Gas chromatography (GC) methods with flame ionization (GC/FID) and mass spectrometry detectors (GC/MS) are available for simultaneous measurement of ethylene glycol and glycolic acid [24–26]. Glycolic acid is then oxidized to glyoxylic by glycolic acid oxidase, or lactate dehydrogenase due to its resemblence of lactate. Ingesstion of agents contanining more than one alcohol or toxic substance should also be considered. The mainstay of treatment is fomepizole, supportive care and resuscitation. Another laboratory parameter which may be useful in assessing ethylene glycol toxicity is the anion gap. Toxicity of diethylene glycol and other glycol ethers is associated with the development of metabolic acidosis. Therapy for EG poisoning is aimed at preventing absorption, increasing excretion, and preventing metabolism of EG. Calcium gluconate may be indicated if complications occur as a result of hypocalcemia, but should otherwise be replaced cautiously and judiciously as exogenous calcium administration may enhance the precipitation of calcium oxylate crystals. This caclium oxalate deposition may predisopose to hypocalcemia, placing patient at risk for tetany, seizures, QT interval prolongation and dysrhythmias. Propylene glycol is also used as a diluent for oral, topical, or intravenous pharmaceutical preparations so that active ingredients can be dissolved properly in the formulation. Given their chemical structural similarities, glycolate can be misinterpreted by some lactate analyzers as lactate . In late presentations, the osmolal gap may not be elevated. When measured in both healthy adults and children, the normal osmolal gap is −2±6 . Oxalic acid then combines with calcium to cause deposition of calcium oxalate in the kidneys, which results in severe renal failure (Equation 18.4): Major complications of ethylene glycol poisoning are metabolic acidosis and renal failure. Ethylene glycol is undergoes multiple metabolic steps, with metabolites glycolic acid and oxalic acid being primarily responsible for acidosis and renal injury, respectively. 2000 Aug, Ng PCY,Long BJ,Davis WT,Sessions DJ,Koyfman A, Toxic alcohol diagnosis and management: an emergency medicine review. Pulmonary infiltration may be observed radiologically, although these changes appear to be non-infective in origin. Without adequate treatment, the patient will deteriorate rapidly with development of severe CNS depression (cerebral edema), convulsions, oliguric renal failure and respiratory problems. Interestingly, in patients poisoned with ethylene glycol, falsely elevated lactate may be observed using blood gas analyzers, but chemistry analyzers usually do not show this false elevation. This should be considered when calculating the osmolar gap, and the true result of the calculation may be +/- 20 compared to the finding. 2009 May 21, McMartin K,Jacobsen D,Hovda KE, Antidotes for poisoning by alcohols that form toxic metabolites. Neither isopropyl alcohol nor acetone can cause metabolic acidosis, and poisoning from these compounds can be less life-threatening than methanol or ethylene glycol poisoning. A mildly elevated osmolal gap is not specific to toxic alcohol ingestions as other drugs and disease processes may result in an osmolal gap. 2017 Dec, Jacobsen D,Hewlett TP,Webb R,Brown ST,Ordinario AT,McMartin KE, Ethylene glycol intoxication: evaluation of kinetics and crystalluria. Frequent measurement of urine production, serum urea nitrogen and creatinine, and blood pH, bicarbonate, ionized calcium, and electrolytes daily or twice daily will help guide fluid and electrolyte therapy (Grauer, 1998). Fomepizole is given intravenously with a loading dose of 15 mg/kg, followed by maintenance dosing of 10 mg/kg every 12 hours for four doses, or until the ethylene glycol concentration is at least less than 62 mg/dL with a normal acid-base status; however, more conservative recommendations of below 25 mg/dL exist. When samples are sent to a referral laboratory, the results may not be available in the time frame needed to assist in making early clinical decisions. Intravenous ethanol formulary is usually 10%, and the loading dose is calculated using the product of the goal plasma concentration (C = 100mg/dL), the volume of distribution of ethanol (V = 0.6L/kg), and the patient’s weight. Therefore, if a loading dose of fomepizole has already been administered, a continuous infusion of 1 to 1.5 mg/kg per hour should be prescribed for the duration of the hemodialysis. The tubular damage caused by EG may be reversible, but tubular repair can take weeks to months. , Fomepizole and ethanol inhibit alcohol dehydrogenase to stop the conversion of ethyelene glycol (and other alcohols) to its toxic metabolites. Fomepizole is an ADH inhibitor, not a competitive substrate, and it does not induce CNS depression (in dogs), diuresis, or hyperosmolality at the recommended dosage. , Like ethanol and methanol, metabolism begins with gastric mucosal alcohol dehydrogenase, and occurs primarily in the liver through serial oxidation by alcohol dehydrogenase and aldehyde dehydrogenase, with each step reducing NAD+ to NADH. The term “toxic alcohols” is a collective term that includes methanol, ethylene glycol, and isopropyl alcohol. The ethylene glycol in antifreeze affects the central nervous system first. Children under the age of 12 made up 686 of the known total 6,374 cases with 13 unknown child age cases. [ncbi.nlm.nih.gov] Symptoms may include nausea, vomiting, convulsions, stupor (decreased level of alertness), or even coma. Ethylene glycol is itself relatively nontoxic. , A patient who has ingested ethylene glycol will present somewhere along the spectrum of asymptomatic with an increased osmolar gap to very ill with end-organ toxicity and anion gap metabolic acidosis. Clinical manifestations of the ethylene glycol intoxication can be divided in three phases: a neurologic stage, with hallucinations, stupor and coma; the second stage is cardiovascular with cardiac failure. Fluid, electrolyte, and acid–base disorders should be corrected and diuresis established, if possible. In Meyler's Side Effects of Drugs (Sixteenth Edition), 2016. Additional disadvantages of ethanol treatment include its metabolism to acetaldehyde, which impairs glucose metabolism and is a cerebral irritant. The American journal of medicine. This is most useful when assessing for toxicity in small, accidental ingestions, usually by children. Acta medica Scandinavica. 1999 Sep 4, Buchanan JA,Alhelail M,Cetaruk EW,Schaeffer TH,Palmer RB,Kulig K,Brent J, Massive ethylene glycol ingestion treated with fomepizole alone-a viable therapeutic option. Acetone is also found in many domestic products, for example, nail polish remover.