Ethylene Glycol Intoxication

Turk, J.L.; Morrell, Louise; Avioli, Louis V.

doi:10.1001/archinte.1986.00360200177029

Cited by 41 publications

(4 citation statements)

References 16 publications

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“…On the contrary, Group B patients presented with an osmolal gap higher than those reported elsewhere. 3,[11][12][13][14][15] The higher ethylene glycol levels in this group can probably account for the increased osmolal gap.…”

Section: Methodsmentioning

confidence: 86%

“…[1][2][3][4][5][6][7][8] The biochemical profile is that of a high anion ([Na]-([Cl] + [HCO3]) and osmolal gap (measured plasma osmolalitycalculated plasma osmolality) metabolic acidosis, acute renal failure and the presence of oxalate as well as hyppurate crystals in the urine. [9][10][11][12][13][14][15][16] Haemodialysis, parenteral ethanol, 4-methylpyrazol and bicarbonate infusions have been shown to be useful in eliminating the toxin, blocking its hepatic metabolism and correcting the initial severe metabolic acidosis. Interestingly enough and to the best of our knowledge, the finding of simultaneous occurrence of true EGI and emerging diabetic ketoacidosis (DKA) has not _________________________________ Correspondence to: Dr. J. Ybarra MD.…”

Section: Introductionmentioning

confidence: 99%

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Ethylene Glycol intoxication with and without simultaneous diabetic ketoacidosis: A report of nine cases and review of the literature

Ybarra¹,

Doñate²,

Pou³

et al. 2005

Int J Diabetes Metab

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Objective: To describe the clinical and biochemical observations made on nine patients with ethylene glycol intoxication (EGI) of whom five presented with simultaneous diabetic ketoacidosis (DKA). Methods: A retrospective chart search for discharge diagnosis including the term ethylene glycol intoxication was conducted at University Hospitals of Cleveland Information Services (Cleveland, OH) from 1986 through 1998. Nine (N=9) patients were identified and subsequently divided into two Groups (A & B). Group A included 5 patients with both DKA and EGI. Group B included 4 patients with EGI without DKA. Clinical manifestations and laboratory tests are summarized for both Groups. Serum specimens for all patients were analyzed for ethylene glycol, propylene glycol, methanol, serum ketones, glucose, pH, electrolytes, liver and kidney function tests, lipase, amylase, cholesterol, triglycerides, C-peptide and glycosylated Hb. Results: Group A patients presented with more severe hyperglycaemia accompanied by increased insulin requirements, glucose toxicity, more severe osmotic diuresis induced severe dehydration, pre-renal azotemia, transient rhabdomyolysis and hypertriglyceridaemia. Their acute renal failure was fully reversible upon discharge. Finally, the length of hospital stay of patients in Group A was significantly longer than that of Group B patients, although mortality rate was reduced. Permanent and irreversible kidney damage requiring haemodialysis was seen in all Group B patients. Conclusions: severe DKA presenting with simultaneous high anion and osmolal gap should prompt suspicion to the hypothetical concomitant EGI, particularly in those patients with a history of alcoholism, depression and past suicidal attempts.

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Section: Methodsmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Ethylene Glycol intoxication with and without simultaneous diabetic ketoacidosis: A report of nine cases and review of the literature

Ybarra¹,

Doñate²,

Pou³

et al. 2005

Int J Diabetes Metab

View full text Add to dashboard Cite

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“…15 These include a large anion gap metabolic acidosis and renal failure. [16][17][18] EtOH inhibits the formation of toxic metabolites of both of these chemicals by competitively inhibiting alcohol dehydrogenase. A target EtOH serum concentration of 100 mg/dL is recommended to inhibit alcohol dehydrogenase, 19,20 but others have suggested that EtOH serum concentrations below 100 mg/dL may be effective.…”

Section: Discussionmentioning

confidence: 99%

A Comparison of the Bioavailabilities of Oral and Intravenous Ethanol in Healthy Male Volunteers

Cobaugh

Gibbs

Shapiro

et al. 1999

Academic Emergency Medicine

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Abstract. Objectives: Ethanol (EtOH), the antidote for methanol and ethylene glycol, is administered by the oral (PO) and intravenous (IV) routes. Serum concentrations (SCs) of 100 mg/dL or more are targeted for clinical effect. This study was completed to validate the assumption that there are minimal differences in SC achieved between these two routes. Methods: Twenty healthy male volunteers were randomized to receive either PO or IV EtOH. Subjects abstained from EtOH for 48 hours before each phase. After a seven-day washout period, the subjects crossed over to the other group. Inclusion criteria were no history of medical problems, age between 21 and 40 years, and actual body weight within 10% of ideal weight. Baseline EtOH SCs were obtained before participation in each phase. Two hours after a standard breakfast, the subjects received 700 mg/kg of PO or IV EtOH. PO EtOH was administered as a 20% solution in juice over 10 minutes. IV EtOH, controlled by an infusion pump, was administered as a 10% solution over 30 minutes. Blood was drawn for EtOH SCs at 45, 75, 105, 135, 165, 225, 285, and 345 minutes after start of the dose. Results: All initial EtOH SCs were 0. EtOH SCs were higher after IV administration. Mean peak SC was 103.6 mg/dL after IV administration and 71.3 mg/dL after PO administration (p < 0.0001). Mean time to peak was 46.5 minutes after IV administration and 103.5 minutes after PO administration (p < 0.0001). Total area under the curve was 17,440 min-mg/dL after IV administration and 13,875 min-mg/dL after PO administration (p < 0.003). The order of treatments did not affect results (p > 0.1). Conclusion: Significant differences exist between the SCs of EtOH as well as the times to peak SC after PO and IV administrations.

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“…A single dose of 80 ml of ethanol 40% was therefore administered via a nasogastric tube and the patient underwent a bicarbonate haemodialysis immediately. After the haemodialysis, ethanol 10% was administered intravenously for 3 days to maintain a blood level of ethanol of 1.2–1.4 g/l (1, 3, 4).…”

Section: Case Reportmentioning

confidence: 99%