21-14: Hypermagnesemia

ESSENTIALS OF DIAGNOSIS

GENERAL CONSIDERATIONS

Hypermagnesemia is almost always the result of advanced CKD and impaired magnesium excretion. Antacids and laxatives are underrecognized sources of magnesium. Pregnant patients may have severe hypermagnesemia from intravenous magnesium for preeclampsia and eclampsia. Magnesium replacement should be done cautiously in patients with CKD; dose reductions up to 75% may be necessary to avoid hypermagnesemia.

CLINICAL FINDINGS

A. Symptoms and Signs

Muscle weakness, decreased deep tendon reflexes, mental obtundation, and confusion are characteristic manifestations. Weakness, flaccid paralysis, ileus, and hypotension are noted. Serious findings include respiratory muscle paralysis, complete heart block, and cardiac arrest.

B. Laboratory Findings and ECG

Serum Mg²⁺ is elevated. In the common setting of CKD, BUN, creatinine, potassium, phosphate, and uric acid may all be elevated. Serum Ca²⁺ is often low. The ECG may show increased PR interval, broadened QRS complexes, and QT prolongation.

TREATMENT

Exogenous sources of magnesium should be discontinued. Calcium antagonizes Mg²⁺ and may be given intravenously as calcium chloride, 500 mg or more at a rate of 100 mg (4.1 mmol) per minute. Hemodialysis may be necessary to remove magnesium, particularly with severe kidney disease.

Long-term use of magnesium hydroxide and magnesium sulfate should be avoided in patients with advanced stages of CKD.