Abstract

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Serotonin syndrome (SS) is a life threatening disorder characterized by autonomic dysfunction, altered mental status and neuromuscular excitation (1). Muscle rigidity and hyperthermia can cause cellular damage and enzyme dysfunction leading to rhabdomyolysis, myoglobinuria, metabolic acidosis and multi-organ failure (1). SS is associated with drugs that decrease serotonin breakdown, reuptake or increase its release (1). CASE PRESENTATION: A 20-year-old male with depression, anxiety and substance abuse, presented with dyspnea for two weeks accompanied by non-productive cough and palpitations. For the past two days he reported insomnia and anorexia. His symptoms began after taking phenylethylamine (40 mg daily) and most recently Katrom (Mitragyna speciosa) for his mood. In addition, he takes perphenazine 2 mg-amitriptyline 10 mg per day prescribed by his psychiatrist for anxiety. Bupropion and sertraline were recently discontinued due to lack of symptomatic improvement. He was hemodynamically stable and afebrile, but he was tachycardic, tachypneic without hypoxemia. His neurological examination was significant for bilateral jerk nystagmus, clonus, tremor and hyperreflexia in all four extremities. Patient met Hunter criteria for serotonin syndrome and was admitted to the intensive care unit. EKG showed sinus tachycardia with normal QT interval. Laboratory showed rhabdomyolysis (creatinine phosphokinase (CK) 5068 U/L), mild transaminitis (ALT 50 U/L, AST 97 U/L) and anion gap metabolic acidosis with a bicarbonate of 8 mmol/L. Renal function was normal without electrolyte disturbances. Serum acetaminophen, alcohol, salicylate and lactic acid levels were normal. Urine drug screen was negative. However, urine organic acid panel was significant for elevated ketones and phenylacetate levels. Patient was placed on an intravenous bicarbonate infusion and benzodiazepines with resolution of neurological symptoms within 2 days. The psychotropic agents were discontinued as well. Acid-base balance and CK levels normalized. DISCUSSION: Multiple medications including herbal supplements increase the risk of SS. Phenylethylamine is an "endogenous amphetamine" metabolized by monoamine oxidase to phenylacetate (2). Additionally, Kratom is an understudied psychoactive plant, with stimulant and opiate effects (3). However, it is unclear how much this drug contributed to the development of symptoms. Literature on the acute toxicity of Kratom is confounded by the concomitant use of other drugs (3). CONCLUSIONS: Early recognition of SS is essential to initiate supportive treatment and stop all potential substances responsible for serotonin mediated toxicity. It is important to recognize herbal medications as a potential cause of SS. Reference #1: Wang RZ, Vashistha V, Kaur S et al. Serotonin Syndrome: Preventing, recognizing, and treating it. Cleveland Clinic Journal of Medicine. 2016; 83 (11): 810-817. Reference #2: Irsfeld M, Spadafore M and PruB B. β-phenylethylamine, a small molecule with a large impact. Webmedcentral. 2014; 4(9): 1-15. Reference #3: Swogger MT and Walsh Z. Kratom use and mental health: A systematic review. Drug and Alcohol Dependence. 2018; 183: 134-140. DISCLOSURES: No relevant relationships by John Makram, source=Web Response No relevant relationships by Haneen Mallah, source=Web Response No relevant relationships by Barbara Mantilla, source=Web Response No relevant relationships by Ximena Solis, source=Web Response No relevant relationships by Victor Test, source=Web Response No relevant relationships by Myrian Vinan Vega, source=Web Response

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