The mainstay for diagnosis of amniotic fluid embolism should be a typical clinical picture such as cardiorespiratory failure of abrupt onset that occurs during the third trimester of pregnancy or around delivery, and which is followed by the development of pulmonary edema and coagulopathy.
Demonstration of trophoblastic and squamous cells in the pulmonary artery vasculature is by no means pathognomonic of this condition. Similar cells have been recovered in the peripheral blood of normal pregnant women and in the pulmonary arterial circulation of patients undergoing pulmonary artery catheterization for a variety of medical indications other than amniotic fluid embolism. Any venepuncture may result in the introduction of adult squamous cells into the venous circulation; unfortunately, there are no reliable histological methods for differentiating adult epidermal from fetal squamous cells derived from the infant's skin and present in amniotic fluid. Other debris of presumed fetal or amniotic origin such as lanugo hair, mucin from meconium, and fat from the vernix caseosa may be demonstrated in the buffy coat of pulmonary arterial blood or in a wedged pulmonary capillary aspirate of patients with amniotic fluid embolism. Special stains are usually required to detect these elements whose diagnostic value remains controversial. In the future, antimucin monoclonal antibody and maternal zinc coproporphyrin I assay may reveal specific markers of meconium entrance into the maternal circulation.
As no single clinical or laboratory finding is pathognomonic of this syndrome, a careful exclusion of other critical illnesses is mandatory ( Table 1 and Tabled).
Table 2 Differential diagnosis of amniotic fluid embolism
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