A CASE OF CATASTROPHIC MAGNESIUM OVERDOSE

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Magnesium toxicity can occur due to decreased excretion or overconsumption and is rare in the general population. Early-onset symptoms of toxicity are nausea, flushing, weakness, and urinary retention. However, severe toxicity and its management is not well-described. We present a case of magnesium overdose with intractable hypotension. CASE PRESENTATION: A 34-year-old male presented to the emergency department after he was found unresponsive in a restaurant in the presence of empty bottles of magnesium supplements and ibuprofen. He was hypotensive, hypothermic, and emergently intubated for airway protection. His serum magnesium level was 11.7mg/dl. He was treated with gastric decontamination, intravenous calcium and admitted to the intensive care unit. Continuous Renal Replacement Therapy (CRRT) was initiated and led to a reduction in the measured serum magnesium concentration. Despite aggressive volume administration and multiple vasopressors, he had refractory shock and severe acidosis. An echocardiogram revealed adequate cardiac function; hence, he was not a candidate for Extracorporeal Membranous Oxygenation (ECMO). A trial of hydrocortisone and methylene blue also yielded no benefit to his distributive shock. His hospital course was further complicated by abdominal compartment syndrome requiring a bedside exploratory laparotomy, aspiration pneumonia, acute respiratory distress syndrome, and disseminated intravascular coagulation. Ultimately, his family elected to transition to comfort care, and the patient passed away on hospital day 4. DISCUSSION: Magnesium competitively blocks the entry of calcium into presynaptic terminals of smooth muscle cells, inhibiting the release of acetylcholinesterase, causing smooth muscle relaxation. In the setting of an overdose, this translates to refractory vasoplegia. Magnesium also alters the polarization of the cytoplasmic membrane in cardiac myocytes, causing lengthening of the action potential, thus predisposing to arrhythmias. While iatrogenic magnesium toxicity has been reported at levels of 3-5mg/dL, a level of >10mg/dL is uncommon. There may be a dose-dependent refractoriness that has not been identified in the literature so far. Treatment of severe magnesium toxicity requires urgent dialysis in conjunction with IV calcium which acts as an antagonist. If there is catecholamine resistance, methylene blue may be used to restore systemic vascular resistance. CONCLUSIONS: Severe magnesium toxicity can present with shock & acidosis. Despite dialysis and aggressive resuscitation, the vasoplegia can be refractory and lead to fatal complications, including respiratory collapse and cardiac arrest. Even with early recognition and treatment, the mortality can be high, and further studies are needed to improve outcomes. REFERENCE #1: Ajib FA, Childress JM. Magnesium Toxicity. [Updated 2021 Jan 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. REFERENCE #2: Cavell GF, Bryant C, Jheeta S. Iatrogenic magnesium toxicity following intravenous infusion of magnesium sulfate: risks and strategies for prevention. BMJ Case Rep. 2015;2015:bcr2015209499. Published 2015 Jul 31. doi:10.1136/bcr-2015-209499 REFERENCE #3: Pietro Delva, Magnesium and cardiac arrhythmias, Molecular Aspects of Medicine, Volume 24, Issues 1–3, 2003, Pages 53-62, ISSN 0098-2997, https://doi.org/10.1016/S0098-2997(02)00091-2. DISCLOSURES: No relevant relationships by Ayesha Azmeen, source=Web Response No relevant relationships by Daniel Condit, source=Web Response No relevant relationships by Angad Deengar, source=Web Response No relevant relationships by Prashant Grover, source=Web Response No relevant relationships by Samantha McPeck, source=Web Response No relevant relationships by Evan Nadler, source=Web Response No relevant relationships by Erin Rosenberg, source=Web Response No relevant relationships by Sharad Sathyan, source=Web Response