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.
(See also Overview of Disorders of Magnesium Concentration.)
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.
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).
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.