Hémostase et grossesse

Abstract

Normal pregnancy is an acquired hypercoagulable and inflammatory state. Hypercoagulability in normal pregnancy is due to increased levels of procoagulant coagulation factors, as well as hypofibrinolysis and decreased levels of natural anticoagulants. In addition, regulation of the maternal immune system contributes to a successful pregnancy outcome. Specific pregnancy diseases are defined by their occurrence in relation with the gravid state and their recovery when gestation ends, after delivery, most of the time in emergency conditions in case of: disseminated intravascular coagulation, thrombotic microangiopathies, such as preeclampsia, HELLP syndrome, or the rare thrombotic thrombocytopenic purpura. On the contrary, diseases that enhance bleeding risk are present before pregnancy when hereditary, or detected at the time of pregnancy when acquired: hereditary diseases include von Willebrand disease, thrombopathies, or conducting state of haemophilia, and acquired states are mainly related to autoimmune diseases, such as immune thrombocytopenic purpura. Various corrections may be performed for pregnancy-induced abnormalities and their management and follow-up are achieved accordingly. Diseases that increase the thrombotic risk involve hereditary thrombophilia (deficiencies of natural anticoagulants, factors V or II mutations), and acquired thrombophilia (antiphospholipids antibodies). Normal pregnancy and post-partum also constitute an acquired thrombotic factor and women with thrombophilic defects have been shown to be at increased risk. There is a consensus that such women with a personal history of thrombosis should receive anticoagulant prophylaxis. A good evaluation of the thrombotic risk is necessary in order to determine the most appropriate anticoagulant treatment. Warfarin crosses the placenta and has a known teratogenic effect (warfarin embryopathy). Hence, prophylaxis of gestational thrombosis mainly relies upon the use of heparin, during pregnancy and post-partum.