Practice ABC of wound healing

Venous and arterial leg ulcers

BMJ 2006; 332 doi: http://dx.doi.org/10.1136/bmj.332.7537.347 (Published 09 February 2006) Cite this as: BMJ 2006;332:347
  1. Joseph E Grey,
  2. Keith G Harding,
  3. Stuart Enoch
  1. research fellow of the Royal College of Surgeons of England and is based at the Wound Healing Research Unit, Cardiff University

    Venous ulceration

    Venous leg ulceration is due to sustained venous hypertension, which results from chronic venous insufficiency. In the normal venous system, pressure decreases with exercise as a result of the action of the calf muscle pump. When the muscles relax, the valves in the perforating veins connecting the superficial to the deep venous circulation prevent reflux and the pressure remains low. The venous pressure remains high, however, in a system where the valves are incompetent.

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    Risk factors for venous ulceration

    Up to 10% of the population in Europe and North America has valvular incompetence, with 0.2% developing venous ulceration. Forty to fifty per cent of venous ulcers are due to superficial venous insufficiency and/or perforating vein incompetence alone with a normal deep venous system.

    There are many risk factors for venous ulceration. Recurrent venous ulceration occurs in up to 70% of those at risk. Many venous ulcers are painful, so appropriate pain relief and advice should be given.

    Examination

    Ninety five per cent of venous ulceration is in the gaiter area of the leg, characteristically around the malleoli. Ulceration may be discrete or circumferential. The ulcer bed is often covered with a fibrinous layer mixed with granulation tissue, surrounded by an irregular, gently sloping edge. Ulcers occurring above the mid-calf or on the foot are likely to have other origins.



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    From left to right: Haemosiderin associated with a venous leg ulcer; lipodermatosclerosis; venous leg ulcer in area of atrophie blanche; wenous leg ulcer with severe “champagne bottle” deformity of the leg



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    Pitting oedema is often present and may predate the ulcer. It is often worse towards the end of the day. Extravasation of erythrocytes into the skin occurs, resulting in the deposition of haemosiderin within macrophages, which stimulates melanin production, pigmenting the skin brown. In long term venous insufficiency, lipodermatosclerosis occurs. This …

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