Language

English

Publication Date

12-1-2022

Journal

Intensive Care Medicine

DOI

10.1007/s00134-022-06877-w

PMID

36074167

PMCID

PMC9453725

PubMedCentral® Posted Date

9-8-2022

PubMedCentral® Full Text Version

Post-print

Abstract

Immunomodulation and immunity from vaccination and natural infection have reduced mortality from coronavirus disease 2019 (COVID-19). However, there are ongoing concerns regarding emerging variants and residual pulmonary sequelae in survivors, given that the lungs are the principal site for the triumvirate of infection, inflammation and injury. The initial waves of acute, severe COVID-19 were profoundly inflammatory, usually manifest as organising pneumonia ± acute respiratory distress syndrome (ARDS). The extent of the fibrogenic potential of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and the modifiability of the pathogenic processes and disease course are unclear. Interestingly patients can develop ‘post-COVID interstitial lung disease’ (PC-ILD) irrespective of having ARDS during the acute phase. Here, we describe our evolving understanding of PC-ILD and the critical need to identify risk factors, including within the critical care setting. We also discuss immunopathomechanisms that may facilitate early intervention to prevent, slow or arrest progression of lung damage e.g. with immunomodulatory and/or anti-fibrotic agents.

Keywords

Humans, COVID-19, Lung Diseases, Interstitial, SARS-CoV-2, Lung, Retrospective Studies

Published Open-Access

yes

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