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Prevalence of phenotypes of acute respiratory distress syndrome in critically ill patients with COVID-19: a prospective observational study.
Sinha, Pratik; Calfee, Carolyn S; Cherian, Shiney; Brealey, David; Cutler, Sean; King, Charles; Killick, Charlotte; Richards, Owen; Cheema, Yusuf; Bailey, Catherine; Reddy, Kiran; Delucchi, Kevin L; Shankar-Hari, Manu; Gordon, Anthony C; Shyamsundar, Murali; O'Kane, Cecilia M; McAuley, Daniel F; Szakmany, Tamas.
  • Sinha P; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA; Department of Anesthesia, University of California San Francisco, San Francisco, CA, USA. Electronic address: pratik.sinha@ucsf.edu.
  • Calfee CS; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA; Department of Anesthesia, University of California San Francisco, San Francisco, CA, USA.
  • Cherian S; Critical Care Directorate, Royal Gwent Hospital, Newport, UK.
  • Brealey D; Division of Critical Care, National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK.
  • Cutler S; Critical Care Directorate, Royal Gwent Hospital, Newport, UK.
  • King C; Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.
  • Killick C; Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.
  • Richards O; Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.
  • Cheema Y; Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.
  • Bailey C; Critical Care Directorate, Royal Gwent Hospital, Newport, UK.
  • Reddy K; Department of Anaesthesiology and Critical Care, Beaumont Hospital, Dublin, Ireland.
  • Delucchi KL; Department of Psychiatry, University of California San Francisco, San Francisco, CA, USA.
  • Shankar-Hari M; ICU support offices, St Thomas' Hospital, Guy's and St Thomas' NHS Foundation Trust, London, UK; School of Immunology and Microbial Sciences, Kings College London, London, UK.
  • Gordon AC; Division of Anaesthetics, Pain Medicine and Intensive Care, Imperial College London, London, UK.
  • Shyamsundar M; Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK; Regional Intensive Care Unit, Royal Victoria Hospital, Belfast, UK.
  • O'Kane CM; Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK.
  • McAuley DF; Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK; Regional Intensive Care Unit, Royal Victoria Hospital, Belfast, UK.
  • Szakmany T; Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.
Lancet Respir Med ; 8(12): 1209-1218, 2020 12.
Article in English | MEDLINE | ID: covidwho-731948
ABSTRACT

BACKGROUND:

In acute respiratory distress syndrome (ARDS) unrelated to COVID-19, two phenotypes, based on the severity of systemic inflammation (hyperinflammatory and hypoinflammatory), have been described. The hyperinflammatory phenotype is known to be associated with increased multiorgan failure and mortality. In this study, we aimed to identify these phenotypes in COVID-19-related ARDS.

METHODS:

In this prospective observational study done at two UK intensive care units, we recruited patients with ARDS due to COVID-19. Demographic, clinical, and laboratory data were collected at baseline. Plasma samples were analysed for interleukin-6 (IL-6) and soluble tumour necrosis factor receptor superfamily member 1A (TNFR1) 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, soluble TNFR1, and bicarbonate levels. Data from this cohort was compared with patients with ARDS due to causes other than COVID-19 recruited to a previous UK multicentre, randomised controlled trial of simvastatin (HARP-2).

FINDINGS:

Between March 17 and April 25, 2020, 39 patients were recruited to the study. Median ratio of partial pressure of arterial oxygen to fractional concentration of oxygen in inspired air (PaO2/FiO2) was 18 kpa (IQR 15-21) and acute physiology and chronic health evaluation II score was 12 (10-16). 17 (44%) of 39 patients had died by day 28 of the study. Compared with survivors, patients who 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 cutoff used to assign class, the prevalence of the hyperinflammatory phenotype was between four (10%) and eight (21%) of 39, which is lower than the proportion of patients with the hyperinflammatory phenotype in HARP-2 (186 [35%] of 539). Using the Youden index cutoff (0·274) to classify phenotype, five (63%) of eight patients with the hyperinflammatory phenotype and 12 (39%) of 31 with the hypoinflammatory phenotype died. Compared with matched patients recruited to HARP-2, levels of IL-6 were similar in our cohort, whereas soluble TNFR1 was significantly lower in patients with COVID-19-associated ARDS.

INTERPRETATION:

In this exploratory analysis of 39 patients, ARDS due to COVID-19 was not associated with higher systemic inflammation and was associated with a lower prevalence of the hyperinflammatory phenotype than that observed in historical ARDS data. This finding suggests that the excess mortality observed in COVID-19-related ARDS is unlikely to be due to the upregulation of inflammatory pathways described by the parsimonious model.

FUNDING:

US National Institutes of Health, Innovate UK, and Randox.
Subject(s)

Full text: Available Collection: International databases Database: MEDLINE Main subject: Respiratory Distress Syndrome / COVID-19 Type of study: Cohort study / Experimental Studies / Observational study / Prognostic study / Randomized controlled trials Limits: Female / Humans / Male / Middle aged Language: English Journal: Lancet Respir Med Year: 2020 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Respiratory Distress Syndrome / COVID-19 Type of study: Cohort study / Experimental Studies / Observational study / Prognostic study / Randomized controlled trials Limits: Female / Humans / Male / Middle aged Language: English Journal: Lancet Respir Med Year: 2020 Document Type: Article