Venous thromboembolism and IVC filters

Abstract

1.6 million people in the EU develop venous thromboembolism every year with 0.5 million deaths. More patients die in the UK from venous thromboembolism (VTE) than combined totals from breast cancer, road traffic accidents and AIDS (NICE 2009). VTE cost for Australia in 2008 was 3.9 Billion Dollars, which was more than the entire cancer treatment spend. Rudolf Virchow (1821-1902) bestowed the name embolus on venous thromboembolism in 1856 when he said “the detachment of larger or smaller fragments from the end of the softening thrombus, which are carried along be the current of blood and driven into remote vessels.” This gives rise to the very frequent process on which I have bestowed the name (EMBOLIA). Virchow also gave his name to Virchow’s Triad, which predisposes to VTE, namely, hypercoagulable states, haemodynamic changes (stasis) and endothelial injury or dysfunction. Pulmonary emboli usually arise from thrombi that originate in the deep venous system of the lower extremities. They can also arise from pelvic, renal, upper extremity veins or right heart chambers. Treatment is by full anticoagulation for all patients suspected of having VTE. This is usually achieved by starting the patient on low molecular weighted Heparin (LMWH) with oral anticoagulation (Warfarin) initiated at the time of diagnosis and LMWH discontinued when the INR is 2.0 for at least 24 h, but no sooner than 5 days after Warfarin therapy has been commenced. In some patients, anticoagulation is either contraindicated or there has been a complication associated with anticoagulation so that it has to be stopped. An inferior vena cava (IVC) filter can be placed in these patients to protect against further pulmonary emboli.