Pressure ulcers are a significant cause of morbidity, mortality, and cost in the United States. The incidence and prevalence of pressure ulcers vary widely from study to study likely due to the differences in reporting and classification. The incidence of pressure ulcers ranges from 0.4 to 38% in acute care, 2.2 to 23.9% in long-term care, and 0 to 29% in home care.¹ The Centers for Disease Control and Prevention (CDC) estimated in 2004 that 11% of nursing home patients had a pressure ulcer.² The estimated cost during a hospital stay related to a pressure ulcer is $43,180, with a total cost of $70,000 to manage a single full-thickness pressure ulcer.³ The total US expenditures for treating pressure ulcers have been estimated at $11 billion per year.⁴ A 2006 report found that there were 503,300 pressure-related hospitalizations in the United States, with 45,500 admissions in which pressure ulcers were the primary diagnosis.⁵ Of those admissions, 1 in 25 ended in death.⁶

Skin wounds may occur from multiple mechanisms. Pressure injuries are caused by unrelieved compression of the skin usually over a bony prominence and result in damage to the underlying tissue. Although there is variability in the pressure needed to cause damage, animal models have suggested that pressures greater than 60 mm Hg lead to profound tissue ischemia.⁷ Measurable histologic changes usually occur at between 2 and 6 hours.⁸ Animal models have also shown that cell death is proportional to the amount of pressure applied, with very high pressure forces eliciting faster cell death. Interestingly, muscle has been shown to be affected before skin. Damage from pressure ulcers often forms internally prior to being evident on the skin and superficial underlying tissue. The overlying skin may appear intact despite significant underlying damage.⁹ Although more than 200 risk factors are described in the literature, the most common factors are immobility, sensory loss, breakdown of skin integrity (influenced by factors such as age, nutrition, and circulation), moisture, and the presence of friction or shearing forces.¹⁰

In 2014, the National Pressure Ulcer Advisory Panel, the European Pressure Ulcer Advisory Panel, and the Pan Pacific Pressure Injury Alliance (NPUAP/EPUAP/PPPIA) defined a pressure ulcer as “localized injury to the skin and/or underlying tissue, usually over a bony prominence, resulting from sustained pressure.” This definition included pressure ulcers associated with shear forces. A number of contributing factors are also associated with pressure ulcers—the primary of which is impaired mobility.¹¹ Although pressure ulcers may occur anywhere, they occur most often over a bony prominence, such as the sacrum, calcaneous, coccyx, heel, and greater trochanter (Fig. 52–1). For the rehabilitation patient, such ulcers may often result from pressure and shear secondary to a cast, brace, orthotic device, or medical equipment.

The rehabilitation patient population is particularly at high risk for pressure ulcer development due to the nature of chronic disability and illness. Many of these patients have neurologic impairment (e.g., spinal cord injury, stroke, brain injury, Parkinson’s disease, and multiple sclerosis), with complications including decreased motor and sensory function, neurogenic bowel and bladder, cognitive deficit, and motor spasticity. Also seen in the rehabilitation setting are patients who are deconditioned by acute illnesses such as cancer, diabetes, cardiac and respiratory diseases, and infection. All these factors are known to contribute to pressure ulcer development.

Ideally, prevention should be the overall goal of pressure ulcer management. Early identification of pressure ulcers or at-risk skin may lead to prevention of further clinical deterioration.¹² Assessment and diagnosis of pressure ulcers begin with a thorough skin inspection. This ideally occurs during the first 24 hours of the patient’s hospital admission and preferably is performed by both the physician and a nurse or the wound care team. Accurate consensus of the assessment must occur among team members. The International NPUAP/EPUAP Pressure Ulcer Classification System is the universally recognized and accepted tool to assess and stage pressure ulcers.⁶ This classification system is based on the depth of penetration of pressure ulcer (i.e., epidermis, dermis, adipose tissue, muscle, and bone; Fig. 52–2). The Agency for Healthcare Research and Quality has published guidelines for pressure ulcer prevention (Table 52–1).¹³

Category/Stage I: Nonblanchable Erythema

Stage I involves intact epidermis with nonblanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching: its color may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler than adjacent tissue. Category/stage I may be difficult to detect in individuals with dark skin tones. This often indicates an “at-risk” individual (a heralding sign of risk; Fig. 52–3).

Category/Stage II: Partial-Thickness Skin Loss

Stage II involves a partial-thickness loss of dermis presenting as a shallow, open ulcer with a red to pink wound bed without slough. It may also present as an intact or open/ruptured serum-filled blister. It presents as a shiny or dry, shallow ulcer without slough or bruising (bruising indicates suspected deep tissue injury). This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation (Fig. 52–4).

Category/Stage III: Full-Thickness Skin Loss

Stage III involves full-thickness loss of the dermis and epidermis. The subcutaneous fat may be visible, but bone, tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. The lesion may include undermining and tunneling. The depth of a stage III pressure ulcer varies by anatomic location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and these ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III pressure ulcers. Bone/tendon is not visible or directly palpable (Fig. 52–5).

Category/Stage IV: Full-Thickness Tissue Loss

Stage IV involves full-thickness loss of the epidermis, dermis, and adipose tissue with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed—often including undermining and tunneling. The depth of a stage IV pressure ulcer varies by anatomic location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and these ulcers can be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon, or joint capsule) making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable (Fig. 52–6).

Unstageable: Depth Unknown

These lesions involve full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore category/stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as “the body’s natural (biological) cover” and should not be removed (Fig. 52–7).

Suspected Deep Tissue Injury: Depth Unknown

The cardinal sign is a purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, and warmer or cooler than adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with optimal treatment (Fig. 52–8).