What will happen if a dog eats mouse poison? - briefly
The dog will likely experience severe toxicity, including internal bleeding, seizures, or organ failure, and requires immediate veterinary emergency treatment. Delayed care dramatically reduces the chance of survival.
What will happen if a dog eats mouse poison? - in detail
If a canine ingests a typical rodenticide, toxic substances enter the bloodstream and interfere with vital physiological processes. The most common agents are anticoagulant compounds (e.g., brodifacoum, difenacoum), neurotoxic chemicals (bromethalin, zinc phosphide), and hypercalcemic agents (cholecalciferol). Each class produces a characteristic pattern of clinical signs, onset times, and required interventions.
Anticoagulant rodenticides block the vitamin K‑dependent clotting cascade. Initial symptoms—weakness, pale mucous membranes, and mild bruising—appear within 24–48 hours. As factor levels decline, spontaneous bleeding may occur in the gastrointestinal tract, lungs, or body cavities, often evident as melena, hematuria, or internal hemorrhage. Laboratory tests reveal prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT). Prompt administration of vitamin K1 (phytonadione) at 5–10 mg/kg orally every 24 hours for 3–4 weeks reverses coagulopathy. Supportive care includes fluid therapy, blood transfusions, and control of active bleeding.
Bromethalin, a neurotoxic agent, disrupts mitochondrial oxidative phosphorylation, leading to cerebral edema. Clinical signs emerge 12–48 hours post‑exposure and may include tremors, seizures, ataxia, and coma. No specific antidote exists; treatment focuses on aggressive decontamination (emesis or activated charcoal within the first two hours) and symptomatic management with anticonvulsants and osmotic diuretics to reduce intracranial pressure.
Zinc phosphide reacts with gastric acid to release phosphine gas, a potent cellular poison. Early manifestations—vomiting, abdominal pain, and respiratory distress—appear within minutes to a few hours. Rapid progression to hepatic necrosis, renal failure, and cardiovascular collapse is common. Immediate gastric lavage, activated charcoal, and supportive intensive care (hemodialysis, hepatic protectants) improve survival odds, but prognosis remains guarded.
Cholecalciferol (vitamin D3) rodenticides cause hypercalcemia by increasing intestinal calcium absorption. Signs develop over 24–72 hours and include polyuria, polydipsia, vomiting, lethargy, and, in severe cases, cardiac arrhythmias and renal failure. Blood work shows elevated calcium and phosphorus levels. Treatment consists of intravenous fluid diuresis, bisphosphonates (e.g., pamidronate), calcitonin, and corticosteroids to lower serum calcium. Continuous monitoring of electrolytes is essential.
Diagnosis relies on a thorough history of possible exposure, identification of the specific product, and targeted laboratory testing (coagulation profile, serum calcium, liver enzymes, toxicology screens). Early veterinary intervention dramatically reduces mortality across all toxin classes. Owners should keep all rodent control products out of reach, store them securely, and seek immediate professional care if ingestion is suspected.