We examined ten femoral veins with duplex ultrasound during total hip replacement to demonstrate the operative manoeuvres which cause venous obstruction and to assess prophylactic measures which may overcome it. Exposure of the acetabulum by distraction of the femur with a hook was less likely to occlude flow than retraction with bone levers. Adequate exposure of the femoral shaft by adduction, flexion and either internal or external rotation caused cessation of flow in all cases. In four cases an A-V Impulse System
Previous dye-infusion experiments on cadavers have suggested that the hindfoot should be divided into four muscle compartments including a newly described ‘calcaneal’ element containing quadratus plantae. Since there are no clinical data to support this proposed division, we re-examined the validity of the infusion experiment. We made infusions of dilute Omnipaque at a constant rate into flexor digitorum brevis of four cadaver feet. We monitored the spread of the infusate by real-time CT imaging and measured the pressures at the infusion site by side-ported needles. In all feet, the barrier between flexor digitorum brevis and quadratus plantae became incompetent at pressures of less than 10 mmHg. Pressure gradients in this range cannot be expected to affect tissue perfusion significantly and independently generate compartment syndromes. These results do not confirm those of previous studies carried out by uncontrolled and unmonitored injections made by hand. Injection studies in cadaver limbs can give dramatically different results depending upon the assumptions made when designing the experiment. The technique cannot adequately act as a model of the physiology of the compartment syndrome. As the existence of a physiologically significant compartmental boundary between flexor digitorum brevis and quadratus plantae is based solely on a cadaver infusion experiment the presence of a ‘calcaneal’ compartment has not been confirmed.
Among 449 patients with leprosy, 40 had clinical and radiographic evidence of neuroarthropathy in 50 feet. These changes were classified into four types according to the joints first involved by major lesions: ankle (25 feet), midtarsal (15 feet), tarsometatarsal (7 feet) and subtalar (3 feet). The progression of joint destruction was different in each type, but despite the severe destructive changes seen in radiographs, the patients had relatively few complaints. The muscles innervated by the peroneal nerve were severely paralysed in ankle and midtarsal types and it seems that, over a long term, repeated trauma and/or abnormal stress may lead to these types of neuroarthropathy. Neuropathy was less severe in the tarsometatarsal type of joint degeneration; the pathogenesis in this type seemed to be mainly direct trauma to the forefoot.
Previous reports have suggested that the blood supply derived from the anterior tibial artery is absent or markedly diminished in 85% of severe, untreated club feet. To investigate these claims, we used a Doppler technique to study the arterial pulses in 40 children with 63 club feet. In feet with mild or moderate deformities the anterior tibial pulse was always present; in feet with severe deformities it was absent in two out of 30 feet in children under three years and in seven out of 18 feet in children over three years. These results confirm that the incidence of pulselessness increases with the severity and duration of deformity, but not to the extent previously suggested by angiographic studies. The significance of these findings is discussed.