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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

25 Pages Posted: 6 Aug 2020

See all articles by Sam Hutchings

Sam Hutchings

King’s College London - School of Immunology and Microbial Sciences

James Watchorn

Department of Inflammation Biology, School of Immunology and Microbial Sciences,Faculty of Life Sciences and Medicine, King’s College London

Francesca Trovato

Department of Inflammation Biology, School of Immunology and Microbial Sciences,Faculty of Life Sciences and Medicine, King’s College London

Salvatore Napoli

Department of Inflammation Biology, School of Immunology and Microbial Sciences,Faculty of Life Sciences and Medicine, King’s College London

Salma F Mujib

Institute of Liver Studies, King’s College Hospital, London

Philip Hopkins

Centre for Human & Applied Physiological Sciences, School of Basic & Medical Biosciences, Faculty of Life Sciences & Medicine, King's College, London

Mark McPhail

Department of Inflammation Biology, School of Immunology and Microbial Sciences,Faculty of Life Sciences and Medicine, King’s College London

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Abstract

Background: 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.

Methods: Prospective observational case control study. 30 patients with COVID-19 admitted to the ICUs of a tertiary hospital were compared to 33 patients with septic shock. Measurements of sublingual microcirculatory flow were performed using Incident Dark Field (IDF) video-microscopy and serial measurements of IL-6 and Syndecan-1 levels were made.

Findings: 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 v 2.9 p 0.02, PPV 88 v 97% p <0.001). IL-6 was higher in patients with septic shock than COVID-19 (1653 v 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 2 pathological groups.

Interpretation: Compared to patients with bacterial sepsis 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. COVID-19 may have a different pathogenesis to bacterial induced septic shock.

Funding Statement: Royal Centre for Defence Medicine (UK Ministry of Defence), 2019; European Society of Intensive Care Medicine Point of Care Ultrasound award, 2019.

Declaration of Interests: All authors declare that they have no conflicts of interest.

Ethics Approval Statement: Yorkshire and Humber (Leeds East) and North West Research Ethics committees (18/YH/0371and 19/NW/0750).

Keywords: COVID-19; septic shock; microcirculation; cytokine; inflammation; endothelium

Suggested Citation

Hutchings, Sam and Watchorn, James and Trovato, Francesca and Napoli, Salvatore and Mujib, Salma F and Hopkins, Philip and McPhail, Mark, Microcirculatory, Endothelial and Inflammatory Responses in Critically Ill Patients with COVID-19 Are Distinct from Those Seen in Septic Shock: A Case Control Study (6/10/2020). Available at SSRN: https://ssrn.com/abstract=3627342 or http://dx.doi.org/10.2139/ssrn.3627342

Sam Hutchings (Contact Author)

King’s College London - School of Immunology and Microbial Sciences ( email )

United Kingdom

James Watchorn

Department of Inflammation Biology, School of Immunology and Microbial Sciences,Faculty of Life Sciences and Medicine, King’s College London

Francesca Trovato

Department of Inflammation Biology, School of Immunology and Microbial Sciences,Faculty of Life Sciences and Medicine, King’s College London

Salvatore Napoli

Department of Inflammation Biology, School of Immunology and Microbial Sciences,Faculty of Life Sciences and Medicine, King’s College London

Salma F Mujib

Institute of Liver Studies, King’s College Hospital, London

Philip Hopkins

Centre for Human & Applied Physiological Sciences, School of Basic & Medical Biosciences, Faculty of Life Sciences & Medicine, King's College, London

Mark McPhail

Department of Inflammation Biology, School of Immunology and Microbial Sciences,Faculty of Life Sciences and Medicine, King’s College London