Circulatory and vascular changes in the hip following traumatic hip dislocation.

An experimental study of the extraosseous and intraosseous vascular and circulatory changes following traumatic hip dislocation in dogs and rabbits is reported. The observations were made by dissection, angiography and histology following posterior dislocation and reduction at varying intervals. Traumatic dislocation of the hip causes extraosseous circulatory disturbance in the hip resulting in intraosseous circulatory deficiency in the femoral head. The sites of the vascular lesions are the extraosseous branches of the femoral circumflex arteries and their extraosseous branches of the epiphyseal and metaphyseal arteries and the retinacular artery of the circulus vasculosus articularis. The types of the vascular damage are irreversible tear of the minority of vessels along the ruptured capsule and teres ligament, and the compression, traction and spasm of the majority of intact vessels which are reversible by early reduction. In prolonged dislocation the circulatory disturbance persists or worsens due to additional pathological changes such as posttraumatic inflammatory changes, fixed deformity in the dislocated position, thrombosis, fibrosis and occlusion of vessels which may eventually cause an ischemic necrosis of the femoral head. Early reduction within several hours after dislocation restores nearly normal regional anatomy and relieves vessels from compression, traction or spasm and restores extra and intraosseous circulation. It also prevents or minimizes thrombosis, fibrosis and occlusion of vessels and avascular necrosis of the femoral head.