Thrombophilia and Pregnancy

Abstract

Pregnancy is a state of hypercoagulation, most likely an adaptive mechanism, in order to reduce the risk of hemorrhage during and after the delivery. There are substantial changes in the haemostatic system during normal healthy pregnancy including rise in clotting factors I, VII, VIII, IX, and X, diminished protein S and fibrinolytic activity and resistance to activated protein C.¹ Reduced fibrinolytic activity is due to fivefold increase in PAI-1 (Plasminogen Activator Inhibitor type 1) levels.² In addition venous stasis increases during pregnancy as the lower-extremity veins dilate due to venous compression by the gravid uterus. Endothelial injury may also occur in antepartum or in postpartum period. The combination of these factors results in 4-5 times increased risk of venous thromboembolism (VTE) in the pregnant and postpartum patients.3 The prevalence of VTE in pregnancy is 0.8-2.0 per 1,000 pregnancies and accounts for 1.1 deaths per 100,000 pregnancies.4 The most important risk factor for women experiencing pregnancy-related VTE is prior personal history of VTE.5 The second most common risk factor is thrombophilia 6 7 Studies have shown that at least 20%, and possibly over 50%, of pregnant patients diagnosed with VTE have thrombophilia.8 There is a growing evidence that women with thrombophilia are also at risk of other vascular pregnancy complications, including recurrent fetal loss, pre‐eclampsia, stillbirths, abruption and intrauterine growth restriction.