Magnesium sulfate Side Effects

Not all side effects for magnesium sulfate may be reported. You should always consult a doctor or healthcare professional for medical advice. Side effects can be reported to the FDA here.

For the Consumer

Applies to magnesium sulfate: crystal, ointment, powder, powder for solution, powder for suspension

In addition to its needed effects, some unwanted effects may be caused by magnesium sulfate. In the event that any of these side effects do occur, they may require medical attention.

You should check with your doctor immediately if any of these side effects occur when taking magnesium sulfate:

Incidence not known
  • Confusion
  • dizziness or lightheadedness
  • fast, slow, or irregular heartbeat
  • low blood pressure
  • muscle weakness
  • skin infection after soaking
  • sleepiness

Some of the side effects that can occur with magnesium sulfate may not need medical attention. As your body adjusts to the medicine during treatment these side effects may go away. Your health care professional may also be able to tell you about ways to reduce or prevent some of these side effects. If any of the following side effects continue, are bothersome or if you have any questions about them, check with your health care professional:

Incidence not known
  • Diarrhea
  • skin irritation after soaking

For Healthcare Professionals

Applies to magnesium sulfate: injectable solution, intravenous solution, oral and topical powder for reconstitution


Electrocardiograph changes with a magnesium sulfate overdose have included increased PR interval, increased QRS complex width and prolonged QT interval.

Generally, magnesium sulfate is well tolerated. However, patient response to elevated serum magnesium levels is highly variable. The majority of adverse effects are associated with excessive serum levels. Rapid bolus infusions (i.e. 2 grams over 5 seconds) may cause cutaneous flushing and transient hypotension due to a direct vasodilating effect. As serum levels exceed 3 to 4 mEq/L, central nervous system depression, lethargy, confusion, disorientation, frank coma, flushing, sweating, dilated pupils, hypotension, flaccid paralysis, depressed reflexes, hypothermia, circulatory collapse and cardiovascular depression may occur. When serum levels exceed 11 to 13 mEq/L, respiratory depression or paralysis, heart block and/or asystole may occur. Intravenous calcium (5 to 10 mEq) quickly antagonizes the effects of magnesium.


Shils and colleagues demonstrated that magnesium repletion can reverse the adverse neurological and gastrointestinal effects associated with hypocalcemia (due to low magnesium levels). Additionally, abnormal EKG changes during hypomagnesemia are most likely due to the associated hypocalcemia and hypokalemia. Six men were induced experimentally with hypomagnesemia and subsequently developed hypocalcemia despite an adequate intake of calcium and vitamin D. Magnesium is essential for proper mobilization of bone/soft tissue calcium and for the cellular retention of potassium. A blinded, controlled study investigated the relationship between maternal administration of intravenous magnesium sulfate (mean exposure 38.3 days, range 10 to 64 days) and radiographic abnormality of neonatal long bones. Maternal mean serum magnesium levels ranged from 4.9 to 6.5 mEq/L. Eleven neonates exposed to magnesium sulfate were compared to 22 unexposed neonates. Chest radiographs were examined by a blinded pediatric radiologist. None of the 22 unexposed neonates had abnormal films. In contrast, 6 of 11 exposed neonates exhibited definite abnormalities (p < 0.001), consisting of transverse radiolucent and/or sclerotic bands. There may be a causal relationship between long-term intravenous magnesium sulfate for tocolysis and abnormal fetal bone development; however, the clinical long-term significance is unknown.

A small, retrospective review reported the presence of radiographic abnormalities (rachitic changes, dental enamel hypoplasia) and hypocalcemia in 5 neonates born to mothers treated with magnesium sulfate (from 4 to 13 weeks prior to delivery). The authors hypothesize that prolonged administration of magnesium sulfate, especially in the second trimester, may suppress fetal parathyroid function leading to rickets.

Metabolic side effects have included hypomagnesemia. Hypomagnesemia may be associated with hypocalcemia and/or hypokalemia leading to neurologic and/or gastrointestinal changes (weakness, lethargy, anorexia, nausea and vomiting). Rare metabolic abnormalities due to hypermagnesemia may include hypocalcemia (due to suppression of the parathyroid hormone) and hypercalciuria. Bone abnormalities in infants have been reported. Hyperkalemia in two pregnant intravenous drug abusers has been reported. Reversible maternal hypothermia occurred in 30-year-old woman receiving magnesium sulfate for tocolysis.


Gastrointestinal side effects have included primarily diarrhea, nausea (Mg levels of 4 to 5 mEq/L), and rare cases of paralytic ileus (Mg levels greater than 5 mEq/L).

Nervous system

Central nervous system depression may occur at higher levels; however, therapeutic serum magnesium levels attained for control of seizure during preeclampsia or eclampsia (4 to 7 mEq/L) have not been shown to be harmful to mother or infant.

One study has reported that magnesium sulfate negatively affects attention and rapid information processing ability but not short term memory or comprehension in patients undergoing preterm labor.

Nervous system side effects from hypermagnesemia result from suppression of neuromuscular transmission in the CNS and at the neuromuscular junction by magnesium. Clinically, serum levels above 4 to 7 mEq/L have lead to decreased deep tendon reflexes, muscle weakness, mental confusion or sedation. At levels of 7 to 10 mEq/L, slower respiratory rates and decreased blood pressure has been reported. At levels of 10 to 15 mEq/L, profound mental depression, areflexia, coma and respiratory paralysis has been a common occurrence. Magnesium has also been reported to have a curare-like effect at the neuromuscular junction at serum levels above 10 mEq/L. Death may occur at any serum level but has been especially common at levels above 15 mEq/L.


A case report described a 65-year-old man who developed ventricular fibrillation following rapid (over 5 seconds) administration of 2 grams of magnesium sulfate for treatment of sustained monomorphic ventricular tachycardia. Ventricular fibrillation developed within 3 minutes of administration. The patient was successfully resuscitated with a single direct current shock; however, the patient died 3 days later. The authors caution against rapid intravenous administration of magnesium sulfate, even in the setting of ventricular arrhythmias.

Cardiovascular side effects of magnesium are due to vasodilation, leading to flushing with rapid infusions and hypotension at serum levels of 7 to 10 mEq/L. Bradyarrhythmias have occurred at levels above 10 mEq/L. Asystole has occurred at levels above 25 mEq/L. The risk of cardiotoxicity from hypermagnesemia is increased in the presence of hypocalcemia, hyperkalemia, acidosis, digitalis therapy, and renal insufficiency. Chest pain and palpitations have also been reported.


Respiratory side effects including respiratory arrest have been reported in patients with extremely elevated serum magnesium levels (> 13 mEq/L). Pulmonary edema occurred after magnesium sulfate administration as a tocolytic, which responded to diuretics.


Ocular side effects have included diplopia (double vision) reported in 2 women receiving magnesium sulfate for tocolysis. A decrease in dosage remedied the adverse effect.


Hypersensitivity side effects have included a dermatological urticarial eruption which cleared when intravenous magnesium sulfate was discontinued. The 2 case reports occurred in obstetrical nurses previously exposed occupationally to magnesium sulfate, but who received a therapeutic dose for preterm labor.


Hematologic side effects have included reports of increased bleeding times after magnesium sulfate infusions in preeclamptic women.

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