We reviewed 41 hips in 40 patients at three to 11 years (average 6.3 years) after Sugioka transtrochanteric rotational osteotomy for non-traumatic avascular necrosis of the femoral head. The clinical results were excellent or good in 23 hips (56%) and the radiological success rate was 56%. Failure was due to fracture of the femoral neck, nonunion of the osteotomy, secondary collapse, or osteoarthritis. Nonunion and femoral neck fracture were more common after the use of the large screws described by Sugioka than with AO blade plates. Secondary collapse was significantly more common when less than one-third of the posterior articular surface was intact (p = 0.002). Postoperative degenerative changes were seen in cases with stage III avascular necrosis. We conclude that success depends to a large extent on the amount and stage of necrosis of the femoral head, but that careful technique and the use of AO hip plates may increase the likelihood of a satisfactory result.

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To determine the vascular architecture of nontraumatic avascular necrosis of the femoral head (ANFH), 38 femoral heads procured from 31 ANFH patients were studied by microangiographic and histologic methods. Microangiography showed that the head was consistently stratified into three zones: the normal vascular, the reparative vascular, and the avascular. Microangiographic abnormalities were closely correlated with the histologic changes in each zone. The extent of the necrotic area proved to depend on the extent and number of involved intraosseous nutrient arteries. Circumscribed necrosis accompanied interruption of the lateral epiphyseal arteries in their intracapital portion. Extensive necrosis resulted from multiple vascular involvement, which included not only the lateral epiphyseal arteries, but also the superior and inferior metaphyseal arteries. Histologic examination of different levels of the nutrient arteries revealed many intraosseous pathologic vascular changes in apposition to the ischemic episode of the femoral head. Interruption of the blood supply causing ANFH occurs in the intracapital arteries probably because of vascular wall damage, and the extent of necrosis depends on the number of the involved nutrient arteries and their proximity to the intracapital site of origin.