When you hear the phrase “rodenticide toxicity,” what’s the first type of toxicity that comes to mind? If you’re like most people, you probably think of anticoagulant rodenticides.

However, there are a variety of different rodenticides that can have toxic effects on pets. As a vet tech, it’s important for you to be familiar with these toxins and know your role in managing possible rodenticide toxicity. 

Telephone Triage

The first step in dealing with possible rodenticide toxicity is often to perform telephone triage. In many cases, owners call the veterinary hospital because they suspect that their pet has ingested a rodenticide. It’s up to you, as the vet tech, to guide the client on what comes next. 

Aim to find out which rodenticide the pet ingested. There are four common types of rodenticides: anticoagulant rodenticides, cholecalciferol, bromethalin, and zinc phosphide. Each rodenticide requires a different treatment, so it’s important to figure out which toxin the pet may have ingested. Your initial advice will likely be to bring the pet in for veterinary care, but knowing what the pet ingested will allow you to prepare the veterinarian and the rest of the team. 

If the owner has the original packaging for the rodenticide, have them bring that packaging to the hospital. If the container is too large to transport, ask the owner to take a photo on their phone. Knowing the active ingredients, concentration, and other label information can be valuable information for the veterinarian. 

Decontamination

Any time a pet has recently ingested rodenticide, decontamination will play a role in treatment. Vomiting is typically induced with apomorphine (dogs) or dexmedetomidine (cats), as long as the patient is alert and mentally aware enough to do so safely. If your patient has ingested a rodenticide containing zinc phosphide, emesis should be induced outdoors; phosphine gas, which is toxic to both humans and pets, will be released with emesis.

Activated charcoal is also often administered to bind toxins remaining in the gastrointestinal tract. Activated charcoal has clear benefits in the treatment of anticoagulant rodenticides, cholecalciferol, and bromethalin. Its benefits are less clear in the treatment of zinc phosphide toxicity, but it may still be recommended. 

Treatment of Specific Rodenticide Toxicities 

Following decontamination, treatment will largely depend on the type of rodenticide that was ingested. Each rodenticide has a different mechanism of action, requiring different treatment approaches. 

Anticoagulant Rodenticides

Anticoagulant rodenticides inhibit the enzyme that reactivates vitamin K, interfering with the production of coagulation factors I, II, VII, IX, and X. Clinical signs of toxicity may take up to a week to develop because the body must first use up its store of already-synthesized clotting factors. When clinical signs do occur, they may include anemia, epistaxis, hemoptysis, hematomas, hemothorax, hyphema, melena, hematuria, weakness, and lethargy. 

Diagnosis is usually based on known exposure and response to vitamin K₁ treatment. If clotting tests are performed, a prolonged prothrombin time (PT), activated partial thromboplastin time (APTT), or thrombin time in the presence of normal fibrinogen, fibrin degradation products, and platelets are suggestive of anticoagulant rodenticide toxicity.

If a patient is already experiencing significant bleeding, whole blood transfusion or fresh or frozen plasma can be administered to replace clotting factors. In most cases, however, patients are treated on an outpatient basis with oral Vitamin K₁. This supplement is typically administered at a dose of 3–5 mg/kg/day, divided into two equal daily doses and given with a fatty treat. Treatment is continued for two to four weeks, depending on the specific anticoagulant rodenticide that was ingested. Three days after the last dose of Vitamin K₁, the patient’s PT should be assessed to ensure that continued treatment is not needed.

Cholecalciferol

Cholecalciferol, or Vitamin D₃, causes hyperphosphatemia and hypercalcemia. Within 36 hours of ingestion, owners may observe early signs such as depression, anorexia, and polyuria/polydipsia. As signs progress, nausea, vomiting, hematemesis, hypertension, renal failure, and cardiac abnormalities may occur. 

Treatment is focused on treating hypercalcemia and hyperphosphatemia. Normal (0.9%) saline is typically administered at 2–3 times the patient’s maintenance rate for diuresis. Furosemide is often administered to promote calcium excretion, prednisolone is used to minimize hypercalcemia, and a phosphorus binder (such as aluminum hydroxide) is administered to decrease phosphorus absorption. Pamidronate may also be used to treat severe hypercalcemia. Treatment should be continued until calcium and phosphorus levels normalize, which may take days to weeks. Renal values should also be monitored closely during treatment.

Bromethalin

Bromethalin is a neurotoxin found in some rodenticides. Ingestion causes cerebral and spinal edema, leading to increased CSF pressure. Signs of acute ingestion in dogs include hyperexcitability, tremors, seizures, CNS depression, hyperthermia, and death. In dogs consuming lower doses, clinical signs may include depression, hindlimb weakness/paresis, ataxia, proprioceptive deficits, and possible tremors. Cats develop the paralytic form of bromethalin toxicity, regardless of the dose ingested.

Bromethalin toxicity treatment relies on supportive care because there is no antidote. Anti-seizure medications should be used as needed. Mannitol and corticosteroids may be used in an effort to control cerebral edema, but these drugs are often not helpful. 

Zinc Phosphide

When zinc phosphide reacts with the acidic pH of the stomach, phosphine gas is produced. Vomiting may result in the inhalation of this phosphine gas, causing acute noncardiogenic pulmonary edema. Zinc phosphide may also be absorbed systemically, causing liver and/or kidney failure. 

Antioxidants, such as N-acetylcysteine and S-adenosyl methionine (SAM-e), are administered to prevent free radical damage caused by zinc phosphide. Supportive care is often needed to control electrolyte abnormalities, hyperglycemia, seizures, and pulmonary edema.

Conclusion 

When a client calls regarding a potential rodenticide toxicity case, it’s important to gather as much information as possible. Don’t jump to conclusions. Instead, take the time to find out which toxin the pet ingested; if the owner is unsure, encourage the owner to find that information on their way to the veterinary clinic. Knowing which toxin was ingested is invaluable in recommending effective treatment and minimizing risks to the veterinary team. With this information, you and the veterinarian can move forward with decontamination and treatment, maximizing the likelihood of a successful outcome for the pet.