Amniotic fluid as a potent activator of blood coagulation and platelet aggregation: Study with rotational thromboelastometry. Issue 172 (December 2018)

• Record Type: Journal Article
• Authors: Oda, Tomoaki; Tamura, Naoaki; Shen, Yi; Kohmura-Kobayashi, Yukiko; Furuta-Isomura, Naomi; Yaguchi, Chizuko; Uchida, Toshiyuki; Suzuki, Kazunao; Itoh, Hiroaki; Kanayama, Naohiro
• Is Part Of: Thrombosis research. Issue 172(2018)
• Page Start: 142
• Page End: 149
• Publication Date: 2018-12
• Subjects: Amniotic fluid -- Blood coagulation -- Fibrinolysis -- Thromboelastometry -- Pregnancy; Thrombosis -- Periodicals; 616.135
• DOI: 10.1016/j.thromres.2018.11.001
• Languages: English
• ISSNs: 0049-3848

Abstract

Abstract: Introduction: Pulmonary thromboembolism (PTE) is a leading cause of maternal death and frequently occurs during early puerperium. Amniotic fluid components are frequently observed in the maternal circulation in parturition; however, it currently remains unclear whether amniotic fluid contamination in maternal blood is related to the high incidence of PTE in early postpartum. Objectives: To examine the influence of amniotic fluid on blood coagulation and fibrinolysis systems with thromboelastometry. Materials and methods: Twenty-one pregnant women were recruited. We used whole citrated blood in ROTEM® (Tem Innovations GmbH, Munich, Germany), including the non-activated assay (NATEM), assessments for extrinsic (EXTEM) and intrinsic pathways (INTEM), fibrin polymerization (FIBTEM), and hyperfibrinolysis (APTEM), with amniotic fluid contamination, and measured the clotting time (CT), clot formation time (CFT), alpha, amplitude at 10 min (A10), maximum clot firmness (MCF), and lysis indices at 30 min (LI30) and 60 min (LI60). Results: Short CT in all assays as well as short CFT, high alpha, and increased A10 and MCF in NATEM were observed with amniotic fluid contamination. A10 and MCF as well as LI30 and LI60 decreased in EXTEM. Decreased LI60 with the mixture of amniotic fluid was not improved by tranexamic acid in APTEM. Conclusions: Amniotic fluid accelerated thrombin production and activated platelet aggregation without inducing hyperfibrinolysis in whole blood. The activated tissue factor pathway with amniotic fluid produced soft and fragile clots due to its influence on platelets, which may be associated with, at least partly, the high incidence of PTE in early puerperium, particularly after cesarean section. Highlights: Amniotic fluid activated blood coagulation and platelet aggregation. Amniotic fluid increased clot firmness by augmenting platelet function. Hyperfibrinolysis was not induced by amniotic fluid contact with maternal blood. Amniotic fluid made clots fragile via an extrinsic pathway in thromboelastometry. These results suggest a relationship with PTE in early postpartum.