Saving Mothers' Lives: - Public Health Agency for Northern Ireland

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5 Amniotic fl uid embolism
of amniotic fl uid embolism 1 . Future clarity may be found in the measurement of complement, which may
be activated following AFE, or the fetal antigen sialyl Tn 2 . The latter can be measured serologically or by
immunocytochemistry on lung tissue but, as yet, is not widely available.
The reasons for the large increase in deaths from AFE for this triennium are not immediately obvious. The
main criterion for diagnosis is the fi nding of fetal squames in the pulmonary vasculature at autopsy. The
improved quality of examination and reporting at autopsy may have resulted in some increase in diagnosis,
providing there is clinicopathological correlation. Such increased ascertainment therefore could account for
some, though not all, of this increase. Excluding the two Late deaths, which had to be classifi ed on clinical
features alone, there were three other deaths in which the diagnosis was made clinically, supported by the
Enquiry assessors, but not confi rmed at autopsy. For example:
A multigravid woman who had a normal pregnancy was admitted in late pregnancy because
of pre-eclampsia. She had labour induced with 3mg of oral prostaglandin followed a few hours
later by a further 3 mg. A rapid labour ensued which resulted in a vaginal delivery with an
incomplete placenta. She was transferred to theatre for manual removal of the placental remains
at which stage her observations were stable. She collapsed an hour or so later and developed
disseminated intravascular coagulation (DIC). She sustained another cardiac arrest shortly
afterwards from which she could not be resuscitated.
At autopsy there were numerous petechial haemorrhages on her serosal surfaces. Extensive histology
demonstrated the features of severe pre-eclampsia but found no retention of products in the uterus and no
evidence of amniotic fl uid embolism was identifi ed within the pulmonary capillaries.
There were another three maternal deaths where the fetal squames were scanty and only detected after
prolonged searching. It is therefore conceivable that these six cases may not have been categorised
as amniotic fl uid embolism in previous Reports. Some of these cases also had an atypical clinical
presentation. For example:
A primigravid woman presented at term in spontaneous labour. She collapsed a few hours later,
just as arrangements were being made for an emergency caesarean section for fetal distress.
She was successfully resuscitated but at operation an excess of blood was found in her abdomen
and an exploratory laparotomy revealed a two centimetre tear on the inferior aspect of the left
lobe of the liver. Despite transfusion and blood products she continued to bleed and, even though
she was transferred to a liver unit, she eventually died.
Her autopsy confi rmed the liver rupture but there was no underlying liver pathology on histology.
Cytokeratin positive squames were found in her lung capillaries as well as in a medium-sized artery on
immunochemistry. Her cause of death was attributed to spontaneous rupture of the liver but it is also
conceivable that vigorous resuscitation caused rupture of the liver in a patient with a bleeding diathesis
from amniotic fl uid embolus.
The women who died
The classical scenario of amniotic fl uid embolism usually involves an older, multiparous woman in
advanced labour who suddenly collapses, develops DIC and dies rapidly thereafter:
A woman with a history of previous normal deliveries had labour induced with 3mg of vaginal
prostaglandin which was repeated a few hours later and labour then rapidly commenced. She
collapsed at the start of the second stage and, following successful cardiopulmonary resuscitation,
an emergency caesarean section was performed. She developed DIC with an estimated blood loss