Although intended to kill rodents, all rodenticides are potentially toxic to nontargeted mammals including humans. Many different compounds have been used to poison rodents throughout history, but in modern times governmental regulation has attempted to limit the most toxic substances in favor of new poisons with reduced environmental impact. Occasionally with today's global market access, foreign or banned formulations have been introduced into regulated markets and caused unexpected poisonings. There is no way to reliably identify a rodenticide based on its color, shape, or size, and mistakenly assuming that an unknown rodenticide is one of the commonly available products could lead to inappropriate treatment. Therefore, it is important to correctly identify the compound when determining an observation time and treatment plan.
The mechanism of action and usual onset of action of the various rodenticides are described briefly in Table II–57.
TABLE II–57.MISCELLANEOUS RODENTICIDESa, b |Favorite Table|Download (.pdf) TABLE II–57. MISCELLANEOUS RODENTICIDESa, b
|Rodenticide ||Mechanism of Toxicity ||Estimated Toxic Dose ||Clinical Presentation ||Onset/Durationa ||Antidote or Specific Treatment |
|Acetylcholinesterase inhibitors (Carbofuran severely restricted in the United States) ||Cholinergic crisis (see Organophosphates) ||Varies by product ||Vomiting, diarrhea, salivation, sweating, bronchorrhea, fasciculations, muscle weakness ||Depends on the specific compound ||Atropine and pralidoxime (see Atropine and Glycopyrrolate and Pralidoxime (2-PAM) and Other Oximes) |
|ANTU ||Covalent binding to pulmonary endothelial cells and hepatic microsomes leads to inflammation and cell damage. ||Unknown ||Sudden onset of white frothy and prolific bronchial secretions, pulmonary edema and hepatotoxicity. Used experimentally to induce acute lung injury in animals ||Onset 1–4 h ||No antidote. Ketamine and midazolam were protective in rat models. Glutathione depletion enhanced toxicity in rats |
|Arsenic (inorganic salts). Severely restricted in the United States ||See Arsenic ||Varies with the form ||Vomiting, watery diarrhea, rhabdomyolysis, cardiac and neurotoxicity ||Onset minutes to hours ||Consider chelation (see Arsenic) |
|Barium carbonate ||Blocks potassium channels (Barium) ||1–30 g ||Vomiting, diarrhea, muscle weakness, profound hypokalemia, ventricular arrhythmias ||Onset 10–60 min ||Restore potassium levels. Oral magnesium sulfate to convert barium ions into insoluble barium sulfate |
|Bromethalin ||Uncouples mitochondrial oxidative phosphorylation targeting the central nervous system leading to cerebral edema and myelin sheath abnormalities. ||Unknown. Human death at 0.33 mg/kg ||Based on animal and limited human data. Mild GI upset possible. CNS target symptoms: hyperexcitability, altered mental status, ataxia, tremor, seizures, coma, cerebral edema, increased intracranial pressure and paralysis ||Dose-dependent onset in animal studies: high dose 2–36 h; lower dose 86 h latency. Time to peak 4 h, half-life 5, 6 days, Vd 0.7 L/kg ||No antidote. Consider multi-dose activated charcoal to interrupt enterohepatic recirculation for the first 2–3 days unless intestinal ileus occurs |
|Chloralose ||Unknown, possibly similar to other chloral sedative–hypnotics, but with additional unidentified neurostimulant action ||Hypnotic oral dose 75 mg; severe toxicity ~20 mg/kg ||Vomiting, bronchorrhea, metabolic acidosis, myoclonus or seizures, coma and ...|