Post-fracture avascular necrosis of the femoral head: correlation of experimental and clinical studies.

Both extraosseous and intraosseous blood supply of the femoral head are susceptible to injury in patients with femoral neck fractures. The injury to the extraosseous vessels is proportional to the amount of displacement at the time of fracture. The major intraosseous vessels are damaged if the fracture extends through the superior lateral portion of the neck or head. There is no apparent significant age difference in adults who develop avascular necrosis following a femoral neck fracture that unites compared with those who do not develop avascular necrosis. The difference in reported incidence of avascular necrosis following femoral neck fracture is probably due to several factors. Impacted and nondisplaced fractures should be reported separately from displaced fractures. Avascular necrosis should be reported following united fractures to avoid the confusion in diagnosis when associated with nonunion. At least two years of follow-up are necessary to diagnose 80% of patients who develop avascular necrosis. The type of internal fixation used does not significantly alter the incidence of avascular necrosis. The amount of vascular damage produced at the time of fracture predetermines which patient will develop avascular necrosis. Additional vascular damage may be produced at the time of internal fixation, especially malrotation of the head. The arthritic changes seen in some patients three or more years after femoral neck fracture seem to be initiated by collapse and fragmentation of small areas of avascular necrosis in or near the weight-bearing portion of the head. The various methods currently available for predicting the vascularity of the head at the time of fracture are not sufficiently quantitative to be used on a routine clinical basis. Biologic factors may explain the difference in the incidence of avascular necrosis in the adult femoral head epiphysis compared with that in the metaphysis and explain why the area of revascularization and reossification of avascular bone is so limited.