In the US, ethylene glycol is the main component of all radiator fluid products. It raises the boiling point and lowers the freezing point of the fluid that passes through the radiator of an automobile.
The colliding properties of the solute cause these variations in the freezing and boiling points. The addition of ethylene glycol keeps the radiator from freezing or overheating depending on the season.
A common addition to radiator fluid is fluorescein dye, which aids mechanics in pinpointing the location of a radiator leak. The fluid’s fluorescein fluoresces when exposed to ultraviolet light.
Some animals are drawn to ethylene glycol because of its sweet flavour. Due to the frequent incidences of ethylene glycol toxicity in dogs and cats that have lapped up radiator fluid, many vets are familiar with this condition.
For both people and animals, ethylene glycol is extremely poisonous if consumed, breathed, or absorbed through the skin.
Ethylene glycol’s main source of toxicity is its metabolic metabolites, which are created after consumption rather than the parent substance itself.
Unmetabolized ethylene glycol causes CNS depression, intoxication, and hyperosmolality that are comparable to those caused by ethanol between 30 minutes and 12 hours after exposure.
Severe anion gap metabolic acidosis with compensatory hyperventilation is caused by ethylene glycol metabolites between 12 and 48 hours.
Epidemiology
In US emergency rooms, ethylene glycol is a quite frequent cause of overdose. In 2022, the American Association of Poison Control Centers received 6079 reports of individual exposures to ethylene glycol found in antifreeze and other vehicle products.
There were 8 recorded deaths, 90 significant outcomes, 352 moderate outcomes, and 901 minor outcomes.
With 4280 single case exposures, ethylene glycol exposure was most prevalent in adults as in prior years while children under the age of six had 424 single case exposures, those age between 6 to 12 had 126, and those age between 13 to 19 had 483.
The AAPCC also recorded 566 isolated exposures to ethylene glycol that did not include a boat, airplane, or automobile, resulting in 13 fatalities and 50 serious consequences.
Anatomy
Pathophysiology
Even while ethylene glycol is a reasonably harmless substance before it is digested, it may nevertheless produce some mental state changes.
The liver and stomach mucosa contain the enzyme alcohol dehydrogenase (ADH), which breaks down ethanol. The cytochrome P-450 mixed function oxidase (MFO) system in the liver is an extra pathway.
Ethylene glycol is then converted to glycolic acid (GA) via interaction with aldehyde dehydrogenase, which builds up and may result in a severe metabolic acidosis.
Blood and other tissues can develop and collect crystals of calcium oxalate. The precipitation of calcium oxalate in the renal cortex causes kidney insufficiency and a reduction in glomerular filtration.
The ADH-catalysed step in the metabolism of ethylene glycol is the rate-limiting step. Ethylene glycol and methanol do not attach to ADH as readily as common ethyl alcohol (ethanol).
Etiology
Causes of ethylene glycol toxicity are as follows:
Suicide attempts
Workplace beverage-container mix-ups
Industrial exposures
Unintentional ingestions
Genetics
Prognostic Factors
Ethylene glycol intake is another important predictor of outcome; higher intakes are linked to more severe metabolic acidosis, kidney damage, and an increased chance of death.
A high anion gap and low serum bicarbonate levels are indicative of the degree of metabolic acidosis, which is thought to be a sensitive measure of severity and is associated with worse outcomes.
An increased risk of renal damage is suggested by the presence of calcium oxalate crystals in the urine, especially monohydrate forms, which show considerable ethylene glycol metabolism.
Clinical History
Collect details including the timing of ingestion, quantity ingested, initial, delayed, and late symptoms to understand clinical history of patients.
Physical Examination
Neurological examination
Respiratory examination
Cardiovascular examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Depending on the amount consumed, the presence of co-ingestants such as ethanol, and individual metabolic variances, the onset of clinical characteristics usually happens within 30 minutes to 12 hours.
Acute symptoms are:
CNS depression, confusion, drowsiness, or ataxia
Differential Diagnoses
Metabolic Acidosis in Emergency Medicine
Alcohol Toxicity
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Determine as much precise information as you can about the ingestion’s identity and time.
If at all feasible, get a digital picture of the substance that was consumed or the bottle or container that contained it. It could be useful to interview those who were there at the ingestion site.
Important information about the patient’s clinical features and the identity of the chemical or chemicals involved can frequently be obtained from the prehospital (EMS) staff.
Nasogastric lavage and activated charcoal are ineffective in treating toxic alcohol poisoning because the alcohols are usually absorbed too quickly for them to be effective.
Give crystalloids intravenously (IV) at a rate of 250–500 mL/h at first to improve renal clearance of the toxin and prevent oxalate deposition in the renal cortices.
Pyridoxine and thiamine are safe adjuncts with no notable drawbacks that aid in the metabolism of ethylene glycol by promoting the generation of benign metabolites.
Promote the use of chemicals that give ethylene glycol a bitter taste to prevent inadvertent intake.
Observe local hazardous waste requirements when disposing of used or surplus antifreeze and related substances.
Describe the correct way to handle and store industrial and automotive chemicals.
Regularly inspect industries to make sure safety regulations should be followed.
Proper awareness about ethylene glycol toxicity should be provided and its related causes with management strategies.
Appointments with specialists and preventing recurrence of disorder is an ongoing life-long effort.
Use of Antidotes
Fomepizole:
Alcohol dehydrogenase is competitively inhibited by antizol (fomepizole). The conversion of ethanol to acetaldehyde is catalysed by alcohol dehydrogenase.
Ethanol:
It inhibits the synthesis of harmful metabolites by competing methanol and ethylene glycol for alcohol dehydrogenase.
Use of Nutrients
Pyridoxine:
A cofactor in the transformation of glycolic acid into non-oxalate molecules is water-soluble vitamin B6. It actively participates in the central nervous system’s GABA production.
Thiamine:
It promotes the conversion of glyoxylate into alpha-hydroxy-beta-ketoadipate.
Hemodialysis is most important procedures used in situations of ethylene glycol toxicity.
An ethylene glycol poisoning patient exhibiting symptoms of cardiogenic shock has been successfully treated with extracorporeal membrane oxygenation (ECMO).
In the US, ethylene glycol is the main component of all radiator fluid products. It raises the boiling point and lowers the freezing point of the fluid that passes through the radiator of an automobile.
The colliding properties of the solute cause these variations in the freezing and boiling points. The addition of ethylene glycol keeps the radiator from freezing or overheating depending on the season.
A common addition to radiator fluid is fluorescein dye, which aids mechanics in pinpointing the location of a radiator leak. The fluid’s fluorescein fluoresces when exposed to ultraviolet light.
Some animals are drawn to ethylene glycol because of its sweet flavour. Due to the frequent incidences of ethylene glycol toxicity in dogs and cats that have lapped up radiator fluid, many vets are familiar with this condition.
For both people and animals, ethylene glycol is extremely poisonous if consumed, breathed, or absorbed through the skin.
Ethylene glycol’s main source of toxicity is its metabolic metabolites, which are created after consumption rather than the parent substance itself.
Unmetabolized ethylene glycol causes CNS depression, intoxication, and hyperosmolality that are comparable to those caused by ethanol between 30 minutes and 12 hours after exposure.
Severe anion gap metabolic acidosis with compensatory hyperventilation is caused by ethylene glycol metabolites between 12 and 48 hours.
In US emergency rooms, ethylene glycol is a quite frequent cause of overdose. In 2022, the American Association of Poison Control Centers received 6079 reports of individual exposures to ethylene glycol found in antifreeze and other vehicle products.
There were 8 recorded deaths, 90 significant outcomes, 352 moderate outcomes, and 901 minor outcomes.
With 4280 single case exposures, ethylene glycol exposure was most prevalent in adults as in prior years while children under the age of six had 424 single case exposures, those age between 6 to 12 had 126, and those age between 13 to 19 had 483.
The AAPCC also recorded 566 isolated exposures to ethylene glycol that did not include a boat, airplane, or automobile, resulting in 13 fatalities and 50 serious consequences.
Even while ethylene glycol is a reasonably harmless substance before it is digested, it may nevertheless produce some mental state changes.
The liver and stomach mucosa contain the enzyme alcohol dehydrogenase (ADH), which breaks down ethanol. The cytochrome P-450 mixed function oxidase (MFO) system in the liver is an extra pathway.
Ethylene glycol is then converted to glycolic acid (GA) via interaction with aldehyde dehydrogenase, which builds up and may result in a severe metabolic acidosis.
Blood and other tissues can develop and collect crystals of calcium oxalate. The precipitation of calcium oxalate in the renal cortex causes kidney insufficiency and a reduction in glomerular filtration.
The ADH-catalysed step in the metabolism of ethylene glycol is the rate-limiting step. Ethylene glycol and methanol do not attach to ADH as readily as common ethyl alcohol (ethanol).
Causes of ethylene glycol toxicity are as follows:
Suicide attempts
Workplace beverage-container mix-ups
Industrial exposures
Unintentional ingestions
Ethylene glycol intake is another important predictor of outcome; higher intakes are linked to more severe metabolic acidosis, kidney damage, and an increased chance of death.
A high anion gap and low serum bicarbonate levels are indicative of the degree of metabolic acidosis, which is thought to be a sensitive measure of severity and is associated with worse outcomes.
An increased risk of renal damage is suggested by the presence of calcium oxalate crystals in the urine, especially monohydrate forms, which show considerable ethylene glycol metabolism.
Collect details including the timing of ingestion, quantity ingested, initial, delayed, and late symptoms to understand clinical history of patients.
Neurological examination
Respiratory examination
Cardiovascular examination
Depending on the amount consumed, the presence of co-ingestants such as ethanol, and individual metabolic variances, the onset of clinical characteristics usually happens within 30 minutes to 12 hours.
Acute symptoms are:
CNS depression, confusion, drowsiness, or ataxia
Metabolic Acidosis in Emergency Medicine
Alcohol Toxicity
Determine as much precise information as you can about the ingestion’s identity and time.
If at all feasible, get a digital picture of the substance that was consumed or the bottle or container that contained it. It could be useful to interview those who were there at the ingestion site.
Important information about the patient’s clinical features and the identity of the chemical or chemicals involved can frequently be obtained from the prehospital (EMS) staff.
Nasogastric lavage and activated charcoal are ineffective in treating toxic alcohol poisoning because the alcohols are usually absorbed too quickly for them to be effective.
Give crystalloids intravenously (IV) at a rate of 250–500 mL/h at first to improve renal clearance of the toxin and prevent oxalate deposition in the renal cortices.
Pyridoxine and thiamine are safe adjuncts with no notable drawbacks that aid in the metabolism of ethylene glycol by promoting the generation of benign metabolites.
Emergency Medicine
Promote the use of chemicals that give ethylene glycol a bitter taste to prevent inadvertent intake.
Observe local hazardous waste requirements when disposing of used or surplus antifreeze and related substances.
Describe the correct way to handle and store industrial and automotive chemicals.
Regularly inspect industries to make sure safety regulations should be followed.
Proper awareness about ethylene glycol toxicity should be provided and its related causes with management strategies.
Appointments with specialists and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Fomepizole:
Alcohol dehydrogenase is competitively inhibited by antizol (fomepizole). The conversion of ethanol to acetaldehyde is catalysed by alcohol dehydrogenase.
Ethanol:
It inhibits the synthesis of harmful metabolites by competing methanol and ethylene glycol for alcohol dehydrogenase.
Emergency Medicine
Pyridoxine:
A cofactor in the transformation of glycolic acid into non-oxalate molecules is water-soluble vitamin B6. It actively participates in the central nervous system’s GABA production.
Thiamine:
It promotes the conversion of glyoxylate into alpha-hydroxy-beta-ketoadipate.
Emergency Medicine
Hemodialysis is most important procedures used in situations of ethylene glycol toxicity.
An ethylene glycol poisoning patient exhibiting symptoms of cardiogenic shock has been successfully treated with extracorporeal membrane oxygenation (ECMO).
In the initial stabilization phase, the goal is to airway, breathing, circulation (ABCs) are assessed and stabilized.
In the diagnostic phase, the goal is to rapid assessment based on history, physical examination, and laboratory tests.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional procedures.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
In the US, ethylene glycol is the main component of all radiator fluid products. It raises the boiling point and lowers the freezing point of the fluid that passes through the radiator of an automobile.
The colliding properties of the solute cause these variations in the freezing and boiling points. The addition of ethylene glycol keeps the radiator from freezing or overheating depending on the season.
A common addition to radiator fluid is fluorescein dye, which aids mechanics in pinpointing the location of a radiator leak. The fluid’s fluorescein fluoresces when exposed to ultraviolet light.
Some animals are drawn to ethylene glycol because of its sweet flavour. Due to the frequent incidences of ethylene glycol toxicity in dogs and cats that have lapped up radiator fluid, many vets are familiar with this condition.
For both people and animals, ethylene glycol is extremely poisonous if consumed, breathed, or absorbed through the skin.
Ethylene glycol’s main source of toxicity is its metabolic metabolites, which are created after consumption rather than the parent substance itself.
Unmetabolized ethylene glycol causes CNS depression, intoxication, and hyperosmolality that are comparable to those caused by ethanol between 30 minutes and 12 hours after exposure.
Severe anion gap metabolic acidosis with compensatory hyperventilation is caused by ethylene glycol metabolites between 12 and 48 hours.
In US emergency rooms, ethylene glycol is a quite frequent cause of overdose. In 2022, the American Association of Poison Control Centers received 6079 reports of individual exposures to ethylene glycol found in antifreeze and other vehicle products.
There were 8 recorded deaths, 90 significant outcomes, 352 moderate outcomes, and 901 minor outcomes.
With 4280 single case exposures, ethylene glycol exposure was most prevalent in adults as in prior years while children under the age of six had 424 single case exposures, those age between 6 to 12 had 126, and those age between 13 to 19 had 483.
The AAPCC also recorded 566 isolated exposures to ethylene glycol that did not include a boat, airplane, or automobile, resulting in 13 fatalities and 50 serious consequences.
Even while ethylene glycol is a reasonably harmless substance before it is digested, it may nevertheless produce some mental state changes.
The liver and stomach mucosa contain the enzyme alcohol dehydrogenase (ADH), which breaks down ethanol. The cytochrome P-450 mixed function oxidase (MFO) system in the liver is an extra pathway.
Ethylene glycol is then converted to glycolic acid (GA) via interaction with aldehyde dehydrogenase, which builds up and may result in a severe metabolic acidosis.
Blood and other tissues can develop and collect crystals of calcium oxalate. The precipitation of calcium oxalate in the renal cortex causes kidney insufficiency and a reduction in glomerular filtration.
The ADH-catalysed step in the metabolism of ethylene glycol is the rate-limiting step. Ethylene glycol and methanol do not attach to ADH as readily as common ethyl alcohol (ethanol).
Causes of ethylene glycol toxicity are as follows:
Suicide attempts
Workplace beverage-container mix-ups
Industrial exposures
Unintentional ingestions
Ethylene glycol intake is another important predictor of outcome; higher intakes are linked to more severe metabolic acidosis, kidney damage, and an increased chance of death.
A high anion gap and low serum bicarbonate levels are indicative of the degree of metabolic acidosis, which is thought to be a sensitive measure of severity and is associated with worse outcomes.
An increased risk of renal damage is suggested by the presence of calcium oxalate crystals in the urine, especially monohydrate forms, which show considerable ethylene glycol metabolism.
Collect details including the timing of ingestion, quantity ingested, initial, delayed, and late symptoms to understand clinical history of patients.
Neurological examination
Respiratory examination
Cardiovascular examination
Depending on the amount consumed, the presence of co-ingestants such as ethanol, and individual metabolic variances, the onset of clinical characteristics usually happens within 30 minutes to 12 hours.
Acute symptoms are:
CNS depression, confusion, drowsiness, or ataxia
Metabolic Acidosis in Emergency Medicine
Alcohol Toxicity
Determine as much precise information as you can about the ingestion’s identity and time.
If at all feasible, get a digital picture of the substance that was consumed or the bottle or container that contained it. It could be useful to interview those who were there at the ingestion site.
Important information about the patient’s clinical features and the identity of the chemical or chemicals involved can frequently be obtained from the prehospital (EMS) staff.
Nasogastric lavage and activated charcoal are ineffective in treating toxic alcohol poisoning because the alcohols are usually absorbed too quickly for them to be effective.
Give crystalloids intravenously (IV) at a rate of 250–500 mL/h at first to improve renal clearance of the toxin and prevent oxalate deposition in the renal cortices.
Pyridoxine and thiamine are safe adjuncts with no notable drawbacks that aid in the metabolism of ethylene glycol by promoting the generation of benign metabolites.
Emergency Medicine
Promote the use of chemicals that give ethylene glycol a bitter taste to prevent inadvertent intake.
Observe local hazardous waste requirements when disposing of used or surplus antifreeze and related substances.
Describe the correct way to handle and store industrial and automotive chemicals.
Regularly inspect industries to make sure safety regulations should be followed.
Proper awareness about ethylene glycol toxicity should be provided and its related causes with management strategies.
Appointments with specialists and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Fomepizole:
Alcohol dehydrogenase is competitively inhibited by antizol (fomepizole). The conversion of ethanol to acetaldehyde is catalysed by alcohol dehydrogenase.
Ethanol:
It inhibits the synthesis of harmful metabolites by competing methanol and ethylene glycol for alcohol dehydrogenase.
Emergency Medicine
Pyridoxine:
A cofactor in the transformation of glycolic acid into non-oxalate molecules is water-soluble vitamin B6. It actively participates in the central nervous system’s GABA production.
Thiamine:
It promotes the conversion of glyoxylate into alpha-hydroxy-beta-ketoadipate.
Emergency Medicine
Hemodialysis is most important procedures used in situations of ethylene glycol toxicity.
An ethylene glycol poisoning patient exhibiting symptoms of cardiogenic shock has been successfully treated with extracorporeal membrane oxygenation (ECMO).
In the initial stabilization phase, the goal is to airway, breathing, circulation (ABCs) are assessed and stabilized.
In the diagnostic phase, the goal is to rapid assessment based on history, physical examination, and laboratory tests.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional procedures.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
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