eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Ethylene Glycol

Daniel C Keyes, MD, MPH, Vice Chair, Academic Affairs, Department of Emergency Medicine, John Peter Smith Health Network; Clinical Associate Professor, Department of Surgery, Division of Emergency Medicine and Toxicology, University of Texas Southwestern School of Medicine

Updated: Aug 21, 2009

Introduction

Background

Ethylene glycol is the major ingredient of almost all radiator fluid products in the United States. It is used to increase the boiling point and decrease the freezing point of radiator fluid, which circulates through the automotive radiator. These changes to the boiling and freezing points result from the colligative properties of the solute (ie, they depend on the number of particles in the solution). Hence, ethylene glycol is added to prevent the radiator from overheating or freezing, depending on the season. Fluorescein dye is often added to radiator fluid to help identify the source of a leak. The fluorescein in the fluid fluoresces when viewed under ultraviolet light.

Ethylene glycol tastes sweet, which is why some animals are attracted to it. Many veterinarians are familiar with ethylene glycol toxicity because of the frequent cases that involve dogs or cats who drink radiator fluid.

Pathophysiology

The toxic alcohols mentioned above (see Background) are parent compounds that exert most of their toxicity by conversion to metabolites. Although the parent compound, ethylene glycol, may cause some alteration of mental status, it is a relatively nontoxic compound before it is metabolized. The metabolites cause the distinctive toxicity associated with this compound.

Knowing the pathway of ethanol metabolism is necessary to understand ethylene glycol toxicity properly. Ethanol is metabolized by the enzyme alcohol dehydrogenase (ADH) pathway, which is located in the liver and gastric mucosa, and by the cytochrome P-450 mixed function oxidase (MFO) system in the liver. The mixed function oxidase component is subject to greater inducibility than alcohol dehydrogenase.

As with ethyl alcohol and methanol, ethylene glycol is metabolized by alcohol dehydrogenase to form glycoaldehyde. Through interaction with aldehyde dehydrogenase, ethylene glycol is then metabolized to glycolic acid (GA). A profound acidosis often ensues and is attributable to the glycolic acid in circulation. The patient may develop hyperventilation that results from acidemia. This glycolate is then transformed into glyoxylic acid. At this point, the molecule may be transformed into the highly toxic oxalate or the safer glutamate or a -ketoadipic acid metabolites. The administration of particular vitamins may promote the formation of these safer metabolites.

With the formation of oxalate crystals in the urine, calcium oxalate crystals form and accumulate in blood and other tissues. The precipitation of calcium oxalate in the renal cortex results in decreased glomerular filtration and renal insufficiency. Calcium is consumed in circulation, and hypocalcemia may occur.

The rate-dependent step of ethylene glycol metabolism is the alcohol dehydrogenase–catalyzed step. Ethyl alcohol binds much more easily to alcohol dehydrogenase than ethylene glycol or methanol does. Because ethanol is the preferential substrate for alcohol dehydrogenase, the presence of ethanol may essentially block metabolism of ethylene glycol. In addition, this enzyme is blocked by the administration of fomepizole (4-methylpyrazole [4-MP]), which is discussed below (see Emergency Department Care). This is the basis of one therapy used in the United States.

Frequency

United States

Ethylene glycol is a relatively common cause of overdose in American emergency departments. In 2007, 4966 single exposure cases were reported to the American Association of Poison Control Centers.¹ Rapid intervention often makes an important difference in the outcome of ethylene glycol toxicity.

Mortality/Morbidity

According to the annual report of the American Association of Poison Control Centers' National Poison Data System in 2007, 878 had minor outcomes, 365 had moderate outcomes, 135 had severe outcomes, and 16 deaths were documented.¹

Age

The annual report of the American Association of Poison Control Centers' National Poison Data System in 2007 documented ethylene glycol exposure in 511 children younger than 6 years, 636 in those aged 6-19 years, and 3132 in those older than 19 years.¹

Clinical

History

• As with all poisonings, ascertain the nature of the oral ingestion by talking with the patient.
• The timing of ingestion is important.
• The product involved is important. Try to obtain the original container of the ingested substance to confirm its identity.
• Determine the timing and quantity of liquor or other ethanol ingestion.

Physical

• After an adequate airway is ensured, monitor vital signs, including temperature and mental status.
• A patient breathing deeply and rapidly may be manifesting the Kussmaul respirations, which are indicative of a severe metabolic acidosis.
• Patients with an altered mental status require rapid assessment and therapy directed at rapidly lethal processes. Ensure and maintain an adequate airway.

Causes

Causes of ethylene glycol poisoning include the following:

• Suicide attempts
• Accidental ingestions (mainly observed in children)
• Workplace beverage-container mix-ups

Differential Diagnoses

Metabolic Acidosis
Toxicity, Alcohols

Other Problems to Be Considered

Any other cause of acute altered mental status

Workup

Laboratory Studies

Patients who ingest ethylene glycol may initially have few, if any, metabolic disturbances. Serum concentrations of ethylene glycol may be measured; however, at some health care facilities, these results are not available for 2 or more days. Thus, ethylene glycol levels are often not determined early enough to be useful in emergency treatment. For institutions that frequently treat ethylene glycol toxicity cases, in-hospital rapid laboratory confirmation may become cost-effective because of the institutional cost-benefit ratio evaluation that compares antidotal therapy, ethanol therapy, and hemodialysis therapy.

A study by Long et al has shown promising and reliable results quickly (in 30 min) using a qualitative colorimetric test (ethylene glycol test [EGT] kit), which is already in use by veterinarians. The test detects ethylene glycol in spiked human serum samples. In this study, sensitivity was 100% (95% confidence interval [CI], 70-100%), and specificity was 88.8% (95% CI, 52-100%).²

• Serum osmolality: Because ethylene glycol levels are not reported in a clinically helpful fashion in most institutions, ethylene glycol exposure level is often estimated through measurement of the serum osmolality. This estimate is obtained by sampling a set of electrolyte levels (eg, BUN, creatinine, glucose) and calculating the expected osmolality in the patient's serum. A serum osmolality is then measured, and the difference between the measured and calculated osmolality (the osmolal gap) is determined. Several formulas are effective for calculating the osmolality from serum electrolytes and other solutes.
  • The most commonly used formula is 2(Na⁺ level) + BUN level/3 + glucose level/18 = calculated osmolality. The sodium level is measured in mEq, and the BUN and glucose levels are measured in mg/dL.
  • The osmolal gap is determined by subtracting the calculated osmolality from the measured osmolality (osmol [measured] - osmol [calculated] = osmolal gap). The serum osmolality must be determined by freezing-point depression rather than by boiling point elevation. This is because, with the boiling technique, the toxic alcohols are vaporized rapidly, and, thus, a falsely low or normal estimate of the osmolality is obtained. Once the osmolal gap is determined, estimating the serum levels of ethylene glycol or another alcohol is possible by applying the following conversion factors: ethylene glycol = 6.2, methanol = 3.2, and ethanol = 4.6.
  • If the ethanol level is measured simultaneously with the electrolyte levels, its contribution can be subtracted to determine an approximate contribution of the toxic alcohol. If the clinician does not wish to memorize the conversion factors, they can be calculated by dividing the molecular weight by 10. For example, the conversion factor for ethanol would be calculated by adding the molecular weight of 2 carbons = 2 X 12, 1 oxygen = 16, and 6 hydrogens = 6. Thus, 24 + 16 + 6 = 46. This divided by 10 reveals the conversion factor for ethanol, which is 4.6. Most clinicians prefer to look these values up in a table.
  • Serum electrolyte levels are also useful later in the course of intoxication because they can reveal the presence of anion gap acidosis. This information may be important when determining the need for dialysis and other interventions. The goal of therapy, however, is to treat the patient before acidosis develops.
• Additional laboratory tests that should be obtained in symptomatic patients include the following:
  • Serum calcium level determination is recommended.
  • Arterial blood gas determination is recommended.
  • Urinalysis: Urine may reveal the presence of calcium oxalate crystals, a sign usually observed late in the process of intoxication. Oxalate crystals typically have the shape of a folded envelope.
  • Another technique, popularized by the television series "ER," is to shine a Wood lamp (UV light) on an early sample of urine. If a sufficient fluorescein level is present in the radiator fluid, the urine fluoresces.³ The urine should be compared to a control sample. If the radiator fluid contains fluorescein, a green-colored glow may be observed in a dark room. This light also may be used to detect possible ethylene glycol on clothing or the patient.

Treatment

Prehospital Care

• Ascertain as much specific information regarding the identity of the ingested substance as possible.
• If possible, obtain the bottle or container that held the ingested substance. Interviewing persons present at the site of the ingestion may be helpful in this regard.
• Obtain intravenous access and administer crystalloid infusions.
• Monitor cardiac function and determine blood dextrose level.
• Airway management is a priority because of the risk of aspiration.
• Evidence-based guidelines on out-of-hospital management of ethylene glycol poisoning are available from the American Association of Poison Control Centers.⁴

Emergency Department Care

Rapidly evaluate patients who present with signs, symptoms, or history of toxic alcohol ingestion; determine serum osmolal gap.

• Obtain intravenous access and laboratory specimens.
• Measure levels of electrolytes, calcium, and magnesium, especially in patients with alcoholism because alcohol is a cofactor in oxalate metabolism.
• Administer crystalloids at 250-500 mL/h IV initially to enhance renal clearance of the toxin and to limit deposition of oxalates in the renal cortices.
• Administer bicarbonate to correct severe acidosis (pH level £ 7.2).
• Pyridoxine and thiamine are cofactors in ethylene glycol metabolism and should be administered parenterally.
• Place symptomatic patients in a monitored setting.
• An ECG may be useful in patients with arrhythmias that may result from hypocalcemia.
• Foley catheterization is usually indicated for patients with altered mental status to monitor urinary output and to allow serial examination of urine for crystals or fluorescence.
• If the serum osmolal gap is not zero, begin antidotal therapy empirically while awaiting confirmation. This is performed with either fomepizole (4-MP) or ethyl alcohol. The latter is usually administered intravenously but may be administered orally in remote settings where emergency hospital care is not immediately available.
• Treatment of patients with suspected ethylene glycol intoxication is indicated in any of the following 3 circumstances⁵ :
  • The plasma level of ethylene glycol is 20 mg/dL or more.
  • The history of recent ethylene glycol ingestion is definite, and the osmolal gap is 10 mOsm/L or more.
  • A history or suspicion of ethylene glycol intoxication and at least 2 of the following are present:
    • Arterial pH level is less than 7.3.
    • Serum bicarbonate level is less than 20 mg/dL.
    • Osmol gap is greater than 10 mOsm/L.
    • Urinary oxalate crystals are present.
• Fomepizole (4-MP [Antizol]) is a convenient antidotal therapy for treatment of ethylene glycol or methanol intoxication. Many emergency departments have adopted routine use of this agent for cases of suspected toxic alcohol poisoning.⁶ Fomepizole is administered with a loading dose and twice-daily intravenous dosing.⁷
  • Fomepizole is advantageous because it does not depress the patient's mental status or airway and needs to be administered only every 12 hours. The main drawback of fomepizole is the cost, which can total thousands of dollars. Because this agent is so expensive, clinicians should check its availability at their institution and discuss the plan for use of this antidote, especially for empiric treatment of cases in which the cause of acidosis is unknown.
  • Fomepizole is equally efficacious for the treatment of methanol intoxication but does not cause any alteration in mental status, hypoglycemia, or respiratory depression.
  • Fomepizole received US Food and Drug Administration (FDA) approval in December 1997.
  • The availability of timely results of laboratory tests can be a problem. Weigh the benefits, risks, and costs of each therapeutical intervention at the treating institution.
• If fomepizole is not used, oral or parenteral ethanol loading can be initiated as a temporizing measure while awaiting test results.
  • A loading dose of ethanol is administered based on body weight, followed by infusion to maintain a serum level of approximately 100 mg/dL.
  • Carefully calculate the loading dose and administration of ethanol antidote to prevent excessive administration. Overly aggressive ethanol administration has reportedly caused cases of apnea that required intubation and mechanical ventilation.
  • When administering ethanol, determine glucose levels by fingerstick collection at regular intervals and confirm with laboratory analysis to detect the hypoglycemia occasionally associated with ethanol therapy.
• Most patients with ethylene glycol toxicity require monitoring in an ICU setting.⁸
• Hemodialysis is used to treat metabolic acidosis or to prevent renal insufficiency.⁹
  • Early in the intoxication, the toxin is present as the parent compound, ethylene glycol. As time passes, toxic metabolites accumulate and the patient develops metabolic acidosis. Eventually, oxalate is deposited in the kidney and elsewhere; renal insufficiency may ensue. Once any of these manifestations occurs, antidotal therapy alone (used to block alcohol dehydrogenase with ethanol or 4-MP) is insufficient to treat the poisoning.
  • Alcohol dehydrogenase–blocking therapy must be accompanied by dialysis to remove the metabolites in these cases. Consulting a nephrologist early in the intoxication is prudent to facilitate the timely initiation of dialysis to these patients. Delays may result in renal failure or other severe complications.
  • Some clinicians have suggested that effective blockade of alcohol dehydrogenase may permit the treatment of ethylene glycol intoxication without dialysis. This has not yet been demonstrated clinically.¹⁰

Consultations

If dialysis is considered, consult a nephrologist as early as possible to allow timely treatment of patients with toxic metabolite accumulation. Antidotal therapy is inadequate by itself in these circumstances, and dialysis should be performed as soon as possible. Consult a poison control center or a medical toxicologist for assistance in management options.

Medication

If the osmolal gap is not zero, begin antidotal therapy empirically while awaiting confirmation.

Antidotes

Avoid overdosing or underdosing of ethanol by frequently monitoring blood ethanol levels.

Ethanol

Goal is to maintain blood ethanol levels 100-150 mg/dL. This completely saturates ADH. May be administered PO or IV. Measuring initial blood level is important; if >100 mg/dL, loading dose may be unnecessary and patient can be started on maintenance dose.
Frequent monitoring of blood alcohol concentrations is important. Adjust dose to reduce methanol levels to <20 mg/dL.

Dosing

Adult

IV loading dose: 7.6-10 mL/kg IV of 10% ethanol (V/V) in dextrose 5% in water over 30 min to achieve blood ETOH concentration of 100-130 mg/dL (21.7-28.2 mmol/L)
Oral loading dose: 0.8-1 mL/kg PO of 95% ethanol in 6 oz of orange juice over 30 min
Average maintenance doses (PO/IV): 0.15 mL/kg/h PO of 95% ETOH; 1.4 mL/kg/h IV of a 10% solution

Pediatric

Administer as in adults; titrate dosing to maintain BAL of 100-150 mg/dL

Interactions

May increase toxicity of benzodiazepines and result in death

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Watch for hypoglycemia, especially in children; adjust dosing during hemodialysis; extreme caution if patient has ingested other CNS depressants; IV may cause thrombophlebitis; PO may cause severe gastritis

Fomepizole (Antizol)

Antidote with better safety profile than ethanol. Easier to dose and administer. In contrast to ethanol, 4-MP levels do not need to be monitored during therapy. The biggest drawback is the cost of the antidote; however, compare the additional expenses of fomepizole with the high degree of required vigilance, occasional treatment failure, and complications seen with ethanol.
Begin fomepizole treatment immediately upon suspicion of EG ingestion based on patient history or anion gap metabolic acidosis, increased osmolar gap, oxalate crystals in urine, or documented serum methanol level.

Dosing

Adult

Loading dose: 15 mg/kg IV over 30 min
Maintenance dose: 15 mg/kg IV q12h until patient is asymptomatic with a normal pH level and the EG level is <20 mg/dL

Pediatric

Not established; suggested dose is proportional to body weight, as in adults

Interactions

PO doses (10-20 mg/kg) have been shown to reduce rate of ethanol elimination by 40% in healthy volunteers; ethanol has been shown to decrease rate of fomepizole elimination by 50%

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not administer as bolus; caution with breastfeeding because no information exists on excretion of medication in breast milk; caution in patients with renal impairment; dosage interval needs to be adjusted during hemodialysis

Nutrients

Pyridoxine enhances metabolism of glyoxylate to glycine. Thiamine catalyzes metabolism of glyoxylate from glycolic acid.

Pyridoxine (Nestrex)

Water-soluble vitamin B-complex, which is a cofactor in conversion of GA to nonoxalate compounds. Involved in synthesis of GABA within CNS.

Dosing

Adult

100 mg IV qid for 2 d

Pediatric

1-2 mg/kg IV in first 24 h of treatment

Interactions

May decrease levodopa, phenytoin, and phenobarbital serum levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

>200 mg/d may precipitate withdrawal effects when medication is discontinued

Thiamine (Thiamilate)

Vitamin B-1 is water-soluble and used in many cellular functions that involve energy formation and use. Promotes conversion of glyoxylate to a nontoxic metabolite, alpha-hydroxy-beta-ketoadipate.

Dosing

Adult

50 mg IV qid for 2 d

Pediatric

0.25-0.50 mg/kg IV on first day of therapy

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Some early reports suggest that IV administration is associated with deleterious effects on cardiovascular function (eg, hypotension), but subsequent studies have not supported this; sensitivity reactions can occur (intradermal test-dose recommended in suspected sensitivity); fatalities have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy, following glucose administration, may occur in patients with thiamine deficiency; administer before or together with dextrose-containing fluids in patients with suspected thiamine deficiency

Follow-up

Further Inpatient Care

• Patients who require antidotal therapy or dialysis require admission to an ICU or other setting with cardiac monitoring and close nursing care.

References

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2. Long H, Nelson LS, Hoffman RS. A rapid qualitative test for suspected ethylene glycol poisoning. Acad Emerg Med. Jul 2008;15(7):688-90. [Medline].

3. LeBlanc C, Murphy N. Should I stay or should I go?: toxic alcohol case in the emergency department. Can Fam Physician. Jan 2009;55(1):46-9. [Medline].

4. [Guideline] Caravati EM, Erdman AR, Christianson G, Manoguerra AS, Booze LL, Woolf AD, et al. Ethylene glycol exposure: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(5):327-45. [Medline]. [Full Text].

5. [Guideline] Barceloux DG, Krenzelok EP, Olson K, Watson W. American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poisoning. Ad Hoc Committee. J Toxicol Clin Toxicol. 1999;37(5):537-60. [Medline].

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8. Green R. The management of severe toxic alcohol ingestions at a tertiary care center after the introduction of fomepizole. Am J Emerg Med. Sep 2007;25(7):799-803. [Medline].

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Keywords

ethylene glycol toxicity, EG, EG toxicity, EG poisoning, radiator fluid, antifreeze, glycolic acid, GA, ethylene glycol poisoning, radiator fluid ingestion, accidental ingestion, ethanol, fomepizole, alcohol toxicity, ethylene glycol intoxication, calcium oxalate crystals, acidosis, glycoaldehyde, ethylene glycol ingestion

Contributor Information and Disclosures

Author

Daniel C Keyes, MD, MPH, Vice Chair, Academic Affairs, Department of Emergency Medicine, John Peter Smith Health Network; Clinical Associate Professor, Department of Surgery, Division of Emergency Medicine and Toxicology, University of Texas Southwestern School of Medicine
Daniel C Keyes, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, and American College of Physicians-American Society of Internal Medicine
Disclosure: Nothing to disclose.

Medical Editor

Miguel C Fernández, MD, FAAEM, FACEP, FACMT, Associate Clinical Professor; Medical and Managing Director, South Texas Poison Center, Department of Surgery/Emergency Medicine and Toxicology, University of Texas Health Science Center at San Antonio
Miguel C Fernández, MD, FAAEM, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, Society for Academic Emergency Medicine, and Texas Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

John G Benitez, MD, MPH, FACMT, FACPM, FAAEM, Associate Professor, Department of Medicine, Clinical Pharmacology Division, Vanderbilt University; Managing Director, Tennessee Poison Center
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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