Although intended to kill rodents, all rodenticides are potentially toxic to other mammals including humans. Many different compounds have been used to poison rodents throughout history, but the introduction of governmental regulations has curtailed the most toxic substances in favor of new agents with reduced environmental impact. Unfortunately, access to global markets can introduce foreign or previously banned products into regulated markets resulting in 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 a commonly available product can lead to inappropriate treatment. Therefore, it is important to correctly identify the compound when formulating a treatment plan. Uncommonly, illicit drugs have been adulterated with rodenticides (eg, strychnine and long-acting anticoagulants).
The mechanism of action and usual onset of action of the various rodenticides are described briefly in Table II-55.
TABLE II-55. 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 |
| 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 | 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 respiratory depression. Potential irritation or burns | Duration ~24 h, possibly longer with higher doses | No antidote. Diazepam reported effective for myoclonus |
| Cholecalciferol (vitamin D3) | Vitamin D analog causes severe hypercalcemia (see vitamins) | 4-5 mg/kg lethal in dogs | Nausea, vomiting, abdominal cramps, hypercalcemia. Toxicity more likely with chronic dosing compared with single ingestion | Onset delayed up to several days especially with repeated dosing | Symptomatic treatment for hypercalcemia |
| Coumarins (warfarin, “superwarfarins”) | See superwarfarins | Varies by product | Prolongs prothrombin time (INR) causing bleeding | Onset 1-2 days; can be prolonged | Vitamin K (see Vitamin K) |
| Crimidine. No longer produced or sold in the United States | Vitamin B6 antagonist: causes GABA deficiency leading to seizures | Less than 5 mg/kg | Limited human data. Vomiting, seizures, and status epilepticus. Pulmonary edema reported | Onset 30-60 min. Duration possibly less than 1 day | IV pyridoxine effective in dogs |
| Fluoroacetate (Compound 1080) and fluoroacetamide (Compound 1081). Severely restricted in the United States | Metabolic poison interferes with Krebs cycle and energy production. (see Fluoroacetate) | Fatal dose 2-10 mg/kg | Vomiting, diarrhea, metabolic acidosis, shock, coma | Onset delayed up to several hours | No established antidote. |
| Hydrogen sulfide | Metabolic toxin and irritant gas (see hydrogen sulfide) | 600-800 ppm rapidly fatal | Rotten egg odor; eye and upper airway irritation; headache, nausea and vomiting; sudden collapse, seizures, coma | Rapid and sudden onset | Nitrites of theoretical but unproven benefit |
| Norbromide | Unique calcium channel blocker capable of causing site-specific vascular effects in the rat that are not demonstrated in other animals | Unknown. Over 200 times more toxic to rats than other animals tested | Very limited data in humans; transient hypotension after oral 300 mg dose in one human report | Onset 1 h. Probably short-lived | No antidote known. Rats demonstrated hyperglycemia reversed by insulin |
| Organochlorines. No longer used in the United States | Lindane, endrin (see Lindane) | Varies by product | Vomiting, tremor, confusion, seizures, coma | Onset within 30-60 min | No specific antidote |
| Phosphide, Aluminum or Zinc | Liberates phosphine gas, which is a highly toxic mitochondrial poison (see phosphine) | As little as 0.5 g aluminum phosphide or 4 g zinc fatal in humans | Vomiting, diarrhea, intractable hypotension, respiratory failure, coma; high mortality rate after suicidal ingestion | Onset of GI symptoms is rapid but cardiopulmonary effects may progress over hours | No known antidote |
| Phosphorus (yellow or white) | Highly corrosive and toxic cellular poison (see phosphorus) | Fatal dose approx 1 mg/kg | Vomiting, abdominal pain, oral and gastric burns, “smoking stools,” seizures, coma, shock, arrhythmias, hepatic and renal failure | Corrosive effects immediate, other effects may be delayed hours or days | No specific antidote |
| Pyriminil (Vacor). Banned in the United States | Nicotinamide disruption: inhibits NADH-ubiquinone reductase and mitochondrial respiration leading to pancreatic B islet cell death, and progressive polyneurotoxicity | Less than 5.6 mg/kg | Transient hypoglycemia followed by diabetes mellitus. Delayed, progressive neuropathies: autonomic (orthostatic hypotension, dysphagia, and dystonia of bowel and bladder); peripheral (neurogenic myopathy, sensory and motor neuropathy); central (cortical and cerebellar dysfunction) | Onset dose dependent: high dose <7 h; smaller dose <48 h. Serious progressive symptoms evolve over weeks and are rarely reversible. Peak absorption 1-6 h | Nicotinamide given as early as possible followed by prolonged maintenance dosing |
| Red squill (Drimia maritima) | Major active toxicant is scilliroside, a bufadienolide cardiac glycoside | Unknown | Emesis, seizures, hyperkalemia, cardiotoxicity purportedly similar to digitalis | Rapid onset of vomiting; cardiac effects may be delayed | Unknown if digoxin-specific antibodies are effective |
| Salmonella enteritidis | “Ratin” no longer used in the United States or Europe because of public health threat of infection in humans | Unknown | Invasive enteric infection (salmonellosis) | Days | Treat as salmonella infection |
| Strychnine | Glycine inhibitor | As little as 16 mg fatal in an adult | Seizure-like tetanic muscle contractions, respiratory failure, rhabdomyolysis (see strychnine) | Onset 15-30 min, duration 12-24 h | No specific antidote. Sedation and neuromuscular paralysis |
| Tetramine (Tetramethylene disulfotetramine). Banned worldwide since 1984 but still illegally produced, found in some Chinese rodenticides | GABAA antagonist | 0.1 mg/kg oral and inhaled | Nausea, vomiting, dizziness, seizure, status epilepticus, and coma. Seizures very difficult to control | Onset appears dose dependent; 30 min is typical, but can be delayed 13 h. Seizures may occur later than other symptoms | Ketamine was successful in human case reports of status epilepticus; high-dose pyridoxine may also enhance effectiveness of benzodiazepines. DMPS effective in animals |
| Thallium. Banned in the United States | Generalized cellular poison (see Thallium) | Minimum lethal dose probably 12-15 mg/kg, although as little as 200 mg has caused death | Vomiting, diarrhea, shock from fluid losses; delirium and seizures; followed by hair loss and peripheral neuropathy. | Onset 12-14 h after ingestion | Prussian blue (see Prussian blue) |
See Table II-55.
The clinical manifestations of poisoning by each of the agents are described briefly in Table II-55.
Depends on the agent and may be very difficult if the identity of the product is unknown. For some agents, such as the superwarfarins (see Warfarin), prolongation of the PT/INR and onset of bleeding may be delayed by 1-3 days. The onset/duration for many of the listed products is an estimation based on acute human poisoning reports and mammalian poisoning studies when human data is lacking. Beware that for some substances the time of onset may be quicker with higher doses and slower with lower doses.