Carpentier P, Magne J L, Sarrot-Reynauld F, Franco A
J Mal Vasc. 1987;12(3):280-4.
In patients with chronic venous insufficiency, tissular damage occurs as a consequence of microcirculatory disturbances. Venular distension, venulo-arteriolar reflex and probably valves in collecting venules are the only microcirculatory protective mechanisms against venous pressure overload. Edema is primarily a consequence of increased capillary hydrostatic pressure. However, the increase of endothelial macromolecular transport and a true lymphatic microangiopathy are important contributive factors. Venous ulceration is hypoxic although the amount of total blood flow is normal in the surrounding tissue. Several hypothesis were proposed for explaining this nutritional steal: arterio-venous shunt vessels have never been shown consistently, peri-capillary fibrin deposition might block oxygen diffusion, and last but not least, the abnormal geometrical arrangement of the capillary bed is facilitating functional shunting. On a therapeutic point of view, behind the classical hemodynamic therapy, the microvascular approach to chronic venous insufficiency supports the use of lymphatic manual drainage for controlling edema and rheologic therapy for improving skin capillary perfusion.