Abstract
Posttraumatic avascular necrosis (AVN) is osteonecrosis from vascular disruption, commonly encountered after fractures of the femoral neck, proximal humerus, talar neck, and scaphoid. These locations have a tenuous vascular supply; the diagnosis, risk factors, natural history, and treatment are reviewed. Fracture nonunion only correlates with AVN in the scaphoid. In the femoral head, the risk is increased for displaced fractures, but the time to surgery and open versus closed treatment do not seem to influence the risk. Patients with collapse are frequently symptomatic, and total hip arthroplasty is the most reliable treatment. In the humeral head, certain fracture patterns correlate with avascularity at the time of injury, but most do not go on to develop AVN due to head revascularization. Additionally, newer surgical approaches and improved construct stability appear to lessen the risk of AVN. The likelihood of AVN of the talar body rises with increased severity of talar injury. The development of AVN corresponds with a worse prognosis and increases the likelihood of secondary procedures. In proximal pole scaphoid fractures, delays in diagnosis and treatment elevate the risk of AVN, which is often seen in cases of nonunion. The need for vascularized versus nonvascularized bone grafting when repairing scaphoid nonunions with AVN remains unclear.