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Practice of Geriatrics
Patricia S. Goode, M.D., M.S.N., E.T., and Richard M. Allman, M.D.
Risk Factors
Pressure ulcers are an all too common problem among the elderly, in that more than 50% of persons with pressure ulcers are over age 70.1 Almost two thirds of pressure ulcers first develop in acute care hospitals. Sixty to seventy percent of these ulcers occur within the first 2 weeks of hospitalization.1 As many as 20% to 33% of patients admitted to nursing homes have a pressure ulcer that is stage 2 or more severe.2,3 and 4 The true costs of pressure ulcer care are difficult to ascertain. Data indicate that patients with pressure ulcers have increased hospital costs, increased lengths of stay, and increased mortality.5,6 and 7
Pressure ulcers can be defined as localized areas of tissue injury that develop when soft tissue is compressed between a bony prominence and an external surface for a prolonged period of time.8 These lesions may present clinically as non-blanchable erythema, blisters, ulcerations, or lesions covered with necrotic eschar. Since pressure is the primary pathophysiologic factor in the development of these lesions, pressure ulcer is the preferred term. Previous terminology includes decubitus ulcer and bedsore, which imply that the lesions occur only when lying down; in fact, some of the most severe pressure-induced cutaneous injuries result from prolonged sitting.
Clinical staging or grading of pressure ulcers helps in guiding clinical management decisions. The National Pressure Ulcer Advisory Panel (NPUAP) has suggested adopting a uniform staging system (Table 22-1). There has been considerable controversy about stage 1 pressure ulcers (nonblanchable erythema, darkening or induration of intact skin), but development of a stage 1 ulcer is associated with the subsequent occurrence of a stage 2 or greater ulcer in nearly 60% of cases.5 Pressure-induced blisters typically occur on the heels and are most often stage 3 if they are unroofed, but this is not recommended because the blister provides a natural “dressing.” Most wounds covered with eschar have full-thickness tissue necrosis and are stage 3 or 4, although these wounds cannot be accurately staged until the eschar is removed.


Pressure is the primary etiologic factor in the development of pressure ulcers. Development of prolonged pressure sufficient to result in ischemic tissue damage is related to the degree of immobility. In a classic study, Exton-Smith and Sherwin9 used a mattress sensor to monitor spontaneous nocturnal movements in patients at an extended care facility. No patient with 51 or more spontaneous nocturnal movements developed a pressure ulcer, but 90% of patients with 20 or fewer movements did.
Muscle and subcutaneous tissue are more susceptible to pressure-induced injury than are epidermal and dermal tissues. Contact pressures of 60 to 70 mmHg for 1 to 2 hours can cause muscle damage.10 Pressures under bony prominences such as the sacrum and greater trochanter can be as high as 100 to 150 mmHg on a standard hospital mattress, and pressures under the ischial tuberosities of a seated person can reach 300 mmHg.11 These pressures are sufficient to decrease the transcutaneous oxygen tension to nearly zero.11 Age-related changes in the skin including thinning of the epidermis, increased skin permeability, flattening of the dermal-epidermal junction, loss of dermal vessels, and loss of elastic fibers may increase the older person’s susceptibility to pressure ulcers.
Other factors such as shear, friction, and moisture can also lead to skin breakdown. Shear is generated when tangential forces are applied to the skin surface, causing the dermis and epidermis to shift laterally with respect to the deeper layers, angulating the blood vessels and reducing the amount of pressure needed to cause vessel occlusion. Shear occurs commonly in the tissues over the sacrum when an individual sits up in a chair or a bed and then slides toward the edge of the chair or the foot of the bed. The sacral skin is held in place by friction, and the underlying blood vessels are stretched and angulated, increasing their susceptibility to pressure-induced necrosis. Friction can lead to blister formation and superficial skin erosions. Moisture causes maceration, and incontinence has been found to be a risk factor in several studies. However, two studies5,7 have examined fecal and urinary incontinence separately and have found that only fecal incontinence is independently associated with development of pressure ulcers.
Periodic use of a risk assessment tool has been found to decrease the incidence of pressure ulcers.12 The Norton Scale, the first such instrument, and the Braden Scale have been evaluated most often with respect to reliability and validity. Patients should be assessed on admission to acute care hospitals, rehabilitation centers, nursing homes, home care programs, and other health care facilities, and then should be reassessed at periodic intervals.13
Awareness of risk factors helps to target preventive interventions to those patients who are most likely to benefit. Risk factors for pressure ulcer development include bedbound or chair-bound status, immobility (i.e., inability to reposition oneself), incontinence, inadequate dietary intake, impaired nutritional status, and altered level of consciousness.13 Risk factors have been shown to vary by setting; hence risk factors for acutely ill patients in hospitals may be quite different from those for chronically ill patients in nursing homes. Prospective studies are needed to more clearly define the pertinent risk factors in each setting.
After risk of pressure ulcers has been identified in an individual either by the presence of multiple risk factors or by the use of a risk assessment tool, preventive measures should be initiated.Table 22-2 summarizes the methods used to prevent pressure ulcers. Prevention programs may include adequate nutrition, proper management of co-morbid conditions including incontinence, and rehabilitation to improve mobility and functional status. Educational programs for caregivers, including physicians, nurses, nursing assistants, and family members, are also important. Multidisciplinary teams have been able to reduce the incidence of pressure ulcers by more than 50% in acute care hospitals.11,14


The traditional recommendation for preventing pressure ulcers is to reposition at-risk patients every 2 hours. Actually, considerable differences exist among individuals in their tolerance of various pressure-time intervals. The frequency of repositioning required depends on the degree of mobility of the patient and the support surface used. At-risk individuals should be monitored carefully for evidence of nonblanchable erythema and skin discoloration or induration (stage 1 pressure ulcer), which indicate the need for more frequent repositioning or the use of more effective pressure-reducing devices. Generous use of soft pillows between the legs, behind the back, and supporting the arms is helpful to maintain proper position.
A right or left 30-degree oblique position, in which the patient’s back is at a 30-degree angle to the support surface, avoids direct pressure on the bony prominences that accounts for 80% of pressure ulcers: the sacrum, ischial tuberosities, trochanters, lateral malleoli, and heels.11 In contrast, lying with the back at a 90-degree angle to the support surface exposes the greater trochanter and the lateral malleoli to pressure. This sidelying position should be avoided in patients who are unable to reposition themselves. The supine position puts pressure on the sacrum and heels, while sitting exposes the tissues over the ischial tuberosities to pressure. Keeping the head of the bed elevated less than 30 degrees decreases shearing forces, so immobile patients whose heads are elevated more than 30 degrees for bathing or eating should be returned to an elevation of less than 30 degrees within 1 to 2 hours unless this is medically contraindicated.
Pressure Reduction
A number of pressure-reducing devices are marketed to prevent and treat pressure ulcers. Synthetic sheepskins and 2-inch convoluted (“egg crate”) foam mattress overlays are very popular and are relatively inexpensive. Although they can increase the patient’s comfort, they cannot decrease pressure sufficiently to prevent pressure ulcers. Information such as indention load deflection (ILD—the amount of force required to compress the foam a given percentage of its original height), density (the weight of a cubic foot of foam), and the support factor (the 65% ILD divided by the 25% ILD) can be useful in selecting appropriate foam products.15 Foam mattress overlays that are specifically designed to prevent pressure ulcers (e.g., BioGard, Derma-Foam, Geo-matt, IRIS) are preferable, since they reduce pressure under bony prominences to levels that are believed to reduce risk. Foam mattress overlays have a one time cost of $30 to $50. As an alternative, the standard hospital mattress may be replaced with a mattress that has pressure-reducing capability at a cost of less than $200 to $750 (e.g., BioCore, DeCube, PressureGuard). This may be a cost-effective solution for high-risk settings such as intensive care units, general medical floors, and orthopedic wards.
Static air mattress overlays (e.g., K-Soft, Sof-Care) have interconnecting air cells that transfer air among cells as a person changes position on them, equalizing pressure. They are inflated to an appropriate pressure (i.e., when the sacrum is not palpable to the examiner’s hand placed beneath the inflated air cells of the mattress overlay). Cost is $25 to $50. Some static overlays have a rental fee of about $25 a day (e.g., ROHO). Dynamic systems, or alternating air mattresses (e.g., AcuCair, BioTherapy, CliniCare, First Step) have air cells that are alternately inflated and deflated by a bedside pump. Water- or gel-filled mattresses and overlays (e.g., Lotus, TenderGEL) are difficult to move and have not been popular in acute care hospitals but may be appropriate in long-term care settings or in the home. One randomized controlled trial demonstrated a greater than 50% decrease in incidence of pressure ulcers with the use of alternating air mattresses or water mattresses compared with the use of conventional hospital mattresses in an acute care hospital.14
Devices such as heel protectors, which are designed to decrease pressure over a localized area, can be useful to reduce pressure over high-risk bony prominences. Patients who are in chairs or wheelchairs for longer than 1 or 2 hours at a time should use an appropriate pressure-reducing chair cushion (e.g., Jay, ROHO, Waffle cushion). These chair cushions have properties similar to those of mattress overlays and can be selected using similar criteria. “Donut” cushions should not be used for pressure relief because they may cause ischemia in the tissues positioned in the center of the donut.13
Skin Care
Proper skin care is an important part of a pressure ulcer prevention program. The skin should be inspected daily and cleansed at regular intervals and after each episode of soiling with a mild cleanser (e.g., Dove soap). Since dry skin is a risk factor for pressure ulcers,5,16 topical moisturizers (e.g., Bard Skin Care Cream, Nivea Moisturizing Lotion, Vaseline Constant Care) should be used to help increase the resistance of the skin to mechanical trauma. More studies are needed to demonstrate whether moisturizers can actually decrease the incidence of pressure ulcers. Maceration also decreases the resistance of the skin to mechanical trauma. Skin should be protected from incontinence and excessive perspiration by the use of a topical moisture barrier (e.g., A & D Ointment, Peri-Care Moisture Barrier Ointment, Restore Barrier Creme). Underpads or briefs that have a quick-drying surface placed against the skin are also helpful in keeping moisture away from skin. Massage over bony prominences has traditionally been recommended as part of a pressure ulcer prevention program. However, there is evidence that massage actually increases the incidence of pressure ulcers by causing deep tissue trauma,17 and it should therefore be avoided.13
Pressure Ulcers in Terminal Conditions
Despite the use of appropriate preventive care, some pressure ulcers may still occur. The skin is the largest organ of the body, and pressure ulcers may be one part of the syndrome of multiple organ failure that accompanies many terminal conditions. Inability to prevent pressure ulcers in terminally ill patients should be considered when the presence of pressure ulcers is used as an indicator of the quality of care.
Treatment of All Stages
Treatment of pressure ulcers is summarized in Table 22-3.18


A carefully recorded assessment of pressure ulcers at the initiation of therapy is mandatory to provide a baseline against which to judge improvement or deterioration. A complete description includes the number of pressure ulcers and, for each ulcer, the location, stage, size (length, width, depth), description of tunneling or undermining, necrotic tissue, odor or exudate if present, and the condition of the surrounding skin (maceration, abrasions, discoloration, induration, if present). Although stage 2 pressure ulcers usually heal in days to weeks, ulcers in stages 3 and 4 may require months to heal completely. Improvement can by judged by a decrease in size (taking undermining into account), a decrease in odor and drainage, a decrease in the amount of necrotic tissue, improved appearance of granulation tissue, and improved appearance of the surrounding skin. Serial photographs may be useful for monitoring. Tools are also available to guide wound assessment and quantify healing.19
The staging system recommended by the NPUAP is useful in guiding initial clinical management but is not intended nor appropriate for monitoring healing. The original tissue layers are not regenerated in a full-thickness wound. Just as a third-degree burn does not become a second-degree and then a first-degree burn as it heals, a pressure ulcer does not progress through reverse staging.
Optimizing nutritional status cannot be emphasized strongly enough and is all too often neglected. The Agency for Health Care Policy and Research (AHCPR) guideline18 suggests as markers of clinically significant malnutrition: a serum albumin level of less than 3.5 g/dL, a total lymphocyte count of less than 1800/mm3, and weight loss of more than 15% or a weight of less than 80% of ideal. Tube feeding or parenteral nutrition should be considered for patients with insufficient oral intake, the goal being 30 to 35 calories/kg/day and 1.25 to 1.50 g protein/kg/day. Protein intake has been shown to be one of the most important predictors of improvement in pressure ulcers. A high-potency vitamin and mineral supplement (e.g., Centrum, Theragram M, Unicap M) should be given daily to all geriatric patients with pressure ulcers owing to the high prevalence of subclinical vitamin and mineral deficiencies in this group. Inadequate data are available to support the routine use of additional vitamin and mineral supplements. Megadose vitamin and mineral therapy may even be harmful to patients because of the toxicity of high levels of the supplement itself (vitamin A) or because of side effects (anorexia with oral zinc supplements).
Stage 1 Pressure Ulcers
The appearance of nonblanchable erythema, other discoloration, or induration over a bony prominence signals underlying tissue injury and mandates an evaluation of the preventive measures currently in use. The use and adequacy of pressure-reducing devices, the frequency and techniques of repositioning, and the adequacy of the patient’s nutritional status should be assessed and any necessary changes made. Topical application of various pressure ulcer treatment products is unnecessary for stage 1 ulcers, since the epidermis is intact. The goal of intervention at this stage is to halt progression of tissue injury before epithelial breakdown occurs, and this is best done by relieving pressure.
Stage 2 Pressure Ulcers
With appropriate intervention, stage 2 pressure ulcers usually heal in weeks without scarring. Patients with pressure ulcers of any stage are at high risk for additional skin breakdown, so attention to all preventive measures described previously is particularly important. Usually stage 2 pressure ulcers are quite shallow, have minimal necrotic tissue, and are not infected. However, they can be quite painful. Local wound care for stage 2 pressure ulcers should maintain a moist, physiologic environment that facilitates granulation and epithelialization and does not disturb healing tissue. Occlusive, vapor-permeable dressings (e.g., Bioclusive, OpSite, Tegaderm) and hydrocolloid dressings (Comfeel, Dermiflex, DuoDERM, Intrasite, Tegasorb) permit accumulation of serous fluid on top of the wound, providing a physiologic environment; they also reduce pain and in controlled trials improve healing of shallow pressure ulcers (stage 2 and shallow stage 3). These dressings should be changed every 2 to 7 days, depending on the wound. More frequent dressing changes increase expense, damage the surrounding skin, and are usually unnecessary.
Stage 3 and 4 Pressure Ulcers
Stage 3 and 4 pressure ulcers generally take months to heal and result in scarring. Ulcers may enlarge initially as necrotic tissue is removed. As for treatment of stage 2 ulcers, general systemic measures such as nutritional support, pressure relief, and management of risk factors are essential.
Positioning patients on a pressure ulcer should be avoided. It cannot be emphasized enough that without relief of local pressure, the pressure ulcer will not heal, and all other therapeutic measures will be futile. Positioning devices such as soft pillows may be used to raise a pressure ulcer off the support surface. A written repositioning schedule should be used. It is particularly helpful to post the schedule on the wall above the patient’s bed. A pressure-reducing surface should be used for all patients at risk for developing additional pressure ulcers. A static support surface may be sufficient for patients who can assume a variety of positions without putting weight on a pressure ulcer. A dynamic support surface is usually necessary for patients who are unable to reposition themselves, for those who completely compress a static support surface (i.e., bottom out), and for those with pressure ulcers on multiple turning surfaces. Some mattress overlays may lift the patient so high that the side rails are not high enough to prevent falls in at-risk patients; caution should be used to select an overlay that is compatible with the bed. A mattress replacement or a specialized bed is another alternative.
Patients with multiple large truncal stage 3 and 4 ulcers, with less than two intact turning surfaces available for repositioning, or with ulcers that fail to heal on a less expensive support surface when all other components of the care plan are optimal, may require the use of a specialized bed. Air-fluidized beds (e.g., Clinitron, FluidAir) contain microspheres of ceramic glass that are covered by a filter sheet. Warm pressurized air is forced up through the glass beads so that they take on the characteristics of a fluid, and the patient floats on the system. Low air-loss beds (e.g., Flexicair, KinAir, Pneu Care Plus) consist of a traditional hospital bed frame fitted with large fabric cushions that are constantly inflated with air. The standard hospital bed frame allows the head of the bed and the bed itself to be raised or lowered, an advantage compared with the air-fluidized bed. The drying effect of the air-fluidized beds (and some dynamic mattress overlays) may be helpful in treating patients with excessive skin moisture, but because it increases insensible fluid losses, the hydration status of the patient requires extra attention. Air-fluidized beds rent for $55 to $100 per day, and low air-loss beds rent for $30 to $80 per day. Low air-loss mattress overlays are available and rent for $20 to $40 per day.
The effectiveness of low air-loss beds has not been compared with that of air-fluidized beds, but both types of beds decrease the healing time of pressure ulcers compared with foam overlays or traditional hospital mattresses. Many beds, overlays, and mattresses are reported to lower pressure under bony prominences to below capillary filling pressure, traditionally considered to be 32 mmHg. However, most of these measurements are made in healthy young volunteers, not in frail elderly patients or patients with neurologic disorders, who may require considerably less pressure to occlude the capillaries. Any pressure-reducing support surface requires monitoring of the patient’s skin to ascertain individual efficacy.
Removal of necrotic debris is the first step in reducing the bacterial content of the wound. Bacterial counts of greater than 100,000 (105) colonies per gram of tissue in pressure ulcers correlate well with impaired wound healing and wound graft failure. Wounds with eschar or large amounts of necrotic debris are best debrided surgically. Debridement is often performed at the bedside with sterile tissue forceps and scissors or scalpel. If there is bleeding, a dry gauze dressing should be applied for several hours before moist therapy is resumed. Lesser amounts of necrotic debris can be removed with irrigation or whirlpool techniques, wet-to-dry saline gauze dressings, or enzymatic debriding agents such as collagenase. Debridement (wet-to-dry dressings, whirlpool, enzymatic agents, and so on) should be discontinued once the wound base is clean to prevent disruption of healthy granulation tissue.
Several issues involving infection and pressure ulcers should be mentioned. The first is culturing. Essentially all stage 2 or more severe pressure ulcers are colonized with bacteria, and routine cultures of a wound that does not appear infected add nothing to the therapeutic plan. Evidence of cellulitis, osteomyelitis, or sepsis is an indication for culturing. Needle aspiration and ulcer biopsy have been recommended as the most reliable culture methods.18 However, if the wound is first thoroughly cleansed with a nonantimicrobial solution and then a 1 cm2 area of the wound base is swabbed for 5 seconds with sufficient pressure to express fluid from the wound tissue, reliable semiquantitative culture data can be obtained.20
Systemic antibiotics are not needed for routine treatment of pressure ulcers but are indicated for patients with cellulitis, sepsis, or osteomyelitis. In addition, since debridement results in transient bacteremia, antibiotics for endocarditis prophylaxis should be administered as indicated. In patients with sepsis or suspected bacteremia, broad-spectrum coverage for aerobic gram-negative rods, gram-positive cocci, and anaerobes is indicated pending culture results. Ampicillin-sulbactam, imipenem, ticarcillin-clavulanate, or a combination of clindamycin and an aminoglycoside is an appropriate choice for initial antibiotic therapy. The mortality of patients with sepsis associated with pressure ulcers is high, so treatment should be aggressive. Prompt, thorough surgical debridement of necrotic tissue is also indicated to remove the source of the bacteremia.
Randomized controlled trials suggest that topical antibiotics such as gentamicin and silver sulfadiazine may help infected pressure ulcers to heal. In contrast, antiseptics such as 1% povidoneiodine, 0.25% acetic acid, 0.5% sodium hypochlorite (Dakin’s solution), and 3% hydrogen peroxide all are cytotoxic to fibroblasts in culture, may impair wound healing, and should not be used in patients with pressure ulcers.18 Topical antibiotics effective against gram-negative, gram-positive, and anaerobic organisms (e.g., silver sulfadiazine, triple antibiotic) may be prescribed for specific purposes such as accomplishing an initial decrease of bacterial wound content or decreasing foul odor, or as a therapeutic trial for ulcers that are not healing despite an optimal multicomponent treatment plan. A fixed treatment period (2 weeks) is recommended to avoid adverse local and systemic effects and selection of antibiotic-resistant bacteria.18
The Centers for Disease Control (CDC) recommends use of drainage and secretion precautions (gloves for touching infective material, gowns if soiling is likely, handwashing before next patient contact, contaminated articles discarded or bagged and labeled before being sent for decontamination and reprocessing) in managing patients with an infected pressure ulcer. If an infection is caused by a multiply resistant organism or if the drainage is not adequately contained by the dressing, contact isolation (which is the same as drainage and secretion precautions with the addition of a required private room) is indicated. Many nursing homes will not accept patients who have positive cultures for a resistant organism.
Stage 3 and 4 ulcers should be protected with a dressing that keeps the ulcer bed continuously moist and the surrounding skin free of maceration. Intact skin can be protected with an ointment-based moisture barrier. Deep ulcers that have been adequately debrided should be lightly packed with a material that does not inhibit healing; saline-moistened gauze is the standard. The gauze should be kept continuously moist and should be remoistened before removal if necessary to avoid disrupting the granulation tissue. Wet-to-dry dressings should be used only to debride wounds and should be discontinued when the wound bed is clean. A variety of alternatives to saline-moistened gauze dressings exist, and randomized placebo-controlled studies are needed to compare the efficacy of these various dressings and to provide specific indications for use of the different types. Some dressings are particularly formulated for the management of ulcers with large amounts of drainage (e.g., Bard Absorption Dressing, Debrisan). Calcium alginate dressings (e.g., Sorbsan) and combination products (e.g., IntraSite Gel) show promise in their ability to create a therapeutic microenvironment and also are easily removed without disrupting granulation tissue.
Miscellaneous topical agents (e.g., sugar, honey, vitamins, zinc, magnesium, aluminum, gold, phenytoin, insulin, yeast extract, aloe vera gel) have been promoted from time to time but have not been evaluated sufficiently to warrant a current recommendation.18 Topically applied growth factors (e.g., recombinant platelet-derived growth factor and basic fibroblast growth factor) have shown promising results, and studies are ongoing. Skin equivalents are also currently undergoing clinical trials. Systemic agents such as vasodilators, hemorrheologics (pentoxifylline), serotonin inhibitors, and fibrinolytic agents cannot be recommended for use in treating pressure ulcers because of lack of data on their efficacy.18 Of the adjunctive therapies (e.g., hyperbaric oxygen; infrared, ultraviolet, and low-energy laser irradiation; and ultrasound), only electrotherapy (electrical stimulation of the wound) has demonstrated sufficient efficacy in treating pressure ulcers. Electrical stimulation is recommended for stage 2, 3, and 4 ulcers that have proved unresponsive to conventional therapy.18 In addition to promoting more rapid healing, electrical stimulation may assist in controlling pain.
Surgical treatment of pressure ulcers includes direct closure, skin grafts, skin flaps, musculocutaneous flaps, and free flaps. Ischiectomy (to remove the underlying bony prominences) can lead to perineal ulcers and urethral fistulas and is no longer recommended.18 Most of these procedures were developed for young patients with spinal cord injuries, although age alone is certainly not a contraindication for surgical treatment. Surgical consultation should be obtained for older persons for whom surgical intervention would be appropriate after considering the patient’s rehabilitative potential and ability to tolerate a surgical procedure including the postoperative immobility required. Postoperative care usually involves the use of an air-fluidized or low air-loss bed for at least 2 weeks. Weight bearing is gradually increased after this time, and close observation of tissue tolerance is needed. Education of patients and caregivers is essential to reduce the high rate (10% to 60%) of recurrence of pressure ulcers following surgical repair.

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Mulder GD, Fairchild PA, Jeter KF (eds): The Clinician’s Pocket Guide to Chronic Wound Repair, 3rd ed. Long Beach, CA, Wound Healing Institute Publications, 1995, pp. 81–96.

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