What will happen if a dog eats a poisoned mouse? - briefly
The dog will absorb the toxin, which can cause vomiting, diarrhea, seizures, cardiac arrhythmias, or organ failure depending on the poison and amount ingested. Immediate veterinary care is required to administer antidotes, supportive therapy, and increase the chance of survival.
What will happen if a dog eats a poisoned mouse? - in detail
When a dog swallows a rodent that has been treated with poison, the toxic agent enters the gastrointestinal tract and begins to be absorbed into the bloodstream. The clinical picture depends on the type of poison, the dose ingested, the size of the animal, and the time elapsed before treatment.
Absorption and distribution
- Oral ingestion allows the toxin to pass through the stomach and small intestine, where it is taken up by the mucosal lining.
- Once in circulation, the substance is carried to target organs (liver, kidneys, heart, nervous system) according to its chemical affinity.
Typical toxic classes and their effects
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Anticoagulant rodenticides (e.g., warfarin, brodifacoum)
- Inhibit vitamin K‑dependent clotting factors.
- Initial signs may be absent for 24–48 hours; later symptoms include petechiae, bruising, hematuria, and prolonged bleeding from wounds or surgery sites.
- Laboratory findings: prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), decreased plasma fibrinogen.
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Bromethalin
- Disrupts mitochondrial oxidative phosphorylation.
- Early manifestations: weakness, ataxia, tremors, seizures.
- Progresses to coma and respiratory failure if untreated.
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Zinc phosphide
- Reacts with gastric acid to produce phosphine gas.
- Causes rapid cardiovascular collapse, respiratory distress, and hepatic necrosis.
- Mortality often occurs within hours.
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Metal phosphides (aluminum, magnesium)
- Generate phosphine similarly to zinc phosphide but with higher toxicity.
- Clinical course: vomiting, abdominal pain, shock, multi‑organ failure.
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Neurotoxic agents (e.g., strychnine, organophosphates)
- Strychnine blocks inhibitory glycine receptors, leading to severe muscle spasms and opisthotonus.
- Organophosphates inhibit acetylcholinesterase, producing salivation, lacrimation, bronchoconstriction, and seizures.
Diagnostic approach
- Obtain a thorough history: time of exposure, suspected rodenticide brand, amount potentially consumed.
- Perform physical examination focusing on mucous membranes, coagulation status, neurologic function, and cardiovascular parameters.
- Run blood work: CBC, serum chemistry, coagulation profile, and specific toxin assays when available.
Therapeutic measures
- Decontamination: induce emesis only if ingestion occurred within 1–2 hours and the toxin is not a caustic agent; administer activated charcoal to bind residual poison.
- Antidotes:
- Vitamin K1 (phytonadione) for anticoagulants, administered orally or intravenously for several weeks.
- N‑acetylcysteine for bromethalin‑induced oxidative stress (experimental).
- Specific anticholinesterase agents (atropine, pralidoxime) for organophosphate poisoning.
- Supportive care: intravenous fluids, blood product transfusions for coagulopathies, anticonvulsants for seizures, oxygen therapy, and intensive monitoring.
- Prognosis: improves markedly with early recognition and appropriate treatment; delayed intervention increases risk of irreversible organ damage or death.
In summary, ingestion of a poisoned mouse initiates a cascade of toxic effects that vary with the chemical class involved. Prompt identification of the toxin, rapid initiation of decontamination, administration of targeted antidotes, and comprehensive supportive care are essential to mitigate morbidity and maximize survival.