COVID-19: Catastrophic Cause of Acute Lung Injury.

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak that began in 2019 and spread rapidly across the globe has been observed to cause acute lung injury and multiorgan system failure. While common symptoms are flu-like, this population has been observed to decompensate at an alarmingly rapid rate to severe hypoxia. SARS-CoV-2 infects host cells by targeting the angiotensin-converting enzyme 2 (ACE2) receptor, which is present on endothelial cells in the lung, heart, kidney, and gastrointestinal tissue. The pathophysiology of acute respiratory distress syndrome (ARDS) in SARS-CoV-2 infection has a component of lung perfusion dysregulation and is described as a "cytokine storm" that causes increased vascular permeability and disease severity. Older adults and those with comorbid conditions, particularly hypertension, diabetes, and history of ischemic heart disease, are especially vulnerable. These high-risk populations are often on angiotensin-modulating therapies, which are theorized to increase ACE2 expressivity, but current evidence for or against discontinuation is equivocal. The standard for SARS-CoV-2 testing is through reverse transcription polymerase chain reaction, which has presented problems due to low sensitivity and possible co-infection with other pathogens. Treatment for ARDS in the setting of SARS-CoV-2 should follow pre-established goals of care and the wishes of the patient and family members or caregivers and consider the high risk for polypharmacy, cognitive decline, malnutrition, and depression, particularly in older adults. Treatment recommendations have outlined ventilation goals to minimize further lung injury. Compassionate use of pharmacologic therapies such as remdesivir has shown promise, and further clinical trials of anticytokine agents are underway.