What is the pathogenesis of acute respiratory distress syndrome (ARDS) in COVID-19?
ARDS is an acute life-threatening inflammation of the lung due to infection, trauma, or inflammatory conditions. Excessive inflammation leads to alveolar damage and increased permeability of endothelial and epithelial cells. This results in protein-rich fluid accumulation in the interstitium and the air space, which causes impaired gas exchange and hypoxemia. Reactive oxygen species, leukocyte proteases, chemokines, and cytokines also contribute to lung injury. The barrier impairment of the lung microvascular barrier is central to the pathogenesis of ARDS.79 Pulmonary vascular endothelial injury in association with the presence of the intracellular virus and disrupted cell membranes contribute to the increase of endothelial permeability. COVID-19 patients with ARDS had a histological pattern of diffuse alveolar damage with perivascular T cell infiltration. In addition, alveolar capillary microthrombi, secondary to endothelial injury, in patients who died of COVID-19 may be an important cause of refractory hypoxia in ARDS.49,74,80,81