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

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3 Pre-eclampsia and eclampsia
Women with pre-eclampsia but who died from other causes are counted and discussed in other Chapters,
including cases of post caesarean section haemorrhage in Chapter 4, iatrogenic haemothorax in Chapter
8, and intracranial haemorrhage that was probably unrelated to pre-eclampsia in Chapter 10. Key learning
points are shown in Box 3.1.
Box 3.1
Learning points: pre-eclampsia and eclampsia
Fulminating pre-eclampsia occurs at term and post term, as well as pre-term.
Systolic blood pressures over 160 mm/Hg must be treated.
Syntometrine should not be given for the active management of the third stage if the mother is
hypertensive, or her blood pressure has not been checked.
The anaesthestist should be given as much time as possible to try to prevent the pressor effects of
intubation in the pre-eclamptic woman, even when there are pressing fetal reasons for urgent caesarean
section under general anaesthesia.
Systolic hypertension
The single major failing in clinical care in pre-eclampsia in the current triennium was inadequate treatment
of systolic hypertension. The sequel, intracranial haemorrhage, occurred in several cases. The following
description is illustrative:
A woman whose early pregnancy blood pressure was 140/70 mm/Hg was normotensive until
mid-third trimester when her blood pressure was found to be 180/100 mm/Hg, with proteinuria
++ and she was admitted for care. Labetalol was started and she was discharged but remained
hypertensive. She was subsequently readmitted with a blood pressure of 160/100 mm/Hg and
proteinuria +++. Over the next 48 hours, her blood pressure remained elevated and reached a
maximum systolic pressure of 205 mm/Hg. The dose of oral labetalol was increased, and low
molecular weight heparin thromboprophylaxis started. After a further 48 hours, she was still
symptomatic and had a blood pressure of 220/110 mm/Hg with disordered liver function.
Magnesium sulphate was started and a single oral dose of nifedipine given. Induction of labour
was unsuccessful and caesarean section was performed. After delivery, her systolic blood pressure
remained elevated between 190 and 205 mm/Hg, on oral labetalol. Neurological signs fi rst appeared
within a day of delivery. Her systolic pressure remained between 180-200 mm/Hg. She became
unresponsive and a CT scan showed a cerebral haemorrhage. She died in the Critical Care unit.
Autopsy showed dual intracranial pathology: cerebral sinus thrombosis as well as the haemorrhage.
This woman had prolonged hypertension with systolic pressures frequently above 200 mm/Hg, and no
effective treatment. There was additional sub-standard care through inappropriate discharge, inappropriate
referral to community midwifery care after discharge on anti-hypertensive medication and inappropriate
delay in delivery.
There is incomplete understanding of the precise mechanisms that link hypertension and haemorrhagic
stroke, both in pregnant and non-pregnant patients, but systolic hypertension is certainly important.
With large pulse pressures, the mean arterial pressure (MAP) may not convey the real threat of a very
high systolic pressure. In the last Report it was suggested that clinical guidelines should identify a
systolic pressure above which urgent and effective anti-hypertensive treatment is required. Since then, a