Severe pre-eclampsia at 33 weeks in a district hospital without neonatal intensive care
A 29-year-old woman, G2P1, is admitted at 33+4 weeks' gestation with a 2-day history of frontal headache and visual flashes. Blood pressure is 168/112 mmHg on two readings 15 minutes apart, and urine dipstick shows 3+ protein. She has right upper quadrant tenderness. Platelets are 88,000/µL, ALT 210 U/L and creatinine 1.1 mg/dL. The cardiotocograph shows a baseline of 150 bpm with reduced variability but no decelerations. The district hospital has magnesium sulphate and labetalol but no neonatal intensive care unit; the special care baby unit can provide CPAP but not surfactant. The tertiary obstetric unit with a level 3 neonatal unit is 3 hours away by road, and an ambulance crew is available. She had a caesarean section for fetal distress in her previous pregnancy.
1. What is the diagnosis, and what are your first drug treatments, with doses?
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This is pre-eclampsia with severe features at 33+4 weeks. The systolic pressure is above 160 mmHg, she has cerebral and visual symptoms, right upper quadrant pain, thrombocytopenia below 100,000/µL and transaminitis - any one of these defines severe disease, and she has several. The creatinine is mildly raised, so renal involvement is beginning.
Start magnesium sulphate for seizure prophylaxis: a loading dose of 4 g intravenously over 20 minutes (diluted in 0.9% sodium chloride), followed by an infusion of 1 g/hour. Magnesium is indicated for severe disease regardless of whether she has already fitted, and does not lower blood pressure appreciably.
Treat the hypertension urgently but not precipitately. Give labetalol 20 mg intravenously over 2 minutes; if the blood pressure remains above 160/110 mmHg after 10 minutes, give 40 mg, then 80 mg at 10-minute intervals to a cumulative maximum of about 300 mg. Oral nifedipine 10 mg is an alternative if intravenous access or labetalol is unavailable. The target is roughly 140–150/90–100 mmHg: bringing the pressure down to normal can critically reduce uteroplacental perfusion. Restrict total fluids to about 80 mL/hour to reduce the risk of pulmonary oedema, and record strict input–output. Give antenatal corticosteroids if delivery can be deferred: either betamethasone 12 mg intramuscularly, repeated after 24 hours, or dexamethasone 6 mg 12-hourly for four doses.
2. Should she be transferred before delivery or delivered in the district hospital? Explain your reasoning.
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The answer depends on whether she can be stabilised and whether there is a maternal indication for immediate delivery - not on the CTG alone, which currently shows reduced variability without decelerations.
Transfer in utero is preferred if, after magnesium and antihypertensives, her blood pressure is controlled, symptoms are settling, platelets and liver enzymes are stable, there is no abruption or pulmonary oedema, and the fetal tracing remains acceptable without decelerations. The reason is neonatal: at 33+4 weeks a baby may need surfactant and level 3 support that this hospital cannot provide, and delivering here commits the neonate to a separate, riskier transfer after birth. Give corticosteroids and transfer to the tertiary unit, where delivery can be planned after the 24–48-hour steroid window if her condition remains stable.
Deliver locally, after stabilisation, if she develops uncontrollable hypertension despite treatment, eclampsia, pulmonary oedema, abruption, disseminated intravascular coagulation, progressive renal or hepatic deterioration, or a non-reassuring fetal heart pattern such as repeated decelerations. In that situation, maternal safety overrides neonatal logistics and the neonate is transferred afterwards. Because she has had a previous caesarean, a trial of labour is unlikely to be advised at this gestation; plan delivery by caesarean section, and make that decision explicitly rather than allowing the transfer debate to delay definitive care. Speak to the tertiary unit before departure, and document who accepted her and the plan for delivery on arrival.
3. What will you monitor for during the magnesium infusion, and how do you respond if toxicity develops?
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Magnesium sulphate has a narrow therapeutic window, and toxicity is predicted by clinical signs in a predictable order: loss of the patellar reflex, then respiratory depression, then cardiac arrest. Monitor respiratory rate, deep tendon reflexes, urine output and oxygen saturation at least hourly, and check serum magnesium if available - but do not rely on levels alone; the bedside signs are the practical trigger.
Because magnesium is cleared renally, reduce or withhold the infusion if urine output falls below about 30 mL/hour (0.5 mL/kg/h) or if creatinine rises. If the reflexes are absent or the respiratory rate falls below 12–16/min, stop the infusion, give oxygen, and prepare calcium gluconate 10% 10 mL intravenously over 10 minutes as the antidote. Inform the anaesthetist and neonatal team early if toxicity occurs, because both mother and fetus can be affected.
Continue magnesium for 24 hours after delivery, or after the last seizure if she fits. Recurrent seizures are treated with a further 2 g intravenous bolus over 5 minutes. After delivery, watch for postpartum haemorrhage, because thrombocytopenia and antihypertensive drugs both increase risk, and continue close blood pressure monitoring for at least 24–48 hours - pre-eclampsia can worsen or first appear after delivery.