Chronic venous ulcers

Abstract

Ulcers of the lower leg secondary to venous insufficiency account for some 85% of all leg ulcers. The proper venous drainage of a leg requires three sets of veins. Thee deep vein surrounded by muscles, the superficial veins, and the veins connecting these two - the perforating or communicating veins. When the leg muscles contract blood in deep veins is squeezed back against gravity to the heart (the calf muscle pump); reflux is prevented by valves. When the muscles relax, with the help of gravity blood from the superficial veins passes into the deep veins via the communicating vessels. If the valves in the deep and communicating veins are incompetent hypertension develops in the deep veins. The calf muscle pump now pushes blood into the superficial veins, where the pressure remains high (venous hypertension) instead of dropping during exercise. This persisting venous hypertension enlarges the capillary bed and forces fibrinogen out through the capillary walls. Patients with these changes develop lypodermatosclerosis and have a high serum fibrinogen and reduced blood fibrinolytic activity. The precapillary fibrin cuff blocks the diffusion of oxygen and nutrients and the overlying skin becomes hypoxic, as a result minor trauma leads to ulcers which are slow to heal.