Bromide is considered an effective anticonvulsant drug for treating primary epilepsy in dogs. Bromide acts on GABA-mediated
chloride ion channels by inducing a competitive displacement of chloride, potentiation of chloride activity and consequent
hyperpolarization and stabilization of excitable neurons. Bromide also inhibits carbonic anhydrase. This element is rapidly
absorbed through the gastrointestinal mucosa, is not bound to serum proteins and readily enters the cerebrospinal fluid. It
is excreted unchanged by the kidneys and is reabsorbed in renal tubules. The half-life in dogs is about 25 days.
Bromide toxicosis (bromism), which involves the ingestion of excessive bromide-containing compounds, is infrequently seen
in dogs. The serum bromide concentration poorly predicts impending bromism in this species. Although reported clinical signs
attributed to bromism in dogs include central nervous system depression, central nervous system hyperexcitability, ataxia,
tetraparesis and paraparesis, there is still uncertainty concerning the risk factors and outcomes associated with bromism
in dogs with idiopathic epilepsy.
A recent retrospective study evaluated the clinical signs, risk factors and outcomes associated with canine idiopathic epilepsy
treated with potassium or sodium bromide.1 The study reports clinical observations in 31 dogs with bromism. The mean (± standard error of the mean [SEM]) serum bromide
concentration in dogs with bromism yielded 3.7 (± 0.3 mg/ml), whereas the mean (± SEM) serum bromide concentration in dogs
without bromism was 1.7 (± 0.1 mg/ml). Clinical experience and results of other studies indicate that in most dogs with idiopathic
epilepsy, a steady-state serum bromide concentration within the range of 1 to 2.5 mg/ml is apparently adequate when phenobarbital
is given in conjunction with bromide. Dogs treated with bromide alone may require a higher (2 to 3.5 mg/ml) serum bromide
concentration.
It is important to note that dogs treated with bromide may have artifactually elevated chloride assays. It is also important
to purchase relatively small bottles of bromide solution (e.g., one-month supply) to avoid elevated bromide concentrations
due to evaporation and possible bromide overdose.
Table 1: Clinical And Neurologic Signs Attributed To Bromism In Dogs
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Neurologic examinations revealed clinical signs suggestive of diffuse intracranial disease, upper motor neuron or lower motor
neuron paraparesis and diffuse motor neuron disease (flaccid tetraparesis); one dog had cerebellar ataxia (Table 1).1 Of the dogs with diffuse intracranial disease, the predominant clinical signs included stupor, coma, bilateral mydriasis
associated with slow and incomplete pupillary light reflexes, head pressing, bilateral thalamocortical blindness, propulsive
pacing and intermittent periods of aggression. Ataxia was present in dogs with tetraparesis or paraparesis. Two dogs with
diffuse motor neuron disease also had a history of regurgitation, flaccid tetraparesis and megaesophagus, and one dog also
had dysphagia.
Suboptimal monitoring of serum bromide concentrations was the most commonly implicated reason for the development of bromism.1 Reduction in renal function, suboptimal treatment monitoring and iatrogenic bromide dosing error may predispose to bromism.
A patient's sex, bromide formulation, bromide dosing interval, total number of prescribed bromide dose changes in the year
preceding referral to the veterinary hospital, concurrent treatment with phenobarbital, phenobarbital dosing interval, concurrent
medications or concurrent disease were not significantly associated with bromism.1 However, for a 5-mg/kg increase in the total daily dose of bromide, the odds of having bromism increased almost fivefold.
In two dogs, iatrogenic bromide dosing errors were identified when the formulation was changed from the potassium salt to
the sodium salt of bromide in order to reduce vomiting associated with bromide administration.1 In two other dogs, the concentration of administered bromide was increased from 250 to 500 mg/ml without a recommended concurrent
volume reduction, resulting in a dosing error. This happened when the prescription was changed to a different compounding
pharmacy.
Exposure to sources of bromide other than bromide compounded for anticonvulsant use may be associated with ingestion of water
from either a bromide-tainted source (e.g., well water) or chemically treated spa water.
All the dogs in this study were treated with a bromide dose reduction. Patients requiring hospitalization were treated with
intravenous administration of physiologic saline solution to induce diuresis and furosemide in a few cases. Breakthrough seizures
were treated with diazepam.2 Induction of diuresis should be performed judiciously and in conjunction with serial monitoring of serum bromide concentrations
to avoid breakthrough seizures. Interestingly, none of the patients in this study that received furosemide experienced breakthrough
seizures.
Rapid clinical improvement with treatment and a satisfactory clinical recovery are expected in most cases of bromism in dogs.
Dr. Bichsel completed his residency in neurology at the University of Georgia in 1984. He is a diplomate of the American College of Veterinary
Internal Medicine and works at the Animal Emergency and Referral Center in Ft. Pierce, Fla.
Dr. Lyman is a diplomate of the American College of Veterinary Internal Medicine and is the founder and president of Animal Emergency
and Referral Center in Ft. Pierce, Fla.
References
1. Rossmeisl JH, Inzana KD. Clinical signs, risk factors, and outcomes associated with bromide toxicosis (bromism) in dogs
with idiopathic epilepsy. J Am Vet Med Assoc 2009;234(11):1425-1431.
2. Trepanier LA. Use of bromide as an anticonvulsant for dogs with epilepsy. J Am Vet Med Assoc 1995;207(2):163-166.
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