Critical Hypermagnesemia Induced by Excessive Milk of Magnesia in Acute Kidney Failure

Introduction: Hypermagnesemia is rare, usually caused by excessive magnesium intake, impaired renal excretion, or both, with most cases being mild and asymptomatic. Here, we present a case of severe Hypermagnesemia in the setting of Peptic Ulcer disease and Acute Renal Failure. Case Description: 68-year-old Male with a history of Heart Failure with Reduced Ejection Fraction, EF 45%, Mobitz II, status-post pacemaker, and prior percutaneous cholecystostomy, normal baseline renal function, presented with nausea, vomiting, and epigastric pain. Initial CT showed pneumonia but no intraabdominal abnormalities. Labs were unremarkable, with a magnesium of 1.5 mg/dL. Suspecting Peptic ulcer disease, he was given 3 doses of 400 mg magnesium oxide and 2 doses of 2400 mg Milk of Magnesia. Thereafter, He left Against Medical Advice (AMA), only to return 12 hours later with worsening abdominal pain, hypotension, and tachycardia. Repeat CT showed large pneumoperitoneum. EKG was notable for paced rhythm and prolonged QTc. He was emergently taken for exploratory laparotomy for suspected duodenal perforation, even before labs could be obtained. Post-op labs showed critically elevated magnesium at 11.6 mg/dL, and serum creatinine at 2.5, with oliguria. He was started on normal saline, with Lasix and calcium gluconate as a temporizing measure. He then underwent urgent intermittent hemodialysis (HD), followed by continuous Renal replacement therapy for 24 hours. Magnesium gradually improved to 4.7, and to 2.5 over the next 24 hours. He admitted to drinking ¾ bottles of Milk of Magnesia after leaving AMA. After discontinuing HD, magnesium levels remained in the normal range, and urine output and creatinine gradually improved. Discussion: Significant exogenous magnesium intake can exceed the kidneys' excretory capacity, especially in cases of renal impairment. Gastrointestinal inflammation can lead to increased absorption. Magnesium levels greater than 10mg/dl can lead to neuromuscular paralysis and even cardiac arrest and require emergent hemodialysis. Calcium gluconate antagonizes hypermagnesemia's neuromuscular and cardiac effects and should be given promptly. This case highlights the need for concise patient history, judicious medication administration, emergent therapies for electrolyte abnormalities, and patient education to prevent risks associated with self-medication and AMA discharges.