This concept addresses coagulopathy and thrombotic risk associated with acute viral infection, framed through Virchow's triad—the classical pathophysiologic model attributing thrombosis to circulatory stasis, an intrinsic hypercoagulable state, and endothelial injury—applied to explain markedly elevated rates of venous thromboembolism observed in critically ill infected patients despite standard prophylactic anticoagulation. It also covers the distinct laboratory signature of this virus-associated coagulopathy (markedly elevated D-dimer with preserved or elevated fibrinogen and only mild thrombocytopenia, distinguishing it from classic disseminated intravascular coagulation) and the risk-stratified approach to anticoagulation intensity based on illness severity. This belongs to hematology, specifically the pathophysiology and management of acquired hypercoagulable states and thrombosis risk assessment in critical illness.
This concept addresses coagulopathy and thrombotic risk associated with acute viral infection, framed through Virchow's triad—the classical pathophysiologic model attributing thrombosis to circulator…