Download: Bromethalin – Toxicology – Merck Veterinary Manual
Bromethalin, a nonanticoagulant, single-dose rodenticide, is a neurotoxin available as bars (blocks), pellets, seed, and a fake worm you can give to Moles.
The net result is cerebral and spinal edema and increased CSF pressure, leading to neurologic dysfunction.
Bromethalin can cause either an acute or a subacute/chronic syndrome, depending on the dose ingested. At doses equivalent to or more than the average lethal dose, dogs may develop an acute convulsant (or high-dose) syndrome resulting in clinical signs within 4–36 hr of exposure; such signs include hyperexcitability, muscle tremors, grand mal seizures, hindlimb hyperreflexia, CNS depression, hyperthermia, and death. The paralytic (subacute or chronic) syndrome is seen at lower doses, and clinical signs may not appear for several days (up to 7 days) after exposure. Initial signs may include depression, hindlimb weakness or paresis, decreased propioception, ataxia, and possible tremors. Muscle weakness often progresses from posterior to anterior muscles. Cats typically develop paralytic syndrome irrespective of dose of bromethalin.
Source: https://www.merckvetmanual.com/toxicology/rodenticide-poisoning/bromethalin
Based on the history of exposure, bromethalin toxicosis should be considered when there is moderate to acute onset of weakness, hindlimb paralysis, tremors, and seizures. Some other toxicologic and nontoxicologic differential diagnoses should include ethylene glycol toxicosis, marijuana ingestion, 2,4-D and other phenoxyacetic acid herbicide toxicosis, copper head snake envenomation (cats), intervertebral disc problems, spinal cord and CNS trauma, and tick paralysis.
The following can be used as a guideline to treat bromethalin exposure in dogs and cats:
At a bromethalin dosage of 0.1–0.49 mg/kg in dogs, or 0.05-0.1 mg/kg in cats, emesis alone within 4 hr of exposure may be adequate. If emesis is not successful, or if > 4 hr have elapsed since ingestion, a single dose of activated charcoal at 1–2 g/kg body wt is indicated. Whenever administering activated charcoal, the clinician must remain aware of the risk of aspiration or hypernatremia secondary to fluid shift into the gut. The clinical signs of acute hypernatremia may mimic those seen with bromethalin toxicosis.
Diazepam, barbiturates, and other anticonvulsant medications should be used to control seizures and other CNS signs. Full recovery may require days to weeks of treatment.
At a bromethalin dosage of 0.5–0.75 mg/kg in dogs, or 0.1–0.3 mg/kg in cats, an initial dose of activated charcoal at 1–2 g/kg body wt should be considered. A repeat dose at half the original dose at 8-hr intervals for a total of three doses can be administered, again being aware of and monitoring for possible hypernatremia.
At a bromethalin dosage of ≥0.75 mg/kg in dogs, or ≥0.3 mg/kg in cats, administration of six doses of activated charcoal over 48 hr (repeat every 8 hr) can be considered to reduce the body burden by interrupting enterohepatic recirculation.
Use of mannitol and corticosteroids has been suggested to treat clinical signs, because they may help manage cerebral edema due to other causes. However, this has not been shown to be very helpful, likely because of the presence of intra-myelin edema. Diazepam, barbiturates, and other anticonvulsant medications should be used to control seizures and other CNS signs. Full recovery may require days to weeks of treatment.
