It is important to recognize that fomepizole is removed by hemodialysis. Individuals at risk include toddlers and young children exploring their environment, alcoholics, and suicidal individuals. 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. Ethylene glycol is itself relatively nontoxic. Similarly, if ethanol has been used as a competitive inhibitor of alcohol dehydrogenase, its dose will have to be doubled because of its removal by hemodialysis. Ethylene glycol's metabolites are responsible for the anion gap metabolic acidosis. Oral dosing may be calculated using the above equation for serum alcohol concentrations by using 100 mg/dL for the serum concentration and then solving for the percentage amount of ethanol ingested. 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. Additional tests to be considered when self-harm is a concern are a complete blood count, transaminases, lipase, pregnancy status, serum or urine ketones, lactate, ethanol and salicylate concentrations. The presence of severe acidosis indicates the active and likely incomplete metabolism of ethylene glycol, with the concern that circulating glycolic acid may be converted to oxalate, which increases the risk of worsened renal function. Prolonged oral use irritates the gastric mucosa. Patients often recover when prompt diagnosis and treatment occur. Fomepizole should be prescribed if there is a clear history of ethylene glycol or methanol ingestion with an osmolal gap above 10 (indicating significant toxicity) or the ethylene glycol or methanol blood level is more than 200 mg/l. The volume of distribution is about 0.7 L.kg. The fluid volume administered should be based on the maintenance, deficit, and continuing loss needs of the patient. [1] According to the Annual Report of the American Association of Poison Control Centers' National Poison Data System, the number of case mentions of ethylene glycol in 2016 was 6,374. Ethylene glycol poisoning can cause acidosis, central nervous system depression, pulmonary edema, acute oliguric renal failure with crystalluria, liver damage due to calcium oxalate deposition, nausea, abdominal pain, and cramping, acute colonic ischemia [34], and papilledema and abducens nerve palsy [35]. Animals may take up to 1 year following EG toxicosis to regain concentrating ability, and some remain isosthenuric. In contrast to methanol poisoning, these patients usually are in coma when hyperventilation is pronounced so there is no subjective feeling of dyspnoea. A 12-hour observation period has been accepted as the standard of care, but it is based on collective experience more than specific data since acidosis is likely to occur earlier than 12 hours.[1]. In severe cases, acute respiratory distress syndrome may develop. The presence of hypocalcemia and calcium oxalate crystals in the urine is suggestive of ethylene glycol poisoning, although their absence should not be used to exclude toxicity [20]. [1][16][17][7][18], Using ethanol as an antidote is more complicated than treatment with fomepizole. The Journal of pediatrics. [24] When ethanol is used as an antidote, it can be difficult to manage, requiring critical care management for close titration and intoxciation with its associated complications, such as encephalopathy and respiratory depression. The anion gap is commonly calculated as follows: The metabolites of ethylene glycol (glycolic acid, oxalic acid) are acids and their accumulation will result in an elevated anion gap. Treatment options for ethylene glycol toxicity include supportive care, fomepizole (Antizole, 4-Methylpyrazole or 4MP), ethanol, dialysis and theoretically, thiamine, pyridoxine and magnesium. 2009 May 21, McMartin K,Jacobsen D,Hovda KE, Antidotes for poisoning by alcohols that form toxic metabolites. The evaluation of the ethylene glycol intoxicated patient should follow a diagnostic approach that utilizes historical and objective data. Early recognition is essential, allowing institution of treatment to inhibit alcohol dehydrogenase with ethanol or fomepizole. Therefore, a methodological approach to the diagnosis needs to be considered in which the patient is monitored for the anticipated effects of toxicity. Ethylene glycol and methanol poisoning may present with nausea, vomiting, abdominal pain, impaired consciousness that may progress to severe metabolic acidosis, AKI, optic nerve damage, convulsions, coma, and ultimately death.

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