Abstract
Purpose:
Community-acquired pressure injuries (CAPIs) are present among approximately 3% of patients admitted to acute-care hospitals. Patients with CAPI are not well represented in the hospital- acquired pressure injury (HAPI) literature because those studies usually exclude patients with CAPI. The purpose of our study was to determine the incidence of HAPI development, and associated risk factors, among critical care patients with CAPI.
Design:
This was a retrospective cohort study.
Subjects and Setting:
We used electronic health record data from adult surgical critical care patients admitted to a level-1 trauma center and academic medical center between 2014–2018.
Methods:
We conducted univariate analysis to compare patients with CAPI who developed HAPI and those who did not, and then used logistic regression analysis to identify independent risk factors for HAPI among patients with CAPI.
Results:
Among 5,101 patients admitted to the surgical critical care units, 167 (3%) patients were admitted with a CAPI. HAPI were four times more common among patients with CAPI compared to patients without CAPI: Among the 167 patients with CAPI, 47 patients (28%) went on to also develop a HAPI, whereas in the 4,934 patients without CAPI, 352 patients (7%) went on to develop HAPI. Upon multivariate logistic regression analysis (n = 151), decreased serum albumin (OR = 0.47, 95% CI = [0.25, 0.85], p = .02) and excessively dry skin (OR = 2.6, 95% CI = [1.1, 6.22], p = .03) were independent predictors of HAPI development among patients admitted with CAPI.
Conclusions:
Results from our study show patients with CAPI are at high risk for HAPI, particularly among patients with decreased serum albumin or excessively dry skin.
Keywords: Pressure Injury, Hospital Acquired Pressure Injury, Community Acquired Pressure Injury, Critical Care
Introduction
Pressure injuries, formerly called pressure ulcers, are areas of injury to the skin and underlying soft tissues that occur as a result of pressure, or pressure combined with shear.1 Hospital-acquired pressure injuries (HAPIs) occur among 6% to 10% of surgical critical-care patients2 and result in a longer length of hospitalization, increased cost, and undue human suffering.3,4
Community-acquired pressure injuries (CAPIs) are present among approximately 3% of patients admitted to acute-care hospitals.5 Patients with a CAPI are not well represented in the HAPI literature because those studies often exclude patients with CAPIs. For example, among 18 studies in a recent systematic review aimed at identifying risk factors for HAPIs among critical-care patients, 10 (56%) excluded patients with a CAPI from the study.2 Furthermore, no studies specifically examined HAPI development among patients with a CAPI. Consequently, little is known about risk factors for subsequent HAPI development in patients with a CAPI.
Purpose
The purpose of this study was to determine the incidence of HAPI development and associated risk factors among patients with a CAPI.
Background
Stage 1 pressure injuries are nonblanchable areas of erythema that may appear differently in people with dark skin pigmentation.6 Stage 1 pressure injuries progress to Stage 2 or worse pressure injuries among about one-third of critical-care patients.7 Stage 2 pressure injuries are open areas with exposed dermis. They may also appear as an intact or ruptured serum-filled blister. Stage 3 pressure injuries present with full thickness tissue loss and visible fat. In a Stage 4 pressure injury, fascia, muscle, bone, tendon, ligament, cartilage, and/or bone are visible or directly palpable. Stage 3 and 4 pressure injuries may include epibole, undermining, and/or tunneling. In unstageable pressure injuries, the wound base is obscured by eschar and/or slough. In a deep tissue injury (DTI), skin may be intact or nonintact with deep red, maroon, or purple discoloration. Finally, mucosal pressure injuries are found on the mucous membranes, for example in the nose, and are typically associated with pressure from medical devices. Mucosal pressure injuries are not staged according to the traditional system because there is no epidermis or dermis in mucosal tissue.8
Pressure injury etiology is multifactorial and results from a combination of pressure (mechanical boundary) and compromised tissue tolerance.9 Most, but not all, pressure injuries are avoidable. Unavoidable pressure injuries occur despite appropriate risk-based intervention when pressure cannot be relieved, or when perfusion is inadequate to support the delivery of oxygen-rich blood to organs, including the skin.10 Among critical-care patients, consistently identified risk factors for HAPIs include advanced age, limited mobility, and altered perfusion.2 Evidence for other factors, including compromised nutrition and general health status, is inconsistent.2
Methods
Design
In this retrospective cohort study, we used electronic health record (EHR) data to identify the incidence of HAPI development and associated risk factors among surgical critical-care patients with a CAPI. The institutional review board approved our study.
Sample and Setting
Study participants were adult patients admitted to the surgical or cardiovascular surgical intensive care units (ICUs) between August 1, 2014, and March 1, 2018, at our study site, an academic medical center and level-1 trauma center in the Intermountain West. Patients admitted to the ICU for fewer than 24 hours were excluded from the study.
Data Discovery and Measures
We worked with the institution’s research-data service team to extract EHR data from the enterprise data warehouse. We verified the data by manually comparing exported data values with patient records, as viewed through the institution’s EHR system, for a sample of 30 admissions. We considered each variable valid when values and date/time stamps matched for 30/30 hand-reviewed cases.
We included a broad set of potentially relevant variables based on a combination of clinician input—including intensivist physicians, surgeons, critical care nurses, and certified wound care nurses—and a review of the relevant literature. Because no studies exist that identify risk factors for HAPIs in critical-care patients with a CAPI, we also reviewed the long-term-care literature. Coleman and colleagues’ conceptual model for pressure injury development served as the theoretical framework for our variable selection.9
Study variables included diagnosis and comorbidities, Braden Scale total and subscale scores, body mass index, fluid balance, laboratory values, vasopressor infusions, nursing skin assessments, duration of mechanical ventilation, and surgical duration. Demographic data included age, race, ethnicity, sex, and hospital mortality. We also collected data on clinical deterioration via the Modified Early Warning Score, discharge disposition, and the discharge LACE score (an indicator of risk for 30-day readmission).
Pressure injuries were staged according to the National Pressure Ulcer Advisory Panel (NPUAP) staging guidelines.11 At the study hospital, critical care nurses conduct a head-to-toe skin inspection once per shift and record information about HAPIs in a structured field in the EHR. A clinical-decision support link in the EHR also provided point-of-care information about the NPUAP stages, and nurses had the option to initiate a certified wound-care nurse consult for any ambiguous stages. Critical-care nurses at this hospital undergo annual training in pressure injury identification and staging.
We defined a CAPI as a pressure injury of any stage identified within 24 hours of admission to the hospital. We included Stage 1 injuries in our analysis because that stage is considered clinically relevant in the critical-care population, with one-third of Stage 1 injuries progressing to more severe stages.7 We also collected data about pressure injury progression, including the most severe stage reached by each pressure injury during the hospital stay.
Analysis
We conducted data cleaning and analysis using R Version 3.3.4.12 To identify variables predicting HAPI development among patients with a CAPI, we did not include values after the HAPI occurred. For example, if a patient was afebrile prior to HAPI development but then went on to develop a fever after the HAPI was recognized, that patient would be considered afebrile for analysis.
Our study purpose was to identify factors associated with subsequent HAPI development among patients admitted to the ICU with a CAPI. We conducted univariate analysis to compare patients with and without a HAPI using a Pearson chi-square or Fisher exact test, as appropriate, for categorical variables. We used a Mann-Whitney U test for ordinal variables and a t test or Mann-Whitney U test for parametric versus nonparametric continuous variables. Next, we used logistic regression analysis. Before building the model, we assessed colinearity with a Pearson correlation matrix and limited the model to variables with correlations < 0.7.13,14 We assessed model fit via McFadden’s Pseudo R square.15
Results
The final sample consisted of 5,101 patients; one patient was excluded from analysis due to incomplete data. The mean length of hospitalization was 12 days (+/– 11 days) and the mean ICU stay was 5 days (+/– 8 days). The patients in the sample were predominantly male (n = 3302, 65%) and White (n = 4265, 84%). The mean LACE index score, a measure of risk for readmission based on length of stay, acuity, comorbidities, and emergency department use, was 10.0 (+/– 2.83), indicating relatively high risk for readmission and associated severity of illness.16 Hospital mortality in the sample was 8% (n = 395).
Patients With a CAPI
CAPIs were present among 3.3 % (n = 167) of patients in the total sample (N = 5101). Patients with a CAPI were older than patients without a CAPI (M = 64 years +/– 15 years versus 58 years +/– 17 years; t(181) = 5.1, p < .000). Patients with a CAPI also had significantly longer duration of hospitalization (M = 14 days +/– 12 days versus 11 days +/– 11 days, t(177) = 2.23, p = .02) but did not have statistically significantly longer ICU stays (M = 7 days +/– 9 days compared with 5 days +/– 8 days, t(177) = 1.6, p = .1).
The 167 patients with CAPIs were admitted with a total of 220 pressure injuries (Figure 1). Among those, 65 (30%) were Stage 1, 88 (40%) were Stage 2, 20 (9%) were Stage 3, 5 (3%) were Stage 4, 26 (12%) were unstageable, and 14 (6%) were DTIs. The most severe stages reached during the hospital stay were as follows: 41 (19%) Stage 1, 94 (42%) Stage 2, 28 (13%) Stage 3, 9 (4%) Stage 4, 25 (11%) unstageable, and 23 (10%) DTI. None of the CAPIs were mucosal pressure injuries.
Figure 1: CAPI.
(N = 167, 200 Pressure Injuries)
HAPI Development Among Patients With a CAPI
HAPI were four times more common among patients with CAPI compared to patients without CAPI: Among the 167 patients with CAPI, 47 patients (28%) went on to also develop a HAPI, whereas in the 4,934 patients without CAPI, 352 (7%) went on to develop HAPI X2 (1, N = 5101) = 25.72, p < .000. Relationships between potential predictor variables and HAPI development are presented in Table 1. Upon multivariate analysis (n = 151), decreased serum albumin (odds ratio, or OR = 0.47, 95% confidence interval, or CI = [0.25, 0.85], p = .02) and excessively dry skin (OR = 2.6, 95% CI = [1.1, 6.22], p = .03) were independent predictors of HAPI development among patients admitted with a CAPI. McFadden’s Psuedo R-squared = 0.16 indicated the data were a good fit for the model.13 The area under the receiver operating characteristic curve was 0.69 (+/– 0.6).
Table 1.
Characteristics Associated With Hospital-Acquired Pressure Injury Development
| Variable | All Patients With a CAPI N = 167 |
Patients Without a HAPI n = 120 |
Patients With a HAPI n = 47 |
Test Statistic |
Missing Data |
|---|---|---|---|---|---|
|
| |||||
| Demographic, Treatment, and Discharge Information | |||||
| Age in years, M (SD) | 64 (15) | 65 (15) | 61 (16) |
T(78) = 1.82 p = .19 |
0% |
| Sex, male, n (%) | 101 (60) | 74 (62) | 27 (57) |
X2 (1, N = 167) = 0.11 p = .74 |
0% |
| Race, White, n (%) | 141 (84) | 104 (87) | 37 (79) |
X2 (1, N = 167) = 0.39 p = .85 |
0% |
| Ethnicity, non-Hispanic White, n (%) | 148 (89) | 107 (89) | 41 (87) |
X2 (1, N = 167) = 0.36 p = .83 |
0% |
| LACE score [30-day readmission risk], M (SD) | 11.2 (2.6 | 10.8 (2.5) | 12.1 (2.6) | U = 2596 p = .003 |
0% |
| Specialty bed, n (%) | 59 (35) | 39 (33) | 20 (43) |
X2 (1, N = 167) = 1.08 p = .3 |
0% |
| Died during hospitalization, n (%) | 31 (19) | 22 (18) | 8 (17) |
X2 (1, N = 167) = 0.00 p = 1.0 |
0% |
| Braden Scale Scores | |||||
| Braden Scale total score, M (SD) | 11.47 (2.48) | 11.4 (2.47) | 11.8 (2.49) | U = 2246 p = .48 |
0% |
| Braden subscale activity, M (SD) | 1.08 (0.39) | 1.05 (0.25) | 1.17 (0.6) | U = 2691 p = .224 |
0% |
| Braden subscale moisture, M (SD) | 2.4 (0.7) | 2.4 (0.72) | 2.5 (0.71) | U = 2765 p = .83 |
0% |
| Braden subscale mobility, M (SD) | 1.8 (0.6) | 1.75 (0.69) | 1.85 (0.66) | U = 2592 p = 0.37 |
0% |
| Braden subscale nutrition, M (SD) | 1.68 (0.55) | 1.61 (0.52) | 1.85 (0.6) | U = 2246 p = .01 |
0% |
| Braden subscale sensory, M (SD) | 2.08 (0.8) | 2.03 (0.82) | 2.19 (0.74) | U = 2520 p = .26 |
0% |
| Braden subscale friction shear, M (SD) | 1.26 (0.5) | 1.25 (0.4) | 1.3 (0.5) | U = 2730 p = .67 |
0% |
| Vasopressor Infusions | |||||
| Received norepinephrine, n (%) | 47 (28) | 25 (21) | 22 (47) |
X2 (1, N = 167) = 0.86 p = .35 |
0% |
| Received vasopressin, n (%) | 47 (28) | 32 (26) | 15 (13) |
X2 (1, N = 167) = 0.32 p = .85 |
0% |
| Received phenylephrine, n (%) | 47 (28) | 45 (38) | 2 (0.04) |
X2 (1, N = 167) = 0.17 p = .67 |
0% |
| Received dopamine, n (%) | 29 (17) | 23 (19) | 6 (13) |
X2 (1, N = 167) = 0.56 p = .45 |
0% |
| Received epinephrine, n (%) | 29 (17) | 23 (19) | 6 (13) |
X2 (1, N = 167) = 0.56 p = .45 |
0% |
| Other Potential Predictors | |||||
| Admission body mass index kg/m2, M (SD) | 30.0 (11) | 30.2 (12.0) | 29.8 (9.7) |
T(98) = 0.20 p = .84 |
4 % |
| Length of stay prior to HAPI, days, M (SD) | 6 (9) | 5 (6) | 8 (14) |
T(54) = −1.6 p = .11 |
0% |
| Fluid balance, daily maximum (ml), M (SD) | 2868 (2375) | 2667 (2104) | 3379 (2923) |
T(65) = 1.52 p = .13 |
0% |
| Maximum MEWS score, M (SD) | 4.9 (2) | 4.6 (2) | 5.6 (1.6) | U = 1962 p = .002 |
0.01% |
| Maximum lactate (mg/dL), M (SD) | 3.9 (3.7) | 3.7 (2.7) | 4.0 (4.0) |
T(102) = 0.56 p = .58 |
9% |
| Maximum serum creatinine (mg/dL), M (SD) | 2.4 (2.0) | 2.5 (2.1) | 2.0 (1.2) |
T(141) = 2.04 p = .04* |
0.01% |
| Maximum serum glucose (mg/dL), M (SD) | 238 (104) | 241 (106) | 231 (101) |
T(85) = 0.55 p = .59 |
0.01% |
| Minimum hemoglobin (g/dL), M (SD) | 8.2 (2.2) | 8.3 (2.3) | 8.1 (2.0) |
T(95) = 0.48 p = .63 |
0.01% |
| Minimum Albumin (mg/dL), mean (SD) | 2.6(0.6) | 2.7(0.7) | 2.4(0.5) |
T(95) = 2.80 p = 0.006** |
9% |
| Longest surgery, min, M (SD) | 108 (128) | 118 (133) | 84 (112) |
T(99) = 1.69 p = .09 |
0% |
| Maximum temperature, °C, M (SD) | 37.8 (0.66) | 37.8 (0.63) | 37.9 (0.73) | U = 2865 p = .80 |
0% |
| Ventilator days, n (%) | 2.0 (4.2) | 1.8 (4.2) | 2.4 (4.3) | U = 2596 p = .39 |
0% |
| Nursing Skin Assessments | |||||
| Thin epidermis with subcutaneous tissue loss, n (%) | 67 (40) | 42 (35) | 25 (53) |
X2 (1, N = 167) = 3.92 p = .05* |
0% |
| Excessively dry skin, n (%) | 20 (12) | 16 (13) | 14 (30) |
X2 (1, N = 167) = 5.14 p = .02* |
0% |
| Skin tear, n (%) | 64 (530) | 26 (22) | 18 (38) |
X2 (1, N = 167) = 4.0 p = .05* |
0% |
| Swollen skin, n (%) | 26 (16) | 16 (13) | 10 (21) |
X2 (1, N = 167) = 1.07 p = .30 |
0% |
| Excessively moist skin, n (%) | 17 (10) | 19 (16) | 8 (17) |
X2 (1, N = 167) = 0.00 p = 1 |
0% |
| Weeping skin, n (%) | 46 (28) | 30 (25) | 16 (34) |
X2 (1, N = 167) = 0.96 p = .33 |
0% |
| Bruised skin, n (%) | 112 (67) | 80 (67) | 32 (68) |
X2 (1, N = 167) = 0.00 p = 1 |
0% |
| Blister present, n (%) | 26 (16) | 19 (16) | 7 (15) |
X2 (1, N = 167) = 0.00 p =1 |
0% |
| Reddened or irritated skin, n (%) | 95 (57) | 66 (55) | 29 (62) |
X2 (1, N = 167) = 0.38 p = .61 |
0% |
| Diagnosis and Comorbid Conditions | |||||
| Charleston Comorbidity Index, M (SD) | 5.0 (3.1) | 5.0 (3.1) | 5.0 (3.3) | U = 2865 p = .88 |
0% |
| Diabetes, n (%) | 80 (48) | 55 (46) | 25 (53) |
X2 (1, N = 167) = 1.21 p = .27 |
0% |
| Paralysis (paraplegia or quadriplegia), n (%) | 47 (28) | 37 (30) | 10 (21) |
X2 (1, N = 167) = 1.41 p = .23 |
0% |
| Heart failure, n (%) | 47 (28) | 28 (23) | 19 (40) |
X2 (1, N = 167) = 0.07 p = .79 |
0% |
| Dementia, n (%) | 12 (7) | 10 (8) | 2 (4) | Insufficient events for analysis | 0% |
| COPD, n (%) | 73 (44) | 52 (43) | 21 (44) |
X2 (1, N = 167) = 0.00 p = 1 |
0% |
Note. CAPI = community-acquired pressure injury; HAPI = hospital-acquired pressure injury; SD = standard deviation; Sp02 = peripheral capillary oxygen saturation; mg = milligram; g = gram; dL = deciliter; U = Mann-Whitney U score; COPD = chronic obstructive pulmonary disease.
The 47 patients with a CAPI developed a total of 77 HAPIs (Figure 2). Among those, at the time of pressure injury detection, 22 (29%) were Stage 1, 28 (36%) were Stage 2, 11 (14%) were Stage 3, 2 (3%) were Stage 4, 8 (10%) were unstageable, and 6 (8%) were DTI. The most severe stages reached during the hospital stay were as follows: 11 (14%) Stage 1, 27 (35%) Stage 2, 15 (19%) Stage 3, 2 (3%) Stage 4, 10 (13%) unstageable, and 12 (16%) DTI. None of the HAPIs were mucosal pressure injuries.
Figure 2: HAPI Among Patients Admitted with CAPI.
(N = 47, 77 Pressure Injuries)
Limitations
The retrospective design limits our study because we were restricted to the data available within the EHR. Additionally, data were obtained from a single site. Results from our single-site sample may not be generalizable to the larger population of surgical critical-care patients.
Our logistic regression model’s area under the receiver operating characteristic was poor to fair in terms of predictive accuracy/discrimination, at 0.69 (+/– 0.6).15 We selected potential predictor variables based on the current literature, clinician input, and Coleman’s conceptual framework. However, since this is the first study to specifically examine risk factors for HAPIs among critical-care patients with a CAPI, it is likely that other, as-yet-unexamined variables are also important predictors.
Discussion
This is the first study examining the incidence of HAPI development and associated factors among critical-care patients admitted to the hospital with a CAPI. Our findings indicate that patients with a CAPI are at increased risk for a HAPI, consistent with prior studies conducted among long-term-care patients17,18 and also with Coleman’s conceptual framework for pressure injury development, which posits that current pressure injury status is a major factor in risk for additional pressure injury development.9 However, the magnitude of the relationship was unexpectedly large: In our sample, patients admitted with a CAPI were four times more likely to develop a HAPI compared with patients who did not have a present CAPI on admission (28% vs. 7%, respectively).
Stage 1 pressure injuries are sometimes excluded from pressure injury studies due to concerns about the clinical relevance of that stage. In our study, nurses identified 65 Stage 1 CAPIs at admission. Among those, 41 (63%) did not progress to a more severe stage, whereas 24 (37%) Stage 1 CAPIs progressed to Stage 2 or worse. Among patients with a CAPI, nurses identified 22 Stage 1 HAPIs and half of those (n = 11) progressed to Stage 2 or worse. Our findings are consistent with a recent study that determined that approximately one-third of Stage 1 HAPIs (31%) progressed to Stage 2 or worse at discharge, underscoring the clinical relevance of Stage 1 pressure injuries.7
Total Braden Scale scores and subscale scores were not related to HAPI development among patients with a CAPI except in the case of the nutrition subscale, where lower risk scores were paradoxically associated with an increased risk for HAPI development. However, all of the patients with a CAPI were at high risk for pressure injury development according to the Braden Scale, with a mean total score of 11.5 (SD = 2.5). The seemingly paradoxical finding that lower-risk Braden Scale nutrition subscale scores were associated with HAPI development is consistent with results from a prior study that showed patients with lower risk Braden Scale nutrition subscale scores, as opposed to high risk, are at increased risk for pressure injury development.19 Moreover, the Braden Scale nutrition subscale score is considered a poor proxy for general nutrition status,20,21 and therefore it is necessary to avoid over-interpretation of the current finding.
Lower levels of serum albumin were an independent risk factor for pressure injury development (OR = 0.47, 95% CI = [0.25, 0.85], p = .02). Albumin is commonly implicated as a risk factor for pressure injury development among critical-care patients.22–24 In their theoretical schema, Coleman and colleagues proposed a causal pathway for pressure injury development in which decreased albumin is both a marker of poor nutrition and a contributor to poor perfusion due to decreased colloid osmotic pressure.9
Although excessively moist skin is an established risk factor for pressure injury development,25 in our study, moisture (measured in two ways: as part of the Braden Scale and also as part of the nursing skin assessment) was not significantly related to HAPI development among patients with a CAPI. Interestingly, in our analysis, excessive skin dryness was an independent risk factor for pressure injury development (OR = 2.6, 95% CI = [1.1, 6.22], p = .03). Ours is the first study of which we are aware that examined dry skin as a risk factor for HAPI development among critical-care patients (with or without a CAPI). However, dry skin has been identified as an independent risk factor for development of pressure injuries in hospitalized patients, and use of skin moisturizers to reduce risk of skin damage is endorsed by NPUAP and the Wound, Ostomy, and Continence Nurses Society.26–28
Advanced age is a common risk factor for HAPIs due to a combination of comorbidities associated with aging and aging-related changes to the skin, such as loss of elasticity.29–33 Among patients with a CAPI, however, no significant relationship appeared between advanced age and HAPI development. That being said, patients with a CAPI were older than patients without a CAPI (64 years +/– 15 years and 58 years +/– 17 years, respectively, t(181) = 5.1, p < .000). Additional study is needed to elucidate the relationship between age, CAPIs, and subsequent HAPI development.
Conclusion
Patients admitted to the ICU with a CAPI are often excluded from studies that examine risk factors for HAPIs, and therefore little is known about risk for a subsequent HAPI among patients with a CAPI. Results from this study show that patients with a CAPI are four times more likely than patients without CAPI to develop a subsequent HAPI (28% vs. 7%, respectively). Decreased serum albumin and excessively dry skin were independent risk factors for HAPIs. Patients with excessively dry skin may benefit from application of moisturizers.
Table 2.
Multivariate Analysis of Risk Factors for HAPI Development Among Patients With a CAPI
| Risk Factor | No HAPI (n = 120) |
HAPI (n = 47) |
β | SE | OR (95% CI) | p |
|---|---|---|---|---|---|---|
|
| ||||||
| Intercept | 0.76 | 0.80 | 2.13(0.45–10.84) | |||
| Albumin (mg/dl), M (SD) | 2.7 (0.7) | 2.4 (0.5) | –0.75 | 0.31 | 0.47(0.25–0.85) | 0.02 |
| Excessively dry skin, n (%) | 16 (13) | 14 (30) | 0.96 | 2.18 | 2.60(1.09–6.22) | 0.03 |
Note. HAPI = hospital-acquired pressure injury; CAPI = community-acquired pressure injury; SE = standard error; OR = odds ratio; CI= confidence interval; SD = standard deviation.
Key Points.
Patients with a CAPI were four times more likely than patients without CAPI to develop a subsequent HAPI (28% vs. 7%, respectively).
Decreased serum albumin and excessively dry skin were independent risk factors for HAPI development among patients with CAPI.
Nurses may consider skin moisturizer for patients with CAPI and excessively dry skin.
Disclosure Statement:
This publication was funded by a grant from the American Association of Critical Care Nurses and Sigma Theta Tau International.
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