THE MICROVASCULAR PATHOPHYSIOLOGY OF CHRONIC VENOUS INSUFFICIENCY

Severe chronic venous insufficiency (CVI) demonstrates as chronic, har d-to-heal wounds of the lower extremity. The wound is the result of po or skin perfusion due to a complex series of pathologic events, often initiated by a deep vein thrombosis (DVT). As years pass, the DVT caus es venous valvular damage and incompetence. The calf muscle pump fails to augment venous return, and venous blood pressure is chronically el evated upon standing. Mechanisms that normally prevent the transmissio n of venous hypertension back upstream to the dermal microcirculation are lost. Early dermal microvascular responses include increased fluid filtration and edema. An inflammatory response induces white cell act ivation and adhesion. It is thought that activated white cells are tra pped in dermal capillaries and increase microvascular permeability. Pl asma proteins leak into the tissue space, increasing the edema. Ischem ic damage to the epidermis leads to epithelial cell necrosis and ulcer ation. The ulcer is often slow to heal, due to inadequate perfusion an d delivery of substrates required for proper wound healing. Current tr eatments aim to improve calf pump function, reduce edema, improve perf usion, and enhance wound healing.