Severe pre-eclampsia at 34 weeks with a falling platelet count: neuraxial or general anaesthesia?

Her platelet count has fallen from 210 to 78 × 10^9/L in 72 hours, which suggests consumption rather than dilution, and her rising ALT and creatinine indicate possible HELLP syndrome. Before any neuraxial block I would check fibrinogen, PT/APTT and consider thromboelastography; fibrinogen 2.1 g/L is borderline and the conventional clotting tests are near normal, but the trend is more important than any single value. ESRA guidance suggests neuraxial anaesthesia can be considered with platelets above roughly 70–80 × 10^9/L when there is no other coagulopathy, but a rapidly falling count plus HELLP materially increases the risk of spinal haematoma. I would not proceed with a single-shot spinal on a count of 78 alone.

The realistic options are: (1) general anaesthesia, accepting the risks of a difficult airway in a BMI-37 patient with airway oedema and a potentially severe pressor response; (2) transfuse one adult dose of platelets to achieve a count above 100 × 10^9/L and then perform spinal anaesthesia, accepting that transfused platelets may be consumed quickly; (3) repeat the count and coagulation after a short interval, though a category 2 caesarean does not allow much delay. Given the falling count, fetal compromise and maternal risk, I would favour general anaesthesia unless the platelet count rises briskly after transfusion and coagulation is normal. I would document the discussion and involve a senior obstetric anaesthetist.

I would place an arterial line before induction and have a second large-bore cannula. The key is to attenuate the sympathetic response without causing hypotension that compromises uteroplacental perfusion. I would pre-oxygenate, use a rapid-sequence induction with propofol and remifentanil or alfentanil, and give esmolol 0.5 mg/kg or labetalol if the systolic pressure rises above 160 mmHg. Magnesium sulphate already provides vasodilatation and some analgesia, and it potentiates non-depolarising neuromuscular blockers, so I would reduce the rocuronium dose and monitor with a train-of-four. I would avoid ketamine and ergometrine, use a smaller tracheal tube with topical lidocaine, and ensure adequate depth before laryngoscopy. After delivery, I would use an oxytocin infusion rather than a bolus to avoid hypotension, and maintain normocapnia. I would monitor for magnesium toxicity with loss of deep tendon reflexes, respiratory depression and oliguria. If severe hypertension persists, a nitrate infusion may be needed, but I would avoid excessive hypotension because cerebral autoregulation is shifted in pre-eclampsia.

Magnesium reduces presynaptic acetylcholine release at the neuromuscular junction and decreases the sensitivity of the post-synaptic membrane, so it potentiates both depolarising and non-depolarising neuromuscular blockers. In practice this means a reduced rocuronium dose, a longer time to complete reversal and the need for quantitative train-of-four monitoring before extubation. If rocuronium is used, sugammadex must be available. Magnesium also has analgesic properties, reduces catecholamine release and can cause vasodilatation, so it may contribute to intraoperative hypotension. Postoperatively, the infusion is usually continued for 24 hours, and I would monitor reflexes, respiratory rate, urine output and magnesium levels if renal function is impaired. Because magnesium is renally excreted, oliguria or a rising creatinine mandates dose reduction or cessation to avoid hypermagnesaemia. I would also be alert to the interaction with calcium channel blockers and to the risk of uterine atony, which is why oxytocin is used cautiously. These effects are predictable from the physiology and should be planned for rather than discovered in the recovery room.