Ethylene glycol intoxication Flashcards
(8 cards)
Which characteristics make EG particularly a deadly toxin
Sweet taste
Rapid absorption through the gastric mucosa
Small volume required for a lethal dose
What is the mechanism of toxicity of EG
Peak plasma concentration of EG are attained within 2-3 h of ingestion and the half-life in plasma is only 3 h
EG itself is only mildly toxic but is rapidly metabolised to more toxic metabolites which can persist for several days within the body
- EG and glycoaldehyde are considered to be principally responsible for the initial CNS signs, both as direct action of the toxin plus concurrent hyperosmolality
All metabolites seem to be cytotoxic to the renal tubular epithelium
Calcium binds with oxalate to form calcium oxalate crystals leading to crystalluria
What are the signs of stage 1 EG toxicity
Starts within 30 min of ingestion and can last up to 12 h
The signs principally relate to CNS
- nausea, vomiting
- depression
- incoordination and ataxia
- seizures and coma with more severe intoxications
Treatment is more likely to be successful if it is initiated at this stage
What are the signs of stage 2 EG toxicity
12-24 h after ingestion
Characterised by clinical signs associated with worsening AKI:
- anorexia
- vomiting
- diarhhea
- GI ulceration
- serum BUN and creatinine start to rise
What are the signs of stage 3 EG toxicity
Occurs after approximately 24 h with the development of oliguria and progression to anuric renal failure
Blood work reveals a high anion gap metabolic acidosis
Ionised hypocalcemia may be seen
Demonstrating fluorescence with a Wood’s lamp in the urine, on the cat’s paws and face may be an aid to diagnosis because fluorscent stains are frequently added to antifreeze substances
What would be your treatment plan for EG toxicity
Early recognition and aggressive treatment are key to the succesful management
Treatment within 6 h of ingestion has the best prospects of influencing outcome by disrupting the formation of toxic metabolites
Disruption of the metabolic pathways is achieved by inhibition of alcohol dehydrogenase activity using either:
- ethanol: 20% ethanol IV as a CRI
- loading dose: 1.3 ml/kg
- CRI: 0.42 ml/kg/h for 48h
- or, 5 ml of 20% ethanol/kg, IV, q6h for five treatments then q8h for four treatments
- fomepizole: 125 mg/kg, IV as a bolus then 31.25 mg/kg, IV, 12, 24 and 36h later
What is the prognosis for EG intoxication
For patients that develop anuric renal failure, the prognosis is grave unless peritoneal or hemodialysis is available
