Traditionally wet-to-dry gauze has been used to dress wounds. Dressings that create and maintain a moist environment, however, are now considered to provide the optimal conditions for wound healing. Moisture under occlusive dressings not only increases the rate of epithelialisation but also promotes healing through moisture itself and the presence initially of a low oxygen tension (promoting the inflammatory phase). Gauze does not exhibit these properties; it may be disruptive to the healing wound as it dries and cause tissue damage when it is removed. It is not now widely used in the United Kingdom. Occlusive dressings are thought to increase cell proliferation and activity by retaining an optimum level of wound exudate, which contains vital proteins and cytokines produced in response to injury. These facilitate autolytic debridement of the wound and promote healing. Concerns of increased risk of infection under occlusive dressings have not been substantiated in clinical trials. This article describes wound dressings currently available in the UK. Low adherent dressings Low adherent dressings are cheap and widely available. Their major function is to allow exudate to pass through into a secondary dressing while maintaining a moist wound bed. Most are manufactured in the form of tulles, which are open weave cloth soaked in soft paraffin or chlorhexidine; textiles; or multilayered or perforated plastic films. They are designed to reduce adherence at the wound bed and are particularly useful for patients with sensitive or fragile skin.

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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.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. ExaminationNinety 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.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.

Most wounds, of whatever aetiology, heal without difficulty. Some wounds, however, are subject to factors that impede healing, although these do not prevent healing if the wounds are managed appropriately. A minority of wounds will become chronic and non-healing. In these cases the ultimate goal is to control the symptoms and prevent complications, rather than healing the wound. It is important that the normal processes of developing a diagnostic hypothesis are followed before trying to treat the wound. A detailed clinical history should include information on the duration of ulcer, previous ulceration, history of trauma, family history of ulceration, ulcer characteristics (site, pain, odour, and exudate or discharge), limb temperature, underlying medical conditions (for example, diabetes mellitus, peripheral vascular disease, ischaemic heart disease, cerebrovascular accident, neuropathy, connective tissue diseases (such as rheumatoid arthritis), varicose veins, deep venous thrombosis), previous venous or arterial surgery, smoking, medications, and allergies to drugs and dressings. Appropriate investigations should be carried out. Wounds are not just skin deep, and accurate assessment is an essential part of treatment

A pressure ulcer is defined by the European Pressure Ulcer Advisory Panel as an area of localised damage to the skin and underlying tissue caused by pressure, shear, or friction, or a combination of these. Pressure ulcers are caused by a local breakdown of soft tissue as a result of compression between a bony prominence and an external surface. They usually develop on the lower half of the body: two thirds around the pelvis and a third on the lower limbs, with heel ulceration becoming more common. Elderly people are the most likely group to have pressure ulcers; this is especially true for those older than 70, up to a third of whom will have had surgery for a hip fracture. Those with spinal injuries form another distinct group, in whom the prevalence is 20%-30% one to five years after injury. Most pressure ulcers arise in hospital, where the prevalence among inpatients is 3%-14%, although it can be as high as 70% in elderly inpatients with orthopaedic problems. The incidence of pressure ulcers in hospitals is 1%-5%. In patients who are confined to bed or to a chair for more than one week, the incidence rises to almost 8%. In long term healthcare facilities 1.5%-25% of patients develop pressure ulcers. Almost a fifth of pressure ulcers develop at home and a further fifth in nursing homes. The prevalence of pressure ulcers in nursing homes is not much higher than in hospitals. Pressure ulceration in elderly patients is associated with a fivefold increase in mortality, and in-hospital mortality in this group is 25%-33%. Estimates of the cost of pressure ulceration to the NHS range from £180m ($318m; €265m) to nearly £2bn a year.

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