Sylvie Hampton, MA, BSc (Hons), DpSN, RGN.
Independent Tissue Viability Consultant in Eastbourne
The skin is the largest organ in the body, weighing 2.7kg in the average adult (Hampton and Collins, 2003). It contains specialised cells and structures and acts as a protective barrier (see Figure 1).
With ageing, the skin becomes thinner, more fragile, and more susceptible to injury. The progressive normal and physiological ageing changes increase the risk for chronic health problems such as a low albumin level or chronic infection that are associated with open wounds and delayed healing (Boynton et al, 1999). Hence, chronic wounds are a frequent problem in elderly people.
The cost of managing chronic wounds in terms of staff time and dressing materials is phenomenal (Benbow, 1995). In chronic wounds, the orderly sequence of events seen in acute wounds becomes disrupted or ‘stuck’ at one or more of the different stages of wound healing (Schultz et al, 2003) and it is at this point that protection of the skin that surrounds the wound takes on an importance in the process of wound healing.
Chronic wounds are characterised by loss of skin or underlying soft tissue and do not progress toward healing with conventional wound-care treatment (Frantz and Gardner, 1994). Care of the skin surrounding wounds is difficult as many factors (see Table, opposite page) can negatively impact on the wound-healing process, leading to recalcitrant wounds (Ennis and Meneses, 2000). Therefore wounds should not be considered in isolation (Dowsett, 2002) or without consideration of the local and systemic factors that will affect healing.
Maceration of the surrounding skin
Excessive wound exudate or other bodily fluids, such as urine or sweat, can cause skin maceration around a wound, which may delay healing and lead to other complications (Cutting and White, 2002). Maceration occurs when fluid is present on the skin for a long period. This may be due to a dressing that is not absorbent enough to contain fluid from the wound or in a dressing that does not ‘lock’ the fluid away. A cycle of moisture, friction, bacteria and breakdown may then be established (Fiers, 1996).
The practitioner must balance wound-healing principles with the possibility that selected treatments may have unwanted consequences. A wound must be kept moist to enable healing (Winter, 1962) and yet moisture can cause maceration (see Box, right).
A study undertaken by Breuing et al (1992) compared wound healing between a liquid-tight vinyl chamber and exposed wounds. Healing of fluid-treated wounds occurred without tissue maceration and showed less inflammation and less scar formation than healing of air-exposed wounds.
Moist wound healing is one of the most frequently used, but least understood, terms in wound care. No reliable operational definition exists of ‘too little’ or ‘too much’ wound surface moisture (Bolton et al, 2000). This lack of definition can lead to ‘wet’ dressings such as hydrogels being used inappropriately. In managing exuding wounds, particularly chronic wounds, failure to deal adequately with exudate can lead to exposure of the peri-wound skin to exudate and hence damage (White and Cutting, 2003). An exuding wound coupled with a wet dressing may increase the fluid loss onto the surrounding skin. Therefore the correct moisture balance - neither too moist nor too dry - at the wound-dressing interface must be achieved (Bishop et al, 2003).
There are two common reasons for excess exudate production (see Figure 2):
- In leg ulcers, hydrostatic pressure in the venous system causes the veins to distend. This widens the cell junctions and permits the passage of fluid into the wound surface (Majno and Joris, 1996). Compression therapy will assist with reversing the pathology that creates the problem
- Most chronic wounds are colonised by bacteria and this causes vaso-permeability to occur, increasing the loss of fluid (Majno and Joris, 1996). Appropriate use of dressings will assist with reducing bacterial colonisation.
Other reasons for fluid loss include diseases that disrupt homeostasis such as low protein levels which can cause fluid imbalance (Majno and Joris, 1996).
In addition to reducing exudate, the surrounding skin can be protected by liquid films which permit adherence of dressings while covering the ‘at risk’ area of skin. Campbell et al (2000) noted reduced skin redness in 96% of patients who were at risk and prevention of maceration in 94% of subjects when a film-barrier was used.
Choosing an appropriate dressing for a patient with a highly exuding wound is important as using the wrong dressing can lead to repeated dressing changes and soiling of clothes and bedding. This may undermine the patient’s faith in care (Anderson, 2002) as well as causing damage to the surrounding skin.
Most chronic ulcers are colonised by bacteria, such as staphylococci, enterococci, with Pseudomonas aeruginosa colonising 20-30% of all venous leg ulcers (Schmidtchen et al, 2003). Bacterial proteinases play a pathogenic role in chronic ulcers and the surrounding tissues. Schmidtchen et al (2003) demonstrated that elastase-producing Pseudomonas aeruginosa isolates degrade human wound fluid as well as human skin proteins.
Figure 3 shows a wound colonised by Pseudomonas aeruginosa which has damaged the local skin surrounding the ulcer. Hypothetically, Pseudomonas aeruginosa could release proteases and cytotoxic substances in the environment of chronic ulcers, thus negatively affecting wound-healing activity (Schmidtchen et al, 2001) and negatively affecting the surrounding skin, as can be seen in Figure 3. Here the pseudomonas has spilled out of the wound in the exudate and has come into contact with healthy tissue, with the potential to cause tissue destruction.
There are many dressings suitable for treatment of colonised wounds (see Table overleaf). Once bacterial colonisation is reduced, the exudate production will be lowered, thus reducing potential ‘overspill’ onto the surrounding skin.
Contact dermatitis is an altered state of skin reactivity induced by exposure to an external agent (Krasteva et al, 1999). ‘Eczema’ and ‘dermatitis’ are often used synonymously to denote a polymorphic pattern of inflammation of the skin characterised by erythematic, vesiculation and pruritus (Krasteva et al, 1999). Allergic contact dermatitis is a common and under-recognised phenomenon in patients with recalcitrant wounds (Siegel, 2000). It may be caused by topical antibiotics, adhesives in dressings, emollients, emulsifiers, and self-administered treatments (Siegel, 2000). Many different types of dressings contain similar components and therefore it is important to check for allergies and avoid the use of dressings with similar components.
It is also possible for a patient to become sensitive to their own exudates (Hampton and Collins, 2003). It is apparent that patients whose wounds are heavily exuding can develop erythema around the wound even under neutral foam dressings. There is a distinctive difference between redness from contact dermatitis and clinical infection. The redness from contact dermatitis has a uniform demarcation line that matches the dressing margins, whereas clinical infection does not have a uniform demarcation line but has an uneven and spreading line.
Emollients are essential in the management of dry skin conditions, but are often underused in general practice (Burr, 1999). The proper use of moisturisers along with rational use of topical corticosteroids is crucial to effective long-term management (Hanifin and Tofte, 1999).
The horny layer of the skin may be removed by tape stripping (Weigmann et al. 2003). A barrier film can be a useful adjunct in the prevention and treatment of injury to skin Campbell et al (2000). Barrier films include Cavilon (3M) and LiquiShield (Medlogic).
Protection of the surrounding skin will reduce the potential for wounds to increase in size. There are many different types of wound dressings available to deal with the colonisation and over-production of fluid within a wound bed. Treating the underlying cause of excessive exudate generation and selecting appropriate dressings are the keys to effective management (Watret, 1997). It is only by becoming familiar with the various presentations of maceration, and with prophylactic treatment measures, that practitioners can avoid the increased costs and morbidity associated with it (White and Cutting, 2003).
The European Pressure Ulcer Advisory Panel’s Pressure Ulcer Treatment Guidelines include the following on dressing use
Use a dressing which maintains a moist environment at the wound/dressing interface. Determine the condition of the wound and establish treatment objectives before selecting dressing, for example grade, wound bed, infection, level of exudate, pain, surrounding skin, position and the patient’s preference.
Dressings should be maintained in situ as long as is clinically appropriate, and in line with manufacturers’ recommendations. Frequent removal could damage the wound bed. Dressings that harden should not be used since they may cause pressure injuries. Dressings may need to be removed daily to ensure that the wound is not getting worse because of inadequate pressure relief.
Leakage or strike-through causes a break in the barrier that the dressing provides to external contamination. Therefore if strike-through occurs the dressing should be changed. If strike-through occurs frequently it may be appropriate to reconsider dressing choice. The use of wound protocols based on good evidence will avoid unnecessary changes of dressing. Regular observation will demonstrate the progress of healing and if there is a need to change treatment objectives.
Available at: www.epuap.org/gltreatment.html
Author’s contact details
Sylvie Hampton, MA, BSc (Hons) DpSN, RGN, Viability Consultant, Tissue Viability Consultancy Service, The Masters Building, Dental Practice Board, Compton Place Road, Eastbourne, East Sussex BN20 8AD; email: firstname.lastname@example.org
Anderson, I. (2002)Practical issues in the management of highly exuding wounds. Professional Nurse 18: 3, 145-148.
Benbow, M. (1995)Extrinsic factors affecting the management of chronic wounds. British Journal of Nursing 4: 9, 534, 536-538.
Bishop, S.M., Walker, M., Rogers, A.A. et al. (2003)Importance of moisture balance at the wound-dressing interface. Journal of Wound Care 12: 4, 125-128.
Bolton, L.L., Monte, K., Pirone, L.A. (2000)Moisture and healing: beyond the jargon. Ostomy Wound Management 46: (suppl 1A), S51-S64.
Bowler, P.G., Jones, S.A., Davies, B.J. et al. (1999)Infection control properties of some wound dressings. Journal of Wound Care 8: 10, 499-502.
Boynton, P.R., Jaworski, D., Paustian, C. (1999)Meeting the challenges of healing chronic wounds in older adults. Nursing Clinics of North America 34: 4, 921-932(vii).
Breuing, K., Eriksson, E., Liu P., et al. (1992)Healing of partial thickness porcine skin wounds in a liquid environment. Journal of Surgical Research 52: 1, 50-58.
Burr, S. (1999)Emollients for managing dry skin conditions. Professional Nurse 15: 1, 43-48.
Campbell, K., Woodbury, M.G., Whittle, H. et al. (2000)A clinical evaluation of 3M no sting barrier film. Ostomy Wound Management 46: 1, 24-30.
Cutting, K.F., White, R.J. (2002)Avoidance and management of peri-wound maceration of the skin. Professional Nurse 18: 1, 33-36.
Dowsett, C. (2002)The role of the nurse in wound bed preparation. Nursing Standard 16: 44, 69-76.
Ennis, W.J., Meneses, P. (2000)Wound healing at the local level: the stunned wound. Ostomy Wound Management 46: (suppl 1A), S39-S50.
Frantz, R.A., Gardner, S. (1994)Elderly skin care: principles of chronic wound care. Journal of Gerontology Nursing 20: 9, 35-44.
Fiers, S.A. (1996)Breaking the cycle: the etiology of incontinence dermatitis and evaluating and using skin care products. Ostomy Wound Management 42: 3, 32-40.
Hampton, S., Collins, F. (2003)Tissue Viability. London: Whurr Publications.
Hanifin, J.M., Tofte, S.J. (1999)Patient education in the long-term management of atopic dermatitis. Dermatology Nursing 11: 4, 284-289.
Krasteva, M., Kehren, J., Sayag, M. et al. (1999)Contact dermatitis II. Clinical aspects and diagnosis. European Journal of Dermatology 9: 2, 144-159.
Lansdown, A.B. (2002)Silver. I: Its antibacterial properties and mechanism of action. Journal of Wound Care 11: 4, 125-130.
Majno, G., Joris, I. (1996)Cells, Tissues and Disease: Principles of general pathology. Oxford: Blackwell Science
Ovington, L.G. (1999)Battling bacteria in wound care. Home Healthcare Nurse 19: 10, 622-631.
Schmidtchen, A., Wolff, H. Hansson, C. (2001)Differential proteinase expression by Pseudomonas aeruginosa derived from chronic leg ulcers. Acta Dermato-Venereologica 81: 6, 406-409.
Schmidtchen, A., Holst, E., Tapper, H., Bjorck, L. (2003)Elastase-producing Pseudomonas aeruginosa degrade plasma proteins and extracellular products of human skin and fibroblasts, and inhibit fibroblast growth. Microbial Pathogenisis 34: 1, 47-55.
Schultz, G.S., Sibbald, R.G., Falanga, V. et al. (2003)Wound bed preparation: a systematic approach to wound management. Wound Repair and Regeneration 11: (suppl 1), S1-S28.
Siegel, D.M. (2000)Contact sensitivity and recalcitrant wounds. Ostomy Wound Management 46: (suppl 1A), 65S-76S.
Thomas, S., Jones, M., Wynn, K., Fowler, T. (2001)The current status of maggot therapy in wound healing. British Journal of Nursing 10: (suppl 22), S5-12.
Watret, L. (1997)Know how … management of wound exudate. Nursing Times 93: 30, 38-39.
Weigmann, H.J., Lindemann, U., Antoniou, C. et al. (2003)UV/VIS absorbance allows rapid, accurate, and reproducible mass determination of corneocytes removed by tape stripping. Skin Pharmacology and Applied Skin Physiology.16: 4, 217-227.
White, R.J., Cutting, K.F. (2003)Interventions to avoid maceration of the skin and wound bed. British Journal of Nursing.12: 20, 1186-1201.
Winter, G.D. (1962)Formation of the scab and rate of epithelialisation of superficial wounds in the skin of a young domestic pig. Nature 193: 293-294.