Pathogenesis of Hypofibrinogenemia in Placental Abruption

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Abstract
THE pathogenesis of hypofibrinogenemia associated with placental abruption continues to be a subject of much conjecture. The most commonly proposed explanation has been intravascular coagulation due to the escape of thromboplastin from the products of gestation into the maternal circulation.1 2 3 4 5 6 Fibrinogen destruction resulting from the activation of circulating plasminogen has also been proposed to account for the fall in circulating fibrinogen.7 8 9 Recently, Stefanini and Turpini10 reported hypofibrinogenemia to follow massive hemorrhage in laboratory animals.Dieckmann,11 who in 1936 first clearly demonstrated that a coagulation defect with severe hypofibrinogenemia occurred with some cases of premature separation of the placenta, suggested that . . .

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