Wound Care for Patients With Darkly Pigmented Skin

Written By: Sam Savage

Published Date: October 20, 2005 Last Edited: October 20, 2005

By Bethell, Elaine

Summary

This article examines the main skin or wound assessment parameters used for patients with darkly pigmented skin. Differences in skin pigmentation are discussed along with the challenges health professionals encounter in clinical practice and why linking theory to practice is vital.

Keywords

Diversity; Pressure ulcers; Transcultural care; Wounds

These keywords are based on the subject headings from the British Nursing Index. This article has been subject to double-blind review. For related articles and author guidelines visit our online archive at www.nursing-standard.co.uk and search using the keywords.

THE SKIN PIGMENTATION continuum varies from light ivory, deep brown, black, yellow to olive, light pink to dark, ruddy pink, or red (Baranoski and Ayello 2004). Lyder (2005) describes patients with skin pigmentation as having ‘diversity in skin tones’. This can pose a challenge to clinicians when they assess patients with wounds or grade 1 pressure ulcers. In patients with darkly pigmented skin the assessment of skin changes for erythema, which is indicative of inflammation, is difficult especially for healthcare professionals and carers who lack training and experience (Bennett 1995, National Pressure Ulcer Advisory Panel (NPUAP) 1998). The usual signs of redness that characterise blanching and non-blanching erythema are difficult to detect. Erythema is characteristic of many skin conditions other than pressure ulcers (Alterescuand Alterescu 1988).

This article examines the key skin or wound assessment parameters necessary for patients with darkly pigmented skin admitted to any healthcare setting. It explores how clinical practice relating to skin or wound assessment incorporating a patient history and physical examination is the same for any patient regardless of age, sex, race or skin colour. However, it is important that an assessment is made by trained practitioners who are a ware of the differences between lightly and darkly pigmented skin. The clinical implications and relative risks are that failure to assess skin adequately and to detect signs of inflammation or non-blanching erythema may lead to the development of a severe pressure ulcer or a life-threatening wound infection.

Assessment provides the key elements regarding the current status of a wound and is essential to the development of all healthcare interventions (Baranoski and Ayello 2004). The management of acute and chronic wounds has evolved into a highly specialised area of practice and this is apparent in the assessment of patients with darkly pigmented skin (Baranoski and Ayello 2004).

Background

The Office for National Statistics (ONS 2002) found that the UK’s minority ethnic population, most of whom have darkly pigmented skin, rose from 3.1 million in 1991 to 4.5 million in 2001-2002 – this equates to 7.6 per cent of the population. It is envisaged that the minority ethnic population in the UK will continue to increase (Bethell 2003a). The ONS also found that many members of this population have lower incomes than other populations and experience ill health, thus placing them at risk of developing pressure ulcers and wound infections. Salcido (2002) states that health care in the United States is beginning to experience a shift in racial and ethnic demographics. In the US, the black and Latino/Hispanic populations are the fastest growing among those aged 85 years and older and are often in poor health (Lyder et al 1998).

The problem for clinicians when assessing patients with pigmented skin is the lack of guidance and/or evidence. A search of Medline, the Cumulative Index of Nursing and Allied Health Literature (CINAHL) and other sources including the European Pressure Ulcer Advisory Panel (EPUAP), NPUAP, the Tissue Viability Society (TVS) and the National Institute for Health and Clinical Excellence (NICE) websites, in addition to conversations with colleagues, demonstrated that guidance cited in the literature primarily relates to pressure ulcers with little on skin and wound assessment (Lyder 1991, Witkowski 1993, Bennett 1995, Flanagan 1996, Lyder 1996, Lyder et al 1998, NPUAP 1998, NICE2001, Bethell 2002, Salcido 2002, Baranoski and Ayello 2004, Scanlon and Stubbs 2004).

Diversity in skin tones

Skin colour or tone depends on four factors: various carotene pigments in the subcutaneous fat, concentration and state of oxygenation of haemoglobin, the presence of other pigments, for example bile, and the amount of melanin present in the epidermis. Melanin is synthesised by melanocytes. These cells are of neuro- ectodermal origin and migrate during development to the epidermis where they remain scattered in the basal layers. The cell bodies of the melanocytes are located between the basement membrane and the basal epithelial cells. The ratio of melanocytes to basal epithelial cells varies from about one in five to one in ten in different regions of the body. They are highest in the skin of the face and external genitalia.

Sunlight promotes melanin synthesis and causes darkening of previously synthesised melanin. Melanin has biophysical and biochemical properties related to its functions in skin. It protects against the damaging effects of ultraviolet (UV) radiation. Tanning or pigment darkening can occur in minutes, probably due to photo- oxidation of pre-existing melanin. There are fewer melanocytes in freckles than in adjacent paler epidermis, but they are larger and more active (Bannister 1995).

Within melanocytes, melanin accumulates in secretory vesicles known as melanosomes. These are disseminated throughout long cytoplasmic processes from where they are transferred to surrounding epithelial cells. The rate of production and the size and shape of melanosomes vary between individuals of one race and between racial groups. Consequently, the pigmented cells of skin are both the melanocytes, which synthesise melanin, and the epithelial cells, which have taken up melanin; commonly the epithelial cells contain much more melanin than the melanocytes. The number of melanocytes is relatively constant between different individuals irrespective of race. Racial variations and differences in skin colour and tone are due to melanocyte morphology and activity, that is, the amount of melanin produced rather than the number of melanocytes present (Bannister 1995).

Wound assessment

A wound is a disruption of normal anatomic structure and function (Lazarus et al 1994), and may be classified as acute or chronic. Baranoski and Ayello (2004) purport that there is no written standard that outlines the type and amount of information to include in a wound assessment; also, no single documentation chart or tool has been designated as the most effective. However, it is accepted generally that a total patient assessment, inclusive of any co- morbid conditions and lifestyle, must form part of a comprehensive wound assessment. A patient history irrespective of skin colour must be systematically documented. A wound assessment is a written record or picture of the progress of the wound, and a cumulative process of observation, data collection, and evaluation. It is a vital component of patient care. An individual wound assessment should include a record of initial assessment, ongoing changes, and treatment interventions (Baranoski and Ayello 2004 ). The effectiveness of interventions cannot be ascertained unless baseline assessment data are compared to follow-up data.

A minimal wound assessment should include a thorough patient examination, aetiology or wound type and wound characteristics such as location, size, depth, exudate, and tissue type. Wounds can be classified using several different approaches, however, this is not within the scope of this article and has been covered elsewhere (Lazarus et al 1994). The pathology or cause of the wound must be determined before appropriate interventions can be implemented. Wounds may have a surgical, traumatic, neuropathic, vascular, or pressure-related aetiology. These factors do not change whatever the patient’s diversity in skin tone.

Physical examination

To accurately detect skin changes in patients, visual assessment must be followed by a thorough physical assessment of the wound and its surrounding skin. The skin surrounding a wound can provide the assessing clinician with valuable information regarding ongoing evaluations and future wound care management (Baranoski and Ayello 2004). Asking patients and/or carers about skin changes can also prove useful. Baranoski (2001 ) advises that a minimal skin assessment should include the following five parameters: colour, temperature, moisture, turgor, and intact skin or presence of open areas.

Palpation should be carried out with the fingers around a wound surface. This may reveal a temperature difference compared with the surrounding skin. Induration and oedema indicate abnormal fluid accumulation, which may suggest further tissue damage, abscess or a wound infection (Baranoski and Ayello 2004).

Changes in normal skin colour and increase in temperature are due to the inflammatory process (Hart 2002). Failure to observe the above may increase the risk of a patient developing a pressure ulcer or wound infection. Therefore, it is important for practitioners to recognise and understand the clinical implications of inflammatory changes.

Inflammation Inflammation is a normal physiological response to tissu\e insult or injury and is integral to microbial resistance (Gardner and Frantz 2004). In surgical wounds, inflammation occurs following an incision and wounding, but should subside within five days post-operatively (Stotts 1998). The inflammatory process is triggered by endogenous (host sources) and exogenous (microbial) mediators. The release of inflammatory mediators results in localised vasodilation and increased blood flow to the injured area. These chemical mediators are key to the inflammatory process. The accompanying increase in vascular permeability promotes a rapid influx of phagocytic cells and antibodies to the wound site. Collectively, these events cause the removal of micro-organisms, debris and bacterial toxins and enzymes. These physiological responses to injury are demonstrated by the signs of inflammation including erythema, heat, oedema and pain (Gardner and Frantz 2004).

Inflammation is either acute or chronic. Acute inflammation is the initial response to tissue invasion or in] ury. Chronic inflammation occurs if the invasion or injury of tissue is not resolved and persists over a long period (Gardner and Frantz 2004).

Erythema The change in usual skin colour results from the dilation of capillaries near the skin’s surface, which is mediated by polymorphonuclear leukocytes, monocytes and macrophages. This phase usually occurs from the time of initial insult to about two to five days’ post-injury. Colour is a proven indicator of a physiological response to injury and a good indicator of a stage 1 pressure ulcer (Lyder 1991). In patients with darkly pigmented skin, erythema is difficult to detect (Bennett 1995). In lightly pigmented skin the presence of erythema is detected by bright or dark red skin, and by darkening in patients with darkly pigmented skin (Gardner and Frantz 2004).

Most clinicians agree that colour and temperature play a major role in the identification and assessment of stage 1 pressure ulcers (Agency for Health Care Policy and Research 1992, Parish et al 1997, EPUAP 1999), and almost all pressure ulcer classifications include erythema as a category (Lyder 1991). However, erythema is not only difficult to detect in darkly pigmented skin, but it is also characteristic of many skin conditions other than pressure ulcers, including allergic reactions and excoriation from faecal incontinence caused by alkaline enzymes in the stool which irritate the skin (Alterescu and Alterescu 1988).

Lyder (2005) suggests using a pen torch to observe changes in skin colour. However, this is a subjective assessment (Matas et al 2001 ). Lyder et al ( 1998 ) report that caregi vers who are not of the same ethnic background as patients may be less sensitive to slight changes in skin colour. This is an important factor to consider in the assessment of patients with darkly pigmented skin (Lyder 1991).

Temperature Skin is usually warm to touch. If it is warmer than usual this could be a sign of inflammation, and an indicator of infection or pressure damage. Increased local blood flow and oedema are followed by engorgement of surrounding vessels and tissues resulting in warmth and redness in the area. Histologically this is due to oedema of the papillary dermis, platelet aggregation in the microcirculation (Barton and Barton 1981), and erythrocyte engorgement of the superficial blood vessels (Witkowski 1993).

Pale and cool skin may be a sign of poor perfusion or ischaemia and may indicate the end stage of non-blanching erythema (Lyder 1991, NPUAP 1998). Histologically this is due to endothelial cell damage, and activation of haemostatic mechanisms that decrease blood flow and potentiate endothelial cell damage which increases the degree of platelet thrombosis and hence ulcer size and severity (Barton and Barton 1981). Witkowski (1993) and Bliss (2000 ) report that a grade 1 pressure inj ury is more likely to have a bluish tinge than reactive hyperaemia, and that this is evidence of irreversible tissue damage. Lyder (1991) reasons that non-blanching erythema must be considered a true criterion of stage 1 pressure ulcers.

Both extremes in temperature are included in the definition of stage 1 pressure ulcers (Lyder 1991). Education and training are required to avoid inaccurate assessment and negative patient outcomes. An increase or decrease in skin temperature is usually detectable by touch (Parish et al 1988, Bliss 2000). Flanagan (1996) states that these temperature changes are slight and detection can be made easier by avoiding the use of gloves. However, Lyder (2005 ) challenges this and argues that in clinical practice a rise in temperature of 1 -2 degrees is difficult to assess with or without gloves; practitioners’ fingers are not usually that sensitive. However, this assessment is important in patients with darkly pigmented skin because of the difficulty in observing colour changes.

Oedema Oedema is one of the physiological signs of inflammation, and is also indicative of heart, liver and kidney failure and venous insufficiency. In the case of suspected pressure ulceration, wound infection, or abscess formation, oedema can be palpated in areas of suspected damage, irrespective of skin pigmentation. Gardner and Frantz (2004) state that shiny, taut skin or pitting impressions in the skin adjacent to any wound but within 4cm of the wound margin indicate oedema. This can be assessed by pressing firmly within 4cm of the ulcer margin with a finger, releasing and waiting five seconds to observe for any indentation (Gardner and Frantz 2004).

Oedema and induration occur because pressure causes separation in the skin layers and allows interstitial fluid to accumulate (Longe 1986). Therefore, both oedema and induration are good indicators of tissue damage. Parish et al (1988) found that at this stage there is engorgement of capillaries and venules in the papillary dermis.

Turgor Skin should quickly return to its original state when it is assessed and palpated. A slow return may indicate dehydration or the effects of ageing. Soft tissue may indicate an underlying infection. Tense skin may indicate lymphoedema and cellulitis. Palpation is useful to assess skin temperature, oedema and turgor of suspected damaged areas.

Moisture It is important to note whether skin is moist or dry during assessment. If it is dry look for hyperkeratosis (flaking and scales). Observe for eczema or dermatitis, psoriasis rashes, leaking oedema, or exudate. These signs may aid diagnosis in patients with cellulitis, lymphoedema or wet gangrene.

No consensus as to what constitutes a minimal skin assessment exists in the literature (Baranoski and Ayello 2004). A skin assessment differs from a wound assessment as it should include observation of the patient’s entire body, not only areas with wounds. Lesions, bruising, absence of hair, shiny skin, callus formation, scars (hypertrophie and keloid scars are more prevalent in patients with darkly pigmented skin (Placik and Lewis 1992)) and signs of venous insufficiency such as haemosiderin deposits (reddish- brown colour), ankle flare and atrophy blanche can be identified. Haemosiderin deposits are often seen on the lower legs of patients with venous ulcers and lightly pigmented skin. However, in patients with darkly pigmented skin the signs of venous insufficiency are difficult to detect and patient history becomes the key to aid diagnosis.

Arterial ulcers often present with the classic signs of hair loss, weak or absent pulses, and thin, shiny, taut skin. Patients with diabetes are prone to callus formations. All of these diagnostic features can be detected during an assessment (Baranoski and Ayello 2004). Physical examination and patient history should reveal why the patient has a wound and, if it is not healing, why healing is not taking place irrespective of age, race or skin colour.

Scarring

Epithelialisation is the regeneration of the epidermis across the surface of a wound ( Bryant 1992 ). As wound migration occurs from the wound edges, the area covered with epithelium is pearly or silver and shiny (Figure 1 ). In darkly pigmented skins the colour of the epithelium will be tonally relevant to normal skin but as with scar tissue in lighter skins it will be different from surrounding undamaged epidermis ( Gray et al 2004 ).

Hypertrophie and keloid scars Hypertrophic (Figure 2) and keloid sears (Figure 3) are abnormalities associated with the maturation phase of healing. Hypertrophic scars occur directly after initial repair, tend to follow the line of the incision and are more common in young patients. Careful placing of incisions along Langer’s lines (incisions are made in natural creases) and fine suture material can avoid excessive scar formation (Centre for Medical Education 1992, Leaper and Gottrup 1998).

Keloids result from formation of large amounts of scar tissue around the site of the wound. This is due to an increase in collagen synthesis and lysis and is also thought to be linked to melanocyte- stimulating hormone (MSH). Often these scars are larger than the wound itself, and even if the scar is excised it is likely to recur (Bale and Jones 2000). Keloid scars may occur some time after healing (Eisenbeiss etal 1998) and are often red (darker in pigmented skin) and prominent. The scar continues to grow and spread, invading surrounding healthy tissue, whereas hypertrophie scars do not. Black AfroCaribbeans are ten times more likely to develop keloid scarring than Caucasians (Lee 1982). The reasons for this are not fully understood. Theories include a deficiency or an excess of MSH, decreased percentages of mature collagen and increased soluble collagen, or blockage of small blood vessels which results in lack of oxygen and contributes to keloid formation (Placik and Lewis 1992). While the lack of a definitive theory demonstrates lack of understanding of the condition, it also indicates that work is being done to find the cause. Determ\ining the cause should mean better preventive medicine and more effective treatment in the future, but there are many problems with inadequate follow up of people with the condition, lack of a clear cut-off from treatment and too few studies, which hamper the search for a cure.

FIGURE 1

Epithelial tissue

FIGURE 2

Hypertrophic scar

FIGURE 3

Keloid scar

The role of MSH in humans is not fully understood (Bennett 1995). However, Mehendale and Martin (2001 ) suggest that a better understanding of melanocyte responses to wounding may suggest ways to prevent post-healing pigmentary disturbances and avoid the necessity for further surgical intervention.

Pressure ulcers

A pressure ulcer has been defined as ‘an area of localised damage to the skin and underlying tissue caused by pressure, shear, friction and/or a combination of these'(EPUAP 1999). They frequently occur over bony prominences (Barton and Barton 1981).

Pressure ulcer aetiology is complex and the costs in terms of patients’ quality of life and NHS resources are significant (Gebhardt and Bliss 1994). Pressure ulcers are a major financial burden to health services as they are common and the cost of prevention and treatment is high. Estimates of the cost of pressure ulcers in the United Kingdom (UK) range from annual costs of 300 million in 1988 (with no supportive data provided) (Waterlow 1988), approximately 60 million in 1991 (Department of Health (DH) 1991), 288 million (1991-1992) (Hollingsworth et al 1997) to 420 million (Centre for Reviews and Dissemination 1995). Other countries also have no definitive costs and there are similar variations in estimates. Annual estimates of costs in the US ranged from $836 million in 1992 (Tomaselli and Granick 2000), to more recent estimates of $1.3 billion (Dealey 2004) and $2.8 billion (Tomaselli and Granick 2000). It would appear that there are no data available that clearly define the costs of pressure ulceration.

The aetiology of pressure ulcer formation is still not fully understood (Bliss 1998) and many areas of assessment and practice remain ineffective (Gebhardt and Bliss 1994) and controversial, including the identification and assessment of grade 1 pressure ulcers.

However, it is now generally accepted that the aetiology of pressure ulcers is a result of two coexisting concurrent processes, pressure and shear, which ultimately cause tissue anoxia (Neumark 1981, Scales 1982, Alterescu and Alterescu 1988, Scales 1990). However, pressure and shear do not account for the whole pathogenesis of pressure ulcers (Barton and Barton 1981, Barton 1983, Bennett and Lee 1988, Bridel 1993, Leigh and Bennett 1994, Bliss and Simini 1999).

The tissues involved in pressure ulcer development are the skin, subcutaneous fat, deep fascia, muscle and bone (Nixon 2001 ). Skin in particular plays an important role (Krouskop 1983, Woolf 1998). The prevalence and incidence of pressure ulcers are highest in older patients (Barbenel et al 1977, Versluysen 1986, Meehan 1990, Clark and Cullum 1992, Meehan 1994, O’Dea 1995, Hagisawa and Barbenel 1999).

If non-blanching erythema has developed, then irreversible damage has been sustained and this will progress to deeper skin layers if pressure is not relieved (James 1998). In American prevalence surveys, dark-skinned African-American patients had the most severe grade 4 pressure ulcers (Meehan 1990, 1994, Meehan et al 1999). This was probably because early non-blanching erythema was not detected and deep tissue injury occurred before action was taken (Bethell 2002). However, difficulties in identifying a stage 1 pressure ulcer or nonblanching erythema in patients with darkly pigmented skin led to the setting up of a special task force in the US to try to address the problem.

A definition of a stage 1 pressure ulcer, with emphasis on redness, was not helpful in assessing patients with darkly pigmented skin (Bennett 1995). It was acknowledged that localised skin colour changes can occur at the site of pressure; these colours differ from the patient’s usual skin colour. The area of skin over a point damaged by pressure may appear darker than the surrounding skin and may feel warmer to the touch, taut, shiny and/or indurated. The patient may complain of discomfort or pain in these areas.

A more specific definition has been approved by the NPUAP (Henderson et al 1997), which incorporates skin temperature, pigmented skin, and purple hues (Box 1). The EPUAP ( 1999) has also acknowledged the problem and offers similar guidance (Box 2), while NICE (2001) emphasises the importance of discoloration (Box 3).

Purple ulcers

The NICE (2001) guidelines only discuss the connection between purplish/bluish areas and pressure damage in relation to people with darkly pigmented skin. The aetiology is the same for all skin types, regardless of pigmentation (Bethell 2003b).

Further controversy arises over ‘purple’ ulcers which are often classified as stage 1 (Torrance 1983, Lyder 1991, Dailey 1992, Witkowski 1993) or even ignored. However, Dailey (1992) described the increasing number of patients admitted with ‘purple’ ulcers as purple-red, ecchymotic – an effusion of blood under the skin causing discoloration – pale ecchymotic, or bruised. The skin may be intact or the epidermis ‘brushed’ off, exposing a discoloured area. These can rarely be reversed. Biopsy specimens of the purple lesions demonstrate haemorrhage and early gangrenous changes (Witkowski 1993).

Purple ulcers appear to be treated less seriously than they should be, especially in patients with darkly pigmented skin where they are clinically difficult to identify (Dailey 1992, Witkowski 1993). Both authors suggest that the main problem is the lack of recognition of the serious nature of these ulcers. However, it is vital that practitioners are aware that the purple patch is the end stage of non-blanching erythema and signifies a full-thickness skin loss, and take appropriate action.

Blanch test

To distinguish between blanching and non-blanching erythema an assessor has to press a finger on the skin. However, while the finger is on the skin there is no means of telling what is occurring immediately beneath the finger. The study of stage 1 pressure ulcers needs reliable measurements (Halfens et al 2001). A simple, more accurate widely accepted means of detecting non-blanching erythema is to use clear glass or a plastic disc to assess whether discoloration blanches or not (Halfens et al 2001).

When gentle pressure is exerted on the skin, blood is temporarily forced out of the area, causing skin to appear white instead of pink. In healthy tissue colour returns swiftly as blood refills the dermal capillaries. This is the basis of the blanch test, which differentiates healthy skin from damaged skin that is non-blanching erythema. In patients with darkly pigmented skin the presence of melanin will ensure that the practitioner or carer carrying out the test will be unable to see the evacuation of blood, followed by the refill; only the melanin will be visible (Matas et al 2001).

Some studies have attempted to distinguish between blanching and non-blanching erythema. Halfens et al (2001) instructed nurses to use a convex glass. Wee et al (2004) used a thumb and a transparent disc. The results from both studies demonstrated that more non- blanching erythema was identified when these tools were used.

Pulse oximetry

Non-invasive pulse oximetry is a popular method of assessing and determining oxygenation status. Good oxygenation is important for wound healing. Adler et al (1998) identified that pulse oximetry may not be as accurate and work as reliably in patients with darkly pigmented skin, compared to patients with less darkly pigmented skin. The effect of skin pigmentation is controversial (Adler et al 1998). However, Adler et al’s (1998) observational study of 274 patients led researchers to conclude that skin pigmentation does not bias or affect the precision of pulse oximetry.

Pressure ulcer risk prediction scores

The Waterlow scale (1988) is the most widely used pressure ulcer assessment tool in the UK while in the US it is the Braden scale (Braden and Bergstrom 1987). Although there is no evidence to question the use of the Braden and Waterlow scales in patients with darkly pigmented skin, there is no definitive evidence that either scale is effective in this population. Lyder et al (1998) carried out a pilot study to examine the validity of the Braden scale in black and Latino/Hispanic elders. Although the study sample was small, statistical analysis revealed that the Braden score significantly under-predicted those participants at risk of pressure ulcers.

BOX 1

National Pressure Ulcer Advisory Panel (NPUAP) definition of grade 1 pressure ulcers

BOX 2

European Pressure Ulcer Advisory Panel (EPUAP) definition of grade 1 pressure ulcers

Lyder et al ( 1998 ) state that clinicians should examine pressure ulcer prediction tools and those variables that place older people at risk in non-white populations, for example, diet. They noted that the diets of black and Latino/Hispanic people differ from the diets of white people. Dietary differences may affect hospitalised patients who are accustomed to traditional foods. This important factor may alter risk scores if patients do not eat. These findings can also be extrapolated to certain areas in the UK, therefore nutritional assessment of patients is vital, particularly in those who have wounds.

BOX 3

National Institute for Clinical Excellence guidance on pressure ulcer development

Conclusion

The NICE (2001) guidelines state that risk assessment should be carried out by personnel who have undergone appropriate training to recognise the risk factors that contribute to the development of pressure ulcers. This applies to any wound assessment. However, few healthcare professionals receive enough formal training and clinical support in this complex area of care (Scanlon and St\ubbs 2004).

The literature reveals that there is more variability in research that attempts to classify the aetiology of grade 1 pressure ulcers than any other grade (Lyder 1991, Hitch 1995). If healthcare professionals and carers aim to prevent a stage 1 pressure ulcer progressing to a more serious potentially life-threatening stage, they must be able to identify it correctly (Lyder 1991). However, it is particularly difficult to recognise a pressure ulcer in its early stage and to ascertain the extent of the damage in patients with darkly pigmented skin (Bennett 1995, Russell and Reynolds 2001).

It is vital that nurses and carers receive appropriate information and training. Educationalists must be clear in their teaching and assess nurses on theory and clinical competence. It is also important that patients are given explanations as to why their skin and bony areas will be palpated and touched to carry out a detailed assessment. Translators may be required.

A means of examining patients’ skin to appropriately diagnose and prevent wounds is required to assist practitioners. A variety of devices are being tested and evaluated and may be suitable to detect alterations in blood flow and other changes specific to ischaemia and reperfusion injury associated with chronic wounds (Salcido 2002). This will aid diagnosis regardless of skin colour, but more so in patients with darkly pigmented skin.

Lyder et al (1998) highlighted that researchers have developed systematic assessment tools and identified pressure ulcer predictive variables without considering ethnic minority groups. The specific risk to patients with darkly pigmented skin should no longer be ignored. Pressure ulcer risk assessment tools that are validated for patients with darkly pigmented skin may be required. Researchers should include significant numbers of ethnic minorities in their investigations of pressure ulcer risk and investigate risk factors specific to these groups (Lyder 1996).

The EPUAP carried out a pressure ulcer prevalence survey, without taking into account patients with darkly pigmented skin (Clark et al 2002). Perhaps the next study could include this patient group as this would help to ascertain the extent of the problem, establish a baseline and enable data to be compared to the US.

Practitioners in the UK and Europe can learn from the guidance cited by American colleagues (Box 1). European practitioners, the EPUAP, Tissue Viability Nurses Association and NICE should promote this guidance in relation to grade 1 pressure ulceration. Salcido (2002) emphasises that patients should not be undiagnosed because of the colour of their skin. Subsequent research in education, wound healing and pressure ulcers should include patients with darkly pigmented skin

Bethell E (2005) Wound care for patients with darkly pigmented skin. Nursing Standard. 20, 4, 41-49. Date of acceptance: June 6 2005.

References

Adler JN, Hughes LA, Vivilecchia R, Camargo CA Jr (1998) Effect of skin pigmentation on pulse oximetry accuracy in the emergency department. Academic Emergency Medicine. 5, 10, 965-970.

Agency for Health Care Policy and Research (1992) Pressure Ulcers in Adults: Prediction and Prevention. Clinical Practice Guideline Number 3. AHCPR, Public Health Service, US Department of Health and Human Services, Rockville MD.

Alterescu V, Alterescu K (1988) Etiology and treatment of pressure ulcers. Decubitus. 1, 1, 28-35.

Bale S, Jones V (2000) Wound Care Nursing: A Patient-centred Approach. Baillire Tindall, London.

Bannister L (1995) Control of pigmentation: integumental system. In Gray H, Williams PL (Eds) Gray’s Anatomy. 38th edition. Churchill Livingstone, London, 388-394.

Baranoski S (2001) Skin: the forgotten organ. 16th Annual Clinical Symposium of Advances in Wound Care. Lake Buena Vista FL, September 20-21.

Baranoski S, Ayello E (2004) Wound assessment. In Baranoski S, Ayello E (Eds) Wound Care Essentials: Practice Principles. Lippincott, Williams and Wilkins, Philadelphia PA, 79-90.

Barbenel JC, Jordan MM, Nicol SM, Clark MO (1977) Incidence of pressure sores in the Greater Glasgow Health Board area. The Lancet. 2, 8037, 548-550.

Barton A (1983) Pressure sores. In Barton A, Barton M (Eds) Pressure Sores. Macmillan, London, 53-57

Barton A, Barton M (1981) The Management and Prevention of Pressure Sores. Faber and Faber, London.

Bennett MA (1995) Report of the task force on the implications for darkly pigmented intact skin in the prediction and prevention of pressure ulcers. Advances in Wound Care. 8, 6, 34-35.

Bennett L, Lee BY (1988) Vertical shear existence in animal pressure threshold experiments. Decubitus. 1, 1,18-24.

Bethell E (2002) Incidence and prevalence data: can we ensure greater accuracy? Journal of Wound Care. 11, 8, 285-288.

Bethell E (2003a) Assessment and prevention of pressure ulcers for patients with darkly pigmented skin. Diversity in Nursing. 1, 1, 34-35.

Bethell E (2003b) Controversies in classifying and assessing grade 1 pressure ulcers. Journal of Wound Care. 12, 1, 33-36.

Bliss MR (1998) Pressure injuries: causes and prevention. Hospital Medicine. 59, 11, 841-844.

Bliss M (2000) Medical management of pressure ulcers. Part 1. European Pressure Ulcer Advisory Panel Review. 3, 1, 18-21.

Bliss M, Simini B (1999) When are the seeds of postoperative pressure sores sown? Often during surgery. British Medical Journal. 319, 7214, 863-864.

Braden B, Bergstrom N (1987) A conceptual schema for the study of the etiology of pressure sores. Rehabilitation Nursing. 12, 1, 8- 12.

Bridel J (1993) The aetiology of pressure ulcers. Journal of Wound Care. 2, 4, 230-238.

Bryant R (1992) Acute and Chronic Wounds: Nursing Management. Mosby, St Louis MO.

Centre for Medical Education (1992) The Wound Programme. University of Dundee, Dundee.

Centre for Reviews and Dissemination (1995) The prevention and treatment of pressure sores. Effective Health Care Bulletin. 2.1. CRD, York.

Clark M, Cullum N (1992) Matching patient need for pressure sore prevention with the supply of pressure redistributing mattresses. Journal of Advanced Nursing. 17, 3, 310-316.

Clark M, Bours G, Defloor T (2002) EPUAP: summary report on the prevalence of pressure ulcers. EPUAP Review. 4, 2, 49-57

Dailey C (1992) ‘Purple’ ulcers. Journal of ET Nursing. 19, 3, 106.

Dealey C (2004) Review of advances in pressure ulcer management since 1992. In Clark M (Ed) Pressure Ulcers: Recent Advances in Tissue Viability. Quay Books, Salisbury, 3-7.

Department of Health (1991) Health of the Nation. HMSO, London.

Eisenbeiss W, Peter FW, Bakhtiari C, Frenz C (1998) Hypertrophie scars and keloids. Journal of Wound Cars. 7 5, 255-257

European Pressure Ulcer Advisory Panel (1999) Pressure Ulcer Treatment Guidelines. EPUAR Oxford.

Flanagan M (1996) How can you accurately assess pressure damage on patients with darkly pigmented skins? Journal of Wound Care. 5,10, 454.

Gardner S, Frantz R (2004) Wound bioburden. In Baranoski S, Ayello E (Eds) Wound Care Essentials: Practice Principles. Lippincott, Williams and Wilkins, Philadelphia PA, 91-116.

Gebhardt KS, Bliss MR (1994) Preventing pressure sores in orthopaedic patients: is prolonged chair nursing detrimental? Journal of Tissue Viability. 4, 2, 51-54.

Gray D, White R, Cooper P, Kingsley A (2004) The wound healing continuum, an aid to clinical decision making and clinical audit. Applied Wound Management Supplement. 9-12. Wounds UK, Aberdeen.

Hagisawa S, Barbenel J (1999) The limits of pressure sore prevention. Journal of the Royal Society of Medicine. 92, 11, 576- 578.

Halfens RJ, Bours GJ, Van Ast W (2001) Relevance of the diagnosis ‘stage 1 pressure ulcer’: an empirical study of the clinical course of stage 1 ulcers in acute care and long-term care hospital populations. Journal of Clinical Nursing. 10, 6, 748-757

Hart J (2002) Inflammation. 2: its rale in the healing of chronic wounds. Journal of Wound Care. 11, 7, 245-249.

Henderson CT, Ayello EA, Sussman C et al (1997) Draft definition of stage 1 pressure ulcers: inclusion of persons with darkly pigmented skin. Advances in Wound Care. 10, 5, 16-19.

Hitch S (1995) NHS Executive Nursing Directorate: strategy for major clinical guidelines: prevention and management of pressure sores. A literature review. Journal of Tissue Viability. 5, 1, 3- 24.

James H (1998) Classification and grading of pressure sores. Professional Nurse. 13, 10, 669-672.

Hollingsworth T, Todd C, Parker M (1997) The cost of treating hip fractures in the 21st century. Journal of Public Health Medicine. 17, 269-276.

Krouskop TA (1983) A synthesis of the factors that contribute to pressure sore formation. Medical Hypotheses. 11, 2, 255-267

Lazarus GS, Cooper DM, Knighton DR et al (1994) Definitions and guidelines for assessment of wounds and evaluation of healing. Archives of Dermatology. 130, 4, 489-493.

Leaper D, Gottrup F (1998) Surgical wounds. In Leaper DJ, Harding KG (Eds) Wounds: Biology and Management. Oxford University Press, Oxford, 47

Lee CP (1982) Keloids: their epidemiology and treatment. International Journal of Dermatology. 21, 9, 504-505.

Leigh IH, Beniiett G (1994) Pressure ulcers: prevalence, etiology, and treatment modalities. A review. American Journal of Surgery. 167, 1A, 25S-30S.

Longe RL (1986) Current concepts in clinical therapeutics: pressure sores. Clinical Pharmacy. 5, 8, 669-681.

Lyder CH (1991) Conceptualization of the stage 1 pressure ulcer. Journal of ET Nursing. 18, 5, 162-165.

Lyder CH (1996) Examining the inclusion of ethnic minorities in pressure ulcer prediction studies. Journal of Wound, Ostomy, and Continence Nursing. 23, 5, 257-260.

Lyder CH (2005) Is pressure ulcer care evidence based or evidence linked? Science of Surfaces Meeting. Warwickshire UK, January 20- 21.

Lyder CH, Yu C, Stevenson D et al (1998) Validating the Braden Scale for the prediction of pressure ulcer risk in blacks and Latino/ Hispanic elders: a pilot study. Ostomy/Wound Management. 44\, 3A Suppl, 42S-50S.

Matas A, Sowa MG, Taylor V, Taylor G, Schattka BJ, Mantsch HH (2001) Eliminating the issue of skin color in assessment of the blanch response. Advances in Skin and Wound Care. 14, 4, 180-188.

Meehan M (1990) Multisite pressure ulcer prevalence survey. Decubitus. 3, 4, 14-17

Meehan M (1994) National pressure ulcer prevalence survey. Advances in Wound Care. 7, 3, 27-38.

Meehan M, O’Hara L, Morrison M (1999) Report on the prevalence of skin ulcers in a home health agency population. Advances in Wound Care. 12, 9, 459-467

Mehendale F, Martin P (2001) The cellular and molecular events of wound healing. In Falanga V (Ed) Cutaneous Wound Healing. Martin Dunitz, London, 28-29.

National Institute for Clinical Excellence (2001) Pressure Ulcer Risk Assessment and Prevention. NICE, London.

National Pressure Ulcer Advisory Panel (1998) Position Statement: Stage 1 Assessment in Darkly Pigmented Skin. www.npuap.org/ positn4.html (Last accessed: September 6 2005.)

Neumark D (1981) Deformation, not pressure, is the prime cause of pressure sores. Care Science and Practice. 1, 41-43.

Nixon J (2001) Trie pathophysiology and aetiology of pressure ulcers. In Morison M (Ed) The Prevention and Management of Pressure Ulcers. Mosby, London, 17-35.

O’Dea K (1995) The prevalence of pressure sores in four European countries. Journal of Wound Care. 4, 4, 192-195.

Office for National Statistics (2002) Final Results on 2001 Census for England and Wales. ONS, London.

Parish LC, Witkowski JA, Crissey JT (1988) Unusual aspects of the decubitus ulcer. Decubitus. 1, 2, 22-24.

Parish L, Witkowski J, Crissey J (1997) The Decubitus Ulcer in Clinical Practice. Springer-Verlag, Berlin.

Placik OJ, Lewis VL Jr (1992) Immunologic associations of keloids. Surgery, Gynecology and Obstetrics. 175, 2, 185-193.

Russell LJ, Reynolds TM (2001) How accurate are pressure ulcer grades? An image-based survey of nurse performance. Journal of Tissue Viability. 11, 2, 67-75.

Salcido RS (2002) Finding a window into the skin. Advances in Skin and Wound Care. 15, 3, 100.

Scales J (1982) Pressure sore prevention. Care Science and Practice. 1, 2, 9-17

Scales J (1990) Pathogenesis of pressure sores. In Bader DL (Ed) Pressure Sores: Clinical Practice and Scientific Approach. Macmillan, Basingstoke, 15-26.

Scanlon E, Stubbs N (2004) Pressure ulcer risk assessment in patients with darkly pigmented skin. Professional Nurse. 19, 6, 339- 341.

Stotts N (1998) Promoting wound healing. In Kinney MR, Packa DA, Dunbar SB (Eds) AACN’s Clinical Reference for Critical Care Nursing. Fourth edition. Mosby, St Louis MA.

Tomaselli N, Granick M (2000) Team approach to a wound care programme. In Bryant R (Ed) Acute and Chronic Wounds: Nursing Management. Mosby, Philadelphia PA, 495-502.

Torrance C (1983) Pressure Sores: Aetiology, Treatment and Prevention. Groom Helm, London.

Versluysen M (1986) How elderly patients with femoral fracture develop pressure sores in hospital. British Medical Journal. 292, 6531, 1311-1313.

Waterlow J (1988) Prevention is cheaper than cure. Nursing Times. 84, 25, 69-70.

Wee V, De Neve B, Grypdonck M, Defloor T (2004) Observation of non-blanchable erythema. EPUAP Review. 6, 2, 48.

Witkowski J (1993) Purple ulcers. Letter. Journal of ET Nursing. 20, 3, 132.

Woolf N (1998) Pathology: Basic and Systemic. WB Saunders, London.

Author

Elaine Bethell is tissue viability clinical nurse specialist, Sandwell and West Birmingham Hospitals NHS Trust, City Hospital, Birmingham. Email: [email protected]

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