COVID-19 pneumonia is characterised by increases in multiple cytokines, including tumor necrosis factor (TNF) and interleukin-6 (IL-6) [16], which are potent activators of the tissue factor (TF)-dependent coagulation cascade [17–19]. Activation of the coagulation system is known to be pro-inflammatory and could drive further increases in inflammation; in tissues with a delicate architecture such as the distal lung, this can be highly detrimental, impairing gas exchange [20] and culminating in acute respiratory distress syndrome (ARDS) [21, 22]. The extensive activation of coagulation in patients with severe COVID-19 could stimulate further inflammation via the mechanisms described below, resulting in a positive feedback loop that maintains high levels of inflammation for a prolonged period. Hence, effective anticoagulation strategies may prevent complications associated with aberrant clotting, attenuate coagulation-induced exaggerated inflammatory responses and potentially reduce the severity and extent of pulmonary infiltrates.