Ice Melts
Now that the colder months are upon us, snow and ice are sure to follow. Soon folks will be using a variety of ice melt products to try and keep sidewalks and driveways safe. House pets can accidentally be exposed to these types of products and experience potentially serious problems because of that exposure.
There are several common ingredients in most commercially available ice melt products, including sodium chloride, potassium chloride, magnesium chloride, calcium salts and urea.
Sodium Chloride: Sodium toxicosis is possible after large ingestions of ice melts, salt, or rock salt. A dose of 4g/kg of sodium chloride can be lethal in dogs. Ingestion can cause gastrointestinal signs, PU/PD, hypernatremia leading to tremors, seizures, tachycardia and metabolic acidosis. Treatment of acute sodium chloride toxicosis primarily involves IV fluids and managing signs. The fluid of choice is either half strength saline + 2.5% dextrose, or 5% dextrose in water. Furosemide may help prevent pulmonary edema during fluid therapy. For hypernatremia occurring over days to weeks, it is important to correct sodium slowly over a period of 48 to 72 hours in order to avoid cerebral edema. The sodium should not be lowered at a rate of more than 0.7 mEq/L/hr. Sodium bicarbonate should be used cautiously when treating acidosis as not to exacerbate hypernatremia.
Potassium Chloride: Ingestion of this ingredient can cause severe irritation to the GI tract, including hemorrhage. Hyperkalemia can also occur, mainly in patients with renal insufficiency. Signs associated with hyperkalemia are vomiting/diarrhea, weakness, hypotension, and abnormal cardiac conduction. Treatment usually begins with dilution, as emesis is controversial. Fluids (LRS or saline) and furosemide or hydrochlorothiazide are used to treat the hyperkalemia. Other recommended treatments include electrolyte, glucose and renal function monitoring.
Magnesium Chloride: Hypermagnesemia can occur after ice-melt ingestion. Hypermagnesemia can cause hypotension, hypophosphatemia, cardiac abnormalities (atrioventricular block, prolonged QT intervals, and bradycardia), weakness, and impaired neuromuscular transmission. Patients with renal insufficiency are more susceptible to developing hypermagnesemia. The LD 50 of magnesium chloride in rats is about 4,000 mg/kg. Dust from products containing magnesium may be irritating and can cause upset stomach. Treatment of magnesium salt ingestion is symptomatic and supportive. Emesis may reduce the amount absorbed if induced within two hours of ingestion.
Calcium Carbonate and Calcium Magnesium Acetate: Acute ingestion of calcium salts is unlikely to increase serum calcium concentrations, because of the requirement of an acidic pH, parathyroid hormone, and vitamin D for absorption. The calcium carbonate and calcium magnesium acetate forms are irritants, and can cause gastritis, while the calcium chloride form is capable of causing severe irritation, including hemorrhage. Treatment is symptomatic and supportive including treatment for severe mucosal irritation with exposure to the calcium chloride form.
Urea: Monogastric animals are not susceptible to urea poisoning but may exhibit increased blood ammonia concentrations. Ruminants and large-bowel fermenters are susceptible because their intestinal microflora provides an ideal environment for the hydrolysis of urea, releasing carbon dioxide and ammonia. Ingestion of urea by dogs usually results in local irritation, and signs of hypersalivation, gastroenteritis, and abdominal pain. Less frequent signs include methemoglobinemia, weakness, and tremors. Managing urea ingestion in monogastric animals includes inducing emesis and monitoring electrolyte concentrations.
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