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
Contributor Information and Disclosures

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.)

References

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

• Foot, Ankle, Knee, and Hip Center
• Total Hip Replacement Introduction
• Total Hip Replacement Preparation