PD Coleridge Smith DM FRCS
Tel: 0870 609 2389 fax: 01753 663964 e-mail: p.coleridgesmith@ucl.ac.uk
Senior Lecturer
Department of Surgery, UCL Medical School, The Middlesex Hospital, London.
Summary
Chronic venous insufficiency (CVI) affects up to 2% of the population in western countries, a prevalence similar to that of diabetes. One in five affected patients suffers leg ulceration at any one time, and patients endure recurrent episodes of ulceration. The cost to healthcare systems is massive: in the United Kingdom it has been estimated that £600 millions per year (US $1000 millions) is spent on the management of legs ulcers.
The pathophysiology of chronic venous insufficiency (CVI) in large veins is well established. Deep or superficial veins become incompetent, permitting reverse flow and resulting in raised pressure in the superficial veins during ambulation.
The reasons why this results in leg ulceration have been discussed for many years. Initially it was suggested that arterio-venous anastomoses deprived the skin of nutrition. Later it was proposed that pericapillary fibrin cuffs prevent oxygen diffusion to the tissues. These suggestions do not provide a complete answer and more recently it has been shown that leucocytes which are trapped in the leg during venous hypertension become activated and cause damage to the endothelium of the lower limb. This probably results in the chronic inflammatory condition of the skin called lipodermatosclerosis. The capillary circulation in this skin is abnormal and susceptible to catastrophic breakdown resulting in leg ulcers.
Our understanding of these processes is incomplete, but further research may lead to identification of factors which could be changed by the use of drugs. Whilst the use of compression bandaging and hosiery will remain the main treatment in patients with CVI, the availability of more active drugs will be of great use.