Clotting Defects in Hemorrhagic Complications of Pregnancy

Abstract

The coagulation defect in premature separation of the placenta, amniotic embolism, and retention of a dead fetus is primarily a defibrination syndrome resulting from pathologic infusion of thromboplastic substances. Secondary fibrinolytic activity, which can occur as a direct result of the clotting process or in response to hemorrhagic shock, causes proteolysis and further loss of fibrinogen and inhibits polymerization of fibrin. However, measures directed largely against this fibrinolytic activity could predispose the patient to severe thrombotic complications. Therefore, therapy should be aimed primarily at replacing the lost clotting factors, inhibiting the hypercoagulable state, and treating shock.