Abstract
Purpose:
The purpose of this study was to identify factors associated with second, subsequent, hospital-acquired pressure injury (HAPrI) formation among surgical and cardiovascular surgical intensive-care-unit (SICU and CVICU) patients with an initial HAPrI.
Methods:
This was a retrospective cohort study. Patients admitted to the SICU or CVICU at a Level 1 trauma center and academic medical center in the western United States between 2014 and 2018 were eligible for the study. Inclusion criteria were development of a HAPrI stage 2 or above, age ≥18, the presence of mechanical ventilation for at least 24 hours, repositioning at least every 2 hours, and documentation of a risk-based HAPrI-prevention plan. The outcome measure was development of a second, subsequent HAPrI ≥ stage 2. Potential predictor variables included demographic factors, shock, Charleston comorbidity score, blood gas and laboratory values, surgical factors, vasopressor infusions, levels of sedation or agitation, Braden Scale scores, and nursing skin assessment data. Independent risk factors for subsequent HAPrI formation were identified using logistic regression analysis.
Results:
The final sample consisted of 226 patients. Among those, 77 patients (34%) developed a second HAPrI. Independent risk factors for subsequent HAPrI formation were decreased hemoglobin (OR= 0.71, 95% CI= 0.53–0.92, p<0.000), Vasopressin infusion (OR= 2.20, 95% CI= 1.17–4.26, p=0.02), and longer length of stay in the ICU (OR= 1.01, 95% CI= 1.00–1.02, p=0.009).
Conclusion:
Patients with a HAPrI are at high risk for second, subsequent HAPrI development. Anemia, Vasopressin infusion, and longer ICU stays are independent risk factors for subsequent HAPrI formation.
Keywords: Pressure Ulcer, Pressure Injury, Critical Care
Hospital-acquired pressure injuries (HAPrIs) disproportionately affect critical care patients,1 with surgical patients2 at the highest risk. Surgical intensive care unit (SICU) and cardiovascular intensive care unit (CVICU) patients who undergo mechanical ventilation are particularly vulnerable to HAPrI,3 likely due to a combination of altered oxygenation and the severe illness that require mechanical ventilation.4–6 High-risk patients who develop a single HAPrI are likely at risk for additional, subsequent HAPrIs; however, the proportion of patients who develop a subsequent HAPrI, and the associated risk factors, are not known. For patients who have a HAPrI already and are mechanically ventilated, it is important for planning care delivery to understand their risk factors for formation of a second HAPrI.7 Risk factors may be used in the future to develop tailored PrI prevention interventions.
The purpose of this study was to describe the risk profiles and identify the factors associated with subsequent hospital-acquired pressure injury formation for surgical and cardiovascular intensive-care-unit patients who are mechanically ventilated.
Methods
Design
This study employed a retrospective cohort study design using electronic health record (EHR) data to identify mechanically ventilated SICU and CVICU patients with HAPrI and determine the characteristics of patients who formed an additional HAPrI. This study had institutional review board approval (IRB # IRB_00111380).
Setting and Sample
Patients admitted to the SICU or CVICU at a Level 1 trauma center and academic medical center in the western United States between 2014 and 2018 were eligible for the study. Inclusion criteria were development of a HAPrI (defined as a pressure injury stage 2 or above, identified at least 24 hours after admission), age ≥18, and the presence of mechanical ventilation for at least 24 hours. Twenty-four hours of mechanical ventilation was chosen to avoid including patients who were briefly mechanically ventilated for procedures, instead focusing on patients whose medical condition required mechanical ventilation. Included patients’ care was consistent with our facility’s skin-care protocol: repositioning every 2 hours or more often and documentation (either initiation or continuation) of a risk-based HAPrI-prevention plan within 24 hours of the first HAPrI detection. Patients with a community-acquired PrI were included if they developed a separate HAPrI at least 24 hours later. Exclusion criteria were pediatric age (<18 years), the absence of at least one HAPrI, <24 hours of mechanical ventilation, repositioning intervals >2 hours apart, and the lack of a risk-based HAPrI care plan in the EHR.
Data Collection and Study Procedures
Data were extracted using a query of our institution’s critical-care datamart using the timeframe between each patient’s first HAPrI detection and ICU discharge. A practicing ICU nurse familiar with the EPIC© EHR system validated 10% of the data obtained in the query in EPIC© to ensure accuracy, including date and time stamps; data were considered valid when 100% of the data points in the query matched the information in EPIC©.
Measures
In concert with the 2019 NPIAP international guidelines, HAPrIs were staged 2–4, DTI, or unstageable.8 We did not include Stage 1 HAPrIs due to concerns expressed about the clinical relevance, given their rapid healing rate.9 In cases where the stage was ambiguous or where the emergence of a HAPrI might have been confused with another source of injury, a certified wound nurse made the final decision. The outcome variable was the development of a second HAPrI in a new anatomic location. HAPrIs on a new anatomic location were chosen to avoid confusion about satellite injuries that occurred near the first injury and were related to the first injury.
Potential predictor variables were identified using a systematic review of the literature10 that was organized around Coleman and colleagues’ conceptual model for PrI etiology.4 Because no studies have identified factors associated with second, subsequent HAPrIs after a first HAPrI, the systematic review was focused on factors associated with first HAPrI. Predictor variables included in our analysis were age,5,10,11 demographic factors,12 diabetes,13 shock (defined as an ICD diagnosis of shock),14 Charleston comorbidity index score, blood gas15 and laboratory values,13 surgical time,16 vasopressor infusion,13,17 levels of sedation or agitation,6,18 Braden Scale scores,19 and data from nursing skin assessments related to fragile skin and edema.20,21
Analysis
To identify factors associated with additional, subsequent HAPrIs, univariate analysis was conducted using a Mann-Whitney U test for ordinal variables and a t test or Mann-Whitney U test for parametric versus nonparametric continuous variables, and a Pearson chi-square or Fisher exact tests, as appropriate, for categorical variables. Next, a logistic regression analysis was conducted. Before building the model, the collinearity was assessed using a Pearson correlation matrix and limited the model to variables with correlations <.70.22 A model fit was assessed via McFadden’s Pseudo R square23 and reported the area under the receiver operating characteristic (ROC) curve.22
Results
Sample
A total of 241 adult SICU and CVICU patients with a HAPrI and >24 hours of mechanical ventilation were identified in the query. Eight of those patients were excluded from the analysis because greater than 2-hour repositioning was documented and seven were excluded because a risk-based HAPrI-prevention plan was not recorded, for a final sample of 226 patients. The characteristics of the sample are presented in Table 1.
Table 1:
Potential Predictor Variables and Second Hospital-Acquired Injury Development
| Variable | All Patients N = 226 |
Patients with Only One HAPrI n = 149 |
Patients with a Second HAPrI n = 77 |
p Value | % of Missing Data |
|---|---|---|---|---|---|
| DEMOGRAPHIC DATA | |||||
| Age, M (SD) | 58 (15) | 58 (15) | 59 (14) | T (163) = –0.44 p = .66 |
0% |
| Sex, male, n (%) | 149 (66%) | 99 (66%) | 50 (64%) |
X2 (1, N = 226) = 0.006 p = .94 |
0% |
| Race, White, n (%) | 179 (79%) | 120 (81%) | 59 (77%) |
X2 (6, N = 226) = 1.56 p = .96 |
0% |
| Ethnicity, non-Hispanic, n (%) | 201 (89) | 132 (89) | 67 (87) |
X2 (1, N = 226) = 0.36 p = .83 |
0% |
| Length of Hospital stay (days), M (SD) | 32 (20) | 29 (19) | 40 (21) | T (139) = –4.08 p < .000 |
0% |
| Length of ICU stay (days), M (SD) | 22 (18) | 18 (14) | 31 (22) | T (108) = –4.57 p < .000 |
0% |
| Died in the hospital, n (%) | 65 (29%) | 40 (27%) | 25 (32%) |
X2 (1, N = 226) = 0.53 p = .46 |
0% |
| LABORATORY DATA | |||||
| Maximum lactate (mg/dL), M (SD) | 4.5 (4.8) | 3.8 (4.3) | 5.8 (5.5) | T(127) = –2.74 p = .006 |
1% |
| Maximum serum creatinine (mg/dL), M (SD) | 2.9 (2.1) | 2.8 (2.1) | 3.1 (2.0) | T(160) = –0.71 p = .48 |
1% |
| Maximum blood glucose (mg/dL), M (SD) | 270 (190) | 249 (185) | 310 (195) | T(147) = –2.25 p = .02 |
0% |
| Minimum hemoglobin (mg/dL), M (SD) | 6.9 (1.4) | 7.2 (1.5) | 6.4 (1.1) | T(200) = –4.41 p < .000 |
2% |
| Minimum Albumin (mg/dL), M (SD) | 2.45 (0.53) | 2.55 (0.54) | 2.48 (0.51) | T(153) = –0.50 p = 0.61 |
18% |
| Minimum arterial PaO2a mmHg, M (SD) | 54 (16) | 60 (17) | 51 (15) | T(137) = –3.45 p < .000 |
0% |
| Minimum arterial pH, M (SD) | 7.29 (0.12) | 7.32 (0.11) | 7.24 (0.12) | T(142) = 4.73 p < .000 |
0% |
| Maximum arterial PaCO2b, M (SD) | 52 (28) | 44 (28) | 56 (28) | T(151) = 3.14 p = .001 |
0% |
| SKIN STATUS | |||||
| Thin epidermis/subcutaneous tissue loss, n (%) | 50 (22%) | 34 (23%) | 16 (21%) |
X2 (1, N = 226) = 0.006 p = .94 |
0% |
| Edema n (%) | 104 (46%) | 69 (46%) | 35 (45%) |
X2 (1, N=226) = 0.04 p = .83 |
0% |
| SURGICAL DURATION | |||||
| Longest single surgery, hours, M (SD) | 1.9 (2.3) | 1.5 (2.0) | 2.5 (2.6) | T(127) = –2.87 p = .004 |
0% |
| VASOPRESSOR | |||||
| Dopamine infusion, n (%) | 18 (8%) | 9 (6%) | 9 (12%) |
X2 (1, N = 226) = 0.04 p = .82 |
0% |
| Epinephrine infusion, n (%) | 104 (46%) | 64 (43%) | 40 (52%) |
X2 (1, N = 226) = 1.31 p = .25 |
0% |
| Norepinephrine infusion, n (%) | 135 (60%) | 84 (56%) | 51 (66%) |
X2 (1, N = 226) = 1.67 p = .19 |
0% |
| Phenylephrine infusion, n (%) | 15 (7%) | 9 (6%) | 6 (8%) |
X2 (1, N = 226) = 0.05 p = .82 |
0% |
| Vasopressin infusion, n (%) | 126 (56%) | 71 (47%) | 55 (71%) |
X2 (1, N = 226) = 10.69 p = .001 |
0% |
| OTHER POTENTIAL PREDICTORS | |||||
| Minimum Braden Scale score M (SD) | 11.7 (2.5) | 11.8 (2.5) | 11.4 (2.5) | T(186) = 0.69 p = .48 |
0% |
| Minimum Rikerc score, M (SD) | 1.95 (1.18) | 2.06 (1.21) | 1.75 (1.10) | T(166) = 1.93 p = 0.05 |
2% |
| Admission body mass index (kg/m2), M (SD) | 31.6 (11.9) | 31.6 (12.7) | 31.5 (10.2) | T(183) = 0.04 p = 0.96 |
1% |
| Comorbid diabetes, n (%) | 102 (45%) | 68 (46%) | 34 (44%) |
X2 (1, N = 226) = 0.05 p = .94 |
0% |
| Charleston Comorbidity Index score, M (SD) | 4.26 (2.93) | 4.19 (2.95) | 4.39 (2.90) | T(156) = 0.49 p = .61 |
0% |
| Shock, n (%) | 197 (88%) | 125 (84%) | 72 (94%) |
X2 (1, N = 226) = 3.37 p = .07 |
0% |
Note: HAPrI = hospital-acquired pressure injury
Partial pressure of oxygen in the blood
Partial pressure of carbon dioxide in the blood
Riker sedation and agitation scale
Second, Subsequent HAPrI Outcome
Seventy-seven patients (34%) developed a second HAPrI. Stages were as follows: 48 (62%) Stage 2, 3 (4%) Stage 3, 22 (29%) DTI, and 4 (5%) unstageable.
Risk Factors for Second, Subsequent HAPrIs
Bivariate relationships between potential predictor variables and subsequent HAPrI development are presented in Table 1. On multivariate analysis, decreased hemoglobin, vasopressin infusion, and longer length of stay in the ICU were independent risk factors for a subsequent HAPrI (Table 2). McFaddens pseudo-R square was 0.18, indicating good model fit,23 and the area under the ROC curve was 0.72, indicating fair discrimination.22
Table 2.
Multivariate Analysis of Risk Factors for the Development of a Subsequent Hospital-Acquired Pressure Injury (HAPrI) Among Patients with an Initial HAPrI
| Risk Factor | One HAPrI (n = 149) |
Two HAPrIs (n = 77) |
β | SE | OR (95% CI) | p |
|---|---|---|---|---|---|---|
|
| ||||||
| Intercept | 0.58 | 1.06 | 1.79 (0.22–15.01) | .58 | ||
| Hemoglobin (g/dl), M (SD) | 7.2 (1.5) | 6.4 (1.1) | 0.14 | 0.14 | 0.71 (0.53–0.92) | <.000 |
| Vasopressin, n (%) | 71 (47%) | 55 (71%) | 0.33 | 0.33 | 2.20 (1.17–4.26) | .02 |
| Length of ICU stay, M (SD) | 18 (14) | 31 (22) | 0.04 | 0.01 | 1.01 (1.00–1.02) | .009 |
Note. SE = standard error; OR = odds ratio; CI = confidence interval; M = Mean; SD = standard deviation.
AROC = 0.72
McFaddens psudeo R2 = 0.18
Discussion
This is the first study to examine associated risk factors for formation of a second HAPrI using a cohort of ICU patients. Results showed that patients with HAPrIs were at high risk for subsequent HAPrI development, despite documented q2 hour repositioning and the presence of a risk-based prevention plan. This finding is consistent with Coleman’s conceptual framework for PrI development, which posits that current PrI status is a risk factor for additional PrI development.4 Independent risk factors for second HAPrI were lower levels of hemoglobin, vasopressin infusion, and longer length of stay in the ICU.
While substantial evidence supports the efficacy of HAPrI-prevention programs in reducing PrI,24,25 most researchers use HAPrI development as the study outcome and do not address the possibility of subsequent HAPrI formation. This is unfortunate, because patients with a HAPrI have an increased vulnerability for additional HAPrI formation, as evidenced by the current study, in which over a third of the patients (34%) went on to develop a second HAPrI. Critical care healthcare teams should be aware that patients with an existing HAPrI are at high risk for additional HAPrIs and require a tailored HAPrI-prevention approach to address modifiable risk factors and, as possible, to mitigate the effects of nonmodifiable risk factors. A one-size-fits-all approach does not appear to be working.
Anemia, or decreased hemoglobin, is a potentially modifiable independent risk factor for subsequent HAPrIs. In the current study, patients with two or more HAPrIs had significantly lower minimum hemoglobin values than patients with only one HAPrI (7.2 g/dl, SD = 1.5, and 6.4 g/dl, SD = 1.1, respectively). Adequate hemoglobin is essential, because hemoglobin represents the body’s oxygen-carrying capacity, which is necessary for oxygen delivery to skin and underlying tissue.26,27 So-called “permissive anemia” is increasingly used in the critical care environment to avoid negative effects associated with blood transfusions.28 However, it is important to consider ischemia-related complications, including HAPrIs, when determining the risks and benefits of blood transufusion.29
In the current study, patients who received Vasopressin were more than twice as likely as patients who did not receive Vasopressin to develop a second HAPrI (OR = 2.20, SD = 1.17–4.26). Vasopressin is a second-line vasopressor that is commonly used in shock states, including septic shock. The finding that vasopressin is associated with increased second HAPrI risk is consistent with prior studies implicating vasopressors and other alterations in perfusion (delivery of oxygen-rich blood) in initial HAPrI development.6,10,17,30,31 The risk associated with vasopressin infusion is likely related to both the tissue-level constricting effects of vasopressor drugs (including the first-line drugs that usually accompany Vasopressin, such as norepinephrine) and the underlying severity of illness and shock state that necessitated vasopressor infusion. Although vasopressors are medically essential and therefore not a modifiable risk factor, use of vasopressors may be used to identify highest-risk patients for maximal preventive intervention.
Patients who developed second HAPrIs had longer lengths of ICU stay than patients who developed only one HAPrI, although the large standard deviations show considerable variability (31 days, SD = 22, and 18 days, SD = 14, respectively; OR = 1.01, 95% confidence interval = 1.00–1.02). Longer length of stay is commonly implicated in HAPrI risk and likely represents both longer durations of exposure and increased severity of illness.5,14,32
Limitations
Results from the current study are from a relatively small sample and a single site, and may not be generalizable to the broader ICU population. We did not differentiate avoidable versus unavoidable HAPrI because prior studies show information—particularly repositioning information—recorded in the EHR may not match real clinical events.33 We also did not differentiate medical-device-related pressure injuries.
Conclusions
The results of this study show patients with a HAPrI to be at high risk in developing a second HAPrI despite the presence of a risk-based PrI-prevention plan, including turning every 2 hours. Additional independent risk factors for a second HAPrI were the presence of anemia, vasopressin therapy, and longer ICU admission, depicting an overall high acuity level. ICU patients who develop an initial HAPrI in the presence of anemia, vasopressin therapy, and extended ICU admissions are at greater risk for developing additional, subsequent HAPrIs. Further research exploring preventive strategies targeting the acute ICU patient with a targeted risk profile centered on HAPrI history is needed.
Financial support:
American Association of Critical Care Nurses Critical Care Grant
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