What will happen if someone eats mouse poison? - briefly
Ingestion of rodenticide that contains anticoagulant compounds triggers uncontrolled internal bleeding, with symptoms such as bruising, blood in urine, and severe weakness appearing within hours to several days. Prompt medical treatment with vitamin K antagonists and supportive care is essential to prevent fatal outcomes.
What will happen if someone eats mouse poison? - in detail
Ingestion of rodenticide introduces toxic compounds that interfere with normal physiological processes. The most common categories are anticoagulant agents, neurotoxic substances, calcium‑disrupting compounds, and phosphide formulations. Each class follows a distinct pathophysiology.
- Anticoagulants (e.g., warfarin‑derived baits) block vitamin K recycling, preventing synthesis of clotting factors II, VII, IX, and X.
- Neurotoxins such as bromethalin impair mitochondrial function, leading to cerebral edema.
- Calcium‑based poisons (cholecalciferol) cause hypercalcemia, damaging kidneys and heart tissue.
- Zinc phosphide releases phosphine gas in the acidic stomach environment, producing cellular respiration failure.
Symptoms appear after a latency that varies by agent. Anticoagulant poisoning typically manifests 24–48 hours post‑consumption with bruising, bleeding from mucous membranes, hematuria, and melena. Neurotoxic exposure produces lethargy, ataxia, tremors, and seizures within hours. Hypercalcemia induces nausea, vomiting, polyuria, and cardiac arrhythmias soon after ingestion. Phosphine poisoning leads to rapid onset of abdominal pain, dyspnea, hypotension, and metabolic acidosis.
Clinical evaluation includes a thorough history of possible exposure, physical examination for bleeding or neurological deficits, and laboratory tests. Coagulation profiles (prothrombin time, activated partial thromboplastin time) identify anticoagulant effects; serum calcium levels detect hypercalcemia; arterial blood gases reveal acidosis in phosphide cases; neuroimaging may be warranted for severe neurotoxic signs.
Treatment strategies depend on the toxin:
- Decontamination – activated charcoal administered promptly reduces systemic absorption.
- Antidotes – vitamin K₁ (phytonadione) restores clotting factor synthesis in anticoagulant poisoning; calcium‑channel blockers and diuretics manage hypercalcemia; there is no specific antidote for bromethalin, requiring supportive care; phosphine toxicity relies on aggressive supportive measures, including ventilation and renal replacement therapy.
- Symptomatic care – blood product transfusions for hemorrhage, anticonvulsants for seizures, and fluid resuscitation for hypotension.
Prognosis correlates with the amount ingested, time to treatment, and toxin class. Early administration of vitamin K₁ improves survival in anticoagulant cases, while delayed care in phosphide poisoning often results in fatal outcomes. Continuous monitoring of coagulation status, electrolyte balance, and organ function is essential throughout recovery.
Prevention emphasizes secure storage of rodent control products, child‑proof packaging, and public education on the dangers of accidental ingestion.