Pressure Ulcers
Localized areas of cellular necrosis, pressure ulcers occur most commonly in the skin and subcutaneous tissue over bony prominences, particularly the sacrum, ischial tuberosities, greater trochanter, heels, malleoli, and elbows. These ulcers—also called decubitus ulcers, pressure sores, or bedsores—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; by then, they have usually caused subcutaneous damage.
Causes
Pressure, particularly over bony prominences, interrupts normal circulatory function and causes most pressure ulcers. 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 body to bacterial invasion and infection.
Shearing force, the force applied when tissue layers move over one another, can also cause ulcerations. This force stretches the skin, compressing local circulation. As an example, if the head of the patient’s bed is raised, gravity tends to pull the patient downward and forward, creating a shearing force. The friction of the patient’s skin against the bed, such as occurs when a patient slides himself up in bed rather than lifting his hips, compounds the problem.
Moisture, whether from perspiration or incontinence, can also cause pressure ulcers. Such moisture softens skin layers
and provides an environment for bacterial growth, leading to skin breakdown.
and provides an environment for bacterial growth, leading to skin breakdown.
Other factors that can predispose a patient to pressure ulcers and also delay healing include poor nutrition, diabetes mellitus, paralysis, cardiovascular disorders, and aging. Added risks include obesity, insufficient weight, edema, anemia, poor hygiene, and exposure to chemicals.
Complications
Bacterial invasion and secondary infection, possibly leading to bacteremia and septicemia, are common complications of pressure ulcers. If the ulcer is large, a continuous loss of serum may deplete the body of its normal circulating fluids and essential proteins. In severe cases, ulcers may extend through subcutaneous fat layers, fibrous tissue, and muscle until reaching the bone.
Assessment
The patient with a pressure ulcer will have a history of one or more predisposing factors. Inspection of an early, superficial lesion notes shiny, erythematous changes over the compressed area, caused by localized vasodilation when pressure is relieved. If the superficial erythema has progressed, you’ll see small blisters or erosions and, ultimately, necrosis and ulceration.
In underlying damage from pressure between deep tissue and bone, you’ll note an inflamed skin surface area. Bacteria in a compressed site cause inflammation and, eventually, infection, which leads to further necrosis. You may detect a foul-smelling, purulent discharge seeping from a lesion that has penetrated the skin from beneath. A black eschar may develop around and over the lesion because infected, necrotic tissue prevents healthy granulation of scar tissue. (See Stages of pressure ulcers.)
Diagnostic tests
Wound culture and sensitivity testing of the ulcer exudate identify infecting organisms.
Serum protein and serum albumin studies may be ordered to determine severe hypoproteinemia.
