Antifreeze Poisoning

Antifreeze or ethylene glycol (EG) is a commonly available coolant for 
most water cooled engines. The availability of the product is slightly 
seasonal in colder climates. However, EG is used year round as an 
antifreeze and summer coolant. Unfortunately, the chemical is very toxic 
and lethal in small amounts to all animals. Dogs and cats are probably 
more susceptible because of their inherent nature to taste everything. In 
particular dogs seem quite willing to try anything if smells or tastes 
reasonable. EG is somewhat sweet to the taste. Newer coolants are now 
available that eliminate the desirable taste but, EG is the predominant 
coolant on the market. 

EG is readily absorbed by the gastrointestinal system. Doses of less than 
1ml per kg. in the cat and 4-5ml per kg. in the dog are fatal if not 
promptly treated. The drug itself is not toxic but, the metabolites of EG 
cause tremendous changes in acid-base balance and produce direct toxic 
effects to the kidneys. In addition, EG metabolic byproducts cause, 
metabolic acidosis, respiratory depression and upset glucose metabolism.

By the time most animals are presented with signs of EG toxicity it is 
often too late to effectively intervene. The prognosis is hourly 
dependent on the interval between ingestion and treatment. Most dogs will 
recover if presented in the first 8 hours and within 4 hour for cats. 
Early signs include vomiting in the first few hours with in coordination 
problems. These signs may actually decrease significantly after 12 hours 
but, by then the outcome is almost always certain and death will follow 
in 2-3 days. After one day, most dogs will begin to show severe signs of 
dehydration from vomiting and increased urination. Signs in the final 
48-72 hours are mostly neurological including, incoordination, 
depression, coma and death.

Therapy for EG poisoning is only effective if employed quickly, ideally 
upon ingestion but no later than 24 hours. Early diagnosis is critical 
for effective therapy and involves measuring serum osmolality which is 
greatly increased in EG toxicity or by employing a commercial test for 
serum EG. If consumption of EG ocurred within 6 hours,  induced vomiting, 
stomach pumping and stomach installation of charcoal adsorbants can be 
effective. However, prevention of absorption of EG is best done within 
the first two hours post ingestion. After EG absorption, stopping  
metabolism of the drug involves preventing the action of the liver enzyme 
alcohol dehydrogenase (ADH). Traditionally, intravenous administration of 
20% ethanol has been employed in conjunction with bicarbonate and 
steroids to counter acid base problems and shock. Ethanol has been 
effective if treatment is given in the first hours after ingestion of EG. 
The doses of ethanol employed to tie up ADH must be repeated every 4-6 
hours over 2 days. Recomended doses of 5 ml/kg. cause severe depression, 
occasionally coma, interfere with clinical assessment and increase the 
difficulty of patient management. 

Currently, a newer drug, 4-methylprazole (4-MP) has proven more effective 
at blocking the action of ADH without the depressive side affects of 
ethanol. If administered early, under 3 hours, nearly all of the EG will 
be eliminated by the kidneys in the original unmetabolized form. This 
drug has been shown to be very effective up to 8 hours after ingestion 
and will provide some benefits even with intervals up to 36 hours. The 
longer the interval between ingestion and treatment the greater the 
amount of kidney damage. Unfortunately, 4-MP does not seem to be 
effective in the cat.

Additional support during therapy includes traditional intravenous fluid 
therapy and acid-base regulation if required. Convalescent therapy may 
include low protein diets to rest the kidneys depending on the damage 
incurred.