Perspectives on Modern Orthopaedics

Use of Glucosamine and Chondroitin Sulfate

in the Management of Osteoarthritis

Andrew A. Brief, MD, Stephen G. Maurer, MD, and Paul E. Di Cesare, MD

Abstract

The goals of osteoarthritis therapy are to decrease pain and to maintain or versy surrounding their use as al-
improve joint function. The pharmacologic treatment of this condition has ternative agents in the treatment of
included the use of aspirin, acetaminophen, and nonsteroidal anti-inflammatory osteoarthritis. The recent literature
drugs. More recently, numerous studies have investigated the potential role of contains some limited evidence on
chondroprotective agents in repairing articular cartilage and decelerating the the efficacy, potential toxicity, and
degenerative process. The reports of limited clinical experience with two of long-term safety of glucosamine
these agents, glucosamine and chondroitin sulfate, as well as the accompanying and chondroitin sulfate for the
publicity in the popular media, have generated controversy. Advocates of these treatment of patients with osteo-
alternative modalities cite reports of progressive and gradual decline of joint arthritis. Health-care professionals
pain and tenderness, improved mobility, sustained improvement after drug should be familiar with that evi-
withdrawal, and a lack of significant toxicity associated with short-term use of dence and should conduct further
these agents. Critics point out that in the great majority of the relevant clinical objective evaluations of their efficacy.
trials, sample sizes were small and follow-up was short-term.
J Am Acad Orthop Surg 2001;9:71-78
Cartilage Structure and
Function
Osteoarthritis is the most prevalent The goals of osteoarthritis therapy Cartilage is composed of a complex
musculoskeletal condition: more are to decrease pain and to maintain extracellular matrix of collagen and
than 70% of the population 65 years or improve joint function. In recent elastic fibers within a hydrated gel
of age or older demonstrate radio- years, numerous studies have in- of glycosaminoglycans and proteo-
graphic evidence of this process,1 vestigated potential chondroprotec-
with an incidence approximately tive agents—substances that are
twice as high in women as in men.2 capable of increasing the anabolic
Dr. Brief is Resident, Department of Orthopaedic
Substantial patient morbidity from activity of chondrocytes while Surgery, New York University–Hospital for
pain and loss of function can be at- simultaneously suppressing the Joint Diseases, New York, NY. Dr. Maurer is
tributed to this disease. Despite the degradative effects of cytokine Resident, Department of Orthopaedic Surgery,
high prevalence of osteoarthritis, its mediators on cartilage. It has been New York University–Hospital for Joint
precise biochemical mechanisms suggested that such agents may Diseases. Dr. Di Cesare is Associate Professor of
Orthopaedic Surgery, Musculoskeletal Research
are not yet completely understood. repair articular cartilage, or at least Center, New York University–Hospital for Joint
Characteristics of osteoarthritic car- decelerate its progressive degrada- Diseases.
tilage include an increase in the tion. Among those substances that
water content and degradation of may possess chondroprotective Reprint requests: Dr. Di Cesare, Department
the extracellular matrix, including properties are chondroitin sulfate, of Orthopaedic Surgery, Musculoskeletal
alteration of the proteoglycans (e.g., glucosamine sulfate, hyaluronic Research Center, New York University–
Hospital for Joint Diseases, 301 East 17th
shorter chains and a decrease in the acid, piroxicam, tetracyclines, corti- Street, New York, NY 10003.
ratio of chondroitin to keratan sul- costeroids, and heparinoids.3 Pub-
fate). These changes predispose to licity relating to the clinical experi- Copyright 2001 by the American Academy of
progressive deterioration, with even- ence with the first two of these Orthopaedic Surgeons.
tual loss of the articular cartilage. agents has created an air of contro-

Vol 9, No 2, March/April 2001 71

Glucosamine and Chondroitin Sulfate for Osteoarthritis
glycans. This specialized network is
stabilized by means of intermolecu-
lar and intramolecular cross-links
that harness the swelling pressure
exerted by the high concentration
of negatively charged aggregates.4
This accounts for more than 98% of
the articular cartilage volume; cel-
lular components constitute the
remaining 2%. The interaction of
these matrix components imparts
the characteristic biomechanical
properties of flexibility and resis-
tance to compression of cartilage.
The collagen component of the car-
tilage matrix is relatively inert, but
the other constituents, such as pro-
teoglycans, undergo a distinct turn-
over process during which the ca-
tabolism and removal of molecules
from the extracellular matrix is in
balance with the synthesis and de-
position of new molecules.5
Proteoglycans—large macromol-
ecules consisting of multiple chains
of glycosaminoglycans and oligo-
saccharides attached to a central
protein core—provide a framework
for collagen and also bind water
and cations, forming a viscous, elas-
tic layer that lubricates and protects
cartilage. The presence of these
negatively charged aggregates im-
parts to the matrix of articular carti-
lage its strong affinity for water and
is hence the most significant factor
that contributes to the biomechani-
cal properties of cartilage. The gly-
cosaminoglycans most common in
human connective tissue include
keratan sulfate, dermatan sulfate,
heparan sulfate, chondroitin sulfate,
and hyaluronic acid. They consist
of amino sugars, which are repeat-
ing disaccharide units composed of
a hexuronic acid (D-glucuronic acid,
iduronic acid, or L-galactose) and a
hexosamine (D-glucosamine or D-
galactosamine).6
Osteoarthritis results in the pro-
gressive catabolism of cartilage
proteoglycans due to an imbalance
between synthesis and degradation.
This relative decrease in the carti-
72
lage proteoglycans alters the affinity
of the cartilage matrix for water and,
in a sense, the ability of water to
easily flow in or out of the joint sur-
face. Such structural changes in the
composition of these molecules have
been shown to have a negative im-
pact on the biomechanical proper-
ties of normal adult articular carti-
lage and synovial fluid, rendering
the articular cartilage vulnerable to
the compressive, tensile, and shear
forces that occur during normal joint
motion. Theoretically, exogenous
administration of glycosaminogly-
cans (e.g., glucosamine sulfate and
chondroitin sulfate) to chondrocytes
will ameliorate this imbalance and
restore, or at least prevent further
damage to, the articular cartilage of
osteoarthritic joints.
Glucosamine (2-amino-2-deoxy-
alpha-D-glucose) is an aminosaccha-
ride that takes part in the synthesis
of glycosaminoglycans and proteo-
glycans by chondrocytes. Glucos-
amine serves as a substrate for the
biosynthesis of chondroitin sulfate,
hyaluronic acid, and other macro-
molecules located in the cartilage
matrix. Chondroitin sulfate is a gly-
cosaminoglycan composed of a long,
unbranched polysaccharide chain of
alternating residues of sulfated or
unsulfated residues of glucuronic
acid and N-acetylgalactosamine.
Chondroitin sulfate chains are
secreted into the extracellular ma-
trix covalently bound to proteins as
proteoglycans. These chains are
components of several classes of
proteoglycans, including aggrecan
(the large-molecular-mass proteo-
glycan within articular cartilage).
These proteoglycans function to
draw water into the tissue, creating
a high osmotic pressure that causes
swelling and expansion of the ma-
trix. The load-bearing properties of
cartilage are attributable to the
compressive resilience and affinity
for water of these high-molecular-
weight compounds that fill the in-
terfibrillar collagen matrix.
Journal of the American Academy of Orthopaedic Surgeons
Pharmacology and
Pharmacokinetics
The compound glucosamine sulfate
can be derived from chitin (the sec-
ond most abundant polymer on
earth) or can be produced by syn-
thetic means. Glucosamine sulfate
is commercially available as an oral
dietary supplement, either alone or
in combination with other ingredi-
ents, including magnesium, cop-
per, zinc, selenium salts, and vita-
mins A and C. Glucosamine is also
commonly formulated with chon-
droitin sulfate. It has been safely
administered to patients with a
variety of medical conditions,
including circulatory diseases, liver
disorders, lung disease, diabetes,
and depression. 7 An injectable
form of glucosamine is available
outside the United States.
Most clinical trials utilize glu-
cosamine sulfate in oral doses of
1,500 mg daily (500 mg three times
daily). Some patients exhibit a
more rapid response with higher
amounts (dosages of up to 1 g three
times daily). Commercial products
carry dosage recommendations of
500 mg three times daily to 1,000
mg twice daily. It has been sug-
gested that individuals with peptic
ulcer disease, those taking diuretics,
and obese patients require a higher
dose of glucosamine sulfate, as they
have been noted to exhibit a below-
average response to 1,500 mg daily.
Such findings imply that dosing
recommendations should be based
on a patient’s weight.
Adverse reactions to oral glu-
cosamine are infrequent and most
often not serious, consisting pri-
marily of gastrointestinal distur-
bances that are reversed after dis-
continuation of treatment.6 Other
complaints include headache, nau-
sea and vomiting, dyspepsia, heart-
burn, constipation, abdominal pain,
edema, pain or a sensation of heavi-
ness in the legs, palpitations, ex-
haustion, and skin reaction.

Glucosamine sulfate is the most
readily available form of glucos-
amine. Glucosamine sulfate is a
small, water-soluble molecule that
is readily absorbed by the gastroin-
testinal tract (90% absorption) by
carrier-mediated transport.8 It is
not clear whether the glucosamine
sulfate molecule is absorbed in its
entirety or is degraded prior to ab-
sorption. Bioavailability in humans
after first-pass metabolism by the
liver is approximately 26% for the
oral preparation, 96% for the intra-
muscular form, and 100% for the
intravenous agent.
The actual metabolic uptake of
orally administered chondroitin
sulfate has been found to be incon-
sistent—possibly because of varia-
tion in the structure, biochemical
properties, and molecular weights
of the various preparations. Baici et
al9 investigated the impact of oral
chondroitin sulfate on the concen-
tration of glycosaminoglycans in
human serum. In that study, chon-
droitin sulfate was not absorbed
either in an intact form or as a sul-
fated oligosaccharide and did not
produce any measurable change in
the total serum concentration of
glycosaminoglycans. The authors
concluded that the theory that orally
administered chondroitin sulfate
alone offers chondroprotection is
biologically and pharmacologically
unfounded.
Morrison10 found the absorption
rate of chondroitin 4-sulfate to be
between 0% and 8%. However, in
another study, 11 when a radiola-
beled preparation of a commercial
chondroitin sulfate preparation
(Condrosulf [IBSA, Lugano, Swit-
zerland]) was administered orally to
both rats and dogs, the rate of ab-
sorption of the radioisotope was
70%, although only 8.5% of the ra-
dioactivity was associated with an
intact molecule of chondroitin sul-
fate. The same authors adminis-
tered Condrosulf to healthy human
volunteers and found both an in-
Vol 9, No 2, March/April 2001
crease in plasma concentrations of
exogenous molecules associated
with chondroitin sulfate and an
increase in hyaluronic acid and sul-
fated glycosaminoglycan content in
synovial fluid. They speculated that
this increase can be attributed, at
least in part, to exogenous chon-
droitin sulfate. Despite the structur-
al similarity between chondroitin
sulfate and heparin, there are at pres-
ent no data suggesting that chon-
droitin sulfate is relatively contra-
indicated if the patient is receiving
anticoagulation therapy.
In vitro experiments have shown
that the administration of glu-
cosamine sulfate to human chon-
drocytes in tissue culture leads to
its incorporation into glycosamino-
glycan composition as well as to the
activation of core-protein synthesis,
thus promoting proteoglycan pro-
duction.12,13 Other reports assert
that the chondroprotective action of
glucosamine is due to enhanced
synovial production of hyaluronic
acid.14 This theory proposes that
the maintenance of normal hyal-
uronic acid levels within joint spaces
may down-regulate the mechanisms
that result in cartilage degradation
and pain in patients with osteoar-
thritis.
When added to chondrocyte tis-
sue cultures, chondroitin sulfate
has been shown to (1) influence the
in vitro growth and metabolism of
glycosaminoglycans; (2) increase
total proteoglycan production by
healthy cells, and (3) inhibit the col-
lagenolytic activity of normal chon-
drocytes.15 Its mechanism of action
may be related to its role as a sub-
strate for proteoglycan synthesis.
Other authors have proposed that
the chondroprotective properties of
chondroitin sulfate and glucos-
amine sulfate are related to the sul-
fate component in both of these
compounds, as sulfur is an essential
element for the stabilization of the
extracellular matrix of connective
tissue.
Andrew A. Brief, MD, et al
The potential role of glucos-
amine as an anti-inflammatory
agent has also been investigated in
studies employing animal models.
According to Setnikar,3 the effects
of oral glucosamine are best de-
scribed as antireactive rather than
anti-inflammatory. Although glu-
cosamine does not appear to be
effective in inhibiting either cyclo-
oxygenase or proteolytic enzymes
involved in inflammation, its anti-
reactive properties are likely due to
its ability to synthesize proteogly-
cans needed for the stabilization of
cell membranes and the production
of intracellular ground substance.
Because the anti-inflammatory
mechanism of action of glucos-
amines is different from that of
nonsteroidal anti-inflammatory
drugs (NSAIDs), it is conceivable
that these two treatment modalities
may work synergistically to allevi-
ate the symptoms of osteoarthritis
in some patients. There is evidence
that glucosamine in combination
with indomethacin, piroxicam, or
diclofenac sodium decreases the
amount of NSAID needed to pro-
duce an antiexudative outcome.16
Chondroitin sulfate may also
possess some anti-inflammatory
potential. Ronca et al17 showed that
although it is less effective than
indomethacin and ibuprofen, chon-
droitin sulfate effectively inhibits
directional chemotaxis, phagocyto-
sis, and the release of lysosomal
contents characteristic of the in-
flammatory response.
Clinical Trials
Glucosamine vs Control
The majority of clinical trials per-
formed to evaluate the efficacy of
glucosamine in the treatment of os-
teoarthritis have demonstrated a
decrease in joint pain, tenderness,
and swelling and an increase in
mobility 7,18-25 (Table 1). In 1981,
D’Ambrosio et al 20 examined the
73
Glucosamine and Chondroitin Sulfate for Osteoarthritis

Table 1
Summary of Results in Glucosamine Sulfate Trials

No. of Follow-up
Author(s) Year Patients Period Complications* Results

Crolle and D’Este7 1980 30 3 wk None Overall symptom score improved by 65%
after week 1, additional improvement by
15% at week 3
Drovanti et al18 1980 80 30 d Few and minor 73.3% reduction in overall symptoms
(nausea, compared with 41.3% in placebo group;
constipation, cartilage specimens from glucosamine
heartburn) group were “smoother” and more
“orderly” than those in placebo group
Pujalte et al19 1980 20 6-8 wk No serious events Considerable alleviation of self-assessed
(dizziness in 1) degree of articular pain, tenderness, and
swelling with glucosamine
D’Ambrosio et al20 1981 30 3 wk None 58% decrease in overall symptoms
during initial week of therapy; additional
13% decline at day 21
Lopes Vaz21 1982 40 8 wk Mild (heartburn, Pain scores were lower for ibuprofen
epigastric pain, compared with placebo at week 1,
abdominal pain, lower for glucosamine compared with
nausea, headache) ibuprofen at week 8
Rovati22 1992 252 4 wk Mild (allergy Reduction in symptoms was 55% in
and GI upset) glucosamine group vs 38% in placebo
group
Müller-Fassbender 1994 199 4 wk 35% ibuprofen, Quicker response time for pain relief
et al23 6% glucosamine, with ibuprofen; ibuprofen benefits
(mild GI upset) stabilized after week 2; patients receiv-
ing glucosamine continued to improve
Reichelt et al24 1994 155 4 wk Well-tolerated Reduction in symptoms was 55% in
glucosamine group vs 33% in placebo
group
Qiu et al25 1998 178 4 wk 16% ibuprofen, At 4 weeks, both glucosamine and
6% glucosamine ibuprofen groups showed reduction
(mild sleepiness, in knee pain (57% vs 51%, respectively)
nausea, GI upset) and swelling (77% and 78%)

* GI = gastrointestinal.

efficacy of glucosamine in a ran-
domized study of 30 patients with a
history of chronic osteoarthritis.
Half received daily intramuscular
injections of 400 mg of glucosamine
sulfate for 1 week, followed by 2
weeks of oral glucosamine sulfate,
1,500 mg (500 mg three times daily).
The other half (control group) re-
ceived daily injections of antiar-
thritic medication containing piper-
azine bisiodomethylate, 100 mg;
piperazine thiosulfate, 100 mg; and
trichloro-t-butanol, 5 mg, for 1
week, followed by 2 weeks of place-
bo. There was a 58% decrease in
overall symptoms during the initial
week of therapy with injectable glu-
cosamine, followed by an additional
13% decline in overall symptoms at
day 21 (P<0.05 and P<0.01, respec-
tively). The composite scores were
markedly lower for glucosamine
compared with placebo (weeks 2
and 3), and the overall scores for
patients receiving placebo therapy
regressed to pretreatment levels by
the completion of the study. Glucos-
amine sulfate was well tolerated,
and no adverse effects were ob-

74 Journal of the American Academy of Orthopaedic Surgeons


served. The limitations of this study
included an absence of efficacy
comparisons between the routes of
administration.
Crolle and D’Este 7 found that
glucosamine sulfate caused a 65%
improvement in overall symptom
score compared with placebo ad-
ministration during week 1, fol-
lowed by an additional 15% im-
provement over the following 2
weeks (P<0.01). No appreciable ad-
verse effects were noted.
A larger, randomized, double-
blind, placebo-controlled study
was conducted in 1980 in Italy by
Drovanti et al. 18 Eighty patients
with established osteoarthritis re-
ceived either oral glucosamine sul-
fate (500 mg three times daily) or
placebo for 30 days. Those treated
with glucosamine sulfate experi-
enced a 73.3% reduction in overall
symptoms, compared with 41.3%
in the placebo group (P<0.001).
Physicians rated the results of glu-
cosamine therapy as excellent or
good in 29 of 40 patients who re-
ceived it, compared with 17 of 40
who received placebo (P<0.005).
Another prospective, double-
blind trial by Pujalte et al19 in 1980
evaluated the use of glucosamine
sulfate in 20 ambulatory patients
with osteoarthritis of the knee. Half
the patients received oral glucos-
amine sulfate, 500 mg three times
daily; the other half received placebo
for 6 to 8 weeks. There was a greater
improvement in overall composite
scores for patients who received
glucosamine sulfate than in those
given placebo (P<0.01). Further
analysis of the results revealed that
80% of the patients who received
glucosamine sulfate, but only 20%
of those who received placebo, ex-
perienced diminished or complete
resolution of joint pain and tender-
ness (P<0.01). Those who were
treated with glucosamine sulfate
encountered earlier relief of pain,
joint tenderness, and swelling than
placebo patients (P<0.01).
Vol 9, No 2, March/April 2001
The largest multicenter, ran-
domized, double-blind, placebo-
controlled parallel-group study was
performed by Rovati22 in Europe.
A total of 252 patients with osteo-
arthritis in the knee were treated
with either oral glucosamine sul-
fate (500 mg three times a day) or
placebo over a 4-week period. Of
the 241 patients who completed the
trial, 55% of those who received glu-
cosamine sulfate had a significant
reduction in symptoms, compared
with 38% who received placebo
(P<0.05).
In the multicenter, prospective,
randomized, placebo-controlled
trial reported by Reichelt et al,24 155
patients received intramuscular
injections of 400 mg of glucosamine
sulfate or 0.9% saline solution bi-
weekly for 6 weeks. Use of NSAIDs,
other analgesics, or oral corticoste-
roids was not permitted. In the 142
patients who completed the study,
there was a significant (P=0.012) dif-
ference in response rate between
patients treated with glucosamine
(55% [40 of 73]) and those treated
with placebo (33% [23 of 69]).
Chondroitin Sulfate vs Control
A number of clinical trials have
examined the effects of chondroitin
sulfate26-32 (Table 2). The most fre-
quently studied therapeutic agents
containing chondroitin sulfate are
derivative products, such as glycos-
aminoglycan polysulfate (Arteparon
[Luitpold, Munich, Germany]), ga-
lactosaminoglycan polysulfate, and
chondroitin sulfate (Condrosulf and
Structum [RobaPharm, Allschwil,
Switzerland]).
In one randomized, double-blind,
placebo-controlled clinical trial, Bucsi
and Poór30 examined the efficacy of
oral chondroitin sulfate (Condrosulf)
in 80 patients with symptomatic
osteoarthritis of the knee. Chondroi-
tin sulfate, 800 mg, or placebo was
given daily for 6 months. At the
completion of the trial, there was a
43% reduction in joint pain in the
Andrew A. Brief, MD, et al
chondroitin sulfate group, compared
with only 3% in the placebo group
(P<0.01). The chondroitin sulfate
group also exhibited significantly
greater improvement in walking
time (P<0.05), and the patients’ pain
scores improved consistently (by
15%, 24%, and 37% at months 1, 3,
and 6, respectively), while the scores
for the placebo group showed little
variation (P<0.01).
Uebelhart et al31 reported the re-
sults of a randomized, double-blind,
controlled trial involving 46 patients
with symptomatic osteoarthritis of
the knee. Chondroitin sulfate was
well tolerated and significantly di-
minished joint pain (P<0.05) and im-
proved overall mobility (P<0.001).
In Rovetta’s double-blind, placebo-
controlled study, chondroitin sul-
fate was given by 50 intramuscular
injections over 25 weeks to 40 pa-
tients with osteoarthritis in the
knee.26 A statistically significant
(P<0.01) therapeutic effect on all
symptoms of joint pain was ob-
served. Oliviero et al27 also reported
favorable effects of chondroitin sul-
fate in diminishing joint pain and
improving mobility when given
both orally and intra-articularly to
elderly patients with osteoarthritis.
In recent studies, several authors
have alleged that, in addition to
providing symptomatic relief, chon-
droitin sulfate is directly responsible
for an increase in cartilage height
and radiographic improvement of
osteoarthritic changes when com-
pared with placebo.31,32 However,
no compelling data exist as yet to
substantiate such claims.
Glucosamine Sulfate or
Chondroitin Sulfate vs NSAIDs
The efficacy and safety of glu-
cosamine sulfate for the treatment
of osteoarthritis have been com-
pared with those of NSAIDs in sev-
eral recent studies. A double-blind,
randomized trial involving 40 out-
patients with unilateral knee osteo-
arthritis compared the efficacy of
75
Glucosamine and Chondroitin Sulfate for Osteoarthritis

Table 2
Summary of Results in Chondroitin Sulfate Trials

No. of Follow-up
Author(s) Year Patients Period Complications Results

Rovetta26 1991 40 25 wk None (drug Higher therapeutic effect on all

“well tolerated”) symptoms of osteoarthritis
Oliviero et al27 1991 200 6 mo 3% “mild” Considerable improvement in both
adverse effects pain and mobility
Morreale et al28 1996 146 3 mo Few, minor NSAIDs gave prompt reduction of
clinical symptoms, but symptoms
reappeared at the end of treatment;
benefits of chondroitin sulfate appeared
later but lasted for up to 3 months after
end of treatment
Bourgeios et al29 1998 127 3 mo No major events Significant (P<0.01) reduction in joint
pain with both doses vs placebo
Bucsi and Poór30 1998 80 6 mo Few, minor (1 GI 43% reduction in joint pain vs 3% in
upset) control group
Uebelhart et al31 1998 42 1 yr None (drug Decreased joint pain and improved
“well tolerated”) overall mobility; also stabilized medial
femorotibial joint width
Verbruggen et al32 1998 119 3 yr Not documented Radiographic demonstration of decrease
in number of patients with “new” erosive
finger-joint osteoarthritis (8.8% vs 29.4%)

glucosamine sulfate and ibuprofen
over an 8-week period.21 Patients
received either glucosamine sulfate,
500 mg, or ibuprofen, 400 mg, three
times daily for 8 weeks. At week 1,
the mean pain score for the ibupro-
fen group was significantly lower
than that for the glucosamine sulfate
group (P<0.01). At week 8, the pain
score for the glucosamine sulfate
group was significantly lower than
that for the ibuprofen group (P<0.05).
Unlike the response to ibuprofen,
the response to glucosamine sulfate
continued to improve throughout the
trial period (P<0.05). The attending
physician rated the overall efficacy
as good in 8 of 18 glucosamine
sulfate–treated patients (44%) but in
only 3 of 22 ibuprofen-treated pa-
tients (14%). The limitations of this
study included small sample size
and short treatment follow-up.
Another randomized, double-
blind, parallel study compared the
efficacy of orally administered glu-
cosamine sulfate and ibuprofen in
199 patients with osteoarthritis of
the knee.23 Patients received daily
doses of ibuprofen, 1,200 mg (400
mg three times daily), or glucos-
amine sulfate 1,500 mg (500 mg
three times daily). A difference with
respect to response time was found
between the groups, with glucos-
amine requiring 2 weeks to achieve
the same degree of pain relief
achieved with ibuprofen in the first
week. As in the previously cited
study, the benefits of ibuprofen
appeared to stabilize after the first
2-week period, while patients taking
glucosamine sulfate continued to
improve in subsequent weeks. At
the end of the treatment period, it
was shown that both agents reached
a similar therapeutic level and that
there was no significant difference in
success rates between the groups:
52% for the ibuprofen group versus
48% for the glucosamine-treated
group (P = 0.67). A significant dis-
parity in the incidence of adverse
effects of the two treatments was
found, however: 35% in the ibupro-
fen group versus 6% in the glucos-
amine sulfate group (P<0.001).
A more recent study from China
was performed on 178 patients with
osteoarthritis of the knee.25 Patients
were randomized into two groups,
one treated for 4 weeks with glu-
cosamine sulfate, 1,500 mg (500 mg
three times daily), and the other
with ibuprofen, 1,200 mg (400 mg
three times daily). At 4 weeks, ad-
ministration of either glucosamine
sulfate or ibuprofen resulted in re-
duced knee pain relative to baseline

76 Journal of the American Academy of Orthopaedic Surgeons


values (by 57% and 51%, respectively)
and knee swelling (by 77% and 78%,
respectively). However, there was
no statistically significant difference
in the effectiveness of the two agents.
Glucosamine sulfate was significantly
(P = 0.01) better tolerated than ibu-
profen as measured by the incidence
of adverse drug reactions (6% in the
glucosamine sulfate group vs 16% in
the ibuprofen group).
Morreale et al 28 compared the
efficacy of chondroitin sulfate in the
treatment of knee osteoarthritis with
that of NSAIDs (diclofenac sodium).
Patients treated with NSAIDs showed
a prompt reduction in clinical symp-
toms; however, these symptoms re-
emerged soon after the discontinua-
tion of therapy. Patients treated with
chondroitin sulfate tablets, despite
having a slower initial response,
exhibited a more favorable outcome
3 months after discontinuation of
treatment.
A notable limitation of all the
aforementioned studies comparing
glucosamine sulfate or chondroitin
sulfate with NSAIDs is the absence
of a control (placebo) group.
Combination Therapy
One recent study examined the
effects of simultaneous administra-
tion of glucosamine and chondroi-
tin sulfate on osteoarthritis. 33 In
a 16-week randomized, double-
blind, placebo-controlled crossover
trial, a combination of glucosamine
hydrochloride (1,500 mg/day),
References
1. Lane NE, Thompson JM: Management
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6A):25S-30S.
2. Hawker G: Update on the epidemiol-
ogy of the rheumatic diseases. Curr
Opin Rheumatol 1997;9:90-94.
3. Setnikar I: Antireactive properties of
“chondroprotective” drugs. Int J Tissue
React 1992;14:253-261.
Vol 9, No 2, March/April 2001
chondroitin sulfate (1,200 mg/day),
and manganese ascorbate (228
mg/day) was given to 34 male sub-
jects from the US Navy diving and
special warfare community with
chronic back pain and radiographic
evidence of osteoarthritis of the
knee or low back. A summary dis-
ease score incorporated physical
examination scores, pain and func-
tional questionnaire responses, and
running times. The study demon-
strated greater effectiveness of this
combination regimen compared
with placebo in symptomatic relief
as measured by the summary dis-
ease score (−16.3% [P<0.05]), pa-
tient assessment of treatment effect
(P<0.05), and visual analog scale
for pain (−28.6% [P<0.05]). This
study neither demonstrated nor
excluded a therapeutic benefit for
this combination of drugs in the
treatment of spinal degenerative
joint disease. In the limited num-
ber of studies on combination ther-
apy, there is no suggestion of an in-
creased incidence of adverse effects
when these two agents are admin-
istered together.
Summary
Glucosamine and chondroitin sul-
fate have been widely acclaimed in
the popular press as a panacea for
the treatment of osteoarthritis.
These agents are proposed to act by
virtue of their chondroprotective
4. Sandy JD, Plaas AHK: Age-related
changes in the kinetics of release of pro-
teoglycans from normal rabbit cartilage
explants. J Orthop Res 1986;4:263-272.
5. Ilic MZ, Haynes SR, Winter GM,
Handley CJ: Kinetics of release of
aggrecan from explant cultures of
bovine cartilage from different sources
and from animals of different ages.
Acta Orthop Scand Suppl 1995;266:33-37.
6. Barclay TS, Tsourounis C, McCart GM:
Andrew A. Brief, MD, et al
properties. Thus far, the vast major-
ity of studies conducted that have
supported both glucosamine and
chondroitin sulfate for the relief of
the symptoms of osteoarthritis have
been based on clinical trials with
short-term follow-up. These stud-
ies have demonstrated a progres-
sive and gradual decline of joint
pain and tenderness, improved mo-
bility, and sustained improvement
after drug withdrawal. In addition,
there are fewer side effects when
compared with other drugs used to
treat the symptoms of osteoarthri-
tis, as well as a lack of toxicity asso-
ciated with short-term use of these
agents.
Many unanswered questions
remain surrounding their long-term
effects (whether beneficial or ad-
verse), the most effective dosage
and route, and product purity. A
well-designed prospective study of
glucosamine sulfate and chondroi-
tin sulfate demonstrating that these
agents are effective for the preven-
tion and treatment of osteoarthritis
has yet to be conducted. Such a lack
of substantial and conclusive evi-
dence underlies the refusal of the
Arthritis Foundation to support
the use of glucosamine sulfate or
chondroitin sulfate for the treatment
of osteoarthritis or any other form
of arthritis. Despite these contro-
versies, patients continue to use
such alternative forms of therapy to
alleviate the painful effects of this
prevalent disease process.
Glucosamine. Ann Pharmacother 1998;
32:574-579.
7. Crolle G, D’Este E: Glucosamine sul-
phate for the management of arthrosis:
A controlled clinical investigation.
Curr Med Res Opin 1980;7:104-109.
8. Setnikar I, Palumbo R, Canali S, Zanolo
G: Pharmacokinetics of glucosamine
in man. Arzneimittelforschung 1993;43:
1109-1113.
9. Baici A, Hörler D, Moser B, Hofer HO,
77
Glucosamine and Chondroitin Sulfate for Osteoarthritis
Fehr K, Wagenhäuser FJ: Analysis of
glycosaminoglycans in human serum
after oral administration of chondroitin
sulfate. Rheumatol Int 1992;12:81-88.
10. Morrison M: Therapeutic applications
of chondroitin-4-sulfate: Appraisal of
biological properties. Folia Angiol
1977;25:225-232.
11. Conte A, Volpi N, Palmieri L, Bahous I,
Ronca G: Biochemical and pharmaco-
kinetic aspects of oral treatment with
chondroitin sulfate. Arzneimittel-
forschung 1995;45:918-925.
12. Bassleer C, Henrotin Y, Franchimont
P: In-vitro evaluation of drugs pro-
posed as chondroprotective agents.
Int J Tissue React 1992;14:231-241.
13. Vidal y Plana RR, Bizzarri D, Rovati
AL: Articular cartilage pharmacology:
I. In vitro studies on glucosamine and
non steroidal antiinflammatory drugs.
Pharmacol Res Commun 1978;10:557-569.
14. McCarty MF: Enhanced synovial pro-
duction of hyaluronic acid may explain
rapid clinical response to high-dose
glucosamine in osteoarthritis. Med
Hypotheses 1998;50:507-510.
15. Pipitone VR: Chondroprotection with
chondroitin sulfate. Drugs Exp Clin
Res 1991;17:3-7.
16. Zupanets IA, Drogovoz SM, Bezdetko
NV, Rechkiman IE, Semenov AN: The
influence of glucosamine on the
antiexudative effect of nonsteroidal
antiinflammatory agents [Russian].
Farmakol Toksikol 1991;54:61-63.
17. Ronca F, Palmieri L, Panicucci P, Ronca
G: Anti-inflammatory activity of chon-
droitin sulfate. Osteoarthritis Cartilage
1998;6(suppl A):14-21.
18. Drovanti A, Bignamini AA, Rovati AL:
Therapeutic activity of oral glucos-
amine sulfate in osteoarthrosis: A
placebo-controlled double-blind inves-
tigation. Clin Ther 1980;3:260-272.
78
19. Pujalte JM, Llavore EP, Ylescupidez
FR: Double-blind clinical evaluation
of oral glucosamine sulphate in the
basic treatment of osteoarthrosis. Curr
Med Res Opin 1980;7:110-114.
20. D’Ambrosio E, Casa B, Bompani R,
Scali G, Scali M: Glucosamine sul-
phate: A controlled clinical investiga-
tion in arthrosis. Pharmatherapeutica
1981;2:504-508.
21. Lopes Vaz A: Double-blind clinical
evaluation of the relative efficacy of
ibuprofen and glucosamine sulphate
in the management of osteoarthrosis of
the knee in out-patients. Curr Med Res
Opin 1982;8:145-149.
22. Rovati LC: Clinical research in osteo-
arthritis: Design and results of short-
term and long-term trials with disease-
modifying drugs. Int J Tissue React
1992;14:243-251.
23. Müller-Fassbender H, Bach GL, Haase
W, Rovati L, Setnikar I: Glucosamine
sulfate compared to ibuprofen in
osteoarthritis of the knee. Osteoarthritis
Cartilage 1994;2:61-69.
24. Reichelt A, Förster KK, Fischer M,
Rovati LC, Setnikar I: Efficacy and
safety of intramuscular glucosamine
sulfate in osteoarthritis of the knee: A
randomised, placebo-controlled, dou-
ble-blind study. Arzneimittelforschung
1994;44:75-80.
25. Qiu GX, Gao SN, Giacovelli G, Rovati
L, Setnikar I: Efficacy and safety of
glucosamine sulfate versus ibuprofen
in patients with knee osteoarthritis.
Arzneimittelforschung 1998;48:469-474.
26. Rovetta G: Galactosaminoglycuron-
oglycan sulfate (Matrix) in therapy of
tibiofibular osteoarthritis of the knee.
Drugs Exp Clin Res 1991;17:53-57.
27. Oliviero U, Sorrentino GP, De Paola P,
et al: Effects of the treatment with
Matrix on elderly people with chronic
Journal of the American Academy of Orthopaedic Surgeons
articular degeneration. Drugs Exp Clin
Res 1991;17:45-51.
28. Morreale P, Manopulo R, Galati M,
Boccanera L, Saponati G, Bocchi L:
Comparison of the antiinflammatory
efficacy of chondroitin sulfate and
diclofenac sodium in patients with
knee osteoarthritis. J Rheumatol 1996;
23:1385-1391.
29. Bourgeois P, Chales G, Dehais J,
Delcambre B, Kuntz JL, Rozenberg S:
Efficacy and tolerability of chondroitin
sulfate 1200 mg/day vs chondroitin sul-
fate 3 × 400 mg/day vs placebo. Osteo-
arthritis Cartilage 1998;6(suppl A):25-30.
30. Bucsi L, Poór G: Efficacy and tolerabil-
ity of oral chondroitin sulfate as a
symptomatic slow-acting drug for
osteoarthritis (SYSADOA) in the treat-
ment of knee osteoarthritis. Osteo-
arthritis Cartilage 1998;6(suppl A):31-36.
31. Uebelhart D, Thonar EJ, Delmas PD,
Chantraine A, Vignon E: Effects of oral
chondroitin sulfate on the progression
of knee osteoarthritis: A pilot study.
Osteoarthritis Cartilage 1998;6(suppl
A):39-46.
32. Verbruggen G, Goemaere S, Veys EM:
Chondroitin sulfate: S/DMOAD (struc-
ture/disease modifying anti-osteo-
arthritis drug) in the treatment of finger
joint OA. Osteoarthritis Cartilage 1998;
6(suppl A):37-38.
33. Dettmer N: The therapeutic effect of
glycosaminoglycan polysulfate (Artep-
aron) in arthroses depending on the
mode of administration [German]. Z
Rheumatol 1979;38:163-181.
34. Leffler CT, Philippi AF, Leffler SG,
Mosure JC, Kim PD: Glucosamine,
chondroitin, and manganese ascorbate
for degenerative joint disease of the
knee or low back: A randomized, dou-
ble-blind, placebo-controlled pilot
study. Mil Med 1999;164:85-91.
 Protrusio Acetabuli: Diagnosis and Treatment

Mark T. McBride, MD, Michael P. Muldoon, CDR, MC, USN,

Richard F. Santore, MD, Robert T. Trousdale, MD, and Dennis R. Wenger, MD

Abstract

Idiopathic protrusio acetabuli is an uncommon disease process with both primary typical orientation for the joint-
idiopathic and secondary forms. It is important to consider all etiologic possibili- reaction force to be 69 degrees from
ties before evaluating treatment options. Diagnosis is made on the basis of an horizontal during the stance phase
anteroposterior radiograph of the pelvis that demonstrates a center-edge angle of gait. McCollum et al4 observed
greater than 40 degrees and medialization of the medial wall of the acetabulum that protrusio acetabuli occurs at 65
past the ilioischial line. For the skeletally immature patient, triradiate fusion degrees from the horizontal in pa-
(occasionally combined with intertrochanteric osteotomy) provides good results. tients with rheumatoid arthritis
For the young adult, valgus intertrochanteric proximal femoral osteotomy is rec- and concluded that the axis of mi-
ommended. In the older adult, this procedure may provide an acceptable result if gration was nearly the same as that
there is minimal arthritis. For patients with more advanced arthritis, total hip of the joint-reaction force during
arthroplasty with lateralization of the cup to a normal position provides a pre- stance.
dictable long-term solution.
J Am Acad Orthop Surg 2001;9:79-88
Etiology

There are a number of theories re-

Protrusio acetabuli, also known as
arthrokatadysis, was first described
by the German pathologist Otto in
1824. A translated excerpt of Otto’s
original report provides a vivid
description:
The right acetabulum protrudes into
the pelvis like half an orange . . . at
the crest corresponding to the center
of the acetabular fossa, is an irregular
circular defect, measuring one and
one-half inches . . . supplying com-
munication between the acetabulum
and abdominal cavity . . . both the
inner aspect of the acetabulum and
the head of the femur are devoid of
cartilaginous covering, and have the
abraded and polished appearance of
some gouty joints.1
Idiopathic, or primary, protrusio
acetabuli is the diagnosis reserved
for patients in whom no causative
factors can be found. It is a diagno-
sis of exclusion; as more underlying
disease states associated with this
condition are recognized, the num-
ber of diagnoses of primary protru-
sio acetabuli continues to decline. In
those cases in which an underlying
cause is identified, the term second-
ary protrusio acetabuli is used. Nu-
merous processes are now known to
cause protrusio acetabuli (Table 1).
The prevalence of the disease
process is unknown, but the natural
history of those with the condition
appears to be one of inexorable
progression of the deformity, corre-
sponding deterioration of function,
and increase in pain. This is pre-
dictable on the basis of Pauwels’
theories of hip biomechanics.2 The
major contributors to the forces
across the hip are (1) body weight,
(2) distance from the center of the
femoral head to the midline, and
(3) femoral neck-shaft angle. Using
basic newtonian statics and a free-
body diagram, one may calculate
the various vector forces acting on
the hip. Egan et al3 calculated the
garding the etiology of primary
protrusio acetabuli. Eppinger pos-
tulated that the condition was sec-
ondary to a chondrodystrophy
Dr. McBride is Resident Physician, Naval
Medical Center San Diego, San Diego, Calif.
Dr. Muldoon is Staff Physician, Naval Medical
Center San Diego. Dr. Santore is Clinical
Chairman, University of California, San Diego;
and Chief Orthopaedic Surgeon, Sharp
Memorial Hospital, San Diego. Dr. Trousdale
is Consultant, Department of Orthopedics,
Mayo Clinic, Rochester, Minn. Dr. Wenger is
Clinical Professor of Orthopaedic Surgery,
University of California, San Diego.
Reprint requests: Dr. Muldoon, Clinical
Investigation Department, Medical Editing
Division, Naval Medical Center San Diego,
Suite 5, 34800 Bob Wilson Drive, San Diego,
CA 92134-1005.
Copyright 2001 by the American Academy of
Orthopaedic Surgeons.

Vol 9, No 2, March/April 2001 79

Protrusio Acetabuli
Table 1
Causes of Secondary Protrusio
Acetabuli
Infectious
Gonococcus
Echinococcus
Staphylococcus
Streptococcus
Mycobacterium tuberculosis
Neoplastic
Hemangioma
Metastatic carcinoma (breast,
prostate most common)
Neurofibromatosis
Radiation-induced osteonecrosis
Inflammatory
Rheumatoid arthritis
Ankylosing spondylitis
Juvenile rheumatoid arthritis
Psoriatic arthritis
Acute idiopathic chondrolysis
Reiter’s syndrome
Osteolysis following hip
replacement
Metabolic
Paget’s disease
Osteogenesis imperfecta
Ochronosis
Acrodysostosis
Osteomalacia
Hyperparathyroidism
Traumatic
Sequelae of acetabular fracture
Surgical error during hip
replacement
Genetic
Trichorhinophalangeal syndrome
Stickler syndrome
Trisomy 18
Ehler-Danlos syndrome
Marfan syndrome
Sickle cell disease
wherein the three plates of the tri-
radiate cartilage remain unfused,
allowing protrusion of the femoral
head medially into the pelvis. 1
Alexander 5 observed that an in-
ward bulge of the acetabulum was
normal in children between the
ages of 4 and 8 years, and favored
80
the theory of Eppinger. He stated
that the “protrusion is reversible,
diminishing stresses after the age
of 8 years, permitting corrections in
the majority of children.” He be-
lieved that protrusio in the adult is
the result of failure of this normal
correction.
Macdonald 6 reported on four
generations of one family affected
by protrusio acetabuli. One index
subject in the first generation had
the condition, as did all three mem-
bers of the second generation. Most
members of the ensuing genera-
tions had borderline cases. A famil-
ial study by Ventruto et al 7 rein-
forced the concept that protrusio
may well be an inherited disease.
Sherlock8 recently published a case
study indicating a link between
acute idiopathic chondrolysis and
primary protrusio acetabuli. In that
study, computed tomographic
scans demonstrated areas of focal
osteonecrosis of the femoral head,
as well as degenerative changes in
the acetabulum, in patients with
idiopathic protrusio acetabuli.
Many of the early reported cases
were secondary to untreated septic
arthritis, particularly gonococcal
and tuberculous infections. The
condition is also known to develop
in patients with defective collagen,
such as those with Marfan or Ehler-
Danlos syndrome, osteogenesis im-
perfecta, or trisomy 18.9-11 There are
numerous reports in the literature of
patients with acetabular deficiency
secondary to metastatic cancer, as
well as in those with neurofibro-
matosis (prevalence of up to 20%).12
In inflammatory arthritides, protru-
sio is very common, occurring in as
many as 15% of those with rheuma-
toid arthritis in the hip and 33% of
those with ankylosing spondyli-
tis.13,14
There are some who feel that in
many cases diagnosed as primary
protrusio acetabuli an overlooked
subtle metabolic abnormality is
actually the cause. Certainly, osteo-
Journal of the American Academy of Orthopaedic Surgeons
malacia and Paget’s disease have
been identified as etiologic factors.
The incidence of protrusio acetabuli
in patients with documented osteo-
malacia may be as high as 50%.14
This is in sharp contrast to the inci-
dence in patients with osteoarthritis,
which is generally estimated to be
about 5%. More information with
respect to bone metabolism and
histomorphometry in patients with
idiopathic protrusio may reveal ad-
ditional risk factors for acquiring
this condition.
In summary, secondary protrusio
acetabuli can have an inflammatory
cause or a noninflammatory cause
(i.e., a metabolic, neoplastic, or con-
nective-tissue disorder). Inflamma-
tory causes lead to destruction and
weakening of the bone surrounding
the hip with resultant migration
along the joint-reaction vector. In
cases with metabolic or connective-
tissue causation, there is a quali-
tative deficiency of the bone. The
thin medial acetabular wall has less
strength than the better supported
bone in the superior portion of the
joint, and when it falls below the
threshold of strength required to
withstand the medial component of
the joint-reaction force, secondary
protrusio occurs. This results in the
medial pattern of migration seen in
these cases. Once the joint-reaction
vector has migrated medial to the
ilioischial line, the rate of progres-
sion increases.
Diagnosis
History and Physical
Examination
As with all other medical prob-
lems, a thorough history and physi-
cal examination are critical. A family
history of similar or related prob-
lems should be well documented.
Because numerous syndromes and
disease states are associated with
protrusio acetabuli, it is important
to do a complete review of systems
 Mark T. McBride, MD, et al

in addition to the musculoskeletal
system. Of particular importance
are the neurologic and cardiovascu-
lar examinations. This will greatly
enhance the likelihood of identify-
ing any underlying cause and
thereby avoiding embarkation on
an injudicious treatment plan. The
symptoms of idiopathic protrusio
frequently first develop in adoles-
cence; therefore, this condition
should be considered in the differ-
ential diagnosis for hip pain in the
teenager.15,16
Patients with protrusio acetabuli
typically present with complaints of
activity-related pain in the groin re-
gion as well as stiffness. Occasion-
ally, the presenting complaint is
knee pain. Arising from a seated
position is a frequent cause of exac-
erbation. There is often a decrease
in both active and passive range of
hip motion, especially in abduction.
Pain may occur with active straight
leg raise or at extremes of motion.
There may be a positive Trendelen-
burg sign secondary to the short-
ened lever arm of the mechanically
disadvantaged abductors. With am-
bulation, there may be an antalgic
gait, a Trendelenburg gait, or both.
Physical manifestations of related
disease processes may or may not
be present.
males and noted that mild coxa vara
is not uncommon. Sotelo-Garza
and Charnley19 used the ilioischial
line on an AP radiograph of the
pelvis as a reference point from
which to measure the location of the
acetabulum. This distance was used
to designate the condition as mild (1
to 5 mm), moderate (6 to 15 mm), or
severe (>15 mm). Gates et al20 com-
pared multiple measurements in a
series of patients with protrusio and
discovered that the teardrop is the
most consistent landmark, varying
little with minor degrees of pelvic
obliquity. They recommended uti-
lizing an X-Y coordinate system
based on the hip center in relation to
the teardrop as the most useful way
to assess and track progression of
protrusio.
Laboratory Studies
It is important to obtain basic
blood tests to facilitate identifica-
tion of a possible underlying cause.
These include complete blood cell
Protrusio
count, erythrocyte sedimentation
rate, rheumatoid factor, antinuclear
antibody, and serum chemistry de-
terminations. If concern regarding
an inflammatory etiology is engen-
dered by the results of this workup,
a synovial biopsy may be required
to make a definitive diagnosis.
Treatment
The key consideration before pro-
ceeding with operative treatment is
identification and treatment of any
underlying disease process. Selec-
tion of the most appropriate surgi-
cal option is based on the patient’s
age and skeletal maturity and the
extent of degenerative changes
visualized on plain radiographs.
Skeletally Immature Patients
Patients with protrusio acetabuli
of noninflammatory origin who
have an open triradiate cartilage
may be considered for surgical tri-
Normal

Radiographs F E
Standard anteroposterior (AP) A A
and lateral radiographs of the pelvis
are critical both to make the diagno- B
sis and to stage the severity of pro-
trusio (Fig. 1). Many early authors
expressed their dissatisfaction with C
the absence of a coherent grading
system. The center-edge angle,
described by Wiberg to grade ace- D
tabular dysplasia, has generally
been adopted; an angle of over 40
degrees is diagnostic of protrusio
acetabuli.17 Armbuster et al18 con-
sidered protrusio to be present if the
Figure 1 Radiographic landmarks used in the diagnosis of protrusio acetabuli: A = iliois-
medial wall of the acetabulum pro- chial (Kohler) line; B, iliopectineal line; C = acetabular wall; D = interteardrop line; E = nor-
truded medial to the ilioischial line mal center-edge angle; F = abnormal center-edge angle indicative of protrusio acetabuli.
by 3 mm in males or 6 mm in fe-

Vol 9, No 2, March/April 2001 81

Protrusio Acetabuli
radiate closure. Steel21 reported a
series of 22 patients with Marfan’s
syndrome and protrusio acetabuli.
Eleven patients (21 hips) under-
went surgical triradiate closure.
The center-edge angle, the appear-
ance of the teardrop, and the rela-
tionship of the acetabulum to the
ilioischial line were evaluated on
plain radiographs of 19 hips at
maturity. On the basis of these fac-
tors, 12 of the 19 hips were consid-
ered to be restored to normal, 4
were reduced to “acetabular deep-
ening,” and 3 were unchanged.
Depending on the neck-shaft
angle of the proximal femur, surgi-
cal triradiate closure may be com-
bined with valgus intertrochanteric
osteotomy (VITO) in an attempt to
establish more normal hip biome-
chanics. Figure 2 demonstrates
successful surgical treatment of
protrusio acetabuli in a skeletally
immature patient who underwent
combined triradiate epiphysiodesis
and proximal femoral valgus oste-
otomy. The 12-year-old girl had no
evidence of a secondary cause for
the condition, and radiographic
A B
Figure 2 A, AP radiograph of the pelvis of a 12-year-old girl with idiopathic protrusio acetabuli. B, Radiograph obtained 2 years after
triradiate cartilage epiphysiodesis and VITO.
82
examination revealed a center-edge
angle of 45 degrees.
Adolescent or Young Adult
Patients
In the skeletally mature young
adult with idiopathic protrusio
acetabuli, the treatment options are
very limited. Historically, surgical
approaches included resection ar-
throplasty and arthrodesis. An ace-
tabuloplasty was described by Smith-
Peterson to treat the condition,22 and
a hanging hip procedure was devised
by Voss.17 Pauwels2 first described
VITO for protrusio and documented
several successful results, providing a
biomechanical rationale for an oste-
otomy to relieve medializing forces
on the affected hip (Fig. 3).
No other series in which VITO
was used for protrusio was reported
until 1973, when Rosemeyer et al23
showed good to excellent results in
21 of 25 hips at 6-year follow-up. A
good result was correlated with
young age as well as with minimal
preoperative arthritis.
In the series of Hooper and
Jones,17 of 57 patients treated by a
Journal of the American Academy of Orthopaedic Surgeons
variety of means, 9 underwent val-
gus osteotomy. The authors reported
fair or poor results in 7 of the 9 pa-
tients with 2- to 7-year follow-up
and concluded that the only opera-
tion with a predictable outcome was
total hip arthroplasty (THA). In a
1978 study, Verburg and Elzenga24
reported good improvement in all 6
patients, with markedly improved
function in the 3 patients evaluated
at a mean follow-up interval of 3
years. These authors noted, as had
Rosemeyer et al, 23 that the best
results were obtained in patients
who were young and had minimal
arthritic changes.
Poss25 has written that the keys
to valgus osteotomy are lateraliza-
tion of the femur to restore me-
chanical alignment and soft-tissue
releases, particularly of the psoas
tendon, to help effect lateralization
and to improve motion of the hip.
The amount of valgus correction is
typically determined on the basis
of the amount of preoperative
adduction present. Generally, a
correction of 20 to 30 degrees is
desirable. Excessive correction can
 Mark T. McBride, MD, et al

Clinical Experience With VITO

Before VITO After VITO The combined experience with
VITO at the Mayo Clinic, Children’s
Hospital San Diego, Sharp Memo-
rial Hospital, and Naval Medical
R R Center San Diego are summarized
in Table 2. A total of 19 hips in 12
patients were treated with VITO
Q
for primary protrusio. One skele-
Q tally immature patient was treated
with triradiate epiphysiodesis as
L
well. All patients had a thorough
L preoperative workup to rule out in-
flammatory disease and metabolic
bone disease. The patient group
consisted of 8 women and 4 men,
25°
ranging in age from 18 to 47 years.
Clinical follow-up was 2 to 33
CCD = 130° CCD = 155° years. Eight hips in 5 patients were
revised to total hip replacement.
The interval from index osteotomy
to primary THA ranged from 10
months to 15 years (Fig. 5). All pa-
tients except the 2 with less than a
Figure 3 Effects of VITO on the medializing force (vector Q) in the hip (CCD = femoral 3-year interval between osteotomy
neck-shaft angle). (Adapted with permission from Pauwels F [ed]: Biomechanics of the
Normal and Diseased Hip. Berlin: Springer-Verlag, 1976, p 245.) and THA were satisfied with the de-
cision to undergo osteotomy. One
patient required revision of bilateral
THAs 21 and 26 years after the ini-
lead to abductor contracture. A tion is performed (Fig. 4). In- tial procedures.
trapezoid-shortening osteotomy creased abductor tension can be A variety of fixation devices were
has been recommended as well, to reduced by an opening-wedge os- used to stabilize the intertrochan-
minimize the limb-length inequal- teotomy of the greater trochanter if teric osteotomies, including AO
ity that occurs when a large correc- necessary. blade-plates, Harris plates, sliding

A B

Figure 4 A, AP radiograph of the pelvis of a 19-year-old man with bilateral protrusio. B, Radiographic appearance 2 years after VITO.

Vol 9, No 2, March/April 2001 83

Protrusio Acetabuli

Table 2
Data on 12 Patients Treated With VITO

Iliopsoas
Patient Age, yr Sex Side Surgery (date) Fixation Correction Release

1 44 F R VITO (6/69) Harris plate 20° Yes

L VITO (6/69) Harris plate 20° Yes
2 47 F L VITO (2/82) Sliding compres- 22° No
sion screw

3 21 M R VITO (5/81) Harris plate 18° No

L VITO (2/81) Harris plate 20° No
4 43 F R VITO (1/81) Harris plate 20° No
5 25 F R VITO (3/65) Triflange nail 15° Yes

L VITO (3/65) Triflange nail 20° Yes

6 33 F R VITO (3/84) Sliding compres- 20° No
sion screw
L VITO (6/84) Sliding compres- 20° No
sion screw
7 14 F R VITO (3/94), Blade-plate 20° Yes
epiphysio-
desis (3/94)
8 19 M R VITO (12/91) Blade-plate 20° Yes
L VITO (6/92) Blade-plate 20° Yes

9 22 F R VITO (3/96) Blade-plate 15° No

L VITO (7/96) Blade-plate 25° No

10 32 M R VITO (6/97) Blade-plate 20° Yes

11 29 M L VITO (6/92) Blade-plate 20° Yes

33 R VITO (4/96) Blade-plate 20° Yes
12 42 F L VITO (5/94) Blade-plate 15° Yes

* Clinical scoring system used: Mayo Hip Score for patients 1-6; Harris Hip Score, patients 7-12.

compression screws, and, in the
earliest cases, triflange nail and a
side-plate and Wainwright spines.
Iliopsoas tendon releases were per-
formed in 11 hips, and in 6 patients
trapezoidal osteotomies were used
to shorten the femur.
One patient had a nonunion that
required bone grafting but went on
to heal uneventfully; no further
surgery other than hardware re-
moval was necessary. One patient
who underwent reoperation for
inadequate correction did relatively
well, but the occurrence of more
symptoms necessitated reoperation.
The third patient with bilateral
osteotomies underwent revision for
a recurrent flexion deformity; heal-
ing eventually occurred, but THA
was required 6 years after the initial
osteotomy. Abduction contractures
were treated with iliotibial band
lengthening at the time of hardware
removal in 1 patient.
Although this series represents a
relatively small number of patients
with varying follow-up who were
treated at different institutions,
some pertinent observations can be

84 Journal of the American Academy of Orthopaedic Surgeons

 Mark T. McBride, MD, et al

Survivorship Survivorship of
Complications Follow-up, yr Result of VITO* Additional Surgery (date) of VITO, yr Primary THA, yr

None 25.9 Poor THA (4/70) 0.8 26

None 25.9 Poor THA (4/70) 0.8 26
Nonunion 12.5 Poor Illiac-crest bone grafting 17.5 …
with repeat fixation;
hardware removal
Inadequate correction 15.3 Good Hardware removal; THA 15.2 1
None 15.5 Good Hardware removal; THA 15.5 1
None 15.5 Poor Hardware removal; THA 6 9
Fixation failure 33.1 Fair Revision osteotomy; 7.3 26
THA; revision THA
None 33.1 Fair THA; revision THA 11.5 21
None 13.3 Excellent None 13.3 …

None 13.0 Excellent None 13 …

None 5.0 Excellent Hardware removal 5 …

None 5.0 Excellent Hardware removal 5 …

None 4.5 Excellent Hardware removal 4.5 …

Abductor contracture 3.1 Good Hardware removal; iliotibial 3.5 …

band lengthening
Abductor contracture 2.8 Good Hardware removal; iliotibial 3 …
band lengthening
None 2.2 Excellent Hardware removal 2 …

None 7.0 Good … 7 …

None 3.2 Excellent … 3 …
None 5.2 Poor THA 3 2

made. Clearly, there is a subgroup
of patients with protrusio acetabuli
who cannot be effectively managed
with osteotomy. On the basis of
this study as well as the work of
Verburg and Elzenga 24 and of
Rosemeyer et al,23 the VITO proce-
dure should not be performed on
patients who are over age 40 years
or who have significant degenera-
tive changes visualized on plain
radiographs. The longest survivor-
ship after this procedure was asso-
ciated with decreased hip motion
and diminished exercise tolerance.
However, the patients remained
satisfied with their results and felt
that they would have gone on to
further surgery earlier if they had
not undergone the osteotomy.
Interestingly, limited preoperative
motion does not preclude a satis-
factory outcome, as several long-
term survivors were quite stiff pre-
operatively. There were no diffi-
culties encountered in conversion
to THA after VITO, and survivor-
ship in this group mirrors the re-
sults reported in the literature for
primary cemented THAs.

Vol 9, No 2, March/April 2001 85

Protrusio Acetabuli
Older Adult Patients
The surgical options for the older
adult with protrusio acetabuli are
VITO or some form of arthroplasty.
The results of VITO in this age
group are less predictable than in
younger patients, especially if there
is radiographic evidence of arthritis.
Wilson and Scott26 and Torisu et al27
reported relatively poor results after
use of bipolar hemiarthroplasty
combined with bone grafting. In
both studies there was a high per-
centage of continued medial and
superior migration at intermediate
follow-up. The authors expressed
concern regarding the longevity of
this approach.
Total hip arthroplasty is the
recommended treatment for the
older adult with protrusio acetabuli
and degenerative changes. Sotelo-
Garza and Charnley19 reported on
the use of THA to treat protrusio in
253 hips and found that the out-
come of cemented THA for protru-
sio was not different from that of
other primary THAs at a minimum
follow-up interval of 60 months.
Ranawat et al28 reported on 35 hips
with protrusio acetabuli secondary
to rheumatoid arthritis that had
been treated with cemented THA
and had been followed up for an
average of 4.3 years. They reported
loosening in 16 of 17 hips recon-
structed with the cup center more
A B
Figure 5 A, AP radiograph of the pelvis obtained 16 years after bilateral VITO. B, Patient subsequently underwent bilateral THA. This
radiograph was obtained 1 year after that procedure.
86
than 10 mm from the anatomic cen-
ter. Of the 13 hips reconstructed
with the cup center within 5 mm of
the anatomic center, none was
loose.
Crowninshield et al29 used finite-
element analysis to identify the vari-
ables affecting stress on the acetabu-
lum after reconstruction for protru-
sio acetabuli. They discovered that
medial cup placement led to high
medial stresses, whereas anatomic
placement resulted in decreased
medial stresses. Furthermore, they
found that reinforcement of the
medial wall with cement and wire
mesh was not effective, but that a
metal-backed component was effec-
tive, due to the superior stress dis-
tribution of the metal cup. Their
data also suggested that a metal
protrusio ring device more reliably
transfers stress from the medial wall
to the rim than does a flanged pro-
trusio cup.
In clinical series, Bayley et al30
and Gates et al 20 confirmed the
importance of restoring the hip to
an anatomic center. They noted
that 50% of reconstructed hips with
a cup center more than 10 mm
from the anatomic hip center had
failed.
Use of bone graft is the opti-
mal method of cup lateralization.
Heywood31 described a technique
whereby the femoral head was
Journal of the American Academy of Orthopaedic Surgeons
used as a graft. The interior of the
femoral head was scooped out, and
a reverse reamer was utilized to
denude the remaining cartilage
from the articular side, which was
then put into the defect of the pro-
truding acetabulum to restore the
hip center. This “concavoconvex”
graft was press-fitted into the medial
wall defect, and an all-polyethylene
cup was then cemented into the re-
constructed socket in the standard
fashion. He reported excellent short-
term results with this technique in a
series of nine hips.
McCollum et al 4 reported the
results obtained by using a similar
technique in a series of 39 hips with
an average follow-up of nearly
5 years. On serial radiographic
follow-up, all grafts had incorpo-
rated without evidence of loosening
or migration. Subsequently, numer-
ous other authors have demon-
strated nearly universal incorpora-
tion of morcellized or fragmented
grafts, both with and without ce-
ment. This results in restoration of
the anatomic center and provides
medial bone stock for potential fu-
ture revision surgery with less graft
preparation time.
The approach most widely used
today is to fill the defect with mor-
cellized graft and then to use a
porous-coated metal cup for the
acetabular reconstruction (Fig. 6).

A B
Figure 6 A, AP radiograph of the pelvis of a 48-year-old man with bilateral protrusio. B, Film obtained 18 months after THA shows
complete incorporation of medial bone grafts.
Porous-coated “deep profile” com-
ponents may be used without bone
graft in mild cases. On occasion,
antiprotrusio cages may be re-
quired for a primary reconstruction.
Ranawat and Zahn32 have recom-
mended the following guidelines:
In cases in which the protrusion is
less than 5 mm, bone graft is not
required. When the protrusion is
greater than 5 mm and there is an
intact medial wall, bone graft with-
out augmentation devices is appro-
priate. If there is gross deficiency of
the medial wall, bone graft with
consideration of additional fixation
devices (hemispherical noncemented
cup with screw supplementation or
antiprotrusio ring) is indicated.
The choice of surgical approach is
determined by surgeon preference;
however, a trochanteric osteotomy
is sometimes required in severe
References
1. Pomeranz MM: Intrapelvic protrusion
of the acetabulum (Otto pelvis). J Bone
Joint Surg Am 1932;14:663-686.
2. Pauwels F; Furlong RJ, Maquet P (trans):
Biomechanics of the Normal and Diseased
Hip: Theoretical Foundation, Technique and
Vol 9, No 2, March/April 2001
cases to facilitate initial femoral
head dislocation. An alternative is
an in situ neck cut to allow mobili-
zation of the femur, followed by re-
moval of the femoral head with use
of a corkscrew.
Summary
Idiopathic protrusio acetabuli is a
rare cause of osteoarthritis in young
adults. Further study of the genetic,
histomorphometric, and anatomic
factors that may contribute to its
development is warranted. The
secondary causes of protrusio must
be identified and managed before
embarking on surgical treatment.
Synovial biopsy may be required
for diagnosis in some cases.
The surgical treatment options
are age-specific. In the skeletally
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Springer-Verlag, 1976, pp 129-169.
3. Egan KJ, Kummer FJ, Frankel VH:
Biomechanics of total hip arthroplasty.
Semin Arthroplasty 1993;4:288-301.
4. McCollum DE, Nunley JA, Harrelson
Mark T. McBride, MD, et al
immature patient with progressive
protrusio acetabuli, triradiate fusion
has been demonstrated to arrest pro-
gression or improve the condition in
the majority of reported cases. Val-
gus intertrochanteric osteotomy is
effective for a select group of young
patients with protrusio. Long-term
pain relief and restoration of func-
tion can be achieved in properly
selected individuals. Furthermore,
osteotomy can delay the need for a
THA for a decade or more. For the
older adult with significant arthritis
as well as protrusio, THA with non-
structural bone grafting of the medial
wall cavity can be effective. This
approach achieves two important
objectives: (1) restitution of bone
stock and (2) lateralization of the hip
center to the anatomic position to
ensure the greatest chance of a du-
rable long-term outcome.
JM: Bone-grafting in total hip replace-
ment for acetabular protrusion. J Bone
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5. Alexander C: The aetiology of primary
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38:567-580.
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6. Macdonald D: Primary protrusio ace-
tabuli: Report of an affected family. J
Bone Joint Surg Br 1971;53:30-36.
7. Ventruto V, Catani L, Celona A,
Fioretti G, Stabile M, Gallo G: Familial
occurrence of protrusio acetabuli
(Otto’s disease): Ten members affected
in four generations. Ital J Orthop
Traumatol 1980;6:423-426.
8. Sherlock DA: Acute idiopathic chon-
drolysis and primary acetabular pro-
trusio may be the same disease. J Bone
Joint Surg Br 1995;77:392-395.
9. Wenger DR, Ditkoff TJ, Herring JA,
Mauldin DM: Protrusio acetabuli in
Marfan’s syndrome. Clin Orthop 1980;
147:134-138.
10. Wenger DR, Abrams RA, Yaru N,
Leach J: Obstruction of the colon due
to protrusio acetabuli in osteogenesis
imperfecta: Treatment by pelvic oste-
otomy—Report of a case. J Bone Joint
Surg Am 1988;70:1103-1107.
11. Ray S, Ries MD, Bowen JR: Arthro-
katadysis in trisomy 18. J Pediatr
Orthop 1986;6:100-102.
12. Joseph KN, Bowen JR, MacEwen GD:
Unusual orthopedic manifestations of
neurofibromatosis. Clin Orthop 1992;
278:17-28.
13. Hastings DE, Parker SM: Protrusio
acetabuli in rheumatoid arthritis. Clin
Orthop 1975;108:76-83.
14. Dwosh IL, Resnick D, Becker MA: Hip
involvement in ankylosing spondyli-
tis. Arthritis Rheum 1976;19:683-692.
15. Bible MW, Pinals RS, Palmieri GMA,
Pitcock JA: Protrusio acetabuli in osteo-
88
porosis and osteomalacia. Clin Exp
Rheumatol 1983;1:323-326.
16. Hughes RA, Tempos K, Ansell BM: A
review of the diagnoses of hip pain
presentation in the adolescent. Br J
Rheumatol 1988;27:450-453.
17. Hooper JC, Jones EW: Primary protru-
sion of the acetabulum. J Bone Joint
Surg Br 1971;53:23-29.
18. Armbuster TG, Guerra J Jr, Resnick D, et
al: The adult hip: An anatomic study—
Part I. The bony landmarks. Radiology
1978;128:1-10.
19. Sotelo-Garza A, Charnley J: The re-
sults of Charnley arthroplasty of the
hip performed for protrusio acetabuli.
Clin Orthop 1978;132:12-18.
20. Gates HS III, Poletti SC, Callaghan JJ,
McCollum DE: Radiographic mea-
surements in protrusio acetabuli. J
Arthroplasty 1989;4:347-351.
21. Steel HH: Protrusio acetabuli: Its oc-
currence in the completely expressed
Marfan syndrome and its musculo-
skeletal component and a procedure to
arrest the course of protrusion in the
growing pelvis. J Pediatr Orthop
1996;16:704-718.
22. Gilmour J: Adolescent deformities of
the acetabulum: An investigation into
the nature of protrusio acetabuli. Br J
Surg 1939;26:670-699.
23. Rosemeyer B, Viernstein K, Schumann
HJ: Follow up study of intertrochan-
teric valgus osteotomy with medial
displacement in cases of primary pro-
trusio acetabuly [sic] [German]. Arch
Orthop Unfallchir 1973;77:138-148.
Journal of the American Academy of Orthopaedic Surgeons
24. Verburg A, Elzenga P: Intertrochan-
teric valgization osteotomy for treat-
ment of primary protrusion of the
acetabulum (Otto-Chrobak pelvis).
Arch Chir Neerl 1978;30:207-215.
25. Poss R: The intertrochanteric osteot-
omy, in Sledge CB (ed): The Hip: Mas-
ter Techniques in Orthopaedic Surgery.
Philadelphia: Lippincott-Raven, 1998,
pp 183-196
26. Wilson MG, Scott RD: Bipolar socket
in protrusio acetabuli: 3–6-year study.
J Arthroplasty 1993;8:405-411.
27. Torisu T, Utsunomiya K, Masumi S,
Maekawa M: Bipolar hip arthroplasty
in rheumatoid arthritis. Clin Orthop
1989;244:188-197.
28. Ranawat CS, Dorr LD, Inglis AE:
Total hip arthroplasty in protrusio
acetabuli of rheumatoid arthritis. J
Bone Joint Surg Am 1980;62:1059-1065.
29. Crowninshield RD, Brand RA, Peder-
sen DR: A stress analysis of acetabu-
lar reconstruction in protrusio ace-
tabuli. J Bone Joint Surg Am 1983;
65:495-499.
30. Bayley JC, Christie MJ, Ewald FC,
Kelley K: Long-term results of total
hip arthroplasty in protrusio acetabuli.
J Arthroplasty 1987;2:275-279.
31. Heywood AWB: Arthroplasty with
a solid bone graft for protrusio ace-
tabuli. J Bone Joint Surg Br 1980;62:
332-336.
32. Ranawat CS, Zahn MG: Role of bone
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acetabuli by total hip arthroplasty. J
Arthroplasty 1986;1:131-137.
 The Limping Child: Evaluation and Diagnosis

John M. Flynn, MD, and Roger F. Widmann, MD

Abstract

A limp is a common reason for a child to present to the orthopaedist. Because of cally between 12 and 16 months of
the long list of potential diagnoses, some of which demand urgent treatment, an age), they have a short stride
organized approach to evaluation is required. With an understanding of normal length, a relatively fast cadence
and abnormal gait, a directed history and physical examination, and the devel- and slow velocity, and a widened
opment of a differential diagnosis based on the type of limp, the patient’s age, base of support in double stance.
and the anatomic site that is most likely affected, the orthopaedist can take a Their hips, knees, and ankles move
selective approach to diagnostic testing. Laboratory tests are indicated when through a small arc of motion. 2
infection, inflammatory arthritis, or a malignant condition is in the differential Until 30 to 36 months of age, chil-
diagnosis. The C-reactive protein assay is the most sensitive early test for mus- dren have neither the balance nor
culoskeletal infections; an abnormal value rapidly returns to normal with effec- the abductor strength to maintain
tive treatment. Imaging should begin with plain radiography. Ultra- single-limb stance for very long.
sonography is particularly valuable in assessing the irritable hip and guiding By 7 years of age, children exhibit a
aspiration, if necessary. mature gait.2
J Am Acad Orthop Surg 2001;9:89-98 The mature gait cycle is com-
posed of the stance phase (initial
contact, loading response, mid-
stance, terminal stance, preswing)
A limp is a common reason for a child sient synovitis) to conditions in and the swing phase, during which
to present to the orthopaedist, often which early diagnosis may be life- the limb is advanced in space to
after first being seen by a primary- saving (e.g., acute leukemia).1 The position the foot for the next heel-
care physician or in an emergency long differential diagnosis (Tables 1 strike. The abductors stabilize the
department. Most parents are keen and 2) may seem daunting, particu- pelvis during stance phase, pre-
observers; they are quick to detect larly when the site of origin is un- venting significant side-to-side
even subtle gait abnormalities and known. However, after obtaining a motion as the opposite limb swings
generally will not wait long to have thorough history and performing a
a limp evaluated. The orthopaedist careful physical examination, the site
is expected to recognize the gait of origin can often be localized and
Dr. Flynn is Assistant Professor of Orthopaedic
abnormality, determine the proba- the differential diagnosis narrowed, Surgery, Unviersity of Pennsylvania School of
ble site of origin, and then develop a thus permitting a well-organized Medicine, Philadelphia; and Attending
good working diagnosis before approach to obtaining additional Surgeon, Division of Orthopaedic Surgery,
ordering selective diagnostic tests. data with selective diagnostic tests. Children’s Hospital of Philadelphia. Dr.
Widmann is Assistant Professor of Orthopaedic
These tests should provide the data Appropriate treatment can then be
Surgery, Weill Medical College of Cornell
for confirming the diagnosis and instituted. University, New York, NY; and Assistant
developing a treatment plan while Attending Surgeon, Hospital for Special
decreasing costs to the health-care Surgery, New York.
system, as well as minimizing pain Normal Gait
and anxiety for the child and parent. Reprint requests: Dr. Flynn, Division of
Orthopaedic Surgery, Children’s Hospital of
Pain, weakness, and mechanical Normal gait is a smooth, rhythmic,
Philadelphia, 34th and Civic Center Blvd,
factors are the primary causes of mechanical process that advances Philadelphia, PA 19104-4399.
limp in children. The etiology of a the center of gravity with a mini-
limp ranges from benign, self-limited mum expenditure of energy. Many Copyright 2001 by the American Academy of
conditions that call for only a diag- aspects of gait change with age. 2 Orthopaedic Surgeons.
nosis and reassurance (e.g., tran- When children begin to walk (typi-

Vol 9, No 2, March/April 2001 89

The Limping Child

Table 1
Differential Diagnosis of Antalgic Gait

<4 yr 4 to 10 yr >10 yr

Toddler’s fracture (tibia or foot)
Osteomyelitis, septic arthritis,
diskitis
Arthritis (juvenile rheumatoid
arthritis, Lyme disease)
Discoid lateral meniscus
Foreign body in the foot
Benign or malignant tumor
Fracture (especially physeal)
Osteomyelitis, septic arthritis, diskitis
Legg-Calvé-Perthes disease
Transient synovitis
Osteochondritis dissecans (knee or ankle)
Discoid lateral meniscus
Sever’s apophysitis
Accessory tarsal navicular
Foreign body in the foot
Arthritis (juvenile rheumatoid arthritis,
Lyme disease)
Benign or malignant tumor
Stress fracture (femur, tibia, foot, pars
intra-articularis)
Osteomyelitis, septic arthritis, diskitis
Slipped capital femoral epiphysis
Osgood-Schlatter disease or Sindig-
Larsen-Johanssen syndrome
Osteochondritis dissecans (knee or
ankle)
Chondromalacia patellae
Arthritis (Lyme disease, gonococcal)
Accessory tarsal navicular
Tarsal coalition
Benign or malignant tumor

through. During normal walking Abnormal Gait lumbar spine, as demonstrated

motion, one foot is always on the
ground. The kinematics of normal
gait has been studied in detail,2,3
establishing normal ranges of joint
motion during different phases of
the gait cycle. The ankle dorsiflexes
at heel-strike, then plantar-flexes to
foot-flat, and then dorsiflexes again
as the tibia moves forward. The
knee is flexed at heel-strike, extends
until toe-off, and then flexes during
swing, allowing clearance of the
foot as it positions for the next heel-
strike. The hip follows a similar
pattern, with slight flexion at heel-
strike, extension through stance,
and then flexion in swing.
Normal gait can be altered by pain,
a mechanical problem, or a neuro-
muscular problem. A child will
adopt an antalgic gait in an effort to
prevent pain in the affected limb.
The single-limb-support phase of
stance is shortened on the painful
extremity, as is the stride length of
the normal opposite limb (to get
back to bearing weight on the well
leg as quickly as possible). A vari-
ant of the classic antalgic gait is the
“cautious” gait of a child with back
pain.4 For example, a child with
diskitis will lose the normal rhyth-
mic flexion and extension of the
when bending to pick up objects off
the floor.5 Another variant of the
antalgic gait is the complete refusal
to walk. This pattern is seen most
often in toddlers and may indicate
a condition causing pain that can-
not be avoided by any of the possi-
ble gait alterations.
Circumduction—excessive hip
abduction, pelvic rotation, and hik-
ing—functionally shortens a limb,
thus enhancing foot clearance dur-
ing swing when there is joint stiff-
ness, particularly in the ankle. 6
Children with a significant limb-
length inequality may “vault” with
the short leg (or toe-walk) to clear

Table 2
Differential Diagnosis of a Nonantalgic Limp

Circumduction Gait/
Equinus Gait (Toe-Walking) Trendelenburg Gait Vaulting Gait Steppage Gait

Idiopathic tight Achilles tendon
Clubfoot (residual or untreated)
Cerebral palsy
Limb-length discrepancy
Legg-Calvé-Perthes disease Limb-length discrepancy Cerebral palsy
Developmental dysplasia of the hip Cerebral palsy Myelodysplasia
Slipped capital femoral epiphysis Any cause of ankle or Charcot-Marie-Tooth
Muscular dystrophy knee stiffness disease
Hemiplegic cerebral palsy Friedreich’s ataxia

90 Journal of the American Academy of Orthopaedic Surgeons


the long leg, rather than circumduct
it. An equinus gait (toe-walking)
occurs when ankle dorsiflexion is
limited. This may result from gas-
trocnemius-soleus spasticity, short-
ening of the Achilles tendon, or
both. Thus, stance phase will be
initiated with toe-strike rather than
heel-strike.
Several abnormal gait patterns
result from muscle weakness or a
neurologic abnormality. A Trendel-
enburg gait results from altered
hip mechanics, particularly abduc-
tor weakness. During stance on the
involved side, the contralateral side
of the pelvis drops. To preserve
balance, the child may lean the
trunk toward the affected side. A
variation of the Trendelenburg gait
is the waddling gait of a child with
bilateral hip dislocation. A “step-
page gait” develops when the ankle
dorsiflexors are weak (e.g., as in
Charcot-Marie-Tooth disease). To
compensate for the weakness, the
child increases knee flexion in the
swing phase to clear the foot. The
foot will slap to the ground because
the ankle dorsiflexors are unable to
decelerate the foot between heel-
strike and foot-flat. An unsteady
gait may result from conditions that
affect balance, such as Friedreich’s
ataxia. Careful initial analysis of
the gait can enhance the specificity
of the remainder of the physical
examination and facilitate localiza-
tion of the origin of the limp.
History
An accurate history may be difficult
to obtain from a young child, and
some or all of the history must be ob-
tained from the parents or primary
caregivers. A brief discussion with
the child, followed by a parental
description of pain complaints and
changes in gait pattern, is invalu-
able in guiding the subsequent
physician-directed evaluation. In
certain circumstances, adolescents
Vol 9, No 2, March/April 2001
John M. Flynn, MD, and Roger F. Widmann, MD
and some children should be ques-
tioned privately, as they may pro-
vide important details regarding
exposure to sexually transmitted
diseases, such as gonococcal infec-
tion, which may not be obtained in
the presence of parents.7 Once the
parent and patient have had an
opportunity to describe the pain
and/or limp in their own terms, the
physician is best prepared to com-
plete the history.
The history should focus on the
character of the limp: the presence
or absence of pain or other localiz-
ing symptoms, the frequency and
duration of symptoms, and the
mechanism of injury, when appro-
priate. A history of ceasing athletic
participation or social play with
friends should raise concern.4 The
absence of pain suggests either neu-
romuscular or metabolic disease or
a congenital or developmental ab-
normality, such as hip dysplasia or
limb-length discrepancy. In a tod-
dler, the absence of pain complaints
may not be particularly helpful,
and the physical examination takes
on greater importance.
The pattern, onset, and duration
of pain may suggest the origin. 4
Acute onset of severe pain over a
few days focuses the evaluation on
trauma, infection, or malignancy,
whereas gradual worsening over
months suggests inflammatory or
mechanical symptoms.8 It is helpful
to characterize the quality of the
pain as constant, intermittent, or
transient. Constant pain is of partic-
ular concern, suggesting an intra-
medullary process, such as expand-
ing tumor or infection. A history of
trauma is readily established in most
circumstances, with some notable
exceptions: pathologic fracture and
child abuse.
It is important to characterize the
timing of pain (e.g., morning pain,
pain after activity, or pain that wakes
the child from sleep). Morning pain
or pain and stiffness after inactivity
are more characteristic of inflamma-
tory joint disorders.8 Pain after activ-
ity may suggest an overuse injury,
such as a stress fracture, or an inter-
nal articular derangement, such as
an osteochondral lesion, a meniscal
tear, or an anterior cruciate ligament
tear. Night pain that wakes a child
from sleep may represent benign
“growing pains,” but the concern is
that it may derive from osteoid oste-
oma or a malignant condition.
Pain relief with nonsteroidal anti-
inflammatory medications may be
characteristic of osteoid osteoma but
is not diagnostic. Referred pain must
also be considered, particularly thigh
or medial knee pain referred from
painful conditions of the hip (e.g.,
slipped capital femoral epiphysis).
Buttock or lateral thigh pain may be
referred from the back. Pain in multi-
ple joints suggests an arthritic process.
A past medical history including
recent trauma or exposure to infec-
tious diseases and use of antibiotics
is helpful in diagnosis. Recent vari-
cella infection may lower systemic
immunity, rendering the child sus-
ceptible to opportunistic bone or
joint infections.9 Failure to achieve
appropriate developmental mile-
stones or, more ominously, deterio-
ration of motor ability warrants fur-
ther neuromuscular or metabolic
evaluation. The review of systems
should seek a history of recent fever,
weight loss, or malaise suggestive of
infection or malignancy. A history
of prior medical evaluation for the
same problem should be sought, and
the pertinent records should be ob-
tained when possible. A complete
history should include questioning
about the family history of neuro-
muscular disease, metabolic disease,
inflammatory arthritis, or infectious
disease exposure.
Physical Examination
The physical examination of the
limping child has three essential
components: the gait exam, the
91
The Limping Child
standing/floor exam, and the table-
top exam. The child should be
dressed in as little clothing as is prac-
tical; gym shorts and bare feet are
ideal. Much can be missed watching
a small child walk in an oversized
gown that extends to the floor.
Gait Examination
The examination area should
offer sufficient space to see multiple
gait cycles. It is important not to be
fooled by an artificial “doctor walk”;
the best chance to see the true limp
is by observing gait when the child
does not know she is being watched,
such as when the child is walking to
the examination room.10 Running
may accentuate the limp or abnor-
mal gait. Subtle weakness or the
upper-extremity posturing of cere-
bral palsy might not be seen until
the child runs. Shoes may provide
valuable clues to gait problems; for
example, a child having trouble
clearing his foot in swing phase may
have excessive toe wear.
It is best to adopt a systematic
approach to the gait examination,
working from the ground up and
watching each limb segment and
joint through several gait cycles.
Trying to simultaneously analyze
every facet of gait is difficult for
even the most experienced clinician,
considering that a typical toddler
takes 180 steps per minute. Note
how the foot strikes the floor—is
there heel-strike, foot-flat, or toe-
strike? A child may walk on the
medial or lateral border of the foot
to protect a sore bone or the site of a
puncture wound or foreign body.
Abnormal limb rotation may be
observed. Metatarsus adductus,
internal tibial torsion, or femoral
anteversion will result in an internal
foot-progression angle. An adoles-
cent with a slipped capital femoral
epiphysis or a young child with an
occult fracture may walk with an
external foot-progression angle.
The next feature to consider is
the symmetry of the stance phase.
92
A unilateral shortened stance phase
is characteristic of an antalgic gait.
The range of motion of each joint
should also be evaluated. Limited
ankle dorsiflexion is seen in chil-
dren with a short Achilles tendon
or a spastic gastrocnemius-soleus.
At the knee, motion should be ob-
served through several gait cycles.
Contracture or spasticity in the
quadriceps or hamstrings or intra-
articular derangement will limit
knee motion. Any frontal-plane ab-
normalities should be noted as well
(e.g., a varus thrust of the proximal
tibia in Blount’s disease). Hip mo-
tion may be abnormal, exhibiting
circumduction, persistent flexion,
or excessive pelvic or trunk motion.
Upper-extremity posturing as well
as difficulty with balance and coor-
dination may suggest a neurovas-
cular origin of the limp.
Standing/Floor Examination
After the history and vital signs
have been taken and the physician
has thoroughly studied the child’s
gait, there are several tests to con-
sider before the tabletop examina-
tion. The spine should be examined
with the child standing, taking care
to note balance in the coronal and
sagittal planes, scoliosis, lumbo-
sacral step-off, pelvic obliquity, and
any cutaneous findings (e.g., café-
au-lait spots, hairy patches, or sacral
dimples). On the forward bend, the
examiner should note a thoracic or
lumbar prominence due to scoliosis.
The Trendelenburg test is per-
formed by having the child stand
on the affected leg with the knee
flexed and the hip extended. The
child may need to rest his hands
against the wall for balance. If the
Trendelenburg test is performed
with hip flexion, the hip flexors can
elevate the pelvis and mask a mild
deficiency of the gluteus medius.4
It may take 20 seconds or more of
continuous testing on the affected
limb before abductor weakness
causes the opposite pelvis to drop.
Journal of the American Academy of Orthopaedic Surgeons
If muscular dystrophy is a possi-
bility, a Gower test is performed by
having the child sit on the floor and
then rise quickly, observing to see if
he uses his hands to substitute for
weak hip extensor muscles. Repeti-
tive single-leg heel raises and toe
raises can be utilized to accentuate
subtle weakness in the foot plantar-
flexors or dorsiflexors.
Tabletop Examination
With the child on the examining
table, one should thoroughly in-
spect for asymmetry, deformity,
erythema, rashes, and swelling.
Puncture wounds or foreign bodies
should be sought on the plantar
surface of the foot in walkers and
on the anterior aspect of the knee in
crawlers. The resting position of
the limb should be noted; for exam-
ple, a child with septic arthritis of
the hip will hold the hip flexed and
externally rotated. Note also any
muscle hypertrophy (e.g., calf hy-
pertrophy in muscular dystrophy)
or atrophy (e.g., global unilateral
atrophy in hemiplegia or quadri-
ceps atrophy in a child with a pain-
ful hip or knee).
Palpation of the lower extremity
to find the point of maximum ten-
derness is often the most valuable
part of the physical examination of a
limping child. Knowing the exact
site of pain dramatically limits the
differential diagnosis and may elim-
inate the need for a bone scan or
other diagnostic test (Fig. 1). Every
joint of the lower extremity should
be taken through its range of mo-
tion, noting pain, contractures, or
muscle spasticity. The patellofemo-
ral joint, a common source of pain
in adolescents, should be tested for
signs of apprehension or pain with
patellar compression during flexion
and extension. The sacroiliac joint is
tested by direct percussion posteri-
orly and by stressing the joint with
the hip positioned in flexion, abduc-
tion, and external rotation (FABER
test). The rotational profile should
 John M. Flynn, MD, and Roger F. Widmann, MD

tional oblique views may reveal

more subtle osseous changes, such
as a minimally displaced tibial frac-
ture (toddler’s fracture) or the peri-
osteal elevation of a stress fracture.
In children who present with a limp
or refusal to bear weight but are too
young to localize pain, plain radio-
graphs of the entire lower extremity
should be obtained (Fig. 2).
Plain radiographs are not particu-
larly helpful in identifying early
bone or joint infections. The early ra-
diographic findings of acute hema-
togenous osteomyelitis include a nor-
mal osseous appearance with subtle
displacement and swelling of the soft
tissues.13 Comparison views may
depict subtle soft-tissue swelling, but
radiographic sensitivity for the early
changes of osteomyelitis is less than
50%.14 The radiographic appearance
of early soft-tissue changes due to
septic arthritis is difficult to interpret
A B and unreliable.15 Early bone or joint
Figure 1 A, A healthy limping toddler presented with reproducible tenderness to palpa-
changes are not typically seen radio-
tion over the midportion of the tibia. Rotational stress to the tibia was also painful. graphically until 10 to 12 days after
Although the radiographs were read as normal, an occult fracture was suspected. B, At 4 the onset of bone or joint infection,13
weeks, radiographs showed periosteal elevation along the medial cortex of the tibia
(arrows), confirming the clinical suspicion of a toddler’s fracture. The child’s symptoms
and the presence of these changes
resolved after 4 weeks in a cast. suggests a significant delay in diag-
nosis.
The triphasic technetium-99m
bone scan is an excellent test for
be documented in children with in- limp, plain radiography should evaluating a limping child when
toeing or out-toeing.11 Appropriate always be performed first, because the history and physical examina-
neurologic testing should also be radiographs are inexpensive, can be tion fail to localize the anatomic site
performed. easily obtained at any hour, and are of pathologic changes (Fig. 3). Bone
Limb lengths should be assessed. both sensitive and specific for a scanning has been demonstrated to
If an inequality is noted, the differ- wide variety of disorders.12 In chil- be superior to the other standard
ence is most accurately determined dren who can localize tenderness, screening tests for infection (tem-
by leveling the pelvis with blocks initial plain radiographs should perature, white blood cell [WBC]
under the short leg. Although a sig- include orthogonal images of the count, erythrocyte sedimentation
nificant limb-length inequality may affected limb that visualize the joint rate [ESR], and plain radiography)
itself alter gait, it also suggests other both above and below the point of in the limping toddler.14 The tech-
potential causes of limping, such as maximum tenderness. A third ob- netium accumulates at the site of in-
hemiplegia and developmental dis- lique view is included when imag- creased blood flow and osteoblastic
location of the hip. ing the ankle or foot if an area of activity in osteomyelitis, stress frac-
suspected pathologic change may tures, occult fractures, neoplasm,
be obscured by bone overlap, mini- and metastases. In suspected early
Radiographic Evaluation mal displacement of fracture frag- bone infection, bone scans have high
ments, or minimal physeal widen- sensitivity (84% to 100%) and speci-
Although the various imaging ing. 12 If the patient can localize ficity (70% to 96%).12,14,16
modalities may each have a role in pain but the initial radiographs of Although the diagnosis of many
the assessment of the child with a the long bones are negative, addi- long-bone infections can be made

Vol 9, No 2, March/April 2001 93

The Limping Child

in clinical practice.17 Other advan-

tages of bone scanning over cross-
sectional imaging modalities include
decreased expense, less need for se-
dation, and the ability to image the
whole body.
Limitations of bone scintigraphy
include difficulty in distinguishing
between bone infarct and osteomy-
elitis in hemoglobinopathies and the
occurrence of false-negative bone
scans in cases of Langerhans cell his-
tiocytosis and some other aggressive
tumors in children.17 Bone scanning
has low sensitivity for septic arthri-
tis, especially when there is adjacent
osteomyelitis, and is therefore not
indicated in this circumstance.
Leukemia may result in increased,
decreased, or no change in tech-
A B netium uptake.14 A “cold” scan (i.e.,
one showing low uptake) in the set-
Figure 2 A, Anteroposterior (AP) radiograph of the hips and pelvis of a 2-year-old girl
with a 2-week history of limping, fever, malaise, and difficulty sleeping through the night.
ting of suspected osteomyelitis is
Periosteal changes (arrow) were noted in the right femur. B, A full-length AP radiograph not necessarily negative; instead, it
of the femur demonstrates the extent of periosteal elevation and geographic medullary may represent bone rendered avas-
canal erosion of the lesion, which on biopsy proved to be eosinophilic granuloma.
cular due to a subperiosteal or end-
osteal abscess. A study of cold bone
scans in pediatric patients with
without scintigraphy, bone scans Prior bone drilling and periosteal osteomyelitis revealed that they had
are particularly helpful in localiz- elevation have been demonstrated more severe bone infections requir-
ing sepsis around the pelvis and experimentally to have no effect on ing more aggressive medical and
the spine—areas that are difficult a subsequent bone scan performed surgical treatment compared with
to examine and where soft-tissue within 24 hours,18 and prior aspira- control children with “hot” bone
changes are difficult to identify.17 tion has not interfered with results scans and osteomyelitis.19

A B

Figure 3 A, AP radiograph of an 8-year-old girl who presented with a limp and the sudden, nontraumatic onset of severe left groin and
thigh pain. The film was read as normal. B, The history, physical examination, and plain radiographs did not allow precise localization of
the process. A bone scan showed decreased uptake in the left femoral head, suggesting Legg-Calvé-Perthes disease.

94 Journal of the American Academy of Orthopaedic Surgeons


Ultrasonography is a valuable
diagnostic tool in the evaluation of
a limping child with an irritable hip
(Fig. 4). Ultrasonography is nonin-
vasive, requires no sedation, and is
typically more accessible and less
expensive than other secondary
radiologic tests. 20 However, if
infection is highly probable, ultra-
sonography should not delay urgent
operative irrigation and debride-
ment. If a hip effusion is noted, the
ultrasonographer can assist with a
guided aspiration and can docu-
ment the intra-articular positioning
of the needle. If ultrasonography is
not available, a possibly infected
hip can be aspirated with fluoro-
scopic guidance.
In one series of 44 patients with
a limp or hip pain and negative
plain radiographs, ultrasonog-
raphy was 100% accurate in pre-
dicting the presence of aspiration-
documented hip effusion.21 Another
larger prospective study of 111 chil-
dren with irritable hips confirmed
that the plain radiograph was of lit-
tle value in the detection of early
hip effusion; in that study, there
was radiographic evidence of effu-
sion in 15% of hips, compared with
sonographic evidence of effusion in
71% of hips.15 Furthermore, Zawin
et al 22 showed that ultrasound-
guided hip aspiration in the radiol-
ogy suite decreased the subsequent
operative time for septic hips by
50%. However, a large prospective
study of 500 painful hips in chil-
dren demonstrated that ultrasound
cannot effectively differentiate
among sterile, purulent, and hem-
orrhagic effusions.23 The authors of
that study concluded that ultra-
sonography of the hip should be
reserved for select cases in which
sepsis is suspected.
Ultrasound evaluation of the irri-
table hip is performed with the
transducer oriented in an oblique
sagittal plane parallel to the long
axis of the femoral neck with the hip
in extension.12 An effusion causes
Vol 9, No 2, March/April 2001
John M. Flynn, MD, and Roger F. Widmann, MD
Femoral
head
Hip capsule
Effusion
A B
Figure 4 A, A 12-year-old girl presented with an antalgic limp on the right and thigh
pain. She had pain with internal rotation of the hip, suggesting an effusion. The plain radio-
graph was normal. B, Sonogram of the right hip shows an effusion. Ultrasound-guided
aspiration yielded purulent fluid. Drainage of the septic hip was performed immediately.
bulging of the iliofemoral ligament, proved to be the most effective im-
so that the joint capsule appears aging modality for bone marrow,
convex; the normal opposite capsule joints, cartilage, and soft tissues
will be concave.22 (Fig. 6, C). It is extremely useful in
Ultrasonography can help con- cases of suspected tumor and stress
firm the diagnosis of osteomyelitis fractures.
on the basis of characteristic early
and late ultrasonographic clinical
features.24 Early changes, such as Laboratory Testing
deep soft-tissue swelling, are fol-
lowed by periosteal thickening. Infection, inflammatory disease, and
Subperiosteal fluid or abscess is seen malignancy all demand rapid diag-
as a later finding 1 to 2 weeks after nosis and treatment, and laboratory
the onset of symptoms. The main testing may assist both in making
value of ultrasound imaging of the the appropriate diagnosis and in
extremity in cases of suspected in- monitoring the efficacy of treatment.
fection is to rule out subperiosteal Laboratory testing is indicated when
abscess.20 a child presents with an acute non-
Cross-sectional imaging, includ- traumatic limp and signs and symp-
ing computed tomography (CT) and toms of fever, malaise, night pain, or
magnetic resonance (MR) imaging, localized complaints. Appropriate
is rarely necessary as an initial tests include a complete blood cell
study in the evaluation of a limping count with differential and determi-
child. Computed tomography is in- nation of the ESR, the C-reactive
dicated specifically for imaging of protein (CRP) and antinuclear anti-
suspected localized abnormalities of body levels, and the rheumatoid fac-
cortical bone (Fig. 5). It may also tor and Lyme titers.
confirm the presence of either a cen- In the setting of bone or joint
tral nidus in cases of osteoid osteoma infection, the WBC count is neither
or the occurrence of a tarsal coalition. sensitive nor specific. Although the
Magnetic resonance imaging has WBC count is elevated in 25% to
95
The Limping Child
A B
Figure 5 A, A 10-year-old soccer player presented with a limp and thigh pain of 4 weeks’
duration. AP radiograph shows a radiodense area in the medial subtrochanteric region.
B, CT scan obtained to better characterize the sclerotic area shows a pattern typical of a
femoral-neck stress fracture. A biopsy was avoided. The pain and limp resolved after 2
months of protected weight bearing.
31% of children with osteomyeli-
tis, 25 normal values for the WBC
count are seen frequently in osteo-
myelitis.26 The differential is more
sensitive and may be abnormal in as
many as 65% of children with osteo-
myelitis and 70% with septic arthri-
tis. The complete blood cell count
may reveal moderate to severe ane-
mia in cases of systemic juvenile
rheumatoid arthritis (JRA), as well
as leukocytosis with active disease.8
Patients with systemic-onset JRA
may present with WBC counts in the
range of 30,000 to 50,000/mm3. The
platelet count may rise considerably
as well.
The ESR is a sensitive indicator
of inflammation and is most helpful
in the diagnosis and follow-up of
bone or joint infection. The ESR
reflects changes in the concentration
of fibrinogen synthesized by the
liver, which increases after 24 to 48
hours and may not return to normal
for 3 weeks with appropriate treat-
ment.27 In one study of previously
well children with new-onset limp,
an ESR elevated to over 50 mm/hr
was associated with a clinically im-
portant diagnosis in 77% of cases.28
The ESR is also a sensitive indicator
96
of infection and is elevated in 90%
of patients with osteomyelitis.16,25
However, early in the course of in-
fection, the ESR may be normal. Ex-
treme elevation of ESR in what ap-
pears to be isolated osteomyelitis
should raise the question of associ-
ated septic arthritis.
C-reactive protein is an acute-
phase protein synthesized by the
liver in response to inflammation.
Unlike the ESR, the CRP level rises
within 6 hours of onset of symp-
toms and returns to normal within 6
to 10 days with appropriate treat-
ment. The CRP level is more sensi-
tive than the WBC count or the ESR
in assessing the effectiveness of
therapy and predicting recovery
from osteomyelitis and septic arthri-
tis.27,29 The CRP value is not influ-
enced by prior aspiration or drilling
of the cortex, and a secondary rise
suggests relapse.29 The CRP level
should be determined on the initial
screening examination if musculo-
skeletal infection is in the differen-
tial diagnosis.
Aspiration and evaluation of joint
fluid should be performed when
joint sepsis is considered in the dif-
ferential diagnosis. Of the large
Journal of the American Academy of Orthopaedic Surgeons
joints, the hip is the most technically
difficult to aspirate. Sedation and
local anesthesia are helpful, and
aspiration under fluoroscopic guid-
ance with arthrography at the com-
pletion of the procedure is recom-
mended to confirm appropriate
spinal needle placement within the
joint.30 Ultrasound-guided aspira-
tion provides similar confirmation of
needle placement. Culture and cell
counts should be obtained in all
cases. A WBC count greater than
80,000/mm3 with a percentage of
polymorphonuclear cells greater
than 75% is highly suggestive of
joint sepsis, although early sepsis
may present with a much lower cell
count.30
The rheumatoid factor and anti-
nuclear antibody levels are deter-
mined when inflammatory arthritis
is a possibility. In practice, JRA is
the most frequently diagnosed pedi-
atric arthritis.31 It must be noted
that the rheumatoid factor test is
positive in only 15% to 20% of chil-
dren with JRA, and is more fre-
quently positive in older children
and children in a poor functional
class. 8 The finding of a positive
antinuclear antibody test is impor-
tant in the identification of children
most at risk for the development of
chronic uveitis, which may result in
blindness if untreated.
Testing for Lyme disease should
be performed on any patient who
presents with acute arthritis and
who lives in or has recently traveled
to an endemic area.32 The presenta-
tion of acute Lyme arthritis may
have considerable overlap with that
of septic arthritis, including fever,
local swelling, pain with range of
joint motion, and an elevated WBC
count in joint aspirate. Serologic
confirmation of Lyme disease is
based on a two-test approach con-
sisting of a preliminary enzyme-
linked immunosorbent assay and a
confirmatory Western immunoblot
assay, which specifically examines
the reactivity of antibodies.32
 John M. Flynn, MD, and Roger F. Widmann, MD

A B C

Figure 6 An 11-year-old girl sustained a suspected distal fibular physeal fracture. AP (A) and lateral (B) plain radiographs of the ankle
taken 10 days after the injury. C, Because of persistent pain and an ESR of 35 mm/hr, an MR imaging study of the distal portion of the leg
was obtained. The appearance of this transverse section at the distal fibula is consistent with fibular osteomyelitis and soft-tissue swelling
with an abscess, which were successfully treated with surgical drainage and antibiotic therapy. Cultures grew Staphylococcus aureus.

Making the Diagnosis
When a limping child is brought for
musculoskeletal evaluation, some
potential diagnoses require urgent
treatment to ensure the best possible
outcome. Some conditions affect all
age groups, but many conditions
have a peak age of onset. Although
there is increasing interest in prac-
tice standardization with use of
algorithms for many musculoskele-
tal conditions, there are so many
exceptions in the evaluation of the
limping child that any single algo-
rithm will be unreliable for all pre-
sentations. Despite this complexity,
there are five essential questions
that the orthopaedist must answer
to direct the evaluation of a limping
child: (1) Is the limp due to pain?
(2) Did the limp develop suddenly
or gradually, or has it always been
there? (3) Is the child systemically
ill? (4) What type of limp does the
child exhibit? (5) Can the problem
be localized (specifically, is there a
point of maximum tenderness)?
The answers to these questions will
narrow the differential diagnosis
and establish the pace of evalua-
tion. 33 Determining whether the
gait is antalgic is the first step in
developing a differential diagnosis
(Tables 1 and 2).
The answers to these five essen-
tial questions direct the evaluation
of different clinical scenarios. For
example, a healthy 4-year-old pre-
sents with the gradual onset of a
painless Trendelenburg gait. Exami-
nation shows that there is unilateral
limitation of hip motion. The work-
up of this limp requires only a plain
radiograph to establish the diagnosis
of Legg-Calvé-Perthes disease or de-
velopmental dysplasia of the hip.
In a very different scenario, an ill
child presents with the sudden
onset of an antalgic gait. Samples
for screening laboratory studies
should be drawn, and plain radio-
graphs should be obtained for ana-
tomic localization. If the site cannot
be localized, a bone scan is valu-
able. An MR imaging study may
add important information, espe-
cially if a malignant condition is
suspected. If septic arthritis of the
hip is a possibility, ultrasound-
guided aspiration may be indicated.
Unfortunately, the presentations
are usually not this straightforward.
The most common challenge is de-
termining whether an acute limp is
due to trauma. A typical case is illus-
trated in Figure 6. The 11-year-old
patient had ankle pain after falling.
Her pain persisted after casting of a
suspected fibular physeal fracture.
The plain-radiographic appearance
remained normal. Her limp was
clearly due to pain, which was wors-
ening with time. Because this was un-
characteristic for trauma, laboratory
tests were obtained, which revealed
an ESR of 35 mm/hr. Because the
process could be localized by pain
and swelling around the distal fibula,
a bone scan was not needed. An MR
imaging study obtained to simultane-
ously evaluate the soft tissues, the
bone, and the ankle joint revealed
osteomyelitis with a soft-tissue ab-
scess. The patient was successfully
treated with surgical drainage and
antibiotics.

Vol 9, No 2, March/April 2001 97

The Limping Child
Summary
Limping children commonly present
to the orthopaedic surgeon, who is
expected to recognize the gait abnor-
mality, determine the probable
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tion. Radiology 1993;187:459-463.
23. Miralles M, Gonzalez G, Pulpeiro JR,
et al: Sonography of the painful hip in
children: 500 consecutive cases. AJR
Am J Roentgenol 1989;152:579-582.
24. Mah ET, LeQuesne GW, Gent RJ,
Journal of the American Academy of Orthopaedic Surgeons
standing of normal and abnormal
gait, the orthopaedist can use the
child’s age and the answers to five
essential questions to develop a dif-
ferential diagnosis and plan a selec-
tive approach to diagnostic testing.
Paterson DC: Ultrasonic features of
acute osteomyelitis in children. J Bone
Joint Surg Br 1994;76:969-974.
25. Faden H, Grossi M: Acute osteomye-
litis in children: Reassessment of etio-
logic agents and their clinical charac-
teristics. Am J Dis Child 1991;145:65-69.
26. Fink CW, Nelson JD: Septic arthritis
and osteomyelitis in children. Clin
Rheum Dis 1986;12:423-435.
27. Unkila-Kallio L, Kallio MJT, Peltola H:
The usefulness of C-reactive protein
levels in the identification of concur-
rent septic arthritis in children who
have acute hematogenous osteomye-
litis: A comparison with the usefulness
of the erythrocyte sedimentation rate
and the white blood-cell count. J Bone
Joint Surg Am 1994;76:848-853.
28. Huttenlocher A, Newman TB: Evalua-
tion of the erythrocyte sedimentation
rate in children presenting with limp,
fever, or abdominal pain. Clin Pediatr
(Phila) 1997;36:339-344.
29. Unkila-Kallio L, Kallio MJT, Eskola J,
Peltola H: Serum C-reactive protein,
erythrocyte sedimentation rate, and
white blood cell count in acute hema-
togenous osteomyelitis of children.
Pediatrics 1994;93:59-62.
30. Morrissy RT, Shore SL: Septic arthritis
in children, in Gustilo RB, Gruninger
RP, Tsukayama DT (eds): Orthopaedic
Infection: Diagnosis and Treatment.
Philadelphia: WB Saunders, 1989, pp
261-270.
31. Cassidy JT, Nelson AM: The frequen-
cy of juvenile arthritis [editorial]. J
Rheumatol 1988;15:535-536.
32. Rose CD, Fawcett PT, Eppes SC, Klein
JD, Gibney K, Doughty RA: Pediatric
Lyme arthritis: Clinical spectrum and
outcome. J Pediatr Orthop 1994;14:
238-241.
33. Choban S, Killian JT: Evaluation of
acute gait abnormalities in preschool
children. J Pediatr Orthop 1990;10:74-78.
 Medial Elbow Problems in the
Overhead-Throwing Athlete

Frank S. Chen, MD, Andrew S. Rokito, MD, and Frank W. Jobe, MD

Abstract

The elbow is subjected to enormous valgus stresses during the throwing motion, pronation-supination through the
which places the overhead-throwing athlete at considerable risk for injury. ulnohumeral and radiocapitellar
Injuries involving the structures of the medial elbow occur in distinct patterns. articulations, respectively. In full
Although acute injuries of the medial elbow can occur, the majority are overuse extension, the elbow has a normal
injuries as a result of the repetitive forces imparted to the elbow by throwing. valgus carrying angle of 11 to 16
Injury to the ulnar collateral ligament complex results in valgus instability. degrees. The osseous configuration
Valgus extension overload leads to diffuse osseous changes within the elbow joint provides approximately 50% of the
and secondary posteromedial impingement. Overuse of the flexor-pronator mus- overall stability of the elbow, pri-
culature may result in medial epicondylitis and occasional muscle tears and rup- marily against varus stress with the
tures. Ulnar neuropathy is a common finding that may be due to a variety of elbow in extension. The remaining
factors, including traction, friction, and compression of the ulnar nerve. stability of the elbow is provided
Advances in nonoperative and operative treatment regimens specific to each by the anterior joint capsule, the
injury pattern have resulted in the restoration of elbow function and the success- ulnar collateral ligament (UCL)
ful return of most injured overhead athletes to competitive activities. With fur- complex, and the radial collateral
ther insight into the relevant anatomy, biomechanics, and pathophysiology ligament complex.1-3
involved in overhead activities and their associated injuries, significant contribu- The UCL complex is composed
tions can continue to be made toward prevention and treatment of these injuries. of three main portions: the anterior
J Am Acad Orthop Surg 2001;9:99-113 bundle, the posterior bundle, and
the oblique bundle (transverse liga-
ment) (Fig. 1). The anterior bundle,
consisting of parallel fibers insert-
The elbow is subjected to tremen- account for up to 97% of elbow ing onto the medial coronoid pro-
dous valgus stresses during over- complaints in pitchers. However,
head activities, which result in spe- athletes who participate in other
cific injury patterns unique to the sports that require similar over-
Dr. Chen is Sports Medicine Fellow, Depart-
throwing athlete. The forces gener- head motion, such as football, volley- ment of Orthopaedic Surgery, University of
ated as the result of repetitive throw- ball, tennis, and javelin throwing, Southern California School of Medicine, Los
ing are primarily concentrated on can be likewise affected. A thor- Angeles. Dr. Rokito is Associate Director,
the medial structures of the elbow. ough understanding of functional Sports Medicine Service, and Assistant Chief,
Shoulder Service, Department of Orthopaedic
Consequently, medial elbow prob- elbow anatomy and the biome-
Surgery, Hospital for Joint Diseases, New
lems predominate in the athlete chanics of throwing is essential to York, NY. Dr. Jobe is Associate, Kerlan-Jobe
engaged in overhead activities. the recognition, diagnosis, and Orthopaedic Clinic, Los Angeles; and Clinical
Although acute traumatic injuries treatment of these specific elbow Professor of Orthopaedic Surgery, University
to the osseous, musculotendinous, injuries. of Southern California School of Medicine.
and ligamentous structures of the
Reprint requests: Dr. Chen, USC Department
elbow may occur, the majority are
of Orthopaedic Surgery, Suite 322, 1510 San
chronic overuse injuries resulting Functional Anatomy of the Pablo, Los Angeles, CA 90033.
from repetitive intrinsic and ex- Medial Elbow
trinsic overload. Baseball players Copyright 2001 by the American Academy of
are the athletes most commonly The osseous anatomy of the el- Orthopaedic Surgeons.
affected; medial elbow symptoms bow allows flexion-extension and

Vol 9, No 2, March/April 2001 99

Medial Elbow Problems in the Overhead-Throwing Athlete
Posterior
bundle
Anterior
bundle
Transverse ligament
Figure 1 The UCL complex consists of
the anterior bundle (functionally the most
important for valgus stability), the posteri-
or bundle, and the transverse ligament
(oblique bundle). The anterior bundle is
further subdivided into anterior and poste-
rior bands, which perform reciprocal func-
tions. (Adapted with permission from
Kvitne RS, Jobe FW: Ligamentous and
posterior compartment injuries, in Jobe FW
[ed]: Techniques in Upper Extremity Sports
Injuries. Philadelphia: Mosby-Year Book,
1996, p 412.)
cess, is functionally the most im-
portant in providing stability
against valgus stress.1,2,4 Its origin
is the inferior aspect of the medial
epicondyle of the humerus. The
anterior bundle is eccentrically
located with respect to the axis of
elbow motion, enabling it to pro-
vide stability throughout the full
range of motion. 3 The anterior
bundle is further subdivided into
distinct anterior and posterior
bands, which perform reciprocal
functions.2,5,6 The anterior band is
the primary restraint to valgus
stress up to 90 degrees of flexion,
and becomes a secondary restraint
with further flexion.6 The posterior
band is a secondary restraint at
lesser degrees of flexion, but be-
comes functionally more important
between 60 degrees and full flex-
ion.5,6 Sequential tightening occurs
within the fibers of the anterior
bundle, progressing from anterior
to posterior as the elbow flexes. 5
The posterior band is nearly iso-
100
metric and is functionally more pect of the joint capsule extending
important in the overhead athlete, from the medial olecranon to the
as it is the primary restraint to val- inferior medial coronoid process.3
gus stress with higher degrees of The musculotendinous anatomy
flexion (N. ElAttrache, MD, F.W.J., of the elbow originating from the
J.G. Rosen, unpublished data). The medial epicondyle includes the
anterior band is more vulnerable to flexor-pronator musculature and
valgus stress with the elbow ex- provides dynamic functional resis-
tended, whereas the posterior band tance to valgus stress.7 From proxi-
is more vulnerable with the elbow mal to distal, this muscle mass
flexed.2,3,5,6 includes the pronator teres, flexor
The fan-shaped posterior bundle carpi radialis (FCR), palmaris lon-
of the UCL complex originates from gus, flexor digitorum superficialis,
the medial epicondyle and inserts and flexor carpi ulnaris (FCU). The
onto the medial margin of the semi- pronator teres and FCR arise from
lunar notch. It is thinner and weaker the medial supracondylar ridge.
than the anterior bundle and pro- The palmaris longus originates
vides secondary elbow stability at from the anterior midportion of the
flexion beyond 90 degrees.1,2,5 The medial epicondyle. The FCU arises
posterior bundle has been shown to from the anterior base of the epi-
be vulnerable to valgus stress only condyle and possesses both humeral
if the anterior bundle is completely and ulnar heads.
disrupted.6 The ulnar nerve is commonly
The oblique bundle, or trans- susceptible to injury during over-
verse ligament, does not cross the head athletic activities (Fig. 2).
elbow joint. Rather, it serves to ex- Proximally, the ulnar nerve passes
pand the greater sigmoid notch as through the arcade of Struthers,
a thickening of the caudalmost as- which is located approximately 8
Biceps
Brachialis
Flexor-pronator Arcade of
mass Struthers
Triceps
Medial intermuscular
septum
Flexor carpi Ulnar nerve
ulnaris Cubital Medial
tunnel epicondyle
Figure 2 The ulnar nerve courses around the medial aspect of the elbow. Proximally, the
nerve passes beneath the arcade of Struthers, runs along the medial intermuscular septum,
enters the cubital tunnel around the medial epicondyle, and passes through the two heads
of the FCU. (Adapted with permission from Boatright JR, D’Alessandro DF: Nerve
entrapment syndromes at the elbow, in Jobe FW, Pink MM, Glousman RE, Kvitne RE,
Zemel NP [eds]: Operative Techniques in Upper Extremity Sports Injuries. St Louis: Mosby-
Year Book, 1996, p 520.)
Journal of the American Academy of Orthopaedic Surgeons

cm proximal to the medial epicon-
dyle. The arcade, running obliquely
and superficial to the ulnar nerve, is
composed of the deep investing fas-
cia of the arm, the superficial fibers
of the medial head of the triceps,
and an expansion of the coraco-
brachialis tendon. The ulnar nerve
then traverses the medial intermus-
cular septum at the midpoint of the
arm as it passes from the anterior to
the posterior compartment. An
anastomotic arterial network con-
sisting of branches of the superior
and inferior ulnar collateral arteries
proximally and the posterior ulnar
collateral artery distally accompa-
nies the nerve as it enters the cu-
bital tunnel.
The floor of the cubital tunnel is
formed by the UCL, whereas the
roof is formed by the overlying arcu-
ate, or Osborne, ligament. The me-
dial head of the triceps constitutes
the posterior border of the tunnel;
the anterior and lateral borders are
formed by the medial epicondyle
and the olecranon, respectively.
After traversing the cubital tun-
nel, the ulnar nerve enters the fore-
arm by passing between the two
heads of the FCU, eventually rest-
ing on the flexor digitorum profun-
dus. The sensory fibers within the
ulnar nerve are located more pe-
ripheral and anteromedial than the
motor fibers and are therefore more
susceptible to injury.8
Biomechanics of Throwing
Although specific techniques of
overhead throwing vary with differ-
ent sports, the overall basic throw-
ing motion is similar. The baseball
pitch has been the most studied and
can be divided into five main stages
(Fig. 3). 3,9-13 Stage I, or windup,
involves initial preparation as the
elbow is flexed and the forearm is
slightly pronated. Stage II, or early
cocking, begins when the ball leaves
the nondominant gloved hand and
Vol 9, No 2, March/April 2001
Windup Early
cocking
Start Hands Foot
apart down
Figure 3 The five main stages of the overhead throwing motion. (Adapted with permis-
sion from DiGiovine NM, Jobe FW, Pink M, Perry J: An electromyographic analysis of the
upper extremity in pitching. J Shoulder Elbow Surg 1992;1:15-25.)
ends when the forward foot comes
in contact with the ground. The
shoulder begins to abduct and exter-
nally rotate. Stage III, or late cocking,
is characterized by further shoulder
abduction and maximal external
rotation, as well as elbow flexion
between 90 and 120 degrees and
increasing forearm pronation to 90
degrees.
Rapid acceleration of the upper
extremity, or stage IV, follows and
is marked by the generation of a
large forward-directed force on the
extremity by the shoulder muscula-
ture, resulting in internal rotation
and adduction of the humerus cou-
pled with rapid elbow extension.
Stage IV terminates with ball release
and occurs over a period of only
40 to 50 msec, during which the el-
bow accelerates as much as 600,000
degrees/sec2.14 Tremendous valgus
stresses are generated about the
medial aspect of the elbow. The
anterior bundle of the UCL complex
bears the principal portion of these
forces; the secondary supporting
structures (e.g., the flexor-pronator
musculature) facilitate transmission
of these forces.7,11 Most elbow in-
Frank S. Chen, MD, et al
Deceleration
Late Acceleration Follow-
cocking through
Maximal Ball Finish
external release
rotation
juries occur during stage IV (accel-
eration) as a result of the concentra-
tion of stresses and loads on the
medial elbow structures.
Stage V, or follow-through, in-
volves dissipation of all excess
kinetic energy as the elbow reaches
full extension and ends when all
motion is complete. Rapid and
forceful deceleration of the upper
extremity occurs at a rate of almost
500,000 degrees/sec 2 over a time
span of 50 msec. 3,9-14 Throwing
curveballs, which theoretically re-
quires elbow deceleration over a
shorter time interval and potentially
results in greater elbow angular
velocities, has not been clinically
shown to have greater adverse
effects on the elbow.13,15
Valgus Instability
Injury to the UCL, initially recog-
nized in javelin throwers, has been
reported to occur with increasing
frequency in other types of over-
head athletes as well. Microtears of
the UCL occur once the valgus
forces generated during the cocking
101
Medial Elbow Problems in the Overhead-Throwing Athlete
and acceleration phases of throwing
exceed the intrinsic tensile strength
of the UCL. Improper throwing
mechanics, poor flexibility, and in-
adequate conditioning result in ad-
ditional cumulative stress transmis-
sion to the UCL complex, leading to
attenuation and eventual rupture of
the UCL.3,15
Evaluation
The diagnosis of valgus instabil-
ity is based on the athlete’s history,
physical examination, and radio-
graphic studies. Patients with acute
UCL injury usually experience the
sudden onset of pain after throw-
ing—with or without an associated
popping sensation—and are unable
to continue throwing. Patients with
chronic injury usually describe a
gradual onset of localized medial
elbow pain during the late-cocking
or acceleration phase of throwing.
Athletes may also describe pain
after an episode of heavy throwing
that results in the inability to subse-
quently throw at more than 50% to
75% of their normal level. Patients
with chronic instability also com-
monly present with ulnar nerve
symptoms. This is due to local in-
flammation of the ligamentous
complex, which produces second-
ary irritation of the ulnar nerve
within the cubital tunnel.3
Physical examination of the elbow
for valgus instability is best per-
formed with the patient seated and
the wrist secured between the exam-
iner’s forearm and trunk (Fig. 4, A).
The patient’s elbow is flexed be-
tween 20 and 30 degrees to unlock
the olecranon from its fossa as a val-
gus stress is applied.8 This maneu-
ver stresses the anterior band of the
anterior bundle of the UCL.3,8,16 It is
important to palpate the UCL along
its course from the medial epicon-
dyle toward the proximal ulna as
valgus stress testing is performed.
Valgus laxity is manifested by in-
creased medial joint-space opening
as compared to the contralateral
102
extremity. Comparison with the un- sion) secondary to flexion contrac-
involved elbow should always be tures (which develop as a result of
performed to differentiate between the repeated attempts at healing
physiologic and pathologic laxity. and stabilization) may also be pres-
Loss of a firm endpoint coupled with ent in cases of chronic valgus insta-
increased medial joint-space opening bility.8 Overall performance by the
with valgus stress is consistent with athlete, however, may not be signifi-
an attenuated or incompetent UCL. cantly compromised, as the throwing
Testing of the functionally more motion does not require full elbow
important posterior band of the extension and can be accomplished
anterior bundle can be accomplished with a flexion arc between 20 and
by the milking maneuver, which is 120 degrees.16
performed by pulling on the pa- Routine radiographs may show
tient’s thumb with the patient’s fore- changes consistent with chronic
arm supinated, shoulder extended, instability, such as calcification and
and elbow flexed beyond 90 degrees occasionally ossification of the liga-
(Fig. 4, B).3 This maneuver gener- ment. Stress radiographs can be
ates a valgus stress on the flexed el- used to confirm instability, especially
bow; a subjective feeling of appre- in apprehensive patients and in pa-
hension and instability, in addition tients in whom the clinical findings
to localized medial-side elbow pain, are equivocal (Fig. 5). Medial joint
is indicative of UCL injury. opening greater than 3 mm is con-
Point tenderness and swelling sistent with instability.2,3
over the UCL vary with the amount Magnetic resonance (MR) imag-
of inflammation and edema present. ing is useful in evaluating ligamen-
The absence of increased pain with tous avulsions, partial ligamentous
wrist flexion, combined with pain injuries, midsubstance tears, and the
localization slightly posterior to the status of the surrounding soft tis-
common flexor origin, differentiates sues.3,17 Computed tomographic ar-
UCL injury from flexor-pronator thrography has also been reported
muscle injury.3,15,16 Decreased range to be useful in the evaluation of the
of motion (loss of terminal exten- UCL complex.
A B
Figure 4 A, Examination of the anterior band of the anterior bundle of the UCL complex
is performed with the patient sitting and the elbow slightly flexed as a valgus stress is
applied to the elbow. B, The milking maneuver, performed with the patient’s elbow flexed
beyond 90 degrees while applying a valgus stress, tests the posterior band of the anterior
bundle of the UCL complex. (Adapted with permission from Kvitne RS, Jobe FW:
Ligamentous and posterior compartment injuries, in Jobe FW [ed]: Techniques in Upper
Extremity Sports Injuries. Philadelphia: Mosby-Year Book, 1996, p 415.)
Journal of the American Academy of Orthopaedic Surgeons

Figure 5 Gravity valgus stress radio-
graphs—taken with the patient supine and
the unsuspended, externally rotated arm
held out at the side to allow the weight of
the forearm to deliver a valgus stress to the
elbow—are a helpful adjunct in the diagno-
sis of valgus instability. (Reproduced with
permission from Miller CD, Savoie FH III:
Valgus extension injuries of the elbow in
the throwing athlete. J Am Acad Orthop
Surg 1994;2:261-269.)
Treatment
Specific treatment programs may
be implemented after the diagnosis
of valgus instability is made. Ini-
tially, a nonoperative treatment pro-
tocol is instituted to reduce inflam-
mation and pain. A brief period of
rest (2 to 4 weeks) is recommended,
coupled with use of nonsteroidal
anti-inflammatory medications
(NSAIDs) and local physical therapy
modalities. Corticosteroid injections
are not recommended, as further lig-
amentous attenuation may occur.
Once the acute inflammation has
subsided, a supervised flexibility
and strengthening program is insti-
tuted, aimed at restoring muscle
tone, strength, and endurance to
provide dynamic elbow stability.
The pronator teres, FCU, and flexor
digitorum superficialis should be
targeted, as they are potentially
important secondary dynamic stabi-
lizers of the elbow.7,9,11,13 Electromy-
ographic analysis has shown maxi-
mal activity of the flexor-pronator
mass during the acceleration phase
of the pitching cycle in healthy ath-
letes; however, in athletes with val-
gus instability, a paradoxical de-
Vol 9, No 2, March/April 2001
crease in activity has been observed
in these muscle groups.10,11 This
finding may be a reflection of the
primary disorder predisposing the
elbow to instability, or may be at-
tributable to muscular inhibition
through a painful feedback loop
arising from injury to the UCL com-
plex.10,11 This situation is similar to
that observed in overhead athletes
with anterior shoulder instability in
which the subscapularis (a dynamic
stabilizer of the shoulder) has been
shown to have decreased activity.10
Strengthening and conditioning of
the flexor-pronator mass may po-
tentially enhance performance by
increasing valgus stabilization and
theoretically increasing functional
protection of the UCL.7,10
A well-supervised throwing and
conditioning program is begun at 3
months, once the athlete has regained
full range of motion and strength.
In addition, an evaluation of the
athlete’s throwing motion is essen-
tial to identify and correct improper
mechanics. Nonoperative manage-
ment instituted at an early stage has
been shown to arrest the progres-
sion of instability and functional
impairment, with as many as 50% of
athletes being able to return to their
preinjury level of throwing.
Surgical intervention is indicated
for competitive athletes with acute
complete ruptures of the UCL or
chronic symptoms secondary to in-
stability that have not significantly
improved after at least 3 to 6 months
of nonoperative management. Op-
erative treatment consists of either
repair or reconstruction of the UCL.
The goals of surgery are to reestab-
lish stability of the elbow and to
allow the athlete to return to maxi-
mal functional levels.3
Direct repair of the UCL is re-
served for acute ligamentous avul-
sions from the humeral origin or
the coronoid insertion.15,16,18 More
commonly, however, chronic repet-
itive microtrauma leads to attenua-
tion and midsubstance tears of the
Frank S. Chen, MD, et al
ligament. The UCL is significantly
scarred and tenuous, precluding an
effective primary repair. In these
cases, graft reconstruction of the
ligament is necessary. Options for
autologous grafts include the ipsi-
lateral or contralateral palmaris
longus tendon, the plantaris ten-
don, a 3.5-mm medial strip of the
Achilles tendon, or a portion of the
hamstring tendons.3,15,16 Allografts
may also be utilized.
Surgical reconstruction begins
with an approach centered over the
medial epicondyle. Care must be
taken to preserve the medial ante-
brachial cutaneous nerve. Next,
while preserving the flexor-pronator
origin on the medial epicondyle, the
common flexor mass is split longitu-
dinally in line with its fibers in its
posterior third near the FCU and
subsequently separated from the un-
derlying ligamentous-capsular com-
plex. The ligament is next inspected
as a valgus stress is applied. The
ligamentous-capsular complex is
then incised to allow access into the
elbow joint. Any osteophytes, loose
bodies, and calcifications should be
removed. Posterior compartment
involvement, if present in cases of
chronic instability, may be addressed
through a separate posteromedial
arthrotomy posterior to the ulnar
nerve.8,16 Loose bodies in the poste-
rior compartment, as well as osteo-
phytes on the posteromedial olec-
ranon margin, may be removed
through this approach.
Next, the anatomic origin and
insertion of the anterior bundle of
the UCL are identified. Osseous
tunnels are then made in the proxi-
mal ulna at the level of the coronoid
tubercle and in the medial epicon-
dyle at the level of the anatomic
UCL origin (Fig. 6, A). A single
entrance hole is made in the medial
epicondyle, with two divergent exit
holes anterosuperiorly. The drill
holes must be placed precisely at
the anatomic origin and insertion
sites of the native UCL to maintain
103
Medial Elbow Problems in the Overhead-Throwing Athlete

Ulnar nerve Ulnar nerve

A B Frontal View Medial View

C D

Figure 6 A, Transosseous drill holes through the medial epicondyle and olecranon are made for preparation of graft passage. Care is
taken to avoid penetration of the posterior cortex of the medial epicondyle to prevent injury to the ulnar nerve within the cubital tunnel.
B, Divergent exit tunnels are placed within the medial epicondyle near the anatomic origin of the anterior bundle of the UCL. C, The
autologous graft is passed in a figure-of-eight fashion through transosseous drill holes in the medial epicondyle and olecranon. D, The
graft is subsequently tensioned and sutured to itself in 45 degrees of flexion and neutral varus-valgus alignment. (Adapted with permis-
sion from Kvitne RS, Jobe FW: Ligamentous and posterior compartment injuries, in Jobe FW [ed]: Techniques in Upper Extremity Sports
Injuries. Philadelphia: Mosby-Year Book, 1996, pp 420-422.)

the isometricity and camlike func-
tion of the reconstructed ligament.
The harvested graft is then placed
in a figure-of-eight configuration
through the transosseous tunnels
and subsequently tensioned and
sutured to itself with the elbow in 45
degrees of flexion and neutral varus-
valgus alignment (Fig. 6, B and C).
The elbow is taken through a full
range of motion, and the graft is
carefully inspected for isometricity,
stability, and contact with the sur-
rounding bone and tissues. A con-
current ulnar nerve transposition
may be performed in cases of con-
comitant ulnar neuritis, ulnar nerve
subluxation, or pathologic nerve
constrictions noted at the time of
surgery.3,16 Routine transpositions
are no longer performed, because of
the risk of nerve injury secondary to
segmental devascularization, intra-
operative compression or traction,
and postoperative scarring.
Postoperative complications most
commonly involve injury to the
medial antebrachial cutaneous and
ulnar nerves. Recurrent instability
secondary to rupture or stretch of
the reconstructed ligament occurs
infrequently.15,16
After a brief period of postopera-
tive immobilization (7 to 10 days),
active shoulder, elbow, and wrist
range-of-motion exercises are initi-
ated. Progressive resistive strength-
ening exercises of the wrist and fore-
arm are begun after 4 to 6 weeks,
including flexion, extension, prona-
tion, and supination. At 6 weeks,
progressive elbow-strengthening
exercises are begun, but valgus
stress of the elbow is avoided until 4
months. Shoulder range-of-motion
exercises are begun early and main-
tained throughout the rehabilitation
period. Strengthening exercises

104 Journal of the American Academy of Orthopaedic Surgeons


emphasizing the rotator cuff are
instituted at 2 to 3 months, begin-
ning with gentle isotonic exercises
and progressing to the use of light
weights.
A progressive throwing program
beginning with light tossing is insti-
tuted at 3 to 4 months. Distance
and speed are gradually increased
as strength, power, and endurance
of the shoulder and elbow muscles
improve. By 6 months, patients may
be allowed to begin lobbing the ball
for a distance of 60 ft using an easy
windup. At 7 months, throwing is
advanced to 50% of maximum ve-
locity; by 8 to 9 months, pitchers are
permitted to return to the mound
and progress to approximately 70%
of maximum velocity. Careful at-
tention is also paid to optimization
of overall pitching mechanics, in-
cluding those motions involving
the torso and lower extremities.
Functional performance, including
rhythm, proprioception, and accu-
racy, is usually maximized by 12 to
18 months after surgery, at which
time most athletes will be able to
return to their preinjury level of ac-
tivity.3,15,16
Results
Jobe et al15 reported on 16 throw-
ing athletes who underwent UCL
reconstruction with ulnar nerve
transposition. Ten (63%) were able
to return to their preinjury level of
activity.
Conway et al16 subsequently re-
ported on 70 procedures in 68 pa-
tients with valgus instability of the
elbow; 14 elbows were treated by
direct repair of the UCL, and 56
underwent ligamentous reconstruc-
tion with use of a free autologous
tendon graft. Ten elbows (71%) in
the direct-repair group and 45
(80%) in the reconstruction group
demonstrated good or excellent
results at a mean follow-up of 6.3
years. Seven patients (50%) in the
repair group were able to return to
preinjury competition levels, in-
Vol 9, No 2, March/April 2001
Frank S. Chen, MD, et al
cluding 2 of 7 professional baseball structures of the elbow. Micro-
players who had not undergone trauma and inflammation of the
previous elbow surgery. In the re- UCL occur, with eventual attenua-
construction group, 38 (68%) were tion and insufficiency of the liga-
able to return to preinjury levels of mentous complex. The elbow be-
competition, including 12 of 16 pro- comes subluxated in valgus during
fessional baseball players who had extension, leading to excessive force
not undergone previous elbow transmission to the lateral aspect of
surgery. The mean time to return the elbow, as well as extension over-
to competition was 9 months in the load within the posterior compart-
repair group and 12 months in the ment (Fig. 7). Compressive and rota-
reconstruction group. Previous tory forces are increased within the
surgery on the elbow was found to radiocapitellar articulation, leading
decrease the likelihood that athletes to synovitis and the development of
would return to their previous level osteochondral lesions (osteochondri-
of function. Twenty-two patients tis dissecans and osteochondral frac-
(40%) in the reconstruction group tures) that can fragment and become
had preoperative symptoms related loose bodies.20,21
to the ulnar nerve, and 15 (22%)
had ulnar nerve symptoms postop-
eratively. Six of these patients had
paresthesias that resolved sponta-
neously, but 8 of the remaining 9
underwent revision procedures on
the ulnar nerve. Two patients were
unable to return to their sport be-
cause of persistent ulnar nerve
symptoms.
In 1997, Jobe and co-workers19
presented follow-up data on 83 ath-
letes (54 professional, 18 collegiate,
and 11 recreational) who under-
went UCL reconstruction without
ulnar nerve transposition. Only 3
patients (4%) had transient ulnar-
nerve paresthesias postoperatively
that completely resolved within 6
weeks. In 1 patient (1%), ulnar neu-
ropathy, including motor weak-
ness, resolved within 6 months
postoperatively. Of the 33 patients
who were evaluated at long-term
follow-up, 27 (82%) had excellent
results, and 4 (12%) had good re-
sults. The mean time for return to
Figure 7 Medial tension overload sec-
full, competitive throwing was 13 ondary to repetitive valgus stress at the
months (range, 6 to 18 months). elbow, resulting in attenuation of the UCL
complex medially, lateral radiocapitellar
compression, and extension overload with-
in the posterior compartment. (Adapted
Valgus Extension Overload with permission from Kvitne RS, Jobe FW:
Ligamentous and posterior compartment
injuries, in Jobe FW [ed]: Techniques in
Medial tension overload secondary Upper Extremity Sports Injuries. Philadel-
to repetitive valgus stress can also phia: Mosby-Year Book, 1996, p 414.)
result in injury to the surrounding
105
Medial Elbow Problems in the Overhead-Throwing Athlete

Evaluation
Athletes may report symptoms
of catching or locking when loose
bodies develop. Medial tension
overload resulting in valgus insta-
bility also leads to extension over-
load of the posterior compartment.
The extension forces generated
during the acceleration and follow-
through phases of the throwing mo-
tion, which are normally absorbed
by the ligamentous, capsular and
muscular structures of the elbow,
are excessively transmitted to the
posterior compartment.7,10-13,20
Repeated impaction of the pos-
teromedial olecranon in the olecra-
non fossa leads to chondromalacia
and subsequent hypertrophic spur
and osteophyte formation, espe-
cially in the medial aspect of the
ulnar notch (Fig. 8). Posteromedial
impingement secondary to en-
A B
croachment on the olecranon fossa
by osteophytes and scar tissue re- Figure 8 Valgus-extension overload of the posterior compartment resulting in traction
sults in pain during the late accel- spurs on the medial aspect of the ulnar notch (A), as well as posteromedial osteophytes
eration and follow-through phases within the olecranon fossa (B). (Reproduced with permission from Miller CD, Savoie FH
III: Valgus extension injuries of the elbow in the throwing athlete. J Am Acad Orthop Surg
of throwing.20,21 These hypertro- 1994;2:261-269.)
phic osteophytes and traction spurs
can frequently be observed on
plain radiographs, especially on the
axial olecranon view. Loose bodies underlying medial elbow stability; olecranon fossa. Undersurface tears
and osteochondral lesions may oc- athletes who have failed conserva- of the UCL can also be visualized,
casionally be seen as well.20,21 tive therapy and have persistent although definitive treatment of the
symptoms attributable to chronic underlying instability cannot yet be
Treatment valgus instability may also be candi- performed arthroscopically.17
Nonoperative treatment consists dates for operative management. Postoperative rehabilitation is
of an initial period of rest, ice, and Elbow arthroscopy has replaced begun early to maintain range of
NSAIDs to alleviate pain and in- formal arthrotomy as the surgical motion as well as to strengthen the
flammation, followed by functional procedure of choice for joint de- elbow gradually. Athletes usually
strengthening of the elbow and fore- bridement and has been shown to progress through a graduated
arm. Stretching, isotonic, isokinetic, have good results with low compli- throwing program that allows them
and isometric strengthening and cation rates in symptomatic pa- to return to full activity within 3
conditioning exercises of the fore- tients.20-22 Chondromalacia of the months.20,21
arm are implemented. As strength ulnohumeral or radiocapitellar joint Reconstruction of the UCL is
improves, the athlete may begin plyo- may be treated with debridement or reserved for athletes with recalci-
metric exercises concentrating on the drilling. Loose bodies and osteo- trant symptoms associated with
flexor-pronator musculature, as well chondritic lesions can also be ad- chronic valgus instability for whom
as an interval-throwing program. dressed. Debridement of hypertro- nonoperative management and less
Surgical intervention is recom- phic synovium or scar tissue can be invasive procedures have failed.
mended for patients who have failed performed as well. Osteophytes and These athletes usually have medial
nonoperative therapy or who have hypertrophic spurs in the posterior elbow instability that potentiates
symptomatic traction spurs or loose and medial aspects of the olecranon symptoms of posteromedial im-
bodies. There is a wide spectrum of can be debrided to decompress the pingement if left unaddressed.

106 Journal of the American Academy of Orthopaedic Surgeons


Timmerman and Andrews17 have
described an undersurface tear of
the UCL that correlates with de-
tachment of the inner layer of the
anterior bundle of the UCL from
either the humerus or the ulna while
the external portion of the UCL
remains intact. These injuries are
usually best visualized arthroscopi-
cally, and can be difficult to diag-
nose clinically or on MR imaging. In
athletes with valgus extension over-
load and underlying chronic insta-
bility secondary to an attenuated,
incompetent UCL, an open recon-
struction of the UCL, along with
adequate joint debridement (which
may require an additional postero-
medial arthrotomy), is necessary to
ensure maximal functional out-
comes.8,17,20
Medial Epicondylitis
Commonly referred to as “golfer’s
elbow,” medial epicondylitis in-
volves pathologic inflammatory
changes of the flexor-pronator mus-
culature. Medial epicondylitis
occurs frequently in pitchers and
other athletes who participate in
activities that impart large valgus
forces to the elbow. In athletes,
however, it is still 7 to 20 times less
common than lateral epicondyli-
tis.23,24 Overload from extrinsic val-
gus stresses and intrinsic muscular
contractions predispose the flexor-
pronator musculature to inflamma-
tion and injury, which commonly
involve the humeral head of the
pronator teres, the FCR, and occa-
sionally the FCU.7,10,23 The prona-
tor teres has been shown in elec-
tromyographic studies to possess
the highest activity level during the
acceleration phase of throwing.
Medial epicondylitis usually begins
as a microtear in the interface be-
tween the pronator teres and FCR
origins, with subsequent develop-
ment of fibrotic and inflammatory
granulation tissue.
Vol 9, No 2, March/April 2001
Evaluation
Typically, patients are aggressive
advanced-level athletes who present
with an insidious onset of medial el-
bow pain worsened by throwing. On
physical examination, they gener-
ally have tenderness over the flexor-
pronator origin slightly distal and
anterior to the medial epicondyle.
Pain is usually exacerbated by re-
sisted wrist flexion and forearm
pronation.23,24 It is also important to
evaluate for concomitant valgus in-
stability, as flexor-pronator overuse
may predispose to medial ligamen-
tous injury.11
Plain radiographs of the elbow
may be normal, although medial
ulnar traction spurs and UCL calci-
fication can be observed in athletes
with associated medial tension over-
load and potential valgus instability.
Magnetic resonance imaging may
demonstrate increased signal within
the musculotendinous structures,
and is a useful adjunct to more
accurately define the underlying
pathologic changes in the adjacent
structures in the athlete with con-
founding medial elbow symptoms.
In addition, in those with recalci-
trant symptoms, MR imaging can be
utilized to evaluate the integrity of
the musculotendinous structures;
full-thickness tears, if present, may
necessitate more aggressive surgical
management.
Electromyographic studies and
cinematography have demonstrated
that athletes with UCL injuries ex-
hibit decreased pronator teres and
FCR activity during the late-cocking
and acceleration phases.11 In pa-
tients with combined valgus insta-
bility and medial epicondylitis,
treatment should be aimed at both
entities to maximize elbow function.
Authors have also reported a high
incidence (up to 60%) of ulnar neu-
rapraxia in patients with medial
epicondylitis.23-26 Therefore, it is
important to evaluate for concur-
rent ulnar neuropathy and, if pre-
sent, to direct treatment toward
Frank S. Chen, MD, et al
both the neuropathy and the epi-
condylitis to optimize the functional
outcome.
Treatment
Initial nonoperative treatment
consists of rest, ice, NSAIDs, and
local modalities. Corticosteroid in-
jections deep to the flexor-pronator
mass may be utilized, although
there is an associated risk of tendon
attenuation with repeated injec-
tions. Recent studies have shown
that steroid injections provide good
short-term (up to 6 weeks) symp-
tom improvement; results beyond
this time frame are no different
from those obtained with physical
therapy and NSAIDs alone.27 The
next phase of nonsurgical treatment
consists of throwing-technique
enhancement and physical therapy.
Splinting or counterforce bracing
may also be a useful adjunct. Re-
habilitation begins with wrist flexor
and forearm pronator stretching
and progressive isometric exer-
cises. Eccentric and concentric re-
sistive exercises are added once
flexibility, strength, and endurance
have improved. A gradual return
to normal activity is subsequently
allowed. Nonoperative treatment of
medial epicondylitis has been
shown by several authors to have
excellent results, with success rates
as high as 90%.23-25
Surgery is indicated for patients
with refractory symptoms that do
not respond to at least 6 months of
a well-supervised therapy pro-
gram. In these cases, a high corre-
lation with full-thickness tendon
tears has been reported.25 The goals
of surgical treatment include de-
bridement of all inflamed and
pathologic tissue, followed by se-
cure tendinous repair. It is also im-
portant to minimize disruption of
the flexor-pronator origin to pre-
vent weakness.
An oblique skin incision is made
over the medial epicondyle, fol-
lowed by incision of the common
107
Medial Elbow Problems in the Overhead-Throwing Athlete

flexor origin at the pronator teres–
FCR interval.25 Care must be taken
to protect the ulnar nerve and the
medial collateral ligament. In-
flamed tissue is then sharply ex-
cised from the undersurface of the
flexor-pronator mass, which is
reattached to the medial epicon-
dyle through multiple drill holes
(Fig. 9).25 After a brief period of
postoperative immobilization (7 to
10 days), gentle passive and active
elbow range-of-motion exercises
are begun. Resisted wrist flexion
and forearm pronation exercises
are instituted at 4 to 6 weeks, fol-
lowed by a progressive strengthen-
ing program. By postoperative
month 4, patients are usually able
to return to their normal activity
levels.23-25
Results
Vangsness and Jobe 25 have re-
ported that surgical debridement
and reapproximation of the flexor-
pronator musculature as treatment
for refractory medial epicondylitis
provides excellent pain relief while
allowing athletes to return to high
functional levels. They reported that
34 of 35 patients (97%) had good or
excellent results, and 30 (86%) had
no limitation in the use of the elbow.
The patients’ mean subjective esti-
mate of elbow function improved
from 39% of normal preoperatively
to 98% postoperatively. Isokinetic
and grip-strength testing revealed
no functionally significant loss of
strength, and all athletically active
patients were able to return to their
sport.25
Gabel and Morrey 26 reported
similar success rates after surgical
treatment of recalcitrant medial
epicondylitis in 26 patients (30
elbows), but found associated ulnar
neuropathy to be statistically corre-
lated with a poor postoperative
prognosis. Of 25 patients with no
or only mild ulnar nerve symp-
toms, 24 (96%) had good or excel-
lent results. In comparison, good
or excellent results were noted in
only 2 of 5 (40%) elbows with asso-
ciated moderate or severe ulnar
neuropathy, even with concurrent
decompression or transposition of
the ulnar nerve. Overall, however,
the authors reported that 26 elbows
(87%) had good or excellent results
at an average follow-up interval of
7 years.

Cutaneous
nerves

(Shoulder )
Incision

( Wrist)

Medial epicondyle
Ulnar nerve
A B

Figure 9 Technique of debridement and reapproximation

of the flexor-pronator musculature for medial epicondylitis.
A, An incision is made in the common flexor origin. B, All
inflamed tissue is sharply excised from beneath the elevated
flexor-pronator mass. C, The flexor-pronator mass is
securely reapproximated to the medial epicondyle.
(Reproduced with permission from Jobe FW, Ciccotti MG:
Lateral and medial epicondylitis of the elbow. J Am Acad
Orthop Surg 1994;2:1-8.)

108 Journal of the American Academy of Orthopaedic Surgeons

 Frank S. Chen, MD, et al

Flexor-Pronator Injuries
and Ruptures
The flexor-pronator musculature
provides dynamic stability to the
medial elbow and may be injured
with repetitive valgus stress. 10-13
Continued activity and throwing
beyond the limits of muscle fatigue
may lead to injury and, occasion-
ally, rupture of the flexor-pronator
musculature.18 These injuries usu-
ally occur during the acceleration
and follow-through stages of the
throwing motion, when forceful
extension of the elbow and prona-
tion of the forearm occur. Patients
generally present with pain and
swelling along the medial aspect of
the elbow. On examination, there
is usually tenderness at the medial
epicondylar origin with pain that
may be exacerbated by wrist flex-
ion and elbow extension. It is im-
portant to evaluate for concurrent
UCL injury. Minor partial injuries
of the flexor-pronator musculature
may be treated with rest, ice, and
NSAIDs. More severe injuries and
complete ruptures that compromise
elbow stability require surgical
repair.18,20
Hypertrophy of the pronator
teres secondary to repetitive activity
may result in compression of the
median nerve and the development
of pronator syndrome. Patients usu-
ally present with fatiguelike pain in
the proximal volar aspect of the fore-
the medial elbow and proximal
forearm that is worsened by in-
creased throwing and activity, typi-
cally forcing pitchers to stop throw-
ing after only a few innings. This
condition can usually be prevented
by adequate warm-up and proper
timing of pitching to ensure ade-
quate rest between workouts.20
Ulnar Neuropathy
Symptoms involving the ulnar nerve
are very common in throwing ath-
letes because of its superficial loca-
tion, making it susceptible to injury.
More than 40% of athletes with val-
gus instability develop ulnar neuritis
secondary to irritation from inflam-
mation of the UCL, and as many as
60% of throwers with medial epicon-
dylitis also have concomitant ulnar
nerve symptoms.8,16,26
Ulnar nerve entrapment results
from both pathologic and physio-
Ulnar nerve
Flexor digitorum profundus
Traction
{ Flexor carpi ulnaris
logic responses to repetitive trau-
ma.28,29 Mechanical factors include
compression, traction, and irritation
of the nerve (Fig. 10).8 Compres-
sion of the ulnar nerve proximal to
the cubital tunnel may be due to a
tight structure (arcade of Struthers
or intermuscular septum) or to
hypertrophy of an adjacent muscle
(anconeus epitrochlearis or medial
head of the triceps). Compression at
the level of the cubital tunnel may re-
sult from osteophytes, loose bodies,
synovitis, or a thickened retinaculum
(Osborne lesion). Compression may
also occur distal to the cubital tunnel
at the FCU aponeurosis or at the
deep flexor-pronator aponeurosis
after the ulnar nerve passes between
the two heads of the FCU.
The pressure within the ulnar
nerve in the flexed elbow and ex-
tended wrist has been shown to be
elevated to more than three times
the resting level.30 This has been
attributed to nerve compression as

arm that gradually worsens with

continued activity. Symptoms are
usually exacerbated by resistance to
pronation of the forearm combined
Compression
{
with wrist flexion. Surgical explora-
tion, including elevation and divi-
sion of the superficial head of the Compression
pronator teres, may be necessary to and traction
{

decompress the median nerve and

provide symptomatic relief.
Although uncommon, compart-
ment syndrome as a result of hy-
pertrophy of the flexor-pronator
musculature has also been reported.
Patients describe pain localized to
Figure 10 Pathologic forces acting on the ulnar nerve during the throwing motion. As
valgus stresses are placed at the elbow, both traction and compression forces are produced
on the nerve during the acceleration phase of throwing. (Adapted with permission from
Boatright JR, D’Alessandro DF: Nerve entrapment syndromes at the elbow, in Jobe FW,
Pink MM, Glousman RE, Kvitne RE, Zemel NP [eds]: Operative Techniques in Upper
Extremity Sports Injuries. St Louis: Mosby-Year Book, 1996, p 521.)

Vol 9, No 2, March/April 2001 109

Medial Elbow Problems in the Overhead-Throwing Athlete
well as to physiologic stretching of
the nerve (the ulnar nerve normally
moves 7 mm medially and elongates
4 to 7 mm during elbow flexion).28,29
As the elbow flexes, increased ten-
sion on the arcuate ligament and the
UCL also increases tunnel pressures.
During the throwing motion, with
further elbow flexion and wrist ex-
tension combined with shoulder
abduction, the intraneural pressure
may be elevated to as much as six
times the resting level.30 Any tether-
ing of the nerve secondary to chron-
ic changes associated with valgus
overload (e.g., scar tissue, calcifica-
tion of the UCL, traction spurs,
degenerative changes in the ulnar
groove) further increases intraneural
pressures.8,28,29,31 Traction on the
nerve may also result from restric-
tion of its normal mobility.28,29 Ad-
ditional friction on the nerve may be
caused by ulnar nerve subluxation
or dislocation, present in up to 16%
of the population.32 As a result, the
cumulative effects of prolonged and
repeated pressure elevations pro-
duce nerve fibrosis and ischemia.
Evaluation
Athletes with ulnar neuropathy
usually present with intermittent
medial elbow pain that may occa-
sionally radiate down the medial
aspect of the forearm into the hand.
As inflammation progresses, they
may also describe clumsiness or
heaviness of the fingers on the in-
volved side, as well as numbness
and paresthesias in the little and
ring fingers. Typically, these symp-
toms resolve with rest and are exac-
erbated by throwing or overhead
activity. Athletes generally do not
complain of weakness in the ex-
tremity—a late finding in ulnar neu-
ropathy—as their performance is
usually affected in the early stages
before the development of motor
changes. Painful popping or snap-
ping sensations may also be experi-
enced by patients with recurrent
nerve subluxations or dislocations.
110
A careful neurologic evaluation
of the neck and upper extremity is
mandatory to rule out more proxi-
mal causes of neuropathy. 8,28,29
Palpation of the ulnar nerve in its
groove through a full range of
motion should be performed to
examine for subluxation or disloca-
tion. The nerve may feel “doughy”
or thickened. Patients usually
exhibit a positive Tinel sign at the
cubital tunnel as well as a positive
elbow flexion test (i.e., reproduction
of pain, numbness, and paresthe-
sias in the ulnar nerve distribution
with maintained maximum elbow
flexion and wrist extension for at
least 1 minute).33 The earliest sen-
sory changes are noted with vibrom-
etry or monofilament threshold
tests. Nerve-ending density tests
(e.g., two-point discrimination) be-
come positive later as the condition
progresses. Motor weakness, if ob-
served, is seen earliest in the intrin-
sic hand muscles, such as the ab-
ductor digiti quinti and adductor
pollicis, because the intrinsic motor
fibers lie more superficial within
the ulnar nerve in the cubital tunnel
and are thus more susceptible to in-
jury. Extrinsic weakness involving
the flexor digitorum profundus and
FCU is usually associated with more
severe and advanced compression,
as the extrinsic motor fibers lie deep
within the nerve and are better pro-
tected.
Plain radiographs of the elbow,
especially the cubital tunnel view,
may be helpful in determining the
presence of any associated patho-
logic changes in the bones. Mag-
netic resonance imaging may be
used to identify the presence of
soft-tissue masses that may be com-
pressing the ulnar nerve, as well as
to evaluate the status of surround-
ing soft-tissue structures.
Electrodiagnostic studies may be
used as an adjunctive diagnostic
tool, usually depending on the se-
verity of the patient’s condition. A
negative electrodiagnostic study,
Journal of the American Academy of Orthopaedic Surgeons
however, does not rule out the diag-
nosis of ulnar neuritis.28,31 Nerve-
conduction velocities across the
elbow are usually decreased only in
cases of advanced or chronic nerve
entrapment. A dynamic electromyo-
gram may be more helpful when
the diagnosis is equivocal and may
aid in differentiating cervical, elbow,
and more distal nerve involvement.
Thermography is currently being
investigated as a diagnostic test for
ulnar neuropathy. However, no con-
clusive evidence has yet been re-
ported.8,28,29,31
Treatment
Nonoperative management of
ulnar neuropathy usually begins
with rest, ice, and NSAIDs. Immo-
bilization of the elbow for a brief
period (2 to 3 weeks) may be neces-
sary, especially in cases of ulnar-
nerve subluxation or dislocation.
Local corticosteroid injections are
not recommended. Although non-
operative treatment has had high
success rates in the general popula-
tion, many athletes—especially
those with associated valgus insta-
bility—experience a recurrence of
symptoms on resumption of throw-
ing and ultimately require surgical
intervention. Indications for sur-
gery include failed nonoperative
management, persistent ulnar-nerve
subluxation, symptomatic tension
neurapraxia, and concomitant me-
dial elbow problems (e.g., valgus in-
stability) that require surgery.
Surgical options include simple
decompression, medial epicondy-
lectomy, and anterior subcutaneous
and submuscular transpositions.
Simple decompression and medial
epicondylectomy have been shown
to have poor results in the overhead
athlete and are thus not recom-
mended. Simple decompression
does not eliminate traction forces on
the ulnar nerve, does not address
pathologic changes within the cu-
bital tunnel, and cannot be per-
formed in the presence of nerve
 Frank S. Chen, MD, et al

instability. Medial epicondylectomy
is associated with high recurrence
rates and destabilizes the nerve,
which may predispose to subluxa-
tion or dislocation. In addition,
injury to the UCL and the flexor-
pronator musculature—important
secondary dynamic stabilizers of the
elbow—may occur, which may lead
to valgus instability of the elbow
with associated decreased forearm
and wrist strength. Anterior subcu-
taneous transposition has been
shown to have satisfactory results in
the athletic population and has the
advantage of minimizing disruption
of the flexor-pronator musculature.34
The subcutaneously transposed
nerve, however, is vulnerable to di-
rect trauma and may potentially de-
velop instability.8,28,29 In addition, the
nerve may become secondarily com-
pressed within the surgically created
subcutaneous fasciodermal sling,
leading to recurrence of symptoms.
Anterior submuscular transposi-
tion of the ulnar nerve decompresses
all potential sites of entrapment
and protects the transposed nerve
from both direct and indirect trau-
ma that may be encountered during
athletic activity. The transposed
nerve lies superficial to the pronator
muscle mass and follows a direct
course deep to the flexor muscle
mass, where it lies adjacent to the
median nerve in a fatty plane. This
surgical approach also allows direct
examination of the UCL and the
underlying elbow joint for osteo-
phytes, loose bodies, and other osse-
ous abnormalities. In patients with
concomitant valgus instability, repair
or reconstruction of the UCL can be
performed concurrently through this
approach.8,28,29,31
A curvilinear incision along the
course of the ulnar nerve, centered
just posterior to the medial epi-
condyle, is made while preserving
the medial antebrachial cutaneous
nerve. The ulnar nerve is dissected
and mobilized proximally from the
arcade of Struthers, which must be
released. A 2- to 3-cm portion of
the medial intermuscular septum is
removed to prevent tethering of the
nerve once it is transposed anteriorly.
The cubital tunnel retinaculum, in-
cluding the arcuate ligament and
the deep flexor-pronator aponeuro-
sis band, is divided. The nerve is
then mobilized distally past the
medial epicondyle, preserving the
motor branches and the vascular
supply of the nerve, and is released
from beneath the FCU aponeurosis
as the nerve passes between the
two heads of the FCU. The flexor-
pronator interval is incised, the
aponeurotic band of the flexor digi-
torum superficialis origin is re-
leased, and the common flexor origin
is elevated off the medial epicon-
dyle. The ulnar nerve is transposed
anteriorly onto the remaining intact
musculature overlying the ligamen-
tous structures. The flexor origin is
then reattached either by direct
suture or through drill holes in the
medial epicondyle (Fig. 11).
A potential disadvantage of sub-
muscular ulnar nerve transposition
is the lengthy postoperative rehabil-
itation period necessary after de-
tachment and reapproximation of
the flexor-pronator origin, which
must be healed before the resump-
tion of throwing. After a 1- to 2-
week period of immobilization, pas-

Ulnar Median Median

nerve nerve nerve
Flexor-pronator Ulnar nerve
mass transposed

Arcade of Arcade of
Struthers, Struthers,
released released
Deep head,
pronator teres Excised segment of
Medial Flexor origin Medial
Medial intermuscular septum
collateral reattached epicondyle
ligaments epicondyle
A B

Figure 11 A, Anterior transposition of the ulnar nerve after elevation of the flexor-pronator mass, leaving the deep head of the pronator
teres and the UCL complex intact. The transposed nerve lies next to the median nerve in a vascular, fatty bed. B, Completed submuscular
transposition with reattachment of the flexor-pronator mass to the medial epicondyle. (Adapted with permission from Boatright JR,
D’Alessandro DF: Nerve entrapment syndromes at the elbow, in Jobe FW, Pink MM, Glousman RE, Kvitne RE, Zemel NP [eds]: Operative
Techniques in Upper Extremity Sports Injuries. St Louis: Mosby-Year Book, 1996, p 526.)

Vol 9, No 2, March/April 2001 111

Medial Elbow Problems in the Overhead-Throwing Athlete
sive elbow range-of-motion exercises
are begun. Active range-of-motion
exercises are initiated at 3 to 4 weeks,
followed by a strengthening program
at 6 weeks. At 8 weeks, a supervised
throwing program beginning with
light tossing is initiated. Full, unre-
stricted activity is usually achieved
by 4 to 6 months after surgery.
The outcome of this procedure
in the athletic population depends
on the degree of preoperative ulnar
nerve involvement and the pres-
ence of associated medial elbow
problems.31 Patients with minimal
sensory complaints and no motor
weakness routinely recover com-
pletely and have an excellent prog-
nosis for return to their previous
level of function. However, less
consistent results have been reported
for patients who exhibit more ad-
vanced motor weakness and mus-
cle wasting. Concomitant medial
elbow problems, such as instability
and degenerative changes, have also
been associated with less consistent
results. Patients with associated
valgus instability should undergo
repair or reconstruction of the UCL
at the time of ulnar nerve transpo-
sition to optimize postoperative
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of the underlying biomechanics and
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also important to recognize that
many of these injuries may occur in
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In general, most symptomatic
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despite a supervised therapy pro-
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construction with an autologous
graft has been shown to yield satis-
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able to return to their previous level
of activity. Advancements and re-
finements in arthroscopic tech-
niques have resulted in improved
and more successful methods of
treatment of valgus-extension over-
load injuries. Continued modifica-
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treatment of ulnar neuropathy and
injuries to the flexor-pronator mus-
culature have also resulted in im-
proved functional results. Common
underlying factors in the enhance-
ment of functional results include
improvements in rehabilitation pro-
grams, which play an integral role
in the restoration of function in
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pathophysiology associated with
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vention and treatment of many
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Perry J, Pink M: An electromyograph-
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injured pitchers with medial collateral
ligament insufficiency. Am J Sports
Med 1992;20:311-317.
12. DiGiovine NM, Jobe FW, Pink M,
Perry J: An electromyographic analy-
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Pink M: Medial instability of the
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17. Timmerman LA, Andrews JR: Under-
surface tear of the ulnar collateral liga-
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22:33-36.
18. Norwood LA, Shook JA, Andrews JR:
Acute medial elbow ruptures. Am J
Sports Med 1981;9:16-19.
19. Thompson WH IV, Jobe FW, Yocum
LA: Ulnar collateral ligament recon-
struction in throwing athletes: Muscle
splitting approach without transposi-
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Shoulder Elbow Surg 1997;7:175.
20. Miller CD, Savoie FH III: Valgus
extension injuries of the elbow in the
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throwing athlete. J Am Acad Orthop
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21. Wilson FD, Andrews JR, Blackburn
TA, McCluskey G: Valgus extension
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22. Andrews JR, St Pierre RK, Carson WG
Jr: Arthroscopy of the elbow. Clin
Sports Med 1986;5:653-662.
23. Jobe FW, Ciccotti MG: Lateral and
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Am Acad Orthop Surg 1994;2:1-8.
24. Ciccotti MG, Lombardo SJ: Lateral
and medial epicondylitis of the elbow,
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1996, pp 431-446.
25. Vangsness CT Jr, Jobe FW: Surgical
treatment of medial epicondylitis:
Results in 35 elbows. J Bone Joint Surg
Br 1991;73:409-411.
26. Gabel GT, Morrey BF: Operative treat-
ment of medial epicondylitis: Influence
of concomitant ulnar neuropathy at the
elbow. J Bone Joint Surg Am 1995;77:
1065-1069.
27. Stahl S, Kaufman T: The efficacy of an
Frank S. Chen, MD, et al
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sixty elbows. J Bone Joint Surg Am
1997;79:1648-1652.
28. Rokito AS, McMahon PJ, Jobe FW:
Cubital tunnel syndrome. Operative
Techniques Sports Med 1996;4:15-20.
29. Glousman RE: Ulnar nerve problems
in the athlete’s elbow. Clin Sports Med
1990;9:365-377.
30. Pechan J, Julis I: The pressure mea-
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Ulnar nerve entrapment syndrome in
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113
 Talus Fractures: Evaluation and Treatment

Paul T. Fortin, MD, and Jeffrey E. Balazsy, MD

Abstract

Fractures of the talus are uncommon. The relative infrequency of these injuries while the lateral articular wall
in part accounts for the lack of useful and objective data to guide treatment. curves posteriorly, such that they
The integrity of the talus is critical to normal function of the ankle, subtalar, meet at the posterior tubercle. The
and transverse tarsal joints. Injuries to the head, neck, or body of the talus can neck of the talus is oriented medially
interfere with normal coupled motion of these joints and result in permanent approximately 10 to 44 degrees with
pain, loss of motion, and deformity. Outcomes vary widely and are related to reference to the axis of the body of
the degree of initial fracture displacement. Nondisplaced fractures have a favor- the talus and is the most vulnerable
able outcome in most cases. Failure to recognize fracture displacement (even area of the bone after injury. In the
when minimal) can lead to undertreatment and poor outcomes. The accuracy of sagittal plane, the neck deviates
closed reduction of displaced talar neck fractures can be very difficult to assess. plantarward between 5 and 50 de-
Operative treatment should, therefore, be considered for all displaced fractures. grees.
Osteonecrosis and malunion are common complications, and prompt and accu- The talus has no muscle or tendi-
rate reduction minimizes their incidence and severity. The use of titanium nous attachments and is supported
screws for fixation permits magnetic resonance imaging, which may allow solely by the joint capsules, liga-
earlier assessment of osteonecrosis; however, further investigation is necessary ments, and synovial tissues. Liga-
to determine the clinical utility of this information. Unrecognized medial talar ments that provide stability and
neck comminution can lead to varus malunion and a supination deformity with allow motion bind the talus to the
decreased range of motion of the subtalar joint. Combined anteromedial and tibia, fibula, calcaneus, and navicu-
anterolateral exposure of talar neck fractures can help ensure anatomic reduc- lar. The tendon of the flexor hallu-
tion. Posttraumatic hindfoot arthrosis has been reported to occur in more than cis longus lies within a groove on
90% of patients with displaced talus fractures. Salvage can be difficult and the posterior talar tubercle and is
often necessitates extended arthrodesis procedures. held by a retinacular ligament. The
J Am Acad Orthop Surg 2001;9:114-127 spring (calcaneonavicular) ligament
lies inferior to the talar head and
acts like a sling to suspend the head.
Inferiorly, the posterior, middle,
Major fractures and dislocations of tion of these fractures is based on and anterior facets correspond to
the talus and peritalar joints are their anatomic location within the the articular facets of the calcaneus.
uncommon. However, fractures of talus (i.e., head, body, or neck). Each Between the posterior and middle
the talus rank second in frequency type has unique features that affect
(after calcaneal fractures) of all both diagnosis and treatment.
tarsal bone injuries. The incidence
of fractures of the talus ranges from Dr. Fortin is Attending Orthopaedic Surgeon,
0.1% to 0.85% of all fractures.1 Anatomy William Beaumont Hospital, Royal Oak, Mich.
Talus fractures most commonly Dr. Balazsy is Fellow, Department of Ortho-
occur when a person falls from a The talus is the second largest tarsal paedic Surgery, William Beaumont Hospital.
height or sustains some other type bone, with more than one half of its
Reprint requests: Dr. Fortin, Suite 100, 30575
of forced dorsiflexion injury to the surface covered by articular cartilage.
North Woodward Avenue, Royal Oak, MI
foot or ankle. The anatomic config- The superior aspect of the body is 48073-6941.
uration of the injury is important widest anteriorly and therefore fits
because of both the function of the more securely within the ankle mor- Copyright 2001 by the American Academy of
talus and its relationship to the ten- tise when it is in dorsiflexion. The Orthopaedic Surgeons.
uous blood supply. The classifica- articular medial wall is straight,

114 Journal of the American Academy of Orthopaedic Surgeons


facets is a transverse groove, which,
with a similar groove on the dor-
sum of the calcaneus, forms the
dorsal canal that exits laterally into a
cone-shaped space, the tarsal sinus.
The tarsal canal is located just below
and behind the tip of the medial
malleolus. These two anatomic re-
gions form a funnel: the tarsal sinus
is the cone, and the tarsal canal is the
tube. Because blood vessels reach
the talus through the surrounding
soft tissues, injury resulting in cap-
sular disruption may be complicated
by vascular compromise of the talus.
Blood Supply
Wildenauer was the first to correct-
ly describe in detail the blood sup-
ply to the talus. His findings were
confirmed by Haliburton et al 2
through gross dissection and micro-
scopic studies on cadaver limbs. In
1970, Mulfinger and Trueta3 pro-
vided the most complete descrip-
tion of the intraosseous and extra-
osseous arterial circulation.
Only two fifths of the talus can
be perforated by vessels; the other
three fifths is covered by cartilage.
The extraosseous blood supply of
the talus comes from three main
arteries and their branches (Fig. 1).
These arteries, in order of signifi-
cance, are the posterior tibial, the
anterior tibial, and the perforating
peroneal arteries. In addition, the
artery of the tarsal canal (a branch
of the posterior tibial artery) and
the artery of the tarsal sinus (a
branch of the perforating peroneal
artery) are two discrete vessels that
form an anastomotic sling inferior
to the talus from which branches
arise and enter the talar neck area.
The main supply to the talus is
through the artery of the tarsal
canal, which gives off an additional
branch that penetrates the deltoid
ligament and supplies the medial
talar wall. The main artery gives
branches to the inferior talar neck,
Vol 9, No 2, March/April 2001
Anteroposterior view
Perforating
peroneal
artery
Anterior
lateral
malleolar
artery
Artery of
tarsal sinus Lateral tarsal artery
Figure 1 Blood supply to the talus.
thereby supplying most of the talar
body. Therefore, most of the talar
body is supplied by branches of the
artery of the tarsal canal. The head
and neck are supplied by the dor-
salis pedis artery and the artery of
the tarsal sinus. The posterior part
of the talus is supplied by branches
of the posterior tibial artery via cal-
caneal branches that enter through
the posterior tubercle.
Extensive intraosseous anasto-
moses are present throughout the
talus and are responsible for the sur-
vival of the talus in severe injuries.
Preservation of at least one of the
three major extraosseous sources can
potentially allow adequate circula-
tion via anastomotic channels. Ini-
tial fracture displacement, timing of
reduction, and soft-tissue handling
at the time of surgery are all factors
that can potentially affect the integ-
rity of the talar blood supply.
Fractures of the Talar
Head
Fractures of the talar head are rare
and often difficult to visualize on
routine radiographs. It is not un-
Paul T. Fortin, MD, and Jeffrey E. Balazsy, MD
Inferosuperior view
Dorsalis
pedis artery Artery of tarsal sinus
Posterior
tarsal artery
Deltoid
artery
Deltoid
artery
Artery of
tarsal canal
Artery of
Medial tarsal artery tarsal canal
Posterior tibial artery
common, therefore, for fractures of
the talar head to go unrecognized.
Coltart,4 in his review of 228 talar
injuries, reported only a 5% inci-
dence of talar head fracture. Most
of these injuries were secondary to
flying accidents. Kenwright and
Taylor5 reviewed 58 talar injuries
and found a 3% incidence of talar
head injury, whereas Pennal 6 re-
ported a 10% incidence among all
fracture-dislocations involving the
talus.
According to Coltart,4 the mech-
anism of injury consists of the
application of a sudden dorsiflexion
force on a fully plantar-flexed foot,
which thereby imparts a compres-
sive force through the talar head.
Another mechanism is thought to
be hyperdorsiflexion, resulting in
compression of the talar head
against the anterior tibial edge. Im-
paction fractures of the talar head
can also occur in association with
subtalar dislocations. Patients usu-
ally give a history of a fall and com-
plain of pain in the talonavicular
joint region. Swelling and ecchy-
mosis may be present, along with
pain on palpation of the talonavicu-
lar joint. Depending on the size
115
Talus Fractures
and degree of displacement of the
fracture fragment, routine radio-
graphs may not identify the frac-
ture; therefore, computed tomogra-
phy (CT) may be needed to define
the extent of the injury.
Initial treatment of nondisplaced
fractures and those involving a
very small amount of articular sur-
face includes immobilization in a
short leg cast for 6 weeks, as well
as rest, ice, and elevation. If the
fragment causes instability of the
talonavicular joint or is displaced,
causing articular incongruency,
open reduction and internal fixa-
tion should be considered. Typi-
cally, a medial approach to the
talonavicular joint is used, carefully
avoiding the posterior tibial tendi-
nous attachment to the navicular.
Dissection must also proceed cau-
tiously over the anterior aspect of
the talar head to avoid disruption
of the blood supply to the head.
Small-fragment subchondral can-
cellous lag screws or bioabsorbable
pins can be utilized to fix the head
fracture. With more severe impac-
tion injuries, bone grafting is occa-
sionally necessary to maintain the
articular reduction.
A B
Figure 2 A, Preoperative lateral radiograph shows a displaced fracture of the talar neck. B, Canale view demonstrates anteromedial and
anterolateral lag-screw placement. C, Postoperative lateral radiograph shows reduction of the talar neck and subtalar joint.
116
Postoperatively, weight bearing
is not allowed for 6 to 8 weeks.
Early range-of-motion exercises can
be initiated if the fixation is stable
and the patient is reliable. Rapid
healing usually ensues with a low
incidence of osteonecrosis because
of the abundant blood supply to the
talar head. The prognosis is good as
long as severe comminution is not
present and anatomic reduction is
obtained.
Not uncommonly, these injuries
go unrecognized, which leads to
loss of medial-column support and
talonavicular joint instability. Small
nonunited head fragments that are
symptomatic and cause limitation
of joint range of motion can be ex-
cised. Nonunions involving a larger
portion of the articular surface
should be treated on the basis of the
overall integrity of the joint surface.
Severe posttraumatic arthrosis may
necessitate talonavicular joint ar-
throdesis. Due to the coupled mo-
tion of the hindfoot joints, fusion of
the talonavicular joint essentially
eliminates motion at the subtalar
and calcaneocuboid joints and
should be considered a salvage pro-
cedure.
Journal of the American Academy of Orthopaedic Surgeons
Fractures of the Talar Neck
Talar neck fractures account for
approximately 50% of all talar frac-
tures. In 1919, Anderson reported
18 cases of fracture-dislocation of
the talus and coined the term “avia-
tor’s astragalus.” He was the first to
emphasize that forced dorsiflexion
of the foot was the predominant
mechanism of injury.
Fractures occur when the narrow
neck of the talus, with its less dense
trabecular bone, strikes the stronger
anterior tibial crest. As forces pro-
gress, disruption occurs through the
interosseous talocalcaneal ligament
and the ligamentous complex of the
posterior ankle and subtalar joints,
leading to eventual subluxation or
dislocation of the body from the
subtalar and tibiotalar articulations
(Fig. 2). With forced supination of
the hindfoot, the neck can encounter
the medial malleolus, leading to
medial neck comminution and rota-
tory displacement of the head.
In the laboratory, it is difficult to
produce talar neck fractures with
forced dorsiflexion alone. Peterson
et al7 experimentally produced these
fractures only after eliminating ankle
C

joint motion by vertical compression
through the calcaneus, forcing the
talus against the anterior tibia. They
felt that these forces could be repro-
duced in an extended leg if the tri-
ceps surae was contracted.
In a study by Hawkins,8 15 of 57
patients (26%) had associated frac-
tures of the medial malleolus. Canale
and Kelly9 found that 11 of 71 pa-
tients (15%) with fractures of the talar
neck had associated fractures of the
medial and lateral malleoli (10 and 1,
respectively). This level of incidence
of malleolar fractures supports the
concept that in addition to dorsiflex-
ion, rotational forces contribute to
displacement of a talar neck fracture.
Displaced talar neck fractures
often occur as a result of high-energy
injuries. Hawkins8 reported that
64% of patients had other fractures,
and 21% had open fractures.
Classification
Hawkins,8 in his classic paper,
described a classification system
that could be correlated with prog-
nosis. He classified fractures into
groups I to III. In 1978, Canale and
Kelly 9 reported on the long-term
results in their series of talus frac-
tures. They referred to the three dif-
ferent Hawkins groups as “types”
and included a type IV not previ-
ously described. The terms “group”
Type I
Figure 3 Classification of talar neck fractures.8,9
Vol 9, No 2, March/April 2001
Paul T. Fortin, MD, and Jeffrey E. Balazsy, MD
and “type” have since been used in-
terchangeably in the literature. 10
The classification for fractures of the
neck of the talus is based on the
radiographic appearance at the time
of injury (Fig. 3).
Type I fractures of the neck of the
talus are nondisplaced. Any dis-
placement is significant and pre-
cludes classification as a type I frac-
ture. The fracture line enters the
subtalar joint between the middle
and posterior facets. The talus re-
mains anatomically positioned with-
in the ankle and subtalar joints.
Theoretically, only one of the three
major blood supply sources is dis-
rupted—the one entering through
the anterolateral portion of the neck.
True type I fractures may be difficult
to see on conventional radiographs,
and CT or magnetic resonance (MR)
imaging may be necessary for con-
firmation. Fractures with clear dis-
placement of even 1 to 2 mm should
be considered type II fractures
rather than type I.
Type II fractures combine a frac-
ture of the talar neck with subluxa-
tion or dislocation of the subtalar
joint. In 10 of the 24 cases reported
by Hawkins,8 the posterior facet of
the body of the talus was dislocated
posteriorly; in most of the remain-
ing cases there was a medial subta-
lar joint dislocation, with the foot
Type II Type III
and calcaneus displaced medially.
Two of the main sources of blood
supply to the talus are injured—the
vessels entering the neck and pro-
ceeding proximally to the body and
the vessels entering the foramina in
the sinus tarsi and tarsal canal. The
third source of blood supply, enter-
ing through the foramina on the me-
dial surface of the body, is usually
spared, but can be injured.
Type III injuries are character-
ized by a fracture of the neck with
displacement of the body of the
talus from the subtalar and ankle
joints. Hawkins8 identified 27 of
these fractures and found that the
body of the talus extruded posteri-
orly and medially and was located
between the posterior surface of
the tibia and the Achilles tendon,
where it can compress adjacent tib-
ial neurovascular structures. The
body of the talus may rotate within
the ankle mortise; however, the
head of the talus remains aligned
with the navicular. All three sources
of blood supply to the talus are
usually disrupted with this injury.
Over half of type III injuries are
open, and many have associated
neurovascular and/or skin com-
promise.
In type IV injuries, the fracture of
the talar neck is associated with dis-
location of the body from the ankle
Type IV
117
Talus Fractures
and subtalar joints with additional
dislocation or subluxation of the
head of the talus from the talona-
vicular joint. In the series of Canale
and Kelly,9 3 of 71 talar fractures
(4%) were type IV injuries, all of
which had unsatisfactory results.
Clinical and Radiologic
Evaluation
Patients with talar neck fractures
present with significant swelling of
the hindfoot and midfoot. Gross
deformity may be present, depend-
ing on the displacement of the frac-
ture and any associated subtalar
and ankle joint subluxation or dis-
location.
A history of a fall from a height
or a forced loading injury (e.g., a
motor-vehicle collision) may be
elicited. A talus fracture may be
only part of the total spectrum of
the patient’s injuries, and a general
trauma survey should be included
in each patient’s evaluation. Particu-
lar attention should also be directed
to the thoracolumbar spine, because
spine fractures have been found in
association with talar neck and
body fractures. Focused evaluation
of the involved foot should include
an assessment of the neurovascular
status as well as the integrity of the
skin over the fracture site. Dis-
placed talar neck fractures often
lead to significant stretching of the
dorsal soft tissues. Prompt reduc-
tion is mandatory to avoid skin ne-
crosis. With fracture-dislocations,
posterior displacement of the body
leads to bowstringing of the flexor
tendons and neurovascular bundle.
Patients can present with flexion of
the toes and tibial nerve dysesthe-
sias. As many as 50% of type III
Hawkins fractures present as open
injuries, with a subsequent infec-
tion rate as high as 38%.11 Hence,
an open fracture must be treated
with urgency.
Radiographic evaluation consists
initially of anteroposterior (AP), lat-
eral, and oblique views of the foot
118
and ankle. This allows classification
of the fracture and an assessment of
associated injuries. The special
oblique view of the talar neck de-
scribed by Canale and Kelly9 (Fig. 4)
provides the best evaluation of talar
neck angulation and shortening,
which is not appreciable on routine
radiographs. This view should be
obtained to assess initial displace-
ment of all talar neck fractures before
embarking on an operative reduction.
Computed tomography is invaluable
for preoperatively assessing talar
body injuries with regard to fracture
pattern, degree of comminution, and
the presence of loose fragments in
the sinus tarsi. The typical CT proto-
col involves 2-mm-thick sections in
the axial and semicoronal planes
with sagittal reconstructions.
Treatment
The goal of treatment of talar
neck fractures is anatomic reduction,
which requires attention to proper
rotation, length, and angulation of
the neck. Biomechanical studies on
cadavers have shown why precisely
reducing talar neck fractures leads
to better outcomes. In one cadaveric
study, displacements by as little as 2
mm were found to alter the contact
characteristics of the subtalar joint,
with dorsal and medial or varus dis-
placement causing the greatest
change. The weight-bearing load
pathway changed, and contact stress
was decreased in the anterior and
middle facets but was more local-
ized in the posterior facet. 12 In
another study, varus alignment was
created by removing a medially
based wedge of bone from the talar
neck. This resulted in inability to
evert the hindfoot, and the altered
foot position was characterized by
internal rotation of the calcaneus,
heel varus, and forefoot adduction.13
The altered hindfoot mechanics with
a talar neck fracture may be one fac-
tor that leads to subtalar posttrau-
matic arthrosis. For these reasons,
open reduction and internal fixation
Journal of the American Academy of Orthopaedic Surgeons
75°
15°
Figure 4 Radiographic positioning for the
oblique view of the talar neck, as described
by Canale and Kelly.9
is recommended for displaced frac-
tures.
Type I Fractures
Truly nondisplaced fractures of
the talar neck can be treated success-
fully by cast immobilization. Care
must be taken to obtain appropriate
radiographs, including a Canale
view, to ensure that there is no dis-
placement or malrotation. A cast is
applied, and weight bearing is not
allowed for 6 to 8 weeks or until
osseous trabeculation is seen on
follow-up radiographs. Nonopera-
tive treatment necessitates frequent
radiographic follow-up to make
certain that the fracture does not
displace during treatment.
Type II Fractures
Initial management of displaced
talar neck fractures should involve
prompt reduction to minimize soft-
tissue compromise. This can often be
performed in the emergency room.
However, repeated forceful reduc-
tion attempts should be avoided.
The foot is plantar-flexed, bringing
the head in line with the body. The
heel can then be manipulated into
either inversion or eversion, depend-
ing on whether the subtalar compo-
nent of the displacement is medial or
lateral.

Anatomic reduction of this frac-
ture is difficult to obtain by closed
means. Rotational alignment of the
talar neck is very difficult to judge
on plain radiographs. Even mini-
mal residual displacement can ad-
versely affect subtalar joint mechan-
ics and is therefore unacceptable.12
Even if closed reduction is success-
ful in obtaining an anatomic reduc-
tion, immobilization in significant
plantar-flexion is typically necessary
to maintain position. For these rea-
sons, operative treatment of all type
II fractures has been recommended.10
Numerous surgical approaches
have been described for talar neck
fractures. The medial approach
allows easy access to the talar neck
and is commonly used. An incision
just medial to the tibialis anterior
starting at the navicular tuberosity
exposes the neck and can be ex-
tended proximally to facilitate fixa-
tion of a malleolar fracture or to
perform a malleolar osteotomy.
Surgical exposure can contribute to
circulatory compromise of the talus.
Care must be taken to avoid strip-
ping of the dorsal neck vessels and
to preserve the deltoid branches
entering at the level of the deep del-
toid ligament.
The disadvantage of the medial
approach is that the exposure is less
extensile than that which can be
achieved along the lateral aspect of
the neck. This limited exposure
makes judging rotation and medial
neck shortening difficult. Medial
neck comminution or impaction can
be underestimated; if either condi-
tion is present, compression-screw
fixation of the medial neck will result
in shortening and varus malalign-
ment. In these circumstances, a sep-
arate lateral exposure allows a more
accurate assessment of reduction and
better fixation.
The anterolateral approach lateral
to the common extensor digitorum
longus–peroneus tertius tendon
sheath provides exposure to the
stronger lateral talar neck. A wide-
Vol 9, No 2, March/April 2001
Paul T. Fortin, MD, and Jeffrey E. Balazsy, MD
enough skin bridge must exist be-
tween the two incisions, and strip-
ping of the dorsal talar neck must
be avoided.
Once the fracture has been re-
duced, it is provisionally stabilized
with Kirschner wires. Two screws
(one medial and one lateral) are in-
serted from a point just off the artic-
ular surface of the head and directed
posteriorly into the body (Fig. 2, B).
Lag screws can be used unless there
is significant neck comminution
that would result in neck shorten-
ing or malalignment when the frac-
ture is compressed. Bone graft is
occasionally necessary to make up
for large impaction defects of the
medial talar neck (Fig. 5, A).
Another alternative for screw
placement is the posterolateral
approach described by Trillat et
al.14 An incision is made lateral to
the heel cord in the interval be-
tween the flexor hallucis longus
Lateral view
Superior view
A B
Figure 5 A, Placement of bone graft into an impaction defect in the medial talar neck.
B, Posterolateral exposure of the talus as described by Trillat et al.14
and peroneal muscles (Fig. 5, B).
This allows safe access to the entire
posterior talar process. Care must
be taken during exposure to avoid
injury to the peroneal artery and its
branches. Most commonly, the
posterolateral exposure is used in
combination with an initial antero-
medial or anterolateral approach
for provisional fracture reduction
and stabilization with Kirschner
wires under image intensification.
The patient is then positioned
prone or on one side, and a postero-
lateral approach is used for place-
ment of cannulated screws for final
fracture fixation. Alternatively, if
anatomic reduction can be accom-
plished with closed manipulation,
posterior-to-anterior screw fixation
can be used through a single poste-
rior approach.
Posterior-to-anterior screw place-
ment provides superior mechanical
strength compared with insertion
Peroneus
brevis
and longus
Flexor
hallucis
longus
Posterior
talus
Screw
placement
Triceps
surae
119
Talus Fractures
from anterior to posterior.15 San-
ders 10 has suggested that screws
can be placed on either side of the
flexor hallucis groove and directed
anteromedially. On the basis of
their findings in a cadaveric study,
Ebraheim et al16 suggested that the
best point of insertion for anterior-
to-posterior screws is the lateral
tubercle of the posterior process.
Pitfalls of posterior-to-anterior
screw fixation include penetration of
the subtalar joint or lateral trochlear
surface, injury to the flexor hallucis
longus tendon, and restriction of
ankle plantar-flexion due to screw-
head impingement. These potential
problems can be minimized by
placement of smaller-diameter coun-
tersunk screws directed along the
talar axis.
Several types of screws have been
used, including solid-core stainless
steel small-fragment lag screws.
Cannulated screws offer the poten-
tial advantage of easier insertion.
Titanium screws have the advantage
of compatibility with MR imaging,
allowing early assessment of osteo-
necrosis.17
Bioabsorbable implants have
several theoretical advantages, but
experience is limited with these
devices. They are not easily visible
on radiographs, resorb over time,
and can be placed through articular
surfaces. These are most often used
in fractures of the talar body but
may be helpful as supplemental
fixation of talar neck fractures.10,18
Screws placed from the talar
head into the body may interfere
with talonavicular joint function if
the screw head is prominent and
near the joint. This often necessi-
tates countersinking the screw head.
Headless lag screws have been
shown to have mechanical proper-
ties comparable to those of small-
fragment compression screws. 19
They have the theoretical advantage
of not interfering with talonavicular
joint function when placed through
the talar head.
120
The timing of operative treat-
ment of type II fractures remains
controversial. There are no data to
suggest that emergent treatment of
type II fractures improves outcome,
but most would agree that they
should be treated with all possible
expediency.
Type III Fractures
Type III fractures, which are
characterized by displacement of
the talar body from the ankle and
subtalar joints, pose a treatment
challenge. Urgent open reduction
is mandated to relieve compression
from the displaced body on the
neurovascular bundle and skin
medially and to minimize the oc-
currence of osteonecrosis. Many of
these injuries have an associated
medial malleolar fracture, which
facilitates exposure. When the
malleolus is intact, medial malleo-
lar osteotomy is often required to
allow repositioning of the talar
body. Careful attention to the soft
tissues around the deltoid ligament
and medial surface of the talus is
necessary, as these may contain the
only remaining intact blood sup-
ply. A femoral distractor or exter-
nal fixator may be applied for dis-
traction of the calcaneus from the
tibia to help extricate the body
fragment. A percutaneous pin may
be placed in the talus to toggle the
body back into its anatomic posi-
tion. Fracture stabilization can be
carried out as described for type II
fractures.
Because nearly half of these frac-
tures are open, meticulous irriga-
tion and debridement is mandated
on an urgent basis. Open type III
injuries are devastating and typi-
cally associated with significant
long-term functional impairment.20
In cases of severe open injury with
extrusion of the talar body, a di-
lemma exists as to whether to save
and reinsert the talar body or to
discard it.10 Marsh et al11 reported
on the largest series of open severe
Journal of the American Academy of Orthopaedic Surgeons
talus injuries. In 12 of 18 cases, the
talus was totally or partially ex-
truded through the wound. Deep
infection developed in 38% of the
patients despite contemporary open
fracture management. The occur-
rence of deep infection was the
major factor contributing to poor
results. There was a 71% failure
rate in patients in whom an infec-
tion developed. In cases of contam-
inated wounds when the talar body
is totally extruded and completely
devoid of soft-tissue attachment,
consideration should be given to
discarding the body fragment and
planning a staged reconstruction.
Type IV Fractures
Type IV injuries are treated in a
manner similar to type III injuries,
with urgent open reduction and in-
ternal fixation. The talar body and
head fragments are reduced and
rigidly fixed. Stability of the talo-
navicular joint is then assessed; if it
is unstable, consideration should be
given to pinning the talonavicular
joint. The significance of this injury
is that osteonecrosis of both the
talar body and the head fragment is
possible.10 As with type III injuries,
urgent treatment is of paramount
importance.
Postoperative Care
Provided stable fixation has been
achieved, early range of motion is
begun once the wounds are healed.
With comminuted fractures and
those with significant instability of
the ankle, subtalar, or talonavicular
joint, consideration should be given
to cast immobilization until provi-
sional healing has taken place (4 to
6 weeks). Weight bearing is de-
layed until there is convincing evi-
dence of healing, which may take
several months.
Complications
The reports of the incidence of
complications vary widely (Table 1).
There is, however, a consistent

Table 1
Complications Following Talar Neck Fractures*
Fracture
Type Osteonecrosis
Type I 0%-13%
Type II 20%-50%
Type III/IV 8%-100%
* Range of cited incidence values in references 1, 4, 5, 6, 8, 9, 11, 23, 25, and 26.
trend for the incidence of complica-
tions to increase with the Hawkins
stage.
Fractures of the Talar Body
Talar body fractures occur less fre-
quently than fractures of the talar
neck. 13 Because fractures of the
talar body involve both the ankle
joint and the posterior facet of the
subtalar joint, accurate reconstruc-
tion of a congruent articular surface
is required.
Evaluation and Classification
It is sometimes difficult to differ-
entiate vertical fractures of the talar
body from talar neck fractures.
Inokuchi et al 21 suggest that the
diagnosis can be accurately pre-
dicted on the basis of the location
of the inferior fracture line in rela-
tion to the lateral process. Frac-
tures in which the inferior fracture
line propagates in front of the lateral
process are considered talar neck
fractures. Fractures in which the
inferior fracture line propagates
behind the lateral process involve
the posterior facet of the subtalar
joint and are therefore considered
talar body fractures.
Plain radiographs often underes-
timate the extent of articular injury.
Computed tomography is neces-
sary to define the fracture pattern,
amount of comminution, and extent
of joint involvement.
Vol 9, No 2, March/April 2001
Degenerative
Joint Disease Malunion
0%-30% 0%-10%
40%-90% 0%-25%
70%-100% 18%-27%
Talar body fractures have been
classified by Sneppen et al22 on the
basis of anatomic location, as follows:
type A, transchondral or osteochon-
dral; type B, coronal shear; type C,
sagittal shear; type D, posterior
tubercle; type E, lateral process; and
type F, crush fractures. Boyd and
Knight23 also proposed a classifica-
tion system for shearing injuries of
the talar body. In their classification
system, body fractures are differenti-
ated according to associated disloca-
tion of the subtalar or talocrural joint.
As with talar neck fractures, talar
body fractures with associated dislo-
cation have a higher incidence of
osteonecrosis. In the simplest sense,
talar body fractures can be divided
into three groups: group I are prop-
er or cleavage fractures (horizontal,
sagittal, shear, or coronal); group II,
talar process or tubercle fractures;
and group III, compression or im-
paction fractures (Fig. 6).
Group I
Figure 6 Talar body fractures. Group I are fractures of the body proper or cleavage frac-
tures (horizontal, sagittal [shown], shear, or coronal). Group II are talar process or tubercle
fractures (lateral talar-process fracture shown). Group III are compression or impaction
fractures of the articular surface of the body.
Paul T. Fortin, MD, and Jeffrey E. Balazsy, MD
Treatment of Talar Process and
Tubercle Fractures
The extent of joint involvement
and the degree of comminution
should be considered when treating
fractures of the talar process or
tubercle. These injuries are often
missed or neglected; this can lead to
significant disability, because such
fractures can involve a substantial
portion of the ankle and subtalar
articular surface. In general, non-
displaced process or tubercle frac-
tures can be treated with casting
and maintenance of non-weight-
bearing status. For displaced frac-
tures with significant articular in-
volvement, consideration should be
given to operative fixation (Fig. 7).
Not uncommonly, however, the
extent of comminution precludes
operative fixation, and fragments
can only be either excised or man-
aged nonoperatively (Fig. 8).
Treatment of Cleavage and
Compression Fractures
Displaced cleavage and crush
fractures of the talar body are opti-
mally treated with anatomic reduc-
tion and internal fixation. Because
these fractures occur beneath the
ankle, a mortise, medial, or lateral
malleolar osteotomy is often neces-
sary to gain exposure to the frac-
ture.16 Once the fracture has been
exposed, temporary Kirschner-wire
fixation is used before final fracture
stabilization with screws. Bioab-
Group II Group III
121
Talus Fractures

A B C

Figure 7 Preoperative CT scan (A) and lateral radiograph (B) showing a displaced posteromedial talar tubercle fracture (arrows).
C, Radiograph obtained after lag-screw fixation.

sorbable pins or subarticular screws
can be helpful (Fig. 9). Severe inju-
ries with significant impaction of
the cancellous bone of the talus may
require bone grafting (Fig. 10).
fractures. Other authors have re-
ported comparable clinical results,
as well as diminished osteonecrosis
and arthrosis, with operative treat-
ment of all displaced fractures.25,26
Complications and Salvage
Osteonecrosis, malunion, and ar-
throsis are the most commonly re-
ported complications after talus

Results

Differences in treatment methods

among reported series and the
small numbers of patients make it
difficult to make valid inferences
regarding the outcome of talus frac-
tures. Contemporary management
with open reduction and internal
fixation of all displaced fractures
has led to improved clinical results.
Canale and Kelly 9 reported only
59% good or excellent results in a
series of 71 fractures followed for
an average of 12.7 years. More than
half of the patients with type II frac-
tures in that series were treated
with closed reduction and casting.
Many of these fractures were com-
plicated by varus malalignment
and subsequent arthrosis. Low et
al24 reported good or excellent re- A B
sults in 18 of 22 patients who un- Figure 8 Plain radiograph (A) and CT scan (B) demonstrate a comminuted lateral talar-
derwent open reduction and inter- process fracture (arrow), which was subsequently treated by excision of fragments.
nal fixation for displaced talar neck

122 Journal of the American Academy of Orthopaedic Surgeons

 Paul T. Fortin, MD, and Jeffrey E. Balazsy, MD

views of the ankle and is useful as

an objective prognostic sign. The
presence of the Hawkins sign is a
reliable indicator that osteonecrosis
is unlikely. The absence of the Haw-
kins sign, however, is not as reliable
in predicting the development of
osteonecrosis.9 A film of the normal
side, taken at the same exposure,
should be available for comparison.
Magnetic resonance imaging is
very sensitive for detecting osteone-
crosis and estimating the amount of
talar involvement. Adipocyte via-
bility produces strong T1-weighted
A B images. With avascularity of bone,
death of marrow adipocytes occurs
early.27 This alters the appearance
of fat signals on the T1-weighted
image. It does not appear that MR
imaging is helpful in assessing os-
teonecrosis until at least 3 weeks
after the time of injury, and false-
negative MR images have been
reported.16,28 The role of MR imag-
ing in the follow-up of both nonop-
eratively and operatively treated
talus fractures has yet to be deter-
mined.
Initial treatment for osteonecrosis
is conservative. It is important to
note that a talus fracture can heal
C D
despite the development of osteo-
Figure 9 A, AP radiograph of a talar body fracture. B, CT reconstruction shows the talar necrosis. The main determinant for
neck component of the fracture (arrows). Postoperative AP (C) and lateral (D) radio- progressing the patient’s weight-
graphs. Medial malleolar osteotomy was required for fracture exposure. Headless subar-
ticular screws were used for fracture fixation. bearing status on the injured extrem-
ity is the presence of fracture heal-
ing. Once radiographic evidence of
healing has been demonstrated, the
fracture. Nonunion occurs infre- the time to recognize its presence is patient may be allowed to bear
quently. within 6 to 8 weeks; however, it may weight.
first be observed on radiographs at It may take up to 36 months for
Osteonecrosis any time from 4 weeks to 6 months revascularization of the talus to
Osteonecrosis is a frequent com- after fracture-dislocation. It usually occur; therefore, prolongation of
plication of talar neck and body frac- presents as relative opacity of the non-weight-bearing status until the
tures and dislocations. Hawkins8 involved bone caused by osteopenia risk of collapse no longer exists is
reported no osteonecrosis in 6 type I of the neighboring bones of the foot not practical. There is no definite
fractures, whereas Canale and Kelly9 secondary to disuse and cessation of evidence to suggest that weight
reported a 13% incidence in 15 type I weight bearing. bearing on an avascular talus will
fractures. Hawkins reported a 42% The Hawkins sign (evidence of contribute to collapse. Hawkins8
incidence in 24 type II fractures and a preserved vascularity of the talus) is stated that collapse of the talus
91% incidence in 27 type III fractures. seen 6 to 8 weeks after the injury. It occurred despite maintenance of
Osteonecrosis is not always easily consists of patchy subchondral enforced non-weight-bearing status
recognized. Hawkins8 stated that osteopenia on the AP and mortise for several years.

Vol 9, No 2, March/April 2001 123

Talus Fractures

Patients with pain and evidence of

osteonecrosis may be offered an off-
loading orthosis, such as a patellar
tendon–bearing brace, which may
limit symptoms. However, these
types of orthotic devices have not
been shown to prevent collapse of the
talar dome in the presence of osteo-
necrosis. It should be noted that
osteonecrosis of the talus is not al-
ways symptomatic, and patients may
function quite satisfactorily without
discomfort despite having radio-
graphic findings of osteonecrosis.
Surgical salvage is indicated only for
patients with intractable symptoms
after nonoperative treatment.
A B Operative treatment of osteone-
crosis after a talus fracture depends
on the location and extent of necro-
sis and the degree of accompanying
arthrosis of the ankle and subtalar
joints. Patchy osteonecrosis with
isolated involvement of one joint is
approached differently than total
body necrosis and collapse. In cases
of limited osteonecrosis with ar-
throsis, arthrodesis of the involved
joint is an effective means of elimi-
nating pain. It is important that
C D any dead bone adjacent to the fu-
sion interface be removed to ensure
successful union. Bone graft is nec-
essary to fill any defect created by
removal of the necrotic bone. In
cases of isolated lateral dome in-
volvement, the fibula can be used
as a strut graft.
Operative salvage in cases of
total body osteonecrosis and col-
lapse is a challenge. Talectomy
alone has been used in such cases
with only minimal success.8,9 Haw-
kins8 reported on 6 patients evalu-
ated an average of 6 years after
talectomy. All patients had prob-
lems related to pain or shortening
of the limb. To address some of
E F the problems with talectomy alone,
a Blair-type fusion has been sug-
Figure 10 AP (A) and lateral (B) plain radiographs show an impacted talar-body frac- gested.10 This involves resection of
ture. Axial CT image (C) and sagittal CT reconstruction (D). AP (E) and lateral (F) radio-
graphs obtained after operative fixation. The medial malleolar fracture facilitated expo- the necrotic talar body fragment
sure to the talar body. The impacted articular segment was elevated and bone-grafted. and fusion of the talar head to the
anterior distal tibia. This has the

124 Journal of the American Academy of Orthopaedic Surgeons

 Paul T. Fortin, MD, and Jeffrey E. Balazsy, MD

potential advantages of limiting the
amount of limb shortening and
preserving some hindfoot motion.
This technique can result in a pain-
less plantigrade foot, but potential
problems include high rates of non-
union at the tibiotalar junction and
late collapse.10
Alternatively, the defect created
by removal of the talar body can be
spanned with tricortical graft be-
tween the distal tibia and the calca-
neus in conjunction with fusion of
the talar head and anterior distal
tibia. This preserves limb length
and limits the risk of late collapse
between the tibia and the calcaneus
(Fig. 11). Another option that has
been recently reported is to leave
the necrotic talar body in place and
span from the tibia to the calcaneus
with bone graft. Kitaoka et al 29
reported union in 13 of 16 patients
treated with this technique.
Nonunion and Malunion
Nonunion is the least frequent
complication of talar neck fracture.
In a review of the world literature
up to 1985,30 the reported incidence
was 2.5%. The differentiation of a
nonunion from a delayed union is
somewhat arbitrary. Consolidation
across the site of a type III talar
neck fracture may take as long as 8
months.30 Treatment of nonunion
is dependent on the presence of co-
existing problems, such as arthro-
sis, osteonecrosis, and infection,
and is injury-specific. Considera-
tion should be given to arthrodesis
when nonunion is associated with
advanced hindfoot arthrosis.
Malunion after inaccurate reduc-
tion of talar neck fractures has a
reported incidence as high as 32%,
with varus malunion occurring most
frequently.9,10 It is difficult to assess
the accuracy of reduction on plain
radiographs; therefore, malunion is
probably more common than re-
ported. Canale and Kelly9 found
that varus malunion occurred most
frequently in Hawkins type II frac-
tures that had been treated in a
closed manner. Type III fractures
were more likely to be treated oper-
atively, and the incidence of mal-
union was less in this group. The
authors stressed the importance of
obtaining adequate radiographs,
particularly the specialized oblique
view that allows assessment of neck
alignment.
Because treatment of talar neck
malunion is difficult, preventing this
complication is important. It has
been recommended that minimally
displaced fractures of the talar neck
can be treated with casting,8,9 but
acceptable amounts of displacement
have been variably defined. Canale
and Kelly9 suggested that 5 mm of

A B C

Figure 11 AP (A) and lateral (B) plain radiographs demonstrate osteonecrosis of the entire talar body. C, Lateral postoperative radio-
graph shows tibiocalcaneal arthrodesis with intramedullary nail fixation. The necrotic talar body was removed.

Vol 9, No 2, March/April 2001 125

Talus Fractures
displacement and 5 degrees of angu-
lation or varus are acceptable. San-
georzan et al12 studied the effect of
malalignment of the talar neck on
the contact characteristics of the sub-
talar joint. Displacement by 2 mm
resulted in changes in the subtalar
contact characteristics. These small
displacements are likely critical and
can lead to altered subtalar joint
mechanics and arthrosis. Therefore,
displaced fractures should be accu-
rately reduced and internally fixed.
With any medial comminution, a
two-incision approach may provide
the best chance for accurate fracture
reduction.
Patients with varus malunion
walk with the foot internally rotated
and often complain of excessive
weight bearing on the lateral border
of the foot. Initial management con-
sists of footwear modification and
use of inserts intended to cushion
the lateral overload.
Surgical treatment of talar neck
malunion is dependent on the status
of the ankle, subtalar, and talonavic-
ular joints. Long-standing varus
malunion with significant arthrosis
and loss of hindfoot motion can be
salvaged with arthrodesis to obtain
a plantigrade foot. At the time of
arthrodesis, the malpositioning of
the foot should be corrected. Pa-
tients with varus malunion typically
have a shortened medial column of
the foot. Correction of the deformity
involves lengthening of the medial
column or shortening of the lateral
column of the foot in conjunction
with derotation of the forefoot.
Occasionally, joint function is pre-
served, and correction of the varus
deformity with talar neck osteotomy
is possible. Monroe and Manoli31
reported a successful outcome after
talar neck osteotomy and insertion
of a tricortical bone graft to restore
medial neck length.
Dorsal malunion can occur when
the body is not properly derotated
during reduction and the head
fragment remains dorsal to the
126
body. This can lead to sympto-
matic impingement of the dorsal
surface of the talus on the distal
tibia and restriction of ankle dorsi-
flexion. In the absence of signifi-
cant arthrosis, resection of the dor-
sal prominence of the talar neck
may relieve symptoms.
Skin Necrosis and Infection
Deep infection and skin slough
are probably the most dreaded com-
plications of severe talar fractures.
Displaced fractures can lead to ex-
cessive tension on the dorsal skin
and subsequent necrosis. Extensive
soft-tissue loss can increase the
chance of infection and often neces-
sitates flap coverage. Prompt re-
duction will help minimize this
potentially disastrous complication
(Fig. 12). Acute, deep infection, such
as septic arthritis, should be treated
aggressively with serial debride-
ment and attempted wound closure
or coverage and prolonged antibi-
otic therapy.20 Chronic deep infec-
tion with bone involvement typically
requires removal of the infected
bone and hardware. Antibiotic-
A B
Figure 12 A, AP plain radiograph shows a Hawkins type III fracture. B, Injury was left
unreduced for 48 hours, which resulted in full-thickness skin loss that necessitated free-
vascularized-flap and skin-graft coverage.
Journal of the American Academy of Orthopaedic Surgeons
impregnated bone-cement spacers
can be used to fill large defects, and
staged reconstruction can be consid-
ered after the infection has been erad-
icated.
Posttraumatic Arthrosis
Subtalar and tibiotalar arthrosis
with limited range of motion is a
frequent residuum of severe talar
injuries. Arthrosis can result from
articular damage at the time of in-
jury or from abnormal joint me-
chanics, as is seen with talar neck
malunion. The exact incidence of
arthrosis for each fracture type is
unknown. In a study of displaced
talar neck fractures, Sanders10 re-
ported that the incidence of arthro-
sis varied from 47% to over 90%.
Arthrosis is often not symptomatic
and is, therefore, probably more
common than has been reported. As
with osteonecrosis, the presence of
arthrosis does not preclude a satis-
factory outcome.
Arthrodesis may be considered
for symptomatic arthritic joints if
bracing and lifestyle modification
do not provide sufficient relief. It is

important not to underestimate the
possibility of osteonecrosis in pa-
tients with arthritis subsequent to
talar injuries. The presence of focal
osteonecrosis may not be apparent
on plain radiographs, and conven-
tional arthrodesis techniques may
fail if large areas of necrotic bone
are not appropriately treated with
bone grafting.
References
1. Santavirta S, Seitsalo S, Kiviluoto O,
Myllynen P: Fractures of the talus. J
Trauma 1984;24:986-989.
2. Haliburton RA, Sullivan CR, Kelly PJ,
Peterson LFA: The extra-osseous and
intra-osseous blood supply of the
talus. J Bone Joint Surg Am 1958;40:
1115-1120.
3. Mulfinger GL, Trueta J: The blood
supply of the talus. J Bone Joint Surg
Br 1970;52:160-167.
4. Coltart WD: “Aviator’s astragalus.” J
Bone Joint Surg Br 1952;34:545-566.
5. Kenwright J, Taylor RG: Major inju-
ries of the talus. J Bone Joint Surg Br
1970;52:36-48.
6. Pennal GF: Fractures of the talus. Clin
Orthop 1963;30:53-63.
7. Peterson L, Romanus B, Dahlberg E:
Fracture of the collum tali: An experi-
mental study. J Biomech 1976;9:277-279.
8. Hawkins LG: Fractures of the neck of
the talus. J Bone Joint Surg Am 1970;52:
991-1002.
9. Canale ST, Kelly FB Jr: Fractures of
the neck of the talus: Long-term evalu-
ation of seventy-one cases. J Bone Joint
Surg Am 1978;60:143-156.
10. Sanders R: Fractures and fracture-
dislocations of the talus, in Coughlin
MJ, Mann RA (eds): Surgery of the Foot
and Ankle, 7th ed. St Louis: Mosby-
Year Book, 1999, vol 2, pp 1465-1518.
11. Marsh JL, Saltzman CL, Iverson M,
Shapiro DS: Major open injuries of the
talus. J Orthop Trauma 1995;9:371-376.
12. Sangeorzan BJ, Wagner UA, Harring-
ton RM, Tencer AF: Contact character-
istics of the subtalar joint: The effect of
Vol 9, No 2, March/April 2001
Paul T. Fortin, MD, and Jeffrey E. Balazsy, MD
Summary
Talus fractures often present as
complex injuries. Optimal diagno-
sis and management require a thor-
ough understanding of the osseous
anatomy and the vascular supply
of the talus. Fractures with signifi-
cant displacement or associated
dislocation require urgent reduc-
talar neck misalignment. J Orthop Res
1992;10:544-551.
13. Daniels TR, Smith JW, Ross TI: Varus
malalignment of the talar neck: Its
effect on the position of the foot and
on subtalar motion. J Bone Joint Surg
Am 1996;78:1559-1567.
14. Trillat A, Bousquet G, Lapeyre B: Les
fractures-séparations totales du col ou
corps de l’astragale: Intérêt du vissage
par voie postérieure. Rev Chir Orthop
Reparatrice Appar Mot 1970;56:529-536.
15. Swanson TV, Bray TJ, Holmes GB Jr:
Fractures of the talar neck: A mechani-
cal study of fixation. J Bone Joint Surg
Am 1992;74:544-551.
16. Ebraheim NA, Mekhail AO, Salpietro
BJ, Mermer MJ, Jackson WT: Talar
neck fractures: Anatomic considera-
tions for posterior screw application.
Foot Ankle Int 1996;17:541-547.
17. Thordarson DB, Triffon MJ, Terk MR:
Magnetic resonance imaging to detect
avascular necrosis after open reduction
and internal fixation of talar neck frac-
tures. Foot Ankle Int 1996;17:742-747.
18. Kankare J, Rokkanen P: Dislocated
fractures of the talus treated with
biodegradable internal fixation. Arch
Orthop Trauma Surg 1998;117:62-64.
19. Wheeler DL, McLoughlin SW: Bio-
mechanical assessment of compression
screws. Clin Orthop 1998;350:237-245.
20. Sanders R, Pappas J, Mast J, Helfet D:
The salvage of open grade IIIB ankle
and talus fractures. J Orthop Trauma
1992;6:201-208.
21. Inokuchi S, Ogawa K, Usami N: Class-
ification of fractures of the talus: Clear
tion to afford the best outcome.
Using a combination of antero-
medial and anterolateral incisions
for fracture exposure facilitates
anatomic reduction. Severe talar
injuries with significant initial dis-
placement remain problematic, and
even aggressive management does
not always lead to a satisfactory
outcome.
differentiation between neck and body
fractures. Foot Ankle Int 1996;17:748-750.
22. Sneppen O, Christensen SB, Krogsoe O,
Lorentzen J: Fracture of the body of the
talus. Acta Orthop Scand 1977;48:317-324.
23. Boyd HB, Knight RA: Fractures of the
astragalus. South Med J 1942;35:160-167.
24. Low CK, Chong CK, Wong HP, Low
YP: Operative treatment of displaced
talar neck fractures. Ann Acad Med
Singapore 1998;27:763-766.
25. Grob D, Simpson LA, Weber BG, Bray T:
Operative treatment of displaced talus
fractures. Clin Orthop 1985;199:88-96.
26. Schulze W, Richter J, Klapperich T,
Muhr G: Functional outcome of surgi-
cal therapy of talus fractures [German].
Chirurg 1998;69:1207-1213.
27. Bobechko WP, Harris WR: The radio-
graphic density of avascular bone. J
Bone Joint Surg Br 1960;42:626-632.
28. Henderson RC: Posttraumatic necro-
sis of the talus: The Hawkins sign ver-
sus magnetic resonance imaging. J
Orthop Trauma 1991;5:96-99.
29. Kitaoka HB, Patzer GL: Arthrodesis
for the treatment of arthrosis of the
ankle and osteonecrosis of the talus. J
Bone Joint Surg Am 1998;80:370-379.
30. Migues A, Solari G, Carrasco NM,
Gonzalez Della Valle A: Repair of
talar neck nonunion with indirect cor-
ticocancellous graft technique: A case
report and review of the literature.
Foot Ankle Int 1996;17:690-694.
31. Monroe MT, Manoli A II: Osteotomy
for malunion of a talar neck fracture:
A case report. Foot Ankle Int 1999;20:
192-195.
127
 Kienböck’s Disease: Diagnosis and Treatment

Christopher H. Allan, MD, Atul Joshi, MD, and David M. Lichtman, MD

Abstract

Kienböck’s disease, or osteonecrosis of the lunate, can lead to chronic, debilitat- Isolated or repetitive trauma to a
ing wrist pain. Etiologic factors include vascular and skeletal variations com- lunate predisposed to injury due to
bined with trauma or repetitive loading. In stage I Kienböck’s disease, plain any of several factors (e.g., bone
radiographs appear normal, and bone scintigraphy or magnetic resonance geometry and vascularity) may lead
imaging is required for diagnosis. Initial treatment is nonoperative. In stage to a fracture or to vascular compro-
II, sclerosis of the lunate, compression fracture, and/or early collapse of the mise. Bone necrosis results in trabec-
radial border of the lunate may appear. In stage IIIA, there is more severe ular fractures and sclerosis. Un-
lunate collapse. Because the remainder of the carpus is still uninvolved, treat- treated, the process continues, with
ment in stages II and IIIA involves attempts at revascularization of the collapse and fragmentation of the
lunate—either directly (with vascularized bone grafting) or indirectly (by lunate. At this stage, carpal height is
unloading the lunate). Radial shortening in wrists with negative ulnar vari- decreased, the capitate migrates
ance and capitate shortening or radial-wedge osteotomy in wrists with neutral proximally, and the scaphoid hyper-
or positive ulnar variance can be performed alone or with vascularized bone flexes (Fig. 1). Abnormal carpal mo-
grafting. In stage IIIB, palmar rotation of the scaphoid and proximal migra- tion, particularly related to scaphoid
tion of the capitate occur, and treatment addresses the carpal collapse. rotation, 3,4 leads to degenerative
Surgical options include scaphotrapeziotrapezoid or scaphocapitate arthrodesis changes throughout the carpus and
to correct scaphoid hyperflexion. In stage IV, degenerative changes are present the radiocarpal joint.
at the midcarpal joint, the radiocarpal joint, or both. Treatment options Patients in early stages of the dis-
include proximal-row carpectomy and wrist arthrodesis. ease rarely seek medical attention.
J Am Acad Orthop Surg 2001;9:128-136 Therefore, the true incidence and
the natural history are not known
with certainty. Nevertheless, the
apparent common pathway in-
In 1910, Robert Kienböck, a Viennese tions.” He recommended excision volves osteoarthritic changes and
radiologist, reported a series of 16 of the bone in the event of severe debilitating pain, which has led to
cases of “traumatic malacia” of the pain and disability. the development of a large and con-
lunate.1 Although others had de- Kienböck’s disease occurs most fusing array of treatment options.
scribed similar anatomic findings in commonly in men aged 20 to 40.2 It
cadaveric specimens, Kienböck’s is rarely bilateral, and patients fre-
was the first clinical report of osteo- quently have a history of wrist trauma.
necrosis of the lunate. He provided The initial symptoms of pain over Dr. Allan is Assistant Professor, Department
of Orthopaedics, University of Washington
radiographic evidence of isolated the dorsum of the wrist in the region
Medical Center, Seattle. Dr. Joshi is Resident,
changes beginning in the proximal of the lunate accompanied by limited John Peter Smith Health Network, Fort Worth,
portion of the lunate and affecting wrist motion may have been present Texas. Dr. Lichtman is Professor and Chair-
the radiolunate articulation, with months to years before the patient man, Orthopaedic Residency Program, John
other areas spared. He described seeks medical attention. Some pa- Peter Smith Health Network, Fort Worth.
the collapse of the lunate, occasion- tients with radiographic evidence of
Reprint requests: Dr. Allan, Department of
ally with fragmentation, and felt severe destruction are relatively
Orthopaedics, Box 356500, 1959 NE Pacific
that this condition was caused by “a asymptomatic; however, most have Street, Seattle, WA 98195.
disturbance in the nutrition of the increasing reactive synovitis and
lunate caused by the rupture of liga- limitation of wrist motion, swelling, Copyright 2001 by the American Academy of
ments and blood vessels during grip weakness, and pain with mo- Orthopaedic Surgeons.
contusions, sprains, or subluxa- tion and eventually at rest.

128 Journal of the American Academy of Orthopaedic Surgeons


Carpal height
Radial inclination
Ulnar variance
Figure 1 Radiographic wrist measurements.
The clinical condition of Kienböck’s
disease, therefore, remains challeng-
ing to both patient and physician.
Etiology
Many direct or indirect causes of
Kienböck’s disease have been pro-
posed. The local vascular and os-
seous anatomy may play a role.
The patterns of lunate blood supply
provide insight into some possible
causes of osteonecrosis of this bone.
There are multiple patterns of arterial
supply,2,5 with the lunate in most
cadaveric specimens receiving con-
tributions from branches entering
both dorsally and palmarly. How-
ever, the lunate was supplied by
only a single palmar artery in 7% of
wrists in one study.6 In addition, in-
traosseous branching patterns vary,
with 31% of specimens in one study
showing a single path through the
bone without significant arboriza-
tion (Fig. 2).6 A lunate with a single
vessel and minimal branching may
be at increased risk of osteonecrosis
after hyperflexion or hyperexten-
sion injuries or a minimally dis-
placed fracture. Of interest, Takami
Vol 9, No 2, March/April 2001
Scapho-
lunate
angle
et al7 reported that severe injuries,
such as lunate dislocation, can oc-
cur without the development of
osteonecrosis or with only a tran-
sient appearance of this condition.
This is because the lunate usually
dislocates palmarly, with a flap of
palmar capsule still attached. All
specimens examined in that study
had at least one palmar vessel;
therefore, the intact flap probably
transmits sufficient vascular supply
to maintain lunate viability.7
Disruption of venous outflow has
also been suggested as a cause of
Kienböck’s disease. In one study,8
in vitro intraosseous pressure mea-
surements within normal and ne-
crotic lunates showed marked in-
Figure 2 Patterns of intraosseous arterial branching in the lunate. (Adapted with per-
mission from Gelberman RH, Bauman TD, Menon J, Akeson WH: The vascularity of the
lunate bone and Kienböck’s disease. J Hand Surg [Am] 1980;5:272-278.)
Christopher H. Allan, MD, et al
creases in pressure in the necrotic
bones, a finding more consistent
with venous stasis than with arterial
compromise. It is unclear whether
this is a cause or a result of the dis-
ease process (the authors of that
study point out that these findings
may be due solely to collapse of the
lunate), but traumatic disruption of
venous outflow may be another fac-
tor in lunate osteonecrosis.
Lunate geometry and local anat-
omy may be important as well. Neg-
ative ulnar variance, first identified
as a factor by Hultén9 in 1928, was
present in 78% of his patients with
Kienböck’s disease, but in only 23%
of the general population. Hultén
suggested that a short distal ulna
led to increased force transmission
across the radiolunate articulation,
contributing to an increased risk of
osteonecrosis. However, D’Hoore
et al10 found no statistically signifi-
cant difference in ulnar variance
when they compared 125 normal
wrists with 52 wrists in patients
with Kienböck’s disease. Several
investigators from Japan11,12 have
noted that negative ulnar variance
occurs with equal frequency in
patients with Kienböck’s disease
and in the general population. A
flattened radial inclination may pre-
dispose to Kienböck’s disease.12,13
Watanabe et al13 noted a tendency
toward smaller lunates in their pa-
tients with the disorder. Thus, neg-
ative ulnar variance and flattened
radial inclination may predispose
certain patients to develop Kien-
129
Kienböck’s Disease
böck’s disease, but neither is likely
to be the sole factor.
Occasional occurrences of Kien-
böck’s disease have been reported
in association with such conditions
as septic emboli, sickle cell disease,
gout, carpal coalition, and cerebral
palsy, as well as corticosteroid use.
However, there is no well-defined
correlation with any systemic or
neuromuscular process that war-
rants screening when considering
the diagnosis.2,14
Thus, the etiology of Kienböck’s
disease seems to involve the inter-
play of multiple factors. Vascular
and skeletal variations may lead to
an at-risk lunate, which, when sub-
jected to traumatic insult, repetitive
mechanical loading, or some other
factor, may develop osteonecrosis.
It is still not clear whether the lu-
nate fracture lines occasionally seen
in early Kienböck’s disease repre-
sent a primary event, or whether
these fractures occur later in the
process, after revascularization and
resorption of necrotic bone cause
structural weakness.15,16
Diagnostic Techniques and
Staging
Kienböck’s disease can occur in
patients of any age and either sex
even if there is no history of prior
wrist problems. Symptoms vary
depending on the stage of the dis-
ease at presentation and may range
from mild discomfort to constant,
debilitating pain. Swelling over the
carpus is common and may occur
palmarly as well as dorsally. Ten-
derness over the dorsum of the
lunate is a frequent finding. Grip
strength may be markedly reduced.
Wrist range of motion may be mini-
mally or severely impaired.
In 1977, Lichtman described a
clinical and radiographic classifica-
tion for Kienböck’s disease, which is
now widely used to stage treatment
and compare outcomes2 (Table 1).
130
Table 1
Stages of Kienböck’s Disease
Stage I Normal radiographs or linear fracture, abnormal but nonspecific
bone scan, diagnostic MR appearance (lunate shows low signal
intensity on T1-weighted images; lunate may show high or low
signal intensity on T2-weighted images, depending on extent of
disease process)
Stage II Lunate sclerosis, one or more fracture lines with possible early
collapse of lunate on radial border
Stage III Lunate collapse
IIIA Normal carpal alignment and height
IIIB Fixed scaphoid rotation (ring sign), carpal height decreased,
capitate migrates proximally
Stage IV Severe lunate collapse with intra-articular degenerative changes at
midcarpal joint, radiocarpal joint, or both
Before the advent of magnetic reso- originally considered to have stage
nance (MR) imaging, radionuclide III disease. Nevertheless, since tri-
scintigraphy was the next diagnos- spiral tomography is not routinely
tic study recommended after plain available, plain radiography and
radiography. Hashizume et al 17 MR imaging (Fig. 3) remain the
have pointed out, however, that MR most common tools for staging
imaging cannot distinguish among Kienböck’s disease.
osteonecrosis, the histologic reactive In stage I, plain radiographs are
interface between living and dead either normal or occasionally dem-
bone, and reactive hyperemia. They onstrate a linear fracture without
suggest that MR imaging is never- sclerosis or collapse of the lunate
theless superior to plain radiog- (Fig. 4). No changes are seen else-
raphy, tomography, or computed where in the carpus. The early-flow
tomography, in defining the early
stage of Kienböck’s disease (Licht-
man stage I), when trabecular bone
has not yet been destroyed. By con-
trast, once lunate collapse has oc-
curred, tomography or computed
tomography best reveals the extent
of necrosis and trabecular destruc-
tion.17
Quenzer et al18 reported that tri-
spiral tomography makes possible
more accurate staging than stan-
dard tomography or plain radiogra-
phy. In a study of 105 patients with
Kienböck’s disease, they noted that
89% of patients with radiographic
stage I disease actually met the
tomographic criteria for stage II; Figure 3 T1-weighted MR image reveals
decreased signal intensity of the lunate in
this “up-staging” was true as well the wrist of a patient with Kienböck’s dis-
for 71% of those with radiographic ease.
stage II disease and 9% of those
Journal of the American Academy of Orthopaedic Surgeons
 Christopher H. Allan, MD, et al

Stage I Stage II

Stage IIIA Stage IIIB

Figure 4 Drawings and radiologic images illustrating staging of

Kienböck’s disease, according to Lichtman.2 In stage I, the trabecu-
lar bone has not yet been destroyed, and plain radiographs either
are normal or demonstrate a linear fracture without sclerosis or
collapse of the lunate. In stage II, findings include increased den-
sity of the lunate, frequently with one or more fracture lines; the
entire lunate may be sclerotic, but lunate height is preserved. In
stage IIIA there is lunate collapse, but carpal height is relatively
unchanged. Stage IIIB is characterized by proximal migration of
the capitate and fixed hyperflexion of the scaphoid (cortical “ring
sign”). In stage IV, arthritic changes are apparent throughout the
radiocarpal and/or midcarpal joint. (Reformatted coronal CT
image depicts both radial styloid and radiolunate degenerative
changes.)

Stage IV

phase of bone scintigraphy may
indicate reactive synovitis. In stage
I, MR imaging is highly suggestive
when there is uniformly decreased
signal intensity on T1-weighted
images in comparison with the
surrounding normal bones. This
change in signal intensity reflects
reduced vascularity of the lunate.19
Caution must be exercised when
partial T1 signal loss is noted, how-
ever. Disorders such as ulnar abut-
ment, fractures, enchondromas, and
osteoid osteoma can cause focal MR
signal changes. In addition, tran-
sient ischemia may cause a general-
ized decrease in lunate signal inten-
sity. T2-weighted images typically

Vol 9, No 2, March/April 2001 131

Kienböck’s Disease
show low signal intensity in Kien-
böck’s disease, but will show in-
creased signal if revascularization is
occurring.20,21 For this reason, MR
imaging may also be used to assess
healing of the lunate after treatment.
Symptoms in stage I resemble those
of wrist sprains and early nonspecific
synovitis.
Radiographic findings in stage
II Kienböck’s disease include in-
creased density of the lunate on
plain radiographs, frequently asso-
ciated with one or more fracture
lines. Density changes in the lunate
are often best appreciated on the
lateral plain radiograph. The entire
lunate may be sclerotic, but lunate
height is preserved. There are no
associated carpal abnormalities.
Clinical findings in stage II are fre-
quently those of chronic synovitis.
Increased density of the lunate
can also occur as a transient finding,
not associated with the typical pro-
gressive changes of Kienböck’s dis-
ease. This is a common finding after
perilunate fracture-dislocations, and
generally resolves with standard
treatment of the initial injury.7
In stage III, the lunate shows col-
lapse. This stage can be divided
into two categories. In stage IIIA, lu-
nate collapse has occurred, but car-
pal height is relatively unchanged.
Lateral radiographs demonstrate a
widened anteroposterior dimension
of the lunate associated with short-
ening in the coronal plane. Neither
proximal migration of the capitate
nor fixed hyperflexion of the scaph-
oid (cortical “ring sign”) is present.
In stage IIIB, these signs of carpal
collapse do appear. In addition,
there may be ulnar deviation of the
triquetrum and either the dorsal or
the volar intercalated segment insta-
bility pattern. Clinical findings are
progressive stiffness in stage IIIA
and signs of wrist instability in
stage IIIB.
In stage IV Kienböck’s disease,
arthritic changes are also apparent
throughout the radiocarpal or mid-
132
carpal joint or both. Symptoms in ease in the same way as stage II and
stage IV are similar to those of de- stage IIIA disease. Nevertheless,
generative arthritis of the wrist, for most clinicians, cast immobiliza-
with more severe swelling, pain, tion (or an equivalent form of wrist
and limitation of motion. immobilization, such as with use of
an external fixator) remains the first
treatment option for stage I Kien-
Treatment böck’s disease. The possibility of
resolution of symptoms does exist;
The value of staging Kienböck’s therefore, a trial of immobilization
disease lies in guiding the selection for as long as 3 months is appropri-
of treatment (Table 2), in predicting ate. In addition, such a period may
the results of treatment, and in allow the restoration of vascularity
comparing the results of different in cases of transient osteonecrosis of
treatment regimens. There is a vast the lunate, helping to distinguish
array of proposed treatments for this entity from Kienböck’s disease.
Kienböck’s disease, but certain Delaere et al22 recently reported
techniques have documented pat- that night splinting during periods
terns of success. These will be dis- of discomfort for patients with
cussed along with alternative pro- stage I, II, or III Kienböck’s disease
cedures for each stage of disease. gave results equivalent to those
obtained with surgical treatment.
Stage I However, the average level of dis-
Many authors report poor results ease severity in the splinted group
with prolonged immobilization as was one stage lower than that in
the primary treatment for stage I the operatively treated group; thus,
disease. 22 For this reason, some comparison was difficult. How-
clinicians elect to treat stage I dis- ever, in another series of 22 nonsur-
Table 2
Options for Treatment of Kienböck Disease
Stage of Disease Treatment
I Immobilization (3 months)
II and IIIA with negative Radius-shortening osteotomy; ulnar
or neutral ulnar variance lengthening; capitate shortening
II and IIIA with positive Direct revascularization + external fixation
ulnar variance or temporary scaphotrapeziotrapezoid
pinning (stage II only); radial-wedge or
dome osteotomy; capitate shortening
with or without capitohamate fusion;
combination of joint-leveling and direct
revascularization procedures
IIIB Scaphotrapeziotrapezoid or scaphocapitate
fusion with or without lunate excision
with palmaris longus autograft; radius-
shortening osteotomy; proximal-row
carpectomy
IV Proximal-row carpectomy; wrist arthrodesis;
wrist denervation
Journal of the American Academy of Orthopaedic Surgeons

gically treated patients with vari-
ous stages of disease,2 17 showed
progression, and 5 had no im-
provement.
When immobilization fails to
reverse the avascular changes, the
process will almost always have
advanced to stage II. In this set-
ting, analysis of ulnar variance is
important.
Stage II or IIIA With Neutral or
Positive Ulnar Variance
Stages II and IIIA are often con-
sidered together, and treatment
options are similar with one major
exception. In stage II, lunate avas-
cularity has developed, but the
bone has not collapsed. Direct re-
vascularization procedures have
their greatest likelihood of success
in this stage.
A number of vascularized pedi-
cle and/or bone grafting procedures
have been described, including vas-
cularized transfers of the pisiform
bone, transfers of segments of the
distal radius on a vascularized pedi-
cle of pronator quadratus, and
transfers of branches of the first, sec-
ond, or third dorsal metacarpal
arteries. 23-25 Our preference has
been to use the second dorsal inter-
metacarpal artery and vein either as
originally described26 or as modi-
fied by suturing it to a corticocancel-
lous graft harvested from the distal
radius.24 Most of the recently de-
scribed vascularized pedicle bone
grafts have the advantage that the
bone graft and vascular pedicle are
harvested together, making the pro-
cedure technically easier. The dor-
sal aspect of the distal radius is sup-
plied by several arterial branches,
which enter the bone via septa be-
tween the extensor compartments.
When these are used, no vein is har-
vested. Because of anatomic varia-
tion, it is best to be aware of the
location of several potential vascu-
larized pedicle bone grafts before
performing such a procedure. Ex-
ternal fixation to unload the lunate
Vol 9, No 2, March/April 2001
after revascularization has often
been used, but temporary pinning
of the scaphotrapeziotrapezoid
(STT) joint or the scaphocapitate
(SC) joint for the same purpose has
also been described.24,25 Outcomes
of the various direct revasculariza-
tion procedures are still being eval-
uated.
Treatment options other than
direct revascularization for patients
with stage II or IIIA disease and
positive ulnar variance include
radial closing-wedge osteotomy,
radial-dome osteotomy, and capitate
shortening with or without capito-
hamate fusion (Almquist proce-
dure).11,13,27 These may be consid-
ered attempts to unload the lunate
to improve its environment for re-
vascularization through decreasing
the shear stress across the radio-
lunate joint. Capitate shortening
(Figs. 5 and 6) is relatively simple,
and good results have been reported
(83% revascularization and healing
of the lunate in one report27). In
addition, a recent biomechanical
study showed that capitate shorten-
ing with capitohamate fusion sig-
nificantly (P<0.05) decreased the
load across the radiolunate articula-
Figure 5 Capitate shortening with capitohamate fusion.
Christopher H. Allan, MD, et al
tion.28 If this procedure is chosen, it
is helpful to ensure that the hamate
is not allowed to abut on the lunate
after shortening of the capitate; if
this appears to be the case, removal
of the proximal tip of the hamate
with a rongeur will correct the
problem.29
Stage II or IIIA With Negative
Ulnar Variance
In patients with stage II or IIIA
Kienböck’s disease and significant
negative ulnar variance, a shorten-
ing osteotomy of the radius may be
performed in an effort to reduce
forces on the lunate. Preoperative
measurement of ulnar variance is
made in order to plan the amount of
radial resection; sufficient bone
should be removed to result in neu-
tral to 1-mm positive ulnar variance.
Positive ulnar variance greater than
1 mm risks abutment of the ulna on
the lunate or triquetrum, which is
manifested by ulnar-sided discom-
fort after surgery.
Horii et al 30 described a two-
dimensional wrist model in which
they assessed the extent of unload-
ing of the radiolunate joint after var-
ious osteotomy procedures. They
133
Kienböck’s Disease
A B
Figure 6 A, Preoperative AP radiograph of the wrist of a patient with stage IIIA
Kienböck’s disease. B, Postoperative radiograph shows fixation of the lunate fracture and
vascularized bone grafting, in addition to capitate shortening.
found that shortening the radius or
lengthening the ulna by 4 mm led to
a 45% decrease in radiolunate load
with only a moderate increase in
force across the midcarpal or radio-
scaphoid joint.
Trumble et al 31 assessed the
effects on lunate loading after ulnar
lengthening, radial shortening, STT
fusion, and capitohamate fusion
without capitate shortening in an in
vitro model. They found that all but
the capitohamate fusion significantly
unloaded the lunate and that wrist
motion was preserved in all except
STT fusion.
In another biomechanical study,
Iwasaki et al4 used a three-dimen-
sional theoretical wrist model. They
demonstrated reduced force across
the radiolunate joint after STT or SC
fusion but not after capitohamate
fusion.
A report on radial shortening per-
formed on 68 patients demonstrated
diminished pain in 93% at an average
follow-up interval of 52 months.32
134
One third of patients had radio-
graphic signs of lunate revasculariza-
tion. Range of motion was improved
in 52% and worsened in 19%. Grip
strength improved in 74% of patients.
Thus, radial shortening is an effective
option for either stage II disease or
stage IIIA disease with negative ulnar
variance. Ulnar lengthening has also
been described, but this requires iliac-
crest bone graft and osteotomy heal-
ing at two sites (each end of the graft)
rather than one.
Stage IIIB
In stage IIIB Kienböck’s disease,
in addition to lunate collapse, there
is loss of carpal height along with
hyperflexion of the scaphoid. Cor-
recting the scaphoid position to its
normal posture of 45 degrees of
flexion followed by fusion to either
the trapezium and trapezoid (STT
fusion) or to the capitate (SC fusion)
theoretically decreases load across
the radiolunate joint, prevents fur-
ther carpal collapse, and stabilizes
Journal of the American Academy of Orthopaedic Surgeons
the midcarpal joint.2,4,15 Some au-
thors advocate proximal-row car-
pectomy; others prefer joint-leveling
procedures. A recent comparison
between STT fusion and proximal-
row carpectomy in advanced Kien-
böck’s disease showed no statistical
difference in grip strength, pain re-
lief, or wrist range of motion.33 In
another comparison, radial short-
ening led to better results than STT
fusion in a group of 23 patients with
late-stage Kienböck’s disease fol-
lowed up for an average of 5 years.34
In stage III, collapse and frag-
mentation of the lunate may cause a
significant synovial reaction. Exci-
sion of the lunate, performed in
addition to a fusion procedure, may
provide pain relief. Some authors
interpose a rolled palmaris longus
tendon to fill the dead space. The
use of silicone prostheses for re-
placement of an excised lunate has
been discontinued due to an un-
acceptably high rate of particulate
synovitis.2
Naum et al35 reported on the use
of titanium implants for this pur-
pose in 16 patients. At an average
follow-up interval of 58 months,
they recorded no loss of motion, an
increase in grip strength, and pre-
vention of further carpal collapse. It
should be noted that the stage of
disease was not described, that
associated intercarpal fusions were
done in 7 of the 16 patients, and that
one implant required reoperation
for subluxation.
Stage IV
In stage IV Kienböck’s disease,
all the findings of stage IIIB (lunate
collapse and fixed scaphoid rota-
tion with loss of carpal height) are
present, along with generalized de-
generative changes throughout the
midcarpal joint, the radiocarpal
joint, or both. At this point, there is
no value in attempting to revascu-
larize or decompress the lunate, nor
in attempting to arrest progression
of palmar flexion of the scaphoid.

Treatment options must be di-
rected at the pancarpal arthritis.
These include proximal-row carpec-
tomy and wrist fusion, as well as
wrist denervation. It should be
noted that severe arthritic involve-
ment of the capitate head is a con-
traindication to proximal-row car-
pectomy, although milder changes
are accepted by some or can be
addressed with an interposed flap
of dorsal capsule between the capi-
tate head and the lunate fossa. 36
Advocates for proximal-row carpec-
tomy claim that it preserves most of
the already limited range of motion,
is simple to perform, and leaves
open the possibility of wrist fusion
at a later date. A 1-cm segment of
the posterior interosseous nerve
within the fourth dorsal compart-
ment can be excised when perform-
ing a proximal-row carpectomy to
minimize postoperative wrist pain.
More complete wrist denervation
procedures have been described for
the treatment of advanced Kien-
böck’s disease. The concept is at-
tractive, but these procedures offer
little advantage in terms of results
over the two former operations.2,15,37
Authors have disagreed on the com-
plete anatomic description of wrist
innervation and therefore on the
best method of denervation.38
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Vol 9, No 2, March/April 2001
Summary
For the past 10 to 15 years, selection
of treatment options for Kienböck’s
disease has been primarily based on
stage and ulnar variance. With
advancements in diagnostic tools
(and corresponding earlier diagno-
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venous drainage before the actual
onset of osteonecrosis. Corrections
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treatment of this disorder has not
been tested. Arthroscopic fusion,
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reasonable applications of this tech-
nique in the near future. The use of
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böck’s disease. Dosage, method of
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Christopher H. Allan, MD, et al
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steps are required to harvest a vas-
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techniques are eagerly awaited. The
concept of temporary unloading of
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SC pinning (rather than fusion) dur-
ing revascularization is a creative
extension of the use of external fixa-
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of treatment options for Kienböck’s
disease.
Kienböck’s disease is an uncom-
mon but potentially debilitating con-
dition. The precise cause and opti-
mal treatment continue to elude
investigators. Nevertheless, increased
attention to evaluation of outcomes
has led to greater ease of decision
making when faced with this diffi-
cult problem. Accurate staging
directs selection of appropriate treat-
ment and allows comparison of
results with other investigators.
New techniques continue to appear,
holding promise for improvement in
all phases of diagnosis, staging, and
treatment.
ic lunate and perilunate dislocations.
Arch Orthop Trauma Surg 1996;115:
104-107.
8. Schiltenwolf M, Martini AK, Mau HC,
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Further investigations of the intra-
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9. Hultén O: Über anatomische Varia-
tionen der Handgelenkknochen. Acta
Radiol Scand 1928;9:155-168.
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J, Fabry G: Negative ulnar variance is
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11. Nakamura R, Imaeda T, Miura T:
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Radial shortening for Kienböck’s dis-
ease: Factors affecting the operative
result. J Hand Surg [Br] 1990;15:40-45.
12. Tsuge S, Nakamura R: Anatomical
risk factors for Kienböck’s disease. J
Hand Surg [Br] 1993;18:70-75.
13. Watanabe K, Nakamura R, Horii E,
Miura T: Biomechanical analysis of
radial wedge osteotomy for the treat-
ment of Kienböck’s disease. J Hand
Surg [Am] 1993;18:686-690.
14. Culp RW, Schaffer J, Osterman AL,
Bora FW Jr: Kienböck’s disease in a
patient with Crohn’s enteritis treated
with corticosteroids. J Hand Surg [Am]
1989;14(2 pt 1):294-296.
15. Linscheid RL: Kienböck’s disease.
Instr Course Lect 1992;41:45-53.
16. Aspenberg P, Wang JS, Jonsson K,
Hagert CG: Experimental osteonecro-
sis of the lunate: Revascularization
may cause collapse. J Hand Surg [Br]
1994;19:565-569.
17. Hashizume H, Asahara H, Nishida K,
Inoue H, Konishiike T: Histopathology
of Kienböck’s disease: Correlation with
magnetic resonance and other imaging
techniques. J Hand Surg [Br] 1996;21:
89-93.
18. Quenzer DE, Linscheid RL, Vidal MA,
Dobyns JH, Beckenbaugh RD, Cooney
WP: Trispiral tomographic staging of
Kienböck’s disease. J Hand Surg [Am]
1997;22:396-403.
19. Ficat RP: Idiopathic bone necrosis of the
femoral head: Early diagnosis and treat-
ment. J Bone Joint Surg Br 1985;67:3-9.
20. Sowa DT, Holder LE, Patt PG, Weiland
AJ: Application of magnetic resonance
imaging to ischemic necrosis of the
lunate. J Hand Surg [Am] 1989;14:
1008-1016.
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21. Desser TS, McCarthy S, Trumble T:
Scaphoid fractures and Kienböck’s dis-
ease of the lunate: MR imaging with
histopathologic correlation. Magn
Reson Imaging 1990;8:357-361.
22. Delaere O, Dury M, Molderez A,
Foucher G: Conservative versus oper-
ative treatment for Kienböck’s disease:
A retrospective study. J Hand Surg
[Br] 1998;23:33-36.
23. Sheetz KK, Bishop AT, Berger RA:
The arterial blood supply of the distal
radius and ulna and its potential use
in vascularized pedicled bone grafts. J
Hand Surg [Am] 1995;20:902-914.
24. Tamai S, Yajima H, Ono H: Revascu-
larization procedures in the treatment
of Kienböck’s disease. Hand Clin
1993;9:455-466.
25. Bochud RC, Büchler U: Kienböck’s
disease, early stage 3: Height recon-
struction and core revascularization of
the lunate. J Hand Surg [Br] 1994;19:
466-478.
26. Hori Y, Tamai S, Okuda H, Sakamoto
H, Takita T, Masuhara K: Blood vessel
transplantation to bone. J Hand Surg
[Am] 1979;4:23-33.
27. Almquist EE: Capitate shortening in
the treatment of Kienböck’s disease.
Hand Clin 1993;9:505-512.
28. Viola RW, Kiser PK, Bach AW, Hanel
DP, Tencer AF: Biomechanical analy-
sis of capitate shortening with capitate
hamate fusion in the treatment of
Kienböck’s disease. J Hand Surg [Am]
1998;23:395-401.
29. Hanel DP, Hunt TR: Capitate shorten-
ing osteotomy: Kienböck’s disease.
Atlas Hand Clin 1999;4:45-58.
30. Horii E, Garcia-Elias M, Bishop AT,
Cooney WP, Linscheid RL, Chao EY:
Journal of the American Academy of Orthopaedic Surgeons
Effect on force transmission across the
carpus in procedures used to treat
Kienböck’s disease. J Hand Surg [Am]
1990;15:393-400.
31. Trumble T, Glisson RR, Seaber AV,
Urbaniak JR: A biomechanical com-
parison of the methods for treating
Kienböck’s disease. J Hand Surg [Am]
1986;11:88-93.
32. Quenzer DE, Dobyns JH, Linscheid
RL, Trail IA, Vidal MA: Radial reces-
sion osteotomy for Kienböck’s disease.
J Hand Surg [Am] 1997;22:386-395.
33. Nakamura R, Horii E, Watanabe K,
Nakao E, Kato H, Tsunoda K: Proxi-
mal row carpectomy versus limited
wrist arthrodesis for advanced Kien-
böck’s disease. J Hand Surg [Br] 1998;
23:741-745.
34. Condit DP, Idler RS, Fischer TJ,
Hastings H II: Preoperative factors
and outcome after lunate decompres-
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Surg [Am] 1993;18:691-696.
35. Naum SC, VanGorp CC, DeHeer DH,
Swanson AB: Titanium lunate implant
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One to nine-year follow-up. Presented
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American Society for Surgery of the
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Surgical considerations. J Hand Surg
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 Neurologic Complications After Lumbar Spine Surgery

M. Darryl Antonacci, MD, and Frank J. Eismont, MD

Abstract

With the increasing complexity and number of lumbar spine operations being occur, rapid recognition and appro-
performed, the potential number of patients who will sustain perioperative com- priate treatment can minimize their
plications, including those that involve neural structures, has also increased. effect.
Neurologic complications after lumbar spine surgery can be categorized by the
perioperative time period during which they occur and by their mechanism of
injury. Although the overall incidence of neurologic complications after lumbar Anatomy
surgery is low, the severity of these injuries mandates careful preoperative plan-
ning, awareness of risk, and meticulous attention to perioperative details. Knowledge of the relevant anatomy
J Am Acad Orthop Surg 2001;9:137-145 is essential to minimizing direct
neural injuries. The spinal cord ter-
minates as the conus medullaris at
the level of the inferior border of L1
Neurologic complications after lum- complications arising from anes- and the superior border of L2.
bar spine surgery may be broadly thesia, patient positioning, surgical Spinal cord tissue is much less tol-
classified by the mechanism of technique, or procedure-specific erant of traction and compression
injury and by the time period dur- risks. Early in the postoperative than the nerve roots are. Even
ing which they occur. The causes of period and up to 2 weeks after sur- minimal manipulation of the cord
injury are generally either indirect gery, neurologic injuries are most may cause profound neurologic
or direct, with the latter including commonly secondary to direct consequences. Focal injury to the
laceration, compression, traction, compression of the neural ele- conus medullaris can cause injury
and avulsion injuries to the neural ments. This is often caused by the to the function of the lower sacral
elements. Such direct causes are mass effect of postoperative hema- roots and result in disturbances in
most commonly the result of a tech- toma, pseudomeningoceles, and bowel, bladder, or sexual function
nical mishap by the surgeon. In- epidural abscesses. After partial with or without other obvious neu-
direct injuries are due to the disrup- diskectomy, retained fragments or rologic deficits in the lower extrem-
tion of the blood supply to the recurrent herniations may also ities.
spinal cord and nerve roots or to the cause neurologic symptoms in this
gradual compression of the neural time period. After 14 days from
elements, as by correction of defor- surgery, recurrent disk herniation
mity or by a postoperative hema- should be considered more likely, Dr. Antonacci is Assistant Professor of
toma. This type of injury is usually although this may occur earlier Orthopaedic Surgery and Director, Spine
Diagnostic and Treatment Center, MCP
the result of ischemia or the disrup- as well.
Hahnemann University School of Medicine,
tion of axoplasmic flow, which pro- To both minimize and prevent Philadelphia, Pa. Dr. Eismont is Professor of
vides neural nutrition. Its causes potential neurologic complications Orthopaedic Surgery, University of Miami
are more difficult to define and are that may occur in association with School of Medicine, Miami, Fla.
often inexplicable. lumbar spine surgery, the surgeon
Neurologic injuries categorized must thoroughly understand the Reprint requests: Dr. Antonacci, Spine
Diagnostic and Treatment Center, Graduate
by the time period during which relevant anatomy and must do
Hospital, 1800 Lombard Street, Philadelphia,
the insult occurs may be intraoper- meticulous preoperative planning. PA 19103.
ative, early postoperative (1 to 14 Additionally, a thorough under-
days), or delayed postoperative standing of the etiology of the com- Copyright 2001 by the American Academy of
(after 14 days) events. Intraopera- plications can decrease their inci- Orthopaedic Surgeons.
tive events are generally related to dence. When complications do

Vol 9, No 2, March/April 2001 137

Neurologic Complications After Lumbar Spine Surgery
The spinal nerve roots, while
more tolerant of mechanical defor-
mation than the spinal cord, are less
tolerant than the peripheral nerves.
The intradural nerve rootlets are
covered by only a thin membra-
nous root sheath, which is perme-
able to cerebral spinal fluid for nu-
trition. 1 In contrast, peripheral
nerves are protected by an epineu-
rium and a perineurium. This, in
addition to a more developed con-
nective tissue layer, makes periph-
eral nerves much less susceptible to
injury than the intrathecal nerve
rootlets.
The results of experimental stud-
ies in dogs suggest that when the
thecal sac is compressed acutely to
45% of its normal area (i.e., to ap-
proximately 75 of the normal 170
mm2), significant nerve-root com-
pression occurs, with measurable
changes in both motor and sensory
function.2 The motor nerve roots
recover more quickly than the sen-
sory roots after the pressure is re-
leased; thus, transient compression
is more likely to affect the sensory
roots. The critical value of 75 mm2
can be used for the radiologic diag-
nosis of central spinal stenosis. Re-
ducing the cross-sectional area of the
thecal sac to approximately 65 mm2
generates a pressure level of about
50 mm Hg in the cauda equina.
Measurable changes in spinal nerve-
root conduction generally occur
between 50 and 75 mm Hg.3 The
effects of compression are related
not only to the duration of compres-
sion and the pressure itself but also
to the rate of onset.4 In the acute
injury setting, rapid application of
compression to the nerve roots
causes more pronounced tissue
changes than slow application. The
application of pressure over multi-
ple spinal levels and the combina-
tion of compression with systemic
hypotension can lower these thresh-
old injury levels.
The pedicle is a constant anatomic
landmark that can be used to locate
138
the exiting nerve root and thus min-
imize the likelihood of inadvertent
injury to it. If the anatomy is aber-
rant, the one constant is the relation-
ship of the pedicle to the nerve root,
which lies along the inferomedial
edge of the pedicle. In cases with
poor visualization of the nerve root,
resection of bone until the pedicle is
visible will aid in the identification
of the exiting nerve root.
During anterior lumbar surgery,
the hypogastric nerve plexus and
sympathetic chain are at risk of
injury. The aorta, the vena cava,
and collateral vessels are preverte-
bral and in close proximity to the
hypogastric nerve plexus. This
nerve plexus is approximately 6 to
8 cm in length along the surface of
the aorta and extends from the
cephalad aspect of L4 (as the supe-
rior hypogastric plexus) to the first
sacral vertebra. As the plexus en-
ters the pelvis, it divides into right
and left divisions, which course dis-
tally and join the inferior hypogas-
tric plexus. These fibers innervate
the seminal vesicles and vas deferens
in the male; injury to these struc-
tures can lead to retrograde ejacu-
lation. Injury to the hypogastric
plexus in approaches to the L5-S1
disk space is minimized by blunt
dissection directly on the anterior
surface of the disk. Sweeping the
prevertebral tissues and hypogas-
tric nerve plexus laterally, rather
than dissecting through these struc-
tures, decreases the risk of injury to
the nerve fibers. The use of bipolar
cautery and limited exposure also
helps to minimize the risk of injury.
The exposure of upper lumbar seg-
ments is not associated with as
high a risk for retrograde ejacula-
tion as the exposure of L5-S1, be-
cause the sympathetic fibers in-
volved lie on the anterior aortic
wall. Injury to the sympathetic
chain, which lies along the anterior
border of the psoas muscle, can
manifest as patient complaints of
contralateral foot coldness. In fact,
Journal of the American Academy of Orthopaedic Surgeons
vasodilatation secondary to this in-
jury causes increased warmth in the
ipsilateral foot.
Preoperative Planning
Failure to recognize variations in
normal anatomy on preoperative
studies may predispose to injury
(e.g., asymptomatic spina bifida).
Such a finding may necessitate a
particularly careful dissection or
alteration in surgical approach.
Similar caution is necessary after
prior laminectomies or with wid-
ened interlaminar spaces. It is
good practice to review all preop-
erative radiographs just prior to
surgery, with special attention to
the variant anatomy in each indi-
vidual case.
In other situations, such as in
patients with high-grade lumbar or
cervical stenosis, preoperative con-
sideration of patient positioning
may help avoid unexpected injury.
For example, patients with cervical
stenosis should be carefully trans-
ferred to the prone position with
their heads in a neutral or slightly
flexed position, or awake position-
ing should be used. In severe cases,
consideration should also be given
to fiberoptic intubation. In patients
with high-grade lumbar spinal
stenosis, use of large Kerrison ron-
geurs should be avoided in favor of
the motorized diamond burr. Un-
der these conditions, placement of
cottonoid pledgets within a tightly
narrowed epidural space should be
avoided.
Prior to surgery, patients should
be instructed to discontinue the use
of anti-inflammatory medications
(for 2 to 3 days) and aspirin (for 2 to
10 days) to minimize intraoperative
and postoperative blood loss. Pa-
tients should also be questioned
about complementary or alternative
medications, such as gingko and
cayenne, which can have effects on
clotting.

Complications Related to
Induction of Anesthesia
and Patient Positioning
The risk of intraoperative neuro-
logic injuries begins with the in-
duction of anesthesia and position-
ing of the patient for surgery. The
incidence of significant neurologic
injury, including complete paraly-
sis, secondary to spinal or epidural
anesthesia has been reported to be
approximately 0.02%.5 Injuries re-
lated to these types of anesthesia are
usually secondary to direct mecha-
nisms. These include laceration by
inadvertent needle placement and
compression of the neural elements
secondary to postinjection hema-
toma. Paralysis can occur in patients
with low-lying spinal cords who
undergo routine epidural or intra-
thecal injections of anesthetic agents.
Peripheral nerve injury secondary
to the placement of intravenous
and arterial lines, although uncom-
mon, can also occur.
Peripheral nerve injuries after
lumbar spine surgery more typically
occur secondary to malpositioning
or improper padding of the patient.
In posterior lumbar surgery, the
patient is usually placed in a prone
position on rolls or on a four-poster
padded frame (e.g., Relton frame)
or Andrews-type table. After posi-
tioning, it is important to ensure
that the abdomen hangs free, so as
to minimize intraoperative blood
loss. Regardless of the type of frame
used, well-padded support is neces-
sary, with care taken to avoid exces-
sive pressure on the chest wall and
pelvis. Extra foam padding of the
posts aids in distributing pressure
uniformly to the patient’s skin and
helps to avoid skin blisters and
burns. Every patient should be
positioned and padded as would be
appropriate for a much longer
duration of surgery than projected.
Direct compressive or traction inju-
ries of upper- and lower-extremity
nerves can occur. In particular, ex-
Vol 9, No 2, March/April 2001
M. Darryl Antonacci, MD, and Frank J. Eismont, MD
cessive pressure or stretch at the
brachial plexus or femoral nerve can
lead to upper- and lower-extremity
nerve palsies, respectively. In the
upper extremity, the ulnar and an-
terior interosseous nerves are par-
ticularly susceptible to external
pressure, as are the peroneal and
lateral femoral cutaneous nerves of
the lower limbs.
In patients with coexistent cervi-
cal and lumbar stenosis, careful
positioning of the head in neutral or
slight flexion is mandatory to avoid
cervical myelopathy or spinal cord
injury, either while transferring the
patient prone or during final posi-
tioning. A Mayfield three-point
head holder provides very reliable
positioning for long-duration sur-
gical procedures and for high-risk
patients. This avoids pressure on
the face and in particular on the
eyes. Ophthalmic injuries have been
reported secondary to excessive
pressure on the eyes, resulting in
permanent blindness in rare in-
stances.6
Direct and Indirect
Surgical Injuries
Direct and indirect injuries related to
surgical technique make up the ma-
jority of intraoperative neurologic
complications. Three factors appear
to predispose to iatrogenic injuries:
the relative inexperience of the sur-
geon, failure to follow meticulous
surgical technique, and a history of
prior surgical procedures on the
patient. In patients with undis-
turbed anatomy, the frequency of
injury should be very rare. If inju-
ries are occurring relatively more
frequently, it is mandatory that the
surgeon reevaluate the surgical
techniques employed (Table 1).
Most neurologic injuries from
direct trauma are related to either
trauma by surgical instruments or
placement of pedicle screws or
hooks. Several principles should be
observed to minimize risks. Appro-
priately sized rongeurs down to 1
mm with a small foot-plate should
be available. When removing bone
or soft tissue, one must always
check to see that the dura has been
dissected free (especially in patients
with rheumatoid arthritis) and that
adequate space is available for the
Kerrison foot-plate. If scarring or
adhesions are present, careful dis-
section with angled curettes or
dural elevators is required. If the
area is too narrow, bone must be
removed from above with either
motorized burrs or osteotomes
before rongeurs can be safely used.
Protection of the dura with cot-
tonoid pledgets should be avoided
in these conditions. Use of magnifi-
cation, such as with loupes or an op-
erating microscope, can be helpful
in difficult situations. In general,
Kerrison rongeurs should be directed
parallel to the exiting nerve root to
avoid transection. Motorized burrs
are passed from medial to lateral to
avoid dural damage. Diamond-
tipped burrs with copious saline irri-
gation can be used safely close to the
dura with a lower risk of laceration.
During diskectomy, the exiting
nerve root must be mobilized me-
dially to expose the herniation. In
large herniations, it may not be pos-
sible to completely mobilize the root
without excessive traction. If that is
the case, the disk should be removed
before complete mobilization. Be-
fore incising the disk anulus, one
should always make sure that the
exiting root has been mobilized and
protected. Meticulous hemostasis is
important to avoid mistaking a
nerve root for a disk fragment. The
smallest pituitary rongeurs should
be used to remove the disk, and they
should be opened only after they
have been inserted in the disk space.
Occasionally, the suction tip can
become nicked by another instru-
ment, such as the burr. The sharp
edge created can cause a dural or
nerve root laceration. For this rea-
139
Neurologic Complications After Lumbar Spine Surgery

compression. Bertrand described

Table 1 the “battered-root” syndrome, in
Basic Spine Surgery Technique
which new-onset numbness after
laminectomy or laminotomy strongly
1. Ensure adequate exposure and lighting suggests intraoperative root injury.5
2. Do not pass instruments over the open wound Excessive compression with cot-
3. Avoid overaggressive bone removal tonoid pledgets, gel foam, or mal-
4. Use the Kerrison rongeur with foot-plate oriented parallel to thecal sac positioned fat grafts has also been
5. Use Kerrison rongeur without upward or downward pressure reported as a source of intraopera-
tive neurologic compromise.7
6. Leave ligamentum flavum intact to protect thecal sac
The incidence of nerve-root avul-
7. Do not pull or tear ligamentum flavum sion injuries has been reported to
8. Release all tissue attachments to dura be approximately 0.4%.5 Forceful
9. Use disposable and undamaged suction tips around thecal sac retraction of a nerve root, especially
10. Be aware of conjoined nerve roots within a stenotic foramen, can be an
11. Use knife to incise anulus only vertically inadvertent cause of a nerve-root
avulsion. This can also occur during
12. Open mouth of pituitary rongeur within disk space
aggressive bone removal. The inci-
13. Avoid use of electrocautery near the dura dence of conjoined nerve roots in
14. Use cottonoid pledgets cautiously the lumbar spine has been reported
15. Use burr in medial-to-lateral direction under direct visualization to be between 2% and 14%,5 and
16. Never manipulate thecal sac above L2 probably is more common than is
17. Never retract thecal sac more than 50% generally acknowledged. Failure to
recognize a conjoined nerve root
18. Consider neurologic monitoring
can result in excessive compression,
19. Do not leave spikes of bone after decompression laceration, or avulsion. Adequately
20. Control bleeding with bone wax, hemostatic agents, and cautery visualizing the nerve-root sleeve
prior to closure and working laterally relative to the
21. Use drains when appropriate nerve root will help to minimize the
22. Have anesthesiologist do Valsalva maneuver before closure incidence of this complication. In
many instances, when the nerve
root cannot be identified or mobi-
lized, it is better to remove more
son, the suction tip should be help loosen any attachments to the bone until the pedicle is exposed
checked and discarded if damaged. dura. Performing bone removal than to place undue traction on the
Other laceration injuries may while leaving the ligamentum neural elements.
occur with the use of osteotomes flavum intact may also serve as an The frequency of dural tears as a
during medial facetectomies and added measure of protection to the complication of lumbar surgery can
during aggressive bone removal thecal sac. be reduced through meticulous
with the rongeur. Tearing or rip- Compression or contusion of the technique. Although identification
ping of the ligamentum flavum nerve roots or cauda equina is of a dural tear is typically made
should be avoided. Particular care another potential type of neurologic after the sudden leak of spinal
is needed when removing the bone injury related to surgical technique. fluid, identification of dural tears
fragments of the medial facet, Excessive thecal sac retraction, that have not yet disrupted the
because the capsule of the facet is especially prior to adequate decom- arachnoid layer is also important.
often adherent to the ligamentum pression of the spinal canal in pa- Most tears can be repaired primarily
flavum or the dura itself. Any tients with lumbar stenosis, can with 5-0 or 6-0 suture with a run-
movement of the dura while bone cause ischemic injuries. As noted ning stitch. Care must be taken to
is being removed, either during previously, compression of the the- avoid incorporating any neural ele-
facetectomy or when a Kerrison cal sac to less than 45% of its cross- ments into the closure. After clo-
rongeur is being used, should alert sectional area can cause changes in sure, a Valsalva maneuver aids in
the surgeon that such an attach- motor and sensory root conduction. the identification of a persistent or
ment may be present. Use of a Poorly visualized nerve roots are residual leak. In these cases, rein-
Penfield or Woodson probe can often subject to such unrecognized forcement of the repair is possible

140 Journal of the American Academy of Orthopaedic Surgeons


with muscle or fat grafts sutured
over the repair to the dura. The
use of fibrin glue, which is derived
from equal volumes of thrombin
and cryoprecipitate, may add to the
reinforcement of tenuous repairs.
Larger defects in the dura may re-
quire patch grafting with a seg-
ment of fascia from the paraverte-
bral muscles. Once the repair has
been made, a watertight closure
without wound drains is required
for the overlying fascia, subcuta-
neous tissue, and skin. Postopera-
tively, patients are typically kept
supine for several days to reduce
the hydrostatic pressure on the
dural repair.
Persistent or residual dural leaks
at the time of initial repair may be
treated by the percutaneous place-
ment of a subarachnoid drain im-
mediately after the procedure. The
placement of a subarachnoid drain
above the dural tear allows diver-
sion of spinal fluid and a decrease in
hydrostatic pressure at the repair
site. Patients should be kept supine
after surgery for as long as 5 days,
and prophylactic antibiotic coverage
should be maintained. Continuous
drainage at a rate of 10 to 15 mL/hr
is recommended. In addition, close
monitoring of spinal fluid levels of
protein, glucose, and cell count is
important until the drain is discon-
tinued. Daily Gram stains and cul-
tures of the collected spinal fluid
should also be obtained.
Complications Due to
Changes in Spinal
Alignment
Neurologic complications some-
times occur without an obvious
intraoperative cause. These indirect
injuries are usually the result of dis-
ruption of the vascular perfusion of
the spinal cord or nerve roots. More
commonly associated with scoliosis
surgery, cord ischemia can occur
secondary to application of exces-
Vol 9, No 2, March/April 2001
M. Darryl Antonacci, MD, and Frank J. Eismont, MD
sive distraction forces to a relatively
rigid spinal deformity. It can also
occur secondary to excessive hypo-
tension. Any change in neurologic
monitoring signals during these
maneuvers should alert the surgeon
to possible neurologic injury. The
degree of correction of the spinal
deformity should be lessened or
completely released, and a return to
baseline of the evoked potentials
should occur before further reduc-
tion is attempted. In some instances,
the removal of the posterior instru-
mentation is indicated. Ischemic
events involving the spinal cord and
neural elements are estimated to
occur in approximately 1 of every
3,000 surgical procedures for sco-
liosis.5
Another procedure with high
risk for neural deficit is reduction of
spondylolisthesis. Decompression
of the neural foramina (especially
at L5) before instrumentation and
avoidance of nerve-root compres-
sion from manual downward pres-
sure during the process of drilling,
tapping, and insertion of pedicle
screws or the placement of rods
reduces the risk of neurologic in-
jury. However, root injury is prob-
ably secondary to effective length-
ening of the root associated with
deformity reduction or to release of
reduction or resection of the sacral
dome (sacral shortening).
Injuries Due to
Instrumentation
The risk of neural injury secondary
to aberrant pedicle-screw place-
ment has been reported.5 A num-
ber of principles should be adhered
to in order to minimize that risk.
The proper starting point should be
identified by using osseous land-
marks or, in cases of severe de-
formity, by directly palpating the
pedicle through a laminotomy.
Once the pedicle has been probed,
it should be checked for inadvertent
perforations. After tapping, the
hole should be checked again for
perforations. Radiography or fluo-
roscopy should be used to evaluate
the placement of screws and the
overall alignment after insertion of
hardware. Intraoperative pedicle-
screw stimulation with electromyog-
raphy is commonly used to ensure
proper pedicle-screw placement.8
Stimulation of the pedicle screw that
results in nerve-root conductivity
below a certain threshold stimula-
tion can be indicative of screw
breakout or pedicle fracture. Re-
orientation or redrilling of the screw
hole is warranted. Fractures of the
pedicle secondary to screw mis-
placement can also cause direct
nerve-root impingement by the frag-
ment of bone.
Patients noted to have postoper-
ative neurologic deficits or leg pain
after the placement of instrumenta-
tion should be evaluated with com-
puted tomography (CT). This is
preferable to magnetic resonance
(MR) imaging because it accurately
demonstrates screw placement.
Questionable screw placement in
the clinical setting of new-onset leg
pain or neurologic deficit is best
managed by reoperation to remove
or replace the device and to ensure
adequate neural foraminal decom-
pression (Fig. 1).
Posterior interbody grafts, or
cages, used during posterior-lumbar
interbody fusions potentially can
dislodge and impinge on the nerve
roots or cauda equina, causing seri-
ous neurologic sequelae. The inci-
dence of this complication is in the
range of 0.3% to 2.4%. 9 Another
problem with such procedures is
the wide exposure required for graft
insertion, with resultant traction
injury or development of instability.
Anterior interbody devices carry
similar risks with regard to incor-
rect placement and dislodgment.
With the placement of anterior in-
terbody fusion devices, injury to the
hypogastric plexus secondary to the
141
Neurologic Complications After Lumbar Spine Surgery

nerve injuries increases with exten-

sion of the incision more than 8 cm
lateral to the posterior superior iliac
spine. The superior cluneal nerves
are cutaneous branches of the proxi-
mal three lumbar nerves and sup-
ply sensation to a large portion of
the buttock after piercing the lum-
bodorsal fascia. Although there is a
large degree of cross-innervation,
numbness or painful neuromas
may develop after laceration. Pal-
pation of the sciatic notch may aid
the surgeon in establishing land-
marks for taking the graft and
A B avoiding injury to the sciatic nerve
Figure 1 Lateral (A) and anteroposterior (AP) (B) radiographs of a 46-year-old man who
or superior gluteal artery. The
underwent anterior diskectomy with bone grafting and posterior fusion with pedicle direction of use of the osteotome or
screws 4 years previously. The patient awakened from surgery with severe left leg pain gouge should always be cephalad
extending to the dorsum of his foot and was subsequently seen by several physicians.
Radiographs demonstrate misplacement of three of the four pedicle screws.
and tangential to the notch.

Complications in the Early

traumatic exposure can result in
retrograde ejaculation in men. The
incidence of injury to the plexus has
been reported to be in the range of
1% to 5% with the use of these de-
vices, especially when utilizing a
laparoscopic approach.10 The risk of
such an injury after open anterior
lumbar fusion surgery has been
reported to be 0.42%.11 Additionally,
malplacement of anterior interbody
devices themselves or expulsion of
disk material posteriorly into the
spinal canal can cause neurologic
compromise, with an incidence of
2% to 4%.10
Bone Graft–Related
Neurologic Injury
The site from which bone graft is
harvested is often the origin of post-
operative pain. Kurz et al12 noted a
15% incidence of pain in the first 3
postoperative months. Frymoyer et
al13 noted this problem in up to 37%
of patients as long as 14 years after
surgery. In many instances, the
postoperative pain was part of a
general pain syndrome. Persistent
pain was more common in patients
in whom the grafts had been taken
from the same side as their preoper-
ative sciatica.
Donor-site pain can also be spe-
cifically related to peripheral nerve
injury. This may be secondary to
involvement of the lateral femoral
cutaneous nerve (meralgia pares-
thetica) during harvesting of ante-
rior iliac crest bone. Nerve symp-
toms may result from entrapment
secondary to scar formation, hema-
toma, or laceration. The variant
anatomy of this nerve as it crosses
the anterior ilium mandates careful
dissection. The incidence of this
complication is reportedly between
1% and 14%.14 Beginning the inci-
sion at a point 3 cm posterior to the
anterior superior iliac spine lessens
the chance of this complication.
When taking a bone graft from
the posterior iliac crest, one should
be aware of the location of the su-
perior cluneal nerves and the sciatic
nerve.12 The risks associated with
bone-graft harvesting from this area
can be significant. The incision
should be parallel to the midline, as
the incidence of superior cluneal
Postoperative Period
A careful neurologic assessment
when the patient awakens from
surgery provides an index exami-
nation to distinguish a deficit that
may have occurred intraoperatively
from one that occurs in the early
postoperative period. Anatomic
correlation of the neurologic deficit
noted on examination with intraop-
erative events often facilitates early
diagnosis. This is often more valu-
able than attempts at postoperative
imaging with CT, MR imaging, or
plain radiography. Evaluation of
perineal sensation and sphincter
tone is also essential, particularly
after high lumbar surgery when the
possibility of spinal cord injury
exists. The development of neuro-
logic symptoms in a patient who
awakened from lumbar surgery
neurologically intact should alert
the surgeon to the possibility of the
development of new neural ele-
ment compression. The importance
of an early accurate baseline exami-
nation cannot be overemphasized,
as diagnostic imaging of the neural
elements with MR imaging or CT

142 Journal of the American Academy of Orthopaedic Surgeons


can be difficult to interpret in the
early postoperative period.
Neurologic deficits that develop
in the early postoperative period (1
to 14 days) usually occur secondary
to retained disk fragments after
diskectomy, postoperative hema-
toma, pseudomeningocele, hernia-
tion of a fat graft, or (rarely) an
epidural abscess. Acute spondy-
lolisthesis secondary to iatrogenic
instability may also present with a
new neurologic deficit. This is more
likely to occur in the late postopera-
tive period; when it does occur in
the early postoperative period, it is
more likely to occur after aggressive
lateral decompressions with viola-
tion of the pars or facet joints. Plain
radiography and CT may be helpful
in the evaluation of this problem.
Recurrent Disk Herniation
After diskectomy for disk hernia-
tion, the incidence of neural com-
pression by a retained or missed
fragment of disk is approximately
0.2%.15 The patient typically awak-
ens from surgery and reports unre-
lieved symptoms of radiculopathy.
Because early postoperative imag-
ing is difficult to interpret, reexplo-
ration based on the clinical exami-
nation findings and symptoms may
be indicated to ensure the removal
of any remaining disk fragment.
Of course, more than one fragment
may be causing residual compres-
sion. At the time of the index proce-
dure, suspicion that a fragment of
disk may have been missed should
be raised by the presence of friable
disk material or multiple fragments.
Epidural Hematoma
The development of a postoperative
epidural hematoma may be associ-
ated with excessive or poorly con-
trolled intraoperative bleeding. Pa-
tients often have few complaints
Vol 9, No 2, March/April 2001
M. Darryl Antonacci, MD, and Frank J. Eismont, MD
initially, but significant increasing
back pain subsequently develops.
This may progress to unremitting
leg pain or even cauda equina syn-
drome in severe cases. Patients with
increasing back or leg pain require
careful monitoring. A complete
neurologic assessment is mandatory,
including a rectal examination and a
check for perianal pin-prick sensa-
tion. If neurologic deterioration oc-
curs, a spinal imaging study, such as
CT-myelography or MR imaging,
should be performed. In obvious
cases, the patient can be immediately
taken to the operating room for
evacuation without imaging. The
presence of an epidural hematoma is
a surgical emergency, requiring
decompression.
Epidural Abscess
In the 2- to 4-week period after sur-
gery, epidural abscess (Fig. 2) be-
comes a potential cause of new-
onset neurologic deficits, although
this is a rare complication. Epidural
abscesses, like hematomas, require
urgent decompression.
Pseudomeningocele
Dural tears that occur during sur-
gery and that are not recognized
and repaired or are inadequately
repaired can result in the formation
of a pseudomeningocele5 (Fig. 3).
With the increased number of oper-
ations for stenosis being performed,
this complication may be more fre-
quent than previously suspected.
The incidence of pseudomeningo-
cele formation is estimated to be
between 0.07% and 2%.8 The prev-
alence of incidental durotomy is
higher, at approximately 4%.8 In-
cidental durotomy is the second
most common cause of lawsuits
after lumbar spine surgery and the
most common complication of re-
peat laminectomy.8
The formation of pseudomenin-
goceles is more common after lum-
bar spine surgery than after cervi-
cal spine surgery. Although small
dural tears can close spontaneously,
many continue to leak and form
pseudomeningoceles. The use of
agents such as Adcon-L may pre-
cipitate continued leakage of unrec-
ognized dural lacerations.16 These
can be noted as a slowly expanding
fluid mass or soft-tissue bulging on
physical examination. Patients usu-
ally present with a progressively
worsening headache. Both the
mass and the headache may in-
crease in magnitude on standing.
Diagnosis is readily made early by
using myelography followed by
CT. Magnetic resonance imaging
may also be helpful in the diagno-
sis, but it may be difficult to differ-
Figure 2 T2-weighted MR image of a 50-
year-old man who underwent posterior
laminectomy. Approximately 3 to 4 weeks
after surgery, severe, unremitting back
pain developed. The image demonstrates
enhanced signal in the disk space with
enhancement anterior to the thecal sac
extending cephalad, consistent with an
epidural abscess. Treatment included irri-
gation and debridement and intravenous
antibiotic therapy.
143
Neurologic Complications After Lumbar Spine Surgery

A B

Figure 3 Lateral (A) and axial (B) MR images of a 55-year-old man approximately 4 to 5 weeks after lumbar laminectomy. He reported a
sudden sharp pain with coughing, and a fluctuant mass was noted in his low back. The images demonstrate a large pseudomeningocele.

entiate a pseudomeningocele from
a postoperative hematoma with
this modality. The onset of neuro-
logic symptoms may present either
insidiously or acutely with pain,
headache, and sudden neurologic
deficit. A neurologic deficit may
occur when one or more nerve
roots herniate out of the dural tear
and become trapped within the
pseudomeningocele.
Treatment of pseudomeningoceles
includes surgical exploration and
repair. Careful dissection is required.
Excision of the cyst is not necessary,
but opening of the cyst to avoid in-
jury to the trapped roots is usually
required before closure and repair.
Summary
Neurologic complications after
lumbar spine surgery are neither
common nor necessarily foresee-
able. With the increasing number
of lumbar spine operations being
performed, the number of patients
who will sustain neurologic injury
can be expected to increase. Be-
cause of the often irreversible and
dramatic nature of these injuries, as
well as the lack of definitive treat-
ments once they have occurred, it
is obviously best to prevent these in-
juries through use of meticulous op-
erative technique, awareness of risk,
and close attention to perioperative
details.

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