Pressure ulcers are localized areas of tissue necrosis that tend to develop when soft tissue is compressed between a bony prominence and an external surface for a prolonged period of time.

The consequences of pressure-induced skin injury range from nonblanchable erythema of intact skin to deep ulcers extending down to the bone.

The common pathway that results in necrosis of the skin is an unrelieved application of pressure to susceptible tissues for a prolonged period of time. The resulting ulcer imposes a significant burden not only on the patient but on the entire health care system.

The staging, epidemiology, pathogenesis, and clinical manifestations of pressure ulcers will be reviewed here. Prevention and treatment are discussed separately.


A number of staging systems have been developed to describe the extent of pressure ulcers. The most commonly used system, proposed by the National Pressure Ulcer Advisory Panel, is described as follows:

Stage 1

Stage 1 is characterized by an observable pressure-related alteration of intact skin which, when compared to an adjacent or opposite site area on the body, may include changes in one or more of the following: skin temperature (warmth or coolness); tissue consistency (firm or boggy feel); and/or sensation (pain, itching).

The ulcer appears as a defined area of persistent redness in lightly pigmented skin; in darker skin tones the ulcer may appear with persistent red, blue, or purple hues.

Stage 2

Stage 2 is characterized by a partial thickness skin loss involving the epidermis and/or dermis. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater.

Stage 3

Stage 3 is characterized by a full-thickness skin loss involving damage or necrosis of subcutaneous tissue which may extend down to, but not through the underlying fascia. The ulcer presents clinically as a deep crater with or without undermining of the adjacent tissue.

Stage 4

Stage 4 is characterized by a full-thickness skin loss with extensive destruction, tissue necrosis, or damage to the muscle, bone, or supporting structures.

These staging systems primarily describe ulcer depth. Wounds also may be characterized on the basis of features such as size, the presence of necrotic tissue, and the undermining of tissue.

Healing scales

Staging systems are also commonly used to monitor and describe pressure ulcers that are healing. However, this practice, known as reverse staging, is not recommended. Healing ulcers do not progress serially from one stage to the next lowest. Instead, they heal through a process that includes granulation, wound contraction, reepithelialization, and scar formation.

The healing process is better described by scales that capture changes in surface area, the extent of necrotic tissue and exudate, and the presence of granulation tissue.

A number of scales have been advocated for use in monitoring the healing of pressure ulcers, including the Pressure Sore Status Tool (PSST) , the Pressure Ulcer Scale for Healing (PUSH) , the Sessing Scale and the Wound Healing Scale.

Given the differences among these staging systems, the scale used should be explicitly described to facilitate effective communication among clinicians responsible for patients with a pressure ulcer. Training in the use of these scales is also required to ensure that ulcers are staged in a consistent manner.

Pathogenesis of pressure ulcers

The development of a pressure ulcer is a complex process that requires the application of external forces to the skin. However, external forces alone are not sufficient to cause an ulcer; their interaction with host-specific factors culminates in tissue damage.

External Factors

External factors that lead to the development of pressure ulcers include pressure, shearing forces, friction, and moisture.


Pressure applied to the skin in excess of the arteriolar pressure (32 mm Hg) prevents the delivery of oxygen and nutrients to tissues, resulting in the accumulation of metabolic waste products. Pressures are greatest over bony prominences where weight-bearing points come in contact with external surfaces.

A patient lying on a standard hospital mattress may generate pressures of 150 mmHg; sitting produces pressures as high as 300 mmHg over the ischial tuberosities.

Pressure in excess of 70 mmHg for two hours results in irreversible tissue damage in animal models. Ulcer formation occurs more rapidly with higher pressures, and intermittent relief of pressure prevents tissue damage.

Pressure over a bony prominence tends to result in a cone-shaped distribution with the most affected tissues located deep, adjacent to the bone-muscle interface. Tissues vary in their susceptibility to pressure-induced injury; muscle is the most susceptible, followed by subcutaneous fat and then dermis.

Thus, extensive deep tissue damage may occur with little or no evidence of superficial tissue injury. A deep necrotic wound may be the first evidence of pressure-induced injury, rather than a gradual progression of an ulcer from stages 1 through 4.

Shearing forces

Shearing forces occur when patients are placed on an incline. Deeper tissues, including muscle and subcutaneous fat, are pulled downwards by gravity, while the superficial epidermis and dermis remain fixed through contact with the external surface.

The result is stretching and angulation of local blood vessels and lymphatics. Shear forces alone may not cause ulceration, but appear to have an additive effect so that in the presence of pressure, more severe tissue damage will occur.


Friction occurs when patients are dragged across an external surface. This results in abrasion with damage to the most superficial layer of skin. Friction is most likely to result in stage 2 pressure ulcers since it does not cause the necrotic changes associated with deep tissue injury; it has only a limited contribution to the development of stage 3 and 4 ulcers.


Exposure to moisture in the form of perspiration, feces, or urine may lead to skin maceration and predispose to superficial ulceration. There are little data regarding the magnitude of the contribution of moisture to pressure ulcer development; some have questioned whether a plausible mechanism exists by which moisture leads to the deep tissue necrosis characteristic of stage 3 or 4 ulcers.

Host factors

A number of host factors may contribute to pressure ulcer development including immobility, incontinence, nutritional status, circulatory factors, and neurologic disease.


Immobility is one of the most important host factors that contribute to pressure ulcer development. Immobility may be permanent (eg, due to spinal cord injury) or transient (eg, during an acute medical illness or from the use of sedatives). There is a high correlation between a lack of spontaneous nocturnal movements and pressure ulcer development in studies using devices that measure body movement .

However, methods to measure immobility in clinical settings are generally not available. Thus, investigators have often relied upon other clinical characteristics as markers for immobility and risk for pressure ulcer development, including functional measures (eg, whether patients are able to ambulate or are bed- or chair-bound) and diagnostic information (eg, a history of a cerebrovascular accident)


Urinary incontinence is frequently cited as a predisposing factor for pressure ulcers. Some studies suggest that incontinent patients have up to a five-fold higher risk for pressure ulcer development

However, these studies have generally not considered the strong correlation between incontinence and immobility. A national survey of nursing home discharges, for example, found that 94 percent of incontinent pressure ulcer patients were bed- or chair-bound.

Urinary incontinence often does not remain as an independent predictor of ulcer development when statistical analyses are performed to account for this correlation. Several studies have suggested that fecal incontinence is a predictor.

Nutritional status

The role of nutritional status in the development of pressure ulcers is uncertain. Animal studies have found that more severe pressure-induced skin destruction occurred in malnourished animals than in well-nourished animals exposed to similar amounts of pressure.

In addition, cross-sectional studies have suggested that patients with pressure ulcers are more likely to have hypoalbuminemia

A wide variety of other nutritional measures have also been examined in prospective studies with inconsistent findings. One study found that lymphopenia was associated with ulcer development in acute hospital patients, but this was not confirmed in long-term care settings.

The strongest nutritional measure predicting pressure ulcer development may simply be whether the patient has adequate dietary intake. It is not clear if interventions to increase dietary intakes, such as initiation of tube feedings or use of dietary supplements, can prevent pressure ulcers; this is awaiting evaluation in well-designed, randomized clinical trials.

Circulatory factors

The role of circulatory factors in the development of pressure ulcers has been increasingly recognized. Some authors have suggested that "pressure sores are not irremediable afflictions of long-stay patients but a sign of acute illness".

Contributing factors to the development of tissue ischemia have been postulated to include hypotension, dehydration, vasomotor failure, and vasoconstriction secondary to shock, heart failure, or medications.

  • Several studies have demonstrated an association between low blood pressure and pressure ulcer development, although this has not been consistently found.
  • A global measure of disease severity, the Acute Physiology, and Chronic Health Evaluation (APACHE) score, has been associated with pressure ulcer development in an intensive care unit, but not among other hospital patients.
  • One study evaluated skin blood flow over bony prominences during surgery. A 500 percent increase in skin blood flow was seen in patients who did not develop a pressure ulcer postoperatively compared to no increase in patients developing a pressure ulcer, suggesting that a failure to increase blood flow in response to extended pressure contributes to ulcer development.
  • Arteriosclerotic disease, particularly of the lower extremities, may contribute to ulcer development either as a result of baseline tissue hypoxia or failure of blood flow to increase in response to pressure.

The precise role of circulatory factors in pressure ulcer development must be further elucidated, although it appears likely that they will have a major role; in the setting of decreased circulation, the pressure applied for less than two hours may be sufficient to cause severe damage.

Neurologic diseases

Neurologic diseases such as dementia, delirium, spinal cord injury, and neuropathy are important contributors to pressure ulcer development. This may in large part be related to immobility, spasticity, and contractures that are common in these conditions.

Sensory loss is also common, suggesting that patients may not perceive pain or discomfort arising from prolonged pressure. The relative contributions of immobility and sensory loss to ulcer development have not been defined.

Other factors

Many other host factors have also been evaluated in an attempt to define their role in pressure ulcer development. Among the demographic factors identified in some studies are older age, white race, and male gender. Specific diagnoses that have been associated with ulcer development include the presence of dry skin, recent lower extremity fractures, diabetes, and cardiovascular disease.

Further studies are required to determine whether these host factors are independent predictors or simply reflect the high prevalence of immobility among frail, elderly patients.


Identification of patients at risk

Knowledge of factors contributing to the pathogenesis of pressure ulcers allows the identification of patients at risk for ulcer development. Preventive interventions may then be targeted to those specific patients.

Two general approaches have been used when developing prediction rules that allow the identification of patients at high-risk for pressure ulcers. The first approach involves the use of clinical judgment to determine patient characteristics and their associated weights. More recently, empirical studies combined with multivariate statistical techniques have been employed.

Assessment of risk for pressure ulcer development is not a one-time activity. Patients should be reassessed periodically, particularly when there is a change in health status.

Norton and Braden scales

The most commonly used prediction tools based upon clinical judgment are the Norton and Braden scales.

  • The Norton scale uses a 1 to 4 scoring system in rating patients in each of five subscales: physical condition; mental condition; activity; mobility; and incontinence. A score of less than 14 indicates a high risk of pressure ulcer development.
  • The Braden scale rates patients in six subscales: sensory perception; moisture; activity; mobility; nutrition; and friction and shear using scores ranging from 1 to 3 or 4. The maximal total score is 23; a score of 16 or less indicates high-risk.

The Norton scale generally identifies more patients at high-risk than the Braden scale. The performance of these scales has been evaluated in a variety of settings; sensitivity typically ranges from 70 to 90 percent and specificity from 60 to 80 percent.

A limitation of these systems is that interrater reliability is low unless performed by trained staff. In addition, it is unclear whether they perform better than clinical judgments of risk. Nevertheless, both the Norton and Braden scales have withstood the test of time and been shown in clinical practice to be useful in predicting patients at risk of pressure ulcer development.

Clinical Manifestation and diagnosis

Pressure ulcers are usually easy to identify by their appearance and location overlying a bony prominence. The exception maybe stages 1 ulcer which can be difficult to recognize, particularly in patients with darkly pigmented skin. They also may be confused with other conditions that cause erythema such as cellulitis.

Eschar often covers deep ulcers, making it difficult to determine whether lesions are stage 3 or 4. In addition, the extent of stage 4 ulcers is often underestimated due to undermining and fistula formation; a relatively small superficial skin defect may mask extensive deep tissue necrosis.


Pressure ulcers may be associated with both medical and psychosocial complications. The medical complications can be life-threatening and are more common with stage 3 and 4 ulcers.

Psychosocial consequences are not often considered. However, patients with pressure ulcers may suffer pain and feel stigmatized by the development of chronic skin ulcers. This could result in depression, social isolation, and decrements in overall health-related quality of life. The extent and magnitude of psychosocial complications have not been well defined in the literature.


Infection is common among patients with pressure ulcers; 4 to 6 percent of nursing home patients develop an infected pressure ulcer.

On the other hand, pressure ulcers are an uncommon cause of fever, and the skin is the source of infection in only 7 to 14 percent of nursing home patients with bacteremia. When pressure ulcers do cause bacteremia, they have been associated with high mortality rates.

Osteomyelitis can occur via direct extension from the wound. This is a relatively infrequent occurrence, although one study suggested that osteomyelitis may be found in over one-third of non-healing pressure ulcers. Radiography often is unable to differentiate osteomyelitis from reactive changes in the bone due to the overlying ulcer.

Technetium bone scans are sensitive but nonspecific. Indium 111-labeled leukocyte scanning may be considered, but is difficult to interpret in the presence of surrounding soft tissue inflammation.

Computed tomography has a low sensitivity but high specificity for the diagnosis of osteomyelitis. Bone biopsy with culture may be necessary to confirm the diagnosis.

Other rare infectious complications of pressure ulcers include septic arthritis, endocarditis, and meningitis. Pressure ulcers may also pose a risk to other hospitalized patients by serving as a reservoir for resistant organisms such as methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and multiply-resistant gram-negative bacilli.

Other complications – Other complications due to pressure ulcers are rare.

  • Sinus tracts may develop that communicate with the deep viscera including the bowel or bladder.
  • Heterotrophic calcification also occasionally occurs.
  • The chronic inflammatory state arising from the ulcer may result in systemic amyloidosis.

Squamous cell carcinoma occasionally develops in a pressure ulcer and should always be considered in patients with a nonhealing wound

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