Ingestion of Synthetic Street Drug 25-I (25I-NBOMe) Causing Type B Lactic Acidosis and Multi-Organ Dysfunction

Matthew L. Friedman, Marcelo Malakooti, Craig Smith, Zena Leah Harris, Mark Wainwright


25I-NBOMe (25-I) is a novel synthetic agonist of the 5-HT2A receptor. It is used recreationally for its psychedelic properties similar to LSD. Side effects include altered mental status, sympathomimetic symptoms, serotonin syndrome and multiple organ injury. We report a case of delayed type B lactic acidosis after ingestion of 25-I. A 16-year-old male presented after being found obtunded. He developed seizures requiring endotracheal intubation. He developed a lactic acidosis about 30 hours after ingestion, peaking at 8.5 mEq/L 38 hours post-ingestion. Concurrently the patient had an elevated mixed venous saturation and decreased arterial-venous oxygen content difference, indicating a type B lactic acidosis. Thiamine, L-carnitine, and coenzyme Q-10 were initiated to treat the metabolic derangement and promote oxygen utilization. Additional treatments included n-acetylcysteine and plasmapheresis. This treatment strategy resulted in reduction in lactate and other markers of organ injury. Arterial-venous oxygen content difference increased to normal levels. The patient made a full recovery. Type B lactic acidosis has been reported previously in a variety of diseases, but never after 25-I ingestion. A novel approach of vitamins and co-factors to support mitochondrial function, n-acetylcysteine and plasmapheresis was employed to treat the lactic acidosis and multi-organ dysfunction successfully.

J Med Cases. 2015;6(3):125-127


Mitochondrial dysfunction; Thiamine; Carnitine; Plasmapheresis; Type B lactic acidosis; 25-I

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