EUROPEAN PRESSURE ULCER ADVISORY PANEL

THE LIMITS OF PRESSURE ULCER SORE PREVENTION
J.C. Barbanel, University of Strathclyde, Glasgow, Scotland and S. Hagisawa, Hiroshima, Japan

Thank you for the opportunity to respond to the comments on our paper of 1999. We are pleased that the paper has led to a debate on the limits of pressure sore prevention, a debate which we believe to be long overdue.

The heading ‘Can pressure ulcer prevention be a waste of time?’ is somewhat unfortunate. Those caring for patients are not omniscient and cannot identify infallibly those patients in whom preventive care will fail; assessment tools provide a warning that the patient is at risk, not a diagnosis that a sore will occur. We believe that all patients who are assessed as being at risk of developing pressure should receive appropriate preventative care and that it is not a waste of time even if it fails to prevent a pressure sore developing.

Both the Editor and Ms Barrois comment on the number of patients who were at risk and the level of risk. This data for those patients who developed pressure sores is shown in Table 1. It is apparent that most of the patients had a very variable Braden Score and this is also true of those who did not develop sores. Patients developing a sore did so when their score was from 8 to 14, although there are too few to make any substantive comment on where to set a risk level (see also our final paragraph). Table 2 shows the pooled data for the three groups of patients. The patients who were in the group who either developed a sore or skin redness had a considerably longer mean stay than did those who developed neither redness nor a sore. The percentage of patients whose Braden Score was 12 or less, 10 or less, or died at sometime during the study, is higher in the patient group who developed a sore than the other groups, but the small patient numbers produce very wide confidence intervals which means these differences are not statistically significant.

The Editor is correct in his statement that the Braden Scale may over predict risk or be inappropriate for the patient population and our paper comments that the outcome of the study ‘may reflect either patient misclassification or the success of the preventive regimen’ but our data does not allow us to decide which of these hypotheses is correct.

Ms. Barrois comments on our statement that skin inspection occurred at least once per day. Those patients with skin redness which persisted for more than thirty minutes had a hydrocolloid dressing applied to the relevant area and this prevented their skin being directly inspected more than once per day. The skin of the at-risk patients without such dressings was inspected when given nursing care, including when the patients were turned. In addition the skin was routinely inspected once per eight-hour nursing shift.

It is rather difficult to respond to the comments of Ms Dealey. Her first paragraph suggested that 95% of pressure sores are preventable; her reference (Waterlow, 1988) shows no evidence to substantiate the claim, but merely quotes another reference (Robertson, 1987). The relevance of the comment to our results is also unclear. It is difficult to respond to her other comments because she makes no specific criticism, but we would reiterate our belief that the preventative regimen we used was an example of the best current practice, and would seem to have been accepted by the other commentators.

The comments of Dr Halfens are much more basic. The initiation of a pressure sore depends on both intrinsic factors (especially the condition of the patient and their tissues) and extrinsic factors (including the overall level of nursing and preventative care). In seeking the limits of pressure sore prevention, we investigated a group of seriously, or terminally, ill patients in whom we believe pressure sores may not be preventable. We are not alone in believing this (e.g., Witkowski and Parish, 1993; Bliss, 2000) and there is evidence that there may actually be microvascular malfunction in such patients (e.g., Haisjacket et al, 1990; Hartl et al, 1988). In order to find a realistic and reliable estimate of the pressure sore prevalences in such patients, it is necessary to ensure that preventative care is the highest achievable. Thus our conclusion is based on an appropriate but specific patient group and what we are convinced is an example of the highest quality nursing care. The preventive care was not discontinued and Dr Halfens’s question and responses may reflect differences in practice and attitudes in Japan and The Netherlands.

It is not possible to simply extrapolate our results to other patient groups, and in our papers we comment in our conclusion that ‘the incidence of pressure sores in this study may approach the lowest achievable in such patients’. We can only comment on the results quoted by Dr Halfens if we have more information. If the number of patients at risk, and the degree of risk, in Holland were similar to those in this study then we can compare the results; if they were significantly different then it is not possible to compare the results and the similarity in prevalence might be coincidental. Unfortunately we do not have this basic information. Perhaps another discussion might be on what information should be provided in incidence and prevalence studies to make them more useful and comparable.

Few people would disagree with the suggestion that pressure sore initiation depends both on intrinsic and extrinsic factors. Logically, it would seem to us that the assessment of pressure sore risk should also depend on extrinsic and intrinsic factors. All the scoring systems we know of are based soley on the intrinsic factors and this may account for the variability and limitation of current scoring systems. Should we be considering a risk scoring system which supplements intrinsic factors by some information on the level of preventive care which may be available?

References:

• Bliss M, Pressure sores – demographic perspectives J. Tissue Viability, 2000 10, 106–115.
• Haisjackl M, Hasibeder W, Klaunzer S, Altenberger H, Koller W. Diminished reactive hyperaemia in the skin of critically ill patients. Crit care Med. 1990 18 813–818.
• Hartl WH, Gunther B, Inthorn D, Heberer G. Reactive hyperaemia in patients with septic conditions. Surg 1988 103, 440–444.
• Witkowski J, Parish L. Skin failure and the pressure ulcer Decubitus 1993, 6(5) 4.
• Waterlow J. Prevention is cheaper than cure. Nursing Times 1988, 84 (25) 69–70.

Table 2. Description of the groups of patients who developed a sore, skin redness or neither during the study period. Patients who were in hospital for longer than the one-year study period are omitted from Mean stay calculation.