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Rodenticides: The old and the new (Proceedings)
Bromethalin is one of the lesser known rodenticides on the market, and poisoning in dogs and cats is most likely underreported.
Bromethalin is one of the lesser known rodenticides on the market, and poisoning in dogs and cats is most likely underreported. Minimum toxic/lethal dose of the bait is approximately 16-25 g/kg BW in dogs and 4.5 g/kg BW in cats. Relay toxicosis may be a concern in cats who are excellent mousers. Bromethalin is an uncoupler of oxidative phosphorylation within the central nervous system, and clinical signs in poisoned animals may mimic many other clinical syndromes. Low dose exposures have been known to cause depression, and hind limb paresis and paralysis. High dose exposures can cause muscle tremors, hyperexcitability, hyperesthesia [which is seen with strychnine, metaldehyde, penitrem A, and organochlorine poisonings], vomiting, dyspnea and seizures. There is generally a delay of several hours to a few days between the time of ingestion and the onset of clinical signs. Treatment recommendations include decontamination of the asymptomatic patients, with particular emphasis on repeated doses of activated charcoal, along with symptomatic therapy based on the patient's need. Despite many different treatment options being tried over the years, most affected patients do not survive. Confirmation of exposure can be done by residue testing of liver, kidney and brain tissue. Histopathologic examination of the brain may show vacuolation and edema of many areas of the white matter.
Anticoagulant rodenticides are still one of the more common poisonings seen in dogs by veterinarians. Despite years of use and careful and poignant label instructions to keep out of reach of pets and children, dogs [less commonly cats] are common culprits of its toxic effects. There are 11 compounds on the market, and greater than 90% of all poisonings are due to the long acting, second generation ones. The most common ones seen by our veterinary teaching hospital are brodifacoum, diphacinone, chlorophacinone, bromadiolone and difethialone and 85% of the poisonings occur in dogs. Despite popular rumors, poisonings are typically the result of direct ingestion of the bait, NOT ingestion of rodents poisoned by the baits. These rodenticides, along with the coccidiostat sulfaquinoxaline, inhibit the enzyme vitamin K epoxidase, necessary in the recycling of vitamin K; clotting factors 2, 7, 9 and 10 are ultimately depleted and inhibition of the clotting cascade occurs. Prolonged clotting times [PT, PTT] will be seen within 24 to 48 hours of ingestion; however, clinical signs associated with hemorrhage may not be visibly present until a few days later.
The most important aspect of these poisonings is that clinical signs, clinical pathological changes, lesions and treatment options will reflect/depend on the site, speed and amount of hemorrhage. Hemorrhage can occur anywhere. Approximately 50% of affected animals will bleed into their lungs, thereby exhibiting depression, epistaxis, weakness, coughing and pallor. The remaining animals can bleed anywhere [e.g., thymus, urinary bladder, spinal cord, post surgical sites, abdominal cavity, retroperitoneal space]; therefore, clinical signs can be quite varied. Anticoagulant rodenticide should always be on the differential list for a patient exhibiting bleeding and abnormal clotting times [PT, PTT, ACT]. Imaging should be considered to localize the location of the hemorrhage, and tapping of the source should only be done after clotting times are assessed. Testing for the rodenticides can be done on blood [antemortem] or liver [postmortem]. Sulfaquinoxaline testing can also be done on liver.
For the exposed but non-bleeding patient, inducing emesis along with repeated doses of activated charcoal and cathartic will help reduce further absorption of the rodenticide. If the exposure dose is high enough [LD50s are reported for some of the compounds], vitamin K1 therapy [1.25-2.5 mg/kg bid with fatty meal, PO; only go SQ with starting dose if patient is vomiting or AC was administered] should be initiated for 2-4 weeks. For the bleeding patient, decontamination procedures are generally not worthwhile due to time delay between ingestion and onset of bleeding. When clotting times are prolonged, plasma transfusions are a necessity. Blood transfusions may be necessary if the patient is severely anemic. Vitamin K1, at 2.5 mg/kg bid with a fatty meal, should be administered for a minimum of 4 weeks. Other supportive measures may include broad spectrum antibiotics, oxygen therapy and exercise restriction. Removing free blood from the thoracic cavity should only be performed where respiratory function is severely compromised. It is recommended that clotting times be re-examined 2-3 days following cessation of vitamin K therapy.
Some of these rodenticides are known to cross the placenta and deleterious effects have been observed in newborn pups. It has also been shown that these compounds can be secreted into the milk, so nursing pups or kittens should be protected by early weaning or administering oral vitamin K1 therapy.
Strychnine containing rodenticides can still be found over the counter in some parts of the US, and can cause an acute onset of severe extensor rigidity, seizures, and death. Many strychnine baits are grain based [wheat, oats, sorghum], and are green/red in color. Onset of signs typically occurs within 15 to 30 minutes of ingestion, and death can rapidly ensue. Many exposures are confirmed postmortem, by testing vomitus/stomach contents for strychnine [though serum and urine can be used antemortem]. Treatment is symptomatic and supportive. Aggressive decontamination procedures, particularly activated charcoal, can significantly enhance the prognosis of the patient. Clinical signs typically abate with 24 to 72 hours.
Zinc phosphide is another rodenticide [also used as an insecticide] that can be found over the counter, but the clinical syndrome is quite different than the previously described rodenticides. Within the acidic environment of the stomach, zinc phosphide releases phosphine gas which is a severe gastrointestinal and systemic toxin. Lethal dose are reported to be around 20-50 mg/kg in most species. The onset of clinical signs is generally quite rapid, and can include severe gastrointestinal pain, vomiting, diarrhea, weakness, depression, recumbency, seizures and death. Death is generally a result of cardiovascular collapse, with pulmonary, hepatic and renal complications. Treatment is symptomatic and supportive in nature, and confirmation of exposure is often difficult due to the dissipation of the gas.
Persistent hypercalcemia and hyperphosphatemia in dogs and cats can be due to ingestion of cholecalciferol-containing rodenticides [or antipsoriatric medication like Dovonex]. Toxicities with the rodenticide can be seen at exposures as low as 2 mg/kg BW. The minimum toxic dose of calcipotriene is 10 µg/kg, and the lethal dose is around 65 µg/kg. The metabolite 1,25-dihroxycholecalciferol causes increased calcium and phosphorus absorption from the intestines, enhanced calcium release from bones, and increased renal distal tubular reabsorption of calcium.
Clinical signs associated with hyperphosphatemia and hypercalcemia develop within 3-5 days after cholecalciferol ingestion, and 4-6 hours following calcipotriene ingestions. Signs may include anorexia, depression, lethargy, vomiting, generalized muscle weakness, PUPD, cardiac arrhythmias and seizures. Death is generally the result of multiple organ failure [renal, GI, cardiac, respiratory, vascular] due to soft tissue calcification. Serum and kidney levels of 25-hydroxycholecalciferol can be evaluated to confirm exposures. Treatment plans should include decontamination procedures if deemed appropriate, calcitonin or pamidronate disodium, diuresis with physiologic saline, furosemide, prednisone or prednisolone, and oral phosphate binders coupled with periodic chem panels and UAs. Treatment can last 2-4 weeks, or longer.
Dorman DC. 2006. Bromethalin. In Small Animal Toxicology, Eds. ME Peterson and PA Talcott, Elsevier Inc., pp. 609-618.
Murphy MJ and Talcott PA. 2006. Anticoagulant rodenticides. In Small Animal Toxicology, Eds. ME Peterson and PA Talcott, Elsevier Inc., pp. 563-577.
Sheafor SE and Couto CG. 1999. Anticoagulant rodenticide toxicity in 21 dogs. J Am Anim Hosp. Assoc 35:38-46.