Pathophysiology of venous leg ulceration.

The currently favoured hypothesis for the link between the raised venous pressure of chronic venous insufficiency and venous ulceration is based on the intermittent inappropriate activation of white blood cells. The damage initiated by the oxidative burst of the leucocyte leads to endothelial dysfunction, interstitial oedema, microthrombi and long-term microcirculatory damage including decreased capillary density. The net result is impairment of the potential for healing and hence ulceration.