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Name: Denise F.
Status: Educator
Age: 40s
Location: N/A
Country: USA
Date: 2002

I teach pet first aid classes, and was speaking out the dangers of pets ingesting antifreeze. One student mentioned that when his dog got into antifreeze, someone quickly gave the dog a shot of vodka and all was fine. I certainly wouldn't condone giving a pet alcohol in my classes cause that too could be considered a poison, however I wondered if there is any chemical basis for why the alcohol seemed to push the ethyglycol through the body without causing any harm.

One shot of vodka will not really do it, but in a pinch, vodka can be used, even IV. Antifreeze is a common cause of poisoning in dogs and cats and, according to a recent report from the American Association of Poison Control Centers it is the second most common cause of fatal poisonings in animals. Antifreeze toxicity is associated with a mortality rate of 59-70% in dogs and with a higher mortality rate in cats. Early diagnosis and treatment of animals ingesting antifreeze is critical. Ethylene glycol is the toxic component in antifreeze. Antifreeze is a commonly used solution, has a pleasant taste, and ingestion of only a small amount causes toxicity. Toxicities are most common in the fall, winter, and spring corresponding to the increased use of antifreeze.

ETHYLENE GLYCOL (EG). Antifreeze solutions are usually ~95% ethylene glycol. The minimum lethal dose of undiluted EG is 6.6 ml/kg in the dog and 1.5 ml/kg in the cat. Ethylene glycol is structurally similar to ethanol and like ethanol is a CNS depressant. Unlike ethanol, ethylene glycol is metabolized to very toxic compounds - glycoaldehyde, glycolic acid, glyoxylic acid, and oxalic acid that cause marked metabolic acidosis and acute renal failure.

The goal of treatment is to prevent the metabolism of EG to its toxic components by inhibiting alcohol dehydrogenase (ADH), the enzyme that initiates the biotransformation of EG.

Ethanol (and even Vodka) has been used to treat EG toxicity because it is a competitive substrate with a higher affinity for ADH than EG. Although no longer the recommended treatment in dogs, ethanol is still the recommended treatment for EG toxicity in cats.

Unfortunately, like EG, ethanol also causes CNS depression which limits its usefulness. Ethanol also has a short half-life as a competitive substrate for ADH so must be given every 4 hours or as a continuous IV drip. Other problems associated with the use of ethanol include its metabolism to acetaldehyde, it worsens the metabolic acidosis by increasing the formation of lactic acid, and worsens the EG-induced osmotic diuresis and serum hyperosmolality.

One suggested protocol is to give 20% ethanol at 5.5 ml/kg IV q 4 hr for 5 treatments then q 6 hr for 4 treatments to try and maintain a serum ethanol level of 50-100 mg/dl. However lower levels of ethanol have been shown to be as effective i.e., giving a 30% ethanol solution at 1.3 ml/kg as an IV bolus followed by continuous IV infusion at 0.42ml/kg/hr for 48 hours. Intraperitoneal injections have been previously reported but are irritating to the peritoneum and offer no advantages over other routes. Fluid therapy and careful patient monitoring are needed with ethanol therapy as the CNS depression can progress to respiratory arrest and coma.

Phillip Raclyn, DVM, CVA

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