Severe Preeclampsia on Magnesium Sulfate: Drowsy with Falling Urine Output
Mrs B is 34 weeks pregnant, admitted 14 hours ago with severe preeclampsia: blood pressure persistently above 160/110 mmHg, headache, 3+ proteinuria, platelets 96 × 10⁹/L, aspartate aminotransferase 88 U/L. She received a 4 g magnesium sulfate loading dose and is maintained on 1 g/hour. At 07:00 she rings the bell. She says the headache is 'splitting' and her vision is blurry. Blood pressure is 174/110 mmHg in both arms, heart rate 92, respiratory rate 12, SpO2 98%, temperature 36.8 °C. She is drowsy but rousable and answers slowly, saying she 'just needs to sleep'. Deep tendon reflexes are 2+ and equal with no clonus. Urine output was 25 mL and then 20 mL in the last two hours; it had been running 50–70 mL/hour. The fetal heart rate is 150 beats/min with no decelerations on the monitor. There is no calcium gluconate on the unit; it is stocked in the central pharmacy.
1. Which findings drive your first ten minutes of action, and in what order? Justify the sequence and state whether the magnesium infusion should be stopped.
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Priority one - treat the blood pressure, because the immediate lethal risk is maternal intracranial haemorrhage. 174/110 mmHg with a headache and visual disturbance is a hypertensive emergency of pregnancy. Call for help (obstetric emergency bell, second midwife, obstetric registrar and anaesthetist), stay with her, position her left lateral, apply continuous cardiotocography, and give the prescribed antihypertensive - labetalol 20 mg IV or hydralazine 5 mg IV - titrated to a target of roughly 140–150/90–100 mmHg. A rapid drop to 'normal' pressures is dangerous because it reduces uteroplacental perfusion.
Priority two - confirm magnesium safety before changing it. Respiratory rate 12 is low-normal, not depressed; reflexes are 2+ and clonus is absent, so the classic triad of magnesium toxicity (loss of reflexes, respiratory depression, oliguria) is only partly present. Do not stop the infusion reflexively, because she still needs seizure prophylaxis - but do not simply continue on autopilot either. The drowsiness plus oliguria means magnesium clearance may be falling. Request a serum magnesium and creatinine urgently, ask the prescriber to consider dose reduction if renal function is impaired, and have calcium gluconate brought to the bedside now.
Priority three - fetal and neurological monitoring with a documented plan for delivery, since severe features at 34 weeks usually mean delivery after stabilisation. The reasoning is that hypotension from over-treatment, seizures from under-treatment and stroke from untreated hypertension are all preventable deaths, so all three tracks run in parallel rather than in sequence.
2. Explain how you would distinguish magnesium toxicity from worsening preeclampsia in this patient, and what data you need before deciding.
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Magnesium toxicity is a depression syndrome that progresses predictably: nausea and flushing first, then loss of the patellar reflex (the earliest reliable sign, usually around 3.5–5 mmol/L), then respiratory depression below about 12 breaths/min, then coma and cardiac arrest. Oliguria and renal impairment accelerate all of this because magnesium is cleared by the kidney.
Worsening preeclampsia is an excitation and endothelial syndrome: unrelieved or worsening headache, visual scotomata or blurring, epigastric or right upper quadrant pain, clonus, rising blood pressure, falling platelets, rising transaminases, and haemolysis. Central nervous system signs here tend towards irritability and hyperreflexia rather than drowsiness.
Applying this to Mrs B: her drowsiness is ambiguous - it fits both. But her reflexes are preserved, clonus is absent, respiratory rate is 12 and she has no nausea or flushing, which makes established toxicity less likely. Her headache, blurred vision and oliguria point more towards severe preeclampsia with renal involvement plus a contribution from reduced magnesium clearance.
Data needed before deciding: serum magnesium level with the local therapeutic range (commonly 2–3.5 mmol/L), creatinine and estimated glomerular filtration rate, urine output trend, hourly reflexes and respiratory rate, continuous SpO2, repeat platelets and liver enzymes, assessment for clonus and epigastric pain, and continuous cardiotocography. The nurse's judgement should be a provisional synthesis pending these results, with the obstetric team informed and involved, not a personal decision to stop a life-saving infusion.
3. Set out your escalation, retrieval and pharmacy plan, including what you request and who you call.
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Calls (in parallel, not in sequence)
- Obstetric registrar now: report blood pressure 174/110, headache, visual symptoms, drowsiness, urine 45 mL over 2 hours, respiratory rate 12, reflexes 2+, no clonus. Ask for a bedside review and a decision on antihypertensive escalation, magnesium rate and timing of delivery.
- Anaesthetist and theatre coordinator: alert them that a 34-week severe preeclampsia may need caesarean section, so airway and blood pressure planning starts early.
- Neonatal unit: warn of a possible 34-week delivery.
- Pharmacy and blood bank: request two ampoules of 10% calcium gluconate 10 mL to the bedside immediately (antidote for magnesium toxicity; 1 g IV over about 10 minutes if toxicity occurs), plus cross-matched blood in case of haemorrhage or HELLP progression.
- Senior midwife or nurse in charge: request enhanced observation, ideally one-to-one, with a written observation chart for reflexes, respiratory rate, urine output and blood pressure every 15 minutes.
Documentation Record the time of each call, who was spoken to, the exact observations quoted, the response and the plan. Note that the calcium gluconate was not on the unit and what was done about it, because that stock gap is a system risk that must be surfaced, not absorbed silently. Use a structured obstetric early warning score to support the escalation and re-score after every intervention.