The Royal Marsden Hospital Manual of Clinical Nursing Procedures - Lisa Dougherty [129]
Pressure ulcers
Definition
Pressure ulcers are areas of localized tissue damage caused by excess pressure, shearing or friction forces (Benbow 2006). The extent of this damage can range from persistent erythema to necrotic ulceration involving muscle, tendon and bone (RCN 2005).
Related theory
The three major extrinsic factors that are identified as being significant contributors in the development of pressure ulcers are pressure, shearing and friction. These factors should be removed or diminished to reduce injury (RCN 2005).
Pressure. The blood pressure at the arterial end of the capillaries is approximately 35 mmHg, while at the venous end it drops to 16 mmHg (the average mean capillary pressure is about 17 mmHg) (Guyton and Hall 2000, Tortora and Grabowski 2008). External pressures exceeding this will cause capillary obstruction as the capillaries close when the pressure between the bed surface and the bony prominence exceeds 16–32 mmHg (Landis 1930, S. Hampton, personal communication, October 2006). Tissues that are dependent on these capillaries are deprived of their blood supply and will eventually become ischaemic and die (Bridel-Nixon 1999, Tong 1999). The pressure near bony prominences can be up to five times greater and is known as the ‘cone of pressure’; thus a surface redness can hide extensive tissue damage nearer the bone. It also explains why a small ulcer can open into a large, undetermined ulcer with overhanging edges and sinus formation (S. Hampton, personal communication, October 2006).
Shearing. This may occur when the patient slips down the bed or is dragged up the bed. As the skeleton moves over the underlying tissue, the microcirculation is destroyed and the tissue dies of anoxia. In more serious cases, lymphatic vessels and muscle fibres may also become torn, resulting in a deep pressure ulcer (Clay 2000, Collier 1999, Simpson et al. 1996).
Friction. This is a component of shearing, which causes stripping of the stratum corneum, leading to superficial ulceration (Johnson 1989, Waterlow 1988). Poor lifting and moving techniques may be a major contributory factor (NICE 2003).
The most common sites for pressure ulcer development are areas where soft tissue is compressed between a prominence (such as the sacrum) and an external surface (such as a mattress or seat of a chair) (Hess 2005).
Evidence-based approaches
Rationale
Pressure ulcers are a major healthcare issue and are associated with pain, infection, prolonged hospital stay and in extreme cases can be a causative factor in a patient’s death (Bennett et al. 2004, RCN 2005). Many pressure ulcers are preventable if there is a systematic and multiprofessional approach to their prevention and continuous assessment of skin integrity (Beldon 2006).
A 3-year clinical audit published in 2009 reported overall pressure ulcer prevalence in UK hospitals of 10.2–10.3%. Over half of pressure ulcers are hospital acquired (57–63%) (Phillips and Buttery 2009). Another study, published in 2004, reported that the mean incidence of pressure damage amongst hospital inpatients in the UK was approximately 40 cases per 1000 admissions in the population at risk (Bennett et al. 2004). NPSA data from 2009 demonstrate that of the pressure ulcers reported to the NRLS each year, 13% were grade 1, 47% were grade 2, 23% were grade 3 and 17% were grade 4 (NHS Institute for Innovation and Improvement 2010, NPSA 2009). See Box 4.3.
Box 4.3 Grades of pressure ulcers
Grade 1: non-blanchable erythema of intact skin.
Grade 2: presents clinically as an abrasion or blister.
Grade 3: superficial lesions.
Grade 4: deep lesions, extensive destruction, tissue necrosis or damage to muscle,