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.
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. 
(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.)
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.)
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.
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