Thromboembolism
Introduction, The thrombotic risk of pregnancy is a consequence of the hypercoagulability resulting from suppressed fibrinolysis and increased levels of procoagulant factors, venous stasis, and, reflecting the likely inevitable trauma to pelvic vessels at delivery, endothelial damage [1]. Therefore, all three factors in Virchow’s triad occur in the course of pregnancy and delivery. Unsurprisingly, the risk is greatest immediately postpartum. The coagulation changes in pregnancy include: coagulation factors increased: factors VII, VIII, andX; von Willebrand factor; fibrinogen, suppressed endogenous anticoagulant activity, reduced protein S, acquired activated protein C resistance, suppressed fibrinolysis, increased plasminogen activator inhibitor types 1 and 2 (type 2 is produced by the placenta). The hypercoagulable state of pregnancy has likely evolved to meet the hemostatic challenge of hemorrhage at the time of miscarriage or childbirth. Indeed, in the developing world, the leading cause of maternal death remains obstetric hemorrhage, but in Western Europe and the USA, where hemorrhage is more likely to be successfully prevented or treated, a leading cause of maternal death is thromboembolic disease, with recent reports from the UK suggesting a decline that is temporally associated with the introduction of greater thrombotic risk assessment and prophylaxis guidelines [2].
