DESCRIPTION
USES
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.
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INTERVENTION CRITERIA
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 All eye exposures 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 Ingestions with intent to harm Symptomatic patients All eye exposures Any patient showing signs or symptoms following skin or inhalational exposure should be assessed at a medical facility. |
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 Inebriation |
Patients accidentally ingesting ethylene glycol should be monitored for 4 hours and may then be discharged into the care of a reliable observer provided:  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) Serum electrolytes including: Calcium Chloride (required for anion gap calculation) Anion gap (elevated in later stages of poisoning) Arterial pH Serum bicarbonate Urinalysis including: Proteinuria Hematuria 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: either A history or suspicion of ethylene glycol ingestion plus any 2 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 or 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. |
Hospital admission is recommended: - For any patient with abnormal biochemistry - In all symptomatic cases Ensure the receiving hospital is able to provide: Advanced care/ICU facilities, and |
TREATMENT
TREATMENT SUMMARY
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 dsyrhythmia 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. Cranial nerve palsies may occur some 4 to 18 days following ingestion and usually spontaneously resolve over weeks to months without specific therapy. Co-factor replenishment with thiamine and pyridoxine is not necessary unless the patient is considered vitamin deficient (e.g. history of alcoholism). |
EMERGENCY STABILIZATION
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. |
CHILD Where the systolic blood pressure is below normal blood pressure ranges for the age group: Age (years) | Normal Systolic Blood Pressure (mmHg) | <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 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. |
Most toxic seizures are short-lived and often do not require intervention. Administer a benzodiazepine as first-line treatment to patients with seizure activity. 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.
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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. However, these may also be due to cerebral ischemia. As administration of dextrose may exacerbate ischemic injury, 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.
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Thiamine dose ADULT 100 mg IV |
Electrocardiograph Electrolytes including: Calcium Magnesium 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 Bicarbonate Serum ethylene glycol concentration |
DECONTAMINATION
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.
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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.
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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 jewellery. Wash the affected area thoroughly with soap and water until all of the contaminant is removed. |
SIGNS AND SYMPTOMS
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. 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. 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. Most deaths occur in this second phase. 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. Calcium oxalate crystals may be detected in the urine of some patients. Renal symptoms may last up to 45 days or more. In addition, cranial nerve palsies that develop in some patients may persist for weeks to months. Convulsions and coma are considered ominous signs. 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. |
Symptoms predominantly occur following ingestion of ethylene glycol. However, toxicity is also possible via dermal, intravenous and intramuscular routes.
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Onset/Duration of Symptoms |
Stage I: Neurological Phase 0.5 to 12 hours post-ingestion Inebriation Euphoria Nausea Vomiting Metabolic acidosis CNS depression Stage II: Cardiopulmonary Phase 12 to 24 hours post-ingestion Hypertension Tachycardia Severe metabolic acidosis Hyperventilation Hypoxia Adult respiratory distress syndrome (ARDS) Congestive heart failure Stage III: Renal Phase 24 to 72 hours post-ingestion Oliguria Acute tubular necrosis Renal failure Hematuria Proteinuria 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. |
| Mild Ethylene Glycol Toxicity | Moderate Ethylene Glycol Toxicity | Severe Ethylene Glycol Toxicity | Nausea Vomiting Inebriation Drowsiness | Mild metabolic acidosis Tachycardia Hypertension Hematuria Proteinuria | Pulmonary edema Congestive cardiac failure Anuria Hyperventilation Severe metabolic acidosis Seizures Multiple organ failure Coma Death |
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CHRONIC EFFECTS
Chronic exposures to ethylene glycol vapor may result in CNS abnormalities and lymphocytosis.
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Do Not Archive. This document is current on day of issue,
NZ: 18.May.2012 |
