3rd April 2024

Pathophysiology

Virchow’s triad describes the pathogenesis of DVT and consists of venous stasis, blood hypercoagulability and vessel wall injury. Immobility contributes to venous stasis. Hypercoagulability may be secondary to genetic factors, acute illness or cancer. Vessel wall injury stimulates circulation of pro-coagulants. 

A VTE is termed provoked, when caused by an environmental or acquired risk factor and unprovoked, in the absence of these factors. This has implications on treatment duration with longer duration of anticoagulation where VTE has been unprovoked. PE usually results from dislodgement of thrombi from a DVT.