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Pressure sore treatment: A literature review
hf. J. Nurs. Stud., Vol. 19, No. 4, pp. 183-191, 1982 Pruned m Great Britain
OOZO-7489/82/04018309 $03.00/O 0 1982 Pergamon Press Ltd.
Pressure sore treatment: a literature review JILL A. DAVID, M.Sc., B.Sc., S.R.N., H.V. Project Leader-Pressure Sore Project, Nursing Practice Research Unit, North wick Park Hospital and Clinical Research Cen Ire, Watford Road, Harrow Middlesex HAI 3UJ, U.K.
There is no lack in the amount of advice, both printed and verbal, available to the nurse inquiring about the treatment* of pressure sores. However, the number of different preparations-l- advocated and the variety of different reasons given to justify their use, suggests that there is little more basis for choice than personal preference, laced with unsubstantiated theory. In addition to the preparations applied to the sore, treatment must also include the devices used to remove the cause (pressure) and all the measures taken to improve the patient’s ability to heal. In the course of writing this review, the author has read around 100 articles which have appeared since 1965; selected because either they mention the treatment of established pressure sores, or they discuss the related subjects of the healing of open wounds, infection and wound healing, and experimental models for the assessment of treatment. Papers on the surgical treatment of sores have been omitted, as these do not come within the nurse’s sphere of influence. The papers to be discussed have been divided into five groups according to content, which lead progressively more deeply towards an understanding of the subject: (1) Lists and discussion of treatments advocated by the authors; (2) Detailed case histories; (3) Small uncontrolled clinical trials; (4) Controlled clinical trials; (5) Related subjects, theory or experimental, which contribute to a greater understanding of the subject. Each group forms an important stage in the development of understanding, though unfortunately it is only rarely that any one treatment can be followed through all the logical stages in this progression. Group 1: Lists and discussion
of treatments advocated
by the authors
The treatment of patients with pressure sores poses a number of problems, not least because every patient is an individual. The sore itself can range in depth from a superficial *Treatment j-preparation
when used in this article refers to anything which is done to the patient refers to any chemical which contacts the sore. 183
or the sore.
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deep fascia or bone; each presenting a range of size and complications such as infection and the presence of necrotic tissue. This is reflected in the range of preparations listed and local policies reported in the first group of papers. Some give descriptions of new methods available (Hodkinson, 1965). Hodkinson’s paper is short and states the advantages the author experienced using a new method (aerosol) for the application of tincture of benzoin, a very old method of treatment. Similarly, less well known methods are described: air current treatment (Davis and Dong Sun Chu, 1974); cold therapy, limited to experience with children (Marshall, 1971); hyberbaric oxygen (Torelli, 1973); topical metronidazole (Jones et al., 1978); hydrotherapy and topical collagenase (Vetra and Whittaker, 1975); gelfoam (Lang and McGrath, 1974); and micropore (Relph, 1976). All adequately describe the method advocated, report success, and give more (Jones et al., 1978) or less (Marshall et al., 1971) convincing evidence to enable the reader to decide if he should try the method for patients in his care. The less dogmatic papers attempt to look more widely at what is available, trying to relate changes in approach or using attitude to a uniform policy for treatment (Morley, 1973), or attempt to classify sores before assigning the patient to a treatment programme (Forrest, 1980). Also within this group come papers which review the treatments available; none are comprehensive, for this would be well-nigh impossible; indeed, the author, to date, has listed more than 90 reported preparations. The best reviews cover many preparations, relate their use to the healing process (Nierman, 1978), and look at the faults in reports such as small numbers and inadequate controls, and the lack of assessment (Morgan, 1975). One of the most useful reviews comes from a group of pharmacists who relate the preparations to the state of the sore and look, to some extent, at what each preparation should achieve (Michocki and Lamy, 1976a). Their extensive list of preparations is divided into groups of like pharmacological action. However, being American, the list includes preparations which may not be available in other countries, and those which are rare or unusual. While it is of interest to know that treatments like gold leaf, topical vitamin A and ultrasound have been used to treat pressure sores, the dearth of information on relatively more commonly used preparations waits to be rectified. A further pitfall with these ‘What to do’ articles is the sometimes presumptuous titles: for example, “Prevention, Assessment and Treatment of Decubitus Ulcers”, appears to offer the complete solution (Mordern and Bayne, 1976). However, in its two pages, prevention fills only a small part, there is no contribution to assessment, and treatment is limited to the authors’ advocated methods. Indeed, no one article could expect to cover all that the nurse needs to know. The more specific papers discuss work in specialist pressure sore units (Hentz, 1979), the requirements of special groups of patients (Isiadinso, 1979), or review a specific treatment regime (Parish and Witkowski, 1980a). For those wishing to look at work done in the more distant past, Russell Grant (1967), in the introduction to a paper on the prototype of the water immersion bed, looks at some of the physical methods used to treat sores. These range from the complete removal of their cause (i.e. pressure), to the work of Sir James Paget, 1873, whose attempts at water flotation were foiled by the lack of suitable waterproof materials in the 19th century. break in the skin to a crater involving
Group 2: Detailed case histories In many ways the detailed case histories offer a greater insight into treatment than the more dogmatic views given in the Group 1 articles. The studies look more deeply at the
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patient as a individual in relation to the problem sore (e.g. Love, 1980), discussing the basis upon which decisions as to the choice of treatment or the preparations used were made. All relate to a ‘problem’ sore or patient, where the long-standing sore treated at home became infected and, following admission, was healed (e.g. Parr, 1979). The endpoint is ‘success’, the general message being, we used it and it worked. The articles thus give very biased information. Nevertheless, in spite of this limitation, these case histories are the testing ground for new ideas and are a necessary preliminary to more rigorous research. In most cases the theoretical basis of the action is described and the method of use clearly stated. But again the title of the written reports is often misleading, not least because the preparation under discussion is omitted; this leads the reader to waste time and money collecting papers which are irrelevant to his line of investigation. Equally, so often the preparations described are either those rarely encountered or those newly developed, including synthetic skin (Synthoderm) (Bayliss, 1979), ultrasound (Fisher, 1976), dextranomer (Debrisan) (McClemont et al., 1979) and karaya (Wallace and Hayter, 1974). An advance on these single descriptive case histories are those concerned with more than one patient, where the information is more organised. These latter reports cover discussion of the relief of pressure by use of the fluidised air bed (Clinitron) (Parish and Witkowski (1980b) and the water bed (Beaufort-Winchester) (Grahame et al., 1973), the second stage in research development following the earlier paper by Russell Grant (1967). A further innovation which enters with the increase in the number of patients studied is the assessment of sores either by culture when infection is probable, or through measurement lesions prior to the initiation and at the end of a period of therapy (e.g. Greene, 1975). In addition, sequential photographs are frequently included as a visual demonstration of the effect of the treatment discussed (Woodbine, 1979; Easterby, 1977). To end this group, one discordant note must be mentioned; Morgan (1976) describes how five paraplegic patients, who, in spite of having sores which healed satisfactorily, failed to learn from the experience, ignored the advice given, and consequently suffered a recurrence of sores. The point to be made is that the occurrence of sores is a problem which has not been fully investigated and yet is far from rare, as is being demonstrated in a study still in progress (Lockett, 1982). The combination of factors underlying the development and quality of healing of sores, given the different treatments used, is a subject as yet untapped. Thus, case histories serve as a source, not only of detailed individual care, but also as areas from which future investigations may be initiated. They are therefore a stepping stone to the next two groups, both of which concern clinical trials. Group 3: Small uncontrolled
clinical trials
One important difference between a clinical trial and a case history is that in the clinical trial the method of treatment and goals are established as part of a schedule to be followed, whereas in the case history the results describe the consequences of everyday practice. The first decision to be made when designing a clinical trial is the choice of preparation or treatment to be tested. Several methods of choice have been employed. Some researchers follow up preparations described in the case history where it has been
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suggested that the preparation is useful (Jacobson et al. 1976; Soul, 1978), or a more extensive study is undertaken involving a variety of wounds having the same characteristics for which the preparation is indicated. Data is collected on a number of possibly therapeutically relevant factors, including the removal of debris, the frequency with which dressings need to be changed, and the changes in pain caused by both the dressing technique and the wound itself. This is a time when lateral thinking and the researcher’s nose for important and unexpected events are of prime importance, for an incident normally considered of minor importance could be the one thing which demonstrates the greater efficacy of a product. One thing which strikes the reader as he looks more critically at the reported trials is that the number of patients included is small, rarely more than twenty. It is always difficult for the researcher studying a single site or area to obtain a sufficient number of patients and/or sores to validate a trial. The prevalence rates of 4-10’3’0 (number of sores at any one time) demonstrated by large scale surveys suggest that a reasonable number of sores will be found (Barbenel et al., 1977; Petersen and Bittmann, 1971). However, the number of new sores of any one type (incidence) may not be sufficient to test out the preparations of interest in the time allowed for the study. The pressure of time leads the researcher to lump together wounds of different etiology, such as venous ulcers, into the same trial (Lee et al., 1979). This would be acceptable if it were possible to distinguish one group from another, but in the study cited the purpose of applying povidone iodine was to reduce infection and promote healing. Initially, there was a dramatic drop in the number of infected sores. But there remained a low number of infected sores throughout; we are not told if these constituted an identifiable group, nor are we told how many of the 18 male outpatients in this study had pressure sores. The organisation of admission to the trial should be predetermined, cases being admitted as they arise or drawn at random. In the study reported by Rao et al. (1975), selected patients with wounds needing debridement had the wounds measured and assessed on a four-point scale for necrosis, inflammation, pus odour and the presence of granulation, before and at weekly intervals after the initiation of treatment with collagenase ointment. But what happened to the parallel group not randomly selected is not recorded, although there would seem to be no reason why records should not have been kept. Consequently no conclusion can be drawn as to the efficacy of the preparation. It is this very lack of systematic study which weakens the value of the uncontrolled trials; they are useful as a pilot study but can offer little more to knowledge than the case history. There is a temptation to draw conclusions; for example, Ramsey (1979), in a study concerned with testing porcine dermis, claimed “we consider that granulations form more quickly”. But there were not the data to substantiate the claim. However, it is important to recognise that an uncontrolled trial is the forerunner to further research, “clinical impressions and results of incompletely controlled studies have strongly suggested that the technique (silicone foam) leads to faster healing than conventional packing” (Wood et al., 1977). Group 4: Controlled clinical trials
The controlled clincial trial is a scientific experiment; its seeds having been sown by the questioning of routine and dogma and its growth nurtured through the preliminary case histories and uncontrolled trials. The value of a controlled trial lies in the extent to which one preparation can be rated against another. To obtain scientific validity there must be sufficent numbers in the trial and control groups to show statistically significant
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differences between the variables measured. The problem of acquiring sufficient numbers of patients for a trial has been mentioned above; to some extent it can be overcome by reducing, where possible, the differences between the groups which could affect the outcome, such as pairing patients (Yucel and Basmajian, 1974). Equally, all patients should receive similar care and pressure relieving aids, even when the treatment to be assessed is a dietary supplement such as zinc (Norris and Reynolds, 1971). The problems which arise when neither of these measures are followed is illustrated by a trial examining the effect of oral metronidazole; the standardised treatments were allowed to be revised as the wound changed (Baker and Haig, 1981). Although well organised, the trial was not controlled and the results were further placed in question because the difficulties in obtaining anaerobic wound samples for culture were not overcome. Diagnosis therefore relied on the very dubious subjective sense of smell; the presence of such bacteria was never confirmed by any independent means, nor was entry of the antibiotic into the area ever established. Yet the diagnosis of anaerobic infection has been successfully achieved (Daltry et al., 1981) and there are reported attempts to assess the penetration of antibiotics into pressure sores, where both clindamycin and gentamicin have been shown to reach the site of infection (Berger et al., 1978; 1981). The definition of endpoints and effective measures of the outcome are essential in any trial, and need to be both simple and accurate. In the study of pressure sores, the direct measurement of the sore area is the parameter most generally acceptable and is obtained by tracing the outline of the sore onto transparent film (Yucel et al., 1974), by measuring the sore diameters (Lee et al., 1979), or by the employment of a graduated scale (Van Ort and Gerber, 1976). Although photographs are frequently used, the difficulties of translating the sore to scale and the problems of measuring curved surfaces on a flat representation lead to inaccuracy unless special three-dimensional photography is employed (Gunnel Eriksson et al., 1979). This three-dimensional photography has the added advantage that it also allows for the computation of depth, the most difficult measurement of all to make, because even though sore grading by tissue involvement gives some idea of depth, with the variation in the tissue damage and its effects on patients the individual results are not comparable. Notwithstanding, knowledge of the tissue damage involved is a relevant factor in the study of pressure sores and researchers could well look at survey data which attempts to standardize assessment of this (Lowthian, 1979). The other method of volume/depth measurement employed is by using wound casts prepared with dental impression material. These casts are then measured by a technique using volume displacement (Lee and Ambrus, 1975). In the trial by Lee and Ambrus, point scales were also employed to assess changes in odour, pus, necrosis and inflammation to compare collagenase ointment against a heat-treated placebo ointment; making this trial not only controlled, but also the only trial to date with a truly blind comparison. Its only shortcoming is the low numbers- 11 patients and 28 sores. A more sophisticated index of infection is possible when a microbiologist joins the team (Rhodes et al., 1979). In the study of Rhodes et al., sores were allocated to infection categories before treatment with karaya gum powder was started. However, the control group leaves much to be desired because sores of patients in this group were treated with any one of a number of unrecorded preparations prescribed by the medical or nursing staff. Such anomalies in the design of a trial need to be recognised by the reader. But in spite of all this, all the papers presented/discussed are of value either to those seeking further information about preparations, or as a guide to those who would like to set up their own trials. Others
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follow up preparations which were the subject of previously described uncontrolled trials, e.g. a study reported by Parish and Collins (1979), who compared dextranomer with other preparations of like effect, namely sugar, egg white and collagenase. Although the numbers in the study were small, 34 ulcers on 17 patients, the results do give us some basis for comparing these particular preparations.
Group 5: Related theoretical and experimental aspects which contribute to a greater understanding of pressure sores
The final group of studies consider, in greater depth, factors which may affect the healing of pressure sores drawing on information from the broader research field of wound healing. The central problem of concern to nurses is that sores do not heal as they would expect. The reason for this poor prediction could be that current concepts about these wounds is incorrect. The individual nurses’s experience in the care of pressure sores is, in practice, usually far less than experience gained in caring for surgically incised wounds. The tendency is, therefore, to generalise the knowledge gained from the experience of the behaviour of incised wounds to pressure sores, including the expectation that pressure sores, like surgical wounds, will close in a matter of days. The justification for this too ready extrapolation is put in question by Barton and Barton (1973) who, in a study of 200 patients, established that pressure sores could be divided into three groups according to the time each sore required to heal. In Group I, sores healed within six weeks; in Group II, they required at least fourteen weeks; and in Group III sores showed little tendency to heal. Each group was also characterised by the patient’s general physical condition. In Group I, patients were “otherwise healthy” apart from the presence of sores; in Group II they were mainly geriatric patients, and in Group III the patients died within a matter of weeks of the sore being assessed. In addition, the sores could be allocated to the three groups before healing had occured or the patient died, by characteristic differences in the skin temperature around the sores. Barton and Barton go on to describe the recorded effects of corticosteroid drugs on the sore diameter, drawing attention to the fact that drugs such as steroids and salicylates which are known to reduce inflammation also inhibit healing in pressure sores. In summary, this study suggests that the patient’s general medical treatment as well as his physical condition must be considered when healing fails. Other research on healing indicates that the anergic or immunologically compromised patient is at risk (Meakins, 1976), as is the debilitated patient whose nutritional demands are increased (Moolten, 1972), when it is also known that the mechanisms involved in collagen formation demand a ready supply of non-storable vitamin C (Taylor et al., 1974). In addition, age, lack of mobility and sensation, all of which have been shown to contribute to sore development (Barbenel et al., 1977) also delay healing and thus affect the outcome of sore treatment; an outcome which may not always include healing. In addition to Barton, Vasile and Chaitin (1972) and Michocki and Lamy (1976b) have shown that a proportion of patients with pressure sores, 33% and 75% respectively, died during the study period. Indeed, Hunt (1973) suggests that endpoint measurements in wound healing are merely the sum of sequential, and often opposing mechanisms and that studies of these mechanisms could offer greater insight. “The investigator must define which of the many properties of wounds he wishes to study and must interpret his results in that context.” With this in mind, the relevance of studies which look at the bactiostatic effects of honey in open granulating wounds (Cavenagh
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et al., 1970), local nutrition in deep wounds (Calver and Stanley, 1980) or compare the effects of drying and occlusion on epidermal healing (Winter, 1978) become apparent; each being applicable to only one stage in the healing process, and relevant to the factors which impede that process for a period of time. Having considered the effect of the patient’s condition on the sore, and the effect of local treatment on healing, it is time to turn to the effect of locally applied preparations on the sore and patient as a whole. Although it has generally been considered that the circulation to pressure sores is poor, assays of antibiotic concentration in granulating wounds and their exudate suggest that there is transport of tissue fluids and their contents outwards from the wounds (Robson et al., 1974). Indeed, absorbent dressings with capillary action, such as dextranomer, will enhance this effect. The absorption of chemicals from the wound surface, although limited in amount, cannot be ruled out, particularly when treatment consists of repeated applications over a considerable period of time. Little work has been devoted to this aspect of treatment, although excessive concentrations of serum iodine have been reported in two patients whose wounds were packed with povidone iodine (Aronoff et a/., 1980). Their recommendation is that serum iodine be monitored when topical povidone iodine is applied to patients with renal insufficiency. The need here may well be for parallel laboratory research in which both the longer established and the newly developed preparations are investigated in experiments using models. Here we could learn from the surgeons who, having noticed that wounds cleansed with surgical soaps developed inflammation and infection, subsequently set up experiments to explore this. What they found was that detergents could be harmful to cartilage, synovia and other soft tissues, harm which could lead to an increased susceptibility to infection, poor wound healing and a loss of joint function in the model animal (Faddis et al., 1977). The use of animal models or tissue culture to test pharmaceutical products for external application is not new, yet many of the traditional preparations used to treat pressure sores which are so familiar to the nurse in practice have not been subject to assessment. Methodology is available for both culture and the production of model sores and would be applicable for the assessment of such preparations (Daniel et al., 1981). Although used in other contexts, one can only conclude that this is an area in nursing where more imaginative research is needed.
Conclusion
At the outset of this review it was suggested that pressure sores present multiple problems. Not only are sores of long duration, but they vary considerably in severity and complication. The patients with sores also vary in age, prognosis and physical status and treatment may directly counteract the patient’s ability to heal. Consequently, there can be no one description of a pressure sore that fully represents the picture and therefore no one standard treatment. The nurse’s objective must be to establish what it is realistic to achieve, determining what might impede this achievement, and then decide on how many impediments could be removed. The all-important question of which of the many preparations available will achieve her purpose is a question which to date has no one answer. But hoefully, with better understanding of both sore and preparation, there will be answers based on rational choices in the future.
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Morgan, J. E. (1975). Topical therapy of pressure sores. Surg. Gynuec. Obstet. 141, 945-947. Morgan, J. E. (1976). Recurrence of pressure ulcers. J. Am. med. Ass. 236, 2430. Morley, M. H. (1973). Decubitus ulcer management-a team approach. Can. Nurse 69, 41-43. Nierman, M. M. (1978). Treatment of dermal and decubitus ulcers. Drugs 15, 226-230. Norris, J. R. and Reynolds, R. E. (1971). The effect of oral zinc sulphate therapy on decubitus ulcers. J. Am. Geriat. Sot. 19, 793-797.
Parish, L. C. and Collins, E. (1979). Decubitus Ulcers: a comparative study. Cutis 23, 106-110. Parish, L. C. and Witkowski, J. A. (198Oa). The bear and the decubitus ulcer. ht. J. Derm. 19, 327-328. Parish, L. C. and Witkowski, J. A. (1980b). Clinitron therapy and the decubitus ulcer: preliminary dermatologic studies. Int. J. Derm. 19, 517-518. Parr, E. (1979). A patient with pressure sores. Nurs. Times 75, 369-372. Petersen, N. C. and Bittmann, S. (1971). Epidemiology of pressure sores. Scund. J. plust. reconstr. Surg. 5, 62-66.
Ramsey, R. (1979). Pressure sores in para and tetraplegic patients. Nurs. Times 75, 361-364. Rao, D. B., Sane, P. G. and Georgiev, E. L. (1975). Collagenase in the treatment of dermal and decubitus ulcers. J. Am. Geriat. Sot. 23, 22-30. Relph, E. J. (1976). Treatment of pressure sores using micropore. Nurs. Times 72, 301. Rhodes, B., Daltrey, D. L. and Chattwood, J. C. (1979). The treatment of pressure sores in geriatric patients. Nurs. Times 75, 365-368. Robson, M. C., Edstrom, L. E., Krizek, T. J. and Groskin, M. G. (1974). The efficacy of systematic antibiotics in the treatment of granulating wounds. J. Surg. Res. 16, 299-306. Russell Grant, W. (1967). Weightlessness in the treatment of bedsores and burns. Proc. R. Sot. Med. 60, 71 I-715. Soul, J. (1978). A trial of debrisan in the cleansing of infected surgical wounds. Br. J. clin. Pructice 32, 172. Taylor, T. V., Rimmer, S., Day, B., Butcher, J. and Dymock, 1. W. (1974). Ascorbic acid supplementation in the treatment of pressure sores. Lancer 2, 544546. Torelli, M. (1973). Topical hyperbaric oxygen for decubitus ulcers. Am. J. Nurs. 73, 494-496. Van Ort, S. R. and Gerber, R. M. (1976). Topical application of insulin in the treatment of decubitus ulcers. A pilot study. Nurs. Res. 25, 9-12. Vasile, J. and Chaitin, H. (1972). Prognostic factors in decubitus ulcers of the aged. Geriatrics 27, 126-129. Vetra, H. and Whittaker, D. (1975). Hydrotherapy and topical collagenase for decubitus ulcers. Geriatrics 30, 53-58.
Wallace, G. and Hayter, J. (1974). Karaya for chronic skin ulcers. Am. J. Nurs. 74, 1094-1098. Winter, G. D. (1978). Oxygen and epidermal wound healing. In Oxygen Transport to Tissue III, I. A. Silver et al. (Eds.), pp. 673-678). Plenum, New York. Wood, R. A. B., Williams, R. H. F. and Hughes, L. E. (1977). Foam elastomer dressing in the management of open granulating wounds: experiences with 250 patients. Br. J. Surg. 64, 554-557. Woodbine, A. (1979). Pressure sores 2: A survey in Macclesfield. Nurs. Times 75, 1128-I 132. Yucel, V. F. and Basmajian, J. M. (1974). Decubitus ulcers: healing effect of an enzymatic spray. Archs. phys. Med. Rehabil. 55, 517-519.
OOZO-7489/82/04018309 $03.00/O 0 1982 Pergamon Press Ltd.
Pressure sore treatment: a literature review JILL A. DAVID, M.Sc., B.Sc., S.R.N., H.V. Project Leader-Pressure Sore Project, Nursing Practice Research Unit, North wick Park Hospital and Clinical Research Cen Ire, Watford Road, Harrow Middlesex HAI 3UJ, U.K.
There is no lack in the amount of advice, both printed and verbal, available to the nurse inquiring about the treatment* of pressure sores. However, the number of different preparations-l- advocated and the variety of different reasons given to justify their use, suggests that there is little more basis for choice than personal preference, laced with unsubstantiated theory. In addition to the preparations applied to the sore, treatment must also include the devices used to remove the cause (pressure) and all the measures taken to improve the patient’s ability to heal. In the course of writing this review, the author has read around 100 articles which have appeared since 1965; selected because either they mention the treatment of established pressure sores, or they discuss the related subjects of the healing of open wounds, infection and wound healing, and experimental models for the assessment of treatment. Papers on the surgical treatment of sores have been omitted, as these do not come within the nurse’s sphere of influence. The papers to be discussed have been divided into five groups according to content, which lead progressively more deeply towards an understanding of the subject: (1) Lists and discussion of treatments advocated by the authors; (2) Detailed case histories; (3) Small uncontrolled clinical trials; (4) Controlled clinical trials; (5) Related subjects, theory or experimental, which contribute to a greater understanding of the subject. Each group forms an important stage in the development of understanding, though unfortunately it is only rarely that any one treatment can be followed through all the logical stages in this progression. Group 1: Lists and discussion
of treatments advocated
by the authors
The treatment of patients with pressure sores poses a number of problems, not least because every patient is an individual. The sore itself can range in depth from a superficial *Treatment j-preparation
when used in this article refers to anything which is done to the patient refers to any chemical which contacts the sore. 183
or the sore.
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deep fascia or bone; each presenting a range of size and complications such as infection and the presence of necrotic tissue. This is reflected in the range of preparations listed and local policies reported in the first group of papers. Some give descriptions of new methods available (Hodkinson, 1965). Hodkinson’s paper is short and states the advantages the author experienced using a new method (aerosol) for the application of tincture of benzoin, a very old method of treatment. Similarly, less well known methods are described: air current treatment (Davis and Dong Sun Chu, 1974); cold therapy, limited to experience with children (Marshall, 1971); hyberbaric oxygen (Torelli, 1973); topical metronidazole (Jones et al., 1978); hydrotherapy and topical collagenase (Vetra and Whittaker, 1975); gelfoam (Lang and McGrath, 1974); and micropore (Relph, 1976). All adequately describe the method advocated, report success, and give more (Jones et al., 1978) or less (Marshall et al., 1971) convincing evidence to enable the reader to decide if he should try the method for patients in his care. The less dogmatic papers attempt to look more widely at what is available, trying to relate changes in approach or using attitude to a uniform policy for treatment (Morley, 1973), or attempt to classify sores before assigning the patient to a treatment programme (Forrest, 1980). Also within this group come papers which review the treatments available; none are comprehensive, for this would be well-nigh impossible; indeed, the author, to date, has listed more than 90 reported preparations. The best reviews cover many preparations, relate their use to the healing process (Nierman, 1978), and look at the faults in reports such as small numbers and inadequate controls, and the lack of assessment (Morgan, 1975). One of the most useful reviews comes from a group of pharmacists who relate the preparations to the state of the sore and look, to some extent, at what each preparation should achieve (Michocki and Lamy, 1976a). Their extensive list of preparations is divided into groups of like pharmacological action. However, being American, the list includes preparations which may not be available in other countries, and those which are rare or unusual. While it is of interest to know that treatments like gold leaf, topical vitamin A and ultrasound have been used to treat pressure sores, the dearth of information on relatively more commonly used preparations waits to be rectified. A further pitfall with these ‘What to do’ articles is the sometimes presumptuous titles: for example, “Prevention, Assessment and Treatment of Decubitus Ulcers”, appears to offer the complete solution (Mordern and Bayne, 1976). However, in its two pages, prevention fills only a small part, there is no contribution to assessment, and treatment is limited to the authors’ advocated methods. Indeed, no one article could expect to cover all that the nurse needs to know. The more specific papers discuss work in specialist pressure sore units (Hentz, 1979), the requirements of special groups of patients (Isiadinso, 1979), or review a specific treatment regime (Parish and Witkowski, 1980a). For those wishing to look at work done in the more distant past, Russell Grant (1967), in the introduction to a paper on the prototype of the water immersion bed, looks at some of the physical methods used to treat sores. These range from the complete removal of their cause (i.e. pressure), to the work of Sir James Paget, 1873, whose attempts at water flotation were foiled by the lack of suitable waterproof materials in the 19th century. break in the skin to a crater involving
Group 2: Detailed case histories In many ways the detailed case histories offer a greater insight into treatment than the more dogmatic views given in the Group 1 articles. The studies look more deeply at the
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patient as a individual in relation to the problem sore (e.g. Love, 1980), discussing the basis upon which decisions as to the choice of treatment or the preparations used were made. All relate to a ‘problem’ sore or patient, where the long-standing sore treated at home became infected and, following admission, was healed (e.g. Parr, 1979). The endpoint is ‘success’, the general message being, we used it and it worked. The articles thus give very biased information. Nevertheless, in spite of this limitation, these case histories are the testing ground for new ideas and are a necessary preliminary to more rigorous research. In most cases the theoretical basis of the action is described and the method of use clearly stated. But again the title of the written reports is often misleading, not least because the preparation under discussion is omitted; this leads the reader to waste time and money collecting papers which are irrelevant to his line of investigation. Equally, so often the preparations described are either those rarely encountered or those newly developed, including synthetic skin (Synthoderm) (Bayliss, 1979), ultrasound (Fisher, 1976), dextranomer (Debrisan) (McClemont et al., 1979) and karaya (Wallace and Hayter, 1974). An advance on these single descriptive case histories are those concerned with more than one patient, where the information is more organised. These latter reports cover discussion of the relief of pressure by use of the fluidised air bed (Clinitron) (Parish and Witkowski (1980b) and the water bed (Beaufort-Winchester) (Grahame et al., 1973), the second stage in research development following the earlier paper by Russell Grant (1967). A further innovation which enters with the increase in the number of patients studied is the assessment of sores either by culture when infection is probable, or through measurement lesions prior to the initiation and at the end of a period of therapy (e.g. Greene, 1975). In addition, sequential photographs are frequently included as a visual demonstration of the effect of the treatment discussed (Woodbine, 1979; Easterby, 1977). To end this group, one discordant note must be mentioned; Morgan (1976) describes how five paraplegic patients, who, in spite of having sores which healed satisfactorily, failed to learn from the experience, ignored the advice given, and consequently suffered a recurrence of sores. The point to be made is that the occurrence of sores is a problem which has not been fully investigated and yet is far from rare, as is being demonstrated in a study still in progress (Lockett, 1982). The combination of factors underlying the development and quality of healing of sores, given the different treatments used, is a subject as yet untapped. Thus, case histories serve as a source, not only of detailed individual care, but also as areas from which future investigations may be initiated. They are therefore a stepping stone to the next two groups, both of which concern clinical trials. Group 3: Small uncontrolled
clinical trials
One important difference between a clinical trial and a case history is that in the clinical trial the method of treatment and goals are established as part of a schedule to be followed, whereas in the case history the results describe the consequences of everyday practice. The first decision to be made when designing a clinical trial is the choice of preparation or treatment to be tested. Several methods of choice have been employed. Some researchers follow up preparations described in the case history where it has been
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suggested that the preparation is useful (Jacobson et al. 1976; Soul, 1978), or a more extensive study is undertaken involving a variety of wounds having the same characteristics for which the preparation is indicated. Data is collected on a number of possibly therapeutically relevant factors, including the removal of debris, the frequency with which dressings need to be changed, and the changes in pain caused by both the dressing technique and the wound itself. This is a time when lateral thinking and the researcher’s nose for important and unexpected events are of prime importance, for an incident normally considered of minor importance could be the one thing which demonstrates the greater efficacy of a product. One thing which strikes the reader as he looks more critically at the reported trials is that the number of patients included is small, rarely more than twenty. It is always difficult for the researcher studying a single site or area to obtain a sufficient number of patients and/or sores to validate a trial. The prevalence rates of 4-10’3’0 (number of sores at any one time) demonstrated by large scale surveys suggest that a reasonable number of sores will be found (Barbenel et al., 1977; Petersen and Bittmann, 1971). However, the number of new sores of any one type (incidence) may not be sufficient to test out the preparations of interest in the time allowed for the study. The pressure of time leads the researcher to lump together wounds of different etiology, such as venous ulcers, into the same trial (Lee et al., 1979). This would be acceptable if it were possible to distinguish one group from another, but in the study cited the purpose of applying povidone iodine was to reduce infection and promote healing. Initially, there was a dramatic drop in the number of infected sores. But there remained a low number of infected sores throughout; we are not told if these constituted an identifiable group, nor are we told how many of the 18 male outpatients in this study had pressure sores. The organisation of admission to the trial should be predetermined, cases being admitted as they arise or drawn at random. In the study reported by Rao et al. (1975), selected patients with wounds needing debridement had the wounds measured and assessed on a four-point scale for necrosis, inflammation, pus odour and the presence of granulation, before and at weekly intervals after the initiation of treatment with collagenase ointment. But what happened to the parallel group not randomly selected is not recorded, although there would seem to be no reason why records should not have been kept. Consequently no conclusion can be drawn as to the efficacy of the preparation. It is this very lack of systematic study which weakens the value of the uncontrolled trials; they are useful as a pilot study but can offer little more to knowledge than the case history. There is a temptation to draw conclusions; for example, Ramsey (1979), in a study concerned with testing porcine dermis, claimed “we consider that granulations form more quickly”. But there were not the data to substantiate the claim. However, it is important to recognise that an uncontrolled trial is the forerunner to further research, “clinical impressions and results of incompletely controlled studies have strongly suggested that the technique (silicone foam) leads to faster healing than conventional packing” (Wood et al., 1977). Group 4: Controlled clinical trials
The controlled clincial trial is a scientific experiment; its seeds having been sown by the questioning of routine and dogma and its growth nurtured through the preliminary case histories and uncontrolled trials. The value of a controlled trial lies in the extent to which one preparation can be rated against another. To obtain scientific validity there must be sufficent numbers in the trial and control groups to show statistically significant
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differences between the variables measured. The problem of acquiring sufficient numbers of patients for a trial has been mentioned above; to some extent it can be overcome by reducing, where possible, the differences between the groups which could affect the outcome, such as pairing patients (Yucel and Basmajian, 1974). Equally, all patients should receive similar care and pressure relieving aids, even when the treatment to be assessed is a dietary supplement such as zinc (Norris and Reynolds, 1971). The problems which arise when neither of these measures are followed is illustrated by a trial examining the effect of oral metronidazole; the standardised treatments were allowed to be revised as the wound changed (Baker and Haig, 1981). Although well organised, the trial was not controlled and the results were further placed in question because the difficulties in obtaining anaerobic wound samples for culture were not overcome. Diagnosis therefore relied on the very dubious subjective sense of smell; the presence of such bacteria was never confirmed by any independent means, nor was entry of the antibiotic into the area ever established. Yet the diagnosis of anaerobic infection has been successfully achieved (Daltry et al., 1981) and there are reported attempts to assess the penetration of antibiotics into pressure sores, where both clindamycin and gentamicin have been shown to reach the site of infection (Berger et al., 1978; 1981). The definition of endpoints and effective measures of the outcome are essential in any trial, and need to be both simple and accurate. In the study of pressure sores, the direct measurement of the sore area is the parameter most generally acceptable and is obtained by tracing the outline of the sore onto transparent film (Yucel et al., 1974), by measuring the sore diameters (Lee et al., 1979), or by the employment of a graduated scale (Van Ort and Gerber, 1976). Although photographs are frequently used, the difficulties of translating the sore to scale and the problems of measuring curved surfaces on a flat representation lead to inaccuracy unless special three-dimensional photography is employed (Gunnel Eriksson et al., 1979). This three-dimensional photography has the added advantage that it also allows for the computation of depth, the most difficult measurement of all to make, because even though sore grading by tissue involvement gives some idea of depth, with the variation in the tissue damage and its effects on patients the individual results are not comparable. Notwithstanding, knowledge of the tissue damage involved is a relevant factor in the study of pressure sores and researchers could well look at survey data which attempts to standardize assessment of this (Lowthian, 1979). The other method of volume/depth measurement employed is by using wound casts prepared with dental impression material. These casts are then measured by a technique using volume displacement (Lee and Ambrus, 1975). In the trial by Lee and Ambrus, point scales were also employed to assess changes in odour, pus, necrosis and inflammation to compare collagenase ointment against a heat-treated placebo ointment; making this trial not only controlled, but also the only trial to date with a truly blind comparison. Its only shortcoming is the low numbers- 11 patients and 28 sores. A more sophisticated index of infection is possible when a microbiologist joins the team (Rhodes et al., 1979). In the study of Rhodes et al., sores were allocated to infection categories before treatment with karaya gum powder was started. However, the control group leaves much to be desired because sores of patients in this group were treated with any one of a number of unrecorded preparations prescribed by the medical or nursing staff. Such anomalies in the design of a trial need to be recognised by the reader. But in spite of all this, all the papers presented/discussed are of value either to those seeking further information about preparations, or as a guide to those who would like to set up their own trials. Others
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follow up preparations which were the subject of previously described uncontrolled trials, e.g. a study reported by Parish and Collins (1979), who compared dextranomer with other preparations of like effect, namely sugar, egg white and collagenase. Although the numbers in the study were small, 34 ulcers on 17 patients, the results do give us some basis for comparing these particular preparations.
Group 5: Related theoretical and experimental aspects which contribute to a greater understanding of pressure sores
The final group of studies consider, in greater depth, factors which may affect the healing of pressure sores drawing on information from the broader research field of wound healing. The central problem of concern to nurses is that sores do not heal as they would expect. The reason for this poor prediction could be that current concepts about these wounds is incorrect. The individual nurses’s experience in the care of pressure sores is, in practice, usually far less than experience gained in caring for surgically incised wounds. The tendency is, therefore, to generalise the knowledge gained from the experience of the behaviour of incised wounds to pressure sores, including the expectation that pressure sores, like surgical wounds, will close in a matter of days. The justification for this too ready extrapolation is put in question by Barton and Barton (1973) who, in a study of 200 patients, established that pressure sores could be divided into three groups according to the time each sore required to heal. In Group I, sores healed within six weeks; in Group II, they required at least fourteen weeks; and in Group III sores showed little tendency to heal. Each group was also characterised by the patient’s general physical condition. In Group I, patients were “otherwise healthy” apart from the presence of sores; in Group II they were mainly geriatric patients, and in Group III the patients died within a matter of weeks of the sore being assessed. In addition, the sores could be allocated to the three groups before healing had occured or the patient died, by characteristic differences in the skin temperature around the sores. Barton and Barton go on to describe the recorded effects of corticosteroid drugs on the sore diameter, drawing attention to the fact that drugs such as steroids and salicylates which are known to reduce inflammation also inhibit healing in pressure sores. In summary, this study suggests that the patient’s general medical treatment as well as his physical condition must be considered when healing fails. Other research on healing indicates that the anergic or immunologically compromised patient is at risk (Meakins, 1976), as is the debilitated patient whose nutritional demands are increased (Moolten, 1972), when it is also known that the mechanisms involved in collagen formation demand a ready supply of non-storable vitamin C (Taylor et al., 1974). In addition, age, lack of mobility and sensation, all of which have been shown to contribute to sore development (Barbenel et al., 1977) also delay healing and thus affect the outcome of sore treatment; an outcome which may not always include healing. In addition to Barton, Vasile and Chaitin (1972) and Michocki and Lamy (1976b) have shown that a proportion of patients with pressure sores, 33% and 75% respectively, died during the study period. Indeed, Hunt (1973) suggests that endpoint measurements in wound healing are merely the sum of sequential, and often opposing mechanisms and that studies of these mechanisms could offer greater insight. “The investigator must define which of the many properties of wounds he wishes to study and must interpret his results in that context.” With this in mind, the relevance of studies which look at the bactiostatic effects of honey in open granulating wounds (Cavenagh
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et al., 1970), local nutrition in deep wounds (Calver and Stanley, 1980) or compare the effects of drying and occlusion on epidermal healing (Winter, 1978) become apparent; each being applicable to only one stage in the healing process, and relevant to the factors which impede that process for a period of time. Having considered the effect of the patient’s condition on the sore, and the effect of local treatment on healing, it is time to turn to the effect of locally applied preparations on the sore and patient as a whole. Although it has generally been considered that the circulation to pressure sores is poor, assays of antibiotic concentration in granulating wounds and their exudate suggest that there is transport of tissue fluids and their contents outwards from the wounds (Robson et al., 1974). Indeed, absorbent dressings with capillary action, such as dextranomer, will enhance this effect. The absorption of chemicals from the wound surface, although limited in amount, cannot be ruled out, particularly when treatment consists of repeated applications over a considerable period of time. Little work has been devoted to this aspect of treatment, although excessive concentrations of serum iodine have been reported in two patients whose wounds were packed with povidone iodine (Aronoff et a/., 1980). Their recommendation is that serum iodine be monitored when topical povidone iodine is applied to patients with renal insufficiency. The need here may well be for parallel laboratory research in which both the longer established and the newly developed preparations are investigated in experiments using models. Here we could learn from the surgeons who, having noticed that wounds cleansed with surgical soaps developed inflammation and infection, subsequently set up experiments to explore this. What they found was that detergents could be harmful to cartilage, synovia and other soft tissues, harm which could lead to an increased susceptibility to infection, poor wound healing and a loss of joint function in the model animal (Faddis et al., 1977). The use of animal models or tissue culture to test pharmaceutical products for external application is not new, yet many of the traditional preparations used to treat pressure sores which are so familiar to the nurse in practice have not been subject to assessment. Methodology is available for both culture and the production of model sores and would be applicable for the assessment of such preparations (Daniel et al., 1981). Although used in other contexts, one can only conclude that this is an area in nursing where more imaginative research is needed.
Conclusion
At the outset of this review it was suggested that pressure sores present multiple problems. Not only are sores of long duration, but they vary considerably in severity and complication. The patients with sores also vary in age, prognosis and physical status and treatment may directly counteract the patient’s ability to heal. Consequently, there can be no one description of a pressure sore that fully represents the picture and therefore no one standard treatment. The nurse’s objective must be to establish what it is realistic to achieve, determining what might impede this achievement, and then decide on how many impediments could be removed. The all-important question of which of the many preparations available will achieve her purpose is a question which to date has no one answer. But hoefully, with better understanding of both sore and preparation, there will be answers based on rational choices in the future.
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References Aronoff, G. R., Friedman, S. .I., Doedens, D. J. and Lavell, K. J. (1980). Increased serum iodide concentration from iodine absorption through wounds treated topically with povidone iodine. Am. J. Med. Sci. 279, 173-176. Baker, P. G. and Haig, G. G. (1981). Metronidazole (‘Flagyl 400’) treatment for chronic pressure sores and ulcers. A coniparison with standard treatments in general practice. Practitioner 225, 569-573. Berbenel, J. C., Jordon, M. M., Nicol, S. M. and Clark, M. 0. (1977). Incidence of pressure sores in the Greater Glasgow Health Board Area. Lance? 2, 548-550. Barton, A. A. and Barton, M. (1973). The clinical and thermographical evaluation of pressure sores. Age Ageing 2, 55-59. Bayliss, D. (1979). A new cure of an old problem. Nur.s. Mirror 149, 34-36. Berger, S. A., Barza, M., Haher, J., McFarland, .J. J., Louie, S. and Kane, A. (1978). Penetration of clindamycin into decubitus ulcers. Anlimicrob. Agenfs Chemother. 14, 498-499. Berger, S. A., Barza, M., Haher, J., Bell, D., Waintraub, S.. Burtyk, M. L. and Kane, A. (1981). Penetration of antibiotics into decubitus ulcers. Antimicrob. Agents Chemother. 7, 193-195. Calver, R. F. and Stanley, J. K. (1980). Enchancement of secondary wound healing by local tissue nutrition. Clin. Trials J. 17, 144-158. Cavenagh, D., Beazley, J. and Ostapowicz, F. (1970). Radical operation for carcinoma of the vulva. J. Obsret. Gynaec, Br. Commonw. 77, 1037-1040. Daltry, D. C., Rhodes, B. and Chattwood, J. G. (1981). Investigation into the microbial flora of healing and non-healing decubitus ulcers. J. c/in. Path. 34, 701-705. Daniel, R. K., Priest, D. L. and Wheatley, D. C. (1981). Etiologic factors in pressure sores: an experimental model. Archs. phys. Med. Rehabil. 62. 492-498. Davis, S. W. and Dong Sun Chu (1974). Air current treatment for decubitus ulcers. Archs. phys. Med. Rehabil. 55, 138-139. Easterby, M. (1977). A treatment for pressure sore5 and stasis ulcers. Nurs. Times 73, 519-520. Fad&, D., Daniel, D. and Boyer, J. (1977). Tissue toxicity of antiseptic solutions: a study of rabbit articular and periarticular tissues. J. Trauma 17, 895-897. Fisher, M. V. (1976). Pressure sores: treatment by ultrasound. Nurs. Times 72, 302. Forest, R. D. (1980). The treatment of pressure sores. J. Int. int. med. Res. 8, 430-435. Grahame, R., Broomhead, I. W.. Chir, M., Burry, H. C., Kemp, W. A. and Morris, A. M. (1973). Treatment of severe decubitus ulcers using the Beaufort-Winchester water bed. Br. J. plust. Surg. 26, 7580. Greene, R. (1975). Ostomy skin barriers for decubitus ulcers. Canadian Nurse 71, 34-35. Gunnel Eriksson, A., Eklond, E., Torlegard, K. and Dauphin, E. (1979). Evaluation of leg ulcer treatment with stereophotogrammetry. Br. J. Dermaf. 101, 123-131. Hentz, V. R. (1979). Management of pressure sores in a Fpeciality center: a reappraisal. Plastic Reconstr. Surg. 64, 683-691. Hodkinson, M. A. (1965). Aerosols in the care ot the elderly. Br. Hosp. J. Social Serv. Rev., 23 April 1965. Hunt, T. K. (1973). Standards for wound healing research. Surgery 73, 153-154. Isiadinso, 0. 0. (1979). Decubitus ulcers in geriatric patients: present status. N. Y. State J. Med. 79, 2027-2029. Jacobson, S., Rothman, U.. Arturson. G.. Ganror, K.. Haeger, K. and Juhlin, I. (1976). A new principle for cleansing infected wounds. Scund. J. pht. reconstr. SurR. 10. 65-72. Jones, P. H., Willis, A. T. and Fergur;on. I. R. (1978). Treatment of anaerobically infected pressure sores with topical metronidazole. Lancef 1, 214. Lang, C. and McCrath, A. (1974). Gelfoam for decubitus ulcers. Am. J. Nurs. 74, 460-461. Lee, B. Y.. Trainor, F. S. and Thoden, W. R. (1979). Topical application of povidone iodine in the management of decubitus and stasis ulcers. .I. Geriat. Sot. 27, 302-306. Lee, L. K. and Ambrus, J. L. (1975). Collagenase therapy for decubitus ulcers. Geriatrics 30, 91-98. Lockett, B. (1982). Personal communication. Love, C. (1980). A problem sore. Nurs. Times 76, 560-564. Lowthian, P. (1979). Pressure sore prevalence. Nurs. Times 75, 358-360. McClemont, E. J. W., Shand, I. G. and Ramsay, B. (1979). Pressure sores: a new method of treatment. Br. J. clin. Practice 33, 21-25 Marshall, R. S. (1971). Cold therapy in the treatment of pressure sores. Physiotherapy 57, 372-373. Meakins, J. L. (1976). Pathophysiologic determinants and prediction of sepsis. Surg. Clin. N. Am. 56,847-857. Michocki, R. J. and Lamy, P. P. (1976a). The care of decubitus ulcers. J. Am. Geriut. Sot. 24, 217-224. Michocki, R. J. and Lamy, P. P. (1976b). The problem of pressure sores in a nursing home population: statistical data. J. Am. Geriaf. Sot. 24, 323-328. Moolten, S. E. (1972). Bed sores in the chronically ill patient. Arch. ph_vs. Med. Rehabil. 53, 430-438. Moolten, S. E. (1977). Bedsores. Hosp. Med. May 1977, 83-103. Morden, P. and Bayne, R. (1976). Prevention, assessment and treatment of decubitus ulcers. Canadian Fam. Physician 22, 1301-1302.
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Morgan, J. E. (1975). Topical therapy of pressure sores. Surg. Gynuec. Obstet. 141, 945-947. Morgan, J. E. (1976). Recurrence of pressure ulcers. J. Am. med. Ass. 236, 2430. Morley, M. H. (1973). Decubitus ulcer management-a team approach. Can. Nurse 69, 41-43. Nierman, M. M. (1978). Treatment of dermal and decubitus ulcers. Drugs 15, 226-230. Norris, J. R. and Reynolds, R. E. (1971). The effect of oral zinc sulphate therapy on decubitus ulcers. J. Am. Geriat. Sot. 19, 793-797.
Parish, L. C. and Collins, E. (1979). Decubitus Ulcers: a comparative study. Cutis 23, 106-110. Parish, L. C. and Witkowski, J. A. (198Oa). The bear and the decubitus ulcer. ht. J. Derm. 19, 327-328. Parish, L. C. and Witkowski, J. A. (1980b). Clinitron therapy and the decubitus ulcer: preliminary dermatologic studies. Int. J. Derm. 19, 517-518. Parr, E. (1979). A patient with pressure sores. Nurs. Times 75, 369-372. Petersen, N. C. and Bittmann, S. (1971). Epidemiology of pressure sores. Scund. J. plust. reconstr. Surg. 5, 62-66.
Ramsey, R. (1979). Pressure sores in para and tetraplegic patients. Nurs. Times 75, 361-364. Rao, D. B., Sane, P. G. and Georgiev, E. L. (1975). Collagenase in the treatment of dermal and decubitus ulcers. J. Am. Geriat. Sot. 23, 22-30. Relph, E. J. (1976). Treatment of pressure sores using micropore. Nurs. Times 72, 301. Rhodes, B., Daltrey, D. L. and Chattwood, J. C. (1979). The treatment of pressure sores in geriatric patients. Nurs. Times 75, 365-368. Robson, M. C., Edstrom, L. E., Krizek, T. J. and Groskin, M. G. (1974). The efficacy of systematic antibiotics in the treatment of granulating wounds. J. Surg. Res. 16, 299-306. Russell Grant, W. (1967). Weightlessness in the treatment of bedsores and burns. Proc. R. Sot. Med. 60, 71 I-715. Soul, J. (1978). A trial of debrisan in the cleansing of infected surgical wounds. Br. J. clin. Pructice 32, 172. Taylor, T. V., Rimmer, S., Day, B., Butcher, J. and Dymock, 1. W. (1974). Ascorbic acid supplementation in the treatment of pressure sores. Lancer 2, 544546. Torelli, M. (1973). Topical hyperbaric oxygen for decubitus ulcers. Am. J. Nurs. 73, 494-496. Van Ort, S. R. and Gerber, R. M. (1976). Topical application of insulin in the treatment of decubitus ulcers. A pilot study. Nurs. Res. 25, 9-12. Vasile, J. and Chaitin, H. (1972). Prognostic factors in decubitus ulcers of the aged. Geriatrics 27, 126-129. Vetra, H. and Whittaker, D. (1975). Hydrotherapy and topical collagenase for decubitus ulcers. Geriatrics 30, 53-58.
Wallace, G. and Hayter, J. (1974). Karaya for chronic skin ulcers. Am. J. Nurs. 74, 1094-1098. Winter, G. D. (1978). Oxygen and epidermal wound healing. In Oxygen Transport to Tissue III, I. A. Silver et al. (Eds.), pp. 673-678). Plenum, New York. Wood, R. A. B., Williams, R. H. F. and Hughes, L. E. (1977). Foam elastomer dressing in the management of open granulating wounds: experiences with 250 patients. Br. J. Surg. 64, 554-557. Woodbine, A. (1979). Pressure sores 2: A survey in Macclesfield. Nurs. Times 75, 1128-I 132. Yucel, V. F. and Basmajian, J. M. (1974). Decubitus ulcers: healing effect of an enzymatic spray. Archs. phys. Med. Rehabil. 55, 517-519.