Hemostatic defects in pregnancy

Abstract

During the past decade there have been numerous reports concerning the role of alterations of the blood coagulation mechanism in the genesis of hemorrhage during pregnancy and the puerperium.1–9 Most frequently hemorrhage due to blood coagulation defects has been reported in cases of severe abruptio placentae, amniotic fluid embolism, or prolonged intrauterine retention of a dead fetus; less attention has been focused on alterations of the hemostatic mechanism due to the transfusion of incompatible blood or associated with a septic abortion.In each of these 5 instances a prominent and clinically most significant alteration of the blood coagulation mechanism is a reduction in the concentration of circulating fibrinogen to a level inadequate for effective hemostasis. Associated with the hypofibrinogenemia may be a slight to moderate reduction in the activity of some of the plasma factors which accelerate clotting. On occasion there also may be thrombocytopenia of sufficient intensity to be clinically important.The present report is concerned with abnormal hemostasis in prolonged intrauterine retention of a dead fetus and more briefly alterations of the blood clotting mechanism in cases of transfusion of incompatible blood and of septic abortion. All methods used have been described in previous publications.9–11