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By James L. Lewis, III, MD

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Hypermagnesemia is a serum magnesium concentration > 2.6 mg/dL (> 1.05 mmol/L). The major cause is renal failure. Symptoms include hypotension, respiratory depression, and cardiac arrest. Diagnosis is by serum magnesium concentration. Treatment includes IV administration of calcium gluconate and possibly furosemide; hemodialysis can be helpful in severe cases.

Symptomatic hypermagnesemia is fairly uncommon. It occurs most commonly in patients with renal failure after ingestion of magnesium-containing drugs, such as antacids or purgatives.

Symptoms and signs include hyporeflexia, hypotension, respiratory depression, and cardiac arrest.


  • Serum magnesium concentrations >2.6 mg/dL (> 1.05 mmol/L)

At serum magnesium concentrations of 6 to 12 mg/dL (2.5 to 5 mmol/L), the ECG shows prolongation of the PR interval, widening of the QRS complex, and increased T-wave amplitude. Deep tendon reflexes disappear as the serum magnesium concentration approaches 12 mg/dL (5.0 mmol/L); hypotension, respiratory depression, and narcosis develop with increasing hypermagnesemia. Cardiac arrest may occur when blood magnesium concentration is > 15 mg/dL (6.0 to 7.5 mmol/L).


  • Calcium gluconate

  • Diuresis or dialysis

Treatment of severe magnesium toxicity consists of circulatory and respiratory support with administration of 10% calcium gluconate 10 to 20 mL IV. Calcium gluconate may reverse many of the magnesium-induced changes, including respiratory depression.

Administration of IV furosemide can increase magnesium excretion when renal function is adequate; volume status should be maintained. Hemodialysis may be valuable in severe hypermagnesemia, because a relatively large fraction (about 70%) of blood magnesium is not protein bound and thus is removable with hemodialysis. When hemodynamic compromise occurs and hemodialysis is impractical, peritoneal dialysis is an option.

* This is the Professional Version. *