How does a rat die from rat poison? - briefly
The anticoagulant poison blocks vitamin K recycling, causing uncontrolled internal bleeding that leads to cardiovascular collapse within 2–3 days. Death occurs when hemorrhage compromises vital organs such as the lungs and brain.
How does a rat die from rat poison? - in detail
When a rodent consumes an anticoagulant rodenticide, the active compound blocks the enzyme vitamin‑K epoxide reductase. This enzyme is essential for recycling vitamin K, which in turn is required for the synthesis of clotting factors II, VII, IX and X in the liver. As the toxin accumulates, the production of functional clotting proteins declines sharply.
Within 24–48 hours after ingestion, the animal’s blood loses its ability to form stable fibrin clots. Minor injuries that would normally seal quickly begin to bleed persistently. Internal hemorrhage appears in the lungs, gastrointestinal tract, pericardium and skeletal muscles. Blood loss leads to hypovolemia, reduced oxygen delivery, and ultimately circulatory collapse.
The clinical progression typically follows this pattern:
- 12–24 h: mild lethargy, reduced appetite, slight tremor.
- 24–48 h: visible bruising, nosebleeds, blood‑tinged urine or feces, difficulty breathing due to pulmonary hemorrhage.
- 48–72 h: extensive internal bleeding, severe anemia, shock, loss of consciousness.
- 72 h+ (if untreated): irreversible organ failure and death.
Some rodenticides act by a different mechanism. Zinc phosphide releases phosphine gas in the acidic stomach environment. Phosphine interferes with cellular respiration by inhibiting cytochrome c oxidase, causing rapid depletion of ATP. The resulting metabolic collapse produces respiratory distress, seizures, and cardiac arrest within a few hours.
Bromethalin, a neurotoxic compound, uncouples oxidative phosphorylation in mitochondria. The toxin raises intracellular cyclic AMP levels, leading to cerebral edema and seizures. Death usually occurs within 24 hours from respiratory failure and severe neurological impairment.
Regardless of the specific agent, the lethal outcome is the result of either catastrophic loss of hemostasis or profound disruption of cellular energy metabolism. The time to mortality varies with the dose, the type of poison, and the animal’s physiological state, but the underlying processes—coagulopathy, hemorrhage, or mitochondrial failure—remain consistent across most formulations.