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Emergency And Acute Medicine - Ethylene glycol poisoning
Basic description
Peak serum concentration occurs in 1–4 hr. The half-life is 2.5–4.5 hr, and less than 20% is excreted unchanged by the kidneys.
Ethylene glycol is metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase to acidic metabolites that ultimately form oxalic acid. Aldehyde and acid metabolites are directly toxic to the CNS, heart, and kidneys.
Etiology
Exposure is typically from ethylene-glycol–containing products such as antifreeze and certain solvents. The minimum reported lethal dose is approximately 30 mL of 100% ethylene glycol.
Diagnosis – signs and symptoms
Cardiovascular: tachycardia, bradycardia, dysrhythmias, hypertension, hypotension.
Cns: inebriation, irritability, ataxia, obtundation, coma, cerebral edema, seizures; may also have peripheral nervous system findings including cranial nerve abnormalities.
Gi: nausea, vomiting, abdominal pain.
Pulmonary: tachypnea, hyperventilation, Kussmaul respirations, pulmonary edema.
Renal: crystalluria and acute renal failure.
Three overlapping stages may be seen:
History
Intentional or unintentional ingestion may be reported. Consider this diagnosis even without a clear history when there is an unexplained high anion gap metabolic acidosis and/or an elevated, unexplained osmol gap.
Physical examination
Tachypnea and altered mental status are common.
Essential workup
Obtain a complete ingestion history. Draw the following simultaneously:
Diagnosis tests and interpretation
Calculate the anion gap: (Na⁺) − (Cl⁻ + HCO₃⁻); normal is approximately 8–12.
Calculate the osmol gap: measured osmolality − calculated osmolarity; an increased gap is generally >10.
Calculated osmolarity: 2(Na⁺) + glucose/18 + BUN/2.8 + ethanol (mg/dL)/4.6.
The osmol gap is most useful early after ingestion (and may be larger with concurrent ethanol ingestion, with less severe acidosis). A normal osmol gap does not exclude ethylene glycol poisoning, especially with late presentation when metabolites drive an anion gap acidosis.
Urinalysis may show envelope-shaped calcium oxalate crystals (specific but insensitive). Absence of crystals does not rule out exposure.
Wood lamp inspection of urine or gastric contents may show fluorescein from antifreeze, but this is insensitive and nonspecific.
Differential diagnosis
Elevated osmol gap: methanol, ethanol, isopropyl alcohol, mannitol/glycerin/propylene glycol/sorbitol, acetone/ammonia, propylene glycol.
Elevated anion gap metabolic acidosis: alcoholic ketoacidosis, toxic asphyxiants (e.g., cyanide/CO/H₂S), acetaminophen-related causes, antiretrovirals (NRTIs), toluene, metformin, uremia, DKA, iron/INH, lactic acidosis, salicylates, starvation ketosis, methanol, ethylene glycol.
Treatment
Prehospital care
Bring containers of suspected substances. Monitor airway and mental status. For dermal exposure, remove contaminated clothing/jewelry and irrigate with soap and water.
Initial stabilization and therapy
ABCs. Provide supplemental oxygen, cardiac monitoring, and IV access with 0.9% saline. For altered mental status, check glucose and consider dextrose, naloxone, and thiamine as appropriate.
Emergency department treatment and procedures
Pregnancy considerations
Fomepizole is class C in pregnancy. Ethanol is not recommended.
Pediatric considerations
Ethanol can cause significant CNS depression and hypoglycemia in children.
Medication
Activated charcoal: 1 g/kg PO.
Dextrose: D50W 25 g IV (peds: D25W 2–4 mL/kg).
Ethanol: oral (via NG) or IV 10% ethanol in D5W per dosing protocols; adjust during hemodialysis.
Fomepizole: 15 mg/kg IV load over 30 min, then 10 mg/kg q12h ×4 doses, then 15 mg/kg q12h until level <25 mg />L; dose adjustments required during hemodialysis.
Magnesium: 25–50 mg/kg IV once (max 2 g).
Naloxone: 2 mg IV/IM (peds: 0.1 mg/kg).
Pyridoxine: 100 mg daily for 2 days.
Sodium bicarbonate: 1–2 mEq/kg IV in D5W.
Thiamine: 100 mg daily for 2 days (peds: 50 mg).
Follow-up and disposition
Admission criteria
Admit all patients with significant suspected or confirmed ethylene glycol ingestion, even if initially asymptomatic. ICU admission is indicated for serious illness, metabolic acidosis, or renal failure. Transfer if fomepizole or hemodialysis is indicated but not available.
Discharge criteria
An asymptomatic patient with isolated exposure may be discharged only if ethylene glycol concentration is undetectable and there is no metabolic acidosis.
Follow-up recommendations
Psychiatric evaluation is indicated after intentional ingestion.
Clinical pearls and common pitfalls
An osmol gap <10 does not exclude ethylene glycol poisoning. treat early with fomepizole when the diagnosis is on table and confirm serum levels available. presentations may show only an osmol gap, while late anion gap. do use absence of urinary crystals or lack fluorescence under a wood lamp to rule out exposure. if confirmation, antidote availability, 24 /> hemodialysis capability is uncertain, transfer to a facility that has all of these resources.
Basic description
Peak serum concentration occurs in 1–4 hr. The half-life is 2.5–4.5 hr, and less than 20% is excreted unchanged by the kidneys.
Ethylene glycol is metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase to acidic metabolites that ultimately form oxalic acid. Aldehyde and acid metabolites are directly toxic to the CNS, heart, and kidneys.
Etiology
Exposure is typically from ethylene-glycol–containing products such as antifreeze and certain solvents. The minimum reported lethal dose is approximately 30 mL of 100% ethylene glycol.
Diagnosis – signs and symptoms
Cardiovascular: tachycardia, bradycardia, dysrhythmias, hypertension, hypotension.
Cns: inebriation, irritability, ataxia, obtundation, coma, cerebral edema, seizures; may also have peripheral nervous system findings including cranial nerve abnormalities.
Gi: nausea, vomiting, abdominal pain.
Pulmonary: tachypnea, hyperventilation, Kussmaul respirations, pulmonary edema.
Renal: crystalluria and acute renal failure.
Three overlapping stages may be seen:
- First stage (1–12 hr): CNS depression, GI symptoms, worsening acidosis, coma, seizures, cerebral edema, tetany or myoclonus from hypocalcemia.
- Second stage (12–36 hr): cardiopulmonary manifestations; many deaths occur in this period.
- Third stage (36–72 hr): oliguria, flank pain, acute renal failure.
History
Intentional or unintentional ingestion may be reported. Consider this diagnosis even without a clear history when there is an unexplained high anion gap metabolic acidosis and/or an elevated, unexplained osmol gap.
Physical examination
Tachypnea and altered mental status are common.
Essential workup
Obtain a complete ingestion history. Draw the following simultaneously:
- Arterial blood gas
- Serum ethylene glycol, methanol, isopropyl alcohol, and ethanol concentrations
- Electrolytes, BUN/creatinine, glucose
- Measured serum osmolality (freezing point depression)
- Serum calcium, phosphorus, magnesium
Diagnosis tests and interpretation
Calculate the anion gap: (Na⁺) − (Cl⁻ + HCO₃⁻); normal is approximately 8–12.
Calculate the osmol gap: measured osmolality − calculated osmolarity; an increased gap is generally >10.
Calculated osmolarity: 2(Na⁺) + glucose/18 + BUN/2.8 + ethanol (mg/dL)/4.6.
The osmol gap is most useful early after ingestion (and may be larger with concurrent ethanol ingestion, with less severe acidosis). A normal osmol gap does not exclude ethylene glycol poisoning, especially with late presentation when metabolites drive an anion gap acidosis.
Urinalysis may show envelope-shaped calcium oxalate crystals (specific but insensitive). Absence of crystals does not rule out exposure.
Wood lamp inspection of urine or gastric contents may show fluorescein from antifreeze, but this is insensitive and nonspecific.
Differential diagnosis
Elevated osmol gap: methanol, ethanol, isopropyl alcohol, mannitol/glycerin/propylene glycol/sorbitol, acetone/ammonia, propylene glycol.
Elevated anion gap metabolic acidosis: alcoholic ketoacidosis, toxic asphyxiants (e.g., cyanide/CO/H₂S), acetaminophen-related causes, antiretrovirals (NRTIs), toluene, metformin, uremia, DKA, iron/INH, lactic acidosis, salicylates, starvation ketosis, methanol, ethylene glycol.
Treatment
Prehospital care
Bring containers of suspected substances. Monitor airway and mental status. For dermal exposure, remove contaminated clothing/jewelry and irrigate with soap and water.
Initial stabilization and therapy
ABCs. Provide supplemental oxygen, cardiac monitoring, and IV access with 0.9% saline. For altered mental status, check glucose and consider dextrose, naloxone, and thiamine as appropriate.
Emergency department treatment and procedures
- Limit absorption: gastric lavage may be considered only in select cases (<1 hr since ingestion, coma, or reported large ingestion). activated charcoal may be given for coingestants but adsorbs ethylene glycol poorly.< />pan>
- Block toxic metabolism: initiate fomepizole promptly when a potentially toxic ingestion is suspected (intentional ingestion, more than a “sip,” or unexplained osmol gap and/or anion gap acidosis with concerning presentation). Do not wait for confirmatory levels if suspicion is high.
- Alternative antidote: ethanol is second-line if fomepizole is unavailable, targeting a serum ethanol level of 100–150 mg/dL, and continuing until ethylene glycol level is ~25 mg/dL.
- Adjunct cofactors: thiamine, pyridoxine, and magnesium may be given to support metabolism toward less toxic pathways (human outcome data are limited).
- Hemodialysis: use to accelerate clearance of ethylene glycol and metabolites. Consider for severe acidosis, persistent metabolic derangements, renal insufficiency, pulmonary edema, cerebral edema, or ethylene glycol concentration >25 mg/dL; continue until level approaches 25 mg/dL and acidosis resolves.
- Correct complications: ensure urine output with IV fluids. Use sodium bicarbonate for severe acidemia (commonly when pH <7.1) to maintain ph in the normal range. monitor and replace calcium as needed because oxalate formation can lower serum calcium.< />pan>
Pregnancy considerations
Fomepizole is class C in pregnancy. Ethanol is not recommended.
Pediatric considerations
Ethanol can cause significant CNS depression and hypoglycemia in children.
Medication
Activated charcoal: 1 g/kg PO.
Dextrose: D50W 25 g IV (peds: D25W 2–4 mL/kg).
Ethanol: oral (via NG) or IV 10% ethanol in D5W per dosing protocols; adjust during hemodialysis.
Fomepizole: 15 mg/kg IV load over 30 min, then 10 mg/kg q12h ×4 doses, then 15 mg/kg q12h until level <25 mg />L; dose adjustments required during hemodialysis.
Magnesium: 25–50 mg/kg IV once (max 2 g).
Naloxone: 2 mg IV/IM (peds: 0.1 mg/kg).
Pyridoxine: 100 mg daily for 2 days.
Sodium bicarbonate: 1–2 mEq/kg IV in D5W.
Thiamine: 100 mg daily for 2 days (peds: 50 mg).
Follow-up and disposition
Admission criteria
Admit all patients with significant suspected or confirmed ethylene glycol ingestion, even if initially asymptomatic. ICU admission is indicated for serious illness, metabolic acidosis, or renal failure. Transfer if fomepizole or hemodialysis is indicated but not available.
Discharge criteria
An asymptomatic patient with isolated exposure may be discharged only if ethylene glycol concentration is undetectable and there is no metabolic acidosis.
Follow-up recommendations
Psychiatric evaluation is indicated after intentional ingestion.
Clinical pearls and common pitfalls
An osmol gap <10 does not exclude ethylene glycol poisoning. treat early with fomepizole when the diagnosis is on table and confirm serum levels available. presentations may show only an osmol gap, while late anion gap. do use absence of urinary crystals or lack fluorescence under a wood lamp to rule out exposure. if confirmation, antidote availability, 24 /> hemodialysis capability is uncertain, transfer to a facility that has all of these resources.
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