Oedema in Chronic Venous Insufficiency: Physiopathology and Investigation

Abstract

Aim:

To review the physiology of the venous system in the leg and the events in the microcirculation of the skin leading to development of the symptoms of chronic venous insufficiency (CVI).

Method:

A review of current literature in the field of CVI has been conducted, with particular reference to the microcirculation and the means of investigating this.

Synthesis:

Venous valvular incompetence and obstruction in the lower limb causes damage to the microcirculation of the skin. The resulting venous hypertension is resisted by the microcirculation. Cutaneous vasomotion alters, with a prevalence of closing periods of the pre-capillary sphincters, limiting capillary hypertension and resulting in capillary haemoconcentration. This phenomenon promotes drainage of fluids from the interstitial spaces and prevents hypoxic damage to the endothelium. In severe CVI this defence mechanism is overwhelmed, vasomotion declines and arteriolar vasoparalysis occurs. The capillary bed is filled and the intracapillary pressure increases. Reduced microcircula-tory perfusion flow velocity favours capillary plugging by white cells. Leucocyte activation damages the endothelium through the release of proteolytic enzymes, oxygen metabolites and lipid oxidation products. Increased permeability of the endothelium allows passage of fibrinogen and results in a perivascular fibrin cuff. Initially this protects the capillary but later blocks oxygen exchange. These events lead to capillary thrombosis with destruction of capillaries with tissue ischaemia and trophic lesions.

Conclusions:

The result of venous hypertension in the large veins of the lower limb is damage to the microcirculation of the skin. This leads to lipodermato-sclerosis and eventually ulceration in some patients.