How does mouse poison affect humans? - briefly
Ingestion or absorption of mouse poison can lead to internal bleeding, organ failure, or neurotoxic effects, depending on whether the product contains anticoagulants, bromethalin, or similar agents. Immediate medical intervention with appropriate antidotes or supportive care is required to prevent serious or fatal outcomes.
How does mouse poison affect humans? - in detail
Rodenticide compounds used to control mice contain active ingredients that can be absorbed by humans through ingestion, inhalation, or skin contact. The most common agents are anticoagulants (e.g., warfarin, brodifacoum), neurotoxicants (e.g., bromethalin, zinc phosphide), and metabolic disruptors (e.g., cholecalciferol). Each class produces a distinct pattern of toxicity.
Anticoagulant rodenticides interfere with vitamin K recycling, preventing synthesis of clotting factors II, VII, IX, and X. Initial symptoms appear 24–48 hours after exposure and include nosebleeds, gum bleeding, blood in urine or stool, and bruising. Laboratory tests reveal prolonged prothrombin time and reduced fibrinogen levels. Without prompt administration of vitamin K1 (phytonadione) and supportive care, severe hemorrhage can occur in internal organs, leading to fatal outcomes.
Neurotoxic rodenticides such as bromethalin block mitochondrial ATP production, causing cerebral edema and increased intracranial pressure. Early signs involve headache, dizziness, nausea, and vomiting. Progression leads to seizures, loss of motor control, and coma. Treatment is largely supportive; no specific antidote exists, so rapid decontamination and intensive monitoring are critical.
Zinc phosphide releases phosphine gas when it contacts stomach acid. Phosphine inhibits cellular respiration, resulting in multi‑organ failure. Clinical presentation includes abdominal pain, respiratory distress, hypotension, and metabolic acidosis. High‑dose exposure often proves lethal despite aggressive supportive measures. No antidote is available; management focuses on ventilation, cardiovascular support, and toxin removal.
Cholecalciferol (vitamin D₃) induces hypercalcemia by increasing intestinal calcium absorption. Symptoms develop within 12–24 hours and consist of nausea, vomiting, polyuria, polydipsia, and confusion. Laboratory analysis shows elevated serum calcium and suppressed parathyroid hormone. Treatment requires intravenous fluids, diuretics, bisphosphonates, and calcitonin to lower calcium levels.
Risk factors for severe poisoning include pediatric exposure, accidental ingestion of bait, occupational handling without protective equipment, and chronic low‑level intake. Prevention strategies involve securing bait in tamper‑proof containers, using low‑toxicity formulations, and providing clear labeling. In cases of suspected exposure, immediate medical evaluation, identification of the specific rodenticide, and initiation of appropriate antidotal therapy are essential to mitigate morbidity and mortality.