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Skin and pressure area care for patients at the end of life
  1. Jane McManus, Deputy Ward Manager
  1. Rugby Ward, St Christopher’s Hospice, London. Email: j.mcmanus{at}stchristophers.org.uk

Abstract

Dying patients are at increased risk of skin breakdown. Skin breakdown in the dying patient may be an inevitable outcome of dysfunction of organs and blood circulation associated with the dying process. This article aims to explain the function and structure of the skin, highlighting factors affecting that structure and function, particularly in relation to the dying patient. Guidelines are offered to assist the healthcare worker to manage skin care for dying patients more effectively, taking into account the inevitability of skin failure that may be a feature of dying. The guidelines, developed by St Christopher’s Hospice, London, are based on clinical research findings and the experience of end-of-life care. They are designed to assist the healthcare worker to assess and cleanse the dying patient’s skin and position the patient to reduce the detrimental effects that may be caused by sustained skin compression. Conflicts of interest: none.

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Patients with advanced illness are at significant risk of skin damage (Henoch and Gustafsson, 2003; Langemo et al, 2007). Cancer patients with cachexia (weakness, debilitation, weight loss and muscle atrophy) are at particular risk due to their catabolic state. Catabolism is a metabolic process by which the body breaks down its own complex molecules in order to release energy. Pressure areas are vulnerable to damage in the catabolic patient because the body’s subcutaneous fat reserves are depleted, which increases the compression of the skin between the bones and a compressing surface. Catabolic patients cannot repair damaged tissue and tend to be protein-malnourished, have reduced oxygen absorption and mobility and dehydration, all of which increase the risk of pressure damage. The skin of patients with reduced intake of nutrition and hydration, whose mobility is compromised, is also vulnerable.

All of the above often occur at the end of life (Langemo et al, 2007) and in patients with advanced disease (Naylor, 2005). Langemo and Brown (2006) use the term ‘skin failure’ to describe hypo-perfusion of the blood vessels in the skin, alongside severe dysfunction or failure of other organ systems. This lack of perfusion and organ failure is often associated with dying (Langemo and Brown, 2006). As such, pressure ulcers occurring at the end of life may not be preventable or respond to treatment (Langemo and Brown, 2006).

One of the challenges of caring for patients with advanced disease is to provide holistic nursing care that promotes the integrity of fragile skin, while attending to the patient’s other symptoms. For example, a breathless patient may wish to sit up in bed or in a chair to ease dyspnoea, but this practice increases pressure and shear forces on the sacrum and heels. A patient in pain may prefer to lie in one particular position, placing particular areas of skin under prolonged pressure, increasing the risk of skin damage. Patient comfort and skin damage prevention strategies can be opposing forces during end-of-life care (Henoch and Gustafsson, 2003).

Providing good skin care at the end of life has three main components:

  • ▶▶ Assessment

  • ▶▶ Cleansing

  • ▶▶ Positioning.

This article will examine these components, but will begin by considering the anatomy and functions of the skin.

Anatomy and function of the skin

The skin consists of three layers, the epidermis, dermis and subcutaneous tissue, known as the subcutis, with blood vessels, nerves, sweat glands, sebaceous glands and sensory receptors (Figure 1).

Figure 1.

Diagrammatic representation of the skin.

The epidermis

The epidermis comprises five layers (Table 1). Epidermal cells are formed in the basal cell layer and then migrate through the spinous and granular layers before reaching the outer horny layer. This process takes about 28 days (Powell and Soon, 2002). By the time the cells reach the horny layer, they are flattened and hardened by the presence of keratin. They have lost their nucleus and become dead cells (Peters, 2005). The stratum corneum provides a protective barrier against physical and chemical attack. It prevents water loss by evaporation and its water-binding ability. It maintains skin elasticity and firmness.

Table 1

Layers of the epidermis

The dermis

The dermis contains blood vessels that supply the epidermal cells with nutrients. It provides structural and nutritional support to the epidermis. The blood circulation of the dermis is essential for body temperature regulation, the provision of oxygen and nutrients to the basal layer of the epidermis and the removal of toxins and waste products (Holloway and Jones, 2005).

Hair follicles, sebaceous and eccrine glands originate from the dermis. The sebaceous glands secrete sebum, an oily substance that lubricates the skin surface and maintains a slightly acidic surface of the skin (between pH 4.0 and 5.5) (Cooper and Gray, 2001). Eccrine glands secrete sweat in response to heat and stress (Holloway and Jones, 2005).

The subcutis

The subcutaneous tissue supports the dermis. It contains adipose (fat) tissue, connective tissue and blood vessels. It insulates the body and protects from physical shock as well as providing a high-energy source when the fat is metabolised (Holloway and Jones, 2005).

The function of skin secretions

Skin secretions and melanin provide chemical protection to the body (Copson, 2006). Melanin is a skin pigment produced by cells called melanocytes. It provides some protection to the skin from the sun’s ultraviolet light. In response to sun exposure melanocytes increase the production of melanin. Sebum (an oily secretion from the sebaceous glands) contains chemicals that can destroy bacteria (Copson, 2006).

The skin is a metabolically active organ. Its protective function is often taken for granted until damage occurs and its integrity is threatened or broken. The various components of the skin have particular functions as shown in Table 2.

Table 2

The function of skin components

Skin integrity

Factors that affect skin integrity are outlined in Table 3. Health problems such as diabetes and underlying skin conditions such as eczema and dermatitis, along with medications such as corticosterioids, may also affect skin integrity (Fore-Pfliger, 2004). From the literature, it would appear that there are three primary contributing factors associated with pressure ulcer development at the end of life:

  • ▶▶ Older age

  • ▶▶ Reduced mobility

  • ▶▶ Reduced physical activity (Galvin, 2002; Henoch and Gustafsson, 2003).

Table 3

Factors affecting skin integrity

Age-related changes to the skin

The epidermis thins by 50% from the age of 60 years (Peters, 2005). The surface between the epidermis and dermis, woven closely together in folds in younger skin, flattens out, increasing the skin’s fragility and susceptibility to shearing (Baranoski, 2000). Changes to the collagen in the dermis also occur making it less elastic and resilient, thus skin becomes looser and more prone to wrinkling (Holloway and Jones, 2005). These changes increase the skin’s fragility and vulnerability. Skin vascularity reduces with age. It tends to become more easily dehydrated. Sebum production and sensation is also reduced in the older person (Desai, 1997).

Incontinence

It is well established that maceration (softening by moisture) of the skin increases the skin’s fragility and threatens its integrity (Gray et al, 2002). Faecal and urinary incontinence can cause skin maceration (Gray et al, 2002). Ammonia in urine is caustic to the skin, causing irritation and damage (Holloway and Jones, 2005). It also acts as a nutrient for bacteria on the surface of the skin, enabling them to multiply (Holloway and Jones, 2005). Pathogenic fungi also grow in the warm, moist environment created by incontinence (Gray et al, 2002) and may be present in fiery, red, itchy and burning skin rashes (Holloway and Jones, 2005).

The provision of good skin care

St Christopher’s Hospice, London, has developed clinical guidance for good skin and wound care (St Christopher’s Hospice Skin and Wound Group, 2006). These have been developed from clinical research and experience of end-of-life care. The guidance has three cornerstones: assessment, cleansing and pressure reduction.

Assessment

The National Institute for Health and Clinical Excellence (NICE) guidelines (NICE, 2003) recommend that skin assessment should include an assessment of the following signs:

  • ▶▶ Persistent erythema (redness)

  • ▶▶ Non-blanching erythema

  • ▶▶ Blisters

  • ▶▶ Discolouration

  • ▶▶ Localised heat

  • ▶▶ Localised oedema and induration (firmness of the soft tissues due to inflammation).

If the erythema blanches (turns white) under light finger pressure, the microcirculation of the skin is intact, indicating the redness has been caused by a rush of arterial blood (hyperaemia) flowing to an area of skin that has been subjected to pressure (Scanlon and Stubbs, 2004). However, erythema that does not blanche indicates that the skin’s microcirculation has been damaged due to the intensity or duration of pressure. This is known as non-blanching erythema or hyperaemia. It is classified as a stage 1 pressure ulcer in most classification systems (Bethell, 2003).

Although looking for signs of erythema may be appropriate for patients with pale skin, in darkly pigmented skin, redness will not be apparent as an early indicator of skin damage (Scanlon and Stubbs, 2004). In this instance, the NICE guidelines (NICE, 2003) recommend noting the following signs:

  • ▶▶ Purplish/bluish localised areas of skin

  • ▶▶ Localised heat that, if tissue becomes damaged, is replaced by coolness

  • ▶▶ Localised oedema and localised induration.

Other changes associated with erythema are also caused by the inflammatory reaction that occurs when tissue is damaged. These include localised oedema, heat and pain. If the damage has caused necrosis (death) of local tissues, the area may feel cool, and there may be a bluish tinge to the skin. If the damage has occurred to an area of soft tissue, the area may feel firm (indurated) due to oedema (Scanlon and Stubbs, 2004).

The St Christopher’s Hospice guidance suggests conducting a pressure ulcer risk assessment on admission, which is reviewed weekly or if the patient’s condition changes. The skin should be visually inspected during every episode of care. The observations and ensuing care requirements should be documented in the notes.

Skin cleansing

The use of soap and water for frequent cleansing of a patient’s skin leads to dryness and reduction of skin integrity (Dealey, 1995). Soap and water cleansing of the skin causes damage by:

  • ▶▶ Increasing the skin’s pH (making it more alkaline) (Kirsner and Froelich, 1998). This may encourage the proliferation of bacteria that prefer an alkaline environment (Voegeli, 2005)

  • ▶▶ Removing sebum and natural moisturising factors from the skin surface (Peters, 2001). This may make the skin more vulnerable to damage from fluids, shear and friction (Peters, 2005)

  • ▶▶ Depositing soap residues on the skin that remain after washing. Soap may also cause chemical irritation through the interaction of perfumes and the skin (Kirsner and Froelich, 1998)

  • ▶▶ Increasing friction damage from repeated drying of the skin after cleansing.

Incontinence dermatitis caused by repeated moistening, further weakens the skin, causing it to become even more susceptible to friction. Guidance from the European Pressure Ulcer Advisory Panel (EPUAP, 1998) and NICE (2003) has acknowledged the importance of skin care in pressure ulcer prevention.

There have been several studies into the use of skin care protocols involving specific skin cleansing agents, barrier creams and films (Bale et al, 2004; Cole and Nesbitt, 2004). These studies have all demonstrated the benefits of skin cleansers that are non-soap-based, used alongside protective barrier creams or films, for the protection of vulnerable skin and the prevention of pressure damage.

The St Christopher’s skin cleansing guidance incorporates earlier work carried out at the hospice that highlighted the advantages of using an emollient, DiproBase (Schering-Plough), as a skin-cleansing and moisturising agent, rather than soap and other moisturising creams. DiproBase cream is an emollient (softens and soothes the skin) containing white soft paraffin, cetostearyl alcohol (emulsifying agent), liquid paraffin, cetomacrogol (emulsifying agent) and chlorocresol (antimicrobial preservative). It feels greasy on application to the skin, but is easily absorbed and provides an oily layer over the epidermis to reduce evaporation of water from the skin.

It is used in the hospice as a cleansing cream (dispersing it in washing water by applying some to a disposable dry cloth which is wrung out in the water to create a milky effect), as well as a moisturiser for the skin. Two or three drops of essential oil can be added to the cleansing solution as a fragrance, if the patient chooses. It is well tolerated by most patients, although the alcohol in DiproBase has been shown to be an irritant to some people’s skin (Peters, 2005).

As a barrier product between the skin and an irritant, such as urine or faeces, Cavilon Durable Barrier Cream (3M) is recommended in small amounts on skin in contact with moist substances, such as urine or faeces (St Christopher’s Hospice Skin and Wound Group, 2006). Over-application of these products may reduce the effectiveness of incontinence pads by clogging or interfering with their absorbency (Williams, 2001). If the skin is broken, Cavilon No Sting Barrier Film may be used instead. Cavilon can last up to 72 hours (Williams, 1998), but this is dependent on the frequency of skin cleansing that is required by the patient.

This guidance has standardised patient hygiene care. There is anecdotal evidence that patient skin integrity has improved since the introduction of the guidance, although a formal evaluation has not yet been conducted. Figure 2 shows the picture of the sacrum and buttocks of a 68-year-old man on admission to St Christopher’s Hospice. Figure 3 shows the same area 5 days after St Christopher’s hospice skin care guidelines had been followed.

Figure 2.

The sacrum and buttocks of a 68-year-old man on admission to the hospice. He was occasionally incontinent of urine and suffered from perspiration. In addition, his sacral area had been subject to friction due to the rough material of the tracksuit trousers that he liked to wear. The skin is roughened and beginning to get excoriated. There is also a small break.

Figure 3.

Five days later. His sacrum and buttocks had been treated in accordance with St Christopher’s Hospice’s good skin care policy, using DiproBase and Cavilon film. The sacral wound had been dressed with a silicone adhesive foam dressing.

Pressure reduction

Although some practitioners recommend turning vulnerable patients every 2 hours (Langemo et al, 2007), the NICE (2003) guidance for pressure ulcer prevention recommends that the frequency of repositioning should be determined by the results of skin inspection and individual needs rather than by a ritualistic schedule.

At the end of life, the patient’s symptoms, such as nausea or pain, may make effective repositioning difficult (Langemo, 2006; Langemo et al, 2007). However, efforts should still be made to minimise skin damage to vulnerable areas of the body. For example, with heels a pillow or heel protectors can be used to create elevation away from the compressing surface.

Some patients may refuse to be turned. While this will challenge carers, the patient’s wishes should be explored and respected.

The St Christopher’s Hospice guidance suggests that patients who are repositioned regularly experience reduced pressure damage and maintain movement in their joints. Repositioning may prevent contractures and provide the psychosocial benefits of human interaction. Patient positions should: be safe; suitable for the individual and their condition; reduce pressure generally, or on areas at particular risk; and be comfortable and acceptable to the patient, allowing for meals, rest periods, treatments and visitors. The frequency of position change will be based on assessment of risk, the general condition of the patient and the equipment to be used.

Conclusion

Good skin care at the end of life should aim to prevent the occurrence of damage where possible, minimising the worsening of that damage if it occurs, by the employment of an effective wound care regime. While the prevention of skin damage resulting from pressure, friction or incontinence should be the primary nursing goal, it is inevitable that some patients will experience a breakdown of their skin integrity at the end of life (Naylor, 2005; Langemo, 2006). Nursing care should then attend to the patient’s physical and psychological needs, providing reassurance and explanations to those who are alongside the patient that, while ‘skin failure’ does occur at the end of life despite good skin care (Langemo, 2006), its effects will be managed as effectively as possible to minimise the negative impact on the patient.

Key Points

  • ▶▶ End-of-life nursing should aim to prevent skin damage.

  • ▶▶ Despite good skin care, dying patients’ skin may still break down.

  • ▶▶ St Christopher’s Hospice has developed guidance on skin care for dying patients.

  • ▶▶ Non-soap-based cleansing products should be used in conjunction with barrier creams to maintain skin integrity of the dying patient.

References

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