Magnesium sulfate is used as a tocolytic and anticonvulsant in parturient patients with preeclampsa/eclampsia. Although it is a very effective medication in this setting it has severe adverse effects at supratherapeutic levels requiring regular monitoring of the patient for sign/symptoms of magnesium toxicity.
Some minor side effects of magnesium are feeling warm/flushed, nausea or vomiting, sedation, dizziness, injection site irritation, and muscle weakness. As the plasma levels increase the muscle weakness becomes more pronounced and there is a marked reduction and then loss of deep tendon reflexes eventually leading to flaccid paralysis and respiratory arrest. This is the result of both decreased release of presynaptic acetylcholine and decreased motor end-plate sensitivity to acetylcholine. This end-plate effect results in an increased sensitivity to both depolarizing and non-depolarizing muscle relaxants. NMDBs have a reduced ED50 and onset time, and increased duration of action. Muscle relaxant doses should be reduced by 25-50%. Fasciculations will likely be absent with succinylcholine administration. Magnesium has cardiovascular effects ranging from hypotension and bradycardia to complete heart block/cardiac arrest. A prolonged PR interval and widened QRS may be seen on EKG. Magnesium administration also increases the risk of post-partum hemorrhage.
Neonates born to parturients receiving magnesium may have magnesium toxicity at the time of delivery resulting in flaccidity, respiratory depression, and apnea. The treatment for magnesium toxicity, in all patients, is intravenous calcium (note: there is approximately three times more calcium in calcium chloride than calcium gluconate). Loop diuretics such as furosemide increase the renal excretion of magnesium.