ABCDs of rodenticides (Proceedings)


Anticoagulants, bromethalin and cholecalciferol (Vitamin D3) are all found in baits marketed for both household and outdoor/industrial areas. In addition, there are a number of baits containing strychnine or zinc phosphide that are labeled for moles, gophers, and similar rodents, that are meant to be placed in burrows or holes.

Anticoagulants, bromethalin and cholecalciferol (Vitamin D3) are all found in baits marketed for both household and outdoor/industrial areas. In addition, there are a number of baits containing strychnine or zinc phosphide that are labeled for moles, gophers, and similar rodents, that are meant to be placed in burrows or holes. These baits are generally packaged in bulk, so larger quantities are often available.


Anticoagulants in use as rodenticides today are almost all second-generation derivatives of either warfarin or indane 1,3-dione. They are active in the liver where they inhibit the activity of vitamin K epoxide reductase, which converts the vitamin K epoxide to the active reduced form. This reduced vitamin K is crucial to activation of clotting factors II, VII, IX, AND X.

The concentration of active chemical in an anticoagulant bait can range from 0.002%-1%, but the vast majority are 0.005%. Container sizes vary, so having the package with label is very useful in estimating exposure. Doses need to be calculated in mg active chemical/kg BWT. If concentration is 0.005%, each gram of bait has 0.05 mg of the active component. When there is uncertainty about the amount consumed, use the amount potentially available to make calculations.

At the ASPCA Animal Poison Control Center we use an exposure of 0.02mg/kg BWT as the dose that triggers treatment and evaluation. If ingestion was witnessed or a window of opportunity places it within a couple hours, we generally start with inducing emesis. If little or no bait is recovered, administration of activated charcoal is next. If the ingested dose is over 0.02 mg/kg and there has been no decontamination, you can simply institute Vitamin K1 without initial testing. We commonly recommend this approach with young animals, as they have smaller stores of clotting factors initially.

Because the body has several day's worth of active Vitamin K stored in the liver (the site of the re-activation activity), there is a delayed onset of effect on blood clotting after ingestion of an anticoagulant. Factor VII has the shortest half-life, so we can get the earliest valid estimate of effect by checking the prothrombin time (PT). The PT is expected to elevate within 24-48 hours post ingestion. A normal PT at 48-72 hours, with no elevation from baseline, is good evidence that there is no need for Vitamin K1 therapy. If the dose is over 10% of the LD50 in a species and there has been no decontamination, you may just recommend the Vitamin K with PT 48 hours after stopping the meds.

When K1 therapy is needed, target dose is 3-5 mg/kg. If there has been a large ingestion or if PT is very high, it is a good idea to repeat the PT after several days. If it is not yet in the normal range, you may need to increase the dose. Repeating the PT 48 hours after the final dose of K1 can determine that treatment has been sufficient.

A witnessed or evidenced exposure is manageable, and the goal is to prevent any bleeding episodes. When the exposure was not witnessed or suspected, diagnosis and treatment are more challenging. Early signs of anticoagulant toxicosis are vague, and depend on the site of a bleed. You may see lethargy, a soft, non-productive cough, intermittent lameness, mild anemia, or even sudden collapse. Frequently there is no obvious hemorrhage. Petechiae and echymoses are more often seen later in the course of illness, after the platelet numbers have been depleted in smaller bleeds. Diagnosis is based on signs, history of possible exposure, and coagulation studies. The PT will be elevated at 24-48 hours.

Therapy depends on the severity of signs shown. Vitamin K1 is started at 3-5 mg/kg BWT, using the higher doses in smaller animals and more severely affected animals. Horses should get about 2 mg/kg, per Beasley (pp914-915, 1997 notes). There is no real need to give via injection unless the animal is not eating. If injecting, use the smallest needle possible and give IM or SQ, not IV. Giving Vitamin K1 via IV significantly increases the risk of an anaphylactic reaction. The dose can be divided bid and given with a small amount of fatty food to aid absorption. If necessary, the injectible form can be given by mouth (very small animal, difficult to pill, capsules not available)

If there has been significant blood loss, these animals may be good candidates for whole blood transfusions, fresh frozen plasma (to replace clotting factors quickly) or Oxyglobin™. Minimize invasive procedures as much as possible to avoid starting new bleeds. If there is a hemothorax with dyspnea, thoracocentesis can be a lifesaver. If a hemothorax is present but there is no dyspnea, continue to monitor, the blood may be resorbed during the course of therapy.

Minimize physical activity throughout therapy, but most stringently during the first 1-2 weeks, until clotting factors have been restored to normal by the Vitamin K. Even mild exercise can initiate a bleeding event when there is a defect in the clotting cascade.


Bromethalin is a neurotoxin that uncouples oxidative phosphorylation in CNS mitochondria. This results in lack of adequate ATP concentration and insufficient energy for maintaining Na+-K+ ion channel pumps. Loss of pump activity results in cerebral and spinal cord edema and a demyelination injury to long nerves. The usual concentration is 0.01% in both pelleted baits and in bait blocks

Bromethalin is rapidly absorbed from GI tract. Effects are mostly neurological, and can mimic a number of different disorders Minimal lethal dose of bait generally reported in dogs is 25 gm bait or 2.5 mg active ingredient/kg BWT. APCC data had documented deaths in dogs at doses as low as 0.96 mg/kg. Cats are far more sensitive to this agent than are dogs. For cats it is only 4.5 gm bait /kg BWT. As most packets are 21 grams, a single packet can be lethal to a 10-pound cat. Interestingly, the toxicity on a dose/kg basis in a bait formulation is much higher than reported based on toxicity studies in which the technical bromethalin was used.

Dogs seem to have both a low-dose and a high-dose syndrome. With lower doses signs may not appear for 72-96 hours, and include hind limb ataxia and paresis, decreased proprioception, loss of deep pain response, vocalizations, patella hyper-reflexia, CNS depression progressing to coma, vomiting, and fine muscle tremors. At or above the mean lethal dose, signs can begin within 12-24 hours and include severe tremors, hyperthermia, extreme hyperexcitability, running fits, hyperesthesia and seizures.

Treatment of clinical signs is directed to controlling cerebral edema, and is mostly frustrating and non-productive. Mannitol, corticosteroids and diazepam may be used. Animals with sub-lethal doses will require good nursing care and supplemental feedings.


Cholecalciferol is a Vitamin D3 analog. It alters calcium metabolism in the body, increasing intestinal absorption and renal tubular reabsorption of calcium and stimulating bone resorption. Clinical signs of intoxication usually develop within 12-36 hours. Early signs include lethargy, weakness, anorexia, polydipsia, polyuria, and vomiting, often with blood. Biochemical alterations include hyperphosphatemia within 12 hours and hypercalcemia within 24 hours of exposure and azotemia (both renal and pre-renal). The elevated calcium levels result in calcification of many tissues, notable renal tubules and iwalls of blood vessels. The elevated calcium also has a direct effect on kidney function, sometimes causing acute renal failure even without mineralizations.

Without an observed exposure, diagnosis can be challenging. Differentials for hypercalcemia must include the normal juvenile state, hypercalcemia of malignancy, a hypoadrenal condition, primary renal failure, primary hyperparathyroidism, and disuse osteoporosis.

Diagnosis of toxicosis is based on history of exposure, clinical signs, serum chemistries and urinalysis. Run baseline chemistries as soon as possible after a known exposure. Pursue GI decontamination if within several hours of ingestion, or if there is evidence of ingestion (chewed box) at unknown time but a still asymptomatic animal.

Treatment is aimed at lowering the serum calcium and phosphorus levels if the product of Ca X Phos is over 60, preventing a rise in these values if still normal, and stopping further calcium mobilization from the bones. IV normal saline at twice maintenance, prednisone and furosemide all enhance calciuria. Monitor serum calcium, phosphorus, BUN and creatinine daily to judge effectiveness of therapy. Especially with a young animal, don't wait for sign to begin to start treating. If calcium levels are rising despite calciuresis, best choice is pamidronate (Aredia™). Unlike salmon calcitonin, it needs to be given only once, with a repeat dose possibly at about 5-7 days. It acts at the level of the osteoclast and is deposited in the bone itself. Dose is 60-90 mg (about 1.3 mg/kg) mixed in 500-700 ml saline and given slowly over 2-4 hours. A drawback can be the expense, about $250-300/60 or 90 mg vial. The advantage is that it works quickly in a majority of dogs. We have also documented the use and rapid response in at least one cat.

Once the pamidronate has been administered, it is important to taper the initial treatments (prednisone, furosemide) and decrease the rate of fluid administration. Continue to monitor calcium, phosphorus, and kidney values during this time. End of therapy will be marked by a return to normal of kidney values and the decrease of calcium x phosphorus levels (in mg/dl) to less than 60.

Zinc Phosphide

Zinc phosphide is an old rodenticide posing as a new one. The dark gray powder in not soluble in water, is commonly sold as a 2%-5% bait, and may be in the form of a paste or tracking powder as well as a grain-based product. In the past several years an oat-based bait labeled for killing prairie voles has been marketed. There is evidently no way to identify this as bait, and not just as oats, once the product is removed from the bag; this has proved lethal to a number of horses.

The phosphide salts are unstable in an acid environment. At gastric pH they degrade rapidly to form phosphine gas. Phosphine gas, when inhaled, results in acute non-cardiogenic pulmonary edema. When absorbed systemically, it is thought to block cytochrome C oxidase, leading to formation of highly reactive oxygen compounds.It is these reactive compounds which cause most of the tissue injury, most severe damageis in tissues with the highest oxygen demand – brain, lungs, liver and kidney.

Lethal doses cattle, sheep, pigs, goats, dogs, and cats range between 20-50 mg/kg. For a 55 pound (25 kg) dog, that would be between 10 grams (0.35 ounce) and 25 grams (just under an ounce) of 5% bait. Severely poisoned animals may die in 3-5 hours. Those who survive longer that 48 hours have a pretty good chance.

Initial signs may vary by species, as well as by the dose. Onset of signs is normally between 15 minutes to 4 hours post ingestion. Vomiting, often with blood, is common. Dogs may show lateral recumbency with whole body tremors and salivation.

Other signs may include anorexia and lethargy. Rapid deep breathing may signal the onset of the pulmonary changes. Abdominal pain, ataxia, and weakness leading to recumbency may follow. Hyperesthesia and seizures may develop that resemble the signs of strychnine toxocosis.

Metabolic acidemia ensues. Other biochemical changes may include depressed serum calcium and magnesium. If there is survival beyond 48 hours an elevated blood urea is common. Hepatic enzymes may elevate after several days as well.

Hepatic and renal damage often may be detected 5-14 days later.

Initial decontamination is tempered by the wish to keep the stomach pH as high as possible to prevent the formation of phosphine gas. If there has been no spontaneous vomiting, it may be better to induce emesis with apomorphine rather than hydrogen peroxide. Giving food, commonly done in order to improve gastric emptying and the response to peroxide, will trigger release of gastric acid and increase the rate of production of phosphine. If you are going to perform gastric lavage, add an alkalizing component like a magnesium and aluminum hydroxide gel to your lavage liquid. Also consider mixing into your activated charcoal preparation.

Supportive care included IV fluids to maintain blood pressure renal perfusion, and gastroprotectants like carafate or kaopectate after decontamination is completed. Corticosteroids won't hurt. Seizures may respond to diazepam, or may require barbiturates or full anesthesia. Since the most severe injury is probably due to action of the oxygen radicals, use of an antioxidant may be useful – consider vitamin C or n-acetylcysteine.

Caution: Phosphine gas released from vomitus or stomach washings can cause significant illness in veterinary personnel assisting animal. Phosphine has been describes as having a spoiled fish or garlic odor. It is detectable at 1-3 ppm in air; maximum allowed in air in occupational situations is 0.3 ppm, so if you can smell it, you are being exposed to a concentration that can be harmful.

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