Preventing Pressure Ulcers and Skin Tears   24  

Elizabeth A. Ayello and R. Gary Sibbald

OVERVIEW

The skin is the largest external organ; so preserving its integrity is an important aspect of nursing care. Performing a risk assessment and implementing a consistent prevention protocol may avoid disruption of the skin integrity, including pressure ulcers or skin tears. Although, pressure ulcers and skin tears may look similar, they are different types of skin injury; skin tears are acute traumatic wounds, whereas pressure ulcers are chronic wounds. It is important, therefore, to assess the wound and to determine the correct etiology so that the proper individualized treatment plan can be implemented.

BACKGROUND AND STATEMENT OF PROBLEM

Pressure Ulcers

Pressure ulcers are a significant health care problem worldwide (Bolton, 2010). They have a significant impact on health-related quality of life (HRQL; Gorecki et al., 2009). The word friction was first eliminated from the definition of a pressure ulcer in the 2009 joint pressure ulcer clinical guideline written by the National Pressure Ulcer Advisory Panel and the European Pressure Ulcer Advisory Panel (NPUAP, EPUAP, 2009). In the most recent international pressure ulcer clinical guideline by the NPUAP, EPUAP and now joined by the Pan Pacific Pressure Injury Alliance the word friction has been eliminated (NPUAP, EPUAP, PPPIA, 2014; Table 24.1). The NPUAP has upheld its position that friction is a superficial force that is not an important etiological factor for pressure ulcers (Brienza et al., 2015). Pressure ulcers are believed to develop as a result of the tissues’ internal mechanical deformation in response to external mechanical loading (EPUAP, NPUAP, & PPPIA, 2014). A case series by Berke (2015) can help clinicians differentiate friction injuries from pressure ulcers, moisture-associated skin damage such as incontinence-associated dermatitis, and other skin problems or injuries.

TABLE 24.1

2014 International NPUAP−EPUAP−PPPIA Pressure Ulcer Definition and Classification System

^aBruising indicates suspected deep tissue injury.

Reprinted with permission from the National Pressure Ulcer Advisory Panel (NPUAP), European Pressure Ulcer Advisory Panel (EPUAP), and Pan Pacific Pressure Injury Alliance (PPPIA, 2014).

The exact combination of pressure, ischemia, muscle deformation, and reperfusion injury that leads to a pressure ulcer remains unclear (NPUAP, EPUAP, & PPPIA, 2014). Most pressure ulcers on adults are found on the sacrum, with heels being the second most common site (VanGilder, Amlung, Harrison, & Meyer, 2009). In a study of hospitalized adults, a hospital-acquired pressure ulcer (HAPU) rate of 4.5% was identified, with the majority of HAPUs on the coccyx or sacrum (41%) with heels and hip/buttock region both being at 23% (Lyder et al., 2012). Data in 2009 from 92,408 U.S. facilities reported an overall prevalence rate of 12.3%, with a facility-acquired rate of 5.0%, which lowers to 3.2% rate when Stage I ulcers are excluded (VanGilder et al., 2009). This same study of 86,932 U.S. acute care facilities reported an overall prevalence rate of 11.9%, with a facility-acquired rate of 5.0%, which reduced to 3.1% when Stage I ulcers were excluded (VanGilder et al., 2009).

Table 24.2 summarizes the number of pressure ulcers by stages from this study (VanGilder et al., 2009). The distribution of pressure ulcers has changed over the years, with the number of Stage I ulcers decreasing and the number of unstageable pressure ulcers increasing to 15%, and suspected deep tissue injury (sDTI) to 9% (VanGilder, MacFarlane, Harrison, Lachenbruch, & Meyer, 2010). The most common site for deep tissue injury (DTI) is the heel (41%) followed by the sacrum (19%) and buttocks (13%; VanGilder et al., 2010).

In hospice patients, in addition to the usual sites on the sacrum and heels, elbows are a common site for ulcers with most ulcers occurring within 2 weeks before death (Hanson et al., 1991). In one hospital’s 10-bed palliative care unit, 5% of their patients developed a Kennedy terminal pressure ulcer (shaped like a pear, over the sacrum, bruise-like discoloration that is yellow and brown-black; Brennan & Trombley, 2010).

Device-Related Pressure Ulcers

Device-related pressure ulcers account for 9.1% of ulcers, with ears being the most common location (Table 24.3; VanGilder et al., 2009). The NPUAP has a position paper specifically on medical device–related pressure ulcers; a one-page educational resource (often referred to as an enabler for practice by educators), to raise awareness of the prevention and treatment of these pressure ulcers that can be downloaded for free from their website (www.npuap.org). Device-related pressure ulcers on the mucosa are not staged using the NPUAP classification system, as mucosa does not keratinalize and therefore the staging definitions cannot be applied (NPUAP position paper on device-related pressure ulcers; NPUAP, EPUAP, & PPPIA, 2014). Because of this ruling, in the United States, the Centers for Medicare & Medicaid Services (CMS) has directed long-term care (LTC) facilities and long-term acute care hospitals (LTCHs) that mucosal device-related pressure ulcers should not be recorded on the resident assessment instrument (RAI) under the pressure ulcer section.

TABLE 24.2

2009 Pressure Ulcer Prevalence by Stages in Acute Care

DTI, deep tissue injury.

Adapted from VanGilder, Amlung, Harrison, and Meyer (2009).

TABLE 24.3

Location of Device-Related Pressure Ulcers

Adapted from VanGilder, Amlung, Harrison, and Meyer (2009).

Pressure Ulcer Risk Factors

No single factor puts a patient at risk of pressure ulcer skin breakdown. The 2014 NPUAP EPUAP PPPIA pressure ulcer clinical guideline confirms what the CMS has required in LTC facilities, LTCHs, and inpatient rehabilitation units, which is that pressure ulcer risk assessment should be comprehensive and should include assessment of all patient risk factors. Clinicians need to go beyond just relaying on validated pressure ulcer risk assessment tools (e.g., the Braden Scale, Norton Scale, and so forth; NPUAP, EPUAP, & PPPIA, 2014).

Nonnemacher et al. (2009) addressed the question of what combination of factors increase the pressure ulcer risk by exploring 12 factors that seem to have the most impact on predicting pressure ulcer risk. Historically, pressure ulcers occur from a combination of intensity and duration of pressure as well as from tissue tolerance (Bergstrom, Braden, Laguzza, & Holman, 1987; Braden & Bergstrom, 1987, 1989). Immobility as seen in bedbound or chair-bound patients and those unable to change body positions can lead to shear, undernourishment or malnutrition, incontinence, friable skin, impaired cognitive ability, and decreased ability to respond to one’s environment, which are some of the important identified risk factors for pressure ulcers (Braden, 1998).

True pressure ulcers need to be distinguished from moisture-associated dermatitis or surface injury in the buttocks region caused by the contact irritation of local friction (Berke, 2015) and moisture factors (Gray et al., 2011). In a large study by Bergquist-Beringer and Gajewski (2011), immobility and incontinence were the two predictors of pressure ulcer development in older persons receiving home care.

A study of 20 hospitals of patients waiting for surgery determined a higher incidence of pressure ulcers for longer surgery waiting times or time in an intensive care unit (ICU; Baumgarten et al., 2003). Most pressure ulcers, in one study of 84 surgical patients, occurred within the first three postoperative days (Karadag & Gümüskaya, 2006). A large study of more than 50,000 hospitalized Medicare beneficiaries reported that 4.5% developed at least one new pressure ulcer during their hospital stay, had higher mortality rates during their hospitalization as well as within 30 days of discharge, and had longer hospital stays (Lyder et al., 2012). The following patient characteristics were found in those who developed HAPUs: a diagnosis of congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), cardiovascular disease (CVD), or diabetes mellitus, and presence of obesity (Lyder et al., 2012). A 2015 study found that in hospitalized patients, immobility, a diagnosis of diabetes mellitus, peripheral vascular disease, and a Braden Scale score of 18 or below were independent predictors for hospital-acquired heel pressure ulcers (Delmore, Lebovits, Suggs, Rolnitzky, & Ayello, 2015).

Patients With Hip Fracture and Pressure Ulcer Risk

In a study of nine hospitals, the cumulative incidence of Stage II or higher pressure ulcer in older adults with hip fractures was 36.1% (Baumgarten et al., 2009). The less time patients waited to go to the operating room (OR) for repair of the hip fracture, the fewer the number of associated Stage IV pressure ulcers (Hommel, Ulander, & Thorngren, 2003). The length of time on the OR table also increased the risk of pressure ulcers in patients with hip fracture (Houwing et al., 2004). Campbell, Woodbury, and Houghton (2010b) found that one third of their sample of patients with hip fracture developed Stage II or higher pressure ulcers. Implementation of a Heel Pressure Ulcer Prevention Program (HPUPP) for orthopedic patients in Canada resulted in complete elimination of heel pressure ulcers compared to the preimplementation level of 13.8% (Baumgarten et al., 2008).

Critically Ill, Intensive Care Unit Patients and Pressure Ulcer Risk

In a case–control study of medical patients in two hospitals, Baumgarten et al. (2008) found that the odds of developing a pressure ulcer were twice as high for those having an ICU stay. In contrast, Shahin, Dassen, and Halfens (2009) found a low incidence of pressure ulcers in their 121 ICU patients as a result of prevention measures, including foam and alternating air-pressure reducing mattresses. Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, physiological criteria, and Glasgow Coma Scale scores are used to predict ICU outcomes, with higher scores indicating poorer outcome; scores were higher in patients who developed pressure ulcers. In contrast, other researchers found no relationship between pressure ulcer development and APACHE II scores (Kaitani, Tokunaga, Matsui, & Sanada, 2010). Shanks, Kleinhelter, and Baker (2008) found that despite the consistent implementation of pressure ulcer prevention protocols in their critically ill patients, the patients who developed more hypotensive episodes were more likely to develop pressure ulcers.

Several authors have published case series that provide emerging support that when polyurethane foam dressings are applied prophylactically on the sacrum of critically ill, emergency department (ED), or medical–surgical (med–surg) patients, there is a reduction in incidence of pressure ulcers (Brindle & Wegelin, 2012; Brindle, 2010; Chaiken, 2012; Cubit, NcNally, & Lopez, 2013; Keily, 2012; Ohura, Takahaski, & Ohura, 2008; Park, 2014; Philbin, Shaw, Walker, & Bishop, 2013; Santamaria et al., 2013; Torrabou et al., 2009; Walsh et al., 2012). Based on their review of the evidence, the 2014 NPUAP, EPUAP, PPPIA Pressure Ulcer Clinical Guideline has provided a recommendation at the B level of evidence to consider using polyurethane foam dressing prophylactically to prevent pressure ulcers on bony prominences such as the heels or sacrum (NPUAP, EPUAP, & PPPIA, 2014, p. 18).

Regulatory and Government Initiatives

Regulatory and government initiatives continuously support the importance of pressure ulcer prevention. Beginning October 1, 2008, CMS no longer reimbursed hospitals at a higher rate for pressure ulcers acquired during hospitalization (CMS Hospital Acquired Conditions, 2011). Recording of location and stage of any Stage III and IV pressure ulcers present on admission (POA) now holds clinicians who are legally responsible for establishing the medical diagnosis accountable for documenting this information in the patient’s medical record; otherwise, the hospital is not reimbursed for the pressure ulcer diagnosis (Russo, Steiner, & Spector, 2006). Data from the Healthcare Cost and Utilization Project (HCUP) statistical review reveal that, over the past years, pressure ulcers have increased in hospitalized patients by 80%, even though the number of hospitalizations during this period of 1993 to 2006 only increased by 15% (CMS Hospital Acquired Conditions, 2011). In the state of New Jersey, Stage III and IV pressure ulcers are now reportable in acute care (New Jersey Department of Health and Senior Services, 2004). Pressure ulcers are one of the 12 targeted areas to reduce harm to hospitalized patients in the United States as part of the Institute for Healthcare Improvement’s (IHI) “5 Million Lives Campaign” launched in December 2006 (IHI, 2006). Therefore, at the beginning of the 21st century, appropriate risk assessment and preventative care take on even more important meanings.

Several successful initiatives to decrease pressure ulcer incidence are reported in the literature (Anderson et al., 2015; Lyder & Ayello, 2009; McInerney, 2008; Pancorbo-Hidalgo, Garcia-Fernandez, Lopez-Medina, & Alvarez-Nieto, 2006). Nurses will find the Agency for Healthcare Research and Quality (AHRQ) toolkit available at www.ahrq.gov/professionals/systems/hospital/pressureulcertoolkit helpful in developing quality initiatives to decrease pressure ulcer incidence (AHRQ, 2012). A summary of successful characteristics of pressure ulcer reduction initiatives can be found in the literature (Niederhauser et al., 2012; Padula, Valuck, Makic, & Wald, 2015).

ASSESSMENT OF THE PROBLEM

When to Do an Assessment

The assessment of the relative pressure ulcer risk is the first step of any individual patient or health care system plan for prevention. Some pressure ulcer clinical guidelines recommend that patients are assessed for pressure ulcer development on admission to a care facility, on discharge, whenever the patient’s condition changes, and then reassessed based on the person’s acuity (NPUAP, EPUAP, & PPPIA, 2014).

Pressure Ulcer Risk-Assessment Tools

Guidelines recommend that a comprehensive assessment for pressure ulcer risk be structured and include evaluation of all relevant risk factors and avoid reliance on just one risk factor or assessment tool total score (NPUAP, EPUAP, & PPPIA, 2014). The assessment should include a history (comorbidities, previous pressure ulcer, medications, and so forth) and physical examination, including skin inspection for skin status, and a pressure ulcer risk assessment using a valid and reliable assessment tool, including subscale scores. Both the Braden (Braden & Bergstrom, 1989) and the Norton Scales (Norton, McLaren, & Exton-Smith, 1962; Norton, McLaren, & Exton-Smith, 1975) are considered reliable and valid. A study of 429 patients in acute care found the modified Braden Scale to be a better predictor than the Norton Scale (Kwong et al., 2005). Although Kottner and Dassen (2010) found that the Braden Scale was more valid and reliable than the Waterlow Scale, they do not recommend either of these scales for ICU patients. Research to create new scales specific to ICU patients continues (Suriadi, Sanada, Sugama, Thigpen, & Subuh, 2008).

The Braden Scale was created in 1987 (Bergstrom et al., 1987) as part of a research study. The scale has six factors and is the most widely used scale in the United States. The first three subscales, sensory/perception, mobility, and activity, address clinical situations that predispose the patient to intense and prolonged pressure. The last three subscales, moisture, nutrition, and friction/shear, address factors that alter tissue tolerance for pressure. Each of the six categories is ranked with a numerical score, with 1 representing the lowest possible subscore and indicating the greatest risk. The sum of the six subscores and the greatest risk is the final Braden Scale score, which can range from 6 to 23.

A low Braden Scale score indicates that a patient is at risk for pressure ulcers. The original onset-of-risk score on the Braden Scale was 16 or less (Braden & Bergstrom, 1987). Further research on older adults (Bergstrom & Braden, 1992) and on persons with darkly pigmented skin (Lyder et al., 1998, 1999) supports a score of 18 or less. Research by Chan, Tan, Lee, and Lee (2005) also determined that the total Braden Scale score was the only significant predictor of pressure ulcers in hospitalized patients. In 2009, Chan, Pang, and Kwong (2009) applied a modified Braden Scale and calculated a cutoff score of 19 in a 107-bed orthopedic department of an acute care hospital in Hong Kong, with 9.1% of patients developing a pressure ulcer. In a retrospective study of intensive care patients in Korea using a cutoff score of 13, the Braden Scale (without a more comprehensive approach to patient-risk assessment) had low to moderate positive predictive performance (Cho & Noh, 2010). Risk was associated with pressure ulcer development in ICU patients who had low Braden Scale scores on the first day of hospitalization and low Glasgow Scale scores (Fernances & Caliri, 2008).

The NPUAP, EPUAP, and PPPIA 2014 clinical guidelines recommend that clinicians not only consider total Braden Scale scores but also address any low subscale scores (these indicate a higher risk) in planning pressure ulcer prevention care. Once high risk is identified, either for overall score or in any low subscales (CMS, 2004), prevention interventions need to be implemented. However, one study determined that in a sample of 792 hospitalized patients with a high risk of pressure ulcer development, only 51% of patients 65 years and older had a preventive device in place (Rich, Shardell, Margolis, & Baumgarten, 2009).

DOES RACE MAKE A DIFFERENCE?

When it comes to severity of pressure ulcers, race may make a difference. Ayello and Lyder (2001) analyzed and summarized the existing data about pressure ulcers across the skin pigmentation spectrum. Blacks have the lowest incidence (19%) of superficial tissue damage classified as Stage I pressure ulcers, and Whites have the highest incidence at 46% (Barczak, Barnett, Childs, & Bosley, 2007). Despite the lower Stage I rate, the more severe tissue injury detected in Stages II to IV pressure ulcers is higher in persons with darkly pigmented skin (Barczak et al., 2007; Meehan, 1990, 1994). Three national surveys identified that Blacks had 39% (Barczak et al., 2007), 16% (Meehan, 1990), and 41% (Meehan, 1994) higher incidence of Stage II pressure ulcers compared to Caucasians. Subsequent studies by Lyder et al. (1998, 1999) continue to support a higher incidence of pressure ulcers in persons with darkly pigmented skin. Fogerty, Guy, Barbul, Nanney, and Abumrad (2009) determined that not only was there a higher prevalence of pressure ulcers, but also that they occurred at a younger age in African Americans as compared to Caucasians.

Inadequate detection of Stage I pressure ulcers in persons with darkly pigmented skin may be a result of clinicians erroneously believing that dark skin tolerates pressure better than light skin (Bergstrom, Braden, Kemp, Champagne, & Ruby, 1996), or that only color changes indicate an ulcer (Bennett, 1995; Henderson et al., 1997; Lyder, 1996; Lyder et al., 1998, 1999; Rich et al., 2009). Research has begun to validate these assessment characteristics in the Stage I definition. In 2001, Lyder et al. (2001) reported a higher diagnostic accuracy rate of 78% using the revised definition compared with 58% with the original definition. Sprigle, Linden, McKenna, Davis, and Riordan (2001) evaluated changes in skin temperature; in particular, that warmth followed by coolness accompanied most Stage I pressure ulcers.

Clinicians should pay careful attention to a variety of factors when assessing a patient with darkly pigmented skin for Stage I pressure ulcers. Differences in skin over bony prominences (e.g., the sacrum and the heels) as compared with surrounding skin may be indicators of a Stage I pressure ulcer. The skin should be assessed for alterations in pain or local sensation. In addition, a change of skin color should be noted; doctors need to be familiar with the range of skin pigmentation that is normal for a particular patient (Bennett, 1995; Henderson et al., 1997).

INTERVENTIONS AND CARE STRATEGIES

Determining a patient’s risk for developing a pressure ulcer is only the first step in providing best practice care. Once risk is identified, implementing a consistent protocol to prevent the development of a pressure ulcer is essential. A nursing standard-of-practice protocol for pressure ulcer prevention is presented later in the chapter to facilitate proactive interventions to prevent pressure ulcers. A change in attitudes of health care professionals may be required to facilitate prevention (Buss, Halfens, Abu-Saad, & Kok, 2004). Educating nursing students (Holst et al., 2010) and nurses in an ICU unit resulted in decrease in pressure ulcers (Uzun, Aylaz, & Karadag, 2009). Several clinical guidelines exist detailing pressure ulcer prevention (NPUAP, EPUAP, & PPPIA, 2014; Wound, Ostomy, and Continence Nurses Society, 2010). Components of a pressure ulcer prevention protocol should minimally include interventions targeting the following: skin care (including addressing moisture and friction), pressure redistribution, repositioning, and nutrition.

Skin Care

Skin that is too dry or too wet has been associated with pressure ulcers. Although there is limited research, dry skin is believed to predispose ulcer formation (Allman, Goode, Patrick, Burst, & Bartolucci, 1995; Reddy, Gill, & Rochon, 2006). The type of cream used on the skin for different parts of the body may make a difference as evidenced by a study of 79 patients treated with dimethyl sulfoxide cream, with an increase in pressure ulcers when this cream was used on the heels as compared to the buttocks (Houwing, Van der Zwet, van Asbeck, Halfens, & Arends, 2008). Other researchers (Stratton et al., 2005) found that a silicone-based dermal nourishing cream reduced the proportion of HAPUs to 0 after 8 months. Each of these creams are lubricating, adding an external ointment layer preventing insensible losses. The stratum corneum has 10% moisture content maintained by a complex structure of a number of chemicals referred to as the natural moisturizing factor (NMF). When the NMF decreases to below a critical level, the skin integrity is lost, with defects occurring between the keratin layers (dry skin, winter itch, eczema craquelé). The second way to moisturize the skin is with humectants (urea, lactic acid, glycerin, ceramides), which actually bind water to the stratum corneum. These substances will sting or burn when applied to open skin because of their hydroscopic properties but this does not indicate an allergy. Skin can also be too wet, causing a macerated stratum corneum, decreasing the cutaneous barrier and subjecting affected individuals to an increased risk of yeast and bacterial infections.

Use of a soft silicone dressing on the sacrum of critically ill patients resulted in zero pressure ulcers in one ICU (Brindle, 2010). Other researchers have reported similar pressure ulcer occurrence reduction when polyurethane foam dressings are placed prophylactically on heels or sacrum (Brindle & Wegelin, 2012; Chaiken, 2012; Cubit et al., 2013; Keily, 2012; Park, 2014; Philbin et al., 2013; Santamaria et al., 2013; Torrabou et al., 2008; Walsh et al., 2012). Hydrocolloid dressings decreased pressure ulcers from nasotracheal intubation (Huang, Tseng, Lee, Yeh, & Lai, 2009). When hydrocolloid or film dressings were applied to the skin under facemasks, there were fewer device-related pressure ulcers (Weng, 2008).

Repositioning and Pressure Redistribution

Because hospitalized patient immobility is a risk factor for the development of pressure ulcers (Lindgren, Unosson, Fredrikson, & Ek, 2004), efforts must be implemented to address pressure. Although repositioning patients is a key intervention to redistribute the pressure and prevent pressure ulcers, the best frequency for turning and repositioning, as well as which support surface to use, remains a challenge (Defloor, De Bacquer, & Grypdonck, 2005; Norton et al., 1975; Young, 2004). Patients on a particular support surface may not have to be repositioned every 2 hours, depending on their tolerance to pressure. There is no one repositioning timetable for all, the timing needs to be individualized (EPUAP & NPUAP, 2009). The use of a wedge-shaped cushion rather than a pillow may be more effective in decreasing pressure ulcers in some patients (Heyneman, Vanderwee, Grypdonck, & Defloor, 2009).

Redistributing pressure is a key pressure ulcer prevention component. When compared to alternating pressure overlays, alternating pressure mattresses reduced length of stay for hospitalized patients, thus decreasing costs as well as having the added benefit of delaying the time at which a pressure ulcer appeared (Iglesias et al., 2006; Nixon et al., 2006).

The incidence of heel pressure ulcers decreased when the appropriate heel-suspending device was used to relieve pressure (Gilcreast et al., 2005). In 2010, a prospective 150-patient, 6-month study by Campbell, Woodbury, and Houghton (2010a), indicated pressure ulcer incidence was being lowered significantly, by 16%, (p = .016) for those who received help with pressure relief interventions. No new pressure ulcers developed in a single study of persons with a body mass index (BMI) greater than 35 who were placed on appropriately sized low air-loss equipment (Pemberton, Turner, & VanGilder, 2009). Clinicians may find the Wound, Ostomy, and Continence Nursing Society (WOCN) evidence-based algorithm for selecting a support surface to be a helpful tool in practice (McNichol, Watts, Mackey, Beitz, & Gray, 2015).

In Australia, where medical grade sheepskin (animal source, not synthetic) is available, one study with some questionable methodology demonstrated that hospitalized patients randomly assigned to the animal-source sheepskin mattress overlay had a 9.6% lower incidence of risk of pressure ulcers compared to the control group, which had a risk of 16.6% (Jolley et al., 2004). The results were that 58 patients developed pressure ulcers (sheepskin group, 21; referent group, 37). The cumulative incidence risk was 9.6% in the sheepskin group (95% CI, 6.1%–14.3%) versus 16.6% in the referent group (95% CI, 12.0%–22.1%). Patients in the sheepskin group developed new pressure ulcers at a rate less than half that of referent patients (rate ratio, 0.42; 95% CI, 0.26–0.67).

Nutrition

There is lack of consensus about the best way to assess nutritional impairment but, generally, consultation by a dietitian for nutritional status, determination of any unintended weight loss, and evaluation of laboratory values, including serum albumin or prealbumin, should be considered. Cordeiro et al. (2005) found that the concentrations of ascorbic acid and alpha-tocopherol were significantly decreased in patients with pressure ulcers or active infection. In a randomized double-blind study on the effect of a daily supplement with protein, arginine, zinc, and antioxidants versus a water-based placebo supplement in patients with hip fractures, there was a 9% difference in the incidence of Stage II pressure ulcers between the nutritionally supplemented group and the placebo group (Houwing et al., 2003). The Cochrane Database reviewed the role of nutrition in pressure ulcer prevention and treatment. The analysis of the database was inconclusive because of the lack of high-quality trials (Langer, Schloemer, Knerr, Kuss, & Behrens, 2003). When and how patients should be nutritionally supplemented to prevent pressure ulcers remains unclear (Houwing et al., 2003; Reddy et al., 2006; Stratton et al., 2005), with contradictions in the literature. The NPUAP nutritional recommendations (NPUAP, EPUAP, & PPPIA, 2014; Posthauer, Banks, Dorner, & Schols, 2015) for pressure ulcer prevention are included in Protocol 24.1.

SKIN TEARS

Skin tears were originally conceptualized as traumatic wounds caused by shear and friction (O’Regan, 2002) when the epidermis is separated from the dermis (Malone, Rozario, Gavinski, & Goodwin, 1991). Extensive work of the ISTAP has provided the following new skin tear definition: “a wound caused by shear, friction, and/or blunt force resulting in separation of skin layers. A skin tear can be partial-thickness (separation of the epidermis form the dermis) or full-thickness (separation of both the epidermis and dermis from underlying structures)” (LeBlanc et al., 2013, p. 460). Because aging skin has a thinner epidermis, a flatter dermal–epidermal junction, and decreased dermal collagen, older persons are more prone to skin injury from mechanical trauma (Baranoski, 2000; Payne & Martin, 1993; White, Karam, & Cowell, 1994). Therefore, skin tears are common in older adults, with more than 1.5 million occurring annually in institutionalized adults in the United States (Thomas, Goode, LaMaster, Tennyson, & Parnell, 1999), although the incidence in acute care is unknown. Skin tears are frequently located at areas of age-related purpura (Malone et al., 1991; White et al., 1994).

Assessment of Skin Tears

The following areas should be assessed for skin tears: shins, face, dorsal aspect of hands, and plantar aspect of the foot (Malone et al., 1991). Besides older adults, others with thinning skin who are at risk of skin tears are patients on long-term steroid therapy, women with decreased hormone levels, persons with peripheral vascular disease or neuropathy (the decreased sensation making them more susceptible to injury), and those with inadequate nutritional intake (O’Regan, 2002).

The three-group risk assessment tool was developed during a research study by White et al. (1994). Because of its length, and awkward format, it is not often used clinically to assess for risk of skin tears (White et al., 1994). Within the tool, there are three groups delineated by the level of risk: Groups 1, 2, and 3 (Table 24.4). Summarizing the components of this tool, the clinician should assess patients for five criteria:

TABLE 24.4

Enabler for Skin-Tear Risk Assessment

Any of these criteria should alert clinicians to institute a skin tear prevention program, especially the presence of skin tears or history in the past 90 days, along with mobility challenges with impaired mentation, skin changes, and physical limitations further increasing the risk.

The recent work of ISTAP affirms the importance of reviewing both intrinsic and extrinsic factors to assess skin tear risk (LeBlanc et al., 2013).

Several authors have suggested protocols to prevent skin tears (Baranoski, 2000; Battersby, 1990; LeBlanc et al., 2013; Mason, 1997; O’Regan, 2002; White et al., 1994). Lacking research in acute care, some nursing home research supports the value of skin ulcer care protocols to reduce the incidence of skin tears (Bank, 2005; Birch & Coggins, 2003; Hanson, Anderson, Thompson, & Langemo, 2005). After changing from soap and water to a no-rinse, one-step bed product, skin tears declined from 23.5% to 3.5% in one nursing home (Birch & Coggins, 2003). Hanson et al. (2005) also found that skin tears could be reduced in two different nursing homes when staff were educated in appropriate skin cleaning and protection strategies. A reduction in monthly average of skin tears from 18 to 11 after using longer lasting moisturizer lotion, sleeves to protect the arms, and padded side rails was reported in yet another nursing home study (Bank, 2005). One study claims a decrease in skin tears when skin is treated with cream (Groom, Shannon, Chakravarthy, & Fleck, 2010).

Interventions for Skin Tears

If a skin tear does occur, it is important to correctly identify it and begin an appropriate plan of care. ISTAP (LeBlanc et al., 2013) has suggested replacing the original three-category Payne–Martin classification system (Payne & Martin, 1993) with their newer and more simplified classification system of three types, as follows:

The usual healing time for skin tears is 3 to 10 days (Krasner, 1991). Although skin tears are prevalent in the older adult patient, there is no consistent approach to managing these skin injuries (Baranoski, 2000; O’Regan, 2002). The extensive work of ISTAP has attempted to provide a research base for consistent care to prevent and treat skin tears worldwide (LeBlanc et al., 2013).

Research is just beginning to provide evidence on the best dressings for skin tears. One study (Edwards, Gaskill, & Nash, 1998) compared the use of four different types of dressings in treating skin tears in a nursing home: three occlusive (transparent film, hydrocolloid, and polyurethane foam) and one nonocclusive dressing of Steri-strips covered by a nonadhesive cellulose-polyester material. The nonocclusive dressing facilitated healing at a faster rate than the occlusive dressings. Another study by Thomas et al. (1999) studied older adult skin tears in three nursing homes and identified that there was a higher rate of complete healing with foam dressings compared to transparent films. ISTAP has published a skin tear product selection guide that directs clinicians to avoid adhesives, hydrocolloids, transparent films and closure strips, and instead consider using lipocolloid mesh, silicone mesh, foam, impregnated gauze, hydrogel, calcium alginate, hydrofibers, or acrylic dressings (LeBlanc et al., 2013).

Goals of care for skin tears include retaining the skin flap if present, providing a moist, nonadherent dressing, and protecting the site from further injury (LeBlanc et al., 2013; O’Regan, 2002). A consensus protocol for treating skin tears based on suggested plans of care has been developed by several authors (Baranoski, 2000; Baranoski & Ayello, 2008; Edwards et al., 1998; LeBlanc et al., 2013; O’Regan, 2002) as well as ISTAP, and can be found in Protocol 24.2.

Stay updated, free articles. Join our Telegram channel

Join