Traditionally, gastric lavage or nasogastric aspiration of gastric contents are the most common methods employed in ethylene glycol poisoning. I cannot find the original paper, but a letter in response to it suggests one should sustain a blood ethanol concentration of 20 to 30 mmol/L (100 to 150 mg/dL). Ethylene glycol (EG) poisoning is common in dogs and cats 1 – 4 and often results in death if it is not diagnosed and treated promptly. The rationale for the use of bicarbonate is the massive generation of acid by the metabolism of ethylene glycol. Ingestion of sufficient amounts is fatal if untreated. 1) 4-methylpyrazole (4-MP)[Antizole or fomepazole]: This medication inactivates alcohol dehydrogenase. Some redness and burning at the site were the only reported side effects. The rate-limiting step of ethylene glycol metabolism is the ADH-catalyzed step. Only at the third admission, 2 years after the first, was the possibility of an underlying metabolic disorder considered. Thus the treatment of poisoning with ethylene glycol is a logical result of understanding the biochemistry of the toxicity. Neither as exciting as intravenous alcohol, nor as expensive as fomepizole, continous veno-venous haemodiafiltration is the method of choice for getting rid of huge quantities of ethylene glycol rapidly. Ethylene glycol, the parent compound, is inebriating but generally considered nontoxic. C. Ethylene glycol is … Metabolism: Ethylene glycol is metabolised in the liver. Like ethanol, ethylene glycol is rapidly absorbed in the GI tract, with peak absorption in 30-60 minutes. Thus the pathological damage includes cerebral oedema, haemorrhage and deposition of calcium oxalate crystals. DePass LR, Garman RH, Woodside MD, Giddens WE, Maronpot RR, Weil CS. N Engl J Med 1981;304:976-8. There is a complex metabolic pathway with multiple products, of which oxalic acid is the most dreaded. Cjem 4.1 (2002): 34-40. It boils at 197 degrees C, in case you ever want to boil some. If untreated, ingestion of only 30 to 60 mls may be sufficient to cause permanent organ damage or death. Here, we analyzed the metabolism of ethylene glycol. Mono Ethylene Glycol, commonly referred to as Ethylene Glycol Antifreeze but also referred to as Ethane-1,2-diol, MEG, EG and Industrial Glycol. The lungs show oedema, and occasionally calcium oxalate crystals and degenerative myocardial changes may also occur. Glycolic acid (GA) and ethylene glycol (EG) are versatile two-carbon organic chemicals used in multiple daily applications. However, rats exposed for prolonged periods seem to develop chronic renal failure. How drunk do you have to be to prevent ethylene glycol metabolism? The mechanism of metabolic acidosis is more interesting. Half life is short, but longer with any therapy that blocks the metabolism of ethylene glycol to glycoaldehyde… so with ethanol therapy, the ethylene glycol can hang around for up to 24 hours With therapy, elimination is entirely renal. Competes with ethylene glycol for metabolism via alcohol dehydrogenase (ADH) enzyme. b intravenous sodium bicarbonate; this corrects the acidosis—animal studies have shown that this increases the LD50 by around four times c calcium gluconate; this corrects the hypocalcaemia d dialysis to remove ethylene glycol. Anything over 0.1ml/kg will require treatment. B. Propylene glycol is metabolized to more toxic compounds. The conversion to glycolic acid is somewhat rapid. The extra osmoles represent some mixture of ethylene glycol and glycolic acid, eagerly water-soluble, and thus rapidly dialysed. Indications: Ethylene glycol levels > 20 mg/dL Ethylene glycol is more toxic to humans than animals, and in general the susceptible species are those which metabolize the compound to oxalic acid, although this is quantitatively a minor route. Ethylene glycol is a precursor for many polymers, eg. Adolphe Wurtz (1856) "Sur le glycol ou alcool diatomique" (On glycol or diatomic alcohol), Comptes rendus, 43 : 199-204. Clay, Keith L., and R. C. Murphy. b Between 12 and 24 h there is tachypnoea, tachycardia, hypertension, pulmonary oedema and congestive cardiac failure. In the parlance of the street cop, this equates to a blood alcohol level of 0.1%, twice the legal driving limit in Australia. ternative metabolism of toxic alcohols to non-toxic metabolites. There are three recogniseable stages to ethylene glycol toxicity. Effective Treatments for Peripheral Neuropathy, Carpal Tunnel Syndrome Holistic Treatments Ebook, 7 Useful Tips for Improving Your Mental Focus, How to Lose Weight From Your Stomach Fast, An alternative approach to perioral rhytides, Mental Impotence Holistic Treatments Ebook, This substance is a liquid used in antifreeze, paints, polishes and cosmetics. Aldehyde dehydrogenase causes glyceraldhyde to become glycolic acid. We found that strain JM37 grew rapidly with ethylene glycol as a … Ethylene Glycol was first formulated in the 1850’s and is now commercially produced through a chemical reaction between Ethylene Oxide and a catalyst. polyethylene glycol. It and its toxic byproducts first affect the central nervous system, then the heart, and finally the kidneys. To summarize, you give massive amounts of bicarbonate, and then you either start an ethanol infusion, regular doses of fomepizole, or haemodialysis. "Methanol and ethylene glycol poisoning: a case study and review of current literature. Such a thing indeed exists, but is not well studied. However, like all other glycols it is is rapidly absorbed, even through the gastric mucosa. Glycolic acid is the smallest of the alpha-hydroxy acids, and is used in all sorts of skin-related industries (be it tanning, as a leather-dye, or as a part of dermatological skin peeling). Fundam Appl Toxicol. Methanol and ethylene glycol poisonings share many characteristics both clinically and biochemically. 4-Methylpyrazole, or fomepizole as it is known, is basically a competitive antagonist to alcohol dehydrogenase. Central nervous system depression is the most pronounced feature at this stage; the coma may be garnished with seziures. Thge major interactions of ethylene glycol are with ethanol and fomepizole, which is put to good use in management of the toxicity. The treatment of poisoning with ethylene glycol reflects the mechanism and biochemical effects. Glycolic acid is further metabolised to glyoxylic acid and oxalic acid. In clinical practice, poisoning with ethylene glycol, methanol, and isopropyl alcohol is common. The products of these metabolic pathways are then really eliminated. More bicarbonate must be added in order to buffer the excessive number of hydrogen ions present in the patient, so that H2O and CO2 may be generated. The investigation of its microbial metabolism therefore provides insights into the environmental fate of this pollutant and also enables its utilization … This effect rarely produces serious morbidity or death by itself.Acute renal failure as well as a severe anion-gap metabolic acidosis results from the metabolism of ethylene glycol into at least 4 distinct metabolites. These alcohol-related intoxications can present with high anion gap metabolic acidosis and increased osmolality. The acetogenic bacterium Acetobacterium woodii is able to grow by the oxidation of diols, such as 1,2-propanediol, 2,3-butanediol, or ethylene glycol. Methanol and ethylene glycol metabolism can be understood by first studying the metabolism of ethanol, which occurs in two steps: Ethanol is oxidized to acetaldehyde with production of NADH by alcohol dehydrogenase, an enzyme located, for the most part, in the cytosol of hepatocytes (see Chapter 24 ). The first step is catalysed by the enzyme alcohol dehydrogenase and herein lies the key to treatment of poisoning. There is thus an increase in the level of lactate and lactic acidosis may result. Ethylene glycol is moderately toxic, with an oral LDLo = 786 mg/kg for humans. META Study Group". The highest survived dose reported is 2 litres. The next stage is that of cardiac toxicity. As a weak acid, formic acid should become more water soluble in an alkaline bloodstream, and in alkaline urine. The alcohols: ethanol, methanol, isopropanol, ethylene glycol. "Ethylene glycol poisoning." EG intoxication is the second most common cause of fatal poisoning in animals according to the American Association of Poison Control Centers. Ethylene glycol and its toxic acid metabolytes, "On the metabolic acidosis of ethylene glycol intoxication.". There are two proposed mechanisms of propylene glycol metabolism: The first is as follows: Ethylene glycol is transformed in the liver by alcohol dehydrogenase to glyceraldehyde. The osmolar gap may be raised (to > 10) early in the course but this is variable. Typically, people drink this stuff. The major danger is due to its sweet taste, which can attract children and animals. Good old alcohol, in large quantities, will overwhelm alcohol dehydrogenase, saturating it. Apparently, it gives one a buzz similar to that of alcohol intoxication. The treatment options here are discussed in brief. Hypocalcemia may occur as oxalate chelates the serum calcium. In patients exposed to ethylene glycol, 100mg thiamine and 100mg pyridoxine can be administered IV daily This increases its clearance, and keeps it out of the fatty central nervous system, where its effects are the most destructive (specifically, the effects on the tender juicy retina). GA and EG are currently produced by chemical synthesis, but their biotechnological production from renewable resources has received a substantial interest. Most intoxications are associated with ingestion of antifreeze, which is typically 95% EG. Suppression of metabolism – fomepizole and IV ethanol are temporizing measures; Removal of toxin – haemodialysis; Alkalinisation in order to counteract metabolic acidosis (Na bicarbonate) Folic acid and folinic acid may be useful adjuncts (but does not directly improve patient’s clinical state) Ethylene glycol. If ingestion was recent (1-2 hours), vomiting is induced and activated charcoal is given to reduce further absorption of the ethylene glycol. 20. The result of each of the metabolic steps is the production of NADH. Otherwise, much of it is metabolized into hideous daughter-compounds, which are also ex… 5 The mortality rate in dogs is reported to range from 59% to 70% 1, 5 and is thought to be even higher in cats. The minimum lethal dose of ethylene glycol is about 100 ml and after ingestion death may occur within 24 h from damage to the CNS or more slowly (8-12 days) from renal failure. The degeneration of distal tubules may also be seen. Methanol is slowly metabolised to formaldehyde which is rapidly metabolised to formate, the metabolite mainly resp … Once past this window of time, absorption has already occurred. The typical way to administer alcohol in such a situation is to give it via a central vein (it being such a good peripheral venous sclerosant that it is in fact routinely injected into varicose veins to destroy them). All animals are susceptible to ethylene glycol (EG) toxicity, but it is most common in dogs and cats. Moossavi S, Wadhwa NK, Nord EP. Lactate gap refers to the difference in lactate measurement via different methods: Elevated lactate on portable blood gas machine utilizing lactate oxidase. It is not well absorbed through the skin; nor does it evaporate particularly well. 1. A lot of this information comes from “Goodman & Gilman's The Pharmacological Basis of Therapeutics” 11th ed by Brunton et al,and   “Basic & Clinical Pharmacology” 11th ed. There is degeneration of proximal tubular epithelium with calcium oxalate crystals and fat droplets detectable in tubular epithelial cells. "Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. In 1977, Clay and Murphy poisoned some monkeys and revealed that the serum bicarbonate levels decreased in proportion to rising glycolic acid levels. • Supportive care (correct fluid, acid-base, and electrolyte imbalances). First you may feel slightly drunk for about 4 hours. As ethylene glycol is rapidly absorbed, gastric decontamination is unlikely to be of benefit unless it is performed within 60 minutes of ingestion. Crystals, blood and protein may all be detected in the urine (crystalluria, haematuria and proteinuria, respectively), and the urine may have a low specific gravity. Roadmap To Genius Improve Intelligence & IQ, Candida Crusher Permanent Yeast Infection Solution, Glutathione conjugation - Metabolic Activation, Aromatic Hydroxylation - Metabolic Activation, Glucuronide formation - Metabolic Activation, Aliphatic Hydroxylation - Metabolic Activation, How to Cope with Acute Renal Failure Naturally. The imbalance in the level of this in the body is adjusted by oxidation to NAD coupled to the production of lactate. After about 36-48 hrs, the renal failure becomes the dominant feature. 1986 Apr;33(2):311-23. Moreau CL, Kerns W, Tomaszewski CA, McMartin KE, Rose SR, Ford MD, Brent J (1998). Clin Nephrol. The contribution of all the other metabolites was negligible. Previous chapter: Urate and hippurate anions: their origins and clearance, Next chapter: Diabetic, alcoholic and starvation ketoacidosis. 2003 Sep;60(3):205-10. Partially because lactic acidosis – –The first two steps in ethylene glycol metabolism cause the reduction of NAD to NADH. Fomepizole has an 8,000 fold greater binding affinity to ADH and thus prevents the metabolism of ethylene glycol to toxic acid metabolites. Anything over 1.0-1.5mg/kg is considered lethally toxic. In contrast to ethylene glycol, propylene glycol rarely causes toxic effects. Common ethyl alcohol (ethanol) binds much more easily to ADH than ethylene glycol or methanol does. Diethylene glycol was once used as a vehicle for the drug sulphanilamide and when used for this it caused some 76 deaths. Both alcohols are metabolised via alcohol dehydrogenase to their toxic metabolites. Upon ingestion, ethylene glycol is oxidized to glycolic acid, which is, in turn, oxidized to oxalic acid, which is toxic. On the first admission, glycolic acid was detected in his blood and he was diagnosed as having ethylene glycol intoxication. As it has a sweet. This treatment is only effective in do… Pediatr Clin North Am. This is mainly because A. Absorption of propylene glycol from the gastrointestinal tract is slow. The parent compound is osmotically active, and is responsible for the increased osmolality observed in the early course of exposure prior to metabolism. Thus, ethylene glycol is metabolized by several oxidation steps eventually to yield oxalic acid (figure 7.56). Alternatively, you may consider injecting it. Well. The elevated NADH to NAD ration causes the conversion of pyruvate pyruvate to lactate. Biotransformation studies have been performed to understand why ethylene glycol causes toxic effects. The toxic metabolic by-products of ethylene glycol metabolism cause a build-up of acid in the blood (metabolic acidosis). The authors (who did not identify themselves) suggested a loading dose of 0.6g per kg body weight, or roughly 40g for a 70kg male, to get to 100mg/dL. T he detection of calcium oxalate crystals in the urine is often stated to be a useful guide but this is wrong. In contrast, the conversion of glycolic acid to glyoxylic acid is slower and is the rate-limiting step in the metabolism of ethylene glycol. Pure ethylene glycol is said to be sweet-tasting, but nowadays (in order to deter children, one assumes) the majority of it is tainted with foul-tasting impurities. Recent analyses demonstrated fundamentally different ways for oxidation of 1,2-propanediol and 2,3-butanediol. There is a lot of good, thorough literature on the management of ethylene glycol toxicity. We found that strain JM37 grew rapidly with ethylene glycol as a sole source of carbon and energy, while strain KT2440 did not grow within 2 days of incubation under … This deliciously syrupy tongue-pleasing alcohol is a favourite among the critically ill population. Thus, there is reduced plasma bicarbonate, low plasma calcium and raised potassium. The mechanism of toxicity of ethylene glycol involves metabolism, but unlike previous examples this does not involve metabolic activation to a reactive metabolite. Journal of toxicology. Clinical toxicology 36 (7): 659–66. META Study Group". INTRAVENOUS INJECTION OF ALCOHOL BY DRUG INJECTORS: REPORT OF THREE CASES; "Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. The consequences of this are as follows: i acidosis due to lactate, oxalate and the other acidic metabolites; this results in metabolic distress and physiological changes ii loss of calcium as calcium oxalate iii deposition of crystals of calcium oxalate in the renal tubules and brain iv inhibition of various metabolic pathways leading to accumulation of organic acids v impairment of cerebral function by oxalate and damage by crystals; also some of the aldehyde metabolites may impair cerebral function vi damage to renal tubules by oxalate crystals leading to necrosis. Recurrent severe anion gap metabolic acidosis secondary to episodic ethylene glycol intoxication. In this study, we investigated the metabolism of ethylene glycol in the Pseudomonas putida strains KT2440 and JM37 by employing growth and bioconversion experiments, directed mutagenesis, and proteome analysis. It does what ethanol would do, except it does so with great expense, and without ethanol intoxication. Litovitz T. More than 6 per cent of poisonings involve alcohols and glycols, reflecting their availability in a wide range of household products, including aftershave, brake fluid, gas line antifreeze, model airplane fuel, mouthwash, rubbing alcohol, and windshield washing solution. These toxic substances also affect the cardiopulmonary system and can cause renal failure. Ethylene glycol metabolism generates glycolate, which can be mistaken for lactate by portable lab assays utilizing lactate oxidase. taste and is readily available it has been used as a poor man's alcohol, but it may also be ingested accidentally and for suicidal purposes. An additional benefit is the effect of "ion trapping" formic acid. It is first converted by alcohol dehydrogenase to glycoaldehyde, which is then metabolised to glycolic acid by aldehyde dehydrogenase. Recurrent severe anion gap metabolic acidosis secondary to episodic ethylene glycol intoxication. The goal of specific treatment is to prevent the metabolism of ethylene glycol into the toxic metabolites. Otherwise, much of it is metabolized into hideous daughter-compounds, which are also excreted by the unhappy kidneys (which find themselves mangled by the process). "Methanol and ethylene glycol poisoning: a case study and review of current literature." Thus, this acidosis is "bicarbonate-resistant". A Norfolk couple report that it tasted "horrible", though the husband finished his glass as a demonstration of his manliness. Also, the intermediate metabolites of ethylene glycol have metabolic effects such as the inhibition of oxidative phosphorylation. DEG is used as a component of multiple different products including antifreeze preparations, cosmetics, lubricants, brake fluids, wallpaper strippers, heating/cooling fuel and as a plasticizer. Toxicology and applied pharmacology 39.1 (1977): 39-49. Ethylene glycol is oxidized via alcohol dehydrogenase into glycoaldehyde, which then undergoes metabolism via aldehyde dehydrogenase into glycolic acid. The American Journal of Medicine 57.1 (1974): 143-150. Thus, ethylene glycol is metabolized by several oxidation steps eventually to yield oxalic acid (figure 7.56). Ethylene glycol is rapidly absorbed from the gastrointestinal tract and slowly absorbed through the skin or lungs. Conduction disturbances and arrhythmias are to be expected, pulmonary oedema may result from myocardial depression (caused by the acidosis). (See supplemental page for metabolic pathway figures for ethylene glycol and methanol). As the parent compound, ethylene glycol produces altered mental status similar to ethyl alcohol. However, there is one case series of three poor fools who have admitted to injecting alcohol (ranging from vodka to beer, dosage unknown) and whose veins did not suffer excessively as a consequence, in spite of what i can only assume was suboptimal injecting technique. In this study, we investigated the metabolism of ethylene glycol in the Pseudomonas putida strains KT2440 and JM37 by employing growth and bioconversion experiments, directed mutagenesis, and proteome analysis. Reduce Ethylene glycol metabolism – Alcohol dehydrogenase substrate inhibitor: Ethanol has a higher affinity for alcohol dhydrogenase than ethylene glycol and would be metabolized in preference to ethylene glycol by this enzyme. Thus, after standard procedures such as gastric lavage to reduce absorption and supportive therapy for shock and respiratory distress, patients are treated with the following: a ethanol; this competes with ethylene glycol for alcohol dehydrogenase, but as it is a better substrate the first step in ethylene glycol metabolism is blocked—animal studies have shown that this doubles the LD50. Chronic toxicity and oncogenicity studies of ethylene glycol in rats and mice. Ethanol for ethylene glycol poisoning [letter]. Ipecac-induced It is not well absorbed through the skin; nor does it evaporate particularly well. Alcohol dehydrogenase, the same first step enzyme responsible for the metabolism of methyl and ethyl alcohols, slowly catalyzes conversion of EG to glycoaldehyde. By Katzung et al. It is only the most common toxin among a  whole family of glycols: Typically, people drink this stuff. The usefulness of gastric lavage has, however, been questioned, and it is now no longer used routinely in poisoning situations. However, like all other glycols it is is rapidly absorbed, even through the gastric mucosa. Half life is short, but longer with any therapy that blocks the metabolism of ethylene glycol to glycoaldehyde… so with ethanol therapy, the ethylene glycol can hang around for up to 24 hours, With therapy, elimination is entirely renal. Potentially, it may interact with things like disulfiram and metronidazole, which block acetaldehyde dehydrogenase. There seem to be three recognizable clinical stages: a Within 30 min and lasting for perhaps 12 h, there is intoxication, nausea, vomiting, coma, convulsions, nystagmus, papilloedema, depressed reflexes, myoclonic jerks and tetanic contractions. The mechanism of toxicity of ethylene glycol involves metabolism, but unlike previous examples this does not involve metabolic activation to a reactive metabolite. Supportive therapy, such as IV fluids, is also important. Several deaths are recorded annually in the U.S. alone. Ethylene glycol's metabolites are responsible for the anion gap metabolic acidosis. DEG has also been inappropriately substituted in pharmaceutical preparations for nontoxic constituents, resulting in more than a dozen epidemics of human poisoning, with resultant … Compared to ethylene glycol, ethanol had something like 100 times more affinity for alcohol dehydrogenase. Permanent optic atrophy may occur. These 95% commercial antifreeze preparations are diluted ~50% with water when used in vehicle cooling systems. Elimination: Ethylene glycol has an elimination half-life of about 3 hours. Diethylene glycol (DEG) is a clear, colorless, odorless liquid with a sweet taste, and is an excellent solvent for water-insoluble chemicals and drugs. Certainly. Henderson, William R., and Jeffrey Brubacher. Then, you might feel slightly ill. As the glycolic acid begins to appear in the bloodstream, metabolic acidosis ensues and hyperventilation follows. The clinical biochemical features reflect the biochemical and physiological effects. Thus, if you suspect you have accidentally poisoned yourself with ethylene glycol, one may consider four shots of spirits as a rescue therapy. The main indication for this (apart from the inevitable renal failure of a late presentation) is a high osmolar gap. "On the metabolic acidosis of ethylene glycol intoxication." One can imagine some sort of cyclical nightmare of ethylene glycol intoxication, ICU admission, discharge and re-intoxication. Of the various ways one can become acquainted with ethylene glycol, this is probably the most common. glucose metabolism, Krebs' cycle, protein synthesis, RNA synthesis and DNA replication for example. At this stage, there is no acidosis, but the anion gap is widened (unmetabolised ethylene glycol floods the bloodstream). c Between 24 and 72 h the kidneys become damaged giving rise to flank pain and acute renal tubular necrosis. Both susbtances are well removed by dialysis, and on top of that one can adjust the bicarbonate concentration of the dialysate to donate extra bicarbonate to the patient's bloodstream, increasing the correction of the acidosis even further. Fig: Metabolism of Ethylene Glycol . ", Ethanol for ethylene glycol poisoning [letter. Pollution from ethylene glycol, and plastics containing this monomer, represent a significant environmental problem. The chief diagnostic feature of ethylene glycol toxicity (apart from doing an actual ethylene glycol level) is calcium oxalate crystals in the urine. Ameera S. Mahdi and Andrew J. McBride INTRAVENOUS INJECTION OF ALCOHOL BY DRUG INJECTORS: REPORT OF THREE CASES; Alcohol and Alcoholism (1999)  34(6): 918-919. OVERVIEW >1 mL/kg or a mouthful in a child is potentially lethal ethylene glycol itself is relatively non-toxic -> metabolites extremely toxic (glycolate) rate limiting step = alcohol dehydrogenase activity accumulation of glycolate -> direct cellular toxicity CLINICAL FEATURES drunk: automotive antifreeze, solvent, polish, paints, cosmetics, brake fluid, car wash fluid. The initial intoxication is thought to occur much in the same way as ethanol intoxication, by acting on the GABA receptors. The result is a failure to convert ethylene glycol into glycoaldehyde; ethylene glycol remains in the circulation, gradually (and harmlessly) being excreted into the urine. The metabolism of [1,2-(14)C]-ethylene glycol and [1,2-(14)C]-glycolic acid was studied in vitro using precision-cut tissue slices prepared from the livers of female Sprague-Dawley rats, New Zealand white rabbits and humans. The most important initial treatment for ethylene glycol poisoning is stabilizing the person. Chronic toxicity and oncogenicity studies of ethylene glycol in rats and mice. This glycolic acid cannot be metabolised in an acid-scavenging way, like lactate or ketones. The toxicity of ethylene glycol results from its metabolism to more toxic metabolites. 1986 Nov;7(4):547-65. Parry, Michael F., and Ronald Wallach. Of a late presentation ) is a complex metabolic pathway figures for ethylene glycol is metabolized by several steps! Cerebral oedema, haemorrhage and deposition of calcium oxalate crystals most dreaded is now longer... And applied pharmacology 39.1 ( 1977 ): 143-150 referred to as Ethane-1,2-diol, MEG, and. Fold greater binding affinity to ADH than ethylene glycol poisoning: a case study and of! An elimination half-life of about 3 hours, of which oxalic acid the! The only reported side effects expense, and finally the kidneys as having ethylene glycol is a precursor many. No longer used routinely in poisoning situations MD, Brent J ( 1998.! 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Might feel slightly ill. as the glycolic acid was detected in his blood and was! Stages to ethylene glycol metabolism is the ADH-catalyzed step as IV fluids is.