Assessing and preventing pressure ulcers

Advances in Skin & Wound Care,  Sep/Oct 2000  by Calianno, Carol

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Pressure ulcers (PUs) are among the most serious skin injuries. Recognizing the magnitude of this problem, the Agency for Healthcare Quality and Research (AHQR, formerly the Agency for Health Care Policy and Research) developed a clinical practice guideline for PU prediction and prevention.1 This guideline recommends identification of at-risk adults and defines interventions for PU prevention.

Staged according to the guideline, PUs may be small or large wounds and may have irregular or clearly defined edges. It is important to note that even in a wound that appears small, the underlying tissue damage may be extensive. Areas covered with necrotic tissue cannot be staged until the tissue has been removed and the depth of the injury can be assessed. See Pressure Ulcers Stages.

What Are the Risk Factors?

Pressure ulcers can be caused by various factors:

intensity of pressure. Intense pressure over a bony prominence, even for a short time, may result in a PU.

duration of pressure. Less intense pressure over a long period of time may also cause a PU.

decreased tissue tolerance. Previous injuries resulting in scar tissue, poor perfusion, and thin, dry skin decrease tolerance to pressure, friction, and shear.

friction. This occurs when 2 forces move against each other. When skin is pulled or dragged over bed linen, the friction of the skin against the linen may cause tissue injury. Abrasions or epidermal stripping from friction can develop in patients who are pulled up in bed, who are in traction, or who wear braces, splints, orthotics, or poorly sized footwear.

shear. Deeper than a friction injury, this occurs when skin and tissue over a bony prominence slide over a hard surface. The skin and subcutaneous structures remain in 1 position because pressure keeps the skin stuck to an outside surface (ie, bed linen). The shearing tears at the skin, subcutaneous layer, and even muscle. Deep tissue and blood vessel damage may occur. Friction and shear forces usually occur together.

moisture. Prolonged moisture on the skin alters pH and decreases skin resiliency.

What Is Reactive Hyperemia?

Transient pressure against the skin causes pallor where blood flow to a specific area has stopped. When the area has been without blood flow more than 1 minute, the area will blanch. When the pressure is relieved, the area becomes reddened or hyperemic as blood flows back and revitalizes the area. This rush of blood back into the area is called reactive hyperemia, the earliest sign of tissue compromise and pressure-related ischemia.

If the pressure is prolonged, reactive hyperemia is not sufficient to revitalize ischemic tissue. In healthy tissue, the skin will blanch if pressure is applied to a hyperemic area as blood is pushed away from the area. It becomes erythemic again as blood rushes back to the area. In compromised tissue, the hyperemic area will not blanch. Nonblanching erythema is a serious sign that tissue is not receiving adequate oxygen and nutrients. This is a Stage I pressure ulcer and should no longer be referred to as reactive hyperemia.

Be especially attentive to assessing reactive hyperemia in dark-skinned patients. Look for increased darkening of the skin over bony prominences and palpate the area for warmth, edema, induration, or hardness.

Who Is At Risk?

The following patients have risk factors for PU development.

Patients with spinal cord injuries have absent or diminished sensations. If they try to reposition themselves, they may experience friction and shear injuries.

Diabetic patients on bed rest are at risk for pressure ulcers. Pay special attention to the lower extremities, especially the heels, because diabetic neuropathy can diminish or destroy foot sensation.

Patients who have had orthopedic surgery, especially those with total hip replacement or femoral fractures, are at high risk. Pressure ulcers have been reported in more than 60% of patients admitted with femoral fractures.

ICU patients with hypotension, especially those with a systolic blood pressure of 60 mm Hg or less, even for a short time, can experience tissue breakdown because of decreased perfusion pressures.

Elderly patients and those with multiple diseases (such as dementia, diabetes mellitus, arteriosclerosis, diseases that require steroid use, or infection) can experience impaired skin integrity and delayed healing.

Patients with a history of previous pressure ulcers are especially at risk. Healed full-thickness wounds have only 80% of the tensile strength of noninjured skin. Areas of scar tissue are more likely to break down than intact skin.

Patients with low ejection fractions have significantly reduced peripheral perfusion and very low capillary closing pressures. Less pressure over a shorter time will produce an injury.

Malnutrition is a significant factor in the development of pressure ulcers. Patients with serum albumin levels less than 3.5 grams/dL are protein deficient. The more severe the deficiency, the greater the risk.

Incontinence increases risk by causing chemical irritation and creating an excessively moist environment. Excoriation and maceration can occur even after a brief episode of incontinence. Patients with fecal incontinence have more than 20 times the risk of pressure ulcers than continent patients.