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Abnormal thrombosis and neutrophil activation increases the risk of hospital-acquired sacral pressure injuries and morbidity in patients with COVID-19
Jatin Narang; Samreen Jatana; Andras K Ponti; Ryan Musich; Joshua Gallop; Angela H Wei; Sokhna Seck; Jessica Johnson; Lynne Kokoczka; Amy S Nowacki; Jeffrey D McBride; Eduardo Mireles-Cabodevila; Steven Gordon; Kevin Cooper; Anthony P Fernandez; Christine McDonald.
Affiliation
  • Jatin Narang; Cleveland Clinic Lerner College of Medicine, Case Western Reserve University
  • Samreen Jatana; Cleveland Clinic
  • Andras K Ponti; Cleveland Clinic
  • Ryan Musich; Cleveland Clinic
  • Joshua Gallop; Cleveland Clinic Lerner College of Medicine, Case Western Reserve University
  • Angela H Wei; Cleveland Clinic Lerner College of Medicine, Case Western Reserve University
  • Sokhna Seck; Cleveland Clinic Lerner College of Medicine, Case Western Reserve University
  • Jessica Johnson; Cleveland Clinic Lerner College of Medicine, Case Western Reserve University
  • Lynne Kokoczka; Cleveland Clinic
  • Amy S Nowacki; Cleveland Clinic
  • Jeffrey D McBride; The University of Oklahoma College of Medicine
  • Eduardo Mireles-Cabodevila; Cleveland Clinic
  • Steven Gordon; Cleveland Clinic
  • Kevin Cooper; University Hospitals Cleveland Medical Center
  • Anthony P Fernandez; Cleveland Clinic
  • Christine McDonald; Cleveland Clinic
Preprint in English | medRxiv | ID: ppmedrxiv-22277374
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 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 COVID-19(+) samples were enriched for innate immune responses, thrombosis, and neutrophil activation genes. SARS-CoV-2 viral transcripts were detected in skin tissue of COVID-19(+) patients with severe disease. 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. One Sentence SummarySARS-CoV-2-induced immune dysregulation contributes to pressure-induced sacral skin ulceration in hospitalized patients with severe COVID-19.
License
cc_by_nc_nd
Full text: Available Collection: Preprints Database: medRxiv Type of study: Observational study / Prognostic study Language: English Year: 2022 Document type: Preprint
Full text: Available Collection: Preprints Database: medRxiv Type of study: Observational study / Prognostic study Language: English Year: 2022 Document type: Preprint
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