Pressure ulcers
Pressure ulcers, commonly called pressure sores or bedsores, are localized areas of cellular necrosis that occur most commonly in the skin and subcutaneous tissue over bony prominences. These ulcers may be superficial, caused by local skin irritation with subsequent surface maceration, or deep, originating in underlying tissue. Deep lesions commonly go undetected until they penetrate the skin; however, by then, they have usually caused subcutaneous damage.
Causes
Most pressure ulcers are caused by unrelieved pressure, particularly over bony prominences, that interrupts normal circulatory function, leading to ischemia of the underlying structures of skin, fat, and muscles. The intensity and duration of such pressure govern the severity of the ulcer; pressure exerted over an area for a moderate period (1 to 2 hours) produces tissue ischemia and increased capillary pressure, leading to edema and multiple small-vessel thromboses. An inflammatory reaction gives way to ulceration and necrosis of ischemic cells. In turn, necrotic tissue predisposes the patient to bacterial invasion and subsequent infection.
The patient’s position determines the pressure exerted on the tissues. For example, if the head of the bed is elevated or the patient assumes a slumped position, gravity pulls his weight downward and forward. This shearing force causes deep ulcers due to ische-mic changes in the muscles and subcutaneous tissues and most commonly affects the sacrum and ischial tuberosities.
Predisposing conditions for pressure ulcers include altered mobility, inadequate nutrition (leading to weight loss and subsequent reduction of subcutaneous tissue and muscle bulk), and a breakdown in skin or subcutaneous tissue (as a result of edema, incontinence, fever, pathologic conditions, or obesity).
Signs and symptoms
Pressure ulcers commonly develop over bony prominences. Early features of superficial lesions are shiny, erythematous changes over the compressed area, caused by localized vasodilation when pressure is relieved. Superficial erythema progresses to small blisters or erosions and, ultimately, to necrosis and ulceration. (See Pressure points: Common sites of pressure ulcers.)
An inflamed area on the skin’s surface may be the first sign of underlying damage when pressure is exerted between deep tissue and bone. Bacteria in a compressed site cause inflammation and, eventually, infection, which leads to further necrosis. A foul-smelling, purulent discharge may seep from a lesion that penetrates the skin from beneath. Infected, necrotic tissue prevents healthy granulation of scar tissue; a black eschar may develop around and over the lesion.
Pressure ulcers are described according to stages:
stage I: skin is red but not broken
stage II: damage extends through the epidermis and dermis
stage III: damage extends to the subcutaneous tissue
stage IV: involvement reaches muscle and, possibly, bone.
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