What happens if a cat eats poison intended for mice? - briefly
Ingesting rodenticide can cause rapid onset of severe toxicity in a cat, leading to internal bleeding, organ failure, seizures, and potentially death; prompt veterinary treatment is critical to improve survival chances.
What happens if a cat eats poison intended for mice? - in detail
If a cat ingests a product designed to kill rodents, the animal is exposed to chemicals that are often far more potent for small mammals than for felines, yet toxicity can be severe. The outcome depends on the active ingredient, the amount consumed, and how quickly veterinary care is obtained.
Rodenticides fall into several categories, each with a distinct mode of action:
- Anticoagulants (e.g., warfarin, brodifacoum): Inhibit vitamin K recycling, leading to progressive loss of blood clotting ability.
- Neurotoxic agents (e.g., bromethalin, chlorophacinone): Disrupt neuronal ion channels or mitochondrial function, causing central nervous system failure.
- Metal phosphides (e.g., zinc phosphide): Release phosphine gas in the acidic stomach, producing cellular damage and respiratory collapse.
- Calcium channel blockers (e.g., diltiazem formulations): Interfere with cardiac conduction and muscle contraction.
Clinical signs appear according to the toxin’s mechanism:
- Anticoagulants: Bruising, petechiae, hematuria, melena, lethargy; coagulation tests become abnormal within 24–48 hours.
- Neurotoxics: Tremors, ataxia, seizures, paralysis; symptoms may emerge within a few hours and progress rapidly.
- Phosphides: Salivation, vomiting, abdominal pain, dyspnea, sudden collapse; respiratory distress can develop within minutes.
- Calcium blockers: Weak pulse, hypotension, arrhythmias, depression; cardiovascular collapse may be immediate.
Veterinary assessment includes a thorough history, physical examination, and targeted laboratory work: complete blood count, coagulation profile, serum biochemistry, and, when indicated, toxicology screens. Imaging is rarely required unless secondary trauma is suspected.
Emergency treatment protocols are toxin‑specific:
- Decontamination: Induce emesis only if ingestion occurred within 1–2 hours and the product is not a caustic acid; otherwise, administer activated charcoal to bind residual poison.
- Anticoagulant poisoning: Give vitamin K1 (phytonadione) orally or intravenously for several weeks; provide fresh frozen plasma or prothrombin complex concentrate for acute bleeding.
- Neurotoxic exposure: Maintain airway protection, control seizures with benzodiazepines, and support circulation with fluids and vasopressors as needed.
- Phosphide ingestion: Administer oxygen, provide intravenous fluids, and consider sodium thiosulfate or other antidotes under experimental protocols; monitor for metabolic acidosis.
- Calcium‑blocker toxicity: Use calcium gluconate boluses, high‑dose insulin‑glucose therapy, and lipid emulsion infusion to counteract cardiac depression.
Prognosis improves markedly with prompt intervention. Mild anticoagulant exposure often resolves with vitamin K therapy, while severe neurotoxic or phosphide poisoning may be fatal despite aggressive care. Factors such as the cat’s size, overall health, and time to treatment heavily influence survival odds.
Preventive measures include storing rodent control products in secured containers, using bait stations inaccessible to pets, and selecting cat‑safe alternatives (e.g., mechanical traps). Regular inspection of areas where bait may be hidden reduces accidental ingestion risk.