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Chronic venous insufficiency starts by promoting the case of events. This results in pathologic venous and tissue changes consequential to chronic venous insufficiency. In this article, chronic venous insufficiency is defined as an abnormal function of the venous system due to venous valvular incompetence with or without associated venous outflow obstruction, which may involve the superficial venous system, deep venous system, or both. Long-term venous hypertension may present by a variety of clinical manifestations in terms of the severity and duration of venous circulation damage. Venous leg ulcer occurs in distal part of the shin, mostly around medial malleolus. The base of the ulcer is often covered by a yellowish fibrin layer. The surrounding skin is hyperpigmented, usually irritated by ulcer secretion, and inflamed. Arterial leg ulcer is caused by arterial insufficiency. It is round-shaped with dry basis and involves deeper structures, up to tendons. The skin is dry, atrophic, cool, pale, smooth, and hairless. Therapy of ulcers is demanding and consists of numerous general measures, topical and/or systemic therapy. Topical therapy consists of cleansing, mechanical debridement, disinfection and stimulation of granulations and epithelialization with prevention of secondary infection. Therapy with currently available bio-occlusive wound dressings is most effective. These dressings are hydrocolloids, hydropolymers, transparent films, alginate, and ionic silver. Vascular protectors, venetonics and antiaggregation medications can be used in systemic therapy.

Introduction: The venous system of lower leg can be topographically divided into two subsystems: superficial (extrafascial) and profound (subfascial). Functionally, we can divide circulation in to macrocirculation (arteries and veins) and microcirculation (arterioles, capillaries, and venules). Blood flow towards heart can be disturbed by different pathological conditions, and than chronic venous insufficiency (CVI) develops. First alterations occurs in macrocirculation, and after some period changes in microcirculation also appear. Those changes are leading to the ultimate stage in CVI--venous ulcer., Results and Discussion: Previous conceptions that alterations in microcirculation in CVI are consequences of venous stasis, high pressure in capillaries and anoxic tissue are still actual. Observations that partial pressure of oxygen is higher in venous blood of lower limbs with ulceration than in limbs without ulceration lead to hypothesis that blood is passing directly from arterioles to venules over arterio-venous temperature-regulating shunts in dermis. Histological and electron-microscopic examinations certain alterations in the structure of capillaries. Raised pressure in these altered capillaries leads to exudation of plasma and fibrinogen in the interstitial space. Soluble fibrinogen is transformed to insoluble fibrin and forms fibrin cuffs. These cuffs are a barrier for normal diffusion of oxygen. Recently, it was observed that blood cells can adhere to the endothelial cells--Leukocyte trapping hypothesis. It can be explained by slower blood flow velocity and also by expression of certain endothelial and leukocyte adhesion molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1). This causes congestion of white blood cells which leads to tissue damage due to secretion of inflammatory mediators.