Hypercoagulability in Pregnancy - Causes

Causes

Pregnancy-induced hypercoagulability is probably a physiologically adaptive mechanism to prevent post partum hemorrhage. Pregnancy changes the plasma levels of many clotting factors, such as fibrinogen, which can rise up to three times its normal value. Thrombin levels increase. Protein S, an anticoagulant, decreases. However, the other major anticoagulants, protein C and antithrombin III, remain constant. Fibrinolysis is impaired by an increase in plasminogen activator inhibitor-1 (PAI-1 or PAI) and plasminogen activator inhibitor-2 (PAI-2), the latter synthesized from the placenta. Venous stasis may occur at the end of the first trimester, due to enhanced compliance of the vessel walls by a hormonal effect.

Also, pregnancy can cause hypercoagulability by other factors, e.g. the prolonged bed rest that often occurs post partum that occurs in case of delivery by forceps, vacuum extractor or Caesarean section. Pregnancy after the age of 35 augments the risk of VTE, as does multigravidity of more than four pregnancies. Several pregnancy complications, such as pre-eclampsia, cause substantial hypercoagulability.

General causes of hypercoagulability, about as common in pregnancy as in the general population, include both acquired ones such as antiphospholipid antibodies, and congenital ones, including factor V Leiden, prothrombin mutation, protein C and S deficiencies, and antithrombin III deficiency.