Ethylene Glycol Toxicity


Practice Essentials

Several toxic alcohols are of medical and toxicological importance; the principal ones include ethanol, ethylene glycol (EG), methanol, and isopropanol. See Alcohol Toxicity. This article discusses ethylene glycol, which is extremely toxic. If untreated, ingestion of ethylene glycol can be fatal.

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 mechanics identify the source of a radiator 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 in dogs and cats that have licked up radiator fluid.

Initially, patients may be asymptomatic, but ethylene glycol is rapidly absorbed (within 1 to 4 hours), and altered mental status and tachypnea then begin to appear as the ethylene glycol is successively metabolized to very toxic compounds. The progression of toxic effects can be roughly divided into the following three stages, although overlap is possible[1] :

Initial treatment includes infusion of crystalloids to enhance renal clearance of the toxic metabolites. Ethyl alcohol has traditionally been used for antidotal treatment, but it has largely been supplanted by fomepizole in the United States.


[2] Like the other toxic alcohols mentioned above, ethylene glycol is a parent compound that exerts most of its toxicity by conversion to metabolites. Ethylene glycol itself may cause some alteration of mental status but 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 understanding ethylene glycol toxicity properly. Ethanol is metabolized by the enzyme alcohol dehydrogenase (ADH), 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.

Like ethyl alcohol and methanol, ethylene glycol is metabolized by ADH. In this step it forms glycoaldehyde. Through interaction with aldehyde dehydrogenase, ethylene glycol is then metabolized to glycolic acid (GA), which accumulates and can cause a profound metabolic acidosis. This glycolic acid is eventually converted into glyoxylic acid, and then into the highly toxic oxalate or the safer glutamate or α-ketoadipic acid metabolites.

Calcium oxalate crystals may 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. The formation of these crystals consumes circulating calcium, and hypocalcemia may occur, though this is uncommon.

The rate-limiting step of ethylene glycol metabolism is the ADH-catalyzed step. Common ethyl alcohol (ethanol) binds much more easily to ADH than ethylene glycol or methanol does. Because ethanol is the preferred substrate for ADH, 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.

Upon oral ingestion, serum concentrations of ethylene glycol peak within 1-4 hours. The elimination half-life (assuming preserved renal function) is 3 hours. When alcohol dehydrogenase is inhibited by ethanol or fomepizole, the elimination half-life increases to about 16 hours.



United States

Ethylene glycol is a relatively common cause of overdose in US emergency departments. Single exposures to ethylene glycol in antifreeze and other automotive products reported to the American Association of Poison Control Centers (AAPCC) rose from 5,282 in 2009 to 5,783 in 2016.[3, 4]


According to the AAPCC's National Poison Data System, in 2016, 934 had minor outcomes, 448 had moderate outcomes, 124 had severe outcomes, and 7 deaths were documented.[4]


The annual report of the AAAPCC's National Poison Data System in 2016 documented ethylene glycol exposure in 495 children younger than 6 years, 191 in those aged 6-12 years, 489 in those 13-19 years, and 4014 in those 20 years and older.[4]


As with all poisonings, ascertain the nature of the oral ingestion by talking with the patient or parents. Points to cover include the following:


See the list below:


Causes of ethylene glycol poisoning include the following:

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 most health care facilities, these results are not available for 2 or more days. Thus, ethylene glycol concentrations are often not determined early enough to be useful in emergency treatment, though they should still be sent to confirm the diagnosis.

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 therapy with fomepizole, ethanol, and hemodialysis. Emergency departments located in larger metropolitan areas may negotiate availability of this test at regional clinical laboratories. It is important to check on this availability at your own clinical site.

The classic laboratory profile of ethylene glycol ingestion is an early osmolar gap (the ethylene glycol serves as an unmeasured osmole) that disappears as an anion gap metabolic acidosis develops (as the ethylene glycol is converted into its acidic derivatives). However, there is a wide range of normal osmolar gaps, and even patients with early presentations after consequential ethylene glycol ingestions may have a normal osmolar gap, so it should never be used to exclude toxicity. Listed below are laboratory tests that will be useful in the setting of ethylene glycol ingestion.

Serum osmolality

Because ethylene glycol concentrations are not reported in a clinically helpful or timely 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 electrolytes and other serum solutes (eg, sodium, blood urea nitrogen [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 in the US is 2(Na+ level) + BUN level/2.8 + 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.

A normal osmolar gap can range from -14 to +10, and potentially toxic ethylene glycol ingestions can be hidden within an apparently normal osmolar gap. Additionally, as described above, the osmolar gap goes away as the ethylene glycol is metabolized. For these reasons, the osmolar gap should never be used to exclude ethylene glycol poisoning. Additionally, moderately elevated osmolar gaps (10-30) are common in sick patients with disease states unrelated to toxic alcohol poisoning, so osmolar gaps in this range are not necessarily indicative of poisoning. However, largely elevated osmolar gaps (greater than 40) are highly suggestive of toxic alcohol poisoning.

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

The following tests should also be obtained in symptomatic patients:

View Image

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

Another technique, popularized by the television series "ER," is to shine a Wood's lamp (ultraviolet light) on an early sample of urine. If a sufficient fluorescein level is present in the radiator fluid, the urine fluoresces.[7, 8] The urine should be compared with 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. It must be stated, however, that this is not a reliable means to confirm or eliminate the possibility of an ethylene glycol ingestion, for a multitude of reasons.[9]

Imaging Studies

Imaging rarely contributes to the specific diagnosis of ethylene glycol intoxication, though thalamic lesions may occur on computed tomography or magnetic resonance imaging scans of the brain in severe poisoning. Imaging may be useful as needed for routine care of these patients.

Other Tests

Other tests that may be useful depending on the clinical status of the patient include electrocardiography (ECG). Use of a Wood's (ultraviolet) lamp has been discussed above. Urine microscopy may be useful for identifying calcium oxalate crystals, as noted above. However, calcium oxalate crystals do not develop in the urine for about 4-8 hours following ingestion and if significant renal insufficiency develops, they may not be present for 40 hours following the ingestion.[10]

Approach Considerations

Guidelines on the medical management of ethylene glycol poisoning are available from the Agency for Toxic Substances and Disease Registry. These include recommendations on prehospital, emergency department, and critical care treatment.[1]

Initial emergency department treatment includes infusion of crystalloids to enhance renal clearance of the toxic metabolites. Ethyl alcohol has traditionally been used for antidotal treatment, but it has largely been supplanted by fomepizole in the United States.

 In centers where fomepizole is available, patients who present early and are without acidosis clinically well can be treated with fomepizole and hemodialysis on a regular floor. Any patients who are ill and acidotic or who present to centers where ethanol is used instead of fomepizole should be treated in an intensive care unit (ICU) or other setting with cardiac monitoring and close nursing care. Patients who present to a facility without those capabilities should be transferred to a facility where hemodialysis and an ICU are available.



Prehospital Care

Emergency medical services should do the following:


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:

Treatment of patients with suspected ethylene glycol intoxication has traditionally been indicated in any of the following three circumstances. First, the plasma concentration of ethylene glycol is 25 mg/dL or more. Second, the patient has a definite history of recent ethylene glycol ingestion (especially if the osmolal gap is 10 mOsm/L or more, though patients with potentially toxic ethylene glycol ingestions may have an apparently normal osmolar gap; see Workup/Laboratory Studies). Third, a history or suspicion of ethylene glycol intoxication and the presence of at least two of the following[11] :

However these criteria may be too conservative; if there is clinical concern or if 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).[12]


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 in the US.[13] Fomepizole is administered with a loading dose and twice-daily intravenous dosing.[14]

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.


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, so serum ethanol concentrations must be checked regularly and the infusion rate adjusted to prevent over- or undertreatment. 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. Other potential adverse effects include hyponatremia, sclerosis of veins, and intoxication (which can be particularly distressing in pediatric patients).

Any patient receiving intravenous ethanol therapy requires ICU monitoring.


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[15] :

Some clinicians have suggested that effective blockade of alcohol dehydrogenase may permit the treatment of ethylene glycol intoxication without dialysis. In one case report,[16] a patient with an initial ethylene glycol level of 700 mg/dL was treated aggressively with fomepizole and was able to avoid dialysis. However, because of the cost of fomepizole and the safety of hemodialysis, the threshold for this approach should be carefully considered on the basis of the clinical setting.


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.

Medication Summary

If ethylene glycol poisoning is suspected, begin antidotal therapy empirically while awaiting confirmation. Antidotes are fomepizole and ethanol. B-vitamin therapy may be used as an adjunct to antidotal therapy.

Fomepizole (Antizol)

Clinical Context:  Antidote with better safety profile than ethanol. Easier to dose and administer. In contrast to ethanol, fomepizole 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, need for intensive care unit monitoring, occasional treatment failure, and complications seen with ethanol.

Begin fomepizole treatment immediately upon suspicion of ethylene glycol ingestion based on patient history or anion gap metabolic acidosis, increased osmolar gap, oxalate crystals in urine, or documented serum methanol level.


Clinical Context:  Goal is to maintain blood ethanol concentrations at 100-150 mg/dL. This completely saturates alcohol dehydrogenase (ADH). May be administered PO or IV, but IV is preferred if available. Measuring initial blood concentration is important; if >100 mg/dL, loading dose may be unnecessary and patient can be started on maintenance dose.

Frequent monitoring of blood ethanol concentrations is important, with adjustment of the infusion rate to maintain the serum concentration in the therapeutic range.

Pyridoxine (Nestrex)

Clinical Context:  Water-soluble vitamin B6, which is a cofactor in conversion of GA to nonoxalate compounds. Involved in synthesis of GABA within CNS.

Thiamine (Thiamilate)

Clinical Context:  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.

Class Summary

Pyridoxine enhances metabolism of glyoxylate to glycine. Thiamine catalyzes metabolism of glyoxylate from glycolic acid. Vitamin therapy is a safe and reasonable adjunct in patients with ethylene glycol poisoning. Regional poison centers may suggest the use of these therapies in certain cases.

What is ethylene glycol (EG) toxicity?What are stages of ethylene glycol (EG) toxicity?What is the pathophysiology of ethylene glycol (EG) toxicity?What is the prevalence of ethylene glycol (EG) toxicity in the US?What should be the focus of clinical history for suspected ethylene glycol (EG) toxicity?Which physical findings suggest ethylene glycol (EG) toxicity?What causes ethylene glycol (EG) toxicity?Which conditions should be included in the differential diagnoses of ethylene glycol (EG) toxicity?What are the differential diagnoses for Ethylene Glycol Toxicity?What is the role of lab testing in the diagnosis of ethylene glycol (EG) toxicity?What is the role of serum osmolality in the diagnosis of ethylene glycol (EG) toxicity?Which lab tests should be performed in symptomatic patients with ethylene glycol (EG) toxicity?What is the role of a Wood's lamp in the diagnosis of ethylene glycol (EG) toxicity?What is the role of imaging studies in the diagnosis of ethylene glycol (EG) toxicity?What is the role of urine microscopy in the diagnosis of ethylene glycol (EG) toxicity?Which organization has published guidelines for the medical management of ethylene glycol (EG) toxicity?What is the initial emergency department (ED) treatment of ethylene glycol (EG) toxicity?What is included in prehospital care for ethylene glycol (EG) toxicity?What are the initial considerations for emergency department (ED) care of ethylene glycol (EG) toxicity?When is treatment for suspected ethylene glycol (EG) intoxication indicated?What is the role of fomepizole (Antizol) in the treatment of ethylene glycol (EG) toxicity?What is the role of ethanol in the treatment of ethylene glycol (EG) toxicity?What is the role of hemodialysis in the treatment of ethylene glycol (EG) toxicity?Which specialist consultations are beneficial to patients with ethylene glycol (EG) toxicity?Which medications are used in the treatment of ethylene glycol (EG) toxicity?Which medications in the drug class Nutrients are used in the treatment of Ethylene Glycol Toxicity?Which medications in the drug class Antidotes are used in the treatment of Ethylene Glycol Toxicity?


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

Disclosure: Nothing to disclose.

Specialty Editors

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

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

Disclosure: Nothing to disclose.

Chief Editor

Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

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

Disclosure: Nothing to disclose.


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.


  1. [Guideline] Agency for Toxic Substances and Disease Registry. Medical Management Guidelines for Ethylene Glycol. ATSDR. Available at October 21, 2014; Accessed: September 25, 2017.
  2. Hodgman M, Marraffa JM, Wojcik S, Grant W. Serum Calcium Concentration in Ethylene Glycol Poisoning. J Med Toxicol. 2017 Jun. 13 (2):153-157. [View Abstract]
  3. 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.
  4. Gummin DD, Mowry JB, Spyker DA, Brooks DE, Fraser MO, Banner W. 2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 34th Annual Report. Clin Toxicol (Phila). 2017 Dec. 55 (10):1072-1252. [View Abstract]
  5. Jeffrey Kraut and Ira Kurtz. Toxic Alcohol Ingestions: Clinical Features, Diagnosis, and Management. Clin J Am Soc Nephrol. 2008. 3:208-225.
  6. Saad Alkahtani, Helen Sammons, and Imti Choonara. Epidemics of acute renal failure in children (diethylene glycol toxicity). Arch Dis Child. 2010. 95:1062-1064.
  7. 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. [View Abstract]
  8. 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. [View Abstract]
  9. 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. [View Abstract]
  10. 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.
  11. [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. [View Abstract]
  12. 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. [View Abstract]
  13. 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. [View Abstract]
  14. 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. [View Abstract]
  15. Divakar Jammalamadaka and Sina Raissi. Ethylene Glycol, Methanol, and Isopropyl Alcohol Intoxication. The American Journal of the Medical Sciences. March 2010. 339:276-281.
  16. 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. [View Abstract]
  17. Carney EW. An integrated perspective on the developmental toxicity of ethylene glycol. Reprod Toxicol. 1994 Mar-Apr. 8(2):99-113. [View Abstract]
  18. Brent J, McMartin K, Phillips S, Burkhart KK, Donovan JW, Wells M, et al. Fomepizole for the treatment of ethylene glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group. N Engl J Med. 1999 Mar 18. 340 (11):832-8. [View Abstract]
  19. Long H, Nelson LS, Hoffman RS. A rapid qualitative test for suspected ethylene glycol poisoning. Acad Emerg Med. 2008 Jul. 15(7):688-90. [View Abstract]
  20. Megarbane B, Borron SW, Baud FJ. Current recommendations for treatment of severe toxic alcohol poisonings. Intensive Care Med. 2005 Feb. 31(2):189-95. [View Abstract]
  21. Sabeel AI, Kurkus J, Lindholm T. Intensified dialysis treatment of ethylene glycol intoxication. Scand J Urol Nephrol. 1995 Jun. 29(2):125-9. [View Abstract]
  22. Soghoian S, Sinert R, Wiener SW, Hoffman RS. Ethylene glycol toxicity presenting with non-anion gap metabolic acidosis. Basic Clin Pharmacol Toxicol. 2009 Jan. 104 (1):22-6. [View Abstract]

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

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

Ethylene glycol.