Key points

• Deep vein thrombosis (DVT) and pulmonary embolism (PE) are the leading causes of preventable in-patient mortality following surgery

• Virchow's triad (stasis, hypercoagulable state, vessel wall injury) forms the basis for DVT formation

• Many DVTs are asymptomatic

• Heparin prevents propagation by its action on antithrombin III

• D-dimer level measurements are useful screening tests

• Heparin must be overlapped with warfarin because of the transient hypercoagulable state induced by warfarin

• Outpatient treatment is carried out with low molecular weight heparin (LMWH) and warfarin

• Newer anticoagulants such as rivoraxaban and dabigatran are now being used for prophylaxis

• Inferior vena cava filters can be used when anticoagulation is contraindicated

Background

DVT and its sequela, PE, are the leading causes of preventable in-hospital mortality. In 1846, Virchow recognized the association between venous thrombosis in the legs and PE. Heparin was only introduced to clinical practice in 1937. Over the last 25 years, considerable progress has been made in understanding the pathophysiology, diagnosis, treatment and prevention of venous thromboembolism (VTE). Many DVTs are asymptomatic and almost half of all fatal cases of PE are associated with asymptomatic DVTs.

Pathophysiology

DVT is multifactorial with interaction between hereditary and acquired risk factors. The Virchow triad (i.e. venous stasis, hypercoagulable state, vessel wall injury), continues to serve as the unifying concept in the pathogenesis of DVT. However the significance of interplay between the elements of Virchow's triad and environmental or acquired risk factors is also important.