Ethylene glycol is most commonly thought of as an automotive radiator antifreeze, but ethylene glycol is also present in high
concentrations in many brake fluids and aircraft deicers. In addition, ethylene glycol is often used in condensers, heat exchangers,
home solar units and portable basketball goal post bases. Ethylene glycol may also be used to winterize toilets in recreational
vehicles and summer homes in colder latitudes. Ethylene glycol is commonly present as a component in household paints, but
it is rarely present in concentrations above 10% and significant ethylene glycol exposure is unlikely unless very large quantities
of paint are ingested. Inks, ink pad, polishes, finger moistening compounds (e.g. Tacky Finger), and other stationery supplies
may contain ethylene glycol. Some ink pens contain relatively high levels of ethylene glycol, but the total volume of ink
is only a few milliliters, so ink pens would only pose an ethylene glycol risk to very small animals such as birds, pocket
pets, or dogs/cats less than 2-3 pounds.
Unfortunately, reliable toxic doses of ethylene glycol have not been established for most animals, including dogs and cats.
Much of the acute toxicity data available is based on doses that cause early deaths from acidosis/intoxication and do not
take into account the fact that many animals may survive the initial stages of toxicosis only to succumb to kidney failure
days later. Because of this, any suspected oral exposure of an animal to radiator antifreeze should be considered a potential
toxicosis, and steps should be taken, through historical and diagnostic information, to attempt to determine the extent of
the exposure. When doubt still exists, the only prudent recourse is to treat as if the ingestion was potentially toxic.
It is important to remember that ethylene glycol is a very potent alcohol; for that reason, many of the signs of ethylene
glycol toxicosis will relate to severe alcohol intoxication. In addition, ethylene glycol is broken down to metabolites (e.g.
oxalic acid) that cause damage to the kidney tubules, resulting in renal failure. Because of the different mechanisms involved
in ethylene glycol toxicosis, clinical signs frequently change throughout the course of the toxicosis. It is sometimes easier
to break the clinical signs noted into 3 different stages, although considerable overlap between these stages may be seen
and some animals will not experience each stage. Death can occur at any stage. The stages are 1) neurologic—the initial inebriation
due to the effects of alcohol on the CNS, 2) cardiopulmonary—due to severe acidosis and electrolyte disturbances, and 3) renal—due
to renal tubular injury from calcium oxalate crystals.
Generally begins within 30 minutes of exposure and lasts up to 12 hours. In mild to moderate cases, this stage may pass quickly
and may not be noted by the pet owner or veterinary staff. Animals are initially ataxic, disoriented, "drunk," stuporous,
hypothermic (especially cats), polyuric, and polydipsic (PD/PU more pronounced in dogs). Coma and death may occur during this
stage, or the animal may appear to partially or fully recover over 3-6 hours. By 6-12 hours, the neurologic status of the
animal may again deteriorate due to development of severe metabolic acidosis from ethylene glycol metabolites. You may see
marked CNS depression, stupor or coma an seizures are possible.
This stage generally occurs 12 to 24 hours following exposure. Signs may be more recognizable in dogs than cats. Tachypnea,
tachycardia, depression, +/- seizures, and pulmonary edema may occur. At this time, a high anion gap and severe metabolic
acidosis are generally present.