Seizure prophylaxis

The results of the Collaborative Eclampsia Trial provide compelling evidence that magnesium sulfate is the anticonvulsant of choice in eclampsia. Women allocated magnesium had a 52 per cent lower risk of recurrent convulsions than those allocated diazepam (13.2 per cent versus 27.9 per cent) and a 67 per cent lower risk than those allocated phenytoin (5.7 per cent versus 17.1 per cent) ( Eclampsia,..Tr!a.! C.P!!§bPEaíi.V®...GI0up 1995). Although there was no difference in maternal mortality between the groups, women treated with phenytoin were more likely to be ventilated, to develop pneumonia, and to be admitted to intensive care facilities ( Eclampsia..

TrialColJaboritive G.roup.199.5.). Magnesium appears to act primarily by relieving cerebral vasospasm, although the drug has several other beneficial maternal effects including the production of the endothelial vasodilator prostacyclin. Recent evidence has also suggested that exposure to magnesium sulfate in utero reduces the risk of cerebral palsy in infants born weighing less than 1500 g.

Maintenance treatment with magnesium sulfate should be started immediately after the initial intravenous bolus. Intramuscular injections are painful and associated with abscess formation in 0.5 per cent (Eclampsy Therefore the intravenous route is preferred. Some authorities recommend a maintenance dose of 2 g/h on the basis that this dose consistently produces serum levels within the therapeutic range (2-4 mmol/l) ( Sibai eL§.L 1981). However, a dose of 1 g/h was used in the Collaborative Eclampsia Trial and until a definite therapeutic benefit has been demonstrated using the higher dose, it is probably appropriate to use the lower dose. Maintenance anticonvulsant therapy should be continued for at least 24 h after the last convulsion.

The first sign of magnesium toxicity is the loss of deep tendon reflexes, which occurs when serum levels exceed 5 mmol/l. This is followed by respiratory depression and ultimately respiratory arrest. In most cases therapy can be monitored safely by hourly measurement of the patellar reflex and oxygen saturation without the need for serum levels. If deep tendon reflexes are absent, further doses of magnesium sulfate should be withheld until reflexes return. Significant respiratory depression should be treated with 1 g calcium gluconate given intravenously. Magnesium is excreted by the kidney, and regular monitoring of serum levels should be considered if the patient is oliguric (urine output below 100 ml in 4 h). If serum levels are not available, consideration should be given to reducing the maintenance dose to 0.5 g/h.

Recurrent convulsions will occur despite administration of magnesium sulfate in 5 to 15 per cent of cases ( Eclampsia,..Tr!a.! CP.!!ibP^iíi.V§...G.roup 1995). In a significant proportion of such cases magnesium levels will be subtherapeutic (Sibai eL§L 1981) and therefore measurement of serum magnesium is advisable. Convulsions should be treated with a further bolus of 2 g of magnesium sulfate. Subsequent management will depend on the serum level and the clinical course. If the level is less than 2 mmol/l, the maintenance infusion should be increased and serum magnesium levels checked every 4 to 6 h. If further seizures occur despite therapeutic levels of magnesium, options include diazepam 10 mg intravenously or thiopental (thiopentone) 50 to 100 mg intravenously. Intubation may become necessary in such women to protect the airway and ensure adequate oxygenation. Further seizures should be managed by intermittent positive-pressure ventilation and muscle relaxation.

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