30.May.2017-Expires: 7 days - Do not archive

Ethylene Glycol

Ethylene Glycol
30.May.2017-Expires: 7 days - Do not archive



Ethylene Glycol




Colorless, odorless, sweet-tasting, hygroscopic liquid.
Molecular Weight
62.07 62.07
Boiling Point
197 degrees C197 degrees C
Melting Point
-13 degrees C-13 degrees C
Specific Gravity (water = 1)
1.1274 1.1274
Vapor Pressure
0.07 mmHg at 20 degrees C 0.07 mmHg at 20 degrees C
Flash Point
111 degrees C111 degrees C
Flammability Limits
3.2 to 5 %3.2 to 5%
Water: soluble
Ethanol: soluble
Glycerol: soluble
Acetic acid: soluble
Acetone: soluble
Ether: slightly soluble
Benzene: insoluble
Chlorinated hydrocarbons: insoluble
Petroleum ether: insoluble
Oils: insoluble[1][2]


Predominantly used as a deicer or antifreeze in cooling systems. Ethylene glycol is also used in hydraulic brake fluids, as a solvent, and as an industrial humectant. Large amounts are used as a chemical intermediate. It may also be used as a glycerin substitute in commercial products including paints, detergents and cosmetics.


Intervention Level


Appropriate medical management and observation in an emergency department is recommended for:
- Any ingestion more than a witnessed lick or exploratory taste (e.g. a small sip)
- Ingestions where the dose is unknown
- Symptomatic patients
- Eye exposures if more than mild, resolving symptoms
Any patient showing signs or symptoms following skin or inhalational exposure should be assessed at a medical facility.


Appropriate medical management and observation in an emergency department is recommended for:
- Ingestions of more than 10 mL of ethylene glycol
- Ingestions where the dose is unknown
- Exposures with intent to self-harm
- Symptomatic patients
- Eye exposures if symptoms are more than mild and resolving
Any patient showing signs or symptoms following skin or inhalational exposure should be assessed at a medical facility.

Observation Period

Observation at Home

If the patient does not require medical observation they can be monitored at home for 8 hours in the care of a reliable observer.
The patient should be medically assessed if any symptoms develop, including:
Slurred speech
Stumbling or difficulty in moving

Medical Observation

Patients accidentally ingesting ethylene glycol should be monitored for 4 hours and may then be discharged into the care of a reliable observer provided:[3]
They are asymptomatic
Venous bicarbonate level is greater or equal to 20 mmol/L (mEq/L)
Serum (or breath) ethanol level is zero in adults


A serum ethylene glycol is the preferred investigation, but is commonly not readily available at most institutions. An ethylene glycol ingestion may be inferred from an increased osmolal gap (in the early stages of intoxication) indicating a solute (glycol) load. However, this test cannot rule out ethylene glycol exposure in the presence of a normal osmolar gap.
Once the glycol is metabolized this level will drop and may be replaced by an increased anion gap, indicating an increased organic acid (glycol metabolite) load, with an accompanying metabolic acidosis. Investigation should therefore include:
Serum ethylene glycol level (where available in a practical time frame ie: 1 to 2 hours)
Serum ethanol level (required for osmolal gap calculation)
Osmolal gap (elevated in early stages of poisoning)
Serum electrolytes including:
Chloride (required for anion gap calculation)
Anion gap (elevated in later stages of poisoning)
Arterial pH
Serum bicarbonate
Urinalysis including:
Examination under UV light (Wood’s lamp) for fluorescence
(Fluorescein contained in many antifreeze solutions and eliminated in the urine will fluoresce when expose to UV light). A negative result does not rule out ethylene glycol exposure (fluoroscein is rapidly eliminated by the kidneys and may have already been excreted prior to presentation. Also, the ingested ethylene glycol may not contain fluoroscein). Care must be exercised when performing this test as plastic containers may exhibit some degree of fluorescence under a UV light. A glass container is preferable and previous experience with visualizing fluoroscein containing urine is useful.
Microscopic examination for crystalluria
(In the later stages of intoxication calcium oxalate crystals may form in the urine)
Presence in the urine of either fluorescein or calcium oxalate crystals indicates ethylene glycol exposure, but their absence does not exclude this poisoning.
If a serum ethylene glycol level measurement is not available a presumptive diagnosis of poisoning may be based on:
A history or suspicion of ethylene glycol ingestion plus any 2 of the following;[4]
Arterial pH < 7.3
Serum bicarbonate < 20 mmol/L (20 mEq/L)
Osmolal gap > 10 mOsm/L
Presence of urinary oxalate crystals
A history or suspicion of ethylene glycol ingestion within the last 1 hour and osmolal gap > 10 mOsm/L
NOTE: Patients, particularly children, presenting within an hour of suspected ethylene glycol ingestion may not have any abnormal surrogate markers of ingestion. In these instances, close observation and serial monitoring of acid-base and renal function status should be performed. Any development of early metabolic acidosis would be highly suggestive of recent ethylene glycol exposure.

Admission Criteria

Hospital admission is recommended:
- For any patient with abnormal biochemistry
- In all symptomatic cases
Ensure the receiving hospital is able to provide:
The specific antidotes (Ethanol or Fomepizole)
Advanced care/ICU facilities, and



Initial management includes airway protection and administration of IV fluids. Gastric decontamination may be performed within 1 to 2 hours of ingestion via nasogastric aspiration provided the airways are protected. Late presenters may exhibit severe acidosis with compensatory tachypnea, treat with: sodium bicarbonate, intubation with hyperventilation (hyperventilate as acidosis will otherwise worsen and may prove fatal), and hemodialysis. Seizures require a benzodiazepine - closely monitor breathing. Administer glucose in those with CNS depression and suspected hypoglycemia (unless rapid glucose screen indicates otherwise); concurrently administer thiamine and multivitamins if alcoholism is suspected.
Effective antidotes exist in the form of either ethanol or fomepizole. Any patient with an elevated osmolal gap and an anion gap acidosis requires aggressive treatment including the administration of an antidote. It is recommended that patients receiving ethanol therapy be monitored in an intensive care setting. Other indications for intensive care include: coma, seizures, renal failure, hypotension, or ethylene glycol level > 8.1 mmol/L (50 mg/dL). Those with significant acidosis or a high serum ethylene glycol level should be hemodialyzed to reverse acidosis and/or reduce glycol and toxic metabolite levels.
Supportive care includes management of acidosis with generous sodium bicarbonate; administration to return base excess to normal within 12 to 24 hours is recommended. Large quantities may be required, and iatrogenic hypernatremia may occur. Hemodialysis will be required in severe cases of acidosis. Calcium administration is only indicated if cardiac dysrhythmia occurs (particularly QT prolongation), or seizures prove unresponsive to management. Correct hypoglycemia, hyperkalemia and hypomagnesemia. Calcium oxalate crystals may form in any organ with resultant multiorgan dysfunction/failure. The kidneys are often afflicted, and close monitoring and support of renal function is required due to the risk of acute renal failure. Should this occur hemodialysis is required until recovery. There is also risk of ARDS, and fluid balance will require careful (possibly invasive) monitoring. Stupor or coma indicates metabolic encephalopathy or cerebral edema.[5] Cranial nerve palsies may occur some 4 to 18 days following ingestion and usually spontaneously resolve over weeks to months without specific therapy.[6][7][8] Co-factor replenishment with thiamine and pyridoxine is not necessary unless the patient is considered vitamin deficient (e.g. history of alcoholism).
For eye exposures, if more than mild, resolving symptoms are present following irrigation, a full ophthalmologic examination should be undertaken, including slit lamp examination and fluorescein staining. If there is evidence of injury an ophthalmologist should be consulted. Treatment should follow standard protocols for the management of eye irritation.
Emergency Stabilization
Enhanced Elimination
Supportive Care
Fluid and electrolytes


Ensure Adequate Cardiopulmonary Function

Emergency stabilization includes appropriate airway management, ensuring intravenous access, cardiac monitoring, and obtaining initial laboratory values.


Ensure the airway is protected (intubation may be required), and administer oxygen. Establish secure intra-venous access.


Hypotension may be significant due to GIT fluid loss, and in such cases fluid replacement should be aggressive where possible, having regard to renal function.
Immediately establish secure intravenous access.
Where the systolic blood pressure is below normal blood pressure ranges for the age group:[9]
Age (years)
Normal Systolic Blood Pressure (mm Hg)
< 1
70 to 90
1 to 2
80 to 95
2 to 5
80 to 100
5 to 12
90 to 110
> 12
100 to 120
Administer normal (0.9%) saline
10 mL/kg IV over 5 to 10 minutes
If the systolic blood pressure does not return to the normal range, give a further 10 mL/kg body weight normal saline over 5 to 10 minutes. If intravenous access cannot be obtained consider intra-osseus access.
Administer a bolus of normal saline if systolic blood pressure is less than 100 mmHg.
Normal (0.9%) saline dose:
10 mL/kg IV over 5 to 10 minutes
If the systolic blood pressure does not return to the normal range, give a further 10 mL/kg body weight normal saline over 5 to 10 minutes.


Most toxic seizures are short-lived and often do not require intervention.[10]
Administer a benzodiazepine as first-line treatment to patients with seizure activity.[10]
Blood glucose concentration should be promptly determined. If the result indicates hypoglycemia, or is unobtainable, 50% dextrose should be administered IV (preceded by thiamine in adults).
Seizures due to ethylene glycol intoxication may prove unresponsive to standard management unless hypocalcemia is corrected.


IV dextrose is indicated (even if blood glucose cannot be quickly measured) in patients with altered mental status, unusual behavior, coma or seizures. Hypoglycemic patients may present with focal neurological deficits.[11] However, these may also be due to cerebral ischemia. As administration of dextrose may exacerbate ischemic injury,[12] it is important to verify hypoglycemia with blood glucose measurement prior to use - unless this would lead to unacceptable delay in administration.
Must be administered to adult patients considered alcoholic or malnourished.

Thiamine dose
100 mg IV

Emergency Monitoring

Electrolytes including:
Chloride (for calculation of anion gap)
Anion gap (elevated later in poisoning)
Serum ethanol concentration (used in calculation of osmolal gap)
Osmolal gap (elevated early in poisoning)
Arterial blood gases including:
Arterial pH
Serum ethylene glycol concentration



Nasogastric Aspiration

Nasogastric aspiration is recommended if the quantity of liquid ingested is both systemically toxic and in sufficient volume to aspirate. As this procedure may increase the risk of vomiting and pulmonary aspiration, the airway must be protected in all patients. Accurate placement of the nasogastric tube must also be ensured in all patients.
Nasogastric aspiration is recommended if the patient has presented early (within 1 to 2 hours) following ingestion of ethylene glycol.

Single Dose Activated Charcoal

Activated charcoal is not considered an effective decontaminant for this ingestion as ethylene glycol is rapidly absorbed from the gastrointestinal tract and has poor binding affinity for activated charcoal. Unless there is concern for coingestants, there is little benefit from activated charcoal administration in ethylene glycol ingestions.


Remove contact lenses. Irrigate immediately with water or saline for at least 15 minutes. If the eye is contaminated with solid particles, the eyelid should be completely everted and any solid material removed as quickly as possible whilst continuing to irrigate. A topical anesthetic may be necessary in some patients, especially children, to enable the patient to open the lids sufficiently for effective irrigation.
If, following irrigation, any of the following are apparent:
Ocular pain (other than mild and resolving)
Erythema (other than mild and resolving)
Decreased visual acuity
Ocular discharge/crusting
The patient should receive a full ophthalmologic examination, including slit lamp examination and fluorescein staining. If there is evidence of injury an ophthalmologist should be consulted.


Remove the patient from the exposure. If respiratory symptoms such as shortness of breath are present, administer oxygen and provide additional support if necessary.


Remove any contaminated clothing or jewelery. Wash the affected area thoroughly with soap and water until all of the contaminant is removed.


Appropriate use of antidotes in glycol poisoning is essential. Ethanol has long been regarded as an effective intervention, though objective data is lacking,[13] and is cheap and available.[14] Fomepizole has proven efficacy,[15] but suffers the disadvantage of expense. Both act by inhibiting alcohol dehydrogenase, thus reducing the metabolic conversion of glycol to toxic metabolites (acids).
Thiamine and pyridoxine may be indicated as therapeutic adjuncts. Theoretically, they act as cofactors in the formation of non-toxic metabolites of ethylene glycol. No data exists to support this assumption, but they may benefit those with a history of ethanol abuse or inadequate nutrition (e.g. those vitamin deficient).



Ethanol is indicated if:[16]
- Reliable history of ingestion of a toxic quantity of ethylene glycol; or
- Plasma ethylene glycol concentration is greater than 3.2 mmol/L (20 mg/dL) or;
- Recent ingestion of greater than 0.2 mL/kg ethylene glycol and presence of osmolal gap of greater than 10 mosm/L or;
- History or clinical suspicion of ethylene glycol poisoning and at least two of the following:
Arterial pH < 7.3
Serum bicarbonate < 20 mmol/L (20 mEq/L)
Osmolal gap > 10 mosm/L
Presence of urinary oxalate crystals

Dose and Administration

Loading Dose
For acceptable efficacy, the blood ethanol concentration should be maintained between 22 and 33 mmol/L (100 to 150 mg/dL). To achieve this both a loading dose and maintenance infusion are required. Either 100% ethanol diluted for intravenous use may be infused, or liquor (e.g. vodka, gin) may be administered orally.
Prior to use of ethanol therapy a blood ethanol determination should be made to identify if the patient has an existing ethanol concentration requiring a modification of the loading dose. Monitoring in an intensive care setting is required during administration.
As ethanol may depress respiration, mechanical hyperventilation is recommended in those with reduced level of consciousness.[17]
Oral ethanol loading dose
To calculate the loading dose of oral ethanol the following equation may be applied:
Dose =  (BEC x wt x Vd) / (C x SpG)
desired blood ethanol concentration (mg/dL)
amount of beverage (mL)
patient’s weight (kg)
volume of distribution (0.6 L/kg)
concentration of alcohol (% v/v)
specific gravity (0.8) [converts % v/v to % w/v]
Note: The term "proof" describing alcohol content of beverages should be halved to obtain the proper % v/v value (e.g. 60 proof = 30% v/v ethanol).
To obtain a therapeutic blood ethanol concentration of 125 mg/dL in a 70 kg patient using whisky (80 proof and therefore 40% v/v ethanol), the loading dose will be:
Loading Dose =  (125 x 70 x 0.6)  /  (40 x 0.8)  = 164 mL whiskey
This should be administered as a 20% or less solution (e.g. diluted with water or fruit juice).
Intravenous ethanol loading dose
To prevent vascular damage when administering intra-venous ethanol the 100% alcohol must first be diluted to either a 5 or 10% solution in 5% dextrose and water (some solutions are ready made).
To reach the desired blood ethanol concentration of 22 to 33 mmol/L (100 to 150 mg/dL) administer:
- 12 to 18 mL/kg of 5% w/v ethanol, over 30 minutes, or;
- 6 to 9 mL/kg of 10% w/v ethanol, over 30 minutes.
(Alternatively, the above equation may be used, using 5 or 10% for concentration (C). Multiply by 0.8 (SpG) ONLY if formulation is % v/v not % w/v).
When diluting 100% alcohol, it’s specific gravity of 0.8 must be taken into account. Therefore, to produce a:
10% w/v solution
Dilute 100% ethanol 8 fold (e.g. one 20 mL vial of 100% alcohol to 140 mL 5% dextrose [making total volume of 160 mL]). This solution may be preferable to reduce fluid load in pediatric patients, or those suffering cerebral edema.
5% w/v solution
Dilute 100% ethanol 16 fold (e.g. one 20 mL vial of 100% alcohol to 300 mL 5% dextrose [making total volume of 320 mL]).
Maintenance Dose
The rate of maintenance infusion will vary due to individual differences in ethanol metabolism.
Different rates of metabolism:[18][19]
Non-alcoholic adult
3.3 to 4.3 mmol/L/h (15 to 20 mg/dL/h)
Alcoholic adult
6.5 to 8.7 mmol/L/h (30 to 40 mg/dL/h)
6.5 mmol/L/h (30 mg/dL/h)
The Loading Dose Equation can be used to calculate both oral and IV maintenance doses. Replace BEC with metabolism rate from the equation. Remember NOT to multiply by 0.8 (SpG) if formulation is already % w/v.
Oral ethanol maintenance dose
The Loading Dose Equation can be used to calculate both oral and IV maintenance doses. Replace BEC with metabolism rate from the equation. Remember NOT to multiply by 0.8 (SpG) if formulation is already % w/v.
E.g. In a non-alcoholic 70 kg adult patient (e.g. elimination rate estimated as 20 mg/dL/h) the maintenance dose using 40% v/v ethanol and the above equation will be:
Maintenance Dose =  (20 x 70 x 0.6) / (40 x 0.8)  =  26 mL/h whiskey
This should be administered as a 20% or less solution (e.g. diluted with water or fruit juice).
Intravenous ethanol maintenance dose
5% w/v solution:
3.6 mL/kg/h
1.8 to 2.4 mL/kg/h
3.6 to 4.8 mL/kg/h
10 % w/v solution:
1.8 mL/kg/h
0.9 to 1.2 mL/kg/h
1.8 to 2.4 mL/kg/h

Antidote Endpoint

Ethanol administration may be discontinued if ethylene glycol levels can no longer be detected or are less than 2.4 mmol/L (15 mg/dL) with a normalized arterial pH - this is likely to take 2 to 3 days given ethylene glycol's half-life of elimination of 17 hours. [16]


Hypoglycemia may occur, especially in children.[20] Once an infusion has been commenced blood glucose concentrations must be determined on a frequent basis (every 20 to 60 minutes). It may be necessary to add dextrose to intravenous solutions, or give glucose if ethanol is being administered orally.[21]


While availability is limited by purchase price, fomepizole appears preferable to ethanol. It is more particularly indicated in those with altered mental status, patients suffering hepatic disease, or those critically ill but lacking confirmation of poisoning. Its administration to pediatric patients avoids the disadvantages of ethanol (e.g. inebriation, hypoglycemia).


Fomepizole is indicated if:
- Plasma ethylene glycol concentration greater than 3.2 mmol/L (20 mg/dL) or;
- Recent ingestion of greater than 0.2 mL/kg ethylene glycol and presence of osmolal gap greater than 10 mosm/L or;
- History or clinical suspicion of ethylene glycol poisoning and at least two of the following
Arterial pH < 7.3
Serum bicarbonate < 20 mmol/L (20 mEq/L)
Osmolal gap > 10 mosm/L
Presence of urinary oxalate crystals
Particular indications:
- Altered mental status
- Hepatic disease
- Critically ill patients lacking confirmation of ethylene glycol toxicity
- Pediatric patients (avoids the inebriation and hypoglycemia that may occur with ethanol administration)

Dose and Administration

Loading dose[22]
- 15 mg/kg diluted in 100 mL of normal saline or 5% dextrose in water and administered by IV infusion over 30 minutes
Maintenance doses[22]
- 10 mg/kg should be administered every 12 hours for 4 doses, then;
- 15 mg/kg every 12 hours thereafter if indicated
Maintenance fomepizole should be administered in the same fashion as the loading dose. Dosing requirements will change if hemodialysis is required – as outlined in the enhanced elimination section.

Antidote Endpoint

Fomepizole may be discontinued when ethylene glycol plasma concentrations are either undetectable, or below 3.2 mmol/L (20 mg/dL) in an asymptomatic patient with a normal pH.[22]

Adverse Effects

Abdominal pain, skin rash, nausea, headache and pain at site of injection have been reported following fomepizole use.[22]


Pyridoxine acts as a co-factor in the conversion of glyoxylic acid to the non-toxic metabolite glycine. While the clinical benefit of pyridoxine administration for the treatment of ethylene glycol poisoning has not been demonstrated in healthy individuals, it is recommended for use in malnourished or alcoholic patients who may have vitamin deficiencies.[16]

Dose and Administration

The formulation should be diluted at least 1 to 5.
- 50 to 100 mg pyridoxine given as an IV infusion over 15 to 30 minutes every six hours
- Continue for two days[23]


Profound peripheral neuropathy may occur after very large single doses[24] or a series of doses (for example a total of > 2 g/kg pyridoxine over a three day period).[25] The sensory (if not motor) disturbances are potentially irreversible.[26]


Thiamine acts as a co-factor in the conversion of glyoxylic acid to the non-toxic metabolite alpha-hydroxy-beta-ketoadipate. While the clinical benefit of thiamine administration for the treatment of ethylene glycol poisoning has not been demonstrated in healthy individuals, it is recommended for use in malnourished or alcoholic patients who may have vitamin deficiencies.[16]

Dose and Administration

- Administer 100 mg IV or IM thiamine every six hours
- Continue for two days[23]



Hemodialysis is a highly effective method to enhance excretion of glycols and their toxic metabolites, reducing duration of antidote use and enhancing patient outcome. The 6-hour half-life of elimination of ethylene glycol may be reduced to 2.5 to 3.5 hours.[27][28][29] In severe poisonings it can be life-saving. If dialysis is prolonged monitor for and treat hypophosphatemia.
Hemodialysis is indicated where:[16]
Clinical signs are deteriorating despite intensive supportive care or;
Metabolic acidosis with pH < 7.25 or;
Acute renal failure or;
Serum ethylene glycol level > 8.1 mmol/L (50 mg/dL) in those not receiving fomepizole therapy.
Ethanol Maintenance
This therapy should continue during hemodialysis. As ethanol is dialysed, infusions must be increased (approximately doubled, possibly tripled) or ethanol added to the dialysate. Further infusion rates must be guided by regular measurement of serum ethanol concentration.
Hemodialysis should be continued in those receiving ethanol until:
Measured serum ethylene glycol concentration is < 1.6 mmol/L (< 10 mg/dL) and renal function is restored and acidosis resolved,[30]
Osmolal gap, anion gap, electrolyte concentrations, acid-base, and renal function have normalized.
To reduce risk of recurrence of toxicity (due to redistribution or continued absorption) consideration should be given to continuation of ethanol treatment for 24 hours after completion of hemodialysis.[30]
Fomepizole Maintenance
The dose of fomepizole must be increased during hemodialysis to compensate losses from the procedure. If the dialysis is started six or more hours after the last administration, the next scheduled dose should be given at the commencement of the procedure. All patients should then receive four hourly administrations for the duration of the treatment.[22]
Hemodialysis should be continued in those receiving fomepizole until:[31]
Acid-base and renal function have normalized;
Signs of systemic toxicity have disappeared, and;
Serum ethylene glycol levels are 3.2 mmol/L (20 mg/dL) or less.
While the procedure is preferably terminated under these conditions it has been reported as safe with ethylene glycol levels above 8.1 mmol/L (50 mg/dL) when associated with fomepizole therapy.[32]
Fomepizole treated patients should continue this therapy following hemodialysis. If a dose has been administered within the last hour a further is not required. Those not having received a dose within 1 to 3 hours should be administered half their next scheduled dose at the completion of dialysis; while those who have not received fomepizole for more than 3 hours should receive their full dose. All should maintain 12 hourly dosing thereafter during the monitoring period.[22]
Post-hemodialysis monitoring
Glycols may redistribute following cessation of hemodialysis causing re-intoxication requiring repeat hemodialysis.[33] Serum osmolal gap, anion gap, acid-base status, electrolytes and renal function should be monitored (2 to 4 hourly) for the next 24 hours.
Patients may suffer acute renal failure as a result of their poisoning and require hemodialysis for some weeks. It is usual (but not inevitable) that full renal function will return.

Urinary Alkalinization

The renal clearance of the acidic metabolites of glycols (such as glycolic acid, a toxic metabolite of ethylene glycol), may be increased by aggressive treatment of metabolic acidosis with sodium bicarbonate due to “ion-trapping” within the kidney.[27]



Plasma glucose
Liver function
Electrolytes including:
Chloride (for calculation of anion gap)
Anion gap (will be increased in later stages of poisoning)
Serum ethanol level (ethanol may influence antidote dose)
Osmolal gap (will be increased in early stages of poisoning)
Blood urea nitrogen (urea)
Fluid output
Arterial blood gas
Serum ethylene glycol level
Head CT (if neurological abnormality)


Metabolic Acidosis

Increased anion gap metabolic acidosis results from the metabolism of ethylene glycol to acidic metabolites, predominantly glycolic acid. It is widely accepted that early and aggressive treatment of acid-base abnormality (pH < 7.3) with potentially large quantities of sodium bicarbonate is life-saving following ethylene glycol intoxication (beware of the potential for hypernatremia).[34][35][36] Bicarbonate may also enhance renal excretion of toxic metabolites by renal “ion trapping”,[27] but may contribute to hypocalemia. It is recommended that base excess be raised to normal within 12 to 24 hours however much bicarbonate that requires.[35] In severe acidosis, use of an antidote to halt production of acidic metabolites, and aggressive hemodialysis are necessary.
Arterial blood gases (pH, bicarbonate, pCO2, pO2)
Plasma lactate
Base excess
Follow standard protocols for the management of metabolic acidosis.
Early use of hemodialysis must be considered, and should be used where cardiorespiratory support and sodium bicarbonate are insufficient to control acidosis.


Acute Renal Failure

Renal failure may occur due to the toxic metabolites of ethylene glycol crystallizing in the presence of calcium and being deposited in the kidneys. Acute tubular necrosis, cortical edema, and other direct toxicity is possible. Signs and symptoms of renal insufficiency predominate at 2 to 3 days post ingestion. Alkalinize the urine and ensure adequate output. Hemodialysis is indicated in the presence of renal failure.
Patients should be monitored for the onset of renal failure:
Urine output
Serum creatinine
Blood urea nitrogen (urea)
Loin pain may occur
Manage following standard treatment protocols for acute renal failure.

Fluid and Electrolytes


Prophylactic calcium or treatment of asymptomatic hypocalcemia is not recommended due to the risk of further precipitation of calcium oxalate in the tissues.[36] Calcium is recommended for patients continuing to seize despite standard anticonvulsant management,[16] or in the presence of cardiac dysrhythmia – particularly prolonged QT interval. (It should be noted that available ionized calcium will rise with increasing acidosis [due to release from plasma proteins] and fall with return to normal serum pH).
Monitor for onset of hypocalcemia with:
Observation for signs and symptoms of hypocalcemia
Serum ionized calcium
Serum electrolytes (hypomagnesemia and hyperkalemia are often also present)


Magnesium is a cofactor with thiamine in the metabolic detoxification of ethylene glycol metabolites. Serum magnesium levels should be monitored and hypomagnesemia corrected.[23]
Serum magnesium
Nausea and vomiting
Lethargy, weakness, fatigue
Manage hypomagnesemia following standard protocols.



Seizure activity unresponsive to standard management is indicative of hypocalcemia, particularly in the presence of calcium oxalate crystalluria, or following administration of sodium bicarbonate (which can lower ionized serum calcium).[16] Supplemental calcium should be provided in such cases.
Observe the patient closely for onset of seizure activity.


All asymptomatic patients should be observed until appropriate investigations have been carried out. If treatment is not required they may be:
- Discharged into the care of a reliable observer, or
- Referred for psychological assessment (if the overdose was intentional)
Symptomatic patients may be considered for discharge once symptoms and toxic sequelae have resolved, and ethylene glycol serum levels have declined to below 3.2 mmol/L (20 mg/dL). In some cases, patients may exhibit transient renal failure, requiring continuing dialysis. Furthermore, ongoing cranial nerve palsies may occur, but typically resolve within weeks to months.


Standard protocols should be used for follow-up of patients suffering renal failure or CNS effects. Psychiatric intervention may be necessary depending on the circumstances of the exposure.


Those patients surviving an initial severe acidosis may face oliguric renal failure and require regular hemodialysis for weeks to months. Fortunately, recovery is expected and very few cases lead to permanent renal failure.[37] The return of renal function is usually signified by an increase in urine output and concomitant decrease in serum creatinine.
Those who develop severe CNS manifestations, including seizures and coma, can recover full neurologic function. Cranial nerve palsies may occur in nerves II, V, VII, VIII, IX and XII, typically resolving over weeks to months.[8]


Symptoms following ethylene glycol ingestion can be divided into three acute stages and one sub-chronic phase.
Initial symptoms of ethylene glycol ingestion are due to the direct toxicity of ethylene glycol. CNS effects predominate and include inebriation (without the alcohol odor on the breath), gastrointestinal upset, and drowsiness. In severe cases, coma, and seizures may develop.[38]
In subsequent phases of intoxication, the various metabolites of ethylene glycol are responsible for the presenting symptoms, which in the second phase of poisoning include, metabolic acidosis and cardiopulmonary symptoms 12 to 24 hours post ingestion.[32] In significant poisonings, severe metabolic acidosis with compensatory hyperventilation can develop with multiple organ failure. Tachycardia, mild hypertension, pulmonary edema, and congestive heart failure are all believed to be due to the deposition of calcium oxalate crystals within the vascular tree, myocardium and the lung parenchyma.[39] Most deaths occur in this second phase.[23]
The renal phase of intoxication, beginning 24 to 48 hours after ingestion, is marked by the predominance of oliguria, acute tubular necrosis, renal failure, and occasionally bone marrow suppression. Hematuria and proteinuria are common. In severe poisonings, renal failure may appear early and progress to anuria.[39] Calcium oxalate crystals may be detected in the urine of some patients. Renal symptoms may last up to 45 days or more.[23] In addition, cranial nerve palsies that develop in some patients may persist for weeks to months.[8] Convulsions and coma are considered ominous signs.[35]
Following inhalation, irritation of the nose and throat can occur. Its low evaporation rate (and vapor pressure) at ambient temperatures make it unlikely to present an acute inhalation hazard in most situations; systemic effects would not typically be expected following inhalation.
Eye exposure to vapors or direct contact with the liquid may lead to eye irritation; significant eye injury would not be expected.
Skin contact is unlikely to cause harm to the skin on brief or occasional contact but prolonged or repeated exposure may lead to irritation. It is possible absorption through the skin could lead to systemic effects following large prolonged exposures.

Routes of Exposure

Symptoms predominantly occur following ingestion of ethylene glycol. However, toxicity is also possible via dermal, intravenous and intramuscular routes.

Onset/Duration of Symptoms

There are three acute stages of ethylene glycol poisoning and one sub-acute stage that may occur[40][41][42]
Stage I: Neurological Phase
0.5 to 12 hours post-ingestion
Metabolic acidosis
CNS depression
Stage II: Cardiopulmonary Phase
12 to 24 hours post-ingestion
Severe metabolic acidosis
Adult respiratory distress syndrome (ARDS)
Congestive heart failure
Stage III: Renal Phase
24 to 72 hours post-ingestion
Acute tubular necrosis
Renal failure
Subacute Stage
Onset several (5 to 20) days after ingestion
Cranial nerve neuropathies
Most deaths are reported in Stage II. The severity of these stages and their progression from one to the other often depends on the amount ingested.

Severity of Poisoning

Mild Ethylene Glycol ToxicityModerate Ethylene Glycol ToxicitySevere Ethylene Glycol Toxicity
Mild metabolic acidosis
Pulmonary edema
Congestive cardiac failure
Severe metabolic acidosis
Multiple organ failure



Exposures via this route are rare due to the low vapor pressure of ethylene glycol at normal temperatures. However, when heated or aerosolized, exposures may occur. Upper respiratory tract irritation, cough and lymphocytosis have been reported.[43]


Ethylene glycol does not significantly irritate the skin. Following severe, prolonged exposures, slight maceration of the skin may result and dermal absorption could occur.[44] Repeated skin exposures may result in sensitivity.[45]


Direct eye contact with ethylene glycol may result in immediate eye irritation with temporary conjunctival inflammation. No significant corneal damage would be expected.[46]



Abdominal pain[47]
Abdominal cramping[23][49]


Inebriation without the smell of alcohol on the breath (unless concomitant exposure) occurs early after ingestion.[50][51] Coma may occur in the first 12 hours, as may seizures[52] and death.[16] Permanent cranial nerve deficits may occur following large ingestions (>100 mL) and usually occur several days after the development of the features of acute toxicity.
Early CNS Toxicity
Slurred speech[53]
Delayed CNS Toxicity
Slurred speech[53]
Facial weakness[53][6]
Anisocoria (unequal pupil diameters)[55]
Facial diplegia[8][56]
Hearing loss[54]
Absent gag reflex[54]
Defects of cranial nerves V, VII, VIII, IX, X[42][57][56][8]
Permanent deficit in gross and fine motor skill[52]
Cerebral edema[58]


Hyperventilation and tachypnea[52]
Adult respiratory distress syndrome[59]
Non-cardiogenic pulmonary edema[50]


Disseminated intravascular coagulation[63]
Methemoglobinemia[64] (rare)


Increased anion gap metabolic acidosis[41]
Increased osmolal gap[35]
NB. A normal anion or osmolal gap does not rule out ethylene glycol ingestion.[34][65]

Fluid and Electrolytes

Hypocalcemia may occur following the combination of ethylene glycol’s oxalate metabolite with serum calcium to form calcium oxalate.


Cardiogenic pulmonary edema[69]
Cardiorespiratory arrest[51]
However, cardiac involvement is generally relatively uncommon.


Myalgia (muscle pain)[51][47]
Increased creatine kinase (CK)[51]


Calcium oxalate crystals may be seen in the urine in some[52] but not all cases.[40][41] Acute renal failure may occur, and in a minority of cases may prove permanent.[50][34]
Acute renal failure[50][34][72]


Dilated or poorly reactive pupils[52][34]
Blurred or edematous optic discs[47][73][74]
Reduced vision[73]
Strabismus (involuntary squint)[47][48]
Oculomotor nerve palsies


General Effects

Chronic exposures to ethylene glycol vapor may result in CNS abnormalities and lymphocytosis.[75]



The major toxic agent in ethylene glycol poisoning is not the parent compound, but the metabolites produced by the action of alcohol dehydrogenase (ADH) on the parent compound.[20]
Ethylene glycol is rapidly metabolized via ADH into glycoaldehyde, which is rapidly converted into glycolic acid by aldehyde dehydrogenase. The rate-limiting step in the metabolism of ethylene glycol is the formation of glyoxylic acid from glycolic acid via lactic dehydrogenase or glycolic acid dehydrogenase. Glyoxylic acid can be either metabolized into non-toxic alpha-hydroxy-beta ketoadipate and glycine via thiamine and pyridoxine respectively, or into oxalate.[23]
The etiology and pathophysiology of the CNS, metabolic, cardiopulmonary, and renal toxicity are primarily due to the formation and accumulation of toxic intermediary metabolites, especially glycolic acid (produces profound acidemia, oxalosis, and renal interstitial edema) and to a lesser but histologically important extent, oxalate production and excretion.[76][77]



The toxic dose is variable in humans. However, the lethal dose for humans is reported to be about 100 mL (1.4 mL/kg) of the concentrate, although survival has occurred with ingestions much higher than this[78][79][68][80] and death has occurred with just 30 mL of the concentrate in adults.[81][82]
The intervention criteria has been derived from a consensus opinion.[83] It was concluded that any ingestion of pure ethylene glycol greater than a witnessed lick or taste in a child or more than a 'swallow' (10 to 30 mL) in an adult warrants referral to an emergency department. For ingestion of lower concentration products (<20%) it was concluded that any ingestion of greater than 0.1 mL/kg of pure substance equivalent warrants referral.

Case Studies

100 ml antifreeze solution (ingested)
13 year old female: normal physical examination 30 minutes post-ingestion Became ataxic and dysarthic and urinalysis revealed calcium oxalate crystals. Serum ethylene glycol concentration was 103 mg/dL
Received ethanol and fomepizole[84]
Recovered discharged after three days.[84]
300 ml antifreeze solution (ingested)
19 year old female (62 kg): nausea, vomiting, drowsiness. Serum ethylene glycol concentration was 134 mg/dL
Received fomepizole[32]
Recovered discharged after four days[32]
450 mL amtifreeze solution (ingested)
60 year old male: coma, hypothermia, metabolic acidosis, aspiration, anuria, seizure
Supportive care, including sodium bicarbonate, oxygen, ethanol infusion, hemofiltration[85]
2,250 ml antifreeze solution (ingested)
27 year old male: somnolence
Received gastric lavage, activated charcoal and intravenous ethanol[68]
Discharged after two days[68]
4,500 ml antifreeze solution (ingested)
58 year old male: metabolic acidosis and increased anion and osmolal gap. Serum ethylene glycol concentration was 791 mg/dL
Received activated charcoal, intravenous ethanol and hemodialysis[68]
Recovered discharged after five days[68]



Ethylene glycol poisoning in animals is relatively common as it has a sweet taste and looks like water. Water drained from a radiator containing ethylene glycol may be consumed unwittingly and relatively low amounts may cause toxicity.
In cats, peak plasma concentrations occur an hour post-ingestion and urine concentrations peak at 3 hours post-ingestion. Cats have the best chance of survival following a lethal dose if the antidote is started within 3 to 4 hours of ingestion.[86]
In dogs, peak plasma concentrations occur 2 to 3 hours post-ingestion and urine concentrations peak at 6 hours post-ingestion. Dogs have the best chance of survival following a lethal dose if the antidote is started within 6 to 8 hours of ingestion.[86]
The sooner antidotal therapy is commenced, the better the outcome.[86] Recovery may take 3 to 5 days. The antidote is only effective at blocking ethylene glycol metabolism. There is no benefit of giving it if the ethylene glycol is already metabolized or if the animal has renal failure. If the animal presents in the final stage of poisoning, with symptoms of renal failure or coma, the prognosis is poor.[86]
Ethylene Glycol:
LD50 Oral, Rat
4,700 mg/kg4,700 mg/kg/[78]
LD50 Oral, Mouse
7,500 mg/kg7,500 mg/kg/[78]
LD50 Oral, Cat
1,650 mg/kg1,650 mg/kg/[87]
LD50 Oral, Dog
5,500 mg/kg5,500 mg/kg/[87]
LD50 Oral, Guinea pig
6,610 mg/kg6,610 mg/kg/[88]
MLD Oral, Cat
1 to 2.5 mL/kg1 to 2.5 mL/kg/[89]
MLD Oral, Dog
4 to 5 mL/kg4 to 5 mL/kg/[89]
MLD Oral, Cattle
2 to 10 mL/kg2 to 10 mL/kg/[89]
MLD Oral, Fowl
7 to 8 mL/kg7 to 8 mL/kg/[89]
LD50 IP, Rat
5,010 mg/kg5,010 mg/kg/[78]
LD50 IP, Mouse
5,614 mg/kg5,614 mg/kg/[78]
LD50 SC, Rat
2,800 mg/kg2,800 mg/kg/[78]
LD50 IV, Rat
3,260 mg/kg3,260 mg/kg/[78]


SI Unit Conversion

To convert an ethylene glycol concentration expressed in mg/dL into mmol/L:
Multiply the mg/dL by 0.1611
To convert an ethylene glycol concentration expressed in mmol/L into mg/dL:
Multiply the mmol/L by 6.2070
Units: 1 dL = 0.1 L
1 ug/L = 0.1 ug/dL
1 ug/dL = 10 ug/L

Toxic Plasma Level

Plasma Ethylene Glycol Concentration
Serum ethylene glycol concentrations at admission are not predictive of outcome. Low pH and low base excess, indicative of toxic metabolites, do predict outcome.[35]
Initial ethylene glycol concentration greater than 20 mg/dL may result in toxic effects.
Initial ethylene glycol concentration greater than 30 mg/dL has the potential to be fatal.[23]
Patients presenting with established signs of acute ethylene glycol toxicity may have relatively low or undetectable serum concentrations of ethylene glycol. It is rapidly metabolized to the toxic metabolites responsible for the development of clinical and biochemical signs of poisoning.
Correlation Of Toxic Concentration And Effect
< 20 mg/dL Low Concentration
20 to 30 mg/dL Moderate Concentration
Mild anion gap metabolic acidosis
Elevated osmolal gap (absence does not rule out toxicity)
> 30 mg/dL Severe Concentration
Severe metabolic acidosis
Multiple organ failure
Ethylene Glycol Toxic Plasma Concentrations
103 mg/dL (1 hour post ingestion)
After approximately 120 mL of antifreeze orally, a 13 year old female had ataxia, dysarthria, calcium oxalate crystals in urine[84]
134 mg/dL (1 hour post-ingestion)
After approximately 300 mL of antifreeze orally, a 19 year old female had nausea, vomiting and drowsiness[32]
222.6 mg/dL (3 hours post ingestion)
After an unknown amount of ethylene glycol was ingested a 35 year old male was exhibiting bizarre behavior, was somnolent and had an elevated osmolal and anion gaps[90]
235.9 mg/dL (24 hours post ingestion)
After an unknown amount of ethylene glycol was ingested a 35 year old male was comatose with calcium oxalate crystals, rhabdomyolysis and transient renal failure[91]
888 mg/dL (3 hours post ingestion)
After an unknown amount of ethylene glycol was ingested a 28 year old male was comatose with hyperventilation, calcium oxalate crystals in urine and acute renal failure[23]
Ethylene Glycol Concentrations in Human Fatal Cases (g/L or g/kg)

(0.3 to 4.3)
(0.3 to 3.9)
(0.2 to 15.1)
(0.2 to 11.3)
(0.6 to 10.8)

Osmolal Gap

The osmolal gap represents the difference between the measured osmolality (osmoles per kilogram solvent) and calculated osmolarity (osmoles per liter of solution).[92][16] When positive, it may indicate the presence of low molecular weight compounds such as alcohols and glycols. A normal osmolar gap does not reliably rule out the presence of a toxic alcohol in the blood stream.
Serum osmolality is generally in the range 270 to 290 mOsm/kg H2O, and should be measured by freezing point depression.[68]
The osmolarity may be calculated using SI units or using Mass (traditional) units.
Osmolarity Calculation Using SI Units
Osmolarity = 2 x sodium[mmol/L] + glucose[mmol/L] + urea[mmol/L] + ethanol[mmol/L]
Urea = BUN (blood urea nitrogen)
Include ethanol if found on serum measurement
Osmolarity Calculation Using Mass (traditional) Units[93]
Osmolarity = (2 x sodium[mEq/L]) + (glucose[mg/dL] /18) + (BUN[mg/dL]/2.8) + (ethanol[mg/dL]/4.6)
All units should be expressed as mg/L
BUN = urea
Include ethanol if found on serum measurement
These equations should also include other compounds such as ethanol or mannitol, if present. This calculation should be undertaken in the earlier phases of intoxication prior to the metabolic removal of alcohols and glycols.
Osmolar gap = Osmolality - Osmolarity
The mean normal osmolal gap has been determined to be approximately < 10 or 15 mOsm/kg H2O (though this range will vary between laboratories).[68] However, there exists considerable variation in osmolar gaps between individuals. Hence, a ‘normal’ osmolar gap does not rule out the presence of an alcohol or glycol.[93] The osmolar gap is most useful in suggesting the presence of suspected glycol or alcohol ingestion when it is significantly elevated (usually > 20 to 30 mOsm/kg).

Anion Gap

The anion gap represents the difference between the sum of measured cations and the sum of measured anions. An elevated anion gap indicates the presence of unmeasured organic acids (including products of the metabolism of alcohols or glycols).
Anion gap = [([sodium]) – ([bicarbonate] + [chloride])]
Potassium is normally omitted from the calculation because its range is relatively small and constant.
All units should be expressed as mmol/L.
A “normal” anion gap may be considered within the range 3 to 11.[94]



The effects of human exposure to ethylene glycol during pregnancy are unknown.
Ethylene glycol has been shown to be teratogenic in animals. Teratogenicity was observed in the absence of maternal toxicity in both rats and mice.
Effects in mice given 1640 mg/kg ethylene glycol by mouth included:[95]
Reduced number of live pups
Decreased pup weight
Malformations including
Craniofacial abnormalities
Neural tube defects (anencephaly, meningomyelocele)
Visceral malformations
Skeletal malformations (fused ribs, abnormally-shaped or missing vertebrae, twisting of spine)[96]
Similar effects were noted in rats[97] but at a higher dose (2500 mg/kg/day).
Inhalational exposure to ethylene glycol may also result in teratogenicity.


It is unknown whether this compound is excreted in human breast milk.



Oral Absorption
Dermal Absorption
Thought to be minimal, but a large prolonged exposure could be significant
10 to 26% transcutaneous absorption has been demonstrated in both animal and human models following prolonged exposure[23]
Onset of Action
CNS effects may occur just 30 minutes after ingestion[40]
Duration of Action
1 to 4 hours[41]


  1. Rapidly in body water
Volume of Distribution
  1. 0.5 to 0.8 L/kg[98]


  1. Liver
  1. Glycoaldehyde, glycolic, glyoxylic acid, oxalate
  2. Glyoxal, formic acid, glycine, oxalomalate, 2-hydroxy-3-oxadipate, 2-oxo-4-hydroygluconate, and malate[99]
Major Metabolic Pathways
  1. By the enzyme alcohol dehydrogenase to glycoaldehyde
Glycoaldehyde is then metabolized to glycolic acid with subsequent conversion to glyoxylic acid and oxalate:


Ethylene glycol initially excreted unchanged in urine (up to 80%)
  1. Glycolic acid and its salts are also excreted in the urine
  2. Carbon dioxide formed by breakdown of metabolites is excreted via the lungs (up to 60% in rabbits)[98]
  1. In absence of ethanol: 3 hours
  2. In presence of ethanol: 17 hours
  3. In presence of ethanol with dialysis: 2.5 hours[28]
  4. In presence of 4-methylpyrazole: 11 to 14 hours
Clearance Rate
  1. Urinary: Estimated at 3.2 mL/kg/min
Potential for Accumulation
  1. Calcium oxalate crystals can accumulate in the kidney leading to renal damage and renal failure



Ethane-1,2-diolEthylene alcoholEthylene dihydrate
Ethylene glycolFridexGlycol
Glycol alcoholGlycolmonomerLutrol-9
M.E.GMonoethylene glycolNorkool
Radiator fluidRampTescol
Ucar 17



Ethylene Glycol:


Ethylene Glycol:


[1] Lewis RJ Sr. Sax's dangerous properties of industrial materials. 9th ed. New York: Van Nostrand Reinhold; 1996. p. 1548.
[2] Budavari S, editor. The Merck index. 12th ed. Whitehouse Station (NJ): Merck & Co; 1996. p. 647.
[3] Jolliff HA, Dart RC, Bogdan GM, Daly FF. Can the diagnosis of ethylene glycol (EG) toxicity be made without serum EG and osmolality values? [abstract]. J Toxicol Clin Toxicol 2000; 38 (5): 539-40.
[4] Brent J. Current management of ethylene glycol poisoning. Drugs 2001; 61 (7): 979-88.
[5] Maier W. Cerebral computed tomography of ethylene glycol intoxication. Neuroradiology 1983; 24 (3): 175-7.
[6] Spillane L, Roberts JR, Meyer AE. Multiple cranial nerve deficits after ethylene glycol poisoning. Ann Emerg Med 1991 Feb; 20 (2): 208-10.
[7] Lewis LD, Smith BW, Mamourian AC. Delayed sequelae after acute overdoses or poisonings: cranial neuropathy related to ethylene glycol ingestion. Clin Pharmacol Ther 1997 Jun; 61 (6): 692-9.
[8] Berger JR, Ayyar DR. Neurological complications of ethylene glycol intoxication. Report of a case. Arch Neurol 1981 Nov; 38 (11): 724-6.
[9] Mackway-Jones K, Molyneux E, Phillips B, Wieteska S, editors. Advanced paediatric life support: the practical approach. 3rd ed. London: BMJ Books; 2001.
[10] Chen HY, Albertson TE, Olson KR. Treatment of drug-induced seizures. Br J Clin Pharmacol 2016 Mar; 81 (3): 412-9.
[11] Wallis WE, Donaldson I, Scott RS, Wilson J. Hypoglycemia masquerading as cerebrovascular disease (hypoglycemic hemiplegia). Ann Neurol 1985 Oct; 18 (4): 510-2.
[12] Browning RG, Olson DW, Stueven HA, Mateer JR. 50% dextrose: antidote or toxin? Ann Emerg Med 1990 Jun; 19 (6): 683-7.
[13] Watson WA. Ethylene glycol toxicity: closing in on rational, evidence-based treatment. [Editorial] Ann Emerg Med 2000 Aug; 36 (2): 139-41.
[14] Wacker WE, Haynes H, Druyan R, Fisher W, Coleman JE. Treatment of ethylene glycol poisoning with ethyl alcohol. JAMA 1965 Dec 13; 194 (11): 1231-3.
[15] Brent J, McMartin K, Phillips S, Burkhart KK, Donovan JW, Wells M, Kulig K. 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.
[16] 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.
[17] Paasma R, Hovda KE, Hassanian-Moghaddam H, Brahmi N, Afshari R, Sandvik L, Jacobsen D. Risk factors related to poor outcome after methanol poisoning and the relation between outcome and antidotes--a multicenter study. Clin Toxicol (Phila) 2012 Nov; 50 (9): 823-31.
[18] Sidell FR, Pless JE. Ethyl alcohol: blood levels and performance decrements after oral administration to man. Psychopharmacologia 1971; 19 (3): 246-61.
[19] Leung AK. Ethyl alcohol ingestion in children. A 15-year review. Clin Pediatr (Phila) 1986 Dec; 25 (12): 617-9.
[20] Bates N, Edwards N, Roper J, Volans G, editors. Paediatric toxicology. London: Macmillan Reference Ltd; 1997. p. 63-9.
[21] Parfitt K, editor. Martindale: the complete drug reference. 32nd ed. London: Pharmaceutical Press; 1999. p. 1344.
[22] Antizol Prescribing Information, USA: Paladin Labs (USA) Inc; April, 2006; [cited 2007 August 1]. URL: http://www.paladin-labs.com/our_products/Antizol_en.pdf
[23] Davis DP, Bramwell KJ, Hamilton RS, Williams SR. Ethylene glycol poisoning: case report of a record-high level and a review. J Emerg Med 1997 Sep-Oct; 15 (5): 653-67.
[24] Harati Y, Niakan E. Hydrazine toxicity, pyridoxine therapy, and peripheral neuropathy. [Letter] Ann Intern Med 1986 May; 104 (5): 728-9.
[25] Albin RL, Albers JW, Greenberg HS, Townsend JB, Lynn RB, Burke JM Jr, Alessi AG. Acute sensory neuropathy-neuronopathy from pyridoxine overdose. Neurology 1987 Nov; 37 (11): 1729-32.
[26] Albin RL, Albers JW. Long-term follow-up of pyridoxine-induced acute sensory neuropathy-neuronopathy. Neurology 1990 Aug; 40 (8): 1319.
[27] Jacobsen D, Hewlett TP, Webb R, Brown ST, Ordinario AT, McMartin KE. Ethylene glycol intoxication: evaluation of kinetics and crystalluria. Am J Med 1988 Jan; 84 (1): 145-52.
[28] Peterson CD, Collins AJ, Himes JM, Bullock ML, Keane WF. Ethylene glycol poisoning: pharmacokinetics during therapy with ethanol and hemodialysis. N Engl J Med 1981 Jan 1; 304 (1): 21-3.
[29] Jacobsen D, Ostby N, Bredesen JE. Studies on ethylene glycol poisoning. Acta Med Scand 1982; 212 (1-2): 11-5.
[30] DaRoza R, Henning RJ, Sunshine I, Sutheimer C. Acute ethylene glycol poisoning. Crit Care Med 1984 Nov; 12 (11): 1003-5.
[31] Sivilotti ML, Burns MJ, McMartin KE, Brent J. Toxicokinetics of ethylene glycol during fomepizole therapy: implications for management. For the Methylpyrazole for Toxic Alcohols Study Group. Ann Emerg Med 2000 Aug; 36 (2): 114-25.
[32] Hantson P, Hassoun A, Mahieu P. Ethylene glycol poisoning treated by intravenous 4-methylpyrazole. Intensive Care Med 1998 Jul; 24 (7): 736-9.
[33] Gabow PA, Clay K, Sullivan JB, Lepoff R. Organic acids in ethylene glycol intoxication. Ann Intern Med 1986 Jul; 105 (1): 16-20.
[34] Blakeley KR, Rinner SE, Knochel JP. Survival of ethylene glycol poisoning with profound acidemia. [Letter] N Engl J Med 1993 Feb 18; 328 (7): 515-6.
[35] Hylander B, Kjellstrand CM. Prognostic factors and treatment of severe ethylene glycol intoxication. Intensive Care Med 1996 Jun; 22 (6): 546-52.
[36] Jacobsen D, McMartin KE. Methanol and ethylene glycol poisonings. Mechanism of toxicity, clinical course, diagnosis and treatment. Med Toxicol 1986 Sep-Oct; 1 (5): 309-34.
[37] Ford MD, McMartin K. Ethylene glycol and methanol. In: Ford MD, Delaney KA, Ling LJ, Erickson T, editors. Clinical toxicology. 1st ed. Philadelphia (PA): WB Saunders Company; 2001. p. 757-67.
[38] Jolliff HA, Sivilotti ML. Ethylene glycol. In: Dart RC editor. Medical toxicology. 3rd ed. Philadelphia (PA): Lippincott Williams & Wilkins; 2004. p. 1223-30.
[39] Haddad LM, Shannon MW, Winchester JF, editors. Clinical management of poisoning and drug overdose. 3rd ed. Philadelphia (PA): WB Saunders Company; 1998. p. 497-500.
[40] BERMAN LB, SCHREINER GE, FEYS J. The nephrotoxic lesion of ethylene glycol. Ann Intern Med 1957 Mar; 46 (3): 611-9.
[41] Curtin L, Kraner J, Wine H, Savitt D, Abuelo JG. Complete recovery after massive ethylene glycol ingestion. Arch Intern Med 1992 Jun; 152 (6): 1311-3.
[42] Factor SA, Lava NS. Ethylene glycol intoxication: a new stage in the clinical syndrome. N Y State J Med 1987 Mar; 87 (3): 179-80.
[43] Wills JH, Coulston F, Harris ES, McChesney EW, Russell JC, Serrone DM. Inhalation of aerosolized ethylene glycol by man. Clin Toxicol 1974; 7 (5): 463-76.
[44] Clayton GD, Clayton FE, editors. Patty’s industrial hygiene and toxicology. 4th ed. New York: John Wiley & Sons; 1994. Volume II, p. 4650.
[45] Rietschel RL, Fowler JF. Fisher's contact dermatitis. 4th ed. Baltimore (MD): Williams & Wilkins: 1995. p. 622.
[46] Grant WM, Schuman JS. Toxicology of the eye. 4th ed. Springfield (IL): Charles C Thomas; 1993. p. 663-9.
[47] FRIEDMAN EA, GREENBERG JB, MERRILL JP, DAMMIN GJ. Consequences of ethylene glycol poisoning. Report of four cases and review of the literature. Am J Med 1962 Jun; 32 (): 891-902.
[48] Vale JA, Bluett NH, Widdop B. Ethylene glycol poisoning. Postgrad Med J 1976 Sep; 52 (611): 598-602.
[49] Hantson P, Vanbinst R, Mahieu P. Determination of ethylene glycol tissue content after fatal oral poisoning and pathologic findings. Am J Forensic Med Pathol 2002 Jun; 23 (2): 159-61.
[50] Karlson-Stiber C, Persson H. Ethylene glycol poisoning: experiences from an epidemic in Sweden. J Toxicol Clin Toxicol 1992; 30 (4): 565-74.
[51] Parry MF, Wallach R. Ethylene glycol poisoning. Am J Med 1974 Jul; 57 (1): 143-50.
[52] Huhn KM, Rosenberg FM. Critical clue to ethylene glycol poisoning. CMAJ 1995 Jan 15; 152 (2): 193-5.
[53] Reddy NJ, Lewis LD, Gardner TB, Osterling W, Eskey CJ, Nierenberg DW. Two cases of rapid onset Parkinson's syndrome following toxic ingestion of ethylene glycol and methanol. Clin Pharmacol Ther 2007 Jan; 81 (1): 114-21.
[54] Mallya KB, Mendis T, Guberman A. Bilateral facial paralysis following ethylene glycol ingestion. Can J Neurol Sci 1986 Nov; 13 (4): 340-1.
[55] Morgan BW, Ford MD, Follmer R. Ethylene glycol ingestion resulting in brainstem and midbrain dysfunction. J Toxicol Clin Toxicol 2000; 38 (4): 445-51.
[56] Fellman DM. Facial diplegia following ethylene glycol ingestion. [Letter] Arch Neurol 1982 Nov; 39 (11): 739-40.
[57] Palmer BF, Eigenbrodt EH, Henrich WL. Cranial nerve deficit: a clue to the diagnosis of ethylene glycol poisoning. Am J Med 1989 Jul; 87 (1): 91-2.
[58] Leth PM, Gregersen M. Ethylene glycol poisoning. Forensic Sci Int 2005 Dec 20; 155 (2-3): 179-84.
[59] Catchings TT, Beamer WC, Lundy L, Prough DS. Adult respiratory distress syndrome secondary to ethylene glycol ingestion. Ann Emerg Med 1985 Jun; 14 (6): 594-6.
[60] Piagnerelli M, Lejeune P, Vanhaeverbeek M. Diagnosis and treatment of an unusual cause of metabolic acidosis: ethylene glycol poisoning. Acta Clin Belg 1999 Dec; 54 (6): 351-6.
[61] Verrilli MR, Deyling CL, Pippenger CE, Van Lente F, Vidt DG, Sivak ED. Fatal ethylene glycol intoxication. Report of a case and review of the literature. Cleve Clin J Med 1987 Jul-Aug; 54 (4): 289-95.
[62] TRIOSI FM. Chronic intoxication by ethylene glycol vapour. Br J Ind Med 1950 Apr; 7 (2): 65-9.
[63] Jobard E, Harry P, Turcant A, Roy PM, Allain P. 4-Methylpyrazole and hemodialysis in ethylene glycol poisoning. J Toxicol Clin Toxicol 1996; 34 (4): 373-7.
[64] Rasic S, Cengic M, Golemac S, Macanovic M. Acute renal insufficiency after poisoning with ethylene glycol. [Letter] Nephron 1999 Jan; 81 (1): 119-20.
[65] Jacobsen D, McMartin K. 4-Methylpyrazole--present status. [Editorial] J Toxicol Clin Toxicol 1996; 34 (4): 379-81.
[66] Brent J. Fomepizole for ethylene glycol and methanol poisoning. N Engl J Med 2009 May 21; 360 (21): 2216-23.
[67] Kralova I, Stepanek Z, Dusek J. Ethylene glycol intoxication misdiagnosed as eclampsia. Acta Anaesthesiol Scand 2006 Mar; 50 (3): 385-7.
[68] Eder AF, McGrath CM, Dowdy YG, Tomaszewski JE, Rosenberg FM, Wilson RB, Wolf BA, Shaw LM. Ethylene glycol poisoning: toxicokinetic and analytical factors affecting laboratory diagnosis. Clin Chem 1998 Jan; 44 (1): 168-77.
[69] Denning DW, Berendt A, Chia Y, Morgan SH. Myocarditis complicating ethylene glycol poisoning in the absence of neurological features. Postgrad Med J 1988 Nov; 64 (757): 867-70.
[70] Amathieu R, Merouani M, Borron SW, Lapostolle F, Smail N, Adnet F. Prehospital diagnosis of massive ethylene glycol poisoning and use of an early antidote. Resuscitation 2006 Aug; 70 (2): 285-6.
[71] Collins JM, Hennes DM, Holzgang CR, Gourley RT, Porter GA. Recovery after prolonged oliguria due to ethylene glycol intoxication. The prognostic value of serial, percutaneous renal biopsy. Arch Intern Med 1970 Jun; 125 (6): 1059-62.
[72] Bobbitt WH, Williams RM, Freed CR. Severe ethylene glycol intoxication with multisystem failure. West J Med 1986 Feb; 144 (2): 225-8.
[73] Ahmed MM. Ocular effects of antifreeze poisoning. Br J Ophthalmol 1971 Dec; 55 (12): 854-5.
[74] Delany C, Jay WM. Papilledema and abducens nerve palsy following ethylene glycol ingestion. Semin Ophthalmol 2004 Sep-Dec; 19 (3-4): 72-4.
[75] Troisi FM. Chronic intoxication by ethylene glycol vapour. Br J Ind Med 1950; 7: 65-6.
[76] Clay KL, Murphy RC. On the metabolic acidosis of ethylene glycol intoxication. Toxicol Appl Pharmacol 1977 Jan; 39 (1): 39-49.
[77] Bove KE. Ethylene glycol toxicity. Am J Clin Pathol 1966 Jan; 45 (1): 46-50.
[78] Lewis RJ. Sax's dangerous properties of industrial materials. 9th ed. New York: Van Nostrand Reinhold; 1996. p. 1548-9.
[79] Johnson B, Meggs WJ, Bentzel CJ. Emergency department hemodialysis in a case of severe ethylene glycol poisoning. Ann Emerg Med 1999 Jan; 33 (1): 108-10.
[80] Stokes JB 3rd, Aueron F. Prevention of organ damage in massive ethylene glycol ingestion. JAMA 1980 May 23-30; 243 (20): 2065-6.
[81] Field DL. Acute ethylene glycol poisoning. [Letter] Crit Care Med 1985 Oct; 13 (10): 872-3.
[82] Widman C. A few cases of ethylene glycol intoxication. Acta Med Scand 1946; 126 (4-5): 295-305.
[83] Caravati EM, Erdman AR, Christianson G, Manoguerra AS, Booze LL, Woolf AD, Olson KR, Chyka PA, Scharman EJ, Wax PM, Keyes DC, Troutman WG. Ethylene glycol exposure: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila) 2005; 43 (5): 327-45.
[84] Boyer EW, Mejia M, Woolf A, Shannon M. Severe ethylene glycol ingestion treated without hemodialysis. Pediatrics 2001 Jan; 107 (1): 172-3.
[85] Hatchett R. A severe and fatal case of ethylene glycol poisoning. Intensive Crit Care Nurs 1993 Sep; 9 (3): 183-90.
[86] Bates N, Rawson-Harris P, Edwards N. Common questions in veterinary toxicology. J Small Anim Pract 2015 May; 56 (5): 298-306.
[87] Concise International Chemical Assessment Document 45: Ethylene glycol: Human health aspects. World Health Organization; 2002. p. 12.
[88] O'Neil M, editor. The Merck index. 14th ed. Whitehouse Station (NJ): Merck & Co; 2006. p. 650-1.
[89] Booth NH, McDonald LE, editors. Veterinary pharmacology and therapeutics. 5th ed. Ames (IA): The Iowa State University Press, 1982. p. 969-72.
[90] Sharma AN. Toxic Alcohols. In: Goldfrank LR, Flomenbaum NE, Lewin NA, et al. Goldfrank's toxicologic emergencies. 7th ed. New York (NY): McGraw-Hill; 2002. p. 980-90.
[91] Darchy B, Abruzzese L, Pitiot O, Figueredo B, Domart Y. Delayed admission for ethylene glycol poisoning: lack of elevated serum osmol gap. Intensive Care Med 1999 Aug; 25 (8): 859-61.
[92] Smithline N, Gardner KD Jr. Gaps--anionic and osmolal. JAMA 1976 Oct 4; 236 (14): 1594-7.
[93] Hoffman RS, Smilkstein MJ, Howland MA, Goldfrank LR. Osmol gaps revisited: normal values and limitations. J Toxicol Clin Toxicol 1993; 31 (1): 81-93.
[94] Winter SD, Pearson JR, Gabow PA, Schultz AL, Lepoff RB. The fall of the serum anion gap. Arch Intern Med 1990 Feb; 150 (2): 311-3.
[95] Lamb JC 4th, Maronpot RR, Gulati DK, Russell VS, Hommel-Barnes L, Sabharwal PS. Reproductive and developmental toxicity of ethylene glycol in the mouse. Toxicol Appl Pharmacol 1985 Oct; 81 (1): 100-12.
[96] Neeper-Bradley TL, Tyl RW, Fisher LC, Kubena MF, Vrbanic MA, Losco PE. Determination of a no-observed-effect level for developmental toxicity of ethylene glycol administered by gavage to CD rats and CD-1 mice. Fundam Appl Toxicol 1995 Aug; 27 (1): 121-30.
[97] Price CJ, Kimmel CA, Tyl RW, Marr MC. The developmental toxicity of ethylene glycol in rats and mice. Toxicol Appl Pharmacol 1985 Oct; 81 (1): 113-27.
[98] Baselt RC. Disposition of toxic drugs and chemicals in man. 5th ed. Foster City (CA): Chemical Toxicology Institute; 2000. p. 306-9.
[99] Clayton GD, Clayton FE, editors. Patty's industrial hygiene and toxicology. 4th ed. New York: John Wiley & Sons; 1994. Volume II, p. 4645-57.

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