C53-48 Beyond the Morning Cup: Severe Caffeine Intoxication Presenting as Metabolic and Electrical Instability

Background Caffeine, a methylxanthine derivative, exerts dose-dependent sympathomimetic and phosphodiesterase-inhibiting effects. In toxic quantities, it amplifies catecholamine release and cyclic adenosine monophosphate (cAMP) activity, leading to widespread metabolic and cardiovascular instability. Although mild caffeine exposures are common, severe intoxication is rare and may imitate septic or metabolic shock. We describe an adolescent with high-dose caffeine ingestion resulting in severe electrolyte derangement and conduction abnormalities, underscoring the pathophysiologic overlap between stimulant toxicity and metabolic collapse. Case Presentation An 18-year-old male with history of major depressive disorder and unspecified mood disorder presented to the hospital one hour after ingesting over 2 g of over-the-counter caffeine tablets. He reported nausea, tremors, diaphoresis, and multiple episodes of non-bloody vomiting. There was no suicidal intent or co-ingestion. His medications included lithium, olanzapine, and fluvoxamine. On arrival, he was alert but agitated with a blood pressure of 142/54 mmHg, heart rate of 91, respiratory rate 25/min, and saturating 99% at room air. Laboratory evaluation revealed severe hypokalemia (2.2 mmol/L), high anion-gap metabolic acidosis (bicarbonate 14 mmol/L, anion gap 27), hyperglycemia (260 mg/dL), and elevated lactate (8.5 mmol/L) with normal renal and hepatic indices. Electrocardiography showed sinus rhythm with pauses, frequent atrial premature complexes, and QTc prolongation to 529 ms.The metabolic findings reflected β-adrenergic hyperstimulation leading to intracellular potassium shift, catecholamine-driven glycogenolysis, and cAMP-mediated lactate accumulation. Management included isotonic fluid resuscitation, aggressive intravenous potassium repletion, and antiemetic therapy. Beta-blockade was deferred due to stable hemodynamics. Lithium and olanzapine were withheld because of QT-prolongation. The patient’s biochemical and electrocardiographic abnormalities normalized within 48 hours of supportive therapy. Discussion This clinical presentation illustrates caffeine’s capacity to trigger a reversible yet life-threatening “ion-shift syndrome” dominated by profound hypokalemia without total-body depletion. Elevated lactate stemmed from adrenergic-driven glycolysis rather than tissue hypoxia, distinguishing this from type A lactic acidosis. QTc prolongation was multifactorial, reflecting hypokalemia, adrenergic surge, and psychotropic synergy. Management required dynamic correction of metabolic disturbances with continuous rhythm surveillance rather than rigid toxicology algorithms. Conclusion Caffeine toxicity should be recognized as a potential cause of severe metabolic acidosis and malignant arrhythmogenic risk, particularly among adolescents with psychiatric comorbidities or polypharmacy. Prompt diagnosis, targeted electrolyte repletion, and careful ECG monitoring are vital for preventing fatal outcomes. This case highlights the growing need for regulation and education around high-dose stimulant products marketed as benign enhancers of alertness. This abstract is funded by: none