Objective: To evaluate the potential role of immunologic mechanisms that in
volve mast cell degranulation (anaphylaxis) or complement activation in the
mechanism of amniotic fluid embolism.
Methods: This study was a case series of nine women with presumed amniotic
fluid embolism and a control group of 22 women who had normal labor. Women
were from community and tertiary referral hospitals in Japan and the United
States. Main outcome measures were maternal peripartum complement levels (
C3 and C4), serum levels of tryptase, urinary histamine concentrations, and
serum levels of a fetal antigen (sialyl Tn).
Results: Serum tryptase and urinary histamine measurements were negative in
women with amniotic fluid embolism; seven of nine had elevated levels of f
etal antigen. All eight who had serum available for testing had abnormally
low levels of complement. Mean C3 level of 44.0 mg/dL and C4 level of 10.7
mg/dL were significantly lower than corresponding postpartum control values
of 117.3 mg/dL and 29.4 mg/dL (P = .018 for C3, P = .012 for C4). Postpart
um C3 and C4 levels decreased by 8% and 5%, respectively, compared with int
rapartum values (P = .003 for C3, P = .021 for C4) but were still within no
rmal range.
Conclusion: Serologic findings suggest a role for complement activation in
the mechanism of amniotic fluid embolism. Laboratory data from this series
did not implicate mast cell degranulation (anaphylaxis) in the pathophysiol
ogy of the disease. (C) 2001 by The American College of Obstetricians and G
ynecologists.