In colder climates, the incidence of EG intoxications is seasonal, with most cases occurring in the fall, winter, and early spring, when antifreeze is added to radiator fluid or when cooling systems are flushed. Serum osmolality can be increased as much as 100 mOsm/kg above normal (280–310 mOsm/kg) within 3 hr of EG ingestion. Vomiting should not be induced in a dog or cat exhibiting neurologic signs because of increased risk of aspiration. Ingestion of sufficient quantities of avocado fruit is most likely to cause myocardial necrosis in which of the following species? As little as one eighth of a teaspoon per pound of body weight in a cat of undiluted antifreeze can result in fatality. To prevent metabolism of EG, the activity of alcohol dehydrogenase is decreased by direct inactivation or by competitive inhibition. The formula 0.3 − (0.5 × kg body wt) × (24 − plasma bicarbonate) is used to determine the dose, in mEq of bicarbonate. Pigs may also have pulmonary edema with tan fluid in the pleural and peritoneal cavities. Acidosis (acidic blood) can also be detected through the biochemistry profile. Treatment is aimed at decreasing absorption of ingested EG, increasing excretion of unmetabolized EG, preventing metabolism of EG, and correcting the metabolic acidosis that occurs with EG metabolism. Absorption through the skin from topical products that contain ethylene glycol has caused toxicity in cats. Ethylene Glycol Poisoning in Dogs. When in doubt, if you suspect your pet has ingested ethylene glycol, immediate veterinary attention is imperative as the prognosis is very poor once clinical signs have developed. Ethylene glycol has been shown to be toxic to humans and is also toxic to domestic pets such as cats and dogs. We’re committed to keeping clients and staff safe during COVID-19 with NEW admittance and check-out processes. Further absorption of EG is prevented by induction of emesis or gastric lavage (or both) within 1–2 hr of ingestion, although the rapidity of EG absorption from the GI tract suggests these procedures may not be beneficial. In addition, a test kit that can be used in the veterinary clinic is available to detect the amount of ethylene glycol present in the bloodstream. This hyperphosphatemia resolves before the onset of EG-induced acute renal failure and azotemia, then recurs when the animal becomes azotemic. Pathophysiology [2] Like the other toxic alcohols mentioned above, ethylene glycol is a parent compound that exerts most of its toxicity by conversion to metabolites. The gastrointestinal tract is the primary route of exposure. Pathophysiology. Left untreated, the animal may die. EG intoxication occurs most commonly in temperate and cold climates, because antifreeze is used both to decrease the freezing point and to increase the boiling point of radiator fluid. Epistaxis and hemoglobinuria have also been seen in cattle that have ingested large doses of EG. Cutaneous absorption from topical products that contain EG has been reported to cause toxicity in cats. Ethylene glycol, the toxic component of antifreeze, causes severe kidney damage. The prognosis varies inversely with the amount of time that elapses between ingestion and initiation of treatment. The active ingredient is ethylene glycol (EG), a clear, odourless liquid with a sweet taste, earning it the name ‘sweet killer’.. Antifreeze is the main source of exposure, but ethylene glycol is also used in a variety of household products including cleaning Partial (focal or multifocal) - total. Clinical signs are dose- and time-dependent and can be divided into those caused by unmetabolized EG and those caused by its toxic metabolites. Ethylene glycol, a sweet-tasting, odorless liquid, is the active ingredient in most automotive antifreeze products. metabolic acidosis. Glycolaldehyde is then rapidly metabolized to glycolic acid. Approximately 50% of ingested EG is excreted unchanged by the kidneys; however, a series of oxidation reactions in the liver and kidneys metabolize the remaining EG. Stage 1 (within 30 minutes of ingestion): The signs include lethargy, vomiting, incoordination, excessive urination, excessive thirst, hypothermia (low body temperature), seizures, and coma. Ethylene glycol exposure can be extremely dangerous, with significant morbidity and mortality if … This damage can be identified in a serum biochemistry profile by increases in the levels of creatinine and BUN (blood urea nitrogen) that are normally removed from the blood by the kidneys. Antifreeze poisoning in cats Antifreeze is found in car radiators and some screen washes, but it is extremely toxic to cats. Many animals will voluntarily drink ethylene glycol if antifreeze is spilled or leaks onto garage floors or driveways. Consumption of the fruit, seed, stem, or leaves of avocados can cause toxicity in animals. Oliguric acute renal failure usually develops between 12 and 24 hr in cats and between 36 and 72 hr in dogs. renal tubules. Ethylene glycol itself may cause some alteration of mental status but it is a relatively nontoxic compound before it is metabolized. By as early as 24 hours after ingestion, insufficient ethylene glycol remains to allow detection on this blood test; however, the damage to your pet’s body from ethylene glycol has already occurred. Hypertension Hypertension vascular pathology → incompetence and leakage of plasma and fibrinogen. Stage 3 (12-24 hours after ingestion): At this stage, signs of severe kidney dysfunction, which is characterized by swollen, painful kidneys and the production of minimal to no urine, may occur. Ethylene glycol (C2H6O2) is a toxic alcohol that is found in various household and industrial agents. Cats do not taste ‘sweetness’ in the same way we do, but still find drinking ethylene glycol attractive. The first of two rate-limiting biotransformation steps is the production of glycoaldehyde from EG by the enzyme alcohol dehydrogenase. Pulmonary edema and hemorrhagic gastroenteritis are common secondary findings in dogs and cats. [emedicine.com] Pathophysiology There is limited data regarding DEG and most information is derived from published experimental studies. Incoordination, excessive urination, excessive thirst, vomiting, and lethargy are amongst the first signs to appear. A urinalysis may also confirm ethylene glycol poisoning and underlying kidney damage by the presence of dilute urine containing blood, protein, cellular casts (plugs of cells which have taken the shape of dying tubules in the kidneys), and calcium oxalate crystals (which are seen with ethylene glycol poisoning). Ethylene glycol poisoning can be fatal if not treated soon after ingestion (within 4 to 8 hours). It is often claimed that cats are attracted to the sweet taste of antifreeze, but as cats cannot taste sweet. Limited information is available on the pathological features of EG poisoning in pet animals, with special emphasis on cats. Polydipsia occurs due to osmotic stimulation of the thirst center, and polyuria occurs due to an osmotic diuresis and decreased production and release of antidiuretic hormone. These 95% commercial antifreeze preparations are diluted ~50% with water when used in vehicle cooling systems. Diagnosis is often difficult because the nonspecific multisystemic signs may appear similar to other types of CNS disease or trauma, gastroenteritis, pancreatitis, ketoacidotic diabetes mellitus, and acute renal failure due to renal ischemia or other nephrotoxicants. The clinical signs associated with ethylene glycol intoxication > “In both dogs and cats, toxic doses of ethylene glycol cause CNS depression followed by acute … These 95% commercial antifreeze preparations are diluted ~50% with water when used in vehicle cooling systems. One-half of this dose should be given IV slowly to prevent overdose, and plasma bicarbonate concentrations should be monitored every 4–6 hr. EG is rapidly absorbed from the GI tract; in dogs, blood concentrations of EG peak within 3 hr of ingestion. The gap is caused by the presence of osmotically active particles (eg, ethylene glycol) in the serum that are not factored into the above equation. It is critical that you bring your cat to a veterinary clinic if you know or even suspect that he has consumed ethylene glycol, or if he is exhibiting any of the early symptoms. Calcium oxalate crystals form within the lumina of tubules as water is reabsorbed from the glomerular filtrate and the pH decreases (smaller numbers of calcium oxalate crystals may also be observed in the adventitia of blood vessel walls throughout the body). Cat, Ethylen glycol, Ethylen glycol toxicity, Pathological findings, Poisoning. There are 15 ml in a tablespoon, so figure1 tablespoon (30 ml) per Papillion could be lethal, and a teaspoon is lethal for a cat. Within 3 hr of ingestion of toxic doses of EG, dogs and cats develop normochloremic metabolic acidosis with an increased anion gap, minimally concentrated or isosthenuric urine with an acidic pH, and marked serum hyperosmolality with an increased osmolal gap. Ethylene glycol poisoning is divided into three stages. If 4-MP is not available, an ethanol regimen (5.5 mL of 20% ethanol/kg body wt, IV, every 4 hr for five treatments and then every 6 hr for four additional treatments) is recommended. In dogs and cats with azotemia or in oliguric acute renal failure, inhibition of alcohol dehydrogenase is of little benefit, because almost all of the EG has already been metabolized. Once absorption has occurred, excretion of EG is increased by fluid therapy designed to correct dehydration and increase urine production. Renal tubular epithelial necrosis with calcium oxalate crystals in the tubular lumina is the characteristic finding of EG intoxication. Phase 1 signs include ataxia and a … Cats that roam outside unsupervised are more likely to encounter ethylene glycol in antifreeze which has been disposed of improperly. Pet Poison Helpline is available in North America by calling 800-213-6680. {ref2}Like the other toxic alcohols mentioned above, ethylene glycol is a parent compound that exerts most of its toxicity by conversion to metabolites. The metabolic acidosis associated with metabolism of EG is corrected by administration of sodium bicarbonate. Most intoxications are associated with ingestion of antifreeze, which is typically 95% EG. –Pathophysiology: Initially a direct effect of ethylene glycol, which in low doses causes euphoria and in high doses causes CNS depression. The difference between measured and calculated (1.86 [Na+ + K+] + glucose/18 + BUN/2.8 + 9) osmolality is referred to as the osmolal gap. Pathophysiology [2] Like the other toxic alcohols mentioned above, ethylene glycol is a parent compound that exerts most of its toxicity by conversion to metabolites. Toxicity: Ethylene glycol is the main toxic ingredient found in most antifreeze products, usually at a concentration of 95-97%.It is an extremely dangerous toxin. Ethylene glycol poisoning is most common in temperate and cold climates because antifreeze is used both to decrease the freezing point and to increase the boiling point of radiator fluid. The best way to confirm ethylene glycol poisoning is by measuring the blood concentration of ethylene glycol. 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