Eclampsia with its precursor preeclampsia is a condition that is rapidly taking the fore front in many countries as the leading cause of adverse maternal outcome, because of gains accruing from ability to curb, the better-understood obstetric haemorrhage. The exact mechanism by which preeclampsia leads to eclampsia remains unclear resulting in difficulty in prediction of individuals with preeclampsia who would develop eclampsia. Magnesium sulphate has been a recognised remedy since the early twentieth century, becoming scientifically proven and increasingly popular in the last two decades. However, the exact mechanism of action of magnesium sulphate in alleviating and preventing seizures still remains elusive and fits have been observed to occur during magnesium sulphate therapy. Better understanding of magnesium homeostasis in pregnancy and improved knowledge of the effects of magnesium sulphate may help unravel the mystery behind the cause and course of eclampsia.
The global incidence of pre-eclampsia has been estimated at 5-14% of all pregnancies while in developing nations, the incidence of the disease ABSTRACT Background: Magnesium sulphate use in the prevention of seizures resulting from preeclampsia and eclampsia is widely accepted. However, several protocols exist worldwide. Aim: To determine serum magnesium levels and associated clinical outcomes in severe pre-eclamptic and eclamptic women treated with magnesium sulphate. Methods: Women, 28-41weeks pregnant or in the puerperium with severe pre-eclampsia or eclampsia, participated in this cross sectional study and their serum magnesium levels were measured using the Atomic Absorption Spectrophotometer (AAS) machine. All participants received the standard Pritchard regimen, including monitoring. Results: Seventy five patients participated in the study. They were mostly overweight (mean BMI 26.38 ± 3.40kg/m 2). Mean pre-treatment serum magnesium level was 1.96 ± 0.29 mg/dL; eclamptics had significantly lower levels (p<0.001). Mean treatment serum magnesium level attained was 5.41 ± 0.58 mg/dL. No evidence of magnesium toxicity was observed. Therapeutic range of serum magnesium was required to prevent seizures, and was attained ≥4-hours after loading dose in most of the eclamptics (74%). All convulsions occurred in the interval between the loading dose and the first maintenance dose; eclamptics had greater risk of convulsing while on treatment (RR=11.56, 95%CI= 0.62-216.36, P=0.049). Conclusion: Low serum magnesium level before or during treatment with magnesium sulphate is a risk factor for convulsion in OAUTHC. The Pritchard regimen has a low risk for toxicity thus administration of magnesium sulphate at peripheral centres before referral may be beneficial in preventing repeat convulsions. Modifications involving additions to the loading dose in eclamptics and fewer number of maintenance doses may be beneficial.
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