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Bromethalin Toxicosis 131

Bromethalin Toxicosis
VetBooks.ir Acute General Treatment Diseases and Disorders

• Symptomatic animals show neurologic
BASIC INFORMATION
deficits: depression, ataxia, paresis, hyperes- • Animals exposed < 4 hours before pre-
Definition thesia, tremors, seizures, stupor, and coma sentation should have emesis induced
A neurotoxic syndrome results from exposure • Less common findings: anisocoria, positional (p. 1188).
to bromethalin-based rodenticides. Incidence nystagmus, Schiff-Sherrington posture, exten- ○ This should be followed with 0-6 doses
of exposure is increasing in the United States sor rigidity, opisthotonus, loss of vocalization of activated charcoal, depending on the
as the second-generation anticoagulant roden- total dosage of bromethalin ingested
ticides have been removed from the market Etiology and Pathophysiology (p. 1087).
and replaced with bromethalin baits. • Bromethalin’s metabolite, desmethylbrometh- • Symptomatic patients
alin, uncouples oxidative phosphorylation ○ Mannitol 1 g/kg IV, then 0.5 g/kg IV q
Synonym in neuronal mitochondria, resulting in 6h and furosemide 2.5-4.5 mg/kg PO q
N-methyl-2,4-dinitro-N-(2,4,5-tribromophenyl)- depletion of ATP synthesis. 6-8h or 0.5 mg/kg/h IV CRI to reduce
6-(trifluoromethyl) benzenamine • Loss of ATP impairs sodium-potassium ion CNS edema. Patients receiving diuretics
pumps. Sodium and fluid accumulate within should be administered intravenous (IV)
Epidemiology the myelin sheaths, resulting in impaired balanced crystalloid fluids and moni-
SPECIES, AGE, SEX nerve conduction. tored for complications associated with
• Exposure is more common in dogs, although • Elevated intracranial pressure contributes to diuretic use.
cats are more sensitive to the toxin. CNS dysfunction. ○ Dexamethasone SP 2 mg/kg IV may also
• Juveniles are believed to be more sensitive. help with cerebral edema.
DIAGNOSIS ○ Unfortunately, the edema is within the
RISK FACTORS myelin sheaths, and these therapies are
• Indiscriminant eating habits Diagnostic Overview unlikely to be efficacious.
• Placement of rodenticide in an area accessible Diagnosis largely depends on history consistent • Control seizures with anticonvulsants such
to pets with exposure to bromethalin-based rodenticide. as diazepam 0.5-2 mg/kg IV, levetiracetam
Owner may notice color of bait passing in stool. 20-60 mg/kg IV, or barbiturates. Patients in
CONTAGION AND ZOONOSIS There are no clinically relevant tests available. status epilepticus or with refractory seizures
Relay toxicosis (toxicity after ingesting poisoned may require general anesthesia.
rodents) is not expected. Differential Diagnosis • Tremors should be treated with methocar-
• Toxic: metaldehyde, strychnine, zinc bamol 50-150 mg/kg IV, titrate up as needed;
GEOGRAPHY AND SEASONALITY phosphide, ethylene glycol, tremorgenic if exceeding 330 mg/kg/day monitor respira-
Exposure is common all year long, but an mycotoxins, hypernatremia, 5-fluorouracil, tory effort
increase in cases is seen in the fall and winter. lamotrigine, macadamia nut, opioids, • Metoclopramide 1-2 mg/kg/day CRI and/
benzodiazepines, serotonergic medications, or enemas may be helpful for animals with
Clinical Presentation muscle relaxants, avermectins ileus.
DISEASE FORMS/SUBTYPES • Nontoxic: traumatic brain injury, infectious • The use of intralipid emulsion remains
Clinical signs and their onset are dose depen- or inflammatory encephalomyelitis, neopla- controversial and is not considered to be
dent for dogs: sia, myasthenia gravis, tick paralysis, botu- part of the standard of care at this time
• Paralytic syndrome (delayed-onset syndrome): lism, polyradiculoneuritis (lipids can increase absorption of some
characterized by decreased conscious pro- toxins, and it is unknown if this happens with
prioception, paresis, ataxia, and depression. Initial Database bromethalin).
More common after an exposure below the • Affected patients show no clinically relevant • Because the prognosis is extremely
LD50 (2.4-5.6 mg/kg for dogs). Signs changes on CBC, serum chemistry, or poor after severe symptoms are recog-
develop 24-86 hours after the exposure. urinalysis. nized, humane euthanasia is a reasonable
• Convulsant syndrome (acute-onset syn- • Cerebrospinal fluid (CSF) analysis will be consideration.
drome): characterized by hyperesthesia, normal or may show mild inflammatory
hyperthermia, tremors, and seizures. Gener- changes. Possible Complications
ally seen in dogs ingesting close to or more • Iatrogenic hypernatremia can occur with use
than the LD50. Signs develop 4-24 hours Advanced or Confirmatory Testing of activated charcoal. Clinical hypernatremia
after exposure. • Histopathologic lesions of brain and spinal can mimic the symptoms of bromethalin
• Cats more commonly develop a paralytic cord consist of spongiosis of the white matter toxicosis. Monitor serum sodium levels
syndrome regardless of the amount of bait with minimal inflammatory response. frequently and provide parenteral and
ingested. • Gas chromatography can be used to detect oral fluids to patients receiving activated
bromethalin in frozen samples of kidney, charcoal.
HISTORY, CHIEF COMPLAINT fat, liver, brain, or stomach contents. • Use antiemetics to help prevent vomiting
• Witnessed or evidenced exposure to and aspiration in symptomatic patients.
bromethalin-based rodenticide TREATMENT • Neurologic deficits in symptomatic animals
• Acute onset of progressive central nervous may be permanent because of neuronal
system (CNS) signs Treatment Overview demyelination and vacuolization.
• Potentially, bait in stool In the unaffected patient with a recent exposure,
treatment is focused on thorough decontamina- Recommended Monitoring
PHYSICAL EXAM FINDINGS tion. In the symptomatic patient, treatment is • Serum sodium if giving multiple doses of
• With very recent exposure, patient is clini- focused on reducing edema in the CNS and activated charcoal
cally normal. managing the symptoms. • Neurologic status over days to weeks

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