Extensive Pulmonary Embolism in late pregnancy associated with Anticardiolipin Antibodies

Abstract

The leading cause of morbidity and mortality during pregnancy and the puerperium is venous thromboembolism. Though uncommon, the risk is five times higher in a pregnant woman than in a non-pregnant woman of similar age.1,2 In pregnancy, all three underlying factors for venous thrombosis are present: hypercoagulability, venous stasis and vascular damage (Virchow's triad). Of these, the most constant predisposing factor is increasing venous stasis due to the pressure of the gravid uterus on the pelvic vasculature. In addition the presence of a thrombophilia, (congenital or acquired) will increase this risk substantially. During pregnancy hypercoagulability is a physiological preparation for the haemostatic challenge of delivery. There are increases in procoagulant factors, such as von Willebrand factor, factor VIII, factor V, and fibrinogen together with an acquired resistance to activated protein C and a reduction in protein S. Increases in plasminogen activator inhibitors impair fibrinolysis. The third factor of this triad, vascular damage, is a possible complication of trophoblastic invasion of the uterine spiral arterioles or of delivery.