Ethylene glycol intoxication: Evaluation of kinetics and crystalluria

Jacobsen, Dag; Hewlett, Tracy P.; Webb, Rhonda; Brown, Stephen; Ordinario, Anacelto T.; McMartin, Kenneth E.

doi:10.1016/0002-9343(88)90024-1

Cited by 132 publications

(56 citation statements)

References 21 publications

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“…Oxidation of the alcohols is first catalyzed by the liver enzyme alcohol dehydrogenase (ADH), this process being a critical step in their biotransformation (12,13,17,(37)(38)(39)(40): Methanol is metabolized to formaldehyde (6,12), ethylene glycol to glycoaldehyde (6,13), propylene glycol (present as DL isomers) to lactaldehyde (41), isopropanol to acetone (4), and ethanol to acetaldehyde (39). Formaldehyde is then metabolized via the enzyme formaldehyde dehydrogenase to formic acid, formate (12,15).…”

Section: Effect Of Alcohols On Serum Osmolality and The Osmolal Gapmentioning

confidence: 99%

“…The serum osmolality can be normal or elevated and is usually the highest within the first several hours after ingestion (13,24,37,38,43). As with methanol, even at this time it may be only slightly elevated.…”

Section: Laboratory Findingsmentioning

confidence: 99%

“…Hyperchloremic acidosis at presentation or with treatment has not been reported. It is postulated that glycolic and not oxalic acid is primarily responsible for the metabolic acidosis (14,38,43,78) based on a strong correlation between the measured glycolate concentration in the blood and the serum anion gap (13,43,78). However, the urinary excretion of oxalate and/or its deposition in tissues could result in an underestimation of its contribution to the metabolic acidosis.…”

Section: Laboratory Findingsmentioning

confidence: 99%

“…Four to 8 h after ingestion of ethylene glycol, calcium oxalate crystals will be present in the urine (38). Crystalluria can persist for as long as 40 h in the absence of renal failure and up to 4 d in its presence (37,38,81).…”

Section: Laboratory Findingsmentioning

confidence: 99%

“…Crystalluria can persist for as long as 40 h in the absence of renal failure and up to 4 d in its presence (37,38,81). The nature of the crystals can change with time: Within the first 4 to 5 h, envelope-shaped calcium oxalate dihydrate crystals are present; between 5 and 7 h, a mixture of monohydrate and dihydrate crystals are present; and after 7 h, only the needle-shaped monohydrate is present (37,38). Hypocalcemia, which is most profound many hours after ethylene glycol ingestion, is frequent at a time when oxalate crystalluria is prominent (13,37).…”

Section: Laboratory Findingsmentioning

confidence: 99%

See 4 more Smart Citations

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

370

326

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Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Table 1. Methanol, ethylene glycol, diethylene glycol, and propylene glycol intoxication and alcoholic ketoacidosis can produce hyperosmolality and metabolic acidosis (3-9). Isopropanol intoxication is usually associated with hyperosmolality alone (4,5). Importantly, several of these disorders can be fatal or produce irreversible tissue damage if they are not quickly recognized and treated appropriately (4 -15). Effect of Alcohols on Serum Osmolality and the Osmolal GapThe normal serum osmolality of 285 to 290 mOsm/L is due to sodium and its counterbalancing ions, bicarbonate and chloride, and glucose and urea. It can be calculated using the following equation:Serum osmolality (mOsm/L) ϭ 2 ϫ Na ϩ ϩ blood urea nitrogen (mg/dl)/2.8 ϩ glucose (mg/dl)/18. The serum osmolality measured by freezing point depression is usually within 10 mOsm/L of the calculated serum osmolality (16). Accumulation of low molecular weight substances in the serum (such as each of the alcohols) will raise the measured serum osmolality above that of the calculated serum osmolality, producing an osmolal gap (4,5,16 -18). The effect of each of the alcohols on serum osmolality is shown in Table 2. Methanol gives rise to the greatest increment in serum osmolality, followed by ethanol, isopropanol, ethylene glycol, propylene glycol, and diethylene glycol in that...

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Section: Effect Of Alcohols On Serum Osmolality and The Osmolal Gapmentioning

confidence: 99%

Section: Laboratory Findingsmentioning

confidence: 99%

Section: Laboratory Findingsmentioning

confidence: 99%

Section: Laboratory Findingsmentioning

confidence: 99%

Section: Laboratory Findingsmentioning

confidence: 99%

See 3 more Smart Citations

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

370

326

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Renal Failure Caused by Chemicals, Foods, Plants, Animal Venoms, and Misuse of Drugs

1990

Arch Intern Med

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Ethylenglykol [MAK Value Documentation in German language, 1991]

2012

The MAK‐Collection for Occupational Health and Safety

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Veröffentlicht in der Reihe Gesundheitsschädliche Arbeitsstoffe , 17. Lieferung, Ausgabe 1991 Der Artikel enthält folgende Kapitel: Allgemeiner Wirkungscharakter Angaben zur Pharmakokinetik Erfahrungen beim Menschen Inhalation Ingestion Wirkung auf Haut und Schleimhaut Tierexperimentelle Befunde Akute Toxizität Subchronische und chronische Toxizität Lokale Wirkung auf Haut und Schleimhäute Reproduktions‐ und Teratogenitätsstudien Untersuchungen zur gentoxischen Wirkung Untersuchungen zur kanzerogenen Wirkung Begründung des MAK‐Wertes

show abstract

Ethylene glycol intoxication: Evaluation of kinetics and crystalluria

Cited by 132 publications

References 21 publications

Toxic Alcohol Ingestions

Toxic Alcohol Ingestions

Renal Failure Caused by Chemicals, Foods, Plants, Animal Venoms, and Misuse of Drugs

Ethylenglykol [MAK Value Documentation in German language, 1991]

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