EUROPEAN PRESSURE ULCER ADVISORY PANEL

MEDICAL MANAGEMENT OF PRESSURE ULCERS.  Part 1
Dr Mary Bliss, London, adapted from a talk given at the Fifth Oxford European
Wound Healing Summer School held at St Anne’s College, Oxford, 28 June – 1 July 2000

The chief medical contribution to the management of pressure injuries should be helping to understand the patho-physiology and principles of prevention. Treatment is mainly carried out by nurses. Healing a pressure sore is no different from healing any other wound providing the condition of the patient permits it and pressure is properly relieved. Plastic surgery may be helpful in selected patients.

Pressure Injuries
What is a pressure injury, and why should it be called an ‘injury’ and not an ‘ulcer’ or ‘sore’? It is because it is an acute (not chronic) wound resulting from tissue death due to ischaemia caused by pressure (Fig. 1). A pressure injury is no different from wounds due to other causes, for example, a blow or a burn. All result in dead tissue which has to be removed by the body (Fig. 2) before healing: granulation, contraction and eventual re-epithelialisation can occur. The sore is merely part of the healing process: it is the acute injury, the reasons for it and how to prevent it that we need to concentrate on.

Effect of pressure
If we press a finger on the back of a hand and then take it away quickly we will see a white spot where the blood has been squeezed out of the capillaries by pressure between it and the underlying bone. Pressure injuries nearly always occur over bony areas of the body where pressure, and therefore tissue distortion, is greatest. The main weight bearing areas in the recumbent body are the sacrum, hips and heels, and in the sitting posture, the ischial tuberosities. But pressure injuries can occur in any part of the body which is subject to pressure, for example, the knee (Fig. 3).

Figure 4 shows the effects of a soft mattress with a catheter spigot (or a wrinkle in a sheet) pressing on the skin of a plump patient. The catheter spigot is causing high localised pressure at the point where it is indenting the skin. This squeezes and distorts the neighbouring capillaries both by direct pressure and by causing shear forces. Shear forces occur at the edges of a compressing object where pressurised and non pressurised tissues met,¹ or where tissue such as skin tries to slide on adjacent structures, for example, subcutaneous tissue or bone.² Together with direct pressure, this causes stretching and blanching (loss of blood flow) in the affected capillary beds. The discomfort caused by interruption of the blood supply by even a small object such as a wrinkle in a sheet is normally so severe that the sufferer will immediately move to relieve it. But if he cannot feel pain, or is too ill to move, the ischaemia may be prolonged sufficiently to cause cell death resulting in a pressure sore.

The soft mattress causes no distortion of the skin other than that due to the catheter spigot. Pressure injuries are always caused by localised objects indenting soft tissue. Pressure which is evenly distributed does not cause tissue distortion and therefore does not cause injury. Divers who are subjected to multiaxial pressures of hundreds of millimetres of mercury, which are equalised inside and outside the body, do not get sores.³

However, there is another source of localised pressure besides the spigot shown in the diagram: a bony prominence (which could be the sacrum or greater trochanter) pressing down under the weight of the skeleton on soft tissue deep inside the body. This large heavy object is causing much greater pressure and tissue distortion than the catheter spigot, with shearing (stretching) forces extending widely into surrounding connective tissues and muscle. The result is blanching of the capillaries with failure of the blood supply in the deep periosteal tissues similar to that caused by the spigot on the skin. If the pressure is unrelieved, these will die, giving rise to a deep pressure sore. Deep sores do not originate in the skin, but in the deep tissues where the pressures due to internal bony prominences are much higher than on the skin itself.⁴ They only secondarily involve the skin as the necrotic tissue forms an abscess which is finally discharged. The extent of the forces caused by large internal bones explains why deep pressure sores are usually more extensive underneath the skin than on the surface and characteristically have overhanging edges. (Fig. 2) This is not due to infection invading deep tissues, but to the distribution of the pressure and shear forces which caused the original injury, the extent of which only becomes apparent as the dead tissue begins to break down. In a thin patient, pressure due to bone will involve the subcutaneous tissues and skin directly, so that the injury will be full thickness from the start.

We should now be able to understand why some types of soft mattress are not able to prevent all sores. Although they may be effective at preventing pressure on the skin, they are not able to prevent deep pressure due to bony prominences inside the body, particularly in sick patients with flaccid tissues in whom pressure is likely to be much higher than in normal people with resilient tissue. Lack of movement, which is required for lymphatic drainage, is also a factor.⁵

Illness
Pressure injuries only occur in sick people. This is frequently overlooked, partly because by the time the sore becomes visible the patient has often recovered from the acute episode which caused the original injury. However, careful enquiry will almost always show that there has been an illness, or exacerbation of a chronic illness, or trauma, in the hours or days preceding a new pressure injury. If we think about it, this must be so. We do not expect to get a pressure sore every time we fall asleep, or even if we have to sit for eight hours in an aeroplane – however uncomfortable this may make us. Even handicapped people who have had strokes or spinal injuries do not usually develop pressure sores whilst they are well, but only following a period of illness, or stress, for example, a urinary tract infection or a respite admission to a hospital or nursing home. So how does acute illness predispose to pressure injury?

Firstly, dehydration, hypotension and some types of muscle paralysis make tissues soft and flabby so that they are less resilient and more likely to suffer distortion with pressure than normal tissue. Secondly, illness reduces the ability to move in response to pressure pain. Thirdly, failure of sensation or of appreciation of pressure pain may be even more important than poor mobility. Patients with motor neurone disease or polio,⁶ which only affect mobility, seldom develop sores whilst patients with multiple sclerosis, Parkinson’s disease or diabetic neuropathy who may be much less paralysed do. These patients have not only had impaired sensation but also abnormalities of the autonomic reflexes which are important for regulating the blood supply. These may be adequate to protect the patient in health but not in illness. This brings us to the fourth, probably most important effect of illness in causing tissue injury: impaired reactive hyperaemia or vasomotor control of the peripheral circulation.⁷

Reactive hyperaemia is the increased blood flow which occurs in an organ which has been rendered ischaemic for any reason. This includes activities which require increased supply of oxygen such as running or digesting as well as the response to ischaemia due to pressure. It causes dilatation of the arterioles, capillaries and venules partly by the action of substances, the chief of which is nitric oxide, produced by the ischaemic endothelial (Lining) cells of the blood vessels and partly by reflex vasodilation. Reactive hyperaemia is the vital process by which the healthy body directs blood to whatever part needs it most at any time of the day and night. Normal capillaries are not inert tubes, but live, dynamic structures which are continually relaxing and constricting in a process known as vasomotion. Vasomotion and reactive hyperaemia have been shown to be impaired both in patients liable to pressure sores⁸ and in very sick people, for example, intensive care patients.⁹

Acute illness, particularly if it is due to sepsis, or trauma, causes inflammatory products, which can paralyse the vascular tree, to be disseminated throughout the body. Although the capillaries are maximally dilated, blood is short circuited from the arterioles to the venules, thus leaving vital areas ischaemic. Reactive hyperaemia, which should be able to direct blood to areas of need is no longer able to work so that cells in these tissues die. Patients with very severe sepsis or trauma can develop widespread vasomotor paralysis causing multi-organ failure and death unless the cause can be effectively treated. It is significant that patients who are most likely to develop multi-organ failure with illness are the same as those most susceptible to pressure injuries: elderly patients with malnutrition, alcohol abuse, diabetes, advanced cancer, terminal illness, sepsis, vascular and neurological disease.¹⁰ Therefore, it is likely that the pathological processes which cause multi-organ failure and pressure injuries are similar, if not identical. Patients who develop pressure injuries usually have evidence of failure of at least one other organ, for example, the brain causing acute confusion, or the gut causing constipation.

It is essential to understand the importance of acute illness in causing pressure injuries in order to develop methods of preventing them. It is not sufficient simply to measure interface pressure, or even deep tissue pressure or tissue oxygen or carbon dioxide levels, in healthy volunteers on support surfaces because the results are likely to be very different from those in a septicaemic patient in an intensive care ward, or in a shocked patient with a new spinal cord injury, or even in a 76 year old patient with a stroke and a urinary tract infection. These are the patients we need to study. It should not be difficult because the skin is an easily accessible organ, but it requires a mind shift away from measuring pressure per se. For example, Laser Doppler flow meters could be used to measure skin blood flow before and after local application of pressure in acutely ill patients with a high pressure sore prediction scores to see how the results differed from those in healthy age matched controls. We might then begin to understand why some types of support systems work better than others.

Prevention
We can prevent sores without fully understanding their patho-physiology, just as we treat many other diseases which we do not understand although we usually treat them better when we do.

The effect of illness in causing pressure injuries explains the need for early intervention to prevent them. In a study of elderly patients with fractures, Versluysen¹¹ found that of 66% of patients who developed sores, 83% developed them during the first five days in hospital. The largest number occurred on the day of operation. In the USA it has been suggested that one quarter of all sores originate on the operating table.¹² Anaesthetics and sedatives which cause sensory loss or inattention, dehydration and low blood pressure, and poor pain relief which inhibits patients from moving, exacerbate the effect of the original illness or trauma. Pressure sore prediction scores are usually unhelpful because the patients’ condition can change within the hour. Patients who may have been relatively fit on admission can become rapidly and highly at risk with increasing shock and dehydration, especially in the peri-operative period. Patients with predisposing conditions such as old age, neurological disease, vascular disease or cancer are particularly vulnerable. Instead of compiling risk assessment scores we need to learn to recognise vulnerable groups and to be prepared to provide adequate pressure relief early for these patients, whatever their ‘score’.

Most important of all, we need to examine patients. First, we need to see if they can turn themselves over in bed because if they can – and while they can – they are unlikely to develop a pressure injury. Second, we need to search for persistent erythema. Unlike the normal blush caused by reactive hyperaemia in a pressure area which usually fades within minutes of changing a patient’s position, persistent erythema may remain for several hours or days. Also known as a Grade 1 pressure sore¹³, it usually has a more bluish tinge than reactive hyperaemia. It is evidence of tissue damage and, depending on the degree of capillary thrombosis and inflammation in the affected area, it may or may not blanch on pressure. Provided pressure, and hence further ischaemia, is immediately relieved, most Grade 1 pressure injuries heal without breaking down; but if pressure is not properly relieved, or if the initial damage has been too severe, they will progress to form a superficial, or, in cases of deep injury, a deep pressure sore. The presence of a Grade 1 sore is irrefutable evidence that the patient is highly at risk of further pressure injury, whatever his risk score or apparent state of health. It needs to be carefully documented and pressure relief must be provided immediately to prevent further damage.