Case Presentation: A 77 year-old male with a past medical history of Parkinson’s disease and hyperlipidemia presented to the emergency department with a two week history of constipation, abdominal pain and distension. His medications include carbidopa-levadopa, entacapone, ropinirole, selegiline and atorvastatin. He also reported taking daily milk of magnesia for the past two weeks. On presentation vital signs were stable and exam was notable for abdominal distension and diffuse tenderness. An abdominal x-ray showed severely dilated loops of bowel consistent with large bowel obstruction. Attempted colonoscopy decompression was complicated by bowel perforation. Decompression was emergently transitioned to exploratory laparotomy, where a large amount of stool was noted in the peritoneal cavity. Patient underwent peritoneal washout and Hartmann’s procedure. Intraoperative course was complicated by development of profound hypotension requiring multiple vasopressors and bradycardia. Given his intraoperative hemodynamic instability, repeat blood tests were sent and revealed a serum magnesium of 13 mg/dL. Repeat tests confirmed the result. Assessment during recovery was notable for decreased responsiveness, absent deep tendon reflexes and persistent bradycardia and hypotension. Dialysis was considered if forced diuresis with furosemide and intravenous fluid did not improve his condition. After forced diuresis, magnesium levels returned to normal, patient’s mental status improved, bradycardia, hypotension resolved and deep tendon reflexes returned.

Discussion: Severe hypermagnesemia has been described in several case reports and case series. In the majority of reported cases, hypermagnesemia is the result of chronic use of magnesium containing laxatives in patients with underlying chronic kidney disease. As the proximal tubule and ascending limb of Henle’s Loop are highly effective at regulating and excreting magnesium, and gastrointestinal absorption via the small and large intestines is inhibited by increased serum levels of magnesium, severe elevations are uncommonly seen. This case is unique in several regards. First, this patient had normal renal function and no evidence of hypermagnesemia on admission. Second, this patient reported only a short duration, two weeks, of magnesium use. Third, and most striking, the patient developed the clinical features of hypermagnesemia, shortly after bowel perforation during attempted colonoscopy decompression. It is the authors’ hypothesis that magnesium absorption occurred directly through diffuse peritoneal absorption of magnesium-containing feculent material.

Conclusions: evere hypermagnesemia is rare, but potentially fatal. Typical features include depressed mental status, decreased deep tendon reflexes, cardiopulmonary depression and occur when magnesium levels are greater than 5 mg/dL. Risk factors include advanced age, chronic kidney disease, magnesium laxative use and Treatment options include loop diuretics, often paired with intravenous fluids, to promote magnesium secretion as well as dialysis, or continuous renal replacement therapy. This case illustrates the rapid development of severely elevated serum magnesium hypothesized to be due to peritoneal absorption of magnesium containing fecal matter following bowel perforation which is not previously described in the literature.