Because of the significant morbidity and mortality associated with pressure ulcers and because they are considered, for the most part, preventable, effective pressure ulcer prevention has been included in hospital patient safety strategies. Caution should be used when making comparisons across hospitals regarding rates of hospital-acquired pressure ulcers because of the discrepancies in data sources. For example, authors of one study found little correlation between each hospital’s administrative incidence data and point-prevalence surveillance data. An examination of Medicare claims data from fiscal year 2009–2010 found that lower-staged pressure ulcers (such as stage I or stage II) on admission which progressed to stage III or stage IV pressure ulcers were reported as present on admission, thus causing underreporting of hospital-acquired stage III and stage IV pressure ulcers.
Pressure ulcer rates are also of concern in long-term care facilities. These facilities must ensure that “a resident who enters the facility without pressure sores does not develop pressure sores unless the individual’s clinical condition demonstrates that they were unavoidable.” An updated version of the standardized assessment used in nursing homes, the minimum data set (MDS), was implemented in 2010 to include direct interviews with the nursing home residents and to recognize resident needs. The pressure ulcer section of the MDS version 3.0 differs from MDS version 2.0 by requiring the assessor to provide pressure ulcers counts and stages [using the National Pressure Ulcer Advisory Panel (NPUAP) definitions] and to provide better tracking of pressure ulcers. It also requires reporting of the number and stage of pressure ulcers at admission. In 2011, CMS provided an updated resource for long-term care facilities to use for pressure ulcer prevention and treatment with the aim of helping facilities reduce the rate of high-risk pressure ulcers.
Pressure ulcers are an international health concern. The European Pressure Ulcer Advisory Panel (EPUAP) and the NPUAP issued a joint definition of pressure ulcers: “localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear. A number of contributing or confounding factors are also associated with pressure ulcers; the significance of these factors is yet to be elucidated.”
The most commonly used category or staging system for pressure ulcers in the United States is the NPUAP classification system, which consists of four pressure ulcer stages and two additional categories: (1) unstageable or unclassified pressure ulcer, and (2) suspected deep tissue injury – depth unknown. The joint EPUAP and NPUAP guidelines began using the term “category” in their classification system for pressure ulcers. Since the term “staging” implies progression from one stage to the next stage, these experts noted that pressure ulcers do not always progress sequentially. The new term “category” was needed to free clinicians from the notion of progression of or reversing stages.
The NPUAP’s category for unstageable or unclassified pressure ulcer was defined as “full thickness loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed.” The actual depth of the pressure ulcer will be either stage III or stage IV after removal of slough and/or eschar in order for the base of the wound to be exposed. Suspected deep tissue injury – depth unknown was defined as “purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear.” This type of injury can occur after prolonged immobilization and lead to a stage IV pressure ulcer. (See Table 36.1 for a complete description of pressure ulcer stages and categories.)
|Category/stage I: Nonblanchable erythema||Intact skin with nonblanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue. Category I may be difficult to detect in individuals with dark skin tones. May indicate at-risk persons.|
|Category/stage II: partial thickness||Partial thickness, loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled or sero-sanginous-filled blister.Presents as a shiny or dry shallow ulcer without slough or bruising.* This category should not be used to describe skin tears, tape burns, incontinence associated dermatitis, maceration, or excoriation.|
|Category/stage III: full thickness skin loss||Full thickness tissue loss. Subcutaneous fat may be visible, but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a Category/Stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have (adipose) subcutaneous tissue and category/stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep Category/Stage III pressure ulcers. Bone/tendon is not visible or directly palpable.|
|Category/stage IV: full thickness tissue loss||Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present. Often includes undermining and tunneling. The depth of a category/stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Category/Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis or osteitis likely to occur. Exposed bone/muscle is visible or directly palpable.|
|Additional categories/stages for the United States|
|Unstageable/unclassified: full thickness skin or tissue loss – depth unknown||Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar are removed to expose the base of the wound, the true depth cannot be determined; but it will be either a Category/Stage III or IV. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as “the body’s natural (biological) cover” and should not be removed.|
|Suspected deep tissue injury – depth unknown||Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or Shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.|
* Bruising indicates deep tissue injury.
Secondary analyses of the Medicare Patient Safety Monitoring System database revealed that 4.5% of Medicare beneficiaries who had been discharged from hospitals during a two-year period (January 1, 2006, to December 31, 2007) developed at least one new pressure ulcer. Compared to those who did not develop a pressure ulcer, patients who developed pressure ulcers were more likely to die while in hospital (risk-adjusted OR 2.81, 95% CI 2.44–3.23); had longer hospital stays (risk-adjusted mean length of stay 11.2 days, 95% CI 10.19–11.4, versus 4.8 days, 95% CI 4.7–5.0); and had higher rates of readmission within 30 days (risk-adjusted OR 1.33, 95% CI 1.23–1.45).
Using data from the National Database of Nursing Quality Indicators® 2010 Pressure Ulcer Surveys, the rate of hospital-acquired pressure ulcers was determined. Among 710,626 adult patients surveyed in 1,419 hospitals in the United States, the rate of hospital-acquired pressure ulcers was 3.6% in all patients and 7.9% in at-risk patients. Odds of having a hospital-acquired pressure ulcer were lower in Magnet® and Magnet®-applicant hospitals. (Note: The ANCC’s Magnet Recognition Program® is “an international organizational credential that recognizes nursing excellence in healthcare organizations.”) In 2009, 3.3% of adult patients in intensive care units developed stage III or stage IV pressure ulcers. In older adults who had surgical repair of hip fractures, the cumulative incidence of pressure ulcers stage II or higher at the third day of hospitalization was 6.2% (95% CI 5.4–7.1). The majority of pressure ulcers were classified as stage II and located in the sacral area or the heel.When these patients were followed from hospital admission to 32 days post-hospitalization, the highest adjusted (for multiple factors, including time) acquired pressure ulcer rate, when compared to the home setting, was in the hospital setting (relative rate 2.2, 95% CI 1.3–3.7).
Racial differences in pressure ulcer incidence have been reported. The incidence of stages II, III, and IV pressure ulcers in black nursing home residents was 0.56 per person-year as compared to 0.35 per person-year for whites. Black nursing home residents had fewer stage I pressure ulcers identified than white nursing home residents, perhaps because of the difficulty in detecting nonblanchable erythema in dark pigmented skin. A systematic review, however, indicated that there is limited evidence for the relationship between race and pressure ulcer development. This systematic review also noted that independent predictors for pressure ulcer development included mobility/activity, perfusion, and skin/pressure ulcer status.
Few data are available regarding the remission or cure rates of pressure ulcers. Sibbald and colleagues recommended that determining “healability” is important before beginning treatment. These authors also noted that healable wounds should be healed within twelve weeks. An instrument to measure pressure ulcer healing for stages II to IV pressure ulcers – Pressure Ulcer Scale for Healing (PUSH 3.0) – is available at the NPUAP website. This instrument helps to quantify several parameters: surface area (as measured by length multiplied by width of the pressure ulcer), exudate amount, and tissue type. This instrument offers an alternative to a practice known as reverse staging. An international group of experts released a consensus document supporting the NPUAP’s position that a healed stage IV ulcer should be classified as a healed stage IV pressure ulcer rather than using a reverse staging technique.
Costs of pressure ulcers prevention and treatment
Available data regarding pressure ulcer surveillance programs in acute care facilities indicate that those programs can lower hospital-acquired pressure ulcer rates and can be cost-saving, with net savings of $127.51 per patient. Costs of treating existing pressure ulcers are high. For example, costs for treating stage I pressure ulcers were reported in 2013 at approximately $2,000, stage II between $3,000 and $10,000, stage III between $5,900 and $14,840, and stage IV between $18,730 and $21,410.
Pressure ulcers cause both acute and chronic pain, are unsightly, and may limit function. Therefore, understanding and measuring patient-reported outcomes is important. Measuring the quality of life of adults living with pressure ulcers has gained importance, and an instrument (PU-QOL) has been developed and tested. It consists of 10 scales: pain, exudate, odor, sleep, movement/mobility, daily activities, vitality, emotional well-being, self-consciousness and appearance, and social participation. This self-reported scale attempts to capture the impact of pressure ulcer prevention and treatment interventions from the affected adult’s perspective. More research about the effects of pressure ulcers on quality of life from the perspectives of the affected adult, family members, and formal caregivers is critically needed.
Tissue injury can be superficial, deep, or a combination of both. Injury to the skin and deep tissue can occur within four to six hours after sustained loading, and clinically detectable pressure ulcers can develop within two to six hours. Emerging evidence indicates that deep tissue injury may occur under intact skin, but the current staging systems do not sufficiently encompass that type of lesion. Pressure to skin over bony prominences – such as the sacrum, heels, trochanters, femoral condyles, malleoli, or ischial tuberosities – may occlude capillary blood flow and lead to tissue death. Shear forces pull and distort skin, underlying tissues, and blood vessels, leading to tissue damage. This can occur when a supine person is raised to a greater than 30-degree angle or when a patient is pulled up in bed without the use of a pull sheet.
A pathway has been described to explain deep muscle injury as hypoxic reperfusion injury. The compressed area between a bony prominence and pressure point is described as the epicenter of injury. The injury could be from high impact over a short time period or from lower impact over a longer time period. As swelling and edema occur, it leads to further hypoxia at the epicenter and hypoxia spreading to the peri-injured tissue. As microcirculation becomes impaired and further ischemia occurs, irreversible damage takes place. The muscle swells within rigid fascia, leading to compartment syndrome, which requires surgical intervention.
Pressure ulcers are subject to bacterial colonization, which can occur as early as 48 hours. Enzymes released by bacteria break down protein that could otherwise aid wound healing. Fluids from chronic wounds exhibit increased protease levels and proinflammatory cytokine levels as well as decreased levels of growth factors. An impaired healing response in older adults with pressure ulcers may be a result of the interplay among several intrinsic and extrinsic factors, including ischemic and oxidant stress, metabolic disruptions, prolonged application of uneven pressure to tissue, and exposure to shear forces and friction.[43, 45] Some pressure ulcers become infected with multidrug resistant organisms that increase risk of bacteremia and death.
In 2007 the Institute for Healthcare Improvement included pressure ulcer prevention in its Five Million Lives Campaign. The overall aim of this two-year campaign was to prevent five million incidents of medical harm in participating hospitals. Pressure ulcer prevention includes identifying at-risk individuals and reliably implementing prevention strategies for these individuals. Elements of prevention are (1) assessing for pressure ulcers at admission into a health-care setting, (2) reassessing pressure ulcer risk daily, (3) inspecting skin daily, (4) managing moisture, (5) optimizing nutrition and hydration, and (6) minimizing pressure.
Several screening tools are available, but the Braden Scale is frequently used in health-care facilities in the United States. It consists of six subscales that measure sensory perception level, skin moisture, level of physical activity, mobility, nutrition, and friction/shear. The sensitivity and specificity of this scale are 57.1% and 67.5%, respectively. Scores on the Braden Scale range from 6 to 23, with the lower scores indicating higher risk of pressure ulcer development. Although the tool tends to overpredict pressure ulcer risk (51), the assignment of risks is as follows: 19 to 23, not at risk; 15 to 18, mild risk; 13 to 14, moderate risk; 10 to 12, high risk; and a score of 9 or lower, at very high risk. This tool has high inter-rater reliability for registered nurses (Pearson r = 0.99, percent agreement 88%).
In people of color, a score of 18 or below on the Braden Scale was accurate in predicting pressure ulcers. A systematic review indicated that the Braden Scale should not be used for surgical patients; there was low predictive validity for pressure ulcer risk.[49, 53] In the critical care setting, four of the six Braden Scale subscales were associated with increased likelihood of developing a pressure ulcer. These included sensory perception, mobility, moisture, and friction/shear subscales. Both patients who did and did not develop pressure ulcers had been classified at risk using the Braden Scale, indicating that more research is needed to differentiate at-risk adults in critical care units. The ability to differentiate between these groups is essential to effectively implement preventive strategies for at-risk patients as recommended by the joint NPUAP and EPUAP expert. The EPUAP and NPUAP joint guidelines recommended a structured and systematic approach to risk assessment (24), although no conclusive evidence exists that a systematic and structured risk assessment tool reduces pressure ulcer incidence.
In home health agencies, clinical judgment had been the most commonly used method to assess pressure ulcer risk, especially before the implementation of Outcome and Assessment Information Set (OASIS). When nurses used clinical judgment about pressure ulcers, they considered patients’ dependency level and self-care abilities. According to OASIS data from five home health-care agencies in the United States from September 2007 to January 2009, the prevalence of pressure ulcers was 1.3%. Newly developed pressure ulcers were associated with the presence of bowel incontinence, activities of daily living (ADL) dependence, being chairfast or bedfast, and having a pressure ulcer upon admission to home care.
Pressure ulcer prevention interventions
In 2009, the EPUAP and the NPUAP issued joint evidence-based guidelines on pressure ulcer prevention and treatment.
There is limited evidence for the use of pressure-redistributing support surfaces (i.e., mattresses, pads, and cushions) to relieve pressure exerted on subcutaneous tissues by body weight when a body part presses against a chair or bed’s surface. These support surfaces may be static (such as a mattress) or dynamic (whereby pressure under the body is varied mechanically). When compared to standard hospital mattresses, foam alternatives reduced incidence of pressure ulcers, as did medical sheepskins when compared to standard care. Using dressings prophylactically to mitigate shear on tissue may enhance pressure ulcer prevention and may reduce pressure ulcer incidence.[60, 61] A consensus panel recommended the use of a five-layer soft silicone dressing for high-risk patients (i.e., patients in the emergency department, intensive care unit, or operating room) as part of a strategy to prevent sacral pressure ulcer development. More research is needed to better understand clinical, quality of life, and economic outcomes of the use of dressings in pressure ulcer prevention.
Repositioning has long been considered the cornerstone of pressure ulcer prevention because repositioning relieves or eliminates interface pressure for the maintenance of microcirculation. There is limited research evidence, however, for repositioning to prevent pressure ulcers, especially in regard to repositioning frequency and position (i.e., 30-degree tilt versus 90-degree position). One study in nursing homes found that a repositioning schedule of every three hours using 30-degree tilt was cost-effective when compared to every six hours using 90-degree lateral rotation. Another study in nursing home residents who were placed on high-density foam mattresses did not find a significant reduction in pressure ulcer incidence when two-, three-, or four-hour turning schedules were used. The EPUAP and NPUAP joint guideline recommended repositioning based on the affected person’s factors, such as tissue tolerance, activity and mobility levels, health status, skin condition, and patient comfort. The use of support surfaces also influences repositioning frequency. To prevent the effect of shear forces, maintaining the head of bed at 30 degrees or less was recommended.
People who sit for long periods of time may not be able to shift their position, including adults with spinal cord injuries. This population is at increased risk of pressure ulcer development.[24, 66] Evidence exists that pressure-redistributing seat cushions prevent pressure ulcers. Results from one study indicated that air-cell-based cushions provided greater reductions in tissue stresses when compared to foam cushions. Wheelchair users should be taught how to reposition while seated to relieve pressure and increase blood flow to the buttocks.
The EPUAP and NPUAP joint guideline recommends providing high-protein mixed oral or tube feeding supplements to adults at risk of pressure ulcer development. This recommendation is supported by direct evidence from trials conducted in humans.
Maintaining a clean wound base is considered important for healing and closure, but a systematic review found no evidence to support specific cleansing solutions or techniques. The authors of the review noted the limited number and low quality of research studies that were reviewed, making recommendations difficult. The EPUAP and NPUAP joint guideline graded the level of evidence for cleansing and debriding pressure ulcers as being supported by indirect evidence and/or expert opinion. These findings highlight the need for clinicians and researchers to work together to conduct and publish high quality research to provide higher levels of evidence on which to base clinical practice.
The NPUAP defined a support surface as “a specialized device for pressure redistribution designed for the management of tissue loads, micro-climate, and/or other therapeutic functions (i.e., any mattresses, integrated bed systems, mattress replacements, overlays, or seat cushions or seat cushion overlays).”
Air-fluidized beds provided moderate-strength evidence of wound improvement when compared to standard hospital beds. In this review, alternating-pressure mattresses and other support surfaces had similar healing rates.
Repositioning to relieve pressure over bony prominences has been a mainstay of pressure ulcer treatment, yet no randomized trials existed to determine its impact on pressure ulcer healing. Keeping the head of the bed at the lowest degree of elevation to avoid shear forces and friction may prevent further pressure ulcer development. The use of a wound electronic medical record that includes photographs of wounds has been recommended as an integral part of treatment.
Multiple options are available for pressure ulcer dressings. The type of dressing is determined by the tissue in the wound bed, condition of skin surrounding the pressure ulcer, and the condition and treatment goals of the affected adult. Type of dressing may change as wound healing progresses. Presence of exudate, necrotic tissue, and infection also can influence dressing choices. In one systematic review, hydrocolloid dressings, compared to gauze dressings, showed greater reduction in wound size. Overall, there is limited evidence for using specific dressings and topical therapies for wound improvement.
Little systematic evidence exists on the effectiveness of enteral and parenteral nutrition in the prevention of pressure ulcers. Several nutritional guidelines are available, which generally recommend conducting a nutritional assessment including weighing the patient, reviewing food and fluid intake, and investigating unexplained weight loss. Other recommendations include recognizing the effects of malnutrition, correcting an underfed status by designing a diet based on 35 kcal/kg, 1.0 to 1.5 g/kg of protein, and 1mL/kcal of fluids, and evaluating the effects of a nutritional intervention. Protein supplementation was found effective in reducing the size, but not in healing, of pressure ulcers.
Electromagnetic therapy for pressure ulcer treatment has been studied, although two systematic reviews concluded that no evidence exists supporting the benefit of this therapy.[72, 79] The use of therapeutic ultrasound for pressure ulcer healing has also been investigated, and no systematic evidence exists regarding the benefits of this treatment. The authors of the preceding systematic reviews noted that further research is needed.
Results of a meta-analysis on the use of electrical stimulation for chronic wound healing indicated that increased wound healing occurred. The proposed mechanism of electrical stimulation on healing is that it restarts or accelerates wound healing by stimulating fibroblasts and increasing the migration of neutrophils and macrophages. Recent reviews indicate moderate evidence for electrical stimulation as an ancillary intervention for wound healing (82) and improved healing rates. A review of hyperbaric oxygen therapy for chronic wounds noted that no trials that involved pressure ulcers were included in the review.