Venous thromboembolism (VTE) is a term that encompasses deep vein thrombosis (DVT) and pulmonary embolism (PE).
Up to one-third of patients with a symptomatic DVT may have an asymptomatic PE.1 Most PEs arise from the legs.1,2
When a PE is present there is ventilation of lung tissue but a lack of perfusion, resulting in impaired gas exchange. This leads to alveolar collapse, due to the reduction in the area of the pulmonary arterial bed. There may be a resultant increase in pulmonary arterial pressure. These sequelae may cause a reduction in cardiac output. If perfusion is impaired to the extent that the collateral bronchial circulation cannot compensate, lung infarction occurs. In the case of a large PE or multiple PEs, the pulmonary arterial pressure can increase to such an extent that right ventricular failure may result.
A thrombus is a mass comprising of platelets, fibrin, red and white blood cells within a blood vessel.3 This can be carried to the pulmonary vasculature.
Causes of non-thrombotic PE include septic emboli, fat, air or amniotic fluid.
Risk factors for VTE include thrombophilia, as per NICE, a previous history of VTE, age >60 years, surgery, obesity, malignancy, immobility, acute medical illness and pregnancy.1