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
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.
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.
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