Prothrombotic risk factors in pregnancy

Pregnancy and puerperium have historically been associated with a significant increase – five-and tenfold vs non-pregnant women, respectively – of the thromboembolic risk, which in turn is the main cause of maternal mortality. Predisposing factors for thrombosis include components of the so-called Virchow’s triad: venous stasis, hypercoagulability and endothelial damage/dysfunction. Venous stasis is secondary to the compression that the uterus exerts on the inferior vena cava and the pelvic veins, to the reduction of the progesterone-mediated venous tone and to the development of varicose veins in the lower limbs; and, sometimes, to a prolonged immobilization. Furthermore, there is a physiological tendency to hypercoagulability, caused by an imbalance between procoagulant and anticoagulant factors, which on the one hand counters the postpartum hemorrhagic risk, while on the other increases the thromboembolic risk. The hypercoagulable profile may be confirmed via global coagulation assessment tests, such as thrombin generation and thromboelastometry/-graphy. The presence of a thrombophilic state – the tendency to develop thrombosis from an inherited or acquired condition – may contribute, alone or in association with other compounding factors, to the added thrombotic risk described in pregnancy. Pregnancy, especially if complicated, also involves endothelial activation, which may trigger thrombotic events, as confirmed by the increased levels of various plasma markers. Finally, the Virchow’s triad is often exacerbated by several thrombotic risk factors, such as a personal history of venous thrombosis, advanced age, obesity, plurality, smoking, hypertension, blood group A and caesarean section.