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Hypermagnesemia is a serum Mg concentration > 2.1 mEq/L (> 1.05 mmol/L). The major cause is renal failure. Symptoms include hypotension, respiratory depression, and cardiac arrest. Diagnosis is by serum Mg concentration. Treatment includes IV administration of Ca 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 Mg-containing drugs, such as antacids or purgatives.
Symptoms and signs include hyporeflexia, hypotension, respiratory depression, and cardiac arrest.
At serum Mg concentrations of 5 to 10 mEq/L (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 Mg concentration approaches 10 mEq/L (5.0 mmol/L); hypotension, respiratory depression, and narcosis develop with increasing hypermagnesemia. Cardiac arrest may occur when blood Mg concentration is > 12 to 15 mEq/L (6.0 to 7.5 mmol/L).
Treatment of severe Mg toxicity consists of circulatory and respiratory support with administration of 10% Ca gluconate 10 to 20 mL IV. Ca gluconate may reverse many of the Mg-induced changes, including respiratory depression. Administration of IV furosemide can increase Mg 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 Mg is not protein bound and thus is removable with hemodialysis. When hemodynamic compromise occurs and hemodialysis is impractical, peritoneal dialysis is an option.
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