Definition and staging
A pressure ulcer is defined as any lesion caused by unrelieved pressure that damages underlying tissue (4). Because pressure is the primary pathophysiologic factor causing skin injury in typical ulcer locations, the term pressure ulcer is preferred to such synonyms as bedsore or decubitus ulcer (5). Typically, these ulcers occur over bony prominences. Because treatment differs, pressure ulcers must be distinguished from other conditions, such as venous stasis ulcers, ischemic lesions, and diabetic foot ulcers (2).
A pressure ulcer is defined as any lesion caused by unrelieved pressure that damages underlying tissue (4). Because pressure is the primary pathophysiologic factor causing skin injury in typical ulcer locations, the term pressure ulcer is preferred to such synonyms as bedsore or decubitus ulcer (5). Typically, these ulcers occur over bony prominences. Because treatment differs, pressure ulcers must be distinguished from other conditions, such as venous stasis ulcers, ischemic lesions, and diabetic foot ulcers (2).
The staging system proposed by the National Pressure Ulcer Advisory Panel and the AHCPR is based on the extent of tissue damage (4). Skin injury from pressure ranges from blanchable erythema of intact skin to loss of full-thickness skin and damage to underlying tissue, including bone (table 1) (4,6). The four-stage system, which does not imply the progress of ulcers from one stage to another in the course of worsening or healing, has limitations (4). For example, stage I ulcers are not true ulcers because the skin is intact, and it can be difficult to delineate them in persons with dark skin. An ulcer cannot be accurately staged until its eschar is removed. Assessment of the skin may require removal of an orthopedic device (4).
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Table 1. Characteristics of pressure ulcers used in staging |
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Stage I
Nonblanchable erythema of intact skin. Discoloration of skin, warmth, edema, or induration may be indicators in dark skin.
Stage II
Superficial ulcers involving loss of the epidermis, dermis, or both. These ulcers can present as an abrasion, blister, or shallow crater.
Stage III
Full-thickness skin loss involving damage to subcutaneous tissue that extends down to, but not through, underlying fascia
Stage IV
Full-thickness skin loss with extensive tissue destruction and necrosis of underlying muscle, bone, tendon, or joint capsule
Adapted from Bergstrom et al (4). |
Assessment should include documentation of anatomic location, stage, and description of size (ie, length, width, and depth). The presence of sinus tracts, undermining, maceration, exudate, or necrotic tissue and the presence or absence of granulation tissue should be noted (6). Pressure ulcers are most often found on the lower part of the body, particularly the bony prominences and weight-bearing surfaces of immobile persons (7). Areas prone to pressure ulcers include the sacrum, greater trochanter, ischial tuberosity, lateral malleolus, calcaneus, occiput, chin, ear, elbow, scapula, and iliac crest. Photographs of pressure ulcers may be considered part of assessment and documentation (8).
Prevalence
Pressure ulcers are common in older adults in the acute care setting, long-term care facilities, and community. Confinement to a bed or chair for a week increases the prevalence of these ulcers by 28% (5). Younger adults with spinal injuries also are vulnerable. When a stage I ulcer develops, the risk of additional ulcers increases tenfold (5). The prevalence of pressure ulcers is 3% to 11% in hospitalized adults, 2.5% to 24% in persons living in long-term care facilities, and up to 17% in adults in the community (5,8,9).
Pathophysiologic factors
When transient pressure interrupts blood flow, the skin becomes pale. If the ischemia lasts for more than a minute, the localized area becomes red or hyperemic, a reversible phenomenon, and blanchable. Nonblanchable erythema suggests capillary extravasation of plasma and red cells; it may be reversible if recognized promptly. Subcutaneous tissues, including muscles, are more sensitive to ischemia than the epidermis and dermis. Hence, pressure ulcers are more extensive than they appear superficially (6).
Risk factors
Identifying persons at high risk for pressure ulcers is vital (table 2). Unrelieved pressure is an essential risk factor that, coupled with inadequate microcirculation, results in tissue damage. Such ischemia is observed in persons of advanced age and in association with malnutrition, diabetes, cancer, terminal illness, sepsis, and vascular and neurologic disease (10). Risk factors are classified as either intrinsic or extrinsic (7,11).
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Table 2. Risk factors for pressure ulcers |
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Intrinsic
Immobility
Limited functional ability
Fecal incontinence
Impaired sensation
Diminished level of consciousness
Poor nutritional status
Age, especially >75 yr
Comorbid conditions, including stroke, Parkinson's disease, fracture, sepsis, prior ulcers
Extrinsic
Pressure
Friction
Shearing
Moisture
Pressure
Friction
Shearing
Moisture |
Intrinsic
This type of risk factor relates to patient status. Immobility, limited functional ability, fecal incontinence, impaired sensation, and diminished level of consciousness place patients at higher risk for pressure ulcers (7,11). Geriatric patients who have fewer than 20 spontaneous nocturnal movements are at greatest risk; ulcers usually are not seen in patients who have more than 50 spontaneous nocturnal movements (5).
Hypoalbuminemia, a decreased lymphocyte count, decreased body weight, and inadequate dietary intake--all factors that suggest malnutrition--are associated with pressure ulcers. Age greater than 75 years appears to be a risk factor because changes in epidermal turnover, dermal thickness, collagen and elastin production, and vascularity occur during healthy aging (5,7). Stroke, contractures, Parkinson's disease, fractures, diabetes, sepsis, and prior ulcers add to the risk (5). Although fecal incontinence is considered a risk factor, the role of urinary incontinence remains controversial (12,13).
Extrinsic
Examples of this type of risk factor are pressure, friction, shearing, and moisture (7,11,14). Pressure, when unrelieved, is the most important factor in the pathogenesis of pressure ulcers. When a person lies on a standard hospital bed, the pressure over the greater trochanters and heels is 50 to 95 mm Hg; while the person is seated, pressure on the ischial tuberosity can be 300 to 500 mm Hg (5). These values are far above the normal capillary filling pressure of 32 mm Hg, and such pressure occludes circulation (11,14). Pressure of 60 to 70 mm Hg for 1 or 2 hours may lead to muscle injury (5,11).
Examples of this type of risk factor are pressure, friction, shearing, and moisture (7,11,14). Pressure, when unrelieved, is the most important factor in the pathogenesis of pressure ulcers. When a person lies on a standard hospital bed, the pressure over the greater trochanters and heels is 50 to 95 mm Hg; while the person is seated, pressure on the ischial tuberosity can be 300 to 500 mm Hg (5). These values are far above the normal capillary filling pressure of 32 mm Hg, and such pressure occludes circulation (11,14). Pressure of 60 to 70 mm Hg for 1 or 2 hours may lead to muscle injury (5,11).
In a healthcare facility, friction can occur when a patient is pulled across support surfaces during transferring and repositioning, causing loss of stratum corneum and the formation of intraepidermal blisters. When the blisters are unroofed, superficial erosions, skin tears, or abrasions (ie, stage II ulcers) become apparent (5,11,14).
Shearing forces are exerted when the skin and subcutaneous tissues slide on each other when the patient's head is elevated more than 30° or when gravity causes a seated patient to slide down. Sliding causes angulation of perforating arterioles, which compromises circulation (5,11,14). Moisture softens the stratum corneum and increases the risk of maceration injury with friction. Acid and bacterial products from urine or feces may contribute to the problem (7).
Impact on morbidity
Pain is a severe or distressing symptom in half of persons who have pressure ulcers, but only a small number receive adequate analgesia (5). Local infection that manifests as cellulitis or osteomyelitis is the most common infectious complication. Osteomyelitis occurs in up to one fourth of nonhealing ulcers (5). Sepsis is associated with high mortality (5). Other complications include bacteremia, endocarditis, meningitis, septic arthritis, sinus tract or abscess, amyloidosis, and squamous cell carcinoma in the ulcer (4).
Prevention
The AHCPR recommendations to prevent pressure ulcers, which are listed in table 3, include risk assessment, measures to relieve pressure, proper skin care and nutrition, and steps to minimize moisture from urinary and fecal incontinence (4).
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Table 3. Prevention of pressure ulcers |
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Risk assessment
Identify person predisposed to pressure ulcers
Measures to relieve pressure
Turn or reposition often
Use positioning devices
Use support surfaces
Static: mattresses or overlays (foam, gel, water, air, sheepskin)
Dynamic: low-air-loss and air-fluidized beds
Nutritional assessment and supplements Skin care
Cleanse with isotonic sodium chloride solution
Avoid rubbing or massaging ulcers
Prevent excessive dryness by avoiding hot water and soap
Protect from excessive moisture
Management of urinary and fecal incontinence
Adapted from the American Medical Directors Association (19). |
Risk assessment
Risk assessment should be performed to identify patients who are bound to a bed or wheelchair and therefore are predisposed to pressure ulcers. The AHCPR guidelines recommend the use of systematic risk assessment tools, such as the Braden scale or Norton scale, and reassessment at regular intervals (4). The Braden scale evaluates the level of sensory perception, skin moisture, physical activity, mobility, food intake, friction, and shear. The Norton scale assesses physical condition, mental state, activity, mobility, and incontinence (8,11,15).
Measures to relieve pressure
Turning and positioning, use of support surfaces, and proper skin care and nutrition can minimize the occurrence of pressure ulcers. Frequent repositioning along with the use of support surfaces helps limit the amount and time of pressure exposure. Observational studies have shown that patients should be turned every 2 hours to limit ischemia to tissues overlying bony prominences. Even seated patients need to be repositioned often to relieve pressure. Individualized and specialized seat cushions are beneficial.
Positioning devices help maintain a position and prevent contact of bony prominences with one another. Because the heel is susceptible, total pressure relief with pillows placed under the calf is recommended. During repositioning, a patient may be placed at 30° angles (oblique position) to reduce pressure on the trochanter. To minimize shearing, the lowest degree of head elevation is recommended. The use of lifting devices reduces friction-associated injury (4,14,15).
Use of support surfaces: The use of a pressure- reducing surface lowers the incidence and severity of pressure ulcers (4,14). Support surfaces are static or dynamic depending on their ability to alternate the tissue interface pressure independent of the patient. Pads, cushions, and most mattress overlays are static; some mattress overlays, special mattresses, and specialty beds (low-air-loss and air-fluidized beds) are dynamic (14). Sheepskin, egg-crate foam, and 2-in foam pads are inexpensive. However, they are unable to reduce pressure sufficiently (5); high-density, 4-in foam overlays are more effective at lowering interface pressure (5).
The use of a pressure- reducing surface lowers the incidence and severity of pressure ulcers (4,14). Support surfaces are static or dynamic depending on their ability to alternate the tissue interface pressure independent of the patient. Pads, cushions, and most mattress overlays are static; some mattress overlays, special mattresses, and specialty beds (low-air-loss and air-fluidized beds) are dynamic (14). Sheepskin, egg-crate foam, and 2-in foam pads are inexpensive. However, they are unable to reduce pressure sufficiently (5); high-density, 4-in foam overlays are more effective at lowering interface pressure (5).
Static air mattresses or overlays feature interconnected air cells that deflate or inflate with patient movements and equalize interface pressure. Dynamic air-filled products have a series of air cells that are alternately inflated and deflated with a bedside pump, intermittently relieving pressure at bony sites (5,14). These alternating-pressure devices decrease skin pressure significantly. Water mattresses are useful to reduce pressure, but they may increase the risk of maceration because they are made of impermeable materials. These mattresses are not often used because they are heavy and may leak (5,14).
A specialized bed should be considered for patients who have multiple large, stage III or IV ulcers to prevent new ulcers and accelerate healing of existing ones (5). Low-air-loss beds consist of air-permeable fabric pillows that are constantly inflated with air, have a drying effect on tissues from a flow of warm air, and allow several different positionings. Air-fluidized beds contain microspheric silicon beads covered by an air-permeable fabric; streams of warm air forced through the beads allow the patient to float on the beads. Considerable variations in dermal-insensible fluid loss that can affect body temperature and hydration necessitate monitoring of these parameters (5,14,16).
Skin care
Systematic skin inspection should be performed at least once a day, and the skin should be cleansed at regular intervals and whenever it is soiled. Hot water and drying soaps are best avoided. To treat dry, flaky, scaly skin, optimum environmental humidity should be maintained and moisturizers used. Areas of redness over bony prominences should not be massaged or rubbed. Mobility through rehabilitation should be encouraged (15).
Nutrition
Nutritional assessment is an important part of evaluation. Pressure ulcers and malnutrition often coexist, but a causal relationship is not well established. A serum albumin level of less than 3.5 g/dL, a total lymphocyte count less than 1,800/microliter, and an unintentional reduction in body weight suggest malnutrition (4).
The goal is to provide about 30 to 35 calories and 1.25 to 1.50 g of protein per kilogram per day (4). A daily high-potency multivitamin and mineral supplement is recommended when micronutrient deficiency is suspected (4). Short-term supplementation with vitamin C (500 mg/day) and zinc (15 mg/day) may promote ulcer healing in the presence of deficiency (2,4).
Although malnutrition is potentially reversible, nutritional support by itself does not invariably lead to the healing of ulcers. The decision to administer parenteral or enteral supplements should be made on the basis of the patient's overall status, life expectancy, and quality of life and the preferences of the patient or caregiver (5,15).
Moisture
Moisture from urine, stool, and perspiration can lead to skin damage (7,15). Bacterial colonization is common in the setting of fecal incontinence. Urinary incontinence should be addressed. Moisture barriers (eg, liquid spray barriers, petroleum jelly, transparent adhesive dressings) are helpful after skin cleansing (15,17).
Treatment
Proper documentation of wound characteristics (see table 1) is essential, along with history taking, physical examination, and assessment of complications (4,18). Comorbid illnesses, such as diabetes, peripheral vascular disease, immune deficiency, collagen vascular disease, malignancy, psychosis, and depression, deserve evaluation (4).
A treatment plan should consist of the previously described preventive measures as well as specific ulcer care, infection control, and monitoring at regular intervals (table 4) (4,18). Patients with cognitive impairment may not complain of pain, but when pain is suspected, analgesic relief is important to improve their quality of life (4,18). Other crucial measures include appropriate wound covering, adjustment of support surfaces, and repositioning.
