Potentially dangerous to a vast array of mammals and birds, anticoagulant rodenticides are a relatively common cause of poisoning in pets and wildlife. Intoxications in nontarget domestic animals and wildlife have resulted from several causes:
direct ingestion of bait product intended for target species
contamination of feed with anticoagulant concentrate
relay toxicosis from ingestion of prey or scavenged carrion
malicious intent (rarely)
Anticoagulant rodenticides come in a variety of formulations with many active ingredients.
First-generation anticoagulant rodenticides (eg, warfarin, coumatetralyl, pindone, chlorphacinone, and diphacinone) generally require multiple feedings by the target species before causing death.
Second-generation anticoagulant rodenticides have LD50's that are 2.5–200 times lower than those of first-generation anticoagulant rodenticides and generally require only a single feeding to result in the death of the target species. Examples include brodifacoum, bromadiolone, flocoumafen, difethiolone, and difenacoum. The toxic-dose calculations in companion animals are widely accepted as based on one-tenth of the lowest reported LD50 for a particular active ingredient in a particular species.
Anticoagulant rodenticides mechanistically inhibit the enzyme vitamin K epoxide reductase, which is crucial in the recycling and production of vitamin K1, a necessary component for clotting factors II, VII, IX, and X. When the hepatic production of these clotting factors is inhibited, prothrombin cannot be adequately converted to thrombin, and coagulopathy results. The serum half-life of the affected coagulation factors ranges from 6.2 to 16.5 hours, and circulating supplies are generally exhausted 24–64 hours after ingestion of a toxic dose of the rodenticide. Elevation of coagulation parameters is thus delayed for 2–5 days after ingestion, with clinical evidence of bleeding typically noted 3–7 days after ingestion of a toxic dose.
Pearls & Pitfalls
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Clinical Signs of Anticoagulant Rodenticide Poisoning
Clinical signs of poisoning by anticoagulant rodenticides are a manifestation of coagulopathy and bleeding. They may include inappetence, lethargy, weakness, epistaxis, respiratory distress (secondary to pleural hemorrhage and resulting hemothorax or pulmonary hemorrhage and resulting hemoptysis), hematoma or petechiation with pallor, cavitary bleeding, hematemesis, melena, hematochezia, hematuria, tachycardia, and hypovolemia. (See images of thoracic and mesenteric hemorrhage.)
Courtesy of Dr. Frederick W. Oehme.
Courtesy of Dr. Frederick W. Oehme.
Atypical clinical signs depend on the location of bleeding and may include joint pain, ataxia, seizures, pharyngeal swelling, tracheal compression, or collapse with consequent respiratory distress. Sudden death, though rare, is also possible.
Decontamination of Anticoagulant Rodenticide Poisoning
For decontamination in nonclinically affected patients with anticoagulant rodenticide poisoning:
Induction of emesis, if ingestion occurred within 4 hours, using the following:
In dogs: apomorphine, ropinirole, or hydrogen peroxide
In cats: dexmedetomidine, hydromorphone, or xylazine
Activated charcoal with a cathartic (eg, sorbitol): 1–2 g/kg, PO as aqueous slurry, repeated without a cathartic as needed at 4- to 8-hour intervals
Not pursued by all clinicians, given the availability of vitamin K1 antidote
Diagnosis of Anticoagulant Rodenticide Poisoning
Diagnostic tests include the following for nonclinically affected patients with anticoagulant rodenticide poisoning:
Baseline PCV and total protein concentration (PCV/TP) or CBC; prothrombin time (PT) and partial thromboplastin time (PTT), or PT
If exposure is questionable and vitamin K1 is withheld: PT 48 hours after ingestion. If PT is elevated, treatment should proceed.
If vitamin K1 is administered: PT 2–3 days after treatment
Diagnostic tests in clinically affected patients include the following:
Baseline PCV/TP or CBC, coagulation profile, cross-match in preparation for transfusion
PT 2–3 days after vitamin K1 treatment
Serial monitoring of PCV/TP and coagulation profiles every 6–12 hours until normalized
Thoracic or abdominal radiographs in the stable patient if clinical signs dictate the need:
For pleural hemorrhage with hemothorax: interlobar fissure lines, extraluminal tracheal deviation or compression
For pulmonary hemorrhage: air bronchogram
For hemoabdomen: loss of serosal detail
Anemia and thrombocytopenia are generally mild to moderate at the time clinical signs of anticoagulant rodenticide poisoning are noted by the animal's owner; however, the extent of anemia can be severe in some cases. PT will elevate first in dogs and cats; PTT will elevate shortly thereafter. By the time clinical evidence of a bleeding event appears, both PT and PTT are typically elevated.
Gastric contents, serum, or plasma can be analyzed for the presence of anticoagulants to confirm a diagnosis. Some veterinary diagnostic laboratories offer an anticoagulant screen to detect most anticoagulant rodenticides available in the market in the serum, plasma, liver, or kidney; however, such screens are rarely performed.
Differential diagnoses when hemorrhage is encountered may include disseminated intravascular coagulation, congenital factor deficiencies, von Willebrand disease, platelet deficiencies, and canine ehrlichiosis.
Treatment of Anticoagulant Rodenticide Poisoning
Treatment for nonclinically affected patients with anticoagulant rodenticide poisoning consists of the following:
Vitamin K1 (2.5 mg/kg, PO, every 12 hours for 28 days, or 5 mg/kg, PO, every 24 hours for 28 days)
The short half-life of warfarin (15 days) indicates that a 2-week course of vitamin K1 is typically sufficient in this less common exposure.
Reassess PT 2–3 days after treatment cessation, and if PT is prolonged, reimplement vitamin K1 for an additional 1–2 weeks, until posttreatment PT has normalized. Assessment of PT while the patient is actively taking vitamin K1 is not necessary unless the patient appears coagulopathic or inconsistent dosing is a concern.
Treatment for clinically affected patients consists of the following:
Fluid resuscitation of the hypovolemic patient, followed by IV fluid therapy at 1.5–2 times maintenance rates until the patient is noncoagulopathic and stable
Vitamin K1 (2.5 mg/kg, PO, every 12 hours for 28 days, or 5 mg/kg, PO, every 24 hours for 28 days)
SC dosing may be considered until the patient can tolerate oral medications. Due to the risk for anaphylactoid reactions, IV administration is not advised unless the product is specifically labeled for veterinary IV administration.
Oral dosing with a fatty meal to enhance bioavailability is preferred so as to decrease the risk of hematoma formation with needle sticks.
Coagulation factors are produced within 6–12 hours after implementing treatment; PT and PTT improve within 12–24 hours.
Transfusion of fresh frozen plasma or whole blood in the coagulopathic patient, depending on availability and patient needs, with a focus on providing necessary coagulation factors
Monitoring of PCV/TP and PT every 6–12 hours until values normalize and the patient is stable. Typical duration of inpatient care ranges from 1 to 3 days.
Supportive measures, such as GI support, antiemetic agents, and oxygen therapy as needed
Restriction of activity until the patient is noncoagulopathic
Key Points
Anticoagulant rodenticide leads to coagulopathy developing within 2–5 days of ingestion.
Vitamin K1 is the antidote.
PT should be checked 2–3 days after completion of treatment to confirm success.
For More Information
Murphy MJ, Talcott PA. Anticoagulant rodenticide. In: Peterson ME, Talcott PA, eds. Small Animal Toxicology. 3rd ed. Elsevier; 2013:435-445.
Brutlag AG. Anticoagulant rodenticides. In: Hovda LR, Brutlag AG, Poppenga RH, Epstein SE, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. 3rd ed. Wiley-Blackwell; 2024:787-794
Buchweitz JP. Anticoagulant rodenticides. In: Gupta RC, ed, Veterinary Toxicology: Basic and Clinical Principles. 4th ed. Elsevier; 2025:597-609.
