A comatose 24-year-old man with blurred vision had metabolic acidosis (pH 6.831), CO
2 tension of 13.6mmHg, bicarbonate of 2.2mEq/l, and an anion gap of 21.7mEq/l. He was intubated and treated with sodium bicarbonate intravenously, then referred to our emergency department. The urine alcohol screening test by methanol detection tube was positive and serum/urine analysis revealed a serum methanol level of 2.7mg/ml and formic acid level of 969.0μg/ml. He underwent 4-hour hemodialysis twice. Non-enhanced CT showed hypodensity bilaterally in the putamen. On hospital day 2, MRI revealed hyperintense lesions in and around the putamen and subcortical white matter on T2-weighted and fluid attenuated inversion recovery (FLAIR). Axial diffusion-weighted (DW) images showed hyperintense lesions in the bilateral putamen and subcortical white matter, indicating cytotoxic edema. Also, short TI inversion recovery (STIR) showed bilateral optic nerve edema. On hospital day 26, MRI showed putaminal necrosis and improvement of optic nerve edema. He gradually became alert from hospital day 4. He could see distant finger movement but still had impaired vision after 1 year. He survived due to our new and rapid way of identifying methanol poisoning by detection tube, and quick hemodialysis. CT/MR image findings also revealed lesions in the basal ganglia, especially the putamen, and cortex.
View full abstract