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      Risk factors for mortality in Asian Taiwanese patients with methanol poisoning

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          Abstract

          Introduction

          Methanol poisoning continues to be a serious public health issue in Taiwan, but very little work has been done to study the outcomes of methanol toxicity in the Asian population. In this study, we examined the value of multiple clinical variables in predicting mortality after methanol exposure.

          Methods

          We performed a retrospective observational study on patients with acute poisoning who were admitted to the Chang Gung Memorial Hospital over a period of 9 years (2000–2008). Out of the 6,347 patients, only 32 suffered methanol intoxication. The demographic, clinical, laboratory, and mortality data were obtained for analysis.

          Results

          Most patients were middle aged (46.1±13.8 years), male (87.5%), and habitual alcohol consumers (75.0%). All the poisonings were from an oral exposure (96.9%), except for one case of intentionally injected methanol (3.1%). After a latent period of 9.3±10.1 hours, many patients began to experience hypothermia (50.0%), hypotension (15.6%), renal failure (59.4%), respiratory failure (50.0%), and consciousness disturbance (Glasgow coma scale [GCS] score 10.5±5.4). Notably, the majority of patients were treated with ethanol antidote (59.4%) and hemodialysis (58.1%). The remaining 41.6% of patients did not meet the indications for ethanol therapy. At the end of analysis, there were six (18.8%), 15 (46.9%), and eleven (34.4%) patients alive, alive with chronic complications, and dead, respectively. In a multivariate Cox regression model, it was revealed that the GCS score (odds ratio [OR] 0.816, 95% confidence interval [CI] 0.682–0.976) ( P=0.026), hypothermia (OR 168.686, 95% CI 2.685–10,595.977) ( P=0.015), and serum creatinine level (OR 4.799, 95% CI 1.321–17.440) ( P=0.017) were significant risk factors associated with mortality.

          Conclusion

          The outcomes (mortality rate 34.4%) of the Taiwanese patients subjected to intensive detoxification protocols were comparable with published data from other international poison centers. Furthermore, the analytical results indicate that GCS score, hypothermia, and serum creatinine level help predict mortality after methanol poisoning.

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          Most cited references 33

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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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            Fomepizole for the treatment of methanol poisoning.

            Methanol poisoning may result in metabolic acidosis, blindness, and death. The inhibition of alcohol dehydrogenase is fundamental to the treatment of methanol poisoning. We performed a multicenter study to evaluate fomepizole, an inhibitor of alcohol dehydrogenase, in the treatment of patients with methanol poisoning. We administered intravenous fomepizole to 11 consecutive patients who presented with methanol poisoning at a participating center. Serial clinical and laboratory studies, including measurements of plasma formic acid and fomepizole, were performed. The outcomes measured were the preservation of visual acuity, the resolution of metabolic acidosis, the inhibition of formic acid production, the achievment of therapeutic plasma concentrations of fomepizole with the dosing regimen, residual illness or disability, and death. Plasma formic acid concentrations were detectable in eight patients, and these concentrations were closely correlated with the initial arterial pH values (r=0.92, P<0.001). In response to fomepizole, plasma formic acid concentrations fell and metabolic abnormalities resolved in all patients. Nine patients survived. Seven patients initially had visual abnormalities, but at the end of the trial no surviving patient had any detectable visual deficits related to methanol poisoning. Fomepizole had few adverse effects. The two patients who died had anoxic brain injury that was present at the time of enrollment. During treatment, methanol had an elimination half-life of 54 hours. Fomepizole appears to be safe and effective in the treatment of methanol poisoning.
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              Methanol outbreak in Norway 2002-2004: epidemiology, clinical features and prognostic signs.

              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
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2014
                2014
                17 January 2014
                : 10
                : 61-67
                Affiliations
                [1 ]Department of Nephrology and Division of Clinical Toxicology, Taipei, Taiwan
                [2 ]Department of Psychiatry, Chang Gung Memorial Hospital and Chang Gung University, Taipei, Taiwan
                [3 ]Department of Nephrology, China Medical University Hospital and China Medical University, Taichung, Taiwan
                Author notes

                *These authors contributed equally to this work

                Correspondence: Tzung-Hai Yen, Department of Nephrology, Chang Gung Memorial Hospital, 199 Tung Hwa North Road, Taipei 105, Taiwan, Tel +886 3 328 1200 ext 8181, Fax +886 3 328 2173, Email m19570@ 123456adm.cgmh.org.tw
                Article
                tcrm-10-061
                10.2147/TCRM.S51985
                3900329
                © 2014 Lee et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Medicine

                mortality, intoxication, wood alcohol, hemodialysis, ethanol

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