Definition

A pressure ulcer is a localized injury to the skin or underlying tissue, usually over a bone prominence, as a result of pressure or pressure in combination with shear [1]. The development of pressure ulcers due to tissue breakdown and cell necrosis is a significant problem for many patients, including the elderly and those with impaired mobility or paralysis. Pressure ulcers are associated with significant morbidity and even mortality; they can cause pain as well as decreased activities of daily living and quality of life [2]. Therefore this is a pertinent issue for many patients in rehabilitation. Furthermore, they are extremely costly; the burden on the U.S. health care system has recently been estimated at $6 to $15 billion per year [3].

Tissue breakdown is referred to by many terms, including decubitus ulcers, pressure sores, ischemic sores, and bedsores. The term pressure ulcer is the most accurate nomenclature to describe both the cause and nature of chronic, nonhealing wounds due primarily to excessive applied pressure. This term is used throughout the chapter.

The incidence of pressure ulcers among patients in acute care hospitals ranges from 1% to 33%, with prevalence rates of 3% to 69% [4,5]. Higher rates have been associated with increasing age and duration of hospital stay in the elderly [6]. In those with spinal cord injury, individuals with paraplegia are more likely to be rehospitalized because of pressure ulcers [7]. The prevalence of pressure ulcers on admission to skilled nursing facilities ranges between 10% and 26% [8,9]. A multicenter study of pressure ulcer incidence in spinal cord injury conducted across the U.S. Model Spinal Cord Injury System [10] found a significant trend toward increasing pressure ulcer prevalence more recently; the most recent period covered by this study was 2002. A consideration of the risk factors in pressure ulcer development is of vital importance because they contribute to the formulation of treatment and rehabilitation strategies. There are many factors that can lead to the development of pressure ulcers. These can be generally classified as intrinsic factors, which are related to the clinical and physiologic profile of the individual, and extrinsic factors, which are primarily attributed to the external environment (Table 148.1). These intrinsic and extrinsic factors can overlap. They highlight the complex nature of the development of pressure ulcers and are indicative of the need for a holistic and systematic approach to prevent their formation.

Intrinsic Risk Factors

Intrinsic risk factors in pressure ulcer development are related to the conditions of the individual patient. Decreased muscle activity and paralysis lead to loss of muscle bulk, thus reducing soft tissue coverage over the bone prominences of the pelvic and other anatomic regions. As muscle bulk decreases, regional vascularity diminishes and the proportion of avascular fatty tissue increases. Loss of normal muscle tone leads to abnormal responses to environmental stimuli, such as applied pressure, thus increasing the risk for blood flow to become compromised.

Furthermore, motor paralysis will directly affect a person’s ability to respond unconsciously to potential noxious stimuli (e.g., fidgeting while sitting or turning while asleep). Reduced mobility also profoundly alters the individual’s ability to consciously perform postural maneuvers necessary to relieve prolonged applied pressure, from weight shifting while sitting to walking. The loss or reduction of mobility may be further complicated by sensory impairment, leading to the absence or alteration of normal perception of environmental stimuli, such as pain or temperature. Patients with impaired sensation or proprioception are at increased risk for pressure ulcer development because they cannot sense the warning signals that precede tissue damage.

The malnourished patient is at increased risk for pressure ulcer development and will also have an impaired response to healing. Normal tissue integrity depends on correct nitrogen balance and vitamin intake. Protein depletion will lead to decreased perfusion and impaired immune response. The presence of an exuding pressure ulcer will cause massive protein loss, and the patient will move into increasingly negative nitrogen balance. The severity of a pressure ulcer can be directly related to the degree of hypoalbuminemia [11]. Fluid balance must also be considered in conjunction with nutritional status because dehydration will decrease cellular nutrient delivery.

Patients with systemic diseases may be at higher risk of pressure ulcers. For instance, those with renal disease and diabetes may be more prone to pressure ulcer formation because of their peripheral vascular status. The cognitive and mental status of an individual may also affect the ability to perform pressure relief for at-risk body areas, hence potentially increasing the risk of pressure ulcer formation.

Bowel and bladder incontinence causing excessive local moisture may alter the microenvironment of the skin surface, making it more susceptible to maceration and skin breakdown.

Extrinsic Risk Factors

The primary extrinsic risk factor is external applied pressure. Body tissues can support high levels of hydrostatic pressure, such as in deep sea diving. When pressure is the same in all directions, there is no resulting tissue damage. However, nonuniform applied pressures cause tissue distortion, leading to localized tissue damage. This will occur when a patient is in contact with an external load-supporting device, such as a bed or wheelchair. The pressure at the interface between the patient and the support surface must be maintained at a level such that the local blood supply and lymphatic circulation are not impaired. This threshold varies between individuals, and a specialized support system is often required in high-risk individuals, such as acute spinal cord–injured patients.

Any external load that can cause tissue distortion is also likely to cause shear stresses. When only shear forces are present, slipping occurs, and tissue damage will be minimized. However, shear and normal applied loads generally tend to occur together. The normal applied load required to occlude blood flow can be halved when shear forces are also present [12]. Significant clinical problems can arise from propping patients up in bed at angles of less than 90 degrees. In contrast, in the side-lying position, it has been found that blood flow is severely impaired by fully lying on the trochanteric region; but at a partial, 30-degree side-lying position, blood flow is maintained [13].

Symptoms

The primary symptoms of a pressure ulcer are due to an area of persistent tissue breakdown involving the skin and underlying tissues. The patients may complain of an open area in the skin, drainage, bleeding, odor, fever, and pain. The severity of pressure ulcers has traditionally been characterized by the extent of breakdown, as described by a staging system.

Physical Examination

Physical examination for a pressure ulcer starts with an overall assessment of the risk factors of the individual and his or her environment. During general examination, evaluation of overall strength, muscle tone, spasticity, range of motion, and presence of contractures is important. Abnormalities in these areas can contribute to both the development and the persistence of pressure ulcers. In addition, it is important to note whether the individual is malnourished, anemic, incontinent of feces or urine, cognitively impaired, or immobile from medical conditions such as stroke or spinal cord injury as well as whether appropriate pressure-relieving surfaces for seating and sleeping have been used. The Braden Scale is a commonly used nursing risk assessment tool to determine whether an individual is at risk for pressure ulcer development [14]. An individual with a score of 18 or lower is found to be at risk. A systematic approach to the examination of the pressure ulcer is necessary to provide accurate assessment and monitoring of the pressure ulcer. The following parameters are to be noted:

• Location of the ulcer

• Size of the pressure ulcer (length to be measured as the maximum measurement craniocaudally; width as the maximum measurement from side to side; depth to be measured at the deepest part of the wound perpendicular to the skin surface)

• Staging of the ulcer

• Presence of undermining or tunneling

• Ulcer bed appearance

• Presence of necrotic materials, slough, eschar, fibrous tissues

• Presence of rolled wound edges

• Presence and amount of drainage (exudate versus transudate)

• Presence of foul odor

• Health of the periulcer tissues, including any surrounding erythema, maceration, edema, or associated fungal infection

Staging of pressure ulcers describes the extent of tissue breakdown at initial examination. There have been multiple staging systems for pressure ulcers. The National Pressure Ulcer Advisory Panel (NPUAP) and European Pressure Ulcer Advisory Panel (EPUAP) have agreed on the following staging system [1].

In addition, the EPUAP/NPUAP recommends use of the following categories/stages.

This staging system can be used only for initial description of the wound. It cannot be used for repeated assessments or reverse staging, primarily because it is not a physiologic description and cannot characterize what is happening in a healing wound. Reepithelialization will occur before lost muscle, subcutaneous fat, or dermis is replaced, resulting in mistakes when healed wounds are staged again.

Care must also be taken in the evaluation of the skin of patients with darkly pigmented skin. Sprigle and colleagues [15] found that erythema in subjects with dark skin is more likely to be nonblanching and to have poor resilience. This indicates that clinicians should use persistence of erythema rather than blanching status to judge incipient pressure ulcers. The staging system defined here includes both visual and nonvisual indicators in the definition of a stage I ulcer, in part to address this issue.

All pressure ulcers are associated with some degree of bacterial colonization, which may or may not lead to local wound infection. The presence of bacterial biofilms in the wound bed may be both a cause and effect of delayed healing [16,17]. Biofilms are typically polymicrobial and are not detected by routine clinical microbiology. They may inhibit healing even in the absence of clinical signs of infection [18]. The possible clinical signs and symptoms of local infection include increasing pain in the wound; erythema, edema, and heat of the periwound area; foul odor; and purulent drainage [19]. Individuals with spinal cord injury may not have intact sensation; in such cases, infected wounds are painless but can cause systemic responses, such as autonomic dysreflexia.

Pressure ulcers also frequently exhibit wound drainage. However, this drainage is not necessarily due to wound infection, and unless it is clinically indicated, routine wound swab culture may not be warranted because this would give a false-positive result. On the other hand, in some cases, increased volumes of exudate may indicate wound infection. Systemic infection may develop if the initial local wound infection is not adequately treated. In such cases, patients may exhibit fever, malaise, and chills. Cellulitis, osteomyelitis, and bacteremia may also develop.