EUROPEAN PRESSURE ULCER ADVISORY PANEL

CAN PRESSURE ULCER PREVENTION BE A WASTE OF TIME?
Further Comments on Hagisawa and Barbenel’s important study (1999)

The limits of pressure ulcer prevention
In the last issue of the EPUAP Review several authors gave their opinions upon the setting of appropriate minimum rates of pressure ulcer occurrence. This debate was sparked by the publication by Hagisawa and Barbenel of apparent limits to pressure ulcer prevention among a defined patient population. In this issue, Ruud Halfens of the University of Maastricht continues the debate. Further commentary on this contentious issue is welcomed. A subsequent issue will contain a response from Hagisawa and Barbanel to the comments offered by EPUAP members.

An angry physician approached a tissue viability nurse about an AIDS patient in a terminal phase, who developed a pressure ulcer: ‘How is it possible that this patient developed a pressure ulcer? You are paid to prevent pressure ulcers!’ The nurse looked at him and answered: ‘As soon as you have cured the patient from AIDS, I guarantee you that I will have him free of pressure ulcers’.

Not all pressure ulcers can be prevented. Although one of the main goals of the EPUAP is to reduce both the incidence and prevalence of pressure ulcers, to what level of occurrence do we want to reduce them? What is a realistic target?

Recently an interesting study from Japan was published in the Journal of the Royal Society of Medicine (Hagisawa & Barbenel, 1999). Pressure ulcer prevalence and incidence were assessed in 275 patients, who were either admitted to a well-staffed internal medicine ward during a 12-month period or who were present on day 1 of the study. Patients scored as being at high risk on the Braden scale (score 16 or less) received active preventive care, weekly assessment and continuous monitoring. The preventive measures included turning the patient every two hours, skin inspection at least once a day, the use of an alternating pressure air cell mattress, keeping the skin clean and dry by bathing, rinsing the perineum after every bowel movement, evaluation of nutritional status and fluid/electrolyte balance, and urinary catheter and bowel management.  In addition careful attention was paid to avoidance of friction when transferring from bed to chair and vice versa. If skin redness was detected that did not resolve within 30 minutes, a hydrocolloid dressing was applied to the reddened area which was continuously monitored until the redness disappeared. So, in fact one could say that ‘best current practice’ was used during this study. Incidence and prevalence figures found were reported to be the lowest achievable for this patient population.

In the study a pressure ulcer was defined as an area of broken skin (stage 2 or higher). The incidence among all patients (both those at high risk and minimal risk) was 4.4 while the prevalence was 5.1%. None of the minimal-risk patients (Braden score 17 or higher) developed a pressure ulcer. For the high-risk patients (n = 36) alone the incidence was 33.3%. Patients who developed a pressure ulcer (n =12) were all severely ill patients: including five patients with Creutzfeldt-Jakob disease, multiple sclerosis and multi-organ failure, and four with lung cancer. 

So this study suggests that even when using ‘best current practice’ with regard to pressure ulcer prevention, the incidence and prevalence of pressure ulcer in this internal medicine ward was 4.4% and 5.1%. While not all pressure ulcers can be prevented, data of such studies are useful to obtain insight into what the lowest, and presumably therefore acceptable incidence and prevalence rates may be.

However, from a broader perspective, I would like to discuss two problems with the study reported by Hagisawa and Barbebel. Can the results be applied to other popula-tions (the question of generalization)? If Stage 1 ulcers had also been considered by Hagisawa and Barbenel then a doubling of the prevalence rate to about 10% would not have been surprising. A 10% prevalence is broadly similar to that reported in other surveys that have considered medical patients. This figure is not completely different to other prevalence rates for this patient population. For example, the Dutch National prevalence study (Bours et al, 1999) reported a pressure ulcer prevalence rate within internal medicine wards of university hospitals of 11.2 % (5.7% without stage 1).  However, considering only those internal medicine wards within non-teaching hospitals the prevalence rate was twice as high, namely 21.5% (10.6% without stage 1). Does the similarity between the prevalence rate reported by Hagisawa and Barbenel, and the data gathered within Dutch teaching hospitals suggest that the prevalence rates achieved within the Dutch internal medicine wards are the lowest achievable? However, the knowledge we have about the preventive measures used in these university hospitals would appear to suggest that practice may not reflect the ‘best available’ and so this suggests that a lower prevalence rate must be possible. From this comparison it would appear that one hospital’s lowest achievable pressure ulcer prevalence rate may not reflect the performance achievable within other care providers or health systems

A more fundamental challenge within Hagisawa and Barbenel’s study was its objective of defining the lowest achievable pressure ulcer incidence and prevalence rates! Although, in theory, all pressure ulcers can be prevented this is not the case in practice for perhaps two main reasons. Firstly, aggressive preventive care may be discontinued for ethical reasons – for example in the terminally ill.  Additionally we do not possess enough knowledge, methods and time to practically protect all patients from pressure and shearing forces. So, does this mean that we do have to search for the lowest achievable rates, and accept that not all pressure ulcers can be prevented? One of the dangers of acceptable occurrence rates may be their use as an excuse for the development of pressure ulcers. In my opinion it is better to investigate why a patient developed a pressure ulcer even where ‘best current practice’ was adopted. Such an approach may give more insight as to why pressure ulcers occur, and this knowledge could be used to guide the development of new and appropriate preventive methods. In Hagisawa and Barbenel, most recruited patients were very ill, and of the twenty-two patients who died, eight died with a pressure ulcer. Perhaps aggressive preventive care ceased as death approached? Or perhaps these patients were so ill that preventive activities were ineffective. Perhaps the pressure ulcers were even the cause of death? The publication offered no information regarding these points.

In conclusion, Hagisawa and Barbenel is a useful study that sets out to determine the lowest achievable pressure ulcer incidence and prevalence rates. However, do we have to accept these minimum rates or must we continue to investigate why patients develop pressure ulcers? In my view the last point should form the basis for our actions and even if determined, and agreed, a lowest achievable occurrence rate should never be accepted as an excuse for the development of a pressure ulcer.

References

• Hagisawa S and Barbenel J, (1999). The limits of pressure sore prevention. Journal of the Royal Society of Medicine, 92, 576–578.
• Bours GJJW,  Halfens RJG and Joosten CMC, (1999). Landelijke prevalentie onderzoek decubitus (National Prevalence Study Pressure Ulcers). Maastricht.