Avascular necrosis (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 years). The disease prevalence is unknown, but estimates indicate that 10,000 to 20,000 new cases are diagnosed in the United States per year, and up to 18% of total hip arthroplasties performed annually are for osteonecrosis of the femoral head.
The arterial supply to the femoral head is principally provided by three sources: an extracapsular arterial ring at the base of the femoral neck, anterior and posterior ascending branches from this ring, and arteries of the ligamentum teres. This arterial supply is well affixed to the femoral neck and is easily damaged with any femoral neck trauma.
AVN may present as nonspecific signs and symptoms. Early in the disease process, the condition is painless; however, patients ultimately present with pain, typically in the groin, and limitation of motion. Although the groin is the most common area of pain, patients may complain of pain in their buttock, knee, or greater trochanteric region.
AVN can be either traumatic or nontraumatic. Traumatic causes are usually very obvious to diagnose. The most common traumatic causes are hip dislocations and displaced femoral neck fractures.
The most common causes of nontraumatic AVN are high-dose corticosteroid use and excessive alcohol consumption. These factors alter lipid profiles and are thought to cause intravascular coagulation. Other causes of AVN include coagulopathies, chemotherapy, chronic liver disease, diabetes, gout, sickle cell disease, hyperlipidemia, pregnancy, radiation, systemic lupus erythematosus, and vasculitis.
Plain radiographs in the early stages may be normal or may show a femoral head lucency and subchondral sclerosis.
As the disease progresses, subchondral collapse (i.e., crescent sign) and femoral head flattening become evident. Further progression of the disease results in femoral head flattening and progressive osteoarthritis. MRI is the study of choice in patients in the early stages of AVN (before collapse) or in patients with suspected AVN but with normal radiographic findings. It can help predict the progression of disease, with smaller and more medial lesions having better outcomes.
Nonoperative treatment for symptomatic AVN is often unsuccessful. 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. NSAIDs may be beneficial for management of the patient’s pain. More recently, antiresorptive agents commonly used for the treatment of osteoporosis have shown some promise. It is thought that these drugs retard the resorptive process in AVN and therefore prevent femoral head collapse.
Surgical treatment of AVN is based on the severity of disease. Small asymptomatic lesions do not warrant surgical intervention and are closely monitored with serial examination.
In symptomatic patients before collapse, the most commonly performed surgical intervention is core decompression. In this procedure, a hole is created through the lateral aspect of the femur, through the femoral neck, and into the lesion. This is done in an attempt to allow for a new blood supply to the devascularized region. Vascularized fibular grafting is an alternative to core decompression, although this is less commonly done.
The outcomes of these procedures are variable.
Osteotomies may be performed in attempt to move necrotic bone away from primary weight-bearing areas in the hip joint, but they have fallen out of favor because they often make subsequent arthroplasty more challenging.
Once the disease has progressed to collapse, the best surgical option is hip replacement. Total hip arthroplasty provides predictable and long-term pain relief for these patients.