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Rodenticide Poisoning

By

Safdar A. Khan

, DVM, MS, PhD, DABVT, ASPCA Animal Poison Control Center, Urbana, Illinois;


Mary M. Schell

, DVM, DABVT, DABT, ASPCA Animal Poison Control Center, Urbana, Illinois

Last full review/revision Oct 2020 | Content last modified Oct 2020

Pets often gain access to rodenticides by eating baits or the poisoned rodents (See also Strychnine Poisoning). Many rodenticides are toxic to pets. Early veterinary intervention in cases of ingestion provides the best chance for successful treatment.

Anticoagulant Rodenticides (Warfarin and Related Compounds)

Anticoagulant rodenticides interfere with blood clotting. They are the most frequent cause of poisoning in pets. Pets may be poisoned directly from baits or indirectly by eating poisoned rodents. Different anticoagulants have different toxicity levels. Some are highly toxic with a single feeding, whereas others require multiple feedings to result in toxicity.

Signs generally reflect blood loss from ruptured blood vessels, including anemia, semisolid masses of blood in the tissues, or bleeding into various areas of the body (the gastrointestinal tract, the eye, the nose, the lungs, or the urine). The animal can develop weakness, lack of coordination, colic, and panting or rapid breathing. Depression and loss of appetite are seen in all species even before bleeding occurs.

Anticoagulant rodenticide poisoning is usually diagnosed based on history of ingestion, blood tests, and a good response to vitamin K1 treatment. Vitamin K1 may need to continue for 2 to 4 weeks. Administration of oral vitamin K1 with a fat-containing ration, such as canned dog food, increases its effectiveness 4 to 5 times as compared with vitamin K1 given by mouth alone. Blood transfusions may be needed if bleeding is severe. Blood clotting should be monitored weekly until values remain normal for 5 to 6 days after treatment stops.

Bromethalin

Bromethalin is a nonanticoagulant rodenticide that can cause either a short- or longterm syndrome. In dogs, sudden, severe effects include hyperexcitability, muscle tremors, seizures, heightened reflexes of the hindlimbs, central nervous system depression, and death about 10 hours after ingestion. Longterm effects are seen with lower dosages and may appear 1 to 4 days after ingestion. This syndrome is characterized by vomiting, depression, lack of coordination, tremors, and a reluctance to stand. The effects may be reversible if exposure to bromethalin is discontinued. Bromethalin toxicosis should be considered when swelling of the brain or paralysis of the hind end is present.

Medical treatment is directed at blocking absorption from the gastrointestinal tract and reducing brain swelling. Using activated charcoal for several days may improve the recovery rate.

Cholecalciferol

Rodenticides containing cholecalciferol are a significant health threat to dogs and cats. Cholecalciferol produces excess calcium in the blood, which results in calcification (hardening) of soft tissue throughout the body. Signs generally develop within 18 to 36 hours of ingestion and can include depression, loss of appetite, passing large amounts of urine, and excessive thirst. As blood calcium concentrations increase, signs become more severe. Vomiting blood and bloody diarrhea may develop. As excess calcium in the blood continues, mineralization of the kidneys results in progressive kidney damage.

Diagnosis is based on history of ingestion, signs, and excess calcium in the blood (see also Disorders of the Parathyroid Glands and of Calcium Metabolism in Dogs : Hypercalcemia (High Blood Calcium Levels)).

Treatment usually includes removing the stomach contents, followed by administration of activated charcoal. Medications that increase urination are given for 2 to 4 weeks. Blood calcium levels should be monitored up to 2 weeks after stopping treatment. A low-calcium diet should be provided. Recently, pamidronate disodium has shown promise in treating dogs with cholecalciferol poisoning.

Zinc Phosphide

Zinc phosphide has been used extensively around farms and barns as a rodent bait and is intended for outside use only. Oat-based bait pellets have been marketed for use against voles but cannot be identified once out of the package, and horses have been fatally poisoned. Lethal doses vary greatly by species, and zinc phosphide is much more toxic to those not able to vomit, such as horses. In stomach acid, this compound degrades and rapidly forms phosphine gas, which is dangerous if inhaled because it causes fluid to accumulate in the lungs. Care must be taken if vomiting is induced in an animal suspected of zinc phosphide poisoning.

Poisoning causes gastrointestinal tract irritation and cardiovascular collapse. Signs begin rapidly and include vomiting, abdominal pain, and aimless running and howling, followed by depression, difficulty breathing, and convulsions. Death is due to respiratory arrest. Diagnosis is based on history of exposure to zinc phosphide, signs, and detection of zinc phosphide in stomach contents. Zinc levels in the blood, liver, and kidneys may be increased. Treatment includes supportive care, fluids, calcium gluconate, and sodium bicarbonate to neutralize stomach acidity.

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