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Ethylene Glycol

Ethylene Glycol
17.Nov.2018-Expires: 7 days - Do not archive

DESCRIPTION

SUBSTANCE NAME

Ethylene Glycol
 

SUBSTANCE CLASS

Glycol
 

USES

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

INTERVENTION CRITERIA

Intervention Level

Child

Medical assessment and observation in an emergency department is recommended for:
- Ingestions greater than a witnessed lick or exploratory taste (e.g. a small sip) of ethylene glycol
- Ingestions where the dose is unknown
- Symptomatic ingestions
- All eye exposures (if symptomatic following flushing)
- Significantly symptomatic patients (more than mild irritation) following skin or inhalation exposure
 

Adult

Medical assessment and observation in an emergency department is recommended for:
- Ingestions of greater than 10 mL of ethylene glycol
- Ingestions where the dose is unknown
- Exposures with intent to self-harm
- Symptomatic ingestions
- All eye exposures (if symptomatic following flushing)
- Significantly symptomatic patients (more than mild irritation) following skin or inhalation exposure
 

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:
Nausea
Vomiting
Drowsiness
Slurred speech
Stumbling or difficulty in moving
Confusion
Decreased urine output
 

Medical Observation

If medical observation is required the patient should be monitored until 8 hours post-exposure for the onset or worsening of symptoms. Patients co-ingesting ethanol should be monitored until 12 hours.
 
If the patient is asymptomatic at the end of the observation period, their venous bicarbonate concentration is greater or equal to 20 mmol/L (mEq/L) and their serum (or breath) ethanol concentration is zero (in adults), and any investigations have been carried out, they may be:
Discharged into the care of a reliable observer, or
Referred for psychological assessment if the overdose or exposure was with intent to self-harm
 

Investigations

Patients, particularly children, presenting within an hour of suspected ethylene glycol ingestion or those who have concurrently co-ingested ethanol may not have any abnormal surrogate markers of poisoning. In these instances, close observation and serial monitoring of acid-base profile and renal function status should be performed. Any development of early metabolic acidosis would be highly suggestive of recent ethylene glycol exposure.
 
Serum ethylene glycol concentration (where available)
Serum ethanol concentration (required for osmolar gap calculation)
Osmolar gap (elevated in early stages of poisoning)
Serum electrolytes including:
Sodium (required for anion gap calculation)
Chloride (required for anion gap calculation)
Bicarbonate (required for anion gap calculation)
Calcium
Potassium
Anion gap (elevated in later stages of poisoning)
Blood gas analysis including:
Serum pH
Creatinine and BUN
Urine output
Urinalysis including:
Proteinuria
Hematuria
Examination under UV light (Wood’s lamp) for fluorescence (present in many antifreeze solutions and with urinary elimination the urine will fluoresce when expose to UV light). A negative result does not completely rule out ethylene glycol exposure.
Microscopic examination for crystalluria (calcium oxalate crystals)
 
If a serum ethylene glycol concentration measurement is not available a presumptive diagnosis of poisoning may be based on:
 
either
 
A history or suspicion of ethylene glycol ingestion plus any 2 of the following;[1][2]
Arterial pH < 7.3
Serum bicarbonate < 20 mmol/L (20 mEq/L)
Osmolar gap > 10 mOsm/L
Presence of urinary oxalate crystals
 
or
 
A history or suspicion of ethylene glycol ingestion within the last 1 hour and osmolar gap > 10 mOsm/L
 
A serum ethylene glycol is the preferred investigation, but is often not readily available. A significant ethylene glycol ingestion may be inferred from an increased osmolar gap (in the early stages of intoxication) indicating a solute (glycol) load. However, a normal osmolar gap cannot rule out ethylene glycol exposure. Once the glycol is metabolized the osmolar gap will drop and may be replaced by an increased anion gap, indicating an increased organic acids (glycol metabolites) load, with an accompanying metabolic acidosis.
 
Presence in the urine of either fluorescein or calcium oxalate crystals indicates ethylene glycol exposure, but their absence does not exclude this poisoning. Calcium oxalate crystals may not be present until the later stages of intoxications. Fluorescein is rapidly eliminated by the kidneys and may have already been excreted prior to presentation. Also, the ingested ethylene glycol may not contain fluorescein. Care must be exercised when checking for fluorescence as plastic containers may exhibit some degree of fluorescence under a UV light. A glass container is preferable and previous experience with visualizing fluorescein containing urine is useful.
 

Admission Criteria

Admission to an intensive care environment is recommended when:
Ethylene glycol concentrations are > 20 mg/dL (3.2 mmol/L)
Those receiving antidotal therapy
Following symptoms occur
Coma
Seizures
Kidney injury
Hypotension
 
Ensure the receiving hospital is able to provide:
The specific antidotes (Ethanol or Fomepizole)
Advanced care/ICU facilities, and
 

TREATMENT

TREATMENT SUMMARY

Initial management includes airway protection and adequate minute ventilation, administration of IV fluids, treating seizures with benzodiazepines or barbiturates, and correcting hypoglycemia (unless rapid glucose screen indicates otherwise); concurrently administer thiamine and pyridoxine to support metabolism of ethylene glycol to less toxic products. Nasogastric aspiration may be performed within 1 hour of ingestion provided the airway is protected. Ethanol and fomepizole are effective antidotes and should be administered to patients as early as possible.[2] Hemodialysis is effective in excreting glycols and their toxic metabolites and should be considered in acute renal failure, severe metabolic acidosis, or if other indications are present. Doses of ethanol and fomepizole need to be increased during hemodialysis.[3][4]
 
Severe acidosis is ideally managed using extracorporeal techniques (e.g. hemodialysis). Intravenous sodium bicarbonate may be considered as an adjunctive treatment for severe acidosis. Hypocalcemia should only be reversed if cardiac dysrhythmia occurs (particularly QT prolongation), or seizures prove unresponsive to management. Hypoglycemia, hyperkalemia, and hypomagnesemia should be corrected. Calcium oxalate crystals may form in any organ with resultant multiorgan dysfunction/failure. The kidneys are often afflicted, resulting in acute kidney injury. There is also a risk of lung injury, and fluid balance will require careful monitoring. Stupor or coma indicates metabolic encephalopathy or cerebral edema.[5] Cranial nerve palsies may occur some 5 to 20 days following ingestion and usually spontaneously resolve over weeks to months without specific therapy.[6][7][8][9]
 
Eye exposures require a 15 minute irrigation with saline or water and if more than mild, resolving symptoms are present following irrigation, an 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
Decontamination
Ingestion
Eye
Inhalation
Skin
Antidote(s)
Enhanced Elimination
Supportive Care
Metabolic
Renal
Fluid and electrolytes
Neurologic
Cardiovascular
Hepatic
Respiratory
 

EMERGENCY STABILIZATION

Ensure Adequate Cardiopulmonary Function

Airway

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

Hypotension

Hypotension may be present due to gastrointestinal fluid loss and alcohol-induced vasodilation, and in such cases fluid replacement with a crystalloid should be performed, having regard to adequate urine output.
 
CHILD
Where the systolic blood pressure is below normal blood pressure ranges for the age group:[10]
 
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.
 
The intraosseous route can be used if IV access is difficult or delayed.
 
ADULT
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.
 
The intraosseous route can be used if IV access is difficult or delayed.
 

Seizure

Administer a benzodiazepine as first-line treatment to patients with seizure activity.[11]
 
Blood glucose concentration should be promptly determined. If the result indicates hypoglycemia, or is unobtainable, supplemental dextrose should be administered IV.
 
Check for hypoxia and electrolyte disturbances. Correct acid base and metabolic disturbances. Seizures due to ethylene glycol intoxication may prove unresponsive to standard management unless hypocalcemia is corrected.
 

Hypoglycemia

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.[12] However, these may also be due to cerebral ischemia. As administration of dextrose may exacerbate ischemic injury,[13] it is important to verify hypoglycemia with blood glucose measurement prior to use - unless this would lead to unacceptable delay in administration.
 
Thiamine
Must be administered to adult patients considered alcohol-dependent or malnourished.[2][14]
 
Thiamine dose
 
ADULT
100 mg IV
 

Emergency Monitoring

Blood pressure
ECG
Respiratory rate
Oxygen saturation
Serum ethylene glycol concentration (if available)
Serum ethanol concentration (used in calculation of osmolar gap)
Osmolar gap (elevated early in poisoning)
Electrolytes including:
Sodium (required for anion gap calculation)
Chloride (required for anion gap calculation)
Bicarbonate (required for anion gap calculation)
Calcium
Potassium
Anion gap (elevated later in poisoning)
Blood gas analysis including:
Serum pH
Creatinine and BUN
Urine output
Urinalysis including:
Proteinuria
Hematuria
Microscopic examination for crystalluria
Blood glucose
Liver function
 

DECONTAMINATION

Ingestion

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 hour) 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.

Eye

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.
 

Inhalation

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

Skin

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

ANTIDOTE(S)

Appropriate use of antidotes in glycol poisoning is essential. Ethanol has long been regarded as an effective intervention, is cheap and available but requires longer periods of monitoring due to the risk of ethanol intoxication. Fomepizole has proven efficacy,[15] but suffers the disadvantage of expense and may not be immediately available. Both effectively act (via different mechanisms) by inhibiting the role of alcohol dehydrogenase in ethylene glycol metabolism, 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. vitamin deficient patients).[2]
 
 

Ethanol

Indications

Ethanol is indicated if:[2]
- 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;
- 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)
Osmolar gap > 10 mosm/L
Presence of urinary oxalate crystals
 

Dose and Administration

For acceptable efficacy, the blood ethanol concentration should be maintained between 22 and 33 mmol/L (100 to 150 mg/dL).[2] 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.[16]
 
Loading Dose
Oral Ethanol Loading Dose
 
To calculate the loading dose of oral ethanol from common concentrations in spirits use the appropriate calculation below. The dose should be administered as a 20% or less solution (e.g. diluted with water or fruit juice).
 
Ethanol %
Dose (mL)
37/37.5%
body weight x 2.5
40%
body weight x 2.3
42%
body weight x 2.2
45%
body weight x 2.04
 
If the concentration of spirits does not match those in the above table the dose can be calculated by clicking here.
 
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).
 
 
Intravenous Ethanol Loading Dose
 
Concentrated ethanol solutions need to be diluted to prevent vascular damage, and reduce fluid load in pediatric patients or those suffering from cerebral edema. To convert concentrated ethanol formulations to 5 or 10% click here.
 
To reach the desired blood ethanol concentration of 22 to 33 mmol/L (100 to 150 mg/dL) administer:
5% v/v ethanol:
15 to 22.5 mL/kg over 30 minutes
10% v/v ethanol:
7.5 to 11.25 mL/kg over 30 minutes.
 
If you have w/v formulations please click here to convert to v/v
 
Maintenance Dose
Oral Ethanol Maintenance Dose
 
Ethanol %
Children (mL/h)
Adults (non-alcoholics) (mL/h)
Adults (alcoholics) (mL/h)
37%
0.61 x body weight
0.41 x body weight
0.82 x body weight
40%
0.57 x body weight
0.38 x body weight
0.76 x body weight
42%
0.54 x body weight
0.36 x body weight
0.72 x body weight
45%
0.5 x body weight
0.33 x body weight
0.67 x body weight
 
This should be administered as a 20% or less solution (e.g. diluted with water or fruit juice).
 
If the concentration of spirits does not match those in the above table the dose can be calculated by clicking here.
 
Intravenous Ethanol Maintenance Dose
 
Concentrated ethanol solutions need to be diluted to prevent vascular damage, and reduce fluid load in pediatric patients or those suffering from cerebral edema. To convert concentrated ethanol formulations to 5 or 10% click here.
 
5% v/v solution:
CHILD
4.5 mL/kg/h
ADULT
Non-alcoholic:
2.25 to 3 mL/kg/h
Alcoholic:
4.5 to 6 mL/kg/h
 
10 % v/v solution:
CHILD
2.25 mL/kg/h
ADULT
Non-alcoholic:
1.125 to 1.5 mL/kg/h
Alcoholic:
2.25 to 3 mL/kg/h
 
If you have w/v formulations please click here to convert to v/v.
 

Antidote Endpoint

Ethanol administration may be discontinued if ethylene glycol concentrations can no longer be detected or are less than 3.2 mmol/L (20 mg/dL) with a normalized arterial pH - this is likely to take 2 to 3 days given ethylene glycol's typical elimination half-life of around 17 hours in the presence of ethanol.[2]
 

Precautions

Hypoglycemia may occur, especially in children.[17] Once an infusion has been commenced blood glucose concentrations must be determined on a frequent basis (every 1 to 2 hours). It may be necessary to add dextrose to intravenous solutions, or give glucose if ethanol is being administered orally.
 
It is recommended that patients receiving ethanol therapy be monitored in an intensive care setting and any decline in respiratory drive countered with hyperventilation.[16]
 

Fomepizole

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, pregnant women, or those critically ill but lacking confirmation of poisoning. Its administration to pediatric patients avoids the disadvantages of ethanol (e.g. inebriation, hypoglycemia).[2]
 

Indications

Fomepizole is indicated if:[2]
 
- Plasma ethylene glycol concentration greater than 3.2 mmol/L (20 mg/dL) or;
- Recent ingestion of a toxic amount of ethylene glycol and presence of osmolar 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)
Osmolar gap > 10 mosm/L
Presence of urinary oxalate crystals
 
Particular indications:[2]
- Altered mental status
- Co-ingestion of other drugs that may cause CNS depression (e.g. opioids, sedatives, antidepressants, anticonvulsants, antihistamines, hypnotics, muscle relaxants)
- Patients taking disulfiram or metronidazole
- Hepatic disease
- Critically ill patients lacking confirmation of ethylene glycol toxicity
- Pregnancy
- Pediatric patients (avoids the inebriation and hypoglycemia that may occur with ethanol administration)
- Inability of local laboratory to measure repeated ethanol concentrations
- Lack of local availability of a facility to monitor the patient closely such as an intensive care unit
 

Dose and Administration

Child
There are no specific dosing recommendations for fomepizole in pediatric patients. Consultation with a medical toxicologist or a Poisons Center for dosing is recommended
 
Adult
Loading dose[3]
 
- 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[3]
 
- 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 patients with a normal pH and resolved signs of systemic toxicity.[3]
 

Adverse Effects

Abdominal pain, skin rash, nausea, headache, dizziness, and drowsiness have been reported following fomepizole use.[3]
 

Pyridoxine (Vitamin B6)

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 alcohol dependent patients who may have vitamin deficiencies.[2]
 

Dose and Administration

The formulation should be diluted at least 1 to 5.
 
ADULT
- 50 to 100 mg pyridoxine given as an IV infusion over 15 to 30 minutes every six hours
- Continue for two days[18]
 

Precautions

Profound peripheral neuropathy may occur after very large single doses[19] or a series of doses (for example a total of > 2 g/kg pyridoxine over a three day period).[20] The sensory (if not motor) disturbances are potentially irreversible.[21]
 

Thiamine

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 alcohol dependent patients who may have vitamin deficiencies.[2]
 

Dose and Administration

ADULT
- Administer 100 mg IV or IM thiamine every six hours
- Continue for two days[18]
 

SIGNS AND SYMPTOMS

Symptoms following ethylene glycol ingestion can be divided into three acute stages or phases.[22][23][6][24] The severity of these stages and their progression from one to the other often depends on the amount ingested and other circumstances (e.g. ethanol co-ingestion). Death can occur in any of the acute stages but most commonly the second stage.[18] Ethanol co-ingestion can delay the onset of toxic effects.[25] Low serum pH, decreased base excess, hyperkalemia at admission, seizures, and coma usually indicate a poor prognosis.[26]
 
Initial symptoms of ethylene glycol intoxication (0.5 to 12 hours after ingestion) are due to the direct toxicity of ethylene glycol. CNS effects predominate and include inebriation (without the alcohol odor on the breath), slurred speech, drowsiness, somnolence, hypotonia, hyporeflexia, ataxia, myoclonic jerks, and gastrointestinal upset. Mild metabolic acidosis may occur. In severe cases, seizures and coma may develop.[27][22][23][28][29][30][31][23][32]
 
In subsequent cardiopulmonary phases of intoxication (12 to 36 hours after ingestion), accumulation of acidic metabolites of ethylene glycol are responsible for the presenting abnormalities including high-anion gap metabolic acidosis and cardiopulmonary symptoms.[33][22][23][30] The anion and osmolar gaps are usually increased, but may be within normal parameters in some patients.[34][24][30] In significant poisonings, severe metabolic acidosis with compensatory hyperventilation or Kussmaul respirations can develop.[6][35][36] Tachycardia, mild hypertension followed by hypotension, 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.[23][37][38]
 
The renal phase of intoxication, beginning 24 to 48 hours after ingestion, is marked by oliguria, flank pain acute tubular necrosis, renal failure, and occasionally bone marrow suppression.[31][35][27] Hematuria and proteinuria are also possible.[27][39] In severe poisonings, renal failure may appear early and progress to anuria.[31][2] Renal symptoms may last up to 45 days or more.[18] Acute renal failure may prove permanent in a minority of cases.[25] Subacute cranial nerve palsies usually occur within 5 to 20 days and may persist for weeks to months.[6][7][8][9]
 
Inhalation of ethylene glycol can cause upper respiratory tract irritation. Systemic effects are not expected unless it has been heated or aerosolized.[40]
 
Eye exposure to vapors or direct contact with the liquid may lead to eye irritation;[41] significant eye injury would not be expected.
 
Brief or occasional skin exposure is unlikely to cause harm to the skin but prolonged or repeated exposure may lead to significant irritation and sensitivity.[42] Skin absorption is limited, and systemic effects are unlikely to develop.[43]
 

Routes of Exposure

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

Onset/Duration of Symptoms

There are three acute stages[23][32][34] and one sequelae stage[8][44][45][46][24][6] that may occur following ethylene glycol ingestion. Most deaths are reported in stage II but can occur at any of the stages.[47] The severity of these stages and their progression from one to the other often depends on the amount ingested and other circumstances (e.g. ethanol co-ingestion).
 
Stage I: Neurological Phase
0.5 to 12 hours post-ingestion
Inebriation
Nausea
Vomiting/hematemesis
Metabolic acidosis/elevated anion gap/elevates osmolar gap
Hypocalcemia
Calcium oxalate crystalluria
CNS depression
Coma
Stage II: Cardiopulmonary Phase
12 to 24 hours post-ingestion
Hypertension
Tachycardia
Tachypnea
Severe metabolic acidosis
Pulmonary edema
Congestive heart failure
Stage III: Renal Phase
24 to 72 hours post-ingestion
Proteinuria
Oliguria
Anuria
Acute tubular necrosis
Renal failure
Sequelae
Onset several (5 to 20) days after ingestion
Cranial nerve neuropathies
 

Severity of Poisoning

Mild Ethylene Glycol ToxicityModerate Ethylene Glycol ToxicitySevere Ethylene Glycol Toxicity
Nausea
Vomiting
Ataxia
Slurred speech
Confusion
Drowsiness
Mild metabolic acidosis
Tachycardia
Hypertension
Hypocalcemia
Calcium oxalate crystalluria
Oliguria
Hematuria
Proteinuria
Pulmonary edema
Anuria
Hyperventilation/Kussmaul respirations
Hyperkalemia
Elevated anion and osmolar gaps
Severe metabolic acidosis
Seizures
Acute kidney injury
Multiple organ failure
Cranial nerve defects
Coma
Death
 

CHRONIC EFFECTS

General Effects

Chronic exposures to ethylene glycol vapor may result in nystagmus, unconsciousness, and lymphocytosis.[48]
 

REFERENCES

 
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[2] 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.
[3] Antizol Prescribing Information, USA: Paladin Labs (USA) Inc; May 2017; [cited 2018 January 4]. URL: http://www.paladin-labs.com/our_products/Antizol_en.pdf
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[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.
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[12] Wallis WE, Donaldson I, Scott RS, Wilson J. Hypoglycemia masquerading as cerebrovascular disease (hypoglycemic hemiplegia). Ann Neurol 1985 Oct; 18 (4): 510-2.
[13] Browning RG, Olson DW, Stueven HA, Mateer JR. 50% dextrose: antidote or toxin? Ann Emerg Med 1990 Jun; 19 (6): 683-7.
[14] Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. Intern Med J 2014 Sep; 44 (9): 911-5.
[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] 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.
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[18] 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.
[19] Harati Y, Niakan E. Hydrazine toxicity, pyridoxine therapy, and peripheral neuropathy. [Letter] Ann Intern Med 1986 May; 104 (5): 728-9.
[20] 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.
[21] Albin RL, Albers JW. Long-term follow-up of pyridoxine-induced acute sensory neuropathy-neuronopathy. Neurology 1990 Aug; 40 (8): 1319.
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[23] BERMAN LB, SCHREINER GE, FEYS J. The nephrotoxic lesion of ethylene glycol. Ann Intern Med 1957 Mar; 46 (3): 611-9.
[24] 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.
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