Describe magnesium sulphate regimen in eclampsia — its aetiology, clinical features and management.

Definition

Magnesium sulphate (MgSO₄) is the drug of choice for the control and prevention of convulsions in eclampsia and severe pre-eclampsia. It acts as a membrane stabiliser and cerebral anticonvulsant and is superior to diazepam and phenytoin in preventing recurrent fits and reducing maternal death.

Regimens

Pritchard (intramuscular) regimen — Loading dose: 4 g of 20% MgSO₄ IV slowly over 3–5 minutes, immediately followed by 10 g of 50% MgSO₄ deep IM (5 g into each buttock). Maintenance: 5 g of 50% MgSO₄ IM 4-hourly in alternate buttocks.

Zuspan / Sibai (intravenous) regimen — Loading 4–6 g IV over 15–20 minutes, then a maintenance infusion of 1–2 g/hour.

A recurrent convulsion is treated with a further 2 g IV bolus over 5 minutes. MgSO₄ is continued for 24 hours after the last fit or after delivery, whichever is later.

Monitoring Before Each Maintenance Dose

• Knee-jerk present (lost above ~10 mEq/L).
• Urine output > 30 mL/hour (magnesium is excreted renally).
• Respiratory rate > 12/minute.

The therapeutic serum level is 4–7 mEq/L. Toxicity: loss of reflexes (> 7 mEq/L), respiratory depression (> 10 mEq/L) and cardiac arrest (> 25 mEq/L).

Mechanism and Advantages

Magnesium acts as a membrane stabiliser and cerebral vasodilator, blocking neuromuscular transmission and reducing cerebral oedema and vasospasm. Compared with diazepam and phenytoin it gives better control of recurrent fits, lower maternal mortality and fewer perinatal deaths, without heavy maternal sedation (the Collaborative Eclampsia Trial). It is also used for seizure prophylaxis in severe pre-eclampsia and for fetal neuroprotection when very preterm delivery is anticipated.

Cautions and Contraindications

Use with care in renal insufficiency (reduce/monitor levels) and avoid in myasthenia gravis and heart block. Keep calcium gluconate and facilities for assisted ventilation ready at the bedside whenever magnesium is being given.

A Note on WHY Mgso4 Monitoring Is So Simple — and So Safe

A reassuring and vital point is understanding why magnesium sulphate, despite its narrow therapeutic margin, is safe enough to be given by a nurse in a peripheral hospital. The answer lies in the orderly, predictable sequence in which toxicity develops. As the serum magnesium rises, the effects appear in a fixed order: the therapeutic range (4–7 mEq/L) gives anticonvulsant protection; the first sign of excess is loss of the patellar (knee-jerk) reflex (~8–10 mEq/L); then respiratory depression (~12 mEq/L); and only at higher levels, cardiac arrest. Because the knee jerk disappears well before respiration is threatened, it serves as an early-warning system requiring no laboratory and no equipment — a tendon hammer and a watch suffice. Hence the rule that before every maintenance dose one confirms that the knee jerk is present, the respiratory rate exceeds 12 per minute, and the urine output exceeds 30 mL per hour (magnesium is excreted renally, so oliguria causes accumulation). If any of these fails, the next dose is withheld; if toxicity is established, calcium gluconate 1 g intravenously is the antidote. Understanding that toxicity announces itself in a fixed, clinically-detectable order explains why this simple bedside checklist makes a potentially lethal drug safe.

Calcium gluconate is the antidote for magnesium toxicity.

• Pritchard regimen: loading 4 g IV (20%) slowly + 10 g IM (5 g into each buttock); maintenance 5 g IM 4-hourly, alternate buttocks.
• Continue for 24 hours after the last fit or after delivery, whichever is later; a recurrent fit is treated with a further 2 g IV.
• Before every dose check: knee jerk present, respiratory rate >12/min, urine output >30 mL/h.
• Toxicity sequence: loss of knee jerk → respiratory depression → cardiac arrest; antidote = calcium gluconate 1 g IV.
• MgSO4 prevents fits but is not an antihypertensive — give labetalol/nifedipine/hydralazine separately; delivery is the definitive cure.