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Femoral Head Avascular Necrosis

Practice Essentials
Avascular necrosis (AVN) of the femoral head is a pathologic process that results from interruption of blood supply to
the bone. AVN of the hip is poorly understood, but this process is the final common pathway of traumatic or
nontraumatic factors that compromise the already precarious circulation of the femoral head. Femoral head ischemia
results in the death of marrow and osteocytes and usually results in the collapse of the necrotic segment. (See also the
Medscape Reference article Imaging in Avascular Necrosis of the Femoral Head, as well as Hip Arthroscopy in
Staging Avascular Necrosis of the Femoral Head on Medscape News.)
Osteonecrosis of the femoral head was first described in 1738 by Munro. In approximately 1835, Cruveilhier depicted
femoral head morphologic changes secondary to interruption of blood flow. Since 1962, when Mankin described 27
cases of AVN, the number of reported AVN cases has increased steadily. (See also the Medscape Reference
article Hip Osteonecrosis.)
Early radiographic findings in femoral head AVN include femoral head lucency and subchondral sclerosis. With
disease progression, subchondral collapse (ie, crescent sign) and femoral head flattening become evident
radiographically. Joint space narrowing is the end result of untreated femoral head AVN.
Magnetic resonance imaging (MRI) is the study of choice in patients who demonstrate signs and symptoms that are
suggestive of AVN but whose radiographs are normal.
Essentially, nonoperative treatment for symptomatic AVN of the hip yields unfavorable results. Small asymptomatic
lesions do not warrant surgical intervention and are closely monitored with serial examination. If symptoms ensue,
repeat imaging and surgical treatment are indicated.
Surgical treatment of AVN can be broadly categorized as either prophylactic measures (to retard progression) or
reconstruction procedures (after femoral head collapse).
For excellent patient education resources, see eMedicineHealth's patient education article Total Hip Replacement.

Epidemiology
Frequency
United States
AVN of the femoral head is a debilitating disease that usually leads to osteoarthritis of the hip joint in relatively young
adults (mean age at presentation: 38 y). The disease prevalence is unknown, but estimates indicate that 10,000-20,000
new cases are diagnosed in the United States per year. [1, 2] Furthermore, it is estimated that 5-18% of the more than
500,000 total hip arthroplasties performed annually are for osteonecrosis of the femoral head. [2]
(See also the Medscape Reference articles Osteoarthritis [in the Orthopedic Surgery section] and Rehabilitation for
Osteoarthritis [in the Physical Medicine and Rehabilitation section], as well as Hip-Spine Syndrome: The Effect of
Total Hip Replacement Surgery on Low Back Pain in Severe Osteoarthritis of the Hip and Hip Pain Predicts Disease
Progression in Osteoarthritis on Medscape News.)

Functional Anatomy
By the time an individual reaches age 13-14 years, the partially ossified bone of the ilium, ischium, and pelvis
coalesce to form a Y-shaped triradial cartilage, which proceeds to fuse by age 15-16 years. The acetabulum is chiefly
spherical in its superior margin and allows for approximately 170º of coverage of the femoral head. The femoral head
is not perfectly spherical, and joint congruity is precise only in the weight-bearing position.
The internal trabecular system of the femoral head is oriented along lines of stress. Thick trabeculae that arise from the
calcar extend into the weight-bearing dome of the femoral head and help resist to compressive loads across the joint.
The arterial supply to the femoral head is principally provided by 3 sources: (1) an extracapsular arterial ring at the
base of the femoral neck, (2) ascending branches of the arterial ring on the femoral neck surface, and (3) arteries of the
round ligament. This arterial supply is well affixed to the femoral neck and is easily damaged with any femoral neck
fracture displacement. Furthermore, nutrient vessels to the femoral head terminate in small arterioles that are easily
occluded with small embolic matter (ie, lipids). (See also the Medscape Reference article Fat Embolism.)
Sport-Specific Biomechanics
Forces that act on the femoral head in vivo are appreciable. Standing on one leg generates a force of approximately 2.5
times the body weight across the loaded hip. Running increases femoral head forces to roughly 5 times the body
weight, whereas simply performing a supine straight-leg raise generates 1.5 times the body weight across the hip joint.
During gait, the maximum pressure occurs in the anterosuperior femoral surface and superior acetabular dome.

History
See the list below:
 AVN may present with nonspecific signs and symptoms.
 Early in the disease process, the condition is painless; however, patients ultimately present with pain and
limitation of motion.
o The pain is most commonly localized to the groin area, but it may also manifest in the ipsilateral
buttock, knee, or greater trochanteric region.
o Painful symptoms are usually exacerbated with weight bearing but are relieved by rest.
Physical
See the list below:
 Passive range of motion of the hip is limited and painful, especially forced internal rotation.
 A distinct limitation of passive abduction is usually noted.
 A straight-leg raise against resistance provokes pain in most symptomatic cases.
 Passive internal and external rotation of the extended leg ("log roll test") may elicit pain that is consistent with
an active capsular synovitis.

Causes
Traumatic AVN is simply a result of mechanical disruption of blood flow to the femoral head. During sports
endeavors, hip dislocation or subluxation is the most frequently reported traumatic means of AVN. A tackle from
behind may cause an anterior hip subluxation in a ball carrier. Likewise, extreme abduction or external rotation may
result in an anterior dislocation in a fallen water-skier.
Similarly, a displaced femoral neck fracture can damage the fragile retinacular vessels, which supply the femoral head
and result in femoral head necrosis. (See also the Medscape Reference articles Femoral Neck Fracture Imaging [in the
Radiology section], Femoral Neck Stress and Insufficiency Fractures [in the Orthopedic Surgery section], and Femoral
Neck Fracture [in the Sports Medicine section].) [3]
Most cases of AVN are atraumatic and include the following [4] :
 Excessive corticosteroid usage and alcohol abuse account for as many as 90% of new cases.
 Intravascular coagulation appears to be the central event associated with nontraumatic AVN. (See also the
Medscape Reference article Disseminated Intravascular Coagulation.)
 Coagulation may occur secondary to extravascular compression (eg, marrow fat enlargement), vessel wall
injury (eg, chemotherapy, radiation), or a thromboembolic event (eg, fat emboli).
 Ischemic insult to the femoral head results in infarcted subchondral bone. In this situation, weakened and
unrepaired necrotic bony trabeculae fail under a compressive load, leading to subchondral collapse (ie,
crescent sign) and, ultimately, articular collapse.
Traumatic causes of femoral head AVN include the following:
 Femoral neck fractures
 Hip dislocation (See also the Medscape Reference articles Hip Dislocation [in the Sports Medicine section]
and Hip Dislocations in Emergency Medicine.)
 Slipped capital femoral epiphysis (See also the Medscape Reference articles Slipped Capital Femoral
Epiphysis Surgery [in the Orthopedic Surgery section] and Slipped Capital Femoral Epiphysis [in the Sports
Medicine section].)
A study by Song et al indicated that in patients aged 50 years or older with valgus-angulated femoral neck fractures,
the risk of AVN of the femoral head and fixation failure after screw osteosynthesis is predicted by the severity of the
initial deformity. Patients with an initial valgus and posterior tilt of greater than 15° (B1.1.2 fracture) were found to
have a 17-fold higher risk of treatment failure than did patients with a tilt in both planes of less than 15° (B1.2.1
fracture). [5]
A study by Maini et al indicated that a complete tear of the obturator externus and/or piriformis muscles is a
significant risk factor for femoral head AVN. [6]

Atraumatic osteonecrosis causes include the following:


 Alcohol abuse – Patients who consume less than 400 mL of alcohol per week have a 3-fold higher risk for
AVN than individuals who do not drink. The risk rises to an 11-fold risk if more than 400 mL per week is
consumed. (See also Alcohol Disorders Common, Largely Untreated Among American Adults and Youth
Exposure to Alcohol Advertising in Magazines --- United States, 2001--2005 on Medscape News.)
 Coagulopathies
 Chemotherapy
 Chronic liver disease (See also the Medscape Reference articles Cirrhosis, Primary Sclerosing
Cholangitis, and Hepatitis B, as well as Health-related Quality of Life of Chronic Liver Disease Patients
With and Without Hepatocellular Carcinoma, Nutritional Support in Chronic Liver Disease, and Health-
related Quality of Life of Chronic Liver Disease Patients With and Without Hepatocellular Carcinoma on
Medscape News.)
 Corticosteroids [7] (See also Corticosteroids Influence the Mortality and Morbidity of Acute Critical
Illness on Medscape News.)
 Decompression sickness (See also the Medscape Reference article Decompression Sickness, as well
as Magnetic Resonance Imaging in Spinal Cord Decompression Sickness on Medscape News.)
 Gaucher disease (See also the Medscape Reference article Gaucher Disease.)
 Gout (See also the Medscape Reference articles Gout Imaging and Gout and Pseudogout.)
 Hemoglobinopathy (eg, sickle cell disease)
 Idiopathic hyperlipidemia (See also the Hyperlipidemia Resource Center on Medscape News.)
 Idiopathic atraumatic osteonecrosis
 Metabolic bone disease (see also Diseases of Calcium Metabolism and Metabolic Bone Disease on
Medscape News.)
 Pregnancy
 Radiation
 Smoking
 Systemic lupus erythematosus (See also the Medscape Reference articles Systemic Lupus
Erythematosus, Physical Medicine and Rehabilitation for Systemic Lupus Erythematosus, and Pediatric
Systemic Lupus Erythematosus, as well as the Lupus Resource Center, on Medscape News.)
 Vasculitis (See also the Medscape Reference article Vasculitis and Thrombophlebitis, as well
as Controversies in Small Vessel Vasculitis - Comparing the Rheumatology and Nephrology
Views and Systemic Vasculitis: State of the Art and Emerging Concepts on Medscape News.)
Diagnostic Considerations
Acetabular labrum tear
AVN of the hip has characteristic magnetic resonance imaging (MRI) and radiographic findings that help differentiate
AVN from the conditions listed above. On MRIs and radiographs, AVN chiefly has anterosuperior femoral head
involvement with a characteristic collapse.
Osteoarthritis (See also the Medscape Reference articles Osteoarthritis [in the Orthopedic Surgery section]
and Osteoarthritis, Primary [in the Radiology section ], as well as the Arthritis Resource Center on Medscape.)
Transient osteoporosis of the hip (bone marrow edema syndrome) (See also the Medscape Reference
article Osteoporosis [in the Rheumatology section], as well as the Osteoporosis Resource Center on Medscape.)

Differential Diagnoses
 Femoral Neck Fracture
 Femoral Neck Stress Fracture
 Groin Injury
 Hip Dislocation
 Hip Fracture
 Hip Tendonitis and Bursitis

Laboratory Studies
See the list below:
 Routine laboratory studies are of little value in the evaluation of femoral head AVN other than to rule out
other conditions that may cause hip pain (eg, rheumatoid arthritis). (See also the Medscape Reference
articles Rheumatoid Arthritis and Juvenile Idiopathic Arthritis, as well as the Rheumatoid Arthritis Resource
Center on Medscape News.)
o Hematologic studies may reveal sickle cell disease, if clinically suspected. (See also the Medscape
Reference article Sickle Cell Anemia.)
o Subtle coagulation disturbances (eg, hypofibrinolysis, thrombophilia) are frequent findings, but the
significant cost and limited availability of the sophisticated coagulation tests that are necessary for
these diagnoses argue against routine screening.
Imaging Studies
See the list below:
 Plain radiographs
o Obtain anteroposterior and frog-leg lateral views of both hips. The high incidence of bilaterality
(>60%) and occult disease in cases of femoral head AVN warrant imaging of the unaffected leg.
o Early radiographic findings include femoral head lucency and subchondral sclerosis.
o With disease progression, subchondral collapse (ie, crescent sign) and femoral head flattening become
evident radiographically. Joint space narrowing is the end result of untreated femoral head AVN.
o Radiographic staging of AVN was first proposed by Ficat and Arlet in the 1960s and later amended in
the 1970s. [8] This 4-stage system delineates the natural history of AVN from normal radiographs
(stage I) to cystic changes and sclerosis (stage II), to subchondral collapse or femoral head flattening
(stage III), and finally to joint space narrowing (stage IV). However, this system does not differentiate
among certain phases in disease progression (eg, subchondral vs femoral head collapse), nor does it
quantify the size and extent of the lesion.
o Steinberg proposed the following staging system, known as the Steinberg Classification System,
which is concise and delineates the progression and extent of AVN involvement more
accurately. [9, 10] This staging system has gained increasing acceptance in the orthopedic community.
 Stage I – Normal radiographs; abnormal MRI or bone scan
 Stage II – Abnormal lucency or sclerotic site in femoral head
 Stage III – Subchondral collapse (ie, crescent sign) without flattening of femoral head
 Stage IV – Flattening of the femoral head; normal joint space
 Stage V – Joint space narrowing, acetabular changes, or both
 Stage VI – Advanced degenerative changes
 Stages I-IV are further subdivided according to the percentage of femoral head involvement:
A (< 15%), B (15-30%), or C (>30%).
 MRI
o MRI is the study of choice in patients who demonstrate signs and symptoms that are suggestive of
AVN but whose radiographs are normal.
o MRI is the most sensitive and specific means of diagnosing AVN. MRI may detect disease as early as
5 days subsequent to an ischemic insult.
o Characteristic MRI findings for AVN of the hip include a low signal intensity band (seen on T1 and
T2 images) that demarcates a necrotic anterosuperior femoral head segment. The extent and location
of femoral head necrosis on MRIs have been studied as predictors of femoral head collapse. Smaller
lesions (less than one fourth the diameter of the femoral head) and more medial lesions (away from
primary weight-bearing areas) predict a better outcome. [10]
 Bone scanning
o Abnormalities may show up on a bone scan before they do on plain radiographs. Bone scan findings
should be supplemented with MRI findings.
o The presence of a photopenic area that is surrounded by increased tracer uptake is the typical
scintigraphic picture for radionuclide imaging.
o Bone scans are considerably less sensitive and less specific than MRI, but the images may be useful if
the use of MRI is contraindicated.
 Computed tomography (CT) scanning
o CT scans confer significant radiation exposure to the patient and are less sensitive than MRI in
diagnosing AVN.
o CT scanning may help delineate early subchondral collapse because the resolution of bony
architecture with this modality is unsurpassed.
 Angiography is an invasive mean of diagnostic confirmation of AVN; it is most useful as an investigational
modality.
Procedures
See the list below:
 Biopsy, angiography, and measuring bone marrow pressure are invasive measures of confirming the diagnosis
of AVN, but these procedures are most useful as investigational modalities.
Treatement
Acute Phase

Physical Therapy
Essentially, nonoperative treatment for symptomatic AVN of the hip yields unfavorable results. Restricted patient
weight bearing with the use of a cane or crutches has not been shown to affect the natural history of the disease and is
useful only in controlling symptoms. Physical therapy provides only symptomatic control and also does little to alter
disease progression.

Medical Issues/Complications
If the AVN is associated with a patient's alcohol use, the clinician is urged to assist the patient in alcohol abstinence.
Patient referral to social services, psychologic or psychiatric counseling, or community outreach is recommended. For
patients with prolonged steroid use, osteoporosis screening is indicated. (See also the Medscape Reference
article Anabolic Steroid Use and Abuse, as well as Alcohol Disorders Common, Largely Untreated Among American
Adults and Predictors of Future Anabolic Androgenic Steroid Use on Medscape News.)
Surgical Intervention
Surgical treatment of AVN can be broadly categorized as either prophylactic measures (to retard progression) or
reconstruction procedures (after femoral head collapse). Small asymptomatic lesions do not warrant surgical
intervention and are closely monitored with serial examination. If symptoms ensue, repeat imaging and surgical
treatment are indicated.
 Prophylactic measures
o The most commonly performed prophylactic surgical intervention is core decompression, whereby
one or more cores of necrotic femoral head bone is removed in order to stimulate repair. [11] Core
decompression is often supplemented with bone grafting (cancellous autograft or structural allograft)
to enhance mechanical support and augment healing. Biologic augmentation of core decompression
includes the addition of demineralized bone matrix, bone morphogenic proteins, or
electric/electromagnetic stimulation. [12] These agents are purported to either enhance bone formation
or decrease bone resorption in the hope of maintaining the structural integrity of the femoral head.
Biologic augmentation of core decompression alone offers therapeutic benefit—if it is instituted
before subchondral collapse (Steinberg stage III). [12] A study analyzed the clinical, functional and
radiological outcome of core decompression and bone grafting in 20 patients with 28 cases of
osteonecrosis of the femoral head (ONFH) up to stage IIB (Ficat & Arlet). The study concluded that
core decompression and bone grafting provide satisfactory outcome when patients are carefully
selected in early stages of the disease (stage I), before the stage of collapse. However patients with
stage II disease had poorer outcomes approximately 50% with improvement. [13]
o The addition of a vascularized fibular graft to core decompression offers promise in cases with more
advanced lesions, but this procedure involves considerable morbidity. One study indicated that
vascularized fibular grafts were more effective in preventing femoral head collapse than
nonvascularized fibular autografts. [14, 15]
o The results of prophylactic measures for femoral head AVN have considerable variation, but certain
generalizations can safely be stated. Namely, the clinical results of core decompression alone
deteriorate with more advanced lesions. [12] The addition of cancellous bone grafting appears to
slightly enhance clinical outcomes if subchondral fracture is present. [14] The addition of demineralized
bone matrix to core decompression confers little (if any) clinical response, and the effects of bone
morphogenic protein remain uncertain.
o The supplemental implementation of electrical stimulation with core decompression has provided
disappointing results. [12] Low-frequency pulsed electric and magnetic fields may offer more promise,
but clinical results thus far are inconclusive. The placement of a structural graft through a core tract
into the femoral head generally yields disappointing results. However, grafts placed into the femoral
neck or directly into the femoral head are more promising. Free vascularized fibular grafting
significantly alters disease progression in precollapse lesions and is even useful in modifying disease
in mildly collapsed and early arthritic hips. [14] The best responses to treatment with pulsed
electromagnetic fields were seen in early Ficat stages, however, further studies are needed. [16]
o Osteotomies are performed in attempt to move necrotic bone away from primary weight-bearing areas
in the hip joint. Osteotomies can be angular or rotational, with the latter proving to be much more
technically difficult. These techniques may delay arthroplasty, but they are best suited for small
precollapse or early postcollapse of the femoral head in patients who don't have an ongoing cause of
AVN. However, osteotomies make subsequent arthroplasty more challenging and, unfortunately,
these procedures are associated with an appreciable risk of nonunion.
o The role of arthroscopy to better stage the extent of disease has emerged. Arthroscopic evaluation of
the joint can help better define the extent of chondral flaps, joint degeneration and even joint collapse
and may help with the temporary relief of synovitis. [17] Arthroscopic-assisted reduction of the head
collapse is experimental at this time.
 Reconstruction procedures
o Despite aggressive management, most hips that undergo collapse ultimately require reconstruction (ie,
replacement). Prosthetic replacement offers the most predictable means of pain relief in advanced
AVN; however, many arthroplasty options are available to meet the challenge of painful arthropathy
in younger patients. [18]
o Femoral resurfacing arthroplasty is gaining acceptance for younger patients. [18] Both the femoral head
and acetablum are "resurfaced" with metal, indicating minimal bone resection. This procedure
circumvents the problem of polyethylene wear. However, technical and design problems with surface
replacements may explain the relatively high failure rate in some clinical series. [19] Nonetheless,
refinements in both technique and design predict improved outcomes.
o Resurfacing arthroplasty remains a controversial procedure that likely will not last a patient’s lifetime.
Current recommendations are that resurfacing is contraindicated if the avascular area exceeds one
third of the femoral head. Furthermore, there is a 1% incidence of femoral neck fracture with this
procedure. Lastly, the issue of metal ion release has spurred much debate, although there are no good
data available to suggest injurious effects. Fortunately, resurfacing arthroplasty likely confers no
significant compromise for subsequent arthroplasty.
o A report on preliminary clinical results of 5 subjects who underwent a total of 7 focal anatomic-
resurfacing implantation procedures for the treatment of osteonecrosis of the femoral head, found that
the alternative technique of focal anatomic hip resurfacing yielded preliminary successful results at 2+
year follow-up. [20]
o Bipolar arthroplasty theoretically decreases shear stress and impact load on acetabular cartilage,
although this concept has not been born out clinically. [18] Persistent groin pain, high rates of
polyethylene wear, and early loosening have mitigated the appeal of this option. Resection
arthroplasty should only be considered in very young patients and in debilitated patients who are at
high risk for infection (eg, patients on dialysis).
o Total hip arthroplasty is perhaps the most commonly performed and successful surgery for advanced
AVN of the hip. However, clinical outcomes are inferior to those of total hip arthroplasty that is
performed for osteoarthritis. Cementless prostheses with an improved design may afford increased
longevity relative to cemented counterparts. Despite recent improvements in prosthetic replacement,
replacement arthroplasty precludes further participation in impact activities (eg, running, jogging)
because these activities greatly decrease implant longevity.
Consultations
Because AVN of the hip is often associated with pronounced medical comorbidities (eg, sickle cell disease, systemic
lupus erythematosus), medical consultation is prudent, particularly during the perioperative period. Furthermore, if no
obvious cause of AVN is seen, medical consultation would be a reasonable measure in order to help discern less
common etiologies. (See Clinical, Causes, above.)

Other Treatment
Injections of cortisone into the hip joint may temporarily alleviate the symptoms of AVN; however, these injections
are not generally recommended because of their invasiveness and short-lasting effects.
A systematic review and meta-analysis reported that regenerative therapies such as mesenchymal stem cell
implantation in the osteonecrotic area, intra-arterial infiltration with mesenchymal stem cells, implantation of
bioactive molecules, or platelet-rich plasma provided a significant improvement in survivorship over time when
combined with core decompression. [30]

Recovery Phase
Medical Issues/Complications
Missed diagnoses, especially of the contralateral hip, are not uncommon. Review radiographs of patients with a
characteristic history, examination findings, and risk factors. If radiographs are negative, order an MRI.
A feared complication of core decompression is subtrochanteric fracture. This adverse event can be somewhat
prevented by fastening the core tract as proximally as possible.
Consider administering low molecular weight heparin (LMWH) for thrombophilic patients; LMWH may aid in
preventing the progression of idiopathic osteonecrosis of the hip. [21]

Medication Summary
Medical therapy for AVN of the hip is principally indicated for relief of discomfort. Nonsteroidal anti-inflammatory
drugs (NSAIDs) and, on occasion, narcotics, form the basis of pharmacotherapy. Investigations into vasoactive lipid-
lowering agents and anticoagulants are ongoing and hold promise [7, 22, 23] (eg, studies suggest low molecular weight
heparin [LMWH] may prevent the progression of idiopathic osteonecrosis of the hip [21] ); however, these medications
are not currently recommended. Inhibition of the vascular endothelial growth factor may hold promise in preventing
femoral head collapse because revascularization compromises bone structural integrity. Because medical
comorbidities are common in patients with AVN, the use of selective cyclooxygenase (COX)–2 inhibitors is
appealing.

Cyclooxygenase-2 inhibitors
Class Summary
These agents inhibit primarily COX-2, an isoenzyme that is induced during pain and in response to inflammatory
stimuli. Inhibition of COX-1 may contribute to NSAID gastrointestinal (GI) toxicity. At therapeutic concentrations,
COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased.

Celecoxib

 View full drug information


Selective COX-2 inhibitor with improved GI tolerability over first-generation NSAIDs.
Return to Play
AVN of the hip is generally a contraindication to sports participation. Even when this condition is successfully treated,
impact sports should be discouraged. The athlete can maintain fitness with pursuits that are easy on the joints, such as
swimming, biking, and using elliptical training devices.

Complications
In most cases, progression from femoral head AVN to femoral head collapse requires arthroplasty.

Prevention
Abstinence from excessive alcohol intake and taking the lowest possible dose of a corticosteroid (when indicated) are
the 2 chief means of AVN prevention.
Patients should also stop or avoid smoking tobacco products, as there is an increased risk of nontraumatic
osteonecrosis of the femoral head, particularly in those who never received oral corticosteroids. [24]
There are some data regarding cholesterol-lowering statin therapy as a means of decreasing the risk of AVN for those
receiving corticosteroids. [7] Given the relatively favorable safety profile of these agents, such therapy should be
considered.
Cutaneous electrical stimulation, in the form of capacitive coupling, is purported by some to have a disease-modifying
effect, although long-term studies are lacking.
Anticoagulation therapy in the form of enoxaparin was shown in one investigation to retard progression of early
AVN. [22] This lends support to the "thrombophilia theory" of AVN disease etiology.
Lastly, the antiresorptive, alendronate, was demonstrated to prevent collapse of early AVN. [23] This finding adds
credence to the argument that the bone's repair response (resorption), rather than the actual infarction, leads to femoral
head collapse and the subsequent morbidity.

Prognosis
If AVN of the femoral head is untreated, progression to subchondral collapse occurs in approximately 67% of
individuals with asymptomatic hips and in more than 85% of those who have symptomatic hips.

Education
Information regarding the deleterious effects of alcohol and corticosteroids on femoral head circulation should be
disseminated to those who are at risk for AVN
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