Anticoagulant rodenticides toxicity in pets

Anticoagulant rodenticides cause coagulopathy by reducing vitamin K1-dependent clotting factors. Second-generation anticoagulants, like brodifacoum and bromadiolone, are more toxic and persist longer in the liver than first-generation compounds such as warfarin and diphacinone, requiring extended treatment. These rodenticides inhibit vitamin K1 recycling, preventing activation of clotting factors (II, VII, IX, X) necessary for blood clot formation, leading to impaired coagulation over time.

• Generalized Hemorrhage: Clotting factor depletion causes ecchymoses and bleeding from multiple sites.

• Gastrointestinal Bleeding: Signs include epistaxis, hemoptysis, hematemesis, melena, or hemorrhagic diarrhea; severe cases may lead to live-threatening anemia.

• Respiratory Symptoms: Coughing, dyspnea, abnormal lung sounds (e.g., moist rales, dull ventral lung sounds), massive pulmonary hemorrhage, hemothorax, exercise intolerance, and acute anemia. Respiratory arrest or sudden death can occur after severe pulmonary bleeding.

• Shock: Blood loss and hypovolemia may result in hemorrhagic shock or hypoxemia. Pericardial effusion can lead to muffled heart sounds, arrhythmias, collapse, and poor cardiac filling.

• Musculoskeletal: Hemarthrosis can cause lameness, and muscle hemorrhage may occur following trauma or injections.

• CNS Signs: Rare bleeding in the brain or spinal canal can cause ataxia, lethargy, blindness, seizures, or paralysis.

• Other Signs: Hematuria, placental hemorrhage (leading to abortion), or vaginal bleeding may be present.

• Thrombocytopenia: Platelet count often decreases to 50,000–150,000 × 10³/μL due to consumptive bleeding.

• Coagulation Tests: Prolonged PT and PTT indicate rodenticide exposure. PT typically prolongs earlier (6–18 hours before PTT) and more extensively, becoming evident 36–48 hours post-ingestion. Both normalize with vitamin K1 therapy.

Detoxification:

• Recent Ingestion: Induce emesis followed by activated charcoal with a cathartic.

• Established Clinical Signs or Coagulopathy: Oral detoxification is usually ineffective but may reduce enterohepatic recirculation of second-generation compounds with activated charcoal.

Acute Care:

• Inpatient Care: Necessary during acute crises; outpatient care can follow stabilization of coagulopathy.

• Hemorrhagic Shock: Use IV crystalloids (20 mL/kg boluses over 15–20 minutes, repeat as needed), colloids, or blood products (pRBC, WB, FFP) to address anemia and replace clotting factors.

• Cardiac Tamponade or Hemothorax: Perform pericardiocentesis or thoracocentesis only if life-threatening dyspnea persists; avoid these procedures if the patient is stabilizing, as blood may reabsorb naturally. Autotransfusion can be an option if no response to therapy.

Antidote:

• Vitamin K1: Administer orally (if no contraindications like vomiting) or subcutaneously (small needle, multiple sites). Oral absorption improves with a fatty meal.

  • Dosage: 2.5–5.0 mg/kg PO daily for 5 days to 6 weeks (adjust based on compound).

  • For second-generation compounds, continue therapy for 3–4 weeks.

Restrict movement in early stages of anticoagulant toxicity to prevent increased bleeding and complications.

Monitor PT for 48–72 hours after stopping treatment. If prolonged, continue vitamin K1 therapy for an additional 1–2 weeks.

• Difethialone: dogs at LD50 = 4 mg/kg, cats LD50 >16 mg/kg.

• Brodifacoum: LD50 = 0.25–2.5 mg/kg.

• Bromadiolone: LD50 = 11–20 mg/kg.

• Chlorophacinone: LD50 = 50–100 mg/kg.

• Warfarin: LD50 = 20–50 mg/kg.

• Diphacinone: LD50 = 3–7.5 mg/kg.

Many rodenticides are toxic to pets, and early veterinary intervention is key for successful treatment. If the patient survives the first 48 hours of acute coagulopathy, the prognosis improves. Continued vitamin K1 therapy is crucial for further recovery.