Pressure ulcers: Epidemiology; pathogenesis; clinical manifestations; and staging

Author Dan Berlowitz, MD, MPH Section Editors Russell S Berman, MD Kenneth E Schmader, MD Deputy Editor Kathryn A Collins, MD, PhD, FACS

Last literature review version 19.1: January 2011 | This topic last updated: August 11, 2009 (More)

INTRODUCTION — Pressure ulcers are lesions caused by unrelieved pressure that results in damage to the underlying tissue. Generally, these are the result of soft tissue compression between a bony prominence and an external surface for a prolonged period of time [1,2]. The consequences of pressure-induced skin injury range from nonblanchable erythema of intact skin to deep ulcers extending to the bone. The ulcer imposes a significant burden not only on the patient, but the entire health care system.

Reducing the prevalence of pressure ulcers is a national goal in the United States (US), as part of the Healthy People 2010 initiative for the nation's health [3]. Knowledge of factors contributing to the pathogenesis of pressure ulcers allows the identification of patients at risk for ulcer development. Preventive interventions may then be targeted to those specific patients.

The epidemiology, clinical manifestations, staging and pathogenesis of pressure ulcers will be reviewed here. Prevention and treatment are discussed

separately. (See "Prevention of pressure ulcers" and "Treatment of pressure ulcers".)

EPIDEMIOLOGY — Pressure ulcers are among the most common conditions encountered in patients acutely hospitalized or requiring long-term institutional care. Estimates of the rates of pressure ulcers vary widely by clinical setting [35]. An estimated 2.5 million pressure ulcers are treated each year in US acute care facilities alone [4,5].

A study based on hospital billing codes showed an increase in the number of hospital stays involving pressure ulcers in the United States by nearly 80 percent between 1993 and 2006 [6]. In more than 90 percent of cases, the pressure ulcer was not the cause of admission. Most patients with pressure ulcers were over age 65 (56.5 percent of patients whose pressure ulcers were the cause of admission, and 72 percent of patients whose ulcers were a secondary condition). More than half of the patients with pressure ulcers required subsequent care in long term care facilities, as compared with 16.2 percent of patients without pressure ulcers. However, as coding practices change over time and this study did not include chart review or direct patient evaluation, the changes in these diagnoses may be overstated.

In general, caution is required in interpreting the reported incidence and prevalence rates for pressure ulcers as the methodology and follow up time varies between studies. Methods of studying and reporting pressure ulcer incidence include direct patient examination [7], use of databases [8], and surveys [9]. The most accurate estimates are probably derived from studies where clinician-researchers directly examined patients. However, these studies tend to be small, often involving only a single facility, making generalizability uncertain. Studies have also differed on whether they included early ulcer stages (stage 1 ulcers). Although stage 1 ulcers are frequently encountered, many trials have elected not to include them since they are difficult to reliably detect. Well-designed studies of the epidemiology of pressure ulcers in various settings are still required [2].

Among patients in acute care hospitals, prevalence rates for pressure ulcers have ranged in most studies from 3 to 15 percent [2,3,7,10]. However, rates may be considerably higher in select groups of hospital patients. As an example, in one report in an intensive care unit, over 50 percent of patients

developed a stage 1 or larger ulcer when managed with a standard mattress bed [11]. A prospective cohort study observed that pressure ulcers developed in 36 percent of elderly patients with a hip fracture [12]. Most pressure ulcers develop during acute hospitalizations, early in the hospital course in spite of the adoption of national pressure ulcer prevention objectives [10,12].

Pressure ulcers also are common among patients admitted to nursing homes, with reported rates ranging from 10 to 35 percent [8,13-15]. Prevalence rates are generally lower (3 to 12 percent) among long-term nursing home residents [8,13,15-18]. Studies using databases have found that 4 to 8 percent of nursing home residents develop a stage 2 or deeper pressure ulcer over six months [8,19]. However, incidence rates (including stage 1 ulcers) as high as 24 percent have been noted when residents were regularly examined [7], with over 70 percent of high-risk patients developing an ulcer [20].

The frequency of pressure ulcers among outpatients has not been well defined. However, they may be common among patients receiving home nursing services [21]. One study reported a 9.2 percent prevalence of stage 2 or higher pressure ulcers in a multistate sample of home care patients [22].

CLINICAL MANIFESTATIONS AND DIAGNOSIS — Pressure ulcers are usually easy to identify by their appearance and location overlying a bony prominence. It is important to distinguish pressure ulcers from ulcers that result from diabetic neuropathy or arterial or venous insufficiency [1]. They also may be confused with other conditions that cause erythema such as cellulitis. Superficial moisture-induced lesions, such as maceration over a bony prominence, should not be labeled as pressure ulcers. Characteristics of lesions that need to be distinguished from pressure ulcers are:

Diabetic neuropathic ulcers are seen in patients with diabetes who have peripheral neuropathy. The diabetic ulcer characteristically occurs on the foot, usually on the ball of the foot over the metatarsal heads or on the top of toes with Charcot deformity [1]. (See "Evaluation of the diabetic foot".)Venous insufficiency ulcers usually occur on the pretibial area of the lower leg or above the medial ankle. Previously known as stasis ulcers, venous insufficiency ulcers are the result of relatively minor trauma and are superficial but are difficult to heal and often chronic. These ulcers are painful when the foot is in a dependent position [1]. (See "Clinical evaluation of lower extremity chronic

. These are sometimes difficult to recognize in darkly pigmented skin. particularly of the lower extremity. Initial description of such lesions as stage 1 may not adequately define their severity Stage 1 — Intact skin with nonblanchable redness of a localized area usually over a bony prominence. pressure-induced necrosis of muscle with intact overlying skin) [26]. STAGING — A number of staging systems have been developed to describe the extent of pressure ulcers. they are not commonly in use [23. and natural history of lower extremity peripheral artery disease". These lesions often appear as a deep-purple bruise and. may be multifactorial with peripheral artery disease predisposing to the development of a pressure ulcer. diagnosis. (See "Clinical features.)Arterial ulcers occur as the result of arterial occlusive disease when arterial blockage causes tissue necrosis. firm or soft.24]. Pedal pulses are diminished or warmer or cooler as compared to adjacent tissue. over the course of a week or more.venous disease". Although other staging systems have been proposed in the past by Shea and Yarkony and Kirk.npuap. may progress to a stage 4 ulcer. section on 'Clinical signs by CEAP category'. The wound bed is dry and pale and the affected foot exhibits dependent rubor and increased pain with elevation [1]. The most commonly used system. The area may be painful.) Pressure ulcers. The development of a stage 1 ulcer should be taken as an indication that the patient is at high risk for more serious ulcer development and intensive preventive measures should be taken. proposed by the National Pressure Ulcer Advisory Panel (NPUAP) is available at (www. The NPUAP system follows (table 1 and figure 1) [25]: 2007 NPUAP staging — These new definitions capture the ongoing debate as to how to stage lesions characterized by deep tissue injury (eg. These ulcers are painful and usually occur over the ankle or bony areas of the foot.

brown or black) in the wound bed. This stage should not be used to describe skin tears. Slough may be present but does not obscure the depth of tissue loss.Stage 2 — Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed. tendon or joint capsule making osteomyelitis possible. In contrast. Bone and tendon is not visible or directly palpable. green or brown) and/or eschar (tan. These ulcers often include undermining and tunneling. The depth of a stage 4 pressure ulcer varies by anatomic location. perineal dermatitis. tendon or muscle. As with stage 3 ulcers. Unstageable — Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow. The depth of a stage 3 pressure ulcer varies by anatomic location. Stage 4 ulcers can extend into muscle and/or supporting structures including fascia. or excoriation. . tape burns. areas of significant adiposity can develop extremely deep stage 3 pressure ulcers. Stage 4 — Full thickness skin loss with exposed bone. ear. the bridge of the nose. tendon or muscle are not exposed. or a shiny or dry shallow ulcer without slough or bruising. The extent of stage 4 ulcers is often underestimated due to undermining and fistula formation. Slough or eschar may be present on some parts of the wound bed. These may also present as an intact or ruptured serum-filled blister. occiput and the malleolus. tan. ear. occiput and malleolus do not have subcutaneous tissue and stage 4 ulcers in these locations can be shallow. without slough. but bone. Exposed bone and tendon are visible or directly palpable. Stage 3 ulcers can be shallow in areas without subcutaneous tissue which include the bridge of the nose. Subcutaneous fat may be visible. Undermining and tunneling may also be seen. a relatively small superficial skin defect may mask extensive deep tissue necrosis. Stage 3 — Full thickness tissue loss. gray. maceration.

The presentation of this stage may include a thin blister over a dark wound bed. firm. shearing forces. friction. The wound may further evolve and become covered by thin eschar. However. boggy. while damage from tourniquet induced ischemia is reversible [29. Deep tissue injury may be difficult to detect in individuals with dark skin tones. mushy. Pressure — Pressure applied to the skin in excess of the arteriolar pressure (32 mmHg) prevents the delivery of oxygen and nutrients to tissues. exposing additional layers of tissue even with optimal treatment. External factors — The four main external factors that lead to the development of pressure ulcers are pressure. external forces alone are not sufficient to cause an ulcer. PATHOGENESIS — The development of a pressure ulcer is a complex process that requires the application of external forces to the skin [27]. warmer or cooler as compared to adjacent tissue. and moisture [27]. their interaction with host-specific factors culminates in tissue damage. making it difficult to determine whether lesions are stage 3 or 4. two hours of compression will result in irreversible muscle damage. .30]. In animal models.Eschar often covers deep ulcers. resulting in tissue hypoxia. and free radical generation [28]. Until enough slough and/or eschar is removed to expose the base of the wound. Evolution may be rapid. The area may be recognized by tissue that is painful. it is increasingly recognized that compressive forces play an important role. the accumulation of metabolic waste products. Suspected deep tissue injury — Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying tissue from pressure and/or shear. While hypoxia has traditionally been considered the main factor in pressure ulcer development. cannot be determined. the true depth. and therefore stage.

Moisture — Exposure to moisture in the form of perspiration. and intermittent relief of pressure prevents tissue damage. Pressure in excess of 70 mmHg for two hours results in irreversible tissue damage in animal models [32]. Ulcer formation occurs more rapidly with higher pressures. Deeper tissues. Tissues vary in their susceptibility to pressure-induced injury. Friction is most likely to result in stage 2 pressure ulcers since it does not cause the necrotic changes associated with deep tissue injury. Thus. sitting produces pressures as high as 300 mmHg over the ischial tuberosities. Pressure over a bony prominence tends to result in a cone-shaped distribution with the most affected tissues located deep. feces. There is little evidence regarding the magnitude of the contribution of moisture to pressure ulcer development [35]. Shear forces alone may not cause ulceration. This results in an abrasion with damage to the most superficial layer of skin. . extensive deep tissue damage may occur with little or no evidence of superficial tissue injury. rather than a gradual progression of an ulcer from stages 1 through 4. are pulled downwards by gravity. and trauma to local blood vessels and lymphatics. A deep necrotic wound may be the first evidence of pressure-induced injury. followed by subcutaneous fat and then dermis [33]. Thus. Friction — Friction occurs when patients are dragged across an external surface. including muscle and subcutaneous fat. but appear to have an additive effect so that in the presence of pressure. while the superficial epidermis and dermis remain fixed through contact with the external surface. muscle is the most susceptible. or urine may lead to skin maceration and predispose to superficial ulceration. Shearing forces — Shearing forces occur when patients are placed on an incline. The result is stretching. it has only a limited contribution to the development of stage 3 and 4 ulcers. more severe tissue damage will occur [34]. A patient lying on a standard hospital mattress may generate pressures of 150 mmHg. adjacent to the bone-muscle interface.Pressures are greatest over bony prominences where weight-bearing points come in contact with external surfaces. the extent of injury to deep tissues is often much greater than perceived from the visible ulcer on the skin surface and the skin changes are just the "tip of the iceberg" [31]. angulation.

Accordingly. However. circulatory factors. Immobility may be permanent or transient [36]. Among nursing home residents. these studies have generally not considered the strong correlation between incontinence and immobility. Urinary incontinence often does not remain as an independent predictor of ulcer development when statistical analyses are performed to account for this correlation. The strongest nutritional measure predicting pressure ulcer development may simply be whether the patient has adequate dietary intake [20. methods to measure immobility in clinical settings are generally not available. Nutritional compromise — Impaired nutritional status is a risk factor for the development of pressure ulcers [38]. incontinence. Some studies suggest that incontinent patients have up to a five-fold higher risk for pressure ulcer development [39].38]. and neurologic disease.or chair-bound [40]. However. for example. Immobility — Immobility is the most important host factor that contributes to pressure ulcer development. A national survey of nursing home discharges. .Host factors — A number of host factors may contribute to pressure ulcer development including immobility. nutritional status. investigators have often relied upon clinical characteristics as markers for immobility. found that 94 percent of incontinent pressure ulcer patients were bed.42]. body mass index below 25 kg/m2 is associated with greater risk of pressure ulcer development [43]. including functional measures. Incontinence — Urinary incontinence is frequently cited as a predisposing factor for pressure ulcers. Several studies have also suggested that fecal incontinence is a predictor of pressure ulcers [41. There is a high correlation between a lack of spontaneous nocturnal movements and pressure ulcer development in studies using devices that measure body movement [37]. such as whether patients are ambulatory or bedbound as well as diagnostic information such as a history of cerebrovascular accident [38].

vasomotor failure. or medications. vasoconstriction secondary to shock. This suggests that a failure to increase blood flow in response to extended pressure contributes to ulcer development. the Acute Physiology and Chronic Health Evaluation (APACHE) score. When vital organs such as the kidneys and the gastrointestinal tract are not receiving adequate perfusion. particularly of the lower extremities. Contributing factors to the development of tissue ischemia have been postulated to include hypotension.Arteriosclerotic disease. heart failure. has been associated with pressure ulcer development in an intensive care unit [11].One study evaluated skin blood flow over bony prominences during surgery [51].A global measure of disease severity. the Comprehensive Severity Index (CSI).Animal studies have found that more severe pressure-induced skin destruction occurred in malnourished animals than in well-nourished animals exposed to similar amounts of pressure [44].46].48]. Several studies have demonstrated an association between low blood pressure and pressure ulcer development. (See "Prevention of pressure ulcers" and "Treatment of pressure ulcers". in . The role of nutrition in prevention and treatment of pressure ulcers is discussed separately. which increases the risk for the development of pressure ulcers.42]. dehydration. although it appears likely that they will have a major role.47. A 5 fold intraoperative increase in skin blood flow was seen in patients who did not develop a postoperative pressure ulcer. compared to no flow increase in patients who developed a pressure ulcer. The precise role of circulatory factors in pressure ulcer development must be further elucidated. but not among other hospitalized patients [49]. may contribute to ulcer development either as a result of baseline tissue hypoxia or a failure of blood flow to increase in response to pressure. was found to be associated with pressure ulcer development among nursing home residents [50]. In addition. cross-sectional studies have suggested that patients with pressure ulcers are more likely to have hypoalbuminemia [38. it is likely that blood flow to the skin will also be decreased. Another illness severity measure. although this has not been consistently found [20.) Skin perfusion — The role of skin perfusion in the development of pressure ulcers has been increasingly recognized [45.

cerebrovascular disease. spasticity. cardiovascular disease. Psychosocial consequences are not often considered.52]. Bacteremia and sepsis can complicate pressure ulcers and lead to increased mortality. pressure applied for less than two hours may be sufficient to cause severe damage. Sensory loss is also common. peripheral vascular disease. However. A partial list includes diabetes. elderly patients. (See "Infectious complications of pressure ulcers". suggesting that patients may not perceive pain or discomfort arising from prolonged pressure. and neuropathy are important contributors to pressure ulcer development. The infectious complications of pressure ulcers are discussed separately. The medical complications can be life threatening and are more common with stage 3 and 4 ulcers. This may be related to immobility. and contractures that are common in these conditions. delirium. only clinically evident infections should be addressed with culture and antibiotic treatment [54]. recent lower extremity fractures. sepsis and hypotension [5. depression and decrements in overall health-related quality of life [53]. COMPLICATIONS — Pressure ulcers may be associated with both medical and psychosocial complications. The relative contributions of immobility and sensory loss to ulcer development have not been defined. Other factors — Many other host factors have also been evaluated to define their role in pressure ulcer development. Wound care disrupts normal activities of daily life and patients often feel stigmatized. patients with pressure ulcers suffer pain and suffer a loss of control over their lives. This results in lifestyle changes leading to social isolation. Further studies are required to determine whether these host factors are independent predictors or simply reflect the high prevalence of immobility among frail. Over one hundred risk factors for the development of pressure ulcers have been identified in the literature [5]. Neurologic diseases — Neurologic diseases such as dementia.the setting of decreased circulation. Infection — All pressure ulcers are colonized with bacteria. spinal cord injury. The extent and magnitude of psychosocial complications have not been well defined in the literature.) .

and death. Interaction of external factors with host-specific factors such as immobility.)External factors that lead to the development of pressure ulcers include pressure. and compromised nutritional status culminates in tissue damage.)Pressure ulcers may be associated with both medical and psychosocial complications.)Knowledge of factors contributing to the pathogenesis of pressure ulcers allows the identification of patients at risk for ulcer development. Other complications — Other complications due to pressure ulcers are rare.Squamous cell carcinoma occasionally develops in a pressure ulcer and should always be considered in patients with a nonhealing wound. sepsis. and moisture. Sinus tracts may develop that communicate with the deep viscera including the bowel or bladder. (See "Infectious complications of pressure ulcers". and multiplyresistant gram negative bacilli [55.Heterotrophic calcification occurs occasionally.) . friction.Pressure ulcers may also pose a risk to other hospitalized patients by serving as a reservoir for resistant organisms such as methicillin-resistant Staphylococcus aureus. incontinence. (See 'Introduction' above and 'Epidemiology' above. (See 'Pathogenesis' above. Preventive interventions may then be targeted to those specific patients. (See 'Staging' above. Reducing the prevalence of pressure ulcers is a national goal in the United States as part of the Healthy People 2010 initiative for the nation's health.)The staging system used to describe the extent of pressure ulcers provides uniform criteria for the classification and treatment of these conditions (table 1).)It is important to distinguish pressure ulcers from ulcers that result from diabetic neuropathy or arterial or venous insufficiency.56]. (See 'Clinical manifestations and diagnosis' above. vancomycin-resistant enterococci. The medical complications are primarily infectious and can lead to bacteremia. SUMMARY AND RECOMMENDATIONS Pressure ulcers are among the most common conditions encountered in patients acutely hospitalized or requiring long-term institutional care. shearing forces. (See "Prevention of pressure ulcers".The chronic inflammatory state arising from the ulcer may result in systemic amyloidosis.

and implications for the future. 3. MD Deputy Editor Kathryn A Collins. PhD. incidence. and leading to significant morbidity and prolonged hospital stays. cost and risk assessment: consensus development conference statement--The National Pressure Ulcer Advisory Panel. 2010 (More) INTRODUCTION — Pressure ulcers are a significant problem in institutionalized elderly patients and critically ill patients. 2. Decubitus 1989. An executive summary of the National Pressure Ulcer Advisory Panel monograph. causing pain. MPH Section Editors Russell S Berman. Thomas DR. 2:24. MD. usually over bony prominences. Pressure ulcers can also result from poorly fitting casts .Use of UpToDate is subject to the Subscription and License Agreement REFERENCES 1. decreasing quality of life. Treatment of pressure ulcers Author Dan Berlowitz. The new F-tag 314: prevention and management of pressure ulcers. 7:523. 14:208. Pressure ulcers are ischemic soft tissue injuries resulting from pressure.1: January 2011 | This topic last updated: April 14. FACS Last literature review version 19. MD. Adv Skin Wound Care 2001. Pressure ulcers in America: prevalence. Pressure ulcers prevalence. J Am Med Dir Assoc 2006. MD Kenneth E Schmader.

Partial thickness loss of dermis. and staging". Accordingly. and staging". but bone. which presents as a shallow open ulcer with a red-pink wound bed. necrotic tissue.or appliances. Wounds should be evaluated for stage. Photographs of all wounds are helpful. is outlined below (table 1 and figure 1). pathogenesis.Deep tissue injury .Stage 2 . These ulcers often include undermining and tunneling. brown. or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound. Subcutaneous fat may be visible. gray.Unstageable . A number of staging systems have been developed to describe the extent of pressure ulcers. exudate. sinus tracts. Stage 2 ulcers may also present as an intact or ruptured serum-filled blister. and the presence of granulation. Other aspects of pressure ulcer evaluation and prevention are discussed separately. cannot be determined. Sloughing may be present but does not obscure the depth of tissue loss. pressure ulcers are considered unstageable when there is full thickness tissue loss and the base of the ulcer is covered by slough (yellow.The skin is intact with non-blanchable redness in a localized area. clinical manifestations. the external appearance of a pressure ulcer may underestimate the extent of injury [1].Full thickness skin loss with exposed bone. There may be undermining and tunneling. tendon or muscles are not exposed. The approach to treatment of pressure ulcers is discussed here. clinical manifestations. Sloughing or eschar may be present on some parts of the wound bed.Full thickness tissue loss. or brown) and/or eschar (tan. (See "Prevention of pressure ulcers" and "Pressure ulcers: Epidemiology.Stage 3 . size. the true depth. green.Deep tissue injury is suspected when .Stage 4 . The most commonly used system. and therefore stage. usually over a bony prominence. tendon or muscle.) ASSESSMENT AND STAGING — The treatment of pressure ulcers begins with a comprehensive assessment of both the patient's general medical condition and the wound.In addition. Soft tissues are more susceptible to injury than skin. without sloughing. Darkly pigmented skin may not have visible blanching. tan.npuap.) Stage 1 . its color may differ from the surrounding area. section on 'Staging'. proposed by the National Pressure Ulcer Advisory Panel (www. (See "Pressure ulcers: Epidemiology.

(See "Prevention of pressure ulcers". clinical manifestations. with a focus on positioning and support to minimize tissue pressure.Provide appropriate local wound care. or cooler as compared to adjacent tissue. The general approach to management of a patient with a pressure ulcer should include the following [2]: Reduce or eliminate underlying contributing factors by providing pressure relief with proper positioning and support surfaces. and adequacy of pain controlPresence of possible complications. mushy. which may include debridement for patients with necrotic tissue. The area may be recognized by tissue that is painful.) GENERAL TREATMENT PRINCIPLES — Preventive measures. (See 'Healing Scales' below. firm. and staging".) . Any ulcer development should underscore the need to review and intensify preventive measures that are already in place. Consider adjunctive therapies. such as negative pressure wound therapyMonitor and document the patient's progress Monitoring — The following parameters of care should be monitored daily and documented [3]: Evaluation of the ulcerStatus of the dressing. boggy. should be provided for all patients. (See "Pressure ulcers: Epidemiology. such as infection Documentation may be facilitated by using one of the scales for healing ulcers (table 2) [3-7]. pathogenesis. warmer. including those with pressure ulcers.there is purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying tissue from pressure and/or shear.) Treatment of pressure ulcers depends on the stage and severity of the ulcer (table 1). if presentStatus of the area surrounding the ulcerPresence of pain. based on the ulcer's characteristics.

is easy to use. and has been shown to be helpful in pressure ulcer management [10. and prognosis [ wound contraction. or breakdown of the surrounding skin should be addressed. infection. quality of life. the Sessing Scale. This scale has been validated. reepithelialization. is the most readily applied tool. Healing Scales — The healing process is best described by scales that capture changes in surface area.14]. and scar formation. Local factors that may be contributing to pain such as ischemia.9]. Initial and on-going pain assessment should be documented using a pain scale. The PUSH tool. extent of necrotic tissue and exudate. Given differences among available staging systems. known as reverse staging. designed to be used in conjunction with the NPUAP Staging System (www. is not recommended [12]. Ulcers heal through a process that includes granulation. The PUSH tool is being considered by the Center for Medicare and Medicaid Services for inclusion in the Minimum Data Set for nursing homes and the Outcome and Assessment Information Set (OASIS) for home care (table 2). including the Pressure Sore Status Tool (PSST) (table 3).11].Appropriate therapeutic goals should be set that consider discharge potential. Pain control — Adequate pain relief should be provided as pressure ulcers can be quite painful [13. The practice of changing the stage as the ulcer heals. the Wound Healing Scale. a stage 4 ulcer remains stage 4 throughout the healing process. A number of scales are available for use in monitoring and documentation of the healing of pressure ulcers. Simple oral non-opioids can be used for mild pain. Thus. the healing scale used should be explicitly described to facilitate effective communication among clinicians responsible for patients with a pressure ulcer. and the Pressure Ulcer Scale for Healing (PUSH) tool [4-7]. Guidelines for managing cancer pain can . Opioid analgesics may be needed for moderate to severe pain. Training in the use of these scales is also required to ensure that ulcers are staged in a consistent manner. and the presence of granulation tissue.npuap.

Nutritional intake should be assessed by a nutritionist.19]. . A retrospective cohort study of 882 patients with pressure ulcers at 95 long-term care facilities demonstrated that total caloric intake of at least 30 kcal/kg promoted healing and decreased the size of stage 3 and 4 pressure ulcers [22]. This assessment may include protein and caloric intake. and minerals. vitamins. In particular. particularly for patients with stage 3 and 4 ulcers [1]. Vitamin C and zinc supplementation are commonly employed to promote healing but their efficacy has not been conclusively demonstrated [19]. However. Wound cleansing and dressing techniques may need to be reconsidered if they are causing severe pain. serum albumin and/or prealbumin. Optimizing both protein and total caloric intake is important. hydration status. Assess and optimize nutritional status — Patients with pressure ulcers are in a chronic catabolic state.24]. nutritional supplementation with enteral and parenteral nutrition is recommended to correct deficiencies [19-21]. Topical opioid preparations have shown some benefit in small randomized trials [15-17]. (See "Assessment of cancer pain". although some authors advocate higher protein intake [ helpful in the setting of pressure ulcers as well [14]. and total lymphocyte count [18]. (See "Nutritional support in critically ill patients: An overview".25].5 g/kg/day. but should not be used as the only method of pain relief [14]. protein.Data do not support nutritional supplementation for patients who do not have nutritional deficiencies [26].) Topical local anesthetics such as lidocaine can provide numbness for a short period of time and can be useful for a specific procedure. most patients will require systemic therapy for pain from pressure ulcers. Extensive debridement should be performed in the operating room as patients may require conscious sedation or general anesthesia for these invasive procedures. Nutritional deficiencies should be corrected. The protein target is usually 1. A number of small randomized trials have evaluated the role of nutritional supplements but methodological flaws and study size preclude confirmation of clinically significant results [2. adequate pain control should be provided for dressing changes and debridement. Increased dietary protein intake also promotes the healing of pressure ulcers [23.)If oral intake is not adequate to ensure sufficient calories.

In a study of 65 hospitalized patients with pressure ulcers. The difference was even greater in patients with large ulcers at baseline.5 cm2). These support devices. patients should be positioned to minimize or avoid all pressure on the wound [27]. while 34 patients received conventional therapy with an air mattress covered by a foam pad and repositioning every two hours [23]. and air fluidized mattresses. none of the studies compared a specialized support surface with a standard mattress [2]. do not require electricity. in the absence of data. such as foam. The efficacy of different specialized support surfaces has been studied in a number of randomized clinical trials with inconsistent results. designed to be placed on top of another support surface.Powered or dynamic support surfaces require electricity. 31 patients were given an air-fluidized bed and repositioned every four hours. . Nevetheless. or water overlays are useful for patients who can assume a variety of positions without bearing weight on the ulcer. there are no randomized trials available to identify whether repositioning makes a difference in the healing rates of pressure ulcers or what the optimal repositioning regimen would be. These supports can be used if the patient can assume a variety of positions without bearing weight on the ulcer. Foam. A randomized trial of 158 hospitalized patients found no difference in pressure ulcer healing between 85 patients on nonpowered support devices and 83 on powered support devices [29]. as defined by the National Pressure Ulcer Advisory Panel Support Surface Standards Initiative. However. low air loss beds. Examples of such beds include alternating pressure mattresses. Air currents or mechanical rotation regulate or redistribute pressure against the body. subjects treated with a low-air-loss bed were 2. Pressure ulcers showed a median decrease in total surface area on the air-fluidized beds. has a large ulcer or ulcers at multiple sites. Specialized powered beds should be considered when the patient cannot readily be repositioned. The latter group also used elbow or heel pads as needed.Mattresses and tissue pressure relief — To date.Overlays are an additional support surface.5 times more likely to heal compared with those using a foam mattress [30]. while increasing in size with conventional therapy (-1. are outlined below [28]: Non-powered support surfaces (previously known as static).In another report of 84 nursing home residents with pressure ulcers. Pressure-relieving support surfaces are also helpful in reducing tissue pressure.2 versus +0. or if the pressure ulcer does not show evidence of healing. air. as a practice with good face value.

Stage 1 ulcers may be dressed with transparent films for protection. Most importantly. are absent. However. Powered beds do carry a high cost. such as fever and leukocytosis. it is uncertain if powered mattresses are superior to non powered mattresses [2]. such as a patient with a severe ulcer who could potentially be discharged home once the ulcer resolved. local .) Stages 3 and 4 — Treatment of wound infections. such as warmth. preventive measures should be reviewed and intensified. Wound infections — Wound infections will impair healing. The costs become particularly significant when considering that treatment for at least two months is typically required [31]. erythema.Given limited data. Surgery is necessary for some full thickness pressure ulcers. instead of a standard mattress. (See 'Dressing choices' below. debridement of necrotic tissue. and appropriate dressings will accelerate healing of Stage 3 and 4 pressure ulcers. Wet-to-dry dressings are avoided since these wounds generally require little debridement. Specialized beds may be most important for selected patients in whom rapid healing of the pressure ulcer is critical in meeting overall treatment goals. when available. ULCER TREATMENT BY STAGE Stage 1 treatment — The development of stage 1 ulcers is a warning that more serious lesions may follow if appropriate preventive measures are not instituted in a timely fashion. specialized support surfaces appear to be of benefit and should be used. Infection of pressure ulcers often presents with local signs of soft tissue involvement. The possible presence of an infection should be considered even if systemic signs. It should again be emphasized that support surfaces alone do not address the underlying issues that lead to pressure ulcers. Stage 2 treatment — Stage 2 pressure ulcers usually require an occlusive or semipermeable dressing that will maintain a moist wound environment [32].

Dressings with absorptive qualities include alginates. topical antibiotics.35]. (See "Infectious complications of pressure ulcers". An appropriate wound dressing can remove excess wound exudate while maintaining a moist environment to accelerate wound healing [36]. and hydrofibers. The infectious complications of pressure ulcers including pathogenesis. Calcium alginates are highly absorptive and are useful for wounds with significant exudate. desiccation. The extent of infection in the bone or soft tissue surrounding the ulcer affects management.) Dressing choices — Dressings serve to protect the wound from trauma and contamination. while desiccation will slow epithelial cell migration. Treatment for infection may require local debridement. patients with deep ulcers should be evaluated for the presence of osteomyelitis. They can be easily cut to shape and do not shed fibers. In particular. and the presence of a foul odor. foams. promoting moist interactive healing [36]. Many different types of dressings are available. or systemic antibiotics [1]. Factors to keep in mind while selecting an appropriate dressing include the presence of heavy exudate. microbiology and treatment are discussed separately. no dressing has been shown to be consistently superior to another in clinical trials [2.Foams provide thermal insulation. purulent discharge.tenderness. Ulcers with heavy exudate — An absorptive dressing should be employed to avoid build up of chronic wound fluid that can lead to wound maceration and inhibition of cell proliferation and healing. and facilitate healing by absorption of exudate and protection of healing surfaces [33]. Although varying circumstances may favor choosing one dressing over another. high absorbency. Excess fluid causes wound maceration. and a moist environment. the manifestations of infection in pressure ulcers can be variable with delayed wound healing being the only sign of infection. Calcium alginates are derived from brown seaweed and form a gel on contact. However. infected or necrotic tissue.34. Foams are useful for sloughy or .

Films are especially useful at the later stages of wound healing when there is no significant exudate [36]. hydrocolloids. transparent films. Randomized trials. however.43]. Choices for a dry wound include saline moistened gauze. and hydrogels.40]. they are good secondary dressings when combined with another product for stage 3 or 4 ulcers (full thickness wounds) or may be used alone for stage 2 ulcers (partial thickness wounds). Five approaches to debridement are available.exudative wounds [36]. They come in a variety of sizes and shapes for use on different parts of the body. compare different methods of debridement but have not focused on the effectiveness of debridement per se [42]. Desiccated ulcers — Desiccated ulcers lack wound fluids. Accordingly.Hydrogels provide a high concentration of water contained in insoluble polymers and provide a good choice for dry sloughy wounds with low levels of exudate.37. They are appropriate for sloughy or exudative wounds [36]. they are often used in combination [13. Thus. Debridement — Necrotic tissue promotes bacterial growth and impairs wound healing.Hydrofibers can also be used for highly exudative wounds and are highly absorbent.Transparent films provide an effective barrier for retaining moisture. A comparison randomized trial of transparent films with hydrocolloid dressing in the management of stage 2 and shallow stage 3 pressure ulcers demonstrated the transparent film dressing improved the ability to assess the ulcer and improved patient comfort although the time to wound closure was nearly identical between the two groups [41]. Saline moistened gauze that is not allowed to dry will promote a moist wound environment. .38]. which provide tissue growth factors to facilitate reepithelialization. although occlusive dressings are equally effective and reduce the nursing time required for wound care [39.Hydrocolloids generally provide an effective barrier for retaining moisture and are useful for promoting autolytic debridement. pressure ulcer healing is promoted by dressings that maintain a moist wound environment while keeping the surrounding intact skin dry [22.36. it would seem that removal of necrotic tissue by wound debridement is an important element of pressure ulcer treatment.

Sterile larvae of the Lucilia sericata fly are utilized [13. caution is required to avoid damaging healthy tissue.41].Enzymatic debridement is done with the topical application of proteolytic enzymes such as collagenase. 50 percent with a stage 3 ulcer. Care should be taken with respect to debridement of the ischial spine as this will potentially affect weightbearing and can lead to breakdown of the ischium on the opposite side.Mechanical debridement is a nonselective method of removing necrotic tissue and debris from a wound. This often works best on wounds with minimal exudate.Sharp debridement involves the use of a scalpel or scissors. The larvae produce enzymes to break down dead tissue without harming healthy tissue.48]. or loose necrotic tissue. slough. Sharp debridement is also used to remove thick eschar and when there is extensive necrotic tissue. Papain was used for debridement in the past but was removed from the US market due to hypersensitivity reactions [47]. This is most commonly done with wet-to-dry dressings. It should not be used in the presence of infection [13. These agents may produce excess exudate and cause local irritation to the surrounding skin [9. Mechanical debridement is best for wounds that contain thick exudate.50]. or tendon. The exception is patients with heel ulcers covered by a thick. This can be considered when sharp debridement is contraindicated due to exposed bone. Sharp debridement is not recommended at this site. and deoxyribonuclease to remove necrotic tissue.Biosurgery or the use of maggots is another effective method of debridement.36. Debridement should stop once necrotic tissue has been removed and granulation tissue is present. and 30 percent with a stage 4 ulcer were ulcer-free at six months with conservative nonoperative . The topically applied enzymes work synergistically with endogenous enzymes to debride the wound. dry eschar. This is the most rapid form of debridement. Surgery for wound closure — Most pressure ulcers are successfully managed using the basic principles of wound care and dressings cited above. because of the proximity of bone [9].Autolytic debridement uses semiocclusive (transparent film) or occlusive dressings (hydrocolloids or hydrogels) to cover a wound so that necrotic tissue is digested by enzymes normally present in wound tissue.36. joint. it is indicated when there is evidence of cellulitis or sepsis.44-46]. Removal of both ischial spines will increase the risk of perineal problems and the formation of urethrocutaneous fistulas [1]. Over 70 percent of patients with a stage 2 pressure ulcer. fibrinolysin. Wet-to-dry dressings will remove both nonviable and viable tissues.36. Two studies from large nursing home chains have collectively followed over 1000 pressure ulcer patients [49.

risk of recurrence. In addition. therapeutic ultrasound. application of growth factors to the wound are being investigated for the treatment of pressure ulcers [56-60]. A fecal diversion via surgical colostomy is occasionally considered to promote wound healing if the site of the ulcer is prone to fecal contamination. this procedure may be associated with a high complication rate in frail elderly patients and is of questionable efficacy [55].management. Procedures may last for up to three hours and result in considerable blood loss: patients must be medically stable prior to surgery. ulcers should be free of devitalized tissue. ulcer site. particularly in those whose quality of life would be markedly improved by rapid wound closure. 77 percent of stage 4 ulcers had healed. Nevertheless. Thus. treatment goals. surgical wound closure is still necessary in some patients. usually requiring staged procedures for skin grafts. Some of these adjunctive therapies are discussed below.51]. skin flaps. Ulcer recurrence rates of 13 to 61 percent have been reported [52-54]. Smokers should be encouraged to stop since continued smoking impairs wound healing and may result in higher rates of recurrence [52]. Procedure selection depends upon patient characteristics. negative pressure wound therapy. Direct wound closure is usually not possible. . A variety of operative procedures are available.62]. Operative repair often results in wound closure. The decision to perform surgery depends upon patient preference. the role of operative repair is still uncertain for many patients. and free flaps [9. and available surgical expertise [1]. Indications for their use remain uncertain [61. In patients followed for two years. and quality of life considerations. although the long-term efficacy is less certain. However. musculocutaneous flaps. Adjunctive therapies — A variety of adjunctive therapies such as electrical stimulation. and patient factors predisposing to pressure ulcer development should be corrected where possible. hyperbaric oxygen.

and increasing the formation of granulation tissue [63-65]. A systematic review of randomized trials of electromagnetic therapy. patients with pressure ulcers tend to have many other comorbid conditions. the surrounding skin. (See 'Assessment and staging' above and "Pressure ulcers: Epidemiology. and staging".Negative pressure wound therapy. Negative pressure wound therapy is discussed in detail elsewhere. (See 'Healing Scales' above. A systematic review of studies of HBO for treating wounds concluded that while HBO may be of benefit for some types of wounds. pathogenesis. also known as VAC therapy. SUMMARY AND RECOMMENDATIONS The treatment of pressure ulcers begins with a comprehensive assessment of both the patient's general medical condition and the wound.)Hyperbaric oxygen (HBO) therapy has been advocated. any possible complications and pain control should be documented. The electric current is provided twice daily through a wound overlay and is believed to promote the migration and proliferation of fibroblasts. there is insufficient evidence. decreasing edema.69] and a meta-analysis [70]. Documentation may be facilitated by using one of the scales for healing ulcers. enhances wound healing by reducing increasing blood flow. pressure ulcers are at best a weak predictor of mortality. PROGNOSIS — Patients with pressure ulcers or those who develop a new ulcer are approximately two to three times more likely to die than patients without an ulcer [72-74].Electrical stimulation. (See "Negative pressure wound therapy". found no evidence of benefit [71]. There have been no studies specifically looking at the treatment of pressure ulcers with HBO. has also resulted in enhanced healing in several small studies [68.)Adequate pain control should be provided for patients with . However. a distinct form of electrotherapy. some serious adverse events were associated with HBO therapy including seizures and pneumothorax [66]. the dressing. A standardized system for staging pressure ulcers should be used to document initial presentation and plan appropriate treatment. A systematic review of three randomized trials found that methodologic limitations and small trail size made it impossible to rule out benefit or harm with ultrasound therapy [67]. clinical manifestations. in which a direct current is applied to the wound.)Close daily monitoring of the pressure ulcer. The development of an ulcer should underscore the need to review and intensify preventive measures.Ultrasound is sometimes used as therapy for pressure ulcers. The underlying study quality was poor. but its efficacy remains uncertain. after adjusting for these other factors.

MOC-PSSM CME article: Pressure sores. JAMA 2008. mechanical debridement (wetto-dry dressings). 3. We suggest use of non-powered support surfaces (eg. Reddy M. autolytic debridement under occlusive dressings. 7:523. (See 'Surgery for wound closure' above. et al. Particular attention should be paid to pain management during wound dressing and debridement. Surgery is necessary for some full thickness pressure ulcers. (See 'Mattresses and tissue pressure relief' above. application of proteolytic enzymes. or biosurgery with sterilized maggots. powered surfaces (eg air-fluidized beds) may be appropriate for selected patients with large or multiple ulcers that preclude appropriate positioning.pressure ulcers. and free flaps may be appropriate in patients whose quality of life would be markedly improved by rapid wound closure.)Nutritional status should be assessed in patients with pressure ulcers and any identified deficiencies should be corrected. dessication. musculocutaneous flaps.)Most patients are successfully managed without surgery. J Am Med Dir Assoc 2006.) Use of UpToDate is subject to the Subscription and License Agreement REFERENCES 1.)Necrotic tissue promotes bacterial growth and impairs wound healing. Thomas DR. Bauer J. 300:2647. Stage 3 and 4 ulcers should be managed by treatment of wound infection if present. (See 'Assess and optimize nutritional status' above. based on wound characteristics including the presence of heavy exudate. or necrotic tissue. Kalkar SR. skin grafts. Plast Reconstr Surg 2008. foam mattresses or overlays) for most patients with pressure ulcers (Grade 2C). (See 'Pain control' above. debridement of necrotic tissue. (See 'Debridement' above. The new F-tag 314: prevention and management of pressure ulcers. and appropriate dressings. 2.)Patients should be positioned and repositioned at least every two hours to relieve tissue pressure. Stage 2 ulcers require dressings to maintain a moist wound environment. We suggest not giving nutritional supplementation for patients without documented nutritional deficiency (Grade 2B). (See 'Ulcer treatment by stage' above. procedures such as direct closure. When cost is not a limiting factor. Treatment of pressure ulcers: a systematic review. Phillips LG. Wound debridement may involve any of five approaches: use of sharp dissection. 121:1.)Dressings are selected. . (See 'Dressing choices' above. Gill SS.)Treatment for stage 1 ulcers should focus on preventive measures and wound protection with transparent film.

Bates-Jensen BM. decreasing quality of life.3].1: January 2011 | This topic last updated: May 4. As of October 2008. Critically ill patients admitted to intensive care units are at particularly high risk of developing pressure ulcers [1]. Ulcer prevention and treatment are cost-effective approaches to improving health status [2. and leading to significant morbidity and prolonged hospital stays. PhD. MD. MPH Section Editors Kenneth E Schmader. Pressure ulcers are among the most common conditions encountered in hospitalized patients or those requiring long-term institutional care. failure to provide appropriate pressure ulcer care may expose providers to significant liability [5. The Pressure Sore Status Tool a few thousand assessments later. . FACS Last literature review version 19.6]. MD Deputy Editor Kathryn A Collins. new Center for Medicare and Medicaid Services (CMS) guidelines in the United States state that hospitals will no longer receive additional payments when patients develop stage 3 or 4 pressure ulcers (table 1) [4]. causing pain. In addition. MD Hilary Sanfey. 2010 (More) INTRODUCTION — Pressure ulcers are a significant problem in elderly and critically ill patients.4. Adv Prevention of pressure ulcers Author Dan Berlowitz. MD.

A comprehensive history and physical examination can identify potentially correctable predisposing factors. and staging are discussed separately. Risk prediction tools and guidelines — Guidelines from the Agency for Healthcare Research and Quality (AHRQ) in the United States have strongly prompted the use of prediction tools to identify at-risk individuals [8. pathogenesis. clinical manifestations. While these guidelines are longstanding. Specific interventions may then be initiated depending upon the measured level of risk [7]. (See "Pressure ulcers: Epidemiology. More recently. empirical studies combined with multivariate statistical techniques have been employed. epidemiology. to target appropriate interventions. Assessment of risk for pressure ulcer development is not a one time activity.Knowledge of factors contributing to the pathogenesis of pressure ulcers allows the identification of patients at risk for ulcer development. Patients should be reassessed periodically. The treatment. Two general approaches have been used when developing prediction rules that allow the identification of patients at high-risk for pressure ulcers. regular follow-up is required to identify changes in clinical status. and daily skin inspections should be performed to detect early evidence of pressure-induced skin damage and alter the care plan as needed [7]. clinical manifestations. their recommendations are still considered relevant to pressure ulcer prevention [9]. Preventive interventions may then be targeted to those specific patients. Pressure ulcer prevention is an ongoing task. is central to preventing pressure ulcers. particularly when there is a change in health status. pathogenesis. The prevention of pressure ulcers will be reviewed here. and staging" and "Treatment of pressure ulcers".) RISK IDENTIFICATION — Identifying patients at risk. The European Pressure Ulcer .9]. The first approach involves use of clinical judgment to determine patient characteristics and their relative importance.

The Braden scale rates patients in six subscales: sensory perception. mobility. Nevertheless. concerns about their positive predictive value have been raised [16. and incontinence (table 3) [11]. prepared jointly by the National Pressure Ulcer Advisory Panel (NPUAP) and the EPUAP are nearing completion. a score of 18 or less indicates high-risk (calculator 1). A score less than 14 indicates a high-risk of pressure ulcer development. The AHRQ Publications Clearinghouse can be accessed on the Internet at www.ahrq.npuap. The maximal total score is 23. The performance of these scales has been evaluated in a variety of settings.Advisory Panel (EPUAP) has also published similar guidelines for the prevention of pressure ulcers [10]. activity. In the larger of . In addition. The Norton scale generally identifies more patients at high-risk than the Braden scale [13].gov. it is unclear whether they perform better than clinical judgment of risk [13. New guidelines.19]. sensitivity typically ranges from 70 to 90 percent and specificity from 60 to 80 percent [14]. mobility.16]. activity. A limitation of these systems is that interrater reliability is low unless performed by trained staff [12]. NPUAP and EPUAP guidelines are also available on the internet at both the Norton and Braden scales have withstood the test of time and have been shown to be useful in clinical practice to predict patients at risk of pressure ulcer development.15. mental condition. Norton and Braden scales — The most commonly used prediction tools are the Norton and Braden scales (table 2 and table 3). and friction and shear using scores ranging from 1 to 3 or 4 (table 2) [12].org and www. Two studies have used empirical data to examine and modify the Norton scale and found that the activity and mobility subscales are sufficient to express the risk for pressure ulcers among hospitalized patients [18. nutrition.epuap. The Norton scale uses a 1 to 4 scoring system in rating patients in each of five subscales: physical condition. moisture.18]. While these scales have been validated [17].

factors associated with the presence of a pressure ulcer do not necessarily predict their development. caution is required in their use. lymphopenia. Thus.In a prospective report of hospitalized patients (n = 286) with activity limitations. immobility. and a recent fracture [21]. medical rather than vascular or orthopedic admission. . dry sacral skin.In a large (n = 1192) multicenter prospective study designed to compare products for ulcer prevention in hospitalized patients. These empirically derived risk factors for predicting the development of pressure ulcers have not been validated in a new sample of patients. mental condition. inclusion of the physical condition. the following factors were associated with increased risk for ulcer development: admission for an acute condition. fecal incontinence. despite the widespread use of risk assessment tools. older age. subsequent studies used a prospective design. there are no randomized trials that evaluate their effect on pressure ulcer incidence [20]. In addition. a history of a cerebrovascular accident. and verification of the other scales in prospective trials is needed.or chair-bound.and chair-bound hospital patients: low serum albumin. and decreased body weight were each associated with the development of a stage 2 or larger pressure ulcer [23]. However. and diabetes [24]. When three or more of these factors were present. three risk factors among 301 admissions were identified: being bed. which included over 2000 patients. In one study at a chronic care hospital. and impaired nutritional intake [22]. Thus. and incontinence subscales resulted in worse performance in identifying pressure ulcer patients than when activity and mobility were used alone [18]. Empirical studies — The first empirical study that attempted to identify factors that could be used for predicting the risk of pressure ulcer development identified three predictors among bed.these studies. low hemoglobin level. Similar analyses evaluating subscales of the Braden scale have not been performed. non-blanching erythema or skin trauma at baseline. the presence of a stage 1 ulcer. Risk assessment tools are best used as an adjunct to clinical judgment [10]. over 13 percent of patients developed an ulcer.

Skin with borderline perfusion at baseline will often develop irreversible changes even with shorter intervals of pressure. and then to the other side. used a database with over 30. or location between the two groups. a two-hour interval is recommended although this is based upon expert opinion in the absence of randomized trials [28-32]. Prevention of progression of a stage 1 pressure ulcer may require more frequent repositioning [34].27]. Turning should be performed successively from the back. with particular attention to vulnerable tissue covering bony prominences such as the sacrum [28]. severity. compared repositioning with alternating time intervals (two hours in a lateral position and four hours supine) with repositioning every four hours [29]. it has been demonstrated that skin erythema can occur in healthy adults in less than two hours on a standard mattress [33]. Typically. There was no statistically significant difference in ulcer incidence. An expected probability of ulcer development can then be calculated for each patient. PRESSURE RELIEF — Pressure relief is the most important factor in preventing pressure ulcers and may be accomplished in two ways: proper patient positioning and appropriate use of pressure-reducing devices. It remains to be established whether this methodology will be clinically useful. Despite the paucity of randomized controlled trials. Patient positioning — Proper positioning of bed-bound individuals is recommended. including a regular turning and repositioning schedule. for example. conducted in 16 elder care nursing homes. The Minimum Data Set has been used to develop a predictive model for nursing homes that considers 17 patient characteristics [26. It is . The aim of repositioning is to reduce interface pressure and maintain microcirculation to areas at risk for pressure ulcers [28].Databases — Large databases have also been used to derive prediction rules. A randomized controlled trial of repositioning. One study. to one side.000 long-term care patients to identify eleven characteristics associated with pressure ulcer development [25].

In addition to regular turning. Timing and positioning should be documented [10]. Chair-bound patients may generate considerable pressures over the ischial tuberosities. It is recommended that: Patients should be placed at a 30 degree angle when lying on their side to avoid direct pressure over the greater trochanter or other bony prominences. the advantage gained by this automated approach to pressure reduction could be offset by the presence of continuous shearing forces. Continuous rotation — Continuous lateral rotation was originally developed to enhance respiratory function in hospitalized patients but has been advocated for the prevention and management of pressure ulcers. using monitoring devices as a reminder.Pillows or foam wedges should be placed between the ankles and knees to avoid pressure at these sites when patients have no mobility at these areas. Patients who are cognitively intact and are able to use their upper extremities can be trained to shift weight even more frequently. Conceptually. and bed tilt angle need to be better defined.The heels require particular attention.The head of the bed should not be elevated more that 30 degrees to prevent sliding and friction injury. Technical parameters such as bed rotation frequency. the position of bed-bound patients is likely to be important. Continuous lateral rotation is achieved with a mechanized bed that continuously rotates around its longitudinal axis.important that repositioning be done gently and properly. pillows may be placed under the lower legs to elevate the heels. . with the assist of devices as necessary to avoid friction and shear forces. Continuous rotation therapy is not likely to replace the need to reposition the patient every two hours but clearly further study is warranted. or special heel protectors can be used. they should be repositioned at least every hour with wheelchair pushups or with tilting of the seat to reduce contact between the patient's buttocks and the seat [35]. Observational studies indicate modest improvements in healing rates when continuous lateral rotation is added to an advanced therapy surface [36].

They work by distributing local pressure over a wider body surface area. and air fluidized mattresses. Adjustable seat cushions contain a honeycomb of air cells that are first fully inflated. foam. overlays. Examples include alternating pressure mattresses. low air loss beds. Powered seat cushions include a motorized blower to circulate the air in the cushion. or a combination of these.28. These products can classified as either non-powered.Powered or dynamic support surfaces require electricity to alternate air currents in order to regulate or redistribute pressure against the body. Foam. Donut cushions should not be used as they increase edema and venous congestion and concentrate the pressure to surrounding tissue [7]. appropriate wheelchair cushions are recommended. or water. The result is that the patient essentially floats on a cushion of air while sitting in the chair.Support surfaces — There are over 100 different support surfaces or pressurereducing products available for bed-bound patients [37]. for example. air. The three main types of seat cushions include gel and foam seat cushions. a six-inch deep foam mattress . Selection of customized chair cushions requires the services of a qualified seating specialist. Non-powered support surfaces (previously known as static) do not require electricity and consist of mattresses that are made of gel. These devices are helpful when the patient is at risk for pressure ulcer development. cannot avoid bearing weight on a pressure ulcer. or water overlays may be used for patients who can assume a variety of positions without bearing weight on the ulcer. In one randomized trial. There is reasonably good evidence that mattress overlays on operating tables decrease postoperative pressure ulcers. non-powered adjustable cushions and powered adjustable seat cushions. For chairbound patients. air. or powered according to the new definitions provided by National Pressure Ulcer Advisory Panel Support Surface Standards Initiative (table 4) [38]. placed under the patient and then partially deflated via a release valve to better conform to the patient's body.39]. or a pressure ulcer is not healing as expected [34].Overlays are support surfaces designed to be placed on top of another support surface. and that specialized foam overlays reduce ulcers in hospitalized patients compared to standard mattresses [10. The efficacy of pressure reducing devices has been illustrated in several studies.

It is less clear how different products compare. the basis for this prediction is unclear. There is minimal evidence from randomized trials to support many of these interventions. A well-designed randomized trial (n = 1972) compared two dynamic devices. except in extremely high-risk patients. One study of air suspension beds in an intensive care unit found that this intervention resulted in a cost savings of over $700 per patient [2].reduced the incidence of pressure ulcers among elderly patients with hip fractures from 68 to 24 percent [40]. risk of ulcer development. The selection of an appropriate device for pressure ulcer prevention must balance a variety of considerations including cost (special beds may cost up to several hundred dollars per day to rent). In another randomized trial. . although patient satisfaction was higher for the mattress [10]. may be cost effective. SUPPORTIVE INTERVENTIONS — In addition to positioning and pressure support devices. patients in an intensive care unit treated on an air suspension bed were less likely to develop a pressure ulcer than patients on a standard mattress (odds ratio 0. and are indicated on the basis of individual patient assessment. Only a few well-designed comparative studies have been performed. found no difference in the number of ulcers or median time for the development of pressure ulcers. though costly. Trials comparing static and dynamic overlays and mattresses report inconsistent results. although more expensive. other interventions to prevent pressure ulcers may be helpful. and other patient characteristics [44].42].41. However. with some but not all trials demonstrating better outcomes for the more expensive dynamic devices [28].18) [2]. may be cost-effective based on predictions of a shorter hospital length of stay that offset the increased cost of the mattress [43]. ease of use. A cost-effective analysis accompanying the trial of the alternating pressure mattress and overlay discussed above suggested the mattress. and they have not consistently demonstrated superiority of one product over another [8.28. Dynamic support devices. since there was no statistical difference in time to development of ulcer between the mattress and overlay. Static devices are acceptable in most situations. alternating pressure mattresses and alternating pressure overlays.

An alternative method is to place absorptive pads under the patient without a diaper so that any incontinence episode can be readily detected and addressed. including: Immobilized patients may benefit from physical therapy. It is generally felt that adequate nutrition may both prevent ulcer formation and promote healing of early stage ulcers [7.Minimize immobility — Encouraging patient mobility is key to the prevention of pressure ulcers. and it is necessary to protect patients who are incontinent from being exposed to urine or feces. underpads or adult briefs. If dietary intake of protein or calories is inadequate. Manage incontinence — Excess moisture can promote breakdown of the skin.34]. the factors compromising intake should be addressed as part of total patient care. individuals at risk of developing pressure ulcers should have a protein intake of approximately 1. Both urine and feces can irritate the skin and make it more susceptible to breakdown [34]. .2-1. Nutrition assessment — Nutritional goals should address any documented nutritional compromise. combined with consistent skin cleansing are adequate for managing incontinence.5 gm/kg body weight daily [34]. Several approaches may be helpful to minimize immobility. (See "Treatment of urinary incontinence". such as sedatives should be stopped. Unless there is a contraindication. An indwelling or condom catheter is sometimes needed when treating an ulcer. Practices for managing urinary incontinence have been described in a Clinical Practice Guideline from the AHRQ [45] and are discussed separately. The tabs can be left open at the sides of the incontinence briefs to allow air circulation.) In general. Formal nutritional assessment should be carried out and a plan of support instituted to address any deficiencies.Severe spasticity may be relieved with muscle relaxant drugs or a nerve block.)Medications contributing to immobility. (See "Chronic complications of spinal cord injury".

In one study of hospitalized patients. the incidence of new pressure sores decreased from 15 to 5 percent after introduction of a staff educational program [51]. and integrity [49]. One study of 331 patients comparing hyperoxygenated fatty acid compound versus placebo in acute care and longterm care patients found that the fatty acid preparation significantly reduced the incidence of ulcers (7.Cleansings should be done at regular intervals to minimize exposure to excess moisture due to incontinence.) Skin care — Skin condition should be inspected and documented daily. The effectiveness of specific nutritional interventions.Skin cleansing should be done with mild cleansing agents that minimize irritation. or wound drainage [8. patients.47]. and families is important in pressure ulcer prevention. . color. Lotions containing fatty acids may protect against friction and pressure as well as reduce hyperproliferative skin growth [50]. had an increased risk for developing pressure ulcers. although questions have been raised about methodological aspects of this study [48].Keeping the skin clean and dry. while avoiding excess dryness and scaling is the primary goal. Education and quality initiatives — Education of clinical staff.46]. turgor.3 percent in the placebo group) [50].Hot water should be avoided. moisture status. and should include information regarding the causes of pressure ulcers and how they may be prevented. will depend on the baseline nutritional status of participants [7. compared to oral nutritional supplementation plus standard diet.Dry sacral skin is a risk factor for the development of pressure ulcers [23].Studies evaluating nutritional supplements or enteral feeding have demonstrated mixed results on rates of pressure ulcer development [41. Skin assessment should include skin temperature.Vigorous massage over bony prominences should be avoided.3 percent in the intervention group versus 17. perspiration. One study in critically ill elderly patients did find that patients who were given a standard diet.10]. (See "Nutritional support in critically ill patients: An overview". Any changes should be recorded as soon as they are observed [10]. such as tube feedings or dietary supplements.

When an ulcer does occur. Rather. Several team-related interventions may be helpful: One member of the nursing unit should be designated as a skin care resource.)We suggest using risk prediction tools to identify patients . however. (See 'Introduction' above.Prompting methods for turning patients at regular intervals should be instituted.No single individual involved in patient care is able to prevent pressure ulcers. the coordinated efforts of clinicians in multiple disciplines is critical for pressure ulcer prevention. It is easy to understand why some failures will occur considering that a single bed-bound patient must be repositioned over 4000 times per year. It is uncertain. SUMMARY AND RECOMMENDATIONS Pressure ulcers are among the most common conditions encountered in hospitalized patients or those requiring long-term institutional care.Barriers to obtaining necessary supplies such as special mattresses and overlays should be minimized. although such efforts need ongoing maintenance to sustain results [53-58]. A survey of pressure ulcer experts indicated that 62 percent disagreed with the statement "all pressure ulcers are preventable" [52]. and additional expertise should be readily available through consultations. or whether some patients may be at such high risk that the pressure ulcer development is unavoidable. whether all pressure ulcers are avoidable when best practices are implemented. problems contributing to its development should be identified and methods for solving these problems implemented. Studies evaluating the implementation of educational programs and continuous quality improvement (QI) practices in nursing homes have shown a reduction in the rate of pressure ulcers. Failures are less common when effective systems for staff education are in place [53]. EFFICACY OF PREVENTION EFFORTS — Implementation of these practices for pressure ulcer prevention can decrease the rate of pressure ulcer development.

at risk for the development of pressure ulcers (Grade 2C). and families along with a team staff approach and supporting policies are essential to reduce the development of pressure sores. Proper positioning and turning techniques should be used to minimize friction and shear forces. Dynamic supports.)Pressure relief is the most important factor in preventing pressure ulcers. We suggest that bed-bound patients be repositioned at least every two hours to relieve tissue pressure (Grade 2C). foam. such as air fluidized beds. (See 'Education and quality ini . (See 'Supportive interventions' above. (See 'Patient positioning' above.)We recommend the use of pressure-reducing products for patients at increased risk (identified by clinical assessment or risk scales) for developing pressure ulcers (Grade 1A). will depend on the availability of resources. nutritional supplementation. and dynamic devices. The choice of product. (See 'Support surfaces' above. may be cost effective in high risk patients. including overlays. patients.)Education of clinical staff. (See 'Risk prediction tools and guidelines' above. gel supports.)Other measures that may be helpful for pressure ulcer prevention in selected patients include limiting immobility (with physical therapy and decreased use of sedatives). and meticulous skin care.