A nulliparous 25-year-old patient presented to Nelson Maternity Unit at 34 weeks gestation. She had seen her midwife two hours earlier because of feeling unwell with a frontal headache for the previous few days, and loose bowels for one week. She had less than usual fetal movements. On the day of admission she had also experienced constant, quite severe epigastric pain. Her midwife had recorded a BP180/120 and urine dipstick of 3+ protein.
The patient had a normal pregnancy to date, no relevant medical problems, though the patient’s mother had pre-eclampsia in both her pregnancies leading to two preterm deliveries.
On arrival at Nelson Hospital, at 3pm, blood pressure (BP) was 180/130 with 3+ protein on urine dipstick. On examination she looked uncomfortable with a tender epigastrium, soft non-tender uterus appropriate for dates, fetal head 5/5 palpable abdominally, brisk reflexes and five beats clonus bilaterally. Vaginal examination showed: cervix 3cm long, closed, posterior, head at station -3, CTG reactive.
Bloods: Hb 153, Hct 0.46 Pt 173, Cr 89, ALT 135, urate 0.52, in other words, haemoconcentrated, mildly abnormal renal and liver function with normal coagulation profile.
Magnesium sulphate infusion was commenced at 3.15pm using 5g in 100ml over 20 minutes loading dose then maintenance rate of 15ml per hour, in other words, 1.5g per hour.
At 3.25pm, labetalol 200mg was given orally, at 4.45pm her blood pressure was still 184/132 so nifedipine 10mg oral stat was given, BP gradually decreased to 154/106. Betamethasone 11.4mg im was given at 6.30pm.
At 6.30pm her blood pressure was 156/108 with very concentrated urine (very abnormal brown sludgy urine) her headache was easing, reflexes 2+, JVP +2.
The patient consented to a caesarean section and the anaesthetist recommended one litre of Hartmann’s solution one hour pre-operation. Because of the imminent spinal/epidural, no further anti-hypertensive was given.
Under a combined spinal epidural a growth-retarded female infant was delivered by routine caesarean section at 8.03pm. Apgar scores were 7, 9 and 10, birth weight 1.695kg and the neonate was admitted to NICU in good condition; the estimated blood loss was 300ml.
While I was closing the second layer of uterus, the patient had a tonic-clonic seizure lasting two minutes, the anaesthetist maintained her airway and administered propofol 20mg, a second bolus of 5g magnesium sulphate was given by the paediatrician under my instructions after a midwife collected it from the eclampsia pack on delivery. An arterial line was placed by the anaesthetist, intrathecal morphine administered pre-removal of epidural and the patient transferred to ICU.
In ICU, intravenous infusion magnesium sulphate 2g per hour was commenced, reflexes were present at every 15-minute check. Methyldopa 250mg orally every eight hours was commenced, as this is believed to be neuro protective. Charted hydralazine if blood pressure >155 systolic or >100 diastolic. Bloods at midnight: Pt 55, APTT 36, magnesium 3.1 (1.6-3.3mmol/l therapeutic), ALT204, Cr111- clexane withheld, note the significant deterioration in coagulation markers, renal and liver function.
Day one post caesarean: normal lochia, the patient reported no headache/epigastric pain and feeling much better. Blood pressure was controlled on methyldopa and two doses iv hydralazine overnight, three beats clonus bilaterally, fluids restricted to 1.5 litres per 24 hours, urine output >20ml per hour and paler colour than pre-caesarean. Her blood tests in the morning were: Hb 111, Pt 47, APPT 32, INR 1.1, ALT 166, Cr104. Evening bloods: Hb94 magnesium 3 (mid target range).
Day two post caesarean: no hydralazine needed, 154/70 maximum blood pressure, feeling well. Hb83, Pt65 normal coagulation profile otherwise, good diuresis, magnesium infusion decreased to 1g per hour and three hours later stopped. In the evening, reflexes were hyperactive and six beats clonus so magnesium restarted at 1mg per hour.
Day three post caesarean: magnesium infusion stopped at 1pm. Blood pressure stable on methyldopa, mobilising Hb75, Pt88 reflexes normal, but clonus four beats persisted.
Day four post caesarean: transferred to ward thanks to steady progress. There was marked bruising around wound. Clexane was started when platelets normalised. Hb normalised without blood transfusion, suggesting the anaemia was reflecting fluid shifts not blood loss. Her subsequent recovery was straightforward.
Magnesium sulphate is used to prevent or stop an eclamptic convulsion, to prevent immediate recurrence of convulsions and to gain time for antihypertensives to function. Magnesium sulphate prevents or controls convulsions by blocking neuromuscular transmission. It decreases the amount of acetylcholine secreted at the end plate by the motor nerve impulse.1 It also causes vasodilation of cerebral vasculature reversing the cerebral ischaemia thought to trigger eclampsia. Magnesium should be used with caution in women with impaired renal function because of the risk of magnesium toxicity and is contra-indicated in patients with heart block or myocardial damage.
Data from the Collaborative Eclampsia Trial2 provided strong evidence that magnesium sulphate is the drug of choice for women with eclampsia. Most Australasian units use intravenous regimes as they are less painful than intramuscular injections. The intravenous regimen used in the trial was 1g per hour with a 4g loading dose, and monitoring was clinical rather than by serum concentrations of magnesium. At 1g per hour, clinical monitoring of reflexes and respiratory rate appeared to be safe without the need to check serum magnesium levels. 1g per hour, 1.5g per hour and 2g per hour are all commonly used regimes. Dose is adjusted according to patient response, clinical signs of toxicity and serum magnesium levels (aim to achieve levels of approximately 1.6-3.3mmol/L).
In this case the 2g per hour magnesium infusion led to levels of 2.8–3.1mmol/L, which is what we wanted in the higher half of the target range as the patient had proven lower levels were not sufficient to prevent her convulsions. Her reflexes were never absent and respiratory rate never low. It would be more usual to give a smaller second loading dose of 2–4g but here the infusion was delayed while the patient was transferred to ICU.
A hypertensive emergency is defined as an acute-onset, persistent (lasting 15 minutes or more), severe systolic (greater than or equal to 160mm Hg) or severe diastolic hypertension (greater than or equal to 110mm Hg) or both in pregnant or postpartum women with pre-eclampsia or eclampsia.3
In a recent case series of 28 women with severe pre-eclampsia and stroke, all but one woman had severe systolic hypertension (greater than or equal to 160mm Hg) just before a haemorrhagic stroke, and 54 per cent died, whereas only 13 per cent had severe diastolic hypertension (greater than or equal to 110mm Hg) in the hours preceding stroke.4 A similar relationship between severe systolic hypertension and risk of hemorrhagic stroke has been observed in non-pregnant adults.5
Intravenous or oral labetalol, intravenous hydralazine and oral nifedipine have all been used to control severe hypertension in pregnant women. Aiming for a systolic blood pressure of less than 150 and diastolic less than 100mmHg is generally recommended.6
In our case, I think that starting with intravenous hydralazine or labetalol would have brought down the patient’s blood pressure faster. Starting the magnesium loading dose was prioritised over administering an intravenous anti-hypertensive. While oral anti-hypertensives are appropriate until an intravenous line is sited I believe once a line is sited intravenous anti-hypertensives should be the top priority.
I have presented an unusual case where our first line 1.5g per hour infusion of magnesium sulphate did not prevent an eclamptic convulsion. I have also emphasised the importance of treating blood pressure first in a hypertensive emergency.
Written informed consent to publish this case report and images was obtained from the patient.