Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients

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-hospi...

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Main Authors: Jatin Narang, Samreen Jatana, András 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
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-03-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2023.1031336/full
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author Jatin Narang
Samreen Jatana
András K. Ponti
Ryan Musich
Joshua Gallop
Angela H. Wei
Sokhna Seck
Jessica Johnson
Lynne Kokoczka
Amy S. Nowacki
Amy S. Nowacki
Jeffrey D. McBride
Eduardo Mireles-Cabodevila
Steven Gordon
Kevin Cooper
Anthony P. Fernandez
Anthony P. Fernandez
Christine McDonald
Christine McDonald
Christine McDonald
author_facet Jatin Narang
Samreen Jatana
András K. Ponti
Ryan Musich
Joshua Gallop
Angela H. Wei
Sokhna Seck
Jessica Johnson
Lynne Kokoczka
Amy S. Nowacki
Amy S. Nowacki
Jeffrey D. McBride
Eduardo Mireles-Cabodevila
Steven Gordon
Kevin Cooper
Anthony P. Fernandez
Anthony P. Fernandez
Christine McDonald
Christine McDonald
Christine McDonald
author_sort Jatin Narang
collection DOAJ
description 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.
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spelling doaj.art-dfe99aa36b6c435987dc627662067f1b2023-03-21T04:42:02ZengFrontiers Media S.A.Frontiers in Immunology1664-32242023-03-011410.3389/fimmu.2023.10313361031336Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patientsJatin Narang0Samreen Jatana1András K. Ponti2Ryan Musich3Joshua Gallop4Angela H. Wei5Sokhna Seck6Jessica Johnson7Lynne Kokoczka8Amy S. Nowacki9Amy S. Nowacki10Jeffrey D. McBride11Eduardo Mireles-Cabodevila12Steven Gordon13Kevin Cooper14Anthony P. Fernandez15Anthony P. Fernandez16Christine McDonald17Christine McDonald18Christine McDonald19Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United StatesDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United StatesDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United StatesDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United StatesCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United StatesCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United StatesCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United StatesCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United StatesMedical Intensive Care Unit, Cleveland Clinic, Cleveland, OH, United StatesCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United StatesDepartment of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, United StatesDepartment of Dermatology, The University of Oklahoma College of Medicine, Oklahoma City, OK, United StatesMedical Intensive Care Unit, Cleveland Clinic, Cleveland, OH, United StatesDepartment of Infectious Disease, Cleveland Clinic, Cleveland, OH, United StatesDepartment of Dermatology, University Hospitals Cleveland Medical Center, Cleveland, OH, United StatesDepartment of Dermatology, Dermatology and Plastic Surgery Institute, Cleveland Clinic, Cleveland, OH, United StatesDepartment of Anatomic Pathology, Pathology and Lab Medicine, Cleveland Clinic, Cleveland, OH, United StatesCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United StatesDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United States0Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United StatesHospitalized 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.https://www.frontiersin.org/articles/10.3389/fimmu.2023.1031336/fullCOVID-19SARS-CoV-2sacral ulcerpressure ulcerthrombotic vasculopathythrombosis
spellingShingle Jatin Narang
Samreen Jatana
András K. Ponti
Ryan Musich
Joshua Gallop
Angela H. Wei
Sokhna Seck
Jessica Johnson
Lynne Kokoczka
Amy S. Nowacki
Amy S. Nowacki
Jeffrey D. McBride
Eduardo Mireles-Cabodevila
Steven Gordon
Kevin Cooper
Anthony P. Fernandez
Anthony P. Fernandez
Christine McDonald
Christine McDonald
Christine McDonald
Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients
Frontiers in Immunology
COVID-19
SARS-CoV-2
sacral ulcer
pressure ulcer
thrombotic vasculopathy
thrombosis
title Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients
title_full Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients
title_fullStr Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients
title_full_unstemmed Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients
title_short Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients
title_sort abnormal thrombosis and neutrophil activation increase hospital acquired sacral pressure injuries and morbidity in covid 19 patients
topic COVID-19
SARS-CoV-2
sacral ulcer
pressure ulcer
thrombotic vasculopathy
thrombosis
url https://www.frontiersin.org/articles/10.3389/fimmu.2023.1031336/full
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