Methanol intoxication with cerebral hemorrhage

M is a highly toxic alcohol with a smell and taste similar to ethanol. Small amount around 50 100 ml causes permanent blindness and severe neurological dysfunction leads to death.1 More than half of methanol related morbidity and mortality is classified as accidental and therefore preventable. In addition, it can be suicidal by ingestion of a variety of commercial paint thinners, gasoline anti-freeze, windshield products, organic solvents, shellac varnish, washer fluid, photocopying fluids, perfumes, and in some eau de cologne. Occasionally, it is due to the fraudulent adulteration of wine or other alcoholic beverages.2 Its ingestion causes high anion gap metabolic acidosis from the production of formic and lactic acids and central nervous system disturbances ranging from inebriation and drowsiness to obtundation, seizure and coma. Selective toxicity of the optic nerve and basal ganglia are well-known features. Bilateral putaminal necrosis is often recognized radiologically in severe methanol toxicity and usually death occurs within 3 days.2 Here, we report a patient presented with severe high anion gap metabolic acidosis due to methanol intoxication who developed intracerebral bleed during treatment. A 47-year-old man was brought to our hospital by ambulance presented with body pain, nausea, vomiting, and blurring of vision one day ago and sudden loss of vision upon arrival to emergency department. Briefly after admission, became unresponsive, Glasgow Coma Scale 4 with dilated non reactive pupils. His blood pressure was 110/60 mm Hg, heart rate was 95/min, respiratory rate was 32/min (Kussmul’s-Kien breathing), and temperature was 36C. An examination of the chest, heart, and abdomen was unremarkable. He was intubated in emergency department and diagnostic work-up started. Chest x-ray was normal, computed tomography of brain showed only atrophic brain changes otherwise normal, (Figure 1), but the Blood Gases showed severe high anion gap metabolic acidosis with the following laboratory results PH 6.78 normal range=7.35-7.45, PaO2=195 normal range=75-100 mmHg, PaCO2=22 normal range=35-45 mmHg, HCO3=3.1 normal range=22-26 mQ/L, anion gap=36 normal range=12. Serum sodium=145 mmol/l normal range=135-145, potassium=5.6 mmol/l normal range=3.5-5, chloride=106 mmol/l normal range=92-112, ALT=172 normal range=37, AST=208 normal range=65, GGT=596 normal range=30, Hepatitis B surface antigen, Hepatitis C antibodies and HIV antibodies are non reactive, the elevated liver enzymes are attributed to the hypotension and hypoperfusion (ischemic hepatopathy). Ultrasound of the abdomen was performed which was unremarkable. Kidney functions, complete blood count, random blood sugar were normal. serum lactate was 7.8 nmol/L normal range=2.4 nmol/L. History from the family was taken; he is smoker, alcohol and drug abuser for almost 3 years. So history, clinical presentation, and laboratory parameters guided us to the diagnosis of methanol intoxication. Toxicology screening was carried out and the result was with methanol level 413 mg/dl normal range <10 mg/dl, salicylate and paracetamol were negative. He was started on intravenous sodium bicarbonate to correct acidosis. Ethanol was added to block formic acid production, while a hemodialysis session without heparin was initiated to help correct the severe acidosis and eliminate both methanol and its metabolites -formic acid. Follow-up arterial blood gases showed improvement of acidosis. Shortly after admission to Intensive Care Unit, he became hypotensive, fluid boluses given and vasopressor started. At the same day, he developed generalized tonic clonic convulsions. Fundus examination revealed oedematous optic disk with dilated peripapillary vessels. Second day to admission, his conscious level deteriorated with Glasgow Coma Scale 3, pupils dilated and fixed. He started to be polyuric (250-300 ml/h), central diabetes insipidus was suspected versus high fluid intake, so ethanol and sodium bicarbonate were stopped. Hemodialysis was continued for 2 hours. Clinical Note