The blood supply to particular segments of certain bones is unique and one directional. Consequently, some specific fracture patterns are especially likely to create an avascular segment of bone. For example, the femoral head is particularly susceptible to osteonecrosis because virtually all the blood vessels to the femoral head traverse the femoral neck. A fracture of the femoral neck disrupts these blood vessels, leaving the femoral head with no blood supply. Because of this fact, displaced femoral neck fractures in children or young adults are surgical emergencies. Similarly, the body of the talus has very few soft tissue attachments and derives virtually all its blood supply from vessels that pass up through the talar neck in a retrograde fashion. A fracture of the neck disrupts these blood vessels and impairs the circulation. Another vulnerable area is the proximal pole of the scaphoid, because its circulation is supplied by blood vessels that enter the distal pole and waist of the bone, thus supplying the proximal pole in a retrograde fashion. A fracture of the waist of the scaphoid, therefore, leaves the proximal pole with inadequate circulation or none at all (see Plate 9-10).
Although the loss of circulation to a major bone segment impairs healing, healing does proceed, because the segment that retains its blood supply often generates sufficient callus to incorporate the avascular segment. Once healing occurs, the body removes the necrotic bone by a process called “creeping substitution.” In this process, osteoclasts proliferate from the vascularized bone into the necrotic segment and remove the dead bone trabeculae. While this is happening, the necrotic segment is weakened and becomes susceptible to collapse. The process of creeping substitution is slow, taking as long as 3 years for the necrotic bone to be removed and replaced with new osteons. Stress applied to the weakened bone during this time causes it to collapse. This phenomenon, called late segmental collapse, removes the normal underlying support for the articular cartilage of the segment, disturbing the congruity of the adjacent joints surfaces and predisposing to osteoarthritis. If excessive stresses are avoided during the process of creeping substitution, the necrotic segment is eventually replaced with strong viable bone, late segmental collapse does not occur, and the risk of osteoarthritis is minimized.
In the early stage of osteonecrosis, when the dead bone is present and not yet replaced with new bone, the avascular segment is characterized by a very dense appearance on radiographs. This apparent increase in density is only relative because the surrounding bone, which is still alive, is undergoing disuse osteoporosis, a normal phenomenon seen in the early stages of fracture healing. Without an adequate blood supply, the necrotic fragment does not become osteoporotic and thus appears relatively dense.
The absence of osteonecrosis can be inferred when Hawkins sign is seen on the radiograph. Hawkins sign is evidence of the resorption of subchondral bone as a consequence of disuse osteoporosis and suggests that the bone segment has adequate circulation, normal bone healing is occurring, and that osteonecrosis has not occurred.
Usually, osteonecrosis is a consequence of the pattern of injury and little can be done to prevent it besides stable anatomic fixation of the fracture. When osteonecrosis is detected, the bone must be protected from excessive stresses until it is fully reconstituted, a process that may take as long as 3 years. During this time, patients should wear a brace or use crutches until radiographs show evidence that the avascular segment has been replaced with new bone. These simple measures reduce the risk of late segmental collapse and the development of osteoarthritis.
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