Imperial College London

Professor Anthony Gordon

Faculty of MedicineDepartment of Surgery & Cancer

Chair in Anaesthesia and Critical Care







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






BibTex format

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},
journal = {The Lancet Respiratory Medicine},
title = {Prevalence of ARDS phenotypes in critically-Ill COVID-19 patients: a prospective observational cohort study},
url = {},
year = {2020}

RIS format (EndNote, RefMan)

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
PY - 2020///
SN - 2213-2600
TI - Prevalence of ARDS phenotypes in critically-Ill COVID-19 patients: a prospective observational cohort study
T2 - The Lancet Respiratory Medicine
UR -
ER -