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Microcirculatory, Endothelial, and Inflammatory Responses in Critically Ill Patients With COVID-19 Are Distinct From Those Seen in Septic Shock: A Case Control Study

Research output: Contribution to journalArticlepeer-review

Sam D. Hutchings, James Watchorn, Francesca Trovato, Salvatore Napoli, Salma F. Mujib, Philip Hopkins, Mark McPhail

Original languageEnglish
Pages (from-to)752-758
Number of pages7
JournalShock (Augusta, Ga.)
Issue number6
Published1 Jun 2021

Bibliographical note

Publisher Copyright: Copyright © 2020 by the Shock Society. Copyright: This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine

King's Authors


ABSTRACT: Critically ill patients with COVID-19 infection frequently exhibit a hyperinflammatory response and develop organ failures; however, the underlying mechanisms are unclear. We investigated the microcirculatory, endothelial, and inflammatory responses in critically ill COVID-19 patients and compared them to a group of patients with septic shock in a prospective observational case control study. Thirty critically ill patients with COVID-19 were compared to 33 patients with septic shock.Measurements of sublingual microcirculatory flow using Incident Dark Field video-microscopy and serial measurements of IL-6 and Syndecan-1 levels were performed. COVID-19 patients had significantly less vasoactive drug requirement and lower plasma lactate than those with septic shock. Microcirculatory flow was significantly worse in septic patients than those with COVID-19 (MFI 2.6 vs 2.9 p 0.02, PPV 88 vs 97% P < 0.001). IL-6 was higher in patients with septic shock than COVID-19 (1653 vs 253 pg/mL, P 0.03). IL-6 levels in COVID 19 patients were not elevated compared to healthy controls except on the day of ICU admission. Syndecan-1 levels were not different between the two pathological groups. Compared to patients with undifferentiated septic shock an overt shock state with tissue hypoperfusion does not appear typical of COVID-19 infection. There was no evidence of significant sublingual microcirculatory impairment, widespread endothelial injury or marked inflammatory cytokine release in this group of critically ill COVID-19 patients.

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