EPI DEM IOLOGY

Drugs & Aging 2 (I): 42-57, 1992 II 70-229X/92/000 1-0042/$08.00/0 © Adis International Limited. All rights reserved. ORA17l

Pressure Sores Epidemiology and Current Management Concepts J.B. Young and S. Dobrzanski Department of Health Care for the Elderly, St Luke's Hospital, and Department of Pharmacy, Bradford Royal Infirmary, Bradford, West Yorkshire, England

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Summary I. Whose Problem? 2. Consequences of Pressure Sores 2.1 Patient Morbidity 2.2 Expense 2.3 The Need for Prevention 3. Epidemiology 3.1 Incidence and Prevalence 3.2 Proximal Femoral Fracture 3.3 Mortality from Pressure Sores 4. Mechanisms of Pressure Sore Formation 4.1 Types of Sore and Sites Affected 4.2 Point Pressure 4.3 Shear and Friction 4.4 Capillary Occlusion 4.5 Spontaneous Movement 5. Prevention of Pressure Sores 5.1 Risk Assessment 5.2 Equipment to Prevent Pressure Sores 5.2.1 Airwave System 5.2.2 Polystyrene Bead Bed System 5.2.3 Other Systems 6. Management of Pressure Sores 6.1 Agents Used to Halt Deterioration of Damaged Skin (Type 1 Sores) 6.2 Debridement 6.2.1 Gauze 6.2.2 Absorbent Microbeads 6.2.3 Creams and Ointments 6.2.4 Enzymatic Debridement 6.2.5 Hydrogen Peroxide 6.2.6 Chlorinated Solutions 6.3 Antiseptics 6.4 Antibiotics 6.5 Dressings 6.5.1 Fabric Dressings

Pressure Sores

53 53 53

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Summary

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6.5.2 Foam Dressings 6.5.3 Calcium Alginate Dressings 6.5.4 Polyurethane Film Dressings 6.5.5 Hydrogels 6.5.6 Hydrocolloid Dressings 6.5.7 Antiodour Dressings 7. Other Treatments 8. The Rational Choice of Treatment

Pressure sores remain common, with a prevalence of 5 tQ 9% and more than 70% occurring in patients over 70 years of age. They are often falsely ascribed to poor nursing care, but can more usefully be regarded as a potentially preventable complication of an acute immobility illness. Prevention involves identification of patients at risk, appropriate nursing care measures and the use of special equipment. Much of the special equipment is excessively complex and not validated by clinical trial work. The airwave system, polystyrene bead bed system and Vaperm® mattress have been best studied and are effective. Management of the established sore involves treatment of the underlying medical condition(s), attention to hydration and nutrition, prevention of further tissue trauma and the use of special dressings and procedures which facilitate the inflammatory repair response. There is considerable doubt about the use of 'traditional' wound applications such as gauze or chlorinated lime and boric acid solution ('Eusol'). An extensive range of newer products is now available but these have not yet been subjected to controlled clinical trials. A useful starting point is to classify pressure sores into 4 clinical types depending on amount of tissue damage and depth of ulcer. The least severe sore (type I) can be protected using polyurethane film dressings. Deeper ulcers (types 2 and 3) can be easily and quickly treated by hydrocolloid or alginate dressings which optimise the local wound environment, thus facilitating tissue repair. However, there may be no satisfactory dressing for sacral (near-anal) sores which are more difficult to treat than those at other body sites because of dressing detachment. Cavity ulcers (type 4) can be managed with silastic foam or hydrocolloid or alginate dressings. Debridement of necrotic material is best done manually by scalpel/scissors, although streptokinase/streptodornase (Varidase Topical®) may also help if used correctly. Antiseptics have little part to play and ulcers are best cleaned with warm normal saline. Systemic antibiotics are indicated only when surrounding cellulitis is present, although metronidazole is useful for malodorous sores.

Pressure sores are not a new phenomenon. They have been found in Egyptian mummies, and John Hunter in the eighteenth century recognised that they were caused by an uneven distribution of body weight (Editorial 1973). Yet, despite considerable progress in the understanding of pressure sore prevention and treatment, they remain a challenge. Indeed, pressure sores have been referred to recently as an epidemic (Livesley 1987) and they have been the focus of a King's Fund Working Party in the United Kingdom (King's Fund Centre 1990).

1. Whose Problem? There are 2 pervading myths concerning pressure sores which arguably impede optimal management. They are both to do with 'ownership' of the problem in the clinical setting. The first is the widely held view that pressure sores are a nursing problem; that pressure sores belong in the territory of nurses. This is an unfortunate view, since in practice it has led to an implied (but erroneous) belief that pressure sore formation equates to poor nursing care. As will be seen, pressure sore for-

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mation is complex and multifactorial. However, this uniprofessional nursing perspective of pressure sores is changing (Sutton & Wallace 1990). The need for a team approach with a medical contribution is increasingly recognised (Editorial 1990). The second aspect of pressure sore folklore is that they are a geriatric problem, the implication being that they are an irritation about which little can be done other than removal of the patient and sore to a department of geriatric medicine. There are several reasons why this view cannot be sustained. Demographic changes, especially for those aged over 80 years, will mean that the trend established during this century of an increasing proportion of elderly people will continue for the next 30 years. The scale of this change has meant that older people are not the exclusive province of departments of geriatric medicine, but that elderly people now comprise the largest group under treatment for most hospital departments. Pressure sores as a complication of acute immobilising illnesses in such patients are therefore a concern of all wards and departments. Moreover, improved primary care and community support increasingly enable sick elderly people to be supported at home. The necessary expertise, techniques and equipment for pressure sore management thus also need to be available in the community. It is now recognised, therefore, that adequate prevention and treatment strategies for pressure sores require not a fragmented disjointed approach, but a centrally planned coordinated district-wide strategy (King's Fund Centre 1990). Unfortunately, few health districts in the UK as yet aspire to meet this challenge, although there are pressing reasons why they should.

2. Consequences 0/ Pressure Sores 2.1 Patient Morbidity Pressure sores are associated with considerable patient morbidity. The lesions are usually painful, distressing and, particularly for frail elderly people, may sufficiently delay active rehabilitation measures to preclude return to independence. This means that the person may be unable to return

home, so that institutional care which is unwanted by the patient becomes necessary. 2.2 Expense Pressure sores are expensive in terms of extra resources utilised. It has been estimated that the costs of pressure sore treatment to the National Health Service in the United Kingdom are £150 million per year (Scales et al. 1982) or approximately £750 000 per district (Livesley 1986). A full thickness sacral sore extends hospital stay by over 25 weeks at an estimated cost of £26 000 (Hibbs 1982). This cost is clearly considerable and includes extra staffing, pharmaceuticals and dressings, and hospital overheads. The opportunity costs (alternative uses of resources) are correspondingly considerable. For example, for each sacral pressure sore which is prevented, it is possible to undertake 16 total hip replacements (Hibbs 1982). The increasingly litigious climate has also prompted some patients or their families to sue Health Authorities when a pressure sore has occurred. Several cases are currently before the UK courts but damages of £100000 have already been awarded against the Health Authority concerned (Robertson 1987). 2.3 The Need for Prevention The above factors reinforce the necessity for a preventive focus to pressure sores. The effects of such a focus, properly resourced and executed, could be dramatic since it has been judged that the large majority of sores are preventable (Hibbs 1982). Currently, however, health authorities seem to have become locked into providing expensive treatments for a potentially preventable condition. Thus, a profound cultural change is needed to disentangle the large sums of money used for treatment and to invest in preventive approaches including readily available effective equipment (Young 1990).

3. Epidemiology 3.1 Incidence and Prevalence The well developed image of pressure sores occurring only in patients in geriatric long stay establishments lingers, but is far from the truth. Sir

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Pressure Sores

Arthur Thompson (1949) in his Lumlean lecture given to the Royal College of Physicians remarked on the infrequency of pressure sores in patients residing in long stay wards. It remains a rare event today. Most pressure sores are to be found in patients in acute hospital wards, although there are few large scale studies which have sought to systematically evaluate the problem. Norton and colleagues (1962) observed 250 consecutively admitted patients to a geriatric unit in the early I 960s. The incidence of pressure sores was 24%, with the large majority occurring during the first 2 weeks, indicating the relevance of acute illness as the major event in the genesis of pressure sores. Prevalence rates have been recorded between 5.3% (hospital study of 2513 patients) [Barbenel et al. 1977] and 8.8% (hospital and community study of 10 710 patients) [Hawthorn & Nyquist 1987]. These studies have demonstrated the particular suseptibility of elderly people. Approximately 70% of pressure sores occur in patients aged over 70 years. However, some groups of younger people have also been highlighted, for example those with cerebral palsy and multiple sclerosis (Barbenel et al. 1977) or spinal cord lesions (Bliss 1988). In the latter group, up to 85% may develop pressure sores (Reuler & Cooney 1981). 3.2 Proximal Femoral Fracture A notable subgroup of the elderly is patients with a fractured neck offemur. The last decade has seen an unexplained epidemic of proximal femoral fracture (Editorial 1989) and it has been paralleled by an epidemic of associated pressure sores. Approximately two-thirds of patients hospitalised with a hip fracture develop pressure sores, especially on the heels (Versluysen 1986). The reasons have been carefully documented and all are related to the hospital environment: prolonged periods lying on high pressure surfaces in casualty and in theatre, and enforced immobility due to pain and traction, compounded by delay in surgical repair, have been identified as the principal factors (Versluysen 1986).

3.3 Mortality from Pressure Sores The mortality directly ascribable to pressure sores is difficult to determined, because for many patients the underlying medical condition(s) are lifethreatening in their own right. Clinically, it is possible to identify those patients in whom pressure sores seem to be a component part of a sometimes protracted terminal illness, and a second separate group of patients who recover from a discrete acute illness but develop pressure sores as a complication of immobilisation. Examples of the first group would be patients with an advanced dementia or with multiple strokes. Classic work by Barton and Barton (1981) has shown how these 2 groups can be distinguished by thermography. Terminal sores (Barton classification type 3) are characterised by lack of thermal gradient between the margins of the sore and the surrounding healthy skin. In a sore with good healing potential (Barton classification type I), a temperature gradient exists with the ulcer margin being hotter by several degrees, indicating the presence of the inflammatory response and revascularisation. Such a classification is useful in a practical sense as it separates those patients for whom palliative care is appropriate and those patients in whom all efforts should be made to accomplish sore healing. There is no doubt, however, that pressure sores are accompanied by increased mortality. The relative mortality risk for elderly people with pressure sores in I study was found to be 5-fold higher than for similar elderly people without sores (Norton et al. 1962). The findings of an audit of deaths of patients with pressure sores revealed several anomalies (Davies et al. 1991). In a group of 107 patients consecutively admitted to geriatric wards, of the 25 patients who died, pressure sores were considered by the auditing team to be the primary cause of death for 6 patients and, for a further 6 patients, a major contributing factor. However, pressure sores were cited as a cause of death in only 2 death certificates. This discrepancy in death certification records concerning pressure sores is likely to produce a considerable underestimation of the importance of the condition in statistics. In-

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Drugs & Aging 2 (J) 1992

deed, in 1986 in the UK, only 171 death certificates recorded pressure sores as a cause of death with 1929 mentions. However, it can be estimated that there should be 20 000 mentions, with several thousand as the primary cause of death (Davies et al. 1991). This remarkable omission is probably explained in part by a professional defensiveness towards pressure sores, but it has disguised the real implications of pressure sores as a potentially lifethreatening condition.

4. Mechanisms of Pressure Sore Formation 4.1 Types of Sore and Sites Affected Pressure sores represent a continuum from an erythematous skin lesion to an open wound extending into the deep tissue. A number of different classification systems have been developed for pressure sores to give an indication of the extent of tissue damage which has occurred (fig. 1). Pressure sores occur most commonly over the sacrum (43%), trochanter (12%), heel (11%), ischial tuberosities (5%) and lateral malleolus (6%) [Petersen 1976]. These locations help explain the pathogenesis of pressure sores, since they are the bony prominences that support the body during lying, sitting and standing. It is when pressure is applied to these strategic points with sufficient intensity and duration that the integrity of the overlying skin becomes compromised and a sore develops. 4.2 Point Pressure It is not pressure per se that is the damaging factor, but the way in which it is applied (Neumark 1981). The body can withstand very high pressures if uniformly applied (for example in deep sea divers), but local, or point, pressure causes compression of subcutaneous structures around the unyielding bony prominence. This subcutaneous tissue distortion results in impairment or occlusion of capillary flow. Hence, a full thickness pressure sore deep within the dermis may originate with only the point of a wedge-shaped segment of damaged tissue presenting itself to the epidermis. Thus, most

Type 1: Nonblanchable erythema of intact skin. Type 2: Partial thickness skin loss in an abrasion, blister or shallow crater.

-hJ....f-1~--

1'"-:__~_-04-'-~~~___ r.-~-.,--A-::-~7..J~-

__

t=::::==::;:::=:::~?t-----

Epidermis Dermis Subcutaneous fat Muscle

Type 3: Full thickness skin loss extending down to, but not through, underlying fascia.

Type 4: Extensive destruction involving damage to muscle, bone or tendon.

_ _'T-~~--- Necrotic matter

Fig. 1. The 1989 American National Pressure Ulcer Advisory Panel classification of pressure sores.

full thickness sores appear to deteriorate shortly after they are first observed because the external visible lesion quickly enlarges to match its deeper base. 4.3 Shear and Friction Tissue deformation can also occur by shear. Shear develops most commonly in semirecumbent patients and is an important factor in many sacral and heel sores. As the semirecumhent patient slowly

47

Pressure Sores

slips down the bed, the mobile skin slides over the bony prominences where it is tethered to the overlying deep fascia. Eventually this relative movement causes stretching and deformation of blood vessels, reducing their cross-sectional area until ischaemia develops. Friction, a component of shear, may contribute separately to pressure sores by stripping superficial skin layers and causing ulceration. The superficial ulceration is liable to infection and may be further damaged if the patient is urinary incontinent. 4.4 Capillary Occlusion When the capillary pressure is exceeded by the externally applied force, tissue ischaemia develops. Animal experiments have shown that intermittent high applied pressure is less damaging to the skin than constant low applied pressure (Dinsdale 1973). The accepted data on capillary blood pressures come from Landis (1931) who measured a mean pressure in healthy volunteers of 32mm Hg in the arteriolar limb, but only 12mm Hg (range 16 to 18mm Hg) in the venous limb. However, it is not simply when these pressures are exceeded that ischaemia and tissue damage ensue. Recent work suggests that the applied surface pressures may be increased 3- to 5-fold at internal bony prominences (Le et al. 1984). There are clear implications for the prevention of pressure sores, particularly when it is realised that the they standard hospital mattress can produce point pressures of up to 150mm Hg (Lindan et al. 1965). Critical capillary occlusion pressures may be lower in thin patients· (Garber & Kouskop 1982). Also, there is evidence that they are lower in older people (Bennett et. al. 1981). This is probably because of changes in tissue tension in the latter. Tissue tension is the natural resistance to distortion within the subcutaneous structures. It acts therefore as a counterforce to externally applied point pressures helping to maintain patency of vessel structures. The interface pressure must exceed the summated value of tissue tension and intraluminal blood pressure for ischaemia to occur. There are 2 principal factors leading to reduced tissue tension

in older people. Firstly, there are age-related changes in the connective tissue making it less elastic and, secondly, older people are very susceptible to salt and water depletion (dehydration) which causes a profound lowering of tissue tension and is an important reason why older people are particularly vulnerable to pressure sore formation (Livesley 1986). 4.5 Spontaneous Movement Consideration of the principles of tissue deformation outlined above highlight the need for the patient to be constantly shifting position when lying or sitting. Exton-Smith and Sherwin (1961) showed the importance of small night-time displacements in the prevention of pressure sores. Healthy individuals moved over 150 times during sleep, while those who developed pressure sores moved less than 20 times each night. A comatose patient would be an obvious example of a bedfast and immobile patient. However, enforced bedfast immobility occurs more commonly on the orthopaedic wards during traction. Diseases such as stroke, which may impair cutaneous sensory awareness, Parkinson's disease in which there is an associated difficulty in axial rotation and painful conditions such as arthritis or postoperative periods all put the patient at risk by producing reduced spontaneous movements. Excessive night sedation may have an additional contributory effect (Crowley 1979).

5. Prevention of Pressure Sores Pressure sore prevention begins with good nursing care. Attention to hydration, nutrition, skin care and incontinence are important. Regular patient turning will restore subcutaneous perfusion and has been shown to produce a 75% reduction in pressure sores with any residual sores being superficial rather than deep (Norton et al. 1962). However, the modem high intensity ward environment, reduced nursing establishments and increased numbers of high risk elderly patients mean that 2 to 3 hour turning must be complemented by other methods (Editorial 1990). It is also difficult to see

Drugs & Aging 2 (I) 1992

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Table I. The range of special beds and mattresses to prevent pressure sore formation Mattress supplements (e.g. Spencoe ) Foam mattresses (e.g. Vaperm 8 ) Ripple mattresses Airwave systems (e.g. Pegasus®) Air support systems (e.g. Mediscuse ) 'Dry' flotation (e.g. Clinitron 8 ) Water beds Mechanical beds (e.g. Mecanaide e )

patient turning as a practical procedure for community patients.

which helps keep the skin dry (Denne 1979). A gelpad cushion has proved effective for protecting the sacrum, even during traction (Hughes 1986). The large range and complexity of some pressure-relieving systems is daunting (table I). Comprehensive reviews of the various systems are available (Bliss 1978; Young 1990), but a major deficiency has been that manufacturers have not been sufficiently active in evaluating their products to sustain their statements of effectiveness prior to marketing. A survey 'bf 48 products revealed that only 2 (the Pegasus® airwave system and the polystyrene bead bed system) have been subjected to randomised clinical trials to confirm their efficacy (Y oung & Cotter 1991).

5.1 Risk Assessment As many as 21 variables have been used to predict the occurrence of pressure sores with 98% accuracy (Williams 1972). Most commonly used indicators, however, are simple, and have been developed empirically and not subjected to vigorous validation or reliability testing. The Norton score was the first to be developed and is still widely used (Norton et al. 1962). Several other risk assessment methods are now available (Barratt 1988). However, none has been shown to have clear advantages over its competitors and the regular effective use of a particular method depends more on the commitment to it by a ward or department. Two points require emphasis. Firstly, there is little point in using a pressure sore risk assessment unless special action is taken for those patients identified as being at high risk for pressure sore formation. Secondly, a patient's condition and circumstances may change and it is important that the risk of pressure sore development is updated on these occasions.

5.2.1 Airwave System This has 2 layers of air cells rather than the I layer of the more familiar type of ripple mattress. The air cells are laid together as vertical pairs to provide up to 20cm of depth (fig. 2). Pressure is alternated by deflating every third cell in turn, each cycle lasting 7.5 minutes. The system is considerably more effective than a large cell ripple bed (Exton-Smith et al. 1982). 5.2.2 Polystyrene Bead Bed System Also of proven effectiveness is the polystyrene bead bed system which can be used on trolleys, theatre tables and hospital mattresses (Goldstone et al. 1982). It produces an instant 3-dimensional

5.2 Equipment to Prevent Pressure Sores The pressure-relieving characteristics of standard hospital mattresses are poor and can be improved by a range of additional products. Sheepskin fleeces reduce shear and improve vapour loss

Fig. 2. Airwave system; easy to use and suitable for preventing sores in high risk patients.

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Pressure Sores

Fig. 3. Low air-loss bed. Used for high risk patients in special departments such as intensive care units.

mould of the body contours which reduces point pressure and tissue deformation.

5.2.3 Other Systems Other systems have been less well studied. The Vaperm@ mattress has pressure-relieving characteristics which are considerably superior to the standard hospital foam mattress (Scales et al. 1982). It is constructed from 5 types of fatigueresistant polyethylene foam, each of varying densities, laid together with pressure-relieving and ventilation channels to produce a composite structure. Large cell ripple mattresses are effective (Bliss et al. 1967), although less so than the airwave system, and continue to suffer from poor reliability and therefore cannot be recommended (Stapleton 1986). Some pressure-relieving systems such as the low air-loss bed (fig. 3) are complex and expensive, but are of particular benefit in intensive care and burn units.

reference to the wound healing process. Many unusual sounding remedies have been proposed (table II). Some continue to have their advocates and have remained in use (Dobrzanski et al. 1983) despite concern that they may harm the patient. There are considerable difficulties with the methodology of trials to evaluate putative treatments. Variability in sore type, underlying disease, nursing care and patient factors need to be addressed. Fernie and Dorman (1976) illustrated some of these difficulties when they 'demonstrated' the apparently beneficial effect of 'healing rays' on pressure sores in a controlled trial. The 'healing rays' were, in fact, ordinary light emanating from a technical-looking machine. The treatment led to faster pressure sore healing because the new treatment approach invoked greater enthusiasm from the healthcare staff resulting in improved care of the test group of patients compared to the controls. The majority of the published studies involving pressure sore treatments have been either case history reports or open uncontrolled assessments. There have been some controlled studies published, but typically these have involved small patient numbers or the nature of the control treatment was not specified. There appear to have been no controlled clinical trials involving more than 100 patients. The aim of therapy is to produce a local wound environment which facilitates wound healing mechanisms. Such an environment is one that is moist, warm, clean and has an adequate blood supply. At the same time, every effort should be made

Teble II. Some proposed remedies for pressure sores

6. Management of Pressure Sores Ringer (1869) mentioned the use of yeast and carrot poultices for pressure sore treatment, and Burney Yeo (1894) recommended a thin plate of silver separated from a zinc plate by leather soaked in vinegar. These 2 illustrations characterise much of the approach to pressure sore treatment namely, treatment based on opinion rather than on objective information gained from clinical trials or

Allantoin from comfrey root Balsam of Peru Benzoin tinctures Chopped carrots Cod liver oil Chlorophyll Egg whites Gold leaf Honey Ice Insulin

Meat extracts Onions Salt baths Sugar Tannic acid Toasts Urea Vitamins A and 0 Washing machine powders (enzymatic)

Drugs & Aging 2 (1) 1992

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to prevent additional trauma to the ulcer site, both through avoiding use of unsuitable treatments and through providing good nursing care to halt further pressure or shearing damage to the existing sore. 6.1 Agents Used to Halt Deterioration of Damaged Skin (Type 1 Sores) There is often practical clinical difficulty in identifYing type 1 sores, since what at first appears to be a superficial area of skin damage may in reality mask massive irretrievable underlying cellular necrosis. However, several types of treatment have been proposed. It has been claimed that heparinoid cream is an effective means of preventing the breakdown of already compromised skin areas into deeper sores (Kataria & Datta 1982), although this requires confirmation. Polyurethane films such as Tegaderm® (3M) or OpSite® (Smith & Nephew) are also commonly applied to reddened skin areas. They reduce friction between skin and bedsheets and prevent skin maceration through their vapour permeable properties (Myers 1982).

directly to the ulcer surface absorbs exudate and becomes fixed by a fibrin network as the wound dries out. Removal of the gauze during a dressing change entails tearing away the scab adherent to the ulcer. This may damage healthy tissue, but will also clear necrotic matter, albeit somewhat painfully. 2. Wet-to-dry debridement. Here, before application to the sore, gauze is soaked in a liquid, usually saline, an an~ptic or a 'debriding' agent, such as the chlorinated solution 'Eusol'. Watersoluble coagulum coating the ulcer will then tend to dissolve and be absorbed by the wet gauze. As the dressing dries, the dry-to-dry debridement situation described above applies. 3. Wet-to-wet debridement. This technique is similar to the wet-to-dry method except that the gauze is not allowed to dry out on the ulcer surface due either to frequent dressing changes or use of an occlusive cover. Wet gauze is not as absorbent as dry gauze, but it is less likely to stick or to cause pain. Any debriding effect is more likely to be due to the liquid carried by the gauze than to any intrinsic mechanical debriding effect of the gauze.

6.2 Debridement Part of the inflammatory response encompasses liquefaction and removal of dead tissue as a prelude to re-epithelialisation. Extensive necrotic matter can be removed rapidly and effectively by surgical debridement. The role of pharmaceutical debriding agents is less well defined. It is not clear if any debriding agents directly liquefY necrotic matter. Some pharmaceuticals may act through the creation of a moist environment at the wound surface that facilitates autodebridement through activation of enzyme systems which are inactive when dry (Frithz 1984). 6.2.1 Gauze Many products used as debriding agents are applied to the sore on gauze, but often it is the gauze which acts as the primary debriding material. Gauze interacts physically with the wound surface and can cause debridement by 3 processes. 1. Dry-to-dry debridement. Dry gauze applied

6.2.2 Absorbent Microbeads Cadexomer iodine [Iodosorb® (Geistlich)] and dextranomer [Debrisan® (Kabi)] microbeads have typically been used on moist ulcers. When sprinkled onto open wounds, these products are thought to act through the formation of a gel which removes fluids, microbes and debris from the wound through capillary forces. The microbeads themselves also absorb wound exudate. The Drug and Therapeutics Bulletin (Editorial 1984) criticised trials on dextranomer microbeads as being poorly controlled and not amenable to statistical analysis. A paste incorporating dextranomer microbeads in macrogol [Debrisan Paste® (Kabi)] is also available. Frithz (1984) applied a 3mm layer of the paste and covered it with an occlusive plastic film. The paste was as effective as nonocclusive enzymatic debridement on moist ulcers and was more effective on dry ulcers. Frithz ascribed the debriding effect of Debrisan Paste® as principally due to occlusion.

Pressure Sores

6.2.3 Creams and Ointments Barton and Barton (1981) recommended the use of cetrimide 0.5% cream applied under Melolin® dressings (Smith & Nephew). Their technique involved surgically debriding the sore and filling it with the cream applied like icing. This was then covered with Melolin® and Micropore tape® (Smith & Nephew). They commented that while initially daily dressing changes might be required, twice weekly dressing changes might be possible as healing progressed. Ilonium® ointment (containing colophony 15.6%, phenol 0.1 %, turpentine oil 8%, venice turpentine 8.1% and thymol 0.03%) [Hamilton Laboratories] and Aserbine® cream (benzoic acid 0.024%, hexachlorophane 0.015%, malic acid 0.36%, salicylic acid 0.006%, propylene glycol 1.7%) [Bencard], which have been marketed for ulcer debridement, require well designed clinical trials to confirm effectiveness and to establish the best way to use these products. 6.2.4 Enzymatic Debridement

Varidase Topical® (containing streptokinase 100 OOOU and streptodornase 25 OOOU) [Lederle] has been used to clean sores covered with a hardened eschar. In vitro experiments have shown that these enzymes do possess measurable lytic effects on wound necroses, crust of fibrinoid purulent exudate and clotted blood, while causing no damage to healthy tissue (Hellgren & Vincent 1977). There are various application techniques for this product. It can be administered via subeschar injection or applied as a gel after being mixed with KY Jelly® (Johnson & Johnson). Most commonly, however, Varidase Topical® is applied on gauze and an occlusive cover is placed on top so as to maintain wet-to-wet debridement and prevent drying out. The necrotic ulcer surface may be 'crosshatched' to expose a greater area of substrate to the effects of the enzyme. Correct application of Varidase Topical®, therefore, requires some technical knowledge and thus it can be easily misused. Controlled clinical trials using a standard application technique are required to show if Varidase Topical® has any beneficial effect in cleaning necrotic sores. As Varidase Topical® should nor-

51

mally be used together with occlusion, it is uncertain to what extent any clinical benefit it may exert results from the occlusion rather than from any direct enzymatic effect causing liquefaction of necrotic matter. 6.2.5 Hydrogen Peroxide

Catalase in body tissue causes hydrogen peroxide 3% solution to froth and presumably dislodge some necrotic tissue. It is uncertain if this is worthwhile or simply 'ritualistic. Hydrogen peroxide may damage healthy tissues, and its use has been associated with the formation of oxygen emboli (Sleigh & Linter 1985). 6.2.6 Chlorinated Solutions 'Eusol' (chlorinated lime and boric acid) and 'Dakin's' (surgical chlorinated soda) solutions were first employed during the First World War (Lorrain Smith et al. 1915). The formulation of'Eusol' has changed over the years and commercially available stabilised sodium hypochlorite solutions such as Milton®, (Richardson-Vicks) diluted 1 in 4 so as to contain 0.25% available chlorine, or Chlorasol® (Seton Prebbles), which contains 0.3 to 0.4% available chlorine, are now in use. Despite widespread use for over 70 years on all types of dirty wounds, it is not clear if these solutions actually work. Typically, chlorinated solutions are applied to pressure sores on gauze using a wet-to-dry dressing technique. It may be that any wound cleansing effect resulting from the use of 'Eusol' ultimately results from the gauze on which they are applied, sticking to the ulcer surface and pulling away necrotic matter when it is removed at dressing changes. 'Eusol' and liquid paraffin, in contrast, is always a wet-to-wet dressing as the paraffin never dries out. With this product, it is tempting to speculate that it is the moist environment created at the ulcer surface which activates autodebridement. It is important to appreciate that chlorinated solutions kill healthy cells (Leaper & Simpson 1986). Ifulcer improvement occurs it may be despite their use rather than because of it.

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Table III. Antiseptics evaluated in open clinical trials

Agent

Reference

Acetic acid Benzoyl peroxide lotion 20% Hydrogen peroxide cream 1.5% Povidone-iodine solution 10% Povidone-iodine ointment Silver nitrate Silver sulfadiazine cream 1%

Phillips et al. (1968) Pace (1976) Millward (1988) Kucan (1981) Lee & Long (1976) Fantus (1935) Kucan (1981)

6.3 Antiseptics It is doubtful if antiseptics have any bactericidal action when used for swabbing (Thomlinson 1987); the contact time between antiseptic and microbe is simply too brief. A bactericidal effect is more likely when a wet-to-wet application technique is employed or where creams or ointments are applied, because more time is provided to achieve bacterial kill. However, when used in this way antiseptics such as merbromin (mercurochrome) may be toxic (Slee et a1. 1979) while gentian violet may be carcinogenic (Food Advisory Committee 1987). Apart from systemic toxicity, antiseptics may also inhibit wound healing locally (Deas et a1. 1986; Lineweaver et a1. 1985). The role of other commonly used products such as chlorhexidine or cetrimide in pressure sore care remains to be elucidated. The case for using antiseptic agents in pressure sore care is therefore not absolutely clear cut. The studies listed in table III show improved healing associated with the use of a range of antiseptic agents on infected sores, but all are either open assessments or when controls are included the patient numbers are small. It is unclear if possible benefit is through direct antibacterial action or because the physical properties of the antiseptic formulations create a better wound healing environment. Some dressings also incorporate antiseptics, such as povidone-iodine in Inadine® (Johnson & Johnson) or chlorhexidine in Bactigras® (Smith & Nephew). These products are used on pressure sores, but their effectiveness has not been assessed.

6.4 Antibiotics An infected sore is a potentially threatening event which demands sensitivity tests and appropriate parenteral antibiotics. A sore which is colonised probably does not require topical antibiotics or antibiotic dressings as these do not enhance healing and may induce microbial resistance (Aycliffe et a1. 1977) or produce allergic reactions, particularly when neomlCcin-based products are used (Fraki et a1. 1979). There has been only 1 published trial where a topical antibiotic other than metronidazole was used on pressure sores. Bendy et al. (1964) performed a randomised controlled trial where the effects of a 'standard' treatment regimen on 9 pressure sores were compared with the effect of the same treatment regimen, plus application of gentamicin cream 0.3% 3 times a day in 14 sores. After 1 week significant healing was seen in all the ulcers in the gentamicin group but in only 3 ulcers in the control group. It was concluded that suppression of bacterial growth was the decisive factor. Topical metronidazole can be effective on infected sores characterised by a foul odour typifying anaerobic infection (Gomolin & Brandt 1983; Jones et al. 1978). A commercially available gel containing metronidazole 0.8% has recently become available (Metrotop®, Farmitalia Carlo Erba). It is intended for once- or twice-daily application. Topically applied metronidazole may be used together with oral therapy (Baker & Haig 1981). 6.5 Dressings The ideal dressing has not yet been produced. Dressings for sacral sores are particularly unsatisfactory. Traditional dressings such as gauze are usually applied as part of a 3-layer system. There is the wound contact layer of gauze, a secondary absorbent covering and then a fixative. However, some modem dressings such as Granuflex® (Convatec) or OpSite® (Smith & Nephew) are 1 component and, hence, in theory are easier to use.

Pressure Sores

6.5.1 Fabric Dressings Gauze, and woven and nonwoven fabric equivalents, are the most common pressure sore dressings used in the United Kingdom on sores of all severities (David et al. 1983). However, there are important disadvantages including shedding of fibres and adhesion to the wound surface with consequent pain and damage to healthy tissues when the gauze has to be removed at dressing changes. Strike through, where exudate leaks through the dressing to contaminate the outside, and failure to maintain an environment conducive to wound healing, are also major drawbacks. Woven silicone fabric dressings, such as NA Silicone® (Johnson & Johnson), paraffin gauze dressings and perforated film dressings such as Melolin® avoid some of these disadvantages, but again there have been no formal clinical trials to demonstrate effectiveness. 6.5.2 Foam Dressings Foam dressings are used principally as cavity wound fillers. Ultimately, it is not known if packing a wound with dressing has any advantage over no packing (Bliss 1990). Foam dressings were designed to provide good conformability to the ulcer surface, while offering the wound some degree of physical protection and comfort. They produce a moist environment conducive to wound healing and absorb wound exudate, thereby allowing prolongation of wearing time. Silastic Foam Dressing® (Calmic) is the best studied of all of the type 4 ulcer cavity fillers (Harding 1985). The dressing is made up of an unpolymerised elastomer fluid which has to be mixed with a catalyst before being poured into the ulcer cavity. There it sets to form a polymerised silicone foam elastomer stent whose contours exactly match those of the ulcer. The stent can act as a dressing for up to a week, but has to be removed, disinfected and replaced twice a day during this period. Technically, therefore, the correct application of this dressing is not straightforward and it may readily be misused. It is not suited to all sores and should not be used in ulcers with large cavities but narrow openings. Lyofoam® (Ultra) is used both as a cavity filler

53

and as a dressing for type 2 and type 3 sores. The Lyofoam sheet is placed against the ulcer, allowing a margin of overlap on to the healthy skin around the sore, and a secondary dressing and fixative are then applied. The dressing maintains a moist wound environment and, relative to gauze, is nonstick. Intrasite Cavity Filler® (Smith & Nephew) consists of absorbent foam granules held in nonadherent (honeycombed surface) perforated film bags. The dressing has been designed to give significant absorbency and conformability while maintaining a moist, nonstick wound-dressing interface. Both this and Lyofoam® are currently undergoing evaluation in clinical trials of pressure sores. 6.5.3 Calcium Alginate Dressings Sorbsan® (Steriseal) and Kaltostat® (BritCair) are products which may be used on exudating sores of any severity. They are comfortable and do not adhere to the ulcer surface as they can be washed off with saline in which they are soluble. Recently, Jeter (1990) reported good pressure sore healing with Sorbsan® in an open assessment study. Several companies have brought out differently designed alginate products, some with an adhesive backing, some woven. The relative merits of these on pressure sores are untested. 6.5.4 Polyurethane Film Dressings These are typically used on minor, shallow sores. Trials assessing OpSite® in pressure sore care have involved small patient numbers and no controls. Manufacturer's data from an open assessment study of Tegaderm® on type I and type 2 sores are available. Data from an unpublished open assessment study of Tegaderm® which involved a larger number are available from the manufacturer. In this study tOO superficial sores in 70 patients were treated with Tegaderm® dressing and there was a 90% successful healing rate. Dressing detachment and leakage is often a problem on all but minor sores. Tegaderm Pouch® Dressing (3M) may be used on type 3 sores. Unpublished data are available from 3M giving details of a trial done on 51 patients

Drugs & Aging 2 (1) 1992

54

with type 3 ulcers where 26 were treated with Tegaderm® dressing and 25 were treated with Tegaderm Pouch® dressing. Although no differences in healing rate were seen, the pouch dressing was more likely to remain in place on the sore than the standard film. In this trial, Tegaderm Pouch® dressings were changed, on average, every 2 days. 6.5.5 Hydrogeis These agents are gels in which water is the major constituent of the disperse phase. They offer a good environment for wound healing, but all require secondary dressings and fixatives to stay in place on the ulcer surface. Geliperm® (Geistlich) has been subject to small open assessments on type 2 and type 3 sores, and Geliperm Granulate® on type 4 sores (data on file, Geistlich). Thomas (1986) has suggested that Scherisorb® (Smith & Nephew) may act as a wound cleaning agent through hydration of nonviable tissues. Further work is required to determine how well these products perform in practice on pressure sores. Scherisorb® and Geliperm Granulate®, like all cavity fillers, are liable to be squeezed out of the ulcer cavity if it is compressed by the patient during sitting, rolling or lying. 6.5.6 Hydrocolloid Dressings In essence, these products become nonadherent absorbent gels when in contact with a moist wound surface. Granuflex® (Duo Dermflexible®) [Squibb] is the best studied. It is convenient and effective for treating type 2 and type 3 sores on the heel, ankle, leg, hip and arm. Granuflex paste® can be used to treat cavity sores, but problems may arise with near-anal sores where dressing detachment, leakage of exudate and squeezing of the paste from a compressed ulcer cavity may prove a problem (Dobrzanski et al. 1990). Comfeel Ulcus® (Coloplast) is a similar product and some data concerning its use on pressure sores were reported by Samuelsen (1986) who used the dressing to treat pressure sores of varying severity in 40 patients. Healing of these sores in 33 patients was complete in an average of 43 days. Larger so-

res took longer to heal with one sore taking 214 days. Tegasorb® (3M) is a recently introduced oval shaped hydrocolloid dressing. The claim that the design of the dressing is such (oval-shaped dressing with thin tapered edges) that it is less prone to edge roll and detachment than other hydrocolloid dressings needs to be validated in independent clinical studies. 6.5.7 Antiodour Dressings Two approaches have been tried. Strong smelling fluid may be used to mask foul odour, and various types of activated charcoal dressing have been marketed, but are untested - perhaps due to difficulties in setting up clinical trials. Chlorophyll is probably ineffective as an antiodour agent (Brocklehurst 1953).

7. Other Treatments Pressure sore care involves many professional disciplines. Plastic surgery may be required for extensive deep sores and has been reviewed elsewhere (Keller & Shaw 1985; Lee & Thoden, 1985). Physiotherapy interventions (Fernandez 1988) and advice from clinical dietitians are similarly important. Correction of anaemia, and vitamin and mineral deficiencies, is vital for wound healing. Deficiency of zinc and ascorbic acid retards wound healing, and it has been shown that supplementation of deficient patients with zinc (Cohen 1968) or with ascorbic acid (Taylor et al. 1974) improves pressure sore healing.

8.. The Rational Choice of Treatment Any decision on how to treat a pressure sore might involve the following considerations: 1. Does the treatment work? 2. Does it provide a good wound healing environment? 3. Is it appropriate for the patient? This review suggests that few products meet these criteria. Most are poorly tested, many do not offer a good wound healing environment and it is

55

Pressure Sores

Table IV. Pressure sore management recommendations Pressure sore type

Recommended management

Type 1

Protect the ulcer from further trauma. Keep clean and observe

Type 2

Clean with saline. Apply hydrocolloid dressing on sore If the dressing edge rolls or detachment occurs consider continued excessive shear and review pressure sore prevention plan. If hydrocolloid dressing still does not remain in place or leaks, use an alginate dressing There may be no satisfactory dressing for near-anal ulcers

Type 3

As for type 2 above Some physical debridement of slough ulcers may be required. On sacral sores if leakage of exudate down natal cleft occurs try alginate dressing, but there may be no satisfactory dressing for near-anal ulcers

Type 4

Clean with saline. Physical debridement of gross quantities of necrotic tissues with scalpel or scissors may be required. Specialist debridement in theatre with antibiotic cover for infection may be necessary for problem ulcers such as trochanteric sores exposing bone and tendon. Hydrogel pastes may be used to facilitate debridement of smaller amounts of dead matter difficult to remove physically Assess the patient's suitability for plastic surgery which may in appropriate circumstances be the treatment of choice. If plastic surgery is not appropriate consider cavity fillers such as: Silastic foam on sores without a narrow opening Alginate dressings Hydrocolloid dressings for ulcers on limbs If dressings on sacral sores become detached through the patient's movements in bed, review pressure sore prevention plan Treatment of a massive sore may take many months. Sometimes treatment is part of terminal care, and products such as charcoal dressings and metronidazole gel for malodorous wounds should be used when aggressive debridement would be inhumane

For all sores

Ensure nutrition is adequate, including minerals, vitamins and iron Try to get the patient fitter, and prevent new sores forming

simply not known how successful most products will be for an individual patient. Selection oftreatment is therefore currently empirical, but a reasonable summary approach has been given in table IV.

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Correspondence and reprints: Dr J.B. Young. Department of Health Care of the Elderly. St Luke's Hospital. Bradford BD5 DNA, West Yorkshire. England.