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Abdurrahman (C 111 12 002)
Shandy Shanaya (C 111 12 133)
Senoaji Srimulyo W.W (C 111 12 264)
Ufi Madina (C 111 11 371)

dr. Ricki

Dr. dr. Muhammad Sakti, Sp.OT (k)




Yang bertandatangan dibawah ini menyatakan bahwa :

Nama :
Abdurrahman (C 111 12 002)
Shandy Shanaya (C 111 12 133)
Senoaji Srimulyo W.W (C 111 12 264)
Ufi Madina (C 111 11 371)

Judul Kasus dan Referat :Avaskuler Necrotic Hip Join

Telah menyelesaikan tugas dalam rangka kepaniteraan klinik pada Bagian Ilmu
Kesehatan Mata Fakultas Kedokteran Universitas Hasanuddin.

Makassar,Januari 2018

Supervisor Pembimbing

Dr.dr. Muhammad Sakti, Sp.OT (k) dr.Ricki


HALAMAN JUDUL................................................................................................ i
LEMBAR PENGESAHAN .................................................................................... ii
DAFTAR ISI .......................................................................................................... iii
A. Introduction ................................................................................................... 4
B. Defenition ..................................................................................................... 4
C. Anatomy ........................................................................................................ 5
D. Epidemiology .............................................................................................. 17
E. Etiology ....................................................................................................... 17
F. Pathomechanism ......................................................................................... 19
G. Classification ............................................................................................... 20
H. Diagnostic ................................................................................................... 24
I. Treatment .................................................................................................... 26
J. Prognostic .................................................................................................... 29
A. Conclucion .................................................................................................. 29

Avascular necrosis (AVN), also known as osteonecrosis, aseptic necrosis or ischemic bone
necrosis is a disease that may affect several dif-ferent bones as a result of temporary or per-
manent loss of the blood supply to these bones. The ischemia causes the death and eventual
collapse of the bone tissue, with its overlying joint surface (1).Koenig was the first to
describe this condition, which he termed osteochondritis dissecans, in 1888. In 1925, Haenish
de-scribed the first case that involved the femoral head. In 1940, the cause of the necrosis was
deemed to be arterial occlusion. Pietrograndi described the first case of femoral head AVN
after steroid use in 1957 (2). Ever since, scien-tists have found out more and more about the
complex physiopathology of this disease which to this days remains largely unknown. The
femoral head is most commonly affected by this disease. Usually, the patients are in their
third, fourth or fifth decade of life at the time of diagnose. Men are more prone to this dis-
ease than women, the sex ratio being about.

Initially, patients are asymptomatic, but, in time, AVN leads to joint destruction, requiring
surgical treatment and, in latter stages, total hip replacement (THR) (2). Although treatment
has been facilitated by using a widely accepted inter-national classification system, effective
earlier di-agnosis using MRI, and more aggressive surgical management, no universally
satisfactory therapy has been developed, even for early disease.

It is essential that AVN of the femoral head is diagnosed early because delaying this
disease by joint preserving measures have a much better prognosis and because the results of
joint replace-ment are poorer in young individuals.

2.1. Definition
Avascular necrosis (AVN), also known as osteonecrosis, aseptic necrosis or ischemic bone
necrosis is a disease that may affect several different bones as a result of temporary or per-
manent loss of the blood supply to these bones. The ischemia causes the death and eventual
collapse of the bone tissue, with its overlying joint surface.Koenig was the first to describe
this condition, which he termed osteochondritis dissecans, in 1888. In 1925, Haenish de-
scribed the first case that involved the femoral head. In 1940, the cause of the necrosis was
deemed to be arterial occlusion. Pietrograndi described the first case of femoral head AVN
after steroid use in 1957. Ever since, scientists have found out more and more about the
complex physiopathology of this disease which to this days remains largely unknown.

The femoral head is most commonly affected by this disease. Usually, the patients are in
their third, fourth or fifth decade of life at the time of diagnose. Men are more prone to this
disease than women, the sex ratio being about.

Initially, patients are asymptomatic, but, in time, AVN leads to joint destruction, requiring
surgical treatment and, in later stages, total hip replacement (THR). Although treatment has
been facilitated by using a widely accepted international classification system, effective
earlier diagnosis using MRI, and more aggressive surgical management, no universally
satisfactory therapy has been developed, even for early disease.

It is essential that AVN of the femoral head is diagnosed early because delaying this disease
by joint preserving measures have a much better prognosis and because the results of joint
replace-ment are poorer in young individuals

2.2. Anatomy
The hip joint (see the image below) is a ball-and-socket synovial joint: the ball is the
femoral head, and the socket is the acetabulum. The hip joint is the articulation of the pelvis
with the femur, which connects the axial skeleton with the lower extremity. The adult os
coxae, or hip bone, is formed by the fusion of the ilium, the ischium, and the pubis, which
occurs by the end of the teenage years. The 2 hip bones form the bony pelvis, along with the
sacrum and the coccyx, and are united anteriorly by the pubic symphysis


The femur is the longest and heaviest bone in the human body. It consists of a superior or
proximal end, a shaft, and an inferior or distal end (see the image below).

The superior end of the bone is the articulating side of the femur to the acetabulum. The
upper femoral epiphysis closes by 16 years of age.

The trabecular bone configuration in the proximal femur obeys Wolff's Law, which states
that bony structures orient themselves in form and mass so as to best resist extrinsic forces.
The principal compressive group, the principal tensile group, the greater trochanteric group,
the secondary tensile group, the secondary compressive group, and, finally, Ward's triangle
can be found.

The superior end of the femur consists of a head, a neck, and greater and lesser
trochanters. The head of the femur is angled superomedially and slightly anteriorly when
articulating with the acetabulum. The head is attached to the femoral body or shaft by the
neck of the femur.

The superior border of the neck begins just lateral to the femoral head and ends distally at
the greater trochanter. The inferior border of the neck begins lateral to the femoral head and
extends to the inferior trochanter. The superior border is shorter and thicker than the inferior
border. The anterior surface of the neck is rough in comparison to the smooth femoral head.
The neck’s posterior surface has a concave appearance. The head and neck are at an angle of
130º (± 7º) to the shaft. The angle is larger at birth and decreases with age.

The greater trochanter is a bony prominence on the anterolateral surface of the proximal
shaft of the femur, distal to the femoral neck. It serves as the insertion site for the gluteus
medius and gluteus minimus. The lesser trochanter is a bony prominence on the proximal
medial aspect of the femoral shaft, just distal to the femoral neck. It serves as the iliopsoas
insertion site.

The intertrochanteric line is a raised area that extends from the greater to the lesser
trochanter anteriorly. This connection posteriorly is called the intertrochanteric crest, which
contains the calcar femorale, another anatomic location on the femoral neck. The calcar
femorale is a vertically oriented plate of dense cancellous bone from the posteromedial
portion of the femoral shaft radiating superiorly toward the greater trochanter.

At birth, each pelvic half consists of 3 separate primary bones: the ilium, the ischium, and
the pubis (see the images below). These bones are joined by hyaline cartilage.

In infants and children, these large parts of the hip bones are incompletely ossified. At
puberty, the 3 primary bones are still separated by a Y-shaped triradiate cartilage centered in
the acetabulum. The primary bones begin to fuse at 15-17 years. Fusion is complete between
20-25 years of age. The fact that these bones were originally separate is fairly undetectable in
adult bones on imaging. Although the parts of the hip bone are fused in adulthood, they are
still referred to by their separate origins


The ilium is the largest part of the hip bone and makes up the superior part of the
acetabulum. The ala provides an insertion point for the gluteal muscles laterally and the
iliacus muscle medially.

Anteriorly, the ilium has an anterior superior iliac spine (ASIS); inferior to this is an
anterior inferior iliac spine. From the ASIS, anteriorly, the iliac crest comes around laterally
and continues posterior to the posterior superior iliac spine (PSIS). The PSIS marks the
superior point of the greater sciatic notch.

The lateral surface of the ilium has 3 rough curved lines: the posterior, anterior, and
inferior gluteal lines. Medially, the ilium has an iliac fossa. Posteriorly, the medial aspect of
the ilium has an auricular surface

The ischium is the inferior aspect of the pelvis. The superior part of the body of the
ischium fuses with the pubis and ilium, forming the posteroinferior aspect of the acetabulum.

The ramus of the ischium joins the inferior ramus of the pubis to form a bar of bone
called the ischiopubic ramus, which constitutes the inferomedial boundary of the obturator
foramen. The posterior border of the ischium forms the lower margin of a deep indentation
the greater sciatic notch. The large triangular ischial spine at the inferior margin of this notch
is a sharp demarcation separating the greater sciatic notch from a smaller rounded inferior
indentation called the lesser sciatic notch.

The bony projection at the inferior end of the body of the ischium and its ramus is the
ischial tuberosity.

The pubis makes up the anteromedial part of the hip bone and contributes the anterior
part of the acetabulum. The pubis has a flat body and 2 rami: superior and inferior.

Medially, the symphyseal surface of the body of the pubis articulates at the pubic
symphysis with the surface of the body of the contralateral pubis. The anterosuperior border
of the united bodies and symphysis forms the pubic crest. The pubic tubercles, small

projections at the lateral ends of this crest where the inguinal ligaments attach medially, are
extremely important landmarks of the inguinal regions. The posterosuperior aspect of the
superior ramus of the pubis is called the pectin pubis.

The obturator foramen is an oval opening formed by the rami of the pubis and the
ischium. The obturator canal houses the obturator nerve and vessels.

As indicated above, the acetabulum is formed from parts of the ilium, ischium, and
pubis. The acetabulum is the cup-shaped socket on the lateral aspect of the pelvis, which
articulates with the head of the femur to form the hip joint.

The margin of the acetabulum is deficient inferiorly. An additional fibrocartilaginous

margin of the acetabulum is referred to as the acetabular labrum. The labrum functions to
deepen the acetabulum, thus holding the femoral head more securely. The lunate is the
articular surface of the acetabulum to the femoral head. The rough depression in the floor of
the acetabulum is the acetabular fossa, which is continuous with the acetabular notch.

The transverse acetabular ligament is located along the inferior aspect of the acetabulum;
it prevents the femoral head from moving inferiorly by deepening the acetabulum inferiorly.

The hip joint contains a strong fibrous capsule that attaches proximally to the
acetabulum and transverse acetabular ligament and distally to the neck of the femur anteriorly
at the greater trochanter (see the image below). Posteriorly, the fibrous capsule crosses to the
neck 1-1.5 cm proximal to the intertrochanteric crest.

Most of the fibers go from the hip bone to the intertrochanteric line, but some deeper
fibers go around the neck, forming the orbicular zone, which holds the femoral neck in the
acetabulum. The anterior capsule of the hip is the strongest and thickest part.

This capsule is composed of 3 ligaments. The iliofemoral ligament, sometimes referred

to as the Y ligament of Bigelow, attaches to the anterior inferior iliac spine and the acetabular
rim proximally and takes an inferolateral direction to insert on the intertrochanteric line
distally. It is the strongest part of the capsule. The iliofemoral ligament prevents
hyperextension of the hip joint during standing by holding the femoral head within the

The ischiofemoral ligament reinforces the capsule posteriorly. It originates on the ischial
part of the acetabular rim and spirals superolaterally to the neck of the femur, medial to the
greater trochanter. This ligament, like the iliofemoral, also prevents hyperextension and holds
the femoral head within the acetabulum.

The pubofemoral ligament reinforces the capsule anteriorly and inferiorly. It begins from
the obturator crest of the pubic bone and passes inferolaterally to join the fibrous capsule of
the hip joint. This ligament prevents overabduction of the hip joint.

An iliopectineal bursa lies anteriorly over the gap in the ligaments, beneath the iliopsoas

There are several additional structures of importance related to the fibrous capsule.
Lining the fibrous capsule is the synovial membrane. It covers the neck of the femur between
the attachment of the fibrous capsule and the edge of the articular cartilage of the head; it also
covers the nonarticular area of the acetabulum, providing a covering for the ligament of the
femoral head.

Retinacula, which contain blood vessels, are deep longitudinal fibers of the capsule that
go superiorly from the femoral neck and blend with the periosteum. The bursa is considered
the synovial extension beyond the free margin of the fibrous capsule onto the posterior aspect
of the femoral neck.

The ligament of the femoral head is weak. It attaches to the margins of the acetabular
notch and the transverse acetabular ligament; its narrow end attaches to the pit in the head of
the femur. Usually the ligament contains a small artery to the head of the femur.

A fat pad in the acetabular fossa is covered with synovial membrane. It fills the
acetabular area that is not filled by the femoral head.


Nerve Sensory Motor
Proximal None in hip and thigh
Genitofemoral L1 – L2
anteromedial thigh Gracilis (anterior division)

Adductor longus (anterior
Adductor brevis
(Anterior/posterior division)
Obturator L2 – L4 Inferomedial thigh
Adductor magnus (posterior
Lateral femoral Psoas major
L2-L3 Lateral Thigh
cutaneous Sartorius
Articularis genu
Femoral L2-L4 Anteromedial thigh Rectus femoris
Vastus lateralis
Vastus intermedius
Vastus medialis
Biceps femoris (long head)
Tibial L4-S3 None in thigh Semitendenosus
Common fibular
L4-S2 None in thigh Biceps femoris (short head)
Posterior femoral
S1-S3 Posterior thigh none
cutaneous nerve


Muscles Action Nerve
Sartorius Hip flexion, external rotation Femoral nerve
Illiopsoas Hip flexion Femoral nerve
Pectineus Hip flexion Femoral nerve
Rectus femoris Hip flexion, leg extension Femoral nerve
Adductor magnus (anterior
Hip flexion, adduction Obturator
Adductor magnus (posterior
Thigh extension Tibial
Gracilis Hip flexion. Internal rotation Obturator
Tensor fascia lata Hip flexion, abduction Superior gluteal nerve
Obturator nerve (posterior
Adductor brevis Hip adduction
Obturator nerve (anterior
Adductor longus Hip adduction
Pectineus Hip adduction, flexion Femoral
Obturator nerve posterior
Obturator externus Thigh external rotation
Gluteus maximus Lateral rotation, extension Inferior gluteal nerve
Piriformis Lateral rotation Nerve to piriformis
Oturator internus Lateral rotation Nerve to obturator internus

Gemellus superior Lateral rotation Nerve to obturator internus
Gemellus inferior Lateral rotation Nerve to quadriatus femoris
Quadratus femoris Lateral rotation Nerve to quadratus femoris
Gluteus medius Hip abduction Superior gluteal nerve
Gluteus minimus Hip abduction Superior gluteal nerve
Semimembranosus Thigh extension, leg flexion Tibial
Semitendinosus Thigh extension, leg flexion Tibial
Biceps femoris, long head Thigh extension, leg flexion Tibial
Biceps femoris short head Thigh extension, leg flexion Common fibular


Artery Branches
Anterior and posterior branches
In femoral triangle, runs in medial thigh
Obturator between vastus medialis and adductor longus,
in adductor canal, through adductor hiatus,
then becomes popliteal artery behind knee
Superficial circumflex iliac
Superficial epigastric

Superficial external pdendal
Deep external pudendal
Deep femoral artery
Descending genicular artery
Articular branch
Saphenous brabch
Medial circumflex femoral, major supply to
femoral neck
Lateral circumflex femoral, also supllies
femoral neck
Deep femoral artery
Ascending branch
Transverse branch
Descending branch
Perforators branches
Artery Course
Obturator Run through ligament of femoral head
Artery of ligament teres Branches from femoral artery in femoral
Deep femoral artery triangle
Medial circumflex femoral
Ascending branch Between pectineus and illiopsoas femoral
Descending branch neck
Lateral circumflex femoral
Ascending branch Runs on quadriatus femoris deep to Sartorius

Cervical branches and rectus femoris to grater trochanter

Retinacular arteries anteriorly

Tranverse branch
Extracapsular branches of anastomosis

Intracapsular branches run along neck, enter

Descending branch bone at base of femoral head

Extencis laterally

Under rectus femoris

2.3. Epidemiology
Approximately 5%-18% of all hip arthroplasties arecompleted on patients with a primary
diagnosis of osteonecrosis. Patients are generally younger adults age35 years to 45 years, and
risk factors for 75%-90% of cases. Males are affected up to three times morethan females,
and bilateral femoral head osteonecrosisis found in up to 75% of cases. Incidence in the late
1990’s was reported to be 10 000 to 20 000 new patientsper year, but this incidence has
almost certainly increasedover the past decade

2.4. Etiology
There are various conditions than can be in criminated as triggers for this disease.
However, almost half of the patients diagnosed present none of these conditions. This type of
avascular necrosis is termed primary, or idio-pathic. All the other forms of this disease are
secondary (2-8). One of the most common rea-sons for secondary avascular necrosis is
prolonged systemic steroid use in high doses (equivalent to 4000 mg of Prednisone) for
extended periods of up to 3 months, or longer. There were cases cited in literature of AVN of
the femoral head after relatively brief periods (7 days) of oral steroids. The mechanism of
action is not yet fully understood, but it is thought to be linked to the hypercoagulable state,
with subsequent impaired fibrinolysis and venous thrombosis in the femoral head. Other
common causes include trauma, blood disorders or decompression disease Taking these facts
into account, AVN can be classified as follows:

1. Primary (idiopathic)
2. Secondary to:
– Trauma

– Fracture of the femoral neck/ Slipped capital femoral epiphysis /Proximal femoral
epiphysiolysis / Dislocation of the femoral head / Epiphyseal compression / Vascular
trauma / Burns/ Radiation exposure

– Hemoglobinopathies

ƒ Sickle cell disease
Hemoglobin S or hemoglobin C hemoglobinopathy

ƒ Polycythemia
– Caisson disease

– Dysbaric osteo-necrosis

– Local infiltrative disease

ƒ Gaucher disease
ƒ Infection
ƒ Neoplasms
– Hypercortisolism

ƒ Corticosteroid medications
ƒ Cushing disease
– Alcohol consumption

– Pancreatitis

– Chronic renal failure

– Cigarette smoking

– Collagen vascular diseases

– Congenital and developmental / Congenital dislocation of the hip / Ehlers-Danlos

syndrome / Heredity dysostosis / Legg-Calvé-Perthes disease

– Fabry disease

– Giant cell arteritis

– Gout and hyperuricemia

– Hemodialysis

– Hypercholesterolemia

– Hypercoagulable states

– Hyperlipidemia

– Hyperparathyroidism

– Intravascular coagulation

– Organ transplantation

– Pregnancy

– Systemic lupus erythematosus

– Thrombophlebitis

– Hemophilia ‰

2.5. Patofisiologi/ Patomechanism

Extraosseous arterial factors are the most important. The femoral head is at
increased risk because the blood supply is an end-organ system with poor collateral
development. Blood supply can be interrupted by trauma, vasculitis (Raynaud disease), or
vasospasm (decompression sickness).

Intraosseous arterial factors may block the microcirculation of the femoral head
through circulating microemboli. These can occur in sickle cell disease (SCD), fat
embolization or air embolization from dysbaric phenomena.

Intraosseous venous factors affect the femoral head by reducing venous blood flow
and causing stasis. These factors may accom-pany conditions such as Caisson disease, SCD
or enlargement of intramedullary fat cells.

Intraosseous extravascular factors affect the hip by the increasing the pressure,
resulting in a femoral head compartment syndrome. For example:
– Fat cells hypertrophy after steroid admin-istration or abnormal cells, such as
Gaucher and inflammatory cells, can encroach on intraosseous capillaries, reducing
intramedullary circulation and contributing to compartment syndrome.

– Repeated microfractures in the weight-bearing segment of the femur may cause
multiple vascular lesions resulting in is-chemia within fragile and poorly repaired
– Cytotoxic factors, such as alcoholism and steroid use, have a direct toxic metabolic
effect on osteogenic cells .
– Decreased concentrations of 1,25 di-hydroxyvitamin D3 can cause a quanti-tative
or qualitative deficiency in the bone architecture, causing the bone to deform under

Extraosseus extravascular (capsular) fac-tors involve the tamponade of the lateral

epi-physeal vessels located within the synovial mem-brane, through increased intracapsular
pressure. This occurs after as trauma, infection, and ar-thritis, causing effusion that may
affect the blood supply to the epiphysis .

2.6. Classification
The 2 most prevalent tools for staging the disease are the Ficat and Arlet, and the Steinberg
staging systems.

Steinberg et al. expanded this staging system, by dividing stage III lesions into femoral heads
with or without collapse or hips with or without acetabular involvement. In addition, they
quantified the amount of involvement of the femoral head into mild (30%), based on
radiographs (TABLE 1).

Ohzono et al. incorporated the concept of location of the lesion, with prognostic
value. In type 1 lesions, there is a line separating the normal femoral head from the affected,
sclerotic part. Depending on the amount of weightbearing area involved, they are classified as
A (60%). Type 2 is a collapsed head without a separating line and type 3 is represented by the
presence of cysts (FIGURE 4). Type 3 A lesions are central, 3 B lesions involve the supero-
lateral aspect of the femoral head. Types 1 A, 1 B, 2 and 3 A have a better prognosis than
types 1 C and 3 B. More recently, a new classification has been completed by ARCO, which
joins the Ficat Arlet staging system, the quantification of involvement (Steinberg) and the
concept of prognosis based on location (Ohzono) (FIGURE 5).
 Stage 0 – Bone biopsy results consistent with osteonecrosis; other test results
 Stage I – Positive findings on bone scan, MRI, or both
- A – <15% involvement of the femoral head (MRI)
- B – 15-30% involvement
- C – >30% involvement
 Stage II – Mottled appearance of femoral head, osteosclerosis, cyst formation, and
osteopenia on radiographs; no signs of collapse of femoral head on radiographic or
CT study; positive findings on bone scan and MRI; no changes in acetabulum
- A – <15% involvement of the femoral head (MRI)
- B – 15-30% involvement
- C – >30% involvement
 Stage III – Presence of crescent sign lesions classified on basis of appearance on
AP and lateral radiographs
- A – <15% cresent sign or <2-mm depression of femoral head
- B – 15-30% cresent sign or 2- to 4-mm depression
- C – >30% crescent sign or >4-mm depression
Stage IV – Articular surface flattened; joint space shows narrowing; changes in acetabulum
with evidence of osteosclerosis, cyst formation, and marginal osteophytes.

2.7. Dagnostic

Avascular necrosis may be asymptomatic and is occasionally discovered following

radiography. Pain in the affected joint, described as throbbing, deep and, often, intermittent
(2), is typically the presenting symptom. Patients with AVN of the femoral head often report
groin or hip pain that can radiate to the buttocks, anteromedial thigh, or knee that is
exacerbated by weight bearing and sometimes by coughing. The pain may initially be mild
but progressively worsens over time and with use. Eventually, the pain is present at rest and
may be present or even worsen at night (7), in which case, it may be associated with morning


o Usually the initial findings are unrevealing.

o In the latter stages of the disease, joint function deteriorates and the following signs may
be found:
 The patient may walk with a limp and may experience loss of range of motion, both
active and passive, most frequently in flexion, abduction, and internal rotation,
especially after collapse of the femoral head.
 The patient may have tenderness around the affected area.
 A neurological deficit may be found (7).
 The Trendelenburg sign may be positive.
 A click may be heard when the patient rises from a chair or after external rotation of
the abducted hip (2).
o Advanced disease leads to joint deformity and muscle wasting (7).

 Plain film radiographic findings are absent in stages 0 and 1 of AVN. A normal
radiograph does not equal a normal hip. A delay of 1-5 years can occur between the
first symptoms and the appearance of radiographic modifications (2). In more
advanced disease, radiographs show sclerosis and changes in bone density. As the
disease progresses, subchondral radiolucent lines (crescent sign), flattening or the
collapse of the femoral head may appear (7).
 CT scan is used to determine the extent of involvement, such as subchondral lucencies
and sclerosis present in the reparative stage (2) (before the collapse of the femoral
head), but it is not as sensitive as MRI in stages 0 and 1. CT is excellent for detecting
femoral head collapse, early degenerative joint disease and the presence of loose
bodies especially when using multiplanar reconstruction (2).
 MRI is the most sensitive means of diagnosing AVN, representing the gold-standard
of noninvasive diagnostic evaluation (FIGURE 1). It has several advantages:
- It allows accurate staging by clearly depicting the size of the lesion.
- It detects asymptomatic lesions (7) that are undetectable on plain radiographs, thus
facilitating early treatment and better response.
- It provides multiplanar imaging and excellent soft tissue resolution (10,11).
- It can demonstrate response of the femoral head to treatment (2).
 Single-photon emission computed tomography (SPECT) is used as an alterna tive for
MRI when the latter cannot be performed or when MRI results are indeterminate.

SPECT is difficult to use because it requires remaining still for long periods of time.
Also, bladder artifacts are a frequent problem (2,10).
Scintigraphic imaging reveals a central area of decreased uptake, surrounded by an area
of increased uptake (the doughnut sign or coldin-hot sign) (2). It indicates the reactive zone
surrounding the necrotic area. The main disadvantages are that it lacks specificity (2) and that
the same image may be encountered in other conditions such as osteoarthritis, fracture, and
inflammatory arthritis. Results are difficult to interpret if disease is bilateral.

Bone biopsy is not routinely used because of the availability of sensitive noninvasive tests
such as MRI (7). It is a valuable diagnostic tool after analyzing the bony fragment extracted
after core decompression.

2.8. Treatment
The goal of the treatment is to keep joints from breaking down, because severe pain
and limitation in movement will occur within 2 years, in the absence of treatment. There are
several options that one can choose from and in order to determine the most appropriate
treatment, one has to take into consideration the age of the patient, the stage of the disease,
the location and amount of bone affected and the underlying cause of avascular necrosis
(unless corticosteroid or alcohol use is stopped, treatment may not work) (1). There are
conservative and surgical methods for treating this disease. Conservative treatments have
been used experimentally alone or in combination, but they rarely provide lasting
improvement. Most patients will eventually need surgery either to delay, or even to repair the
joint permanently (1).

Conservative Treatment
During the early stages of AVN, a physician may begin treatment by having patients limit the
amount of weight they place on the affect- ed joint. Limited activity or crutches will likely be
recommended to slow the damage caused by AVN. Range-of-motion exercises may be done
by a physical therapist or by the patients themselves. is can improve and maintain the joint’s
range of motion. € e reduction of weight, together with prescribed medications, can be an
elective way to avoid or delay surgery for some patients. When surgery is indicated, one
of two pro- cedures is typically performed—either a core decompression or a total hip
Statin therapy, bisphosphonates (6,12,13) or nonsteroidal anti-inflammatory drugs
may be helpful. – In some early cases, reduced weight bearing, limiting activities or using
crutches can slow the damage caused by avascular necrosis and permit natural healing (1).
However, these patients run a risk of 85% of femoral head collapse (2). Protected weight-
bearing may be effective when the involved segment is smaller than 15% and located far
from the weight-bearing region (5).– Range-of-motion exercises are helpful for maintaining
joint function (1). – Electrical stimulation is thought to induce bone growth (1).

Surgical Treatment
Core decompression is achieved by removing the inner layer of bone (1) and provides
immediate pain relief by reducing pressure in the bone, decreasing vascular engorgement and
inflammation and relieving the compartment syndrome (2). It enhances the process of
creeping substitution and also encourages the formation of new blood vessels, thereby
increasing blood flow to the bone (1). It is indicated in people with early stages of avascular
necrosis, before the collapse of the head and when less than 30% of the femoral head is
involved (2). Core decompression is also effective for pain relief (11) and helps delay the
need for arthroplasty, acting as a joint preserver. – Bone grafting uses healthy bone from one
part of the patient and transplants it to the diseased area. After the failure of nonvascularized
grafts, present-day grafts (called vascular grafts) include an artery and veins, increasing the
blood supply to the affected area (1). Bone grafting can be combined with core
decompression, acting together towards stopping the cycle of ischemia. It is indicated in early
stages of the disease and, when it is successful, it can ensure lifelong survival of the femoral
head, in the absence of foreign body– associated complications. If unsuccessful, the
procedure allows the patient to retain the option of total hip arthroplasty in the future (3)

Osteotomy is a procedure by which the bone is reshaped to reduce stress on the affected area.
It requires a longer recovery period and limited activities for 3 to 12 months after surgery.
This procedure is most effective for patients with advanced avascular necrosis and those with
a large area of affected bone (1). Intertrochanteric and transtrochanteric rotational
osteotomies aim at bringing an intact area of bone and cartilage to the weight-bearing area of
the femoral head and, at the same time, at improving blood supply (biotrophic effect) (5,14).
The consensus is that femoral osteotomies should be performed in more advanced stages of
the disease (II or III Ficat-Arlet), but that they should be limited to patients with Kerboul
necrotic angle (sum of angles bordering the sequestrum on antero-posterior and lateral X-ray
views) inferior to 200°. Historically, 25-30 years ago, varisation, with or without
medialisation osteotomies were thought to be sufficient, but later, flexion (Kempf) or
rotational (Sugioka) osteotomies began to gain ground. One possible problem with
osteotomies is that they may make conversion to total hip arthroplasty more difficult
technically and less successful on a long-term period.
Arthroplasty. Most patients address an orthopaedic surgeon in advanced stages of the
disease, after femoral head collapse. Total joint replacement is the treatment of choice in the
final stages of avascular necrosis or when the joint is irreversibly destroyed (1). The
procedure can be done in numerous fashions, according to the surgeon’s preference. The
surgeon may use various approaches (antero-lateral, Hardinge, postero-lateral, minimal
invasive, etc.) and may employ an even broader array of implants. Classic total hip
endoprostheses (cemented or, preferably, cementless) account for the majority of implants
used but surgeons and patients alike turn more and more towards resurfacing arthroplasty
(14), a procedure that holds several advantages. Unlike classic implants that employ a friction
couple of metal on polyethylene, or ceramics or, more recently, Oxinium heads on
polyethylene cups, resurfacing arthroplasty employs a metal on metal friction couple that is
the nearest to the normal hip joint. By this technique, the acetabulum is replaced with a
cementless metal cup, very similar to its classic predecessor, but instead of removing the
entire head and femoral neck (as is the case with classic implants), the femoral head is
prepared by removing its cartilage and a thin layer of bone, thus preserving most of the bone
stock. A large diameter femoral implant is cemented (usually larger than 44 mm), which
ensures a superior stability against dislocation. Also, the design of these implants ensures an
even better range-ofmotion, that can sometimes be crucial for young, active patients. Also,
resurfacing arthroplasty preserves more of the patient’s bone stock, a feature that becomes

increasingly more important, taking into account the patients’ young age, meaning that he/she
will probably require a second and sometimes even a third intervention (15) sometime later.
Total hip arthroplasty, be it classic or resurfacing, yields excellent results, with
immediate and long-lasting pain relief (4) and allows early mobilization and a quicker return
to an active lifestyle. However, several authors have observed that there is an earlier failure
of total hip replacement in osteonecrosis than in age-matched patients with other diagnosis.
This is probably because of abnormal remodeling of bones and subsidence of prosthesis
becauseof the poor bone quality of the proximal femur. Other factors may in-clude ongoing
systemic disease, defects in mineral metabolism, use of steroids, high level of activity in
young patients and increased body weight. Over the years, as our knowledge of this disease
has improved, several surgical and conservative methods of treatment have been perfected.
Their goal is to preserve the femoral head and prevent its collapse for as long as possible
keeping in mind at the same time that the maximal and definitive treatment is total hip
replacement. Efforts should be made to delay the moment when arthroplasty is needed,
without compromising the chance of a straight-forward hip replacement. Although there have
been extensive studies regarding avascular necrosis of the femoral head, we still know little
about its pathogenesis, and therefore about the best method to treat this disease. Future
medical treatment should be aimed at the cause of this disease, thus slowing down or even
stopping the evolution of avascular necrosis and thus delaying as much as
possible the need for surgery.

2.9. Prognostic
Hip-preservation should be effective in the patients in whom17,18: (i) a diagnosis has been in
stage I or II and available technical skills and treatment options are appropriate; (ii) the
osteonecrosis is of M or C type; and (iii) the osteonecrosis is of L1 type and appropriate
treatment has been provided. Patients with disease in the pre-collapse phase who receive
timely treatment are expected to achieve good prognosis, whereas in patients with a longer
duration of collapse (>6 months), the prognosis is difficult to predict20,25. In patients with
ONFH of the same phase and type, younger (<35 years) patients have a better prognosis than
older patients; thus, the indications for treatment can be more flexible in young patients.