Front Page VSPN Message Boards Chat Library Continual Education Search MyVSPN Help Frequently Asked Questions Send us Feedback! Industry VetQuest Search & Referral and Classifieds The Pet Care Forum Y2Spay
Menu bar   Go to the Portal
Back Print Save Bookmark in my Browser Top of Page. Front Page : Library : Rodenticides
Small Animal Toxicoses - Rodenticides

Charlotte Means, DVM, MLIS

Rodenticides are one of the most common poisonings in veterinary medicine. Of available commercial rodenticides, anticoagulant, bromethalin, and cholecalciferol rodenticides are the most likely to be encountered in practice. The mechanism of action, clinical signs, diagnosis, and treatment are unique to each class of rodenticide. Because of these differences, a veterinarian must obtain a good exposure history. Accurate identification of a rodenticide requires obtaining the trade name of the product, the generic active ingredient, and the concentration of the active ingredient. The EPA registration number can also be used to accurately identify a rodenticide. In most cases, the color and formulation (blocks versus place packs) do not provide accurate clues to the type of rodenticide.


Sources: First generation anticoagulants include coumarin, warfarin, and indandione compounds. First generation anticoagulants generally have a shorter time frame when they are biologically active. Frequently, multiple feedings are required to produce toxicosis. Formulations and concentrations vary widely but frequently range from 0.025 to 0.005%. Commercial warfarin brands include D-Con, Warf, and Prolin. Indandione products include pindone (Pival, Tri-ban) and chlorophacinone (Rozol, Ramik, Patrol.)

Second generation anticoagulants have increased single feeding lethality. These products also have a much greater biologically active time frame. Brodifacoum is the most common active ingredient used and is usually found in 0.005% concentrations (D-Con Mouse Prufe II, Talon-G). Bromadiolone is found in brands such as Contrac, Maki, and Hawk. Diphacinone is found in Ramik, Tomcat, and Ditrac. It is important to remember many companies produce more than one type of rodenticide. Many brands, due to space, are not listed in the proceedings.

Mechanism of action: Anticoagulants inhibit epoxide reductase, causing a loss of vitamin K regeneration. This results in depletion of vitamin K, which leads to the inhibition of coagulation synthesis. The vitamin K dependent factors are II, VII, IX, and X. The presence of circulating clotting factors, synthesized prior to the exposure, causes the delay in clinical signs. Generally 3-7 days are required before clotting factors are exhausted and clinical signs are seen.

Toxicity: Toxicosis is dependent on the dose and the susceptibility of the species. All species are susceptible if the correct dose is ingested. Relay toxicosis (poisoning by eating a poisoned animal) is unlikely unless a large percentage of the diet consists of rodents or other prey species, which might be ingesting rodenticides. Other factors, which enhance toxicity, include oral antibiotics; highly protein bound drugs, liver disease or compromised liver function, as well as age. The very young and the very old are considered to be more susceptible. Toxicity is possible when a dose is ingested greater than or equal to 1/10 of the LD50. When a range in toxicity is given, always calculate from the lowest reported number.

Reported oral LD50 for some anticoagulants
Anticoagulant Dog Cat Pig
Warfarin 5-50 mg/kg or 3 mg/kg for 5 days 5 mg/kg or 3 mg/kg for 5 days 3 mg/kg, lethal dose at 1 mg/kg for 5 days
Pindone 5-75 mg/kgrry    
Chlorophacinone 3-20 mg/kg 15 mg/kg 150 mg/kg
Brodifacoum 0.2-4 mg/kg 25 mg/kg 0.5 mg/kg
Bromodiolone 0.5-15 mg/kg 15 mg/kg 150 mg/kg
Diphacinone 0.9-8 mg/kg 15 mg/kg 150 mg/kg

Trigger dose for second generation anticoagulants is 0.02 mg/kg. Ingestions of multiple small doses over a period of several days may equal a single acute toxic dose. A trigger dose is the dose when decontamination and/or treatment is necessary.

Clinical signs: There is generally a gradual onset and signs are often vague. Initial signs often include lethargy, weakness, +/- anorexia. Owners often miss these signs or just note exercise intolerance. As bleeding progresses, signs reflect the site of bleeding. Bleeding into the joints causes lameness and swollen joints. Epistaxis, rectal bleeding, and bruising can be present but these signs are not the most common presentations. Animals are often found acutely dead. Owners frequently present a dog because of dyspnea and coughing. Bleeding into the thoracic cavity is quite common.

Clinical diagnosis: Exposure history, clinical signs, and a prolonged PT (prothrombin time) or PIVKA will generally provide a diagnosis. The PT will test both the intrinsic and extrinsic coagulation pathways. The PT will be prolonged before clinical signs of disease occur. In a recent exposure, three PT tests are recommended: baseline, 48, and 72 hours. Do not give vitamin K while running the PT because this can alter the test results. In cases where there is no known exposure but an anticoagulant toxicosis is suspected, a complete coagulation profile should be run.

On necropsy, massive internal hemorrhage and a lack of a post-mortem heart blood clot is generally present. Plasma, frozen stomach contents and a frozen post-mortem liver sample may also be checked for the presence of anticoagulants.

Treatment: Decontamination is the first line of defense. Emesis can be quite successful if vomiting is induced within the first four hours post exposure. Activated charcoal and a saline cathartic are also effective in preventing absorption.

Prophylactic vitamin K1 can be given. Vitamin K1 is very similar to natural vitamin K and works rapidly. Vitamin K1 is dosed at 3-5 mg/kg, divided dosage. Although warfarin may only require 14 days of prophylactic therapy, many of the newer anticoagulants will require at least 30 days of treatment. Vitamin K can be given with a small amount of canned food to increase absorption. A PT should be run 48 hours after the last dose of Vitamin K1 to ensure that no bleeding will occur. There are cases where treatment with vitamin K was required for 8 weeks. Vitamin K is well absorbed orally and in an asymptomatic animal is just as effective as injectable.

If an animal is symptomatic, treatment is symptomatic and supportive. Whole blood transfusions or plasma may be required to replace clotting factors. In cases of thoracic bleeding, chest tubes may be required. Oxygen, cage rest, and nutritional support are also important factors in convalescence. Higher doses of vitamin K may be required for several days after a bleeding episode. Monitor PT times to ensure the animal is producing adequate clotting factors.

Differential diagnoses: When an animal is presented with a hemorrhagic crisis, other rule outs should be considered, particularly if the animal does not respond will to vitamin K1. Autoimmune thrombocytopenia, disseminated intravascular coagulation, von Willebrandís, hemophilia, and liver disease are some of the differentials which should be considered.


Sources: Bromethalin rodenticides are increasing in popularity and usage. There are many brands available including Trounce, Assault, and Vengeance. Bromethalin was developed for use against warfarin resistant rodents. Bromethalin is classed as a diphenylamine compound. Bromethalin baits are frequently the same colors as anticoagulants and will be formulated as place packs and bars, like anticoagulants. The most common concentration is 0.01% bromethalin.

Mechanism of Action: Bromethalin causes the uncoupling of oxidative phosphorylation in CNS and liver mitochondria. This results in a decrease in ATP and alters Na/K ATPase. This leads to a functional inhibition of ion channel pumps which causes a gradual inability to maintain osmotic gradients. Fluid buildup results in cerebral edema. Decreased nerve impulse conduction occurs concurrently due to a marked increase in cerebral spinal fluid pressure.

Toxicity: Bromethalin is a somewhat slow acting, progressive neurotoxin. There are 2 syndromes that occur with bromethalin. The first occurs at high doses (at or above the LD50) and is characterized by an acute syndrome occurring within 24 hours post exposure. At lower doses, the clinical syndrome is gradual and progressive and may be delayed 3-14 days post exposure. The minimum lethal dose in the dog is about half the LD50 (2.5 mg/kg in the dog), and the minimum toxic dose is about a quarter of the LD50 (1.5 mg/kg in the dog)

Oral LD50 for bromethalin:
     Dog: 4.7 mg/kg
     Cat: 0.5-1.8 MG/KG
     Pig: 0.25 mg/kg
     Rabbit: 13 mg/kg

Clinical signs: Dose dependent signs are related to effects on the CNS. The high dose, or acute, syndrome produces muscle tremors and seizures, hyperexcitability, ataxia and paddling, hyperthermia, potential loss of vocalization, and forelimb extensor rigidity (Schiff-Sherrington.) A low dose exposure produces ataxia, posterior paresis which can be ascending, hyporeflexia, muscle tremors, CNS depression, and vomiting.

Clinical diagnosis: Exposure history and clinical signs are the most frequently used method to diagnose bromethalin toxicity. EEG changes may show a marked voltage depression and abnormal high-voltage slow-wave activity. There is no readily available test for tissue analysis. Histopathology is characterized by a diffuse spongiosis of the white matter caused by fluid-filled vacuoles in the myelin sheath.

Treatment and Management: There is no specific antidote. Aggressive decontamination is the single most important element of treatment. Typically, doses of 0.5 mg/kg or less require emesis or a single dose of activated charcoal. Doses from 0.5 to 1.0 mg/kg require emesis and 2 doses of activated charcoal. For doses > 1 mg/kg, emesis and multiple doses of charcoal (TID X 48 hours) are recommended. Emesis after 4 hours post exposure is generally ineffective.

Once clinical signs have developed, treatment is symptomatic and supportive. Cerebral edema is treated with mannitol, furosemide, and steroids. Tremors and seizures are treated with diazepam or a barbiturate. Prognosis is grave if the acute syndrome or severe signs in the delayed syndrome occur. In cases of mild toxicosis, signs generally resolve over 2-4 days with good nursing and supportive care.

Differential diagnosis: Infectious diseases such as rabies, distemper or any encephalitis should be considered as a rule out. Other toxins causing similar signs include strychnine, organophosphate or carbamate insecticides, chlorinated hydrocarbon insecticides, permethrin, as well as metaldehyde or illicit drugs.


Sources: There are many commercial brands, including Quintox, Rampage, and Hyperkil. Cholecalciferol is vitamin D3. Most baits contain 0.075% cholecalciferol.

Mechanism of action: Cholecalciferol is bioactivated to calcitrol which causes a marked increase in serum calcium ( can be >16 mg/kg.) This leads to a metastatic calcification. The calcification is found in the kidney, liver, heart, aorta, and the GI tract. The rise in blood calcium concentration is due to increased intestinal absorption of calcium, increased bone resorption of calcium, and increased renal tubular resorption of calcium. Renal failure results from vasoconstriction and renal ischemia secondary to hypercalcemia, as well as calcium deposition.

Toxicity: Cholecalciferol toxicosis is dose and age dependent. Younger animals are at greater risk for toxicity than older animals. Based on clinical cases, the minimum toxic dose is 0.5-3 mg/kg and the minimum lethal dose is 4.5 mg/kg. Real life cases differ dramatically from the technical LD50 of 88 mg/kg in the dog. The trigger dose for treatment in the dog is greater than or equal to 0.1 mg/kg.

Clinical diagnosis: Exposure history and hypercalcemia are the hallmarks of cholecalciferol toxicosis. Calcium generally elevates by 24 hours, following a hyperphosphatemia at 12 hours. Without medical intervention, calcium continues to rise over 70 hours. Additional laboratory abnormalities will include a marked azotemia, hyposthenuria, proteinuria, and glycosuria.

Necropsy findings usually show pitted and mottled kidneys with increased calcium concentrations and multifocal areas of calcification. There may be other soft tissue areas of mineralization, especially in the heart and aorta. Renal calcium to phosphorus ratios can differentiate between cholecalciferol and ethylene glycol toxicosis. Testing for cholecalciferol in bile or kidneys is performed at Michigan State University.

Clinical management and treatment: Management is intense, time consuming, and expensive. A symptomatic animal should always be stabilized first.


     <4 hours post ingestion: emesis and repeated doses of activated charcoal (2-3 doses q 8-12 hours)

     >4 hours post ingestion: activated charcoal (do not use if animal is vomiting); start on IV saline at twice maintenance for 24 hours or until calcium levels are determined.

Laboratory Monitoring:

Baseline calcium, phosphorous, BUN, creatinine; complete serum profile in elderly animals or those with pre-existing disease.

If Ca, P, BUN, Cr are normal on presentation, monitor q 12 hours X 4 days. If 96-hour calcium is normal, no additional treatment required.

If Ca, P, BUN, and/or Cr are abnormal on presentation, go to hypercalcemia management.

Monitor the Ca X P product: if > 60, then soft tissue mineralization is likely. Multiply the calcium level (in mg/dl) times the phosphorous level (in mg./dl). Some labs report values in units other than mg/dl; convert to mg/dl before computing.

Hypercalcemia Management I (preferred)-pamidronate is a biphosphonate used in humans to treat hypercalcemia of malignancy.

  • IV normal saline; twice maintenance, forced diuresis
  • Furosemide-2.5-4.5 mg/kg PO TID to QID or 5 mg/kg/hr via CRI; avoid thiazide diuretics since they reduce renal excretion of calcium.
  • Dexamethasone-1 mg/kg IV or SQ QID or Prednisone-2-3 mg/kg PO BID
  • Pamidronate (Aredia‚)-1.3-2 mg/kg; dilute in normal saline and administer IV over a two hour period.

Hypercalcemia Management II: This is a less desirable protocol since in the ASPCA Animal Poison Control center experience, calcitonin is not consistent in its ability to lower serum calcium, and some dogs become refractory to calcitonin. Additionally, in experimental dogs, concurrent use of pamidronate and calcitonin resulted in greater soft tissue mineralization than when either drug was used alone.

  • IV normal saline; twice maintenance, forced diuresis
  • Furosemide-2.5-4.5 mg/kg PO TID to QID or 5 mg/kg/hr via CRI; avoid thiazide diuretics since they reduce renal excretion of calcium.
  • Dexamethasone-1 mg/kg IV or SQ QID or Prednisone-2-3 mg/kg PO BID
  • Salmon Calcitonin (calcimar‚) 4-7 IU/kg SQ TID

Once Ca levels have stabilized:

  • Wean off fluids and monitor Ca, P, BUN, Cr at least every 24 hours. If BUN and Cr are elevated, treat for acute renal failure. If calcium levels start to rise, re-institute fluid therapy and consider another dose of pamidronate.
  • Switch to oral dexamethasone and furosemide and wean off as long as the dog is BAR.
  • Amphogel-60 mg/kg PO TID as needed if phosphorus level remains elevated.
  • Closely monitor appetite-development of anorexia may indicate the calcium level has risen.
  • If calcium, P, BUN, Cr, remain normal, recheck q 24 hours for 5-7 days, then every 2-3 days for an additional 2 weeks, and then a final test one month post exposure.

Differential diagnosis: Other causes of hypercalcemia should be considered. These rule outs include paraneoplastic disease, pseudohyperparathyroidism (most commonly observed with canine lymphosarcoma and prostatic carcinoma), secondary hyperparathyroidism, juvenile hypercalcemia and primary hyperparathyroidism. Diseases such as pyometra, diabetes, and renal disease can also mimic cholecalciferol toxicosis.

Date Published: June 11, 2001

Address (URL):

Back Print Save Bookmark in my Browser Top of Page. Front Page : Library : Rodenticides

800.700.4636  |  |  530.756.4881  |  Fax: 530.756.6035
777 West Covell Blvd, Davis, CA 95616

Copyright , Veterinary Information Network, Inc.