ORTHOPAEDICS
Osteonecrosis of the femoral head Diagnosing and treating a rare condition BY PAUL HOOGERVORST, MD, AND EDWARD CHENG, MD
O
steonecrosis (also known as avascular necrosis, aseptic necrosis, ischemic necrosis, and atraumatic/non-traumatic necrosis) is characterized as a bone infarct with dead osteocytes due to numerous possible etiologies. While the exact pathophysiology is unknown, etiologic risk factors most often are corticosteroids, ethanol, trauma, and diseases such as lupus erythematosus (SLE) and sickle cell disease. The final common pathway most likely involves a compromised blood supply to the osteocyte with loss of normal bone remodeling. This often occurs adjacent to a joint surface, resulting in subchondral fracture with bony collapse and cartilage delamination leading to disabling osteoarthritis. Although any bone can be affected, the most frequently affected sites are the femoral head, proximal humerus, distal femur, proximal tibia, ankle, elbow, lunate (Kienbock’s disease), navicular (Köhler’s disease or Mueller Weiss syndrome) and metatarsals (Freiberg’s disease).
Epidemiology Osteonecrosis of the femoral head (ONFH) has an incidence of 10,000 to 30,000 new cases annually in the US. It is estimated that 5%–12% of all total
hip arthroplasties (THA) are performed because of ONFH. Although most hip arthroplasties are performed for degenerative joint disease in older individuals, osteonecrosis often affects younger adults, which is especially problematic as joint replacements at this age are not durable enough to last a lifetime.
Pathophysiology Traumatic ONFH can be a sequela of childhood disorders such as slipped capital femoral epiphysis, or secondary to events such as hip dislocation or displaced femoral neck fractures. Disruption of the arterial vasculature supplying the femoral head causes ischemia. Non-traumatic ONFH, however, is not secondary to a mechanical injury but instead related to various biologic insults that are not completely understood. Proposed explanations include intraosseous adipocyte hypertrophy compressing marrow microcirculation (steroids, ethanol), direct cellular toxicity (chemotherapy, radiation therapy, smoking), and coagulopathic states (pregnancy, sickle cell crises, thrombophilia, and hypofibrinolysis). Studies have clearly shown presence of an elevated intraosseous pressure, perhaps due to marrow fat hypertrophy or inflammatory response. Of the known factors associated with ONFH, glucocorticoids and alcohol exposure are the most common. Although several studies have shown a dose-dependent relationship between glucocorticoid exposure and osteonecrosis, a threshold dose for developing osteonecrosis is unknown. However, the relative risk for developing osteonecrosis is 4.5 times greater for every 10 mg increase in oral steroids for renal transplant patients and 1.3 times greater for every 20 mg increase in the non-transplant population. There is some evidence to show that even a short oral course of steroids for less than one week (methylprednisolone dose >300 mg) subjects individuals to a tenfold higher risk for having osteonecrosis. It is important to discuss this side effect with patients when prescribing these types of medications. Other risk factors for ONFH are sickle cell disease, SLE, acute lymphoblastic leukemia, Caisson disease, Gaucher’s disease, and HIV. However, in some patients it is idiopathic as a clearly identifiable risk factor is absent.
Symptoms Treatment outcomes are better when performed in the early stage of disease, yet this is difficult as most patients are asymptomatic at this time. Therefore, it is imperative to maintain a high level of suspicion in high-risk groups. Treatment is directed at preventing femoral head subchondral fracture and collapse, thereby preserving the native joint. Once subchondral fracture occurs, disabling osteoarthritis almost always ensues. Pain, of varying intensity, is the most common presenting symptom in ONFH. It is experienced in the groin, thigh, or buttock and may be related to weight bearing or activity. Approximately two-thirds of patients endorse pain at rest and one-third acknowledge night pain. Findings during physical examination are largely nonspecific. In later stages of disease, once a subchondral fracture develops, a limp may be present and exam findings are similar to any patient with end-stage arthritis. These commonly are a limited, painful range of motion, particularly during internal rotation and abduction.
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APRIL 2020 MINNESOTA PHYSICIAN
