after, 2-hydroxyethoxyacetaldehyde (C4H8O3) is metabolized by the enzyme aldehyde dehydrogenase (ALDH) into the weak acid 2-hydroxyethoxyacetic acid (HEAA) with chemical formula C4H8O4. Later on, HEAA leaves the liver through the bloodstream, being partially filtered in the kidneys for elimination. Mechanisms Based on available literature, scientists suggest unmetabolized DEG and HEAA are partially reabsorbed through glomerular filtration. As a consequence, the concentrations of the weak acid HEAA and metabolites may cause renal delay, leading to metabolic acidosis and further liver and kidney damage. Signs and symptoms The symptoms of poisoning typically occur in three characteristic intervals: First phase: Gastrointestinal symptoms such as nausea, vomiting, abdominal pain, and diarrhea develop. Some patients may develop early neurological symptoms like altered mental status, central nervous system depression, coma and mild hypotension. Second phase: In one to three days after ingestion (and dependent on dose ingested), patients develop metabolic acidosis, which causes acute kidney failure, oliguria, increasing serum creatinine concentrations, and later anuria. Other symptoms reported and secondary to acidosis and/or kidney failure are: hypertension, tachycardia, cardiac dysrhythmia, pancreatitis, hyperkalemia or mild hyponatremia. Final phase: At least five to ten days after ingestion, most of the symptoms are related to neurological complications, such as: progressive lethargy, facial paralysis, dysphonia, dilated and nonreactive pupils, quadriplegia, and coma leading to death. Treatment Fomepizole or ethanol should be quickly administered to prevent diethylene glycol being metabolized to the compound or compounds that cause the real damage. Fomepizole: an alcohol dehydrogenase (ADH) inhibitor with 8,000 times more affinity than ethanol. This treatment has minimal adverse effects because of constant serum concentration. However, it is a very expensive medication (approximately $3,000 U.S. per treatment). Ethanol: ethanol is a competitive ADH substrate. A constant blood concentration of 1 to 1.5 g/L (corresponding to 0.5 to 0.75 mg/L in the breath) should be maintained to acceptably saturate the enzyme. An initial dose of 0.6 to 0.7 g ethanol per kilogram body weight should be given (ca 0.8 mL/kg or 0.013 fl.oz./lb). This will cause ethanol intoxication. To avoid adverse effects, frequent serum monitoring and dosage adjustments should be done. For late diagnosis where ethanol or fomepizole is ineffective, because DEG has already been metabolized, hemodialysis becomes the only treatment available. Hemodialysis may either be administered alone or in combination with ethanol or fomepizole. Prognosis The prognosis depends on prompt diagnosis and treatment due to the high mortality rate DEG intoxication produces. Patients