COVID-19 Infection: Implications for Perioperative and Critical Care Physicians

Abstract

Healthcare systems worldwide are responding to Coronavirus Disease 2019 (COVID-19), an emerging infectious syndrome caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus. Patients with COVID-19 can progress from asymptomatic or mild illness to hypoxemic respiratory failure or multisystem organ failure, necessitating intubation and intensive care management. Healthcare providers, and particularly anesthesiologists, are at the frontline of this epidemic, and they need to be aware of the best available evidence to guide therapeutic management of patients with COVID-19 and to keep themselves safe while doing so. Here, the authors review COVID-19 pathogenesis, presentation, diagnosis, and potential therapeutics, with a focus on management of COVID-19-associated respiratory failure. The authors draw on literature from other viral epidemics, treatment of acute respiratory distress syndrome, and recent publications on COVID-19, as well as guidelines from major health organizations. This review provides a comprehensive summary of the evidence currently available to guide management of critically ill patients with COVID-19.

Fig. 1.

SARS-CoV-2 virus particles visualized by transmission electron micrograph. Viral particles are shown in blue-green with yellow viral envelope. This image was captured and color-enhanced at the National Institute of Allergy and Infectious Diseases Integrated Research Facility (Fort Detrick, Frederick, Maryland) and used under creative commons license agreement.

Fig. 2.

Coronavirus biology. Notable coronavirus structural proteins include the spike protein (S), which mediates receptor binding and fusion, the viral membrane protein (M), and the nucleocapsid protein (N). After binding of the viral spike protein to the angiotensin converting enzyme-2 (ACE2) receptor, virions enter cells either by receptor-mediated endocytosis or direct fusion with the cell membrane. Endocytosis is a potential target of chloroquine, which prevents endosomal acidification that triggers viral membrane fusion. Chloroquine may also modify ACE2 terminal glycosylation and inhibit coronavirus binding. Viral RNA is then transcribed to generate polyproteins pp1a and pp1ab that are cleaved by a protease to generate the viral replication machinery. These polyproteins are cleaved to form replication-transcription protein complexes (RTCs) by a viral protease 3-chymotrypsin-like protease (3CLpro). 3CLpro has been postulated to be a target of human immunodeficiency virus protease inhibitors lopinavir or ritonavir, although in silico studies have questioned this theory. Viral RNA is replicated and transcribed in double membraned vesicles (DMV) in replication-transcription protein complexes, which include the RNA-dependent RNA polymerase that is the putative target of remdesivir. Viral mRNA is then translated and virions are assembled in the endoplasmic reticulum and golgi.