Venous and arterial leg ulcers

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Abstract
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. View this table: In this window In a new window 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. 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 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 is characterised by the dermis and subcutaneous tissue becoming indurated and fibrosed with the lack of pitting oedema; the skin also becomes atrophic, loses sweat glands and hair follicles, and becomes variably pigmented (ranging from hypopigmented to hyperpigmented). Severe lipodermatosclerosis may lead to atrophie blanche—white fibrotic areas with low blood flow. Lipodermatosclerosis often precedes venous ulceration. As a result of lipodermatosclerosis, a rigid woody hardness often develops, which at its worst may result in the leg resembling an “inverted champagne bottle.” Venous eczema (erythema, scaling, weeping, and itching) is also common and is distinct from cellulitis. Typical venous leg ulcer over the medial malleolus (left) and venous leg ulcer over malleolus with a fibrinous base (right) View this table: In this window In a new window Features of venous eczema and cellulitis This is the second in a series of 12 articles Management Compression is the mainstay of venous ulcer management (see also 11th article in this series). Graded compression, with greatest pressure (about 40 mm Hg) at the ankle, tapering off to lower pressure (about 18 mm Hg) below the knee, increases the limb hydrostatic pressure and concomitantly reduces the superficial venous pressure. Various compression bandage systems are used. These include the single and multilayer elastic banadage system, short stretch bandage, and elasticated tubular bandages (for example, Tubigrip). Compression with pneumatic devices (for example, Flowtron) has been used to promote healing of venous ulcers in patients with oedematous legs. Patients should be warned to remove the compression if they notice any side effects (such as numbness, tingling, pain, and dusky toes) and seek advice. View this table: In this window In a new window Choice of dressing Sharp debridement of non-viable tissue may expedite healing of venous ulcers and can be done in the primary care setting. Surgery is normally indicated to correct superficial venous disease in an attempt to prevent ulcers from recurring. Shave therapy (excision of the whole ulcer) followed by skin grafting, or skin grafting alone, may be useful in patients where other treatments have failed. Unhealthy venous leg ulcer before debridement (left) and sharp debridement of venous leg ulcer (right) Venous leg ulcers often become infected (see 10th article in this series for how to detect signs of infection). The most common organisms include Staphylococcus aureus, Pseudomonas aeruginosa, and β-haemolytic streptococci. Initially, these should be treated empirically (with broad spectrum penicillin or macrolide or quinolone antibiotics) until definitive culture and sensitivities are available. Infection should be treated with a two week course of antibiotics. Topical antibiotics should be avoided owing to the risk of increasing bacterial resistance and contact dermatitis. Associated venous eczema should be treated with topical steroids and emollients. The eczema may be secondarily infected and require systemic antibiotic therapy. View this table: In this window In a new window Compression stockings Once the venous ulcer has healed, it is essential that patients follow simple advice aimed at preventing the recurrence of the ulcer: this includes wearing compression stockings, skin care, leg elevation, calf exercises, and adopting a suitable diet. The reported annual recurrence rate of venous ulcers (20%) is strongly influenced by patient adherence. Local “leg clubs” (www.legclub.org) may help to reduce this rate. Compression stocking