Authors: Spagnolo P, Balestro E, Aliberti S, Cocconcelli E, Biondini D, Casa GD
PMID: 32422177 PMCID: PMC7228737 DOI: 10.1016/S2213-2600(20)30222-8
Abstract
As of May 6, 2020, nearly 3·7 million people have been infected and around 260 000 people have died from coronavirus disease 2019 (COVID-19) worldwide.1 Almost all COVID-19-related serious consequences feature pneumonia.2 In the first large series of hospitalised patients (n=138) with COVID-19 in Wuhan, China, chest CT showed bilateral ground glass opacities with or without consolidation and with lower lobe predilection in all patients.3 In this series, 36 (26%) patients required intensive care, of whom 22 (61%) developed acute respiratory distress syndrome (ARDS).3 The mechanisms through which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes lung damage are only partly known, but plausible contributors include a cytokine release syndrome triggered by the viral antigen, drug-induced pulmonary toxicity, and high airway pressure and hyperoxia-induced acute lung injury secondary to mechanical ventilation. To date, about 1·2 million people worldwide have recovered from COVID-19, but there remains concern that some organs, including the lungs, might have long-term impairment following infection (figure). No post-discharge imaging or functional data are available for patients with COVID-19.
Keywords: pulmonary fibrosis, COVID-19
