Although the precise mechanism inducing DIC from AFE remains unclear, it is probably
multifactorial. In vitro, amniotic fluid decreases whole blood clotting time, produces a
“thromboplastin-like effect”, induces platelet aggregation and activates the complement
cascase.73 The current hypothesis is that, in AFE, the presence of tissue factor in amniotic
fluid activates the extrinsic pathway by binding with factor VII, and this triggers clotting by
activating factor X, with the subsequent development of a consumptive coagulopathy.74–76
The activation of the clotting cascade in the pulmonary vasculature may cause generation of
microvascular thrombosis, which could then cause vasoconstriction.74 Additional data report
that high levels of a latent form of plasminogen activator inhibitor type 1 in amniotic fluid
can be reactivated by a denaturing agent in maternal circulation, leading to DIC.77 Recently,
it has been proposed that DIC may be a secondary result of complement activation rather
than the direct introduction of pro-coagulants into the maternal circulation.56
Although the precise mechanism inducing DIC from AFE remains unclear, it is probablymultifactorial. In vitro, amniotic fluid decreases whole blood clotting time, produces a“thromboplastin-like effect”, induces platelet aggregation and activates the complementcascase.73 The current hypothesis is that, in AFE, the presence of tissue factor in amnioticfluid activates the extrinsic pathway by binding with factor VII, and this triggers clotting byactivating factor X, with the subsequent development of a consumptive coagulopathy.74–76The activation of the clotting cascade in the pulmonary vasculature may cause generation ofmicrovascular thrombosis, which could then cause vasoconstriction.74 Additional data reportthat high levels of a latent form of plasminogen activator inhibitor type 1 in amniotic fluidcan be reactivated by a denaturing agent in maternal circulation, leading to DIC.77 Recently,it has been proposed that DIC may be a secondary result of complement activation ratherthan the direct introduction of pro-coagulants into the maternal circulation.56
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