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Methanol Induced ST Elevation and Brain Death

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A6926 - Methanol Induced ST Elevation and Brain Death
Author Block: E. Chow1, A. Khosla2, L. Berman3; 1Norwalk Hospital, Norwalk, CT, United States, 2Internal Medicine Resident, Norwalk, CT, United States, 3Norwalk Hosp, Norwalk, CT, United States.
Introduction:Methanol is commonly found in industrial solvents and anti-freeze with ingestion whether accidental or intentional leading to variety of symptoms. Symptoms range from GI upset to headaches, central nervous depression, seizures, and in more serious cases blindness and death.
Case:52 y/o male with a history of hypertension, chronic alcohol abuse presented with substernal chest pain. Pain was non-radiating with no associated diaphoresis or shortness of breath. The pain was worsened with exertion and relieved with rest. Upon arrival he was hemodynamically stable with a normal physical exam. Initial EKG showed ST elevations in leads V-1V3 with subsequent development of reciprocal changes in the inferior leads on repeat EKG. The patient was taken for immediate cardiac catheterization for presumed ST elevation MI. During the procedure he became increasingly lethargic and bradycardic requiring endotracheal intubation. Catheterization showed no evidence of stenosis, with patient transferred to the ICU. CT brain was negative for acute hemorrhage, stroke or midline shift.
His initial labs were significant for WBC:16.3, K:7.1 Cr:1.57, Anion gap:36, Bicarbonate:5, lactic acid:5, troponin: 0.09, serum osmolarity: 437, Osmolar gap:152, pH:6.78. Initial CT brain was negative for acute hemorrhage, stroke or midline shift. Methanol level:339, ethanol: negative, isopropyl alcohol: negative
Given the degree of acidosis and elevated methanol level, fomepizole was administered and emergent hemodialysis started. His repeat exam was notable for absence of brainstem reflexes, with repeat CT brain revealing global hypoxic ischemic brain injury with bilateral attenuation of the lentiform nuclei.Given the lack of improvement despite aggressive care, the family withdrew care and the patient passed away.
Discussion:Methanol toxicity is thought to be secondary to accumulation of formic acid, with evels greater than 200mg/L considered to be toxic. Apart from severe acidosis, EKG changes have also been reported, with the most common being tachycardia and prolonged QTc. Common findings on CT scan include generalized edema and less commonly bilateral putaminal hypodense lesions. While uncommon, there should be low threshold for further investigation when there is a metabolic acidosis, high anion gap and osmolar gap in order to avoid irreversible toxicity such as blindness or death. Even with rapid recognition and treatment, acute deterioration can still occur. To our knowledge, this is the first documented case of ST elevation associated with methanol intoxication, highlighting the difficulties of diagnosing and treating methanol intoxication.
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