Massive platelet-rich thrombus formation in small pulmonary vessels in amniotic fluid embolism: An autopsy study.

OBJECTIVE

To identify pulmonary/uterine thrombus formation in amniotic fluid embolism (AFE).

DESIGN

Retrospective, observational.

SETTING

Nationwide.

POPULATION

Eleven autopsy cases of AFE and control cases.

METHODS

We assessed pulmonary and uterine thrombus formation and thrombus area in AFE and pulmonary thromboembolism (PTE) as a control. The area of platelet glycoprotein IIb/IIIa, fibrin, neutrophil elastase, citrullinated histone H3 (a neutrophil extracellular trap marker) and mast cell chymase immunopositivity was measured in 90 pulmonary emboli, 15 uterine thrombi and 14 PTE.

MAIN OUTCOME MEASURES

Pathological evidence of thrombus formation and its components in AFE.

RESULTS

Amniotic fluid embolism lung showed massive thrombus formation, with or without amniotic emboli in small pulmonary arteries and capillaries. The median pulmonary thrombus size in AFE (median, 0.012 mm ; P < 0.0001) was significantly smaller than that of uterine thrombus in AFE (0.61 mm ) or PTE (29 mm ). The median area of glycoprotein IIb/IIIa immunopositivity in pulmonary thrombi in AFE (39%; P < 0.01) was significantly larger than that of uterine thrombi in AFE (23%) and PTE (15%). The median area of fibrin (0%; P < 0.001) and citrullinated histone H3 (0%; P < 0.01) immunopositivity in pulmonary thrombi in AFE was significantly smaller than in uterine thrombi (fibrin: 26%; citrullinated histone H3: 1.1%) and PTE (fibrin: 42%; citrullinated histone H3: 0.4%). No mast cells were identified in pulmonary thrombi.

CONCLUSIONS

Amniotic fluid may induce distinct thrombus formation in the uterus and lung. Pulmonary and uterine thrombi formation may contribute to cardiorespiratory collapse and/or consumptive coagulopathy in AFE.