TL;DR: With the advent of newer cholecalciferol and bromethalin-based rodenticides, therapeutic failures may occur more commonly, necessitating more broad-based and often more intensive therapeutic measures.
Abstract: Rodenticides continue to be the cause of a significant number of animal poisonings each year. Anticoagulants are the most commonly encountered rodenticides, and poisonings are often successfully managed with vitamin K1 and blood transfusions. However, with the advent of newer cholecalciferol and bromethalin-based rodenticides, therapeutic failures may occur more commonly. Cholecalciferol rodenticides produce severe life-threatening hypercalcemia, which may result in dystrophic mineralization of the kidney, stomach, and other organs. Bromethalin is an uncoupler of oxidative phosphorylation, producing increased cerebrospinal fluid pressure. Clinical signs of bromethalin poisoning include depression, hind-limb paresis, paralysis, tremors, and, occasionally, seizures. Unlike the case of anticoagulant rodenticides, there is no specific antidote (e.g., vitamin K1) for these newer rodenticides, necessitating more broad-based and often more intensive therapeutic measures.
TL;DR: The effects of administration of a commercially available extract of Gingko biloba (EGB) on bromethalin-induced brain lipid peroxidation and cerebral edema in adult male Sprague-Dawley rats was determined and treatment was associated with a statistically significant decrease in clinical sign severity.
Abstract: The effects of administration of a commercially available extract of Gingko biloba (EGB) on bromethalin-induced brain lipid peroxidation and cerebral edema in adult male Sprague-Dawley rats was determined. Gingko biloba extract was given (100 mg/kg) by gavage immediately after bromethalin (1.0 mg/kg) administration. Rats were euthanatized at 24 hours after dosing. Brain lipid peroxidation was determined by measurement of brain malonaldehyde-thiobarbituric acid chromophore (MDA-TBA) concentration, brain sodium concentration, and brain water content. Treatment of bromethalin-dosed rats (10/group) with EGB was associated with a statistically significant (P less than 0.05) decrease in clinical sign severity, compared with bromethalin-dosed saline solution-treated rats. All rats given bromethalin and saline solution developed clinical signs of toxicosis including CNS depression, hind limb weakness, ataxia, paralysis, and coma. Some rats given bromethalin and EGB developed clinical signs, however, none developed hind limb paralysis. The brain MDA-TBA concentration (2.4 +/- 0.5 delta MDA-TBA concentration/mg of protein), percentage of water in brain tissue (80.3 +/- 0.30%), and brain sodium concentration (6.68 +/- 0.21 mg/g of dry weight) were significantly increased in rats given bromethalin and saline solution, compared with control rats given saline solution (1.0 +/- 0.1 delta MDA-TBA concentration/mg of protein; 78.1 +/- 0.33% water in brain tissue; 4.83 +/- 0.30 mg of brain Na+/g of dry weight) and rats given bromethalin and EGB (1.6 +/- 0.2 delta MDA-TBA concentration/mg of protein; 79.3 +/- 0.31% water in brain tissue; 5.37 +/- 0.34 mg of brain Na+/g of dry weight).(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: Clinical evidence of successful treatment with ILE as an antidote for previously unpublished toxicities (amlodipine, carbamate, methamphetamine, and dextroamphetamine sulfate), additional evidence of success in treating baclofen and ivermectin toxicosis, as well as unsuccessful treatment of bromethalin and organophosphate toxicities.
Abstract: The objective of this retrospective study was to describe the responses to treatment with intravenous lipid emulsion (ILE) and the outcomes for a variety of severe intoxications. This case series includes 10 client-owned animals, 9 dogs and 1 cat, that underwent treatment with ILE for a variety of severe intoxications over a 4-year period. History, physical examination findings, clinical signs, clinicopathological test results, treatment, response to treatment, and outcome were recorded. Eight of the 10 patients survived to discharge. The toxicities included in this case series were baclofen, ivermectin and spinosad plus milbemycin oxime, baclofen and tadalafil, carbamate, methamphetamine, dextroamphetamine sulfate, amlodipine, bromethalin, and organophosphate. The two patients who died were intoxicated with bromethalin and an organophosphate. Six of the 10 patients developed lipemia secondary to ILE administration, and there were no other known adverse effects. Overall, ILE was a safe therapeutic option. This case series provides clinical evidence of successful treatment with ILE as an antidote for previously unpublished toxicities (amlodipine, carbamate, methamphetamine, and dextroamphetamine sulfate), additional evidence of success in treating baclofen and ivermectin toxicosis, as well as unsuccessful treatment of bromethalin and organophosphate toxicities.
TL;DR: Intravenous lipid emulsions (ILEs) were used with increasing frequency in both human and veterinary medicine to treat numerous acute systemic toxicities and to the authors' knowledge, this is the first report describing treatment of bromethalin ingestion with ILE.
Abstract: Bromethalin is a central nervous system toxin currently incorporated into several different rodenticides. In 2008, the EPA requested that manufacturers phase out second-generation anticoagulant rodenticides. In response, manufacturers began to increase production of bromethalin-based rodenticides. It is likely that pet exposure to bromethalin will increase in the future. Bromethalin has no known antidote and tends to deposit in fat. Intravenous lipid emulsions (ILEs) are being used with increasing frequency in both human and veterinary medicine to treat numerous acute systemic toxicities. A 4 yr old spayed female Pit bull terrier was presented following witnessed ingestion of bromethalin rodenticide by the owners. Decontamination was unsuccessful and ILE was started. Serum was frozen at -80°C before and 1 hr after completion of ILE. In rats, the half-life of desmethylbromethalin, the toxic metabolite, has been reported at 5.6 days and 6 days, and it is likely to be similar in dogs. The only intervention between the pre-lipid serum sample and the post-lipid serum sample was the administration of ILE, and the serum desmethylbromethalin levels were reduced by 75% (from 4 ppb to 1 ppb) during this time. To the authors' knowledge, this is the first report describing treatment of bromethalin ingestion with ILE.