QUARTERLY BEAT / APRIL 2025
crisis, clinicopathologic monitoring is necessary every 3-4 days thereafter for 2-3 weeks, until bone marrow function returns to normal. 4-7
false positives for EG may be from other drugs such as propylene glycol, sorbitol, mannitol, alcohol, etc. Treatment for EG toxicosis includes antidote therapy, aggressive IV fluid therapy, monitoring urine output and clinicopathologic parameters, anti- emetic therapy, and symptomatic supportive care. The antidote, fomepizole (also known as 4-MP), is expensive but lifesaving when administered to dogs within the first 8-12 hours of ingestion. In cats, the antidote must be administered within 3 hours of ingestion to be effective. 8-9 Dosing for 4-MP is significantly different between dogs and cats. For dogs, the dose of 4-MP is: 20 mg/kg, IV, first dose; 15 mg/kg at 12 hours; 15 mg/kg at 24 hours; 5 mg/ kg at 36 hours. For cats, the dose of 4-MP is: 125 mg/kg, IV, first dose; 31.25 mg/kg IV at 12 hours; 31.25 mg/kg IV at 24 hours; 31.25 mg/kg at 36 hours. Ethanol can also be used as an antidote if fomepizole is not available, as it competes with alcohol dehydrogenase, thereby preventing metabolism of EG into its more toxic metabolites. A 7% of ethanol is made by removing 175 ml from a 1L bag of saline and adding 175 ml of an 80-proof vodka. If 190 proof grain alcohol is available, a 7% solution can be made by removing 74ml from a 1L bag of saline and adding 74 ml of the grain alcohol. Remember to use only “clear” alcohols on patients (e.g., grain alcohol, vodka, etc.). The dose of ethanol in dogs and cats is a loading dose of 8.6 ml/kg (600 mg/kg) 7% ethanol slow IV then continue with a CRI of 1.43 ml/kg/hr (100 mg/kg/hour) IV as a CRI for 24-36 hours. Regardless, antidote therapy must be started immediately to ensure good outcome. Once a patient has already developed azotemia, the prognosis is generally poor to grave without hemodialysis. EG toxicosis should be suspected in any patient with unexplained neurologic signs, metabolic acidosis or an elevated anion gap ((Na+ + K+) – (Bicarb + Cl-) >25). Any combination of these signs should prompt the administration of an EG blood test. The detection of calcium monohydrate oxalate crystalluria is virtually diagnostic for EG toxicosis. Be aware that ethylene glycol testing is only accurate within approximately the first 24 hours, as false negatives may be found thereafter due to complete metabolism of the EG to its more toxic metabolites. On veterinary specific EG tests, rare false positives for EG may be from other drugs such as propylene glycol, sorbitol, mannitol, alcohol, etc. ORGANOPHOSPHATES/CARBAMATES: Thankfully, carbamates and OPs are rarely seen now; the acutely seizing patient is rarely a result of this toxicosis nowadays. That’s likely a result of the Environmental Protection Agency (EPA) removing many of these dangerous insecticides off the market (replacing them with pyrethrins and pyrethroids instead). However, some products (particularly rose or plant fertilizer/insecticide combination products, cattle ear tags, etc.) still exist. 10-11 Add to the fact that gardeners often mix these dangerous chemicals with additional bone or blood meal (which is highly palatable to pets), thus resulting in increased ingestion of the toxin. Carbamates and OPs work by competitively inhibiting acetylcholinesterase and pseudocholinesterase (e.g., the enzymes that breaks down acetylcholine), which prevents
ETHYLENE GLYCOL (EG): Accidental or malicious poisoning with ethylene glycol (EG) is common, as the public is generally well aware of its toxic nature. Sources of EG include automotive antifreeze (radiator coolant, which typically contains 95% EG), windshield deicing agents, motor oils, hydraulic brake fluid, developer solutions, paints, solvents, etc. 8,9 As little as 4.4 ml/kg can result in severe acute kidney injury (AKI) in canine patients, while as little as 1.4 ml/kg can result in AKI in feline patients (based on high concentration EG products). 8,9 Ethylene glycol is metabolized by the body to highly poisonous metabolites (including glycoaldehyde, glycolic acid, and oxalic acid), which lead to severe AKI secondary to development of calcium oxalate crystalluria. 8,9
THREE STAGES OF ETHYLENE GLYCOL POISONING STAGE 1: This occurs within 30 minutes to 12 hours
and looks similar to alcohol poisoning. Signs of ataxia, hypersalivating, vomiting, seizuring, and polyuria/polydipsia are seen. 8,9
STAGE 2: This occurs within 12-24 hours post- exposure, 8 and clinical signs seem to
“resolve” to the pet owner; however, during this time frame, severe internal injury is still
occurring. Signs of ataxia may seem to improve during this stage, but signs of dehydration, tachycardia, and tachypnea may be seen. STAGE 3: In cats, this stage occurs 12-24 hours after
ethylene glycol exposure. 8,9 In dogs, this stage occurs 36-72 hours post-ingestion. 8 During this stage, severe AKI occurs secondary to calcium oxalate crystalluria. Severe anorexia, depression, hypersalivation, uremic halitosis, coma, vomiting, and seizures may be seen.
Any patient suspected of EG toxicosis should have an EG blood test, venous blood gas, and urinalysis performed. Evidence of a positive EG test, metabolic acidosis, elevated anion gap, and presence of calcium oxalate crystalluria is consistent with EG toxicosis, and prompt therapy is indicated. Be aware that EG testing is only accurate within approximately the first 24 hours, as false negatives may be found thereafter due to complete metabolism of the EG to its more toxic metabolites. With EG testing, keep in mind that the toxic metabolites of EG are not typically detected on routine EG testing – only ethylene glycol itself. On veterinary specific EG tests, rare
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