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Ethylene Glycol Toxicity Treatment & Management

  • Author: Daniel C Keyes, MD, MPH; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Jun 24, 2016
 

Prehospital Care

Emergency medical services should do the following:

  • 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.[9]

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Emergency Department Care

Rapidly evaluate patients who present with signs, symptoms, or history of toxic alcohol ingestion; determine serum osmolal gap. The prehospital (EMS) personnel often can provide important details regarding the identity of the chemical(s) involved and the clinical characteristics of the patient.

Considerations in emergency department (ED) care include the following:

  • Many patients with ethylene glycol ingestions are extremely obtunded and are at high risk of aspiration; endotracheal intubation may need to be considered.
  • Obtain intravenous access and laboratory specimens.
  • Activated charcoal and nasogastric lavage have no role in toxic alcohol poisoning; typically the alcohols will be absorbed too quickly for either of these modalities to have any efficacy.
  • Measure levels of electrolytes, calcium, and magnesium, especially in patients with alcoholism because alcohol is a cofactor in oxalate metabolism. Obtain ethylene glycol level if you have access to this at your institution or locally.
  • 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); this of course should be done in conjunction with addressing the underlying cause of the acidosis.
  • Pyridoxine and thiamine are cofactors in ethylene glycol metabolism and some advocate the use of these agents. They may be administered parenterally.
  • Place symptomatic patients in a monitored setting.
  • An ECG may be useful to detect arrhythmias that may result from hypocalcemia. With low serum calcium, the QT interval may also be prolonged.
  • 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. Contemporary treatment of this poisoning is most commonly done with fomepizole alone and not alcohol.

Treatment of patients with suspected ethylene glycol intoxication has traditionally been indicated in any of the following three circumstances. First, the plasma level of ethylene glycol is 20 mg/dL or more. Second, the history of recent ethylene glycol ingestion is definite, and the osmolal gap is 10 mOsm/L or more. Third, a history or suspicion of ethylene glycol intoxication and at least two of the following are present[10] :

  • Arterial pH less than 7.3
  • Serum bicarbonate level less than 20 mg/dL
  • Osmol gap greater than 10 mOsm/L
  • Oxalate crystals in the urine

However these criteria may be too conservative; if there is clinical concern or if your laboratory testing will take an extended amount of time to return it is advisable to initiate therapy earlier. A review of 121 ethylene glycol poisoning cases found that patients who did not receive an antidote (ethanol and/or fomepizole) until more than 6 hours had passed had higher odds of dying or having prolonged renal insufficiency (odds ratio 3.34).[11]

Fomepizole

Fomepizole (Antizol) is a convenient antidotal therapy for treatment of ethylene glycol or methanol intoxication. Fomepizole received US Food and Drug Administration (FDA) approval for use in ethylene glycol intoxication in December 1997, and it appears to have largely supplanted ethanol as the antidote of choice in toxic alcohol exposures.[12] Fomepizole is administered with a loading dose and twice-daily intravenous dosing.[13]

Fomepizole is equally efficacious for the treatment of methanol intoxication but does not cause any alteration in mental status, hypoglycemia, or respiratory depression.

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.

The availability of timely results of laboratory tests can be a problem. Weigh the benefits, risks, and costs of each therapeutic intervention at the treating institution.

Ethanol

If fomepizole is not used, oral or parenteral ethanol loading is less commonly used 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, as hypoglycemia is occasionally associated with ethanol therapy.

Hemodialysis

Hemodialysis is used to treat metabolic acidosis or to prevent renal insufficiency.

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 fomepizole) 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.

Traditional dialysis indications include the following[14] :

  • pH < 7.25
  • Acute renal failure
  • Ethylene glycol level >50 mg/dL
  • Serum glycolic acid >8 mmol/L

Some clinicians have suggested that effective blockade of alcohol dehydrogenase may permit the treatment of ethylene glycol intoxication without dialysis. In one case report,[15] a patient with an initial ethylene glycol level of 700 mg/dL was treated aggressively with fomepizole and was able to avoid dialysis.

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Consultations

It is highly recommended to include the regional poison center (or a toxicologist) in the management of these patients. The telephone number for certified poison centers anywhere in the United States and Puerto Rico is 1-800-222-1222.

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.

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Contributor Information and Disclosures
Author

Daniel C Keyes, MD, MPH Associate Chair, Academic Affairs, Department of Emergency Medicine, St Joseph Mercy Hospital; Clinical Faculty, Emergency Medicine Residency, University of Michigan Medical School; 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, American College of Physicians-American Society of Internal Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and 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.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Texas Medical Association, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Abid A Kagalwalla, MD Resident Physician, Department of Emergency Medicine, St Joseph Mercy Hospital, University of Michigan Health System

Abid A Kagalwalla, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Giffin SL. 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 27th Annual Report. Clin Toxicol (Phila). December 2010. 48:979-1178.

  2. Mowry JB, Spyker DA, Brooks DE, McMillan N, Schauben JL. 2014 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 32nd Annual Report. Clin Toxicol (Phila). 2015. 53 (10):962-1147. [Medline]. [Full Text].

  3. Jeffrey Kraut and Ira Kurtz. Toxic Alcohol Ingestions: Clinical Features, Diagnosis, and Management. Clin J Am Soc Nephrol. 2008. 3:208-225.

  4. Saad Alkahtani, Helen Sammons, and Imti Choonara. Epidemics of acute renal failure in children (diethylene glycol toxicity). Arch Dis Child. 2010. 95:1062-1064.

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

  6. Winter ML, Ellis MD, Snodgrass WR. Urine fluorescence using a Wood's lamp to detect the antifreeze additive sodium fluorescein: a qualitative adjunctive test in suspected ethylene glycol ingestions. Ann Emerg Med. 1990 Jun. 19(6):663-7. [Medline].

  7. Wallace KL, Suchard JR, Curry SC, Reagan C. Diagnostic use of physicians' detection of urine fluorescence in a simulated ingestion of sodium fluorescein-containing antifreeze. Ann Emerg Med. 2001 Jul. 38(1):49-54. [Medline].

  8. Stephen M.S. Ting, Irene Ching, MRCP, Harikrishnan Nair, MRCP, Gerald Langman, et al. Early and Late Presentations of Ethylene Glycol Poisoning. American Journal of Kidney Diseases. June 2009. 53:1091-1097. [Full Text].

  9. [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].

  10. [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].

  11. Lung DD, Kearney TE, Brasiel JA, Olson KR. Predictors of Death and Prolonged Renal Insufficiency in Ethylene Glycol Poisoning. J Intensive Care Med. 2013 Dec 26. [Medline].

  12. Ghannoum M, Hoffman RS, Mowry JB, Lavergne V. Trends in toxic alcohol exposures in the United States from 2000 to 2013: a focus on the use of antidotes and extracorporeal treatments. Semin Dial. 2014 Jul. 27(4):395-401. [Medline].

  13. Corley RA, McMartin KE. Incorporation of therapeutic interventions in physiologically based pharmacokinetic modeling of human clinical case reports of accidental or intentional overdosing with ethylene glycol. Toxicol Sci. May 2005. 85(1):491-501. [Medline]. [Full Text].

  14. Divakar Jammalamadaka and Sina Raissi. Ethylene Glycol, Methanol, and Isopropyl Alcohol Intoxication. The American Journal of the Medical Sciences. March 2010. 339:276-281.

  15. Buchanan JA, Alhelail M, Cetaruk EW, Schaeffer TH, Palmer RB, Kulig K, et al. Massive ethylene glycol ingestion treated with fomepizole alone-a viable therapeutic option. J Med Toxicol. 2010 Jun. 6(2):131-4. [Medline]. [Full Text].

  16. Carney EW. An integrated perspective on the developmental toxicity of ethylene glycol. Reprod Toxicol. 1994 Mar-Apr. 8(2):99-113. [Medline].

  17. Jeffrey Brent. Fomepizole for Ethylene Glycol and Methanol Poisoning. The New England Journal of Medicine. May 2009. 360:2216-2223.

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

  19. Megarbane B, Borron SW, Baud FJ. Current recommendations for treatment of severe toxic alcohol poisonings. Intensive Care Med. 2005 Feb. 31(2):189-95. [Medline].

  20. Sabeel AI, Kurkus J, Lindholm T. Intensified dialysis treatment of ethylene glycol intoxication. Scand J Urol Nephrol. 1995 Jun. 29(2):125-9. [Medline].

  21. Sari Soghoian, Richard Sinert, Sage Wiener, Robert Hoffman. Ethylene Glycol Toxicity Presenting with Non-Anion Gap Metabolic Acidosis. Basic & Clinical Pharmacology & Toxicity. January 2009. 104:22-26.

 
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Oxalate crystals. Courtesy of John D Schaldenbrand, MD, Department of Pathology, St Joseph Mercy Health System, Ann Arbor, MI.
Ethylene glycol.
 
 
 
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