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Magnesium-containing laxatives are commonly used in elderly patients for the treatment of constipation; however, excessive magnesium absorption, particularly in individuals with impaired renal function, may result in severe hypermagnesemia that can lead to life-threatening complications. Non-occlusive mesenteric ischemia (NOMI) is a rare but often fatal condition characterized by intestinal hypoperfusion without major arterial occlusion and is typically associated with systemic hypotension and low-flow states. We report the case of an 83-year-old female with a history of hypertension and chronic neurological sequelae who presented to the emergency department with altered mental status, abdominal pain, hypotension, and bradycardia following rectal administration of a magnesium-containing laxative. Laboratory analysis revealed severe hypermagnesemia (8.56 mg/dL), acute kidney injury, metabolic acidosis, elevated lactate (10 mmol/L), leukocytosis, and markedly increased inflammatory markers. Contrast-enhanced abdominal computed tomography demonstrated diffuse small bowel wall thickening with decreased mural enhancement and mesenteric edema, while CT angiography showed patent mesenteric arteries without occlusion, findings consistent with non-occlusive mesenteric ischemia. Despite aggressive fluid resuscitation, vasopressor therapy, broad-spectrum antibiotics, and emergency surgical resection of necrotic bowel segments, the patient developed multiorgan failure and died on postoperative day nine. Severe hypermagnesemia in elderly patients with renal impairment may therefore lead to profound hemodynamic instability and systemic hypoperfusion, potentially contributing to the development of NOMI; early recognition of hypermagnesemia, prompt measurement of serum magnesium levels, and aggressive management are essential to reduce morbidity and mortality. In addition, the markedly elevated inflammatory markers raise the possibility of a mixed shock state, in which both hypermagnesemia-induced cardiovascular depression and a concomitant septic process may have contributed to systemic hypoperfusion and the development of non-occlusive mesenteric ischemia.