Chronic venous insufficiency is the result of an impairment of the main venous conduits, causing microvascular changes. The driving force responsible for the alterations in the microcirculation is probably the intermittently raised pressure propagated from the deep system into the capillaries. The capillaries are dilated, elongated and tortuous and their endothelium is injured (irregular luminal surface, increased cytopempsis, dilated interendothelial spaces). Through the latter an increased extravasation can be observed, leading to an enlarged pericapillary space, oedema in the interstitial tissue and to the clinical finding of swelling. Haemoglobin from extravasated erythrocytes and erythrocyte fragments in the pericapillary space is degraded to haemosiderin which is responsible for hyperpigmentation. Microthrombosis in the capillaries causes microinfarction and micronecrosis. Skin areas with severe microangiopathy have reduced numbers of perfused nutritional capillaries and are characterized by a low transcutaneous (tc) PO2. The increased blood flow in the deeper skin layers does not contribute to nutrition of the superficial skin layers. The microvascular ischaemia is patchy and appears to be the main factor determining trophic changes and venous ulceration. The process of microinfarction and micronecrosis is followed by the formation of a granulation tissue, proliferation of capillaries and fibroblasts and finally wound healing by formation of scar tissue destroying the microlymphatic network. Clinically this process leads to lipodermatosclerosis, atrophy and in its most extreme form to ulceration where the compensating mechanisms are no longer able to repair the damage.