Environmental Medicine Integrating a Missing Element into Medical Education (1995) / Chapter Skim
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Case Study 23: Methanol Toxicity
Case Study 23: Methanol Toxicity
Pages 473-492
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From page 473... ...
Methanol is sometimes used as an ethanol substitute by alcohol abusers. :~ The shift to alternative motorfuels may signif cantly increase both acute and chronic methanol exposures in the general population.
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From page 474... ...
Medical history includes coronary artery bypass surgery at age 63 with subsequent medical management of stable angina and atransurethral prostatectomy at age 65with no recurrence of obstructive symptoms. Current medications include nitroglycerine patches used before exercise (with no patches used in the previous 4 days)
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From page 475... ...
. Data regarding methanol levels in drinking water are lacking.
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From page 476... ...
O Persons Ingesting adulterated alcoholic beverages are at great risk of methanol toxicity. O Foiat~deficient persons are potentially at increased risk for toxicity after methanol exposure.
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From page 477... ...
O lUbthanol is oxidized in the liver to formaldehyde, then formic acid, which contributes to the profound metabolic acidosis seen in acute methanol poisoning. O Most methanol is eliminated via the lungs as carbon dioxide.
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From page 478... ...
Alcohol dehydrogenase, the enzyme responsible for the first step of methanol metabolism, has an approximately ninefold greater affinity for ethanol than for methanol. Administration of ethanol blocks the oxidation of methanol, preventing the lethal synthesis of formaldehyde and formic acid and increasing the amount of methanol that is eliminated unchanged {now approximately equal amounts in urine and exhaled breath)
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From page 479... ...
In swvhrore of acute methanol Intoxication. O Chronic exposures to methanol have not been thoroughly studied, although anecdotal reports of chronic vlaual effects have been pubilshed in the medical literature.
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From page 480... ...
In suspected inhalational and dermal exposures, emphasis should be placed on identifying specific methanol-containing products (e.g., canned fuel, windshield washer solution, duplicator fluid, shellac thinner, alternative fuels) and on documenting unusual conditions of prolonged and extensive skin contact or inhalation.
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From page 481... ...
These include the following: Blood methanol and blood ethanol Arterial blood gases Serum electrolytes (Na+, K+, Cl-, HCO3-) and calculation of anion gap BUN and serum creatinine Serum glucose Serum ketones Serum osmolarity and calculation of osmolar gap Urinalysis CBC 8 481 ENVIRONMENTAL MEDICINE
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From page 482... ...
O Immediately after an acute exposure, a blood methanol level serves as the best predictor of the "verity of the cilnical course. O Chronic methanol exposure can be documented by measuring urinary methanol.
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From page 483... ...
L Lactic acidosis E Ethanol (alcoholic) ketoacidosis, ethylene glycol poisoning S Salicylate overdose Of the various pathophysiobgic states and toxic agents listed above, only diabetic ketoacidosis, ethanol ketoacidosis, and methanol and ethylene glycol poisoning produce elevations of both the anion and osmolar gaps.
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From page 484... ...
Methanol intoxication, like that of ethylene glycol, acetaminophen, and lithium, may deceive the clinician by the initial lack of severe toxic manifestations. For recent, suspected methanol ingestions, gut decontamination ,, ...
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From page 485... ...
In cases of suspected methanol exposure, the following are indications for starting an intravenous ethanol infusion: a blood methanol level of greater than 20 mg/dL; a history of ingesting more methanol than 0.4 mung body weight; any ingestion history, with delayed access to toxicologic testing; or metabolic acidosis with otherwise unexplained elevated anion and osmolar gaps, especially if eye symptoms are present. Ethanol, usually as a 10% solution (10 mL of 100% ethanol in 90 mL of 5% aqueous dextrose)
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From page 486... ...
O Patients chronically exposed to methanol should be treated symptomatically. Ch - ~/ Additional information for the case study: Consistent with acute methanol intoxication, the patient's arterial blood gases indicate a pH of 7.25; bicarbonate is 10 mEq/L, pCO2 23 mm Hg, and pO2 92 mm Hg.
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From page 487... ...
However, under EPA's generic standards for the synthetic organic chemical manufacturing industry, all volatile organic chemical (VOC) emissions, including methanol releases, are to tee kept to atechnologically feasible minimum.
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From page 488... ...
* ACGIH = American Conference of Govemmental Industrial Hygienists; EPA = Environmental Protection Agency; FDA = Food and Drug Administration; NIOSH = National Institute for Occupational Safety and Health; 0SHA = Occupational Safety and Health Administration PEL (Permissible Exposure Limit)
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From page 489... ...
Serum formate concentrations in methanol intoxication as a criterion for hemodialysis. Ann Intern Med 1986;104:200-3.
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From page 490... ...
Acute visual loss in this age group can occur with central retinal artery or vein occlusion, internal carotid emboli, vitreous hemorrhage, retinaUmacular hemorrhage, retinal detachment, temporal arteritis, cerebrovascular accidents of the posterior circulation, acute angle-closure glaucoma, idiopathic optic neuritis, head trauma, and carbon monoxide and methanol poisoning. Of these conditions, only cerebrovascular events, head trauma, temporal arteritis, and carbon monoxide and methanol poisoning commonly affect vision bilaterally.
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From page 491... ...
are indicative of methanol intoxication of potentially life-threatening severity. Appropriate therapeutic intenrentions for methanol intoxication include intravenous ethanol infusion, sodium bicarbonate and folate administration, and hemodialysis.
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From page 492... ...
produces an elevated osmolar gap: methanol, ethanol, ethylene glycol, acetone, and isopropanol. Although several drugs can potentially contribute to the osmolar gap (e.g., salicylates, paraldehyde, and chloral hydrate)
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