Abstract: TH-PO181
Severe Hypermagnesemia-Induced Ischemic Colitis in a Patient with AKI
Session Information
- Drug Events Trainee Case Reports
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 902 Fluid and Electrolytes: Clinical
Authors
- Levy, Rebecca, Montefiore Medical Center, New York, New York, United States
- Prudhvi, Kalyan, Montefiore Medical Center, Bronx, New York, United States
- Thakkar, Jyotsana, Montefiore Medical Center, Bronx, New York, United States
Introduction
Severe hypermagnesemia is a rare complication seen with laxative/antacid overdose, usually in patients with acute kidney injury(AKI). We present a case of marked hypermagnesemia leading to ischemic colitis with perforation, pancreatitis and multi system organ failure in a patient with AKI.
Case Description
A 54 year old female with hypertension, asthma, and chronic neurogenic bladder presented with abdominal pain and vomiting for one day. She was taking magnesium hydroxide 1200mg four times a day for constipation. She was hypotensive on arrival with blood pressure of 70/50mmHg. Labs were remarkable for AKI with serum creatinine of 6.8mg/dL (baseline 0.9mg/dL) and severe hypermagnesemia (>10mg/dL, baseline of 2.2mg/dL about one month ago). Other significant lab findings were microangiopathic hemolytic anemia (MAHA) and lactic acidosis. She was intubated, started on vasopressors and admitted to the intensive care unit. CT abdomen revealed free air suggestive of perforation, reactive pancreatitis and ischemic colitis. Emergent exploratory laparotomy was performed which showed cecal ischemia. She also received plasma exchange for for MAHA which was stopped after three treatments given normal ADAMTS13 activity. Continuous renal replacement therapy (CRRT) was started for hypermagnesemia and oliguria. Her renal function and hypermagnesemia improved and she was weaned off CRRT.
The etiology of AKI was presumed to be multifactorial in the setting of obstructive uropathy from neurogenic bladder, acute tubular necrosis from hypotension and thrombotic microangiopathy. Severe hypermagnesemia was attributed to high dose oral magnesium supplementation in the setting of AKI. She showed significant improvement in her follow up labs in renal clinic two months later with magnesium level of 2.2mg/dL and serum creatinine of 0.9mg/dL.
Discussion
Hypermagnesemia is known to induce hypomotility of gut leading to ileus, colitis, intestinal perforation and toxic megacolon, especially in the setting of AKI. Our patient developed severe refractory hypermagnesemia requiring CRRT complicated by ischemic colitis, bowel perforation and reactive pancreatitis. High index of suspicion for these bowel complications is warranted if patients present with hypermagnesemia and abdominal symptoms.