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      Ethylene glycol poisoning: a rare but life-threatening cause of metabolic acidosis—a single-centre experience

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          Abstract

          Background.

          Intoxication with ethylene glycol happen all around the world and without rapid recognition and early treatment, mortality from this is high.

          Methods.

          In our study, we retrospectively analysed six cases of ethylene glycol intoxication in our department. We measured ethylene glycol or glycolate levels, lactate levels and calculated the osmolal and anion gap.

          Results.

          Data from six patients admitted to the nephrology department between 1999 and 2011 with ethylene glycol poisoning are reported. All patients were men. The mean pH on admission was 7.15 ± 0.20 and the anion and osmolal gap were elevated in five of six patients. Four patients had an acute kidney injury and one patient had an acute-on-chronic kidney injury. All patients survived and after being discharged, two patients required chronic intermittent haemodialysis. Interestingly, at the time of admission, all patients had elevated lactate levels but there was no linear regression between toxic levels and lactate levels and no linear correlation was found between initial lactate levels and anion gap and osmolal gap.

          Conclusions.

          The initial diagnosis of ethylene glycol poisoning is difficult and poisoning with ethylene glycol is rare but life threatening and needs rapid recognition and early treatment. Therefore, intoxication with ethylene glycol should not be misdiagnosed as lactic acidosis in patients with metabolic acidosis and elevated lactate levels.

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          Most cited references16

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          American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poisoning. Ad Hoc Committee.

          Fomepizole (4-methylpyrazole, 4-MP, Antizol) is a potent inhibitor of alcohol dehydrogenase that was approved recently by the US Food and Drug Administration (FDA) for the treatment of ethylene glycol poisoning. Although ethanol is the traditional antidote for ethylene glycol poisoning, it has not been studied prospectively. Furthermore, the FDA has not approved the use of ethanol for this purpose. Case reports and a prospective case series indicate that the intravenous (i.v.) administration of fomepizole every 12 hours prevents renal damage and metabolic abnormalities associated with the conversion of ethylene glycol to toxic metabolites. Currently, there are insufficient data to define the relative role of fomepizole and ethanol in the treatment of ethylene glycol poisoning. Fomepizole has clear advantages over ethanol in terms of validated efficacy, predictable pharmacokinetics, ease of administration, and lack of adverse effects, whereas ethanol has clear advantages over fomepizole in terms of long-term clinical experience and acquisition cost. The overall comparative cost of medical treatment using each antidote requires further study.
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            1999 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System.

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              Derivation and validation of a formula to calculate the contribution of ethanol to the osmolal gap.

              We sought to evaluate the relationship between osmolal gap and serum ethanol level and derive a formula that can be used clinically to calculate the expected osmolal gap in the presence of ethanol. Some investigators have noted that the residual osmolal gap appears to increase as the ethanol level increases, and thus it is important to determine the exact relationship between these 2 values. In part 1, a convenience sample of emergency department patients undergoing serum ethanol determination had sodium, urea, and glucose levels and osmolality determined on the same blood sample, and values were prospectively recorded. Predicted osmolality excluding ethanol was calculated with the following formula: 2 Na (mEq/L) + (Urea [mg/dL])/2.8 + (Glucose [mg/dL])/18. The osmolal gap was determined by subtracting the calculated serum osmolality excluding ethanol from the measured serum osmolality. Linear regression analysis was then used to derive a formula for the relationship between ethanol and the osmolal gap. This formula was then prospectively validated on a second convenience sample of patients. In part 2, we repeated this experiment in vitro by adding known amounts of ethanol to serum. We derived the formula to calculate the contribution of ethanol to the osmolal gap by using 98 observations. The mean ethanol level was 197.8 mg/dL (SD 138.5), with a range of 0 to 538.2 mg/dL. The relationship between ethanol and osmolal gap was linear, with a Pearson coefficient of correlation of 0.99. Linear regression analysis generated a model with the following formula: Osmolal gap=(Ethanol [mg/dL])/3.7 - 0.35 or, in SI units: Osmolal gap (mOsm/kg)=1.25 (Ethanol [mmol/L]) - 0.35 The 95% confidence interval (CI) for the multiplicative factor was 1/3.58 to 1/3.80 (or, in SI units, 1.21 to 1.28). The 95% CI for the additive constant was -2.19 to 1.50. We prospectively validated our formula on 128 patients. The mean residual osmolal gap for this group of patients was 0.84 mOsm/L (SD 5.65; range, -18.40 to 17.85 mOsm/L). The results of the in vitro experiments were similar. Our data suggest that the best formula for the calculation of the contribution of ethanol to osmolality is as follows: Ethanol (mg/dL)/3.7 or, in SI units: 1.25 (Ethanol [mmol/L])
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                Author and article information

                Journal
                Clin Kidney J
                Clin Kidney J
                ndtplus
                ckj
                Clinical Kidney Journal
                Oxford University Press
                2048-8505
                2048-8513
                April 2012
                : 5
                : 2
                : 120-123
                Affiliations
                Department of Internal Medicine, Division of Nephrology, Robert-Bosch Hospital, Stuttgart, Germany
                Author notes
                Correspondence and offprint requests to: Joerg Latus; E-mail: Joerg.latus@ 123456rbk.de
                Article
                10.1093/ckj/sfs009
                4235595
                25503773
                a914fa28-8f32-4748-b249-7dde0ac0a248
                © The Author 2012. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com
                History
                : 07 September 2011
                : 17 January 2012
                Page count
                Pages: 4
                Categories
                Original Contributions
                Original Articles

                Nephrology
                acute kidney injury,ethylene glycol poisoning,lactate levels
                Nephrology
                acute kidney injury, ethylene glycol poisoning, lactate levels

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