Editorial: Preventing VTE: Part 3-the pregnant patient

Pregnancy and delivery present unique and profound challenges to a woman's hemostatic system. Successful pregnancy requires avoidance of serious hemorrhage during implantation, placentation, and throughout gestation. The greatest hemostatic challenge, however, is after delivery of the placenta. At that instant, around 120 spiral arteries, denuded of their muscular envelopments, are shorn open while transporting 12% of a woman's cardiac output every minute. The body copes with this extraordinary situation with hemostatic adaptations that are both local and systemic.

Local puerperal hemostasis is mediated by a combination of contraction-induced vessel compression and thrombus formation induced by the abundant tissue factor (thromboplastin) in the decidua.¹ Underscoring the decidua's crucial importance to uterine hemostasis is the profound obstetric hemorrhage that occurs when decidualization is absent or impaired (for example, in ectopic and cesarean scar pregnancy, placenta previa and accreta, and abdominal pregnancies).

But clearly this system is not foolproof, because hemorrhage remains the second leading cause of maternal death and accounts for 17% of these deaths.³ Conversely, hemostasis is often too efficient: VTE is the leading cause of maternal mortality, accounting for 20% of deaths.³ Indeed, VTE is 10 times more likely during pregnancy and the puerperium-or 1/1,500-than the background risk for women of reproductive age.

Risk of thrombosis in pregnancy is further exacerbated as the enlarging uterus compresses the inferior vena cava and pelvic veins, producing venous stasis in the lower extremities, and deep vein capacitance increases under the influence of hormones. Obesity, infection, and surgery heighten the risk. And the stakes are raised five- to sixfold in women with thrombophilias such as factor V Leiden (FVL) and the prothombin G20210A gene mutation (PGM).^4,5 Indeed, maternal thrombophilias likely account for more than 80% of VTE in pregnancy.^4,5 Moreover, a personal or family history of VTE increases thrombophilia-associated risks up to fiftyfold!⁵ The estimated risk of VTE among pregnant FVL heterozygotes who have no personal or strong (firstdegree) family history of VTE is only 0.2%, but exceeds 10% in patients with such a history.^5,6

How can we prevent pregnancy-associated VTEs? For pregnant women with a prior episode, risk of recurrence is highly dependent on the presence of thrombophilia and the type of risk factors that led to the previous event.⁷ Screen these patients for thrombophilias and review the clinical details of the prior VTE episode in detail. In my opinion, antepartum prophylactic heparin is not necessary during pregnancy for women whose prior VTE was associated with a nonrecurring risk factor (such as surgery while on OCs) other than pregnancy and who do not have a documented thrombophilia or current major risk factors (such as obesity, superficial thrombophlebitis, or prolonged bed rest).⁷ They should, however, receive postpartum anticoagulation, since that is when most pregnancy-associated fatal pulmonary emboli occur. Conversely, both antepartum and postpartum thromboprophylaxis are warranted in patients with a prior VTE who have a thrombophilia, prior unexplained VTE, or current major risk factor.

I would also screen patients with strong family histories but no personal history of VTE for the most common and thrombogenic thrombophilias (that is, FVL, PGM, antithrombin, protein C and S deficiencies). Given the up to fiftyfold higher rate of VTE during pregnancy among thrombophilic women with such a family history, antepartum anticoagulation should be strongly considered, and postpartum therapy is a must if any of these disorders are detected.