Magnesium sulfate has been assigned to pregnancy category A by the FDA. Studies in pregnant women have not shown evidence of fetal risk if magnesium sulfate is administered during any trimesters of pregnancy. However, because studies cannot completely rule out the possibility of harm, magnesium sulfate injection is only recommended for use during pregnancy when benefit outweighs risk.
Newborns may show signs of magnesium toxicity (i.e. respiratory and/or neuromuscular depression) if the mother has received intravenous magnesium sulfate prior to delivery (especially if for a period of longer than 24 hours). Equipment for assisted ventilation as well as intravenous calcium should be immediately available for the first 24 to 48 hours after delivery. One study has reported that maternal magnesium sulfate treatment is associated with reduced brain blood flow perfusion in preterm infants. However, intravenous magnesium sulfate did not lead to lower neonate apgar scores in a study of women treated for pre-eclampsia even though the newborn's cord level indicated hypermagnesemia. The mean cord magnesium level (5.3 mEq/100 mL) was equivalent to the mean maternal serum level. Cord serum magnesium levels do not usually correlate with infant toxicity. The Collaborative Perinatal Project monitored 50,282 mother-child pairs, 141 of which had been exposed to magnesium sulfate during pregnancy. No reports or evidence were found linking congenital birth defects with magnesium sulfate. A study of 7000 offspring of mothers treated for pre-eclampsia noted no adverse effects due to magnesium sulfate therapy in the fetuses or newborns. One study compared the newborn of women with pregnancy-induced hypertension who received magnesium sulfate with women who did not receive treatment. Neurologic behavior in the infants was similar in both groups except that the exposed group had decreased active tone of the neck extensors the day after birth. Long-term infusions of magnesium (such as those used for tocolysis) may lead to persistent hypocalcemia and congenital rickets in the fetus. Case reports of 2 women receiving 9 or 14 weeks of intravenous magnesium therapy prior to delivery noted bony abnormalities. Slight hypocalcemia occurred in one infant. Both infants were treated with intravenous calcium for 3 to 5 days and then given bottle feedings without added calcium or vitamin D. The only noted physical abnormality at 3 year follow-up was dental enamel hypoplasia in one infant. Fetal hypermagnesemia may have decreased parathyroid hormone release and lead to fetal hypocalcemia. The combination of in-utero acquired magnesium sulfate and gentamicin (administered after birth) may lead to respiratory depression in the newborn. The mechanism of this interaction is not known. Animal studies have confirmed this drug interaction.
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