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Part 1. Causes of pressure ulcers

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VOL: 98, ISSUE: 11, PAGE NO: 41

Krzysztof S. Gebhardt, PhD, RGN is clinical nurse specialist, pressure ulcer prevention at St George’s Healthcare NHS Trust, London



A pressure ulcer can be described as localised, acute ischaemic damage to any tissue caused by the application of external force (either shear, compression, or a combination of the two).

Pressure ulcers are also known as ‘bedsores’, ‘decubitus ulcers’ and ‘decubiti’ although these names are now rarely used as it is recognised that the ulcers are not, in the main, caused by lying or being in bed. Pressure sores is the term used commonly in the UK. Some authors refer to pressure damage to encompass pressure injuries that are not open wounds (such as blisters and non-blanching erythema).

Distortion or deformation damage is probably the most accurate description. Pressure ulcers is a term used widely in the USA and other countries and has been accepted as the Europe-wide term by the European Pressure Ulcer Advisory Panel (EPUAP).

Direct causes

Pressure ulcers occur when soft tissues (most commonly the skin) are distorted in a fixed manner over a long period. This distortion occurs either because the soft tissues are compressed and/or sheared between the skeleton and a support, such as a bed or chair when the person is sitting or lying, or because something is pressing into the body, such as a shoe, surgical appliance or clothing elastic. Blood vessels within the distorted tissue are compressed, angulated or stretched out of their usual shape and blood is unable to pass through them. The tissues supplied by those blood vessels become ischaemic.

The precise nature of the changes that take place in ischaemic tissue is not fully understood (Bliss, 1998; Nixon, 2001) but if ischaemia persists for a sufficient length of time, necrosis takes place. This is the start of a pressure ulcer and, in particularly susceptible patients, pressure ulcers can occur within one to two hours (Kosiak, 1958; Reswick and Rogers, 1976).

As well as occluding blood flow, tissue distortion also obstructs lymphatic flow, which leads to accumulation of metabolic waste products, proteins and enzymes in the affected tissue. It is suggested that this can also initiate tissue damage, although the precise mechanisms are not fully understood (Reddy, 1990).

Because living tissues are not static, the way they are distorted changes over time. When constant pressures are maintained, soft tissues mould themselves to accommodate the external shape. Known as tissue creep (Dodd and Gross, 1991), it may reduce external pressures but may also exaggerate internal distortions. This effect and the internal deformation of tissues under pressure in general is significantly greater in paraplegic patients (Reger et al, 1990).


It is important to understand that the application of pressure in itself does not cause damage. Divers and soft-bodied sea organisms can operate at great depths of water with no risk of pressure damage. Although the external pressures can be extremely high, they do not cause tissue distortion because they are uniform. It is only when pressure becomes non-uniform and pressure gradients occur between adjacent areas of tissue that distortion occurs and the potential for pressure damage arises (Neumark, 1981).

Areas particularly prone to pressure damage are bony prominences, such as the heels, ankles, hips and elbows, which have a thin covering of soft tissue. Large compressive forces are concentrated when the body is supported on these pressure points, due to the small surface area and the fact that there is little padding to dissipate those forces.

Depth of tissue is not necessarily the determining factor, however. Although the soles of the feet have a thin covering of soft tissue, they have a vasculature that is particularly well-adapted to withstand considerable distorting forces. On the sacrum and buttocks, on the other hand, although there is a relatively thick covering of soft tissue and a wide supporting surface, the blood vessels are not adapted for weight-bearing, which means that even with fairly light compression, pressure ischaemia can develop rapidly.

When a compression occurs, pressure is applied from at least two sides (Fig 1). This is the reason why pressure damage can present in two distinct clinical patterns. Tissue distortion and superficial damage occur with pressure on the skin surface, particularly if the supporting surface is uneven. If this is maintained for a prolonged period, it may still result in extensive damage as successive layers of tissues are destroyed. Superficial pressure ulcers caused by compression with minimal shearing, tend to have a characteristic regular outline, and can often be matched easily to the shape of the underlying bony prominence (Fig 2) or the object that caused the ulcer.

The most serious pressure damage usually occurs as a result of the deformation in the deep tissues near the underlying bony prominence. Because the pressures can be much higher than at the skin/support interface (Sangeorzan et al, 1989; Le et al, 1984) and because larger blood vessels are more likely to be affected, necrosis of a large volume of tissue often takes place. When the supporting structures of the skin have been destroyed, parts of the skin become non-viable and die subsequent to the primary deep tissue destruction. As the non-viable skin breaks down, a cavity filled with necrotic tissue is revealed (Fig 3).


Shearing of soft tissue occurs when forces moving in different directions are applied to the same tissue mass. For example, if a person is sitting up in bed, the skeleton tends to move towards the feet as gravity drags the upper part of the body downwards (Fig 4). However, at the skin/support interface, frictional forces resist the movement of the body. The tissues between the skin and the skeleton are therefore distorted, and any blood vessels running through the area become sheared along with the rest of the tissue. Because shearing occludes flow more easily than compression (for example, it is easier to cut off flow in a water hose by bending than by pinching it), shear can be considered to be even more significant than pressure in the causation of pressure ulcers (Goossens et al, 1993). 

Areas of the body particularly susceptible to shearing include ischial tuberosities, heels, shoulder blades and elbows. These are areas on which the body is frequently supported when in a position (such as sitting or lying semi-recumbent) which allows forward slide. Superficial pressure ulcers caused by shearing tend to have a jagged and uneven appearance (Fig 5).


Friction, as well as pressure and shear, is also frequently cited as a cause of pressure ulcers (Allman, 1997). This is, of course, true in the indirect sense that friction is necessary to generate shearing forces. However, it is often taken in the broader sense of causing direct tissue damage, for example, when blisters are caused by a patient being dragged up a bed with a rough sheet. However, this type of injury is an acute mechanical and heat trauma and the aetiology is quite different to that of pressure ulcers. Friction is not, therefore, a direct cause of pressure ulcers, although it is clearly possible that skin weakened by pressure ischaemia may be more susceptible to friction, and the two will act together to hasten skin breakdown.

The reactive hyperaemia cycle (Fig 6)

Unlike in water, all animals on land are unsupported by the medium (air) they find themselves in. Therefore, all soft-bodied animals must develop mechanisms to ensure they do not suffer damage when their tissues are distorted by contact with whatever is supporting them. Despite this being an essential requirement of survival on dry land, little or no research seems to have been done to identify what physiological mechanisms exist to prevent pressure damage.

However, it is reasonable to assume that tissue distortion, when it occurs, causes ischaemia. This in turn stimulates protective movements to relieve distortion, and circulatory activity which aims to restore normal blood perfusion in the affected areas. The majority of protective movements are reflexes and the person is unaware of making them. However, if these prove insufficient to relieve ischaemia, the central nervous system is stimulated by discomfort and ultimately by severe pain. This generally ensures that pressure is relieved before permanent damage has been done.

Once circulation has been restored, a dilatation of local capillaries and increased blood flow takes place, referred to as reactive hyperaemia. This presents superficially as a bright pink transitory patch on the skin, often called blanching erythema because it blanches on pressure unlike the dull red non-blanching erythema that indicates tissue damage (Bliss, 1998). Reactive hyperaemia rapidly restores oxygen and carbon dioxide balance and flushes out waste products. Erythema then subsides as tissues are restored to their resting state. Additionally, healthy individuals make frequent major postural changes during sleep and small adjustments on average every 11.6 minutes (Keane, 1978).

Apart from restoring tissues to their resting state after an ischaemic episode, the circulatory system has a direct role in optimising perfusion of the tissues during distortion. Studies have shown that adaptive changes occur in the microcirculation in response to repeated loadings of tissue (Bader, 1990), although little is known about their triggers and mechanisms.


When the reactive hyperaemia cycle ceases to function adequately, a pressure ulcer will almost certainly develop unless preventive action is taken. There are three potential causes of pressure ulcers: loss of movement, failure of reactive hyperaemia and loss of sensation. The creation of a pressure ulcer can involve one, or a combination of these factors.


Immobility, in the absence of additional factors, is rarely the primary cause of pressure ulcers. To cause pressure ulcers independently, the immobility has to be profound (such as that which occurs in the end stage of motor neurone disease or in some cases of multiple sclerosis). Even small bodily movements such as leaning forward or side to side when seated are usually sufficient to give adequate pressure relief.

Patients with ill-fitting plaster casts can be placed in the same category, as they cannot move away from the pressure which is causing distortion of their tissues. Patients with profound immobility but intact sensation rarely develop pressure ulcers when they can still communicate. The pain of tissue ischaemia ensures that these patients frequently ask for their position to be changed. Patients with orthopaedic casts should be encouraged to report any discomfort and pain.

Failure of reactive hyperaemia

In patients with a failure of reactive hyperaemia, the tissues are no longer able to recover from ischaemic episodes, and pressure ulcer prevention is probably most difficult in this group. Failure of reactive hyperaemia can occur in very sick and dying patients in whom there is insufficient peripheral blood pressure to refill capillary beds emptied by compression. Clinically, this presents as white patches in pressure areas which do not change colour rapidly to the red of reactive hyperaemia, as they would in a healthy person. Rather, the white patches remain for many minutes before slowly returning directly to a more normal skin colour with little or no reactive hyperaemia being observable. Similar effects can be seen in critical care patients who are on high doses of inotropes, such as adrenaline.

Another group within this category are some patients who have sustained neurological damage. They present with repeated pressure ulceration of the same part of the body (for example, one buttock, but never the other). There may not be any differences in the external pressure loading, postural faults or activity patterns that would explain the differences in pressure tolerance between the two buttocks. However, careful measurement of tissue responses to repeated pressure loading by percutaneous oximetry reveals that reactive hyperaemia is abnormal. There is an absence of a positive adaptive response, and a reduction in oxygen tension with each successive application of pressure (Bader, 1990). This effect is difficult to explain, as reactive hyperaemia is not thought to be controlled primarily by the nervous system (Michel and Gillot, 1990).

Since individuals in the same diagnostic category can have either a normal or pathological circulatory response to repeated loading (Bader, 1990), this may well explain why some patients are more prone to pressure ulceration than others with the same diagnosis (Sacks et al, 1988).

Loss of sensation

This is probably the most common cause of pressure ulceration. The person affected cannot feel the discomfort and pain normally caused by prolonged tissue distortion, does not have reflex protective responses to this type of stimulation and is not stimulated to make protective movements by discomfort or pain. The problem may arise in one of two ways. First, among other things it may be due to damage or severance of the nervous system. This damage may be:

- Congenital (for example, spina bifida);

- Traumatic (for example, spinal injury);

- A disease process (for example, ischaemic damage to the spine following rupture of an aortic aneurysm, metastatic disease, peripheral neuropathy secondary to diabetes or leprosy, and neurological diseases);

- Iatrogenic causes (for example, spinal anaesthesia, and local nerve block).

Interestingly, when spinal injury occurs at a higher level causing quadriplegia, the affected person is at less risk of pressure ulcers than a paraplegic (Hirose, 2001). This is probably because in the quadriplegic, the reflex loops of the lower spine are less affected and reflex protective responses against pressure damage remain intact.

Second, the central nervous system may be affected. This may be due to unconsciousness or brain damage. The latter manifests in some patients who have sustained head injuries, have brain diseases such as Alzheimer’s disease or have had long-term treatment for psychiatric conditions such as depression or schizophrenia. Although there is apparently adequate sensation, circulation and mobility to prevent pressure ulcers, the brain seems to suppress protective reflexes and disregards sensory warnings of tissue ischaemia. These patients may or may not feel ischaemic pain but even if they do, they do not make appropriate movements to relieve pressure.

Combined pathology

The reactive hyperaemia cycle rarely breaks down due to one factor acting in isolation (Table 1). The diabetic patient with neuropathy of the feet is likely to have abnormal circulatory function in that area. The paralysed patient with a spinal injury will have lost sensation and the ability to move the affected areas. The ventilated patient in the critical care unit is unable to feel or move due to anaesthesia while the peripheral circulation may be compromised by the administration of inotropes.

Chronic and acute susceptibility

To formulate effective plans for the prevention and management of pressure ulcers it is important to understand that regardless of aetiology patients at risk of pressure damage fall into one of two groups - those who are acutely susceptible and those who are chronically susceptible.

Acute susceptibility arises due to sudden illness or trauma or due to an operative procedure. It is likely to be of relatively short duration (usually no more than two weeks) and once the underlying causes are resolved, the patient will usually be susceptible no longer. For example, a patient admitted for surgery may only require high-dependency care for a short period on the day of the operation and overnight but will not be susceptible the following day when no longer ventilated and sedated. Following an acute episode, however, the patient may remain chronically susceptible if the acute episode causes permanent damage to the body’s defence mechanisms against pressure damage. For example, immediately following spinal injury there is an acute phase when there is very high susceptibility (Byrne and Salzberg, 1996). This resolves after a period of time but the patient remains susceptible to some degree for the rest of their life.

Chronic susceptibility will last for a prolonged period of time due to permanent damage caused by trauma or by degenerative disease. Examples include people with spinal or head injuries, patients who have had a cerebrovascular accident and have residual hemiplegia, those with progressive neurological disease (multiple sclerosis, Alzheimer’s disease), diabetic neuropathy and congenital neurological conditions, such as spina bifida.

Chronic susceptibility can be exacerbated by acute episodes. For example, an illness such as a chest or urinary tract infection may reduce tissue tolerance to pressure and increase susceptibility acutely for the duration of the illness.

The significance of pressure ulcers

Pressure ulcers are recognised as having the potential to cause significant harm to the individuals who suffer them, and their prevention and management also consumes large slices of health care budgets. Furthermore, failure by health care professionals and organisations to prevent or manage pressure ulcers appropriately is increasingly the subject of litigation.

To the individual, the consequences of sustaining an ulcer range from mild discomfort and inconvenience to a dramatic reduction in quality of life caused by devastating and painful injuries of huge size (Fig 7), or even death through septicaemia or osteomyelitis.

The costs of pressure ulcers remain the subject of a debate that is not particularly well grounded in factual information. Regardless of exact figures, it is recognised that expenditure is high both on treatment of existing ulcers and on their prevention. The debate, sparked by the suggestion in The Costs of Pressure Sores (Touche Ross and Co, 1993) that treating patients who develop pressure ulcers is cheaper than preventing the ulcers in the first place is perhaps somewhat sterile. The NHS and health care professionals have a clear mandate and ethical imperative to prevent morbidity and mortality and that includes morbidity and mortality caused by pressure ulcers, regardless of whether it is more expensive to prevent them or not. There is little doubt, however, that prevention is expensive. In fact, expenditure on pressure-relieving devices is one of the five largest expenditures in the NHS non-pay budget.

All health care professionals have a responsibility to ensure that this expenditure is used wisely. This requires them to have adequate and up-to-date knowledge of the aetiology, prevention and management of pressure ulcers. All the more so, since litigation is rising throughout the NHS and ignorance is no defence in the eyes of the law. The legal consequences of poor pressure area care can be extremely costly in terms of finance and reputation to organisations, and professionally devastating for individual clinicians.

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