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

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15 Pathology
At autopsy there were numerous petechial haemorrhages on serosal surfaces and pallor of the renal
cortex. Extensive histology demonstrated the features of severe pre-eclampsia. There were no lacerations
in her genital tract and no retained products were found, neither was any evidence of amniotic fl uid
embolism identifi ed within the pulmonary vessels. Despite this, death was given as an anaphylactic
reaction against amniotic fl uid.
In 11 of the remaining deaths there was good clinicopathological correlation. In two there was an atypical
clinical presentation and amniotic fl uid embolus was not suspected clinically but was demonstrated at
autopsy. For example:
A mother presented at term in spontaneous labour with fetal distress. Arrangements were being
made for an emergency caesarean section when she became unrousable. She was resuscitated
and at operation there was an excess of blood in her abdomen. 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 from the site, though not elsewhere, and
despite transfer to a liver unit, she died.
A thorough and detailed autopsy confi rmed the liver rupture with no underlying liver pathology on histology.
Cytokeratin positive squames were found in her lung capillaries on immunochemistry. The cause of death
was attributed to spontaneous rupture of the liver with the amniotic fl uid emboli thought to be resuscitation
‘artefact’ but it is also conceivable that the vigorous resuscitation caused rupture of the liver in a patient
with a bleeding diathesis from amniotic fl uid embolus.
These cases illustrate our poor understanding of the underlying mechanisms surrounding AFE and the
consequent diffi culties for making an accurate diagnosis. There is evidence that foetal squames can
be found in the maternal pulmonary circulation without initiating the clinical syndrome 4 suggesting that
there is either an idiosyncratic response or a threshold effect. In the majority of cases the diagnosis will
be obvious both clinically and pathologically and frequently foetal squames will be visible in the maternal
pulmonary circulation on routine histological stains. There are obviously cases at both ends of the clinical
and pathological spectrum when very careful clinicopathological correlation is a necessity. In these
situations immunocytochemistry for foetal squames is mandatory and will usually resolve the dilemma. It
is possible that foetal squames are a surrogate marker for other components of amniotic fl uid that trigger
an immunological reaction in a susceptible individual 5 . Consequently, in situations where the clinical and
pathological fi ndings lack concordance further investigations are indicated. An immunological reaction
to the foetal sialyl Tn antigen has been found and the essence of this antigen can be demonstrated
by immunocytochemistry 6, 7 . In the light of our current knowledge, this would be an appropriate further
investigation for such diagnostic conundrums.
Box 15.2
Pathology learning points: AFE
The diagnosis of amniotic fl uid embolism needs careful and critical pathological evaluation.
Diffi cult cases require detailed immunocytochemical studies for fetal squames and possibly for fetal mucins.
Sepsis
Puerperal sepsis is increasing in incidence. The Health Protection Agency’s enhanced surveillance of all
Group A streptococcal infections in 2003 identifi ed a total of 2085 cases with an overall mortality of 27%.
Three per cent of the total cases were women with puerperal sepsis 8 . In this Report the deaths of 19 deaths
women have been directly attributed to sepsis. Overall the most common predisposing factor was an