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.
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).
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.
Pressure ulcers are obvious on physical examination. Wound culture and sensitivity testing of the exudate in the ulcer identify infecting organisms and antibiotics that may be needed. If severe hypoproteinemia is suspected, total serum protein values and serum albumin studies may be appropriate.
Treatment should relieve pressure on the affected area, keep the area clean and dry, and promote healing. (See Special aids for preventing and treating pressure ulcers.)
❑ Assess the skin of bedridden patients every 4 hours for possible changes in color, turgor, temperature, and sensation. Examine an existing ulcer for any change in size or degree of damage. When using pressure relief aids or topical agents, explain their function to the patient.
❑ Prevent pressure ulcers by repositioning the bedridden patient at least every 2 hours. To minimize the effects of a shearing force, use a footboard and don’t raise the head of the bed more than 60 degrees. Also, use a draw or pull sheet to turn the patient or to pull him up. Keep the patient’s knees slightly flexed for short periods. Perform passive range-of-motion exercises, or encourage the patient to do active range-of-motion exercises if possible.
❑ To prevent pressure ulcers in immobilized patients, use pressure relief aids on their beds.
❑ Provide meticulous skin care. Keep the skin clean and dry without the use of harsh soaps. Gently massaging the skin around the affected area — not on it — promotes healing. Rub moisturizing lotions into the skin thoroughly to prevent maceration of the skin surface. Change bed linens frequently for patients who are diaphoretic or incontinent. Use a fecal incontinence bag for incontinent patients.
❑ Clean ulcers with noncytotoxic solutions that don’t kill or damage the cells. (Solutions such as sodium hypochlorite, acetic acid, povidone-iodine, and hydrogen peroxide are cytotoxic and shouldn’t be used.) Dressings, if needed, should be porous and lightly taped to healthy skin. Debridement of necrotic tissue may be necessary to allow healing. One method is to apply open wet dressings and allow them to dry on the ulcer. Removal of the dressings mechanically debrides exudate and necrotic tissue. Other methods include surgical debridement with a fine scalpel blade and chemical debridement using proteolytic enzyme agents.
❑ Encourage a high-protein diet — supplemented with vitamins, minerals, and fluids — sufficient to maintain body weight and promote healing. Consult with a dietitian regarding a diet that promotes granulation of new tissue. Encourage the debilitated patient to eat frequent, small meals that include protein and calorie-rich supplements. Assist weakened patients with their meals.
Review other book chapters online related to Bedsores:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
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