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DIAGNOSIS AND TREATMENT

Pressure Ulcers in the Nursing Home

right arrow David M. Smith, MD

15 September 1995 | Volume 123 Issue 6 | Pages 433-438

Objective: To review the literature on the causes, epidemiology, prevention, and treatment of pressure ulcers in nursing homes and to summarize this information for clinicians caring for nursing home residents.

Data Sources: A MEDLINE search of English-language articles published between 1980 and October 1994 using the terms decubitus ulcer and elderly. References from identified articles were also examined.

Study Selection: Articles were excluded if the title indicated that patients were not nursing home residents (unless data from nursing homes were limited or unavailable), that patients were not elderly, or that the ulcers were related to peripheral vascular disease or neuropathy.

Data Extraction: Selected studies either contained original data or were meta-analyses. Prevalence studies were required to have an identifiable denominator; risk factor and incidence studies were required to have an identifiable cohort and a specified duration of follow-up. Preference was given to risk factors identified through multivariate analyses. Studies of preventive and therapeutic interventions were required to have an identifiable control group; preference was given to randomized controlled trials.

Data Synthesis: Seventeen percent to 35% of patients have pressure ulcers at the time of admission to a nursing home, and the prevalence of pressure ulcers among nursing home residents ranges from 7% to 23%. Among high-risk patients, the incidence of pressure ulcers is estimated to be 14/1000 patient-days. Residents at higher risk for developing ulcers are those who have limited ability to reposition themselves, can-not sense the need to reposition, have fecal incontinence, or cannot feed themselves. Occlusive dressings are as effective and less costly than traditional wet-to-dry saline dressings for treating earlier stages of pressure ulcers. There is no consensus on the use of specialized beds in the nursing home for promoting the healing of advanced-stage ulcers or for reducing the incidence of ulcers in high-risk patients. Specific interventions should not detract from careful, total assessment and management of the patient.

Conclusions: Pressure ulcers in the nursing home are common problems associated with significant morbidity and mortality. Because resident characteristics can identify residents likely to develop ulcers, preventive measures can be implemented early. Therapy for advanced stages of pressure ulcers is expensive and prolonged. Involvement of the physician with the multidisciplinary nursing home team is essential for prevention and therapy.


Now the bedsore on his buttock has come from having been too long a time lying on it, without moving himself [1]. Ambroise Paré, circa 1569

Although many advances have been made in the prevention and treatment of pressure ulcers, some principles implicit in the cure were recommended in 1569, including concern for the total welfare of the sickest and most dependent persons [1]. For the physician caring for nursing home residents, this principle implies an understanding of the causes, epidemiology, effective methods for the prevention and treatment of pressure ulcers, and the role of the physician within a multidisciplinary team. This review focuses on these areas.


Methods
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The MEDLINE database was searched for English-language articles published between 1980 and October 1994 using the terms decubitus ulcer and elderly. Articles identified through this search were excluded if the title clearly indicated that the article pertained to one of the following: 1) patients other than nursing home residents, except in articles for which data on nursing home residents were limited or unavailable; 2) patients younger than age 65 years; 3) ulcers related to peripheral vascular disease or neuropathy; or 4) specific surgical interventions. Pertinent articles cited as references in the identified papers were also reviewed. Reviewed articles were excluded if they did not meet the above criteria, described methods without patient data, or were reviews without meta-analyses.

Prevalence studies were required to have an identifiable denominator. Cohort (prospective and retrospective) studies of risk factors were selected in preference to cross-sectional studies. Incidence studies had to have an inception cohort and a specified follow-up period. If incidence figures were not provided, incidence was computed from the mean or median duration of follow-up. Preventive and therapeutic interventions were required to have an identifiable control group; preference was given to randomized controlled trials.


Definitions
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A pressure ulcer is a localized area of soft-tissue injury resulting from compression between a bony prominence and an external surface. There is now consensus on the use of the term pressure ulcer rather than synonyms such as decubitus ulcer or bed sore [2]. In the nursing home population, pressure ulcers are frequent, largely preventable, and, in the early stages, readily responsive to treatment. In the advanced stages, pressure ulcer treatment is problematic and associated with substantial morbidity and complications.

There is also consensus that four ulcer stages Figure 1 are useful for reporting prevalence and guiding therapy [2]. Stage 1 consists of nonblanchable erythema with intact skin. Erythema is redness of the skin produced by congestion of the capillaries. The difference between redness caused by capillary congestion and extravasation of blood with tissue damage is the blanching characteristic. Erythema is the initial reactive hyperemia caused by pressure, and nonblanchable erythema represents a stage 1 pressure ulcer. Reactive hyperemia completely disappears within 24 hours of relief of pressure; this characteristic helps to distinguish it from stage 1 pressure ulcers [3]. However, many believe that reactive hyperemia can be distinguished from nonblanchable erythema within 2 hours of relief of pressure. The latter condition represents tissue injury and heralds skin ulceration.



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Figure 1. Classification of pressure ulcers. Stage 1, nonblanchable erythema. Stage 2, partial-thickness skin loss. Stage 3, full-thickness skin loss. Stage 4, full-thickness skin loss with extensive destruction. (Figure adapted with permission from Braun JL, Silvetti AN, Xakellis GC. What really works for pressure sores. Patient Care. 1992; 28:63-74.).

 

Stage 2 is characterized by partial-thickness skin loss, that is, the epidermis is interrupted as an abrasion, blister, or shallow crater. Stage 3 features full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend to, but not through, the underlying fascia. The ulcer appears as a crater, with or without undermining of adjacent tissue. In stage 4, there is full-thickness skin loss with extensive destruction; tissue necrosis; or damage to muscle, bone, or supporting structures (for example, a tendon or joint capsule).

These staging definitions have two limitations: 1) Assessment of stage 1 is difficult in patients with darkly pigmented skin; and 2) accurate staging of a pressure ulcer with an eschar is difficult until the eschar has sloughed or the wound is debrided [2].


Causes
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The amount and duration of pressure are the primary contributing factors to development of pressure ulcers. This time-pressure relation was shown in dogs, in which ischemic ulcers developed with 500 mm Hg of pressure applied for only 2 hours or 150 mm Hg applied for 10 hours. However, microscopic changes occurred in tissues when they were subjected to as little as 60 mm Hg of pressure for only 1 hour [4]. These pressures are clinically relevant: healthy persons seated on a flat board generate pressures of 300 to 500 mm Hg under their buttocks. A 2-inch-deep foam pad reduced this pressure only to 160 mm Hg [5]. Just lying in a hospital bed generates heel-to-bed pressures of 50 to 94 mm Hg when the patient lies supine [6-8] and femoral trochanter-to-bed pressures of 55 to 95 mm Hg when the patient lies on one side [6, 7, 9, 10]. These pressures exceed the normal intracapillary pressures of 12 to 32 mm Hg [11] and thus are sufficient to produce local occlusion, ischemia, and hypoxia. Lying on the sacrum or femoral trochanter can decrease the transcutaneous oxygen tension from 80 mm Hg to 13 mm Hg [12]. Thus, the amount of pressure needed to produce tissue damage and pressure ulcers is readily present in all patients confined to a bed or chair.

Other factors proposed as etiologic agents include shearing force and friction. Friction is the rubbing of one body against another; it occurs when the patient is dragged across the bed and may result in an abrasion or skin tear. Shear is the stress from applied force that causes two parts of a body to slide on each other. This can be generated when the skin remains stationary and the underlying tissue moves. Shear occurs when the head of the bed is raised and the patient slips down and when the patient slides down in a chair. In elderly patients, the sitting mechanics result in shear that is on average three times that generated in healthy young adults [13]. The force of stretching or bending blood vessels may produce ischemia. It has been shown that with shear, less pressure is needed to produce ischemic occlusion [14, 15].

Recent reports suggest that acute illness and systemic and local circulatory conditions may also be etiologic factors in the development of pressure ulcers. For example, blood flow recovery time was delayed in elderly nursing home residents who developed pressure ulcers compared with residents without ulcers [16]. In addition, ulcer development was associated with lower diastolic blood pressures and other risk factors in a cohort of nursing home residents [3]. Finally, among a cohort of patients admitted to an intensive care unit, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores were found to be markers of a high risk for developing pressure ulcers [17]. In APACHE II, 12 routine physiologic measurements and previous health status are used to provide a general measure of disease severity [18]. Thus, acute illness and associated hemodynamic factors may play a casual role in pressure ulcer development. The postulate, which deserves further study, is that decreased perfusion may cause ischemia and lead to ulcers.


Epidemiology
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Data on the epidemiology of pressure ulcers in the nursing home Table 1 show the magnitude of the problem and help guide prevention and therapy. Seventeen percent to 35% of patients have ulcers when admitted to the nursing home [3, 19-22]. Most of these patients are transferred from acute-care hospitals [19, 21, 22]. Because of this high prevalence, a complete examination of each patient for ulcers at the time of admission to the nursing home is essential. The reported prevalence of pressure ulcers among residents in nursing homes ranges from 7% to 23% [19, 21, 23-25]. One study reported an average prevalence of 8.9% among 51 nursing homes in 11 states [19]. Even at the lower range of prevalence, pressure ulcers are one of the more common problems facing physicians in nursing homes. Among patients with ulcers, the average prevalence of each stage [19] is shown in Table 1. The combined prevalence of stage 1 and stage 2 ulcers is 65%. When patients are followed very closely (such as in an incidence study [3]), as many as 98% of the developing ulcers are first detected at stages 1 and 2. With careful assessment, most ulcers can be identified in early stages, when they can be treated most easily.


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Table 1. Epidemiologic Data on Pressure Ulcers in the Nursing Home

 

Ulcers develop over the buttocks (ischial tuberosities) more frequently in patients who are chair-bound. The other sites of bony prominence are subjected to pressure when patients are lying supine or on their side (Figure 2). Pooled data reported from three nursing homes indicate that about 80% of ulcers develop over the sacrum or coccyx, hips (femoral trochanter), buttocks (ischium), and heels [25-27]. Thus, for bed- and chair-bound patients, it is important to examine sites below the waist. The average number of ulcers reported per patient ranged from 1.6 to 2.5 [25-27].



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Figure 2. Positions of the bed-bound patient. In the supine position (top), the body weight is placed on the bony prominence of sacrum or coccyx and heels. In the lateral position (middle), the weight is placed on the prominence of the hips and malleoli of the ankles. These exposures can be avoided by propping the patient in the 30-degree lateral position (bottom) with pillows.

 

Several reports on the incidence of pressure ulcers from nursing home databases are now available [19, 28, 29]. These data were obtained by assessing all residents at 3- to 6-month intervals. The computed incidence from these studies of 0.20 to 0.56/1000 patient-days Table 1 may be low because stage 1 ulcers were not included. Some investigators exclude stage 1 pressure ulcers from their studies because of the potential difficulty of reliable identification for research purposes [19, 30-32]. In a 2-week prospective cohort study of patients at risk (Braden Scale score less than 17), the incidence of pressure ulcers (including stage 1) was 14/1000 patient-days [3]. For comparison, the incidence among all admissions to an adult intensive care unit was 28/1000 patient-days [33]; high-risk patients (APACHE II score more than 15) admitted to an intensive care unit had an incidence of 52/1000 patient-days [17]. Among patients destined to develop ulcers after nursing home admission, most ulcers occur in the first 7 to 14 days [3], perhaps because the patients were still recovering from an acute event. Thus, it is imperative that patients at risk be recognized at admission to the nursing home and that preventive interventions be started as soon as is feasible.


Prevention
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Good evidence suggests that many pressure ulcers are preventable. The following are three general guidelines for prevention: 1) Identify patients at higher risk for developing ulcers; 2) implement preventive measures appropriate for the level of risk; and 3) follow high-risk patients closely and reassess patients when functional status decreases.

Identifying Patients at Risk

Because pressure ulcers rarely develop in ambulatory patients, those who are bed- or chair-bound are targeted for assessment of risk factors. Risk factors for developing ulcers, derived from cohort studies [3, 28, 34-37], are listed in Table 2. Each risk factor has varying levels of severity, and many patients will have more than one risk factor. Thus, both the severity of a risk factor and the number of risk factors characterize the level of risk.


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Table 2. Risk Factors for Pressure Ulcers among Bed- or Chair-Bound Elderly Persons

 

Because the development of pressure ulcers depends on the length of time pressure is applied, immobility is the major risk factor. Although all patients who are bed- or chair-bound have some degree of mobility impairment, the severity ranges from complete immobility to the ability to reposition independently. Patients may not reposition themselves because they cannot move or cannot sense the discomfort associated with not moving. Patients who cannot move include those with spinal cord injury, fracture, Parkinson disease, stroke, and deconditioning from a severe illness. Physical restraints used in the bed or chair impair movement and also may directly cause pressure [34]. Examples of sensory loss that impair sensing the need to reposition include peripheral neuropathy, spinal cord injury, stroke, and coma from any cause. Sedated patients, such as those who are chemically restrained, also may not sense a need to reposition themselves. Although inability to move and inability to sense the need to move are separated in these examples, it is more common to find patients who have both immobility and sensory loss, such as a patient with hip fracture who is sedated to relieve pain.

Malnutrition has been linked to the development of pressure ulcers. In prospective cohorts with multivariate analyses, lower dietary protein intake [3] and inability to feed oneself [28] have been found to be independent predictors of ulcer development. Although these clinical findings of nutritional intake are clinically obvious, they are not only independent predictors but also the earliest signs of malnutrition. With continued poor intake, other markers of malnutrition, such as hypoalbuminemia or low vitamin C levels, may later occur. This observation is supported by the relation of hypoalbuminemia to the presence of pressure ulcers that has been seen in crosssectional studies [37, 38] but has not been an independent predictor in the longitudinal cohort investigations [3, 37]. Thus, when identifying patients at risk for developing pressure ulcers, physicians should concentrate on assessing intake rather than other traditional markers, such as the serum albumin level.

Urinary and fecal incontinence have been considered to be predictive of pressure ulcers, at least since the development of the early predictive instruments [39]. However, the independent contribution of incontinence in predicting pressure ulcers has not been consistently shown in three cohort studies [3, 28, 37]. Urinary incontinence was not found to be a significant risk factor in these studies except as a component of skin moisture in the Braden Scale, which includes five other factors [3]. Fecal incontinence was significant in one of the three studies [28], not independently observed in another [3], and not significant in the third [37]. The lack of consistency may be related to the use of different measures of fecal incontinence [28, 37] or confounding with mobility measures. Despite these findings, it would seem prudent to consider patients with mobility problems and fecal incontinence as being at higher risk for tissue damage than patients not exposed to moisture and bacterial contamination.

In most nursing homes, assessment of risk for pressure ulcer is a routine component of interdisciplinary patient care. In many nursing homes, part of the required admission protocol is the Minimum Data Set for Nursing Home Resident Assessment and Care Screening [40]. The Minimum Data Set includes determination of the presence or absence of pressure ulcers and risk factors on admission, and it provides a mechanism for communicating risk assessment among members of the care team.

Some nursing homes prefer using standardized risk assessment instruments [39, 41]. The Braden Scale [41] has six items (sensory perception, activity, mobility, skin moisture, friction, and nutrition) that contain three to four grades each. Scores are continuous; those of 16 or 17 indicate mild risk, and those of 12 or below indicate high risk [3]. The Braden Scale has been compared with the Norton Scale [39] in the same population, with a Cohen {kappa} statistic for agreement in classification of 0.73 [42]. These scales provide a systematic method for quantitative risk assessment and a method for interdisciplinary team communication. When used in cohorts of high-risk patients in hospitals (in whom the incidence of developing ulcers is about 20% over 10 to 14 days or about 14/1000 patient-days), the sensitivity of both scales was 83%, the specificity was 63% and 64%, respectively, and the calculated positive predictive value was 36% and 37%, respectively [43]. When used alone, these scales may not be helpful in populations at much lower risk. For example, among the nursing home population, the incidence of patients developing ulcers may average 0.5/1000 patient-days Table 1, or about 1% over 14 days. If the same sensitivity and specificity are used, the positive predictive value would be 2%. Thus, the information gained from using these scales in low-risk populations (all residents) is limited. For this reason, many physicians choose to use these scales only for higher-risk populations, such as bedbound patients.

Preventive Measures

Choosing the number and intensity of preventive measures appropriate for the level of risk requires clinical judgment. Preventive measures include reducing or eliminating factors contributing to the development of ulcers: prolonged pressure, amount of pressure, friction, shear forces, malnutrition, and fecal incontinence.

Physicians treating patients with mobility problems need to completely assess the medical conditions that limit the patients' ability to reposition or to sense the need for repositioning. This includes obtaining relevant history, physical examination, and laboratory data and then treating identified conditions or risks. Although the process of complete evaluation and management of medical conditions is important, any prolonged pressure must be relieved immediately. The choice of methods to relieve prolonged pressure depends on the extent of sensory loss and immobility. For patients with severe sensory losses, a standard method is turning the patient every 2 to 3 hours [39] so that the patient's weight does not rest on bony prominences [12]. The objective is to prevent the patient from lying supine (a position in which the sacrum and heels bear weight) and on one side (a position in which the femoral trochanter bears weight) (Figure 2). Pillows are used to prop the patient at a 30-degree lateral position (Figure 2, bottom), and positions are rotated from side to side every 2 to 3 hours. Although protecting the sacrum and hips, 30-degree lateral turning places pressure on the knees and the medial and lateral malleoli. To protect these areas, pillows should be inserted between the ankles and knees.

The intervention prevents prolonged pressure and relieves the amount of pressure by using pillows. Pillows are one example of devices that relieve pressure over prominent bony surfaces by distributing the weight over a wider area using the principle of displacement. The wider the area of weight distribution, the less pressure will be exerted on one point. Thus, the best pressure-relieving device may be a water bed, but this is impractical in care settings.

Categories of pressure-relieving devices are listed in Table 3 [44, 45]. Static overlays and pressure-reducing mattresses are not attached to motors and do not contain moving parts. They are made of or contain gel, foam, water, or air. A 2-inch-deep foam mattress does not significantly reduce pressure over the trochanter [6, 10]; however, a 4-inch-deep foam mattress reduces pressure by 30% [10] compared with regular hospital beds. Among elderly patients in three different settings, a 4-inch-deep solid foam mattress reduced the incidence of pressure ulcers compared with 3- or 4-inch-deep convoluted foam mattresses [46]. In addition, compared with a regular hospital bed, a 6.5-inch-deep foam mattress reduced the incidence of pressure ulcers (68% and 24%, respectively) among elderly patients admitted to the hospital with femoral neck fractures [47]. Other static mattresses reduce pressure by 40% to 70% [6, 7, 10] but are more expensive [48]; in addition, little information on efficacy in actual prevention of ulcers is available.


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Table 3. Devices and Dressings Available for Preventing and Treating Pressure Ulcers

 

Dynamic (alternating air) mattresses relieve pressure by the use of multiple air cushions with alternating air pressure controlled by a pump. These mattresses are more costly than static mattresses and are more complex to operate, but those with 6-inch-diameter air tubes were effective in preventing pressure ulcers [43]. Kinetic or oscillating beds can rotate the patient in a complete circle and are used for high-risk patients with spinal cord injury. Low air-loss beds provide pressure relief using air cushions that allow air to escape through multiple pores. These beds reduced the incidence of pressure ulcers among patients admitted to an intensive care unit [17] but have not been compared with solid foam mattresses. Thus, for high-risk patients in the nursing home, the most inexpensive and effective pressure-relieving products for prevention are 4- to 6-inch-deep solid foam mattresses.

The bony prominences of the heels are vulnerable, frequently neglected areas. When the patient is in the 30-degree lateral position (Figure 2, bottom), the heels can be protected with pillows. When the patient is lying supine, pillows can be placed under the legs to elevate the heels and relieve pressure. Special heel protectors and other pressure-relieving devices are appropriate for patients who cannot change the position of their lower extremities. Some of these heel protectors are constructed of foam and are inexpensive, but their effectiveness in prevention has not been shown. More expensive heel protectors (or boots) have posterior splints for the leg that lift the heel off of contact surfaces; these protectors are more appropriate for treatment or prevention in very-high-risk patients.

Chair-bound patients who cannot sense the need for repositioning require intensive efforts for relieving pressure. The pressures located over ischial prominences are larger, and the potential area for distributing weight is smaller. Measures of pressure reduction of cushions varied so widely among patients that specific recommendations could not be made [49, 50]. Thus, cushions need to be individually selected and prescribed for each patient [51]. Many rehabilitation therapists and nurse specialists have been trained to evaluate patients and prescribe these devices. Doughnut-type devices or ring cushions are to be avoided because they compromise blood flow to areas of bony prominence. Seated patients should be repositioned frequently (that is, every hour) or, if feasible, trained to shift weight every 15 minutes.

Preventive measures for shear and friction include maintaining the head of the bed at the lowest elevation consistent with medical conditions, using a trapeze or bed linen (lift sheet) for moving the patient, and paying careful attention when the patient is being positioned. The use of skin moisturizers for dry skin may be considered. Advances have been made in ways to assess and manage fecal incontinence and malnutrition. Detailed discussion of these problems and interventions is beyond the scope of this review.

Follow-up and Reassessment

Patients should be followed up to determine whether the preventive interventions are working, that is, to observe whether pressure ulcers develop. In high-risk patients, pressure points should be monitored daily. If ulcers develop and are recognized early (for example, at stage 1), the number or intensity of preventive interventions can be increased and therapy can be begun immediately with expectations that the ulcers will resolve within days. The objective is to avoid advanced stages of ulcers associated with major morbidity.

Changes in patients' medical conditions may affect their level of risk for developing pressure ulcers. Thus, risk factors for pressure ulcers should be reassessed after any change in condition to decide whether the intensity of preventive measures must be increased or decreased. Even patients not previously at risk should be periodically assessed (3 to 6 months) for the presence of risk factors for pressure ulcers. This is a routine staff procedure in most nursing homes.


Treatment
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Therapeutic measures should be appropriate for each stage Figure 1 and should be consistent with the therapeutic goals for the patient. Many therapeutic interventions are the same as preventive interventions.

Stage 1: Nonblanchable Erythema

Perhaps the most important facet of therapy is shifting the attitudinal approach from "this is the minimal stage of disease" to "this is the warning that advanced stages will soon appear unless interventions are immediately implemented." Interventions initiated early may produce a cure within days, whereas delay may result in progression to advanced stages within the same period; cure may then take months. Thus, careful examination of patients to detect early stages of disease is imperative. On the basis of the epidemiology of pressure ulcers Table 1, the careful examination process should start on the day of admission to the nursing home. The common sites below the waist deserve special attention.

To treat stage 1 ulcers, risk factors and current preventive measures should be reassessed. When preventive measures are in place, the intensity or number of measures discussed above for prevention should be increased (for example, increased frequency of turning, a more potent pressure-relieving device [Table 3], increased mobility through trapeze bars or physical therapy, or increased nutritional repletion). These measures alone may be sufficient for stage 1. As an alternative, polyurethane dressings applied every 1 to 10 days can protect the area from additional friction. The transparent polyurethane dressings are evenly coated on one side with a synthetic adhesive. These semipermeable films are permeable to water vapor, oxygen, and other gases and are impermeable to water and bacteria. They maintain a moist interface for healing but allow some exudate to be lost by transmission of water vapor. With appropriate treatment, most nonblanchable erythema lesions can be expected to heal by 2 weeks.

Stage 2: Partial-Thickness Skin Loss

All therapeutic interventions for nonblanchable erythema are also appropriate for stage 2 pressure ulcers. Because a defect is present in this stage, the wound should be inspected and monitored for signs of secondary infection (surrounding erythema, warmth). For stage 2 ulcers, polyurethane dressings are more effective and less costly than saline wet-to-dry dressing [52]. Further, saline wet-to-dry dressings (a debridement dressing) are rarely indicated for this stage.

Stage 3: Full-Thickness Skin Loss

A difficulty with stage 3 (and stage 4) lesions is that the extent of disease may not be evident because of covering necrotic material or eschar. To establish the extent of disease and promote healing, the necrotic material must be removed. Debridement may be done by experienced primary care physicians when the eschar is small. When the eschar is large, surgical consultation should be considered. Because physical debridement can be associated with bacteremia [53], prophylactic antibiotic agents should be used for patients with implanted prosthetic devices. For smaller eschars, topical application of enzymatic debriding agents is effective [54]. The eschar should be scored so that the penetration and effectiveness of topical debriding agents are increased. These enzymes must not touch the surrounding area because they irritate healthy skin. Applications should be stopped when the eschar sloughs.

Loose material can be effectively debrided by applying wet-to-dry saline dressings every 8 hours. Wet-to-dry dressings are primarily used for debridement. Although ulcers may heal with these dressings, the dry dressing may remove or disrupt the granulation tissue and delay healing when the lesion is clean with a granulating base. Polyurethane and hydrocolloid dressings are more effective for healing stage 3 pressure ulcers [52, 55-58]. Hydrocolloid dressings are impermeable to gas and moisture. In contrast to polyurethane, hydrocolloid dressings absorb exudate and are changed more frequently, that is, every 1 to 4 days. Hydrocolloid dressings are less costly [57, 58] and more effective [55, 56, 58] than the wet-to-dry dressings, which are changed three times a day.

In the deeper stage 3 and stage 4 wounds, hyrodrocolloid dressings alone are not appropriate. These deeper wounds need to be packed with materials according to the amount of exudate. For dry wounds with minimal exudate, the less absorptive hydrogels are recommended. Continuous moist soaks with normal saline may be used, with care taken to ensure that the dressing does not become dry; healthy tissue is removed when dried dressing is changed. For wounds with significant exudate, the more absorptive dressings, hydrophilic foam, alginates, or saline-impregnated gauze are indicated for packing. Packings are changed daily.

Among patients with several or large ulcers, there is no consensus on the use of costly but effective specialized beds, that is, low-air-loss or air-fluidized beds Table 3, for treatment in the nursing home. In hospitalized patients, the relative odds for showing improvement were 5.6-fold greater with air-fluidized beds compared with air mattresses covered with a 1.9-cm-deep foam pad after a follow-up of 13 days [59]. In nursing home residents, low-air-loss beds compared with 10-cm-deep corrugated foam pads resulted in a threefold reduction in the ulcer area during a follow-up of 37.5 days [60]. Among patients receiving home care, air-fluidized beds did not improve healing compared with usual care (that is, various pressure-reducing mattresses), but the costs of the beds were offset by reduced hospital days [61].

However, in nursing homes not using low-air-loss beds, 20% to 30% of stage 3 and stage 4 ulcers completely heal [19]. Bennett and colleagues [62] advocated not prescribing specialized beds for most patients within the first 30 days of admission to a nursing home. This review showed that many patients, who are prescribed special beds shortly after admission, were extremely ill at that time, died of unrelated conditions during the first 30 days, and received no discernible benefit. A trial of intensive total-patient therapy with close monitoring (weekly linear measurements of size and depth) would provide objective evidence of healing, nonhealing, or worsening and the need or absence of need for special beds. Further, if specialized beds are prescribed, they should be used for at least 60 days before their use is discontinued because of a lack of therapeutic response [62].

If aggressive therapy is consistent with the overall goals for the patient, and if the severe ulcers do not heal or worsen with intensive but conservative therapy, specialized beds should be seriously considered. The constraint for not prescribing specialized beds earlier is the expense ($50 to $100 per day) [62]. The degree to which these costs can be offset by potential benefits of avoiding surgery, reducing nursing home stay, or avoiding hospital readmission requires further clinical trials with long follow-up periods.

If patients with large defects are candidates for surgery, consultation with plastic surgeons for consideration of skin grafting is appropriate, depending on the goals for the patient and response to conservative therapy. Patients with large defects in the sacral area and urinary incontinence may require catheterization. Both venous and arterial insufficiency need to be assessed for pressure ulcers on the lower extremity.

Stage 4: Full-Thickness Skin Loss with Extensive Destruction

Stage 4 ulcers usually require surgical consultation for initial physical debridement. Completion of debridement can be done with wet-to-dry dressings or repeated debridement. For some patients, whirlpool baths facilitate debridement. Clean, deep ulcers require packing, as discussed for stage 3 ulcers.

When the wound is clean and granulation tissue evident, grafting procedures may be considered. The selection of patients for surgical procedures to close pressure ulcers is difficult. In elderly patients with severe cognitive dysfunction and other chronic disabilities, the rates of surgical complications, recurrences, and new ulcer formation can outweigh any benefit of surgery [63]. Moss and La Puma [64] reported that aggressive treatment of advanced pressure ulcers is often inconsistent with the overall goals for the patient. Because elderly patients with advanced pressure ulcers are often terminally ill, Moss and La Puma emphasized the importance of defining the overall goals of therapy for the patient: Is the goal to prolong life, restore normal function, avoid burdensome therapies, or relieve pain and suffering? Alternatively, in patients with moderate dysfunction and comorbid conditions, surgical treatment may be preferred [65] if it is compatible with treatment goals and the patient's ability to tolerate surgery.

Careful attention to serious wounds should not detract from continued assessment and management of the other factors, including general medical conditions, immobility, fecal incontinence, and malnutrition. Too frequently, aggressive care interventions are used without attention to basic care, such as nutritional assessment [66]. This latter aspect of care is important, and recent good clinical trials have shown the effect of specific nutrients. For example, at least two studies showed that a higher protein intake is related to more rapid healing of pressure ulcers [59, 67]. In addition, ascorbic acid supplements have been shown in a randomized, double-blind clinical trial to significantly improve ulcer healing [68].

Newer Forms of Therapy

Recent clinical trials of low-intensity direct current [69] for treating pressure ulcer in stages 2 and 3 and of topical growth factor [70, 71] for treating ulcers in stages 3 and 4 have shown increased healing rates. These studies suggest promising new areas for clinical investigation.


Outcomes
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Local Infection

Pressure ulcers are chronically contaminated wounds. Local infection is usually well controlled by relief of pressure, debridement, dressings, and other general measures of care. Although higher bacterial counts per gram of tissue are associated with delayed healing, unproven antiseptic or antibiotic topical applications should be avoided because they may be toxic to fibroblasts and impair formation of granulation tissue [72]. Few studies have shown efficacy of topical antibiotic agents. One study reported that gentamicin cream applied to ulcers reduced bacterial counts and improved healing [73]. Ulcers with a foul odor are probably infected with anaerobic organisms. Some reports suggest that topical metronidazole may be effective in reducing the foul odor and bacterial counts of these ulcers [74, 75]. However, until efficacy is better shown, topical antibiotic agents should have no role [72].

Sepsis

Among hospitalized patients, the combination of bacteremia and pressure ulcers has been associated with a mortality rate of 50% [76]. Thus, if sepsis is suspected in nursing home residents, the patient should be transferred to the hospital when this move is consistent with the patient's treatment goals. In patients with stage 3 and 4 pressure ulcers and clinical manifestations of sepsis (fever, chills, confusion, and hypotension) without a definable cause, it must be assumed that the primary source of infection is from the wound. Because swab specimens frequently reflect surface colonization, a deep-tissue biopsy specimen for culture should be obtained when feasible [77], in addition to blood cultures.

Blood cultures frequently grow multiple microbial organisms [72] and have included Pseudomonas aeruginosa, Bacteroides fragilis, and Staphylococcus aureus. Thus, when sepsis is thought to be related to the pressure ulcer before culture results are obtained, antibiotic therapy should cover anaerobic organisms, gram-negative bacilli, and gram-positive cocci.

Osteomyelitis

Because ulcers develop over bony prominences, osteomyelitis is a potential complication [78]. The diagnosis is more likely when the ulcer involves bone surface or when healing is delayed. However, clinical evaluation for osteomyelitis is often inaccurate. Appropriate diagnostic procedures, which may include pathologic examination of bone tissue [79], should be pursued to justify a prolonged course of antibiotic therapy. Ulcers located over joints also merit close attention for potential development of septic arthritis.

Mortality

Patients admitted to nursing homes with pressure ulcers have a mortality rate of 50% at 1 year compared with a 27% mortality rate in those without ulcers. Thirty-five percent of patients developing an ulcer within 3 months of admission die within 1 year compared with 25% who do not develop ulcers [19]. In patients with pressure ulcers, death is more likely to be related to cardiovascular disease, respiratory disease, or cancer than a complication of the pressure ulcer [26]. These data show the frailty of patients with or developing ulcers and the need for total patient care.

Costs

In an acute-care facility, the average variable costs (additional costs incurred to treat pressure ulcers) have been estimated to be $1300 per patient or $80 per day [80]. If the patient was admitted specifically for treatment of pressure ulcers, room costs were included; the average variable costs then increased to $3746 per patient. In the nursing home, the average variable costs were estimated to be $751 per patient and $5.35 per day (range, $0 to $128 per day) [81]. For some individual nursing home residents, costs may range from $4255 to $23 300 per patient [82]. These costs were estimated from the institutional perspective and are conservative from the patient perspective. For example, costs of the primary physician are not included, nor are the costs before or after institutionalization at that facility or the costs of the stay being prolonged because of the ulcer. Also, the costs not directly related to pressure ulcer treatment, such as costs of physical therapy to improve mobility, were not included. Further, the estimates from the nursing home did not include pressure-relieving devices nor hospitalizations for pressure ulcers [81]. Thus, from the patient perspective, treatment costs can be significantly higher, thus providing incentive for early prevention and treatment.


Multidisciplinary Care and Other Resources
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Pressure ulcers are a multidisciplinary care problem. Before-and-after studies have shown effective prevention with multidisciplinary teams for systematic risk assessment, implementation of preventive and therapeutic measures, education of patients and staff, and monitoring of incidence [24, 83]. The teams include medicine, surgery, nursing, rehabilitative therapy, dietetics, and surgical subspecialties. Nursing staff play a major role in coordinating systematic preventive interventions. Nursing homes have established protocols for these interventions using the steps outlined above. Some interventions require physician orders, whereas others are automatically implemented. Dietitians are valuable resources for nutritional assessments and recommendations for supplements and methods for providing nutrition. Rehabilitation therapists are resources for improving mobility and devising or recommending protective and pressure-relieving devices. Physicians should be familiar with team function and organization and with established protocols. This will facilitate their roles as team participants, as more effective communicators, and as leaders in therapeutic interventions.

Recent and excellent resources for risk assessment, prevention, and treatment are the clinical practice guidelines Pressure Ulcers in Adults: Prediction and Prevention and Treatment of Pressure Ulcers. These booklets contain descriptions of risk assessment tools, further details on skin care, an algorithm for prevention, details of treatment, and an extensive list of references. Both of these booklets have illustrated companion pamphlets for patient education that explain pressure ulcers, their prevention, and treatment in lay language. These resources were developed by the Agency for Health Care Policy and Research (AHCPR) and the National Pressure Ulcer Advisory Panel. They can be obtained by calling the AHCPR Clearinghouse at (800)-358-9295.


Trends over Time
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As shown in this review, considerable information is now available on effective preventive and therapeutic interventions for pressure ulcers. It could be postulated that application of current knowledge and skills to practice sites would eventually reduce the prevalence and incidence of pressure ulcers. However, data from the National Hospital Discharge Survey [43, 84-87] show that among persons 65 years of age and older, the prevalence of pressure ulcers [ICD-9-CM code 707.0], as any of all listed diagnoses, has more than doubled over the past 10 years Figure 3, whereas the total number of discharges for older persons is constant or decreasing. The increasing prevalence of pressure ulcer diagnoses among discharged patients may be due to 1) coding changes when the prospective payment system was implemented in 1983, 2) an increased proportion of very old persons [those aged 85 years], 3) more invasive procedures being done in older persons at risk for complications, 4) the ineffectiveness of preventive and therapeutic interventions for pressure ulcers, or 5) the lack of implementation of effective interventions. Whatever the reason, these data do not provide evidence for a reduction in the prevalence in hospitals.



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Figure 3. Pressure ulcer prevalence at hospital discharge over time. The bar graph shows the trend over time for discharges from short-stay hospitals in the United States for persons age 65 years and older per 100 000-persons. The total discharges for all diagnoses are indicated by the hatched bars with reference to the right vertical axis. The discharges for which a pressure ulcer (ICD-9-CM code 707.0) was any of all listed diagnoses are indicated by the solid black bars with reference to the left vertical axis.

 

Whether the prevalence of pressure ulcers on admission to nursing homes or the prevalence among nursing home residents nationally is increasing or decreasing over time is unknown. A brief report from a multifacility group involving as many as 68 nursing homes suggests that the prevalence of pressure ulcers has remained stable over 10 years despite the increasing acuity of admissions [88]. Thus, application of current knowledge and skills may be having an effect. With the development of large databases for nursing homes [19, 29], more data on the prevalence for nursing home residents will become available. Such data will allow further judgments on the effectiveness of current practices in reducing the prevalence of pressure ulcers throughout the nation.

From the Richard L. Roudebush Veterans Affairs Medical Center; Indiana University School of Medicine; and the Regenstrief Institute for Health Care, Indianapolis, Indiana.


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For affiliations and current author address, see end of text.
Acknowledgments: The author thanks Drs. Christopher Callahan, Jeffrey Darnell, Terrance Drake, and David Wilcox for review of drafts; David Gregory for the illustrations; and Jane Egan, RN, Terryl Adams, RN, Gayle Redmon, the Skin Care Resource Team of Wishard Memorial Hospital, and Rebecca York for technical assistance.
Requests for Reprints: David M. Smith, MD, Richard L. Roudebush Veterans Affairs Medical Center (111GIM), 1481 West Tenth Street, Indianapolis, IN 46202.
Current Author Address: Dr. Smith: Richard L. Roudebush Veterans Affairs Medical Center (111GIM), 1481 West Tenth Street, Indianapolis, IN 46202.


References
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