9 years) and
lumbar closure (9–10 years).17,28,30 Early closure due to a dys-
plasia (e.g., achondroplasia), infection, metabolic disease, or
trauma may lead to canal stenosis.3,28
The thoracolumbar junction is comparable to a “stress
riser” because of the motion change between the relatively
rigid thoracic spine and the mobile lumbar spine, which
increases the risk of injury at this level. Seat belt usage, espe-
cially if the chest strap is not adapted to the child, increases
the risk of Chance fractures.
Secondary ossification centers variably appear at the tips of
the spinous, transverse, and other processes during adoles-
cence (Fig. 18-12). Avulsion or undisplaced chondro-osseous
disruptions in these areas could be interpreted as ligamen-
tous injuries because they are so difficult to visualize radio-
graphically. Secondary ossification also appears at the same
time in the cartilaginous “ring” apophysis within the vertebral
end-plate (Fig. 18-13). This area is involved in the vertical
growth (i.e., height) of the vertebral body.
Each of the facets has an epiphyseal analogue, with growth
plate, undifferentiated hyaline cartilage, and articular carti-
lage. These areas are hypothetically susceptible to injuries
analogous to physeal fractures in long bones.
The individual vertebral bodies enlarge circumferentially
by the process of perichondrial and periosteal apposition
Anatomy 715

A B

FIGURE 18-12. Secondary ossification in the developing spine. (A) Transverse process (arrow). (B) Spinous process (arrow).

FIGURE 18-13. (A) Superior and inferior ring apophyses of C7 in a
12-year-old child (arrows). (B, C) Thoracolumbar development. (B)
At 7 years. Note the greater degree of ring apophyseal maturation
in the upper thoracic spine. (C), At 14 years. Note the extensive
D
development of ring ossification. (D) Anterior ring apophyseal ossi-
fication in the lumbar vertebra. Abnormal development may lead to
Scheuermann’s kyphosis in a manner similar to Blount’s disease
(response to increased pressure).
716 18. Spine

those with early quadriplegia secondary to spinal cord

trauma, the vertebral body may grow disproportionately in
height, with the result that the vertebral bodies become rel-
atively tall and thin, with biconvex end-plates and decreased
disk spaces.2,32
The sacral vertebra, which are fused as a composite bone,
have ossification patterns comparable to those of the other

FIGURE 18-14. Comparison of metaphyseal undulations in the tho-

racic vertebrae of a 7-year-old human (A) and an adolescent
dolphin (B). The latter species forms a complete end-plate,
whereas the former species forms an incomplete marginal plate
(ring). Asymmetric undulation in the human may be a factor in the B
development of scoliosis. (B) The matching complete end-plate
(secondary, or epiphyseal, ossification center) is adjacent to the
centrum. Also note the central remnant (ghost) of the notochord
(arrow).

and grow vertically by endochondral ossification, with the

vertebral end-plates functioning similarly to other physes. It
has been said that the “ring” apophysis does not contribute
to vertical growth of the vertebral body; it is true, as this par-
ticular structure represents a secondary ossification center
like that in a long bone (Figs. 18-14 to 18-16). However, it is
contiguous with a slow-growing physis covering the superior
and inferior surfaces of each vertebral body.38
Normal values for the vertebral body height/sagittal diam-
eter ratio and the vertebral height/disk space height ratio
have been developed.2 Such values assume significance only C
with full maturation of the osseous vertebra. Normal weight- FIGURE 18-15. Ring apophyses in an 11-year-old boy. (A) Anterior
bearing appears to affect vertical growth and keeps it in a view. (B) Oblique view. (C) Appearance of radial undulations after
normal relation to the anteroposterior diameter. In patients removal of ring apophysis. These undulations are probably adap-
who do not have normal upright or walking posture, such as tations to rotational stresses.
Response of the Developing Spine to Trauma
FIGURE 18-16. Transverse section of a thoracic vertebra of a cape
water buffalo. The “ring apophysis” extends posteriorly, where it
meets the neurocentral synchondroses.
vertebra. Cartilage runs along the margins apposed to the
sacroiliac joint. Growth cartilage is part of this structure,
which allows the possibility of chondro-osseous separation
similar to a growth plate fracture in a long bone.
The basic pattern of blood supply to the spinal cord is
established at birth.4,7,12,23 Segmental arteries supply relatively
discrete sections of the cord.6 These vessels may supply ante-
rior or posterior sections without a great deal of anastomotic
communication.6 The cervical and lumbar cord enlarge-
ments receive relatively greater numbers of blood vessels and
may be more sensitive to temporary hemodynamic disrup-
tion. The lumbar enlargement is often referred to as a water-
shed region because of its dependence on the artery of
Adamkiewicz.7,9,19,33 Disruption of this specific artery has
extreme consequences (especially paralysis).
These penetrating vessels also send branches to the verte-
bra. The supply of the posterior elements and anterior
bodies are essentially separate and remain so even after
FIGURE 18-17. Extradural and intradural venous circulation in the
thoracic vertebra of a 2-year-old child. Disruption of these vessels
may play a role in compressive hematoma formation.
717
FIGURE 18-18. Appearance of vertebral primary ossification, carti-
laginous end-plates, and disk material of the lumbar vertebra at
full term.
closure of the neurocentral synchondroses.10,14,31 Central
arteries usually enter the vertebral body both anteriorly and
posteriorly.28 A significant venous supply leaves the vertebral
body posteriorly, creating venous plexi (Fig. 18-17) that may
be disrupted, causing an extradural hematoma, which may
cause cord compression.
The intervertebral disk (Fig. 18-18) is supplied by encir-
cling vessels that enter the periphery of the disk. Vessels also
penetrate the enlarging vertebral end-plate.38 Venous return
from the disk tends to go into the vertebral body.34
Response of the Developing Spine
to Trauma
Spinal fractures in children have distinct differences from
those in adults. Such differences result from the child’s
inherent resilience to trauma and the potential for altered
growth and development subsequent to a discrete injury, a
major factor that may dramatically improve or worsen the
initial postinjury result. The principal differences observed
in children are the relatively benign clinical course, the
potential for some gradual restoration of the vertebral
body height when anteriorly wedged, and the development
of progressive spinal deformity when there is end-
plate (physeal) injury, facet physeal injury, or paraly-
sis.39,41,42,44,46,47,49–52,54–58,60–66,68,70–72,74–76,78 Fractures, dislocations,
and fracture-dislocations of the spine in infants and children
718
are relatively uncommon compared to their occurrence in
adolescents and adults, who are more likely to be exposed to
the major trauma mechanisms that usually cause spinal frac-
tures. Knowledge about spinal and spinal cord injuries has
been obtained primarily from experience with the adult pop-
ulation. There are far fewer reports concerning comparable
injuries in children. A significant number of the reports
pertain to the cervical spine, which in children is injured
much more frequently than other regions of the spine.
Fractures of the lower cervical and thoracolumbar spine and
spinal cord injuries are less common in children than in
adults.
Henrys and colleagues reviewed 1299 vertebral traumatic
lesions; among them were 631 cervical lesions, of which only
12 were in children under 15 years of age (1.9%).57 The pro-
gressive incidence of osseous injuries in the 6- to 15-year age
group reflects the gradual acquisition of adult features of
reduced flexibility and increasing exposure to more severe
injury mechanisms.
Fracture-dislocations, which usually result from severe vio-
lence, account for the most severe neurologic complications.
Of the six children with fracture-dislocations reported by
Henrys and colleagues, five had significant neurologic com-
plications, and one died.57
Hubbard reviewed 42 cases of spinal injury in children
ranging in age from 17 months to 17 years; two-thirds were
stable, and one-third were unstable.62,63 None of the patients
with stable injuries had neurologic trauma. Of the 14
patients with unstable lesions, however, eight had neurologic
damage (six to the spinal cord and two to a nerve root). The
neurologic injuries were of immediate onset, with the excep-
tion of one patient who sustained injury to the nerve roots
2 days after the initial trauma owing to a redislocation. Of
the eight who suffered neurologic damage, there was cervi-
cal injury in four, thoracolumbar injury in three, and lumbar
injury in one. Radiographs obtained 6 months after injury
revealed scoliosis following stable thoracic, thoracolumbar, or
lumbar injuries associated with hyperflexion force. However,
the scoliosis was only slightly progressive and measured less
than 10°, eventually becoming balanced with time. With
unstable injuries, abnormal alignment was often present on
the initial radiograph and progressed unless early surgical
fusion was undertaken.
Dislocation of spinal segments is rare in children because
the ligaments are generally stronger than the bone. However,
displacement may occur without spinal cord injury; and in
fact, in some cases there is no radiographic evidence of frac-
ture. Separation of the centrum from an end-plate may be
evident only as apparent widening of a disk space. Similarly,
unilateral or bilateral facet disruption may occur in regions
such as the thoracolumbar junction because of intrinsic lig-
amentous laxity. Again, such disruption may be free of con-
comitant spinal cord injury.61
Children have a growth plate and cartilage similar to an
epiphysis associated with each of the four facet joints. Injury
can theoretically involve these regions and certainly has been
seen by me during open reductions of thoracic and lumbar
fractures. Morphologic and histologic studies are lacking,
however, even in Aufdermaur’s classic pathologic study.40 We
have had the opportunity to assess some of these injuries in
skeletally immature large zoo animals.
18. Spine
Normal anteroposterior and lateral alignments of the spine
are contingent on the chondro-osseous anatomy, ligaments,
truncal musculature, and effect of gravity.3,16 The extent of dis-
ruption of perichondrium and periosteum into which these
soft tissues components attach also affects stability. Because of
the possibility of radiolucent injury, the spine must be immo-
bilized until actual or occult injuries are appropriately evalu-
ated. The large size of the child’s head may cause excessive
flexion on a flat immobilization board (Fig. 18-19).45,59
At any specific level of a motion segment where injury
occurs, stability depends primarily on the interrelation
between the anterior, middle, and posterior chondro-
osseous and ligamentous columns. In a traumatized spine,
the extent of damage to these columns determines the
overall stability during the acute and chronic phases. It is
often difficult to assess accurately the amount of stability in
the adult spine. It is even more difficult to assess the
degree of intrinsic or remaining stability of the cartilaginous
portions of the immature spine. The goal of treatment,
whether operative or nonoperative, is still the same: spinal
stability. Failure to achieve this goal may result in progressive
deformity.
In adults spinal deformity is considered a preventable
complication of fractures and fracture-dislocations of the
axial skeleton provided there is judicious use of bracing or
instrumentation and fusion. In the child, however, a differ-
ent situation arises, as damage to end-plate growth mecha-
nisms may not be obvious and may slowly lead to subsequent
deformity during the various periods of growth (especially
adolescence). Whether dealing with acute injury or pro-
gressive secondary changes due to growth deformity, associ-
ated morbidity may significantly limit the ultimate physical
and neurologic rehabilitation of the spine and spinal cord-
injured child and adolescent months or even years following
the original injury. The complex reconstructive surgery that
is often required to correct deformities and relieve symp-
toms is not without potentially serious risk to the child or
adolescent. These risks must be considered before choosing
surgical approaches, especially in skeletally immature chil-
dren. Some methods of stabilization may be difficult or inap-
propriate in the young child.
The clinical picture for patients with stable injury is charac-
teristically benign and not usually associated with long-term
problems, strongly suggesting that initial treatment for more
than a few months may not be required.62 However, long-term
follow-up to skeletal maturity may help identify the patient
who is likely to develop a growth abnormality. Such studies
must be encouraged in centers caring for these children. The
absence of spontaneous interbody fusion or disk narrowing
probably relates to a healthy intervertebral disk and its
inherent ability to withstand stress in the child.
There may be variable, incomplete restoration of vertebral
body height in thoracolumbar fractures, but it is less likely
following cervical compression fractures.62 There is a differ-
ence in the ultimate growth (height) capacity of the cervical
spine versus the thoracolumbar spine during growth spurts
that may be a major factor in this potential tendency of one
region, but not the other, to restore height. The cervical ver-
tebrae approximate adult height sooner than the thoracic
and lumbar vertebrae. It is important to realize that complete
restoration of vertebral height does not always occur in any
Response of the Developing Spine to Trauma
FIGURE 18-19. Concept of large head causing spine
flexion (top). The support for the body should be
higher (middle, bottom).
segment of the developing spine, in contrast to generaliza-
tions that such complete recovery of height usually occurs.
Gunshot Injury
Spinal and spinal cord injuries consequent to gunshots are
becoming increasingly prevalent, particularly among urban
children.43,69,79 These injuries are approached similarly to
those in adults and are described in more detail in Chapter
9. The most serious consequence in a child is that dissolu-
tion of lead by the cerebrospinal fluid may lead to toxic levels
of lead systemically, with subsequent neurodevelopmental
consequences.48,53,77
Preexisting Disease/Deformity
There are many congenital malformations of the cranio-
vertebral junction that should not be confused with
traumatic lesions.80–116 Anomalies characterized by single or
multiple ossification centers must be differentiated from trau-
matic fragmentation. Well-marginated, distinct ossification
centers may be seen anterior to the dens above or below the
arch of the atlas. There may be unilateral or bilateral clefts in
the ring of the atlas, usually in the posterior arch but rarely in
the anterior arch. These clefts vary from small defects
(spina bifida occulta) to agenesis of half or even the entire
posterior ring.
There are a number of congenital and acquired orthope-
dic vertebral problems, especially those involving the various
skeletal dysplasias. In addition, due consideration should be
given to evaluating these children, just as much as a child
719
with Down syndrome, before they participate in various
types of athletic activities. Underdevelopment of the
dens (hypoplasia) and C1–C2 instability are relatively
common.80,83,103,105 Children with severe osteogenesis imper-
fecta may also develop micro- and macrofractures, leading to
severe deformity (see Chapter 11).
Evaluation for an acute injury to the neck or back may be
the first indication of a congenital spinal deformity.112 In the
illustrated case of a child sustaining a hyperflexion in-
jury (Fig. 18-20), there was concern that the wedging was trau-
matic. However, a bifid, congenitally deformed vertebral body
was found on computed tomographic (CT) scan, with no evi-
dence of posterior disruption. Children and adolescents with
congenital deformities such as Klippel-Feil syndrome (Fig. 18-
21) may develop neck or back pain during sports, which may
lead to the initial diagnosis of congenital spine deformity.
Once such deformities are diagnosed they may affect the
appropriateness of continuation in a given sports activity.99,108
Sherk and Nicholson reported a fatal injury in an abnormal
cervical spine.158
Children with Klippel-Feil syndrome and other congenital
deformities may be at significantly increased risk for spinal
cord injury.88 Elster reported a case of quadriplegia following
minor trauma in a patient with preexisting Klippel-Feil syn-
drome.94 Strax and Baran also reported cases of traumatic
quadriplegia on an acute basis.112 Many of these children do
not present for diagnosis until they are engaged in some sport-
ing activity that makes them develop neck pain or subtle to
obvious neurologic findings, at which point evaluation reveals
the abnormality. Most neurologic problems develop slowly.
Any patient with a diagnosis of Klippel-Feil syndrome should
720 18. Spine

A FIGURE 18-21. This 9-year-old patient presented with neck pain

while playing soccer. Her only motion segment was C3–C4.

create an increased moment arm at C7–T1, leading to facet

displacement (Fig. 18-22).

Down Syndrome
Over the past 20 years there has been increasing recognition
of actual and potential cervical instability in children with
Down syndrome.117–167 Much of it has come about because of
increased assimilation of these individuals into family units
and the rise of activities such as the Special Olympics.

B
FIGURE 18-20. A 10-year-old boy with back pain after hyperflexion
injury. Lateral view showed apparent wedging, which suggested a
compression fracture. (A) Anteroposterior view shows widening of
the pedicles and a central lucency (arrow). (B) Computed tomo-
graphic scan showed a bifid vertebral body (arrow). The ligaments
had been strained, but no fractures occurred. The “compression”
was part of the congenital deformity.

be thoroughly screened for potential instability through

hypermobile segments that develop to accommodate lack of
motion in the fused segments.

Scoliosis
Children who have had fusion and instrumentation for sco-
liosis may be at increased risk for spinal trauma following an
accident.89,114,116 Particularly, a high thoracic fusion may
FIGURE 18-22. C6–C7 disruption in an automobile accident victim
who had undergone previous Harrington instrumentation to T1 for
scoliosis. Closed arrows show widening of spinous processes;
open arrow shows facet joint disruption.
Pathobiology 721

FIGURE 18-23. Histologic section of the occiput to C4 in a patient
with Down syndrome. A progressively waddling gait had been
evident for more than 2 years. Stabilization was refused by the
family. Severe upper cord/medulla attenuation is evident.
The most potentially serious problem is intervertebral
instability that leads to acute or progressive compression of
the spinal cord (Fig. 18-23). It may occur at the occipitoat-
lantal joint, the altlantoaxial joint, or both. This instability is
probably a consequence of abnormal collagen, rather than
acute ligament failure. Children with various types of dyspla-
sia and who are involved in accidents obviously deserve close
evaluation of their cervical spine. Great care should be taken
when evaluating what represents a preexistent anatomic
variant or abnormality versus trauma-related disease.
The consensus is that if an atlas-dens interval (ADI) of
4.5 mm or more is present or if significant odontoid hypopla-
sia exists, at-risk sports should be avoided. When significant
myelopathic signs accompany an increased ADI, C1–C2
fusion should be undertaken. These children seem to be at
greater risk to resorb any grafted bone.156 Postoperative halo-
vest immobilization is also recommended because of the
hyperactive nature of these children. There is an excellent
overview of screening indications and frequency in the
AAOS monograph.885
Pathobiology
Aufdermaur presented a detailed morphologic investigation
of spinal injuries in 12 children under 18 years of age who
were examined after accidental deaths.40 Each of the spines
was completely dissected for evaluation. He also removed 20
intact spines from juveniles of similar age groups who had
died from nontraumatic causes (e.g., cancer, drowning) and
subjected them to similar mechanical stress testing. A fre-
quent finding was the tendency for the injuries to have
occurred through the region of the subcondylar (end) plate
and hypertrophic cartilage, creating a physeal injury ana-
logue (Fig. 18-25). Aufdermaur believed that because there
was a high likelihood of such growth mechanism injury the
most likely radiographic sign, if any, would be widening of
the intervertebral space.40 Such widening may not be readily
apparent on routine radiography, as these injuries often
reduce spontaneously after deforming forces are dissipated.
Stress views might elicit the instability, but this procedure
could be dangerous to the spinal cord. Magnetic resonance
imaging (MRI) would be more likely to detect areas of
altered signal intensity associated with hemorrhage and
edema near the vertebral end-plate. This technique has
been used to detect occult physeal injuries in the limbs (see
Chapters 5–7).
Aufdermaur’s cases involved injuries to the following
areas: cervical spine (seven cases), thoracic spine (four
cases), and lumbar spine (one case).40 In 10 instances the
injury was due to a traffic accident, and in two instances the
spine was hyperextended during childbirth. Clinically,

Pathologic Fractures
Children may have acute onset of neck pain that is attributed
to some activity. The (treating) physician must be aware of
the possibility of unusual conditions such as an eosinophilic
granuloma or a spinal cord tumor.
Patients with chronic conditions, such as juvenile rheuma-
toid arthritis (Fig. 18-24), leukemia, or renal osteodystrophy,
may develop back pain. It is usually due to pathologic frac-
tures in the osteoporotic/osteopenic bone. Treatment is
generally symptomatic (medication, orthotics). Successful FIGURE 18-24. Multiple compression fractures in a 9-year-old
treatment of the predisposing cause also obviously affects the boy with systemic juvenile rheumatoid arthritis on high dose
continuation or recurrence of these pathologic fractures. steroids.
722
FIGURE 18-25. Injuries of the immature spine found during autopsy
following traumatic deaths (usually vehicular versus pedestrian).
(A) Cervical (arrow). (B) Thoracic; this is a Chance injury equiva-
however, a spinal fracture was suspected only once. In the
other 11 cases, the spinal injury was not diagnosed until
autopsy. In all cases, death occurred within 1.0–1.5 days of
the accident. In nine of the cases the spinal injuries did not
contribute to death; in three cases, however, there were sig-
nificant cervical, epidural, and subdural hematomas and
associated brain injury that probably were related to the
cause of death. In two cases the anterior longitudinal liga-
ment was ruptured; and in three cases the supraspinous and
intraspinous ligaments, ligamentum flavum, and capsules of
the posterolateral joints were ruptured, as were the carti-
laginous end-plate and the longitudinal ligaments. Histolog-
ically, the fracture lines involved the growth zone almost
exclusively. Four patients had multiple-level cartilage plate
injuries. The top end-plate was injured in 12 patients and the
bottom end-plate in 6. Histologic findings were similar for
cervical, thoracic, and lumbar vertebrae.
This study by Aufdermaur introduced the anatomic
concept of occult injury to the developing spine. He empha-
18. Spine
lent (arrow). (C) Lumbar (arrow). Each is a separation through the
end-plate.
sized that separation of an end-plate from the incom-
pletely ossified vertebral body could occur, leading to
considerable angular displacement when injurious forces
were maximal. As such displacing forces dissipated, the
angulation accordingly reversed, effectively (spontaneously)
closing the fracture gap. With the maximum morphologic
deformity, traction or compression injury to the spinal cord
could occur. This phenomenon has become accepted in
the pediatric orthopaedic and spinal literature as spinal
c ord injury without obvious radiologic abnormality
(SCIWORA).
Animal Fractures
Animal models of spontaneous fractures of the immature
spine offer another method of understanding the
pathoanatomy of these injuries and the occurrence of
SCIWORA. We have studied a number of such physeal frac-
ture analogues.73
 Pathobiology 723

broken through the atlas not only at the posterior synchon-

A placed, hinging apart so the displacement was not readily
B A colobus monkey was the victim of physical abuse by
FIGURE 18-26. C1 fracture in an immature giraffe. (A) Transverse
section shows anterior injury and intraosseous hemorrhage. (B)
Histologic section shows the anterior fracture through the
synchondrosis.
drosis but also at the right anterior synchondrosis.
A 3-day-old Thompson’s gazelle ran head first into an
abutment. The animal developed progressive paralysis over
the ensuing hours and as a result was killed. Initial radio-
graphs of the cervical spine showed a C2 fracture of the
dens. Dissection revealed hemorrhage in the upper cervical
paravertebral tissues and an additional fracture involving the
superior articular facet of C2 (Fig. 18-27). The facet fracture
appeared nondisplaced on the radiograph, and there was no
disruption of the articular surface morphologically. This dis-
crepancy was attributable to the fracture traversing a region
of subarticular cartilage. The facet joint was minimally dis-
evident on the radiograph.
A 5-month-old giraffe was acutely paralyzed after running
into a fence. Radiographs revealed a type 2 physeal fracture
traversing the dentocentral synchondrosis with a right artic-
ular facet Thurstan Holland fragment. This fragment was
partially separated from the physis (Fig. 18-28).
In another injured giraffe the spinal cord was completely
severed at the level of a dens fracture and was additionally
compressed by a hematoma distally at the C2–C3 junction.
Interestingly, most of the hematoma was on the dorsal side
of the cord, whereas the fractures were on the ventral side
(Fig. 18-29).
another colony member, sustaining a fracture-dislocation
at the thoracolumbar junction. This fracture propagated
through the posterior elements and exited in two directions:
(1) through the vertebral body T12, along the neurocentral

As in the skeletally immature human, the most commonly

injured regions in the specimens were the cervical spine (five
fractures) and lumbar spine (five fractures), followed by
the thoracic spine (four fractures).73 All fractures in these
skeletally immature specimens propagated along chondro-
osseous growth regions. The atlas and axis were disrupted
through their synchondroses, whereas the other vertebrae
usually were fractured along the end-plate physes. These
end-plate physeal fractures also propagated variably into the
neurocentral synchondroses when the mechanism of injury
was extension-distraction. Distinct spinal cord injury was
noted in four animals.
A “Jefferson fracture” injury was noted in a 2-month-old
giraffe (Fig. 18-26). The animal became progressively ataxic
following a traumatic delivery and was killed several weeks
after the observed injury when no recovery was evident.
Dissection revealed organized hematoma anterior to the
ring of C1. Radiographs of the atlas demonstrated a thin sub-
chondral separation in the posterior synchondrosis, a closed
left anterior synchondrosis, and a normal right anterior syn-
chondrosis. Morphologic examination of the atlas revealed
hemorrhage in the right anterior synchondrosis and subperi-
osteal hemorrhage extending along the spinal canal to the
posterior synchondrosis with resulting cord compression.
Histology demonstrated hemorrhage and chondro-osseous
separation in the right synchondrosis, providing evidence FIGURE 18-27. C2 fracture in a gazelle. As in the child, the dens
that it was an analogue of a “Jefferson fracture” that had fracture line followed the dentocentral synchondrosis (arrows).
 724
synchondroses, across the inferior end-plate and interverte-
bral disk, exiting anteriorly along the superior end-plate
of L1; and (2) through the inferior end-plate of T11 (Fig. 18-
30). Although these fractures appeared to traverse only the
superior end-plates, further inspection revealed that these
fractures also propagated along the neuro-central synchon-
droses toward the inferior end-plates. This pattern has
recently been described in a case of child abuse.677
Type 3 inferior end-plate fractures of the lumbar spine were
sustained by a camel and a zebra (Fig. 18-31). Dissection
revealed hemorrhage extending into the intervertebral disk.
Histologic examination revealed that the fracture traversed
the primary spongiosa of the body, technically making it a type
4 growth mechanism fracture. The injury also propagated
across a portion of the intervertebral disk.
A B
18. Spine
FIGURE 18-28. (A) Facet fracture of C2 in a
5-month-old giraffe that was a chondro-osseous
separation.
Diagnosis
Diagnosis includes accurate evaluation of the level and
extent of injury to chondro-osseous and nervous system
tissues and the contiguous muscular and vascular structures.
Early assessment is essential, as it is the baseline against
which the effectiveness of any therapeutic manipulation or
development of complications is evaluated. Early assessment
comprises inspection and palpation, accurate determination of
neurologic function or dysfunction, and radiographic examina-
tion. The initial neurologic examination should be com-
pleted before the patient undergoes radiologic evaluation.
Radiographs or other types of diagnostic imaging should be
obtained progressively in accordance with neurologic find-
ings and with appropriate protection.
FIGURE 18-29. SCIWORA in a giraffe. A
fracture is evident at the top of C2
(arrow), but no obvious osseous injury
is seen at C3. (A) Slab section showing
a hematoma posterior to the spinal
cord. (B) Higher power view showing
cord deformity and a smaller area of
hemorrhage anterior to the cord. The
intraosseous hematoma of the C3
proximal metaphysis suggests occult
injury (bone bruising) with incomplete
fracture.
Diagnosis
FIGURE 18-30. Physeal fractures of L1 and L4 (arrows) in an infant
monkey. These fractures propagated along the superior end-plate
physis and turned to follow the neurocentral synchondroses.
Although a rare injury in children, it has been reported and may be
more common because of lack of familiarity with the pattern of
injury.
A B
FIGURE 18-31. End-plate physeal fracture (type 3) in an adolescent zebra. (A) Radiograph. (B) Slab section. (C) Histologic section.
725
Inspection may reveal associated soft tissue injury.
Abrasion of the face suggests cervical hyperextension
injury, possibly with a rotatory component; and abrasion
of the upper neck suggests hyperflexion of the dorsal
spine. Scalp contusion or laceration may indicate an axial
loading component in addition to the aforementioned
angular, shear, and rotatory components. Palpation may
reveal a local area of tenderness. The presence of a palpable
gap may indicate disruption of the posterior ligaments and a
potentially high degree of instability. Neurologic evaluation is
of primary importance, as damage to the spinal cord is the
main complication. Of the 18 patients reported by Henrys
and colleagues, seven had neurologic injuries.57 Of subluxa-
tions of C1 and C2, two resulted in decerebration; and one
patient with subluxation of C1–C2 presented with a transient
paresthesia of the left arm, secondary to a football injury.
Detailed neurologic examination should be repeated fre-
quently, since changing, especially worsening neurologic pat-
terns may require aggressive action, and improvements may
encourage waiting. Motor function in the awake, cooperative
patient should be described so subsequent observers are
able to assess the improvement or gradual loss of neurologic
patterns or function. Loss of deep tendon reflexes generally
parallels loss of motor function. In the unconscious patient,
facial grimacing when in pain, in the absence of withdrawal of
the extremities and loss of deep tendon reflexes, suggests
cord injury. In the cervicodorsal region, the spinous process
lies about two segments above the corresponding spinal
segment (i.e., the spinous process of C5 overlies the C7 cord
level). In the dorsolumbar region, as many as 11 spinal seg-
ments may lie between the spinous processes of T10 and L1.
Complete loss of motor and reflex function immediately
following injury and associated with sensory loss is generally
consistent with similar motor level loss and involves all
sensory modalities, including deep pain. In the Brown-
Sequard syndrome, loss of touch and proprioception occurs
on the same side as the motor loss; in contrast, analgesia
C
726
occurs on the contralateral side and, because of the manner
in which pain fibers cross the sensory level for pain, usually
two to three levels below the motor level.
In the anterior spinal artery syndrome, touch and proprio-
ception may be preserved but there is loss of other long tract
functions. This situation occurs because the posterior cord
(i.e., dorsal and dorsolateral columns) may be supplied by
relatively separate branches of the posterior spinal artery.
Preservation of touch and proprioception has no predictive
value for motor recovery, especially in the young child.
Preservation of sacral sensation is seen occasionally in
central cord injuries because of the peripheral location of the
sacral portion of the spinothalamic tract. Its predictive value is
questionable in children, in whom the recovery potential is
often remarkable compared with similarly injured adults.
In contrast, preservation of patchy areas of sensation or
appreciation of deep pain indicates that motor loss may
be secondary to spinal shock. Spinal shock remains a
misunderstood phenomenon. Deep tendon reflexes cannot
be elicited, and there is flaccid paralysis below the level of
the lesion. Sphincter tone generally is minimally affected,
and there is urinary retention. If the injury is not severe,
reflexes gradually return, voluntary micturition is reestab-
lished, and motor recovery begins within hours or days of
injury. If the cord injury is severe, recovery of reflexes is
accompanied by reflex facilitation that may occur within
hours or days, unaccompanied by any evidence of sensation
or voluntary motor activity. In infants, the reflex activity of
the isolated cord may be almost indistinguishable from
normal motor function.
Pain in a root distribution, often accompanied by sensory
dysfunction, reflex loss, and motor weakness, is generally a
reliable indicator of the level of injury. However, preciseness
may not be as possible in the frightened, traumatized child
as in the adult. Because recovery of function is more likely
following decompression, early diagnosis of root entrapment
is essential. The value of functional recovery in any of the
FIGURE 18-32. (A) Spine injury evaluation in an adolescent does
not adequately show C7. (B) Better view of C6–C7 shows anterior
displacement of C6 and superior end-plate fracture of C7 (arrow).
18. Spine
roots of the brachial plexus cannot be overemphasized, espe-
cially in the child.
A common situation in which spinal injury may be over-
looked or the extent of damage not appreciated is the poly-
traumatized child with head or major thoracoabdominal
injury. Any severe head trauma caused by a rotation, flexion,
or extension force directed against the head is capable of
causing injury to the cervical spine, cervical spinal cord, or
both. Failure to immobilize the unconscious child ade-
quately can lead to irreversible spinal cord damage.
Unconscious patients with facial injuries or patients who
are vomiting may have to be transported on their side to
prevent aspiration of blood or vomitus. These patients
often require support of the cervical area by manual or halter
traction, which is applied to the head. A neutral spine position
generally is adequate; and in the case of a suspected cervical
spine injury, the head should be supported laterally to
prevent rotation or sideways motion. With lower spine injury,
a small support under the affected area or lumbar lordotic
curve may be required to support the spine in a neutral posi-
tion without applying stress to the injury.
The position of the relatively large, posteriorly directed
head of a young child must be considered to prevent cervi-
cal hyperflexion when the child is transported on a flat
immobilization board (Fig. 18-19).67
Diagnostic Imaging
Radiographic evaluation must be accomplished with regard
for potentially severe and unstable injuries and must include
prior adequate immobilization of the spine.173,175,177 Radio-
graphs should show the exact nature of the lesion. The area
of involvement, as suspected or defined by neurologic exam-
ination, must be included in the films. One of the most fre-
quent errors when evaluating suspected injury of the cervical
spine is failure to obtain good visualization of the C7 and T1
vertebral bodies (Fig. 18-32). Anteroposterior and lateral
(C) Reduction and posterior fixation. Note the end-plate fracture
(arrow). This small fragment is the vertebral equivalent of a
Thurstan Holland metaphyseal sign.
Diagnosis
tomograms may be helpful; and oblique views may be nec-
essary. A CT scan, MRI, or three-dimensional reconstruction
of either may also be indicated.172,183,202
The radiology of the developing spine of children
differs considerably from that in adults, especially in the
cervical region. Lack of awareness of the normal, variant,
and traumatically altered roentgenographic appearances
may lead to misdiagnoses in pediatric patients.168,170,171,176,178,
180,182,185–187,189,191,193,196,197,203
Common transient developmental
features and more unusual normal variants may be mistaken
for spinal trauma in children. The multiple primary and sec-
ondary ossification centers and their intervening synchon-
droses are often mistaken for evidence of fracture, avulsion,
or fragmentation.
Naik measured the sagittal and interpedicular diameters
of the cervical spinal canal on radiographs of normal
infants.187 He assessed the difficulty obtaining accurate mea-
surements and mentioned a new method for measuring the
sagittal diameter. Naik’s values may be consulted for the
interpretation of trauma, even though his main purpose was
to assess possible congenital defects.
In young children the lateral thoracic or lumbar spinal
radiograph occasionally shows a vertically oriented, lucent
cleft. This cleft may represent the more anteriorly placed
neurocentral synchondrosis (Fig. 18-8). A similar cleft may
also represent a bifid vertebrae (Fig. 18-20). Morphologic
variations in the lumbosacral region are common. Lum-
barization of the first sacral segment to form a sixth lumbar
vertebrae or bilateral or unilateral fusion of L5 to the sacrum
is often seen. Incomplete osseous fusion of the neural arch
of L5 or S1 (or both) is common in children, with a 50%
incidence in some populations. A gradual decrease in inci-
dence occurs throughout childhood, but remains relatively
high, even in adolescence.
Certain anatomic regions are of significant concern:
1. Variations resembling subluxation due to displacement of
vertebrae.179 Anterior displacement of the second or third cer-
vical vertebrae, resembling a true subluxation, is relatively
common in children less than 7 years of age. Less frequently,
similar displacement is seen between the third and fourth cer-
vical vertebrae. On lateral roentgenograms, overriding of the
atlas on the dens and apparent widening of the space between
these two structures is seen in about 20% of normal children.
There is apparent subluxation of C2 and C3 in 20% of normal
children and absence of lordosis in the cervical spine in about
15%.59 Absence of uniform angulation, absence of cervical
lordosis, and absence of flexion curves have also been
reported in a high percentage of normal, asymptomatic chil-
dren. All of these signs are suggestive of, but do not necessar-
ily specifically indicate, ligamentous or other soft tissue injury.
2. Variations resembling spasm and ligamentous injury due to
curvature of the cervical spine. An absence of uniform angula-
tion between adjacent vertebrae and an absence of a flexion
curvature of the spine between the second and seventh cervi-
cal vertebrae are seen on lateral roentgenograms obtained
with the cervical spine in flexion.
3. Variations resembling fractures related to skeletal growth
centers.169 The cartilaginous plate of the dens (dentocentral
synchondrosis) frequently persists beyond the age of 5 years
and may resemble an undisplaced fracture (Fig. 18-4).
Normal anterior “wedging” of an immature vertebral body
727
(especially in the cervical region) may seem to be a com-
pression fracture. Spinous process secondary centers may be
confused with avulsion fractures during adolescence.
An evaluation of clinical observations and findings that
might increase the reliability of obtaining diagnostically sig-
nificant films in children with potential cervical spine injury
found that no single clinical predictor had a sensitivity of
100% when considered in isolation.189 A clinical assessment
consisting of a complaint of neck pain or involvement in a
vehicular accident with head trauma would have correctly
identified all cases of cervical spine injury. If this informa-
tion had been used prospectively in this study, the number
of cervical spine radiographs could have been reduced by
approximately one-third.189
Hyperextension injuries often reduce spontaneously, espe-
cially in the resilient spine of a child. Swelling of the pre-
vertebral fat stripe may be the only indication of this occult
injury (Fig. 18-33).129,188,198,201 Another indication of such an
injury is a small piece of bone pulled away from the anteroin-
ferior edge of the ossifying vertebral centrum at the point of
separation of the end-plate, anterior longitudinal ligament,
and annulus.
In the young child, radiologic diagnosis is further compli-
cated by the relative elasticity of the cartilaginous spine and
supporting ligamentous structures, which may deform suffi-
ciently to allow severe cord damage at impact, but with subse-
quent absence of radiographic evidence of fracture or
dislocation when the child is evaluated posttraumatically.
Evaluation by CT has increased in frequency. The method
is obviously useful for defining the complete morphology of
the fracture and to assess fragments compromising the spinal
canal. However, because of the nature of the developing
skeleton, significant fracture components may not be readily
visible (i.e., a fracture involving the cartilage). Summers and
Galli showed that CT scans required a cut interval of 3 mm
or less to detect occult fractures of the cervical spine during
screening.196
Wojcik and associates presented preliminary studies on
three-dimensional CT analysis of acute cervical spine trauma
and thought that computer-integrated three-dimensional
images obtained from CT data were considerably superior to
observer mental integration of individual CT images.202 They
did not give the ages of their patients, but at least one of the
cases involving a child showed an excellent reconstruction.
However, such reconstruction must be put in proper per-
spective. The decreased visualization of incompletely ossified
skeletal elements in young children must be considered
during any process of interpretation.
The MRI technique has obviously become increasingly
important for detailed evaluation of children with obvious
fracture and evidence of cord or root damage.181,184,199 As
when diagnosing chondro-osseous injuries, the interpreting
physician should have some familiarity with the normal
anatomy of the developing spinal cord.190 MRI can
show noncontiguous cord injury, especially in the cervical
spine.195 These studies are also useful for delineating post-
traumatic changes in the spinal cord over time.174,192,194
Perhaps the most important use of MRI acutely is to define the
cord injury and an occult fracture in SCIWORA.192
Weng and Haynes assessed flexion-extension MRI in chil-
dren.200 Patients with instability also had neurologic mani-
728
A B
FIGURE 18-33. (A) Subluxation of the upper cervical spine. The
prevertebral fat stripe, however, is normal. (B) Four-year-old child
who sustained a head and neck injury. The prevertebral fat stripe
festations and underwent surgery. Patients without spinal
cord compression on MRI did not demonstrate neurologic
compromise.
Subluxation
The fulcrum of motion of the normal cervical spine in chil-
dren under the age of 8 years is C2–C3, rather than the more
distal C5–C6 fulcrum of the adult.212,216 A flexion film of the
18. Spine
is markedly widened. No radiologically evident vertebral injuries
were noted.
cervical spine frequently seemingly shows the second
segment “misaligned” relative to the third. This condition is
usually termed pseudosubluxation and is generally a normal
finding in children (Fig. 18-34). Failure to recognize this fre-
quent (common) normal variation is responsible for many
erroneous concepts and dictated reports regarding the rela-
tion of subluxation of the cervical spine; it causes a major diag-
nostic problem when the finding is noted in children who
have sustained actual or perceived neck trauma.206,209, 211,218
Communication between the radiologist and treating
FIGURE 18-34. (A) Pseudosubluxation in a
normal child. The C2–C3 joint is most
involved. Note the differences in the
planes of the facet joint surfaces of C3–C4
versus C6–C7. (B) Anterior pseudosublux-
ation of the upper cervical spine.
SCIWORA
physician is extremely important for the diagnosis of variation
versus injury.
Subluxation of the cervical vertebrae without associated
fracture or spinal cord injury occurs frequently in chil-
dren.204,205,208 Anterior displacement (especially rotatory) of
the atlas on the axis is a common pattern. Many of these
cases occur spontaneously; and although local infection has
been cited as a predisposing factor, the high incidence of
upper respiratory infection in the age group most frequently
encountered (6–12 years) makes this relation statistically
difficult to establish.214
The facet joints of the upper cervical vertebrae are
more horizontal than those of the lower cervical vertebrae,
with this variation being more pronounced in the young
child (Fig. 18-9). This angulation changes to a more
oblique orientation as the cervical spine matures. Some
laxity of the transverse ligament must occur for the atlas to
slide forward on the axis. Although asymptomatic cases in
children have been reported in which the distance between
the anterior arch and dens is in excess of 3.5 mm, most
authors agree that 3.0 mm is the upper limit of normal for
children.204
Bailey noted that infants and children should show a
normal step-off of as much as 2–3 mm at the level of the
second and third cervical vertebrae.168 Similarly, the gap
between the posterior portion of the anterior arch of the
adolescent and the anterior portion of the dens may increase
with motion. In normal adults it does not usually move more
than 2 mm, but in normal children even a 5 mm excursion
in flexion may be normal. Furthermore, when the neck is in
extension, the arch may appear to move posteriorly and may
seem to lie on top of the dens. This may occur because of a
combination of ligamentous laxity and the curvilinear angu-
lation of the anterior portion of the dens.
Hypermobility of the cervical spine in young children
may be noted at the C2–C3 and C3–C4 levels on lateral
roentgenograms obtained with the neck in full flexion.214
Anterior subluxation of up to 4 mm may be normal. The
diagnosis of abnormal motion should be made only when
the radiographic finding of subluxation is accompanied by
clinical evidence of muscular spasm and pain, generally
with limitation of lateral extension of the neck. Evidence of
soft tissue swelling with anterior tracheal displacement is
sometimes present. Tomography may be helpful for
demonstrating fractures not readily apparent on the plain
films.
Children who have normal pseudosubluxation and
normal vertebral epiphyses do not require extensive and
aggressive treatment. An awareness of the normal anatomy
of the pediatric cervical spine should prevent overtreatment.
Seemingly abnormal radiographic findings should be accom-
panied by appropriate physical signs to warrant prolonged
traction, casting, or surgery under the misconception that
serious (actual) injury exists. Dunlap and colleagues
reported 12 children between the ages of 3 and 8, only one
of whom had a well-documented traumatic injury.286 Alto-
gether they reviewed 47 children and found 8 with marked
subluxation of C2–C3. They believed that children with these
normal variations should not be subjected to extensive
orthopaedic treatment unless there is a supporting history
of sufficient injury to the neck and clinical examination
729
bears out the significant probability that these variations are
traumatic subluxations.
Intervertebral (disk space) calcification may be found
during the evaluation of acute trauma or pain in chil-
dren.207,210,215,217 It is usually an asymptomatic, fortuitous
finding that should direct the physician to look closely
for other etiologies of the pain. Diskitis, which is really
vertebral osteomyelitis in children, may also present as rela-
tively acute pain sometimes associated (seemingly) with an
injury.213
Grisel Syndrome
Differentiation of a traumatic subluxation from an in-
flammatory subluxation constitutes a major diagnostic pro-
blem.219–244 Grisel syndrome (torticollis and atlantoaxial
subluxation in children) infrequently follows a major injury.
More often it is associated with the hyperemia and local
edema that follow pharyngitis, otitis, tonsillar abscesses,
osteomyelitis, tuberculosis, and tumors, which may permit
stretching of ligaments, so even normal neck motion
produces atlantoaxial displacement.
SCIWORA
As alluded to several times in this chapter the child often
presents to the emergency room with obvious neurologic
injury, but screening, if not detailed imaging studies,
fail to reveal an obvious fracture that could be associated
with the neurologic injury. This has been termed spinal
c ord injury without obvious radiologic abnormality
(SCIWORA).245,246,251,252,254,260–268 MRI may show occult
intraosseous edema (bone bruising) compatible with a spon-
taneously reduced end-plate fracture. Another possible
mechanism is hypermobility, causing a traction cord injury.
This mechanism may be significant in the cervical spine or
thoracolumbar junction. Others have suggested some type
of vascular injury as an etiologic factor.247–250,253,255–259
In sequential MRI studies (Fig. 18-35) in patients with
cervical cord injury without bony injury (SCIWORA), 70%
of the patients had a major cord injury detected by MRI
at the C3–C4 level. Three patterns of signal changes were
observed. Enhancement of the damaged cord was observed
on gadolinium-enhanced MRI, and the palsy in these
patients was more severe than that of those without enhance-
ment. This probably represents necrosis, absorption, and
reorganization of the spinal cord and suggests that the
injury is permanent. Another imaging finding was a high-
intensity signal in the dorsal column that appeared 2–3
months after injury and then disappeared by 6 months. This
probably represents wallerian degeneration of the corti-
cospinal tract.
An analysis of 71 patients with cervicothoracic trauma
found 7 (10%) patients with clinical or MRI evidence of non-
contiguous spinal cord injury and either more than one neu-
rologic level or a cord lesion remote from the suspected or
actual major imaging abnormality.299 The second lesion was
probably due to cord stretching after local tethering at the
first level. Three of the patients had a small extramedullary
hematoma at the distant cord lesion.
730
A B
FIGURE 18-35. This child was admitted with paralysis of the lower extremities but no evident osseous injury (SCIWORA). (A) Magnetic
resonance imaging (MRI) scan shortly after admission showed a focal cord lesion. (B) Three weeks later. (C) Four months later.
Basic Treatment Guidelines
A number of unique problems are encountered during treat-
ment of infants, children, and adolescents with major spine
and spinal cord injuries. With any closed, nonoperative treat-
ment regimen, the spinal osseous deformity should be
reduced and adequately protected from redisplacement or
increasing deformity during the period of physiologic reac-
tion, repair, and consolidation of the anterior, middle, or
posterior columns. Surgical techniques used in adults for
external stabilization, operative stabilization, and anatomic
reduction may be inapplicable in children because of the dif-
ferences in skull and spine morphology and the biome-
chanical resistance, musculature, and ligamentous stability,
all of which must be considered when treating significant
spinal chondro-osseous injury.
Unstable fractures should be treated with traction and, if
necessary, internal fixation. As with the long bones, liga-
mentous rupture is probably infrequent. Most fractures,
including obvious or occult end-plate injuries, stabilize by
osseous healing. With thoracic and lumbar injuries, fusion
may be needed for subsequent growth displacements. Insta-
bility complicating superimposed congenital anomalies may
require fusion.
Laminectomy has been used frequently but often indis-
criminantly. In general, it is not usually indicated in children.
Laminectomy may be appropriate if there is a discrete block
on myelography, CT scan, or MRI and especially if it is associ-
ated with worsening neurologic signs. For removal of impor-
tant posterior elements, extensive laminectomy may become
a major factor in posttraumatic kyphotic deformity. If
laminectomy is indicated, every effort should be made to keep
the facet joints and capsules intact. This operation, as an iso-
lated procedure, has limited use for early management of
closed spinal injuries in children.
18. Spine
C
Specific aspects of treatment are discussed in the ensuing
sections on anatomic regions. Acute and chronic injuries
and posttraumatic consequences are also discussed.
Halo Fixation
The use of a halo may present distinct problems in the
child.269–278,280–282 Halo fixation pins should be placed
anterolaterally and posterolaterally, where the bones are
usually the thickest. Insertion of halo pins in the temporal
fossa region is not recommended because: (1) it is relatively
thin; (2) there is a cranial suture; and (3) the temporal
muscles may be penetrated, resulting in pain with mastica-
tion and during episodes of exaggerated facial expressions
(which occur with regularity in children). The anterior
portion of the skull should be avoided because of thin bone
dimensions and the underlying frontal sinus. The thickest
location is directly posterior, but this is not an ideal location
for pin placement because patients may lie on this pin when
supine.
A limited CT scan may be used to select the best bone to
accommodate the pins. Often one has already been obtained
as part of the trauma evaluation. Another suggestion for
decreasing the risk of pin complications is to use a larger
number of pins (eight) instead of the usual four.
As with application of head-halter or cranial traction in
children, overdistraction may occur when the halo-vest is
used.279 Adequate positioning of the cervical vertebra must
be checked carefully after the device is applied.
Dormans et al. reviewed complications in children immo-
bilized in a halo vest.272 The halo was not used in conjunc-
tion with operative arthrodesis of the cervical spine in 24
patients (65%). The other 13 patients (35%) were being
treated for trauma. Complications occurred in 68% of the
patients. The most common problem was pin-site infection
Specific Injuries
(22/25). Grade II infections (purulent drainage) developed
more frequently in patients over 11 years of age. Children
younger than 10 years tended to have nonpurulent drainage
at the pin sites and pin loosening. Additional complications
included dural penetration, transient injury to the supraor-
bital nerve, and three disfiguring pin site scars.
Goodman and Nelson reported a 15-year-old boy who
developed a brain abscess while being immobilized in a halo
orthosis for a neck fracture.276 Their case and at least one
other may have been due to tightening of a halo pin several
weeks after placement.
Specific Injuries
As mentioned previously, the cervical spine appears to be the
most commonly involved spinal component injured in the
skeletally immature patient, especially the child under 10
years of age.283–309 Fractures and dislocations of the upper cer-
vical spine, in particular, occur with a greater incidence in
children than in adults. Lesions of the atlas and axis were
noted in 16% of cervical spine injuries in adults, whereas they
constitute almost 70% of cervical spine injuries in children.
Locked facets, which are common in adults, are infrequent in
children. Facet physeal fracture, however, may occur as the
analogue, similar to tibial spine/anterior cruciate ligament in
the knee. It is probably associated with ligament laxity. An
underlying congenital abnormality (e.g., Klippel-Feil syn-
drome) may be a predisposing cause of injury. Fuch et al.
reported several cases of high cervical spine injuries in chil-
dren restrained in forward-facing car seats.288
Abuse
Abuse during infancy may also cause significant spinal
injury.310–317 The upper cervical spine is not resistant to major
torsional stresses under these circumstances, and injury may
occur proximal to the tethering of the large brachial nerve
roots. The relatively heavy infantile head is poorly supported
by cervical musculature. Accordingly, the upper cervical
spine is highly vulnerable to repeated shaking, especially in
the battered child syndrome. These infants probably have a
higher risk of SCIWORA, especially in the shaken baby syn-
drome. Firmly gripping the infant around the thorax may
lead to costotransverse injury that is difficult to diagnose (see
Chapter 11), and it may be accompanied by canal hemor-
rhage or disruption of cord vascularity.
Birth Injury
The youngest patients with upper spine lesions have been
newborns in whom autopsy has revealed atlantooccipital and
atlantoaxial disruption, fracture of the dens, and transection
of the cord. These injuries can occur as anticipated obstet-
ric complications of difficult deliveries. Obviously, efforts
should be made to minimize the risk of occurrence.
Birth trauma probably is a common cause of spinal cord
injury in infants.318–376 Most injuries involve breech extrac-
tion and sustained laceration of the spinal cord without a
roentgenographically evident injury to the spine (i.e.,
another cause of SCIWORA).318,322,333,349,351,367,370–373 Spinal
731
cord injury may also result from an accident to the neonate
or infant (e.g., child abuse). In the young infant the verte-
bral column is extremely elastic, certainly more so than the
spinal cord, which is tethered by nerve ends and blood
vessels. During delivery it is possible to prolong longitudinal
traction sufficiently to distract the neck without producing
permanent or evident injury to the chondro-osseous struc-
tures or dura, yet go beyond the tensile resilience of the
spinal cord, which can tear within the intact dura and spinal
column.
Yates showed that trauma to the cervical spine at birth
could result in damage to the cervical portions of the verte-
bral artery.375 There was evidence of distortional trauma but
no evidence of major fracture or dislocation to the cervical
spine. The lesions could be classified into four main groups:
(1) extradural, dural, subdural, and subarachnoid hemor-
rhage; (2) tears and hemorrhages in the nerve roots and
spinal ganglia; (3) evidence of hemorrhage around one or
both of the vertebral arteries in the form of a crescentic,
adventitial hematoma or massive hemorrhage encircling the
vessel; and (4) spinal cord lesions that consisted of contu-
sion and bilateral necrosis of the lateral columns. Vertebral
artery hemorrhage may be an important cause of perinatal
mortality and morbidity. Many cases of cerebral palsy alleged
to be caused by anoxic spells may be explicable on the basis
of vertebral artery trauma and ischemic cerebral, cerebellar,
and cord damage at birth.
Ligamentous laxity permits a longitudinal force to sepa-
rate adjacent vertebral bodies sufficiently that breech deliv-
eries may cause total anatomic transection of the cervical
cord without apparent fracture-dislocation of the spine.
The cervical musculature, so important to the stability and
alignment of the adult cervical spine, is still not fully
developed in the infant. Thus, distracting and displacing
forces at the time of injury are less likely to be checked by
the patient. After injury, protective muscular splinting is less
effective.
These infants have difficult diagnostic patterns. Present-
ing symptoms may be a fever of unknown origin due to loss
of temperature-regulating mechanisms. Reflex movements
may be mistaken for voluntary movements. These infants
may have respiratory distress resulting from paralyzed inter-
costal muscles. Typically, if the child has had a cord transec-
tion, painful stimuli above the level of the transection do not
induce movement in the limbs affected below the cord tran-
section. Stimulation below the sensory level elicits reflex
withdrawal but does not usually produce any irritable
response in the infant.
Clinically, there are two primary neurologic syndromes
seen in infants who sustain major cervical cord injury at
birth. The first type is secondary to complete disruption of
the spinal cord, and the clinical picture seen immediately
after birth is that of a completely flaccid, areflexic infant with
spinal shock. Within a few weeks to several months, the
infant loses the flaccidity and areflexia and becomes hyper-
reflexic and hypertonic. The second type of neurologic syn-
drome is seen in the infant who remains flaccid, rather than
becoming spastic or hyperreflexic. This syndrome probably
results from further damage to the lower cord by the dis-
ruption of the vascular supply, which leads to anoxia and
infarction.
732 18. Spine

Occipital Fracture
Cottalorda et al. described an occipital condylar fracture in
a 15-year-old girl.379 They found only 36 cases reported since
Bell first described the injury in 1817. Occipital fractures are
unusual in young children.377,379–382 When they occur the
potential for growth damage must be considered, as there
are chondro-osseous growth regions in the occipital bone
and occipital condyles.27 In contrast, most of the cranial and
facial bones enlarge by membranous ossification and are less
susceptible to disruption of normal growth dynamics.
Nonoperative treatment is the usual method. Care must
be taken to assess the extent of bleeding, as a contiguous sub-
dural hematoma may have to be evacuated.378

Occipitoatlantal Dislocation
In adults the anatomy of the atlantooccipital joint provides
considerable stability.399 However, the relatively small size of
the occipital condyles, the large space of the atlantooccipi-
tal joints, and the relatively horizontal plane of these joints
in infants and young children make the relation between
the atlas and occiput less stable, particularly in exten-
sion injuries.399 Congenital defects also may predispose to
injury.383,390,393 A progressive inclination of the occipitoat-
lantal joint develops with skeletal maturation. Therefore dis-
location without fracture is possible in children.394,398,400,404,407
Spontaneous, nontraumatic occipitoatlantal subluxations
may also be due to various inflammatory diseases (see Grisel
Syndrome, above).
In children the (sagittal or coronal) diameter of the cer-
vical portion of the spinal canal is approximately 22 mm at
the first cervical vertebrae.397 Hypermobility in this joint may
be confusing.412 The major changes of growth occur in the
surrounding bones. The susceptible areas of neurologic
dysfunction associated with occipitoatlantal injury are the
caudal cranial nerves, brain stem, proximal portion of the
spinal cord, and upper three cervical nerves.
Total dislocation of the atlantooccipital articulation is
a rare, usually fatal injury often associated with transec-
tion of the medulla oblongata or the spinal medullary
junction.386,387,405,410,411 The vertebral artery may also be
damaged.384 There is displacement of the occipital condyles
from the superior facets of the atlas along with retropha-
ryngeal swelling (Fig. 18-36). The relation of the dens to the
basiocciput and that of the posterior arch of the atlas to the
posterior rim of the foramen magnum are distorted.
There is little information available regarding patients
who sustain and, particularly, survive this injury,388,391,398,403,406
although young children appear most likely to do so.398,401,402
The clinical and neurologic manifestations vary and include
cardiorespiratory arrest, motor weakness, quadriplegia, tor-
ticollis, pain in the neck, vertigo, and projectile vomiting.443
A 6-year-old child demonstrated significant irregularities in
pulse and respiration. When the head was extended, they dis-
appeared. After recovery there were no neurologic seque-
lae.392 Gabrielson and Maxwell reported a partial dislocation
in which the patient initially demonstrated cranial nerve dys-
function and long tract signs, but the only residual neuro-
logic deficit was anesthesia over the distribution of the
greater occipital nerve.391 Evarts described traumatic occipi-
FIGURE 18-36. Atlantooccipital dislocation in a 14-year-old. This
case was fatal owing to lack of spontaneous respiration.
toatlantal dislocation in an 11-year-old boy who had acute
respiratory distress, stridor, palsy of the sixth left cranial
nerve and both twelfth cranial nerves, and a left hemipare-
sis.389 The patient had both brain stem and cord involvement
initially, but only a partial left lateral rectus paresis and a pos-
itive left Babinski reflex persisted.440 It is evident that a wide
spectrum of neurologic abnormalities may be encountered
with occipitoatlantal dislocation, from minimal involvement
of the brain stem or proximal spinal cord to sufficient
dysfunction to result in immediate death.
Sponseller and Cass reported two children who survived
atlantooccipital dislocation.408 In both children (4 and 11
years of age) an occiput to C2 fusion was successfully
undertaken. Others have also reported survival of this
injury.384,385,389,409,413,494,497,499
Conservative management (with a halo) has succeeded
in some young children, although surgical fusion may be
required in older children and adolescents because of the
difficulty obtaining and maintaining reduction.389,392,395,408
The initial treatment of this dislocation is to relieve
any respiratory distress by endotracheal intubation, tra-
cheostomy, or cervical traction. Care must be taken not to
increase any displacement with cervical traction, a phenom-
enon more likely in the child than the adult. Monitoring
the occipitoatlantal relation with lateral roentgenograms is
essential.
Atlas Fractures
Atlas fractures in children are infrequent.416,417,420,
421,423–425,427–430,432–434,436,438,480,486,495
Birth injury and congenital
defects may be associated with C1 injury.416 In fact,
congenital abnormalities may be misdiagnosed as atlas
fractures.414,415,418,419,422,426,431,435,
Specific Injuries 733

FIGURE 18-37. C1 fracture. (A, B) Lateral mass fracture (arrows) is evident on lateral and open mouth views. (C) Computed tomogra-
phy (CT) scan shows the fracture clearly (arrow).

Indirect trauma usually causes these injuries.437 The

occiput and multiple muscle layers protect the immature
atlas. Fractures ordinarily require reasonably direct axial
transmission force through the skull to concentrate stresses
on the atlantal components. Direct blows on the head,
accordingly, may produce axial compression of the atlas by
forcing the occipital condyles downward into the lateral
masses of the atlas. If the lower cervical spine remains suffi-
ciently rigid, the lateral masses are displaced centrifugally,
albeit minimally (Fig. 18-37). The force may also comminute
the lateral masses and rupture the transverse ligament. Axial
compression of the skull and cervical spine with hyperex-
tension of the head may also shear the posterior arch of
the atlas at its weakest point, through the groove of the ver-
tebral arteries. Detachment of the posterior arch of the atlas
leaves it subjected to upward displacement by the pos-
teroinferior oblique muscles, but the lateral masses are not
displaced because they generally remain securely attached to
the anterior arch.
Usually there is both anterior and posterior injury of the
ring. In young children this disruption is usually through the
neurocentral synchondroses (Fig. 18-38).425 If the force is
applied eccentrically, there may be only a single fracture.
However, if one synchondrosis is involved, it is likely the
other is also involved as an occult (microscopic) injury
that is not readily evident radiologically (Fig. 18-26). A
fracture may occur within the anterior ossification center
(Fig. 18-39).
Patients usually complain of a sensation of instability,
severe suboccipital discomfort, and pain. Pharyngeal soft
tissue swelling and fat pad displacement are not usually
prominent features. Spinal cord damage may occur.
Because of the difficulty visualizing this region with routine
roentgenographic projections, other imaging methods FIGURE 18-38. (A) Fracture (arrow) through one of the neurocen-
become essential. CT scanning, in particular, allows excellent tral synchondroses. (B) Several months later healing has closed
visualization of the entire ring and is probably the best the disrupted facet, although the other facet remains open. Note
method for demonstrating the pattern of injury and degree of that this is anteriorly displaced and probably “hinged” at the other
fragment displacement. It is also helpful for determining the synchondrosis.
extent of healing during follow-up evaluation.
Treatment consists of a (Minerva) cast or rigid orthosis
(e.g., Somi) for approximately 6–8 weeks followed by a
removable cervical orthosis for the child with minimal dis-
734 18. Spine

disorders such as a syrinx or cord tumor must be sought as

part of the differential diagnosis.
On rotation of the head, instead of the atlas moving on
the axis, the two moved together. Fielding and Hawkins
described 17 cases of irreducible atlantoaxial subluxation.455
The striking features were delayed diagnosis and persistent

FIGURE 18-39. Fracture within the anterior ossification center

(arrow), rather than the synchondrosis.

placement (in whom facet capsules/ligaments and atlantoax-

ial ligaments are probably intact). Serial CT scans allow
assessment of progressive healing of the injury. The older
child or adolescent may require application of a halo vest.
Infrequently, surgical fusion is necessary.427

Rotatory Subluxation of the Atlantoaxial Joint

Rotatory subluxation or dislocation, rather than fracture of
the atlantoaxial articulation (Figs. 18-40, 18-41), is one of the
more common lesions in children with injuries to the atlas
and axis.439–486 The injury mechanism may seem relatively
innocuous in small children.
Isolated atlantoaxial subluxation or dislocation may be
secondary to rupture of the transverse ligament (Fig. 18-42),
skeletal dysplasia, Down syndrome, inflammation (tonsilli-
tis), pharyngitis, or juvenile rheumatoid arthritis (see previ-
ous sections). However, traumatic rupture of the transverse
ligament is rare, as the more mechanically vulnerable dens
usually fails at the neurocentral synchondrosis before the lig-
aments do.446 More importantly, the normal ligamentous
laxity may allow displacement without necessarily incom-
pletely or completely tearing the ligament.
With atlantoaxial displacement, the atlas moves anteriorly,
which increases the distance between the anterior arch
of the atlas and dens and decreases the canal space. Such
displacement may significantly damage the spinal cord
or medulla.449 The maximal normal distance in flexion or
neutral position in children is 3–4 mm, decreasing to 2 mm at
skeletal maturation.466 Pathologic inflammation may produce
increased laxity of the ligaments (e.g., in Grisel syndrome),
and there may be rotatory and anterior displacement.
The presenting symptom of patients with atraumatic sub-
luxation is usually an isolated complaint of torticollis.445
C
Radiographic studies should be obtained for any child whose
cervical spasm and pain do not respond rapidly with con- FIGURE 18-40. (A) Torticollis associated with a locked rotatory sub-
ventional therapy. With the most common type, anterior uni- luxation. (B) CT scan of counterclockwise (arrows) locked rotatory
lateral displacement, the head may be turned away from the subluxation of C1 on C2 (= dens). (C) CT scan of clockwise locked
affected side, and neck movements are limited. Signs and rotatory subluxation of C1 on C2. The transverse ligament may be
symptoms of cord compression are infrequent. Underlying strained, but most likely it is intact.
Specific Injuries
FIGURE 18-41. Torticollis and rotatory subluxation of C1 on C2 in
a 7-year-old child. It was gently “unlocked” by controlled traction
with the patient awake. The anteroposterior view of the spine con-
trasts with the lateral view of the skull.
clinical and roentgenographic deformities. All patients pre-
sented with torticollis and restricted, often painful neck
motion. Seven young patients had long-standing deformity
and flattening of one side of the face. These investigators
thought that cineroentgenography was particularly helpful
for making the diagnosis. Real-time fluoroscopy should also
be considered.
Excessive mobility of the atlas and axis has been
reported.441,455,480 This mobility may exist as an independent
abnormality or with other regional malformations, such as
Klippel-Feil syndrome. The abnormally mobile atlantoaxial
joint associated with a hypoplastic dens does not necessarily
give rise to symptoms in the upper part of the cervical spine.
Because of the absence of the dens, this excessive mobility
may be compatible with minimal if any risk, with the excep-
tion of acute trauma.
Rotatory subluxation of the atlantoaxial joint is a relatively
common problem in a child with an upper respiratory infec-
tion and differs from the fixed pattern. Associated hyper-
emia affects ligaments that support the upper cervical spine
and makes the atlantoaxial joint temporarily unstable. Sub-
luxation is produced by twisting the neck suddenly or rotat-
ing it beyond its normal range. The child presents with
painful torticollis accompanied by marked spasm of the ster-
nocleidomastoid muscle. The child may support the head
with the hands or may prefer to be recumbent. There is local
tenderness of the atlantoaxial joint when the posterior
aspect of the neck is palpated. Neurologic examination is
done to rule out spinal lesions.
Rotatory fixation of the atlantoaxial joint may occur with
a minor accident, such as a blow to the head or an automo-
bile collision. The child complains of pain and stiffness in
the neck and may have occipital neuralgia and torticollis
(Fig. 18-40). Patients with atlantoaxial rotatory fixation
may also develop a compensatory counterclockwise occipi-
toatlantal subluxation.448
735
Open-mouth anteroposterior roentgenograms show that
the dens is asymmetrically placed between the lateral articu-
lar masses of the atlas. The diagnosis is confirmed by addi-
tional open-mouth views obtained in various degrees of
rotation. It cannot be emphasized too strongly that correct
diagnosis of traumatic displacement depends on the analy-
sis of a pair of true right-angle films of the atlas. The crucial
observation on the lateral film is the distance of the dens
from the anterior arch of the atlas. Overriding of the artic-
ular surfaces of the atlas is not significant, as it may be pro-
duced by changing the angulation of the roentgenographic
beam. If the subluxation is minimally evident on routine
radiographs, CT views may be used to demonstrate the
altered C1/C2 relations and whether one or both facet joints
are disrupted (one is more likely if the transverse ligament
is intact).
Ebraheim et al. studied the effect of atlantoaxial rotation
on canal size.452 Anterior translations of the atlas of 3,4, and
5 mm led, respectively, to canal decreases of 85%, 80%, and
75% of normal. If rotation was then added to the deformity,
more significant changes occurred. A 40° degree rotation
coupled with an 8-mm anterior displacement resulted in the
canal area being only one-fourth normal.
Most rotatory deformities of the atlantoaxial joint are
usually temporary and correctable.544,556 Treatment consists
of continuous traction with a head halter. The subluxation
may spontaneously reduce within a few days, as the muscle
spasm subsides. In some cases gentle reduction is attempted
with the patient awake but adequately sedated. One should
try to avoid attempting to reduce this lesion with the patient
under general anesthesia. Evoked potential monitoring is
done whenever possible. After reduction the patient is sup-
ported with a cervical collar, orthosis, cast, or halo, depend-
ing on the etiology and severity of the injury.
For more severe injuries, treatment may include skull or
halter traction followed by atlantoaxial arthrodesis (Fig. 18-
43), as necessary.521,522 Of 13 patients so treated in one study,
11 showed good results, 1 showed fair results, and there was
insufficient follow-up of the other patient. One other patient
died while in traction as the result of cord transection that
was produced by further rotation of the atlas and the axis
FIGURE 18-42. (A) Anterior subluxation of C1 on C2. The trans-
verse ligament has to be disrupted.
 736
(despite traction). After fusion, other segments may exhibit
increased mobility.
The most challenging problem is the chronic, essentially
fixed subluxation that does not reduce in traction or fol-
lowing gentle manipulation. It may be necessary to consider
an atlantoaxial fusion in situ in the displaced position,
accepting the extent of deformity. Alternatively, removal of
some of the displaced facet may allow rotational correction,
which should be followed by fusion.
Dens Fracture
Fracture of the dens is infrequent in children who are
less than 7 years old and especially infrequent in those
who are less than 3 years of age.487,489,490,495,496,499,503,504,
512,514,523,527,529,531–533,535,536,539,540,544
In a large series of dens frac-
tures (60 patients), only five were between the ages of 3 and
6 years.536
A B
18. Spine
FIGURE 18-43. (A) C1–2 fusion for
chronic, painful rotatory subluxation. (B)
Postoperative subluxation of C1–C2 on
C3. It is probably due to attenuation of
facet capsules and the interspinous
ligament.
In most recognized instances of dens fracture in children,
there is major trauma. Most of these fractures are diagnosed
readily on the basis of early roentgenograms (Fig. 18-44),
although swelling or widening of the retropharyngeal soft
tissue space may be the only diagnostic sign in some young
children. Furthermore, the injury mechanism may be rela-
tively “benign” and the radiographs seemingly normal, a
factor that may explain an initially missed diagnosis and the
subsequent origin of the os odontoideum.
There is a difference in the levels at which the axis frac-
tures in the adult and the young child (Fig. 18-7).537,539 The
lateral radiograph in adults shows that the fracture line
usually lies at or above the level of the articular facets,
whereas in the young child the fracture line is generally
below these facets, within the body of the bone (vertebral
centrum). Displacement of the dens may be recognized on
the lateral film. The fracture line propagates along the
region of the physeal plate, although it may involve bone
FIGURE 18-44. (A) Dens fracture in a
5-year-old boy. (B) Healing after 7
weeks in a Minerva jacket.
Specific Injuries 737

FIGURE 18-45. (A) Dens fracture in a 6-year-old

child. (B) MRI shows cord injury, but in the lower
cervical cord several segments distal to the fracture.
This may be a cord traction phenomenon, rather
than SCIWORA, at the level of cord injury.

A B

on the dens side compatible with a type 1 or 2 growth reportedly a potential complication in the adult. Delayed
mechanism fracture.527 Blockey and Purser believed that the myelopathy may be due to a long-term instability.488,493
dens fracture in young children was always an epiphyseal Open-mouth views may be significant, but lateral and
separation.490 anteroposterior tomographic views are also helpful. Care
There is no diagnostic clinical syndrome for a dens frac- must be taken not to misinterpret the closing dentocentral
ture. The symptoms and signs may be few and so indefinite synchondrosis as a fracture (Fig. 18-46). Displacement is
that the diagnosis is missed. There may be little pain, but usually minimal, making the diagnosis more difficult.
usually there is some stiffness in the neck. The immediate In most cases, with minimal or no displacement, treatment
pain may be severe and often is referred to the occipital is conservative with strict bed rest, initial cervical traction for
region. It may be accentuated with any attempt to move the comfort, and a subsequent rigid collar (e.g., Somi brace).
head. Classically, the child supports the head with the hands With displaced lesions, with or without neural deficit, treat-
to prevent any movement and often describes a feeling of ment may have to be modified.496 Manipulation and a
the head “falling off.” The neck may be held twisted (acute Minerva cast have been used, as has skeletal traction fol-
torticollis). lowed by a halo cast. The ease of reduction, stability with
Seimon presented children with dens fractures and traction or cast support, early callus formation, and prompt
described what he considered an important diagnostic clin-
ical sign.535 In each, injury to the cervical spine was suspected
from the description of the trauma mechanics, but initial
roentgenograms failed to reveal any fracture. The patients
were comfortable when lying supine or when fully erect, and
each child strongly resisted any attempt to hyperextend the
neck. With extension, the anterior arch of C1 courses along
the anterior dens, which would cause micromotion at the
fracture site. This symptom is a valuable clinical sign when
injury to the dens is suspected, as these fractures usually
occur with a flexion mechanism. The radiograph may or may
not demonstrate forward displacement of the dens relative
to the C2 vertebral centrum.
The most common minor neurologic complication is
damage to the greater occipital nerve, with referred pain to
the occiput.490 Obviously, the most serious complication is
the immediate damage, followed by the potential for chronic
damage to the spinal cord or medulla oblongata.514,541 The
level of neurologic (spinal cord) injury may not be at the
same level as the dens fracture (Fig. 18-45). One child had FIGURE 18-46. Apparent fracture of the dens (arrow) that is actu-
pyramidal signs with absence of the abdominal reflexes and ally the dentocentral synchondrosis remnant. The absence of con-
extensor plantar responses.490 None of these cases was as- tiguous retropharyngeal swelling should lead one to suspect a
sociated with delayed-onset paraplegia, although this is structural variation, rather than trauma.
738
healing in most cases offer a good prognosis in these
patients. Surgical (manipulative) reduction or fusion rarely
is necessary. In older children and teenagers, the synchon-
drosis at the base of the dens is fused with the body of the
axis, and injuries are essentially the same as those of an adult.
In general, basilar and apical fractures heal well when
reduced and stabilized, whereas fractures of the dens above
the level of the atlantoaxial articular facets tend to remain
unstable and often require posterior C1–C2 fusion.521
Remodeling in children after C1–C2 fusion has a tendency
to form kyphosis but to gradually remodel. Surgery is rarely
necessary in a young child.521 In rare instances an anterior
approach is used.492
Like epiphyseal separations in other parts of the body, the
separated dens is purported to unite readily. In the two cases
reported by Blockey and Purser, union occurred in 7 and 13
weeks, respectively; and at the end of 3 years the clinical and
radiologic appearances were normal.490 Dens fractures in
children older than 7 years closely resemble those in adults,
especially regarding the likelihood of delayed healing.
Although there is a high incidence of pseudarthrosis or
avascular (ischemic) necrosis in adults, these conditions do
not seem to be serious complications in skeletally immature
patients.524 Undisplaced fractures at the base of the dens
within the substance of the body of the axis have a satisfac-
tory potential for healing. Fractures higher in the dens and
displaced fractures, particularly those displaced posteriorly,
have a much higher pseudarthrosis rate and usually require
some type of fusion after reduction.
Late atlantoaxial instability may complicate even a mini-
mally displaced dens fracture. Follow-up must be accurate
and maintained until the child stops growing (Fig. 18-47).
FIGURE 18-47. This 5-year-old child was being evaluated for a
“fall.” Screening of the cervical spine revealed an old odontoid frac-
ture that had healed in a displaced position. A detailed interview
showed a similar presentation after a “fall” 2 years previously. Child
abuse was eventually diagnosed as the cause.
18. Spine
Os Odontoideum
Several anomalies are associated with abnormal
flexion/extension motion between C1 and C2: hypoplasia of
the dens, hypoplasia with an os odontoideum, simple short-
ening of the dens resulting from failure of the terminal
ossification center to develop, and total agenesis of the
dens.498,507,509,513,516,517,522,526 Pizzutillo et al. reported an inter-
esting case in which one of the paired primary ossification
centers failed to develop.530
In the past, os odontoideum was thought to represent a
deformed dens that failed to unite with the body of C2. This
theory neglects the fact that the base of the normal dens is
lower than the plane of the C1–C2 joints, although the os
odontoideum complex may have a protrusion extending
above the articular facets. The os odontoideum has also been
considered a hypertrophic remnant of the proatlas associ-
ated with hypoplasia of the dens in the absence of the distal
ossification center.
Trauma, often unrecognized, undoubtedly plays a sig-
nificant role in the eventual development of an os odon-
toideum in the child and the adult (Figs. 18-48,
18-49).491,497,500,502,506,518,519,524,525,534,545 Cases of apparent con-
genital absence of the dens have been reported frequently,
although in some cases there were reports of definite trauma
prior to definitive diagnosis.501,510,515,536,538 Other reports
describe the disappearance of the central portion of the dens
in the child.535 In these cases roentgenograms obtained
shortly after injury revealed no fracture, whereas abnormal-
ities were found when the patients were reevaluated.
Seimon’s patients were 22 and 35 months old at the time of
their injuries.535
Gwinn and Smith reported 27 cases of acquired and con-
genital absence of the dens.513 In more than half of these
patients there had been antecedent trauma. Associated
abnormalities of the cervical spine were present in five cases.
Gillman described a case of congenital absence of the dens
that was discovered after the patient sustained a head
injury.509 Freiberger and colleagues suggested that although
some cases of an absent dens were congenital, some may be
due to unsuspected trauma.504
Verska and Anderson described an identical twin with an
os odontoideum after trauma, with the other twin having a
normal cervical spine and no history of trauma.543 Another
report found an os odontoideum in both twins.520
Resorption of the basilar portion of the dens occurred in
three reported cases in which injury of the dens was not rec-
ognized and treated. It produced the appearance of com-
plete absence in one patient and the appearance of an os
odontoideum in the other two patients.500
It seems that the disappearance of the lower portion of
the dens is an example of nonunion and fibrous replace-
ment of the bone, not unlike the traumatic acquisition of
lumbar spondylolysis (L5) in gymnasts. A similar situation is
chondro-osseous fracture of the carpal navicular (scaphoid)
leading to a radiologically bipartite scaphoid (see Chapter
17). Certainly, an untreated fracture through a cartilaginous
growth plate in a mobile area of the body such as the dens
may go on to nonunion, especially if it is inadequately immo-
bilized or not immobilized at all. If the dens is not seen radio-
graphically, it does not necessarily mean there is a loss of all
 A

FIGURE 18-48. (A, B) Os odontoideum in a 10-year-old boy. (C)

Fusion of C1–C2 to stabilize this injury.
C
FIGURE 18-49. (A) Unstable C1–C2 relation due to nonunion (os
odontoideum) of a dens fracture in a 12-year-old boy. (B) It was
treated by posterior fusion and wiring. The latter broke owing to
delayed union. (C) Final result after augmentation of the bone graft
and removal of the broken wire.

739
740 18. Spine

FIGURE 18-50. (A, B) Fracture of pedicle and lateral mass (arrow) of C2. (C) Seemingly comparable case. However, this linear defect
was present bilaterally and probably represented a congenital defect (arrow).

tissue with a cystic defect. In a child, roentgenograms
are obtained after suspected or definitive dens fracture to
demonstrate whether union has occurred or unforeseen
problems have arisen (3–4 weeks and 3–4 months after any
suspicious injury).
When an os odontoideum is found, the first treatment step
is a detailed evaluation of cord function, intrinsic stability,
and the potential for cord compression acutely or chroni-
cally. This assessment may be done by assessing lateral MRI
images in flexion and extension. If there is abnormal mobil-
ity or evidence of actual or potential cord damage, C1–C2
fusion should be considered (see Fig. 18-48 below).497,511,521
Fractures of the Body and Neural Arch of the
Axis (C2)
Fractures of the body and neural arch of the axis, compared
with dens or atlas fractures, are infrequent and generally
heal satisfactorily with nonoperative treatment.494,505,508 Con-
genital pseudarthroses, however, may complicate (confuse)
the diagnosis (Figs. 18-50, 18-51).522,528,542 Nordstrom and
associates reported a 9-year-old girl with familial spondylolis-
thesis of C2 and C3.528 Her father had similar vertebral
abnormalities. Her condition was not discovered until she
presented with a complaint of mild, localized neck pain after
having fallen.
The posterior portion of the spinous process may be frac-
tured through bone (Fig. 18-52) or as a chondro-osseous
fracture of the tip (which has a cap of epiphyseal cartilage).
The osseous fracture may extend to one or both laminae.
The latter situation may lead to partial instability.
Upper Cervical Fracture-Dislocation
As previously mentioned, the focus of flexion-extension in the
young child is at C2–C3. It does not shift to the lower cervical
spine until after 7–8 years of age if not the second decade of
life. The laxity of ligaments may allow facet displacement
without fracture (Fig. 18-53). Displacement may be enough to
cause a jumped (locked) facet. End-plate (apophyseal)

A B C

FIGURE 18-51. (A) Apparent pedicle fracture of C2 (arrow) in a case of child abuse. (B) Four months later. (C) Eight months later.
Specific Injuries
FIGURE 18-52. Fracture of the spinous process of C2.
injuries may also occur. Closed reduction in tongs or a halo
should be attempted, followed by fusion (if indicated).
Because an anterior (body) fracture is a significant part of this
injury, this portion may allow some osseous healing. The use
of a Minerva cast or rigid orthosis should be considered, fol-
lowed by careful evaluation of residual posterior ligament
instability, before considering posterior fusion.
Lower Cervical Fracture-Dislocation
The remainder of the cervical spine, with the exception
of pseudosubluxation, is less frequently involved after
trauma in children under 10 years.546–554,556,558–560,562,564,566,
570,571,573,576,578–581,584,586,588,590,595–600,602,604,637,660,688
Compression
A B
FIGURE 18-54. (A) Traumatic subluxation of C2 on C3. An anterior fragment is evident. (B) Ossification is progressing toward C2 several
weeks later.
741
FIGURE 18-53. C2–C3 fracture-dislocation with locked facets. A
small fragment (solid white arrow) is probably from the anteroinfe-
rior body (open white arrow) of C2.
fractures of the cervical spine vertebral centra are unusual
in children.577 Congenital deformity may also predispose to
injury.568,574,582,593,594
There is usually associated disruption of the posterior lig-
aments that allows vertebral body (anterior) displacement
(Fig. 18-54). Posterior ligament disruption is often recog-
nized preoperatively with a lateral roentgenogram that
demonstrates widening of the spaces between the posterior
spinous processes. This widening may be evident only with
application of longitudinal traction. Therefore a lateral
roentgenogram made with the patient in traction may be
necessary to diagnose accurately whether the posterior liga-
ments are intact after injury to the immature cervical spine.
Loss and lordosis are variable radiologic findings.561 If
742 18. Spine

flexion-stress continues, the superior portion of the vertebral

body may be additionally compacted to create a wedged ver-
tebra (Fig. 18-55).
In infants and younger children, reduction of a cervical
fracture-dislocation with halter or skeletal traction usually
suffices, and surgical stabilization is not always necessary.
This treatment generally takes 6–12 weeks in skeletal traction
or a halo and another 6–8 weeks in a rigid orthosis or cast.563
Skeletal traction by any one of several devices is often diffi-
cult to maintain in young children because of the thin outer
table of their skulls.592 Tantalum wire, threaded between burr
holes, may be effective for treating children under 3 years of
age. The halo cast in small children has the advantage of
rigid external fixation coupled with ease of application and
ample surgical approach. Its use in children appears to be
without significant complication.
With tongs or a halo cast, meticulous attention to the sites
of pin insertion is necessary to prevent superficial infection.
Periodic roentgenograms of the skull are necessary for early
detection of penetration of the inner table or osteomyelitis.
Complaints of local pain, especially if severe, always suggest
penetration of the inner table.
Stability is restored by ligamentous and chondro-osseous
healing if the neck is held in a reduced position. If subsequent
roentgenographic examination suggests a recurrent displace-
ment, a limited two- to three-level posterior fusion with wires
and autogenous bone grafts secures fixation in most instances FIGURE 18-55. Wedging of C6 in flexion due to a hyperflexion injury
(Fig. 18-56). Spontaneous fusion at the fracture site is less in a 12-year-old boy. Note the appearance of the superior and infe-
likely in adolescents, and fusion may be needed as often as it is rior ring apophyses despite the retained wedging, which has not
used in adults. Disturbance of the growth of the anterior remodeled 18 months after injury.
centrum, coupled with the disruption of the posterior liga-
ments, may cause these injuries to remain unstable. Without children, as they may damage the superior and inferior end-
fusion, these patients may develop kyphotic deformities. plates (Fig. 18-57).587,601
Techniques of anterior interbody fusion were originally Limited posterior fusions are more appropriate in skele-
developed to treat degenerative cervical spine disease.583 tally immature patients.565,572 When undertaking posterior
These techniques are generally contraindicated in young fusion of the cervical spine in children, it should be noted

FIGURE 18-56. (A) Instability of C4 on C5. Note the narrowing of the interspace (arrow). (B) Similar case with involvement of two inter-
vertebral levels was treated by wiring three spinous processes.
Specific Injuries 743

FIGURE 18-57. (A) Compression fracture of

C5 (open arrow). Note the posterior widen-
ing (solid arrow), suggesting both anterior
and posterior injury. (B) Initial treatment in a
brace failed to correct the deformity. (C) It
was then correctly stabilized by posterior
interspinous wiring. (D) It was thought that
anterior fusion was also indicated, a proce-
dure not appropriate in such a skeletally
immature individual. Surgical elevation of
the anterior longitudinal ligament and the
anterior vertebral cartilage to expose the
incompletely developed central ossification
caused fusion not only of C4–C6 (solid
arrow) but also of C2 and C3 (open arrow),
leading to a major growth abnormality.

C D

that cadaveric bone grafts in children are less likely to result
in posterior cervical fusion.591 Autogenous iliac bone graft is
significantly superior for use in children, athough even it
may be resorbed. Furthermore, young children have limited
amounts of such bone for grafting.
Combined anterior and posterior fusion has also been
advocated in adults. However, when the injury is primarily
posterior, the anterior longitudinal ligament usually is intact
in the young child, in whom it is a thick structure. It proba-
bly is unwise to remove this ligament because it is the final
stabilizing structure in a posterior to anterior disruption.
Anterior approaches should be minimized in children
because of these significant anatomic differences.
Treatment for a fracture or fracture-dislocation of the
cervical spine below the axis in children usually does not
necessitate laminectomy. Progression of a neurologic deficit
while the child is under direct observation is a relative indica-
tion for evaluation with MRI or CT. A child who presents with
a nonprogressive deficit is unlikely to benefit from decom-
pression. The addition of posterior decompressive laminec-
tomy, allegedly done to relieve pressure in the damaged spinal
cord, may involve removal of posterior ligaments, and it
increases the degree of instability that may have been caused
initially by the osseous injury. Because spinal cord injury fre-
quently extends over several levels, decompression of only
one or two segments is inadequate unless there is active pro-
gression of the neurologic deficit. In addition, the multiple-
level laminectomy has adverse consequences from the
standpoint of cervical spine stability in children, resulting in
a severe swan-neck deformity (Fig. 18-58).555,557,575,589,603 If
laminectomy has been undertaken, the facet joints usually are
stabilized with wiring and bone graft.
Occasionally, a child or adolescent sustains trauma to the
cervical spine that produces little or no osseous damage and
has no neurologic consequence. Ligamentous injury may
render the cervical spine unstable, though, an event that is
undetected initially and then is either untreated or under-
treated. Because of the lack of obvious osseous damage, treat-
744 18. Spine

FIGURE 18-59. Multiple avulsions of the spinous processes of C6,

C7, and T1. Only the latter (T1) healed. The other two were painful
nonunions.

A Cervical End-Plate Injury

Physeal injuries of the cervical spine (Figs. 18-60, 18-61) are
uncommon injuries usually caused by hyperextension of the
cervical spine.567,569 Significant violence is the usual mecha-
nism, most often due to an automobile accident or diving
into shallow water. In infants, child abuse involving severe
shaking may completely disrupt an interspace through one
of the end-plates.

B
FIGURE 18-58. Resection of stabilizing fulcrum elements may lead
to major deformity. (A) Appearance after performance of a multiple
laminectomy. (B) Swan-neck deformity 4 years later.

ment may be minimized, and the instability persists or even

progresses.

Spinous Processes
Hyperflexion injuries may lead to avulsion of the cartilagi-
nous tips that are responsible for elongation of the spinous
processes. Whether initially recognized at the time of injury
or later, these particular injuries have a high rate of delayed
and nonunion (Fig. 18-59). If they become painful, resection FIGURE 18-60. Double-level end-plate fractures (arrows). Note the
may be necessary. subluxations in the upper cervical regions.
Specific Injuries
FIGURE 18-61. (A) Inferior end-plate frac-
ture of C2 (arrow). (B) Healing.
The injury usually involves the inferior growth region
(end-plate).567,569 The uncinate processes may biomechani-
cally protect the superior region, making the inferior end-
plate the weaker link relative to fracture susceptibility.
Histologic examination (Fig. 18-62) of a case showed con-
comitant microscopic disruption of the superior end-plate of
C3.569 Stanley et al. described two examples of superior end-
plate injury.592
With some of these injuries it is difficult to imagine, when
the anterior borders of the vertebra above and below the
FIGURE 18-62. (A) Epiphyseal fractures of the cervical spine. The
arrow with the asterisk points to the C2 end-plate, which has sep-
arated from the centrum (C). The intervertebral disk, demarcated
by the two open arrows, is intact. However, the interspace of
C3–C4 (solid arrow) is probably partially disrupted by hyperexten-
sion. (B) Histologic specimen. The arrow with the asterisk points
745
avulsed ossification center maintain their normal anatomic
alignment, that the entire growth plate and epiphysis have
been involved, as would be expected with a classic type l
physeal injury. Accordingly, it is possible that a type 3 injury
(Fig. 18-63) affecting only the anterior portion of the growth
plate and epiphysis may be an appropriate concept for some
of the “adolescent” injuries. In animals these anterior end-
plate injuries certainly are type 3 growth mechanism injuries
(Fig. 18-31), sometimes with an additional type 1 extension.
Furthermore, when the posteroinferior “ring apophysis” is
to the C2 end-plate, which has separated from the centrum. Note
that the intervertebral-apophyseal region is beginning to separate
(open arrow) from the C3 centrum, as it did above at C2. There is
also disruption of the inferior subchondral plate of C3 (solid
arrows).
746
FIGURE 18-63. (A) Type 3 growth mechanism end-plate injury in an adolescent. (B) Traumatic end-plate separation (arrow) in an ado-
lescent cadaver.
injured in adolescent lumbar spines, CT scanning shows a
type 3 fracture, rather than involvement of the entire end-
plate. The type l injury (Figs. 18-64, 18-65) more charac-
teristically involves the infant or young child. Such an
age-related difference in injury response patterns is certainly
consistent with the variability of comparable physeal injuries
in the long bones.
Most of the reported patients are adolescents, an obser-
vation suggesting age-related susceptibility during the stages
of physeal maturation and closure.567,569 However, Aufder-
maur, during postmortem examinations, found cervical end-
plate fractures in children from birth through adolescence,
implying that the injury pattern is not so much related to the
extent of chondro-osseous maturation as it is to our inability
FIGURE 18-64. (A) Type 1 end-plate growth mechanism injury in
an infant. PL = Posterior longitudinal ligament; AL = Anterior longi-
tudinal ligament. Anteroposterior (B) and lateral (C) views of such
18. Spine
to diagnose the undisplaced injury radiographically in young
patients.40
The secondary ossification center of a cervical vertebra
appears relatively late. Evaluation and diagnosis of the injury
thus may be difficult, if not impossible, before its appear-
ance. The infrequent secondary ossification center of a cer-
vical spine vertebra may be mistaken for a fracture fragment
by an inexperienced observer. In contrast, diagnosis of a
displaced ring apophysis is relatively easy on the lateral
roentgenogram. The secondary ossification center is ante-
riorly displaced, and there is usually contiguous soft tissue
swelling. Although secondary ossification centers are present
in children 6–10 years of age, these centers most often first
appear in the cervical spine when children are 10–12 years
an injury following an automobile accident, showing complete sep-
aration of C6 from C7 (arrows).
Specific Injuries
FIGURE 18-65. Traumatic separation of the centrum of C5 (solid
arrow) from the posterior element (open arrow). This injury had to
occur through the neurocentral synchondroses.
of age. Accordingly, if this injury were to occur before such
secondary ossification, the diagnosis would have to be
deduced from soft tissue swelling anterior to the vertebral
body; and treatment would be rendered empirically on the
basis of neck pain following significant trauma. MRI may
offer an alternative diagnostic modality in the affected young
patient. The separation involves angular displacement and is
difficult to diagnose radiographically. Moreover, it probably
FIGURE 18-66. (A) End-plate fracture (arrow). (B) Subsequent ossification of the annulus (arrow).
747
reduces spontaneously. As in older patients, when C7–T1
lesions are evaluated, it is imperative that the radiographic
views adequately visualize the lower margin of C7 and the
C7–T1 interspace.
The injury may occur at various levels in the cervical spine.
The four patients studied by Keller had C2 or C3 inferior end-
plate involvement.567 In contrast, two of our patients had more
caudal involvement of the inferior end-plates (C6 and C7),
and a third patient had involvement of the inferior end-plate
of C3.567 In two of Keller’s patients the avulsion occurred at
a single level, and in the other two it occurred at two levels.
Multiple-level involvement was evident radiographically in
one of my cases and histologically in another.569
Type 3 injuries heal rapidly within a few weeks. The perios-
teum, which is integrally related to the anterior longitudinal
ligament, is pulled away from the inferior portion of the ver-
tebrae associated with the fracture. During childhood this
structure is osteogenic, and if it is surgically elevated it may
lead to rapid fusion of the cervical vertebrae anteriorly. Such
a response lessens with increasing spinal maturity. Keller
described uneventful healing with anterior “osteophytes” in
three patients and incomplete bridging of the interspace
(Fig. 18-66) in a fourth patient.567 The bridging occurred
within the anterior longitudinal ligament. Premature closure
of the growth plate may lead to deformity or interspace nar-
rowing (Fig. 18-67).
Keller did not describe flexion-extension lateral views, so
it is difficult to say if there was any long-term injury to the
contiguous soft tissues in those patients.567 In our patients,
there was definite loss of normal cervical flexion at the
injured levels. However, the long-term consequences of
these motion losses—particularly whether they eventually
predispose to spondylytic changes or disk space narrowing—
are currently unknown owing to the lack of a sufficient
number of patients followed for extended times after such
injuries.
748
FIGURE 18-67. Narrowing of the posterior part of the C5–C6 inter-
space with anterior ring apophysis formation (arrow). This child had
been a victim of child abuse 7 years before this film was obtained
to evaluate neck pain following a football injury.
Type 1 growth mechanism injuries may be fatal, although
not necessarily acutely. Small children may be easily overdis-
tracted because the end-plate, ligaments, and spinal cord are
often all transected, leading to quadriplegia (Fig. 18-65).
Cervical traction must be closely monitored. If the infant or
small child survives, fusion of the disrupted vertebrae is
essential.
Injury to the Thoracic Spine
Injury to the vertebral elements of the developing thoracic
spine is relatively infrequent compared to other, more
mobile regions.608,610 Most of these injuries result from
vehicular accidents. Falls from a height and sporting acci-
dents are less common causes. Child abuse is a common
mechanism. Congenital lesions may also mimic thoracic
spine trauma.612
Because these fractures are often subtle or reduce spon-
taneously, additional diagnostic clues should be sought.
Widening of the mediastinum, similar to the prevertebral fat
stripe seen with a cervical injury, may be a good indicator of
possible thoracic spine injury.605
Inspection of the back frequently reveals abrasions and
contusions, which give a clue to the mechanism of injury.
Palpation may elicit tenderness of the paravertebral muscu-
lature and spinous processes, but palpable widening of the
interspinous distance does not usually occur. Neurologic
symptoms and objective neuromuscular findings are typically
absent. Traumatic ileus may accompany even a minor injury.
Excluding rib fractures, associated skeletal injuries are not
particularly helpful for the diagnosis and may often con-
tribute to a delay in appropriate treatment.
The intrinsic elasticity of the region, coupled with the pro-
tective effect of the rib cage to prevent excessive translational
movements of the thoracic spinal components, maximizes
the abnormal stresses necessary to cause fracture or disloca-
tion. In the thoracic region, especially in young children,
18. Spine
injury to the spinal cord occurs more often without associated
vertebral fracture, although significant translation may occur
without cord damage.611 The thoracic cord appears to be sus-
ceptible to injury because of its relatively narrow canal and
tenuous blood supply (artery of Adamkiewicz).
A relatively rare cause of thoracic spinal cord dysfunction
in a child is blunt trauma to the abdomen. This injury usually
relates to interference with the abdominal aorta and its
branches, particularly the artery of Adamkiewicz, which
arises at T11 and is a particularly important feeder to the
spinal cord. Most patients with this condition have complete,
permanent interruption of cord function.
Ruckstuhl et al. described 26 children and adolescents
with 65 vertebral fractures.610 Most of the fractures occurred
in the mid-thoracic spine. Fractures of the vertebral body
with sagittal wedge deformity alone had a better prognosis
than those with concomitant sagittal and frontal wedge
deformities. Those in the first group self-corrected partially
or completely during subsequent growth, but improvement
in the wedge deformity was present in only about one-third
of the patients in the second group. When the end-plates
were fractured, there was no correction, and there was a dis-
tinct lack of vertebral growth. Severe destruction of the car-
tilaginous end-plates and intervertebral disk led to fusion of
the corresponding segments. An increase in wedge defor-
mity was observed twice. Slight axial deviations of the inter-
vertebral disks following vertebral body fractures were
compensated during growth in most cases. Unstable frac-
tures may be difficult to control, even with a thoracolum-
bosacral orthosis.712
Wedge fractures of the thoracic vertebral bodies, usually
of minor degree, are relatively common (Figs. 18-68, 18-69).
The intrinsic elasticity in children, in contrast to that in
adults, allows these injuries to occur without major damage
to the posterior elements, thus causing an intrinsically more
stable injury.607 The posterior and anterior longitudinal lig-
aments are usually intact, although some posterior damage
may allow subluxation (Fig. 18-70). Wedge fractures occur in
the thoracolumbar junction more commonly than fractures
localized to only the thoracic or lumbar spine. Compression
of two or more vertebrae occurs frequently in children.
The presence of a healthy intervertebral disk, in combi-
nation with well-mineralized bone, is likely to be responsible
for the finding of multiple anterior compression fractures.
When a normal disk is present, the injurious force applied
to the spine may be transmitted from one vertebral body to
an adjacent one. The “normal” intervertebral disk might also
explain the infrequency of disk space narrowing and the
absence of spontaneous interbody fusion in this group of
children, although disk space injury may still occur.
Instability of the thoracic spine after injury depends on the
degree of damage to the posterior elements: chondro-
osseous, ligamentous, or both.607 If these posterior structures
remain intact, the fracture is probably stable. When a
fracture of the articular processes or rupture of the posterior
ligaments occurs, the injury is potentially unstable. A fracture
is grossly unstable when the posterior elements are com-
pletely disrupted and vertebral body displacement and dislo-
cations are present on roentgenographic examination.
Simple bed rest is generally indicated, as most children
with hyperflexion thoracic compression fractures are asymp-
Specific Injuries 749

FIGURE 18-68. (A) Mild compression fracture (arrow) of a thoracic vertebra. (B) Appearance 1 year later, with some reconstitution of the
anterior height (arrow).

tomatic within a few weeks. External support is appropriate.
Activity is gradually increased, depending on the patient’s
symptoms. Spinal fusion or internal stabilization is rarely
necessary in this region in a child but should be considered
in patients, especially older ones, with residual instability.609
Follow-up through spinal skeletal maturity is warranted to
assess potential delayed development of scoliosis or kyphosis
due to end-plate damage. An acquired “bar” may form and
lead to a situation similar to an uncompensated congenital
scoliosis. Pseudomeningocele has also been reported.606
Follow-up radiographs after compression fractures of the
immature spine show varying degrees of restoration of ver-
tebral body height (Figs. 18-68, 18-69). The extent of restora-
tion is directly related to the severity of the fracture and the
age of the patient at the time of injury. In children under 10
years of age with moderate compression injuries, some
reconstitution of the vertebral body may occur. Children
with severe fractures or those injured when older usually
show some permanent asymmetric wedging of the vertebral
bodies with concave end-plates and deformity of the anterior
contour of the bodies.
In a review of 59 patients who had sustained thoracic frac-
tures during childhood, most of which were localized to the
mid-thoracic area, more than 50% had no evidence of post-
traumatic growth or response changes during their follow-
up examinations. The number of posttraumatically altered

FIGURE 18-69. (A) Crush fracture of T12. (B) Incomplete growth recovery 3 years later.
750
FIGURE 18-70. Anterior subluxation of T11 on T12 (arrow) with mild
wedging of T12.
vertebral bodies was significantly lower than the number of
those primarily injured.60
Anteroposterior radiographs often reveal scoliosis follow-
ing a hyperflexion thoracic injury. Typically, the scoliosis is
a balanced thoracolumbar curve apically centered at the
fractured area. From a prognostic standpoint, the deformity
is less than 10° and only slightly progressive.
In patients with unstable injuries, with or without paraly-
sis, this same potential for growth and development, com-
bined with the instability of the fracture, may lead to a
progressive spinal deformity.
Facet Fractures
The facets not only are comprised of an articular cartilage
surface, they also have a variable amount of epiphyseal and
physeal cartilage. These regions are initially integrated with
the neurocentral synchondroses but gradually become sepa-
rate, not unlike the gradual separation of the capital femoral,
greater trochanteric, and lesser trochanteric regions of the
proximal femur. These regions are capable of sustaining an
injury pattern similar to a long-bone physeal fracture. Such
facet injuries may involve any region of the spine: cervical,
thoracic, lumbar, or sacral. This pattern has been docu-
mented in animal specimens (Figs. 18-27, 18-28) but is not
well documented in children. That it is a separation of the
cartilaginous facet away from the metaphyseal bone equiva-
lent makes radiographic demonstration difficult if not
impossible.
Because there are growth plates associated with each of
the four facets present in each vertebra, involvement leading
to physeal damage would affect symmetric growth and could
contribute to a scoliotic deformity.
Scheuermann’s Disease
The combination of fixed kyphosis of the thoracic spine with
radiographic changes of vertebral wedging, end-plate
18. Spine
irregularity, and narrowing of the intervertebral disk space
with or without intervertebral disk herniation is commonly
referred to as Scheuermann’s disease.613–619,621,622,626,629,632,633
Although less common, lumbar and thoracolumbar forms of
Scheuermann’s juvenile kyphosis have been described (Fig.
18-71)622 and characteristically produce more pain than the
thoracic type.618,620,624,627,635
The exact etiology of this “disease” is unknown.619,
621,623,625,630,634
Alexander proposed that it is a traumatic stress
spondylodystrophy that is sequential upon traumatic growth
arrest and end-plate fractures (perhaps single and micro-
scopic) that occurs during the heightened vulnerability of
the adolescent growth spurt.613 Once one fracture has
occurred, an insidious compounding of the deformity may
ensue, with adjacent vertebrae being affected by abnormally
applied static loads that increasingly cause pathologic stress
failure in the anterior region.
In specimens of juvenile Scheuermann’s osteochondrosis,
Aufdermaur showed that there were foci of various sizes in
the cartilaginous end-plates that displayed disruption of the
collagen fibers.614–617 These findings, coupled with an alter-
ation and occasional absence of the growth zone, were
thought to result in the typical deformation of the vertebral
bodies through a disturbance of collagen or ground sub-
stance biosynthesis.
The role of strenuous physical activity or repetitive injury
in the pathogenesis of these lesions has been sug-
gested.625,629–631 I have seen it in adolescents engaged in rig-
orous overhead (e.g., military press) body building. Several
of these patients had a significant kyphotic deformity.
Greene et al. presented 19 adolescent patients with
mechanical-type back pain and vertebral changes consisting
of intervertebral disk herniation, disk space narrowing, and
minimal wedge deformity.624 Most of the symptoms and signs
were located at the thoracolumbar junction, and a specific
strenuous activity or traumatic event was clearly associated
with the onset of symptoms in 16 of the 19 patients. Despite
the thoracic involvement, none of these patients had a pro-
gressive kyphotic deformity. A number of authors have noted
that juvenile kyphosis was more often associated with hard
physical labor or weight lifting before 16 years of age, similar
to that initially reported by Scheuermann.620,622,632,633 Micheli
found similar lumbar changes in young rowers and sug-
gested that the etiology was stress injury to the vertebral
growth plates, which is a more realistic etiology.627 Others
have supported this concept.623,626,635
The concomitant presence of spondylolysis and spondy-
lolisthesis in many patients supports the contention that
abnormal stresses were applied to the spine (thoracolumbar
and lumbar) in Scheuermann’s disease.624 Further support
for this being a stress-related, potentially reversible phe-
nomenon is the reconstitution of vertebral height following
the initiation of treatment.
Treatment should be symptomatic for mild deformity.
A hyperextension brace should be used for more severe
deformation.628 Surgery is sometimes necessary.
Injury to the Thoracolumbar Junction (T12–L1)
The thoracolumbar junction is a major motion segment
during flexion and extension. The ligamentous laxity of
the child increases susceptibility to facet displacement
Specific Injuries
FIGURE 18-71. (A) Scheuermann’s disease of vertebral end-plates (arrows). (B) Deformity of multiple levels (arrows), especially L3.
(C) Healing Scheuermann’s lesion (arrow) during hyperextension brace treatment.
(Figs. 18-72, 18-73), which may occur in the absence of frac-
ture or spinal cord injury. These children should be carefully
assessed for stability and then treated with spica cast immo-
bilization. If there is cord damage, early posterior fusion may
be indicated.
Injuries secondary to flexion-rotation result in classic
fracture-dislocations of the thoracolumbar spine. Antero-
posterior and lateral roentgenograms reveal fractures of the
articular processes (i.e., facet injuries), a lateral shift of
the spinous process, increased interspinous distance, and
forward displacement of the superior vertebral fragment.
Fusion is usually necessary.
Careful neurologic evaluation determines the presence of
spinal cord or nerve root injury. Because the end of the
spinal cord lies opposite the lower border of the first lumbar
vertebra; fractures below this level may cause only nerve
root, rather than specific cord, injury. With fractures at the
thoracolumbar region, however, special attention is needed
to determine whether complete or incomplete division of
751
the spinal cord, with or without nerve root involvement, has
occurred. Complete loss of voluntary power and loss of sen-
sation in all areas supplied by the sacral segments, in asso-
ciation with a bulbocavernosus or anal skin reflex, usually
indicates a complete injury of the spinal cord.
Fracture-dislocations at the thoracolumbar junction are
frequently unstable. Early fusion is the treatment of choice
in these cases. Whether early operative decompression has
any role in the treatment of spinal cord or nerve root injuries
believed to be complete at impact remains controversial.
Operative decompression is indicated when there is a pro-
gressive neurologic deficit associated with partial spinal cord
or nerve root injury.
Chance Fracture
Chance described a horizontal shearing fracture, principally
in adults, in which a relative anterior displacement of the
superior vertebral fragment is common.641 Typically, the
 752
A B
injury in children involves the twelfth thoracic and first to
third lumbar vertebrae (Figs. 18-74 to 18-76).636,637,644,646,659,664
The history and physical examination do not vary signifi-
cantly from those of patients with flexion-rotation injuries,
with one exception: abdominal contusion caused by a seat
belt, which may lead to a temporary paralytic ileus or other
intraabdominal injuries.640,647,649,650,654,655,658,660,662,668 These par-
ticular lumbar injuries may be associated with lap seat
belts,639,642,643,645,648,650,651,653,656–658,660,665–667,669–672 with tension
stress primarily responsible for the injury. Because the frac-
tures are characterized by disruption of the posterior and
anterior elements, they are potentially unstable. Injuries
secondary to tension result in longitudinal separation of the
FIGURE 18-73. (A) Hyperflexion injury in a 4-year-old. T12 is ante-
riorly crushed; but more important, it has a posterior (pedicle) frac-
ture as well as facet disruption and probable fracture. (B) Lateral
18. Spine
FIGURE 18-72. (A) Flexion injury of the thoracic
spine in a 10-year-old boy. (B) Complete tran-
section of the spinal cord.
posterior elements. Minimal if any anterior compression of
the involved vertebral body may occur in children. Voss et al.
reported three children with Chance fractures from the
same accident.671 All three had a different anatomic variant.
One was rendered paraplegic.
Neurologic injury appears to be infrequent in children
with this injury. Winter and Jani reported a child who pre-
sented with total paraplegia after a hyperflexion injury due
to a seat belt.672 The child subsequently had a complete
return of neurologic function.
Of 33 reported cases of Chance fracture in one study, only
8 occurred in adolescents and 1 in a young child.638 The child,
a 6-year-old, was treated with a body cast; at 7 months after
tomogram shows the fracture and dislocation. (C) Anterior tomo-
gram accentuates the disruption of both facet joints.
Specific Injuries 753

FIGURE 18-74. (A) Moderate crush of L3, with posterior extension (arrow). It is a variation of a Chance fracture. (B) Posteriorly displaced
Chance fracture (arrows) in a 5-year-old child.

A B
FIGURE 18-75. (A) This lateral film showing a Chance fracture neurologically intact. (B) Limited fusion and stabilization was
variant (T12–L1) was not obtained until 5 days after injury. The undertaken.
child had already undergone laparoscopy and laparotomy. He was
754 18. Spine

A B
FIGURE 18-76. (A) CT three-dimensional reconstruction of a Chance fracture in a 13-year-old girl. (B) MRI showing posterior soft tissue
disruption.

injury there was complete healing of the lumbar spine, full

range of motion, no evidence of instability in flexion or
extension, and no neurologic problems. It is interesting
that this case involved L4, whereas all other reported
Chance fractures involved L3 or above.768 Only Ritchie
and colleagues661 and Rogers et al.663 have reported other
young patients, between 10 and 14 years of age. An analogue
of the Chance fracture is a perched facet injury (see Fig.
18-73).
When the vertebral end-plate and growth mechanism are
involved, a progressive kyphotic deformity may ensue. It may
require surgical stabilization (Fig. 18-77).652

Injury to the Lumbar Spine

The lumbar region is infrequently involved in significant
injury until the adolescent period, when the maturing spine
assumes more of the biomechanical characteristics of the
adult spine.673,678,680,681 Minor and moderate wedge fractures
may be seen at all levels (Figs. 18-78 to 18-80). The region is
capable of significant translation with a fracture-dislocation,
thus increasing the likelihood of spinal cord or, especially,
nerve root injury.691 Physeal (end-plate) fractures may
involve the lumbar spine during adolescence. Such injuries
may lead to disruption of the interspace with progressive
fusion of the vertebrae (Fig. 18-81). Multiple lumbar frac-
tures are not uncommon, and MRI may be required to detect
occult lesions.686
Glass et al. assessed 35 children with lumbar spine
injuries.684 Most of them (27 of 35, 77%) were restrained by a FIGURE 18-77. Pedicle screw fixation of a Chance fracture in a
14-year-old boy.
lap-style safety belt. Abnormalities were not detected with
thick-section CT scans in 20 (57%) of the cases. Lumbar spine
radiographs must also be obtained in such cases.
Specific Injuries 755

FIGURE 18-78. (A) Lateral view of a mild compression fracture of L2 (arrow). (B) Anteroposterior view showing asymmetric crush (arrow).
This injury may lead to asymmetric growth and scoliosis.

A B

FIGURE 18-79. This 3-year-old girl climbed on the front of a family on the T2-weighted MRI scan suggested multiple vertebral involve-
entertainment center, which fell forward, causing a hyperflexion ment. Four years later she has had virtually no change in the
injury. (A) Multiple lumbar fractures are evident. (B) Focal edema shapes of L4 and L5 vertebral bodies.
756
FIGURE 18-80. Compression fracture of L5 in a lap seat-belted
8-year-old girl. Her aorta was also transected. This seemingly
innocuous fracture was associatd with complete paraplegia.
Burst fractures may occur in the lumbar area (Figs. 18-82,
18-83). The mechanism of injury is a compression force
transmitted directly along the line of the vertebral bodies.
One of the end-plates ruptures, and the disk is forced into
the body of the vertebrae, causing it to burst. The posterior
elements often remain intact. A fragment of the vertebral
FIGURE 18-81. (A) Irregular end-plates 7 months after hyperflexion injury. (B) Progressive narrowing 18 months after the injury. It should
not be confused with diskitis.
18. Spine
body or disk extending posteriorly, compromising the spinal
canal, may cause neurologic damage.
Children who sustain burst fractures at or before puberty
tend to develop mild progressive angular deformity at the site
of the fracture if not surgically stabilized. Operative treatment
achieves and maintains correction of the deformity, Non-
operative treatment of a burst fracture is a viable option in
neurologically intact children, but bony deformity (scoliosis,
kyphosis and body collapse) may occur. Residual deformity
following operative and nonoperative management does not
correlate with symptoms or function at follow-up.
Chatani et al. described a 16-year-old boy who had been
in a motor vehicle accident.679 The vertebral body of L4
was displaced anteriorly in front of L5; and the posterior
elements of L3 and L4 were split away from their respective
vertebral bodies and remained posteriorly.
Variations in developmental anatomy of the lumbosacral
junction may predispose to soft tissue and osseous injury that
may be associated with severe back pain.674,675,682,692,695,696
Some of the pain may be due to disk herniation at the level
of the radiologic variant or just above it.675,696
Acute pedicle fractures may occur685,690,694 They are usually
chronic in nature and represent stress fractures due to repet-
itive athletic activities.
Isolated fractures that involve the neural arch, facet, or
transverse process account for the remainder of stable
injuries.689,690,693 The most common mechanism of injury is a
direct blow. Facet and neural arch fractures are treated best
with an external support until evidence of healing is obtained
by clinical and radiographic evaluation. With fractures of the
transverse process, external support may or may not be used,
depending on the patient’s discomfort with activity.
Postural reduction is the best initial treatment. Pillows,
sandbags, pelvic slings, and various traction techniques may
be used, depending on the availability of equipment and the
type of fracture.
Specific Injuries 757

manipulation with or without the administration of

anesthesia is indicated. If the fracture remains unre-
duced following manipulation, open reduction should be
considered.

B
FIGURE 18-82. (A) Burst fracture with retropulsion of T12. (B)
During placement of the inferior hook and reduction a pedicle frac-
ture became evident. It may have been partial failure of the bone
due to the accident that was worsened by the procedure. The hook
was inserted at a lower level.

The effect of this initial treatment on the injury must be

carefully and frequently assessed by neurologic and radio-
graphic examination. The CT scan may be helpful for
predicting neurologic deficits.683 Changes are made in the
patient’s posture until reduction is achieved. If reduction
of the fracture is not adequate by postural methods, gentle
B
FIGURE 18-83. (A) Flexion injury of L1 in a 14-year-old girl. (B) MRI
showing retropulsion and cord/root injury.
758
FIGURE 18-84. Nonunion of a lumbar transverse process fracture.
Patients with minimal or no neurologic injury can usually
be fitted with external supports and allowed to ambulate if
acceptable reduction has been maintained for a period of
3–6 weeks. Paravertebral callus, when seen on roentgeno-
graphic examination, is helpful for determining the stability
of the fracture and the time when external supports may be
discontinued. Most fractures become intrinsically stable by
12 weeks; flexion and extension films should be obtained at
such time to determine soft tissue stability and any motion
within the fracture itself.
In prepubertal children, supports should be well padded,
removable, and utilized until most of the spinal growth has
occurred (14 years in girls and 16 years in boys). This
approach usually prevents progressive spinal deformity.
If nonoperative treatment fails because of instability or
progressive spinal deformity, operative fusion is indi-
cated.676,687 The surgical procedure (anterior, posterior, or
combined) and the type of internal fixation utilized, if any,
is best determined on an individual basis. Any nerve root
FIGURE 18-85. Spondylolysis of L5 in a gymnast.
18. Spine
impingement must be decompressed at the neuroforamina.
Postoperative immobilization in a spica cast that includes at
least one leg is often essential. Close follow-up of possible
growth deformity is necessary, particularly if the child is just
entering the adolescent growth spurt.
Patients with significant residual neurologic deficit, with
or without severe spinal deformity, continue to require
special care to obtain maximal independence in the com-
munity. Physical findings of decreased mobility and neuro-
muscular abnormalities are directly proportional to the
extent of the residual structural and neurologic damage.
Transverse and Spinous Process
Peripheral areas of the lumbar vertebrae may be injured.
The mechanism may be a direct blow or tensile avulsion.
Either may occur as an isolated injury or as part of a
more extensive fracture. The spinous process has a carti-
laginous cap that may be avulsed, or a fracture may occur
through the osseous portion of the spine. Similarly, the trans-
verse process may sustain an osseous or chondrosseous
fracture. In either instance the injury may progress to
nonunion (Fig. 18-84). Fragment excision is indicated only
for severe pain.
Spondylosis
A somewhat controversial topic is whether spondylolysis has
a traumatic etiology.696,701,703,708,710,711,713,716–722,724,725,730,733,735,
739–745,748
Wiltse and Jackson believe that most, if not all,
patients with spondylolysis (Figs. 18-85, 18-86) have a stress
fracture through the pars interarticularis.720–723,745,748 I agree
with this concept. Not every symptomatic patient has com-
plete bilateral spondylolysis. The pars may be attenuated
(plastic deformation) leading to a thin structure (Fig. 18-87).
Only one side may have a defect. Sclerosis (without fracture)
may occur that is probably reactive bone to subcortical
failure or stress in the pars.
In one study patients with unilateral spondylolysis had
reactive sclerosis and hypertrophy of the contralateral
pedicle.740 This study pointed out the importance of differ-
FIGURE 18-86. Bilateral spondylolysis in an anatomic specimen.
Specific Injuries 759

FIGURE 18-87. (A) Attenuated pars. (B) Contralateral spondylolysis.

entiating pars injuries from osteoid osteoma and, further- Restriction of vigorous athletic activity is essential until the
more, that the unilateral hypertrophy was probably a physi- lesion has healed.707,715,746 Use of a brace may alleviate symp-
ologic reaction to stress from the contralateral unstable toms.723,731 In the study by Letts and colleagues, the lesion
neural arch. The increased sclerosis may make this region was bilateral in 4 patients and unilateral in 10.730 Five of the
susceptible to subsequent failure if the evocative forces unilateral lesions healed with immobilization in a thora-
continue.704–706,712,727,738 columbar orthosis. In none of the patients with bilateral
Miyake et al. analyzed facet orientation in the lumbar lesions or the other five unilateral lesions did healing take
spine in 144 boys without pars defects and 104 boys with pars place, despite 3 months of similar immobilization.
defects.732 They found no difference in growth in the two
groups up to 13 years of age. After that age, however, the
Spondylolisthesis
growth of the facet joints in patients with a pars defect was
significantly retarded. Miyake et al. thought that the facet When failure (spondylolysis) has involved both sides, the risk
changes were due to altered development as the defect of a progressive spondylolisthesis then arises (Figs. 18-89,
developed and were not the cause of the defect.
There is a potential inability of the posterior elements
of the lower lumbosacral vertebrae to respond appro-
priately to stress, leading to fracture of the pars inter-
articularis in adolescent athletes.714,723,726,728 Repetitive
training and competition exercises involving flexion-
extension of the lumbar spine stress this region. In vitro
cyclic stress loading easily produced fractures of the pars inter-
articularis after approximately 1500 cycles of applied force
involving a vertebral column taken from a 14-year-old
child.716,717
Jackson et al. described the condition in young athletes
(adolescents).721 In a study of 100 female gymnasts, 11 had
radiologically evident spondylolysis, 6 of whom also had at
least a grade 1 spondylolisthesis (Fig. 18-88).702 Of the 89
without radiologic disease, 19 had episodic lumbar pain. Low
back pain in any young athlete should be a warning
sign.697,698,707,737
A routine lumbosacral spine series, which should include
oblique views, does not necessarily rule out a developing pars
defect. A technetium bone scan is a valuable tool for diag-
nosing these lesions.736 In unusual circumstances of chronic
pain and a negative bone scan, a single-photon emission
computed tomography (SPECT) scan may delineate the
presence and level of injury.697,699 CT scans may also be FIGURE 18-88. Traumatic spondylolisthesis in an adolescent
beneficial.729 gymnast. Bilateral spondylolysis is also present.
760 18. Spine

A B

FIGURE 18-89. (A) Spondylolisthesis that became symptomatic in a football player. (B) MRI showing stenosis.

18-90), especially if the evocative activity (e.g., gymnastics)
is continued.702,709,734,747 This posttraumatic spondylolysis/
spondylolisthesis progression tends to be painful, in contrast
to congenital spondylolisthesis. Spondylolisthesis has also
been reported on the newborn, although a difficult delivery
could not have been considered the cause.700
Stress Fractures
Other areas may sustain stress fractures without developing
spondylolysis. Unilateral stress fracture may occur in the
pedicle (Fig. 18-91). Another variation is a stress fracture in
the pedicle with a laminar fracture on the opposite side.
Lumbar Apophyseal Injury
Avulsion of the posterior portion of the lumbar end-plate
(apophysis) is being increasingly recognized as a cause of
low back pain in adolescents (Figs. 18-92 to 18-96).749–795
The apophyseal lesion represents a type 3 or type 4 growth
mechanism injury in which a portion of the disk and ring
apophysis, with or without an accompanying “metaphyseal”
fragment, is displaced posteriorly into the spinal canal (Fig.
18-95). This fragment then variably impinges on the lum-
bosacral roots.
Because of the association of the injury with sports such
as gymnastics and weight lifting, attention is often directed

FIGURE 18-90. Traumatic spondylolisthesis in a 10-year-old fol-

lowing a tobogganning injury. FIGURE 18-91. Pedicle stress fracture.
Specific Injuries
FIGURE 18-92. (A) Posterior epiphyseal injury
that may mimic disk herniation. It is a type 3 or
type 4 growth mechanism injury of the inferior
end-plate. (B) Appearance of undisplaced pos-
teroinferior ossification (arrow).
to more common causes of pain (e.g., Scheuermann’s
disease), which may precede or coexist with an avulsed frag-
ment (Fig. 18-93). The uniform complaint is back pain. It is
rarely accompanied by associated sensory or motor loss.
Ikata et al. reviewed 37 patients under 18 years of age
who had lesions of the lumbar posterior end-plate.767 All
but one were active in sports, and most were seen for
back pain. Abnormalities were most frequent at the
inferior rim of L4 and the superior rim of the sacrum.
Adjacent intervertebral disks showed a decrease in signal
intensity. Ikata et al. thought that the posterior end-plate
lesion should be regarded as a vertebral nonarticular
osteochondrosis.
When there is a fracture of the lumbar vertebral apoph-
ysis, CT scanning is the ideal diagnostic test (Fig. 18-94), as
it is sometimes difficult to see the osseous portion on a lateral
film. The CT scan shows the size of the fragment and the
extent of canal compromise. Experimental end-plate frac-
tures are extremely difficult to visualize.
Surgical excision is recommended. Otherwise, the dis-
placed lesion may heal to the vertebral body, effectively
narrowing the spinal canal by causing spinal stenosis
(Fig. 18-96).
A usual version of an apophyseal/synchondrosis injury
is shown in Figure 18-97. The vertebral centrum may be
rotated away from the superior end-plate and the neuro-
central synchondroses.73,677 This is also illustrated in a
primate “child abuse” case (Fig. 18-30), and a cervical injury
(Fig. 18-65). This injury pattern may be more frequent than
we realize because of the diagnostic difficulty.
761
Disk Herniation
Acutely herniated disks are unusual in children under 16
years of age (Fig. 18-98). Fewer than 200 disk protrusions
have been reported in patients 16 years of age or
younger.796–838 Trauma appears to play an important etiologic
role in lumbar disk herniation in the child or adolescent.
Such trauma may result from contact sports, a fall, or an
automobile-related injury. Noncontact sports such as weight
lifting have also been implicated. There may be an accom-
panying fracture of a portion of the vertebral end-plate
because of the dense attachments of the annulus, and this
structure (rather than the disk) may be the cause of any
block.
It is uncommon for children with lumbar disk (or end-
plate) protrusions to have the usual signs and symptoms asso-
ciated with comparable adult disk herniation. Low back pain,
limitation of motion on forward flexion, a peculiar gait, and
limitation of straight-leg raising are common signs. Pain is
not a prominent complaint. Neurologic findings are rare.
The physician should be aware of congenital deformities of
the posterior elements.
A delay in diagnosis often occurs because many of these
patients have pain in the lower limb, rather than in the back.
In one study discrete clinical neurologic changes were found
in only 19 of 55 patients.823 This low incidence of nerve root
compression is in agreement with the findings of other
reports and probably represents (1) significant resistance of
maturing neurologic tissue to nerve root compression and
(2) the lack of chronic impingement through osteophyte
FIGURE 18-93. Attention to a Scheuermann’s lesion (solid arrow)
led to the diagnosis of this lesion as the cause of back pain. The
real cause was a displaced end-plate fracture (open arrow) in this
teenage weight lifter.

FIGURE 18-94. (A) Displaced end-plate fragment (arrow). (B) CT

scan of the injury (arrow).

FIGURE 18-95. (A, B) Histopathology

of end-plate avulsions surgically
excised. (B) Note that the physeal sep-
aration (arrow) extends into the frag-
ment.

762
Spinal Cord Injury
FIGURE 18-96. Lateral view of 24-year-old football player/weight
lifter with chronic back pain since adolescence. The posteriorly dis-
placed end-plate healed in its canal position, causing stenosis.
formation in addition to the disk material. Secondary
changes in the nerve, over time, may predispose it to greater
reaction to acute injury.
Magnetic resonance imaging may be utilized to evaluate
adolescent disk herniation (Fig. 18-98). Gibson and asso-
ciates noted that 15 of their 20 patients had multiple disk
abnormalities, which suggested that there was an underlying
diasthesis in those patients who developed disk herniation,
a finding that is certainly compatible with progressive
multiple-level involvement in adults.811
Lorenz and McCulloch reported the use of chemonucle-
olysis for herniated nucleus pulposus in adolescents, utiliz-
ing the procedure in 55 patients between the ages of 13 and
19 years.823 The procedure was considered an alternative to
diskectomy and was performed only after the patient failed
to respond to previous conservative management. One
patient had an anaphylactic reaction. Chemonucleolysis did
not relieve the symptoms in 11 of the 55 patients, all of whom
subsequently required surgical excision of the disk. Of the
remaining 44 patients, 27 had no subsequent back pain. The
other 17 had occasional backaches but did not require any
specific or prolonged treatment.
Injury to the Lumbosacral Region
The regions of major motion capacity change (i.e., the
thoracolumbar and lumbosacral junction) may be sites of
increased susceptibility to injury, often seemingly innocuous
at the onset. This is especially true at the lumbosacral junc-
tion, where anatomic variations may predispose to debilitat-
ing pain (Figs. 18-99, 18-100).
A rare injury involves facet dislocation at the L5–S1 junc-
tion.847,853 This trauma pattern is usually associated with
cervical injury but may also occur in the thoracolumbar
junction and lumbar vertebrae. The cervical facet obliquity
predisposes to subluxation, but the lumbar facets are more
vertical. Disruption of part of the facet joints by fracture
probably contributes to the injury mechanism.
763
Berguiristain et al. described a 5-year-old boy with a trau-
matic L5–S1 dislocation (traumatic spondylolisthesis).839 No
fracture was evident. Eight years later no significant defor-
mity was evident.
Injury to the Sacrum and Coccyx
Injuries to the sacrum and coccyx are infrequent (Figs.
18-101, 18-102) and are usually produced by direct vio-
lence.840–842,844,846,849,852 They may be difficult to recognize
radiographically because of the patterns of ossification in the
region.843 Neurologic damage must be assessed carefully.850
Treatment should be symptomatic, even if displaced.
Involvement of the sacroiliac joint is covered in detail in
Chapter 19. Sacral injuries (Fig. 18-103) often accompany
pelvic fractures. Regular CT views are best for visualizing
them.
Stress fractures of the sacrum may also occur (Fig.
18-104).844,845,848,851
Spinal Cord Injury
Injury to the Spinal Cord
Injury without fracture or open injury may result in concus-
sion, contusion, infarction of the cord, or anterior spinal
cord damage.868,870,873,874 This condition is often referred to as
SCIWORA: spinal c ord injury without obvious radiologic
abnormality.860,867 The mechanism of injury is a matter of
conjecture. Most likely a displaced type l injury of a carti-
laginous end-plate springs back into position and heals with
no or few radiographic signs (Fig. 18-105). Another possible
mechanism for this particular injury of the young spine is
that the excessive mobility may stretch the spinal cord over
a hyperextended or hyperflexed region (even fractured but
spontaneously reduced) and contuse the anterior portion of
the cord (Fig. 18-106), similar to the mechanism in the more
rigid spine of an adult. Children with complete paraplegia
who have no radiographic signs of injuries may have asso-
ciated rib fractures or a fractured spinal transverse process.
Paraplegia may be spastic or flaccid. Spinal cord injury has
been reported in the newborn following umbilical artery
catheterization.859
Fewer than 5% of patients with traumatic paraplegia are
children.854–857,863,866,872,875,879,882,908,918,923 The decreased fre-
quency of concomitant spinal cord injuries does not mean
that childhood back injuries should not be taken seriously.
The child’s spine is more mobile than that of the adult, so
force is more easily dissipated over a greater number of seg-
ments. It is interesting that cord injury without evident frac-
ture, which is rare in adults, represents about one-fourth of
all injuries in children with neurologic damage. This obser-
vation is especially evident with cord injury in the neonate
and with that caused by child abuse. The efficacy of steroids
in lessening the extent of injury has not been adequately
assessed in children.858 Similarly, acute laminectomy may not
be particularly helpful in the child.865
Because of the lack of radiologic findings, it is imperative
to proceed with further evaluation. MRI offers the best
method for detecting occult fractures, cord injury, and
hematoma.861,869,876 MRI evaluation is also important in brain-
 764
A
injured children.871 Children with head trauma may also
have an injured cord. The diagnosis may be difficult if not
impossible by routine methods. MRI is also useful for detect-
ing posttraumatic lesions such as spinal cord cysts.862
Vertebral or spinal cord damage should be suspected in
any unconscious child with an injury that is likely to cause
flexion or rotation of the spine, in the awake child who com-
plains of loss of sensation or motor power below a transverse
level of the body, and in any injured child who complains of
localized vertebral pain or tenderness or of pain radiating
along radicular distributions. Examination must be done
without moving the possible areas of spinal column instabil-
ity. Intubation in a child with a cervical spine injury is best
accomplished via the nasotracheal route, and tracheostomy
18. Spine
FIGURE 18-97. (A) Apparent posterior dis-
placement of T12 posterior to T11. (B) MRI
suggests an apophyseal separation. (C)
CT scan shows fracturing through the neu-
rocentral synchondroses.
B
may be indicated if intubation cannot be accomplished
without extending or manipulating the neck.
Spinal shock and the resulting loss of sympathetic vaso-
motor tone may complicate a general evaluation and mimic
the symptoms of shock from internal bleeding.877 Rapid
restoration of normal blood pressure is essential to preserve
cord function and may be accomplished by vasoconstrictors
or blood volume expanders. A subsequent drop in blood
pressure suggests blood loss rather than loss of vasomotor
tone, and the source should be sought in the abdominal
cavity, thoracic cavity, pelvis, or fracture in an extremity.
Abdominal reflexes may be absent, and guarding or com-
plaints of abdominal pain may not occur in the patient with
a high cord lesion.
Spinal Cord Injury 765

suggested, but that the general outcome was good, with a

favorable prognosis most likely when admission evaluation
showed good hand function, hyperesthesia, Lhermitte’s
sign, and normal perianal sensation.864 Lhermitte’s sign is
a sudden, shooting paresthesia or paresthesia-like electric
shocks spreading down the body or into the limbs on flexion
of the neck.

FIGURE 18-98. MRI of a herniated nucleus pulposus in a 12-year

old gymnast.

Spinal cord injury associated with spinal shock may

produce urinary retention and overdistension of the
bladder, which may be avoided by using an indwelling
catheter.899,902 Recovery from spinal shock is usually accom-
panied by the development of autonomic micturition. If
urinary tract infection has been avoided and sphincter tone
remains intact (i.e., the level of injury is above S2), inter-
mittent catheterization has proved to be a reasonable means
of achieving socially acceptable continence. The older
paraplegic child may be instructed in the technique of
self-catheterization. For the quadriplegic and younger para-
plegic child, instruction of a family member, usually the
mother, may be accomplished with relative ease. The low rate
of urinary tract infection associated with intermittent
catheterization has been well documented. Pharmacologic
and surgical methods that increase bladder capacity without
causing loss of external sphincter tone are available but not
necessarily applicable in each involved child.906,909 Such pro-
cedures may enable the child to attend a full day of school
without undue concern. Bowel control is relatively easy to
accomplish by means of diet and the use of suppositories. All
the complications of flexor spasm frequently seen in patients
with high cord injury are due to facilitation of local reflexes.
Overflow into visceral channels may also produce a “mass
reflex” phenomenon. This reflex phenomenon remains one
of the least understood areas of spinal cord injury manage-
ment. Dorsal myelotomy and sectioning anterior roots have
not been consistently useful for this condition.907,917 No avail-
able pharmacologic agent has proved useful in the more dif-
ficult cases. Variable success has been reported with a variety
of agents in the less severe forms of the disorder.
Merriam and associates reviewed 77 patients with trau- FIGURE 18-99. (A) Partial sacralization of L5 (arrow). (B) This girl
matic central cord syndrome and found that atypical fell a few months later during a gymnastics routine, developing
variations were more common than the existing literature severe pain, spasm, and scoliosis.
766 18. Spine

FIGURE 18-100. Painful partial sacralization of the right side of L5

in a 15-year-old female softball pitcher.

FIGURE 18-102. Displaced sacral fracture in a 10-year-old girl who

fell from a ski lift.

FIGURE 18-103. (A, B) CT views of sacral fractures (arrows) com-

FIGURE 18-101. Anteroposterior (A) and lateral (B) views of a dis- plicating pelvic injuries.
placed sacral fracture (arrow).
 Spinal Cord Injury 767

siderable variation in the extent of initial damage. One study

reported 31 such children, 18 of whom died. Most of the
patients survived long enough to be admitted to the hospi-
tal, presenting with symptoms of incomplete hemiplegia
(almost 50%).
With complete cord lesions, with or without fracture, the
incidence of spinal deformity, lordosis, kyphosis, or scoliosis
is higher when the lesion involves the upper thoracic or cer-
vical regions. There is muscle imbalance, the onset of para-
plegia is early in life, and laminectomy is often performed.
Bracing is difficult, and spinal fusion is usually required.
Because progressive angular kyphosis may damage cord
functions in partial lesions, early fusion is usually indicated.
With extensive thoracic and lumbar lesions, it may be nec-
essary to use appropriate instrumentation.
Autonomic dysreflexia is a syndrome that occurs in
A patients with spinal cord lesions at or above the sixth tho-
racic level. It is characterized by exaggerated autonomic
responses to stimuli that are usually innocuous in unaffected
persons. The spinal cord lesion is above the sympathetic
splanchnic visceral outflow. The stimuli that may initiate the
reflex include bladder or bowel distension, visceral inflam-
mation, skin irritation, and pain. The initiating afferent
stimuli travel to the spinal cord and trigger a gross sym-
pathetic reflex in the caudal stump. Sympathetic efferent
motor fibers complete the reflex and cause arteriolar spasm
of skin and splanchnic vessels, resulting in severe paroxysmal
hypertension. Vasomotor and sudomotor activity below the
level of the cord lesion are caused by other efferent sympa-
thetic fibers. Marked hypertension may be associated with a
sudden rise in intracranial pressure and may lead to severe

FIGURE 18-104. Stress fracture of sacrum. (A) CT scan showing a

stress fracture. (B) MRI showing extensive changes of altered
signal intensity due to interosseous edema.

It seems to be widely assumed, in classic central cord syn-

drome, that the anatomy and neurophysiology of the human
spinal cord are accurately known. This is far from true in
children who are still in variable stages of neurologic devel-
opment, maturation, and acquisition of various reflex path-
ways. The extent of a given central cord injury cannot always
be anatomically deduced, and the degree of permanent
neurologic deficit varies considerably.
Infarction results in complete, permanent, flaccid para-
plegia below the mid-thoracic level.870,877 The blood supply
of the thoracic cord depends significantly on the artery of
Adamkiewicz. Anastomosis of the spinal vessels between the
first and eleventh intercostal arteries is highly variable and
may result in infarction of a major portion of the cord (Fig.
18-106). Because the whole cord is malfunctioning the para-
plegia is flaccid, in contrast to spastic paraplegia, which is
produced by a segmental lesion.
With thoracic injuries the prognosis for recovery is
essentially nonexistent. Most of these injuries are fracture- FIGURE 18-105. Fatal thoracic end-plate injury (arrow). Note that
dislocations. It may be assumed that the cord is severely the hemorrhage in the spinal cord extends several levels above
damaged or transected initially. Cervical injuries show con- and below the fracture.
768
headaches. The vasodilatation above the cord lesion also
leads to hyperhidrosis, most often on the forehead, and
vasodilatation of the nasal mucous membranes, resulting
in nasal congestion. Infants and toddlers, if not older chil-
dren with relatively early onset of SCIWORA, may be pre-
disposed to develop latex allergy similar to children with
myelodysplasia.
Late Sequelae
Spinal injury prior to the completion of vertebral growth
may lead to unequal growth and progressive defor-
mity.880,883,886,888,989,892,894,896,898,904,905,910–912,919–922 Theoretically,
premature asymmetric epiphyseal (end-plate) closure com-
parable to epiphyseal injuries in the appendicular skeleton
is responsible for the unequal growth. With lateral wedge
compression fractures in children, mild scoliosis is the rule
and significant nerve damage and progression are the excep-
tions. In one study, any residual of anterior wedge compres-
sion fractures incurred by adolescents was difficult to find
radiographically at follow-up averaging 16 years, leading
18. Spine
FIGURE 18-106. MRI of the cervical cord of a 2-
year-old child injured in a vehicular accident. (A)
Spinal cord hemorrhage (arrow) at 48 hours. (B)
Axial view of hemorrhage (arrows) at 48 hours.
(C) Appearance at 5 days (arrow). (D) At 5
weeks. Resolution of hemorrhage reveals
partial cord transection (arrows). The little girl is
left with a complete C5 paralysis.
to the conclusion that unequal growth from an epiphyseal
injury was rare.60 However, other studies and my own expe-
rience show that vertebral height is not always completely
restored. Osseous bridging may also occur.
Although injury to the vertebral column that results in
cord damage is not common in the young child or adoles-
cent, when it does occur the effect of continuing growth on
subsequent behavior of the fractured vertebral column must
be considered. The normal growth rate slows to a steady rate
after the age of 3 years until the growth spurt of puberty.
Griffiths followed a boy who initially had a cervical injury
at the age of 8 years, with an incomplete Brown-Sequard
lesion.897 His initial injury was a flexion type, with fractures
through the vertebral bodies of C3, C4, and C5. Approxi-
mately 2 years later he began to show evidence of a kyphotic
deformity. Four years after the injury his gait pattern was
deteriorating, and both of his legs showed increasing spasm.
Again, a further degree of kyphosis was noted. Surgery was
refused. Postmortem examination showed well-preserved
disk spaces without evidence of anterior callus formation
compatible with an attempt at spontaneous fusion. On the
Spinal Cord Injury
basis of the experience in this case, Griffiths subsequently
treated fractures with an anterior cervical fusion when he
found them in the young adolescent. I disagree. Posterior
fusion is probably a more appropriate approach in the
skeletally immature individual. The posterior elements are
relatively mature in mid-childhood, whereas the anterior
end-plates may grow until late adolescence.
Deformation of a vertebral body may result in angular
deformity. The most frequent deformities are kyphosis, sco-
liosis, and kyphoscoliosis. More than a 30% loss in anterior
height has the potential for an increasing late deformity, as
there may be unrecognized disruption of the posterior ele-
ments (i.e., the interspinous ligaments) and unrecognized
(occult) end-plate injury similar to that described in long-
bone physeal injuries. Alterations in vertebral body shape
and deformities below the site of injury are probably the
result of unequal pressure that results from neuromuscular
imbalance during normal epiphyseal growth.
The late onset of progressive neurologic deficit is
usually associated with the extension of a posttraumatic
syringomyelia (Fig. 18-107) or the development of a kypho-
sis or scoliosis with associated cord injury.881,887 Because both
lesions are potentially surgically correctable, early diagnosis
is indicated to avoid further extension of an already disabling
injury.
The effects of acquired neuromyogenic disorders are
determined by the level and degree of spinal cord injury
and the age of the patient at the time of injury. The
relentless progression of spinal deformity in the untreated
pediatric patient with acquired paraplegia exemplifies the
effects of asymmetric muscle tension and spasm, fascial con-
traction, chronic posturing, and gravity on the unsupported
growing spine. Almost any combination of deformities is
possible. Pelvic obliquity, which may result from contracture
above and below the pelvis, makes treatment even more
difficult.893,922
FIGURE 18-107. (A) Edema 36 hours after
injury. (B) Four months later a syrinx is
evident. A B
769
After management of the acute episode of spinal cord
injury, an orthopaedist’s primary concern is prevention
of subsequent spinal deformation. In a detailed review of
64 juvenile patients who were followed for more than 6
months after injury, spinal deformity, scoliosis, kyphosis, or
lordosis were noted in approximately 91%. Girls up to 12
years and boys up to 14 years who had cervical or thoracic
injuries developed significant spinal deformity with pelvic
obliquity, which may lead to a loss of sitting balance that
requires the use of the upper extremities for trunk support,
pressure sores on the ischium, and subluxation or disloca-
tion of the hip on the “high” side of the pelvis.893,922 Children
with lumbar lesions are less apt to develop significant
spinal deformity, especially one requiring surgical interven-
tion. Most patients with scoliosis had complete lesions, and
almost all of those with incomplete lesions had minimal
return of function. Scoliosis was the most frequent primary
spinal deformity noted. Kyphosis was generally thoracolum-
bar, and lordosis was either thoracolumbar or lumbar.
Pelvic obliquity did not accompany primary kyphosis or lor-
dosis. When it occurred with the scoliosis, it frequently
impaired sitting balance. Nonoperative treatment of spinal
deformity, employing external support, should be initiated
when the potential for spinal deformity exists. In young
children it should be prior to radiologic evidence of fixed
deformity.
Spinal deformity per se is not an indication for surgery
except in an immature patient with a progressive posttrau-
matic deformity despite bracing or a deformity of more than
40°.902 The goals of surgical treatment are to prevent increas-
ing deformity and its sequelae, relieve the symptoms of
mechanical instability, improve spinal alignment through
correction of the deformity, and reverse (or at least halt)
increasing neurologic dysfunction.
Scoliosis following hyperflexion injury is probably also
due to open epiphyses. The development of scoliosis is
770
most likely related to unequal compression of the vertebral
end-plates. This condition probably causes an incomplete
cessation of longitudinal growth or asymmetric stimulation
of epiphyseal growth. These processes may continue.
This slowing or stimulation of osseous development in the
patient who has a stable spinal fracture without neuromus-
cular deficit also explains why the scoliosis is only mildly
progressive.
With scoliosis due to acquired paraplegia, the currently
used principles and techniques of instrumentation are
applicable. If there is also pelvic obliquity and lumbar kypho-
sis or lordosis, the fusion mass must extend proximally at
least two levels above the injury and distally as an inter-
transverse process fusion of the sacrum. Cotrel-Dubousset,
TSRH, or unit rod instrumentation, as well as a number
of other instrumentation systems, offer a stable fixation
method. It may be necessary to release the lumbodorsal
fascia, iliotibial band, or periarticular hip joint contractures
preoperatively.
When there is radiologic evidence of progressive spinal
deformity in the growing child receiving nonoperative treat-
ment, surgery should be considered. Posterior spinal fusion
was the surgical procedure of choice for scoliosis. The fusion
should extend to the sacrum to prevent pelvic obliquity,
which is a consistent finding in those patients with fixed sco-
liosis. Instrumentation of the lumbosacral joint with either
the transsacral bar or an enlarged sacral alar hook is desir-
able. Pseudarthroses may be common, indicating the need
for extensive lateral exposure and decortication to the ends
of the transverse processes.
With progressive kyphosis, when the deformity exceeds
60° and appears rigid, Kilfoyle and colleagues recommended
anterior spinal fusion at the apex of the deformity, followed
by a posterior spinal fusion with compression rods.906 This
decision was based on the frequent observation of loss of
correction or pseudarthrosis formation at the apex of the
kyphotic deformity when only one procedure was used. Pro-
gressive lordotic deformity, which generally includes the
lumbosacral joint, may be satisfactorily corrected and stabi-
lized by posterior spinal fusion. However, when lordosis is
severe or more than 100°, rigid anterior spinal fusion is
probably a better approach, but it must be appended with a
posterior fusion, as anterior extension to the sacrum is not
possible.
In addition to treating the deformity, bracing improves
function by restoring sitting balance and freeing the upper
extremities for activities other than trunk support. Any
orthoses must be well padded to protect the anesthetic skin,
easily removable to allow frequent skin checks, and easily
adjustable to allow for growth. A thoracolumbosacral ortho-
sis brace is best here and should be used in all patients with
spinal lesions above T10. For the levels below T10 a remov-
able axillary-level, high-body jacket is used. Nonoperative
treatment is more apt to be successful in the older child with
a scoliotic deformity than in the patient with kyphosis alone.
Failure usually is seen in the uncooperative patient and in
those with moderate or severe spasticity.
The paraplegic and less often the quadriplegic patient is
at risk of developing pathologic fractures in the osteoporotic
bone.901 These fractures may be difficult to detect because
of loss of symptoms such as pain. The increased emphasis
18. Spine
on sports for the disabled (e.g., wheelchair sports) may
increase the likelihood of extremity injury in the involved
child or adolescent. Fractures may heal with significant
amounts of heterotopic bone, particularly if spasticity is
present.895,913,914,924
Patients with a spinal cord injury have lower bone densi-
ties (compared to their nondisabled peers) ranging from
56% to 65% of normal.878,885,891,900,903,915 Those with a history
of fractures have significantly lower bone density.
Great care must be taken to observe the hips carefully so
subluxation or dislocation does not occur.922 Growth abnor-
malities are more subtle in their presentation. Myelotomy or
rhizotomy may relieve some of the spasticity that contributes
to these structural contractures.907 Botox or baclofen may be
effective in the young patient and the adult.
The patient with loss of sensation following cord injury
is uniquely vulnerable to the development of decubiti.
Irreversible local necrosis may be seen after only 3–4 hours.
The use of mattresses designed to distribute pressure areas
is helpful for preventing decubiti, but the most important
factors are frequent turning and good skin care.
Development of a decubitus ulcer may delay rehabilitation
weeks or months. The injury frequently occurs during the
first few hours after admission, when the attention of the
medical and nursing staff is directed to other matters. Early
and continued attention to this important parameter of
nursing care provides incalculable benefit for long-term
management of these patients.
Chao and Mayo followed 40 children with spinal cord
injury with an average age at presentation of 9 years and a
mean follow-up of 4 years.890 There were 2 cervical, 13 tho-
racic, and 5 lumbar injuries. Bladder management included
11 patients with reflex voiding and 29 patients given
combined anticholinergic medication with intermittent
catheterization. Video-urodynamics showed good function
and preservation of the urinary tract in 25 of 28 patients.
Failure was equated with noncompliance to the recom-
mended voiding regimens. The authors recommended
annual renal ultrasonography and video-urodynamic studies
every 1–2 years.
Physical therapy should be directed at maximizing
function by preventing contractures and by the use of
braces and assistive devices. In general, physical therapy
should be combined with a program of occupational therapy
aimed at making the child independent in the activities of
daily life. Early enrollment in a rehabilitation program
is instrumental in a child’s rapid return to family and
community.
Triolo et al. have applied functional neuromuscular stim-
ulation to children with spinal cord injuries.925 They found
that the procedure required a major commitment from the
patient and family but when used selectively improved the
patient’s standing, walking, and hand grasp.884
Obvious causes of treatment failure include (1) incom-
plete reduction; (2) incorrect assessment of stability with
resultant insufficient quality and duration of spinal orthotic
protection; and (3) neglect of patients with skeletally stable
injuries but a cord deficit.
Assimulation back into the family and school is not easy.
A team effort and counseling are often appropriate. The
willingness to return to school varies remarkably.916
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788
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869. Schwartz A. Spinal cord infarction: MRI and MEP findings in
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871. Sneed RC, Stover SL. Undiagnosed spinal cord injuries in
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872. Sneed RC, Stover SL, Fine PR. Spinal cord injury associated
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873. Tator CH. Review of experimental spinal cord injury with
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874. Tator CH, Fehlings MG. Review of the secondary injury theory
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875. Wilberger JE Jr. Spinal Cord Injuries in Children. Mount
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876. Wittenberg RH, Boetel U, Boyer HK. Magnetic resonance
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878. Abramson AS. Bone disturbances in injuries to the spinal cord
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19
Pelvis
Engraving of immature hemipelvis. (From Poland J. Traumatic Sep-
aration of the Epiphyses. London: Smith, Elder, 1898)
he child’s pelvis is a complex structure that includes
T the termination of the spine (sacrum and coccyx). Mul-
tiple growth regions are present throughout the devel-
oping pelvis. These regions are the equivalents of the
epiphyses of the long bones. Secondary ossification within
these epiphyses and apophyses may be confusing when eval-
uating the possibility of fracture. These regions certainly may
be fractured at the chondro-osseous interface to create a
physeal injury.
The developing pelvic bone, especially the ilium, may be
quite flexible, a factor that allows considerable deformation
without obvious fracture. Rebound following deformation
may create a false sense of security when evaluating the
extent of injury. Such deformation also puts contained soft
tissue structures at risk for injury. The potential for urethral,
790
gynecologic, bladder and rectal injuries must be assessed
carefully, even when the radiologic appearance of the pelvis
does not suggest severe injury.
Anatomy
Each hemipelvis initially forms from three primary centers
of ossification located within the chondral anlagen of the
ischium, pubis, and ilium. The primary ossification centers
of these anlagen converge within the acetabulum to delin-
eate the triradiate cartilage (Fig. 19-1). The triradiate carti-
lage is a composite of the epiphyses of three contributing
anatomic (embryologic) structures that comprise each
hemipelvis.5,6 The particular chondro-osseous interrelations
allow continual integrated growth and hemispheric expan-
sion of the acetabulum commensurate with the progressive
spherical growth of the capital femoral epiphysis. During
adolescence secondary centers of ossification develop within
the “arms” of the triradiate cartilage (Figs. 19-2, 19-3). These
arms should not be misconstrued as fracture fragments
during the evaluation of a pelvic injury during childhood or
adolescence (Fig. 19-4). This modified growth region (trira-
diate cartilage) normally undergoes physiologic epiphy-
siodesis at approximately 12–14 years in girls and 14–16 years
in boys. Damage to the triradiate growth mechanism may
lead to deformity of the acetabulum (e.g., a shallow acetab-
ulum), especially if such an injury occurs in a young child
(under 10 years of age).
Within each arm of the triradiate cartilage the physeal car-
tilage is bipolar, being directed toward two of the three com-
ponent pelvic bones. The germinal zone runs along the
central portion of each arm. Small blood vessels are also
present within this central region of the cartilage. Extending
from the central germinal zone toward each metaphysis are
the dividing and hypertrophic zones. These zones are not
as wide as they are in longitudinal bones, reflecting the
less rapid rates of endochondral ossification occurring
within the triradiate physes. The capacity for continued
growth and endochondral ossification within this structure
may be damaged by certain fracture patterns.
The intrapelvic side of the triradiate cartilage is covered
by perichondrium and a thick layer of fibrous tissue.6
Anatomy
FIGURE 19-1. Anterior (A) and lateral (B) developing pelvis,
showing relative areas of bone (white) and cartilage (stippled).
IL = ilium; IS = ischium; P = pubis; S = symphysis pubis; T = trira-
diate cartilage. (C) Exploded view to emphasize analogy of each
component bone to a long bone and how several “epiphyses” fuse
to form the triradiate cartilage. Similar “epiphyseal” fusions form
the ischiopubic junctions and the symphysis pubis. E = epiphysis;
M = metaphysis; D = diaphysis.
FIGURE 19-2. Early developmental patterns of the triradiate carti-
lage. (A) Duplication of the standard anterior view of the acetabu-
lar segment and composite bones from the pelvis of a stillborn
791
Traumatic stripping of the periosteal attachments in this
region may result in abundant formation of callus and can
contribute to the intrinsic stability. Because of such
periosteal tissue this region may rapidly form a small or large
osseous bridge if injured.
The composite radiolucency of the two superior arms of
the triradiate cartilage is usually visualized on the standard
anteroposterior roentgenogram of the pelvis. However, the
appearance of the triradiate cartilage is shown best by a
direct roentgenogram through the acetabulum (Figs. 19-2,
19-3). In the clinical setting, such a roentgenogram is diffi-
cult to obtain because of the obliquity of the acetabulum
and the superimposed presence of the capital femoral ossi-
fication center. Routine internal and external oblique
roentgenograms (e.g., Judet views105) may assist in visualiz-
ing different portions of the triradiate cartilage, allowing
reconstruction of the entire unit for diagnostic or follow-
up purposes. Computed tomography (CT) may also offer
improved three-dimensional reconstruction of the region. It
is important to understand the anatomy of this cartilage, as
it represents the “epiphyseal” ends of the iliac, pubic, and
ischial rami and may be variably disrupted when these bones
are also fractured in other anatomic regions. The seeming
absence of a concomitant fracture in a childhood single-
ramus injury, in contrast to the double-ramus concept in
adults, may be explained by the fact that a physeal injury
(separation) may also be present at the triradiate cartilage,
the cartilage of the pubic symphysis, or the ischiopubic syn-
chondrosis. If displacement is minimal (or even occult),
such an injury pattern may be virtually impossible to detect
by routine radiography.
The anatomic os acetabuli (i.e., the equivalent of
secondary epiphyseal ossification centers) appear within
the triradiate cartilage when the child is 12–14 years
of age and fuse by 16 years. These secondary centers
coalesce with the peripheral radiographic os acetabulum
neonate. Note the extent of the acetabular, A, and triradiate, T, car-
tilage. (B) Direct view of acetabulum to show the true appearance
of the triradiate cartilage.
792 19. Pelvis

(Figs. 19-4, 19-5), which is a normal secondary ossification

center located along the margins of the acetabulum.5,7,8 The
peripheral os acetabulum may be avulsed traumatically, espe-
cially with posteriorly directed hip dislocations (see Chapter
20). During late adolescence the triradiate ossification
centers fuse with the peripheral center.
The ischium and pubis also have an additional ongoing
interposed bipolar growth cartilage within the inferior
ramus. Fusion of this particular region normally occurs
between the ages of 4 and 7 years. Fusiform enlargement of
this ischiopubic junction during physiologic closure is often
evident radiographically.1,2,4 Caffey and Ross reported that
fusion could occur any time between 4 and 12 years of age
and was often preceded by irregularity of ossification. The
latter is most frequent between the ages of 5 and 8 years and
may be asymmetric in 22% of normal patients.1
Kloiber et al. noted that the bone adjacent to the unfused
ischiopubic synchondrosis has a structure and vascular
anatomy comparable to that of the metaphysis of long bones
of children and thus is a potential site of injury or
osteomyelitis.4 Normal variability in the radiographic and
scintigraphic appearance of the synchondrosis may make the
evaluation of images difficult. Just prior to fusion the normal
synchondrosis may show a combination of expansion and
irregular ossification. The age of fusion varies and, in the
same patient, often proceeds asymmetrically, negating or
minimizing the value of comparison with the opposite side.
Correspondingly, increased asymmetric activity has also been
described in bone scintigraphy in normal patients.
Enlargement of the ischiopubic junction has been variably
described as normal, an osteochondrosis, a stress fracture,
infection, or malignancy. In children in the 6- to 10-year
range irregularity of this area should be considered a

FIGURE 19-3. Later development of the triradiate cartilage. (A) At

12 years, prior to the development of secondary ossification. (B)
At 14 years, with development of secondary ossification centers
in the arms of the triradiate cartilage (arrows). Serial sectioning
shows the morphology (C) of these centers.

FIGURE 19-4. CT scan of the acetabulum in a 14-year-old boy

being evaluated for pelvic trauma following a motor vehicle acci-
dent. Secondary ossification centers are present within the triradi-
ate cartilage and the anterior (open arrow) and posterior (solid
arrow) rims.
Anatomy 793

FIGURE 19-5. Normal peripheral acetabular ossification character- ture of the adjacent anteroinferior spine. (B) Complete rim ossifi-
istic of adolescence. (A) Beginning formation along the superior cation with posterosuperior continuity with the triradiate ossifica-
rim (arrow), which should not be confused with an avulsion frac- tion (arrow).

normal variation of skeletal maturation. It should not be

misinterpreted as a healing fracture, even though the radio-
graphic appearance may be suggestive of callus formation
or reactive new bone caused by osteomyelitis or neoplasia.4
However, in the older child, particularly one with pain in the
groin region, any apparent increased bone formation in
the ischiopubic junction should be considered a possible
stress fracture, infection, or neoplasia. A bone scan showing
asymmetric radionuclide uptake may help make a specific
diagnosis. Chondro-osseous fractures may occur through
this region or the symphysis when there is a triradiate frac-
ture and a rotational displacement of the pubis, ischium,
or both.
The normal, maturing ischial tuberosity may appear irreg-
ular and may be mistaken for a fracture, infection, or
tumor, especially if the patient presents with excessive reactive
bone formation several weeks after injury. Because secondary
ossification is often not present until midadolescence, the
only indication of a traction injury, with or without displace-
ment, may be cystic change in the metaphyseal-equivalent
region.
The iliac crest and spines are cartilaginous until adoles-
cence (Fig. 19-6). Secondary centers of ossification appear
along the anterolateral iliac crest when the child is approxi-
mately 13–15 years old. Posterior advancement continues
until the posterior iliac spine is reached. Fusion of crest ossi-
fication to the rest of the ilium occurs by 15–17 years,
although complete fusion may be delayed until 25 years.
Alternatively, after the ossification center first appears, sepa-
rate ossification may proceed from a posterior center, with
the central portion being ossified at a later date as the two FIGURE 19-6. Slab section of the pelvis showing the anterosupe-
centers grow toward each other. rior iliac spine (open arrow) and the anteroinferior iliac spine (solid
The anterosuperior iliac spine develops from the anterior arrow) above the acetabulum. A portion of the ischial synchondro-
apophysis of the iliac crest. This area ossifies at about age 15 sis is evident below the acetabulum.
years and unites completely with the ilium between 20 and
25 years. Several muscles originate or insert on the antero-
superior iliac spine, including the sartorius, tensor fasciae
lata, and gluteus medius.
 794
A uncovering of the femoral head with subsequent capital
B than comparable adult organs. The juvenile pelvis may
FIGURE 19-7. Development of the symphysis pubis. (A) Radio-
graph of a slab specimen from a 14-year-old, showing the normal
undulated appearance that progressively develops. It should not
be misinterpreted as an inflammatory process. (B) Morphologic
slab sections of the immature pubic symphysis showing undulated
epiphyseal cartilage on either side of central fibrocartilage (which
remains in adults) and extension of the epiphyseal cartilage along
the ramus to the ischiopubic synchondrosis (arrows).
There may be a secondary center of ossification at the
anteroinferior iliac spine, appearing at 13–15 years and
fusing at 16–18 years. This is evident more commonly in boys
than girls and may be contiguous with secondary ossification
extending from the acetabular margin.
The symphysis pubis is a growth region connecting the two
hemipelves anteriorly. As an epiphyseal analogue it may be
injured, comparable to epiphyseal fractures of the long
bones. The normal endochondral ossification process may
be associated with an irregular, undulated appearance that
should not be confused with that due to trauma (Fig. 19-7).
“Widening” of the symphyseal region is highly variable and
19. Pelvis
depends on the degree of maturation of chondral into
osseous tissue.3
General Considerations
The pelvis of the child differs from that of the adult in that the
bone, cartilage, and joints (sacroiliac, symphysis pubis, trira-
diate, ischiopubic) are more pliant (Fig. 19-8) and susceptible
to separation (fractures) at the chondro-osseous interfaces.
This greater volume of cartilage and the less brittle bone
provide a significant buffer for energy absorption, much like
the developing skull and its sutures. Accordingly, pelvic
osseous fractures are less common than in adults.9–45 When
fractures do occur, the contiguous radiolucent cartilage may
be damaged (often occultly) at the time of injury or later, par-
ticularly if the fracture heals in such a way that abnormal
forces result in altered growth. As an example, the triradiate
cartilage may be damaged microscopically (i.e., not radiolog-
ically evident), leading to acetabular maldevelopment and a
morphologic situation similar to developmental hip dysplasia.
A displaced fracture of the ischiopubic ring (essentially revers-
ing an innominate or similar pelvic osteotomy) may lead to
femoral subluxation. The presence of growth cartilage along
several pelvic margins allows avulsion fractures to occur (type
3, 4, and 7 growth mechanism injuries, as described in
Chapter 6). These fractures are comparable to epiphyseal-
physeal injuries in a long bone and are subject to all the
potential acute and long-term complications. Leg length dis-
crepancy may be a problem when a hemipelvis is shifted supe-
riorly and may lead to scoliosis during the adolescent period
owing to the posttraumatic pelvic obliquity and the relative
leg length discrepancy.
The developing chondro-osseous pelvis is more resilient
than that in an adult and therefore affords less rigid pro-
tection to the contained viscera, which because of immature
fibrous capsules and stroma may be damaged more easily
undergo considerable elastic and plastic distortion without
actual fracture. Therefore organ damage may occur with
little subsequent roentgenographic evidence of the severity
of the maximum degree of chondro-osseous trauma.
FIGURE 19-8. Plastic deformation of the ilium following direct pelvic
trauma in a 7-year-old boy. The anterior cortex is deformed but
intact, whereas the posterior cortex is plastically deformed and
cortically disrupted.
General Considerations
The identification of a pelvic fracture in a child, particularly
if displaced, thus assumes even more clinical significance.
The array of injuries, including genitourinary ones, is
roughly proportional to the severity of the pelvic fracture
pattern.
Reed reviewed 84 cases of pelvic fractures in children, more
than 80% of which were due to vehicular accidents33; 39%
were unstable. The most frequent type was the diametric frac-
ture, in which there was a fracture of the ilium or sacrum or
sacroiliac separation, combined with a pubic fracture anteri-
orly on either the same or the opposite side. However, many
diametric fractures in children are stable, because the poste-
rior fractures are often undisplaced or incomplete epiphyseal
separations through the sacroiliac region with a considerable
degree of retained soft tissue (periosteal and ligamentous)
continuity and stability. The other injuries, most of which
were isolated pubic fractures, were stable. Sixteen patients
had associated visceral injuries. Eighteen had transient micro-
hematuria, but none had significant injuries to the genitouri-
nary tract. Eleven had gross hematuria, and all had major
injuries to the lower urinary tract or the kidney. Two patients
had severe intracranial injuries. One-third of the patients sus-
tained fractures of other bones, the most common being the
femur and the skull. Four children had acetabular fractures
through the triradiate cartilage, a pattern that must be closely
sought as it is easy to overlook.
Fractures of the pelvic components must be placed in
proper perspective. During the initial phase the orthopaedist
must be acutely aware of potential injury to the intrapelvic
and intraabdominal visceral and vascular contents, rather
than the obvious osseous injuries.55–102 Osseous damage
often assumes secondary importance until internal tissue
injuries are completely evaluated and treated as necessary.
Massive retroperitoneal bleeding following pelvic fracture
produces high morbidity and mortality in victims of blunt
trauma, no matter what their age. Although less common in
children, hemorrhage still represents a significant potential
complication.46–54
Quinby reported 20 pediatric patients with fractures of the
pelvis,32 19 of whom were involved in vehicular accidents.
The patients were divided into three treatment groups.
Group 1 (six patients) did not require laparotomy; the pelvic
fractures were relatively mild and essentially undisplaced
(including one mild separation of the sacroiliac joint); and
none showed clinical shock or required blood transfusion.
Group 2 (nine patients) all underwent laparotomy for vis-
ceral injuries accompanying the pelvic fractures. All but one
of the patients with organ lacerations were in this group.
One of the children died. Group 3 (five patients) all had
massive retroperitoneal and pelvic hemorrhage with severe
pelvic fractures. All group 3 patients had extensive disrup-
tion of the sacroiliac joint. All were in clinical shock, with
one of the patients dying while control of hemorrhage was
attempted during laparotomy. Two others died within 24
hours of surgery, and another died 36 hours postoperatively.
The amount of blood replacement from admission to either
death or recovery was 3500–8000 ml, which represented
175–400% of the estimated volumes. Vascular injuries were
combined arterial and venous and were both specific and
diffuse. Four of these children had no femoral pulse. In all
cases there was injury to the primary branches of the iliac
795
artery near the disrupted sacroiliac joint. There was also
diffuse bleeding from injured muscle and bone. Thus among
20 patients there were five deaths: one due to associated
brain injury, three to uncontrolled major vascular lacera-
tions, and 1 to a mixture of possible causes but primarily
hemorrhage.
Bond et al. studied children consecutively admitted to a
regional pediatric trauma center with blunt trauma.56 Fifty-
four of the children (2.4% of 2248 injured children) had an
injury to the pelvis. Only 13 of these 54 children had a con-
comitant abdominal or genitourinary injury. Nine of the chil-
dren required transfusion, and nine required exploratory or
reparative surgery. Six children died. The location of the frac-
ture was strongly associated with the probability of abdominal
injury; 80% of children with multiple pelvic fractures had a
concomitant abdominal or genitourinary injury, compared
with only 33% involvement when there was an isolated frac-
ture of the ilium or pelvic rim, and 6% with isolated pubic frac-
tures. According to their study, the probability of abdominal
injury and associated pelvic injury was less than 1% for iso-
lated pubic fractures, 15% for iliac or sacral fractures, and
60% for multiple fractures of the pelvic ring. They noted that
in adults the two major conditions leading to death from
severe pelvic fracture were hemorrhage and subsequent infec-
tion of the intrapelvic hematoma. In contrast, children with
pelvic fractures usually died from complications of an associ-
ated head injury.
Garvin et al. reviewed 36 pediatric patients who were clas-
sified using Torode and Zieg’s system.14,41 They also classified
the severity of injury using the Modified Injury Severity Score
(MISS). Associated injuries occurred in 67% of the patients,
with a long-term morbidity or mortality in 30%. They
stressed the high probability of minimal bony injury being
associated with life-threatening visceral injuries and morbid-
ity. The most common concomitant organ system involved
was musculoskeletal, with 18 long bone fractures in 11
patients. The abdomen was the second most common site of
injury (11 patients). Six injuries involved the prostatic
urethra (n = 3) and spine (n = 3). Two patients with prostat-
ic urethral injuries were still incontinent. The third patient
died of sepsis. Two of the spinal injury patients had perma-
nent neurologic sequelae. One was monoplegic secondary
to lumbosacral plexus injury. The second patient eventually
underwent a hemipelvectomy after a sacral plexus injury,
femoral neurovascular disruption, and subsequent fungal
fasciitis that eventually necessitated the procedure. There
were lacerations or severe contusions in two livers, two
kidneys, two vaginas, two rectums, and one spleen. However,
a partial splenectomy was the only major abdominal surgery
required. Three patients sustained closed head injuries.
None of them had permanent damage from the associated
injury. None of the eight patients had involvement of the
sacroiliac joint. None underwent surgery. They found that
all patients with long-term morbidity had a fracture classified
as ring disruption. However, the morbidity was never attrib-
uted to the pelvic bone injury but, rather, to the other
nonosseous injuries the patient sustained.
Lacheretz and Herbaux questioned whether unstable ring
fractures in children should ever be treated surgically.19 They
reviewed 126 cases, 10 of whom had acetabular involvement.
They classified the other 116 cases according to Tile.40 There
796
were 80 stable fractures (type A), 29 unstable transverse frac-
tures (type B), and seven unstable transverse and vertical
fractures (type C). They found that all type A and B fractures
healed by conservative means. Only in type C fractures was
there a need to consider closed reduction with external
fixation or surgical intervention.
McLaren et al. studied long-term pain and disability after
displaced pelvic ring fractures.25 All patients were adults.
They found that in 43 patients with high-energy pelvic frac-
tures 5 years or more earlier, the occurrence of chronic pain
and the functional outcome was related to residual deformity
of the pelvic ring. Among the patients with no residual defor-
mity (i.e., a displacement of less than 1 cm), 88% had no
serious pain and 82% had normal function. However, among
the patients with residual deformity, with the displacement
being more than 1 cm posteriorly, 70% had serious pain and
only 70% had normal function. They recommended defini-
tive reduction and stabilization as early after the injury as
possible. Schwartz et al. found that near-anatomic reduction
in children gave the best functional/pain results 2–25 years
after pelvic fracture.37 Remodeling in children, however,
makes mandatory anatomic reduction of the pelvis and
sacroiliac joints less necessary. Remodeling does not correct
upward displacement of a hemipelvis at the sacroiliac
junction.
Having treated many pelvic disruptions in children, I
have observed that the patients with hemipelvic displace-
ments of more than 1–2 cm may have minimal problems as
a child but frequently develop pain and discomfort during
adolescence and their early adult years when they are fol-
lowed for an extended period of time. The leg length
inequality often requires treatment. Back pain becomes
a significant problem with further growth and increasing
physical demands.
Diagnosis
The accurate diagnosis of pelvic injuries is difficult only on
the basis of clinical findings. Children tend to be at the
extremes, with either a relatively simple pelvic injury or mul-
tiple trauma. Variable levels of consciousness may limit the
response to pain. Physical examination should include pelvic
compression, which may elicit pain. The absence of pain,
however, does not effectively rule out injury because of pos-
sible lumbosacral plexus and spinal cord injury. Posterior
subluxation of the ilium on the sacrum at the sacroiliac joint
is generally missed because the patient is usually supine,
especially if severely injured. The region may not be exam-
ined with sufficient care, particularly when there are multi-
ple injuries. Soft tissue injury—abrasions, lacerations,
ecchymoses—should increase the index of suspicion. The
perineum should be examined carefully.
As reasonable a neurologic examination as possible should
be undertaken, depending on the level of consciousness of
the patient. In particular, sacral sensation should be tested.
Many nerve injuries are missed because detailed initial
neurologic examination is neglected or cursory, especially in
the child with life-threatening injury. The lumbosacral
plexus is closely related to the sacroiliac joint; there may be
some neural damage when the “joint” is dislocated or sepa-
19. Pelvis
rated. The lumbosacral trunk, the superior gluteal nerve,
and the obturator nerve may be stretched or even disrupted.
Intrathecal rupture of the roots of the cauda equina may
be produced by traction. Chondro-osseous distortion or
displacement may be greater at the time of the accident
than when the child presents for treatment. The actual
extent of tissue deformity may cause stretch (traction) nerve
injuries.
Adequate radiographic examination is critical. However,
always remember that this static radiographic appearance
may not indicate the maximum deformity that was attained
when the injury was actually occurring. A gonad shield
should not be used during the initial screening, as it may
obliterate areas that need to be critically evaluated. The
anteroposterior view of the pelvis that adequately demon-
strates the pelvic ring is not always acceptable for determin-
ing fracture details because of the normal lumbar lordosis.
The best view in the anteroposterior position may be
oblique, depending on how much curvature there is in the
spine.80 An inlet or downshot view is obtained 30° off the ver-
tical, with the cone aimed distally to demonstrate bursting of
the ring. Other projections (e.g., Judet’s views) may provide
important information about fragment displacement, espe-
cially in the adolescent.105
Computed tomography (Figs. 19-9 to 19-11) offers the best
method for detecting subtle injuries and defining the spe-
cific fracture anatomy more precisely.30 For example, appar-
ent sacroiliac disruption was actually a chondro-osseous
disruption comparable to a type 1 or 2 growth mechanism
injury of a long bone. CT scanning is also useful for detect-
ing inward or outward winging hinged at the sacroiliac joint
(Fig. 19-10), as well as the diagnosis of posterior displace-
ment of an ilium (Fig. 19-11).
Magid et al. discussed the role of two- and three-dimen-
sional CT imaging in the evaluation of acetabular and pelvic
fractures in pediatric patients.23 Using standard technology,
the acquired images may be rotated through multiple posi-
tions in any 360° sequence until the best view is obtained.
This capability is important, as conventional films may not
provide the optimum view or because the injured young
patient may be unable or unwilling to comply with position-
ing maneuvers. Furthermore, colonic air and solid contents
may obscure the posterior pelvic ring. Magid et al. noted that
much of the recent trend toward more conservative, less
invasive management of patients with abdominal or thoracic
trauma is related to the ability to document adequately the
extent of injury by CT rather than resorting to exploratory
laparotomy or laparoscopy.
Magid et al. found that three-dimensional CT recon-
struction was useful in 50% of the cases in terms of better
fracture definition, 56% in terms of deciding between con-
servative or operative management, 46% in terms of select-
ing the ideal operative approach, and 30% in terms of
selecting the hardware to be used for the operation.23 CT
also provides a convenient, noninvasive method for follow-
up of a complex pelvic fracture.
Although CT imaging provides additional information for
evaluating traumatized patients, not every pediatric patient
with pelvic trauma requires such a study. Particularly,
patients with simple, stable injuries to the symphysis or ante-
rior ring that were readily evident on routine films did not
Types of Pelvic Fracture 797

Types of Pelvic Fracture

Adult pelvic fractures may be simply classified according to
the direction of the impact force: anteroposterior compres-
sion, lateral compression, vertical shear, or a combination
of these forces. Such classification correlates well with the
presence or lack of pelvic stability and the appropriate treat-
ment requirements. This classification, however, is not as
easily applied to children as it is to adults because of the
presence of multiple regions of physeal and epiphyseal-
equivalent cartilage, all of which have additional injury
failure patterns.
Fractures of the immature pelvis may be classified into
four basic groups: (1) stable fractures with continuity of
the pelvic ring; (2) unstable fractures with disruption of the
pelvic ring anteriorly, posteriorly, or both; (3) fractures of
the acetabulum especially involving the triradiate cartilage;
and (4) avulsion (apophyseal) fractures, often resulting from
muscular avulsion rather than direct violence. The most
common pelvic osseous fracture in children, constituting
almost 50%, is a ramus fracture, with most being unilateral
and primarily involving the superior (pubic) ramus. The
basic fracture types are shown in Figures 19-12 to 19-15.

FIGURE 19-9. (A) CT scan shows that the apparent sacroiliac sep-
aration seen on the routine anteroposterior film was really a type
2 growth mechanism with separation at the chondro-osseous inter-
face, leaving a small Thurstan Holland fragment (arrow) from the
ilium. (B) Similar case but with a posterior Thurstan Holland frag-
ment (arrow). This hemipelvis had been internally rotated by direct
impact from an automobile bumper.

A
require scanning. The two- and three-dimensional CT
images are most useful in pediatric patients with complex
injuries in whom the full definition of injury is essential to
determine whether external fixation or operation was nec-
essary. Contrast in the bladder or intravenous pyclograply
does not interfere with the CT scan and usually delineates
any extravasation.
Scanning by CT is also useful for follow-up of disruptive
pelvic injuries (Fig. 19-10). It allows evaluation of the extent
of healing and residual anatomic deformity. Magnetic reso-
nance imaging (MRI) probably has limited use in pelvic
fractures, as osseous detail is better visualized in a CT scan.
However, intraabdominal and intrapelvic soft tissue injury,
hematoma accumulation, and so on may be discerned and
documented. Furthermore, cartilaginous damage (e.g., avul-
sion of an unossified anteroinferior iliac spine) may become B
evident. FIGURE 19-10. (A) Outward winging of left ilium (curved arrow) due
Because of the increased amount of trauma often incurred to a chondro-osseous disruption of the sacroiliac joint. A small
during adolescence, multiple injuries may occur. In posterior iliac fragment is evident (straight arrow). (B) CT scan 3
particular, a hip dislocation may also occur with pelvic months after right hinging injury. Remodeling of the iliac side of the
fractures. sacroiliac joint is evident.
 A
FIGURE 19-11. (A) Posterior displacement of the ilium (large arrow)
in a 12-year-old girl. Small anterior accessory ossifications of the
sacrum (small arrows) are normal and should not be construed as
fractures. (B) Posterior shift of the left hemipelvis. Note the poste-
FIGURE 19-12. Stable fracture patterns. (A) Infolding of the iliac
wing, which is analogous to a type 4 growth mechanism injury and
may cause irregularity of crest development. Type 1 or 2 growth
mechanism injuries of the iliac crest may occur, although such avul-
sion patterns are unusual. Direct contusion (type 5 growth mech-
anism injury) may also occur. (B) Fractures of the ischiopubic rami
are rarely displaced significantly in a child because of extensive
cartilage and strong periosteum. In fact, the chondro-osseous frac-
ture response in a child may allow fracture of only one ramus, a
highly unusual injury in adults. The examiner should always look
for accompanying disruption of the sacroiliac joint, symphysis
pubis, or triradiate cartilage.
798
B
rior accessory ossification centers of the sacrum (arrows). The shift
of this accessory center on the left implies a chondro-osseous sep-
aration, rather than a sacroiliac dislocation.
FIGURE 19-13. Unstable fracture patterns. (A) Rami fractures may
be accompanied by displacement of the medial ischiopubic frag-
ment from the symphysis (stippled areas) and periosteum (lined
area). The fragment is externally rotated, hinging at the fracture
site. This is a type 1 growth mechanism fracture. If the fragment is
not reduced, the relatively intact periosteal tube makes bone
(membranous and some endochondral) to fill the defect. Alterna-
tively, the ramus fracture may extend to the triradiate cartilage and
allow inward hinging of the ramus. (B) “Malgaigne” fracture of the
immature pelvis. The true sacroiliac joint (*) is intact, but a chondro-
osseous separation occurs on the iliac side, mimicking a sacroil-
iac disruption radiographically (see Figure 19-12). The inferior
disruption may be a type 1 symphysis-ischiopubic separation or
fracture of the rami. The relatively free hemipelvis is then displaced
superiorly, but soft tissue (periosteal) constraints generally limit the
degree of displacement.
Types of Pelvic Fracture
FIGURE 19-14. (Left) Crush injury to the triradiate cartilage (arrows)
Translation may also occur. (Right) Ossifying region of the acetab-
ular rim may be avulsed. This injury may occur prior to ossifica-
tion, as an accompaniment to hip dislocation. The diagnosis is
extremely difficult in such a situation and should not be confused
with normal ossification patterns (see Chapter 20).
In contrast to adult pelvic disruption, pelvic fractures in
children are less likely to be significantly displaced; most are
stable, including diametric fractures in which the posterior
fractures tend to be incomplete. This stability is the result of
the relatively thick periosteum and the frequent involvement
of chondro-osseous regions with partial zone of Ranvier dis-
ruption in children. Many of these injuries are analogous to
physeal-metaphyseal injuries. They have intrinsic stability
because some of the periosteal sleeve is intact. Fractures are
also likely to be incomplete (i.e., greenstick) due to the
resilient nature of the immature bone.
Stable Pelvic Ring Fractures
Wing of the Ilium
The wing of the ilium may be displaced outward, inward,
upward, or downward (Fig. 19-16). The pull of muscles on
this fragment may be reduced by abduction and flexion. This
type of fracture, which is not common in children, is a result
of direct force against the pelvis, causing disruption of the
iliac apophysis or an infolding of the pliable wing of the
ilium. Altered iliac crest development may occur.
FIGURE 19-15. Avulsion fracture patterns of iliac and ischial
regions in which secondary ossification centers normally develop.
799
FIGURE 19-16. Fracture of the iliac wing, with infolding of the ante-
rior portion (solid arrow) and some comminution of the superior
metaphyseal region (open arrow).
The infolding may cause a splitting injury of the iliac crest
apophysis along the rim or at the iliac spines. Such disrup-
tion may lead to subsequent growth distortion of the iliac
wing or elongation (prominence of an iliac spine).
Ischiopubic Rami
If one ramus is fractured, or both rami on the same side (Figs.
19-17 to 19-21), the patient usually may be treated sympto-
matically. If only one ramus is fractured, the physician must
always remember to look carefully for concomitant injury
completing the fracture somewhere within the pelvic ring.
Particularly, the possibility of a “physeal” fracture at the junc-
tion of the involved ramus with the triradiate or symphyseal
cartilage should be assessed. Confirmation of a concomitant
chondro-osseous injury may not adversely affect the intrinsic
fracture stability. However, separation that allows angulation
renders the ramus fracture unstable (see ensuing section).
These injuries are relatively stable, as a portion of the
periosteal sleeve is intact. Significant displacement may
require manipulative (closed) or operative reduction. The
intact periosteal tube allows new bone formation, which fills
the “displacement” gap, again lessening the need for reduc-
tion. Evaluation is also particularly important at the sacroiliac
joint. However, because the pelvic components are resilient in
the child, a solitary ramus fracture is possible, whereas in the
adult a fracture is invariably completed through contraposed
portions of the ring. Even multiple fractures of three or four
800
B se is not disrupted but, rather, is a “physeal fracture ana-
FIGURE 19-17. (A) Minimally disrupted pubic ramus fracture (solid
arrow). The ischial radiolucency (open arrow) is the normal syn-
chondrosis, not a fracture. (B) Multiple fractures of both rami.
FIGURE 19-18. (A) Fracture of the superior pubic ramus (solid
arrow). There also was concern for the triradiate region (open
arrow), as it appeared offset, but it was a variation due to the pro-
jection. Three years later there was no evidence of triradiate growth
19. Pelvis
rami (see Fig. 19-23, below) may be reasonably stable in a
child because of the dense ligamentous, periosteal, and
cartilaginous continuities.
Separation of the Symphysis
The changing size and irregular undulation of the symphysis
region during growth must always be borne in mind. Fre-
quently, an injury to this area must be diagnosed by physical
examination (e.g., pain, overlying ecchymosis), as there
may be little radiographic evidence. These separations are
physeal injuries with separation of the ramus metaphysis
from the epiphyseal and fibrocartilage of the symphysis
(Figs. 19-22 to 19-25). In children, diastasis of the pubic sym-
physis is by separation of the bone–cartilage junction on one
or both sides, rather than by disruption of the fibrous joint,
as in the adult.
Radiographic diastasis of the pubic symphysis may occur
in children without resultant instability of the sacroiliac
joints posteriorly, presumably because of the elasticity of the
bony pelvis, partial disruption of the anterior sacroiliac joint,
or triradiate fracture. The sacroiliac joint in the young child
may split anteriorly at the bone–cartilage interface of either
the posterior ilium or sacrum.
More importantly, a displaced ramus with separation at the
pubic symphysis is more likely to fail additionally within the
triradiate cartilage (i.e., the other end of this bone), rather
than posteriorly at the sacroiliac joint. This difference
between ramus fractures in adults and children is extremely
important.
Webb et al. described use of a two-hole fixation plate for
traumatic diastasis of the symphysis pubis.44 All of their
patients were skeletally mature. The need to use such fixa-
tion in a child is unlikely, particularly as the symphysis per
logue.” However, early application of plate fixation restored
the disrupted anterior pelvic ring, contributed to early
immobilization of the patients, and made reduction of the
injury. (B) A catheter was inserted, dye was injected, and dis-
placement of the bladder (arrows) by retropubic hematoma was
evident.
Types of Pelvic Fracture 801

FIGURE 19-19. (A) Fractures of all four rami. (B)

CT scan showed that the right pubic ramus
fracture (arrow) did not involve the triradiate
cartilage.

A B
FIGURE 19-20. (A) Four ramus fracture, with hinging of the left rami at the triradiate cartilage. (B) Appearance 1 year later. Note the
remodeling of the ramus fractures. The left triradiate cartilage has a medial osseous bridge (arrow).
802 19. Pelvis

Fractures of the Anterior Arch (Fig. 19-26)

Crush injuries in the anteroposterior direction may cause
fractures of both rami bilaterally to give a floating segment.
In the child, a variation of this injury is fractures of both rami
but with an ipsilateral separation of the bone from the sym-
physeal cartilage or the triradiate cartilage. The fragment
may be displaced posteriorly to cause bladder displacement
or damage. Disruption of the symphysis pubis is usually asso-
ciated with separation of the bone (i.e., metaphysis) away

FIGURE 19-21. Fracture at the junction of pubic and ischial rami at

the symphysis. The other end of the fracture is a chondro-osseous
separation at the ischial synchondrosis.

concomitantly disrupted sacroiliac joint easier. A child is

more likely to have a concomitant injury at the triradiate car-
tilage than at the sacroiliac joint. Open reduction back into
the periosteal sleeve, with repair of periosteum, with or
without temporary pin fixation, may be considered. The pin
should be percutaneous, bent at 90° and removed at 2–3
weeks to avoid the risk of breakage or migration. An exter-
nal fixator applied to the ilia can close the anterior chondro-
osseous fracture (not diastasis) as effectively as a plate.
Because the fracture is a growth mechanism injury it usually
stabilizes within a few weeks.

Unstable Pelvic Ring Fractures

Separation of the Symphysis Pubis, Accompanied
by Partial Disruption at the Sacroiliac Joint
(Figs. 19-24, 19-25)
With separation of the symphysis pubis, the ring is disrupted
and opened anteriorly at the symphysis. The posterior sepa-
ration at the sacroiliac joint may be due to disruption of the
anterior capsule of the joint or an epiphyseal iliac fracture.
Comparable epiphyseal separation at the sacrum may occur
but is less likely because of developmental patterns of the
sacrum.
The supine position aggravates the deformity, and the
child may be more comfortable lying on his or her side. Fre-
quently, placement of a pelvic sling relieves symptoms. This
sling may allow some control of the pelvic diastasis, as the
FIGURE 19-22. (A) Stable separation of the right sacroiliac region
straps may be crossed to increase compression. Compression (open arrows) and ipsilateral separation of the symphysis (solid
immobilization with a sling or a spica should be maintained arrows). This roentgenogram was obtained 2 months after injury
for 6–8 weeks, depending on the age of the child, to ensure and shows subperiosteal new bone at the sacroiliac joint and sub-
adequate ligamentous or chondro-osseous union at the sym- periosteal and endosteal bone at the symphysis. (B) At 6 months
physis and to prevent late spreading. more bone is evident adjacent to the symphysis.
Types of Pelvic Fracture 803

ple system injury may preclude use of this method, as rigor-

ous attempts at reduction may precipitate further retroperi-
toneal hemorrhage or nerve damage (traction or avulsion)
and are thus contraindicated. Traction with 10–15 pounds,
usually requiring a skeletal pin, may be necessary to reduce
the fracture. After reduction is achieved, which is usually

FIGURE 19-23. Reduction of a symphyseal diastasis with a small

plate. The posterior screws are not sufficiently across the sacroil-
iac separation.

from the cartilage and thick periosteal sleeve. The separa-

tion gap may subsequently be filled in by endochondral bone
formation. The segment may be displaced posteriorly
(usually by impact), superiorly because of the rectus abdom-
inis muscles, or inferiorly because of the adductors and
hamstrings.
A pelvic sling should not be used in this situation, as it may
cause inward compression of an unstable ramus. Children
with this injury should be rested supine and placed in a semi-
Fowler’s position to relax the abdominal and adductor
muscles. Treatment is maintained for 3 weeks, depending on
the degree of displacement. Disruption of this region must
be carefully assessed, particularly with regard to urethral and
bladder injuries (Fig. 19-27). Thickened periosteum may not
be damaged completely, so major fragment displacement is
not common in children. External fixation may be consid-
ered. If the fragment is displaced into the pelvis, injuring or
potentially injuring the bladder, consider using some type of
stabilization.

Vertical Shear
With vertical shear the ring is broken in front and in back,
and the free hemipelvis is shifted upward, inward, or outward
(Fig. 19-28). The free pelvic segment is displaced by spasm
of the muscles whose origin is fixed to the floating piece
FIGURE 19-24. (A) Externally rotated right hemipelvis with a green-
(e.g., the psoas, adductors, gluteus maximus, lateral abdom- stick iliac fracture of the left side. Note the marked widening of the
inal muscles). If upward displacement is sufficient, leg length symphysis. (B) Treatment with pelvic external fixation. (C) The right
discrepancy may result. hemipelvis had been externally rotated through the sacroiliac joint
Such fractures may be treated by skeletal traction using a (curved arrow). The left hemipelvis had a fracture near the sacroil-
pin through the distal femoral metaphysis. However, multi- iac joint (straight arrow).
FIGURE 19-25. (A) Marked eversion of the right hemipelvis with a tures. (B) CT scan shows external rotation (arrow) of the
posterior fracture and sacroiliac “disruption.” The left hemipelvis hemipelvis through the sacroiliac joint.
has an upward shift through the sacroiliac joint and ramus frac-

FIGURE 19-26. (A) Four weeks after multiple trauma, causing (arrows). (B) Two months later, significant membranous bone is
a right-sided Malgaigne injury and subperiosteal rotational dis- filling the intact periosteal tube along the ramus displacement.
placement of the contralateral rami, there is new bone formation

FIGURE 19-27. (A) Severely damaged pubic ramus is separated and was injuring the bladder. Open reduction was done during
from the symphysis and hinging at the triradiate cartilage. (B) CT bladder repair.
scan showed that this fragment was directed into the pelvic cavity

804
General Management Guidelines
FIGURE 19-28. (A) Vertical shear fracture with probable involve-
ment of the triradiate cartilage. The iliac fracture (open arrows),
combined with pubic and ischial fractures (closed arrow), allowed
within a week, the position should be held. Countertraction
should be maintained to prevent the child from inadver-
tently placing the injured leg in relative abduction. Open
reduction is rarely indicated.
Bucket Handle Injury
With a bucket handle injury the pelvic ring is broken in front
and back, and the floating pieces are rotated so the iliac crest
is displaced medially and the ischial tuberosity laterally. This
condition may be combined with some vertical shear. This
type of injury, in effect, causes the reverse of an innominate
osteotomy and thereby “uncovers” the femoral head. Again,
this injury should be treated by skeletal traction or an exter-
nal fixator whenever possible. It is important to reduce this
deformity, as uncovering the femoral head, particularly in
the young child up to 8–9 years of age, may cause relative
or actual dysplasia of the acetabulum by the time growth is
finished.
Lateral Compression
Lateral crushing injury folds the wing of the pelvis, hinged
posteriorly on the sacroiliac joint or hinged anteriorly at the
pubis. However, the free edge of the fragment may be dis-
placed centrally. When a child is run over, one ilium may be
rotated externally at the sacroiliac joint and the other
hemipelvis rotated internally.
Traction may be applied through the hip joint and proxi-
mal femur in an attempt to reduce it over time. Such reduc-
tion takes approximately l week and should be followed by
maintenance of bed rest. Open reduction may be indicated,
particularly in the small child in whom skeletal traction is
not readily applicable. External fixation with a pelvic frame
may also be used. Using the “lengthening” attachments,
winging of a hemipelvis may be gradually reduced to a
normal (or near-normal) anatomic position.
805
rotation of the “free” fragment. (B) Four years later there is obvious
altered growth of the acetabulum.
General Management Guidelines
Osseous Injuries
Pelvic fractures may be accompanied by other skeletal
injuries. Because many pelvic injuries are caused by direct
blows and vehicular trauma, fractures of the proximal femur,
hip dislocation, and spinal fractures may occur. Such injuries
should not be overlooked during the initial evaluation.
Associated injuries may require much more treatment than
the pelvic fracture itself.
With stable injuries, function is minimally impaired.
Usually the basic pelvic ring is undisplaced or minimally dis-
placed. Comfort, the primary treatment goal, is attained
most effectively by bed rest (frequently mandated by accom-
panying injuries). Reduction, either closed or open, is rarely
necessary, particularly in the young child, because of the
extent of remodeling that will occur and the possibility of
damaging intrapelvic structures.
However, given the inherent instability of posterior dis-
ruption of the pelvis, closed reduction and minimal external
fixation are recommended when displacement is evident
(Fig. 19-29). Fixation frames allow easier nursing care
and access to management of soft tissue damage and
catheters.27,35 However, external fixation must be used care-
fully in the young child, as placement of threaded pins or
screws through apophyseal regions (e.g., iliac crest) may
cause localized physeal damage. Because the chondro-
osseous nature of these fractures allows relatively rapid
healing, fixators do not have to remain in place in a child as
long as they would in an adult. It may be necessary to use
limited internal fixation (Fig. 19-30).
One of the most common complications is leg length
inequality secondary to a shifted hemipelvis (Fig. 19-31).
Vigorous manipulation in the child to reduce the superior
shift anatomically may not be appropriate and may cause
recurrent bleeding or genitourinary damage. Remodeling,
806
FIGURE 19-29. (A) Unstable fracture of the pelvis. (B) It was stabilized with external pelvic fixation.
as in long bones, may alter such relations in a positive way.
Nonunion and delayed union are uncommon complications
of childhood pelvic injuries.35 Limb lengthening may be cor-
rected at a later date. Because the discrepancy is usually less
than 2 cm most children may be treated effectively with a
lift and, if indicated, an appropriately timed contralateral
epiphysiodesis.
Vascular Injuries
Despite having a distribution of pelvic fractures sites similar
to that of adults, only 5 of 372 children in four separate inves-
tigations died as a result of hemorrhage.14,20 Possible expla-
nations for reduced bleeding from pelvic fractures in
children have anatomic bases. First, the periosteal tissues
appear to be more adherent to the underlying bone in the
FIGURE 19-30. Combined use of an external pelvic fixation device
with internal stabilization of a fracture-separation of the sacroiliac
region.
19. Pelvis
child, which may limit the displacement and thus lessen the
likelihood of disruption of major vessels that course over and
around the pelvis. Second, children’s vessels are much more
vasoconstrictive, which potentially helps limit hemorrhage
from smaller vessels.
McIntyre et al.52 reviewed 57 pelvic fractures in children.
Eighteen required blood transfusion within 48 hours (i.e.,
one-third of patients). Skeletal fixation was applied in ten of
these patients and was believed to control bleeding in six.
Pelvic arteriography was used to identify arterial hemorrhage
in three patients, all of whom underwent successful
embolization to control the bleeding.
Shock may accompany severe pelvic fractures and is
usually hemorrhagic rather than neurogenic (see Chapter
10). Appropriate volume replacement, transfusion, and tem-
porary postponement of laparotomy or laparoscopy until the
FIGURE 19-31. Five years after a severe pelvic fracture in a head-
injured patient with multitrauma, there is a permanent upward
shift of the right hemipelvis and clinically evident leg length
inequality.
General Management Guidelines
circulatory and volume status are stable are strongly recom-
mended. A delay in the repair of visceral or arterial injuries
is probably less serious than the crisis of cardiac arrest during
an exploratory operation performed while the general cir-
culation is in a tenuous state. The sacroiliac region of the
child and adolescent seems to be the point where the vessels
and nerves are most susceptible to significant injury. If this
area is disrupted, there should be concern for laceration of
vessels up to the size of the iliac artery. Shock poorly respon-
sive to volume replacement and pressor agents in the pres-
ence of a rapidly enlarging abdomen, with absence of one
or both femoral pulses, should be cause for immediate sur-
gical exploration (e.g., laparoscopy), rather than delay. It is
a good surgical principle not to disturb stable retroperitoneal
hematomas, regardless of their size but, rather, to control the
specific visceral or vascular lacerations. CT and MRI scans
may be more efficacious than abdominal taps for identifying
large hematomas. In addition to being a method of repair,
limited laparoscopy may be helpful for diagnosis.
Certain fractures have been correlated with specific vas-
cular injuries. Lacerations or avulsions of the common exter-
nal iliac vessels are associated with disruption of the ilium or
separation of the sacroiliac joint. In children, disruption of
the posterior pelvis has been associated with avulsion of the
superior gluteal artery.32
Sources of external hemorrhage should be sought around
the urethral meatus, vagina, and anus. Abdominal and rectal
examinations are essential. Pulses in the lower extremities
must be assessed carefully by palpation. Doppler studies
should be obtained if a pulse cannot be felt.
When the sacroiliac joint is separated and pulses in one
leg are diminished or absent, a major branch of the internal
iliac artery has probably been disrupted.49 The child gener-
ally is in profound shock and requires rapid transfusion of
blood in massive quantities. This type of injury is associated
with high mortality, even in children. The importance of
concealed hemorrhage due to fractures of the pelvis cannot
be overstated. In one case, a 7-year-old child lost more than
half of his blood volume into such a hematoma.53 The pos-
sible consequences of allowing continued rapid retroperi-
toneal blood loss, such as intraperitoneal rupture with
exsanguination, prolonged jaundice, renal failure, coagu-
lopathy, and prolonged ileus, should be avoided.
Autopsy studies of 200 consecutive fatally injured pedes-
trians showed that 45% had pelvic fractures, and all had
significant retroperitoneal bleeding.47 The hemorrhage
accompanying pelvic fracture was the direct cause of death
or contributed substantially to the fatal outcome. In contrast,
in a similar study of 500 pedestrians who did not succumb to
their injuries, only 4% sustained pelvic fractures.
Hemorrhage may be intraperitoneal or extraperitoneal.
Intraperitoneal bleeding often necessitates control by
laparotomy or laparoscopy. Extraperitoneal bleeding is
much more difficult to control, and explorative surgery and
attempts to ligate vessels may be difficult. The bleeding often
originates from branches of the obturator artery that supply
the pubic rami.51
The magnitude of blood loss may go unrecognized.
Operative attempts at stemming hemorrhage are frequently
unsuccessful because identification of the primary bleeding
site is difficult. Opening the peritoneum when tamponade
807
has occurred may increase blood loss substantially. In addi-
tion, if the hemorrhage is eventually controlled, the risk of
later sepsis within the hematoma is enhanced (especially if
there has been accompanying urethral or bladder injury).
Success with internal iliac artery ligation has been variable.
In fact, the morbidity associated with retroperitoneal explo-
ration and arterial ligation may outweigh the risk of nonop-
erative management with continued blood replacement.
Angiographic evaluation of bleeding associated with pelvic
fracture and treatment by selective embolization of clotted
blood to sites in the vicinity of the fractures (usually branches
from the obturator artery along the pubic rami) have been
described in adults and more recently in children.46,48,50,51
This technique may be considered a nonoperative approach
to massive pelvic hematomas,54 when contrasted with the
hazards of surgical exploration. The technique involves arte-
rial catheterization on the side opposite the trauma. A flush
aortogram is performed with the catheter at the level of the
renal arteries, with the urinary tract visualized as well. Selec-
tive celiac axis arteriography then follows to evaluate the liver
and spleen. For embolization, the catheter is advanced prox-
imally to the obturator artery, and pieces of Gelfoam (mixed
with contrast material) or autologous clot may be injected
into the obturator artery under fluoroscopic control.
For detecting occult vascular problems MRI angiography
may help.31 New spin echo sequences may allow visualization
of regional anatomic structures contiguous to metallic
devices.
Abdominal Organs
Injury to the bowel is an uncommon complication of child-
hood pelvic fracture and probably occurs in fewer than 3%
of cases.56,62 In contrast, a reactive ileus and gastric dilatation
(air swallowing) are common, especially in children. A naso-
gastric tube may be used if such complications are present.
Children have a propensity to swallow air when injured.
Accordingly, gastric dilatation per se does not indicate a
definite bowel injury.
Entrapment of bowel between osseous fragments of the
pelvis has been reported.55,57,62,63 Everett described a 5-year-
old boy who sustained a fractured pelvis with dislocation of
the left sacroiliac joint.61 Small bowel obstruction subse-
quently developed. At exploration, the apparent fracture-
separation of the sacroiliac joint was a type 1 growth
mechanism injury in which the cartilage at the sacroiliac
joint had retained normal continuity, whereas the osseous
portion of the ilium had hinged away, allowing small bowel
to herniate into this area. The bowel became entrapped
when the fracture spontaneously reduced after the injurious
forces dissipated.
Nimityongskul et al. reported an 8-year-old who had small
bowel incarceration associated with a central fracture dislo-
cation of the hip.64 Again, the bowel was entrapped when the
temporarily widened fracture spontaneously reduced, pro-
gressively leading to perforation of the bowel, infection of
the hip joint, separation of the capital femoral epiphysis, and
osteomyelitis of the femoral shaft (Fig. 19-32).
In the long term, if there is severe disruption of the ante-
rior ring, especially when it is rotated and disrupted by a
symphysis pubis diastasis, the inguinal ligament may be dis-
808
A
B
C
FIGURE 19-32. (A) Central fracture dislocation. (B) Closed reduc-
tion. The widening of the joint space was due to entrapped bowel.
(C) Result after infection supervened (coliform bacteria).
rupted and a hernia may ensue. Similarly, disruption along
the region of the iliac crest may lead to a lumbar or abdom-
inal hernia.
The liver is the second most commonly injured intraab-
dominal organ in pediatric patients.58,59 The need for oper-
ative therapy for liver lacerations in children is controversial.
Further discussion of liver and spleen injury may be found
in Chapter 13, as these organs are also frequently injured
with rib and thoracic trauma.
Perineal avulsion may be associated with genitourinary
and rectal injury.60 Stabilization of the pelvic injury may con-
tribute substantially to the necessary reconstruction of these
19. Pelvis
tissues and organs. Perineal trauma is associated with mor-
tality rates of 32–58%, which are improved by control of
hemorrhage and sepsis.
Neurologic Injuries
Neurologic injury may occur at several levels, particularly
when the sacroiliac region is disrupted.65,66 The nerve roots
may be stretched or avulsed at the spinal foramina. Injury to
the sciatic nerve as it courses past the acetabulum is unusual,
primarily because these injuries usually leave an intact
periosteum that protects the nerve. If the sciatic nerve is
injured, some degree of function may be permanently lost.
Children with residual nerve damage, no matter what the
final level, may have major problems with recurrent frac-
tures, Charcot-like joints, soft tissue contractures, and
decubiti. Relative osteoporosis may significantly weaken the
metaphyseal areas, predisposing to growth mechanism and
metaphyseal fractures (see Chapters 6, 10, 11).
Incomplete injuries to the lumbosacral plexus, especially
stretch injuries, are relatively easy to overlook when evaluat-
ing more life-threatening aspects of a traumatized child.
Lesions around the areas of the sacral roots are often painless.
Because of overlap of sensory fields it may not be easy to detect
discrete sensory loss, and there may be subtle motor damage
that results in problems around the hip region and distally.
Urologic Injuries
Disruption of the symphysis or displaced fractures of the
pubic rami may cause injury to the bladder and
urethra.68,77,83,87 Complete urologic evaluation with urethrog-
raphy, cystography, and an intravenous pyelogram may be
required (Figs. 19-33, 19-34).
Hendren and Peters noted that with multiple trauma the
urinary tract is second only to the central nervous system in
terms of the frequency of injury.80 Injuries to the lower
genitourinary tract and perineum account for about 1% of
pediatric trauma center admissions. In one study 10% had
urethral injuries and one-third had head injuries.21
About 10–25% of bladder injuries are due to penetrating
trauma, especially when the bladder is full at the time of
injury.70,72,82 Allison reported that 17% of pelvic fractures are
associated with rupture of the bladder or urethra.67 The latter
injury is potentially serious (Fig. 19-33B). The degree of
bladder trauma may be classified into four groups: (1) contu-
sion; (2) extraperitoneal rupture; (3) intraperitoneal
rupture; and (4) combined extraperitoneal and intraperi-
toneal rupture.
Suprapubic tenderness may be associated with a contusion
or tear of the bladder wall. A catheter should be placed
through the urethra; if it proves difficult, a tear of the
urethra should be suspected. Should the catheter enter the
bladder without difficulty, a major urethral injury can usually
be excluded. If the urine is blood-stained, cystography may
be performed by injecting dye into the bladder through the
catheter and looking for extravasation of the dye beyond
the bladder outline. Detailed management of major urinary
tract injuries—bladder or urethral tears—should be left to
the discretion of the urologic surgeon. If it is necessary to
make a suprapubic approach to the urethra to place a stent,
it may be possible to perform, concomitantly, a better reduc-
General Management Guidelines
FIGURE 19-33. (A) There is no obvious pelvic fracture. Intrapelvic
bleeding has displaced the bladder. (B) Extravasation of dye from
a bladder tear.
tion of the fracture fragment.69 However, metallic internal or
external fixation should be used cautiously, as there is a risk
of bladder infection during the early postinjury course.
Osteomyelitis by hematogenous or direct spread is a com-
plication to be avoided.
Cystography is one of the best methods for revealing
damage. With contusion, the bladder is generally elevated,
deviated from the midline, teardrop-shaped, and there is no
dye extravasation. With extraperitoneal injury, the cystogram
shows that the base of the bladder is obscured, and there are
small to extensive lines of contrast within the fascial planes.
With intraperitoneal rupture, there is contrast around the
bowel and an hourglass-shaped bladder; there may also be
contrast in and around the abdominal organs. It is impor-
tant to evaluate the ureters and kidneys as well.73 Retrograde
FIGURE 19-34. Multiple rami injuries (curved open arrows) were associated with bladder injury (A, straight arrows) and urethral injury
(B, arrow).
809
B
cystourethrography permits this type of study. Excretory
urography is also beneficial. Intravenous pyclography is an
easy way to obtain basic information.
Urethral trauma is infrequent in children but may be
caused by blunt or penetrating trauma. Boys are more likely
to be injured than girls.86,88 Tears are more common than
complete severance of the urethra.74 The most significant
injury is disruption of the urethra close to the apex of the
prostate.77,78,81,84 The puboprostatic ligament is ruptured, and
the bladder is displaced upward and posteriorly. In a rupture
below the urogenital diaphragm, the extravasation of dye
is often contained within Buck’s fascia.79 Urethral injury
should always be suspected and ruled out in any child with
a pelvic fracture. There is usually an inability to void, and fre-
quently blood is seen at the urethral meatus. A retrograde
810
urethrogram should be obtained, as it can demonstrate
the area of tear or severance with extravasation of contrast.
Multiple projections may be required.
Impotence may complicate urethral injury in the male
patient.85 Gibson reported impotence in 37% of their
patients with urethral injury, the largest percentage occur-
ring in patients with rupture of the membranous prostatic
portion.76 These studies were done in adults, however, and
there are no long-term studies of young children who have
had comparable pelvic fractures to determine whether they
eventually exhibit similar problems once they reach sexual
and physical maturity. Gibson further noted that fertility was
frequently impaired, and that only 14% of the adult patients
had subsequently fathered children.75 I sent questionnaires
to male patients who had sustained significant anterior pelvic
injury, with 11 responses. None had difficulty with erection
or ejaculation. Four were married, but only one patient
had been unable to have a child. Evaluation in this instance
showed extensive scarring.
Dhubuwala et al. found impotence following pelvic frac-
ture in 26 patients including a 7-year-old boy.71 They believed
the impotence was caused not by disruption of the prostatic
membranous urethra but, rather, by disruption of the neu-
rovascular supply to the penis.
Obstetric/Gynecologic Injuries
There is a possibility of future obstetric problems if the pelvic
outlet is significantly narrowed or distorted owing to a dis-
placed fracture. Again, long-term studies in immature girls
who sustain pelvic fractures have not been conducted to
ascertain whether there is a significant risk of such a com-
plication and increased need for cesarean section. Heinrich
et al. noted the association of an open pelvic fracture
coupled with vaginal laceration and pelvic diaphragmatic
rupture in a 4-year-old.89
Acetabular Fractures
Treatment of a pediatric patient with a fractured acetabulum
is determined by the general condition and associated
injuries. Most authors have advised conservative treatment,
especially in the child. In contrast, Judet and colleagues rec-
ommended greater emphasis on surgical repair, but their
series included only skeletally mature patients.105 From this
series, it appeared that conservative treatment was better for
inner wall or posterior acetabular fractures. Superior frac-
tures had poor results whether treatment was nonoperative or
operative. The most important factor seemed to be reestab-
lishment of the superior dome and extraction of any loose
fragments of bone, cartilage, or muscle that might be herni-
ated into the defects, thereby reconstituting a normal relation
between the femoral head and acetabulum. The future of the
hip depends primarily on the condition of the weight-bearing
portions of the acetabulum and femoral head, the potential
for the development of ischemic necrosis in either the acetab-
ulum or femoral head, an accurate femoral-acetabular rela-
tion, and intrinsic stability of the joint.
Heeg and coworkers reviewed 23 acetabular fractures in
patients younger than 17 years of age.102–104 Good or excellent
19. Pelvis
functional results were achieved in 21 patients, and radio-
graphic healing was good or excellent in 16. Conservative
treatment gave consistently good results with fractures
with minimal initial displacement, stable posterior fracture
dislocations, and type 1 and 2 triradiate physeal carti-
lage fractures. Less favorable results were seen with type 5
triradiate fractures and comminuted fractures, but no
operation was better than any other. Unstable posterior
fracture-dislocations and irreducible central fracture-
dislocations usually require operative treatment, but the
results may still be unsatisfactory.
Peripheral Fractures
Peripheral acetabular fractures are often associated with dis-
locations of the hip in the adult. However, because of the
structure of the child’s acetabulum—particularly the pliable
cartilaginous components such as the labrum—dislocations
of the hip often occur without concomitant acetabular frac-
ture or at least a radiologically evident (i.e., osseous) one
(see Chapter 20). In the older child, posterior dislocation is
more likely to displace an osseous acetabular fragment than
is the less common anterior dislocation (Fig. 19-35). The
chance for displacement of an acetabular fragment is also
influenced by the relative extent of ossification of the pos-
terior and anterior walls. Any acetabular fracture that accom-
panies a hip dislocation should be reduced as accurately as
possible, as it is an intracapsular injury in the child. Whether
there are fragments within the joint is not always easy to
determine, as portions of radiolucent cartilage may be dis-
placed into the joint, particularly when there is separation
of the fibrocartilaginous acetabular labrum away from
the main hyaline cartilage. Any suggestion of limitation of
motion or failure to attain complete, concentric reduction
(widening of the radiolucent cartilage or joint space) should
make one suspicious of this possibility. An arthrogram is
FIGURE 19-35. Posterior acetabular fracture, along with some
central propagation just posterior to the triradiate cartilage.
Acetabular Fractures
often of benefit diagnostically. Oblique radiographs with
the pelvis rotated 45° (both right and left oblique views)
must be obtained to reveal the posterior acetabulum in
profile. Depending on the age of the patient, the os acetab-
ulum must be considered a source of roentgenographic
“fracture” (Fig. 19-5). Large superior fragments should be
viewed with caution and must be followed carefully through
skeletal maturity in case they lead to subsequent acetabular
dysplasia and hip subluxation. CT evaluation is often
definitive.
The problem of concomitant hip dislocation and periph-
eral acetabular fracture, especially with displacement of the
osseous or cartilaginous fragment into the joint, is discussed
in Chapter 20.
Central Injuries
The femoral head is infrequently driven centrally into the
pelvis in children prior to adolescence, probably because of
the resilience of this area compared to other portions of the
pelvis (Fig. 19-36). Watts described total dislocation of the
acetabulum through the triradiate cartilage anteriorly and
the sacroiliac joint posteriorly in a 12-year-old child; it was
A such hinging to occur. It is often due to an unrecognized
B
FIGURE 19-36. (A) Central fracture with a split through the closing
or recently closed triradiate cartilage. (B) CT scan.
811
FIGURE 19-37. Superior acetabular fracture (nontriradiate).
successfully treated by open reduction and internal fixa-
tion.43 The fracture may involve the weight-bearing superior
portion, lateral to the triradiate cartilage (Fig. 19-37).
Triradiate Injuries
Traumatic disruption of the acetabular triradiate physeal car-
tilage is an infrequent injury.91,92,95,97,100–104,106,110,111,114–117,119,121
Ljubosic described 13 patients with premature closure of the
triradiate cartilage consequent to injury to the acetabu-
lum.109 Jurkovskj found 2 epiphyseal injuries of the acetabu-
lum among 237 fractures of the pelvis in children.106 Bryan
and Tullos reported 3 cases in 52 pelvic fractures; only one
patient demonstrated significant growth disturbance.10 Of
the 84 pelvic fractures in children reviewed by Reed, 4 had
evidence of acetabular triradiate involvement.33
It is my experience that triradiate fracture is often overlooked in
many children with seemingly solitary ramus fractures. If a ramus
fracture is displaced, there must be another injury that allows
chrondro-osseous separation at one or more arms of the tri-
radiate cartilage. Such displacement, which may be subtle, is
better detected by CT scans than routine radiography of
the pelvis.
If one of the pelvic bones (pubis or ischium) in a child is
displaced and rotated at the symphysis pubis, it must hinge.
In adults the hinging is usually through the sacroiliac
joint; in the skeletally immature patient, however, rather
than injury to the entire hemipelvis, the forces may be sum-
mated at the triradiate cartilage, disrupting a portion (or all)
of the triradiate end and the symphyseal end. Lateral com-
pression forces in an adult may produce a hemipelvic
disruption, whereas the child may sustain a quadrant dis-
ruption with rotatory disruption of the ischiopubic and
triradiate units.
812
These fractures are usually undisplaced and infrequently
require open reduction. However, when a displaced type 2
growth mechanism is observed and CT scan shows joint dis-
ruption, open reduction may be indicated.
Injuries to the triradiate cartilage constitute physeal
trauma comparable to fractures involving the physes of lon-
gitudinal bones. The potential for this injury should always
be assessed whenever a single ramus fracture is noted.
However, the bipolar anatomy of the triradiate cartilage and
the lack of ossified epiphyses until late adolescence may
make classification of these injuries difficult. During adoles-
cence the appearance of multiple secondary ossification
centers may make diagnosis confusing. Three basic patterns
occur that are similar to physeal fractures elsewhere in the
developing appendicular skeleton.
The first pattern is a shearing-type injury due to a blow to
the ilium or the proximal end of the femur that causes a type
1 or 2 injury at the interface of the two superior arms of the
triradiate cartilage and the metaphyseal spongiosa of the
ilium (Figs. 19-38 to 19-42). A triangular medial metaphyseal
fragment (Thurstan Holland sign) may be present. This frag-
ment effectively splits the acetabulum into a superior (main
weight-bearing) one-third and an inferior (minimally weight-
bearing) two-thirds. The germinal zones contained within
the bipolar physes would be unaffected by such a fracture
mechanism, and so continued growth would be expected.
Comparable disruption between the triradiate arms and the
metaphysis of either the ischial or the pubic ramus is theo-
19. Pelvis
retically possible. Type 1 and type 2 injuries appear to carry
a favorable prognosis for continued (relatively) normal
growth.
The second pattern is a displaced ramus fracture (more
often involving the pubic ramus) in either the diaphyseal
(analogous) segment or the metaphysis at the symphysis.
The fulcrum of rotation becomes the inferior arm of the tri-
radiate cartilage along with the anterior or posterior portion
of the superior arm (contingent on whether the pubic or
ischial ramus is involved). This rotational component at the
physeal–metaphyseal interface of the triradiate cartilage is
analogous to a displaced growth plate fracture in a long
bone. Furthermore, there has to be subchondral separation
from the contiguous articular cartilage (Fig. 19-41). They are
usually type 1 or 2 growth mechanism injuries.
The third pattern of disruption causes a type 5 injury
pattern, either as a primary injury (Fig. 19-43) or as part of
the aforementioned type 1 or type 2 pattern. Such a type 5
injury may be difficult if not impossible to detect on the
initial roentgenogram, although narrowing of the triradiate
space suggests the possibility. The variability of the radio-
graphic appearance of the triradiate cartilage makes assess-
ment of “width” changes difficult (even with a CT scan).
Accordingly, one must look for osseous bridging several
months after the injury. Premature closure of the triradiate
cartilage appears to be the usual outcome of a type 5 injury;
and, depending on the age of the patient at the time of
initial injury, it may cause progressive acetabular dysplasia
FIGURE 19-38. (A) Bilateral type 2 growth mech-
anism injuries (arrows) of the triradiate cartilage.
(B) Extent of healing 2 months later.
Acetabular Fractures 813

germinal zones necessary for continued growth. A vascular

injury may be the real cause of premature closure (variation
of a type 5 injury), rather than crushing of germinal cells.
Furthermore, microscopic type 4 shear fractures and com-
minution (see Chapter 6) may be factors.
During the final normal stages of closure of the triradiate
cartilage, severe trauma to the pelvis may result in a fracture
through one or more of the regions of the arms of the trira-
diate cartilage (Fig. 19-42). This pattern during late adoles-
cence is analogous to the Tillaux fracture of the distal tibia,
with the remodeling bone plate creating a region of tempo-
rary susceptibility to fracture until osseous remodeling across
the physeal region is well under way. During this stage sec-
ondary (epiphyseal analogue) centers occur within the trira-
diate cartilage (Figs. 19-3 to 19-5). These ossification regions
should not be confused with a fracture or comminution in an
adolescent being evaluated for acute pelvic trauma.
Pina-Medina and Pardo-Montaner reported an unusual
combination of triradiate cartilage fracture associated with
transphyseal separation of the femoral head.113
Figure 19-50 (below) shows a representative patient who
sustained growth injury to the triradiate cartilage. Potential
injury may only be suggested contingent on the degree of
trauma and possible limitation of movement. The diagnosis
may have to be made retrospectively.120 Narrowing of the
triradiate cartilage and displacement are difficult to detect
roentgenographically, especially when other pelvic compo-
nents are damaged.
These fractures are usually undisplaced and infrequently
require open reduction. However, when a displaced type 2
growth mechanism is observed and CT scan shows joint
disruption, open reduction may be indicated.
The major subsequent problem is disparate growth of the
acetabulum and the femoral head (Fig. 19-44). The femoral
head continues to grow, whereas the normal mechanism
of concomitant hemispheric expansion of the acetabulum
cannot occur responsively. Growth may occur only at the
periphery. Such growth at the periphery becomes increas-

FIGURE 19-39. (A) Type 2 injury of the left acetabulum in a 2-year-

old child. (B) Similar injury in a 13-year-old. (C) Internal fixation.

(Fig. 19-44). The earlier in life any premature closure occurs,

the greater is the potential for change in acetabular mor-
phology with subluxation and lateralization of the less
affected or unaffected femoral head.
Growth mechanisms about the pelvis are dependent on an
adequate vascular supply. It is feasible that trauma disrupts
significant portions of the blood supply to the central ger-
minal zone of the bipolar physis, further contributing to
permanent disruption of growth. This region, like other FIGURE 19-40. Pubic ramus fracture extending to the triradiate car-
epiphyses, is penetrated by cartilage canals that supply the tilage. Note the anterior greenstick fracture of the opposite side.
814 19. Pelvis

A B

FIGURE 19-41. Apparent type 1 injury of the triradiate (pubic-ischial shell at the anterior acetabular wall. The ramus is hinged at the tri-
arm) with rotation of the fragment toward the bladder. (B) Posteri- radiate cartilage.
orly displaced fracture of the pubic ramus leaving a subchondral

ingly subjected to pathologic pressure from the femoral
head, causing eversional deformation, not unlike that seen
in developmental hip disease. When the fracture occurs
during adolescence, subsequent growth-related changes in
acetabular morphology and congruency of the hip joint are
unlikely. However, in young children, especially those who
are less than 10 years old, acetabular growth abnormalities
are a complication of this injury and may result in a shallow
acetabulum similar to that seen in patients with develop-
mental dysplasia of the hip.
Trousdale and Ganz thought that the radiographic
appearance of posttraumatic acetabular dysplasia was dis-
tinctly different from developmental dysplasia.120 The acetab-
ular teardrop width and inner wall of the acetabulum were
significantly enlarged, with lateralization of the femoral
head.
By the end of skeletal maturity, disparate growth increases
the incongruence of the hip joint and may lead to progres-
sively more severe subluxation of the proximal femur.
Acetabular reconstruction may be necessary to correct the
gradual subluxation of the femoral head. Variable irregular-
ities of growth at the proximal end of the femur may also
occur. Whatever the etiology, once the bridge is formed it
acts as a bone graft across the acetabular physis. Experi-

FIGURE 19-42. (A) Thurstan Holland fragment evident only on the Judet view. (B) Internal fixation.
Acetabular Fractures 815

FIGURE 19-43. (A) Attention to a subtrochanteric fracture led to failure to assess a triradiate injury. (B) Three months later a bridge is
forming. (C) CT view of the osseous bridge (arrow). (D) Fourteen months later. The parents refused bridge resection.
816
mentally, a bone graft across a physis may cause distortion or
arrest of growth that ceases only when the graft (progres-
sively) breaks, is resorbed, or is replaced by nonosteogenic
material.101 Theoretically, if the osseous bridge were removed
surgically, growth would resume and the normal shape of the
acetabulum might be preserved. However, the rapid devel-
opment of the osseous bridge and progression to closure of
the triradiate cartilage suggest that resection of the bridge
and implantation of fat or some other interpositional mate-
rial, as recommended for injuries to long bone physes, may
not have much success in this particular anatomic region.
Presumably, there are different degrees of damage to the tri-
radiate cartilage, so variable inhibition of growth may occur.
Peterson and Robertson reported the first resection of a tri-
radiate growth arrest.112
The growth physes of the three pelvic bones extend con-
tinuously from the triradiate cartilage laterally into the
discrete acetabular peripheral physis. Fusion of the triradi-
ate cartilage may still leave the peripheral physis intact.
Depending on the age of the child at the time of injury, this
acetabular growth plate continues to grow, effectively enlarg-
ing the acetabulum laterally (i.e., circumferentially and
posteriorly). The medial wall of the acetabulum becomes
thicker and the acetabulum more shallow. Concomitantly,
as the femoral head expands and is displaced laterally and
superiorly (subluxates), it exerts increased pressure against
the superior part of the acetabulum, impairing normal
endochondral ossification and increasing the acetabular
index, similar to the mechanism of developmental dysplasia
of the hip.
Reconstructive surgery may be necessary in some of these
children and must be individualized to the specific injury,
concomitant pelvic deformation from other fractures, and
the degree of anticipated growth. Shelf augmentation pro-
cedures offers a solution in many of these cases.
None of the reported patients with triradiate fracture had
significant pain in the hip at skeletal maturation, although
one did have some pain with exertion at extremes of motion
during the physical examination. Blair and Hanson reported
a patient who was originally injured at the age of 4 years
when he sustained a fracture of the left femur, right pubis,
and diastases of the pubic symphysis, right sacroiliac joint,
and left triradiate cartilage.91 Premature bridging was
19. Pelvis
FIGURE 19-44. Growth arrest leading to a shallow
acetabulum.
present in the triradiate cartilage 2 months after the injury.
At 14 years he was having significant pain in the hip, and
evaluation showed subluxation of the hip. By the age of 16
the pain required a Chiari osteotomy. Rodrigues noted
growth arrest following injury to the triradiate cartilage,
causing a miniacetabulum.115 Similar growth arrest has been
reported by Hallel and Salvati.101
Experimental closure of the triradiate cartilage, with
gradual acetabular dysplasia, has been reported.90,93,
94,96,98,99,101,107,108,118
Gepstein and associates found no signifi-
cant difference in acetabular dysplasia or hip displacement
resulting from fusion of all three limbs versus selective fusion
of the ilioischial limb.98 Delgado-Baeza and coworkers have
shown that experimental traumatic lesions of the iliac and
pubic regions of the triradiate cartilage of the acetabulum in
rats produced interference with the pubic growth plate that
eventually caused acetabular dysplasia and dislocation of the
hip.93,94,99 Although their primary emphasis was to look at
damage that could lead to some of the changes seen with
developmental dysplasia of the hip, obviously the traumatic
nature is germane for evaluating the results from injury to
this region during trauma. With severe disruption of growth,
a shallow acetabulum results, with progressive subluxation if
not dislocation of the hip.
Avulsion Fractures
Avulsions are the most common type of pelvic chondro-
osseous injury in the child and especially in the adolescent
athlete. Most may be treated by rest, relief from weight-
bearing with crutches, muscle relaxants, and cessation of the
evocative athletic activity for several weeks. These regions
may be avulsed prior to the appearance of secondary ossifi-
cation (which frequently does not appear until late adoles-
cence). In such absence of definitive radiologic diagnosis,
the injury must be strongly suspected clinically, and treat-
ment should be directed toward the presumptive injury.
Several weeks later the diagnosis may be confirmed by the
appearance of “metaphyseal” callus (Fig. 19-45). Because of
the thick periosteum and perichondrium, these fractures are
not usually significantly displaced. Postinjury muscle func-
tion is generally not impaired by eventual healing in a mildly
Avulsion Fractures
FIGURE 19-45. (A) Appearance of the ischial tuberosity following a
“split” injury during water skiing. Note a small linear crack sugges-
tive of fracture (arrow). (B) Three weeks later some reactive bone
displaced position, even if a fibrous, rather than osseous,
union results owing to the persistent tensile forces. However,
significant displacement, which is much less common, may
cause functional insufficiency (inefficiency) of the involved
muscles and may require open reduction or reconstruction
(i.e., shortening) for optimal muscle function. Complica-
tions are unusual, as these fractures are ordinarily associated
with minor athletic stress, rather than major trauma.
When a musculotendinous unit is subjected to excess
stress, whether an acute overload or a less forceful but re-
petitive application, the contraction or contractions may be
transmitted to the apophysis. This may result in a fracture at
either the chondro-osseous interface or through a segment
of the subchondral bone. The excessive, invariably repetitive
demands of adolescent athletics make this age group espe-
cially susceptible to avulsion fractures.
Various studies suggest that iliac spine avulsions are the
most common, whereas others list ischial injuries as more
frequent.159 Frequency is not as important as suspicion and
recognition by the clinician.
The basic treatment protocol is to stop the evocative activ-
ity, prescribe rest (including bed rest), prescribe nonsteroidal
drugs, recommend appropriate positioning of the leg, and
gradual resumption of activity. There should be protected
weight-bearing with crutches. Most avulsion fractures may be
managed nonoperatively, with attention directed at minimiz-
ing tension in the musculotendinous insertion.
Confusion with neoplasia or even osteomyelitis may be
likely when there is irregular radiodensity and radiolucency.
If a biopsy is done, the callus may be misinterpreted as
an osteosarcoma.161 Such a mistake may lead to unnecessary
and costly evaluation and to inappropriate, even ablative
surgery.
For competitive adolescent athletes conservative treat-
ment of pelvic avulsion injuries may cause difficulties,
despite good functional results. The disadvantages include
a relatively long period of immobilization, use of crutches,
817
(arrow) confirms the diagnosis. (C) Four months later the area is
beginning to remodel.
risk of reinjury, alteration of functional length of
involved muscles, disruption of normal training regimens,
and the risk of missing a significant part of a sport
season.
Iliac Crest
Butler and Eggert reported a fracture of the iliac crest as a
variation of “hip pointer,” which is usually defined as an iliac
crest contusion.122 Their patient sustained a direct blow to
the crest from a football helmet. Clancy and Foltz reviewed
iliac crest apophysitis and thought that it was a significant
cause of disability in the adolescent athlete.123 They reported
13 cases of anterior iliac crest apophysitis and 3 cases of stress
fractures of the anterior iliac apophysis in adolescent
runners.
Godshall and Hansen reported a case of incomplete avul-
sion fracture of the iliac epiphysis resulting from a sudden,
severe contraction of the abdominal muscle associated with
abrupt directional changes while running.124 They were
unable to find any comparable cases, although they subse-
quently saw a 16-year-old boy with a similar injury. They
thought this particular condition in adolescent athletes
could be confused with the “hip pointer,” or a contusion of
the iliac crest.
Symptoms may occur acutely or, at the other end of the
spectrum, may persist for months following questionable
injury. Some adolescent athletes have a posterior iliac crest
apophysitis with pain localized at the posterior iliac crest
(Fig. 19-46). This condition may be duplicated by resistance
to abduction with the hip flexed and the patient lying on the
unaffected side.
Roentgenograms are frequently unremarkable. One often
must seek subtle differences in contour or physeal width.
Variable radiolucencies within the iliac crest apophyseal ossi-
fication center are common, just as they are in the calcaneal
apophysis (see Chapter 24); they are not indicative per se of
818
FIGURE 19-46. Adolescent complaining of “hip pointer” after a football tackle. (A) There is mild separation (arrow) of the iliac ossifica-
tion center on the right. (B) Fracture through crest ossification (arrow) following a direct blow to the pelvic rim.
either an avulsion fracture or a fracture within the ossifica-
tion center.
To avoid the risk of further avulsion and more serious
damage, crutches should be used for 5–7 days, followed by
limited physical activity for approximately 4 weeks. Patients
treated by rest and discontinuation of their usual athletic
activity generally have complete relief of symptoms within
4–6 weeks and are able to resume training programs at that
point.
More significant trauma may avulse significant portions of
the iliac crest (Fig. 19-47). The more violent the trauma, the
greater is the risk of damage to growth potential, creating
underdevelopment of the iliac wing. McDonald showed that
growth disturbance of the ilium may be associated with pre-
mature fusion of the sacroiliac joint.24
Physeal avulsion of a nonossified iliac crest may result in
intestinal obstruction because of a lumbar hernia or entrap-
ment of bowel segments.55,61 Damage to the iliac crest physis
during early childhood may lead to growth discrepancy
(Fig. 19-48). Olney et al. found that experimental splitting of
the rabbit iliac apophysis significantly affected growth of the
ilium.125 Altered iliac growth, development, and attainment of
FIGURE 19-47. Subchondral equivalent of an iliac apophysis avul-
sion. This 4-year-old boy was severely injured when pinned under
the tire of a large truck.
19. Pelvis
a normal shape and orientation might negatively affect the
origin and vector efficiency of the adductor muscles, which
could, over time, affect the biomechanics of the hip.
Iliac Spines
The anterosuperior iliac spine (ASIS) serves as the attach-
ment of the sartorius muscle and some of the tensor
fascia lata; and the anteroinferior iliac spine (AIIS) is the
attachment for the rectus femoris muscle. The muscles
arising from either spine cross two mobile joints, both of
which are major hip flexors and may be under extreme
force during vigorous athletic activity or during an accident.
Either iliac spine may be avulsed.126–169 The anterosu-
perior spine is probably injured more often than the
anteroinferior spine. The classic presentation is an adoles-
cent sprinter who feels a sudden, sharp pain in the groin
upon leaving the starting blocks. Less commonly repetitive
stress of training may lead to insidious prodromal micro-
failure that can go on to complete avulsion (similar to the
patterns of slipped capital femoral epiphysis and Osgood-
Schlatter’s lesion).
FIGURE 19-48. Adolescent who as an infant had sustained an
injury to the left pelvis when thrown from a car during an accident.
The left hemipelvis is hypoplastic; and the entire pelvis is rotated,
with displacement of the symphysis. The injury appeared to involve
only a portion of the iliac crest (arrow), as the acetabulum formed
in a reasonably normal manner.
Avulsion Fractures
FIGURE 19-49. Fractures of the superior iliac spine. (A) Direct blow, with mild displacement. (B) Avulsion following a direct blow.
(C) Injury of the anterosuperior iliac spine with downward displacement.
Two mechanisms of injury have been proposed. The first
is a forceful contraction of the sartorius and tensor fasciae
lata muscles against a hyperextended trunk (e.g., while
running, playing soccer), such as at the start of a race or
while slipping. The second is the sudden, repetitive move-
ments of short sprints. This injury pattern most frequently
affects adolescent runners. Essentially the two joints are
moving in opposite directions simultaneously.
Most patients complain of acute pain, which is usually
severe enough to cause them to stop the activity. Pain is
increased during active movement of the hip. A snap was felt
by the patients in 45% of cases. Swelling and tenderness are
often present.
FIGURE 19-50. (A) Avulsion injury of the supe-
rior iliac spine (arrow) in a 14-year-old sprinter
who sustained a tear coming out of the starting
blocks. (B) Appearance 7 weeks later with callus
formation.
819
C
Diagnosis may be difficult. In a young child the spine may
be cartilaginous, and thus impossible to detect with routine
radiography. The adolescent usually has a fracture through
the equivalent of metaphyseal bone, pulling off the cartilage
and enough osseous tissue to be detected radiographically.
Rarely, a secondary ossification center is evident in a carti-
laginous disruption in the adolescent.
Usually these fractures do not separate significantly,
although in rare instances they may be displaced several
centimeters, especially when the trauma is repetitive (Figs.
19-49, 19-50). Hamsa described a displaced superior iliac
spine that had led to formation of an osseous bar extending
down from the pelvis.190 Chronic, repetitive avulsion may
820
FIGURE 19-51. (A,B) Elongated superior iliac spine after break dancing. (C) Mechanism is the traumatic (repetitive) equivalent of
surgical bone lengthening by chondrodiatasis.
lead to formation of an extensively elongated superior spine
(Fig. 19-51).138,154
Treatment includes rest, minimal weight-bearing with the
use of crutches, and discontinuation of athletic activities for
4–6 weeks. If a significant separation has occurred, open
reduction may be indicated. However, open reduction and
internal fixation are rarely needed (Fig. 19-52).
Walking on crutches for 1–2 weeks and abstaining from
vigorous activities yield the best results. The average
duration of disability is approximately 20 days. Pain should
be absent before evocative athletic activities are resumed.
Irving reported two cases of exostosis formation after
traumatic avulsion of the AIIS.144 This particular injury
19. Pelvis
(Figs. 19-53, 19-54) is much less common than other
avulsion fractures around the pelvis and should not be con-
sidered myositis ossificans. This enlarged reactive bone must
be interpreted carefully.
Exostosis formation of either the ASIS or AIIS is due to
acute or chronic traction avulsion of the cartilaginous
apophysis. The intervening gap is filled in with endo-
chondral bone (chronic traction) or a combination of
membranous and endochondral bone (acute avulsion).
In the chronic situation the repetitive minimal avulsion/
traction duplicates the same phenomenon as with
limb lengthening through the growth plate (i.e.,
chondrodiatasis).
Avulsion Fractures 821

FIGURE 19-52. (A) Avulsion of the anteroinferior spine. (B) Internal fixation.

FIGURE 19-53. (A) Avulsion of the inferior iliac spine (arrow). (B) Avulsion of the combined inferior spine and acetabular rim ossification
center. (C) Four months later extensive healing is evident.
822
FIGURE 19-54. Exostosis formation following anteroinferior spine
injury in a 6-year-old child. There was no evidence of osseous
spine injury during initial major pelvic trauma. In retrospect, the car-
Ischial Tuberosity
Injury to the ischial tuberosity has been discussed fre-
quently,170–232 and Hamada and Rida presented an excellent
review.189 Irregularity of the apophysis of the ischial tuberos-
ity is termed Kremser’s disease. The typical patient is a young
adolescent athlete. This area may be avulsed (Fig. 19-55),
which may lead to nonunion although not necessarily a
symptomatic one (Fig. 19-56).200,206
FIGURE 19-55. (A) Avulsion of the ischial tuberosity with early bone formation (arrow). (B) At 7 weeks extensive bone formation is
evident.
19. Pelvis
tilaginous inferior spine had avulsed. New bone formation (arrow)
is evident 3 weeks after injury and 8 months later (arrow) (B).
(C) Five years later.
Ischial apophysiolysis is often diagnosed only after con-
siderable time. In these delayed cases, commonly the pre-
cipitating injury is not considered significant by either the
patient or the physician.
The mechanism of injury appears to be the action of the hip
flexors on the pelvis, transmitted across the femoral head as a
fulcrum, which tends to elevate the ischium. This elevation is
counteracted by the hamstring muscle, which pulls downward
and laterally, a force neutralized by the sacrosciatic ligaments.
Avulsion Fractures
A B
FIGURE 19-56. (A) Avulsion of the ischial tuberosity 10 months after injury. (B) Three years later. Sitting was painful. This fragment was
subsequently excised.
Therefore the degree of displacement of the ischial apophysis
depends on the specific role of these ligaments. The most
likely conditions for the injury are attained when a powerful
muscle contraction takes place in the hamstrings with the
pelvis fixed in flexion and the knee in extension. These con-
ditions commonly occur with hurdling and gymnastics,
although many other sports are associated with the injury. For
example, in the boy shown in Figure 19-45, the injury was
acquired during water skiing when he did an inadvertent split
while both skis were in contact with the water.
From an anatomic standpoint, an avulsion is likely to be
partial (incomplete). The ischial tuberosity is roughly divisi-
ble into two portions, one for insertion of the hamstrings
and the other for insertion of the adductor magnus. Thus
the pattern of injury in a high hurdler could be different
from that in a dancer doing a split.
Diagnosis often is difficult in these children. Figure 19-45
shows an absence of any significant area, although the small
crack, coupled with the history, should make one suspicious.
FIGURE 19-57. Open reduction of an avulsion
of the ischial tuberosity. (A) Original injury.
(B) Postoperative appearance.
823
Yet later, with formation of new bone, the diagnosis became
obvious. Watanabe and Chigira described a detailed study
with serial CT scans showing avulsion of small bone frag-
ments that subsequently enlarged (in the unossified carti-
laginous apophysis, similar to the Osgood-Schlatter injury
pattern).228 They also found that MRI studies strongly sup-
ported the concept of an avulsion fracture.229
Treatment may vary. Most patients with ischial apophysi-
olysis do well with rest and a protective program. Ideally,
osseous union is demonstrable by roentgenography before
strenuous exercises are again permitted. Milch’s study indi-
cated it may require up to 2–4 years in the younger age
groups.209 Failure to follow a protective program could result
in avulsion fracture of the apophysis from a subsequent
undisplaced injury. The possibility of contralateral involve-
ment should always be kept in mind.
Avulsion fractures with significant separation (1 cm or
more) probably should be reduced anatomically by closed or
open reduction (Fig. 19-57). An attempt at closed reduction
824
probably is worthwhile and may be possible with direct pres-
sure over the tuberosity. Open reduction of an avulsion frac-
ture is a relatively straightforward procedure. Attachment
may be made with cancellous screws. Pruner and Johnston
discussed the use of fixation of the ischial tuberosity when it
was displaced.215 Wootton et al. also recommended open
reduction and internal fixation for significantly displaced
fractures.231 Their cases were associated with marked chronic
disability after delay in diagnosis and nonunion of the frac-
ture. Howard and Piha suggested that avulsions with more
than 2 cm displacement needed operative reduction and
fixation.194
An untreated avulsion fracture may unite spontaneously or
may form a fibrous union with subsequent enlargement of the
tuberosity.219 The symptoms include inability to sit comfort-
ably on the enlarged, nonunited tuberosity and pain, with
associated discomfort in the back or limb especially while
involved in excessive activity.21,214,221 The subsequent enlarge-
ment of the tuberosity may be irregular enough to suggest a
tumor, and a diagnosis of osteogenic sarcoma or Ewing’s
sarcoma has been rendered in some cases. Sciatic-type pain is
not a general feature of the older, chronic lesions; and if this
symptom is encountered, one should rule out a coexistent
herniated intervertebral disk before attributing neurologic
symptomatology to this lesion.
Chronic injuries, when symptomatic, may be treated
by excision of the ununited fragment and repair of the
tendinous origin of the hamstrings or by fixation and
bone graft. I prefer resection and musculotendinous
reattachment.
Other Pelvic Injuries
Stress Fracture
The increased emphasis on competitive sports not only puts
skeletally immature individuals at risk for the previously
described avulsion injuries, it also may lead to unusual avul-
sions and stress fractures. As discussed in the section on
anatomy, the pubic symphysis and ischiopubic synchondro-
sis are areas of progressive chondro-osseous growth and mat-
uration. Repetitive use may cause strain and lead to chronic
FIGURE 19-58. Stress fracture (arrow) of the pubic ramus.
19. Pelvis
FIGURE 19-59. Stress fracture of the left ischial synchondrosis
(arrow). The right ischial synchondrosis is physiologically closed
although still slightly enlarged.
fatigue manifesting as pain (i.e., an incomplete or micro-
scopic fracture of the evolving chondro-osseous interface).
These stress fractures (Fig. 19-58) should be treated symp-
tomatically, with the emphasis on decreasing or stopping the
evocative activity.
Ischiopubic Osteochondrosis
The ischiopublic osteochondrosis region may be the site of
stress fractures in young joggers and runners (Fig. 19-59).
Such fractures are nondisplaced.213 These injuries are more
frequent in females, which may be due to differences in
pelvic anatomy and running styles. The increased participa-
tion of young individuals in these sports leads to similar
symptoms (groin/thigh pain) but with radiolucency/radio-
density or enlargement of the synchondrosis.
Treatment is symptomatic. Temporary cessation of the
physical activity for 2–3 weeks usually alleviates the pain.
Preactivity stretching may lessen muscle pull at the pelvic
attachment.
Pubic Symphysis
In the adolescent the onset of midline pain at the symphysis
may be due to a fatigue (tension) failure of the chondro-
osseous origin of the gracilis muscle.237 Changes (radio-
graphic) usually involve only one side of the symphysis. It is
referred to by several names: osteitis pubis, pubic symphysi-
tis, osteochondritis of the symphysis pubis, adductor injury,
and gracilis syndrome.
Pain may be in the groin, perineum, or medial thigh and is
usually gradually insidious in its onset. On examination there
may be discrete tenderness at the symphysis. Radiographic
proof is contingent on a cartilaginous avulsion (radiolucent)
or a piece of subchondral bone along with a cartilage frag-
ment. Fragment displacement is not significant. Reactive
bone may form in the gap (similar to other apophyseal pelvic
avulsions), sometimes leading to a small “exostosis.” Chronic
motion may also cause erosive irregularities in the bone
margin, akin to gymnast’s wrist (see Chapters 12, 16). In
Wiley’s case the bone fragment was excised.237 Histology was
compatible with chronic avulsion failure. Others have
reported similar cases in adolescent athletes.233–236
References
Meralgia Paresthetica
Edelson and Stevens239 and MacNichol and Thompson240
reviewed children and adolescents with meralgia pares-
thetica. It was usually associated with injury during sports
activities. Bilateral involvement is common. The average
duration of symptoms was 24 months. In about half of the
cases the diagnosis was missed initially. Predisposing factors
appeared to include previous pelvic osteotomy and pelvic
fracture. The usual pain was over the anterior or lateral
thigh.
Pain reproduced by direct palpation of the nerve (inferior
to the ASIS) and a trial injection of lidocaine (Xylocaine)
usually produced transient relief of symptoms. Pain
decreased normal activities, including sports. Several were
eventually treated with decompression of the lateral cuta-
neous nerve. Surgery revealed thickened fascial constrictive
bands. Previously unrecognized repetitive (stress) avulsion of
the ASIS may present with chronic pain attributed to
meralgia paresthetica.238,241
References
Anatomy
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children: some normal roentgenologic findings. AJR 1956;
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2. Cawley KA, Dvorak AD, Wilmot MD. Normal anatomic variant:
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3. Gamble JG, Simmons SC, Freedman M. The symphysis pubis:
anatomic and pathologic considerations. Clin Orthop 1986;
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5. Ogden JA. Hip development and vascularity: relationship to
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normal child: anatomical, histological, and roentgenographic
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830 19. Pelvis

Meralgia Paresthetica
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20
Hip
Engraving of the adolescent hip. (From Poland J. Traumatic
Separation of the Epiphyses. London: Elder, Smith, 1898)
he relevant anatomy of the acetabulum is presented
T
in Chapter 19, and aspects of proximal femoral devel-
opment are presented in Chapter 21. However, certain
morphologic structures relate directly to the hip joint
and the specific problems encountered during traumatic
dislocation of the hip joint in the skeletally immature
individual.
Anatomy
The capsule inserts along the chondro-osseous junction
of the pelvis, making the cartilaginous acetabular labrum
intracapsular.1 This is evident as the “rose thorn” in arthro-
graphic studies. The femoral capsular insertion along the
intertrochanteric margins totally encapsulates the develop-
ing capital femur and femoral neck, creating an enveloping
“spherical” structure comprised of synovium, capsule, and
dense ligamentous condensations (Fig. 20-1). The capsule
has intrinsic laxity that allows considerable displacement of
the joint components if the suction effect is disrupted. The
allowable displacement may be significant (Fig. 20-2). Joint
effusion following trauma, similar to pus in septic arthritis,
may accumulate rapidly, break the suction effect, and
hydraulically stretch the capsule.
The iliofemoral ligament (ligament of Bigelow), which
may be an obstacle to reduction, resembles an inverted Y.
The ligament is often referred to as the Y-ligament. The
apex of the ligament is the thickened longitudinal fibers of
the capsule originating from the anterior inferior iliac spine
and traversing the anterior aspect of the hip joint to attach
to the anterior intertrochanteric line (Fig. 20-3). Distally, this
fibrous band broadens and separates into two relatively dis-
tinct bands. The iliofemoral ligament normally limits hyper-
extension and lateral rotation of the hip joint. The ligament
is under maximum tension in extension, which also may
increase intracapsular pressure, especially when a posttrau-
matic hemarthrosis is present.2,3 The capsular confinement
is used as a rationale for the need to perform capsulotomy
for hip dislocation or femoral neck fracture to decompress
a posttraumatic hematoma. Placing the hip in flexion,
however, either in bed in balanced suspension or in a cast
may alleviate much of such pressure without having to
release the fluid operatively or percutaneously. Furthermore,
the capsule is usually torn with traumatic hip dislocation,
allowing extracapsular extravasation of blood into the con-
tiguous soft tissues.
Tears may involve the midcourse of the ligament because
the ligamentous attachments into the cartilage and bone
are dense. Buttonhole displacement through a capsular tear
may impose constricting restraints to closed reduction
and necessitate open reduction (Fig. 20-4). The Y-ligament
may become taut during dislocation and thus become a
significant impediment to closed reduction.
When the capsule is torn, it is likely that the tear is closer
to the pelvic attachment than to the thicker femoral attach-
ments. Such avulsion may include marginal bone (Fig. 20-5)
and cartilaginous labrum from the acetabulum. In young
children only cartilage may be involved, making routine
radiographic diagnosis difficult. Such avulsions are analo-
gous to growth mechanism injuries in the long bones.
831
832
FIGURE 20-1. Appearance of the hip joints in a 7-year-old child.
The right hip capsule has been cut along the femoral insertion to
emphasize the contour and anterior extent of this structure. The
solid arrow depicts the demarcation between the labrum and cap-
sule. Essentially, the capsule extends the hemispheric acetabulum
to create an enveloping structure that is approximately three-fourths
of a sphere. The left hip capsule has been cut to emphasize the
posterior intertrochanteric line (open arrows). This portion does not
extend as far along the femoral neck as the anterior portion.
FIGURE 20-2. Once the suction effect is broken, the proximal femur
may be displaced from the acetabulum. The capsule allows
considerable displacement before constraining the femoral head.
FIGURE 20-3. Y-Ligament of Bigelow. (A) In flexion, the ligament
relaxes. (B) In extension, the ligament is taut.
20 Hip
The iliopsoas tendon may be displaced behind the dislo-
cated femoral head and may indent the capsule, as with
developmental hip dislocation (Fig. 20-4). Such displace-
ment may present a major obstacle to closed reduction.
Other muscles in the direct path of the dislocating femoral
head may be stretched or partially torn. The external rotator
muscle group (obturator externus and internus, piriformis,
and quadratus femoris) is either partially or completely torn,
along with the posterior part of the capsule. The femoral
head occasionally pushes between the short external rotators
without tearing them. The gluteus maximus, medius, and
minimus muscles are stretched and pushed backward by
the femoral head, which usually lies deep to these muscles,
similar to the distortion caused by developmental hip dislo-
cation. These muscles and tendons may, by a buttonhole
effect, prevent or impede reduction.
The ligamentum capitum femoris may limit the extent of
displacement of the femoral head, no matter what the age
of the patient,3,4 but it has to rupture to allow complete acute
anterior or posterior dislocation. Accordingly, any blood
supply from the ligament into the femoral head is disrupted.
The significance of this particular blood vessel system to the
overall hemodynamics within the femoral head is unknown,
although it does not appear to be a major supply.1–3
Incidence
Hip dislocation in children has been frequently reported,
although a large number of the reports are case studies.5–82
Epstein reported 75 dislocations in 74 skeletally immature
patients over a practice span of 48 years.19,21 They repre-
sented 9% of an overall series of 830 hip dislocations in
patients of all ages. Approximately 75% of the young patients
were boys and 25% were girls. The right and left hips were
almost equally involved. There were 11 dislocations in the
2- to 4-year age group, 13 in the 5- to 7-year age group, 18 in
the 8- to 12-year age group, and 33 in the 13- to 15-year age
group. Of these dislocations, 67 were posterior, 8 were ante-
rior, 4 were accompanied by ipsilateral femoral fractures,
and 1 was not recognized for 2.5 months.
FIGURE 20-4. (A) Effect of buttonholing through the capsule. (B)
Effect of a displaced iliopsoas tendon on preventing reduction. The
structure marked by lines is the acetabulum.
Posterior Dislocation
A B
FIGURE 20-5. (A) Peripheral secondary ossification (arrows). It
may be fractured as an equivalent of a physeal fracture when the
hip dislocates. (B) Computed tomography (CT) scan shows
the continuity of the secondary ossification of the anterior rim and
The Pennsylvania Orthopaedic Society collected 51 cases
of hip dislocation in skeletally immature patients: 41 were
posterior, 8 were anterior, and 2 were central.63,64 Nine
patients had associated fractures of the acetabulum, femoral
head, or greater trochanter. These particular concomitant
injuries strongly influenced the prognosis. Five additional
patients had associated ipsilateral tibial or femoral shaft
fractures; these injuries did not influence the final results in
four instances but did delay diagnosis and treatment of the
hip injury.
Using multivariate analysis to assess reported cases of hip
dislocation in patients under 16 years of age, 87% were poste-
rior, and the male/female ratio was 4 : 1. Minimum trauma is
more likely to cause dislocation in those 8 years old or
younger. The young child has increased susceptibility to
minimal injury because of relative ligamentous laxity and the
biologic plasticity of the fibrocartilaginous acetabular margin.
After 8 years of age, hip dislocation is associated with increas-
ingly forceful mechanisms. Overall, approximately 15% of
children have a concomitant fracture, with the femoral dia-
physis or greater trochanter being the most common.
Types of Dislocation
Traumatic dislocation of the hip may be classified according
to the position of the displaced femoral head relative to the
acetabulum. They are depicted in Figure 20-6 and are sub-
sequently illustrated with patient radiographs.
Posterior iliac. The femoral head lies posterosuperiorly
along the lateral aspect of the ilium, usually with a significant
portion of the femoral head above the acetabular roof and
lateral edge (Figs. 20-7 to 20-9).
Posterior ischial. The femoral head is displaced pos-
teroinferiorly and lies adjacent to the greater sciatic notch
(Figs. 20-10, 20-11).
833
the triradiate cartilage. A seemingly separate posterior osssifi-
cation center is also evident. These ossification variations must
be distinguished from a peripheral fracture complicating a hip
dislocation.
Anterior obturator (anterior-inferior). The femoral head
lies near the obturator foramen. The perineal type is an
extremely inferiorly displaced form of anterior dislocation.
Anterior pubic (anterior-superior). The femoral head is dis-
placed anterosuperiorly along the superior (pubic) ramus.
Central. There is a comminuted fracture of the central or
superior portion of the acetabulum with displacement of the
femoral head and acetabular fragments into the pelvis. This
injury is unusual in a child and often involves disruption of
the triradiate cartilage Alternatively, the acetabular roof is
split superiorly, at a variable distance from the superior arms
of the triradiate cartilage. These patterns are discussed in
detail in Chapter 19.
Inferior. There is a dislocation with the femoral head lying
directly inferior to the acetabulum (Fig. 20-12). It may be
referred to as luxatio erecta when the head is directed com-
pletely inferior and the femoral shaft is longitudinally
aligned with the spine (Fig. 20-13).
Medial. A medial segment of the femoral head may remain.
This type of comminution is rare in children. In the adult it
is classified as a type 4 injury (see Chapter 21).
Slipped capital femoral epiphysis (SCFE). With dislocation of
the hip in association with separation of the capital femoral
epiphysis, the capital femur may remain in the joint while
the femoral neck “dislocates”; or the capital femur may be
totally extracapsular but is displaced at the time of disloca-
tion or with reduction.
Posterior Dislocation
Mechanism of Injury
The trauma sustained with a posterior dislocation varies
considerably. One of the most striking observations is the
frequently benign nature of the injury that causes hip dislo-
cation in an infant or young child. In contrast to the
834 20 Hip

FIGURE 20-6. Types of dislocation.

FIGURE 20-7. Bilateral traumatic dislocation

(arrows).
Posterior Dislocation 835

FIGURE 20-8. (A) Posterior iliac dislocation in a 6-month-old

infant. This injury is rare but may be distinguished from a
developmental hip dislocation by the history (an accident)
and normal acetabulum. With trauma a fracture of the prox-
imal femur is more likely. Often such dislocations in this age
group are due to a septic process. (B) Posterior iliac dislo-
cation in a 3-year-old child.

FIGURE 20-10. Posterior ischial dislocation in a 3-year-old child.

B
FIGURE 20-9. (A) Direct posterior dislocation of the left hip in a 4-
year-old boy. Note the widening of the cartilage space medially and
“rotation” of the femoral head. (B) After closed reduction.
836
FIGURE 20-11. Posteroinferior dislocation in a 7-year-old child.
significant force usually required to dislocate the adult hip,
seemingly trivial injuries may have the same result in younger
age groups.
Because minor injuries can cause traumatic dislocation of
the hip in children under 5 years of age, the dislocation
may be missed because of a lack of suspicion of the
possibility of such injury. These injured children may present
with a complaint of knee pain through referred pain from
the hip disorder. This is a well-known stumbling block in the
diagnosis of any hip disorder in children and certainly can
occur even with an acute hip dislocation.
The immature acetabulum has much pliable cartilage.
Joint laxity is also common in young children. Often minimal
force is required to subluxate the proximal femur to the
acetabular rim, while little additional applied force is re-
quired to subsequently dislocate the femoral head completely
from the acetabulum. As age increases, greater portions of the
acetabulum progressively ossify, and there is a gradual lessen-
ing of joint laxity, so more violent trauma is necessary to
produce the same type of injury and is more likely to create
associated osseous damage at the acetabular periphery.
In Epstein’s series, however, most of the hip dislocations
20 Hip
were due to relatively severe trauma. About 60% involved
vehicular accidents, 5% occurred during football, and 30%
involved less severe trauma, such as falling down stairs or
tripping.21
Diagnosis
Most posterior dislocations are of the iliac type, with the
femur positioned between the sciatic notch and the acetab-
ulum. High iliac and ischial posterior luxations are less
common in children. On rare occasions, bilateral traumatic
dislocation of the hips (Fig. 20-8) occur.9,21,72
With posterior iliac dislocations, the deformity has a typical
appearance. The involved lower limb is held in flexion,
adduction, and internal rotation. There is shortening of the
limb. The femoral head may be palpable in the gluteal region.
The child generally is in severe pain and unable to stand
or walk. Motion of the hip is usually painful and guarded by
muscle spasm. The motions of extension, abduction, and
external rotation are markedly restricted and painful.
Flexion and internal rotation posturing of the hip are primar-
ily produced by tension in the Y-ligament of Bigelow.
Because this injury is often sustained while the child is
sitting in a car with the hip flexed, the femur, patella, and
upper end of the tibia must also be evaluated for concomi-
tant injury. Dislocation of the hip, even in children, may be
missed if there is an ipsilateral femoral fracture. These are,
however, comparatively infrequent concomitant injuries in
children relative to those in adults.
Knee pain may be present as a consequence of pain radi-
ating down the obturator nerve. The nerve may be stretched
in either anterior or posterior dislocations. Sciatic nerve
injury may arise because of impact, attenuation, or dis-
placement by the posteriorly dislocated femoral head.
Because the anterior portion of the nerve is usually affected,
dysfunction (sensory, motor, or both) is most likely evident
in the distribution of the perineal nerve. Nerve function, or
lack of it, must be carefully documented before and after
reduction. Neurologic injury, which usually resolves sponta-
neously, occurs in 3% of children.30,75,80 A thorough neuro-
logic examination of the sciatic nerve is an integral part of
both pre- and postreduction testing.
Delayed Diagnosis
If a dislocated hip is found more than 24 hours after injury,
a bone scan or magnetic resonance imaging (MRI) should
FIGURE 20-12. Inferior dislocation in a 10-year-old
child.
Posterior Dislocation
FIGURE 20-13. Luxatio erecta of the left hip.
be done to assess potential femoral (ossification center and
physis) head viability. General anesthesia and muscle relax-
ation should be used, as soft tissue contraction begins early
and may preclude reduction by the usual closed methods
without medications.
If the traumatic dislocation has been present for more
than a few weeks, adequate prereduction evaluation is essen-
tial. It should include a detailed neurologic examination,
as the sciatic nerve may be under chronic stretch. Arthrogra-
phy may determine whether fibrotic tissues are filling the
acetabulum, and dye may flow through a residual capsular
tear to delineate the shape of the femoral head. MRI may
afford the same anatomic information. Open reduction
is usually necessary to remove soft tissues within the acetabu-
lum. Any capsular rent should be repaired to prevent
recurrent dislocation.
Delayed diagnosis is more likely to occur in underdevel-
oped countries57 or in association with ipsilateral diaphyseal
femoral fracture. Skeletal traction followed by closed or
open reduction was the most frequent method of treatment.
However, the incidence of osteonecrosis was high. A reduc-
tion probably should be attempted as long as 6–9 months
after the traumatic incident, especially if the apparent cause
was relatively benign. There probably should be no arbitrary
time limit between injury and possible reduction.
Even a poor result from closed or open delayed reduction
may be acceptable. It prevents proximal migration, may
lessen soft tissue contractures, and decreases the amount of
muscle atrophy. The restored anatomy, even if osteonecrosis
and collapse develop, still makes total hip replacement a
viable possibility and technically easier if soft tissues are
stretched to normal length rather than being contracted
from chronic displacement.
Roentgenography
Roentgenography usually discloses the specific pattern of
dislocation. It is imperative that adequate films be obtained
to rule out associated fractures, especially of the triradiate
cartilage or the acetabular margin (see Chapter 19). The
entire hip region must be roentgenographed when any
fracture of the femur is present to rule out concomitant
hip dislocation, femoral shaft fracture, or both.
Barquet reported six retroacetabular dislocations.6 He
837
stressed the difficulty of diagnosing this particular disloca-
tion pattern in children, as standard frontal roentgenograms
may show a seemingly normal “concentric” projection of the
capital femoral physis and acetabulum. Other authors have
also described this problem.15,123 A true cross-table lateral
view of the pelvis should demonstrate any posterior or ante-
rior displacement. Computed tomographic (CT) scanning
also usually shows this displacement pattern. CT scanning is
useful for revealing small rim fragments, whether in or out
of the joint, before and after reduction. Completely carti-
laginous fragments may be difficult to identify on CT scan-
ning but should be suspected if there is asymmetry of the
cartilage space width (“joint” width).
Improved imaging techniques have become available. The
definition of CT scans is of much better quality. The method
allows good definition of posterior acetabular rim fractures
and intraarticular loose bodies. Three-dimensional CT is
being used increasingly for the evaluation of pelvic trauma,
although its use in young children may be misleading because
of the “irregularities” of the immature ossification center.22
Although MRI does not provide significant further infor-
mation regarding the basic anatomy of the hip dislocation,
it may reveal the status of altered hemodynamics and allow
better prediction of the likelihood of subsequent ischemic
changes. It is more useful in the postreduction patient
with joint space widening to assess interposed capsule or
cartilage. Bone scans may show immediate changes, but
there may also be a delayed reaction. Similarly, the use of
MRI to detect acute vascular compromise may be limited—
even though of benefit several weeks to months later.
Treatment
Early reduction, preferably within 8–12 hours, is important
to lessen the risk of potential sequelae such as ischemic
necrosis. Closed reduction of uncomplicated, acute poste-
rior dislocations is almost always possible, leaving open
reduction for only a small number of neglected cases and
those irreducible, acute dislocations that are usually due to
some type of capsular or musculotendinous interposition.
The chief obstacle to reduction of a posterior hip dislocation
is usually the iliofemoral ligament. Other possible impedi-
ments to closed reduction are the piriformis tendon, an
inverted labrum, or an osteocartilaginous fragment.
838
The following common methods for closed reduction of
posterior dislocations utilize the principle of hip flexion,
which should cause the Y-ligament to relax and bring the
femoral head adjacent to the acetabular margin near the
capsular rent.
Method of Stimson
Using the method of Stimson (Fig. 20-14), the patient is
placed prone, with the lower limb hanging free from the end
of the table. The pelvis is immobilized by pressing down on
the sacrum. The knee is then flexed to 90°, and pressure is
applied just below the bent knee. Gentle rocking, rotatory
motions of the limb, and direct pressure on the femoral head
and trochanter assist in the reduction. This method is not
forceful and utilizes the weight of the limb to help in the
reduction. If necessary, a sandbag may be strapped to the leg
to relax tight muscles gradually. If this procedure is done
with the patient under adequate anesthesia with appropriate
muscle-relaxing agents, excessive force is not usually neces-
sary and should be avoided to prevent complications such as
iatrogenic slipped capital femoral epiphysis.
Method of Allis
Using the method of Allis (Fig. 20-15), the patient is placed
in a supine position, and the pelvis is immobilized by press-
ing on the anterosuperior spine. The hip and knee are both
flexed to 90°, with the thigh maintained in slight adduction
and medial rotation. Direct vertical traction is applied
with the forearm behind the knee, lifting the femoral head
over the posterior rim of the acetabulum and through the
rent in the capsule into the acetabular socket. The hip and
knee are then gradually extended. Soft tissue resistance is
20 Hip
FIGURE 20-14. Closed reduction using the method
of Stimson.
encountered occasionally and may be relaxed by increasing
the degree of hip adduction and internal rotation. If the hip
cannot be extended easily after the reduction, there proba-
bly is soft tissue interposition, and another attempt at closed
reduction should be undertaken before resorting to open
reduction.
Method of Bigelow
Using the method of Bigelow (Fig. 20-16), the patient is
placed supine, and countertraction is applied. The thigh is
adducted and internally rotated, the hip is flexed to 90° or
more, and longitudinal traction is applied in the line of the
deformity. These motions convert an iliac displacement to
an ischial displacement by running the femoral head along
the posterior margin of the acetabulum and relaxing the
Y-ligament. The femoral head is freed from the short exter-
nal rotators by gently rotating and rocking while distally
directed traction is maintained. This maneuver allows lever-
ing the femoral head into the acetabulum.
It may be wise to use general anesthesia or a muscle relax-
ant with any of these methods, particularly in the older child.
Attempts to reduce an acute hip dislocation with the patient
under analgesia, or a combination of analgesia and a drug
such as diazepam, may not allow sufficient muscle relaxation
for a mechanically easy reduction. Because most dislocations
are posterior, attempts to reduce the hip without adequate
relaxation could result in the femoral head being pushed
backward against the posterior acetabular rim, comparable
to the mechanism in chronic SCFE. Because of morphologic
constraints, reduction of an anterior dislocation would not
be as likely to cause such a complicating displacement of the
femoral head.
Posterior Dislocation
FIGURE 20-15. Closed reduction using the method
of Allis.
If two or three attempts at closed reduction (with adequate
muscle relaxtion) are unsuccessful, an open reduction
should be considered. An associated acetabular fracture
with displacement of the fragment lessens the likelihood
of a satisfactorily closed reduction. Either the fragment
mechanically impairs the reduction, or the reduction is
unstable. Thus if a significant fracture fragment is
FIGURE 20-16. Closed reduction using the circum-
duction method of Bigelow.
839
present, open reduction and fracture stabilization are often
indicated.
Following closed reduction my preference is 2–3 days in
traction (balanced suspension) with the hip flexed 30° or
more. The stability is verified by active push–pull testing
under fluoroscopy. If the hip is stable, non-weight-bearing
ambulation is continued for a month.
840
If there is an accompanying fracture, the relative stability
may be assessed fluoroscopically while confirming the reduc-
tion. Traction, with or without a skeletal pin, is instituted for
2–3 weeks. The stability is reassessed fluoroscopically.
Some authors have recommended hip joint aspiration
under image intensification.68 The concept is to decrease the
volume of intracapsular hematoma that might lead to vascular
occlusion. Although theoretically this concept is sound, the
dislocation more often than not causes a capsular tear that
allows decompression of contained fluids. I do not routinely
aspirate the hip in a patient with a traumatic hip dislocation.
Postreduction Care
It is imperative that a satisfactory, anatomic reduction be
confirmed by fluoroscopy or routine radiography. It verifies
the concentric reduction or delineates any widening of the
radiolucent cartilage space (compared to the opposite side)
that should make one suspect an interposed cartilaginous or
chondro-osseous fragment. It can also demonstrate compli-
cations such as a postreduction SCFE. The acetabular rim
should also be reassessed for any injuries. My preference is
to obtain a CT scan as well to assess any acetabular fracture
or fragment interposition.
There is little agreement on immediate postreduction
treatment. Most surgeons use some sort of immobilization
that lasts a few weeks to about 2 months. This immobiliza-
tion may be achieved by bed rest or spica cast. I use traction
for approximately 3–10 days in balanced suspension, with
the hip flexed about 30° to relax the capsule and Y-ligament.
A period of about 3 weeks of subsequent immobilization is
probably sufficient to allow initial healing of capsular and
soft tissue structures. It may be accomplished by use of a hip
spica cast or an orthosis that restricts certain ranges of
motion, especially flexion. Small children may be treated
with abduction orthoses (e.g., Scottish Rite orthosis).
The presence of synovial irritation should be one of the
guidelines to determine when the child is allowed out of bal-
anced suspension or protected weight-bearing activity. So
long as acute synovial irritation or pain is present, the child
should probably be in traction and suspension, not in a cast.
If symptoms of synovial irritation recur after the resumption
of progressive weight-bearing, the patient is again placed in
traction, balanced suspension, or at least restrained from
weight-bearing; and diagnostic studies are undertaken to
determine the cause of the recurrent pain.
It is difficult to assess the importance of the duration of
the non-weight-bearing period; recommendations range
from a few days to 3 months. A correlation between the
period of non-weight-bearing and the frequency of ischemic
necrosis was proposed by Funk,27 but according to other
authors there is absolutely no correlation.26 Hammelbo174
recommended that weight-bearing should be avoided for
2–3 months, although most patients start weight-bearing 2–3
weeks after release from traction or casting. Children are
invariably noncompliant about the status of anything other
than full weight-bearing.
In children under the age of 6 years, despite their excel-
lent prognosis, it is probably advisable to attempt to dis-
courage weight-bearing for at least a month, after which
gradual resumption of activity may be permitted. Children
20 Hip
over the age of 6 years should not bear weight for an addi-
tional period of several more weeks but should engage in
muscle range of movement and strengthening programs.
When persistent symptoms (e.g., synovitis) are present, this
period should be further prolonged. However, it should be
noted that almost all children resume full activities and full
weight-bearing promptly after removal of any restrictive
device, regardless of advice to the contrary.
Results
Epstein described the results in 44 posterior dislocations with
an average follow-up of 78 months. Of these children, 24 had
excellent results, 11 had good results, and 9 had fair to poor
results. Invariably, these patients were severely injured and
usually had concomitant chondral or chondro-osseous injury
that complicated the dislocation.19
The final results in the Pennsylvania series showed 43
normal hips and 8 abnormal hips. However, the predictive
value was tentative, as only 18 of the 51 patients had attained
skeletal maturity. After reviewing the literature, as well as
their series, these investigators thought that one-third of the
children had, or would have, abnormal hips or poor results
by the time they reached skeletal maturity.64
Any child who has sustained a traumatic hip dislocation
should be followed regularly, both clinically and radiographi-
cally, to anticipate and document complications as early as
possible. Ischemic necrosis may not become radiologically
evident until 6 months or more following the dislocation.
An MRI or bone scan 2–3 months following the hip injury
may allow early diagnosis of osteonecrosis. Prior to this time,
reactive changes to the dislocation may create “false” findings.
Patterns of ischemic necrosis complicating the closed
treatment of developmental hip dysplasia may not cause
significant morphologic deformity until the adolescent
growth spurt. Similarly, follow-up of traumatic hip disloca-
tion patients should be considered complete only when the
patients are skeletally mature.
Anterior Dislocation
Traumatic anterior dislocation constitutes roughly 10% of all
pediatric hip dislocations.83–104 Barquet reviewed 111 trau-
matic anterior dislocations of the hip in children.84 The inci-
dence of traumatic anterior hip dislocation, unlike that of
posterior dislocation, is no different between children and
adults. Anterior hip dislocations are usually extrusions of the
femoral head through the joint capsule, often terminating
as a large bulge in the inguinal region.
The most important causal factor is forced abduction and
external rotation. Anterior and central dislocations may also
be caused by a direct blow to the greater trochanter. Ante-
rior dislocation is often sustained in a fall from a height, with
the impact being a direct blow on the posterior aspect of the
abducted and externally rotated thigh.
Anterior hip dislocations may be classified as pubic (supe-
rior) or obturator (inferior) (Fig. 20-17). An avulsion frac-
ture of the greater trochanter may accompany an anterior
dislocation. Direct anterior dislocation may be difficult to
diagnose (Fig. 20-18).
Anterior Dislocation
A
FIGURE 20-17. Anterior pubic dislocation. (A) Acute injury, with a
greater trochanteric fragment (arrow). (B) Greater trochanter
remained attached to the periosteal sleeve and gluteal muscula-
ture. (C) Greater trochanter underwent premature epiphysiodesis,
leading to an elongated femoral neck and valgus at skeletal matu-
With anterior dislocations, the hip is usually held in
abduction, external rotation, and some flexion. There is
fullness in the region of the obturator foramen, where
the femoral head may be palpable. The motion of the hip
is markedly restricted, with almost no adduction and exter-
nal rotation. It is often difficult to palpate the greater
trochanter.
FIGURE 20-18. Direct anterior dislocation. It
was initially missed, despite the obviously
widened space between the teardrop and the
femoral head in the right hip.
841
B
C
rity (6 years later). Most likely, the medial displacement of the main
fragment disrupted the normal medial and lateral circumflex circu-
lation to the greater trochanter. The capital femur exhibited no evi-
dence of ischemic necrosis.
The nerve most likely to be damaged is the femoral nerve.
Careful evaluation of its function is essential before and after
reduction.
With an uncomplicated anterior dislocation, prompt
closed reduction generally gives a good result. Unlike poste-
rior dislocations, there is not a good osseous fulcrum available
to assist in the reduction. The iliofemoral ligament lies
842
across the displaced femoral neck. The patient is placed
supine, the knee flexed to relax the hamstrings, and the hip
adducted and brought into increasing flexion (Fig. 20-19).
The femoral head is gradually brought opposite the tear in
the capsule, through which it is levered into the acetabular
socket. Longitudinal traction is then applied in the line of the
axis of the femur, and lateral traction is applied concomitantly
at the level of the femoral head. The hip may be rotated inter-
nally as it is adducted to try to achieve reduction.
Failure of initial closed manipulation, which is unusual,
may be due to interposition of the torn capsule, a button-
hole lesion of the capsule, or iliopsoas interposition behind
the femoral head.93–95 Open reduction may be necessary in
such situations.
Younge and Lifeso described a 16-year-old boy who had
sustained an anterior dislocation of the hip when he was 10
years old. An open reduction was attempted but led to a poor
result. He eventually underwent hip fusion.104 Four other
examples of anterior hip dislocations occurring 5 months to
12 years before definitive diagnosis are in the literature.91,96
When the greater trochanter is avulsed concomitantly (see
Fig. 20-22, below), open reduction may be essential to restore
chondro-osseous morphology. Such an avulsion pattern rep-
resents a type 3 or 4 growth mechanism injury to the
trochanteric region. Internal fixation of the trochanter
should be used and may be removed once healing occurs.
20 Hip
FIGURE 20-19. Method for closed reduction of an
anterior dislocation.
Acute occlusion or damage of the femoral artery, vein,
or both may occur.85,87,92,102 Nerubay reported a 15-year-old
boy who sustained an anterior dislocation of the hip, bilateral
fractures of the pubic rami, and a fracture of the ischium.97 At
surgery the femoral head was found to be compressing the
femoral artery against the inguinal ligament, completely
occluding flow. The patient developed severe ischemic necro-
sis 2 years after his injury. Bonnemaison and Henderson85 and
Hampson92 observed cases of venous obstruction.
Inferior Dislocation
Inferior dislocation, sometimes referred to as luxatio erecta
(Fig. 20-13), is rare in children.105–110 The mechanism of
injury probably consists of a combination of flexion, abduc-
tion, and internal rotation. All reported cases have been
reduced closed. Recurrent dislocation and osteonecrosis
have occurred.108
Central Dislocation
Central dislocations are discussed in Chapter 19. They are
most often associated with disruption of the triradiate carti-
lage in the skeletally immature patient.
Associated Injuries 843

Associated Injuries
Femoral Fracture (Diaphysis)
Concomitant dislocation of the hip and fracture of the
femoral shaft may not be diagnosed acutely. The simultane-
ous occurrence of hip dislocation and femoral shaft fracture
has also been reported in children.111–113,115–123 Missing such
a concurrence is as inappropriate as missing a Monteggia
injury in the forearm (see Chapter 16). In 42 cases of
dislocation of the hip with ipsilateral fracture of the femur,
the dislocation was recognized at initial examination in only
15 cases. In most cases the diagnosis was not made until 4–6
weeks later.111
Vialas used open reduction of the hip dislocation followed
by traction for both the hip dislocation and femoral fracture
in a 5-year-old girl.122 The outcome was satisfactory.
FIGURE 20-20. Split femoral head in a 15-year-old boy. It is a
variant of the adult type 4 injury.
Fracture of the Femoral Head
Kelly and Yarbrough described posterior dislocation of the
hip with a portion of the femoral head remaining within the
acetabulum.114 This remaining fragment possessed attach- cruciate ligament in the knee. The stability of the hip should
ments of the ligamentum (capitis) femoris. They described be assessed fluoroscopically. If necessary, the avulsed liga-
27 patients, the youngest being a 20-year-old. This injury is ment is excised (including the avulsed fragment).
not generally associated with the immature skeleton,
although it certainly may occur (Fig. 20-20). Like the frac- Traumatic Separation of the Capital
ture of Tillaux (see Chapter 23), it is most likely to occur
when the capital femoral physis is undergoing closure.
Femoral Epiphysis
Open reduction, particularly with excision of the The capital femur may be injured during a hip disloca-
medial head fragment (even though it is relatively non- tion,124–143 and the injury may involve a partial physeal sepa-
weight-bearing), produced inferior results compared with ration that is easy to overlook when there is a seemingly more
those obtained with either open reduction with internal obvious hip dislocation (Fig. 20-21). The femoral head may
fixation or closed reduction. Epstein described a 6-year-old remain within the confines of the acetabulum, with the
girl who underwent closed reduction.21 At follow-up 13 years femoral neck and greater trochanter being displaced later-
later the fragment had reattached to the neck to form an ally (Fig. 20-22). The capital femur may be displaced from
exostosis that blocked full flexion and adduction. the acetabulum and significantly separated from the femoral
A variation of segmental femoral head fracture occurs neck.
when the attachment of the ligamentum teres detaches.144 The capital femur may also be displaced during reduction
This is analogous to a tibial spine avulsion of the anterior of a posterior dislocation (Fig. 20-23). Fiddian and Grace

FIGURE 20-21. (A) Hip dislocation associated with type 1 physeal fracture in a 2-year-old. (B) Follow-up at 6 months shows physeal
narrowing. (C) Mild coxa magna 11 months later.
844 20 Hip

FIGURE 20-22. (A) Anteriorly dislocated femoral neck with located femoral head. (B) Open reduction.

reported two patients in whom there was a traumatic dislo-
cation of the hip with separation of the capital epiphysis.132
In both cases the slip occurred during the subsequent
attempted closed reduction of the traumatic hip dislocation.
However, the capital femoral physis may have been micro-
scopically damaged during the dislocation (occult physeal
injury), rendering it more mechanically susceptible to
macro-injury from relatively minor forces than it would have
otherwise been.
Open reduction is virtually always necessary. It is difficult
to consider how closed reduction might be possible. In fact,
several reported cases occurred while attempting closed
reduction. In these instances the femoral neck reduced
into the acetabulum, leaving the femoral head behind
(extracapsular).
The importance of gentle manipulative reduction of a hip
dislocation, with the patient under general anesthesia and
with adequate muscle relaxation, must be emphasized to
avoid such an unusual complication. Capital femoral dis-
placement, whether part of the original injury or a compli-
cation of the reduction, requires gentle restoration of
anatomy and (under anesthesia) fixation.
Barquet and Vécsei reported a case of traumatic disloca-
tion of the hip with accompanying dislocation of the capital
femoral epiphysis. Because of severe fat embolism, the
patient’s dislocated femoral head was not reduced into the
hip until approximately 4 weeks after injury. The result 11
years later was poor.125
Osteonecrosis has developed in all reported cases of this
combined injury, with the exception of one case that became

FIGURE 20-23. (A) Slipped capital femoral epiphysis complicating attempted reduction of a hip dislocation. (B) Ischemic damage and
collapse 11 months later.
Associated Injuries 845

infected and required removal of the femoral head. Accord-

ing to Mass and colleagues, none of the patients with this
injury have had a good result.138
Fifteen reported patients with at least 2 years of follow-up all
developed osteonecrosis. In one case the dislocated capital
epiphysis was never successfully reduced. Interestingly, this
capital femoral epiphysis developed osteonecrosis while the
capital femur was in its unreduced extracapsular position.
Pedina-Medina and Pardo-Montaner reported a variation
in which a traumatic SCFE, with displacement of the femoral
head from the acetabulum, was associated with a fracture of
the triradiate cartilage.139 Barquet and Vécsei divided the
condition into (1) dislocation with complete separation
and displacement of the epiphysis and (2) dislocation with
incomplete separation of the epiphysis.125 FIGURE 20-25. (A) Posterior acetabular fracture with separation.
This was treated with open reduction and internal fixation.
Acetabular Fragments
The chondro-osseous periphery of the acetabulum may be
fractured during the hip dislocation or subsequently during
attempted reduction (Figs. 20-24, 20-25). Following any
reduction, roentgenograms should be obtained to confirm
the completeness of the reduction of both the hip disloca-
tion and the acetabular fragment.
Sometimes associated fractures of the margin of the
acetabulum are not readily evident on prereduction films
but become evident after reduction.144–164 Shea and associ-
ates described two cases illustrating problems of displaced
unossified and ossified acetabular margins.162 Any widening
of the cartilage (“joint”) space relative to the contralateral
hip should arouse a suspicion of soft tissue or cartilage inter-
position (Figs. 20-26, 20-27) and the need for exploratory
arthrotomy and excision of interposed tissue. Kaelin
reported a 7-year-old boy who had locking of the hip after a
minor fall.154 The major finding was marked widening of the
radiolucent space.
Bennett and Cash encountered a nonconcentric reduc-
tion of the hip in a 7-year-old boy 6 days after closed reduc-

B
FIGURE 20-24. Acetabular rim fracture (arrow) in a teenager. FIGURE 20-26. Retained chondro-osseous fragments (arrows).
846 20 Hip

FIGURE 20-28. Untreated hip dislocation with acetabular injury.

This patient also had a lumbosacral plexus nerve injury, with
permanent muscular impairment and a Charcot joint at the hip.

FIGURE 20-27. Interposed fragment (arrow). This injury was an Frich and coworkers found that arthroscopy was useful for
avulsion of the ligamentum capitum femoris (ligamentum teres).
diagnosing and removing intraarticular fragments and labral
tears.149 However, the application of arthroscopy to the hip is
still controversial.
Santora et al. described six adolescents with intraarticular
tion and casting.145 CT scans suggested posterior soft tissue
loose bodies diagnosed 2 months to 2 years after hip trauma.
interposition. During injection of contrast for an arthrogram
All were treated with excision. Four were symptom-free, and
a spontaneous concentric reduction occurred abruptly,
two had occasional pain.161
along with outflow of dye from the inferior aspect of the
Failure to stabilize a peripheral acetabular injury may
capsule.
lead to chronic instability and severe, destructive joint
If closed (i.e., concentric) reduction is unsuccessful or if
changes (Fig. 20-28). Using CT scanning, Rashleigh-
there are unstable chondro-osseous acetabular fractures,
Belcher and Cannon described a lesion of the posterior
open reduction may be necessary. A posterior or lateral
acetabulum due to a posterior dislocation with no associ-
approach is best for visualizing the damaged areas. Large
ated fracture.160 Exploration of the hip, because of recurrent
acetabular fragments are secured, but fixation pins or screws
dislocation, revealed disruption of the posterosuperior
should not damage the triradiate cartilage. Any capsular rent
acetabular labrum with formation of a pouch between
is repaired.
the posterior acetabular wall and the external rotator
An intraarticular fragment may not be recognized until
muscles. They thought that it resembled a Bankart-
after the reduction. Care is taken to ensure that the intra-
type lesion of the shoulder. Repair was done using a bone
articular distances (cartilage space widths) are bilaterally
block.
equal after reduction, as this may give an early indication
Tears of the acetabular labrum, which certainly can occur
that soft tissue or cartilaginous interposition is present,
with a dislocation, are usually accompanied by a small frag-
possibly indicating a need for open reduction and removal
ment or involve the secondary ossification marginal process.
of the continued tissue. An arthrogram may show the
These small fragment/labral tears may be detected by CT
interposed tissue. Demonstration of this interposed tissue
scan. Pure labral tears are more difficult to diagnose. Nishii
may not be easy in the child whose injury has been
et al. used contrast-enchanced MRI, with continuous leg trac-
acutely reduced, as tears in the capsule may allow extravasa-
tion to delineate such tears successfully.158
tion of dye, which makes interpretation of the arthrogram
In all the reported cases, the chronic labral injury was asso-
difficult.
ciated with subsequent acetabular dysplasia. A constant early
Relocation of the femoral head may disrupt the periph-
radiologic sign was a cyst above the lateral aspect of the
eral acetabular epiphysis or labrum and displace either tissue
acetabulum. The cysts occurred as a consequence of abnor-
into the acetabulum, comparable to the way the femoral
mal stresses imposed by the uncovered lateral portion of the
head may also be displaced from the neck. The size and con-
femoral head.
sistency (cartilage or partially ossified tissue) of the epiphy-
seal fragment vary and make radiographic diagnosis difficult.
Persistent widening of the medial cartilage space and con-
tinued pain and limitation of motion should alert the physi-
Complications
cian to the need for further studies. CT scans may be useful
Ischemic Necrosis (Osteonecrosis)
for delineating interposed cartilage fragments, even after
reduction. If one has to resort to MRI, arthrotomy is proba- A significant long-term complication is vascular compromise
bly justifiable instead. eventuating in ischemic osseous and physeal/epiphyseal
Complications 847

FIGURE 20-29. (A) Ischemic necrosis (arrow) with central collapse of the femoral head following previous dislocation. (B) Recovery 7
months later.

changes (Figs. 20-29 to 20-32).165–187 Fineschi reviewed
approximately 150 cases and found 16 complicated by
ischemic necrosis.23 This figure concurs with that of the
Pennsylvania Orthopaedic Society; their reported incidence
of ischemic necrosis was only 4%.63,64 Epstein reported a
6% incidence.19 Robertson and Peterson thought that if
ischemic necrosis was not evident by 15 months after the
injury it probably would not develop.72
Elmslie described ischemic necrosis of the femoral head
secondary to traumatic dislocation and termed it coxa
plana.169,170 Goldenberg described “Perthes” disease follow-
ing hip dislocation; it most likely was ischemic necrosis.172
Undoubtedly, comparisons with the Legg-Calvé-Perthes
(LCP) lesion are not appropriate because one is a more
chronic kind of condition. However, the roentgenographic
patterns and delayed presentation are often similar in com-
parable age groups.
Glass and Powell presented a study of 47 children who
sustained posterior traumatic hip dislocations.30 Their inci-
dence of ischemic necrosis was approximately 20%. The
average follow-up was 28 months. Of 26 children under the
age of 10 years, 1 developed ischemic necrosis. Of the 21
children aged 10 years or over, 5 were so affected. There was
premature epiphyseal fusion in only one child.
There seems to be an age variation with regard to suscepti-
bility to posttraumatic ischemic necrosis. This complication
appears to be infrequent in children under 6 years of age,
whereas in older children the frequency is probably about
10%. The observation is sometimes made that the young
patient has some protection against the complication of
ischemic necrosis. This protection is probably due to the
anatomic particularities of the circulation and continuity
of the proximal femoral epiphysis, the greater amount of
epiphyseal cartilage, and the relative positions of capsular

A B
FIGURE 20-30. (A) Ischemic changes on both sides of the joint 11 months after hip dislocation. (B) Ten months after a hip dislocation
there is ischemic involvement of the physis and ossification center.
848 20 Hip

not appear until adolescence, even though the vascular

insult may have been rendered within the first few months
of life.167
Once the patient has gotten over the acute healing phase,
usually 2–3 months after the injury, a baseline bone scan may

FIGURE 20-31. (A) Mild ischemic change (arrow). (B) MRI localizes
the lesion (arrow).

insertion to blood vessels in the various age groups. This

complication has also been attributed to changes in the
function of the artery of the ligamentum capitis femoris,
which is usually completely disrupted. It seems more likely
that the age-related differences relate to the volume of
ossification within the capital femoral epiphyseal cartilage. B
The developing osseous centrum is a more vascularly
dependent structure than is the surrounding unossified
cartilage.180,181,187 The greater the mass of epiphyseal bone at
the time of injury, the more is the normal vascular demand, so
the bone is less likely to withstand prolonged ischemia.
Macrovascular and microvascular patterns also change
significantly with age.
The patient who sustains a posterior dislocation usually
tears the capsule in the direction of the longitudinal fibers
and does not usually destroy the area where the blood supply
courses. The capsular rent allows decompression; therefore
there usually is no buildup of hematoma under pressure
within the joint. Furthermore, the intracapsular course of
vessels should not be seriously compromised by this type of
dislocation.
Of all the reported cases of ischemic necrosis, only two C
were first diagnosed more than 2 years after the injury.173 The FIGURE 20-32. Appearance 4 months after traumatic hip dis-
final prognosis should be reserved until the patient reaches location. (A) The hip appears normal, although the child has inter-
skeletal maturity, as unanticipated changes may occur during mittent complaints of hip and groin pain. (B) One year later a sub-
the adolescent growth spurt. Some of the subtle changes of chondral fracture is evident. (C) MRI shows evidence of
ischemic necrosis that complicate the developmental hip do osteonecrosis.
Complications
be obtained to see if there is any decrease in the blood supply
to the affected femoral head. Serial radiographic review
should continue until skeletal maturity to detect any devel-
oping problems, particularly long-term changes in the
femoral head, as some changes do not manifest until the
growth spurt.
Magnetic resonance imaging may also help delineate the
extent of vascular damage. Poggi et al. reviewed 14 patients
who had an MRI evaluation after hip dislocation (only one
was under 18 years).183 Eight of the hips had abnormal
marrow within 6 weeks after injury, but progression to radio-
logically evident damage occurred in only three patients.
Repeat MRI studies in the other five patients showed
resolution of the process. They did not differentiate between
bone bruising (contusion) and osteonecrosis. They also
noted the MRI was not reliable during the first week after
injury, nor was it useful for predicting which patients would
progress to osteoarthritic change. In some cases MRI may
be detecting contusion and hemorrhage similar to the bone
bruise of the distal femur (see Chapter 22).
Li and Hiette used a specialized technique of contrast-
enhanced fat saturation MRI to study the pathophysiology
of osteonecrosis (nontraumatic).176 They believed that early
nontraumatic osteonecrosis was associated with hyperemia,
an increase in capillary permability rather than acute devas-
cularization, or both, and that diffuse marrow edema was
the initial finding. Trauma could easily cause comparable
changes.
If ischemic necrosis should occur, the first step is prohibi-
tion of or protected weight-bearing to try to prevent osseous
collapse during the revascularization period. Osteotomy may
also be beneficial, as it may align the head in a more effec-
tive weight-bearing position and enhance revascularization
and venous outflow.
A complication that is not stressed in the literature is the
development of coxa magna, which is probably caused by
injury-induced hyperemia to the capital femur. If this com-
plication causes acetabular-femoral incongruity, there may
be a predisposition to subsequent osteoarthritis.
Chronic vascular complications of anterior dislocation are
rare. The incidence of ischemic necrosis of the femoral head
after anterior dislocation was reported by Brav as 9% in 62
cases, although these patients were primarily adolescents and
adults.86 Litton believed that ischemic necrosis was a rarity
with anterior dislocation because the main vessels supplying
blood to the femoral head were posterior.95 Although
damage to the posterior capsule is less likely with this injury,
the fact that the femoral head is often buttonholed through
a piece of tight anterior capsule may cause direct pressure
from the capsular rent and the displaced iliopsoas tendon
on some of the vessels. This condition can predispose to a
greater risk of vascular injury if urgent reduction of the dis-
location is not carried out.
Recurrent Dislocation
A less frequent complication is recurrent dislocation.188–202
Choyce described five cases of recurrent dislocation.168
Mauck and Anderson reported a 6-year-old boy who had a
subsequent dislocation 13 months after the initial injury.51
Morton cited five cases of recurrent dislocation.53 The
849
reports of the Pennyslvania Orthopaedic Society mentioned
only one case.63,64 With few exceptions, all children suffering
the complication of recurrent dislocation appeared to be
under 8 years of age at the time of initial injury. One
child developed ischemic necrosis following the recurrent
dislocation.
The longest interval between recurrent dislocations was
7 years, with a 1.5-year follow-up after the second dis-
location.199 The average time between the initial and final
dislocation was 2 years, and the shortest interval between suc-
cessive dislocations was 1 month. Based on these findings,
Simmons and Elder suggested that a minimal period of
follow-up is 2 years.199
An important causal factor of recurrent dislocation may
be inadequate immobilization of the hip after reduction,
with consequent incomplete healing of the capsular damage
(Fig. 20-33). Liebenberg and Dommisse thought that the
mechanism was incomplete healing of a posterior capsular
defect, particularly if the reduction was delayed.196 If there is
incomplete healing, a false cavity with synovial lining may
develop and communicate with the true joint. Synovial fluid
may then flow freely between the two regions.
Treatment, following definitive diagnosis, consists of exci-
sion of the pouch and repair of the capsular defect. The hip
is immobilized for 4–6 weeks with a hip spica cast to allow
complete healing.
Simmons and Elder reported a case of a 5-year-old child
who sustained a posterior dislocation of the hip. On subse-
quent occasions 5, 7, and 9 months afterward, the femur
redislocated as a result of minimal trauma.199 Exploration
revealed a large herniation of the posterior joint capsule,
laxity, and a large capsular tear deep to the quadratus
femoris muscle. This tear was successfully closed without
significant problems or subsequent recurrent dislocation.
FIGURE 20-33. Recurrent dislocation in a 12-year-old boy. CT
arthrogram shows extravasation of dye through a large posterior
capsule defect.
850
Dall and colleagues87 and Scudese103 reported cases of
recurrent anterior dislocation. The complication appears
less prevalent with anterior dislocations than following
posterior dislocations.
Routine hip arthrography after the initial dislocation in a
child has not been advocated, but it may have some merit
for detecting hips that might redislocate by localizing a large
defect in the joint capsule. If the results of arthrography
suggest a capsular defect, repair should be considered. The
operation is done in such a way that the capsular tear or
stretch is demonstrated and specifically repaired.
Osteochondrosis
An 8-year-old boy developed osteochondrosis of the upper
femoral epiphysis 3.5 years after his original posterior dislo-
cation.203 This condition may represent a focal variation of
ischemic necrosis.
Myositis Ossificans
Myositis ossificans is a rare complication in the normal child.
It is more likely in the patient with concomitant head injury.
When it does occur, the process must be allowed to mature
completely before resection is attempted.
Periarticular calcification was present in Nerubay’s97 case
and was previously reported by Aggarwall and Singh in all
six of their reported unreduced anterior hip dislocations.83
Brav found an incidence of 11% among 228 posterior dis-
locations but none with anterior dislocations.86
Neurologic Deficits
Neurologic deficiency was the most frequent complication in
the series by Pearson and Mann.62 Although all experienced
some degree of functional recovery, only one patient had
complete recovery of nerve function. Epstein reported three
cases of neurologic deficiency: two patients with full recov-
ery, although one still had weakness in the great toe exten-
sor 21 years after the injury.21 These deficits all accompanied
posterior dislocation and involved variable sensory or motor
deficiency of the sciatic nerve. Injury accompanying poste-
rior dislocations may be due to the marked internal rotation
of the hip that occurs at the time of dislocation. Sciatic injury
may cause serious long-term consequences (Fig. 20-28).204
Osteoarthritis
It is essential to follow hip-injured children beyond skeletal
maturity. Long-term changes not evident during the early
posttraumatic period may subsequently become significant
osteoarthritis. Epstein reported six such cases.21 Severe
injuries in young children may lead to this complication even
before skeletal maturity is attained.
Chronic Hip Pain
The choice of treatment for the patient with disabling hip
pain consequent to complications of childhood hip disloca-
tion is difficult, especially as some available treatment modal-
20 Hip
ities involve major risks and compromises for a young
patient. Certainly, total joint replacement, a bipolar pros-
thesis, and an endoprosthesis are not reasonable initial alter-
natives in a skeletally immature patient who is otherwise
healthy. For the child sufficiently disabled to warrant surgi-
cal relief of hip pain, the essential options available (other
than acceptance of the pain) are pelvic or femoral osteotomy
or hip fusion.205–210
Fulkerson presented a comprehensive long-term follow-up
of hip fusions done for disabling hip pain in children.206 One
of the significant findings was that following hip fusion there
was a tendency for the fused hip to progressively adduct. This
observation was true of each and every hip fused in skeletally
immature patients. The average increase of adduction was
10°, usually occurring within 2 years after the initial fusion.
The reasons for this postoperative increase in adduction have
not been identified, but certainly growth at the trochanteric
epiphysis and lateral capital epiphysis can contribute. The
hips were fused in 20°–40° of flexion, which is allowable in a
more active child.206 Rotational alignment was not a problem,
and fusion near neutral rotation was generally accepted.
The results of adolescent hip fusions are satisfactory. Many
of these children returned to vigorous physical activities
and normal life styles. Fusion of the hip certainly does not
negate the possibility of subsequent conversion to a total hip
arthroplasty.210
Obstetric “Dislocation”
All presumed acute dislocations of the hip in the newborn
have been found to be fractures across the entire proximal
femoral metaphysis and physis. This type of injury was
produced easily when attempting acute dislocation of the
hip in stillborns and infants (see Chapter 21). Traumatic
dislocation of the femoral head in the newborn is essentially
nonexistent because the ligaments that reinforce the capsule
are strong (although they may be hyperlax during the
perinatal period because of the influence of maternal
hormones). In cases of excessive trauma, as from energetic
traction during delivery, epiphysiolysis or fracture of the
femoral metaphysis may be produced. Elizalde reported
two cases he believed were true dislocations of the hip, but
the roentgenograms indicated that the most likely diagnosis
was a fracture through the transepiphyseal region.211 In
contrast to developmental hip dysplasia, these injuries are
painful if the leg is manipulated. They are discussed in detail
in Chapter 21.
Any neonate who returns to the hospital and is found to
have a traumatic “hip dislocation” deserves careful evalua-
tion. First, the true diagnosis is probably a fracture-separation
of the entire proximal femoral epiphysis. Second, and much
more important, a skeletal survey and detailed physical exam-
ination must be done. This infant is most likely the victim of
child abuse, not unrecognized obstetric trauma.
Snapping Hip Syndrome
Many children and adolescents who pursue athletics or
dance (e.g., ballet) on a highly competitive basis develop
References
repetitive, painful snapping in the hip.212–215 One of two
syndromes may be present. The most common is the exter-
nal variant, caused by the posterior border of the iliotibial
band or the outer border of the gluteus maximus impinging
on the greater trochanter with hip rotation. The less
common internal variant is usually attributed to the iliopsoas
tendon temporarily impinging on the femoral head, anterior
hip capsule, or iliopectineal eminence.212,214
Symptoms with the external variation are a snapping sen-
sation and lateral thigh pain. The internal variant exhibits
palpable or audible snapping in association with anterior
inguinal pain.
Vaccaro et al. used contrast imaging of the iliopsoas bursa
(an anatomic extension of the hip joint) to pinpoint the
impingement during fluoroscopy.215 Therapeutic injection
into the iliopsoas bursa was found to alleviate pain in a
significant number of patients.
Voluntary Habitual Dislocation
Recurrent voluntary or habitual dislocation of the hip in
children, in the absence of a well-defined antecedent dislo-
cation, is unusual.216–227 There may be predisposing factors
such as paralysis or collagen disorders (see Chapter 11). In
the latter situation the repetitive displacement continues
because of capsular distortion (attenuation) and loss of
support of surrounding tissues.
Children with voluntary dislocation probably have an
intact capsule and reasonable contiguous soft tissue support.
These factors cause decreased intracapsular pressure as the
femur displaces from the acetabulum, causing liberation of
gas into the joint.225 It typically produces what is referred to
as a “vacuum arthrogram” and is due to the physics princi-
ple of cavitation (release of dissolved gas with a change in
applied pressure). This phenomenon is pathognomonic of
habitual dislocation.
These children also have clinical “clunks.” However, this
sign may occur with recurrent dislocation due to other
causes or the snapping hip syndrome.
As with nursemaid’s elbow the phenomenon decreases
over time. Expectant treatment and parental education are
ususally sufficient. An intertrochanteric derotation osteotomy
was used in one patient.224
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Acetabular Fragment
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157. Lieberman JR, Altchek DW, Salvati EA. Recurrent dislocation
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161. Santora SD, Stevens PM, Coleman SS. Intraarticular loose
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the hip in children. J Pediatr Orthop 1986;6:215–219.
163. Sprenger TR. Fracture of the acetabulum in a 14 year old
patient. Orthop Rev 1984;13:709–716.
164. Wilchinsky ME, Pappas AM. Unusual complications in
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Ischemic Necrosis
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167. Bucholz RW, Ogden JA. Patterns of ischemic necrosis of the
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171. Fairbank HAT. Case of pseudo-coxalgia following traumatic
dislocation in a boy. Proc R Soc Med (Sect Orthop) 1924;17:40.
172. Goldenberg R. Traumatic dislocation of the hip followed by
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174. Hammelbo T. Traumatic hip dislocation in childhood. Acta
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175. Kleinberg S. Aseptic necrosis of the femoral head following
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179. Mutschler HM. Sekundare Oberschenkelkopf-necrose nach
traumatischer Ausrenkung des Huftgelenkes bei einem 14
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181. Ogden JA. Changing patterns of proximal femoral vascularity.
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185. Scholder-Dumur C. Necrose de la tete femorale a la situe
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186. Shim SS. Circulatory and vascular changes in the hip follow-
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187. Trueta J. The normal vascular anatomy of the human femoral
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Recurrent Dislocation
188. Aufranc OE, Jones WN, Harris HH. Recurrent traumatic
dislocation of the hip in a child. JAMA 1964;190:291–294.
189. Body J. Luxation recidivante de la hanche chez un garcon de
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190. Duytjes F. Recurrent dislocation of the hip joint in a boy. J
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191. Gaul RW. Recurrent traumatic dislocation of the hip in chil-
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194. Hohmann D. Recidivierende traumatische Huftluxation beim
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198. Niloff R, Petrie JG. Traumatic recurrent dislocation of the hip:
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Nerve Injury
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206. Fulkerson JP. Arthrodesis for disabling hip pain in children
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21
Femur
Engraving of a specimen of type 1 growth mechanism fracture of
the distal femur. (From Poland J. Traumatic Separation of the
Epiphyses. London: Smith, Elder, 1898)
he femur is the longest bone in the human body. It
T must develop appropriately at both the proximal and
distal ends to allow coordinated musculoskeletal
activity at the hip and knee. Subtle as well as major al-
terations of development consequent to trauma may
alter normal bone and joint morphology and adversely
affect the biomechanics of a specific joint if not the entire
leg.
Anatomy
Proximal Femur
Development of the proximal femoral chondro-osseous
epiphysis and physis is probably the most complex of all the
appendicular skeletal growth regions.12 Figure 21-1 illustrates
several stages in the development of the proximal
femur. Perhaps the two most important features are (1)
the continuity of epiphyseal and physeal cartilage along
the posterosuperior neck throughout much of postnatal
development and (2) the intracapsular course of the limited
capital femoral blood vessels. Fortunately, significant growth
mechanism injury secondary to direct trauma or selec-
tive vascular damage to the area is infrequent. When it
does occur, however, complications assume great impor-
tance for subsequent morphology and hip and leg
biomechanics.
Secondary ossification usually begins in the capital femur
by 4–6 months postnatally (range 2–10 months). This
process is a centrally located sphere of ossification that
expands centrifugally, eventually conforming to the hemi-
spheric shape of the articular surface by the time the child
is 6–8 years old and forming a discrete subchondral plate
that follows the capital femoral physeal contour. The ossifi-
cation center is dependent on an intact vascular supply;
and any temporary or permanent decrease in blood flow,
as might be sustained with a femoral neck fracture, has
variable effects on the ability of capital femoral ossifica-
tion to continue normal maturation and chondro-osseous
transformation.
Femoral Neck
Throughout most of the development the capital femoral
and trochanteric epiphyses have a cartilaginous continuity
along the posterior and superior portions of the femoral
neck (Fig. 21-2).12 Although this region gradually thins as the
child grows, it is essential for the normal latitudinal growth
of the femoral neck (Fig. 21-2) and, in part, the normal
decrease in anteversion. Damage, as with a femoral neck frac-
ture, may seriously impair the capacity of these cartilaginous
neck regions to develop normally. This posterosuperior
857
858
FIGURE 21-1. Slab sections showing proximal femoral develop-
ment. (A) At 2 months a contiguous epiphysis encompasses the
capital femur and greater trochanter. The intrinsic vascularity of the
capital femoral cartilage is evident. (B) At 8 months the capital
femoral ossification center is developing, and the femoral neck
femoral neck cartilage is radiolucent. Hence the true extent
of a femoral neck fracture may be underdiagnosed if only
the osseous fracture line is considered. The blood vessels
course along the posterosuperior femoral neck. However,
they have a variable intracartilaginous course, which makes
them more susceptible to fracture if the injury to the sub-
capital or neck region propagates into or through this
cartilage.
Selective growth along the capital femorointertro-
chanteric physis establishes a discrete femoral neck. The
primary spongiosa initially formed during neck develop-
ment is not completely oriented to biologic forces across the
hip joint. The more responsive secondary spongiosa begins
to form the typical trabecular patterns oriented to compres-
sion and tension forces. This process becomes more promi-
nent during the second decade of life. The area between
these major osseous patterns is often referred to as Ward’s
triangle.
The development of the femoral neck brings about
changes in the contour of the capital femoral physis. Initially,
the femoral neck is transversely directed (Fig. 21-1); but
during the first year there is preferential growth in the
medial, and middle sections. As these regions develop, the
capital femoral physis becomes more medially (varus) and
21. Femur
(metaphysis) is forming. (C) At 8 years undulations are developing
in the capital femoral physis. (D) At 12 years there is a normal
indentation of the ossification center at the site of attachment of
the capital femoral ligament (L); the capital femoral physis is exten-
sively undulated, and a mammillary process (arrow) is evident.
posteriorly oriented, which eventually may predispose to
slipped capital femoral epiphysis. Lappet formation, undu-
lations, and mammillary processes develop in the physis (Fig.
21-1), again becoming more evident after 10 years of age.
These processes and contours serve to “anchor,” or stabilize,
the capital femoral epiphysis to prevent displacement due to
biologic shear stresses.
Greater Trochanter
Ossification begins in the greater trochanter at 5–7 years
(Fig. 21-3) and is initially present directly above the
trochanteric physis. With further development, ossification
proceeds cephalad into the remainder of the epiphysis.
This cartilaginous portion may be injured without obvious
roentgenographic evidence. Epiphysiodesis of the greater
trochanter occurs at 14–16 years (usually later than in the
capital femoral physis).
The greater trochanter typically is considered a “traction
apophysis,” but this is a simplistic misconception. The bio-
mechanical forces are usually schematically depicted as
traction applied at the tip of the trochanter. In reality, there
are multiple muscle attachments and forces on the entire
surface, including attachments of the quadriceps (vastus
Anatamy
FIGURE 21-2. (A) Progressive proximal femoral development. A
segment of physeal cartilage (arrows) is present along the
posterosuperior femoral neck throughout most of development. It
is necessary for widening of the femoral neck and posteriorly
directed growth of the femoral neck to spontaneously decrease the
A B
FIGURE 21-3. (A) Development of trochanteric ossification in an 8-
year-old child, showing the irregular margins of secondary ossifi-
cation and the extensive cartilaginous nature of the trochanteric
epiphysis, especially proximally at the tip. (B) Later stage (12
859
B
amount of anteversion. (B) Transverse section through the proxi-
mal femur showing the capital femoral epiphysis and the posterior
cartilaginous continuity (arrows) with the unossified greater
trochanter.
C
years) showing an accessory (tertiary) ossification center. (C)
Histologic section through the greater and lesser trochanters in
a 15-year-old boy.
860
lateralis) and the posteriorly located external rotators
(gemelli, piriformis). There is also overlying compression
from the tensor fascia and muscle. The summated vector
force is compression, which is reflected in the histologic
appearance of the greater trochanteric physis.
Growth occurs through the trochanteric physis and inter-
stitial expansion. True growth does not occur proximally,
as some have suggested. Rather, this presumed proximal
growth is, in reality, an expansion of ossification into the
already formed cartilage. Magnetic resonance imaging
(MRI) readily shows such unossified, but well-formed,
trochanteric cartilaginous morphology.
Lesser Trochanter
The lesser trochanter does not usually ossify until adoles-
cence (Fig. 21-3). Fusion occurs between 15 and 19 years.
This region is subject to high tensile stresses from the
attached iliopsoas tendon and represents a traction apoph-
ysis. Overgrowth may occur owing to chronic stress, as with
cerebral palsy.
Proximal Vascularity
The blood supply to the proximal femur varies with the
extent of skeletal maturation.6,7,8,10,11,18,19 A vascular loop
circles the capsular insertion at the base of the femoral neck,
adjacent to the greater trochanter. A limited number of
vessels cross the capsule and extend toward the capital
femur. Their course is defined by morphology. A short
femoral neck is present in the infant, whereas the teenager
has an elongated neck. Essentially, a small group of vessels
traverses the inferior femoral neck to a retinacular re-
flection, entering the medial side of the capital femoral
epiphysis. Another group of vessels courses along the super-
oposterior portion of the developing femoral neck. Some of
these vessels may become encased in the cartilage along
the femoral neck. This posterosuperior vascular grouping
enters the lateral side of the capital femoral epiphysis and
becomes the dominant blood supply. Unfortunately, because
of the close proximity to, or even incorporation into, the
femoral neck cartilage, these vessels are at risk for disruption
whenever the femoral neck or capital femur sustains a
fracture.
The greater trochanteric blood supply is derived from
the aforementioned extracapsular loop and other vascular
systems. It is not particularly susceptible to traumatically
induced vascular damage. Accordingly, trauma that affects
capital femoral circulation creates a situation comparable to
the ischemic necrosis seen with developmental hip dysplasia,
namely, disruption of capital femoral growth and maturation
coupled with normal growth and maturation of the greater
trochanter. This causes variable morphologic change to the
proximal femur, contingent on the age of the patient and
the extent of vascular disruption.
Femoral Diaphysis
The diaphysis is a long cylinder of heavy, compact bone com-
posed of progressively modeled and remodeled osteon struc-
ture. The femoral diaphysis is the only region to have
21. Femur
significant osteon conversion of woven (fetal) bone during
the perinatal period. The lack of well-defined osteons prob-
ably is a factor in the rapid healing associated with perinatal
and infantile femoral fractures. The diaphyseal bone nor-
mally is bowed anteriorly and laterally. Treatment methods
for femoral shaft fractures should be directed at some
restoration of this anterolateral bowing, even when the frag-
ments are left overriding. The linea aspera is a sturdy, ele-
vated ridge that extends along the posteromedial surface of
the femoral shaft. This ridge acts as a thickened buttress, pro-
viding strength and serving as a longitudinal musculofascial
attachment.
The circulation of the diaphysis and the proximal and
distal metaphyses is derived from the nutrient artery and
from a peripheral circulation around each metaphysis.
Vessels derived from the nutrient artery course toward each
end of the bone, supplying small vessels to the marrow and
endosteal circulation. At each end the vessels ramify to create
a more retiform network within the metaphysis. These
vessels end as vascular loops that abut the hypertrophic cells
of the growth plate, and they contribute to the chondro-
osseous transformation of these cells.
Distal Femur
The epiphyseal ossification center of the distal femur is
usually present at birth if the infant is full term. Expansion
occurs relatively rapidly to fill both condylar regions (Fig.
21-4).5,13 This area is the largest and most actively growing
epiphyseal-physeal unit in the body, contributing almost 70%
of the length of the femur and 40% of the entire leg. It fuses
with the metaphysis at 14–16 years of age in girls and 16–18
years in boys. The distal epiphysis, which includes the entire
articular surface of the lower end of the femur, serves as the
origin of part of the gastrocnemius muscle.
The distal femoral physis is essentially a transverse plane
at birth. As the infant commences walking and places
increased weight-bearing and shearing forces across the
knee, the distal femoral physis develops macroscopic undu-
lations. Viewed from the anteroposterior projection, there
appear to be two convexities directed toward the epiphyseal
ossification center (Fig. 21-5). There is a central peak or apex
directed toward the metaphysis. In the lateral view a similar
binodal contour is evident. In three-dimensional terms there
are four convex protuberances of the metaphysis and physis
extending toward the epiphyseal ossification center. These
extensions are directed at dissipating shearing and rotatory
stress within the physis. In large animals that run and leap,
the extension of these cones may be dramatic (see Chapter
1). The physis also exhibits microscopic undulations and
mammillary processes, which represent further biomechan-
ical adaptation to applied loads. Peripherally, physeal/epiph-
yseal lappet formation is evident and is most pronounced
anteriorly in the patellofemoral groove.4
The distal femoral metaphysis is the site of numerous
developmental (maturational) variations (Figs. 21-6 to 21-8)
that should not be misconstrued as due to trauma. Fibrous
cortical defects have been recognized as normal variants
(Figs. 21-7, 21-8), although small pathologic fractures some-
times occur in these defects. Another relatively common
lesion is the avulsive cortical irregularity. Although usually
Proximal Femoral Injuries
FIGURE 21-4. Roentgenographic development of the distal femur.
(A) Serial sections from a 3-year-old child (accident victim). Note
the differences in the physeal/metaphyseal contours. There is a
torus fracture in the distal metaphysis (arrows). (B) Irregular medial
benign in appearance, these radiologically apparent cor-
tical erosions are sometimes suggestive of destructive or
infiltrative lesions such as osteomyelitis or osteogenic
sarcoma.1–3,14,15,17,20 The distal femoral metaphyseal “lesion” is
almost exclusively located on the posteromedial aspect of the
femoral condyle, above the adductor tubercle (Fig. 21-7).
This portion of the medial ridge is the site of insertion of a
portion of the transverse fibers of the adductor magnus
aponeurosis. Intense bone remodeling usually occurs con-
tinuously in this region during periods of rapid skeletal
growth. The cortex of the bone may be affected by this con-
stant remodeling, so excessive mechanical stress produces
microavulsions of the relatively porous cortical bone. These
microavulsions may elicit a hypervascular, fibroblastic
response, which in turn stimulates osteoclastic activity and
bone resorption. In this way, a cycle of microfracture–resorp-
tion–microfracture is established. The rapid appearance and
subsequent regression of the lesion and its common occur-
rence in active, adolescent boys suggest a mechanically
induced lesion that may be a tension stress failure.
The circulation of the distal femur is multifocal.4,9,16 Small
vessels enter the epiphysis medially, laterally, and posteriorly.
The main circulatory input/output is through the posterior
femoral notch. As in the capital femoral epiphysis and spinal
cord, there are “watershed” areas in the condyles (especially
medially) that have limited circulation, and they may be sus-
861
ossification (arrow) is evident in this specimen from a 7-year-old.
(C) Femur from a 15-year-old showing early stages of physiologic
epiphysiodesis.
ceptible to ischemic changes eventuating in osteochondritic
lesions.
Proximal Femoral Injuries
Although proximal femoral fractures are infrequent injuries
in the immature skeleton, they have received considerable
attention in the literature.21–244 These fractures are more
common in boys, with the male/female ratio approximately
3 : 2. Fractures may occur at any age, with the highest inci-
dence being at 11–12 years. Proximal femoral fractures may
occur at birth and must be isolated diagnostically from devel-
opmental hip dysplasia. The injury may also occur in an
abused infant (Fig. 21-9). Because considerable violence is
required to fracture the proximal femur in older children
and adolescents, there are often accompanying injuries.
During adolescence an acute injury represents one segment
of the spectrum of slipped capital femoral epiphysis. Patho-
logic fractures (see Chapter 11) may occur in many diseased
states, including renal osteodystrophy, fibrous dysplasia,
bone cysts, hypothyroidism, juvenile rheumatoid arthritis,
septic arthritis, and malignancies.
There are several important differences between proximal
femoral fractures in adults and those in children. Because
the combined periosteal-perichondrial region is much
862 21. Femur

FIGURE 21-6. (A) Slab section showing irregularity of development

of the medial side of a secondary ossification center. (B)
FIGURE 21-5. Undulating nature of the distal femoral physis. These Roentgenogram showing similar irregularity along the inferior
are 5-mm serial slab sections of the same specimen. The contour region. These variations are normal.
variability affects physeal fracture patterns.

FIGURE 21-7. (A) Roentgenogram of 6-year-old child showing irregularity of the distal femoral metaphysis medially at the adductor
insertion (arrows). Compare this cortex with the lateral cortex. (B) Sclerotic and porotic bone characteristic of this region.
Proximal Femoral Injuries
A
FIGURE 21-8. Typical posterior fibrous cortical defect. (A) MRI shows the osseous demarcation and continuous fibrous tissue. (B) CT
shows indentation of the posteromedial cortex.
stronger in children, fractures are not always significantly dis-
placed. In addition, the presence of the cartilaginous
intraepiphyseal bridge along the superior and posterior
aspect of the neck tends to prevent displacement of the
physis unless this cartilage is also significantly disrupted, a
factor that is impossible to discern with standard roentgeno-
graphic techniques. Damage to this region of cartilage may
affect development of the femoral neck. A potential com-
plication, ischemic necrosis, may affect, specifically or in
combination, the epiphysis, the metaphysis, and the physis.
The violence of the initial injury is generally blamed for the
FIGURE 21-9. Type 1 injury of the capital femur in a 10-month-old
victim of child abuse. The capital femur was completely dislocated.
863
high incidence of ischemic necrosis in children (as high as
80–90% in some series, with an average of 40%). Direct
damage to the vessels coursing along or within the
intraepiphyseal cartilage may also be a factor.
Children generally readily tolerate the duration of cast
immobilization necessary to attain acceptable union with an
undisplaced or reduced fracture. However, malunion of the
developing femoral neck is a real hazard if only casting
is used. Like the lateral condylar fracture of the distal
humerus, the femoral neck fracture has a reasonable risk of
loss of reduction or nonunion in a young child because of
the relatively constant micromotion even while in a cast.
When a displaced or potentially unstable fracture is reduced
and held in a cast, insidious, progressive coxa vara may still
occur. The hardness of a child’s bone and the small size of
the femoral neck often limit the choice of fixation devices.
Pins or screws of small caliber should be used. If transphy-
seal pins are necessary (as they often are), they must be
smooth in the region that crosses the physis. Threaded fixa-
tion devices should not cross the physis. When fracture
healing problems arise in a child, endoprosthetic replace-
ment is usually not an available solution. Accordingly, avoid-
ance of complications, especially ischemic necrosis, becomes
paramount.
Classification
Proximal femoral fractures in children may occur at differ-
ent levels along the femoral neck (Fig. 21-10). However,
because the femoral neck is actively elongating and matur-
ing, certain types cannot occur at young ages, and any given
type may vary morphologically with age.
The type I injury can assume several patterns contingent
on the age of the patient and the presence of predisposing
disease conditions, such as a tumor or rickets. During the
neonatal period and the first year of life, the entire proximal
femoral chondroepiphysis, including the capital femur, the
864
FIGURE 21-10. (A) Types of fracture of the femoral neck: type I,
transphyseal injury; type II, transcervical injury; type III, cervi-
cotrochanteric injury; type IV, peritrochanteric injury. A type I injury
is transphyseal during infancy, but in the older child and adoles-
cent the fracture splits the capital femoral and intraepiphyseal seg-
ments so a type 3 growth mechanism injury occurs. In pathologic
conditions (e.g., renal rickets) the presence of the metaphyseal
intraepiphyseal region, and the greater trochanter, traumat-
ically separates as a contiguous, complete unit. The lesser
trochanter may or may not be included depending on the
patient’s age and the mechanism of injury. As is discussed
later, increased medial disruption may cause localized type
5 injury with the potential for temporary or permanent
growth arrest and a progressive traumatic coxa vara. As the
anatomic femoral neck develops, the type I fracture pattern
changes and increasingly localizes only to the capital femoral
region. The fracture line may extend across the intra-
epiphyseal cartilage and along the capital femoral physis or
partially along the capital femoral physis and into the
metaphysis of the femoral neck. During adolescence
the type I fracture involves the capital femoral physeal–
metaphyseal interface, crossing the remnants of the intra-
epiphyseal region; this is an acute slipped capital femoral
epiphysis.
Type II (transcervical) is a fracture through the midpor-
tion of the femoral neck. Type III is cervicotrochanteric,
through the base of the femoral neck. Type IV is peri-
trochanteric, between the base of the femoral neck and
lesser trochanter. The latter injury essentially follows the
capsular insertions. Obviously, the length of the femoral
neck affects which pattern is present at any given age.
A more realistic classification in children, because of the
changing length of the neck, would be: I, physeal fracture;
II, intracapsular neck fracture; and III, intertrochanteric
fracture (at the capsular insertion or extracapsular). The dis-
21. Femur
fragment indicates a type 4 growth mechanism injury. (B–E) Age-
related variations of type I fractures. (B) Type l growth mechanism
injury in an infant. (C) Type 3 growth mechanism injury in a 4-year-
old child. (D) Type 3 growth mechanism injury in an adolescent
(acute slipped capital femoral epiphysis). (E) Type 4 growth mech-
anism injury in a 7-year-old.
tinction between transcervical and cervicotrochanteric is dif-
ficult to distinguish until adult morphology is reached at
skeletal maturity.
Although limited development of the length of the neck
affects the pattern of fracture, at least from the standpoint
of defining types II, III, and IV, treatment is essentially the
same; and the risks of complications such as ischemic necro-
sis and coxa vara are reasonably similar for all patterns. It
is important to remember that there is a variably thick
cartilaginous continuity along the posterosuperior neck
(Fig. 21-2), and that most femoral neck fractures undoubt-
edly propagate into and through this area, essentially
making types II, III, and IV each a type 4 growth mechanism
injury, which requires reasonably accurate anatomic
reduction to prevent or minimize subsequent growth
deformity.
Transphyseal Injury (Type I)
A transphyseal fracture of the proximal femur of a young
child is infrequent.* Such fractures occur insidiously in
patients with myelomeningocele.142 With the exception of
birth trauma, these children often sustain multiple trauma.
Transepiphyseal fractures infrequently are associated with
dislocation of the capital femoral epiphysis from the acetab-
ulum (see Chapter 20).
* Refs. 37–39,83,107,117,173,180,184,186,193,233,237.
Proximal Femoral Injuries
FIGURE 21-11. Type 1 injury with widening of the physis of the left capital femur (arrow).
This injury pattern may be difficult to diagnose in the
young child (Fig. 21-11). The diagnosis must often be made
as a clinical assumption, as roentgenographic corroboration
may be lacking or difficult to visualize. The distinction from
developmental hip dislocation may be difficult when the
child is first seen, as a roentgenogram may show only upward
and lateral displacement of the femoral shaft. A septic hip
may also be difficult to distinguish from a traumatic lesion
due to child abuse, particularly because both conditions can
cause fever (blood in a joint may cause a temporary febrile
response).
Milgram and Lyne obtained postmortem specimens from
children who died of disease without osseous involvement.142
Manipulative epiphyseal separation was produced by simul-
taneously rotating and bending the specimens. Microscopi-
cally, the zone of disruption was variably through the
hypertrophic cell layer.
Radiographically, the separation occurs at the physis and
may or may not be associated with displacement from the
A
FIGURE 21-12. (A) Transphyseal fracture in an 11-month-old infant
(unrestrained passenger in a motor vehicle accident). (B) Fracture
was reduced under anesthesia, proved to be unstable, and was
865
neck (Fig. 21-12). Because of anatomic constraints there may
be only widening of the physis (Fig. 21-11). In the lateral
view, the neck of the femur may be displaced forward in rela-
tion to the epiphysis, comparable to the type of external rota-
tion that occurs with slipped capital femoral epiphysis. In
some patients only widening of the physis is seen, without
significant displacement. Wide displacement is uncommon
because the periosteal and perichondrial attachments are
usually intact. Displacement may occur only in certain ways
because of the epiphyseal continuity along the posterosupe-
rior surface of the neck. Displacement of the proximal frag-
ment is most likely to be posterior.
Treatment must be individualized. Many of these fractures
are minimally displaced (if at all) and clinically stable, which
may be determined by ranging the hip under fluoroscopy.
Thus whenever possible, conservative, nonoperative treat-
ment is instituted, with resultant growth deformities cor-
rected at a later date. If the fracture line is undisplaced or
minimally displaced, the hip may be immobilized in a spica
B
treated with a single smooth percutaneous pin, which was removed
6 weeks later. There was no subsequent growth arrest 3 years after
the injury.
866
A B
FIGURE 21-13. (A) Child abuse led to fracture of the proximal femur in this 7-month-old baby. (B) Mild deformity and concavity of the
physeal metaphyseal interface at age 1 year.
cast, with the affected side in moderate abduction, neutral
extension, and mild internal rotation. If displaced more than
one-fourth of the physeal length, a gentle closed reduction
with the patient under general anesthesia may be consid-
ered. In the older child, if displacement is significant and a
manipulative reduction has to be undertaken, or if the frac-
ture appears unstable to fluoroscopic examination, it may be
necessary to fix the fracture internally with smooth pins that
penetrate the epiphysis and then immobilize the hip in a
spica cast. Four to six weeks is usually required to achieve
osseous union sufficient to allow discontinuation of the
casting. The pins should be left outside the skin or in the
subcutaneous tissues so they can be removed within 4–8
weeks, at which time the physeal injury should be mechani-
cally stable (although not necessarily stable for active,
normal weight-bearing).
The potentially poor prognosis of these lesions must be
emphasized to the parents. The prognosis may be guarded
because of damage to the physis at the time of the injury,
which may represent a localized type 5 injury, or because of
vascular injury that eventually leads to radiographic evidence
of ischemic necrosis (Fig. 21-13). Each patient must be care-
fully followed by periodic roentgenograms for the possible
development of the complications of ischemic necrosis, coxa
vara, or premature fusion of the physis. Premature fusion
may occur even though there is no ossification center in the
epiphysis at the time of the injury. Early treatment of com-
plications by appropriate osteotomy may salvage the hip.
Using fat interposition after resection of the osseous bridge
in this particular region would not be easy and has not been
reported.
Neonatal Injury (Type I)
Although infrequent, fractures involving the proximal femur
in the neonate must be diagnostically differentiated from
developmental hip dysplasia or infection (septic hip or
21. Femur
proximal femoral osteomyelitis). Numerous authors have
reported one or more cases of this injury.39,142,162,163,189,228,245–289
The injury involves the entire proximal femoral epiphysis,
which at birth is comprised of the capital femur, greater
trochanter, and lesser trochanter. These regions do not
become anatomically separate until several months after
birth.
These particular proximal femoral fractures usually occur
during a difficult delivery (Fig. 21-14), such as those involv-
ing breech or footling presentations. Michail and colleagues
described obstetric separation of the upper femoral epiph-
ysis and the appearance of the ossification center of the
femoral head 15 days after birth; it was believed to be a con-
sequence of the injury. They emphasized that “the existence
of an obstetric (traumatic) dislocation of the hip has never
been demonstrated,”266 a concept with which I completely
agree.
Prevot et al. reported obstetric disruption of the upper
femoral epiphysis.275 They noted that the fracture occurred
even though the delivery was by cesarean section. Three
patients were treated with traction followed by a hip spica
cast, and one patient had a pin osteosynthesis. Two patients
had an excellent result, but two patients had increased exter-
nal rotation of the leg.
Fairhurst opened the hip of a 10-day-old baby who was the
product of a difficult delivery and breech extraction.257 They
directly observed a severely displaced fracture between the
cartilaginous head and neck and the osseous metaphysis. It
was reduced and percutaneously pinned. There was normal
development of the hip.
Meier reported two cases of children with epiphysiolysis
consequent to birth trauma.265 One of these children died
several weeks later. An autopsy showed marked callus for-
mation around the shaft with a fracture through the region
just below the common growth plate. Pfeiffer272 and Trues-
dell287 described similar autopsy findings. Harrenstein
manipulated hips of newborn cadavers and found that “the
Proximal Femoral Injuries 867

FIGURE 21-14. (A) This injury to the proximal femur occurred during birth. The hip appears to be dislocated. (B) Arthrogram shows an
intact hip joint, and the hip eventually developed normally. The injury was a fracture, not a dislocation.

line of cleavage passed below the cartilage of the femoral of a normal-appearing acetabulum, one should be suspicious
head.”258 of a fracture. Developmental hip dysplasia may be con-
Duplication of the lesion in stillborn cadavers shows that sidered because of the superolateral displacement of
the fracture is usually a type 1 growth mechanism injury tra- the femur. However, the acetabulum usually has a normal
versing the entire physis underneath both the capital femur acetabular index in a neonate with a proximal femoral
and the greater trochanter (Fig. 21-15).269,270 The periosteal fracture.
sleeve is intact posteriorly and still attached to the proximal Whenever possible, the diagnosis should be made before
physis. There may be comminution (rather than crushing) fracture callus is evident (Fig. 21-16), as any anatomic defor-
of the epiphysis, physis, and metaphysis medially. Such mity is undoubtedly irreducible at that stage. Subperiosteal
longitudinal splitting and separation along cell columns, ossification around the proximal metaphysis gives irrefutable
with these separations extending through the germinal zone evidence of the injury. Usually, such callus formation is
and into the epiphysis, creates multiple, microscopic type evident within 8–14 days. This callus may be considerable,
3 and 4 physeal injuries. Such findings of cellular micro- depending on both the extent of periosteal stripping at
disruption afford a more plausible explanation of prema-
ture growth arrest than the previously hypothesized type
5 mechanism of cellular crush injury within the terminal
zone. Animal models have shown similar histologic
damage.270
Acute traumatic dislocation of the femoral head in the
newborn is essentially nonexistent because the ligaments and
capsule, although they may be lax during the perinatal
period owing to the influence of selective maternal hor-
mones, are still biomechanically stronger than the proximal
femoral physis. Any unstable (i.e., subluxating or dislocat-
ing) hip found during examination is invariably the result of
chronic, progressive intrauterine deformation, and cartilagi-
nous, ligamentous, and capsular distortion and stretching.
The clinical symptoms are characteristic. Swelling is rea-
sonably constant in the inguinal crease, gluteal area, and
proximal thigh. The newborn holds the leg in external rota-
tion, flexion, and adduction, usually avoiding and resisting
movements of the leg. Irritability during diaper changing is
usually evident. Considerable pain, often with crepitation, is
elicited, an important finding when distinguishing a fracture
from developmental hip dysplasia, which is invariably pain-
free. An almost constant feature appears to be pseudoparal-
ysis of the affected limb. However, the “paralysis” rapidly
disappears as the fracture becomes nonpainful through early
healing and callus stabilization.
Roentgenograms usually show lateral displacement of
the proximal femoral metaphysis (Fig. 21-14). The displace- FIGURE 21-15. Experimental proximal femoral fracture. Posterior
ment may be slight and difficult to interpret. If the metaph- displacement associated with stripping of the posterior periosteum
ysis appears to be displaced laterally, in the presence (arrow).
868
FIGURE 21-16. Extensive subperiosteal new bone. Note that the
shaft is laterally displaced. The radiolucent proximal (capital) femur
is still in the acetabulum.
the time of injury and how much continued motion the
injury was subjected to until and after the diagnosis was
made. Stripping and subperiosteal bleeding that further
elevate the periosteum are present because the injury invari-
ably occurs prior to the neonate receiving a prophylactic
vitamin K injection.
Because the diagnosis is difficult when the clinical and
routine radiographic findings are minimal, other diagnostic
studies may be indicated. Arthrography may define the
injury (Fig. 21-14). Injected dye should outline the anatom-
ically located capital femur, although there may be extrava-
sation of dye beyond the capsule, especially medially, where
some of the metaphysis is normally within the capsular
boundaries. Any joint fluid removed at the time of arthrog-
raphy should be cultured to rule out an infectious process.
Ultrasonography may be used to make the diagnosis. Diaz
and Hedlund described the use of sonography to diagnosis
traumatic separation of the proximal femoral epiphysis in a
patient with myelomeningocele.251
Experimental observations regarding the periosteal sleeve
are important. This structure is intact posteriorly and dis-
rupted anteriorly, allowing the proximal metaphysis to “but-
tonhole” through the tear. The posterior attachment of the
21. Femur
periosteum to the physeal periphery may be used to advan-
tage during traction and reduction to introduce intrinsic
stability, similar to the soft tissue continuity used in other
areas (e.g., dorsally displaced fracture of the distal radius
fracture). This practice contributes to fracture stability and
prevents overreduction.
Traction seems to be the easiest method for controlling
the fracture and is certainly the reasonable choice for initial
management. The child is carefully placed in Bryant’s
traction with the hips flexed to 90° and the knees flexed
15°–20°. Skin traction straps should extend to the upper
thigh. Only 1 pound (or less) may be necessary for gentle
suspension of the legs in this position. This position usually
corrects varus displacement and takes advantage of the pos-
teriorly intact periosteal tissue. Once the child is pain-free
(usually only a few days), an abduction pillow splint or
Pavlik’s harness may be used. Casting is used if the afore-
mentioned methods are unsuccessful. The abduction device
usually may be discontinued 4–6 weeks later. The rapid rate
of healing supports conservative therapy. The long-term
results are usually excellent, with a low incidence of growth
complications.
Subsequent coxa vara has been described by a few
authors.247,258,260,261,265,267 Some degree of coxa vara was usually
evident early in the healing phase because of the anatomy of
the displacement. Usually such a varus deformity corrects
itself within a few months and is followed by normal proxi-
mal growth, although it may persist as long as 4 years after
the injury.259,267 Some cases of congenital and infantile coxa
vara are actually missed cases of neonatal epiphysiolysis or
even intrauterine disruption.261,267
Cases of ischemic necrosis have been described following
this specific neonatal fracture in the literature, but the
anatomy of the fracture relative to the blood supply makes
it unlikely. The fracture line is primarily extracapsular (sub-
trochanteric) and away from the main blood supply, which
is proximal to the injury and should be relatively undis-
turbed.270,280 In fact, the capital femoral ossification center
may appear earlier than normal owing to a hyperemic, not
ischemic, vascular response to the injury.266
Acute Slipped Capital Femoral Epiphyseal
Injury (Type I)
Slipped epiphysis of the capital femur (SCFE) may occur
with traumatic hip injury or dislocation.290–318 These injuries
are serious and are associated with a high incidence of com-
plications. SCFE may also occur acutely without a concomi-
tant dislocation. The distinction between acute and chronic
cases of SCFE may be difficult. By definition, only slips seen
within 3 weeks of the onset of symptoms and particularly
after definable trauma are considered acute.291
This injury may occur in children with preexistent mild
(chronic) slips or beginning (prodromal) symptoms. The
femur undergoing physiologic and biomechanical changes
that predispose it to eventual slipping may be acutely
stressed, causing more significant displacement (Fig. 21-17).
Acute slips of the proximal femoral epiphysis are usually
characterized by abrupt onset of severe pain, limitation of
motion, external rotation deformity, and the inability to bear
Proximal Femoral Injuries
FIGURE 21-17. Acute-on-chronic slipped capital femoral epiphysis
(SCFE). This patient had intermittent thigh pain for a month, fol-
lowed by an acute increase in pain when he misjudged the height
of a school bus step.
weight on the affected limb in association with a specific trau-
matic event (Fig. 21-18).
The acute cases do not differ significantly from the more
common chronic type with regard to age, sex, or body build,
except for the patients having concomitant hip dislocation.
Prodromal symptoms of a dull ache or pain during the
affected or ipsilateral knee may be present for extended
periods, suggesting that acute slips do not necessarily occur
only during the early phase of epiphysiolysis. In fact, Barash
and associates showed a roentgenogram obtained 10 months
prior to an acute slip, demonstrating early epiphysiolysis that
had not been treated with prophylactic pinning.291
When symptoms have been present prior to the acute slip-
ping or earlier roentgenograms showed mild slipping, there
is little doubt that trauma only acutely precipitates further
displacement. Prodromal symptoms were recorded in all
patients reported by Fahey and O’Brien and in 60 of 89 acute
cases reported in the literature.299 Lack of complaints,
however, does not exclude the possibility of mild asympto-
matic slipping. It may be difficult to ascertain the relative
importance of trauma in an adolescent without previous
symptoms, especially when acute displacement of the capital
femoral epiphysis is seen after a moderate to severe injury.
Fahey and O’Brien believed that in only 17 cases from the
literature was trauma the exclusive causal factor, and most of
these cases occurred in the younger age group rather than
in the group for which slip was characteristic.299 The trauma
sustained was usually severe, and associated injuries were fre-
quently present. Of the reported cases, there were eight with
complete dislocations of the capital femur from the acetab-
ulum (see Chapter 20).
869
Several authors have described lateral slipping of
the capital femoral epiphysis (epiphyseal coxa valga).298,299,
301,307,310,315,318
It seems likely that this direction of slipping
occurs in the older child in whom there is a thin remnant of
cartilage along the posterior femoral neck that allows the
capital femur to be pushed laterally as it is slipping posteri-
orly. Rothermel also thought that the slip tended to occur
more frequently in patients with a horizontally oriented
growth plate.310
Some form of gentle closed reduction may be attempted
for acute slipping, but closed reduction is not uniformly
successful for repositioning. In general, most cases may be
treated with balanced suspension, an internal rotation strap,
and bed rest. Operative manipulation should be used cau-
tiously. Fahey and O’Brien thought that the results of their
10 cases supported the observation that gentle manipulation
was the preferred method of reduction, believing that the
earlier closed reduction is attempted, the more likely it is to
succeed in repositioning the femoral head, with minimal risk
of vascular damage.299 Traction is usually carried out with the
hip in extension, which is a position that may increase joint
pressure and predispose to vascular problems in an acutely
injured and possibly effused joint. When traction or bal-
anced suspension is used, with or without derotation straps,
I believe that the hip should be flexed at least 30°. Gentle
reduction attempts in the operating room should have the
hip flexed 90°.
Dietz noted that gentle reduction of acute or acute on
chronic severe SCFE was generally recommended.297 Dietz
attempted to study gentle reduction using longitudinal trac-
tion with medial rotation. Only 5 of 13 hips had discernible
reduction with this method, and one developed ischemic
necrosis. In review, however, this hip had been distracted
from the acetabulum by excessive longitudinal traction.
Casey et al. also described a similar technique and noted that
longitudinal traction with medial rotation was an acceptable
approach.295
FIGURE 21-18. Acute SCFE following a fall. The patient had had
no prodromal symptoms. It was reduced over 2 days in traction
(split Russell’s with derotation strap) and subsequently pinned.
870 21. Femur

tively. The pins were removed 14 months following surgery,

at which time there was an area of lucency at the base of the
right femoral neck, and the patient had coxa vara with a neck
shaft angle of 100°. Tomograms showed a fracture, and it was
treated conservatively. The second patient developed a left
femoral neck fracture and coxa vara, despite having a pin in
place. She subsequently required a vascularized pedicle bone
graft. The authors studied heat production during reaming
for cannulated screws and postulated that the fractures prob-
ably developed through areas of osteonecrosis secondary to
thermal injury.
Acute slip may occur as a complication of a hip dislo-
cation or its attempted reduction (see Chapter
20).293,294,300,302,306,311,312 An SCFE may also complicate a frac-
ture of the femoral neck or diaphysis that has been left in
nonanatomic alignment.308

Femoral Neck Fractures

FIGURE 21-19. Femoral neck fracture, type III injury pattern
(arrow). The fracture was undisplaced, and the child was treated
with immobilization in a cast. The fracture did not appear to extend
completely across the neck (metaphysis), thereby decreasing the
likelihood of intraepiphyseal cartilage injury.
In children, femoral neck and intertrochanteric fractures are
the most frequent levels of injury (Figs. 21-19 to 21-22).
Ratliff reviewed 71 cases of femoral neck fractures of patients
under 17 years of age.182,184,186 The highest incidence of the
injury appeared to be in the 11- to 13-year range. There were
2 physeal fractures, 39 cervical fractures, 26 basal fractures,
and 4 intertrochanteric fractures; 22 were undisplaced and
49 were displaced fractures.

Aadalen et al.290 and Casey et al.295 reported the ability to

Pathomechanics
obtain reduction in acute-on-chronic SCFE. Jerre, in con- Various muscle forces may lead to varus or valgus deforma-
trast, found successful manipulative reduction present in tion of the fragments relative to each other (Fig. 21-23). The
only 19 of 26 patients (73%).304 Schein successfully reduced iliopsoas tends to move the greater trochanter proximally,
three acute hips with traction and internal rotation.313 Based medially, and anteriorly and rotates it externally. The gluteus
on the literature, ischemic necrosis probably occurs in maximus moves the femur proximally, medially, and pos-
10–20% of cases with acute slips no matter what the treat- teriorly and rotates it externally. The external rotators rotate
ment, and traction and reduction appear safe so long
as excessive weight is not used that might result in hip joint
distraction.
Closed reduction should probably not be attempted if a
period of more than 1 week has elapsed since the probable
acute episode. In situ extraarticular fixation with threaded
pins or screws is indicated. The postoperative management
consists of avoiding weight-bearing for 3–4 weeks, followed
by a gradual increase in weight-bearing. The main compli-
cation, other than ischemic necrosis, is subtrochanteric frac-
ture after pin removal, especially if they were in the lateral
cortex. Pins are usually removed to avoid future difficulties.
Titanium pins are avoided, as they may be difficult to
remove. Biomechanical studies suggest that internal fixation
devices reach peak efficacy at 6 months and that surround-
ing bone begins to weaken progressively after that while the
bone “incorporates” the plate, pins, or screws into “normal”
stress patterns. Pin removal is controversial and not without
complications, but I usually remove them within a year of
insertion. Other methods of stabilizing the hip, such as the
use of a transphyseal bone peg, may be considered to avoid
the necessity of removing the pins at a later date.
Baynhamn et al. described two patients who developed FIGURE 21-20. Femoral neck fracture with a varus tilt. The sever-
femoral neck fractures as a complication of in situ pinning ity of injury and displacement place this patient at high risk for
for an SCFE.292 The first patient developed pain postopera- ischemic necrosis.
Proximal Femoral Injuries 871

A B

FIGURE 21-21. (A) Femoral neck fracture in a 9-year-old boy. (B) It was reduced and the fracture stabilized by percutaneous screws
(and a hip spica).

A B
FIGURE 21-22. This 8-year-old girl was involved in a bicycle–car femoral neck fracture. (B) The femoral neck fracture was reduced
accident. She sustained bilateral femoral diaphyseal, unilateral and stabilized with a cannulated screw that stopped short of the
femoral neck and proximal tibial physeal fractures. (A) CT of the physis.

FIGURE 21-23. Varus and valgus neck deformities

in femoral neck fractures. Arrows in (A) show the
major vectors of the deforming forces.
872
the femur and shift it medially. Thus, in theory, four mus-
cular forces contribute to the medial shift and three to exter-
nal rotation. However, the iliopsoas basically neutralizes the
opposite action of the gluteus maximus and external rota-
tors. Therefore after most fractures the greater trochanter is
pulled upward, rotated externally, and shifted medially. This
displacement tends to take place regardless of the exact
anatomic position of the fracture line.
Diagnosis
The diagnosis is generally not difficult. There is a history of
a severe injury, following which the patient complains of
sudden pain in the hip and usually cannot stand or walk.
However, greenstick or impacted fractures and stress frac-
tures may allow some weight-bearing. The injured limb is
usually held rigidly and in varying degrees of external rota-
tion and slight adduction, and it may be flexed to allow some
relief of capsular distension by hematoma. When the frac-
ture is displaced, the patient is generally unable to move the
hip actively. Shortening of 1–2 cm may be present. Generally,
there is marked restriction of passive motion of the hip,
particularly flexion, abduction, and internal rotation. The
diagnosis is confirmed by roentgenograms, which should
be obtained in both anteroposterior and lateral views. The
direction of the fracture line, the degree of traumatic coxa
vara, and the amount of posterior tilt should be noted, as
well as whether the femoral head is retained in the ace-
tabulum in its normal location (the distal fragment is usually
displaced upward and anteriorly or into slight external
rotation).
It is important to remember that the fracture is evident
only through the osseous portion of the neck. The fracture
may propagate further through the intraepiphyseal cartilage,
extending across the rest of the superoposterior femoral
neck (Fig. 21-2).
Treatment
Excellent results are generally, although not universally,
achieved with undisplaced fractures, no matter how they are
treated. Undisplaced fractures in children have some inher-
ent stability, possibly because the contiguous cartilage of the
pertense or prior femoral neck is not completely disrupted.
The safest way to treat them is by a hip spica with the leg
held in internal rotation flexion and abduction for 8–12
weeks. This practice is usually sufficient, especially in the
young child. The stability may be assessed fluoroscopically
prior to applying the cast; and it is imperative that the frac-
ture be radiographed regularly (at 1, 3, and 6 weeks) to assess
it for insidious displacement. After 6 weeks the likelihood
of displacement is minimal provided healing is progressing
and there is no progressive varus deformation. A spica cast
cannot maintain hip stability in most instances when the frac-
ture is not intrinsically stable.
Anatomic alignment may be progressively (insidiously,
nonpainfully) lost and may lead to displacement and a
greater incidence of complications, particularly coxa vara. As
a general rule, if Pauwel’s angle (fracture line) is less than
40°, such fractures may be treated by a spica cast without
weight-bearing. Inclusion of both legs may be necessary for
21. Femur
a particularly active child. Frequent roentgenograms are
essential. If there is significant loss of anatomic position, the
fracture probably should be fixed internally (percutaneous
pinning).
For displaced fractures, the eventual risks of coxa vara
and ischemic necrosis increase significantly. Manipulation
with the patient under anesthesia generally corrects the
displacement, but it may be easily lost once the traction
has been released. Initial reduction of a fracture may be
obtained by counteracting muscle forces acting in the
trochanteric area. A condition as close to anatomic reduc-
tion as possible should be attained.
Anatomic alignment, achieved closed reduction, may be
maintained by internal fixation with percutaneous small,
threaded or nonthreaded pins, which should stop short of
the physis. Again, a hip spica cast is also applied to provide
additional immobilization. The importance of internal fixa-
tion in maintaining reduction when Pauwel’s angle is greater
than 40° cannot be overemphasized.
Although it has been stated that pinning in a young child
may enhance the risk of ischemic change, there is no reason
for the blood vessels to be damaged so long as the pins are
kept within the femoral neck. Should ischemic changes
occur, they are most likely caused by the original injury
(damage to vessels coursing along the femoral neck), rather
than by the surgical intervention.
The relatively short neck of the femur in a young child
sometimes makes fixation difficult. The best type of internal
fixation relates to the differing anatomy. Large-diameter
nails may cause distraction of the fragments, are often diffi-
cult to drive into the dense bone (compared with adult
bone), and may lead to fragmentation and propagation
of the fracture or to premature epiphysiodesis. I prefer
threaded fixation pins or screws that stop short of the capital
femoral physis. It is rarely necessary to cross the growth plate,
except with fractures less than 1 cm from the physis. In such
cases smooth pins should be used, with the pins being
removed as soon as possible to avoid interfering with subse-
quent growth. However, continued growth in the capital
femur may occur, such that the epiphysis progressively grows
away from the pin ends, leaving them in the metaphysis.
Threaded pins that cross the growth plate may enhance the
risk of premature epiphysiodesis. A lag-screw through a
predrilled and tapped hole also offers a good fixation
method, but it requires placing a relatively large device and
displacing much bone, and the lag-screw should not cross
the physis.
Displaced femoral neck fractures should be treated by
gentle closed reduction under fluoroscopy followed by inter-
nal fixation with two or three threaded pins, with any pin
crossing the plate being smooth. Age is not a factor with this
suggested treatment modality. This treatment should be fol-
lowed by the use of a supplementary hip spica cast.
If adequate reduction cannot be achieved or if after reduc-
tion Pauwel’s angle is still more than 50°–60° with a con-
sequently high shearing stress, a subtrochanteric valgus
osteotomy may be considered. In this situation, an anterior
approach or extension of the exposure with direct visualiza-
tion of the fracture may allow adequate reduction. If the
capsule is opened, it should be opened anteriorly, and great
care should be taken not to place any instruments forcefully
Proximal Femoral Injuries
through the fracture line into the posterior region or around
the neck for exposure, as such placement may damage the
major circulatory systems to the femoral head.
Some intertrochanteric fractures in the child may be
reduced and held in traction. When callus is present at 2–3
weeks, a hip spica may be applied. An indication for inter-
nal fixation is irreducibility or inability to hold the fracture
in traction because of concomitant injuries, particularly
those involving the central nervous system. Open reduction
may be difficult. Ischemic necrosis does not carry the same
potential risk as with higher neck fractures, and the tendency
toward varus deformity is more easily overcome than with
proximal fractures. Fixation should avoid the greater
trochanteric physis. Generally, pins should be placed so they
parallel the neck cortices. Thus, the entry points on the
lateral cortex should be below the greater trochanteric physis.
Results
Canale and Bourland reviewed 61 fractures, including 5
transepiphyseal, 27 transcervical, 22 intertrochanteric, and 7
subtrochanteric fractures.50 Among them, 55% had good
results, 20% fair results, and 25% poor results. The use of
internal fixation appeared to reduce the complications
of nonunion and coxa vara. Ischemic necrosis caused most
of the poor results. There were 26 patients who developed
necrosis, 13 developed a coxa vara deformity, and 4 had
nonunion. Of 54 hips with adequate follow-up, 33 (62%)
showed premature capital physeal closure compared to the
opposite hip. Canale and Bourland believed that subtro-
chanteric osteotomy was not indicated as a reparative pro-
cedure, as recommended by Ratliff.182,184,186
McDougall observed equally good or bad results from con-
servative or operative methods.139 However, these statistics
were misleading because all the intertrochanteric fractures
were treated conservatively by casts or traction, whereas
the transcervical fractures were usually treated by internal
fixation.
Leung and Lam129 reassessed some of the patients origi-
nally reported by Lam.123,124 They were able to evaluate 41 of
the 92 children between 13 and 23 years after injury.
Although the early clinical results reported by Lam 3–5 years
after treatment showed excellent clinical results despite a
high incidence of complications, the subsequent review
showed that 83% of the patients had a radiographic abnor-
mality and 24% had pain, a limp, or leg shortening. This type
of study is indicative of what needs to be done following most
childhood skeletal injuries, especially those involving an
epiphysis or physis. Long-term effects—a decade or more
after skeletal maturity is attained—give more realistic results
regarding the likelihood that osteoarthritis, joint dysfunc-
tion, or other chronic problems may develop.
Complications
There is a high incidence of complications independent of
the therapeutic approach. Complications of varying severity
develop in about 50% of children with fractures of the
femoral neck. Such complications include (1) coxa vara, (2)
ischemic necrosis, (3) delayed union, (4) nonunion, (5) leg
length inequality, and (6) epiphyseal slip. The incidence of
873
ischemic necrosis has ranged from 16% to 45%. The inci-
dence of coxa vara has ranged from 25% to 55%. Nonunion
occurs in approximately 10–33% of cases. Of 189 cases
reported in five large series, one or more of these compli-
cations developed in 60% of the patients.72,184,186,189,216 This
fracture is one of the more challenging childhood injuries.
Ischemic necrosis is the major complication.67,111,216 In one
series this complication developed in 30 patients (42%); the
fragments had been displaced in 26 patients, whereas in 4
patients there was no displacement.111 Ischemic necrosis is
usually apparent within a year after injury, although radio-
graphic signs of necrosis may not be obvious for as long as 2
years after the injury.139 Earlier diagnosis may be detected
with MRI.
The basic cause of necrosis is presumed to be damage
to or occlusion (partial, temporary) of the posterosuperior
and posteroinferior vessels passing along the neck of the
femur. It is not clear whether ischemia results from complete
division of all vessels, kinking of those vessels that remain
intact, or tamponade by hemarthrosis within the hip capsule
(Figs. 21-24, 21-25).
Weber et al. stressed the importance of pressure exerted
on the blood vessels by the hematoma formed within the
capsule after a proximal femoral fracture and stated that it
may be a significant factor in reducing the blood supply.231
They recommended that the capsule be opened and the
pressure thereby alleviated. Kay and Hall have argued that
the hip should be aspirated to prevent tamponade of the
vessels.111 This concept remains controversial.
Vegter and Lubsen showed that temporary vascular occlu-
sion for 6 hours resulted in necrosis of trabecular bone in
rabbit femoral heads.229 Only 2 hours of increased intracap-
sular pressure was necessary to result in a much more
complex picture of trabecular osteocyte death. They con-
cluded that transient occlusion due to this type of pressure
phenomenon could cause cellular death despite intact per-
fusion of the bone. Such fractional osteonecrosis was char-
acterized by necrosis of some trabecular osteocytes, whereas
the vascular and bone-forming marrow tissue seemed to
remain alive. This observation probably can be explained by
a difference in susceptibility to ischemia of the various cell
types within the epiphysis.
Melberg and colleagues showed that joint pressures in
adults were less than 20 mmHg when the hip fracture was
unreduced. When the hip was extended and internally
rotated, however, the pressure rose to values exceeding
the normal arteriolar pressure, with a peak pressure of
135 mmHg. Prolonged reduction maneuvers with the hip
joint in extension and internal rotation may create intra-
capsular pressure increases high enough to temporarily jeop-
ardize the circulation of the femoral head. They believed
their findings did not support the hypothesis that hip joint
tamponade per se was the common etiologic factor for the
development of femoral head necrosis after femoral neck
fracture; rather, the position maintained during the treat-
ment was more likely to be responsible.141
There appear to be three basic roentgenographic patterns
of ischemic necrosis (Figs. 21-26, 21-27). One is a total
involvement of the epiphysis, physis, and metaphysis extend-
ing from the level of fracture. The second is anterolateral
involvement, comparable to Legg-Calvé-Perthes disease, with
874 21. Femur

A B
FIGURE 21-24. (A) Femoral neck fracture treated by closed reduction and fluoroscopically directed percutaneous internal fixation. (B)
Development of ischemic (avascular) necrosis 11 months after the injury.

presumed involvement of only the metaphysis and an intact,

FIGURE 21-25. Femoral neck fractures, showing how the fracture
propagates into the intraepiphyseal cartilage. They may attenuate
or transect the posterosuperior vessels, especially with varus
deformation, yet leave the posteroinferior vessels relatively
undamaged.
uninvolved epiphysis. The third type represents involvement
of the anterior vessels from the lateral circumflex artery.
The method of treatment seems to be a factor in the
development of ischemic necrosis. Of fractures treated con-
servatively, 35% were complicated by this problem, in con-
trast to only 27% of those treated by internal fixation.
Extreme abduction of the hip during the treatment of devel-
opmental dislocation of the hip certainly decreases circula-
tion, and it is significant that with some of the recommended
conservative methods of casting the fractured hip is forced
into extreme positions to reduce the fracture. After reduc-
tion the affected hip should be brought into 30°–40° of
abduction and moderate flexion to lessen mechanical
impingement and attenuation of vessels. Similarly, following
internal fixation the hip should not be immobilized in ex-
treme positions.

FIGURE 21-26. Vascular disruption with varus and

valgus injuries.
Proximal Femoral Injuries
FIGURE 21-27. Ischemic (avascular) necrosis patterns. (A) Total
involvement of the capital femoral epiphysis, physis, and metaph-
ysis (all vessels). (B) Anterolateral involvement (probably of only
This complication may occur after undisplaced or dis-
placed fractures of the femoral neck in children. Chong and
coworkers believed that the most important prognostic
factor was the degree of displacement at the time of injury.
They reported an incidence of ischemic necrosis of 50%.56 I
tend to agree with this concept that vascular damage occurs
at the time of injury.
Femoral neck fractures appear more likely to undergo
necrosis than do intertrochanteric fractures. Displaced
transepiphyseal fractures have the poorest prognosis, with
development of avascular necrosis in 80% of the involved
patients. The incidence of ischemic necrosis in those who
are 10 years of age or younger is 21%, whereas in those over
10 years of age it increases to 47%.
These “at risk” children should have a bone scan 3–4
months after the injury, with the scan repeated approxi-
mately 1 year after the injury to look for possible delayed vas-
cular damage or compromise. A bone scan may be difficult
to interpret because of the new bone formation from the
healing fracture and the changes in the femoral head con-
sequent to injury and immobilization. Ischemia is usually
detectable on a scan within the first few months and proba-
bly always within a year, at which time radiographic changes
are also becoming evident. The first signs of ischemic necro-
sis are that the head does not become osteoporotic and that
it does not grow and mature compared with the opposite
side. The cartilage space widens. These signs are present
long before fragmentation and deformity of the head, com-
parable to Legg-Calvé-Perthes disease. MRI is of questionable
value because of the artifactual changes due to the internal
fixation.
If there is any suggestion of ischemic change or if
roentgenographic changes seem to be gradually appearing,
premature epiphysiodesis of the greater trochanter should
be considered to minimize the overgrowth and loss of the
normal articulotrochanteric distance.
Premature fusion of the capital femoral physis is some-
times an early sign of ischemic necrosis. Premature fusion
may result in shortening of the lower limb and a relative coxa
vara. This situation may lead to a short neck and a weak lever
arm for the hip abductor muscles, shortened leg, and limi-
tation of abduction resulting from overgrowth of the greater
trochanter. It appears reasonable to implicate specific
ischemic involvement to selected regions of the physis, along
875
the posterosuperior vessels). (C) Metaphyseal involvement only,
with unaffected capital femoral epiphysis and physis.
with continued growth in other regions, similar to the avas-
cular necrosis encountered in the various patterns following
closed and open treatment of developmental dislocation of
the hip.216
In contrast, an increase in circulation consequent to the
trauma may produce a coxa magna, which is poorly covered
if the acetabulum does not also overgrow congruously. This
development is a good prognostic sign, as it implies more
than adequate circulation, rather than ischemia.
Coxa vara is a common complication.68 Lam reported 23
instances in 75 fractures.124 The deformity developed in frac-
tures during the immediate postinjury period in 18 patients
and as a late complication in 5. It may be caused by several
factors: (1) failure to reduce the fracture; (2) loss of align-
ment in the hip spica because of inadequate immobilization
or delayed union; and (3) ischemic necrosis and premature
fusion of the capital femoral physeal plate, in which instance
relative discrepancy of growth between the capital femur and
greater trochanter may result in a progressive decrease in the
neck–shaft angle. The clinical signs of coxa vara are promi-
nence and elevation of the greater trochanter, shortening of
the limb, decreased hip abduction, and gluteus medius limp.
Treatment usually consists of a subtrochanteric abduction
(valgus) osteotomy. If the capital femoral epiphyseal plate is
prematurely fused, the relative varus deformity recurs with
continued growth of the trochanter. It is reasonable to
consider a greater trochanteric epiphysiodesis at the time
of the abduction osteotomy. The resultant leg length dis-
crepancy may require arrest of the contralateral distal
femoral epiphysis at the appropriate age (or ipsilateral leg
lengthening).
Delayed union or nonunion may develop with femoral
neck fractures. It occurs in about 85% of the cases with a
Pauwel’s angle of more than 60° (Fig. 21-28), particularly
when treated conservatively by cast immobilization alone. In
those treated by internal fixation, the fracture fragments
may be separated by the threaded portion of a large pin.
Nonunion should be treated by bone grafting and sub-
trochanteric abduction osteotomy aimed at converting the
fracture angle from one of shearing or tensile stress to one
of compression. With delayed union, abduction osteotomy is
adequate. Usually it is unnecessary to insert a bone graft as
well. When evaluating these patients prior to considering
surgery, a bone scan is useful for determining if there is ade-
876
C description may cause damage to the blood vessels along the
FIGURE 21-28. (A, B) Femoral neck fracture left in varus. (C)
Simulation of such nonunion and coxa vara after a femoral neck
fracture.
quate blood supply to the proximal portion, particularly in
the metaphysis.
A rare complication of coxa vara is the subsequent devel-
opment of an SCFE during adolescence.204
Stress Fractures
Stress fractures of the femoral neck are relatively common
in young men in their early twenties but less likely prior to
skeletal maturity. Wolfgang described a stress fracture of the
femoral neck in a 10-year-old child.241 There are two types of
stress fracture of the femoral neck. The transverse type
appears as a small lucency in the superior part of the femoral
neck and often becomes displaced. This type is less likely in
a child, in whom there is still epiphyseal cartilage along the
neck. The second, a compression type that appears as a haze
of callus on the inferior aspect of the femoral neck associ-
ated with slight varus displacement, is more likely to occur
in a young patient.
21. Femur
Ipsilateral Proximal/Diaphyseal Fracture
Double level fractures of the femoral neck and diaphysis are
infrequent in the child. The femoral neck fracture has the
same potential problems as the isolated injury. It should be
stabilized first. The diaphyseal fracture may be treated by
closed or open means. However, a cast (immediate), open
reduction, and plating or an external fixator are also rea-
sonable alternatives.
Trochanteric Injuries
Greater Trochanter
Injuries to the greater trochanter (Fig. 21-29) generally
occur as a result of a direct blow or a hip disloca-
tion.329,332,338,340,341,346,349–351,358,359,362 The greater trochanter
may be avulsed by sudden contraction against resistance
in the gluteus medius and minimus muscles. Such a frac-
ture is usually undisplaced or minimally displaced. With
more severe injury, the chondro-osseous fragment is
retracted proximally, posteriorly, and medially (see Fig. 21-
35, below).
Care must be taken not to interpret a small accessory ossi-
fication center at the tip of the greater trochanter as an avul-
sion fracture. This finding usually is a normal variation in
the tip of the greater trochanter that appears in children
7–10 years of age (Fig. 21-3).
Depending on the age of the patient at the time of
trochanteric injury, part of the fracture most likely occurs
through the intraepiphyseal cartilaginous continuity
between the capital femur and greater trochanter. This
posterosuperior femoral neck and lead to ischemic changes
in the femoral head as a consequence of the injury.346 If the
trochanter is avulsed from the lateral femoral metaphysis, an
additional complication may be premature fusion of the
physis with continued growth of the capital femur to create
an elongated femoral neck (see Chapter 20).
Treatment is closed reduction if the fracture is minimally
displaced. When significant displacement occurs, tension
band wiring or transphyseal fixation may be indicated
(Fig. 21-30).
Churchill et al. found that there were few anastomoses
between the vessels of the greater trochanter and those of
the adjacent cancellous bone of the shaft.326 They believed
that ischemia of the greater trochanter could thus contribute
to nonunion following trochanteric osteotomy. The studies
by Churchill et al. suggested that even in the adult the
greater trochanter has a separate blood supply after bony
fusion to the shaft.326 This is not unexpected. When one ana-
lyzes MRI studies in young to middle-aged adults there often
is residual independence of the circulation of the metaphy-
seal and diaphyseal bone from the epiphyseal and apophy-
seal regions. A relatively avascular plane physiologically
separates the two circulatory patterns even well after skele-
tal maturation.
Linhart et al. described a 12-year-old girl who sustained an
apparent isolated fracture of the greater trochanter.346 The
patient was treated conservatively, and approximately 6
months later she was noted to be developing ischemic necro-
Trochanteric Injuries
A B
FIGURE 21-29. (A) Greater trochanteric fracture (arrow). (B) Healed avulsion (arrows) of the greater trochanter. (C) Trochanteric injury
accompanying a femoral neck fracture.
sis of the capital femur. This is the only reported case of this
complication. Probably there was avulsion of the main
branch of the lateral retinacular vessels as they coursed along
the posterosuperior femoral neck. These vessels or even the
main circumflex may have been significantly injured by the
pattern of fracture.
Lesser Trochanter
Wilson and colleagues366 reviewed 78 cases of this injury;
90% occurred in adolescents, usually following the appear-
ance of the secondary ossification center in the lesser
trochanter.319–325,327,328,330,331,333–339,342–345,347–349,352–366 The avul-
sion of the lesser trochanter usually occurs with hyperexten-
sion and abduction of the hip. It often occurs in boys playing
running games when they stop suddenly to avoid a fall or
collision.
FIGURE 21-30. (A) Avulsion of the greater trochanter (arrow). (B) Reduction with tension band wiring. (C) Follow-up showed that the
lesser trochanter was also involved (arrow).
877
C
It is also common in hurdlers, and it may occur coming
out of starting blocks in a sprint race. There is a sudden snap
in the groin, immediate pain, and an inability to stand erect
comfortably. Climbing stairs is difficult. Some hip flexion
may be retained because the iliacus portion has a broader
insertion, and the psoas portion inserts directly into the tip
of the lesser trochanter.
There is pain along the inner thigh, a limp, and frequent
inability to flex the thigh, with deep-seated tenderness in the
region of the lesser femoral trochanter. External rotation is
a common finding. These findings are comparable to those
of slipped capital femoral epiphysis. Patients usually are able
to support the weight of the body on the injured limb, but
the inability to bring the leg forward comfortably and the
associated pain may interfere with walking or other activities.
The inability to flex the hip when in a sitting position is
usually diagnostic of the loss of power.335 It is conceivable that
 878
A B
some degree of flexion is possible if some periosteal attach-
ments of the trochanter remain intact. Good functional
results have been obtained by merely immobilizing the limb.
There have been no long-term complications, even if an
apparent fibrous union developed.
Roentgenograms must be obtained with the thigh in exter-
nal rotation to rotate the lesser trochanter into an adequate
view. Usually the lesser trochanter is avulsed and upwardly
displaced, although not necessarily completely separated
from the femur (Fig. 21-31). Obviously, the lack of a
secondary ossification center makes the radiographic diag-
nosis difficult.328,334 MRI may be useful in such situations
(Fig. 21-32).
FIGURE 21-32. MRI showing avulsion of the lesser trochanter and
surrounding tissue edema (acute injury).
21. Femur
FIGURE 21-31. (A) Avulsion fracture (arrow) of
the lesser trochanter in a female gymnast. (B)
Follow-up 1 year later showing extensive bone
formation.
The displaced fracture heals with minimal if any disability.
Most of these fractures respond simply to rest and decreased
activity. The patient is kept in bed with the hip in flexion
until comfortable and then allowed to ambulate with
crutches and a three-point partial weight-bearing gait. Immo-
bilization in a cast is rarely necessary. Open reduction is not
usually indicated.328,366
Parisel reported an avulsion of the lesser trochanter that
eventually healed with elongation of the trochanter.356
Dimon reviewed 30 fractures of the lesser trochanter,328 22
of which occurred during vigorous sports. He noted that 26
of the 30 patients were treated symptomatically. Two were
treated with a spica cast and two with open reduction. He
further found that beginning resumption of athletic activi-
ties was possible by 6–8 weeks.
Subtrochanteric Fractures
Little attention has been given to children’s subtrochanteric
fractures, with these injuries generally grouped with frac-
tures of the proximal third of the femur.367,368,370–373 These
particular fractures are usually the result of a direct blow
during an automobile accident or athletic activity. Unlike
most children’s fractures, many have some degree of com-
minution, along with overriding and anterior and varus
angulation.367,370,372 Kehr and Starke thought that sub-
trochanteric fractures in children differed from those in
adults in that there was usually a simple fracture line and
much less likelihood of comminution of the fragments.371
These fractures in children are difficult management
problems because of the tendency of the proximal fragment
to be displaced into a flexed, abducted, and externally
rotated position consequent to muscle forces (Fig. 21-33).
Moreover, remodeling is not as extensive in this region, and
malalignment may remain as a permanent deformity
(Fig. 21-34).
Treatment initially may consist of skeletal traction with a
distal femoral (metaphyseal) pin. Skin traction is rarely suf-
Subtrochanteric Fractures 879

FIGURE 21-33. (A) Subtrochanteric fracture in an 8-year-old child. deformation due to subtrochanteric fracture. Arrows show deform-
Overriding has been accentuated by varus and flexion of the ing vectors.
proximal fragment. (B) Final healed position. (C) Abduction flexion

ficient, except in a very young child. The leg is placed in trac- the capital femoral physis. A uniaxial external fixator is also
tion with 90° of hip flexion and 90° of knee flexion. This feasible.
positioning tends to counter both flexion and abduction of Regardless of the method of treatment, virtually all sub-
the proximal fragment. Use of less than 90° of hip flexion trochanteric fractures in children and adolescents develop
may make alignment difficult. Frequent roentgenograms adequate osseous union. Mild anterior angulation and some
may be necessary to be certain that adequate alignment is varus or valgus alignment of the fractures may persist. In
maintained. Traction may be followed by casting or a cast- young children angular deformity may self-correct to a sig-
brace.368 Frequent radiographs are necessary to determine if nificant extent, whereas in older children little change in
the angulation increases in the cast. The average duration of
traction and cast immobilization is 9–12 weeks.
Because of instability, costs of traction (i.e., prolonged hos-
pitalization), and frequent verification of position by radia-
tion exposure, alternative methods are gaining popularity.
My preference is a uniaxial fixator. Depending on the level
of the fracture, one or more fixator pins may have to be
placed in the greater trochanteric epiphysis or the femoral
neck. The use of a longitudinal rod and locking screws is
contraindicated in young patients because of potential
damage to the greater trochanteric physis.
Older patients (adolescents) with subtrochanteric frac-
tures that cannot be adequately controlled by traction may
be candidates for open or closed reduction and internal fix-
ation. The possibility or necessity of using open reduction is
particularly increased if it is difficult to control the fracture
because of the associated head injury.367 The choice of a fix-
ation technique is difficult if the physes of the greater
trochanter and capital femur are still functional. An
intramedullary nail is contraindicated if it must traverse por-
tions of still functional trochanteric and intraepiphyseal
physes. One method is a compression side plate and screw
fixation, a method routinely and effectively used for elective
subtrochanteric osteotomy in children and adolescents. Care
must be taken not to damage the trochanteric physis.
An alternative is the use of flexible rods, usually inserted
retrogradely from the distal femoral metaphysis, across the
fracture, and into the femoral neck but not impinging on FIGURE 21-34. Malunion of a subtrochanteric fracture.
880
A B
FIGURE 21-35. Cervicopertrochanteric fracture. (A) Injury. (B) Four months later.
alignment occurs with growth. In none of the children was
this angulation or rotation at the fracture site a significant
functional problem, although there should be some concern
for the child with increased varus and posterior direction of
the growth plate that might increase susceptibility to slipped
capital femoral epiphysis.205
The spontaneous correction of leg length inequality
by growth stimulation is better in children under 10 years
of age, and an overriding of 10–15 mm is acceptable. In
contrast, in teenage children there is little remodeling or
compensation for shortening after a subtrochanteric
fracture.
Gamble et al. described a subtrochanteric fracture varia-
tion they classified as a transverse cervicopertrochanteric
fracture (Fig. 21-35).369 The injury was just above the lesser
trochanter but below the greater trochanter. It should be
considered a variant of the subtrochanteric fracture.
Femoral Shaft Fractures
Diaphyseal fractures of the femur are relatively frequent in
children and must be considered serious injuries because of
the blood loss and potential shock accompanying the
primary trauma. Such fractures often result from violent
injuries, especially automobile accidents, and great care
must be taken to rule out associated injuries as well as neu-
rologic and vascular complications.374–731
Femoral shaft fractures in children may behave differently
from similar fractures in adults. The important points to con-
sider are (1) early consolidation, often with considerable
callus formation, especially in young children; (2) a reactive
increased rate of longitudinal growth of the femur for
21. Femur
approximately 1 year (even the tibia may similarly respond);
and (3) spontaneous but limited correction of axial defor-
mity without corresponding rotational correction. Because
femoral shaft fractures in children generally heal easily and
satisfactorily, conservative (i.e., nonoperative) treatment has
usually been advocated.
The most frequent site of diaphyseal fracture is the middle
third, where normal anterolateral bowing of the diaphysis
is at its maximum. This area is most commonly subjected
to direct violence; injuries involve the proximal third less
commonly and the distal third least frequently. Greenstick
fractures may occur but are more frequent in the distal me-
taphysis. Fractures that result from obstetric trauma usually
occur in the middle third of the shaft and ordinarily are
transverse. Child abuse femoral diaphyseal fractures tend to
be spiral.
Hedlund and Lindgren studied 851 femoral shaft fractures
in children and adolescents, reporting that the maximal inci-
dence was in children 2–5 years of age and the total inci-
dence was 2.6 times higher in boys than in girls. The cases
were about equally divided between fractures caused by falls
and fractures caused by traffic accidents. Falls were the most
common cause in children under 3 years of age.493
Nafei et al. studied the incidence of femoral shaft fractures
in children in a Danish urban population from 1977 to
1986.585 There were 144 femoral shaft fractures in 138 chil-
dren less than 15 years of age. The boy/girl ratio was 2.8: 1.0.
The incidence rate was 28 per l00,000 child-years. Young chil-
dren less than 3 years of age had the highest incidence per
year. The most common etiologies were trauma due to traffic
accidents (43.1%) and falls (42.2%).
Proper emergency care, such as initial gentle handling
and adequate splinting of the fracture, is extremely impor-
Femoral Shaft Fractures
tant to prevent shock and further injury to soft tissues. Any
movement of the acutely injured limb is usually painful. An
efficient means of immobilization is the Thomas splint,
which must be appropriately sized to the child.
Pathomechanics
The displacement of the fracture fragments depends on the
breaking force, the pull of the attached muscles, and the
force of gravity acting on the limb. The severity of violence
and the strong pull of muscles cause fracture fragments to
be completely displaced, leading to variable amounts of over-
riding. The distal fragment is usually laterally (externally)
rotated. With fractures of the upper third of the femoral
shaft, the proximal fragment is pulled into flexion by
the iliopsoas, abduction by the gluteus medius and minimus,
and external rotation by the short external rotators and
gluteus maximus. The shorter the proximal fragment, the
greater is the degree of displacement. The distal fragment is
drawn proximally by the hamstrings and quadriceps femoris
muscles and medially by the adductors. Thus the upper end
of the distal fragment tends to lie posterior and medial
to the proximal fragment, which is in flexion, abduction,
and external rotation. Displacement of fragments in
a middle third diaphyseal fracture does not follow as regular
a pattern. The tendency is for the proximal fragment to be
in flexion and the distal fragment to be displaced for-
ward. When the fracture level is in the upper half of
the middle third, the proximal half may be abducted.
When the break is in the lower half, it tends to abduct.
Displacements are not necessarily constant, however;
they depend on the relative insertion and the strength
of muscles, factors that change considerably as the child
grows.
Diagnosis
A history of injury with resultant local pain, tenderness, and
swelling, inability or reluctance to move the affected limb,
deformity, shortening, abnormal mobility, lateral rotation of
the limb, and crepitus render the diagnosis evident. The
patient should be examined gently to avoid unnecessary
pain. Neurovascular status in the lower limb must be care-
fully assessed and recorded because injury to the femoral
vessels, sciatic nerve, or both may occur, especially from pos-
terior displacement of the distal fragment. Because femoral
shaft fractures often result from major violence, it is imper-
ative that the general condition of the patient be evaluated.
The patient should be carefully examined to detect any
damage to the abdominal, pelvic, and genitourinary area,
any cranial injuries, or other fractures or hip dislocation.
The last-named injury must be ruled out carefully with a
good film of the hip joint. It is inappropriate to finish treatment
of a fracture of the femur and discover that the hip has been dislo-
cated for the entire duration of treatment. Similarly, the knee
should be examined to rule out injury, such as an anterior
cruciate ligament avulsion (see Chapter 22).
Roentgenograms are necessary to determine the exact
level and nature of the fracture. They should not be done
until the patient has been properly examined, subsequently
881
immobilized on a Thomas splint (or similar device), and
given adequate medication for relief of pain and muscle
spasm.
Khalil described an unusual complication in which there
was a comminuted midshaft femoral fracture with the but-
terfly fragment ending up in the subcutaneous abdominal
tissue, having been telescoped into that region at the time
of the original fracture.532
Treatment
Soft tissue injury inevitably accompanies a femoral shaft frac-
ture. Excessive hemorrhaging with a blood loss of 500 ml or
more may occur. The sources of bleeding may be branches
of the profunda femoris artery, which course around the pos-
terior and lateral surfaces of the femoral shaft, the vessels of
the muscles that envelop the femur, or the medullary vessels
of the bone. Occasionally, the femoral artery is damaged.
Major damage to the femoral artery, necessitating repair, is
one of the situations in which internal fixation is definitely
indicated in a child, as it minimizes the tension of the suture
line of the vascular repair.
Hypotension is not usually present in children in whom
the closed femoral fracture is the only major injury and in
whom there is no major vascular injury.338 Only one-third of
the children have a clinically significant change in hemat-
ocrit, with most averaging a 4% drop. Children with femoral
fractures in whom hypotension or a rapid drop in hematocrit
develops should be promptly evaluated for an alternative
source of significant blood loss (e.g., abdominal, retroperi-
toneal, intrapelvic).
Ostrum et al. reviewed 100 patients who had either an iso-
lated femoral shaft fracture or a femoral shaft fracture in
addition to other non-shock-producing fractures of minor
injuries.600 They found that femoral fractures alone or in
combination with other minor injuries should not be con-
sidered the cause of hypotensive shock in the traumatized
patient. For any traumatized patient who presents with a
closed femoral shaft fracture and hypotension, an alternative
source of hemorrhage should be sought.
There is no routine treatment for displaced femoral fractures in
children. A decision must be made regarding what type of
acute reduction, traction, or fixation is indicated for the spe-
cific injury complex in a given patient. One must consider
the age and weight of the patient; local soft tissue trauma;
the type and location of the femoral fracture; other injuries
to the head, thorax, and abdomen; and additional fractures
of the same or opposite leg.
Several principles should be applied to the treatment of
femoral shaft fractures in children: (1) The simplest form
of satisfactory treatment usually is the best. (2) If possible,
the initial treatment should be maintained. (3) Absolute
anatomic reduction may not be essential for adequate long-
term function. (4) Restoration of longitudinal and rotational
alignment is more important than the positions of the frac-
tured surfaces relative to each other. (5) The more growth
remaining in the fractured femur, the more likelihood it is
that normal osseous architecture can be restored as the bone
remodels. (6) Overtreatment is usually worse than under-
treatment. (7) The hope that all deformities in children will
882 21. Femur

correct themselves spontaneously is no excuse for ignoring be monitored closely for the development of vascular and
any deformity that could be corrected by simpler means and neurologic skin complications. Circulatory problems are the
manipulation. Shortening of less than 2 cm, angulation of most serious. Bryant’s traction is not completely safe in chil-
less than 15°, and minimization of rotation are the major dren; tight dressings and abnormal pressure may impair cir-
goals to achieve with nonoperative treatment. culation and lead to Volkmann’s ischemic contracture, even
in the normal limb that is also being treated.401,426,592 There
are three basic patterns of circulatory insufficiency: (1)
Traction
ischemic fibrosis of the muscles of the lower leg with patches
Several types of skin and skeletal traction may be used; each of sensory loss and almost complete paralysis of the muscle
has its advantages and advocates. The simplest, safest, most distal to the knee, particularly the short toe flexors; (2)
effective method for a child, for a given fracture, and for a involvement characterized both by the aforementioned
particular age group should be the treatment of choice. changes and by circumferential necrosis of the skin and
Bryant’s traction, properly applied and carefully watched, is underlying muscles in the calf; and (3) gangrenous changes
appropriate for children weighing less than 18 kg (25 lb) in the foot and ankle in addition to circumferential necrosis
or under 2 years of age. For children weighing more, of the calf.
Russell’s traction (or a modification thereof) is probably For children older than 2 years of age, there are several
used most commonly. The increased emphasis on decreas- types of traction: (1) skin traction with the knee in exten-
ing the time of hospitalization has led to a deemphasis on sion; (2) suspension skeletal traction with the knee in
traction. However, the methods are safe and are often used in flexion; and (3) 90°–90° skeletal traction with a pin through
parts of the world where internal or external or fixation are not the distal femur or the proximal tibia.413,425,515,572,587 I prefer
available. the distal femoral pin, as it avoids risk to the tibial tuberos-
The fracture fragments should be longitudinally aligned ity with premature growth arrest (Figs. 21-36, 21-37). It also
as near to a normal anatomic relation as possible. Angula- avoids traction across the knee joint, which may have sus-
tion exceeding the normal range by more than 15°–20° tained occult soft tissue injury (e.g., to the anterior cruciat
should not be accepted. The surgeon should strive for as ligament). In general, traction is employed to maintain
complete correction of rotational deformity as possible and alignment until there is adequate callus for stability (i.e., the
should try to achieve angulation that does not exceed 10° in callus and fracture site are no longer tender, and the femur
the medial or lateral direction, 10° anteriorly, and 5° poste- moves as a unit on manipulation). The leg may be effectively
riorly. This objective requires frequent radiographic evalua- immobilized in a hip spica cast without loss of the reduction
tion of the fracture and adjustment of the traction. The or position.
child should not be subjected to frequent manipulations Because of its effectiveness and simplicity, 90°–90° skeletal
simply to correct minor angulation. traction with a pin through the distal femur is frequently
In infants and children up to 2 years of age, Bryant’s trac-
tion is probably satisfactory, provided there is no spasticity
and contracture of the hamstrings and provided that the hips
may be easily flexed to 90° with the knees in slight flexion.
Traction should be applied to both legs. The legs (knees
slightly flexed) should be wrapped from upper thigh to the
malleoli, with padding (e.g., lamb’s wool or soft cotton)
placed over the malleoli to prevent undue pressure. The
same amount of weight should be applied to each leg and
should be sufficient to lift the infant’s pelvis until the sacrum
is slightly elevated from the mattress. One must be cautious
not to overpull a small infant. The position of the fracture
must be checked by periodic roentgenograms so distraction
of the fragments is avoided. Medial bowing caused by an
excessive pull of the hip abductors may be corrected by
decreasing the amount of weight on the affected limb and
increasing traction on the contralateral normal limb,
thereby tilting the pelvis and countering the pull of the hip
abductors. The expectation that an osseous deformity during
childhood will correct itself spontaneously with growth and
remodeling is not an acceptable excuse for ignoring it, espe-
cially if correction may be obtained by simple traction mod-
ification. Callus forms rapidly in young children; at 2–3
weeks after trauma the tenderness disappears and the frac-
ture is probably stable enough to allow removal of the limb
from traction and to place it in a hip spica for an additional
6–8 weeks.
Bryant’s traction should not be used in children over 2 FIGURE 21-36. Effect of a traction pin being too close to the growth
years of age or those weighing over 25 lb. The patient must plate.
Femoral Shaft Fractures
FIGURE 21-37. (A) Recurvatum secondary to pin damage. (B) Recurvatum even with pin (arrow) located below and behind the
tuberosity.
used (Fig. 21-38). Alignment of the fracture is achieved and
maintained, as there is essentially one vector of traction. The
pin through the distal femur provides good rotational
control of the fracture fragments. The gastrocnemius, ham-
string, and iliopsoas muscles are relaxed by the flexed posi-
tion of the hip and knee, making alignment of the fracture
fragments relatively easy.
Other advantages of 90°–90° traction are that it promotes
dependent drainage, the thigh is readily accessible for clini-
cal evaluation of alignment with the use of portable
roentgenographic equipment, and it facilitates change of
dressings and wound inspection in infected or open frac-
tures. A threaded Steinmann pin or large K-wire is inserted
2 cm proximal to the adductor tubercle and distal femoral
physis. Injuring the physis must be avoided. Pushing the skin
slightly upward while inserting the wire through should
prevent undue traction on the skin when the weights are
applied. Sterile dressings are placed over the skin incisions,
and a traction bow is applied, with the pin under tension. A
below-knee cast may be applied, with the ankle in a neutral
position. This cast should be well padded in the popliteal
area, the dorsum of the foot, and the ankle to prevent pres-
sure sores. Traction ropes suspend the lower leg in a hori-
zontal position, and the knee is in 90° of flexion. The
traction forces act vertically, in line with the longitudinal axis
of the femoral shaft.
Angulation and rotation may be corrected by shifting the
overhead traction in the appropriate direction. If additional
external support is necessary in an unstable fracture, coap-
tation splints may be employed. Slings with l–2 kg of traction
may be applied over the fracture site to control lateral or
anteroposterior angulation.
The position and alignment of the fracture fragments
must be checked by periodic roentgenograms. Distraction of
the fragments should not occur. In children between 2 and
10 years of age, side-to-side (bayonet) apposition, with
883
0.5–1.0 cm overriding, is an ideal position. Overriding
should not exceed 1.5 cm in infants and adolescents. End-to-
end apposition is more desirable because of the decreased
likelihood of overgrowth.
Traction is continued for 2–4 weeks until the callus is no
longer tender and the femur moves as a unit. When ade-
quate callus is evident on the roentgenogram and the patient
is comfortable with limb movements, he or she is placed in
a hip spica cast. The affected thigh should be in 10° of abduc-
tion or in neutral position, with the opposite hip in moder-
ate abduction to facilitate perineal hygiene. The fractured
thigh should not be in marked abduction, as the pull of the
strong adductors may cause lateral bowing. The pin in the
femur may be removed or incorporated into the cast, accord-
ing to preference.
Humberger and Eyring described a method of 90°–90°
skeletal traction with the Kirschner wire inserted through the
proximal tibia.513 This method is not recommended. The traction
pin may injure the apophysis of the tibial tuberosity. A wire
in the proximal tibia does not provide direct control of the
femur, as does a wire through the distal femoral metaphysis.
Furthermore, patients treated with 90°–90° traction and a
proximal tibial traction pin may exhibit knee subluxation or
dislocation, genu recurvatum, progressive knee pain, and
prolonged rehabilitation.572
Bjerkreim and Benum reported seven cases of genu recur-
vatum after tibial traction for femoral shaft fracture. Six of
the patients eventually required corrective osteotomy. The
anterior part of the growth plate may be damaged, as may
be that part under the tibial tuberosity.397 Only a small
amount of damage need occur to the growth plate to lead
to an osseous bridge sufficient to cause angular deformity.
Although it is expected that large deformities occur only
with large growth slowdowns, it should be realized that even
with type 6 injuries a small peripheral osseous bridge may
lead to a major angular deformity in this particular region.
 884 21. Femur

such as knee pain, knee joint, subluxation, or growth

disturbance.
Suspension traction is preferred by many orthopedic sur-
geons for older children and adolescents, as skin traction is
often unsatisfactory in the older child. Skeletal traction is
applied with a K-wire inserted through the distal femur
(Fig. 21-39). The thigh and leg are supported on a felt pad
covered with a stockinette and are placed on a Thomas splint
with a Pearson attachment. With the hip in 35°–40° of
flexion, the Thomas splint is placed against the ischial
tuberosity and supported by sufficient weight to balance the
limb. The traction ropes on the Thomas ring should prevent
the splint from sliding distally. The level of the Pearson
attachment should be just above the knee joint level so the
knee can be flexed approximately 30° to relax the ham-
strings. A traction rope with sufficient weight on the distal
A end of the Pearson attachment supports the weight of the
leg. By adjusting the weights the limb may be counterbal-
anced so it moves comfortably with the patient. The foot of
the bed is elevated so the weight of the patient’s body acts
as countertraction.
With midshaft fractures the tendency is toward posterior
angulation. To prevent this and to restore the normal ante-
rior bowing of the femur, the slings under the thigh should
be taut and the knee in flexion to relax the gastrocnemius
muscle. If there is persistent posterior angulation, a pad may
be placed underneath the thigh at the fracture site; alterna-
tively, a sling with direct overhead vertical pull at the appro-
priate level may be employed. Medial or lateral angulation
may be corrected by aligning the distal fragment with the
proximal one, which may be accomplished by shifting the
position of the ends of the Pearson attachment proximally
or distally on the Thomas splint, by changing the direction
of the pull, or both. Rotation may be controlled by adjusting
the suspension.
Mital and Cashman advocated the use of skeletal traction
for 2–3 weeks, followed by cast-brace application and ambu-
lation.576 They followed 28 children who had been treated
with this method. Their ages ranged from 2 to 14 years. The
average time for cast-brace application was 20 days after trac-

B
FIGURE 21-38. (A) The 90°–90° skeletal traction positioning with
the lower leg in a cast. (B) Early callus formation in a patient in
skeletal traction.

Bowler et al. reported two cases of premature closure of

the anterior portion of the proximal tibial physis with genu
recurvatum in patients who had sustained closed femoral
fractures.406 In neither case had a tibial traction pin been used.
One patient had been treated with distal femoral pin trac-
tion and the other with skin traction and a spica cast.
Havránek et al. used a single screw in the proximal tibia
for skeletal traction for femoral shaft fractures.490 It was
inserted into the tibia perpendicular to the surface and well
below the tibial tubercle physis. There were no complications FIGURE 21-39. Skeletal traction combined with splint.
Femoral Shaft Fractures
FIGURE 21-40. Variation of Russell’s skin traction applicable to
femoral fractures in children.
tion, and the average time in the cast-brace was an additional
6.5 weeks.
Russell’s skin traction is preferred by some as a method
for treating femoral shaft fractures in children (Fig. 21-40).
The medial and lateral adhesive traction strips extend from
the ankle to a foot plate with a pulley on its inferior surface.
There should be two pulleys at the foot of the bed and one
overhead. A well-padded sling is placed underneath the
knee. The traction rope extends from the sling to the over-
head pulley, which is distal to the knee joint, so the rope is
directed upward and distally at an angle of 25°, passing over
the superior pulley attached to the end of the bed to which
the skin traction straps are fixed and back again over the
inferior pulley at the foot of the bed, where 2–5 kg of weight
is suspended. The lower limb rests on two pillows arranged
so the knee is in 30° of flexion, the thigh is supported, and
the foot clears the mattress. The foot of the bed is raised
to provide countertraction. The vertical traction force is
FIGURE 21-41. Straight-leg traction method.
885
roughly equal to the amount of weight used, whereas the
horizontal traction force is equal to approximately twice the
amount of weight. The vertical and horizontal forces create
a paralellogram of forces, with the resultant force in line with
the long axis of the shaft of the femur.
Russell’s traction is often preferred because of the ease
with which it may be applied, but there are potential prob-
lems: (1) peroneal nerve palsy with resultant footdrop due
to pressure by the knee sling in the region of the common
peroneal nerve; (2) development of posterior bowing at the
fracture site due to lack of effective external support under
the thigh (often it is necessary to apply an additional sling
underneath the thigh with vertical traction to restore the
normal anterior bowing of the femur); (3) the difficulty
of nursing care and the need for careful vigil to ensure that
the correct traction is maintained; and (4) the child’s
pain, which initially may be greater than that with 90°–90°
traction.
Split Russell’s traction may be used instead of the original
Russell’s traction with its 2 : 1 ratio forces. With split Russell’s
traction, skin traction is applied in the longitudinal axis of
the limb, and a balanced sling with a vertical force is placed
under the distal femur or knee and suspended by weights to
support the part and supply the necessary resolution of
forces. External rotation of the leg is controlled with medial
rotation traction straps.
A relatively simple hip flexion-knee extension method may
be used for children up to 8 years of age (Fig. 21-41). The
leg is placed in a Thomas splint. Skin traction is carefully
applied up to the fracture site. The splint is initially placed
at 40°–50° but may be adjusted if further flexion deformity
is present in the proximal fragment. Up to 7 lb of skin trac-
tion may be tolerated by this method. Rotation is initially
controlled by allowing the leg to assume a natural, comfort-
able position. If necessary after a few days, rotation may be
controlled by a derotation strap placed across the knee or by
restraining the foot. However, the child usually controls rota-
tion spontaneously as he or she begins to move about the
bed when swelling and pain subside.
Foy and Colton described four patients with irreducible
distal-third femoral shaft fractures.465 They were irreducible
886
because either the proximal or distal end of the fracture was
found to be buttonholed through the lateral intramuscular
septum. Continued anatomic separation of the bone ends
may indicate entrapped quadriceps muscle. A small expo-
sure allows the bone to be manipulated out of the envelop-
ing muscle and back into the periosteal sleeve. The patient
may be placed back in traction, casted, or treated with skele-
tal fixation.
Rauch et al. described the use of a Weber vertical exten-
sion frame for treating femoral fractures in young children
to control rotation.620 They reported good results in eight
patients.
Immediate Casting
Because of increasing hospitalization costs, there has been
an emphasis on casting femoral fractures in children as soon
as possible.376,432,499,516,566,649,662,663,711,712 This approach may
include “immediate” application of a cast, which is probably
best for infants and young children. For older children, a
brief period of traction or suspension should probably
precede casting.
Dameron and Thompson described closed reduction and
immediate double hip spica immobilization as a preferred
method for treating infants and young children.438 Their
method is as follows. Under aseptic conditions and with the
patient under general anesthesia, a K-wire is inserted distal
to the proximal tibial epiphysis of the affected side. The foot
on the uninjured side is secured by strapping it to the foot-
piece of the fracture table. Traction is applied to the frac-
tured thigh and normal leg while the pelvis is steadied
against the well-padded perineal post. The pull on the distal
fragment should be in line with the proximal fragment.
Roentgenograms are obtained to determine the alignment
of the fracture fragments. If there is any angulation, it is cor-
rected by altering the direction of the traction forces. A well-
molded double hip spica cast is then applied to include both
feet, incorporating the K-wire in the plaster. The cast is left
on for 6–8 weeks. If the method is used for adolescents, an
additional 2–4 weeks of immobilization may be necessary for
solid bony union. The K-wire placement in the tibia has
the same potential risks as when it is used for traction. The
use of a K-wire is not essential if the cast is applied with
the patient under anesthesia and with adequate muscle
relaxation.
The method I prefer is as follows. The small infant or child
is casted on the infant spica frame; the fracture table may be
used for the older child or adolescent. Adequate cast
padding and felt strips are applied. In the young child I also
use the Gortex cast liner. A short leg cast is first applied to
the injured leg, and then the pelvis and opposite leg are
casted. Once these casts are hardening, the assistant puts
traction on the injured leg (through the short leg cast); ade-
quate reduction is verified fluoroscopically, and the remain-
der of the cast is applied to the injured leg. After completion
of cast application the position of the fracture fragments is
verified by fluoroscopy.
The end results in 53 patients treated by this method, with
an average duration of follow-up of 6.9 years, showed no
deformity, abnormality of gait, or limitation of hip and knee
21. Femur
motion in any of the patients. The fractured leg was,
on average, not significantly longer than the normal leg.
Complications of malunion, delayed union, nonunion,
Volkmann’s contracture, and gangrene were not encoun-
tered. Dameron and Thompson recommended this method
for treating femoral shaft fractures.438 The chief advantage
of this method is that it decreases the duration of the hos-
pital stay, which has obvious financial benefits. However,
in the older child, maintenance of reduction is sometimes
difficult, requiring close supervision by repeated
roentgenograms and wedging of the cast to correct angula-
tion should it occur.
Some studies have concluded that cast-bracing femoral
fractures should be restricted to fractures in the distal third
of the shaft because of the difficulty of controlling varus
and anterior angulation with proximal shaft frac-
tures.409,432,482,544,567,576,664 In the study by Gross and colleagues,
of the 72 femoral fractures treated with immediate cast-
bracing, 22 resulted in excessive residual angulation or short-
ening.482 These injuries were primarily mid- and proximal
shaft fractures. Scott et al. reported that 4 of 14 femoral shaft
fractures treated by cast-bracing had excessive angulation or
shortening.649
Before considering casting, a push-pull evaluation under
fluoroscopy may yield important information.410 The amount
of overriding in an emergency room film or in traction may
not reflect the extent of soft tissue damage, which may allow
further shortening in the cast. Accordingly, prior to casting
(but after anesthesia) the distal fragment is pushed proxi-
mally. If overriding is less than 3 cm, a cast may be tried. If
more than 3 cm of overrriding results, this patient is proba-
bly not a good candidate for immediate casting. Other
methods (e.g., traction or operative) to reasonably maintain
length should be considered.
Hughes et al. assessed the psychosocial aspects when hip
spica casts were used to treat femoral fractures.512 Work inter-
ference was identified by families as the major problem. For
families with two working parents, a mean of 3 weeks time
off work is necessary. None of the children was accepted into
schools in spica casts, and home tutoring became necessary.
However, none of the children in the study fell behind class
permanently (only two temporarily). No child required phys-
ical therapy beyond simple instruction in walking, and 12 did
not even have this. The mean time to independent walking
following cast removal was 5 days and to running 25 days.
Skills returned faster in the young children. All aspects of
spica treatment were easier for the preschool children.
Weiss et al. reviewed 110 consecutive pediatric femoral
shaft fractures treated with early hip spica cast application.720
Four patients developed peroneal nerve palsy. All palsies
resolved with immediate cast removal.
No matter what type of casting is used, immediate removal
of the entire cast is not recommended. The child develops
contractures and ligament tightness while in the cast. I prefer
to remove the uninjured leg side and the injured side to
above the knee. This practice allows reattainment of motion
in the uninjured leg and knee motion on the injured side.
Two to three weeks later the rest of the cast is removed, and
hip motion is begun. This regimen decreases the likelihood
of refracture.
Femoral Shaft Fractures 887

Pavlik Harness
Stannard et al. detailed the use of the Pavlik harness for treat-
ing 16 femur fractures sustained between birth and 18
months of age. Stable union was evident within 5 weeks. The
indications included fracture of the proximal and middle
thirds of the femur, nonambulatory infants less than 4
months old at the start of treatment or small size of selected
patients after 6 months of age, and shortening of less than
2 cm.668

Results
No matter what the method of traction or casting, these frac-
tures generally heal well and rapidly in children. Roentgeno-
graphically evident callus formation occurs within 2–3 weeks
in infants, 4 weeks in children, and 5–6 weeks in adolescents
(Figs. 21-42, 21-43). Such callus formation accompanied by
subsidence of pain usually indicates that the patient in trac-
tion is ready for a spica cast. Casting is necessary inasmuch
as the callus is biologically plastic and may still deform if too
much muscular activity is allowed, even in a spica cast. Cast
removal should be based on clinical and roentgenographic
appearance. The absence of pain on compression of the frac-
ture site is an important sign. As a general rule, the amount
of time (in weeks) needed for sufficient healing to begin pro-
tected activity out of the cast relates to the patient’s age. For
example, fractures in a 10-year-old child take about 10 weeks
for adequate healing; those in a 16-year-old child take about FIGURE 21-42. Typical healing pattern shows subperiosteal new
16 weeks. bone confined by a tissue plane, associated with irregular callus
around the fracture site, at which much of the periosteum pre-
Functional recovery to preinjury status is usually more
sumably was disrupted.
rapid in children than in adults, although they may limp for

FIGURE 21-43. (A) Early subperiosteal to endosteal

healing pattern. (B) Result 16 months later.
888
a long time afterward owing to leg length inequality and
weak thigh musculature. This situation is often disturbing to
relatives and parents, but an explanation of the reasons
usually allays concerns. Leg length inequality, rotational dif-
ferences, and muscular weakness may be routinely expected
following these injuries.
Operative Methods
The operative treatment of femoral shaft fractures in chil-
dren generally has been considered unnecessary and to be
avoided as much as possible.538,548,583,618,682,696 Perfect anatomic
reduction of fracture fragments is less important in the child
than in the adult, as most malunions are corrected with
growth and remodeling, union occurs rapidly, pseudarthro-
sis is rare, and there is a tendency toward spontaneous cor-
rection of deformities. There is, however, an increasing
advocacy for the use of internal or external skeletal fixation,
especially in the older child. Some of this emphasis is due to
the desire to decrease the length of hospitalization. However,
these methods may allow more rapid rehabilitation of the
injured child or adolescent.
Betterman et al. reviewed 270 femoral shaft fractures and
thought that surgical intervention or some type of external
fixation should be considered after 7 years of age and defi-
nitely used after age 12.395
Of 191 children in a series reported by Viljanto and
associates, 45 (18%) were treated by surgery (18 by
intramedullary nailing, 16 by other means of osteosynthesis,
and 1 with a crushed extremity by primary amputation).696
No infections occurred. The mean longitudinal overgrowth
of 9.8 mm did not differ significantly from that of 10.7 mm
in nonoperatively treated patients. It is interesting that over-
growth was less in those treated by intramedullary nailing
than in those treated by other means of osteosynthesis. These
investigators preferred intramedullary nailing, recommend-
ing it for the following situations or groups of patients: trans-
verse fractures that involved the middle third of the femoral
FIGURE 21-44. (A) Intramedullary rodding of a femoral fracture. (B) Subsequent growth deformity of the proximal femoral neck with
increased valgus of the capital femur and premature epiphysiodesis of the greater trochanteric physis.
21. Femur
shaft; pathologic fractures; patients in whom primary con-
servative treatment had not led to an acceptable position;
when there were vascular or neural injuries together
with shaft fractures and large soft tissue defects; for mul-
tiple injuries of the same and other limbs; or the uncon-
scious, neurologically injured patient in whom traction
and casting may be difficult due to spasticity.696 Mohan
thought that further indications for open reduction
included muscle interposition and gross instability of the
fracture.577
Some methods of osteosynthesis may be contraindicated
in skeletally immature patients, as they may damage the
physis along the femoral neck (Fig. 21-44) and may also
create distal problems. Ischemic necrosis may also occur
(Fig. 21-45). Raisch showed that intramedullary nailing may
impinge against the distal epiphyseal plate, resulting in
retarded growth of the extremity.618 This may be avoided by
proper choice of nail length and the use of locking screws
to prevent migration. In contrast, Griessman479 and
Kuntscher548 suggested that operative treatment by means of
internal fixation did not cause a harmful reaction in chil-
dren and could therefore be carried out equally well in both
children and adults.
When there is an open fracture of the femur, the wound
is thoroughly débrided of all foreign material and any
damaged tissue excised. After copious irrigation the wound
should be left open and the leg placed in 90°–90° skeletal
traction to increase spontaneous drainage. Appropriate
antibiotics and tetanus antitoxin are administered. There
is no justification for immediate internal fixation when the
fracture is open. An open fracture does not ordinarily
require a longer period to consolidate in a child, but an
external fixator should be considered for the open femoral
fracture.
Reeves et al. evaluated 90 adolescent patients with 96
femoral fractures.623 Fifty-two fractures were treated with
rigid internal fixation. Forty-four fractures underwent trac-
tion and subsequent casting. The traction casting group had
Femoral Shaft Fractures
A B
FIGURE 21-45. (A) Ischemic necrosis of the femoral head (partial) after femoral rodding. (B) Ischemic necrosis of the femoral head
following closed treatment of a femoral fracture.
a mean hospitalization of 26 days. The operative group had
a mean stay of 9 days and had fewer complications. The
authors concluded that femoral shaft fractures in adoles-
cents could be operatively treated with excellent results and
fewer complication.
Intramedullary Rodding
The use of intramedullary rodding, with or without reaming,
has been advocated for the treatment of femoral shaft frac-
tures in children during the second decade of life. Part of
this advocacy has been based on various statements that pre-
mature growth arrest either does not occur, or if it does
occur, it does not lead to functional problems. Herndon
et al. described 21 fractures in adolescents treated by
intramedullary nailing; none of the patients developed pre-
mature growth arrest.502 Reeves et al. treated 33 adolescent
patients with intramedullary rods and did not observe any
trochanteric growth disturbances.623 In neither study was it
clear whether patients were followed to skeletal maturity.
Valdiserri and colleagues reported that medullary nailing
did not cause adverse effects provided it was carried out in
children older than 8–9 years of age.691 If it was done before
that time, there were significant problems with trochanteric
arrest and a marked valgus deformity. Knittel and Romer
reported 47 cases of children who had intramedullary
pinning with Rush’s rods.539 They noted that there was a 2-
to 20-mm increase in length (average 9.4 mm) compared
with the opposite side. In some children there was shorten-
ing of 1–15 mm (average 4.6 mm).
Cases of trochanteric apophyseal arrest have been
reported.503,530,729 All reported growth arrests have been
asymptomatic. Ziv and coworkers concluded that proximal
889
reaming should be avoided in the growing child and that
femoral head necrosis could be a potential complication of
reaming, as the area of the circumflex artery might be
impaired.729
Beaty et al. described the use of interlocking intra-
medullary nails in 30 patients aged 10–15 years.392 Two of
the patients had an overgrowth of more than 2.5 cm. None
had angular or rotational malunions, and there were no
trochanteric growth alterations. They noted two important
complications: leg length discrepancy and avascular necrosis
of the femoral head. The average leg length discrepancy
was 0.5 cm. Because of the risk of ischemic necrosis, they
recommended that dissection be limited to the base of
the femoral neck and into the piriformis fossa–greater
trochanter junction; it should not extend into the posterior
capsule of the midportion of the femoral neck.
Raney et al. studied skeletally immature patients who
developed premature closure of the greater trochanteric
physis consequent to placement of an intramedullary rod
for primary treatment of the femoral diaphyseal fracture
(Fig. 21-44).619 Each patient developed increased femoral
neck valgus when compared to the contralateral hip. None
of these patients developed functional disability, although
one had a radiographic subluxation. Anatomic specimens
demonstrated the likelihood of traversing a portion of the
greater trochanteric physis. These authors recommended
that other methods of fracture treatment, either operative or
nonoperative, be considered in skeletally immature patients
who have not entered the final phase of maturation char-
acterized by subchondral sclerosis along the greater
trochanteric physis.
The diameter of most rods exceeds the size of the physeal
defect that could be associated with a high incidence of pre-
890
mature growth arrest (see Chapter 7). Any defect larger than
0.25 inch generally leads to formation of an osseous bony
bridge across the physis.
Extensive analysis of development of the proximal femur
shows not only that active growth is present in the greater
trochanteric physis, but the physis extends toward the capital
femur well into the second decade, with this extension being
posterior and superior along the femoral neck. Further-
more, although there is appositional enlargement of the
trochanter through its perichondrium, the “growth” that has
been attributed to the end of the trochanter was, more prop-
erly, proximal (upward) expansion of the secondary ossifica-
tion center into the already formed but still unossified
cartilaginous portion of the trochanter.
Premature fusion of the growth plate of the greater
trochanter has been used as a method of altering the
mechanics of proximal femoral growth for deformities such
as coxa plana and vara in patients with Legg-Perthes disease
or developmental dysplasia of the hip, and in patients who
have developed a deformity secondary to septic arthritis of
the hip or proximal femoral osteomyelitis. The stipulated
aim of such greater trochanteric epiphysiodesis was “redi-
rection” of growth into a “valgus” pattern.
Operative damage to the greater trochanter during
osteotomy for developmental dysplasia of the hip has led to
a long valgus femoral neck without significant disturbance
of acetabular development. Premature closure of the greater
trochanteric epiphysis has also been described as a compli-
cation following traumatic avulsion of this structure and
led to the development of an elongated valgus femoral neck
(see Chapter 20).
Because children enter growth spurts at different stages
and skeletal maturity does not always correlate with chrono-
logic age, the use of intramedullary rods that cross the
greater trochanteric physis should be used with caution. Cer-
tainly, a child who is in the middle or at the end of the growth
spurt and who has evidence of thickening of the subchon-
dral plates on either side of the physis of the greater
trochanter and capital femur could undergo placement of
an intramedullary rod without significant consequence.
An effort should be made to evaluate the skeletal age and
extent of maturity in any patient for whom treatment of a
femoral shaft fracture with an intramedullary rod is consid-
ered. For children who have not yet entered their (pre)ado-
lescent growth spurt, alternative methods of fracture
treatment should be considered. It is safer to consider inter-
nal fixation with a plate and screws, internal fixation with
small rods (e.g., Enders nails) that do not cross a physis, or
placement of an external fixator that may be kept in place
until the fracture has healed or that may be removed when
the fracture is stable and replaced with a cast, cast-brace, or
full contact orthosis.
Galpin et al. reported the use of intramedullary nailing in
37 fractures.469 Twenty-two patients with an average age of 12
years 9 months were treated with reamed nails, whereas
fifteen patients at an average age of 6 months were treated
with nonreamed nails. Fractures united within 6–12 weeks.
None of the patients developed avascular necrosis. One
patient required excision of heterotopic bone to restore
function. Galpin et al. particularly looked at changes in the
articulotrochanteric distance (ATD) and found five patients,
21. Femur
two 11-year-olds and three 13-year-olds, at the time of injury
and surgery in which the ATD had increased an average
of 1.7 cm (range 1.2–2.5 cm); all five had undergone reamed
intramedullary (IM) nailing. None of the nonreamed
nailings sustained trochanteric growth arrest. When using
small rods such as Rush rods, the authors recommended
at least two rods to obtain rotational and angular stability.
Six patients treated with reamed nailing developed
myositis.
Grundes and Reikeras studied the effect on blood flow on
healing in rats with closed versus intramedullary nailing of
femoral fractures.483 Reaming had no acute impact on the
bone blood flow, whereas reaming combined with a fracture
reduced total bone blood flow by half and reduced cortical
diaphyseal flow to approximately one-fourth. At 4 weeks the
bending strength, rigidity, and fracture energy of the frac-
tures treated by closed medullary nailing were greater than
those treated by open nailing; but by 12 weeks there were no
differences in the mechanical parameters.
Pape et al. assessed the effect of pulmonary damage after
intramedullary femoral nailing in traumatized sheep.605,606
They found that nailing after severe shock and lung contu-
sion caused further lung damage as a result of polymor-
phonuclear leukocyte activation and triglyceride embolism.
These effects were significantly less if the nailing was per-
formed without prior reaming.
Blitzer and Hamilton monitored oxygen saturation during
reaming and intramedullary nailing of 15 femoral frac-
tures.399 There was no statistically significant drop in oxygen
saturation during the procedure.
Kao et al. described 10 pudendal nerve palsies (15%)
among 65 intramedullary nailings.526 All palsies were tran-
sient. The authors noted that the patient should be informed
preoperatively of this risk.
Nontrochanteric Rodding
Mann and associates described closed reduction and
intramedullary Ender’s nailing (Figs. 21-46, 21-47) of
femoral fractures in children.562 The average time to inde-
pendent ambulation was 7.1 days. No patient had an angular
deformity of more than 10° in any plane. No patient had clin-
ically evident loss of motion, leg length discrepancy, or radio-
graphic evidence of growth disturbance. It is important,
when placing the nails, that the entry point be proximal to
the distal physis. An image intensifier should be used to iden-
tify the distal physis. For fractures distal to the midshaft, nail
insertion is performed in a proximal to distal direction. The
proximal portal for Ender’s nailing is distal to the greater
trochanteric physis on the lateral cortex. Again, the image
intensifier is used to identify this insertion point. The distal
insertion is used for fractures proximal to the midshaft.
Passage of the nail should be stopped at least 1 cm away from
the physis at the opposite end.
Bourdelat and coworkers treated children between the
ages of 6 and 14 with flexibile medullary nailing, principally
through a descending route from the subtrochanteric
region.403–405 They found the results to be satisfactory.
Heinrich et al. described the use of Ender’s nails in chil-
dren 6 years of age or older.496,497 They found that three
points of fixation should be established around the fracture,
Femoral Shaft Fractures 891

common reason for fixation was to simplify nursing care and

rehabilitation of children who had associated severe head
injury or polytrauma. Twenty-three fractures healed within
an average of 11 weeks. Leg length discrepancy was not a
clinical problem in any of the patients. Interestingly, when
using this rigid fixation method with the AO compression
plate, 75% of the fractures healed by periosteal callus for-
mation, not primary bone healing, which reflects the activ-
ity (hyperactivity) of the periosteum in the child. Despite
instructions of the contrary, many children begin weight-
bearing as tolerated as soon as possible after their injury.
Although it certainly increases the risk of plate breakage, the
stimulus of early weight-bearing probably enhances early
periosteal callus formation, despite the use of rigid plates.
One 14-year-old boy with unrecognized medial cortex com-
munition experienced plate breakage 6 weeks after opera-
tion. Ward et al. also noted, when reviewing the literature,
that there was a plate breakage rate ranging from 3% to 15%,
with most series reporting an incidence of 6–7%. They
thought that the most important factors contributing to
plate breakage in the pediatric/adolescent population were
unrecognized medial cortex comminution, early weight
bearing, and premature return to full activity. Interestingly,
these authors recommended that reamed intramedullary
nailing rather than plate fixation be used for adolescents
over 12 years of age. One of their patients in whom the plate
was removed sustained a stress fracture through the empty

FIGURE 21-46. Single flexible rod used after failure of an external

fixator.

or the intramedullary canal must be stacked with multiple

nails to prevent angulation. Any failure to stack the canal or
achieve multiple fixation points increased the risk of angular
deformity. They thought that subtrochanteric and proximal
third fractures should be stabilized retrogradely with inser-
tion through a single site in the distal femoral diaphysis. In
general, two divergent C-configuration nails or one standard
C- and one S-configuration nail approximately 5 cm distal to
the fracture usually provides sufficient fixation. Noncom-
minuted isthmus fractures should be stabilized through a
single approach from either the medial or lateral aspect of
the distal femur, with the nail stacked to fill the medullary
canal at the site of the fracture. The distal one-third and com-
minuted middle one-third of femur fractures should be sta-
bilized with at least one retrograde C-configuration nail
inserted from the medial metaphysis and one from the
lateral. They further thought that children 6–10 years old
should be stabilized with 4 mm flexible nails. They noted that
4.5 mm flexible nails were too stiff for use in pediatric
patients.

Plate Fixation
Ward et al. reviewed children who underwent compression
plate fixation for a diaphyseal femoral fracture.710 The most FIGURE 21-47. Double rod fixation of a femoral diaphyseal fracture.
892
screw hole 2 months after plate removal following blunt
trauma from a bicycle accident.
Kregor et al. evaluated plate fixation of femoral shaft
fractures in multiply injured children.542 They reviewed 15
fractures (9 closed, 6 open). There were no infections and
were radiographically healed at an average of 8 weeks. The
plates were removed at an average of 10 months (range 3–24
months). After the index operation, overgrowth of the
injured femur averaged 0.9 cm (range 0.3–1.4 cm).
External Fixator
The external fixator offers a relatively simple, minimally
invasive method of stabilizing a femoral shaft fracture (Fig.
21-48). The method is especially useful in the presence of
multiple trauma, head injury, and a comatose state or open
fractures. Two to three pins are placed proximal and distal
to the fracture. Additional pins may be inserted into large
comminuted fragments.
The device chosen depends on the preference of the
surgeon. Several are available. Their purported biomechan-
ical attributes and differences probably are not a factor in
the biologically plastic immature skeleton.
The main potential problems are pin tract inflammation
leading to osteomyelitis and refracture after removal of the
FIGURE 21-48. Uniaxial fixation.
21. Femur
fixator. To lessen the risk of the latter, the same method used
for limb lengthening may be applied. The device is removed,
but the pins are left in place for up to a week. If the patient
develops pain, the fixator may be readily reapplied. After 5–7
days the radiograph is repeated to see if any stress-induced
radiolucency is developing at the fracture site. The pins are
then removed.
Other Considerations
Strickland and Wittgen reported a case of pathologic frac-
ture of the femoral shaft 55 years after circumferential
banding.675 The size of the band was only about 50% of the
final diameter. There was occlusion of the medullary canal
with compact bone. The band probably was responsible for
the formed compact bone occluding the area. Occlusion of
the medullary cavity may predispose to pathologic fracture
in children by increasing the brittleness of the otherwise
hollow bone.
Complications
Vascular Problems
Arterial injuries associated with femoral shaft fractures
present management problems. A slow arterial leak may not
be readily recognized owing to the presence of normal pulse
and capillary filling. Dehne and Kriz reported five cases of
unrecognized slow arterial leakage.444 In three patients
amputation became necessary because of the delayed diag-
nosis. Increasing limb girth, absent or diminishing pulse,
and progressive neurologic signs in the presence of a closed
fracture strongly suggest arterial injury and indicate the
need for prompt arteriography. The collateral circulation
varies widely in its capacity to maintain viability in the limb.
It may be possible to treat young children with skeletal trac-
tion following vascular surgery, although internal fixation is
usually done. The use of internal fixation has been advo-
cated because a more stable fracture site adds protection to
arterial repair.247 Internal fixation may prolong the surgical
procedure and increase the risk of infection; and dissection
of soft tissue for insertion of the plate may produce increased
venostasis and potential loss of collateral circulation. I prefer
an external fixator in these situations.
Because of vascular damage to one or more branches of
the deep femoral artery, significant intracompartment bleed-
ing may occur. It may lead to a compartment syndrome that
must be assessed and, when necessary, decompressed.
False aneurysm has been described following a closed
femoral fracture in a child.451,593,651
Bone Length/Overgrowth
Leg length inequality is the most frequent result of femoral
shaft fractures during childhood.375,387,442,450,478,568,688 Staheli
studied 84 patients followed for 2–16 years after nonopera-
tive treatment of closed femoral shaft fractures.665 Tibial
length was not affected greatly by the femoral fractures,
although some reactive overgrowth may occur even in the
tibia. Among the 17 patients sustaining fracture during
infancy, no late significant femoral inequality was observed.
Among the children 2–8 years of age, 25% showed inequal-
Femoral Shaft Fractures
ity. Among children 8–12 years old, significant inequality was
observed in 44%. Growth acceleration was less consistent in
this age group. Fractures in the proximal third and oblique-
comminuted types were also associated with relatively more
growth acceleration.
Differences in limb length following femoral shaft frac-
tures may result from excessive overriding or distraction of
the fragments or from stimulation of linear growth. These
differences usually stabilize within the first year after injury
and do not change significantly thereafter. However, in chil-
dren under 2 years of age and in adolescents, the normal
growth stimulation is not as dramatic as in children of the
middle childhood years. The infant and young child heal
rapidly. During adolescence there are fewer years of growth
remaining to correct a deformity. Thus in these two age
groups, minimal overriding should be accepted.
The relative tension of the periosteum sleeve is a normal
physiologic control factor; it changes with age and becomes
more “adult” in character during adolescence. The potential
control and interplay between periosteal tension and growth
rates at the physis are undoubtedly affected. Periosteal strip-
ping without fracture may promote overgrowth. Further-
more, larger initial fragment displacements may stimulate
increased overgrowth through a temporary decrease in
periosteal tension.
The extent of overgrowth is not predictable in the indi-
vidual patient. Since Truesdell’s original description, many
authors have observed that the relative lengthening of the
fractured femur averages approximately 1 cm.688 This extent
of overriding of fracture ends is most commonly accepted as
a treatment goal and normal biologic response.
Shapiro documented femoral overgrowth after femoral
shaft fractures with sequential orthoroentgenograms in 74
patients followed until skeletal maturity.652 The femoral over-
growth averaged 0.92 cm (range 0.4–2.7 cm) and was found
to be independent of age, level of fracture, or position of the
fracture at the time of healing. Ipsilateral tibial overgrowth
averaged 0.29 cm (range 0.1–0.5 cm) and added to the
length discrepancy. About 78% of the overgrowth had
occurred during the first 18 months after fracture. By 18
months after fracture only 12% of the patients had com-
pleted the overgrowth, and by 3.5 years after fracture 85%
had completed this overgrowth. In 9%, the overgrowth con-
tinued throughout the remaining growth period, although
at a slower rate than during the first 18 months following
fracture.
Overgrowth is a physiologic process associated with both
the increased vascularity of the physes of the involved bone
produced by healing and changes in tension in the periosteal
sleeve. This observation now appears amply confirmed, espe-
cially as overgrowth occurs regardless of the position of frac-
ture healing and in virtually all patients, indicating that it is
an obligatory phenomenon rather than one compensating
for shortening. It also often involves the ipsilateral tibia,
which would be related to temporarily increased vascularity,
as the periosteum is obviously intact. The phenomenon also
occurs with humeral and tibial fractures. Kellernova and
associates demonstrated increased vascularity to the entire
limb following experimental tibial fracture.528
Hehl et al. studied posttraumatic limb shortening after
conservative and operative treatment of diaphyseal femoral
fractures in children.495 They treated 120 fractures in 116
893
children. The treatment of choice was conservative in young
patients with overhead traction in the 1- to 3-year-old child
and Weber traction in a 3- to 8-year-old child. Operative treat-
ment was usually used in older children. Plate fixation was
performed in children 5–16 years of age, and external fixa-
tion was used in children 2–14 years of age. Measurements
showed a mean limb length increase of 5.5 mm following
overhead traction and 7 mm for 90°–90° traction. Following
plate fixation it was 5.5 mm and following external fixation
8.5 mm. Their results did not show any statistically significant
differences for the various treatment methods regarding the
likelihood of overgrowth.
Corry and Nicol studied 50 children roughly 1.9 years after
injury.436 There was a mean 6.9 mm of overgrowth. Age was
the only influential variable, with overgrowth being less in
children under 4 and 7 years of age. The authors thought
that much less shortening should be accepted than is com-
monly recommended.
Hougaard studied 67 femoral shaft fractures.509 He could
not demonstrate any relation between shortening at the time
of healing and the magnitude of overgrowth 2 years later.
Nor was he able to demonstrate any relation among sex, age,
type of fracture, level of fracture, and magnitude over-
growth. The mean overgrowth was 10.8 mm and the largest
26 mm. Almost all the children who healed with little short-
ening showed no angulation, whereas almost all of the
femoral fractures that healed with considerable shortening
had some angulation. The importance of angulation with
respect to shortening after femoral shaft fractures in chil-
dren had not been previously emphasized.
Stephens et al. reviewed 30 skeletally mature patients who
had isolated closed femoral shaft fractures during childhood
that had been treated conservatively.671 When the fracture
had occurred between the ages of 7 and 13 years, the limb
overgrew about 1 cm. These authors found that excessive
fracture overlap at the time of injury but not at time of union
increased limb overgrowth. Angulation of the fracture
remodeled in children injured when they were under 10
years of age. The authors recommended that in the 7- to 13-
year-old patient treatment should aim at a 1 cm overlap at
union and correction of any angular deformity in children
over 10 years of age.
Angulation/Bowing
Restoration of the normal anterolateral bow should also be
a goal, no matter what the treatment method. Residual angu-
lation may worsen in a cast. Angular deformities should be
minimal. The degree of remodeling and restoration of lon-
gitudinal alignment is unpredictable and less likely the closer
the fracture is to the middle of the bone (Figs. 21-49, 21-50).
The greatest amount of anticipated axial correction was cited
by Nonnemann, according to whom axial deviation up to 30°
tended to correct spontaneously.594 Lateral displacement
may correct varus deformity on an average of up to 40% and
valgus deformity up to 60% of the initial angular defect,
whereas antecurvatum and recurvatum may correct nearly
70% of any original deformity over 10°.697 Viljanto et al. con-
sidered the relatively slow and limited correction of varus
and valgus deformities the most significant finding.697
Wallace and Hoffman studied remodeling of the angular
deformity of femoral shaft fractures in children.708 They
894 21. Femur

FIGURE 21-49. (A) Excessive malunion in an infant (7 months). (B) It was partially corrected and healed by callus. (C) Eight months
later a mild deformity was present. Significant angular deformities are likely to correct themselves only in this young age group.

reviewed 28 children with unilateral middle third fractures
who had angular deformities of 10°–26° after union. At an
average follow-up of 45 months after the injury, the average
correction was 85% of the initial deformity; 74% of the cor-
rection occurred at the physes, and only 26% at the fracture
site. They concluded that in children under 13 years of
age malunion of as much as 25° in any plane can remodel
sufficiently to give normal alignment at the joint surfaces,
even though the bone per se may continue to appear
deformed.
Shaft fractures left with angular deformities have a possi-
bility of long-term complications, such as slipped capital
femoral epiphysis.
Rotation
Rotational deformity may occur with any of the traditional
methods of treatment.607,705 A study of rotational deformities
27–32 years after injury found persistent rotational disability
in only one case and refuted the established view that

A B
FIGURE 21-50. (A) Angular malunion in a young child (19 months). This degree of deformity should not be accepted in children older
than 6–8 years of age. (B) Lack of angular correction, although there is obvious remodeling. It has led to a recurvatum.
Distal Femoral Metaphyseal Injuries
rotational displacement is incapable of spontaneously cor-
recting.408 Hagglund et al. showed that the mean anteversion
difference of 9.6° between the fractured and uninvolved
sides after femoral shaft fracture decreased to 5.6°, suggest-
ing that children have an ability to correct some rotational
deformity by continued growth.486
Strong et al. showed that in malrotated femoral fractures
created in rabbit models there was 55% improvement of mal-
rotation by 4 weeks.676 This may not extrapolate to humans
because of different biomechanical forces.
Muscle Function
Isometric and dynamic measurements of quadriceps func-
tion in children with femoral fractures revealed a significant
reduction of strength in the affected leg.439,500 This function
is rarely used as a criterion for assessing the therapeutic
results, particularly in children. The status of the muscles
after femoral fractures has often been evaluated by mea-
surements of leg circumference, but direct measurements of
quadriceps function have not been carried out. There also
was a greater reduction of strength the more distally the frac-
ture was located. This factor should be taken into account
during the rehabilitation of patients. Miller and associates
reported severe loss of muscle function in a child sustaining
ischemic fibrosis of the lower leg that was a complication of
femoral fracture.573 Muscle herniation also may complicate
healing as well as return of function.
Hennrikus et al. studied muscle strength in the quadriceps
muscle following femoral fracture.500 They examined the
patients an average of 33 months after injury; 39% of the
patients had a persistent deficit in the strength of the quadri-
ceps on testing with the Cybex machine. Six patients (18%)
had a deficit according to the one leg hop for distance test.
Forty-two percent had a loss of 10° of flexion. The amount
of maximum displacement of the fracture as seen on the
initial radiographs appeared to be the only factor that was
significant for predicting weakness. Despite the weakness as
tested, none of the patients had a clinical problem. A sub-
clinical deficit in the strength of the quadriceps may be
related to damage sustained by the muscle at the time of the
fracture.
Refracture
Refracture of the shaft of the femur is an infrequent com-
plication. Saimon reviewed 21 patients ranging in age from
7 to 58 years and found that the incidence of refracture was
highest in those in the 16- to 20-year range.635 He thought
that excessive emphasis on restoration of knee movement
after removal of the cast was a factor because of muscular
tightness, particularly in the quadriceps. Rigorous rehabili-
tation is rarely necessary in children and adolescents. The
amount of overriding of the fragments did not seem to be
related in any way to the liability to refracture. Careful clin-
ical assessment of the degree of union is important when
considering discontinuation of bracing or casting. It is not
sufficient only to palpate the callus gently to apply stress to
the bone. Firm pressure and strong stresses to the bone
should be applied, because if the bone cannot withstand
these maneuvers, it almost certainly cannot withstand the vig-
895
orous mobilization of the child. Radiologic criteria of “ade-
quate” union are more difficult to define. In some cases
refracture occurred despite the presence of a great deal of
callus.635 The radiologic demonstration of “warning” cracks
is obviously of great importance and indicates the need for
further immobilization.
Nerve Injury
Concomitant injury to the sciatic nerve does not affect the
rate of fracture healing. However, the remainder of the bone
may become excessively osteoporotic and susceptible to frac-
ture following removal of the cast.
Growth Arrest
Hunter and Hensinger reported an 11-year-old child with a
comminuted spiral fracture of the femoral shaft.514 Growth
arrest occurred in all physes of the extremity, with the excep-
tion of the distal fibular epiphysis. This instance of multiple
premature epiphyseal closure after a seemingly uncompli-
cated fracture of the femoral shaft appears to be unique, par-
ticularly as there was no detectable neurovascular injury to
the affected extremity and no history or clinical evidence of
direct trauma to the physes. They thought that some gener-
alized vascular or neural disturbance seemed to be the most
reasonable explanation for the monomelic growth arrest.
Myositis
Steinberg and Hubbard showed that heterotopic ossification
after femoral intramedullary rodding was a significant com-
plication of the procedure.669 A statistically significant
increase of myositis ossificans was found in males when there
was an increased delay from injury to surgery and in patients
requiring prolonged intubation because of multiple injuries.
The heterotopic ossification tended to be present in the dis-
sected tissues for the approach to the intratrochanteric
region for insertion of the rod.
Distal Femoral Metaphyseal Injuries
Distal femoral metaphyseal injuries are relatively common.
The fracture line is usually transversely oriented. Torus
(greenstick) fractures are frequent (Fig. 21-51) and must be
treated carefully, as angular deformity (varus or valgus) may
be introduced at the time of injury, comparable to supra-
condylar humeral injuries, and may not be readily recog-
nized during diagnosis or treatment. The fracture may
also be complete but undisplaced. Again, the degree of
compression deformity of a portion of this fracture must
be watched. The fracture may be displaced, but this is
an uncommon injury in this region. There may be com-
munition, with extension (longitudinally) of the fracture
from the primary trabecular fracture toward the physis
(Fig. 21-52).
The gastrocnemius muscle is the chief deforming force.
The muscle arises (by two heads) from the posterior surface
of the distal femur and angulates the distal fragment poste-
riorly toward the popliteal space. Either fragment may
896 21. Femur

requires correction at the inception of treatment. Residual

malunion may require a corrective osteotomy.

Distal Femoral Epiphyseal Injuries

Distal femoral epiphyseal injuries are common, especially in
adolescents.732–802 They were once termed “cartwheel”
injuries because the prevalent mechanism of injury involved
jumping onto large-wheeled wagons. The literature of the
nineteenth and early twentieth centuries called attention to
the high incidence of injuries in the distal femoral epiphysis
caused principally by horse-drawn vehicles. Boys who
attempted to jump on wagons frequently caught one of the
lower limbs in the wheel spokes and sustained a hyperex-
tension injury. Automobile, bicycle, skateboard, go-kart, and
athletic injuries have superseded the horse-drawn wagon.

Obstetric Injury
Type 1 distal femoral epiphyseal plate separation is an infre-
quent obstetric injury. Nevertheless, it is an important clini-
cal entity because it may remain undiagnosed or be
FIGURE 21-51. Torus metaphyseal fracture. misdiagnosed as dislocation, septic arthritis, osteomyelitis, or
pseudoparalysis. A strong hyperextension force on the knee
may produce rupture of the periosteum, causing displace-
ment.781 An audible snap may be felt. The infant is usually
impinge on the popliteal vessels and nerves, partially occlud- irritable upon examination. Crepitation may be felt during
ing or compressing them or even causing some degree of lac- examination.
eration. Careful assessment of neurovascular function is The radiograph may be interpreted as normal unless
essential following injury and during care. The proximal careful attention is paid to the position of the distal femoral
fragment may be driven into the quadriceps femoris muscle epiphysis relative to the metaphysis (Fig. 21-53). Otherwise,
and may cause significant damage to the vastus intermedius, assess the tibia relative to the femoral axis. This particular
with subsequent scarring, restriction of flexion, and fibrosis.
The fragment may become entrapped (buttonholed) within
the muscle.
For the displaced fracture, treatment should consist of
reducing any angular deformity followed by application of a
long leg cast with 10°–15° of knee flexion. This cast should
be maintained for 3–4 weeks, at which time a cylinder (knee
extension) cast or knee immobilizer may be applied to begin
protected weight-bearing. Knee stiffness is not a major
concern in the young child, although a hinged cast may be
used to allow some knee motion in the adolescent who
requires longer casting because of the extended time of
healing.
For the undisplaced fracture, casting may be used. Fre-
quent checks are necessary to be certain that angular defor-
mation, resulting from the pull of the gastrocnemius, does
not occur. Mild knee and ankle flexion should relax the
muscle. If the fracture is unstable or there is any neurovas-
cular compromise, the patient should be placed in skin or
skeletal traction; alternatively, percutaneous fixation can be
used followed by a cast.
If the fracture cannot be controlled effectively, percuta-
neous pinning or an external fixator should be considered.
One of the pins may be placed transversely across the epiph-
yseal ossification center if there is not enough metaphysis
between the fracture and physis to accept more than one pin. FIGURE 21-52. MRI of a distal femoral metaphyseal fracture.
These fractures usually heal rapidly and without major Extensive hemorrhage is evident proximal to the fracture line.
complications. Angular deformity, especially in the There is also a bone bruise in the medial portion of the distal
varus/valgus plane, does not correct spontaneously and femoral ossification center.
Distal Femoral Epiphyseal Injuries
FIGURE 21-53. (A) Birth fracture of the distal femur. (B) “Reduc-
tion.” (C) Extensive subperiosteal bone. Note the loss of reduction.
(D) At 6 months the right side is healing well, but the left side is
suggestive of a developing problem. (E) Right side at 18 months
897
I
showing mild physeal irregularity. (F) Left side developed central
arrest. (G) Growth arrest at 2 years. (H) Resection of bridge. (I)
MRI 4 years later. The elongated “migration” tract of the resected
bridge is readily evident.
898
FIGURE 21-54. Type 1 growth mechanism injury patterns.
injury is much more readily diagnosed because the epiphysis
usually undergoes ossification at 38–40 gestational weeks,
providing an anatomic marker. Ultrasonic examination of
the affected area may demonstrate not only the injury but
also the presence of subperiosteal hematoma, which may be
extensive.
The treatment of this type of injury during the newborn
period is usually relatively simple. When only minimal to
moderate displacement of the epiphysis is noted, immobi-
lization with a splint for 2–3 weeks is necessary. When there
is marked displacement, gentle reduction should be under-
taken. If the reduction is not stable, a spica cast may be
applied. Pin fixation may be used. Reparative bone forma-
tion is rapid and usually effective for stability (clinical) within
about 2–3 weeks. Long-term follow-up is absolutely necessary
because of the significant risk of physeal damage.
A B
FIGURE 21-55. (A) Complete displacement of a type 1 physeal
injury. The epiphyseal fragment was displaced posteriorly. (B)
Arteriogram shows complete vascular occlusion. Primary vascular
21. Femur
Classification
Several patterns of growth mechanism injury may affect the
distal femoral physis and epiphysis. Certainly, types 1 and 2
are relatively common. Types 3 and 4 may occur with a rel-
atively significant frequency and may be difficult to diagno-
sis. Types 5 and 6 are infrequent. Type 7 is common as either
an acute osteochondral fragment or the more common
chronic osteochondritis dissecans (see Chapter 22). Type 7
is also present as a sleeve fracture. Intraepiphyseal fracture
or bone bruising is now being described frequently by uti-
lizing MRI to assess painful injuries without obvious radio-
logic abnormality. These injuries fit the broad category of
type 7 growth mechanism injury pattern. Type 8 (Peterson
version) may also occur. (see Fig. 21-52.)
Type 1 injuries involve a fracture that traverses the entire
physeal–metaphyseal interface (Fig. 21-54). This involve-
ment of the entire physis requires the fracture to follow a
contour that becomes increasingly undulated during ado-
lescence. The undulation increases the risk of focal cell
damage and subsequent growth impairment.
Because of the major undulations the central “peak” is at
risk for focal injury. The direction of epiphyseal displace-
ment varies: anterior, posterior, varus, and valgus. Severe
displacement may be associated with vascular injury
(Fig. 21-55). However, displacement may be minimal and
may be indicated only by slight physeal widening or me-
taphyseal buckling. With child abuse, the distal femur is fre-
quently injured. The only diagnostic finding may be a small
peripheral metaphyseal flake (Fig. 21-56) caused by the
curvilinear peripheral extension of the physis over the me-
taphysis (corner sign).
Type 2 injury is the most common pattern (Fig. 21-57).
Hyperextension injuries lead to anterior displacement of the
epiphysis underneath the patella (Fig. 21-58). Varus or
repair was necessary. The physeal fracture was reduced and sta-
bilized by Kirschner wires.
Distal Femoral Epiphyseal Injuries 899

FIGURE 21-56. (A) Metaphyseal “beak” fracture (arrow) characteristic of type 1 physeal injury due to child abuse. (B) Schematíc of
this injury.

FIGURE 21-57. Type 2 injury.

FIGURE 21-58. (A) Type 2 hyperextension injury. (B) Appearance after closed reduction.
900 21. Femur

FIGURE 21-59. (A) Type 2 valgus injury with greenstick injury of the lateral metaphyseal component. (B) One year later.

valgus displacements are associated with metaphyseal

fragments of variable size (Fig. 21-59). Posterior metaph-
yseal fragment fracture is the least frequent pattern. The
central metaphyseal peak probably plays a role in redi-
recting the propagating fracture proximally into the
metaphysis.
Type 3 injuries involve either the medial or the lateral
condyle (Figs. 21-60 to 21-62). On rare occasions, a posterior
(quadrant) condylar element is involved. These injuries may
be difficult to diagnose and may require stress roentgenog-
raphy (Fig. 21-63). Small pieces of the articular surface and
subchondral bone may be fragmented and displaced into the
joint.
Type 4 injuries may involve the medial or lateral condyle,
or both (Fig. 21-64); or they may occur in conjunction with
a type 3 injury (Fig. 21-65). The fragment tends to be dis-
FIGURE 21-60. Type 3 injury.

A B
FIGURE 21-61. (A) Type 3 injury of the posteromedial portion of the distal femur. (B) Treatment was open reduction and internal
fixation.
 A B
FIGURE 21-62. (A) Severe comminuted type 3 injury with both anterior and posterior fragment displacement. (B) Open reduction was
stabilized with internal fixation.

FIGURE 21-63. (A, B) Stress testing. (C, D) Nonstress view (C) and stress view (D).
901
902
FIGURE 21-64. (A) Unicondylar type 4 injury (left), which can occur
medially or laterally. Bicondylar type 4 injury (right). (B) Bicondy-
lar, or T-type injury.
FIGURE 21-66. (A) Type 4 injury. (B) Transverse fixation following open reduction.
21. Femur
FIGURE 21-65. Combined type 3 and 4 injuries.
placed proximally to a variable degree (Figs. 21-66 to 21-68).
When both condyles are involved, the fragments not only are
proximally displaced but also split apart. Similarly, types 3
and 4 injuries may occur concomitantly (Fig. 21-69). There
is a high incidence of osseous bridge formation, especially
in the smaller lesions (Fig. 21-70).
In other cases, there is initial growth slowdown and irreg-
ularity in the secondary ossification center. Some of the
type 3–4 combinations may constitute the triplane pattern of
fracture.
Type 5 injuries are uncommon and more likely to occur
in patients with other disorders, such as myelomenginocele.
Lombardo and Harvey described a fracture of the proxi-
mal tibial metaphysis and diaphysis extending as a type
4 injury into the proximal tibial epiphysis but also leading
to an initially unrecognized type 5 injury of the distal
femur.774
Type 6 injuries may include glancing blows that lead to
destruction of a small peripheral segment (Fig. 21-71), which
may lead to eventual formation of a physeal bridge. Other
mechanisms, such as burns, osteomyelitis, or irradiation,
may also contribute to this injury. Hyperextension injury
may also damage areas where the capsule, periosteum, and
Distal Femoral Epiphyseal Injuries 903

A B
FIGURE 21-67. (A) Lateral type 4 injury. (B) Open reduction and internal fixation.

FIGURE 21-68. (A) Anteroposterior view of a type 4 injury. (B) Lateral view. (C) Computed tomographic (CT) scan. (D) Fixation.
904 21. Femur

FIGURE 21-69. (A) Type 4 injury of the medial condyle. It proved to be a combined lateral type 3 and medial type 4 injury. (B) Reduc-
tion. (C) Growth arrest of the type 3 side.

FIGURE 21-70. (A) Early bridge formation in a peripheral type 4 injury. (B) Appearance 6 months later. (C) Tomogram of bridge. (D)
Resection and fat transplant.
Distal Femoral Epiphyseal Injuries 905

FIGURE 21-72. Type 7 injury: undisplaced (A); displaced (B); and

posterior involvement (C).

perichondrium blend, leading to formation of a solitary

osteochondroma.
Type 7 injuries involve fragments of the femoral condyles
(Figs. 21-72, 21-73) that vary considerably in size. Alterna-
tively, there may be a sleeve fracture of cartilage and sub-
chondral bone (collateral ligament injury analogue);
irregular ossification appears later. Bone bruising (Figs.
21-74, 21-75) occurs within the substance of the epiphyseal
trabecular bone. The involvement may be within a condyle,
at the periphery (in conjunction with a sleeve injury), or at
an articular surface. The latter pattern may be a precursor
of an osteochondritis dissecans lesion.
With type 8 injuries the main fracture is a metaphyseal
injury. Longitudinal extensions propagate distally toward the
physis, where the fracture further extends transversely along
the physeal–metaphyseal interface.

FIGURE 21-71. (A) Type 6 injury to the peripheral zone of Ranvier.
(B) Hyperextension type 6 injury of the posterior distal femoral and
proximal tibial physes, leading to formation of osteochondromas
posteriorly.
Pathomechanism
Distal femoral epiphyseal injuries may be grouped according
to the etiologic mechanism: (1) abduction; (2) adduction;
(3) hyperextension; and (4) hyperflexion. These four basic

FIGURE 21-73. (A) Acute type 7

fracture of the posterior femoral
condyle (arrow). (B) Chronic type
7 injury. Note the osteochondritis
dissecans (arrow).
906
FIGURE 21-74. Type 7 injury of the medial distal femoral epiphysis.
There is increased signal intensity within the trabecular bone
extending to the subchondral bone medially.
mechanisms are not isolated, often existing in combination,
and are accompanied by variable rotation.
Abduction Type
An abduction injury, caused by a blow to the lateral side of
the distal femur, frequently occurs in athletes. It is the same
type of stress that causes medial soft tissue injuries (especially
meniscal and ligamentous) in an older patient. The result is
generally a type 2 physeal injury, in which the periosteum is
ruptured on the medial side and the distal femoral epiphysis
is displaced laterally with a lateral fragment of the metaph-
ysis. It is usually associated with rotation. This fracture may
reduce spontaneously and may be missed initially if the tri-
angular piece of metaphyseal bone is small. One should care-
fully scrutinize the roentgenogram and, if indicated, take
additional abduction stress views to detect the lesion. MRI
may also delineate the metaphyseal propagation.
Adduction Type
An adduction injury is caused by a medial blow or an indi-
rect injury. The epiphysis is medially displaced as a type 1 or
2 injury pattern. With the addition of a rotational compo-
nent, a type 3 or 4 injury may occur.
Hyperextension Type
A hyperextension injury was the most common variety in the
past because of wagon-wheel injuries, and it is still seen in
vehicular accidents. The distal femoral epiphysis is displaced
anteriorly by the hyperextension force and by the pull of the
quadriceps muscle. The posterior periosteum is torn, and
21. Femur
the fibers of the gastrocnemius are stretched or partially
torn. The triangular metaphyseal bone fragment and the
intact periosteal hinge are anterior, although the latter struc-
ture is modified by synovial extension into the suprapatellar
pouch. The distal end of the femoral shaft is displaced pos-
teriorly and may injure structures in the popliteal region.
Grogan and Bobechko presented an interesting photograph
of the mechanism of injury of hyperextension of the knee in
a patient with a type 2 fracture of the distal femoral epiph-
ysis.765 The injury was sustained while landing during a track
and field event (long jump).
Hyperflexion Type
Posterior displacement of the distal femoral epiphysis, a
hyperflexion injury, is rare. It usually results from a forceful
flexion injury caused by a direct blow to the distal femur.
Diagnosis
The usual history is a relatively violent injury with severe pain
and inability to bear weight on the leg. The knee is markedly
swollen and tense, and the limb is abnormally angulated.
There may be a joint effusion, depending on where the frac-
ture line propagates and if there is extension into the joint,
either through the intercondylar region or through the
suprapatellar extension of the synovium and capsule. Neu-
rovascular function must be examined closely.
These injuries are particularly prone to partial to complete
spontaneous reduction following cessation of the evocative
force. The diagnosis may be suspected on the basis of a
slightly widened growth plate or a fracture extending into
the metaphysis. Oblique projections are sometimes as reveal-
ing as stress roentgenograms.
Undisplaced type 1 and 2 epiphyseal fractures of the distal
femur in the adolescent athlete may mimic injury to the knee
ligaments. Roentgenographic examination with the knee
under stress often reveals the diagnosis, thereby avoiding
FIGURE 21-75. Medial condylar bone bruise.
Distal Femoral Epiphyseal Injuries
unnecessary arthrotomy and indicating appropriate treat-
ment.
Simpson and Fardon reported three cases that initially
appeared to be pure ligamentous injuries until stress films
were obtained.797 They noted that one type 3 injury had been
misdiagnosed as a ligamentous disruption. Rogers and asso-
ciates described a “clipping injury” fracture of the epiphysis
in the adolescent football player as an occult lesion of the
knee.789 They described seven cases of type 3 and one of type
2, all of which were definitively diagnosed with stress films.
It is important to realize that ligament injury may also be
present with an epiphyseal injury. MRI should be considered
if such concomitant ligamentous injury is suspected.
Treatment
In general, these fractures are variably stable injuries, most
of which require some degree of force to effect a reduction.
Manipulation in the emergency room may increase the
already considerable pain. Accordingly, reductions under-
taken in the operating room under more ideal anesthetic
conditions are more likely to be anatomic. The following
general recommendations should be considered:
1. Displaced distal femoral fractures should be treated
with early anatomic reduction under general anesthesia. Sta-
bility is then checked fluoroscopically. Unsuccessful or unsta-
ble closed reduction should be followed by open reduction
with fixation or closed reduction with percutaneous fixation.
2. Following fracture reduction some type of internal fix-
ation is the most effective method of maintaining anatomic
reduction. Percutaneous smooth K-wire fixation is tradi-
tional. However screw fixation, provided the immature
physis is not violated, is acceptable, especially for type 2, 3,
and 4 injuries.
3. Long leg cast immobilization is usually inadequate for
maintenance of fracture reductions if no internal fixation
has been employed. A fracture not internally fixed should
be closely followed to allow early intervention if reduction is
lost. A hip spica may be more appropriate.
4. Patients and families should be made aware of the high
potential for late complications related to physeal damage.
FIGURE 21-76. (A) Type 3 injury. (B) Open reduction and fixation with transcondylar screws.
907
It necessitates periodic examination until the child reaches
skeletal maturity.
The position for immobilization of type 1 and 2 injuries is
usually determined by the characteristics of the original dis-
placement. If there is anterior displacement of the distal
fragment, the patient is treated by reduction with traction
followed by immobilization in flexion. With posterior dis-
placement, the patient is treated by reduction and immobi-
lization in extension. Any medial or lateral displacement
should be corrected by appropriate manipulation. Factors
affecting the choice of treatment should include the ease of
obtaining and maintaining reduction, the amount of
swelling, the body habitus, and the presence of associated
injuries.
Treatment may also include skeletal traction, traction fol-
lowed by cast immobilization, and immediate application of
a long leg cast. Percutaneous pin fixation is also effective as
an adjunct. As pointed out by Bassett and Goldner, treatment
of these injuries must be individualized.737
Hyperextension-type fractures present two problems of
management: (1) potential injury to the popliteal vessels and
nerves; and (2) the difficulty of achieving and maintaining
reduction, as the plane of displacement and the plane of the
knee joint motion are the same. There is an adequate lever
arm to grasp the distal fragment effectively. A closed reduc-
tion is attempted first and, if successful, is followed by
casting. Flexion may be necessary to maintain anatomic
reduction, although swelling in the popliteal region may
prevent the use of much flexion.
Recurrence of anterior displacement is usually caused by
immobilization with insufficient flexion. If necessary, pins
may be used to stabilize the fracture.
The posteriorly displaced distal femur (hyperflexion-type
fractures) must be reduced by pulling the distal epiphysis
anteriorly. This fracture must be immobilized in extension
and should not be immobilized in a position of semiflexion.
Immobilization varies, with a mean of 7 weeks (range 3–16
weeks).
Type 3 injuries invariably require open reduction (Fig.
21-76). This procedure includes an arthrotomy or
arthroscopy so there is accurate restoration of articular
908
anatomy. Fixation, as much as possible, should be directed
transversely across the epiphyseal ossification center frag-
ments. Smooth pins may be placed across the physis. Alter-
natively, transversely directed fixation may affix the free
fragment to the nonfractured condyle.
Type 4 fractures usually require open reduction and inter-
nal fixation with smooth K-wires (if the physis is crossed) or
screws directed from the metaphyseal fragment with the
uninjured metaphysis. An arthrotomy or arthroscopy is a
recommended part of the procedure to gauge restoration of
the articular surface and to remove any small fragments that
could potentially form loose bodies. Failure to reduce and
fix the fragment adequately may result in malunion or
nonunion.
Treatment of the type 7 injury is discussed in Chapter 22.
Results
These fractures generally heal rapidly. However, when they
involve a child or adolescent with any significant remaining
growth potential, this region probably has the highest rate
of complications. Most patients with more than 1 year of devel-
opment remaining demonstrate some type of a growth disturbance:
focal arrest or slowdown of longitudinal growth. Lee and col-
leagues emphasized that at least 90% of patients with this
type of injury have some degree of shortening.773 Stephens
et al. thought that growth disturbance was an all-or-none
phenomenon.798 Fortunately, many patients are nearing
skeletal maturity and do not exhibit major growth deformity
as a consequence.
Prognosis based on the growth mechanism classification
alone is not reliable. The development of deformity appears
to be related to the severity of the injury mechanism, the
degree of initial displacement of the fracture, the ease and
exactness of the reduction, the type of fracture, and the age
of the patient. There undoubtedly are focal areas of physeal
damage due to the multiple undulations of this physis. The
central “peak” seems particularly susceptible.
Complications
The sequelae of distal femoral physeal fractures include leg
length discrepancy, varus or valgus angulation, limitation of
knee motion, and quadriceps atrophy. The primary problem
is leg length discrepancy, which may occur even in the
absence of obvious premature epiphysiodesis because of a
generalized slowdown (rather than a complete arrest) of
growth relative to the contralateral distal femur. It is imper-
ative to follow these patients to skeletal maturity to docu-
ment this type of complication adequately, even when the
fracture appears to heal satisfactorily.
Neer reported a 42% incidence of leg length discrep-
ancy.778 Cassebaum and Patterson noted a 25% incidence.748
The combined series of Nicholson and Neer revealed that
40% of patients had leg length inequality.778,780 Lombardo
and Harvey reviewed 34 fractures of the distal femur
and found an average limb length discrepancy of 2 cm in
36% and a varus or valgus deformity of more than 5° in
33%.774 Twenty percent of the patients required some
type of reconstructive procedure, such as an osteotomy,
epiphysiodesis, or both. Other complications include
21. Femur
limitation of knee motion, ligament laxity, and quadriceps
atrophy.
Riseborough and associates, studying 66 distal femoral
physeal fractures, found that leg length discrepancies in
excess of 2.4 cm or leading to contralateral distal femoral
physeal arrest occurred in 37 patients (56%) and that
angular deformity requiring corrective osteotomy occurred
in 17 patients (26%).786 Central growth arrest occurred in 13
patients (20%) and was associated primarily with type 1 and
2 growth mechanism injuries. The development of this arrest
had an excellent predictive value for progressive limb length
discrepancy. Fractures in the juvenile age group (2–11 years)
were almost invariably caused by severe trauma and had the
poorest prognosis. Of 23 injuries in juveniles, 19 resulted in
growth problems. In contrast, fractures in the adolescent age
group, those 11 years old or older, were caused by less exten-
sive trauma and were most often associated with sports
injuries. However, 50% of these individuals also had growth
problems.
The distal femoral epiphyseal growth plate contributes
70% of the longitudinal growth of the femur and 40% of the
length of the lower extremity. Any injury that completely
or partially arrests growth potential may lead to significant
shortening or angular deformity of the extremity. The
younger the child at the time of injury, the greater the
potential for these undesirable complications. If one of these
sequelae becomes evident during long-term follow-up,
appropriately timed epiphysiodesis or lengthening, as well as
osteotomy or even resection of the bridge, may serve to min-
imize the disability, the deformity, or both.
As noted previously, the undulated contour of the growth
plate and the mechanisms of injury—whether varus, valgus,
anterior, or posterior—introduce combined shearing–
compression forces into the physis as it is displaced. If a large
metaphyseal fragment is present, it is less likely that prob-
lems will occur than when shearing across the entire “trans-
verse” plane of the epiphysis takes place (Fig. 21-77).
The distal femoral epiphyseal cartilage plate is prone to
growth disturbances not generally seen roentgenographi-
cally with equivalent injuries at other sites (Figs. 21-78,
21-79). This finding specifically relates to differences in the
contour of this particular physis that predispose to certain
FIGURE 21-77. Effect of undulation. Arrows show the central
physeal area with a proximal fragment, which disrupts physeal
continuity.
 Distal Femoral Epiphyseal Injuries 909

A,B C

D E
FIGURE 21-78. Effect of grating impingement in type 1 (A–C) and type 2 (D, E) injuries. The microscopic physeal damage leads to pre-
mature growth arrest.

A B
FIGURE 21-79. Growth arrest and osteonecrosis in the type 3 fragment of a type 3/type 4 fracture.
910
FIGURE 21-80. (A) Angular deformity due to premature closure of the lateral physis. (B) Progressive changes 6 months later.
kinds of injury. Fortunately, many epiphyseal injuries to the
distal femur occur at an age when little potential for major
longitudinal growth remains. Microscopic disruption of the
germinal cartilage cells or blood vessels seems to be the most
logical explanation for this cessation of growth. Usually pre-
mature epiphysiodesis is evident within 6 months after the
injury. The rapidity of the phenomenon indicates both a
direct effect of the injury and a gradual growth deceleration
process.
Mäkelä et al. studied injury to the distal femoral growth
plate. A central drill-hole defect of variable size was used.775
They found that destruction of 7% of the cross-sectional area
of the physis resulted in permanent growth disturbance.
Varus-valgus angular deformities may result from partial
or complete unicondylar epiphysiodesis (Fig. 21-80). Treat-
ment is dictated by the anticipated remaining growth. If less
than one-third of the area of the physis is involved, bridge
resection may be considered. An epiphysiodesis in the other
condyle may also be completed. Correction of angular
deformity by osteotomy may be necessary.
Thompson and Mahoney reviewed 28 fractures of the
distal femoral growth plate and showed that complications
were more frequent in displaced than nondisplaced frac-
tures.682 No fractures treated with internal fixation displaced,
whereas 38% of the fractures reduced without fixation sub-
sequently displaced during casting. The authors were unable
to demonstrate that gentle reduction under general anes-
thesia offered any additional protection against subsequent
physeal arrest.
Concomitant Ligament Injury
Bertin and Goble reviewed 29 cases of epiphyseal injuries
about the knee and found that 50% of the patients had
ligament instability at follow-up evaluation an average of 66
months following the original injury.740 Of the 29 patients,
16 had distal femoral injury; and 6 of the 16 patients also
had ligament insufficiency. Proximal tibial physeal fractures
21. Femur
were noted in 13 of the patients, and 8 of them had ligament
laxity. They concluded that ligament insufficiency was prob-
ably a reasonably common concomitant injury to the physeal
fracture of the knee. They also reported a complex proximal
tibial physeal fracture associated with medial collateral liga-
ment rupture that resulted in genu valgum and early degen-
erative osteoarthritic changes.
Buess-Watson et al. thought the Salter classification to be
of little prognostic value at the knee, as type 2 fractures (in
their series) were usually followed by asymmetric growth
arrest.744 They also stressed that associated ligament injuries
were not rare (43%) and deserved more attention.
Floating Knee
The floating knee has received little attention in chil-
dren.803,804 The injury comprises combined fractures of
the ipsilateral femur and tibia (Fig. 21-81). In children,
fractures through the growth plates of the distal femur
or proximal tibia, along with a similar physeal fracture
on the other side of the knee or a metaphyseal or diaphyseal
fracture in the contraposed bone, create many analogous
situations.
Letts and associates reviewed 15 children with this com-
bined injury pattern. They found that there was a high
incidence of floating knee in childhood cyclists, and they
proposed a treatment protocol.804 For a type A injury, in
which both the femoral and the tibial fractures are diaphy-
seal and closed, open reduction and internal fixation of the
tibia and balanced skeletal traction for the femur are rec-
ommended. For a type B injury, in which one fracture is di-
aphyseal, one fracture is metaphyseal, and both are closed,
open reduction and internal fixation of the diaphyseal frac-
ture and balanced skeletal traction (or casting) for the me-
taphyseal fracture are recommended. For a type C injury, in
which one fracture is diaphyseal and the other is an epiphy-
seal displacement, it is recommended that the epiphyseal
Floating Knee 911

FIGURE 21-81. Types of floating knee. (A) Diaphyseal injuries. (B)

Diaphyseal-metaphyseal pattern. (C) Epiphyseal-diaphyseal
pattern.

injury be reduced and internally fixed and the other frac-

ture be treated with traction or casting, as indicated. For a
type D injury, in which one fracture is open, débridement
and external fixation are recommended for the open tibial
fracture, with femoral traction for the open or closed frac-
tured femur. For a type E injury in which both fractures
are open, external fixation of the tibial fracture and trac-
tion or external fixation of the femur are recommended.
Results were worst when both fractures were treated
nonoperatively.804
Any treatment plan has exceptions. If it is essential that
the child be mobilized as quickly as possible, internal fixa-
tion of both femoral and tibial fractures may be indicated
(Fig. 21-82). The type of internal fixation may also depend
on the equipment available, the experience of the surgeon,
and the age of the child. In older children, intramedullary
nailing of the femur or tibia may be more appropriate than
plate fixation. In children under 6 years of age, it may be
possible to obtain a stable closed reduction of the tibia that
may be held with a cast while the femur is treated with trac-
tion. Because fractures of the femur in children may be
managed safely and effectively by traction, it seems unwar-
ranted to open this fracture, unless necessary, for the well-
being of the child.
Lett et al.’s basic premise was that with fractures of the
ipsilateral femur and tibia, no matter what the area of
involvement, at least one fracture should be stabilized. They
thought that such fixation was most appropriate for the tibia.
Letts et al. did not believe that routine internal fixation of
both fractures should be performed in children, as it may
result in overgrowth and is occasionally complicated by
osteomyelitis.804
Bohn and Durbin reviewed 44 ipsilateral femur and tibial
fractures in 42 children and adolescents.803 One patient died FIGURE 21-82. Adolescent with a femoral diaphyseal fracture asso-
from head injury, and one patient had fat embolism syn- ciated with a type 2 epiphyseal fracture. Both were treated with
drome. The age was found to be the most important variable open reduction and internal fixation.
912
related to the clinical course. Of the 15 patients less than 10
years of age, 3 had an early complication. The average time
to complete weight-bearing was 13 weeks, and the average
combined femoral and tibial overgrowth was 1.8 cm. Of the
15 children who were more than 10 years old, 8 had an early
complication. The average time to full weight-bearing was
20 weeks, and there was variable femoral and tibial growth.
The juxtaarticular pattern of fracture was associated with the
highest incidence of early and late problems. Most children
who were younger than 10 years were treated successfully
with closed methods, but limb length discrepancy developed.
Children older than 10 years were treated successfully with
reduction and fixation, but they had a high rate of compli-
cations. There is a high incidence of concomitant injuries to
the ligaments of the knee resulting in long-term dysfunction.
Of 19 patients with long-term follow-up, only 7 had normal
function without major problems. The remainder had a com-
promised result due to limb length discrepancy, angulated
deformity, or instability of the knee, particularly ligamentous
instability.
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Am 1948;30:103–115.
791. Rumlova E, Vogel E. Dislocated supracondylar femoral frac-
tures, slipped epiphyses and epiphyseal fractures in children.
Z Kinderchir 1983;38:48–50.
928
792. Schneider T. Spatergebnisse der kuntschernagelung am
junglichenden Knocher. Arztl Wochenschr 1950;5:846–849.
793. Shulman BH, Terhune CB. Epiphyseal injuries in breech deliv-
ery. Pediatrics 1951;8:693–700.
794. Shivley JL. Genu recurvatum after femoral fracture. Contemp
Orthop 1990;21:577–580.
795. Sideman S. Traumatic separation of the lower femoral epiph-
ysis. J Bone Joint Surg 1943;25:913–916.
796. Siebler G. Frakturen des distalen Femur. Hefte Unfallheilkd
1988;200:468–470.
797. Simpson WC Jr, Fardon DF. Obscure distal femoral epiphyseal
injury. South Med J 1976;69:1338–1340.
798. Stephens DC, Louis E, Louis DS. Traumatic separation of the
distal femoral epiphyseal cartilage plate. J Bone Joint Surg Am
1974;56:1383–1390.
799. Tessore A, Pollono F. Il distacco dell’epifisi inferiore del
femore. Minerva Ortop 1966;17:35–43.
21. Femur
800. Torg JS, Pavlov H, Morris VB. Salter-Harris type III fracture of
the medial femoral condyle occurring in the adolescent
athete. J Bone Joint Surg Am 1981;63:586–591.
801. Vogt P. Die traumatische Epiphysenfrennung und deren
Einfluss auf des Langenwachstum der Rohrenknochen. Arch
Klin Chir 1878;22:343–349.
802. Wajanavisit W, Orapin S. Biplane fracture of distal femoral
epiphysis: a case report. J Med Assoc Thai 1994;77:501–504.
Floating Knee
803. Bohn WW, Durbin RA. Ipsilateral fractures of the femur and
tibia in children and adolescents. J Bone Joint Surg Am
1991;73:429–439.
804. Letts M, Vincent N, Gouw G. The “floating knee” in children.
J Bone Joint Surg Br 1986;68:442–446.
22
Knee
Engraving of a fracture involving the adolescent knee. (From
Poland J. Traumatic Separation of the Epiphyses. London: Smith,
Eder, 1898)
he developmental patterns of the distal femoral and
T proximal tibial epiphyses are detailed, respectively, in
Chapters 21 and 23. The other anatomic structures of
the knee joint include the patella, the quadriceps expansion
and patellar tendon, the medial and lateral menisci, the com-
ponent ligaments (collateral and cruciate), and the capsule.
These structures are discussed in this chapter.
Anatomy
Patella
The patella is a large sesamoid bone that, with the exception
of the articular surface, lies within the tendinous expansion
of the quadriceps femoris muscle. The lower third of the
patella is covered by a large fat pad and synovial reflection,
and it is extra-synovial (Figs. 22-1, 22-2). Synovial recesses
extend between the fat pad, patella, and tibia (Fig. 22-2).
The patellar tendon is also separated from the synovial joint
by this fat pad. The patellar tendon progressively blends
into both the inferior patella and tibial tuberosity by fibrous
to fibrocartilaginous to cartilaginous tissue. Mature fibers
attaching the tendon directly into bone are not present until
late adolescence, when both of these structures have finished
chondro-osseous transformation and maturation.
Initially the patella is completely cartilaginous and thus
radiolucent in the preschool child.8,14 Primary patellar ossi-
fication begins around 5–6 years of age, although small foci
may be evident as early as 2–3 years. The initial chondro-
osseous transformation is usually typified by multiple small
foci that rapidly coalesce (Figs. 22-3, 22-4), similar to sec-
ondary ossification in the trochlear region of the distal
humerus.12 Patellar ossification occurs centrifugally within
the mass of epiphyseal cartilage that is well vascularized by
cartilage canals and is thus comparable to postnatal epiphy-
seal (secondary) ossification in long bones. Sometimes there
is a distinct origin between the inferior and superior portions
of the early ossification center, which may be mistaken for
a fracture. Similarly, multifocal ossification should not be
misconstrued as a comminuted fracture in a young child
being evaluated for knee trauma. Ossification progressively
expands toward the various margins. Ossification rapidly
proceeds to the anterior surface, where periosteum initially
forms. In contrast, the posterior, inferior, medial, and lateral
margins retain a chondro-osseous interface, with peripheral
perichondrium and posterior articular cartilage. During
adolescence the anterior, medial, and lateral cortical bone
of the expanding ossification center becomes confluent with
the fibrous tissue of the quadriceps tendon and progressively
creates a dense continuity between tendon and subchondral
bone through Sharpey’s fibers. Until skeletal maturation,
these chondro-osseous interfaces remain as areas mechani-
cally susceptible to tensile forces and thus may incur avulsion
fractures.
Developing patellar ossification is usually irregular at the
margins, not unlike the expanding distal femoral ossification
center.12 Because of this normal variability of marginal ossi-
fication, a diagnosis of osteochondrosis or osteochondritis
929
FIGURE 22-1. Coronal (A) and sagittal (B) sections of the patella,
capsule, and proximal tibia from a 6-year-old child. Cartilage occu- FIGURE 22-2. Coronally split knee from a 10-year-old boy showing
pies much of the mass of the patella. A small focus of ossification a well-ossified patella. Note how the synovium covers the fat pad.
(solid arrow) is present. The retropatellar fat pad (F) covers much
of the lower pole of the patella. The open arrow indicates the
medial collateral ligament. Note how it blends into the epiphyseal
cartilage and the capsule (c).

FIGURE 22-3. Cadaver specimens showing

progressive patellar development. (A) At 2
years, no ossification is present. However,
air/cartilage contrast outlines the patella
in the lateral view. (B) Early ossification
in a 6-year-old, which is often multifocal.
(C) Multifocal ossification then begins to
C coalesce.

930
 Anatomy
A B
FIGURE 22-4. Ossification rapidly proceeds centrifugally to fill out
the cartilaginous patella. Anatomic (A) and serial histologic (B) sec-
tions show enlargement of the patellar ossification center. Note
how the ossification replaces the anterior cartilage before the pos-
of the patella, or even fracture, solely on the basis of the
roentgenographic appearance, must be made with caution.
Accessory ossification centers may develop, particularly in
the superolateral portion of the bone. A separate ossification
center of the inferior pole probably does not exist. Instead,
one must consider the diagnosis of a Sinding-Larsen-
Johansson lesion, the patellar equivalent of the Osgood-
Schlatter lesion. After 10 years of age the patellar subchon-
dral bone becomes more smooth and develops a distinct,
shell-like appearance with a thin plate of bone surrounding
the patellar trabecular bone.
When a normal, mature patella is sectioned transversely,
the medial and lateral articular surfaces are approximately
FIGURE 22-5. (A) Normal patella/tendon measurements. Insall’s
measurement is the ratio of patellar length (PL) to tendon length
(TL). (B) Specimen of the knee of an 8-year-old showing problems
931
C
terior cartilage. (C) MRI of patellar ossification in a 6-year-old boy.
Note the anterior position of ossification within the cartilaginous
patella.
equal and subtend reasonably equivalent angles. However, if
the immature patella does not track properly (e.g., sublux-
ates laterally), the cartilage may gradually deform (plastic
deformation) and the subsequently appearing ossification
center “mirrors” the antecedent, deformed cartilaginous
precursor. This eventually leads to the unequal osseous
angles characteristic of a chronically maltracking, subluxat-
ing, or dislocating patella.
The patella may be situated relatively high or low. Nor-
mally, the distance from the lower pole of the patella to the
tendinous insertion on the tuberosity should equal the sagit-
tal length of the patella (Fig. 22-5). More than 20% varia-
tion probably indicates an abnormal patellar position,6,10,11
of such measurement, even in a skeletally immature cadaver. The
tuberosity, in particular, is not well defined.
932
although these measurements and ratios are not realistic
in the growing child. Depending on the age and extent
of chondro-osseous transformation, there are significant
amounts of epiphyseal cartilage at both the superior and
inferior patellar poles and the tibial tuberosity, such that the
sagittal length of the ossified patella and the distance from
the patellar ossification center to the tibial tuberosity ossifi-
cation center may be considerably different from the actual
patellar and tendon lengths.
The patella, similar to any epiphysis, is a mass of cartilage
interlaced with an intrinsic vascular system within cartilage
canals. When ossification expands toward the anterior
surface, discrete intraosseous vessels penetrate and supply
the ossification. A number of vessels penetrate from around
the periphery of the patella.13
Meniscus
The menisci assume their characteristic shape during pre-
natal development.4,5 The major postnatal changes are
progressively decreased vascularity, morphologic growth
commensurate with enlargement of the distal femur and
proximal tibia, and accommodation of this growth to chang-
ing femorotibial contact.4,5,7 Weight-bearing obviously affects
these postnatal changes, which are accompanied by changes
at the cellular level and in the extracellular matrix. The
progressive decrease in vascularity obviously affects the in-
flammatory response stage after an injury. The lateral menis-
cus tends to have more developmental variation, but at
no time is it normally discoid. Anterior extensions from
both menisci to the anterior cruciate ligament and to each
other are a residual of their common origin. The transverse
anterior (intermeniscal) ligament between the menisci
may be a source of some discomfort in children complain-
ing of anterior knee pain. The more fixed medial meniscus
possesses important peripheral capsular attachments, includ-
ing the thickened medial capsular ligament and postero-
medial capsular complex. The more mobile lateral meniscus
has no attachment posterolaterally at the popliteus tendon
recess. There may be a communication to the proxi-
mal tibiofibular joint. The meniscofemoral ligaments of
Humphrey and Wrisberg are variable, both as to size and
presence.
The microscopic structure and collagen fiber alignment
of the menisci change over time due to changes in weight-
bearing function and applied mechanical loading.2,3,9 Most
of the fibers are arranged in circumferential fashion in the
long axis of the meniscus. Other radially directed fibers are
located mainly on the surfaces of the meniscus, more on the
tibial than the femoral side, and probably act as tie rods
resisting longitudinal splitting. A few radial fibers change
direction and run in a vertical fashion through the substance
of the meniscus. These patterns undergo changing patterns
as the child begins ambulation. There are no studies relative
to how they change, particularly during adolescence, when
there are both significant morphologic (size) changes in the
knee and often excessive demands of athletic activity.
The meniscus of the infant is a relatively vascular struc-
ture.4,5 As weight-bearing commences, the more central
regions lose their microvascularity. However, peripheral vas-
cularity is retained and allows the likelihood of spontaneous
22. Knee
repair of an incomplete tear in the skeletally immature
individual.1,5,7
Ligaments and Capsule
Throughout most of development the cruciate ligaments
blend into the epiphyseal cartilage of the distal femur (inter-
condylar notch) and proximal tibia (tibial spines). There is
a progressive transition of fibrous, fibrocartilaginous, and
cartilaginous tissues. Only during late adolescence do the
cruciate ligaments insert directly into the maturing ossifi-
cation centers through the development of Sharpey’s
fibers. Accordingly, childhood cruciate injuries usually are
chondro-osseous failures, rather than intraligamentous
ruptures.
It is commonly taught that the medial and lateral collateral
ligaments attach primarily into the distal femoral epiphysis
and proximal tibial metaphysis, an anatomic configuration
that, accordingly, makes the distal femur more susceptible to
epiphyseal-physeal injury. The ligaments blend densely into
the distal femoral epiphyseal perichondrium. However, dis-
section of skeletally immature knees shows that the deep col-
lateral ligaments also attach directly into the proximal tibial
epiphyseal perichondrium (Fig. 22-6). Some of the more
superficial collateral fibers do continue onto the metaphysis,
as does the pes anserinus. The classic concept that the collateral
ligaments have no tibial epiphyseal attachments is thus incorrect.
The increased susceptibility to injury is more likely due to
the moment arm of any applied deformation force, along
with the extent of forceful muscular contracture.
The suprapatellar pouch normally extends under the
quadriceps. Developmental variations of the synovium
(plicae) in this region may lead to compartmentalization of
this pouch (plica syndrome) and chronic knee effusions.
The posterior capsule has minimum redundancy. There are
no normal communications from the posterior capsule into
the popliteal space other than along the popliteal tendon
and the communication to the proximal tibiofibular joint.
Popliteal cysts in children may develop without a discrete
communication with the knee joint.
General Examination
Any child or adolescent presenting for the evaluation of
an acute or chronic knee injury must be evaluated carefully
for possible congenital abnormalities as well as the more
typical traumatic lesions that are most often present in young
adults.15–23 Although the injuries commonly afflicting adults,
such as a meniscal tear or anterior cruciate ligament
injury, are much less frequent in the skeletally immature
patient, such lesions do occur. Extensive amounts of carti-
lage make normal diagnostic methods less likely to be
specific. They also increase the likelihood of chondro-
osseous disruption, which may or may not be accompanied
by a variable layer of subchondral bone. Bleeding within
epiphyseal bone (bone bruising) is a real phenomenon
that is probably prevalent in children, especially with direct
blows to the knee. Magnetic resonance imaging (MRI) is
the only way to establish this diagnosis unequivocally. Such
studies are indicated when routine imaging fails to indicate
Diagnostic Imaging
FIGURE 22-6. Superficial (A) and deep (B) collateral ligament
attachments. Note the fibular collateral ligament (FCL), pes anser-
inus (PES), tibial collateral ligament (TCL), the deep medial col-
lateral ligament (MCL), and lateral collateral ligament (LCL). The
the cause of acute or persistent symptoms following knee
trauma.
Flanagan et al. showed that even minor knee injuries
cause pain and functional problems.18 Rest, ice, and anti-
inflammatory medications are the usual initial treatment.
Range of motion exercises should be started as soon as pos-
sible, preferably after an accurate diagnosis has been made.
Stretching and strengthening exercises for involved muscle
groups provide pain relief and help prevent recurrence.
Even minor knee trauma may lead to subluxation due to
quadriceps atrophy or tightening of (contracture) of the
lateral retinaculum.
Stanitski et al. showed that in 70 children aged 7–18 years
with acute traumatic knee hemarthrosis there was a high inci-
dence of intraarticular lesions22,23: 47% of preadolescents
(age 7–12 years) had meniscal tears and 47% had anterior
cruciate ligament tears. Among the adolescents (age 13–18
years), 45% had meniscal tears and 65% had anterior cruci-
ate ligament tears. Osteochondral fractures accounted for
7% of the lesions. Stanitski et al. thought that meniscal and
anterior cruciate ligament damage was common in children,
especially adolescents. They noted that accurate examina-
tion of acute intraarticular injury is arduous. Young patients
may be limited historians with regard to the mechanism of
injury. Guarding secondary to pain may significantly limit
the range of motion and stability testing.
Diagnostic Imaging
When evaluating injury to the knee, the patella is best seen
in either the lateral or tangential projections. In the antero-
posterior view, because of the normal position of the patella
overlying the distal femoral metaphysis and epiphysis, much
of the patella is obscured especially when the ossification
center is small. However, this anteroposterior view may be
933
C
collateral ligaments attach to the epiphyseal perichondrium of the
proximal tibia, not the metaphysis. (C) The distal femur has been
removed to show the anterior, medial, and lateral capsular reflec-
tions and collateral ligaments in an 11-year-old boy.
the best way to visualize a bipartite patella. Oblique views
may also allow adequate visualization of the superolateral
region.
Because the epiphyseal regions of the younger child
contain more radiolucent cartilage than during the adoles-
cent period, the evaluation of suspected internal derange-
ment of the knee becomes more challenging.32 Only a thin
piece of subchondral bone may be associated with a large
cartilaginous fragment in a lesion such as osteochondritis
dissecans, an acute osteochondral fracture, or a patellar
sleeve fracture. If the knee is placed in the usual diagnostic
positions, especially tangential views, portions of the anterior
proximal tibia or tibial tuberosity ossification centers may
appear to be an osteochondral fragment. The apparent
lucency is the physis of the tuberosity, which parallels the
roentgenographic beam in this particular view.28
Children normally have a greater degree of ligamentous
laxity than adults. It enchances the likelihood of phenom-
ena such as “vacuum arthrography,” which is due to cavita-
tion of gas from joint fluid when stress is applied. Such
cavitation may outline all or part of the joint and should not
be misinterpreted as a loose body, chondro-osseous fracture,
or open injury.
Arthrography is useful in the child’s knee because of the
extensive radiolucency.27,31 Cartilage damage may have little
involvement of contiguous subchondral bone, and may be
depicted only by single- or double-contrast arthrography.
This procedure may be undertaken as a diagnostic study in
a child prior to using more invasive procedures such as
arthroscopy. However, knee arthrography is rapidly being
supplanted by MRI.
Computed tomographic (CT) scanning may be useful to
define complex fractures of the distal femur. Such fracture
“definition” is important to plan proper reduction and fixa-
tion. Certain fractures of the patella and femoral condyles
may be visible only with a CT scan. The subluxated, dislo-
934
FIGURE 22-7. MRI scan of a 9-year-old demonstrating posttrau-
matic knee effusion. It fills the suprapatellar pouch and elevates
the patella away from the condyles. A bone bruise is evident in the
patella.
cating, or dislocated patella may also be assessed with CT
scanning.
Magnetic resonance imaging is becoming a more clini-
cally useful tool for evaluating the skeletally immature
knee.24,26,29,30,33 Unfortunately, the younger the child the
more likely is sedation or anesthesia necessary to maintain
the “stillness” necessary to accomplish a meaningful study.
Because MRI is helpful for diagnosing pathology within
the knee, it is important to be familiar with the MRI appear-
ance of normal anatomic variants that might be confused
with meniscal tears such as the transverse geniculate liga-
ment, the hiatus of the popliteus tendon, and the menis-
A B
FIGURE 22-8. Bone bruising. (A) Medial femoral and tibial intraepiphyseal involvement after vehicular (bumper) impact to the knee. (B)
Medial involvement after being struck by a baseball bat.
22. Knee
cofemoral ligaments.24 Such familiarity must also include
variations of chondro-osseous transformation and matura-
tion in the child and adolescent. Meniscal fragments may be
difficult to detect on MRI, even though clinically significant,
and one of the easier injuries to overlook.25 MRI may not reli-
ably exclude articular cartilage injury.30 Evolving sequencing
methods may allow such delineation in the future.
There is significant variation in the MRI appearance
within the patellar tendon.29 Many changes may represent
subclinical injury. Changes in signal intensity within this
tendon may also occur secondary to joint effusions, anterior
cruciate ligament tears, or strain (microinjury) within the
patellar tendon itself.
The MRI scan is useful for evaluating the presence of effu-
sion or hemarthrosis (Fig. 22-7). The presence of significant
distension of the capsule by fluid should make the physician
search carefully for an anatomic lesion responsible for such
fluid increase. The posterior distension of the joint capsule
may cause the patient to complain of posterior knee pain
and may even be misdiagnosed as a popliteal cyst.
Perhaps the most important use of MRI is for delineating
obscure or occult intraepiphyseal fractures of the knee (Figs.
22-8, 22-9). The knee, like the wrist, is an area of frequent
injury in an active child. Competitive, increasingly physically
demanding team sports put the knee at risk for direct impact
injuries and chondro-osseous interface tensile failure. Chil-
dren and adolescents often present with a painful knee,
with or without joint effusion, only to have a “normal”
radiograph. MRI allows a more definitive diagnosis in the
enigmatic patient.
The incidence of chondral injury within the femoral
condyles may eventually become the most important clinical
consequence of the MRI evaluation. The potential role of
the initial injury in the development of progressive chondral
injury is uncertain. Acute, transarticular load injuries to the
calcified cartilage–bone interface generate no initial abnor-
malities on the surface articular cartilage. The initial con-
cussive blow might exceed some supraphysiologic threshold
Arthroscopy
A B
FIGURE 22-9. (A) Transverse MRI scan showing a peripheral bone bruise (arrow) after a shearing injury to the knee. (B) Five months
later the lateral chondro-osseous transformation is irregular.
and lead to progressive chondral damage. Another possibil-
ity is that the osseous lesion might heal into a stiffer sub-
chondral plate than the previously normal bone. The
decreased compliance might then generate greater stiffness
in the articular cartilage and predispose to lesions such as
osteochondritis dissecans.
Arthroscopy
The diagnosis of traumatic disorders of the knee presents
special problems in the pediatric population. The index
of suspicion for internal derangement, particularly menis-
cal or ligament substance tears, is often low. The history
of the injury is often inadequate in young children. Physi-
cal findings may be nonspecific. Arthroscopy may be
advantageous in children, as it provides evidence of sig-
nificant internal derangements, confirms serious articu-
lar damage, and allows the inception of appropriate
therapy.34–57
Although arthroscopy is not a substitute for a careful
history and physical examination, adequate historical and
physical findings may be difficult to elicit and are often non-
specific in children. In the preadolescent, provision of
historical data often becomes the burden of the parents.
With increased sports involvement at earlier ages by larger
numbers of children and the increased emphasis on sports
participation by girls, a higher incidence of minor to signif-
icant knee injuries is expected. In one study group, 31% had
a major hemarthrosis.41
In preadolescent patients only 55% of the preoperative
clinical diagnoses were confirmed at arthroscopy. The
younger the patient, the less correlation there was between
findings of arthroscopy and the preoperative clinical diag-
nosis. Even in the adolescent, arthroscopy facilitated a more
complete diagnosis. Meniscal injury was frequently over-
diagnosed in both children and adolescents. In the preado-
lescent group with meniscal pathology as the preoperative
diagnosis, the knee is often normal at arthroscopy. During
935
adolescence chondromalacia is the most common arthro-
scopic finding.38 There was also an “unanticipated” inci-
dence of anterior cruciate ligament structural damage in the
preadolescent patient. Even in the child, hemarthrosis is a
harbinger of significant intraarticular insult to the knee and
is a requisite for an accurate diagnosis so specific treatment
may be undertaken.
Ziv and Carroll reviewed 156 arthroscopic examinations in
children with knee complaints; 43 of these patients and ado-
lescents were under 12 years of age.57 In 93% of the cases
arthroscopy was useful for preventing unnecessary arthrot-
omy, providing additional anatomic findings and biopsy
material. In only 5% of their cases did the arthroscopy fail
to provide additional information. There were no complica-
tions from the procedure. Arthroscopy is an effective diag-
nostic tool for children; it is easier to perform owing to the
relative joint laxity, and it allows visualization of the anatomic
structures, whether normal or abnormal. Although most
initial reports of arthroscopy in children emphasized its diag-
nostic potential, treatment (arthroscopic surgery) should be
done when indicated.
The results of arthroscopy in patients older than 13 years
of age were not dissimilar to those reported in adults.47
However, when patients under 13 years of age were analyzed,
the presumptive clinical diagnosis was confirmed in only
27% of patients. Some children had significant damage to
the articular cartilage that probably had been worsened by
the delayed diagnosis of a meniscal tear. Progressive degen-
erative arthritis of the knee, often seen with undiagnosed
meniscal lesions in adults, may be the outcome of similar
lesions in the child. The still unossified epiphyseal cartilage
is biologically plastic and may readily deform when repeti-
tively exposed to an anatomic abnormality such as a mobile
meniscal flap (tear), a joint mouse, or a foreign body. This
problem is typically evident during the relatively rapid
change from a spherical to a bullet-shaped femoral head in
developmental hip dysplasia.
Harvell et al. reviewed 310 knee arthroscopies in 285 chil-
dren. The preoperative clinical diagnoses were correlated
936 22. Knee

with arthroscopic findings in only 55%;41 35% of this group

were found to have additional pathology that had not been
anticipated preoperatively. In adolescents (13–18 years),
70% of the clinical diagnoses were confirmed arthroscopi-
cally; additional pathology was also found in 25% of this
group.
Romdane et al. described the formation of a pseudo-
aneurysm of the popliteal artery following arthroscopic
meniscectomy in an 8-year-old boy.52 They alluded to the fact
that popliteal artery injury was rare in children.

Knee Dislocation
Complete dislocation of the knee is infrequent in children
and adolescents. It must be clinically and radiographically
distinguished from a completely displaced type 1 distal
femoral physeal fracture. The trauma usually necessary to
produce dislocation is more likely to cause a fracture of the
distal femoral or proximal tibial epiphysis.61,63 Dislocation is
usually accompanied by variable disruptions of the unossi-
fied epiphyseal cartilage, capsular soft tissues, and ligaments
and frequently by neurovascular damage, which must be
accurately diagnosed so appropriate repairs may be insti-
tuted. The complication of gangrene is usually avoidable,
although an incompletely patent popliteal artery may cause
ischemia, which may worsen with growth and increasing
functional demands. Vascular complications are usually
preventable if the initial diagnosis and treatment are
adequate.60,64,65
Because the clinical appearance of a dislocated knee
may be indistinguishable from the appearance of a sig-
nificantly displaced physeal/epiphyseal fracture, radio-
graphic evaluation is essential. It allows rapid diagnosis that
allows intelligent reduction if neurovascular compromise
is evident during the antecedent physical examination.
MRI may help to accurately define the specific soft tissue
injuries.66
Dislocation may occur in any direction (Figs. 22-10, 22-11).
Particularly, a rotational dislocation may occur, leaving some
of the soft tissues intact (Fig. 22-12).58
FIGURE 22-10. Dislocation of the knee with anterior femoral dis-
placement in a 12-year-old boy.
The posterior tibialis and dorsalis pedis pulses should be
evaluated thoroughly in any child with knee dislocation. If
they are not present, the dislocation must be reduced as
quickly as possible and the distal circulation immediately
reevaluated. If at this point the circulation is still not normal,
the popliteal artery should be assessed. Arteriography pro-
vides additional information, although the location of the
lesion should be obvious. Intimal damage may be more easily
diagnosed by arteriography. If performed, arteriography
should not prolong the interval between injury and com-
pletion of surgical exploration, repair, or anastomosis
beyond 6–8 hours. Postoperatively, the patient must be mon-
itored closely for compartment syndrome. Even if no vascu-
lar damage occurs, the patient must be monitored closely.
Normal circulatory dynamics are disrupted while the knee
remains dislocated. The rapid restoration of arterial inflow
following reduction may not be accompanied by normal
venous/lymphatic outflow. This situation increases capil-

FIGURE 22-11. (A) Knee dislocation with posterior femoral dis- imal fibular epiphysis did not reduce (arrow). Several days later this
placement in a 14-year-old boy. The arrow indicates a concomitant fracture was reduced surgically, and at the same time the fibular
type 3 fibular growth mechanism injury. (B) Initial reduction was collateral ligament was reattached to the femoral condyle (the lig-
successful. However, the concomitant type 3 fracture of the prox- ament avulsed along with a segment of epiphyseal cartilage).
Knee Dislocation
A B
FIGURE 22-12. (A) Dislocation of the knee with medial displace-
ment of the femur. The distal femur is also rotated, whereas the
patella still appears attached to the tibia. The tibia, soft tissue, and
patella resemble that in Figure 22-6C. It was reduced and treated
nonoperatively. (B) Fourteen months later there is medial instabil-
ity (widening of the joint space during stance). Laterally, it has
lary perfusion into the interstitial space with subse-
quent increased hydrostatic pressure within the myofascial
compartments.
The collateral circulation about the knee is variable, espe-
cially from the standpoint of being able to sustain completely
the rigorous functional activity of the lower leg of an ado-
lescent. The femoral-popliteal artery is variably fixed to the
femur at the adductor hiatus and tibia by a fibrous arch.
Within the popliteal region, the artery gives rise to the genic-
ulate branches. Although these arteries eventually anasto-
mose with the branches of the anterior tibial recurrent
artery, they may not provide adequate blood supply to main-
tain the functional needs of the lower leg musculature of an
active child or adolescent, even though the resting circula-
tory demands may be adequate. An acute popliteal artery
injury, particularly one associated with concomitant damage
to some of the smaller vessels, hardly allows time for com-
pensatory hypertrophy of collateral circulatory patterns. In
some cases the viability of the musculature and skeleton,
even at rest, is not adequately provided by an acute circula-
tory deficiency, which may lead to Volkmann’s ischemia in
the lower leg.
Vascular repair should be completed within 6–8 hours from
the time of injury to avoid amputation or the subsequent
chronic ischemic problems of relative functional insufficiency.64
Of the patients not treated within that defined time period,
86% went on to amputation and two-thirds of the remaining
14% had chronic ischemic changes. Even if the artery was
repaired after 8 hours, many of these patients required even-
tual amputation of the leg.64
Following vascular repair it is essential that the lower leg
be closely observed for compartment syndrome. Even if the
artery is intact, one must be alert to the appearance of this
syndrome as the consequences of muscle infarction and sub-
937
undergone ossification within the sleeve of lateral cartilage that had
been avulsed as a sleeve chondro-osseous fracture when the rest
of the epiphysis displaced medially. The lateral collateral ligament
was intact, as the original injury was a peripheral fracture rather
than a ligament tear.
sequent lower leg and foot dysfunction obviously affect
rehabilitation of the reduced knee.
Cummings et al. described an unusual syndrome of
popliteal artery entrapment in children.59 The symptoms of
vascular insufficiency were caused by an anomalous course
of the popliteal artery or anomalous muscles’ impingement
on it. Surgical excision of the fibrous band that is often
present is the recommended treatment choice. A similar
phenomenon could feasibly occur after knee dislocation if
extensive posterior scarring occurred.
During vascular repair extensive reconstruction of
the knee ligaments usually should not be undertaken, as
it would increase the swelling, tissue damage, and potential
for further damage to the collateral circulation. At the time
of arterial repair, reasonably complete fasciotomies are
recommended because of the marked increase in mus-
cular compartment swelling after restoration of the
circulation.
Knee dislocation usually heals well if it is reduced imme-
diately (closed reduction). However, adequately docu-
mented follow-up of young children less than 10–11 years of
age with this injury is rare.61 Acute surgery should not be
undertaken in children except under well-defined circum-
stances (neurovascular damage, in particular). Reconstruc-
tive surgery should be deferred for several months to allow
assessment of healing. Cruciate ligament reconstruction
must be approached cautiously prior to skeletal maturity.
Collateral ligaments may heal well because the failure may
be a peripheral sleeve fracture (Fig. 22-12) that heals by
fracture healing, not by ligament healing.
Figure 22-11 shows a 14-year-old boy who sustained a knee
dislocation and a concomitant fibular epiphyseal fracture.
He was treated with a closed reduction. The epiphyseal frac-
ture of the fibula did not reduce commensurate with the
938
reduction of the knee dislocation. Several days later the
lateral side of the knee was explored and the fibular fracture
reduced. The lateral collateral ligament was repaired where
it directly avulsed from the femoral epiphysis. There was no
repair of the medial collateral ligament. Follow-up 5 years
later showed a knee that was sufficiently functional to allow
him to play competitive football.
If there is well-defined abnormal capsular laxity after the
child goes through a subsequent period of development, the
knee may be explored and a formal repair undertaken.
When these procedures are done, care must be taken to
restore the normal anatomic relations and not damage car-
tilage along the epiphyseal margins or physis. The pes anse-
rinus attaches along the medial metaphysis of the proximal
tibia; and during reflection for a repair it should be elevated
away with the periosteum, with which it is confluent, and
reflected proximally. Such a procedure may damage the
physeal periphery (zone of Ranvier) and lead to a localized
osseous bridge and angular growth deformity of either the
main tibial or tuberosity physes.
Cooper et al. noted that complete knee dislocation usually
causes disruption of both the anterior and posterior cruci-
ate ligaments.58 However, they described four cases of com-
plete knee dislocation without posterior cruciate ligament
disruption. All their patients sustained either anterior or
anteromedial dislocation with anterior cruciate ligament dis-
ruption and collateral ligament injury. An intact posterior
cruciate ligament obviously affects treatment options
favorably.67
Knee Subluxation
Ferris described a syndrome of congenital snapping knee
by habitual anterior subluxation of the tibia in extension.62
In each instance, the tibia subluxated anteriorly on the
femur when the knee was extended and reduced sponta-
neously during flexion. All patients had dysplastic features
in the knee and had different clinical syndromes (e.g.,
Larson syndrome, congenital short tibia). The authors did
not use MRI to look at the morphology of the cruciate liga-
ments.
Patellar Dislocation
Patellar displacements are relatively common in children
and adolescents when the entire spectrum of acute and
chronic subluxation and dislocation is considered. However,
complete dislocation of the patella is infrequent in a physi-
cally normal, skeletally immature individual.82 In contrast, in
children with predisposing factors (e.g., Down syndrome,
muscular dystrophy, arthrogryposis), other neuromuscular
abnormalities or excessive ligament laxity dislocation may be
frequent and repetitive.80 Chronic or habitual subluxation
often mimics dislocation in terms of subjective complaints.
Some children with neurologic disorders, such as hyperac-
tivity or attention deficit syndrome, voluntarily dislocate the
patella as an attention-getting maneuver.
McManus et al. reviewed 55 cases and thought that most
children with acute dislocation of the patella demonstrated
roentgenographic signs of patellofemoral dysplasia, suggest-
22. Knee
ing that most of the acute dislocations occurred in the knees
of children who had some preexistent anatomic variation or
abnormality.82 Acute dislocations simply add further damage
to the dysplasia and result in the knee becoming increasingly
symptomatic. The early onset of recurrent dislocation
undoubtedly affects development of the cartilaginous patella
and femoral condyles. Repetitive displacement leads to
lateral tightening and medial attenuation in the retinacular
tissues and may impede lateral condylar development of the
femur.
Acute lateral dislocation may be caused by a direct blow to
the medial side of the patella or twisting, muscular contrac-
tions when the knee is placed in valgus stress. The disloca-
tion may be complete or incomplete (Fig. 22-13). Acute
lateral displacement must be accompanied by a variable
degree of soft tissue injury to the medial patellar retinacu-
lum or avulsion of a portion of the medial chondro-osseous
tissue (Figs. 22-14 to 22-16). There is usually hemorrhage
within the joint.
The laterally displaced patella often reduces sponta-
neously, or it may be pushed back inadvertently. The
orthopaedic surgeon rarely sees the patella in its dislocated
state. The knee is maintained in some flexion with a definite
limitation toward full extension. Unless the patient presents
with the patella dislocated, the diagnosis must be made on
an historical basis; it is often difficult to distinguish from
chronic subluxation.
If the patient is seen acutely, the diagnosis should be
evident clinically. Radiography of the dislocation may be
done to confirm the diagnosis and rule out other fractures,
but, radiography is more important after reduction.
Gilbert et al. described medial retinacular tears that also
included osteochondral fragments by utilizing MRI.77 They
described bone bruising of the lateral aspect of the distal
lateral femoral condyle, probably due to the impingement at
the time of the dislocation. Condylar osteochondral injury
may also occur.89,90
Ordinarily, reduction of an acute dislocation is easy. The
hip is flexed to relax the rectus femoris, and the knee is grad-
ually extended and the patella pushed medially into its
normal position. General anesthesia is rarely necessary.
There is usually effusion in the knee joint, but aspiration is
not necessary unless the swelling is painful. Because the
patella usually does not redislocate easily, the knee should
be radiographed following reduction, with good views to
determine if there are any obvious osteochondral fractures
from the condyles or patella, and whether they are intra-
articular. It may not be possible to obtain a complete
roentgenographic examination at the time of acute injury,
as a sunrise view may be uncomfortable.
Following reduction, adequate radiographic views should
be attained to look for peripheral avulsions, especially medi-
ally. The disruption of soft tissues on the medial side, as the
patella displaces laterally, may occur within the retinacular
tissues. Prior to skeletal maturity there may be a chondro-
osseous separation along the edges, especially medially (see
Patellar Fractures, Sleeve Fracture, below). If some of the
subchondral bone is avulsed, the diagnosis may be made
before or after treatment. If the separation is purely carti-
laginous, diagnosis of a true patellar fracture, in contrast to
a soft tissue injury, may be difficult. In such cases the avulsed
Patellar Dislocation 939

C
FIGURE 22-13. Complete lateral dislocation of the patella. (A)
Oblique. (B) Sunrise. (C) MRI.

segment eventually ossifies and may give the appearance C

of a bipartite patella or peripheral nonunion. If significant FIGURE 22-14. Anterior (A) and sunrise (B) views of an avulsion
separation of such fragments can be detected after the initial fracture of the lateral margin (arrow) of the patella following acute
dislocation. (C) MRI of a similiar case involving the medial side.
reduction, the treating surgeon should consider tension
band fixation if a sufficient gap (more than 2–3 mm)
persists.
Acute surgical intervention is indicated only in the patient
who exhibits significant concomitant soft injury or when
940 22. Knee

FIGURE 22-15. Medial and lateral sleeve avulsions in a patient who

sustained an acute dislocation followed by multiple recurrences of
subluxation and dislocation. Note the lateral position of the patella
in the intercondylar notch.

there is displacement of the patella or a fragment into the

joint, which occurs when the quadriceps muscle contracts
strongly after the blow. The failure is usually at the chondro-
osseous junction.
Roger et al. noted that traumatic lateral dislocations with
FIGURE 22-16. (A) Appearance of a minimally discernible acute
internal rotation of the patella may be unreducible because medial avulsion (arrow). (B) One year later the avulsed area has
they involve locking of the patella on the lateral femoral further ossified.
condyle.87 These authors believed that reduction could be
achieved by applying a downward force to the lateral aspect
of the patella, reducing the rotational deformity and unlock-
ing the medial patellar facet. This type of locking and diffi-
culty of reduction is more likely to occur in older patients may be more effective if done electively, after the knee has
(adolescent) than in the more loosely ligamentous child. recovered from the acute injury.70
The limb is placed in a cylinder cast or knee immobilizer Rarely is the patella displaced medially. Miller et al.
for 3–6 weeks. The aforementioned imaging evaluation pro- reported traumatic medial dislocation of the patella in a
cedure is repeated during the subsequent recovery phase child.83 Interestingly, all three of their patients had under-
after return of sufficient motion to allow adequate position- gone lateral retinacular release for chronic knee pain or
ing for roentgenographic examination. recurrent lateral patellar subluxation.
During the reparative (immobilization) phase, a contrac-
ture may develop in the iliotibial band and lateral retinacu-
Intraarticular Dislocation
lum, leading to further lateralization. This accentuates the
tendency for the patella to then chronically subluxate or dis- Intraarticular dislocation of the patella is unusual in chil-
locate following acute dislocation (Fig. 22-17). In the patient dren.69,71–76,78,79,83–86,88 The lesion occurs in skeletally immature
with a chronically subluxating or dislocating patella, surgery individuals because the soft tissue attachments to the patella

FIGURE 22-17. Sunrise view of repetitive lateral dis-

location (curved arrow) of the patella, with a residual
medial remnant (straight arrow).
Chronic Subluxation
FIGURE 22-18. (A) Lateral roentgenograms of intraarticular dislocation (arrow) of the patella. (B) Postreduction film showing early irreg-
ular ossification (arrow) 4 months after the injury.
are more lax, and mobility is greater; with direct trauma to
the flexed knee the cartilage and soft tissues may be stripped
relatively easily from the osseous patella (i.e., at or near the
chondro-osseous interface). In adults a comparable injuri-
ous force would most likely cause a fracture.
There are two basic types of intraarticular dislocation. The
most common type involves the patella being torn loose from
the quadriceps mechanism, with or without the superior
cartilage (i.e., a sleeve fracture), so it lodges in the femoral
intercondylar notch, with its articular surface directed
toward the tibia (Fig. 22-18). With the other type, which is
rare, the inferior portion of the patella is separated from the
patellar tendon and cartilage (again, a sleeve fracture), and
pushed posteriorly into the intercondylar notch. Alioto and
Kates68 and Levin81 have described a vertical intraarticular
dislocation.
The mechanism of injury is probably a direct blow ini-
tially displacing the patella into the intercondylar notch;
the dissection of the patella from the extensor mecha-
nism undoubtedly occurs when the quadriceps contracts
strongly from the blow. The failure is at the chondro-osseous
junction.
Additional associated lesions should be sought with both
types of intraarticular dislocation. The quadriceps tendon
may be ruptured completely, or the patellar tendon may be
partially torn from the tibial tuberosity. Tears of the cruciate
and collateral ligaments may also occur.
Some authors believe that this type of dislocation is
secondary to rupture of the quadriceps tendon. Frangakis
described an 11-year-old boy who fell while running, striking
his left knee against the edge of a step.76 In this case the
quadriceps tendon was intact and there was associated
ligamentous laxity. Frangakis thought that a ruptured
quadriceps tendon, although it may occur, was by no
means necessary for this type of dislocation to manifest in a
child.
Closed reduction is generally not effective. Open reduc-
tion should be the primary procedure, if only to inspect the
extent of injury and repair both soft tissue and chondro-
osseous damage.
941
Habitual Dislocation
As for the shoulder, certain children become habitual dislo-
caters of the patella. These children have frequent displace-
ment, sometimes several times a day. Many have underlying
personality disorders (e.g., hyperactive behavior, attention
deficit syndrome) and may repetitively dislocate the joint to
get someone’s attention. These patients rarely have soft
tissue or chondro-osseous disruption as in the patient who
has an acute traumatic dislocation. Instead, they attenuate
medial retinacular tissues and contract lateral retinacular
tissues.
Treatment may be difficult. Obviously, treatment of any
behavioral problem to try to decrease the “need” to demon-
strate dislocatibility is necessary. Muscle strengthening and
orthotics are minimally effective. In fact, the behavioral
problem is likely to make the child inattentive to the thera-
pist’s efforts. Lateral retinacular release (arthroscopic) with
or without vastus medialis advancement is usually necessary.
Dabezies and Schutte reported a 2-year-old with chronic
habitual dislocation of the patella in whom there was a sig-
nificant contracture of the iliotibial band (probably con-
genital) that was divided along with advancement of the
vastus medialis muscle.96 I have encountered significant
iliotibial band thickening in children with hypoplasia of the
femur along with the characteristic lateral condylar hypopla-
sia. Surgical release was necessary in most cases to correct
patellar maltracking that became increasingly problematic
during the limb lengthening process.
Chronic Subluxation
Chronic subluxation of the patella is a common knee disor-
der, especially in adolescent girls.92,94,99,101,102,110 A significant
number of subluxations and recurrent dislocations of the
patella in the young child or adolescent are associated with
a congenital or developmental deficiency of the extensor
mechanism, the femoral condyles, or the shape of the patella
and femoral notch (groove).97,98 Such deficiencies of the
942
extensor mechanism may be divided into three categories:
(1) abnormalities of patellofemoral configuration; (2) defi-
ciencies of the supporting muscles or guiding mechanism;
and (3) malalignment of the extremity relative to knee
mechanics. Often deficiencies in more than one category
contribute to patellar instability.95 Wiberg and Baumgartl
have described various types of patella based on relative
degrees of sloping of the medial and lateral articular facets
in the sunrise view.114 Such measurements are variably applic-
able to the incompletely ossified patella. Transverse MRI
views may allow such measurement of the unossified carti-
lage.111 Weakness of the anteromedial retinaculum, dystro-
phy or weakness of the vastus medialis obliquus muscle, and
hypermobility of the patella due to poor muscle tone also
constitute predisposing factors. Genu recurvatum may cause
laxity of the extensor mechanism. Patella alta and tightness
of the lateral retinaculum also predispose the patella to sub-
luxation or dislocation.
Posttraumatic tightness in the lateral rectinaculum may
lead to chronic subluxation following an acute patellar dis-
location. This probably occurs because of the medial soft
tissue disruption.
Moller et al. induced chondromalacia in rabbits by surgi-
cal patellar subluxation.106 The experiment included 20
immature and 20 mature rabbits. The tibial tuberosity was
laterally displaced. At 6 weeks after surgery all the nonoper-
ated knees appeared microscopically normal. Histologically,
cartilage degeneration was evident on the experimental side.
By 3 months macroscopic changes were evident in 5 of the
10 mature rabbits but not in the immature rabbits. Moller et al.
thought that this model suggested the importance of mal-
alignment in the development of patellofemoral cartilage
degeneration. The initial lesion of the cartilage was primar-
ily a change in the ground substance of the intermittent
zones, alone or in association with surface defibrillation.
Alteration of glycosaminoglycans may occur in knees during
experimental femoral lengthening. Altered mechanics due
to subluxation may change joint reaction forces sufficiently
to affect the matrix, creating molecular and cellular
changes that alter the consistency of the cartilage, begin-
ning the cycle of softening and breakdown consistent with
chondromalacia.
Early changes in chondromalacia patella may heal by car-
tilaginous or fibrous metaplasia, which may account for the
resolution of clinical symptoms.93 In view of findings of the
response of cartilage cells to increased pressure with disso-
lution of cartilage matrix to excessive pressure (see Chapter
1), simple surgical procedures, such as lateral retinacular
release to decrease pressure, may be effective prior to skele-
tal maturity.
Symptoms may be vague. Chronic patellar instability is fre-
quently confused with meniscal injury and certainly should
be considered in all patients with relatively nonspecific knee
complaints. Limited use of the knee in these painful stages
may lead to chondromalacia.
The patella may forcefully reduce if it has been partially
displaced onto the lateral condyle and cause injury to
the medial patellar articular surface or intercondylar
region of the medial femoral condyle. Damage may also be
intratrabecular (i.e., bone bruising), which could affect
the physiology of the deeper layers of unossified hyaline
cartilage.
22. Knee
Thompson et al., in a study of injuries to the
patellofemoral joint after acute transarticular loading, found
significant changes in the subchondral bone when a fracture
was not identifiable on conventional radiographs.112 They
further found that under certain conditions there was a
potential for repair of the histopathologic abnormalities and
restoration of normality to the articular cartilage and sub-
chondral bone.
Diagnosis is usually by history, as the patella is rarely com-
pletely displaced. Maltracking may be evident on physical
examination. It is more important, as suggested by Yates and
Grana,32 to base the diagnosis of patellofemoral pain on a
precise history and physical examination rather than relying
on the radiographic appearance and measurements.
The primary difficulty when treating patellofemoral pain
syndrome in children has been the inability to translate dis-
tinct problems recognized during the physical examination
into a specific clinical classification. Yates and Grana used a
classification system based on etiology rather than symptoms
and thought it was a better guide for treatment.32 They
believed that most patellofemoral pain in children was
caused by trauma or malalignment syndromes (or a combi-
nation of the two) and could usually be managed success-
fully with nonoperative methods. The classification of
patellar disorders proposed by Merchant104 is a clinically rel-
evant system that helps the clinician categorize complaints
and physical findings in a manner based on etiology. The
chondromalacic lesion seen in a young patient as a result of
trauma usually is associated with flaps, chondral separations,
or osteochondral fractures, in contrast to the soft fibrillated
lesions seen in adults.
Roentgenograms may show patellar deformation and a
less prominent lateral femoral condyle (Fig. 22-19). The
radiographic diagnosis is sometimes subtle and difficult in
young children or adolescents. Anteroposterior views are not
particularly remarkable. A lateral view obtained with the
knee at 30° to assess certain relations has resulted in the
concept of the line of Blumensaat.114 Insall and Salvati also
described the length of patella to length of tendon ratio.100
However, these assessments require a completely ossified patella and
tibial tuberosity; otherwise they are inaccurate. Similarly, tangen-
tial views such as the Hughston view require almost complete
ossification of the femoral condyles and patella to create
accurate lines.
Reikeras and Hoiseth measured the relations of the
patellofemoral joint with a knee in extension in 43 normal
adults.109 They did not find any significant differences
between men and women. They noted that CT scans of the
upper and lower halves of the patellofemoral joint showed
variations in the sulcus angle, the congruence angle, and
the lateral patellar angle. They found that individual varia-
tions were great, especially for the congruence angle, and
that there were variations apparent in the patellofemoral
relations from the proximal to the distal parts of the
joint that may be reflected in different degrees of knee
flexion. However, it must be remembered that these mea-
surements in still ossifying femoral condyles and patellas in
a skeletally immature child or adolescent may be misleading
if they are treated as arbitrary measurements. Ando et al.
described a method using CT scans to measure the rectus
femoris/patellar tendon Q-angle compared with conven-
tional methods.91
Chronic Subluxation
A congruence angles; adults did not exhibit a similar change.
B releases in 33 adolescent patients and analyzed 24 of these
C
FIGURE 22-19. (A) Sunrise view of patellar subluxation. (B) CT
scan. (C) MRI. Note the “short” lateral retinaculum and the atten-
uated medial tissues.
Nietosvaara and Aalto used ultrasonography to evaluate
patellar tracking and found significant changes of mal-
tracking in early flexion as a predisposing factor to patellar
subluxation and dislocation, especially when compared
with normal knees.107 The Q-angle was wider and the
patellar position more lateral and proximal than in the
normal knee.
Initial treatment is immobilization when the patient is
acutely symptomatic and a rigorous exercise program subse-
quently. Failure of conservative therapy should lead to con-
sideration of surgery.113
943
O’Neill et al. studied 30 patients, including 13 skeletally
immature patients, in a prospective study designed to evalu-
ate the effect of isometric quadriceps strengthening exer-
cises on the patellofemoral pain syndrome.108 Each of these
patients had an anatomically normal knee with no history of
trauma. The authors found that an equal number of skele-
tally immature patients and adults had a decrease in peri-
patellar pain. However, 5 of 17 adults had to limit their
physical activities, whereas no adolescent patient had to limit
activity after the exercise program. Furthermore, eight skele-
tally immature knees had a more than 5° change in their
O’Neill et al. recommended immediate inception of an iso-
metric progressive resistance quadriceps program with ilio-
tibial band and hamstring stretching exercises to alleviate
the patellofemoral pain syndrome. Two of the skeletally
immature girls required arthroscopic lateral releases after 6
months of exercise therapy. Patellar bracing and antiinflam-
matory medications had failed to lessen the pain. One
patient did not experience a decrease in the pain after the
release. Long-term compliance with an exercise program was
the major problem.
Micheli and Stanitski performed 41 lateral retinacular
patients 8–16 months after surgery.105 None of these patients
had undergone surgery until they had had a minimum of 3
months of supervised nonoperative management emphasiz-
ing flexibility and static strengthening of the quadriceps and
hamstrings. The authors found that lateral knee retinacular
release did not interfere with the permanent alignment of
the extensor mechanism in the skeletally immature individ-
ual and recommended the procedure for patients who do
not have evidence of significant patellar malalignment, who
are skeletally immature, and who fail a supervised, consci-
entious preoperative therapeutic program.
Lefort et al. described 93 knees in 74 children and ado-
lescents, ranging in age between 9 and 20 years who were
operated on because of patellofemoral instability.103 In 76
knees there was intractable patellofemoral pain, and in 17
cases there had been one or more episodes of patellar dis-
location. All patients had been subjected to rigorous physi-
cal therapy that had failed. In 14 instances a vastus medialis
advancement was performed coupled with lateral retinacu-
lar release; in 71 knees there was transfer of the patellar lig-
ament. Altogether 85 knees were followed for an average of
6 years: 45 were completely free of symptoms; 34 had resid-
ual pain; and 6 patellas redislocated. The authors believed
that patellar tendon realignment was more effective than
vastus medialis transfer.
Bonnard et al. described translation of the medial third of
the patellar tendon combined with lateral retinacular release
in 16 patients (27 knees).94 They found that the results were
excellent in 60% and good in 20%. There was no evidence
of growth disturbance of the tibial tuberosity.
Transposition of the tibial tuberosity medially to effect
a better biomechanical axis of the patellofemoral joint is
frequently advocated for chronic patellar subluxation.
However, its use in children who have not yet attained skele-
tal maturity may be associated with premature epiphysiode-
sis of the anterior portion of the proximal tibial physis.
Rosenthal and Levine studied the effects of tibial tubercle
transplantation in skeletally immature children (16 patients
944
with 20 transplantations).258 Many of these children had neu-
romuscular disorders, with cerebral palsy being the most
common. Six had recurrent lateral dislocation of the patella.
The procedures were performed when the children were
under 11 years of age. All were treated by transplanting the
tibial tuberosity. Three patients sustained a fracture through
the operative site. Growth continued in the contiguous prox-
imal tibial epiphysis in many of these cases, with resultant
further distal “migration” of the transplanted tuberosity. In
all cases, however, the tibial tuberosity epiphysis failed to
develop normally after transplantation.
Ligaments
Ligament injury must be considered in the differential
diagnosis of any child sustaining knee trauma, even though
fractures, especially physeal injuries, are more likely
to occur.119,126,136,144,148,154,156,162,168,175,183,187 A physeal fracture
may occur in combination with a ligament injury. Congenital
ligament deficiencies may not become evident until the
child substains an acute injury.124,147 However, such deficien-
cies are usually associated with other congenital deficiencies
(e.g., anterior cruciate ligament absence in a hypoplastic
femur or fibular hemimelia). Another factor is the degree
of laxity around a joint, which is significant in young
children (Fig. 22-20) but becomes progressively less as
physeal closure is approached. Injury to the ligaments of
the knee in children less than 14 years old is uncommon,
presumably because the resilience and strength of the liga-
ments are greater than those of the chondro-osseous inter-
faces, physis, and bone. However, utilizing arthroscopy to
evaluate acute hemarthrosis reveals that ligamentous tears
probably occur more often in children than is currently
appreciated.39
Baxter assessed normal pediatric knee ligament laxity,
examining 464 normal knees in 232 children between the
FIGURE 22-20. Ligamentous laxity in a 9-year-old boy. (A) Valgus stress. (B) Accentuated recurvatum. (C) Accentuated drawer test.
Some degree of hyperlaxity is not uncommon in children.
22. Knee
ages of 7 and 14 years.118 A progressive decrease in the
absolute value of both translation and rotation laxity was
evident as the age of the child increased. Significant differ-
ences between right and left knees of the same patient were
not seen, nor did there appear to be any sex-related differ-
ence in laxity. Simple clinical testing to evaluate loose joint-
edness is believed to be of some value for identifying
children who might be at greater risk of joint injury during
competitive sports.157 Attempts to predict athletic injury rates
in children and adolesents in this fashion have produced
conflicting results.140,142 The absolute value of the measure of
translation in the anterior, posterior, and varus-valgus plane
decreased progressively from age 7 to 14 years. The transla-
tion index showed the same progressive decrease, as did rota-
tional maneuvers. Thus as the child ages, the knee ligament
laxity clearly changes. Interestingly, Baxter confirmed the
long-standing impression that the ligaments of a child who
was large for his or her age appeared to be tighter than those
in the small, aesthenic child of the same age.118 The inci-
dence of disruption of knee ligaments in the older child or
adolescent is increasing. Reasons probably relate to more
vigorous participation in athletic activities and increased
awareness of the possibility of ligamentous lesions in this age
group that has led to the increased application of diagnos-
tic modalities such as arthroscopy and MRI. The belief
that open physes invariably fail before supporting liga-
ments is not always true. When the child is undergoing phys-
iologic epiphysiodesis during adolescence, the ligaments
do increase their relative propensity to failure compared to
the physis.
Numerous factors are involved at the site of ligament
failure, including the histologic structure, attachment to
bone or cartilage, degree of chondro-osseous maturation in
the epiphysis, and physeal anatomy.167,190 The rate of strain
and the site and direction of the application of force related
to the position of the knee when the strain is applied are
important.128,167 The relation of the attachment of the col-
Ligaments
FIGURE 22-21. (A) Patient with joint injury and
avulsion of the tibial spine. (B) Stress films of both
knees showed widening of the medial joint space
(arrow) of the right knee due to a medial collateral
ligament tear. Comparision should be done
because of the normally increased ligament laxity
in children.
lateral ligaments and joint capsule to the physis influences
the site of injury.
Combinations of physeal separation and ligamentous dis-
ruption may occur (Fig. 22-21). Kennedy and Grainger
reported a 14-year-old who suffered a type 3 physeal injury
and avulsion of the anterior cruciate ligament from the tibial
spine; reduction of the physeal injury alone would not have
controlled the existing instability.153 When physeal separa-
tions are diagnosed in the adolescent, be alert to the fact that
ligamentous damage may accompany the chondro-osseous
lesion.
Bertin and Goble studied 29 cases of epiphyseal separa-
tions and found that 14 of the patients also had ligament
instability at follow-up an average of 66 months after
injury.119 Of 16 patients with distal femoral fractures, 6 had
ligament insufficiency, and 8 of 13 proximal tibial physeal
fractures had associated ligamentous injuries. These authors
concluded that a physeal fracture about the knee did not
exclude obvious or occult ligament damage and, in fact, was
associated with a high incidence of ligament injury.
Kannus and Jarvinen reviewed 32 patients who sustained
a substantial knee ligament injury during adolescence when
their knee physes were open.152 All were treated nonopera-
tively and reexamined an average of 8 years after the injury.
There were 25 partial tears and seven complete tears. After
partial tears injuries, the functional results were excellent or
good, although static instability had not improved signifi-
cantly from the initial posttraumatic examination. The long-
term results of complete injuries were poor because of
chronic functional instability, with continuous symptoms
945
and, in some, posttraumatic osteoarthritis. The poor results
from complete injuries suggest that every patient with open
physes and a complete tear of one or more ligaments should
be treated acutely or subsequently by operation.
Lipscomb and Anderson described a method of recon-
struction in adults and used their method for adolescent
patients, not noting any disturbances of growth with the graft
crossing either the tibial or the femoral physes.158 Further
clinical outcome research in this particular field is needed.
In addition, irrespective of the type of injury, it seems that
during adolescence the extent of damage to the ligaments is
the most important factor for the long-term prognosis and
that which of the specific ligaments is involved is only of
secondary importance.
In the study of Clanton et al., despite primary surgical
repair followed by 6 weeks of immobilization, some degree
of ligament laxity persisted, suggesting that such injuries in
children are analogous to ligament injuries in adults.126
Although some degree of objective knee ligament laxity may
persist, it may not be associatd with subjective symptoms of
instability. Always compare laxity to the opposite side because
of the normal laxity in children and adolescents.
Collateral Ligaments
Few patients under 14 years of age with collateral ligament
injuries have been reported.115,122,135,169,170,182 Hyndman and
Brown described 15 cases of acute knee ligament injuries in
children between the ages of 9 and 15 years.144 One of the
youngest children reported was a 4-year-old boy who sus-
946
tained an isolated traumatic rupture of the medial collateral
ligament; the site of the rupture was the midportion, rather
than the origin or insertion of the medial collateral liga-
ment.150 O’Donoghue described a 6-year-old girl in a series
of 82 patients; she was the only patient in his series less than
15 years of age.169
The initial examination must be undertaken carefully, as
it is probably the evaluation that leads to major decisions for
or against surgery. Medication may be appropriate to ensure
relaxation.
The medial structures are tested with the knee in exten-
sion and at 30° of flexion (Fig. 22-21). The examination
includes a thorough check for rotatory instability. The ante-
rior drawer sign must be sought with the knee tested in
neutral, internal, and external rotation. This sign is best
elicited by having the patient lie supine with the knee flexed
to 90°. The foot should be on the table to minimize depen-
dent stretch in the cruciate ligaments, as happens when the
knee hangs over the side of the table. Instability of the lateral
side is less common but may be more disabling. The lateral
compartment tends to be capable of a greater amount of
physiologic widening, and comparison should be made with
the contralateral uninjured side.
After standard history, physical examination, and
roentgenograms, several other diagnostic alternatives
are available to delineate the lesion.196 Aspiration of the knee
may allow a more thorough examination, especially when
a local anesthetic is instilled. Stress roentgenograms may
be obtained. Examination under anesthesia may help.
Arthroscopy is another useful tool. MRI may delineate a tear
(Fig. 22-22).
Stress roentgenograms of a relaxed patient allow accept-
able initial evaluation of potential acute instability (Fig. 22-
FIGURE 22-22. Tear of the medial collateral ligament in a 15-year-
old female gymnast following an uneven bars dismount.
22. Knee
21). Kennedy and Drainger has published guidelines for
limits of medial side widening,153 but they were for skeletally
mature individuals; great care must be taken when using
these as guidelines for children inasmuch as the normal car-
tilage space width is greater owing to incomplete ossification
of the entire epiphysis, and the child’s knee joint exhibits a
certain amount of normal laxity.
If a fracture is obvious, it is less likely that there is con-
comitant collateral ligament injury. However, if the stress
only opens the joint, an isolated ligament injury is more
probable. Look for peripheral disruption of the secondary
ossification center, which may be an extremely small
fragment (Fig. 22-23) that attaches to the ligament (sleeve
fracture concept).
Acute treatment should be conservative in the skeletally
immature individual, especially as the fragment heals to the
rest of the epiphyseal ossification center by osseous union.149
Conservative treatment consists of immobilization with the
knee in approximately 30°–40° of flexion and no weight-
bearing for 3–6 weeks. There are no certain indications for
surgical repair even in the adolescent patient. Specific sur-
gical treatment of the ligaments depends on the particular
pattern of instability.
Pellegrini-Stieda Lesion
In the adolescent a medial collateral ligament avulsion may
pull a portion of the femoral epiphysis away from the con-
tiguous ossification center. Such a fragment may be radiolu-
cent. However, the normal chondro-osseous maturation
process may lead to formation of a seemingly separate
“ossicle,” referred to as the Pellegrini-Stieda lesion (Figs.
22-24, 22-25).173,174,186,193 The lesion may be continuous with
the metaphysis or epiphysis through connective tissue. If
the lesion is tender, however, a pseudarthrosis is likely and
may require surgical exploration, fixation, or removal.
Segond Lesion
The Segond lesion is the analogue of the Pellegrini-Stieda
lesion, involving an avulsion from the lateral tibial epiph-
ysis.120,130,138,145,155 It was originally described by Segond in
1879.181 The lesion, which may be lateral or medial, is an
avulsion of a cartilaginous peripheral fragment, which may
or may not contain some of the contiguous subchondral
bone (Fig. 22-26).
Felenda and Dittel described a Segond fracture from the
lateral tibial condyle in 11 patients.134 They noted that all
patients showed additional major ligamentous damage, and
10 patients had a concomitant injury of the anterior cruci-
ate ligament along with the lateral collateral ligement. They
noted that this “harmless” lateral capsular sign should be a
warning to undertake further diagnostic measures, particu-
larly arthroscopic or MRI examination.
Cruciate Ligaments
Anterior Cruciate Ligament
Children who have nontraumatic anterior cruciate ligament
(ACL) insufficiency fall into two groups. The first group
Ligaments 947

FIGURE 22-23. (A) Avulsion of the deep portion of the

lateral collateral ligament has included an osteo-
chondral fragment (arrow) from the tibial epiphysis.
This is the site of the collateral ligament attachment.
(B) Medial osteochondral fragment (arrow) from
the distal femur. (C) These osteochondral fragment
fractures, are analogous to ligament disruption in
children and adolescents. The tibial lesion is referred
to as a Segond fracture, and the femoral lesion is
referred to as a Pellegrini-Stieda lesion.

FIGURE 22-24. Early (A) and later (B) stages of Pellegrini-Stieda

lesions.

FIGURE 22-25. Tear of the medial collateral ligament and chondro-

osseous lateral fracture, creating the equivalent of a lateral collat-
eral ligament tear.
948
FIGURE 22-26. Medial Segond lesion equivalent. Early
development.
has the laxity in conjunction with generalized joint laxity
throughout the upper and lower extremities. They usually
have a 1+ to 2+ positive anterior drawer sign bilaterally but
no associated symptomatology. Such generalized laxity must
be considered when evaluating knee injuries in children.
Examination of the opposite uninjured knee is essential to
establish a baseline for ligamentous laxity in any child. The
other group with nontraumatic insufficiency has congenital
absence of the anterior cruciate ligament, which is often
associated with other congenital abnormalities of the
extremity, such as congenital dislocation of the knee, proxi-
mal femoral focal deficiency, and fibular hemimelia. Radio-
A B
FIGURE 22-27. This 16-year-old boy sustained a femoral fracture
in an automobile accident. He was treated with an intramedullary
rod. During postoperative rehabilitation he complained of knee pain
and intermittent effusion. (A) A fragment is barely evident (arrow)
22. Knee
graphic analysis of the intercondylar eminence often shows
aplasia of the intercondylar eminence in congenital absence
of the ACL.137 Eilert reported that most knee problems in
children younger than 12 years of age are usually congenital
in origin, whereas those in children older than 12 years
are more often related to trauma.38 Similarly, in a series of
patients younger than 13 years of age who underwent knee
arthroscopy, Morrissy et al. found that only 36% had a
history of trauma.47
Complete cruciate ligament injuries are infrequent in
children.117,125,131,143,144,146,151,159,163,172,185,189,192,197 Instead, the lig-
ament usually fails at the chondro-osseous transition, which
most often affects the tibial spine (see Chapter 23) but may
also involve the femoral attachment (Fig. 22-27). Robinson
and Driscoll reported a single case in which both femoral
and tibial insertions of the ACL were avulsed as fractures.176
More recently it has been stressed that there is an associ-
ation of avulsion of the intercondylar eminence with other
ligamentous injuries to the knee in children.191 For example,
Hyndman and Brown reported seven cases of avulsion of the
tibial spine, all of which were associated with other liga-
mentous disruptions of the knee.144 Bradley et al. reported
six cases of medial collateral ligament (MCL) disruption in
children younger than 12 years of age; three of the patients
had associated ACL injuries.122 Accordingly, when an
anterior tibial spine avulsion is evident radiographically,
associated collateral knee ligamentous injuries must be
assessed. The ACL also should be assessed, either by
arthroscopy if doing a reduction or after healing if closed
treatment is used.
Clanton et al. reported nine skeletally immature
patients.126 Despite thorough initial physical and roentgeno-
graphic evaluations, the full extent of the lesions was deter-
mined only during surgery in seven of the nine patients.
The intercondylar eminence of the tibia was avulsed in five
patients, four of whom had associated collateral ligament
injuries and a positive anterior drawer sign.126 This associa-
tion in children must be emphasized. Whereas Meyers and
“within” the distal femoral ossification center. (B) MRI delineated
the femoral avulsion fragment and the damaged anterior cruciate
ligament.
Ligaments
A B
FIGURE 22-28. (A) MRI of an anterior cruciate tear in an adolescent. The tear, at arthroscopy, was in the midportion. (B) Anterior drawer
test duplication during an MRI scan.
McKeever163 noted no associated collateral ligament injuries
in children with tibial spine avulsions, Zaricznyj197 and
Hyndman and Brown144 described concomitant collateral-
cruciate damage.
Magnetic resonance imaging (Fig. 22-28) may be used
to evaluate presumptive acute ACL injury.132,177 Among 18
knees 28 osseous lesions were detected by MRI in 15 knees,
but none of them had been detected by radiography or
arthroscopy.133 These lesions can best be described as bone
bruising of various degrees and particularly were areas of
edema or hemorrhage as well as occult (i.e., undisplaced)
tibial spine fractures.
Speer et al., using MRI in patients with cruciate ligament
injuries, showed accompanying osseous injury associated
with acute tears of the ACL.184 Altogether 83% (45 of 54) of
the knees had an osseous contusion directly over the lateral
femoral condyle terminal ligament attachment. The lesion
was highly variable in size and imaging intensity, although
the most intense signal was always contiguous with the sub-
chondral plate. They reported one patient, a 14-year-old,
with an open distal femoral physis in which the superior pro-
gagation of the abnormal signal was limited by the physes.
There is general agreement that a diminished signal on
T1-weighted images and an increased signal intensity on
T2-weighted images depends on the occurrence of micro-
trabecular injury and subsequent hemorrhage and fluid
transudation at the site of the injury.
Panjabi et al. studied subfailure injury of the rabbit ACL.171
The overall strength of the ligament, however, did not
change. The shape of the load-displacement curve, espe-
cially at low loads, was significantly altered.
Aspiration of the hemarthrosis and successful closed
reduction by extension of the knee followed by immobiliza-
tion in extension have produced good results in ACL/tibial
spine injuries.179 Persistent displacement of the tibial emi-
nence following closed reduction may block knee extension
and cause knee laxity. The elevated tibial spine effectively
shortens the ACL, altering its function and strength. Laxity
949
in the anteroposterior plane increases with time owing to
stretching of the secondary capsular restraints.121 Therefore
residual displacement after an attempted closed reduction
requires anatomic reduction. Furthermore, there is no evi-
dence to suggest that knee ligaments in children have the
potential to heal any better than those in adults.128
Injury to the cruciate ligaments in children, excluding
avulsion of the tibial spine, may initiate a syndrome of cru-
ciate insufficiency when nonoperative treatment is used.
DeLee noted that posttraumatic ACL insufficiency, acute or
chronic, was unusual in children younger than 14 years.129
Details of the treatment of the avulsed tibial spine are
covered in Chapter 23.
Wasilewski and Frankl reported an 11-year follow-up of a
patient who had an osteochondral avulsion fracture of the
femoral insertion of the ACL.194 It was treated by an open
procedure. Follow-up at 11 years showed an asymptomatic
patient with a stable knee.
McCarroll et al. described 40 patients under the age of 14
with an open physis who had midsubstance tears of the
ACL.161 Sixteen were treated conservatively with rehabilita-
tion, bracing, and counseling on activity modification, and
the remaining 24 underwent arthroscopic examination and
an extraarticular or an intraarticular reconstruction based
on growth potential. The average follow-up was 26 months.
In the conservative group 6 of 16 patients subsequently
underwent arthroscopy for meniscal tears, and only 7
patients returned to sports, with all of the patients experi-
encing recurrent episodes of instability, effusions, and pain.
In the surgical group, 12 medial and 6 lateral meniscal tears
were found at arthroscopy. All 24 of the patients returned
to sports activity, and 22 of 24 were still competing. The
two remaining patients suffered reinjury 3 years after their
surgery. The authors recommended arthroscopic examina-
tion under anesthesia in a young patient with an ACL tear.
These authors specifically excluded patients with avulsion
of the intercondylar eminence or associated ligamentous
damage.
950
Perhaps the most controversial aspect of repair of an ACL
tear prior to skeletal maturity is the potential risk of distal
femoral or proximal tibial physeal damage and growth arrest
from the tunneling process, the bone plugs, or the interfer-
ence screw. The size of the usual tunnels exceeds the
size of reported experimental physeal defects that are likely
to lead to a significant transphyseal bridge. The place-
ment of a soft tissue graft (e.g., hamstring tendon) through
the tunnel probably has little effect on preventing such
bridging.
Most studies with adequate long-term follow-up show that
the results of ACL repair are similar to those attained in
young adults and are not accompanied by growth arrest that
adversely compromises skeletal maturation.116,164,195 Most
adolescents, especially athletic females, who undergo ACL
repairs are close to skeletal maturity, which minimizes the
risk of growth abnormality even if a bony bridge or complete
epiphysiodesis occurs.
Alternative methods that do not utilize transphyseal drill
holes may also be undertaken in skeletally immature
patients.123 However, these may not duplicate knee joint
mechanics as well as the tunneled graft.
The problem with any of the aforementioned methods
and studies is that very few children under 12 years of age
are included in the study cohorts. The risk of transphyseal
procedures may increase with the decreasing skeletal matu-
rity of the ACL deficient patients.
Schaefer et al. described a 4-year-old child with an ACL
injury who was followed for 11 years.180 Repair was attempted
4 months after injury. Five years later the surgical repair had
failed with evidence of complete disruption, suggesting that
these injuries and attempts at surgical repair are neither
benign nor successful in every patient.
Mylle et al. used screw fixation for ACL avulsion.165 This
screw crossed the physis and led to an anterior growth arrest
with development of recurvatum, leading the authors to
suggest a new technique with smaller screws that did not
cross the growth plate.
A B
FIGURE 22-29. Posterior cruciate ligament injuries. (A) Posterior subluxation stress film. (B) Avulsed fragment-femoral attachment. (C)
MRI showing anterior displacement of the femur.
22. Knee
Graf et al. found eight meniscal tears (four medial, four
lateral) in six patients with ACL tears.141 Of the 12 patients
in the study, 7 sustained further meniscal damage an average
of 15 months (range 7–27 months) after the initial injury.
Posterior Cruciate Ligament
The posterior cruciate ligament (PCL) originates as a broad,
flat band from the posterior portion of the proximal tibia
just distal to the physeal plate. PCL injury is much less fre-
quent than ACL injury (Fig. 22-29). Sanders et al. reported
acute insufficiency of the PCL in two children, noting that it
usually detached from the femur along with a chondral frag-
ment, whereas tibial spine/ACL injury is the more classic
presentation.178 Crawford treated two patients with avulsion
of the PCL.127 One underwent surgical repair and did well;
the other was treated nonoperatively and had unacceptable
instability. Mayer and Micheli also reported an 11-year-old
with a similar injury and result.160
Suprock and Rogers reported a 4-year-old boy who trau-
matically avulsed his PCL.188 The ligament was avulsed from
its femoral osseous attachment, along with a piece of carti-
lage. The posterior horn of the medial meniscus is often
avulsed, and there was a tear of the meniscotibial ligament.
The PCL was reattached with absorbable sutures placed
through a drill hole into the medial femoral epiphysis. It was
done fluoroscopically to avoid crossing the physes. The medi-
al meniscus and the meniscotibial ligament injuries were also
repaired. Two years later the patient had laxity of the PCL
compared to the other side, but he was asymptomatic.
Goodrich and Ballard reported a patient with a closed
right distal femoral diaphyseal fracture who also had a PCL
avulsion with a bony fragment that was not noted until the
patient was placed in traction.139 They noted that this type of
injury had been described previously.122,126,160 Clanton et al.
described two patients with PCL avulsed from the femur.126
Sanders et al. also added two cases avulsed from the femoral
origin.178
C
Patellar Fractures
Patellar Fractures
Fractures may occur when a direct blow is applied to the
patella or during displacement or relocation of a patellar
dislocation. A direct blow may cause the patella to impact
against the femoral condyles and cause a splitting fracture,
which is more likely in an adolescent than a younger
child, in whom the resilience of the primarily cartilaginous
patella usually protects it from major osseous injury. Bone
bruising or chondro-osseous separation (sleeve fracture)
may occur. A sudden, powerful contraction of the quadriceps
mechanism may cause an avulsion fracture through a
segment of the chondro-osseous margins. Fractures of the
patella must be adequately differentiated from developmen-
tal “variations,” such as a bipartite patella.220 Medial and
lateral patellar fractures may follow subluxation or, more
often, dislocation of the patella. Peterson and Stener
reported an interesting case showing that the cause of the
ectopic bone around a patella in a 12-year-old boy was due
to avulsions of the medial and lateral margins of the patella
produced by the medial and lateral longitudinal patellar
retinacula.232 They further showed that not only were these
retinacular portions of the tendons of the vastus medialis
and lateralis into the patella, they constituted a direct fibrous
connection of considerable strength between the patella and
the tibia and thus are capable of producing avulsion
fractures.
Only 1% of patellar fractures involve patients under 15
years of age.198,201,207,208,211,214,226,231,234,235,236,238,242 The youngest
reported patient is a 2-year-old child. It is common for the
diagnosis to be missed or delayed, especially if the patella is
not ossified or is minimally ossified. Ronget235 and Hallo-
peau218 both reported cases in which the diagnosis was not
made until several months after fracture.
Ray and Hendrix reviewed 185 patients who had defined
patellar fractures.233 Of the 185 there were 12 between 8 and
A B
FIGURE 22-30. (A) Anterior and posterior chondro-osseous fractures following direct impact to the knee during a fall. (B) Appearance 8
months later.
951
16 years of age, accounting for a 6.5% incidence in skeletally
immature individuals. All the young patients were male, at
an average age of 12.7 years. Sleeve fractures were the most
common type (n = 5) followed by transverse fractures (n =
4). Of the 12 cases, 10 required operative management.
Previous injury to the knee with compromised quadriceps
mechanism and function may also be a predisposing factor.
These fractures often occur in children who take part in
activities that require forceful extension of the knee with the
quadriceps contracting against resistance. There is an asso-
ciation of this type of injury with high-jumping.204,239,243 Inter-
estingly, in Houghton and Ackroyd’s series, the injury always
involved the “take off” leg, with no direct trauma to the knee
in any case.221 Chronic or acute on chronic patellar failure
may occur with certain neuromuscular diseases (e.g., cere-
bral palsy).
Roentgenograms usually define the fracture best in the
lateral projection (Figs. 22-30 to 22-33). Because of the thick-
ness of the hyaline cartilage and articular cartilage, there
may be an incomplete separation of the articular cartilagi-
nous portion of the patella, even though the patella appears
separated within the osseous portion. Elasticity of the carti-
lage allows hinging, similar to the incomplete fracture of the
lateral condyle. In rare instances the patellar tendon may
be avulsed from the tibial tuberosity, rather than a fracture
of the patella itself. Usually a small osseous fragment is
evident.199,202,209,237
Treatment of the transversely fractured patella in a child
should follow the same principles as in an adult.205,215,228,241
Undisplaced or minimally displaced fractures should be
treated by immobilization of the knee in extension in a
cylinder cast. Fractures with significant separation of the
fragments require open reduction and repair of the torn
quadriceps expansions. Circumferential fixation through the
soft tissues, rather than the patella, is less likely to disrupt
growth patterns in the patella.
FIGURE 22-31. (A, B) Incomplete and complete fractures of the midportion of the patella. (C) Undisplaced fracture of the patella. (D)
Displaced fracture (arrow) that was treated by open reduction.

FIGURE 22-32. Patellar fracture showing involvement of the inferior pole (A) and the superior pole (B). (C) Fracture of the inferior pole.

FIGURE 22-33. (A) Anteroposterior view was interpreted as a tibial spine injury. (B) However, the lateral view showed that it was an
avulsed inferior pole injury.

952
Patellar Fractures
FIGURE 22-34. Radiologic nonunion of a patellar fracture. Quadri-
ceps function was still good because the soft tissues were rea-
sonably intact. The fragments moved as a unit from flexion to
extension.
Tension band fixation of the superficial region is often suf-
ficient to restore anatomy and not cause separation at the
articular surface.200
Failure to diagnose and adequately treat these injuries may
result in an established nonunion between the superior and
inferior fragments (Fig. 22-34), although there may be suffi-
cient intrinsic healing of the quadriceps expansion to stabi-
lize the extent of separation of the fragments. Nonunion may
lead to unusual patellar morphology.210
Maguire and Canale described 66 children with patellar
fractures.227 Twenty-four had adequate long-term follow-
up with results that were good in 13, fair in 8, and poor in
3. Children with fractures of the ipsilateral femur, tibia,
or both and those with comminuted displaced fractures
had the poorest results. Altogether 40% of the fractures in
their series were incurred in motorcycle or automobile
accidents, and 13% were associated with ipsilateral fractures
of the tibia, femur, or both. Comminuted fractures were the
most common pattern in adolescents. A significant number
of the fractures were open. These data are indicative of
high-energy trauma. Open reduction and internal fixation
produced good results. No growth disturbances were noted
after the use of cerclage wires. Absorbable sutures, and/or
temporary transfixation pins may be better in a growing
child.
Stress Fracture
Dickason and Fox described a transverse stress fracture of
the patella in a child athlete.213 They noted that stress frac-
tures have been described in only three animals: thorough-
bred race horses, greyhounds, and humans.213 Such a
condition, also termed overuse syndrome, is defined as a
953
partial or complete fracture of bone due to an inability to
withstand nonviolent stress applied in a rhythmic or
repeated subthreshold manner.
Devas described three children with stress fractures of the
patella; in two there was a crack along the lateral side, and
the other case was a transverse fracture.212 These injuries
occurred during vigorous athletic activity. Devas believed
that patellar stress fractures in children were seldom severe
enough to require operative treatment. However, there may
be significant problems associated with the articular surface
of the patella that one must look for and evaluate thoroughly
before stating that it will be a normal joint. Treatment is dis-
continuation of the repetitive evocative activity.
Iwaya and Takatori reported three cases of lateral longi-
tudinal stress fractures of the patella.222 They were in young
children, and all healed with discontinuation of athletics. It
appears that this injury is due to excessive stress applied
through the vastus lateralis.232
Teitz and Harrington described two patients with patellar
stress fractures due to activities that required prolonged
isometric quadriceps contraction and relatively constant
knee flexion.240 They noted that these injuries have been
described in patients with cerebral palsy166 and in adolescent
athletes.207,212,213,219,222,239 The authors concluded that the
stress fractures occurred because of repeated bending
moments that initiated a fracture on the superficial surface
of the patella. Those whose activities require frequent knee
flexion and quadriceps use, either isotonically or in sudden
bursts, are at risk for these injuries. Children are likely to fail
at the lower pole of the patellar or the attachment of the
tendon into the tuberosity (Sinding-Larsen-Johansson or
Osgood-Schlatter lesions). Such patients presenting with
knee pain and superficial patellar tenderness should
undergo radiographic examination and possible bone scan
to identify early stress fractures of the patella before the
injuries become complete fractures.
Sleeve Fracture
A patellar injury pattern unique to children is the sleeve frac-
ture.206,217,225,234,244 The diagnosis may be missed because the
distal osseous fragment may be sufficiently small to be min-
imally detectable radiographically.221 An extensive sleeve of
cartilage may be pulled from the main body of the osseous
patella, with or without an osseous fragment from the distal
pole. The small size of the osseous fragment may belie the
actual size of the more peripheral radiolucent cartilaginous
component.
When the patellar tendon disrupts in children, it usually
does so at the upper or lower pole, rather than intersti-
tially.219,232 Although avulsion of the tibial tuberosity has been
reported, avulsion of the lower pole of the patella is more
common.218 These cases tend to occur in children partici-
pating in sporting activities that require vigorous extension
of the knee, often without proper warm-up or progressive
conditioning.
Avulsion fractures may involve any segment of the patellar
periphery, with the anatomic extent of the injury not always
appreciated on the initial diagnostic film, as minimal bone
may be present in the avulsed fragment, especially in young
patients.217 This makes the diagnosis difficult because of
954 22. Knee

FIGURE 22-35. Various types of patellar sleeve fracture.

the radiolucency of the concomitantly disrupted, unossified
peripheral cartilage that comprises the rest of the frag-
ment. These fractures separate at the interface between sub-
chondral bone and nonossified cartilage or involve this
layer of the subchondral bone along the biosusceptible
margin.
The patterns of avulsion (sleeve) fracture are classified as
follows (Fig. 22-35).
Inferior: The fragment involves the lower pole of the patella
(Figs. 22-36 to 22-39). It is usually caused by an acute
injury. A more chronic injury is the Sinding-Larsen-

A B
FIGURE 22-36. (A) Sleeve fracture in a 10-year-old. This close-up segment of the patella is nonarticular and is covered by the
view shows bone avulsion (arrows) at the chondro-osseous sepa- retropatellar fat pad.
ration interface. (B) Thin linear sleeve fracture (arrows). This
Patellar Fractures 955

FIGURE 22-37. Sleeve fracture with displacement.

FIGURE 22-38. (A) Acute sleeve fracture. (B) Extent of healing 3

months later.

FIGURE 22-39. (A) Several weeks prior to

this displaced sleeve fracture, a “normal”
radiograph was reported. (B) Five weeks
later even more ossification was evident.
It was eventually resected.
956 22. Knee

FIGURE 22-40. (A) Superior sleeve fracture (arrow). (B) Superior sleeve fracture (arrow). (C) Displaced superior sleeve fracture. This
film was obtained several weeks after the acute onset of symptoms while broad-jumping.

Johansson lesion, although it may be considered an The avulsed patellar osseous fragment, which may be only
incomplete variation of an insidious avulsion (chronic a thin piece of bone, invariably includes an important
stress injury) analgous to the Osgood-Schlatter lesion. “sleeve” of cartilage that should be accurately reduced to
Superior: The fragment involves the superior pole of the reestablish the articular surface of the patella. Houghton
patella (Figs. 22-40, 22-41). It appears to be the least and Ackroyd recommended the importance of (adequate)
common pattern.203 fixation.221 Conservative treatment with extension or hyper-
Medial: The fragment involves most of the medial margin of extension immobilization may lead to marked deformity of
the patella. The most likely mechanism is that of an acute the patella with elongation of the patella and restriction
chondral separation from the ossified patella when the of eventual knee movement. Fixation allows more rapid
bulk of the patella dislocates laterally. The cartilaginous rehabilitation.
rim stays medially with the retinaculum. This rim eventu- The diagnosis is suggested by the frequent absence of a
ally undergoes osseous transformation as a separate direct blow, a sudden giving way, severe pain in the knee, and
ossicle.
Lateral: This lesion is often described as a bipartite
patella or dorsal defect of the patella. It may be a
chronic stress lesion resulting from repetitive tensile pull
from the vastus lateralis muscle during the process of
chondro-osseous transformation. As in the accessory na-
vicular (see Chapter 24), a “congenital” bipartite patella
may become symptomatic owing to acute or repetitive
stress. It is an occult separation along the cartilage sepa-
rating the ossification centers. However, acute disruption
of the entire lateral margin, in conjunction with similar
injuries to the medial and inferior margins, has been
described.
All the margins (superior, inferior, medial, lateral) are sub-
jected to varying amounts of tensile pull through the quadri-
ceps mechanism, patellar tendon, and retinacular tissues.
The peripheral chondro-osseous transformation margin is
often radiographically irregular and may have small acces-
sory foci of ossification that are progressively incorporated
into the main center. The marginal bone is irregularly
formed and not initially mechanically adapted. Accordingly,
it is susceptible to fracture along any patellar margin, com-
parable to a physeal fracture in the metaphyseal primary
spongiosa. FIGURE 22-41. Superior pole sleeve avulsion with displacement.
Sinding-Larsen-Johansson Lesion 957

difficulty or inability to bear weight. Active extension of Sinding-Larsen-Johansson Lesion

the knee may not be possible. Frequently, a gap is palpa-
ble at the involved margin of the patella. This gap is a The Sinding-Larsen-Johansson (SLJ) lesion is comparable to
particularly valuable clinical sign, as the peripheral frag- partial separation of the tibial tuberosity (Osgood-Schlatter
ment of avulsed bone and cartilage may not be easily lesion), affecting the patella at the attachment of the patel-
detectable radiographically (Fig. 22-39). There may be an lar ligament inferiorly.216,245–252 The type of trauma is consis-
effusion. Diagnosis may be delayed, particularly if irregular tent with a chondro-osseous fatigue (stress) fracture with
ossification is interpreted as a developmental variation. The disturbance of normal ossification patterns. The patient is
avulsion becomes obvious when progressive ossification usually an active boy in the 10- to 14-year age group who com-
occurs, although reactive bone is minimal (as bone is not yet plains of pain in the knee accompanied by a limp. Bilateral
present in one of the fracture fragments), and there is symptoms are relatively common. As with the Osgood-
limited periosteum. Flexion/extension lateral films should Schlatter lesion, there may be bilateral involvement radio-
be obtained. In fact, because much of the peripheral patella graphically but only unilateral symptoms. The lesion may
is cartilage around a centripetally expanding osseous center, coexist with an Osgood-Schlatter lesion (Fig. 22-42).
perichondrium is the primary peripheral tissue until Examination shows tenderness and occasional swelling
adolescence. located at the inferior or superior pole of the patella.
No matter which margin is involved, displaced fracture Radiographs may reveal fragmentation at the inferior
may include partial to complete disruption of the quadriceps pole, or there may be anteroinferior extension on the patella
mechanism, although the disruption may not be severe (Figs. 22-43, 22-44). The inferior pole may develop an
enough to compromise function, especially after healing. overenlarged appearance comparable to the deformity seen
One of the primary purposes of exploration is to assess the in the tibial tuberosity. As with the Osgood-Schlatter lesion,
extent of involvement of the articular cartilage. The avulsed the roentgenographic appearance is not necessarily related
patellar fragment may include an important segment to the severity of the symptoms.
(sleeve) of cartilage that must be accurately reduced to estab- Kalebo et al. used ultrasonography to detect partial rup-
lish the articular surface of the patella. The superior and tures in the proximal part of the patellar ligament (jumper’s
inferior fractures in particular may involve nonarticular car- knee).247 A cone-shaped, poorly echogenic area exceeding
tilage, especially inferiorly where the region is covered by a 0.5 cm in length in the center of the patellar tendon, in com-
large retropatellar fat pad. bination with localized thickening, proved to be a reliable
Closed treatment with the knee extended is used indicator of jumper’s knee. The site of attachment of the
when minimal displacement exists. Conservative treat-
ment with immobilization may lead to deformity. Elonga-
tion of the patella and restriction of eventual knee move-
ment may occur if the extent of separation of radiolucent
cartilage is not adequately considered. Attenuation of
the inferior region on a chronic basis may lead to, or be
diagnostically confused with, a Sinding-Larsen-Johansson
lesion.
Widening of the fracture gap usually indicates a need for
surgical stabilization. Open reduction should be performed
when there is fragment displacement to minimize the poten-
tial complications of extensor lag and nonunion. Fixation
also allows more rapid rehabilitation. Jacquemier et al.
reported three patients with sleeve fractures.223 Surgical
repair was undertaken in two; transient ischemic changes
developed in both patients (one required secondary patel-
lectomy). In a third patient, not treated operatively, exten-
sive ectopic bone developed within the knee, and function
was decreased.
Despite the initial delay in the diagnosis of many of these
avulsion fractures, healing often occurs without significant
functional disability. Because the patellar ossification center
is surrounded by cartilage, much of the outer surface is
perichondrium, rather than periosteum. Ossification pro-
ceeds peripherally, but only on the anterior surface does
it reach the “edge” and become associated with a tissue
change to periosteum. Accordingly, the usual childhood
osteogenic subperiosteal callus response is minimal in these
injuries. Primary healing of trabecular bone is the mecha-
nism of repair. If minimal chondro-osseous transformation FIGURE 22-42. Asymptomatic, healing Sinding-Larsen-Johansson
exists in the avulsed fragment, this repair process may be lesion (SL, arrow) in a child who presented with tibial tuberosity
delayed. pain compatible with an Osgood-Schlatter lesion (OS, arrow).
 958
patellar ligament at the inferior pole of the patella is by far
the most common location of jumper’s knee, although other
sites have been reported. The various entities of patellar ten-
donitis, jumper’s knee, and SLJ probably represent a spec-
trum of similar pathomechanical processes.229.230
Sinding-Larsen-Johansson “disease” is a chronic traction
lesion. As with any traction “epiphysitis,” treatment is
directed at the symptoms and the probable inciting cause.
This condition should be treated with rest for a sustained
period of 3–6 weeks using extension immobilization, fol-
lowed by progressive quadriceps mechanism strengthening.
A B
22. Knee
FIGURE 22-43. Sinding-Larsen-Johansson
(SLJ) lesions (arrows) in a 9-year-old (A)
and a 13-year-old (B).
The lesion tends to be self-limited but may remain insidi-
ously active during skeletal growth. Because the involved
area is nonarticular and separated from the joint by the fat
pad, joint changes other than chondromalacia are unlikely.
Treatment of SLJ is conservative, with the symptoms
usually running a course of 2–14 months. A knee immobi-
lizer or cylinder cast is applied for 3–4 weeks in the patient
with acute or severe pain. The patient with less severe
symptoms is treated with a prescribed rehabilitation proto-
col and antiinflammatory drugs. These patients often have
tight hamstrings and relatively weak hip flexors, such that
FIGURE 22-44. (A) Delayed healing in a patient
who continued to play sports despite pain. (B)
Appearance 4 years later.
Sinding-Larsen-Johansson Lesion
FIGURE 22-45. (A) Proximal pole SLJ
lesion in a 12-year old. (B) Chronic
proximal SLJ lesion in a 14-year-old
female gymnast.
A B
stretching and strengthening of these muscle groups
becomes necessary. Cessation of the evocative activity is
essential.
Radiographic incorporation of the ossific lesion of the
anterior/inferior pole to the rest of the patella is not a pre-
requisite for activity resumption. Clinical healing with
absence of pain and tenderness is a more appropriate end-
point. This is followed by a gradual, progressive, directed
strengthening of the quadriceps-patella mechanism. The
severity of the lesion must not be underestimated on the
basis of a seemingly benign radiographic appearance.
Patients treated conservatively may develop prominence of
the patella.
The problem may persist to the end of skeletal maturity,
may lead to irregular development of the lower end of the
patella, and may even be associated with the development of
a radiographic “loose body,” although there is usually fibrous
or fibrocartilaginous continuity.
Proximal Pole Lesion
The SLJ lesion is well recognized in the distal pole of the
patella, but similar changes may occur in the proximal pole
(Fig. 22-45). The radiographic appearances result from trac-
tion exerted through the ligamentous attachments of the
quadriceps muscle into the superior edge of the patella.
The patients reported by Batten and Menelaus, ages 10
and 11, presented with anterior knee pain.245 Batten and
Menelaus thought that the lesion represented (1) an abnor-
mality of ossification of the proximal pole of the patella; (2)
avascular necrosis related to the poor blood supply of this
portion as described by Scapinelli13; or (3) the result of trac-
tion on the superior pole of the patella or a combination of
any of these possibilities.245 However, the abnormal repetitive
traction (overuse) response is the most likely explanation. In
one patient who was followed for 2 years there was restora-
959
tion of the normal trabecular pattern and only minimal alter-
ation in the contour of the bone at the end of the pathologic
process.
Association with Neuromuscular Disorders
Rosenthal and Levine reported 88 patients with spastic cere-
bral palsy and found 10 instances of variable fragmentation
of the distal pole of the patella.258 In addition, 12 knees,
including the uninvolved ones, exhibited changes in the
tibial tuberosity compatible with an Osgood-Schlatter lesion.
Excessive tension in the quadriceps mechanism, usually in
the presence of a significant knee flexion contracture,
appeared to be the cause of the lesions. Of the fragmented
patellas, four healed after hamstring release and correction
of the flexion deformity. The association between fragmen-
tation of the distal pole of the patella and cerebral palsy was
further emphasized by Kaye and Freiberger, who described
fragmentation of the patella in seven patients ranging in age
from 7 to 15 years.253 They thought that the patellar frag-
mentation was traumatic, with the flexion contractures and
spasticity causing chronic, abnormal stresses and repetitive
microtrauma (to the inferior chondro-osseous interface).
It seems feasible that this lesion is a more extensive version
of the SLJ lesion with an osteochondral or sleeve-type frac-
ture pulling away slowly as a chronic separation (Fig. 22-46).
Rosenthal and Levine supported the contention that elon-
gation of the patellar tendon and the secondarily high posi-
tion of the patella seen in spastic patients represented
adaptive changes caused by prolonged increased tension
during the phases of rapid growth, particularly in the pres-
ence of a knee flexion contracture and crouched-gait ambu-
lation.258 In their study of the results of surgical advancement
of the insertion of the patella tendon in patients with cere-
bral palsy, Roberts and Adams found one spontaneous frac-
ture of the patella in a patient who had not sustained any
 960
A B
trauma and proposed that overactivity of the quadriceps had
caused the avulsion fracture.257 If the tension in the exten-
sor mechanism in a growing child is prolonged and of suffi-
cient grade, a high-riding patella or stress fragmentation of
the distal pole of the patella or tibial tuberosity may occur,
especially in the presence of a knee flexion contracture.
Perry and coworkers showed that the quadriceps force
required to stabilize the flexed knee during stance in chil-
dren with cerebral palsy was proportional to the angle of
the knee flexion; and that for each degree of flexion, the
required force increased an average of 6%.256 Therefore a
flexion contracture of 30° may cause forces of 210% of body
weight.255
Lloyd-Roberts et al. discussed avulsion of the distal pole of
the patella in cerebral palsy as a cause of the crouched-knee
gait.254 It should be emphasized that such avulsion may occur
painlessly, although pain may subsequently develop. During
long-term follow-up it seems that these individuals are pre-
disposed to develop unusual contours of the patella and an
apparent bipartite nature that may become progressively
painful with chondromalacia, osteoarthritis, or both. When
this lesion affects the individual, there is usually pain in one
or both knees. Knee flexion increases, and the child may
support the knee with a hand. There may be acute local ten-
derness at the distal pole. Treatment with bilateral hamstring
releases or lengthening and progressive correction of the
flexion deformity by serial splints is indicated. Only two of
eight patients in the Lloyd-Roberts et al. series required
removal of the fragment. Most responded to soft tissue
flexion contracture release.
Bipartite Patella
The bipartite patella is a variation of ossification that often
must be distinguished from an acute or chronic (stress) frac-
ture,259–281 which is sometimes difficult. Theoretically, a bipar-
tite patella may be the result of a nonunited avulsion fracture
or failure of primary and accessory ossification centers to
22. Knee
FIGURE 22-46. (A) Attenuated, curvilinear
patella with inferior SLJ lesion in a child with
cerebral palsy (CP). (B) Similar CP patient with
a crouched knee gait and episodic pain. She
had an acute onset of pain while walking and
was unable to extend the knee. The inferior
pole has acutely fractured through an area
rendered chronically susceptible.
fuse. Smooth articular cartilage usually covers the area of
roentgenographic discontinuity (radiolucency) on the inner
(joint) surface.
Bipartite patellas have been anatomically grouped.276 Class
I involves the distal patellar pole, class II the lateral margin,
and class III the superolateral pole (Fig. 22-47).224 Sympto-
matic cases tend to be class III. Class I appears to be, realis-
tically, the end result of the Sinding-Larsen-Johansson lesion.
Class II seems likely to follow traumatic subluxation or dis-
location in the child or adolescent (see Sleeve Fracture,
above).
The accessory ossification center in bipartite patellae
usually appears around 12 years of age, although occasion-
ally it is seen in children as young as 8 years of age. It may
persist into adulthood. Ruggles reported an autopsy case of
a 63-year-old man with bilateral involvement.275 It is unilat-
eral in 57% of patients, and it is more common in males than
females.279
The histologic appearance of surgical and anatomic
specimens (Figs. 22-48 to 22-50) is similar to that described
in specimens of the Osgood-Schlatter lesion, a factor
strongly suggesting a chronic, chondro-osseous, tensile
failure in some patients. It is also similar to the histologic
changes reported in symptomatic patients with a tarsal
accessory navicular (see Chapter 24). One of the weakest
areas of the developing skeleton is the margin between an
FIGURE 22-47. Anatomic classification of Saupe for bipartite
patella. (I) Inferior. (II) Lateral. (III) Superolateral.
Bipartite Patella 961

FIGURE 22-48. (A) Bipartite patella

(arrows) from an 11-year-old. (B) Bipar-
tite patella (arrows) from a 14-year-old.
(C) Slab roentgenogram showing multi-
ple accessory ossification in the supero-
lateral region. (D) Slab section of bipartite
patella (arrows).

expanding ossification center and the overlying cartilage,
similar to the weakness at the physeal–metaphyseal interface.
Excessive tensile force, whether applied to the superolat-
eral patellar pole (bipartite patella), inferior patellar pole
(Sinding-Larsen-Johansson lesion), or tibial tuberosity
(Osgood-Schlatter lesion), may partially separate (avulse)
a segment of incompletely developed cartilage that eventu-
ally ossifies, thus appearing as an “accessory” or separate
region of ossification. Similar postavulsion ossification
certainly appears in the avulsed tibial spine in the skele-
tally immature patient. This bipartite fragment subse-
quently may fuse to the remainder of the ossifying patella,
or it may be separated by an area of irregular cartilage and
fibrocartilage.

A B

FIGURE 22-49. (A) Irregular ossification of a bipartite patella. Note the superolateral involvement. (B) Histology.
962
FIGURE 22-50. Lateral (A) and transverse (B) histologic sections of a bipartite patella (arrows).
Smillie thought that most bipartite patellas represented
nonunion of marginal fractures due to poor blood supply.277
However, histologic changes do not support vascular
ischemia as an etiologic factor.273
Few patients have undergone roentgenographic studies of
the patella prior to showing the bipartite patella. One patient
had a normal patella 10 weeks before injury and eventual
evidence of a bipartite patella.264 In another case a
roentgenogram obtained 5 years earlier did not show a bipar-
tite patella.260 Bourne and Bianco cited cases in which knees
that appeared normal on radiograph later developed bipar-
tite patella.261
Most patients with a bipartite patella are asymptomatic,
despite the obvious radiographic entity (Figs. 22-51, 22-52).
It is comparable to patients with Sinding-Larsen-Johansson
or Osgood-Schlatter lesions in whom the radiographic
changes often are fortuitous findings during evaluation of
the knee. However, it is becoming increasingly evident that
many patients with a bipartite patella are symptomatic (Figs.
22-53, 22-54). The pain associated with symptomatic bipar-
tite patella presents in one of two characteristic ways: (1)
gradual onset during activity (usually repetitive athletic activ-
ity); and (2) sudden onset after an acute injury. When onset
of pain is related to direct trauma, the activity tolerance is
less, and the need for treatment becomes more intense. The
cause of pain is assumed to be micromotion in the abnormal
synchondrosis. In one study the articular surface was intact
in all but two of the operated patients, and only one patient
had chondromalacia.281
Figure 22-54 shows a bipartite patella that was asympto-
matic until the patient fell acutely, striking the knee on the
ground. He developed lateral knee pain. The bipartite lesion
appeared displaced, and MRI showed focal edema/hemor-
22. Knee
rhage in the lateral condyle due to chronic impingement by
the fragment.
Direct or indirect trauma (e.g., “traction epiphysitis”) to
the interface between the main and accessory ossification
centers has been a frequent hypothesis.278,279 The cartilage
interface may weaken the patella, making a stress fracture
more likely at this site. Because cartilage has limited repair
capacity, painful nonunion develops. When extrapolating
from various studies, it appears that fewer than 2% of
patients with bipartite patellas ever have sufficient symptoms
to seek orthopaedic care.
Scapinelli analyzed the blood supply of the patella and
showed it was compromised in the upper and outer lateral
quadrants. This may account for the poor healing and ten-
dency to form a superolateral bipartite defect or even not
healing after acute or repetitive trauma.13
Weaver studied 21 cases of bipartite patalla. The most
common physical finding was localized tenderness over the
superolateral pole.281 All the patients were athletes and expe-
rienced a gradual onset of pain while training or an onset of
symptoms after a defined injury. Those patients with a trau-
matic onset had a much lower activity tolerance and were less
likely to be managed nonoperatively.
Todd and McCally suggested that direct or indirect trauma
to the interface between the main and accessory ossifications
could render the area symptomatic.278 Benedetti and Canapa
thought that repetitive microtrauma to the zone of inter-
posed cartilage was responsible for the changes of frag-
mented fibrocartilage calcification and necrosis.260
A technetium bone scan may be helpful in rendering a
diagnosis of a chronic stress fracture (Fig. 22-55). When
using a bone scan, the lateral view is important. Normally
there is increased activity at the physeal–metaphyseal junc-
Bipartite Patella 963

FIGURE 22-51. (A) Patient with bilateral inferior bipartite patellas. (B) Patient was treated for 4 weeks with cylinder cast immobilization.
The “bipartite” patella was healing. (C, D) Anteroposterior views of superolateral bipartite patellas.

tion of the distal femur. The superolateral pole may overlie
this region, such that normal uptake of the femur would
obscure abnormal uptake of the patellar pole. The lateral
view removes such overlap.
Initial treatment consists of immobilization for 3–4 weeks
in a knee brace, knee immobilizer, or a cylinder cast.
The next step is progressive muscle rehabilitation and
strengthening.
Echeverria and Bersani showed that acute fracture of the
superolateral patella clinically and radiographically simu-
lated a symptomatic bipartite patella.264 The ability to differ-
entiate between symptomatic bipartite patella and an acute
fracture has therapeutic implications. A minimally displaced
acute fracture would be expected to heal uneventfully if
immobilized in a cylinder cast. However, if the fracture was
mistaken for a bipartite patella and isometric or isotonic

FIGURE 22-52. Bilateral bipartite patellas in an

asymptomatic patient.
964 22. Knee

A B
FIGURE 22-53. (A, B) MRI views of a bipartite patella.

exercises are initiated, it is theoretically possible that a
fibrous nonunion could result.
Excision of the painful, tender accessory ossification
center that fails to respond to initial nonsurgical treatment
is recommended. The accessory region is often relatively
small, and its removal interferes minimally with normal func-
tion of the patellofemoral joint and quadriceps mechanism.
Larger fragments may involve significant portions of the
articular surface. Screw or pin fixation and curettage of the
cartilage between the main bulk of the patella and the acces-
sory ossification center, rather than resection, should be con-
sidered. Such treatment, however, has not been reported in
a significant number of patients. Angulation of the fragment
is another reason for excision.
Weaver described painful bipartite patella in 21 patients.
Sixteen were treated by fragment excision, three of whom
had minor residual symptoms. The three youngest patients
(10, 11, and 14 years) were treated nonsurgically.281 Halpern
and Hewitt reported improvement in a patient after excision
of the accessory ossification center.267 Similarly, Green
reported three patients, one 13 years old and two each 15
years, all of whom, because of incapacitating pain, were
treated with excision of the accessory ossification region.
Their symptoms were relieved.266
Bourne and Bianco examined 16 patients with sympto-
matic bipartite patella.261 In nine patients the pain began fol-
lowing specific trauma, and in seven the onset was insidious.
All patients had pain related to activity. The average age at
surgery was 14 years 6 months, with an average postoperative
follow-up of 7 years. Fifteen of the patients were markedly
improved; one was not. Bourne and Bianco did not note any
changes of the patellofemoral articular surfaces after frag-
ment excision. Of the 16 patients, 12 had nonoperative treat-
ment for more than 6 months prior to surgical excision.
Dorsal Defects
Dorsal defects of the patella probably have an origin similar
to that of the bipartite and multipartite patella.263,268,269,280 Van
Holsbeeck et al. thought that all of these defects represented
a stress-induced disruption of normal ossi-fication patterns,
rather than a posttraumatic subarticular cyst, and that the
initial lesion was probably a traction lesion at the insertion of
the vastus lateralis (Figs. 22-56 to 22-58).280

A B
FIGURE 22-54. (A) Bipartite patella present for 6 years in a highly competitive athlete. (B) MRI shows bone bruising from chronic impinge-
ment of a fragment.
Bipartite Patella 965

FIGURE 22-55. (A, B) “Hot” scan (arrows) of a

patient with bilateral bipartite patella radiographi-
cally, Only one side was symptomatic, as cor-
roborated by the bone scan.

FIGURE 22-56. (A) Development of bipartite

patella or dorsal defect. (B) Dorsal defect
of patella. (C) Combination of dorsal defect
and bipartite patella.
966
FIGURE 22-57. Dorsal defect of the patella. It was associated with
maltracking.
Angiography of the patella showed a lack of arterial pen-
etration from within the bone toward the cartilaginous
superolateral margin.279 Poor vascular supply combined with
stress phenomena at the insertion of a strong vastus lateralis
muscle are probably the causative mechanisms leading to
irregular ossification in this region.
The concept of plastic deformity of the cartilaginous pre-
cursor of the patella allows two possibilities: (1) a deformity
at the stage of the cartilaginous precursor, with subsequent
formation of a multipartite patella; and (2) a deformity
occurring at the stage of partial ossification of the patella, in
which a displaced fragment of cartilage is partially devascu-
larized, causing a delay in the ossification of this segment of
the patella. This delay in ossification could be identified
radiographically as a dorsal defect of the patella.
Fabellar Fracture
Dashefsky reported a 13-year-old boy who sustained a frac-
ture through the sesamoid bone behind the knee.282 This is
FIGURE 22-58. (A) Tomograph of a dorsal defect with enclosed ossification. (B) Lateral view. (C) CT scan.
22. Knee
an unusual cause for pain but certainly one that should be
considered in a knee that proves difficult to diagnose and is
associated with considerable posterior pain beyond obvious
physical signs.
Popliteus Injury
The popliteus muscle is tendinous at the origin from the
lateral side of the proximal distal femoral epiphysis. It runs
intracapsularly deep to the fibular collateral ligament but
external to the lateral meniscus. It has additional insertions
into the periphery of the lateral meniscus and the proximal
fibular epiphysis through the cruciate ligament complex.
McConkey and others283–286 have described avulsion of the
popliteus tendon. It usually follows a twisting injury of the
knee, with the development of effusion and the presence of
an osteochondral (epiphyseal sleeve) fracture in the lateral
gutter. Open reduction and internal fixation are usually
required.
Osteochondral Fractures
Osteochondral fractures of the medial or lateral femoral
condylar articular surfaces may be caused by a direct blow or
rapid lateral subluxation or dislocation of the patella, often
accompanied by spontaneous reduction.288,290,394,399,408 These
injuries may also involve the medial surface of the inter-
condylar notch, although this is commonly the site of a more
chronic lesion, osteochondritis dissecans. The fracture frag-
ment may be visualized as a loose body, although it is not
always easy to visualize it in young children. The separation
through the subchondral bone may leave a thin layer that is
difficult to visualize.
Kennedy divided these fractures into two types: (1) exoge-
nous, in which the condyle strikes an external, direct shear-
ing force; and (2) endogenous, in which there is a twisting
injury with contact between the tibia and the condyle that
causes the lesion.10 Kennedy included an additional mecha-
nism in which, because of patellar dislocation or subluxa-
tion, there is a fracture of the lateral femoral condyle. The
Osteochondritis Dissecans
FIGURE 22-59. (A, B) Lateral and anteroposterior views of a large osteochondritis fragment in a 13-year-old girl. (C) Appearance 4 years
later following operative treatment.
exogenous lesion tends to result from direct shearing
trauma, whereas the endogenous lesion tends to result from
a combination of rotatory and compression forces. In adults
a compressive or rotatory force appears to be dissipated
through the tide mark between calcified and uncalcified car-
tilage where the subchondral bone is not involved. In con-
trast, in adolescents the subchondral bone is penetrated, and
an osteochondral fracture results.
Diagnosis of these injuries is sometimes difficult.
Nonstandard projections may be misleading and suggest
the diagnosis of a loose body, when in reality the tibial
tuberosity is visualized. Because the epiphyseal regions of
the young child contain more radiolucent cartilage than
is seen during adolescence, the evaluation of suspected
internal derangement of the knee is even more difficult.
Chronic osteochondral fragmentation (osteochondritis dis-
secans) is more common than a meniscal tear in these
age groups.
The knee should be aspirated. The presence of fat glob-
ules suggests intraarticular fracture through the subchondral
plate. Treatment consists of arthroscopy or arthrotomy, eval-
uation of the loose fragment, and shaving of the sites of
origin or reinsertion and fixation (by small metallic or poly-
glycolic acid-biodegradable pins) if a large fragment is
found, particularly one that involves a joint surface (Fig. 22-
59). A small fragment may be fixed or removed, especially if
it involves a nonarticular surface. The inability to determine,
with certainty, the size of the dislodged fragment preopera-
tively, the large weight-bearing area often discovered at
operation, and the subsequent internal derangements of
the knee resulting from ignored fragments warrant this
approach. Replacement is indicated if the fragment or frag-
ments are “fresh,” if the osseous components are viable, and
if the host area is weight-bearing and surgically accessible. A
period of delay as limited as 10 days between the accident
and surgery may compromise the result because the area
begins to fill in with fibrous and fibrocartilaginous tissue,
requiring trimming of the fragments or curetting to achieve
a reasonable fit. Fixation pins should not be left protruding
into the joint, as they may provoke a synovitis, pannus for-
mation, and joint stiffness.
967
Osteochondritis Dissecans
Kennedy preferred to differentiate osteochondral fractures
from osteochondritis dissecans.10 The exact cause of the
latter lesion is not known,294,297 but it may represent a com-
bination of microtrauma and ischemic disease, as proposed
by Olsson’s studies of similar lesions in animals (see Chapter
7). Osteochondritis dissecans is seen frequently in children
during the growth spurt, particularly in children who are
taller than average.295,309
The most frequent example of this injury pattern outside
the knee is the subchondral fracture of Legg-Calvé-Perthes
disease (see Chapter 11). There may be similarities: trauma
leading to ischemia, attempted healing, and then subchon-
dral fracture in the biomechanically susceptible bone.
Large, rapidly growing animals such as the giraffe, zebra,
horse, elephant and cape buffalo may develop these lesions,
usually during the equivalent of the adolescent growth spurt
(Fig. 22-60). This is not unexpected in view of the size of the
bone and articular surface and the repetitive cutting, twist-
ing, and leaping that the knee joint is subject to during
normal activity. We have found similar osteochondritic
lesions in various other joints, including the large facet joints
of the giraffe’s cervical spine.
Green and Banks suggested that the disease starts when
both subchondral bone and contiguous trabecular bone
become ischemic.297 The cartilage remains healthy because
of synovial nutrition and continues to grow (thicken). The
necrotic bone is gradually replaced and resorbed (Fig. 22-
61). Until this occurs, osseous replacement of the thicken-
ing cartilage does not. This situation may cause loss of
mechanical subchondral support of the cartilage, with sub-
sequent softening and degeneration. Trauma, a relatively
common occurrence during adolescence, may then disrupt
the region and subsequently transform the lesion into a dis-
placed fragment (Fig. 22-62).
Injured human articular cartilage tends to disrupt along
the junction of calcified and uncalcified cartilage, leaving
the osteochondral junction undisturbed. The child and ado-
968
FIGURE 22-60. Osteochondritis in a juvenile (14-year-old) Indian
elephant. This lesion is probably present in many animal species.
The elephant is relatively unique among quadrupeds in that it walks
with an upright pelvis and extended knee.
lescent have less calcified cartilage, so tangential forces,
whether normal repetition or acute trauma, are directed to
the subchondral region.293 As in other areas of epiphyseal-
physeal cartilage, the normal failure mode is through bone
or the bone–cartilage interface, not the more resilient
cartilage.
Theories invoking trauma have suggested that there was
an impingement between the tibial spine on the lateral
(intercondylar) aspect of the medial condyle,296 which was
further supported clinically and experimentally by Smillie.277
The initial fracture the authors proposed was a subchondral
fracture with intact articular cartilage overlying the infarcted
bone, with subsequent normal use leading to eventual
motion of the fragment in its bed and final propagation of
the fracture through the articular surface. The fact that
investigators were not able to accomplish this fracture exper-
imentally in human cadavers does not necessarily rule out
the proposed mechanism as a cause, particularly as these
A B
FIGURE 22-61. MRI view of early (A, B) and chronic (C) osteochondritis dissecans.
22. Knee
studies were carried out in adult cadavers, and the relation
of articular cartilage, hyaline cartilage, and epiphyseal ossi-
fication in the developing knee may allow different anatomic
and biomechanic mechanisms.276 Forces transmitted
through the patella also have been postulated to cause sub-
chondral fractures eventuating in the dissecans lesion of the
medial femoral condyle. Support for this theory has come
from the experimental work of Aicroth.289
In contrast, others have strongly suggested ischemia to
that area of the developing ossification center, with isolation
of a necrotic fragment of bone unable to bear weight in a
proper fashion. Several authors have suggested that a sepa-
rate ossification center may exist for that position of the
medial femoral condyle typically involved with the dissecans
lesion, and that roentgenographic visualization is no more
than a representation of this normal variation in epiphyseal
growth and development.10,277 Irregularity of ossification in
this region may make certain children more susceptible.
Olsson was able to show that irregularities in the develop-
ment of the cartilage with thickening of the cartilage in the
area eventually formed a dissecans lesion.304
Henderson and Houghton thought that osteochondral
fractures are an important cause of knee morbidity in chil-
dren and contribute to delayed or failed diagnosis.299
Routine plane radiographs are often unreliable as the bony
fragment may be sufficiently small to be barely visible, even
to the most suspicious observer. If not diagnosed properly,
osteochondral fracture may give rise to pain, instability,
and locking of the knee over the short term, with subse-
quent irreparable damage and premature degeneration.
Arthroscopy and MRI can delineate these lesions, particu-
larly ones that are a chondral (minimally osseous) separation
with little epiphyseal bone attached to the cartilage
fragment.303
The increased use of MRI scans that demonstrate in-
traosseous bone bruising (accumulation of edema and hem-
orrhage) suggest that a focal injury may be more common
than we realize (Fig. 22-61). This edema may cause localized
trabecular bone cell death as a causal mechanism. The lack
of vascularity means that normal chondro-osseous transfor-
C
Osteochondritis Dissecans
FIGURE 22-62. (A) Anteroposterior view showing undisplaced osteochondritis (arrow). (B) One week later during a basketball game the
fragment displaced (arrow). It was subsequently removed.
mation cannot occur, so the cartilage focally thickens. Even-
tually the combination of changes is mechanically weak and
nonsupportive of activity. A subchondral crack begins
(as in Legge-Calvé-Perthes disease) and causes pain. If
the child continues activity the fracture may propagate, loos-
ening the fragment further and causing reactive changes
such as synovitis. Healy reported a patient with a 3-year
history of knee pain but no evidence of disease by routine
radiography. Significant osteonecrotic lesions were evident
on MRI.298
Adam et al. thought that MRI is the diagnostic method of
choice for the determination of fragment stability and is
probably the diagnostic method of choice for the early lesion
that may show up on MRI but is not evident with standard
radiography.287 Their experiments suggested that MRI may
reveal the various stages of the healing process of osteo-
chondral fragments. Furthermore, MRI gives more infor-
mation about the healing process and the viability of the
interface than does histology. They believed that clinical
studies using contrast-enhanced (e.g., gadolinium) MRI
sequences were necessary to confirm these findings. The
FIGURE 22-63. (A) Loose body (arrow) behind the patella. It was
probably a small osteochondritis dissecans fragment. The parents
refused arthroscopic removal. Eleven years later the patient pre-
969
gadolinium should be injected into the joint, rather than
intravenously, to give the best results.
Treatment for the young patient with a nondetatched
fragment should be conservative, often with no more than
restriction of symptom-producing activities. The older
patient with a detatched fragment (Fig. 22-63) is treated best
by arthroscopy or arthrotomy with excision of the fragment
and removal of joint debris.291,302,306 Fragments that involve
weight-bearing areas should be replaced and fixed.310 In
either case, the subchondral bone at the base of the
defect should be drilled to stimulate a fibroblastic-
fibrocartilaginous response.
Arthroscopy may be used to fix these lesions, running the
pin into the condyle to a subcutaneous position so that they
may be removed, if necessary, when the lesion heals. Womb-
well and Nunley showed the use of Herbert screws to provide
fixation of osteochondritis dissecans fragments under com-
pression and allow early motion.312 However, the use of
these screws is not without risk. Further collapse of the
lesion, especially if it is large, may cause loosening of the fix-
ation (Fig. 22-64). Biodegradeable pins may also be used.
sented with chronic knee pain and effusion. (B) Radiograph. (C)
MRI. The fragment was finally removed arthroscopically.
970
A B
D E
FIGURE 22-64. This 9-year-old boy presented for an evaluation of
chronic knee pain and effusion. He was otherwise normal. Subse-
quent MRI failed to reveal any spinal or spinal cord pathology. (A)
Initial presentation. There is relative radiolucency in the medial
condyle. (B) MRI, however, showed extensive medial edema and
changes with an unexpected area of penetration of the physis. (C)
Four months later the involvement is more extensive. He was
When the lesion is diagnosed before or after epiphyseal
closure and there is objective evidence of looseness of the
fragment and functional disability, the defect is best treated
by open or arthroscopic reduction and fixation of the frag-
ment until healing occurs. In knees with a long-standing
lesion in which the loose fragment has become smaller than
the crater and in which fixation and healing of the fragment
would not restore a congruous joint surface, the lesion is best
treated by excision of the fragment. Mosaic cartilage graft-
ing awaits adequate outcome studies to see if it is effective
and whether it should be applied to the young patient. Sim-
ilarly, culture and replacement of cartilage cells is an intrigu-
ing but unproved treatment for skeletally immature patients.
Plaga et al. studied the fixation of osteochondral fractures
in rabbit knees with a fibrin sealant, polydioxanone (PDS),
pins, and Kirschner wires.305 They found that all of the
animals treated with Kirschner wire fixation healed versus
22. Knee
C
treated by arthrotomy. The joint surface was relatively intact but
indented. A bone graft was inserted through a separate trans-
epiphyseal (medial) approach. (D) The large fragment was fixed
with Hebert screws. (E) Ten weeks after surgery there is collapse
and penetration of the screws. While awaiting admission for
removal of the screws, one completely dislodged and migrated. All
screws were removed. He currently has a painful knee.
86% of the PDS group and only 50% of the fibrin sealant
group.
Adam et al. assessed the stability of surgically induced
osteochondral fragments of the femoral condyle by MRI
experimentally in dogs.287 Their MR images were compared
with the histopathologic findings. They created loose and
stable fragments. With the loose fragments, a well-defined
line of high signal intensity was evident between the
fragment and the epiphysis. Histologic examination revealed
vascularized granulation tissue at the interface. Stable frag-
ments showed a similar but irregularly defined line on
MR sequences and no enhancement after injection of con-
trast medium. Histologic examination in these specimens
showed no granulation tissue at the interface but intact
bone trabeculae within the completely repaired fracture.
They thought that contrast-enhanced MRI (T1-weighted
sequence) allowed exact delineation of the line of separation
Osteochondritis Dissecans
of unstable versus stable fragments. They noted that the dif-
ference, which could not be well defined histologically, prob-
ably reflected differences of binding or distribution of
protons in the healing osteochondral fragments.
Brown et al. studied the effects of osteochondral defect
size on cartilage contact stress.292 They were full-thickness
osteochondral defects in the weight-bearing area of both
femoral condyles. The defects were progressively enlarged
from 1 mm to 7 mm. All specimens showed a tendency for
contact stress concentration at the rim of the defect, and
the contact stress distribution became progressively more
nonuniform around the defect rim as the diameter was
enlarged. They noted that these contact stress elevations at
the rim were probably insufficient to inhibit defect repair or
to cause degeneration of surrounding cartilage.
Twyman et al. studied 22 knees of patients who had osteo-
chondritis dissecans diagnosed before skeletal maturity.311
The patients were followed prospectively into middle age.
One-third of them had radiographic evidence of moderate
to severe osteoarthritis at an average follow-up of 33 years,
with only half having either a good or excellent functional
result. Osteoarthritis was more likely to occur if the defect
was large or affected the lateral femoral condyle. This
finding was in contrast to that of Linden’s retrospective study
of 23 immature knees followed for an average of 33 years in
which he believed osteochondritis dissecans in children was
rarely complicated by osteochondritis.301
A review of 83 patients with 95 involved knees followed for
2–31 years identified factors that may influence treatment
and long-term prognosis.300 Altogether 16 underwent non-
surgical treatment; 65 had surgical treatment; and 2 had
nonsurgical treatment of one knee and surgical treatment of
the other. Of the 22 knees that were treated nonsurgically,
15 were treated before and 7 after distal femoral epiphyseal
closure. Of the 73 knees that were treated surgically, 23 were
treated before epiphyseal closure and 50 after closure. A
total of 77% of the knees in the surgical group and 82% of
those in the conservatively treated group were rated excel-
A B
FIGURE 22-65. (A) Patellar osteochondritis dissecans. (B) MRI.
971
lent or good at long-term follow-up. The average scores in
both groups were higher for knees in which the osteochon-
dritic defect was small and in which treatment was under-
taken before epiphyseal closure. In the surgical cases the
results were better when the fragment healed in place,
compared to the ones in which the fragment was removed.
Hughston and coworkers concluded that when osteochon-
dritis dissecans is diagnosed before epiphyseal closure the
physical findings are often negative, and there is no func-
tional disability.300 The lesion is best treated conservatively by
continuing normal activity supplemented by quadriceps-
strengthening exercises, rather than by immobilization
and rest.
Patella
Osteochondritis of the patella has also been described.294
This lesion may involve varying areas of the medial and
lateral articular facets, with the medial articular facet being
involved more often (Figs. 22-65 to 22-67). The lesion also
tends to involve the inferior, rather than the superior, half
of the patella. Ischemic necrosis may be a major causal
factor.277 The patellar blood supply primarly enters the lower
pole and proceeds proximally.13 Thus if this lesion were
related to defects of blood supply, one would expect more
lesions in the upper pole than in the lower pole.
As discussed earlier for the femoral condyles, MRI studies
show areas of focal edema following direct blow injuries. It
is feasible that similar changes of focal ischemia ensue, even-
tually leading to microcompromise of tissue interfaces.
The indication for surgery is a loose osteochondral frag-
ment that is either partially or completely detached from the
articular surface. Excision of the affected area with drilling
of the subchondral bone usually gives good results. Loose
bodies should be removed.
Renu et al. followed 12 patients with osteochondritis dis-
secans of the patella.307 The lesion was bilateral in three
patients. All patients were initially treated conservatively,
972
with complete relief of symptoms in five. In the other seven
patients the fragments were excised and the defect was cu-
retted and drilled. At follow-up after 2–8 years, these patients
had no restriction of activities and no pain.
Open Knee Injuries
Lacerations around the knee joint should be treated with a
high degree of suspicion for penetration of an object into
the knee joint.316,317 Lacerations around the patellar tendon
may not necessarily enter the joint. Instead, they may be
totally within the fat pad around and behind the patellar
tendon and therefore extrasynovial. For any case that is sus-
picious of penetration into the knee joint, a diagnosis should
be made as accurately as possible because the joint should
be débrided and irrigated adequately to prevent infection
and serious secondary changes. If the joint has been entered
by the laceration, there frequently is air within the joint
A
FIGURE 22-67. (A, B) Apparent loose body in the knee. It was a displaced patellar osteochondral fracture fragment.
22. Knee
FIGURE 22-66. (A) Osteochondritis of the patella
(arrow) in a 13-year-old girl with bilateral involve-
ment. (B) Semiloose fragment.
(Fig. 22-68). However, there may be the appearance of an
“air” arthrogram due to an associated osteochondral fracture
with bleeding and fat from the underlying epiphyseal ossifi-
cation center. A dye (e.g., methylene blue) may be injected
into the knee joint; it usually leaks out of the laceration tract
if there is a communication into the joint.
The correct diagnosis of retained foreign bodies accom-
panying small wounds about the knee demands a high index
of suspicion. Because falls and wounds around the knee are
a common occurrence in children, especially in the 4- to 8-
year range, parents often defer medical advice, thinking that
the pain and swelling will subside and that nothing could
have entered the deep tissues or joint (see Chapter 9). Bio-
logic structures (e.g., thorns, wood) may penetrate the skin
and even the joint but may come out as the child gets up
from the ground.313–315 If the patient or parent attempts to
remove them, small pieces may break off and remain within
the joint or extracapsular tissues. Unfortunately, most of
these objects are radiolucent. If they remain in the joint they
B
Synovial Plications
FIGURE 22-68. (A) Example of intra-
capsular gas (intrasynovial). (B) Gas is
confined to the fat pad (extrasynovial).
A B
may serve as a mechanical or chemical irritant, creating a
foreign body reaction or even pyarthrosis (see also organic
foreign bodies in the foot, Chapter 24).
Any child presenting with a history suggestive of penetra-
tion of a foreign object into the knee may exhibit only
painful range of motion and joint swelling. Elevation of tem-
perature, white blood cell counts, or the erythrocyte sedi-
mentation rate may be absent. If routine roentgenograms
are negative, xerography is helpful. MRI is also helpful for
delineating soft tissue or intraarticular foreign bodies and
the surrounding areas of reactive inflammation and edema.
History and clinical examination may be entirely negative.
Following local wound care, tetanus therapy, and antibiotics
(if indicated), roentgenograms are mandatory. A knowledge
of synovial recesses and suprapatellar pouch anatomy of the
knee enables one to determine if a foreign body is lying in
or communicating with the intracapsular space. Once rec-
ognized, the intracapsular foreign body must be removed.
The desire to avoid a general anesthetic, to avoid a scar on
the knee, or fear of not being able to locate a foreign body
should not be contraindications, especially if one considers
the potential damage to articular surfaces that may occur if
the foreign body is left within the joint. Small retained frag-
ments (e.g., glass) may become “stuck” in certain regions,
such as a posterior recess, and create low grade, chronic pain
and even a localized lesion with bursal fluid.
Potential problems with intracapsular foreign bodies
include septic arthritis and osteomyelitis, mechanical trauma
to the articular cartilage, physeal trauma, and growth dis-
turbance as a result of the effects of any of the preceding on
the physis. Articular cartilage lacerations heal poorly (often
not at all) and may initiate early secondary arthritic changes.
Synovial Plications
The knee of the developing fetus is divided by thin synovial
membranes into medial and lateral compartments and a
suprapatellar pouch. The medial and lateral compartments
973
of the knee joint are separated by a membranous partition
that involutes so the knee joint becomes a single cavity.
Failure of involution may result in a plica. The incidence of
these plicae, within the general population is estimated to
be 20%.318–328
Plicae are classified as suprapatellar, mediopatellar, or
infrapatellar, according to the corresponding anatomic
regions of the knee (Fig. 22-69). Any one or combination
of these plicae may exist within a given knee. The most
common plica of clinical significance is the suprapatellar
plica, which may be subclassified into transverse, transverse
with porta, medial, and lateral. Infrequently, the entire
septum dividing the inferiorly placed medial and lateral
compartments from the suprapatellar pouch persists into
adult life as a transverse suprapatellar plica. This septum
exists with an irregularly shaped opening called the porta
(Fig. 22-70). A small remnant of this transverse septum may
persist as a medial or lateral suprapatellar plica.
The “porta” plica may create the most problems in a
growing child. The porta may effectively block fluid freely
communicating between the (lower) knee joint and the
suprapatellar pouch. The porta may also affect patello-
femoral tracking. Such a lesion may be diagnosed with
arthrography (Fig. 22-70) or MRI (Fig. 22-71). Perhaps the
worst result I have seen from this type of plica was in an 11-
year-old girl who underwent complete medial meniscectomy
for persistent joint effusion (alleged diagnosis was hyper-
mobile meniscus). The effusion recurred, and the same
surgeon removed the lateral meniscus completely. She was
referred with continuing chronic effusion. Arthrography
and arthrotomy revealed a thick porta with a 4- to 5-mm
opening, effectively dividing the knee into two compart-
ments. This undoubtedly was the cause of the effusions, and
it was resected with disappearance of effusion. Unfortu-
nately, the prospects for this girl’s knee was bleak, as she has
no menisci. At 27 years of age she has severe degenerative
osteoarthritis.
Persistence of the infrapatellar plica represents the most
common plica of the knee joint.328 It usually has a narrow
974
femoral origin in the intercondylar notch and widens as it
sweeps through the inferior joint space to attach distally to
the infrapatellar fat pad. Posteriorly, it borders but does not
necessarily attach to the anterior cruciate ligament.
Although the infrapatellar plica may be found in its entirety,
22. Knee
FIGURE 22-69. Synovial plica. These thickened
bands of tissue remain after incomplete embry-
ologic formation of the knee joint.
frequently only a fenestrated septum or series of fibrous
bands is all that remains.
Variable folds of the synovial membrane occasionally
extend from the upper tibial fringe at the infrapatellar fat
pad to the undersurface of the suprapatellar synovial plica-
FIGURE 22-70. (A, B) Plica (solid arrows) extend-
ing across the suprapatellar pouch. It caused
chronic synovitis and knee effusions for 2 years.
(C) The open arrows in (B) and (C) indicate the
communication.
Synovial Plications
FIGURE 22-71. MRI of a symptomatic suprapatellar synovial plica.
tions.320,323 Such a plica sometimes snaps back and forth over
the condyle as the knee goes from full extension to full
flexion, symptomatically duplicating the problems of a torn
anterior horn of the meniscus. Most synovial folds are con-
stantly being tensed and relaxed during joint movement.
They contain a large portion of elastic fibers to facilitate the
changing shape and length and may be detached easily con-
sequent to trauma.
Most synovial plicae are asymptomatic and are likely to
be incidental findings during arthroscopy, arthrotomy,
arthrography, and MRI. They contain elastic tissue that
allows them to slide over the femoral condyles during
flexion and extension. However, inflammation with associ-
ated edema and thickening may cause symptoms when
the plica becomes relatively inelastic as it snaps over the
femoral condyle. Trauma usually is the precipitating
cause of these inflammatory changes. The trauma may
be direct or indirect. Indirect trauma may be secondary to
other derangements within the knee. Alternatively, a symp-
tomatic plica may be associated with increased demands
made on the knee from excessive exercise or competitive or
recreational athletics. The initial inflammatory change in a
synovial plica, if not corrected, may progress to an intense
synovitis with replacement of elastic tissue by fibrous ele-
ments. Erosive changes of the articular cartilage of the knee
may ensue.
The size and the extent of the plicae depend on the
degree of reabsorption of the various communicating bands
separating the cavities.329 Part of Johnson et al.’s study was to
evaluate why plicae that had been present since birth usually
were associated with the onset of symptoms that were delayed
until adolescence.324 A discrete injury preceding the pain was
found in only 13% of the knees, which contrasted with the
975
report of Hansen and Boe322 in which there was a 50% preva-
lence of previous trauma. Many patients in the Johnson et
al.324 study had symptoms that were incurred during sports
and appeared to have been precipitated in the structured
sports activity undertaken during early adolescence. It is pos-
sible that the elasticity of the plicae diminishes with age or
that the adolescent growth spurt in some way changes a
mechanical relation between the synovial tissue and the
movement of the femoral condyle during flexion of the
knee. It is equally conceivable that the plicae do not grow
and change as readily as the rest of the knee during the ado-
lescent growth spurt.
Characteristically, the patient gives a history of trauma to
the knee by a twisting injury, followed by joint effusion and
pain. Symptoms are comparable to those of internal
derangement of the knee: snapping, instability, pain, and
swelling.
Physical examination may confirm the presence of joint
effusion. Tenderness may be elicited over the femoral
condyle or about the patella. Flexion and extension move-
ments of the knee may cause crepitation of the patella; and
at times an audible snap is heard as the plica courses over
the femoral condyle. A symptomatic plica is often palpated
as a tender band-like structure paralleling the medial border
of the patella in the suprapatellar region.
The plicae syndrome has been associated with anterior
pain as well as clicking, catching, locking, or pseudolocking
of the knee. It may mimic acute internal derangement of the
knee. Symptoms are due to the plicae bow stringing across
the femoral condyle during flexion.
Single- or double-contrast arthrography is an imaging
method for evaluating a possibile plica (Fig. 22-70). MRI also
offers a way of assessing soft tissues such as plica (Fig. 22-71).
Thickening extending from the patella, in the presence of
physical findings, should indicate a plica.
Patients presenting with symptomatic plicae are initially
treated with rest, antiinflammatory agents, and local heat fol-
lowed by muscle strengthening/stretching exercises. Young
children, whose symptoms are of short duration and most
commonly associated with repetitive trauma, generally
respond to conservative therapy. Patients whose symptoms
are of long duration may not respond to conservative
therapy and may require operative intervention. Pathologic
plica may be excised by operative arthroscopy.
Johnson et al. described 30 patients with 45 involved knees
who had a specific diagnosis of synovial plicae syndrome.324
Patients were selected for arthroscopy only if the symptoms
had continued unabated after a course of physical therapy.
Patients were randomly selected for diagnostic arthroscopy
alone or arthroscopy with division of all plicae. At the time
of follow-up, the authors noted that improvement had
occurred in only 29% of the knees in which the plicae had
not been divided, in contrast to improvement in 83% of the
patients in which the plicae had been divided. Altogether
48% of the knees that had not undergone arthroscopic divi-
sion initially were treated with a subsequent arthroscopic
operation to evaluate the plicae; 70% of these knees
improved after subsequent division of the plicae. They con-
cluded that synovial plicae of the knee are a definite cause
of anterior pain in children and adolescents and that they
respond well to division.
976
Meniscal Injuries
Meniscal injuries are uncommon in young children but
become increasingly prevalent during adolescence. Trau-
matic injury of a previously intact normal medial meniscus
in a child below the age of 10 is infrequent.330–378 Smillie
stated that his youngest patient was a 3-year-old girl.277 Volk
and Smith described a tear of the medial meniscus in a 5-
year-old boy.376 Schlonsky and Eyring reported lateral menis-
cus tears in three patients aged 4, 6, and 7 years.369 Only one
was a tear in a discoid lateral meniscus. Fairbank thought
that internal derangements of the menisci in adolescents
and children usually occurred only in congenitally abnormal
menisci.348
The average annual incidence of symptomatic meniscal
lesions in children increased from 0.7 to 2.5 per 10,000
during 1960–1965 to 2.5 per 10,000 during 1980–1985 in
Malmö, Sweden.330 Soccer was the predominant cause of the
lesions, and the increased incidence of the diagnosis was
associated with the introduction of arthroscopy rather than
any change in the extent of sports exposure.
The orthopaedist must render an accurate diagnosis by
ruling out lesions that mimic meniscal tear; confirm the tear
with arthrography, MRI, or arthroscopy; and then, if possi-
ble, define the type and extent of the tear along with other
predisposing causal factors.341,346 Only when all information
is available should any consideration of surgical removal
(partial meniscectomy) be undertaken in a skeletally imma-
ture patient.
Zaman and Leonard reported the results of meniscectomy
in 59 knees of 49 children.378 In 10 children menisci had
been removed from both knees, and in two knees both
medial and lateral menisci had been removed. The average
age at surgery was 13 years. The average length of follow-
up was 7.5 years. They found three definable groups at
follow-up. In group 1 the children were symptom-free as
young adults; this included 25 knees, 21 of which had a
definite abnormality of the meniscus. Group 2 included
those with symptoms present only during sporting activity;
there were 11 knees in this group, and there was no clear
relation between the symptoms and an abnormality of the
meniscus. In group 3 there were symptoms during normal
activity; 23 patients comprised this group, and 16 had no
abnormality of the meniscus when it was removed. The
authors stressed that in one-third of all cases the meniscus
was normal at the time of operative assessment. Despite such
a finding, the normal meniscus was removed in each
case. They stressed that meniscectomy in children was not a
benign procedure, particularly in view of the fact that long-
term radiologic changes were present in 43 of the knees, and
only 42 were symptom-free at follow-up. Only 27% had
normal radiographs at follow-up. The results in girls were
worse than in boys. A definite relation existed between poor
results and complete removal of normal menisci. Zaman and
Leonard recommended that if a normal meniscus is found
it must not be removed. Other sources of joint derangement
such as chondromalacia, patellar subluxation, or plica
syndrome should be sought as the cause of the patient’s
complaints.
22. Knee
Manzione followed 20 children and adolescence with
isolated meniscal tears for an average of 5.5 years after
surgery.360 All other ligamentous injury patients were
excluded. Sixty percent of the patients had unsatisfactory
results.
It has been suggested that meniscectomy in pediatric
patients may be followed by regeneration of a fibrocartilagi-
nous meniscus.347 Clinical studies, however, have yielded con-
flicting results. I did not find any evidence of regeneration
of meniscal tissue in 11 patients who underwent MRI studies
5–9 years after total medial or lateral meniscectomy.
The relatively high proportion of poor results, the persis-
tence of symptoms in many of the children, and the fact that
many children with a provisional diagnosis of a meniscal
lesion improve without operation underlines the need for
careful selection before advising meniscectomy in young
children. The diagnosis must be made only after careful con-
sideration, including arthroscopy. A child presenting with
symptoms of a damaged meniscus must be given a fair trial
of conservative treatment before any surgery is contem-
plated. Indications for surgery are recurrent locking of the
knee with a definite history of injury that is well documented
by arthrography, MRI, or arthroscopy.
In children complete excision is certainly not the treat-
ment of choice for torn menisci.356,362 Every effort should be
made to repair the previously normal meniscus. Patients
with small tears and with tears not causing any block to move-
ment appear to do better with nonoperative treatment.
The important contributions made by the meniscus to knee
stability and load transmission must not be forgotten.352
When the meniscal tear causes abnormal knee mechanics,
operative treatment is warranted. Increasing evidence
demonstrates that partial meniscectomy, when possible, is
the procedure of choice. In adults the concepts of menis-
cal preservation by partial meniscectomy are gaining accep-
tance owing to the decreased incidence of subsequent
degenerative joint disease and the maintenance of joint
stability.343,351,355,358,359,361,365
Surgical repair of peripheral tears is a viable alternative to
meniscectomy in selected cases. The studies concerning
changing vascularity in the meniscal periphery suggest that
repair is a feasible procedure in the young child.5 Only in
those cases in which damage to the meniscus is extensive or
totally within the body should total meniscectomy be con-
sidered in the pediatric patient.
Wroble et al. studied the long-term effects of meniscec-
tomy in children and adolescents.377 Thirty-nine patients
younger than 16 years who had been treated with a total
meniscectomy had an average follow-up of 21 years; 71% of
the patients reported pain, 68% stiffness, 54% intermittent
swelling, and 41% “giving way.” Approximately half the
patients described progression of symptoms. Only 27% were
asymptomatic, and only 10% noted significant limitations;
62% had limitations in sporting activities. Altogether 12%
underwent further knee surgery, and 90% of the patients
had abnormal roentgenograms. Wroble et al. concluded that
treatment of a torn meniscus in the child should be conser-
vative and nonoperative whenever possible. With peripheral
meniscal lesions, repair appears to provide good results and
is the treatment of choice. If a lesion is not repairable, partial
Meniscal Cyst
excision is preferable to total meniscectomy. It is axiomatic
that normal menisci not be removed, particularly the alleged
hypermobile meniscus.
Busch reviewed meniscal injuries in children.340 The most
common lesions are longitudinal (vertical) tears and periph-
eral detachments, with a posterior horn of the meniscus
being most commonly involved. Bucket handle tears typically
occur in the older teenage patients. The involvement is
fairly evenly divided between the lateral and medial
side, although series with a large number of lateral tears
typically contain greater numbers of torn lateral discoid
menisci. Spontaneous healing of meniscal tears may occur,
especially in younger patients. King described four cases with
demonstrable scarring of the periphery as a result of a
healed meniscus tear.357 This is in part due to the vascularity
of the peripheral margin of the meniscus, particularly in
the adolescent. He noted that despite the common concep-
tion that ligament injuries do not occur adolescents with
open growth plates sustain anterior cruciate ligament tears
that are difficult to recognize and that probably account for
some of the poor results after meniscal injuries. He also
pointed out that the fat pad can become abnormally fibrotic
and may contain distinct fibrous bands that may mimic a
torn meniscus.
Abdon et al. described a long-term follow-up study of total
meniscectomy in children.331 They studied 89 children at an
average of 16.8 years after surgery. Although 74% were
pleased with the outcome, only 58% had objectively satisfac-
tory results according to two scoring systems. Significantly
poor results followed lateral meniscectomy. Minor instabili-
ties were recorded in 45% of the patients and major insta-
bility in 15%.
Vangsness et al. studied 47 patients with diaphyseal frac-
tures of the femur.375 Following femoral nailing, all patients
had an examination under anesthesia followed by
arthroscopy. There were 12 medial meniscal injuries and 13
lateral meniscal injuries. Ligamentous laxity was found
977
Meniscal Cyst
Following a conservatively treated meniscal tear, a skeletally
immature patient may develop a meniscal cyst (Fig. 22-72).384
Kinura et al. described a 14-year-old boy with a cyst associ-
ated with a bucket handle tear of the medial meniscus.381
These injuries should be treated arthroscopically to
decompress the cyst and repair the capsular-meniscal defect.
Flynn and Kelly recommended excision of the cyst and the
meniscus.379 However, this was during prearthroscopic days,
and today it is more feasible to try to resect the cyst and
repair any tear. The cyst may be decompressed through the
substance of the meniscus or through a separate incision
over the cyst.
Glasgow et al. treated 69 patients with 72 cystic lateral
menisci through arthroscopic surgery.380 Meniscal tears were
observed in all patients. Their results were good to excellent
in 89% of the patients.
Mills and Henderson described 20 patients with medical
meniscal cyst in a series of almost 7500 knee arthroscopies.382
Eighty-five percent had a coexistent meniscal injury. Treat-
ment of the cyst was by direct open resection in 12 and
arthroscopic evaluation during meniscectomy in 7. They
thought that medial meniscal cysts were an important but
underdiagnosed cause of knee pain. Treatment should be
directed toward both the meniscal lesion and the cyst, which
may require direct open surgery.
Parisien reported 24 patients with meniscal cysts associ-
ated with tears of the meniscal cartilage.383 All were treated
arthroscopically with partial meniscectomy and cyst decom-
pression.
VanderWilde and Peterson described 11 patients ranging
in age from 4 to 18 years with meniscal cysts.385 They thought
that MRI was a useful tool for diagnosing the cyst (Fig.