anion gap ethylene glycol poisoning

Background: Ethylene glycol toxicity is a well-known cause of acute kidney injury (AKI) and high anion gap metabolic acidosis. Over time, as ethylene glycol (osm active) gets metabolized to glycolic acid (acid metabolite), the osmol gap will decrease while the anion gap increases Lactate Gap Glycolic acid is structurally very similar to lactic acid , and can be misread by the POC testing in the ED, and give a falsely elevated lactic acid level These alcohol-related intoxications can present with high anion gap metabolic acidosis and increased osmolality. 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. 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. 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. Large doses and unusual circumstances are necessary for the development of propylene glycol toxicity. Studies have suggested In clinical practice, poisoning with ethylene glycol, methanol, and isopropyl alcohol is common. Unlike ethylene glycol, propylene glycol does not produce nephrotoxicity in humans. Calcium oxalate crystalluria may be observed as early as 3 and 6 hr after ingestion in cats and dogs, respectively. Metabolism of ethylene glycol to organic acids, and increased production of lactate, are responsible for the increased gap. Propylene glycol poisoning is marked initially by CNS depression and an elevated osmolal gap and, later, by an increased anion gap. Patients who have ethylene glycol poisoning characteristically have an elevated anion gap and osmolal gap. Acute ingestions present with altered sensorium and an osmolal gap. 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. The diagnosis is usually suggested by a high anion gap metabolic acidosis and an elevated osmolal gap in the setting of a suspected ingestion. 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. Ethylene glycol poisoning classically presents as a metabolic acidosis with an increased anion gap. If large doses of ethylene glycol are ingested, poisoning is accompanied by metabolic acidosis, with onset occurring within 24 hours after ingestion. Ethylene glycol is found in many household products and is a common toxic ingestion. Ethylene glycol classically produces an elevated anion gap metabolic acidosis. Rarely, the osmolal gap may be close to normal which can delay the diagnosis or lead to a misdiagnosis. 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. We report a series of patients with ethylene glycol toxicity with a component of non-anion gap metabolic acidosis without known associated confounding factors. Elevated osmolal gap, high anion gap and calcium oxalate crystals are findings suggestive of ethylene glycol poisoning, but are not pathognomonic of it. 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