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    • Methanol (methyl alcohol, wood alcohol) • absorbed through the skin or from the respiratory or gastrointestinal tract and is then distributed in body water. • Elimination : by oxidation to formaldehyde, formic acid, and CO2: --- methanol toxicity is probably due to folate-dependent production of formate and not to methanol itself or to formaldehyde, the intermediate metabolite
    • Clinical effects • • • • Inebriated but lack of euphoria. 1-72 hrs of latent period. Fatal dose 60-240 ml. Vertigo ,nausea,vomiting, diarrhea,abdominal pain,dyspnea,agitation. • Blurred vision,photophobia,↓ visual acuity • Bradycardia, blindness, seizures,coma.
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    • • Physical examination constricted visual field,fixed &dilated pupils, retinal edema & hyperemia of disk respiratory apnea ,opisthotonus,& seizure in ptatients dying of Methanol intoxication.
    • • Lab finding high anion gap acidosis (correlates with mortality) high osmolar gap serum methanol> 20 mg/dl symptoms > 50 mg/ dl serious > 100 mg/ dl ocular signs
    • Presentation: 08:30h • Case: 28 years old male presented with methanol ingestion. • History: • Lots of alcohol the night before “very drunk”.At ~7am accidentally drank ½ pint water bottle containing pure methanol. Felt unwell,nausea,blurred vision, abdominal discomfort
    • Initial Biochemistry: Na 137 Alb. ~10.00 h 46 Glucose 6.0 PH 7.38 K 4.o Prot. 84 Ethanol< 2.2 H ion 42 Cl 101 Glob. 38 Amylase 87 PCO2 5.2 HCO3 27 ALP. 81 PO2 12.2 Urea 3.6 Bili. 20 Std.HCO3 24.0 Creat. 102 ALT. 18 BE -0.8 A. Gap 13 GGT. 23 FIO2 21% Osmo.measured = 0.335 Osmo.calculated = 284 Osmolal Gap = 51
    • Initial Treatment • 1L Normal Saline. • 200 ml oral Ethanol (Loading dose ). • 20 ml / h oral Ethanol (Maintenance dose). Treatment Protocol • Methanol > 6 mmol /L (200 mg /L). Ethanol • Methanol > 16 mmol /L (500 mg /L). Haemodialysis
    • Outcome • After 3 days transferred off ITU . • Underwent reviewed by ophalmology , Biochemistry , ABG’S remained unchanged and unremarkable from admission. • Discharged 6 days after admission.
    • Ethanol • Ethanol has approximately 10 times greater affinity for alcohol dehydrogenase than does methanol. Therefore ethanol competitively inhibits the metabolism of methanol to its toxic metabolite, formate, by occupying the receptor sites of alcohol dehydrogenase.
    • Use of Ethanol in Pregnant Patients • The adverse reproductive effects associated with ethanol are not expected to occur following the use of ethanol as an antidote for methanol poisoning during the second and third trimester . • The use of any alcohol during the first trimester is more controversial because of the association of fetal alcohol syndrome.
    • the Use of Ethanol in Children • Children are more susceptible to development of hypoglycemia during methanol intoxication compared with adults, so the use of fomepizole instead of ethanol is a theoretical advantage.
    • • Flushing and hypotension may occur if ethanol is administered and the patient has also received disulfiram, metronidazole, or chlorpropamide. • Ethanol should beused with caution in patients with hepatic disease and the oral administration of ethanol preferably should be avoided when there is a recent history of gastrointestinal ulcers.
    • Fomepizole • Has been shown to be a potent inhibitor of alcohol dehydrogenase, If administered soon after exposure.
    • Use of Fomepizole in the Pregnant Patient Fomepizole should be administered to pregnant or breast-feeding women only after careful consideration of the risks and benefits, including the alternative of administering ethanol.
    • Ethanol vs Fompepizole Ethanol: - Oral or IV - CNS depression - Difficult titration - Frequent levels - Hypoglycemia Fomepizole: - IV - No CNS depression - Easy dosing - No levels to monitor - More predictable pharmacokinetcs - No Hypoglycemia - Cost
    • Haemodialysis - methanol>20-50mg/100ml. - acidosis not responsive to bicarbonate. - formate levels > 20 mg/100ml. - visual impairment. - renal impairment.
    • • Sodium bicarbonate (acidosis). • Folate therapy : Folinic acid, , is the reduced form of folic acid. In vivo, it is converted rapidly to tetrahydrofolic acid derivatives that are the primary bioactive and storage forms of folate in the body. • Folate enhances formic acid metabolism, and is thereby postulated to reduce toxicity.
    • TreatmentSupportive therapy:SeizuresDiazepam 5-10 mg slow IV (max rate: 5 mg/min); may repeat every 5-10 min (MAX dose: 30mg)Lorazepam 0.1 mg/kg slow IV (max rate: 2 mg/min); may repeat in 5-15 min (Usual MAX dose: 8mg)Phenobarbital 10-20 mg/kg IV over 10 min (rate <100mg/min); may repeat in 20 min intervals as needed (MAX dose: 30mg/kg)Midazolam 0.15-0.3 mg/kg IM; may repeat every 10-15 min as needed Metabolic acidosis Sodium bicarbonate 1-2mEq/kg IV, repeat as neededCofactor therapyFolinic acid (leucovorin) 1mg/kg IV every 4-6 hours until resolved, ORFolic acid 50mg IV every 4-6 hours until resolved.
    • The end