BACKGROUND: Hypermagnesemia is a rare condition that is usually iatrogenic. Magnesium oxide (MgO) ingestion by constipated patients with prolonged colonic retention contributes to hypermagnesemia. Treatment of hypermagnesemia includes discontinuation of the magnesium use, gastrointestinal (GI) decontamination, and removal of magnesium from the serum by dialysis. Calcium acts as an antagonist in hypermagnesemia. CASE REPORT: A 72-year-old woman presented with constipation and MgO ingestion. The patient was brought to our department due to altered mental status and progressive general weakness. Laboratory tests showed a magnesium level of 6.2 mEq/L. Bradycardia and hypotension developed with rebound hypermagnesemia after incomplete dialysis. Abdomen computed tomography showed hyperdense MgO tablets retained in the colon. A magnesium-free laxative was used for GI decontamination. Despite the use of high-dose inotropics and an elevated trigger for transcutaneous pacing, the cardiac performance improved minimally. Although our patient responded to calcium administration with hemodynamic improvement, prolonged hypotension and decreased perfusion led to hypoxic encephalopathy. CONCLUSION: This report demonstrates that MgO tablets retained in the GI tract without adequate decontamination result in continuous absorption and rebound of hypermagnesemia. This report also addresses the importance of GI decontamination in the treatment of hypermagnesemia.
BACKGROUND: Hypermagnesemia is a rare condition that is usually iatrogenic. Magnesium oxide (MgO) ingestion by constipatedpatients with prolonged colonic retention contributes to hypermagnesemia. Treatment of hypermagnesemia includes discontinuation of the magnesium use, gastrointestinal (GI) decontamination, and removal of magnesium from the serum by dialysis. Calcium acts as an antagonist in hypermagnesemia. CASE REPORT: A 72-year-old woman presented with constipation and MgO ingestion. The patient was brought to our department due to altered mental status and progressive general weakness. Laboratory tests showed a magnesium level of 6.2 mEq/L. Bradycardia and hypotension developed with rebound hypermagnesemia after incomplete dialysis. Abdomen computed tomography showed hyperdense MgO tablets retained in the colon. A magnesium-free laxative was used for GI decontamination. Despite the use of high-dose inotropics and an elevated trigger for transcutaneous pacing, the cardiac performance improved minimally. Although our patient responded to calcium administration with hemodynamic improvement, prolonged hypotension and decreased perfusion led to hypoxic encephalopathy. CONCLUSION: This report demonstrates that MgO tablets retained in the GI tract without adequate decontamination result in continuous absorption and rebound of hypermagnesemia. This report also addresses the importance of GI decontamination in the treatment of hypermagnesemia.