eMedicine Specialties > Sports Medicine > Hip

Femoral Head Avascular Necrosis

John D Kelly IV, MD, Associate Professor of Orthopedic Surgery, Vice Chairman, Department of Orthopedic Surgery, Temple University; Consulting Surgeon, Temple Children's Hospital and Shriner's Hospital for Surgery
David Wald, DO, FACOEP, Assistant Program Director, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Temple University School of Medicine

Updated: Nov 6, 2007

Introduction

Background

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 eMedicine article Avascular Necrosis, Femoral Head, as well as Hip Arthroscopy in Staging Avascular Necrosis of the Femoral Head on Medscape.)

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 eMedicine article Osteonecrosis, Hip.)

For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center. Also, see eMedicine's patient education article Total Hip Replacement.

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 eMedicine articles Osteoarthritis [in the Orthopedic Surgery section] and 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.)

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 eMedicine 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.

Clinical

History

• 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

• 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 eMedicine articles Femoral Neck, Fractures [in the Radiology section], Femoral Neck Stress and Insufficiency Fractures [in the Orthopedic Surgery section], and Femoral Neck Fracture [in the Sports Medicine section].)
• Most cases of AVN are atraumatic and include the following³ :
  • 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 eMedicine articles Disseminated Intravascular Coagulation [in the Emergency Medicine section] and Disseminated Intravascular Coagulation [in the Hematology section].)
  • 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 eMedicine articles Hip Dislocation [in the Sports Medicine section] and Dislocations, Hip [in the Emergency Medicine section].)
  • Slipped capital femoral epiphysis (See also the eMedicine articles Slipped Capital Femoral Epiphysis [in the Orthopedic Surgery section] and Slipped Capital Femoral Epiphysis [in the Sports Medicine section].)
• 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.)
  • Coagulopathies
  • Chemotherapy
  • Chronic liver disease (See also the eMedicine articles Cirrhosis, Primary Sclerosing Cholangitis, and Hepatitis B [in the Gastroenterology section], 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.)
  • Corticosteroids⁴ (See also Corticosteroids Influence the Mortality and Morbidity of Acute Critical Illness on Medscape.)
  • Decompression sickness (See also the eMedicine article Decompression Sickness, as well as Magnetic Resonance Imaging in Spinal Cord Decompression Sickness on Medscape.)
  • Gaucher disease (See also the eMedicine article Gaucher Disease, as well as Treatment Interruption in Gaucher Disease Can Cause Irreversible Complications and High-Dose Enzyme Therapy Speeds Response of Type 1 Gaucher Disease on Medscape.)
  • Gout (See also the eMedicine articles Gout [in the Radiology section], Gout [in the Rheumatology section], Gout [in the Orthopedic Surgery section], and  Gout and Pseudogout [in the Emergency Medicine section].)
  • Hemoglobinopathy (eg, sickle cell disease)
  • Idiopathic hyperlipidemia (See also the Hyperlipidemia Resource Center on Medscape.)
  • Idiopathic atraumatic osteonecrosis
  • Metabolic bone disease (see also Diseases of Calcium Metabolism and Metabolic Bone Disease on Medscape.)
  • Pregnancy
  • Radiation
  • Smoking
  • Systemic lupus erythematosus (See also the eMedicine articles Systemic Lupus Erythematosus [in the Rheumatology section], Systemic Lupus Erythematosus [in the Physical Medicine and Rehabilitation section], and Systemic Lupus Erythematosus [in the Pediatrics section], as well as the Lupus Resource Center, on Medscape.)
  • Vasculitis (See also the eMedicine 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.)

Differential Diagnoses

Femoral Neck Fracture
Femoral Neck Stress Fracture
Groin Injury
Hip Dislocation
Hip Fracture
Hip Overuse Syndrome

Other Problems to Be Considered

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 eMedicine 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 eMedicine articles Osteoporosis [in the Rheumatology section], as well as the Osteoporosis Resource Center on Medscape.)

Workup

Laboratory Studies

• 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 eMedicine articles Rheumatoid Arthritis [in the Physical Medicine and Rehabilitation section], Rheumatoid Arthritis [in the Rheumatology section], and Juvenile Rheumatoid Arthritis [in the Pediatrics section], as well as the Rheumatoid Arthritis Resource Center on Medscape.)
  • Hematologic studies may reveal sickle cell disease, if clinically suspected. (See also the eMedicine articles Sickle Cell Anemia [in the Pediatrics section] and Pediatrics, Sickle Cell Disease [in the Emergency Medicine section].)
  • 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

• 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.⁵ 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.^6,7  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.⁷
• 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

• 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 eMedicine article Anabolic Steroid Use and Abuse, as well as Alcohol Disorders Common, Largely Untreated Among American Adults, Alcohol Abuse and Dependency, and Predictors of Future Anabolic Androgenic Steroid Use on Medscape.)

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.⁸ 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.⁹ 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).⁹
  • 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.¹⁰
  • 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.⁹ The addition of cancellous bone grafting appears to slightly enhance clinical outcomes if subchondral fracture is present.¹⁰ 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.⁹ 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.¹⁰
  • 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.¹¹  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.¹²
  • Femoral resurfacing arthroplasty is gaining acceptance for younger patients.¹² 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.¹³ 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.
  • Bipolar arthroplasty theoretically decreases shear stress and impact load on acetabular cartilage, although this concept has not been born out clinically.¹² 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.

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.

Medication

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^4,14,15 ; 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

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

Dosing

Adult

200 mg PO qd

Pediatric

Not established

Interactions

Coadministration with fluconazole may cause an increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations.

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Category D in third trimester of pregnancy; may cause fluid retention and peripheral edema; caution in patients with compromised cardiac function, hypertension, and conditions that predispose to fluid retention; caution in the presence of severe heart failure and hyponatremia because circulatory hemodynamics may deteriorate; NSAIDs may mask the usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs that suggest liver dysfunction. Controversy exists as to whether or not COX-2 agents at the 200 mg PO qd dose inhibit fibrinolysis.

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.

There are some data regarding cholesterol-lowering statin therapy as a means of decreasing the risk of AVN for those receiving corticosteroids.⁴ 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.¹⁴ This lends support to the "thrombophilia theory" of AVN disease etiology.

Lastly, the antiresorptive, alendronate, was demonstrated to prevent collapse of early AVN.¹⁵ 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.

Miscellaneous

Medicolegal Pitfalls

• The clinical appearance of AVN of the hip may be mistaken for less worrisome conditions, such as synovitis or a labral tear. A missed diagnosis invites potential legal action because the earlier AVN is diagnosed, the more predictable the treatment. Obtaining a thorough patient history and physical examination, as well as an MRI in the face of negative radiographs, helps to circumvent missed diagnoses and legal action.

References

1. Lavernia CJ, Sierra RJ, Grieco FR. Osteonecrosis of the femoral head. J Am Acad Orthop Surg. Jul-Aug 1999;7(4):250-61. [Medline].

2. Vail TP, Covington DB. The incidence of osteonecrosis. In: Urbaniak JR, Jones JR, eds. Osteonecrosis: Etiology, Diagnosis, Treatment. Rosemont, Ill: American Academy of Orthopedic Surgeons; 1997:43-9.

3. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am. Mar 1995;77(3):459-74. [Medline].

4. Pritchett JW. Statin therapy decreases the risk of osteonecrosis in patients receiving steroids. Clin Orthop Relat Res. May 2001;386:173-8. [Medline].

5. Arlet J, Ficat P. [Non-traumatic avascular femur head necrosis. New methods of examination and new concepts] [Polish]. Chir Narzadow Ruchu Ortop Pol. 1977;42(3):269-76. [Medline].

6. Steinberg ME. Avascular necrosis: diagnosis, staging, and management. J Musculoskel Med. 1997;14(11):13-25.

7. Steinberg ME. Diagnostic imaging and the role of stage and lesion size in determining outcome in osteonecrosis of the femoral head. Techniques in Orthopaedics. Mar 2001;16(1):6-15. [Full Text].

8. McGrory BJ, York SC, Iorio R, et al. Current practices of AAHKS members in the treatment of adult osteonecrosis of the femoral head. J Bone Joint Surg Am. Jun 2007;89(6):1194-204. [Medline].

9. Ciombor DM, Aaron RK. Biologically augmented core decompression for the treatment of osteonecrosis of the femoral head. Techniques in Orthopaedics. Mar 2001;16(1):32-8. [Full Text].

10. Katz MA, Urbaniak JR. Free vascularized fibular grafting of the femoral head for the treatment of osteonecrosis. Techniques in Orthopaedics. Mar 2001;16(1):44-60. [Full Text].

11. McCarthy J, Puri L, Barsoum W, et al. Articular cartilage changes in avascular necrosis: an arthroscopic evaluation. Clin Orthop Relat Res. Jan 2003;406:64-70. [Medline].

12. Ivankovich DA, Rosenberg AG, Malamis A. Reconstructive options for osteonecrosis of the femoral head. Techniques in Orthopaedics. Mar 2001;16(1):66-79. [Full Text].

13. Squire M, Fehring TK, Odum S, Griffin WL, Bohannon Mason J. Failure of femoral surface replacement for femoral head avascular necrosis. J Arthroplasty. Oct 2005;20(7 suppl 3):108-14. [Medline].

14. Glueck CJ, Freiberg RA, Sieve L, Wang P. Enoxaparin prevents progression of stages I and II osteonecrosis of the hip. Clin Orthop Relat Res. Jun 2005;435:164-70. [Medline].

15. [Best Evidence] Lai KA, Shen WJ, Yang CY, et al. The use of alendronate to prevent early collapse of the femoral head in patients with nontraumatic osteonecrosis. A randomized clinical study. J Bone Joint Surg Am. Oct 2005;87(10):2155-9. [Medline].

16. DeLee JC. Fractures and dislocations of the hip. In: Rockwood CA, Green DP, Bucholz RW, eds. Rockwood and Green's Fractures in Adults. 4^th ed. Philadelphia, Pa: Lippincott-Raven; 1996:1661-9.

17. Etienne G, Mont MA, Khanuja HS, Hungerford DS. Nonvascularized bone grafts for osteonecrosis of the femoral head: current concepts and techniques. Techniques in Orthopaedics. Mar 2001;16(1):39-43. [Full Text].

18. Kim SY, Kim YG, Kim PT, et al. Vascularized compared with nonvascularized fibular grafts for large osteonecrotic lesions of the femoral head. J Bone Joint Surg Am. Sep 2005;87(9):2012-8. [Medline].

19. Urbaniak JR, Barnes CJ. Meeting the challenge of osteonecrosis in adults. J Musculoskel Med. 2001;18:395-403.

Keywords

aseptic necrosis, ischemic necrosis, AVN of the femoral head, osteonecrosis

Contributor Information and Disclosures

Author

John D Kelly IV, MD, Associate Professor of Orthopedic Surgery, Vice Chairman, Department of Orthopedic Surgery, Temple University; Consulting Surgeon, Temple Children's Hospital and Shriner's Hospital for Surgery
John D Kelly IV, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Society for Sports Medicine, Arthroscopy Association of North America, Eastern Orthopaedic Association, Pennsylvania Orthopaedic Society, and Philadelphia County Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

David Wald, DO, FACOEP, Assistant Program Director, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Temple University School of Medicine
David Wald, DO, FACOEP is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Gerard A Malanga, MD, Associate Professor, Department of Physical Medicine and Rehabilitation, New Jersey Medical School; Director of Pain Management, University of Medicine and Dentistry at New Jersey, Overlook Hospital; Director of Sports Medicine, Mountainside Hospital
Gerard A Malanga, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

CME Editor

Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

Chief Editor

Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago
Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

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