Background: Amniotic fluid (AF) embolism is a rare, life-threatening obstetric syndrome with a high mortality rate. It is almost always associated with disseminated intravascular coagulation, but the pro-coagulant mechanism of amniotic fluid is still not clear.

Aims: To investigate pro-coagulant mechanisms of blood clotting activation by amniotic fluid.

Methods: Fresh AF samples were collected by amniocentesis from 7 patients. Plasma-based fibrin generation assays with donor pooled plasma (n=12), and plasmas deficient in factors XII, IX, XI, VII, V, X were used to characterize the pro-coagulant activity of amniotic fluid. Differential centrifugation was used to assess the pro-coagulant activity of different AF fractions. Flow cytometry was used to determine microvesicle count and analyze CD41+, TF+ (CD142+), and Annexin5+ populations.

Results: In normal plasma, AF at 1% concentration shortened clot time from 50 to 6 minutes on the average. This effect was not prevented by either corn trypsin inhibitor, or active site-inhibited factor VIIa, or their combination. AF was able to efficiently clot plasmas with severe deficiencies of factor XII, IX, or XI. The clotting time was prolonged in factor V- and, to a lesser degree, in some batches of factor VII-deficient plasma. AF did not cause coagulation in factor X deficient plasma. Although fluid fraction and cell fraction of AF possessed some clotting capacity, the predominant part of the activity was associated with the microvesicle fraction. Flow cytometry analysis revealed that most microvescles were Annexin5+ and CD142+, with few CD41+ events.

Conclusions: Our findings suggests the mechanism wherein amniotic fluid activate coagulation cascade via a microvesicle fraction at the factor X/V and/or factor VII level.

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ISTH Congress Abstracts - https://abstracts.isth.org/abstract/mechanisms-of-blood-clotting-activation-by-amniotic-fluid/