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METHANOL POISONING Management with Ethanol MECHANISM OF ACTION METHANOL FORMALDEHYDE FORMIC ACID ALDEHYDE DEHYDROGENASE ALCOHOL DEHYDROGENASE MECHANISM OF ACTION METHANOL FORMALDEHYDE FORMIC ACID ACIDOSIS Early stage of poisoning ACIDOSIS TISSUE HYPOXIA LACTIC ACID PRODUCTION CIRCULATORY FAILURE GENERAL TOXICITY INCREASED FORMIC ACID TOXICITY OCULAR TOXICITY INHIBITION OF MITOCHONDRIAL RESPIRATION CIRCULUS HYPOXICUS SIGNS AND SYMPTOMS INITIAL INEBRIATION - ESPECIALLY IF ETHANOL COINGESTED AFTER 12 - 24 HOUR DELAY - PROGRESSION TO ACIDOSIS AND OTHER SIGNS AND SYMPTOMS MAY BE FURTHER DELAY WITH CONTINUED INGESTION OF ETHANOL SIGNS AND SYMPTOMS CNS - INEBRIATION PROGRESSING TO COMA, CONVULSIONS RETINAL - BLURRED VISION, PHOTOPHOBIA, VISUAL ACUITY LOSS, DILATED NON-REACTIVE PUPILS, OPTIC NERVE HYPERAEMIC - BECOMING OEDEMATOUS GIT - NAUSEA, VOMITING CARDIAC - TACHYCARDIA, HYPERTENSION PROGRESSING TO HYPOTENSION AND CARDIOGENIC SHOCK RESPIRATORY - TACHYPNOEA INVESTIGATION BLOOD METHANOL LEVEL! ABG - METABOLIC ACIDOSIS OSMOLAL GAP - INCREASED (METHANOL) ANION GAP - INCREASED (FORMIC ACID, LACTIC ACID) BLOOD ETHANOL MAGNESIUM, AMYLASE, POTASSIUM TREATMENT HAZARD ASSESSMENT ABC’s TOXICOKINETICS ABSORPTION DISTRIBUTION METABOLISM ELIMINATION TOXICODYNAMICS SUPPORTIVE CARE TREATMENT BICARBONATE (AGGRESSIVE TREATMENT) CAN REVERSE VISUAL IMPAIRMENT REDUCES MOVEMENT OF FORMATE TO THE CNS MAY REQUIRE 400 TO 600 MMOL DURING FIRST FEW HOURS CORRECTION OF METABOLIC ACIDOSIS REHYDRATION MECHANISM OF ACTION METHANOL FORMALDEHYDE FORMIC ACID ALDEHYDE DEHYDROGENASE ALCOHOL DEHYDROGENASE METHANOL FORMALDEHYDE FORMIC ACID ALCOHOL DEHYDROGENASE ALDEHYDE DEHYDROGENASE ETHANOL X ALDEHYDE ACETIC ACID MECHANISM OF ACTION TREATMENT MAINTAIN BLOOD ETHANOL LEVEL OF 100 - 150 mg/dl LOADING DOSE BEWARE OF EXISTING ETHANOL LEVEL MAINTENANCE DOSE TITRATED AGAINST RATE OF ELIMINATION NON-ALCOHOLIC 15 - 20 mg/dl/h CHRONIC ALCOHOLIC 30 - 40 mg/dl/h CHILD 30 mg/dl/h E