[Chronic venous insufficiency and compression therapy]. / Hronicna venska insuficijencija i kompresivna terapija.

INTRODUCTION: Disorders of venous circulation are among most frequent diseases in the human population. During recent years there has been increased interest in physiopathology of chronic venous insufficiency (CVI), due to development of more accurate diagnostic methods and new therapeutic techniques. Considering patophysiology of CVI and its consequences the crucial points are stasis and reflux of blood flow, with increase of intravascular pressure. CLASSIFICATION AND THERAPY OF CVI: Empirical experience and theoretical models suggest that progression of the disease can be stopped or reverted by correction of stasis. Today, this is the main direction in all therapeutic approaches. Compression therapy represents the most successful conservative technique. In this article we are presenting basic principles of the compression therapy of CVI. Evidence for the physiologic effect of compression therapy are decrease of edema, softening of lipodermatosclerosis, acceleration of venous flow, decrease in venous volume, blood shift into central compartments, reduction of venous refluxes, influence on arterial flow and improvement of microcirculation and lymph drainage. There are several types of compression devices: elastic stockings, elastic bandages, inelastic bandages, intermittent pneumatic compression devices. Other advantages of compression therapy are decrease of hospital treatment and better quality of life for patients with CVI.

[Microcirculatory changes in chronic venous insufficiency]. / Mikrocirkulatorne promene u hronicnoj venskoj insuficijenciji.

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.