The most common forms of venous thromboembolic (VTE) diseases encountered during pregnancy and the postpartum period include deep venous thrombosis (DVT), pulmonary embolism (PE), septic pelvic thrombophlebitis (SPT), and ovarian vein thrombosis (OVT). Thromboembolic disease is a major contributor to both perinatal and maternal morbidity and mortality worldwide. The World Health Organization (WHO) estimates that VTE accounted for 3.2% of maternal deaths between 2003 and 2012.1 A large part of the strategy for reducing maternal morbidity and mortality from VTE lies in a systematic approach to thromboprophylaxis, and there is evidence that progress is being made.
Data from the 1990s suggested that VTE had surpassed hemorrhage and hypertension as leading causes of maternal mortality in developed countries.2 In 2004, the Royal College of Obstetricians and Gynaecologists recommended thromboprophylaxis during pregnancy, labor, and after normal vaginal delivery for women in the United Kingdom (UK).3 The time period from 2006-2008 was the first time in the prior two decades that VTE was not the leading direct cause of death in the UK.4 In 2011, the American College of Obstetricians and Gynecologists (ACOG) updated the Practice Bulletin on Thromboembolism in Pregnancy to include recommendations for thromboprophylaxis for all patients undergoing cesarean delivery including the use of pneumatic compression devices or pharmacologic prophylaxis.5 In the United States, between 2011 and 2013, 9.2% of maternal mortality was attributable to thrombotic PE making it the sixth most common cause of maternal mortality.6
The most recent data from the National Inpatient Sample indicate that the rates of DVT and PE are currently 0.4 and 0.2 per 1000 delivery hospitalizations. Interestingly, since 1994, the rate of DVT among US women has decreased by about one third, while the rate of PE has doubled.7
The cornerstones of VTE management lie in ongoing systems-based strategies for prevention, a high index of suspicion, and prompt treatment. This chapter reviews the etiology, diagnosis, treatment, and prevention of VTE.
A practical and user-friendly version of the complex regulatory pathways of hemostasis and fibrinolysis is presented in Figure 7-1.
Hemostatic and fibrinolytic pathways. The primary initiator of coagulation is tissue factor (TF) which is not normally expressed by cells in contact with the circulation (ie, endothelial cells). Following vascular disruption, perivascular, cell membrane–bound TF complexes with plasma-derived factor VII or its more active form (VIIa) to directly convert factor X to Xa. TF/VIIa can also indirectly generate Xa by converting factor IX to IXa, which, in turn, complexes with factor VIIIa to convert X to Xa. Factor Xa, once generated, complexes with its cofactor, Va, to convert prothrombin (factor II) to thrombin (IIa). Thrombin activates platelets and cleaves fibrinogen to generate fibrin monomers, which spontaneously polymerize and are cross-linked by thrombin-activated factor XIIIa to form a ...