51. Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients.
- Author
-
Narang J, Jatana S, Ponti AK, Musich R, Gallop J, Wei AH, Seck S, Johnson J, Kokoczka L, Nowacki AS, McBride JD, Mireles-Cabodevila E, Gordon S, Cooper K, Fernandez AP, and McDonald C
- Subjects
- Humans, SARS-CoV-2, Retrospective Studies, Ulcer, Neutrophil Activation, Incidence, Hospitals, COVID-19 epidemiology, Pressure Ulcer epidemiology, Thrombosis epidemiology, Thrombosis etiology
- Abstract
Hospitalized patients have an increased risk of developing hospital-acquired sacral pressure injury (HASPI). However, it is unknown whether SARS-CoV-2 infection affects HASPI development. To explore the role of SARS-CoV-2 infection in HASPI development, we conducted a single institution, multi-hospital, retrospective study of all patients hospitalized for ≥5 days from March 1, 2020 to December 31, 2020. Patient demographics, hospitalization information, ulcer characteristics, and 30-day-related morbidity were collected for all patients with HASPIs, and intact skin was collected from HASPI borders in a patient subset. We determined the incidence, disease course, and short-term morbidity of HASPIs in COVID-19(+) patients, and characterized the skin histopathology and tissue gene signatures associated with HASPIs in COVID-19 disease. COVID-19(+) patients had a 63% increased HASPI incidence rate, HASPIs of more severe ulcer stage (OR 2.0, p<0.001), and HASPIs more likely to require debridement (OR 3.1, p=0.04) compared to COVID-19(-) patients. Furthermore, COVID-19(+) patients with HASPIs had 2.2x increased odds of a more severe hospitalization course compared to COVID-19(+) patients without HASPIs. HASPI skin histology from COVID-19(+) patients predominantly showed thrombotic vasculopathy, with the number of thrombosed vessels being significantly greater than HASPIs from COVID-19(-) patients. Transcriptional signatures of a COVID-19(+) sample subset were enriched for innate immune responses, thrombosis, and neutrophil activation genes. Overall, our results suggest that immunologic dysregulation secondary to SARS-CoV-2 infection, including neutrophil dysfunction and abnormal thrombosis, may play a pathogenic role in development of HASPIs in patients with severe COVID-19., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Narang, Jatana, Ponti, Musich, Gallop, Wei, Seck, Johnson, Kokoczka, Nowacki, McBride, Mireles-Cabodevila, Gordon, Cooper, Fernandez and McDonald.)
- Published
- 2023
- Full Text
- View/download PDF