INTRODUCTION — Pressure-induced skin and soft tissue injuries 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 time, although increasing attention is being paid to medical device-related pressure injury. The consequences of pressure-induced skin and soft tissue injury range from nonblanchable erythema of intact skin to deep ulcers extending to the bone.
Pressure-induced injuries impose a significant burden not only on the patient but on the entire health care system. Reducing their frequency is an important component of current goals for patient safety, as evidenced by the Institute for Healthcare Improvement (IHI) 5 Million Lives Campaign and the decision by the United States Center for Medicare and Medicaid Services to not reimburse hospitals for the treatment of hospital-acquired pressure-related injuries [1-3].
Knowledge of factors contributing to the pathogenesis of pressure-induced skin and soft tissue injury allows the identification of patients at risk for ulcer development such that preventive measures may then be targeted to those specific patients. The epidemiology, pathogenesis, risk factors, and risk assessment of pressure-induced skin and soft tissue injury will be reviewed here. Prevention and treatment are discussed separately. (See "Prevention of pressure-induced skin and soft tissue injury" and "Clinical staging and general management of pressure-induced skin and soft tissue injury".)
CLASSIFICATION AND TERMINOLOGY — The National Pressure Injury Advisory Panel (NPIAP) made changes to their classification (table 1) in April 2016 and suggested using the terminology "pressure injury" instead of "pressure ulcer" to describe these wounds. Issues surrounding classification and terminology for pressure-induced skin and soft tissue injury are reviewed separately. (See "Clinical staging and general management of pressure-induced skin and soft tissue injury", section on 'NPIAP staging'.)
EPIDEMIOLOGY — Pressure-induced skin and soft tissue injuries are among the most common conditions encountered in acutely hospitalized patients or those requiring long-term residential care. The incidence varies widely by clinical setting [4-6]. An estimated 2.5 million pressure-induced injuries are treated each year in acute care facilities in the United States alone [4,5].
Methods of studying and reporting their incidence and prevalence include direct patient examination [7], use of databases [8], and surveys [9]. These studies tend to be small and often involve only a single facility, making generalizability uncertain. Shorter hospital stays may also mean that many pressure-induced injuries are missed. Caution is required when interpreting the reported incidence and prevalence rates since the methodology and duration of follow-up varies between studies. Studies have also differed on whether they included superficial ulcer stages (stage 1 ulcers (table 1)). Although stage 1 pressure injuries are frequently encountered, many epidemiological studies have elected not to include them since they are difficult to reliably detect. The most accurate estimates are derived from studies where clinician-researchers have directly examined the patients. A large study from England highlighted how a wound audit involving direct examination identified many more pressure-induced injuries compared with other reporting systems [10].
One study based on hospital billing codes showed an increase in the number of hospital stays involving pressure-induced injuries in the United States by nearly 80 percent between 1993 and 2006 [11]. In more than 90 percent of cases, the pressure-induced injury was not the original cause of admission. Most patients were over age 65. More than one-half of the patients with pressure-induced injuries required subsequent care in long-term care facilities, compared with only 16.2 percent of patients without pressure-induced injuries. However, as coding practices have changed over time, and since this study did not include chart review or direct patient evaluation, changes identified may be overstated. Later studies using hospital databases have shown lower rates. Among over 4 million inpatients in the University HealthSystem Consortium from 2008 to 2012, incidence rates declined from 11.8 per 1000 inpatients to 0.8 per 1000 inpatients [12]. Among over 750,000 hospitalizations at Kaiser Permanente hospitals in southern California, an incidence rate of 0.22 percent was noted [13]. Another study that looked at hospital-acquired pressure injury rates using databases from 2009 to 2014 found similar low rates with improvement over time. However, rates in the database were one-twentieth the rate seen in medical records, and much of the improvement was related to fewer superficial pressure injuries [14]. Inaccuracies in coding and the present on admission (POA) coding continue to be highlighted and raise concerns that reported rates using administrative databases are too low [15].
The International Pressure Ulcer Prevalence Survey has been conducting one-day cross-sectional surveys at a large number of hospitals since 2006. The United States data from 2018 to 2019, which included 296,014 patients from 914 acute care hospitals, reported a pressure injury prevalence of 9 percent with a hospital-acquired rate of 2.6 percent [16]. These rates represented a decline from 2006 but have plateaued since 2015. Among patients in intensive care units (ICUs), the prevalence was 14 percent with a hospital-acquired rate of 6.9 percent. These results contrast with the DecubICUs study, which used a similar methodology in examining 13,254 patients from 117 ICUs in 90 different countries [17]. They reported a prevalence of 22.8 percent with an acquired rate of 13.3 percent in North American ICUs. Reasons for the differences between the two studies are uncertain.
Pressure-induced injuries also are common among patients admitted to nursing homes, with reported rates on admission ranging from 10 to 35 percent [8,18-20]. Prevalence rates are generally lower (3 to 12 percent) among long-term nursing home residents [6,8,18,20-23]. Studies using databases have found that 4 to 8 percent of nursing home residents develop stage 2 or deeper pressure injuries over six months [8,24]. However, incidence rates (including stage 1 injuries) as high as 24 percent have been noted when residents were regularly examined [7], with over 70 percent of high-risk patients developing a pressure-induced injury [25]. New models of nursing home care that emphasize culture change to promote more resident-centered care have not been associated with worsening rates of development [26].
The frequency of pressure-induced injuries among outpatients has not been well defined. However, they may be common among patients receiving home nursing services. One study reported a 9.2 percent prevalence of stage 2 or higher pressure injuries in a multistate sample of home care patients [27]. A retrospective review that evaluated the Outcome and Assessment Information Set (OASIS) in 1.94 million patients at the time of enrollment in a home care program found a prevalence of 7 percent [28]. Among home care patients without a pressure-induced injury on admission, another study noted a 6.3 percent incidence of ulcer development during the home care [29].
PATHOGENESIS — The development of a pressure-induced injury is a complex process that requires the application of external forces to the skin [30]. However, external forces alone are rarely sufficient to cause an ulcer; rather, the interaction of these forces with host-specific factors is what ultimately leads to tissue damage. Consideration then needs to be given to the mechanical boundary conditions (magnitude and duration of applied loads) and the tolerance of the individual, which is impacted by factors such as tissue morphology and its capacity for repair [31]. Even the shape of bony protuberances (eg, ischial tuberosity) may be important, with a more angular shape resulting in higher applied loads.
The traditional teaching is that the development of pressure-induced injury is due to a combination of pressure (force per unit area), friction, shearing forces (gravity effect on friction), and moisture, but other factors may contribute; friction and moisture may have a limited role [30].
Pressure applied to the skin in excess of the arteriolar pressure (32 mmHg) may prevent the delivery of oxygen and nutrients to tissues, resulting in tissue hypoxia, accumulation of metabolic waste products, and free radical generation [32,33]. Pressure in excess of 70 mmHg for two hours results in irreversible tissue damage in animal models [34]. Ulcer formation may occur more rapidly with higher pressures. A synthesis of clinical, animal, and in vitro studies has suggested that pressure-induced injuries may develop with one to four hours of sustained pressure load [35]. This explanation, though, is overly simplistic, as illustrated by the fact that in animal models, two hours of compression will result in irreversible muscle damage, whereas damage from tourniquet-induced ischemia over the same period of time was reversible [36]. Later research emphasizes the importance of deformation of deep tissues resulting from pressure and shear, which may directly cause cell death as a result of loss of cytoskeletal integrity [36,37]. Deformation-induced cell death may combine with tissue hypoxia, edema, inflammation, and reperfusion injury to result in additional injury [38].
Tissues vary in their susceptibility to pressure-induced injury, with muscle being the most susceptible, followed by subcutaneous fat and then dermis [33]. Thus, extensive deep tissue damage can occur with initially little or no evidence of superficial tissue injury. A high-stage pressure-induced injury is initiated as a deep tissue injury that may then progress to the surface. There is little evidence to suggest that high-stage pressure injuries develop as a gradual progression from stage 1 through stage 4 [39,40]. (See "Clinical staging and general management of pressure-induced skin and soft tissue injury", section on 'Staging'.)
Pressures are greatest over bony prominences where weight-bearing points come in contact with external surfaces, which can include immobilization devices [41]. A patient lying on a standard hospital mattress may generate pressures of 150 mmHg. Sitting produces pressures that are 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, adjacent to the bone-muscle interface. Thus, 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" [42].
Shearing forces occur when patients are placed on an inclined surface, such as with head elevation (figure 1). Patients may slide over 7 cm to the foot of the bed [43]. Deeper tissues, including muscle and subcutaneous fat, are pulled downward by gravity, while the superficial epidermis and dermis remain relatively fixed through contact with the external surface. The result is stretching, angulation, and trauma to local blood vessels and lymphatics along with additional tissue deformation. Shear and friction forces have an additive effect such that in the presence of pressure, more severe tissue damage will occur [39].
Superficial lesions (eg, skin maceration, moisture-associated dermatitis, abrasions) are primarily the result of moisture and friction and should not be considered pressure-induced injuries [39,40]. Exposure to moisture in the form of perspiration, feces, or urine with resulting skin maceration may predispose to superficial ulceration [44]. In addition, moisture decreases stratum corneum stiffness and mechanical strength and increases the coefficient of friction so that skin is more adherent to its contact surface. This results in greater deformation and shear forces being transmitted to the subcutaneous tissues with increased likelihood of deep tissue injury [45].
RISK FACTORS — Over 100 risk factors for the development of pressure-induced skin and soft tissue injuries have been identified in the literature [5]. Risk factors can be divided into those that impact the magnitude and duration of pressure and those that affect individual susceptibility and tolerance [31]. The most important factors include immobility, malnutrition, reduced perfusion, and sensory loss, which are discussed below.
Other risk factors have included cerebrovascular disease, cardiovascular disease, recent lower extremity fractures, incontinence, and diabetes [5,46-51]. But whether these are independent risk factors or simply reflect the high prevalence of immobility among frail, older adult patients is not known for certain. As an example, urinary incontinence is frequently cited as a predisposing factor, with some studies suggesting that incontinent patients have up to a fivefold higher risk [47]. However, there is a strong correlation between incontinence and immobility. A national survey of nursing home discharges found that 94 percent of incontinent patients with pressure-induced injuries were immobilized [48]. Urinary incontinence often does not remain as an independent predictor of pressure-induced injury in multivariate analysis.
In health care settings in which most patients are temporarily immobile, such as in critical care units or during surgery, additional factors need to be considered. Among patients undergoing general anesthesia, an additional risk factor for pressure-induced skin and soft tissue injury is longer duration of surgery [46]. Among available studies that have looked at other intraoperative factors, anesthesia variables have not definitively been associated with subsequent development of pressure-induced skin and soft tissue injury. Some of these include hypotension, use of vasopressors, and body temperature, among others. Appropriate positioning and padding of pressure points, which are standard, during surgery are important. Among patients in a surgical critical care unit, body mass index, hemoglobin albumin, creatinine, glucose, lactate, age, and surgical time were contributors to pressure injury development [52]. (See "Patient positioning for surgery and anesthesia in adults" and "Prevention of pressure-induced skin and soft tissue injury", section on 'Support surfaces'.)
Immobility — Immobility is the most important host factor that contributes to development of pressure-induced skin and soft tissue injury. Immobility may be permanent or transient [53]. There is a high correlation between a lack of spontaneous nocturnal movements in studies using devices that measure body movement [54]. However, methods to measure immobility in clinical settings are generally not available. Accordingly, investigators have often relied upon clinical characteristics as markers for immobility, including functional measures such as whether patients are ambulatory or not as well as clinical information such as a history of cerebrovascular accident [55].
Malnutrition — Malnutrition is also a risk factor for the development of pressure-induced skin and soft tissue injuries. 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 [56]. In addition, cross-sectional studies have suggested that patients with pressure-induced injuries are more likely to have hypoalbuminemia [50,55].
It is unclear which nutritional measures best predict risk, although prealbumin levels are often used in clinical practice. There is no lab value that gives an indication of risk. The strongest nutritional measure may simply be whether the patient has adequate dietary intake and can maintain his/her weight [25,55,57]. Among nursing home residents, lower body mass index has been shown to be a strong predictor (<25 kg/m2) [58]. A meta-analysis reported that being underweight (body mass index <18.5) was also associated with greater pressure injury incidence and prevalence [59].
The role of nutrition in prevention and treatment of pressure-induced skin and soft tissue injury is discussed separately. (See "Prevention of pressure-induced skin and soft tissue injury" and "Clinical staging and general management of pressure-induced skin and soft tissue injury".)
Reduced skin perfusion — The role of inadequate skin perfusion has been increasingly recognized [60,61]. One study evaluated skin blood flow over bony prominences during surgery [62]. A fivefold intraoperative increase in skin blood flow was seen in patients who did not develop a postoperative pressure-induced injury, compared with no increase in skin blood flow in patients who did develop a pressure-induced injury. This suggests that a failure to increase blood flow in response to prolonged pressure contributes to ulcer development.
In the setting of decreased perfusion, pressure applied to the skin for less than two hours may be sufficient to cause severe damage. When vital organs such as the kidneys and the gastrointestinal tract are not adequately perfused, blood flow to the skin will also be decreased, which increases the risk for the development of pressure-induced injuries. Factors that contribute to reduced perfusion include volume depletion, hypotension, vasomotor failure, and vasoconstriction (secondary to shock, heart failure, or medications), and underlying peripheral artery disease. Several studies have reported an association between low blood pressure and pressure-induced injuries, although this has not been consistently found [25,63,64]. Atherosclerotic peripheral artery disease, particularly of the lower extremities, may contribute to ulcer development as a result of baseline tissue hypoxia or a failure of blood flow to increase in response to pressure.
Beyond individual diseases such as stroke, peripheral vascular disease, or diabetes, measures of overall comorbidity burden may predict pressure-induced injury development [13]. Global measures of disease severity that capture abnormal vital signs and labs are associated with pressure-induced injuries. The Acute Physiology and Chronic Health Evaluation (APACHE) score has been associated with pressure-induced injuries in the intensive care unit [65] but not among other hospitalized patients [66]. The Laboratory-Based Acute Physiology Score, Version 2 (LAPS2) was predictive of development of pressure-induced injury in a large sample of hospitalized patients [13]. Another illness severity measure, the Comprehensive Severity Index (CSI), has been associated with the pressure-induced injuries among nursing home residents [67].
Sensory loss — Neurologic diseases such as dementia, delirium, spinal cord injury, and peripheral neuropathy are important risk factors for the development of pressure-induced skin and soft tissue injuries. Sensory loss among these patients is common, suggesting that patients may not perceive pain or discomfort arising from prolonged pressure. Other contributors are immobility, spasticity, and contractures, which are common in these conditions.
RISK PREDICTION — Identifying at-risk patients is central to preventing pressure-induced skin and soft tissue injuries. However, the effectiveness of formal risk assessment instruments compared with less standardized methods has not been clearly established [68,69]. A comprehensive history and physical examination should identify potentially correctable predisposing factors. Regular follow-up is required to identify any changes in the patient's clinical condition, and daily skin inspections should be performed to detect early evidence of pressure-induced skin damage. Depending upon the measured level of risk, specific interventions may then be initiated or altered accordingly [70]. (See 'Risk factors' above and "Prevention of pressure-induced skin and soft tissue injury".)
Guidelines from several agencies have prompted the use of prediction tools [71-73]. The National Pressure Injury Advisory Panel (NPIAP) and European Pressure Ulcer Advisory Panel (EPUAP) have published these guidelines online for the use of risk assessment in the prevention of pressure-induced injuries [71,72]. These longstanding recommendations are still considered relevant to prevention of pressure-induced injuries [74]. However, there was little evidence that use of a risk prediction tool, when linked to specific interventions based on the identified risk, resulted in fewer pressure-induced injuries when compared with actions based on nursing assessment [69,75,76].
Norton and Braden scales — The most commonly used prediction tools are the Norton and Braden scales (table 2 and table 3). It is important to recognize that these risk assessment tools only cover a limited range of risk factors. They are best used in conjunction with clinical judgment [77].
●The Norton scale uses a 1 to 4 scoring system in rating patients in each of five subscales (table 3): physical condition, mental condition, activity, mobility, and incontinence. A score <14 is indicative of a high risk.
●The Braden scale rates patients in six subscales (calculator 1): sensory perception, moisture, activity, mobility, nutrition, and friction and shear using scores ranging from 1 to 3 or 4 (table 2) [78]. The maximum score is 23; a score ≤18 is indicative of high risk.
The Norton and Braden scales are generally useful for predicting which patients are at risk for developing pressure-induced skin and soft tissue injuries. The Norton scale generally identifies more patients at high risk than the Braden scale [79]. One limitation is that interobserver reliability is low unless examination is performed by trained staff [78]. Although these scales have been validated [80], concerns have been raised about their positive predictive value [76,81-83]. Sensitivity typically ranges from 70 to 90 percent, and specificity is from 60 to 80 percent [84].
Two studies have found that the activity and mobility subscales are sufficient to express the risk for pressure-induced injuries among hospitalized patients [83,85]. Inclusion of the physical condition, mental condition, and incontinence subscales worsened performance in the larger of these studies, which included over 2000 patients [83]. Similar analyses evaluating subscales of the Braden scale have not been performed, and verification of the other scales in prospective trials is needed. However, the ability of the Braden scale to identify high-risk patients in the intensive care unit and during surgery is limited [86-88]. This likely reflects the high degree of immobility among patients in these health care settings.
Empirical studies — Given the lack of evidence that any prediction tool outperforms nurses' assessment, many studies have attempted to derive empirically based rules that can be used to predict risk [89,90]. The value of these in clinical practice, though, remains uncertain.
One retrospective review identified three predictors among immobilized hospital patients: low serum albumin, fecal incontinence, and a recent fracture [50]. However, retrospectively identified factors associated with the presence of a pressure-induced injury are not necessarily predictive of their development. Subsequent studies have used a prospective design to identify constellations of risk factors.
●In one study at a chronic care hospital, three risk factors among 301 admissions were identified: being immobilized, a history of a cerebrovascular accident, and impaired nutritional intake [55].
●In a prospective report of hospitalized patients with activity limitations (n = 286), the presence of a stage 1 pressure injury, lymphopenia, immobility, dry sacral skin, and decreased body weight were each associated with the development of a stage 2 or larger pressure injury [66]. When three or more of these factors were present, over 13 percent of patients developed an ulcer.
●In a large (n = 1971) multicenter prospective study designed to compare products for prevention of pressure-induced injury in hospitalized patients, the following factors were associated with increased risk: admission for an acute condition, medical rather than vascular or orthopedic admission, nonblanching erythema or skin trauma at baseline, older age, low hemoglobin level, and diabetes [91].
●In a study of 1524 long-term care residents, 29 percent of residents developed a new pressure-induced injury during the 12-week study period [67]. Factors associated with pressure-induced injury development included a higher initial severity of illness, history of recent pressure-induced injury, significant weight loss, oral eating difficulties, the use of catheters, and the use of positioning devices.
●In a study of 3233 patients, independent risk factors for the development of pressure-induced injuries in the first two days following admission included older age, male sex, dry skin over a bony prominence, incontinence, difficulty turning in bed, residing in a nursing home, prior hospitalization in the past six months, and poor nutritional status [92].
●Among 12,650 outpatients aged 60 or over and followed for up to 40 months, older age, male sex, admission to a long-term care facility, history of a previous pressure-induced injury, diabetes, falls, cataracts, renal insufficiency, and peripheral artery disease were associated with the development of a new pressure-induced injury [93].
Machine-learning techniques are increasingly being applied to enhance the prediction of pressure injury development [52,94,95]. The extent to which they will result in improved models remains uncertain.
Databases — Large databases have also been used to derive prediction rules. One study, for example, used a database with over 30,000 long-term care patients to identify 11 characteristics associated with pressure-induced injury development [24]. The Minimum Data Set has been used to develop a predictive model for nursing homes that considers 17 patient characteristics [58,96]. An expected probability of developing pressure-induced injury can then be calculated for each patient; however, it remains to be established whether this methodology will be clinically useful. Increasingly, machine learning approaches are being applied to develop prediction tools for pressure injury development, with two recent applications occurring in the intensive care unit [52,86].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic wound management" and "Society guideline links: Pressure-induced skin and soft tissue injury".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Pressure sores (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Pressure-induced skin and soft tissue injuries are among the most common conditions encountered in acutely hospitalized patients or those requiring long-term institutional care. Reducing the prevalence of pressure-induced injuries is a national goal in the United States as part of the Healthy People 2010 initiative. (See 'Introduction' above and 'Epidemiology' above.)
●External factors that lead to the development of pressure-induced injuries include pressure, shearing forces, friction, and moisture. Interaction of external factors with host-specific factors such as immobility, incontinence, and compromised nutritional status culminates in tissue damage. Decreased skin perfusion resulting from hypotension, shock, or peripheral artery disease is increasingly recognized as an important cause. (See 'Pathogenesis' above.)
●Knowledge of factors contributing to the pathogenesis allows the identification of patients at risk for development of pressure-induced skin and soft tissue injury. Preventive interventions may then be targeted to those specific patients. (See 'Risk factors' above.)
●We suggest using risk prediction tools to identify patients at risk for the development of pressure-induced skin and soft tissue injuries (Grade 2C). Among the available risk prediction tools, the Braden scale may be the best choice in the United States, given widespread familiarity with it. Depending upon the measured level of risk, specific interventions may then be initiated or altered accordingly. (See 'Risk prediction' above.)
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