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      A Systematic Review of Ethanol and Fomepizole Use in Toxic Alcohol Ingestions

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          Abstract

          Objectives. The optimal antidote for the treatment of ethylene glycol or methanol intoxication is not known. The objective of this systematic review is to describe all available data on the use of ethanol and fomepizole for methanol and ethylene glycol intoxication. Data Source. A systematic search of MEDLINE and EMBASE was conducted. Study Selection. Published studies involving the use of ethanol or fomepizole, or both, in adults who presented within 72 hours of toxic alcohol ingestion were included. Our search yielded a total of 145 studies for our analysis. There were no randomized controlled trials, and no head-to-head trials. Data Extraction. Variables were evaluated for all publications by one independent author using a standardized data collection form. Data Synthesis. 897 patients with toxic alcohol ingestion were identified. 720 (80.3%) were treated with ethanol (505 Me, 215 EG), 146 (16.3%) with fomepizole (81 Me, 65 EG), and 33 (3.7%) with both antidotes (18 Me, 15 EG). Mortality in patients treated with ethanol was 21.8% for Me and 18.1% for EG. In those administered fomepizole, mortality was 17.1% for Me and 4.1% for EG. Adverse events were uncommon. Conclusion. The data supporting the use of one antidote is inconclusive. Further investigation is warranted.

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          American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning.

          , J Vale, E P Krenzelok … (2001)
          Almost all cases of acute methanol toxicity result from ingestion, though rarely cases of poisoning have followed inhalation or dermal absorption. The absorption of methanol following oral administration is rapid and peak methanol concentrations occur within 30-60minutes. Methanol has a relatively low toxicity and metabolism is responsible for the transformation of methanol to its toxic metabolites. Methanol is oxidized by alcohol dehydrogenase to formaldehyde. The oxidation of formaldehyde to formic acid is facilitated by formaldehyde dehydrogenase. Formic acid is converted by 10-formyl tetrahydrofolate synthetase to carbon dioxide and water. In cases of methanol poisoning, formic acid accumulates and there is a direct correlation between the formic acid concentration and increased morbidity and mortality. The acidosis observed in methanol poisoning appears to be caused directly or indirectly by formic acid production. Formic acid has also been shown to inhibit cytochrome oxidase and is the prime cause of ocular toxicity, though acidosis can increase toxicity further by enabling greater diffusion of formic acid into cells. Methanol poisoning typically induces nausea, vomiting, abdominal pain, and mild central nervous system depression. There is then a latent period lasting approximately 12-24 hours, depending, in part, on the methanol dose ingested, following which an uncompensated metabolic acidosis develops and visualfunction becomes impaired, ranging from blurred vision and altered visual fields to complete blindness. For the patient presenting with ophthalmologic abnormalities or significant acidosis, the acidosis should be corrected with intravenous sodium bicarbonate, the further generation of toxic metabolite should be blocked by the administration of fomepizole or ethanol and formic acid metabolism should be enhanced by the administration of intravenous folinic acid. Hemodialysis may also be required to correct severe metabolic abnormalities and to enhance methanol and formate elimination. For the methanol poisoned patient without evidence of clinical toxicity, the first priority is to inhibit methanol metabolism with intravenous ethanol orfomepizole. Although there are no clinical outcome data confirming the superiority of either of these antidotes over the other, there are significant disadvantages associated with ethanol. These include complex dosing, difficulties with maintaining therapeutic concentrations, the need for more comprehensive clinical and laboratory monitoring, and more adverse effects. Thus fomepizole is very attractive, however, it has a relatively high acquisition cost. The management of methanol poisoning includes standard supportive care, the correction of metabolic acidosis, the administration of folinic acid, the provision of an antidote to inhibit the metabolism of methanol to formate, and selective hemodialysis to correct severe metabolic abnormalities and to enhance methanol and formate elimination. Although both ethanol and fomepizole are effective, fomepizole is the preferred antidote for methanol poisoning.
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            American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Methanol Poisoning

            Edward Krenzelok, J. Allister Vale, Hannah Cooper … (2002)
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              Methanol outbreak in Norway 2002-2004: epidemiology, clinical features and prognostic signs.

              O Hunderi, Ilse Jacobsen, A-B Tafjord … (2005)
              Knowledge on methanol poisoning does mainly come from clinical studies. We therefore report epidemiological, clinical and prognostic features from the large methanol outbreak in Norway in 2002-2004 where the new antidote fomepizole was the primary antidote in use. Combined prospective and retrospective case series study of 51 hospitalized patients who were confirmed poisoned with methanol, of whom nine died. In addition, eight patients died outside hospital. Most patients were admitted in a late stage and because of symptoms. Treatment consisted of alkali, fomepizole (71%) and haemodialysis (73%). The median serum methanol was 25.0 mmol L-1 (80 mg dL-1) (range 3.1-147.0 mmol L-1), median pH was 7.20 (6.50-7.50), and median base deficit 22 mmol L-1 (range 0-31). The most frequent clinical features reported were visual disturbances (55%), dyspnoea (41%), and gastrointestinal symptoms (43%). Twenty-four per cent were comatose on admission, of whom 67% died. There was a trend towards decreasing pCO2 with decreasing pH amongst the patients surviving. The opposite trend was demonstrated in the dying; the difference was highly significant by linear regression analyses (P 28 mmol L-1) upon admission were strong predictors of poor outcome. Early admission and ability of respiratory compensation of metabolic acidosis was associated with survival.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Emerg Med Int
                Journal ID (iso-abbrev): Emerg Med Int
                Journal ID (publisher-id): EMI
                Title: Emergency Medicine International
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-2840
                ISSN (Electronic): 2090-2859
                Publication date (Print): 2013
                Publication date (Electronic): 31 January 2013
                Volume: 2013
                Electronic Location Identifier: 638057
                Affiliations
                1Department of Emergency Medicine, Dalhousie University, Room 377, Bethune Building, 1276 South Park Street, Halifax, NS, Canada B3H 2Y9
                2Division of Critical Care Medicine, Department of Anesthesia, Dalhousie University, Room 377, Bethune Building, 1276 South Park Street, Halifax, NS, Canada B3H 2Y9
                3Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, BC, Canada V6T 1Z3
                Author notes

                Academic Editor: Robert W. Derlet

                Article
                DOI: 10.1155/2013/638057
                PMC ID: 3574646
                PubMed ID: 23431453
                SO-VID: d1ccc7d7-1110-4fe5-afc2-1e1b8370fff0
                Copyright © Copyright © 2013 Lorri Beatty et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 1 October 2012
                Date accepted : 25 December 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Emergency medicine & Trauma
                Data availability:
                ScienceOpen disciplines: Emergency medicine & Trauma

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