MANAGEMENT OF ETHYLENE GLYCOL TOXICITY
Dr. Valarie Pallatto

It is that time of year, when we see an increase in the number of cases of ethylene glycol toxicities.  This is due to the fact that people are winterizing their cars, so there is an increase in access to ethylene glycol for our pets.  Unfortunately, ethylene glycol exceeds any other type of intoxication in case fatality.

What is ethylene glycol?

It is a sweet, sometimes colorless, odorless, water soluble liquid, which is used as antifreeze or as solvent.  It may be bright green in color.  The most common sources of ethylene glycol are antifreeze, film developing fluids, and plants (beets, lamb's quarter, and rhubarb).  Plants cause toxicity more commonly in  ruminants and herbivores.  Antifreeze is the most common source for house pets. 

There are products available such as "LowTox" and "Sierra"  which are propylene glycol based products.  These products are not as harmful to pets, and they are just as effective for car winterization.

Why is ethylene glycol (EG) toxic?

There are two routes by which ethylene glycol causes harm to animals.  The first is a direct effect on the central nervous system.  EG is rapidly absorbed via the gut, and is able to cross the blood brain barrier causing a narcotic or euphoric effect.  The other route by which EG causes harm, is after it is metabolized by the liver.  EG metabolites cause a very serious toxicity in which the renal system is most severely affected.

EG is maximally absorbed from the GI tract within 1 to 4 hours following consumption.  EG is nearly all metabolized to glycoaldehyde, by 12 to 24 hours post ingestion. (Fig. 1)  Metabolism occurs mainly in the liver and secondarily in the kidneys.  Cats metabolize EG much faster than dogs, so it is literally a race against time, when trying to save a cat from EG toxicity.  There are three important steps in the metabolism of EG that are critical in monitoring and treating the patient:

1. Conversion of EG to glycoaldehyde: This is important because this is the step you are going to try and prevent with treatment.  The metabolites are the source of renal damage.

2.  Formation of glycolic acid and glyoxylic acid: Acids cause severe metabolic acidosis, which diminishes myocardial contractility and can predispose the heart to ventricular arrhythmias and ventricular fibrillation.

3.  Glycoaldehyde, glycolic acid, glyoxylic acid, calcium oxalate, and hyppuric acid all have cytotoxic effects on the renal tubular cells.

What are the toxic doses of EG in dogs and cats?

Cats- 1.4 mls/Kg
Dogs- 4-5 mls/Kg

History:
The owner sees the animal drinking antifreeze, or drained radiator fluid.  The animal is vomiting, depressed, may have signs of incoordination.  Question the owner about recent antifreeze change, or garage access, etc.  Keep in mind, that toxicity is more common in winter months, and in dogs due to their indiscriminate eating habits.

Clinical Signs:
There are four systems affected: CNS, GI, Cardiopulmonary, and Renal.
There are 3 stages in which clinical signs occur:
Stage 1:  (0 to 12 hours post ingestion): vomiting, ataxia, depression, muscle fasiculations, head tremors, or seizures (alcohol intoxication)
Stage 2:  (12 to 24 hours post ingestion): Cardiopulmonary effects; increased respiratory rate and effort due to pulmonary edema
Stage 3:  (also occurs in the 12 to 24 hour post ingestion period): can be oliguric, anuric, or PU/PD, azotemic, abdominal pain, vomiting, severely depressed, uremic.

Clinical Pathology:
CBC: usually displays polycythemia (dehydration) and an inflammatory leukogram (inflammation from GI and kidney irritation).
Chemistry Profile:
Azotemia in the face of isosthenuria, which indicates renal failure.
Hyperphosphatemia from decreased glomerular filtration and the presence of phosphates in EG
Hypochloridemia from loss via vomiting
Hypocalcemia due to loss from renal failure and calcium oxalate formation
Hyperglycemia from catecholamine release.
Hyperkalemia from transcellular shifting
Hyperproteinemia from dehydration
Blood Gas analysis: Metabolic acidosis with respiratory compensation, high anion gap, which indicates titration acidosis and presence of uremic acids and ethylene glycol metabolites.
U/A: isosthenuric (S.G. 1.008- 1.012), decreased pH (» 6), 1+- 2+ protein, 1+ glucose, crystalluria (calcium oxalate and hippurate) (Fig 2 and 3 )
Increase in serum osmolality.  Use the following equation to calculate osmolality:

Normal osmolality  is 280 to 310 mOsm
In- House ethylene glycol test by Pharmacal (Phone # 850-476-9462)  Running this test takes approximately 30 minutes, and it must be run within 12 hours of EG ingestion.  The test detects EG in blood.

Ultrasound can be used to increase the diagnostic confidence level in cases of ethylene glycol poisoning.  Finally, there is also

(Continued on page 11)