Pressure ulcersBMJ 2006; 332 doi: http://dx.doi.org/10.1136/bmj.332.7539.472 (Published 23 February 2006) Cite this as: BMJ 2006;332:472
- Joseph E Grey,
- Keith G Harding,
- Stuart Enoch, research fellow
- Royal College of Surgeons of England and is based at the Wound Healing Research Unit, Cardiff University.
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.
The four main factors implicated are interface pressure, shear, friction, and moisture.
When pressure of short duration is relieved, tissues demonstrate reactive hyperaemia, reflecting increased blood flow to the area. However, sustained high pressure leads to decreased capillary blood flow, occlusion of blood vessels and lymphatic vessels, and tissue ischaemia.
These changes are ultimately responsible for necrosis of muscle, subcutaneous tissue, dermis and epidermis, and consequent formation of pressure ulcers. An external pressure of 50 mm Hg may rise to over 200 mm Hg at a bony prominence, leading, with time, to deep tissue destruction, which may not be evident on the surface of the skin. Regular relief from high pressures in the at-risk patient is essential to prevent pressure ulceration.
Shear force is generated by the motion of bone and subcutaneous tissue relative to the skin, which is restrained from moving due to frictional forces (for example, when a seated patient slides down a chair or when the head of a bed is raised more than 30°). In such circumstances the pressure needed to occlude the blood vessels is greatly reduced. In elderly patients, a reduced amount of elastin in the skin predisposes to the adverse effects of shear.
Friction opposes the movement of one surface against another. Frictional forces may lead to the formation of intraepidermal blisters, which in turn lead to superficial skin erosions, initiating or accelerating pressure ulceration. Such forces occur, for example, when a patient is dragged across a bed sheet or as a result of ill fitting prosthetic devices or footwear.
This is the fourth in a series of 12 articles
Most pressure ulcers are avoidable
An excessively moist environment caused, for example, by perspiration, urinary or faecal incontinence, or excessive wound drainage increases the deleterious effects of pressure, friction, and shear. It also causes maceration of the surrounding skin, which compounds these factors. Friction and moisture exert their greatest effects in areas of high pressure: the effects of friction are up to five times worse if moisture is present.
Among the various classification schemes for pressure ulceration, the one developed by the European Pressure Ulcer Advisory Panel (EPUAP) uses a simple, four grade classification. No “ideal” classification system exists; the EPUAP's grade 1 ulceration, for example, may be difficult to detect in people with darkly pigmented skin. Eschar (dried, black, hard, necrotic tissue) covering a pressure ulcer prevents accurate grading. Undermining of adjacent tissue, and sinus wounds, commonly occur and can affect grading as well as healing.
Prevention and treatment of pressure ulcers
Age alone is not a risk factor; rather, it is the problems common in elderly people that are associated with pressure ulceration. These include hip fractures, faecal and urinary incontinence, smoking, dry skin, chronic systemic conditions, and terminal illness. The effects of all risk factors should be minimised through their optimal management.
Immobility (the inability to reposition without help) and limited activity are probably the major risk factors for pressure ulcers and may occur for various reasons. Elderly people are particularly prone to such problems. Sensory deficits give rise to altered ability to perceive the pain and discomfort associated with persistent local pressure, and this leads to reduced frequency of repositioning.
Being confined to bed or to a chair significantly increases the risk of pressure ulceration; appropriate pressure relieving surfaces should be provided. Individuals with increased limb tone (spasticity) may benefit from interventions such as physiotherapy, muscle relaxants (for example, baclofen), nerve block, or surgery. Care should be taken with the use of sedatives, analgesics, and drugs that cause alteration in skin blood flow, such as antihypertensives.
A correlation exists between the degree of malnutrition and the extent and severity of pressure ulceration. In addition, malnutrition slows the healing of pressure ulcers. Measures of nutritional status predictive of pressure ulceration include a recent decrease in body weight, decreased triceps skin-fold thickness, and lymphocytopenia (< 1.8×109). Serum albumin concentration may be used as a surrogate marker, though its relatively long half life does not provide an accurate reflection of nutritional status. More sensitive markers include serum prealbumin and transferrin concentrations; testing for these, however, is not routinely available.
A systematic evaluation of risk factors will help to identify patients at risk of pressure ulceration. These individuals should be assessed regularly, and the risk assessment scales should be used as an adjunct to, not a substitute for, clinical judgment. Several risk assessment scales are currently used but vary in the risk factors assessed. The guidelines from the UK National Institute for Health and Clinical Excellence (NICE) state, however, that the provision of pressure relieving devices should also be based on cost considerations and an overall assessment of the individual, not only on risk assessment scores.
Regular inspection of the skin of patients at risk of pressure ulcers should focus particularly on areas around bony prominences. Excess moisture from, for example, urinary or faecal incontinence, perspiration, or wound drainage should be minimised. Patients confined to bed should be turned at least every two hours, the frequency reflecting the type of support surface used and the degree of risk.
Most patients are nursed on a standard hospital mattress. However, those at risk may need to be nursed on a “static” pressure relieving mattress or mattress overlay, which should not be able to “bottom out”—that is, the mattress should not provide less than 2.5 cm of support).
Dynamic mattresses, air-fluidised mattresses, and dynamic overlays provide alternating pressure relief in a cyclical fashion. They are suited to patients at high risk, including those in whom contact of the pressure with the mattress is unavoidable, those with very large or several ulcers, and those with non-healing ulcers.
Direct (“kissing”) contact of bony prominences such as the knees and ankles should be avoided by use of cushions or foam wedges. Excess abnormal pressure on the heels should be off-loaded using pressure relieving devices. The patient should not be positioned on the femoral trochanter. Pressure and friction should be minimised by maintaining the head of the bed at less than 30° and using appropriate lifting devices rather than dragging patients during transfer and repositioning.
When sitting in a chair or wheelchair, a patient at risk of pressure ulcers should use a pressure relieving cushion to reduce pressure, ensure good sitting balance, and provide comfort. The patient should be encouraged to shift position every 15-30 minutes. If they are unable to do this independently they should be repositioned at least hourly. “Doughnut” or ring cushions should not be used as they may exacerbate rather than prevent the risk of ulceration.
Debridement and dressings
Necrotic or sloughy pressure ulcers should be debrided to promote healing and to enable the stage of the ulcer to be assessed accurately. Devitalised tissue can be removed at the bedside by sharp debridement with a scalpel; local anaesthetic may be needed. Formal surgical debridement may be necessary for extensive grade 3 or 4 pressure ulcers. These ulcers may also require plastic surgery to reconstruct the area. Dressings are the mainstay of treatment of pressure ulcers. Other treatments, including larval and vacuum assisted closure therapies, may be beneficial (see penultimate article in the series).
All pressure ulcers will be colonised with bacteria. Only signs of clinical infection should prompt bacterial culture to confirm the organism and antibiotic sensitivities. Secondary bacteraemia or septicaemia may complicate pressure ulceration, and each of these conditions is associated with increased mortality. Antibiotics are often started empirically, reflecting the site and depth of the pressure ulcer. A chronic, indolent, non-healing wound may reflect the development of underlying osteomyelitis, the flora of which is often Gram negative or anaerobic (treatment of infection is discussed in a later article). Rarely, amyloidosis or malignancy may arise as a result of chronic pressure ulceration.
The ABC of wound healing is edited by Joseph E Grey (), consultant physician, University Hospital of Wales, Cardiff and Vale NHS Trust, Cardiff, and honorary consultant in wound healing at the Wound Healing Research Unit, Cardiff University, and by Keith G Harding, director of the Wound Healing Research Unit, Cardiff University, and professor of rehabilitation medicine (wound healing) at Cardiff and Vale NHS Trust. The series will be published as a book in summer 2006.
Competing interests For series editors' competing interests, see the first article in this series.