Imperial College London
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Professor Anthony Gordon

Faculty of Medicine, Department of Surgery & Cancer

Chair in Anaesthesia and Critical Care
 
 
 
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Contact

 

anthony.gordon

 
 
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Location

 

ICUQueen Elizabeth the Queen Mother Wing (QEQM)St Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Sinha:2020:10.1016/S2213-2600(20)30366-0,
author = {Sinha, P and Calfee, CS and Cherian, S and Brealey, D and Cutler, S and King, C and Killick, C and Richards, O and Cheema, Y and Bailey, C and Reddy, K and Delucchi, KL and Gordon, A and Shankar-Hari, M and Shyamsundar, M and O'Kane, CM and McAuley, DF and Szakmany, T},
doi = {10.1016/S2213-2600(20)30366-0},
journal = {The Lancet Respiratory Medicine},
pages = {1209--1218},
title = {Prevalence of ARDS phenotypes in critically-Ill COVID-19 patients: a prospective observational cohort study},
url = {http://dx.doi.org/10.1016/S2213-2600(20)30366-0},
volume = {8},
year = {2020}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Rationale: In non-COVID-19 ARDS, two phenotypes, based on the severity of systemic inflammation, have been described. The hyperinflammatory phenotype is known to be associated with increased multi-organ failure and mortality. In this study, we aimed to identify these phenotypes in COVID-19 ARDS.Methods: Patients with ARDS due to COVID-19 at two U.K. ICUs were recruited to the study. Demographic, clinical, and laboratory data were collected at baseline. Plasma samples were analysed for Interleukin-6 (IL-6) and soluble tumour-necrosis-factor receptor-1 (sTNFR-1) using a novel point-of-care assay. A parsimonious regression classifier model was used to calculate the probability for the hyperinflammatory phenotype in COVID-19 using IL-6, sTNFR-1 and sodium bicarbonate levels. Data from this cohort was compared to patients with ARDS recruited to a UK multicentre, randomised controlled trial of simvastatin (HARP-2).Results: 39 patients were recruited to the study. Median PaO2/FiO2 was 18 kpa (IQR: 15 – 21) and APACHE II score was 12 (IQR: 10 – 14.5). 17/39 patients (44%) had died by day 28 of the study. Patients that died were older and had lower PaO2/FiO2. The median probability for the hyperinflammatory phenotype was 0.03 (IQR 0.01 – 0.2). Depending on the probability cut-off used to assign class, the prevalence of the hyperinflammatory phenotype was between 10-21% (4-8/39) which is lower than in HARP-2 (186/539, 35%). Mortality in the hyperinflammatory phenotype was 5/8 (63%) and 12/31 (39%) in the hypoinflammatory phenotype. Compared to matched patients recruited to HARP-2, in COVID-19 levels of IL-6 were similar, whereas sTNFR-1 was significantly lower.Summary: In this exploratory analysis of 39 patients, ARDS due to COVID-19 is not associated with higher systemic inflammation and is associated with a lower prevalence of the hyperinflammatory phenotype compared to historical ARDS data.
AU  - Sinha,P
AU  - Calfee,CS
AU  - Cherian,S
AU  - Brealey,D
AU  - Cutler,S
AU  - King,C
AU  - Killick,C
AU  - Richards,O
AU  - Cheema,Y
AU  - Bailey,C
AU  - Reddy,K
AU  - Delucchi,KL
AU  - Gordon,A
AU  - Shankar-Hari,M
AU  - Shyamsundar,M
AU  - O'Kane,CM
AU  - McAuley,DF
AU  - Szakmany,T
DO  - 10.1016/S2213-2600(20)30366-0
EP  - 1218
PY  - 2020///
SN  - 2213-2600
SP  - 1209
TI  - Prevalence of ARDS phenotypes in critically-Ill COVID-19 patients: a prospective observational cohort study
T2  - The Lancet Respiratory Medicine
UR  - http://dx.doi.org/10.1016/S2213-2600(20)30366-0
UR  - https://www.sciencedirect.com/science/article/pii/S2213260020303660?via%3Dihub
UR  - http://hdl.handle.net/10044/1/81051
VL  - 8
ER  -
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