anion gap ethylene glycol poisoning

Ethylene glycol classically produces an elevated anion gap metabolic acidosis. In clinical practice, poisoning with ethylene glycol, methanol, and isopropyl alcohol is common. However, it is a rare presentation in Australia with only 22 cases reported in 2014. In addition, when a serum ethylene glycol concentration cannot be confirmed, it is especially important to rule out salicylate toxicity. We report a series of patients with ethylene glycol toxicity with a component of non-anion gap metabolic acidosis without known associated confounding factors. We report a case of ethylene glycol ingestion with a near-normal osmolal gap. The diagnosis is usually suggested by a high anion gap metabolic acidosis and an elevated osmolal gap in the setting of a suspected ingestion. Ethylene glycol is found in many household products and is a common toxic ingestion. Patients who have ethylene glycol poisoning characteristically have an elevated anion gap and osmolal gap. Calcium oxalate crystalluria may be observed as early as 3 and 6 hr after ingestion in cats and dogs, respectively. Rarely, the osmolal gap may be close to normal which can delay the diagnosis or lead to a misdiagnosis. Studies have suggested If large doses of ethylene glycol are ingested, poisoning is accompanied by metabolic acidosis, with onset occurring within 24 hours after ingestion. Propylene glycol poisoning is marked initially by CNS depression and an elevated osmolal gap and, later, by an increased anion gap. As previously mentioned, the major metabolites of ethylene glycol are organic acids which are not only responsible for cellular injury but also cause the raised anion gap that is seen in those with significant, established, ethylene glycol poisoning. Unlike ethylene glycol, propylene glycol does not produce nephrotoxicity in humans. Metabolism of ethylene glycol to organic acids, and increased production of lactate, are responsible for the increased gap. The true toxicity of ethylene glycol is mediated by its metabolites, which are responsible for the increased anion gap metabolic acidosis, renal tubular damage, and crystalluria seen later in ingestions. Acute ingestions present with altered sensorium and an osmolal gap. tients with ethylene glycol poisoning classically present with severe metabolic acidosis, accompa- nied by an increased anion gap.‘*‘-5 Metabolism of ethylene glycol to organic acids,4.5 and produc- tion of excess lactate,5 are responsible for this elevation in anion gap. We report the case of an alcohol user who consumed ethanol and ethylene glyc … The gap is caused by the presence of osmotically active particles (eg, ethylene glycol) in the serum that are not factored into the above equation. No specific cut-off in the osmolal gap can be used to rule in or rule out ethylene glycol poisoning, as they can be high or normal depending on the timing of its consumption and metabolism. These alcohol-related intoxications can present with high anion gap metabolic acidosis and increased osmolality. Ethylene glycol poisoning classically presents as a metabolic acidosis with an increased anion gap. Background: Ethylene glycol toxicity is a well-known cause of acute kidney injury (AKI) and high anion gap metabolic acidosis. Large doses and unusual circumstances are necessary for the development of propylene glycol toxicity. When ethylene glycol toxicity is being considered in a patient presenting with an anion gap metabolic acidosis, the patient should be evaluated for acute renal injury. 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