Abstract
This manuscript describes a fatal case of a 45-year-old man who presented with severe chest pain, hypertension (198/115 mmHg), and electrocardiogram changes mimicking acute coronary syndrome (ACS) 30 h after ingesting adulterated alcohol. Uniquely, chest pain was the sole initial manifestation, without visual disturbances, gastrointestinal symptoms, or any other classic methanol features, creating a clinically convincing ACS mimic. Despite negative coronary CT angiography, dual antiplatelet loading therapy (aspirin 300 mg and clopidogrel 300 mg) was administered based on clinical suspicion of ACS, together with low-molecular-weight heparin. Three hours later, the patient developed sudden unconsciousness with unequal pupils. Arterial blood gas analysis revealed severe high-anion-gap metabolic acidosis (pH 7.08, anion gap 34 mEq/L). Toxicology confirmed methanol poisoning (blood concentration 206.85 mg/dL). The diagnosis was prompted only after two coworkers presented simultaneously with visual symptoms and bilateral basal ganglia lesions on CT-a constellation not previously reported as the diagnostic trigger in ACS-mimicking methanol poisoning. Head CT showed subarachnoid hemorrhage, which rapidly progressed to massive right basal ganglia hemorrhage (9.0 × 3.3 cm) with intraventricular extension and surrounding hypodensity consistent with necrosis. Despite hemodialysis, ethanol infusion, and emergency craniotomy, the patient died 2 weeks later. Coagulation studies revealed acidosis-induced coagulopathy (PT 15.2 s, activated partial thromboplastin time 38.6 s, INR 1.3). Critically, what distinguishes this case from prior reports of methanol-associated basal ganglia hemorrhage is the synergistic pro-hemorrhagic state created by the combination of dual antiplatelet therapy (irreversible platelet inhibition), low-molecular-weight heparin (antithrombin III potentiation), and acidosis-induced coagulopathy, superimposed on methanol-induced endothelial injury-a fatal pharmacotoxicological interaction not previously described in a single case. Emergency physicians should consider toxicological etiologies in undifferentiated chest pain with metabolic derangements and obtain early arterial blood gas analysis to avoid such fatal diagnostic errors.