Hospital-Acquired Pressure Injuries and Acute Skin Failure in Critical Care: A Case-Control Study.

PURPOSE: The purpose of this study was to examine clinical characteristics and risk factors for critically ill patients who develop pressure injuries and identify the proportion of validated unavoidable pressure injuries associated with the proposed risk factors for acute skin failure (ASF). DESIGN: Retrospective case-control comparative study. SUBJECTS AND SETTING: The sample comprised adult critically ill participants hospitalized in critical care units such as surgical, trauma, cardiovascular surgical, cardiac, neuro, and medical intensive care and corresponding progressive care units in 5 acute care hospitals within a large Midwestern academic/teaching healthcare system. Participants who developed hospital-acquired pressure injuries (HAPIs) and patients without HAPIs (controls) were included. METHODS: A secondary analysis of data from a previous study with HAPIs and matching data for the control sample without HAPIs were obtained from the electronic health record. Descriptive and multivariate logistic regression analyses were conducted. RESULTS: The sample comprised 475 participants; 165 experienced a HAPI and acted as cases, whereas the remaining 310 acted as controls. Acute Physiology and Chronic Health Evaluation (APACHE II) mean score (23.8, 8.7%; P < .001), mortality (n = 45, 27.3%; P = .002), history of liver disease (n = 28, 17%; P < .001), and unintentional loss of 10 lb or more in 1 month (n = 20, 12%; P = .002) were higher in the HAPI group. Multivariate logistic regression analysis identified participants with respiratory failure (odds ratio [OR] = 3.00; 95% confidence interval [CI], 1.27-7.08; P = .012), renal failure (OR = 7.48; 95% CI, 3.49-16.01; P < .001), cardiac failure (OR = 4.50; 95% CI, 1.76-11.51; P = .002), severe anemia (OR = 10.89; 95% CI, 3.59-33.00; P < .001), any type of sepsis (OR = 3.15; 95% CI, 1.44-6.90; P = .004), and moisture documentation (OR = 11.89; 95% CI, 5.27-26.81; P <.001) were more likely to develop a HAPI. No differences between unavoidable HAPI, avoidable HAPI, or the control group were identified based on the proposed ASF risk factors. CONCLUSION: This study provides important information regarding avoidable and unavoidable HAPIs and ASF. Key clinical characteristics and risk factors, such as patient acuity, organ failure, tissue perfusion, sepsis, and history of prior pressure injury, are associated with avoidable and unavoidable HAPI development. In addition, we were unable to support a relationship between unavoidable HAPIs and the proposed risk factors for ASF. Unavoidability of HAPIs rests with the documentation of appropriate interventions and not necessarily with the identification of clinical risk factors.

Hospital-Acquired Pressure Injuries in Critical and Progressive Care: Avoidable Versus Unavoidable.

BACKGROUND: Despite prevention strategies, hospital-acquired pressure injuries (HAPIs) continue to occur, especially in critical care, raising the question whether some pressure injuries are unavoidable. OBJECTIVES: To determine the proportion of HAPIs among patients in critical and progressive care units that are unavoidable, and to identify risk factors that differentiate avoidable from unavoidable HAPIs. METHODS: This study used a descriptive retrospective design. Data collected included demographic information, Braden Scale scores, clinical risk factors, and preventive interventions. The Pressure Ulcer Prevention Inventory was used to categorize HAPIs as avoidable or unavoidable. RESULTS: A total of 165 patients participated in the study. Sixty-seven HAPIs (41%) were unavoidable. Participants who had congestive heart failure (odds ratio [OR], 0.22; 95% CI, 0.06-0.76; P = .02), were chemically sedated (OR, 0.38; 95% CI, 0.20-0.72; P = .003), had systolic blood pressure below 90 mm Hg (OR, 0.52; 95% CI, 0.27-0.99; P = .047), and received at least 1 vasopressor (OR, 0.44; 95% CI, 0.23-0.86; P = .01) were less likely to have an unavoidable HAPI. Those with bowel management devices were more likely to have an unavoidable HAPI (OR, 2.19; 95% CI, 1.02-4.71; P = .04). When length of stay was incorporated into the regression model, for each 1-day increase in stay, the odds of an unavoidable pressure injury developing increased by 4% (OR, 1.04; 95% CI, 1.002-1.08; P = .04). Participants who had a previous pressure injury were 5 times more likely to have an unavoidable HAPI (OR, 5.27; 95% CI, 1.20-23.15; P = .03). CONCLUSIONS: Unavoidable HAPIs do occur; moreover, when preventive interventions are not documented and implemented appropriately, avoidable HAPIs occur.

Can the identification of an idle line facilitate its removal? A comparison between a proposed guideline and clinical practice.

BACKGROUND: There are 250,000 cases of central line-associated blood stream infections in the United States annually, some of which may be prevented by the removal of lines that are no longer needed. OBJECTIVE: To test the performance of criteria to identify an idle line as a guideline to facilitate its removal. METHODS: Patients with central lines on the wards were identified. Criteria for justified use were defined. If none were met, the line was considered "idle." We proposed the guideline that a line may be removed the day following the first idle day and compared actual practice with our proposed guideline. RESULTS: One hundred twenty-six lines in 126 patients were observed. Eighty-three (65.9%) were peripherally inserted central catheters. Twenty-seven percent (n= 34) were placed for antibiotics. Seventy-six patients had lines removed prior to discharge. In these patients, the line was in place for 522 days, of which 32.7% were idle. The most common reasons to justify the line included parenteral antibiotics and meeting systemic inflammatory response (SIRS) criteria. In 11 (14.5%) patients, the line was removed prior to the proposed guideline. Most (n = 36, 47.4%) line removals were observed to be in accordance with our guideline. In another 29 (38.2%), line removal was delayed compared to our guideline. CONCLUSIONS: Idle days are common. Central line days may be reduced by the consistent daily reevaluation of a line's justification using defined criteria. The practice of routine central line placement for prolonged antibiotics and the inclusion of SIRS criteria to justify the line may need to be reevaluated. Journal of Hospital Medicine 2016;11:489-493. © 2016 Society of Hospital Medicine.

Unavoidable Pressure Ulcers: Development and Testing of the Indiana University Health Pressure Ulcer Prevention Inventory.

PURPOSE: Despite prevention strategies, hospital-acquired pressure ulcers (HAPUs) continue to occur in the acute care setting. The purpose of this study was to develop an operational definition of and an instrument for identifying avoidable/unavoidable HAPUs in the acute care setting. METHODS: The Indiana University Health Pressure Ulcer Prevention Inventory (PUPI) was developed and psychometric testing was performed. A retrospective pilot study of 31 adult hospitalized patients with an HAPU was conducted using the PUPI. RESULTS: Overall content validity index of 0.99 and individual item content validity index scores (0.9-1.0) demonstrated excellent content validity. Acceptable PUPI criterion validity was demonstrated with no statistically significant differences between wound specialists' and other panel experts' scoring. Construct validity findings were acceptable with no statistically significant differences among avoidable or unavoidable HAPU patients and their Braden Scale total scores. Interrater reliability was acceptable with perfect agreement on the total PUPI score between raters (κ = 1.0; P = .025). Raters were in total agreement 93% (242/260) of the time on all 12 individual PUPI items. No risk factors were found to be significantly associated with unavoidable HAPUs. CONCLUSION: An operational definition of and an instrument for identifying avoidable/unavoidable HAPUs in the acute care setting were developed and tested. The instrument provides an objective and structured method for identifying avoidable/unavoidable HAPUs. The PUPI provides an additional method that could be used in root-cause analyses and when reporting adverse pressure ulcer events.

The leukocyte integrin gene CD11d is repressed by gut-enriched Kruppel-like factor 4 in myeloid cells.

The myeloid-specific leukocyte integrin CD11d encodes the alphaD subunit for the alphaDbeta2 receptor. A yeast one-hybrid screen showed that a longer isoform of gut-enriched Kruppel-like factor 4 (GKLF) we term GKLFa interacts with the CD11d promoter. Purified GST-GKLFa protein was shown to bind within the -61 to -44 region that overlaps a binding site for the CD11d transcriptional activators Sp1 and transforming growth factor beta-inducible early gene-1 (TIEG1). Transfection of GKLF/GKLFa in myeloid cells reduced CD11d promoter activity, whereas, down-regulation of GKLF/GKLFa with small interfering RNAs led to up-regulation of CD11d expression. Differentiation of myeloid cells with phorbol ester led to activation of the CD11d promoter and reduced occupancy of the promoter by GKLF/GKLFa but an increased occupancy by TIEG1 in vivo. Binding of GKLF/GKLFa, Sp1, and TIEG1 to the CD11d promoter in vivo is dependent on their zinc finger DNA binding domains. GKLFa physically associates with the histone deacetylases (HDAC) 1 and 2, and both HDACs are bound to the CD11d promoter in vivo but released after exposure of myeloid cells to phorbol ester suggesting that GKLF/GKLFa recruits HDACs to effect repression.

The zinc finger transcription factor transforming growth factor beta-inducible early gene-1 confers myeloid-specific activation of the leukocyte integrin CD11d promoter.

CD11d encodes the alpha(D) subunit for a leukocyte integrin that is expressed on myeloid cells. In this study we show that the -100 to -20 region of the CD11d promoter confers myeloid-specific activation of the CD11d promoter. Transforming growth factor beta-inducible early gene-1 (TIEG1) was isolated in a yeast one-hybrid screen using the -100 to -20 region of the CD11d promoter as bait. Purified GST.TIEG1 protein was able to bind within the -61 to -45 region that overlaps a shorter binding site for Sp1. Transient overexpression of TIEG1 activated the CD11d promoter specifically in myeloid cells, whereas, down-regulation of TIEG1 with small interfering TIEG1 RNA also down-regulated expression of CD11d. In vivo, TIEG1 does not physically interact with Sp1. Cotransfection and electrophoretic mobility shift analyses of TIEG1, Sp1, and Sp3 revealed that TIEG1 competes with these Sp proteins for binding to overlapping sites in the CD11d promoter. Although TIEG1 and Sp1 are ubiquitously expressed in myeloid and non-myeloid cells, chromatin immunoprecipitation assays revealed differential occupancy of the CD11d promoter by these factors. In undifferentiated myeloid and non-myeloid cells, occupancy of the CD11d promoter by TIEG1 is similar. Upon differentiation of myeloid cells and subsequent up-regulation of CD11d expression, TIEG1 occupancy increases. In contrast, occupancy by TIEG1 remains low in non-myeloid cells exposed to phorbol ester. We propose that up-regulation of CD11d expression following differentiation of myeloid cells is mediated through increased binding of TIEG1 binding to the CD11d promoter.