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