Femoral Head Avascular Necrosis 

Updated: Oct 22, 2018
Author: John D Kelly, IV, MD; Chief Editor: Craig C Young, MD 

Overview

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.

 

Presentation

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.

    • The pain is most commonly localized to the groin area, but it may also manifest in the ipsilateral buttock, knee, or greater trochanteric region.

    • 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.)

 

DDx

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

 

Workup

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.)

    • Hematologic studies may reveal sickle cell disease, if clinically suspected. (See also the Medscape Reference article Sickle Cell Anemia.)

    • 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

    • 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.

    • Early radiographic findings 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.

    • 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.

    • 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

    • MRI is the study of choice in patients who demonstrate signs and symptoms that are suggestive of AVN but whose radiographs are normal.

    • 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.

    • 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

    • Abnormalities may show up on a bone scan before they do on plain radiographs. Bone scan findings should be supplemented with MRI findings.

    • The presence of a photopenic area that is surrounded by increased tracer uptake is the typical scintigraphic picture for radionuclide imaging.

    • 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

    • CT scans confer significant radiation exposure to the patient and are less sensitive than MRI in diagnosing AVN.

    • 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.

 

Treatment

Acute Phase

Rehabilitation Program

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

    • 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]

    • 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]

    • 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.

    • 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]

    • 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.

    • 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

    • 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]

    • 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.

    • 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.

    • 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]

    • 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).

    • 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

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 (Celebrex)

Selective COX-2 inhibitor with improved GI tolerability over first-generation NSAIDs

 

Follow-up

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.

 

Questions & Answers

Overview

What is femoral head avascular necrosis (AVN)?

What are early radiographic findings indicative of femoral head avascular necrosis (AVN)?

What is the role of MRI in the evaluation of femoral head avascular necrosis (AVN)?

What is the prevalence of femoral head avascular necrosis (AVN) in the US?

What is the anatomy of the femoral head relative to femoral head avascular necrosis (AVN)?

What are the sport-specific biomechanics of the femoral head avascular necrosis (AVN)?

Presentation

What are the signs and symptoms of femoral head avascular necrosis (AVN)?

What are the physical findings characteristic of femoral head avascular necrosis (AVN)?

What is the role of trauma in the etiology of femoral head avascular necrosis (AVN)?

What are the atraumatic causes of femoral head avascular necrosis (AVN)?

What types of trauma cause femoral head avascular necrosis (AVN)?

What are risk factors for femoral head avascular necrosis (AVN)?

What is the role of atraumatic osteonecrosis in the etiology of femoral head avascular necrosis (AVN)?

DDX

How is femoral head avascular necrosis (AVN) differentiated from acetabular labrum tear?

What are the differential diagnoses for Femoral Head Avascular Necrosis?

Workup

What is the role of lab studies in the evaluation of femoral head avascular necrosis (AVN)?

What is the role of radiography in the diagnosis of femoral head avascular necrosis (AVN)?

What is the Steinberg Classification System for femoral head avascular necrosis (AVN)?

What is the role of MRI in the diagnosis of femoral head avascular necrosis (AVN)?

Which invasive procedures are performed in the diagnosis of femoral head avascular necrosis (AVN)?

Treatment

What is the role of physical therapy in the treatment of femoral head avascular necrosis (AVN)?

What are possible complications of prolonged steroid use in the treatment of femoral head avascular necrosis (AVN)?

What is the role of surgery in the treatment of femoral head avascular necrosis (AVN)?

Which prophylactic interventions are used in the management of femoral head avascular necrosis (AVN)?

Which reconstruction procedures are performed in the treatment of femoral head avascular necrosis (AVN)?

Which medical comorbidities of femoral head avascular necrosis (AVN) may require a specialist consultation?

What is the role of cortisone injections in the treatment of femoral head avascular necrosis (AVN)?

What are the medical concerns during the recovery phase of femoral head avascular necrosis (AVN)?

Medications

What is the role of drug treatment for femoral head avascular necrosis (AVN)?

Which medications in the drug class Cyclooxygenase-2 inhibitors are used in the treatment of Femoral Head Avascular Necrosis?

Follow-up

What are activity restrictions during the treatment of femoral head avascular necrosis (AVN)?

When is arthroplasty indicated in the treatment of femoral head avascular necrosis (AVN)?

How is femoral head avascular necrosis (AVN) prevented?

What is the prognosis of untreated femoral head avascular necrosis (AVN)?

What information should patients at risk for femoral head avascular necrosis (AVN) receive?