… A reasonable endpoint for dialysis is correction of metabolic acidosis and reduction of EG level to less than 50 mg/dL. Nearly half of these deaths were due to ethylene glycol or methanol. Early haemodialysis is indicated for patients who exhibit multi-organ dysfunction and persistent metabolic acidosis despite ADH inhibition. It is nontoxic itself but is converted to toxic metabolites in the liver: Glycolic acid (->glycolate anion) is the major contributor to the often severe high anion gap acidosis … Background: Ethylene glycol toxicity is a well-known cause of acute kidney injury (AKI) and high anion gap metabolic acidosis. The chief cause of metabolic acidosis is glycolic acid, which is a product of ethylene glycol metabolism. Ethylene glycol is a colorless sweet tasting solvent which is used in antifreeze solutions. Editor: Anthony J. Hemodialysis accomplishes three immediate goals. presented with metabolic acidosis and acidemia after ethylene glycol ingestion, but with only a relatively minor increase in the anion gap. We report a series of patients with ethylene glycol toxicity with a component of non-anion gap metabolic acidosis without known associated confounding factors. It will correct metabolic acidosis, and reduce both ethylene glycol levels and the toxic EG metabolites. This patient had a component of non-anion gap metabolic acidosis as demonstrated by a gap, or delta ratio (DR) of less than 1. This acidosis is caused primarily by the accumulation of glycolic and glyoxylic acids, although oxalic acid and excess lactic acid may be contributing factors. However, it is a rare presentation in Australia with only 22 cases reported in 2014. Ingestion of ethylene glycol indirectly results in central nervous system compromise, cardiopulmonary depression, and renal failure 1. A retrospective review of Poison Control Center records were … 8.6.2: Ethylene Glycol Poisoning. – –Removes ethylene glycol and glycolate effectively Indications: – –Ethylene glycol concentration>500mg/L or presence of severe metabolic acidosis, renal failure, severe electrolyte imbalance, or generally deteriorating A retrospective review of Poison Control Center records were searched more than 8 years (2000-2007) for ethylene glycol and antifreeze. The poisoning causes disturbances in the body’s chemistry, including metabolic acidosis (increased acids in the bloodstream and tissues). Once absorbed from the gastrointestinal tract, which occurs rapidly, ethylene glycol is converted to glyoxylic acid and oxalic acid which are the compounds responsible for toxicity, and metabolic acidosis 1. We report a series of patients with ethylene glycol toxicity with a component of non-anion gap metabolic acidosis without known associated confounding factors. Ethylene glycol classically produces an elevated anion gap metabolic acidosis. Ethylene glycol toxicity is important to recognize because of its conversion to acid metabolites that can cause a metabolic acidosis and renal toxicity. Oxalic acid is another byproduct, which causes acute tubular necrosis and degrades opportunities for acid-base recovery. Ethylene glycol poisoning is primarily treated with ADH inhibitors, fomepizole or oral ethanol [4,5]. Treatment is multifactorial, but if implemented early can prevent some of these complications. Non-anion gap metabolic acidosis is occasionally reported Ethylene glycol and methanol themselves are not toxic, but their metabolites cause inebriation, nausea and vomiting, metabolic acidosis, hemodynamic instability and seizures. Ethylene glycol is a traditional cause of high anion gap metabolic acidosis, and occupies the "E" spot in the MUDPILES mnemonic. 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