Rat Poisoning (Rodenticide Toxicity)

1. Anticoagulant Rodenticides (Most Common)

First-Generation: Warfarin-Based

• Mechanism: Inhibits vitamin K epoxide reductase, blocking synthesis of clotting factors II, VII, IX, and X (the vitamin K-dependent factors). This leads to a bleeding diathesis.
• Toxicity: A single small ingestion in children is typically insignificant. Significant coagulopathy requires either a large single dose or repeated exposures over several days.
• Onset: Anticoagulant effect begins within 12-48 hours.
• Half-life: ~42 hours.

Second-Generation: Superwarfarins (Most Potent, Most Common)

• Mechanism: Same as warfarin but far more potent and longer acting.
• Onset: Coagulopathy within 24-48 hours after intentional ingestion.
• Duration: A single ingestion of brodifacoum can cause marked anticoagulation for weeks to months due to its ~120-day half-life.
• Key diagnostic trap: Superwarfarins are NOT detected by standard warfarin assays. Specific reference laboratory assays are needed.

Indandione Derivatives

Clinical Features (All Anticoagulants)

• Easy bruising, prolonged bleeding from cuts
• Epistaxis (nosebleeds), hemoptysis
• Hematuria, hematemesis, rectal bleeding
• Intracranial hemorrhage (severe cases)
• Unexplained coagulopathy - especially in children or depressed patients who deny ingestion

Lab Findings

• Elevated PT/INR (primary marker)
• Large doses may also prolong aPTT
• Check INR at baseline, 12-24 hours (warfarin), and 24-48 hours (superwarfarin)

Treatment

2. Non-Anticoagulant Rodenticides

Bromethalin (Second Most Common Ingested Agent in U.S.)

• Mechanism: Uncouples oxidative phosphorylation in the CNS, causing cerebral edema.
• Clinical features: Hind limb weakness/paralysis, tremors, seizures, coma. Onset may be delayed 1-4 days.
• Treatment: Supportive. Activated charcoal. No antidote. Mannitol for cerebral edema.

Zinc Phosphide

• Mechanism: Reacts with stomach acid to produce phosphine gas, a potent mitochondrial toxin. Also damages blood vessels and blood cells.
• Clinical features: Loss of appetite, vomiting, diarrhea, abdominal pain, rapid breathing, lethargy, convulsions, paralysis, coma, death.
• Hazard: Phosphine gas can off-gas from vomitus - a real danger to healthcare workers. All treatment must occur in a well-ventilated space.
• Treatment: Supportive. No specific antidote.

Strychnine

• Mechanism: Competitive antagonist of glycine (the inhibitory neurotransmitter) at postsynaptic motor neurons in the spinal cord and brainstem. This causes uncontrolled muscle excitation.
• Clinical features: Restlessness, muscle twitching, painful muscle spasms, opisthotonos (arching of the back), trismus (jaw clenching), inability to swallow, facial cramping, respiratory failure and death.
• Treatment: Airway control, minimize all sensory stimulation (light, sound, touch can trigger spasms), activated charcoal, benzodiazepines/barbiturates. Neuromuscular blockade if necessary. Avoid gastric lavage - can precipitate seizures.

Sodium Fluoroacetate (1080)

• Mechanism: Blocks the Krebs cycle (citric acid cycle), halting cellular energy production.
• Clinical features: Nausea, vomiting, lactic acidosis, seizures, coma, ventricular arrhythmias (VT/VF), pulmonary edema, hypocalcemia.
• Treatment: Activated charcoal, seizure and dysrhythmia control. Glycerol monoacetate, calcium gluconate, sodium succinate may be used. Toxicologist consultation required.

Thallium Sulfate

• Mechanism: Binds mitochondrial sulfhydryl groups, interfering with oxidative phosphorylation.
• Clinical features (classic triad): Painful ascending peripheral neuropathy, gastrointestinal symptoms, and alopecia (hair loss - appears 2-3 weeks post-ingestion).
• Treatment: Prussian blue (binds thallium in the gut), supportive care.

Cholecalciferol (Vitamin D3)

• Mechanism: Mobilizes calcium from bone, increases intestinal calcium absorption → hypercalcemia.
• Clinical features: Delayed 36-48 hours. Anorexia, weakness, vomiting, polyuria/polydipsia, acute renal failure (2-3 days post-exposure), soft tissue calcification.
• Treatment: IV fluids, loop diuretics, calcitonin, bisphosphonates, corticosteroids.

Barium Carbonate / Salts

• Mechanism: Inhibits potassium channels → severe hypokalemia.
• Clinical features: Vomiting, diarrhea, abdominal pain, muscle weakness, paralysis, cardiac arrhythmias, respiratory failure. Onset within ~8 hours.
• Treatment: Activated charcoal + sodium/magnesium sulfate (converts barium carbonate to less toxic barium sulfate), aggressive potassium replacement.

Arsenicals

• Mechanism: Binds sulfhydryl groups on proteins, disrupting multiple enzyme systems.
• Clinical features: Dysphagia, nausea/vomiting, bloody diarrhea, muscle cramps, QT prolongation, cardiovascular collapse, altered mental status, seizures, late peripheral neuropathy.
• Treatment: Activated charcoal + chelation with succimer or dimercaprol (BAL).

Pyriminil (Vacor) - now banned in the U.S.

• Mechanism: Destroys pancreatic beta cells through nicotinamide antagonism, impairing NAD/NADH synthesis.
• Clinical features: Permanent insulin-dependent diabetes mellitus, autonomic neuropathy.

Tetramine (TETS)

• Mechanism: Blocks GABA receptors in the CNS.
• Clinical features: Rapid onset - headache, nausea, dizziness, then seizures and respiratory failure. Very lethal (~6-12 mg can kill an adult).
• Treatment: Benzodiazepines or barbiturates for seizures. No antidote.

General Approach to Any Rodenticide Ingestion

1. Identify the agent - retrieve packaging if possible; do not assume "just rat poison."
2. Stabilize airway, breathing, and circulation.
3. Activated charcoal - useful in most cases if within 1-2 hours of ingestion (avoid in strychnine/seizure risk until airway secured).
4. Specific antidotes where available (Vitamin K for anticoagulants; chelation for arsenic/thallium; Prussian blue for thallium).
5. Contact Poison Control (US: 1-800-222-1222) for guidance.
6. Serial monitoring - INR for anticoagulants; electrolytes, renal function, and neurological status for others.