Neutrophil extracellular traps might propagate inflammation and microvascular thrombosis in patients with COVID-19 and severe acute respiratory distress syndrome.60 Along with IL-33, IL-1, TNF, and other cytokines, neutrophil extracellular traps might increase endothelial permeability and induce a procoagulant phenotype in endothelial tissues by inducing expression of tissue factor,61, 62, 63 thus representing a possible link between hyperinflammation and hypercoagulability that could account for D-dimer elevation, pulmonary thrombosis, and microvascular manifestations affecting the heart, kidneys, and small bowel seen in patients with critical COVID-19.64, 65 Endothelialitis and endothelial dysfunction would also account for predominant exudative-phase diffuse alveolar damage characterised by hyaline membranes and fibrin deposits typically observed in patients with COVID-19 and severe acute respiratory distress syndrome.4