Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 21-14: Hypermagnesemia + Key Features Download Section PDF Listen +++ ++ Almost always the result of advanced stages of chronic kidney disease (CKD) and impaired magnesium excretion Antacids and laxatives are underrecognized sources of magnesium Pregnant patients may have severe hypermagnesemia from intravenous magnesium therapy for preeclampsia and eclampsia Magnesium replacement should be done cautiously in patients with CKD, and dose reductions up to 75% may be necessary to avoid hypermagnesemia + Clinical Findings Download Section PDF Listen +++ ++ Muscle weakness Decreased deep tendon reflexes Mental obtundation Confusion Weakness, even flaccid paralysis Ileus, urinary retention, hypotension In severe cases, respiratory muscle paralysis or cardiac arrest + Diagnosis Download Section PDF Listen +++ ++ Serum magnesium is elevated In the common setting of CKD, elevated blood urea nitrogen, serum creatinine, phosphate, and uric acid; serum K+ may be elevated Serum Ca2+ is often low ECG may show increased PR interval, broadened QRS complexes, and peaked T waves, probably related to associated hyperkalemia + Treatment Download Section PDF Listen +++ ++ 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)/min Hemodialysis or peritoneal dialysis may be necessary Long-term use of magnesium hydroxide and magnesium sulfate should be avoided in patients with advanced stages of CKD