Keith F. Cutting, MN, RMN, RN, DipN (Lond), CertEd(FE).
Principal Lecturer, Buckinghamshire Chilterns University College, Chalfont St Giles
Information on the following pages is brought to you as a joint initiative between Professional Nurse and the Journal of Wound Care. This will be a regular feature in each issue of Professional Nurse - offering a selection of the latest evidence-based practice in tissue viability. This paper is based on an article first published in Journal of Wound Care, April 1999 (8: 4, 200-201). To subscribe to the Journal of Wound Care, call 01858-438847 (£37 personal). Maceration is defined as the softening and breaking down of skin resulting from prolonged exposure to moisture (Anderson, 1998). It was first described by Charcot in 1877.
|Information on the following pages is brought to you as a joint initiative between Professional Nurse and the Journal of Wound Care. This will be a regular feature in each issue of Professional Nurse - offering a selection of the latest evidence-based practice in tissue viability. This paper is based on an article first published in Journal of Wound Care, April 1999 (8: 4, 200-201). To subscribe to the Journal of Wound Care, call 01858-438847 (£37 personal).|
Maceration is defined as the softening and breaking down of skin resulting from prolonged exposure to moisture (Anderson, 1998). It was first described by Charcot in 1877.
Causes of maceration
Maceration is caused by excessive amounts of fluid remaining in contact with the skin or the surface of a wound for extended periods. This fluid may be produced by the wound itself or it may be a result of urinary incontinence (Charcot, 1877) or excessive sweating. Excessive exposure to moisture may not only cause a wound to deteriorate but may also lead to breakdown of the skin. There is also a strong relationship between excessive skin moisture, whatever the source, and the development of pressure sores (Jordan and Clark, 1977; Thyagarajan and Silver, 1984). Cochrane (1990) states: ‘Skin should be kept clean and dry to prevent maceration because damp skin breaks down more easily under axial pressure and shear forces.’
The constituents of exudate from acute and chronic wounds vary. Chronic wound exudate contains proteases, which break down protein and will actively damage what may be otherwise healthy tissue (Hofman, 1997). Maceration is thus most likely to occur in chronic wounds such as leg ulcers, pressure sores, diabetic foot ulcers, fungating wounds and burns, particularly where occlusive therapy is used inappropriately (Figures 1-4).
Patients who are bedbound and are incontinent of urine are at risk of developing lesions on the buttocks or sacrum. In obese people, lesions may also occur between folds of skin. When maceration occurs, this may lead to an increase in the overall size of the lesion, accompanied by excoriation and pain (Nelson, 1997).
The formation of exudate
The normal wound healing response of inflammation leads to the development of local oedema. Histamine, released from damaged cells as a result of injury, causes plasma leakage from blood vessels and, as a consequence, oedema forms in adjacent tissues. This exudate seeps from the wound surface, initially taking the form of a clear, serous liquid. Later, it becomes more viscous and opaque, as it contains leucocytes and other constituents such as albumin, macrophages and cellular debris (Thomas, 1997a).
Although there is limited understanding of exudate formation, Thomas (1997b) lists some of the factors that may influence its production (Box 1).
When a wound deteriorates, it may exhibit an increase in exudate production, accompanied by soiling of clothes or bedclothes, a change in odour, and possibly leakage from dressings.
The optimal level of exudate for a wound - The optimal level of exudate required to facilitate healing has not yet been determined. In addition, it varies with different types of wound. Increased levels of wound exudate may promote bacterial wound colonisation (Armstrong and Ruckley, 1997), particularly in wounds that are not appropriately managed. However, despite the possibility of dressings becoming soaked and ‘strike-through’ providing potential access for bacteria, there is little evidence to support the theory that this increases the risk of infection.
Moist wound healing has been shown to reduce the time required to heal a wound (Winter, 1962), but this work was carried out on partial-thickness wounds. It is therefore unclear whether or not this approach to management is appropriate for all types of wounds during all stages of healing.
Management of maceration
Exudate volume is traditionally categorised as light, moderate or heavy; however, this is a subjective approach which leads to problems with dressing selection (Thomas et al, 1996). Developing and improving the fluid-handling properties of dressings remains a major challenge.
Occlusive therapy, using films, foams and hydrocolloids, is synonymous with moist wound healing. However, modern fibrous dressings such as alginates and hydrofibres also offer moist wound healing. Hydrofibres have a gel block and prevent lateral wicking; they capture and contain exudate directly above the wound without compromising healthy skin (Armstrong and Ruckley, 1997).
Avoiding maceration from dressings - Occlusive therapy is often blamed for maceration and/or infection. However, maceration is a complication of moist wound healing only if the dressing regimen is used inappropriately. For example, it is important not to exceed the wear time beyond which the dressing can adequately cope with the production of exudate.
Dressing choice should reflect exudate levels, site and condition of the wound. To avoid or reduce maceration, hydrofibre or alginate dressings may be used to cover the peri-ulcer area generously and absorbent pads can then be applied as a secondary dressing to provide additional absorption.
Exudate from venous leg ulcers and resulting maceration of the skin can be controlled with compression therapy and elevation of the limb where clinically indicated.
Some practitioners advocate the use of Eosin as an astringent (Morgan, 1997) to dry macerated peri-wound skin. Others may use potassium permanganate on the wound itself to promote drying of the wound. It should be remembered that neither of these two approaches has been evaluated in comparative clinical trials.
If the wound is deteriorating, an evaluation of management and a careful assessment of the wound and the quantities of exudate produced should be carried out at every dressing change. The possible presence of infection should also be considered. Additionally, zinc paste bandages and zinc oxide paste BP are of value in providing protection to the skin by acting as a barrier agent. Patch-testing 48 hours before application is advisable in order to avoid sensitivity reactions.
Changing the type of dressing without a clinical reason should be avoided.
Use of medication - Antimicrobial agents have a role to play in preventing and/or managing maceration. Some practitioners use iodinated dressings to control heavily exuding wounds that are at risk of causing maceration of the surrounding skin. There is some empirical support for this approach but only if they are used for a short time, as prolonged use may interfere with resolution of the wound.
Corticosteroids are anti-inflammatory and vaso-constricting, and their use is controversial. When managing leg ulcers they appear chiefly to be of benefit on the peri-ulcer skin when wet eczema is present. There does not appear to be any evidence to support their use on the wound bed.
In general, the following rules of wound management should be followed to avoid or reduce maceration:
- Select dressing(s) according to exudate level
- Estimate the optimal wear time as objectively as possible
- Recognise and treat any infection
- Use compression therapy and elevation for appropriate leg ulcers.
Anderson, K.N. (ed.). (1998) Mosby’s Medical Nursing and Allied Health Dictionary St. Louis, Mo: Mosby-Year Book.
Armstrong, S.H., Ruckley, C.V. (1997)Use of a fibrous dressing in exuding leg ulcers. Journal of Wound Care 6: 7, 322-324.
Charcot, J.M. (1877)On Diseases of the Nervous System (63, 126). Sydenham: New Sydenham Society.
Cochrane, G. (1990)The severely disabled. In: Bader, D.L. (ed.). Pressure Sores: Clinical practice and scientific approach. London: Macmillan.
Hofman, D. (1997)Exudate: a nursing perspective. European Tissue Repair Society Bulletin 4: 2, 1-7.
Jordan, M.M., Clark, M. (1977)Report on Incidence of Pressure Sores in the Patient Community of the Greater Glasgow Health Board Area. Glasgow: University of Strathclyde.
Morgan, D.A. (1997)Formulary of Wound Management Products (7th edn). Haslemere: Euromed Communications.
Nelson, A. (1997)Is exudate a clinical problem? In: Cherry, G., Harding, K. Proceedings, Joint Meeting, European Wound Management Association and European Tissue Repair Society. Management of Wound Exudate. London: Churchill Communications Europe.
Thomas, S. (1997a)Assessment and management of wound exudate. Journal of Wound Care 6: 7, 327-330.
Thomas, S. (1997b)Exudate: who needs it? In: Cherry, G., Harding, K. Proceedings, Joint Meeting, European Wound Management Association and European Tissue Repair Society. Management of Wound Exudate. London: Churchill Communications Europe.
Thomas, S., Fear, M., Humphreys, J. et al. (1996)The effect of dressings on the production of exudate from venous leg ulcers. Wounds 8: 5, 145-150.
Thyagarajan, C., Silver, J.R. (1984)Aetiology of pressure sores in patients with spinal cord injury. British Medical Journal 289: 1487-1490.
Winter, G.D. (1962)Formation of the scab and rate of epithelialisation of superficial wounds in the skin of the young domestic pig. Nature 193: 293-294.