Rodenticide Toxicity

Summary

Rodenticide toxicity is a very common issue for pet and wildlife medicine, alike. The ubiquitous use of a variety of highly toxic compounds to control unwanted rodent populations has historically proved a problem for a wide variety of animals.

This occurs either because pets and wildlife are drawn to the bait (which contains the toxin in a highly palatable form). Alternatively, they may prey upon (and ingest) the already-poisoned rodents. This latter process of poisoning is referred to as "relay toxicosis."

Note: While relay toxicosis is a common cause of exposure among wildlife, it is not considered a common source of toxicity for dogs and cats (this is likely because the rodents killed are not typically ingested).

The problem of rodenticide toxicity is made far worse by the fact that the baits are comprised of many different compounds with many different sorts of packaging. Moreover, pet owners are often misled into believing some are safe for use around pets.

The following are the most common forms of rodenticide, and make no mistake, they are all potentially lethal (some more than others):

Zinc, calcium, and aluminum phosphides
While these poisons are more typically included in mole or gopher baits, mouse and rat baits may use them, too. These kill by releasing phosphide gasses inside the animal, leading to painful abdominal distension and liver damage.
Bromethalin
This extra-lethal toxin kills by causing deadly swelling of the brain (cerebral edema). The toxic dose for this particular poison is very low, especially for cats!
Cholecalciferol (Vitamin D3)
This highly toxic compound is gaining traction in the rodenticide marketplace. It works by increasing calcium and phosphorus levels, thereby causing acute kidney failure. As for the above compounds as well, no specific antidote is available to reverse its effects.
Anticoagulants
Long-acting compounds that "thin" the blood by preventing it from clotting are traditionally the most common approach to killing rodents. Though it may seem exceptionally cruel, it is arguably less so than the above three. Having said that, this toxin has killed more dogs and cats than any other rodenticide; In part, because it is so insidious, killing pets many days or weeks after exposure with almost no advance symptoms to show for it.
Luckily, this class of rodenticides does have an antidote (namely, prescription-strength Vitamin K1). Sadly, many patients are diagnosed long after they've consumed the toxin. For a large percentage of these unfortunate pets, the antidote arrives too late to exert its life-saving effects.

Clearly, rodenticides are among the worst possible toxins for pets: tasty, stealthy, effective, and quite deadly.

Symptoms and Identification

The clinical signs of rodenticide poisoning depend on the type ingested. Knowledge of their consumption is, of course, the primary sign of potential poisoning, but that's not always possible. Which is why I've listed their various clinical signs below:

Zinc, calcium, and aluminum phosphides
Immediate effects (depending on the ingested dose):
- Painful abdominal distension
- Non-productive retching
- Vomiting
- Shock and collapse
Bromethalin
Within 2 to 24 hours (depending on the ingested dose):
- Tremors
- Seizures
- Ataxia (loss of balance)
- Paralysis
- Collapse
- Sudden death
Cholecalciferol (Vitamin D3)
Within 1 to 4 days after ingestion (depending on the ingested dose):
- Lethargy and depression
- Poor appetite
- Vomiting
- And other signs consistent with acute renal (kidney) failure
- Anticoagulants
  Within 48 hours to two weeks (depending on the ingested dose):
  - Weakness and pale gums (because of internal bleeding)
  - Coughing and difficulty breathing (due to pulmonary bleeding)
  - Vomiting and diarrhea (with or without blood)
  - Nosebleeds
  - Bruising
  - Bloody urine
  - Poor appetite
  - Bleeding from the gums
  - Collapse
  - Sudden death

The following tests and procedures may be undertaken as part of the diagnostic process for all kinds of rodenticide intoxication:

Physical examination
CBC (complete blood count)
Chemistry (biochemical screen)
Blood clotting (coagulation) profile
Fecal examination (for bleeding)
Urinalysis
EKG
Abdominal and chest X-rays
Abdominal ultrasound and/or echocardiography

Affected Breeds

There is no known breed predisposition to the toxic effects of any of the above-listed rodenticides.

Treatment

Pets who ingest rodenticides require immediate treatment. If the ingestion is identified immediately (within an hour or two of exposure), vomiting is typically induced.

Note: This may be done at home if the veterinarian's office is far away, but always consult with your veterinarian or a board-certified toxicologist (available at one of the many pet poison hotlines readily accessible on the Web) to determine the appropriate means of inducing vomiting in a home environment.

In the case of zinc, calcium, and aluminum phosphides, great care must be taken not to expose the veterinarian, staff and pet owner to the release of gas that may ensue after vomiting.

All animals who have ingested any amount of rodenticide must be taken to a veterinarian immediately, regardless of whether vomiting has been productively induced or not. Obtaining the product's packaging before heading to the veterinarian is a crucial part of the process.

When there is a specific antidote available, as with the long-acting anticoagulants, prescription-strength K1 should be administered quickly and serially for up two weeks (or more, depending on the particular kind of anticoagulant).

When there is no known antidote, as with the other three forms of rodenticide, patients must be treated supportively. Most pets hospitalized for supportive care post-ingestion receive the following as part of their supportive care regimen:

Aggressive decontamination via gastric lavage may be required (under anesthesia), especially for phosphide exposure
Intravenous fluid administration and electrolyte support
Activated charcoal (to reduce absorption of the toxin and speed its transit through the gastrointestinal tract)
Gastroprotectants (drugs to support the GI tract) after vomiting and/or gastric lavage
In the case of cholecalciferol treatment, critical care hospitalization for up to a week may be required to counteract this poison's long-lasting effects. Head elevation and mannitol administration (among other approaches) are all used to reduce brain swelling.

Sadly, many pets may succumb in spite of treatment.

Veterinary Cost

The cost of toxic exposure depends on the dose received, the ability to induce vomiting immediately after ingestion, and the type of rodenticide consumed. It's difficult to say exactly, but most owners can assume that an episode of rodenticide ingestion may cost as little as $500 and as much as $1,000 a day or more for patients in need of critical care.

Prevention

Rodenticide intoxication is 100% preventable. Unfortunately, many pet owners are still in the dark about the severity of rodenticides.

References

Casteel SW, Bailey EM Jr. A review of zinc phosphide poisoning. Vet Hum Toxicol 1985;28(2):151-154.

Chugh SN, Aggarwal HK, Mahajan SK. Zinc phosphide intoxication symptoms: analysis of 20 cases. Int J Clin Pharmacol Ther 1998;36(7):406-407.

Merola V. Anticoagulant rodenticides: deadly for pests, dangerous for pets. Vet Med 2002;97:716-727.

Morrow C. Cholecalciferol poisoning. Vet Med 2001;96:905-911.

Murphy MJ. Rodenticides. In: Howard JL, ed. Current veterinary therapy 3: food animal practice. Philadelphia, Pa.: WB Saunders Co, 1993;282-286.

Osweiler GD. Toxicology. Rodenticides. Philadelphia, Pa.: Williams and Wilkins, 1996;275-296.

Rodenberg HD, Chang CC, Watson WA. Zinc phosphide ingestion: a case report and review. Vet Hum Toxicol 1989;31(6):559-562.

Wilson R, Lovejoy FH, Jaeger RJ, et al. Acute phosphine poisoning aboard a grain freighter. Epidemiologic, clinical, and pathological findings. J Am Med Assoc 1980;244(2):148-150.