Lars Schröder1,2, Astrid Hellmund3, Ulrich Gembruch3, Waltraut Maria Merz3. 1. Department of Obstetrics and Gynecology, Medical Faculty, University Hospital Cologne, Kerpener Straße 34, 50931, Cologne, Germany. lars_schroed@gmx.net. 2. Department of Obstetrics and Prenatal Medicine, University Bonn Medical School, Bonn, Germany. lars_schroed@gmx.net. 3. Department of Obstetrics and Prenatal Medicine, University Bonn Medical School, Bonn, Germany.
Abstract
INTRODUCTION: Amniotic fluid embolism (AFE) continues to be a rare, enigmatic condition with high maternal mortality. It is characterized by cardiovascular compromise, loss of consciousness or other neurologic symptoms, and coagulopathy. The latter is usually treated according to existing protocols for consumptive coagulopathy. METHODS: Serial analyses of a panel of hemostaseological parameters were performed in three consecutive cases of AFE that occurred at our institution. RESULTS: All mothers and neonates survived without major sequelae. Disproportionately low levels of fibrinogen and factor five, and exorbitantly elevated D-dimers were present in all cases, whereas markers of consumptive coagulopathy, platelets and antithrombin in particular, were only slightly reduced. DISCUSSION: Our results support hyperfibrinolysis as contributing factor of AFE-associated coagulopathy. We, therefore, propose a treatment algorithm which includes early use of tranexamic acid and transfusion of red blood cells and fresh frozen plasma, adding fibrinogen if hemostasis is not readily achieved.
INTRODUCTION:Amniotic fluid embolism (AFE) continues to be a rare, enigmatic condition with high maternal mortality. It is characterized by cardiovascular compromise, loss of consciousness or other neurologic symptoms, and coagulopathy. The latter is usually treated according to existing protocols for consumptive coagulopathy. METHODS: Serial analyses of a panel of hemostaseological parameters were performed in three consecutive cases of AFE that occurred at our institution. RESULTS: All mothers and neonates survived without major sequelae. Disproportionately low levels of fibrinogen and factor five, and exorbitantly elevated D-dimers were present in all cases, whereas markers of consumptive coagulopathy, platelets and antithrombin in particular, were only slightly reduced. DISCUSSION: Our results support hyperfibrinolysis as contributing factor of AFE-associated coagulopathy. We, therefore, propose a treatment algorithm which includes early use of tranexamic acid and transfusion of red blood cells and fresh frozen plasma, adding fibrinogen if hemostasis is not readily achieved.