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Potassium Bromide Used
Alone
and as an Adjunct to Phenobarbital
compiled and written by
Guardian Angel Robin Welty

Potassium
bromide (KBr) is a salt that breaks down into its basic components, potassium
and bromide, when it comes in contact with water. Once
in the brain, the bromide component becomes negatively charged ions and causes
the brain cells to also become negatively charged.
It’s this negative state which seems to inhibit the excitability of nerve cells
and helps to prevent the cells of the brain from firing in a random and
haphazard manner. This is how potassium bromide helps
to control seizures.
KBr is an old drug and was used to treat human epileptics over 200 years ago,
but over the passage of time and the discovery of new anticonvulsants, KBr
apparently became less popular. However, potassium bromide is becoming
more popular today to treat canine epilepsy and has been shown to be effective
especially in dogs with seizures that are resistant to standard therapies
including phenobarbital (Pb).
POTASSIUM BROMIDE AS AN ADD ON DRUG TO PHENOBARBITAL
Phenobarbital is what many veterinarians choose first when an anti-seizure
drug is indicated for a dog. Phenobarbital has been successfully used in dogs
for decades and has always been considered a relatively safe drug. Only
recently has it been recognized that 20% of the dogs on Pb therapy develop liver
dysfunction which can result in death if not properly treated. As a result, KBr
is now becoming the first drug of choice for veterinarians. KBr
and Pb are often used together to achieve control with dogs whose seizures are
not well controlled by phenobarbital alone.
The use of potassium bromide appears to be relatively safe in dogs even when
used over months or years and monitored correctly. Unlike PB, which is processed
through the liver, KBr is broken down through the kidneys and does not have any
known liver toxicity.
WHAT ABOUT KBr ALONE AS AN ANTICONVULSANT?
I know there are many List members who only use potassium bromide on their dogs
and have had good success. Here is what Lauren Trepanier, DVM, Ph.D. of Cornell
University has to say about this:
“The relative efficacy of bromide alone compared to phenobarbital alone is still
not clear. In the handful of epileptic dogs that we have treated with bromide
from the time of initial diagnosis, bromide appears to be quite
effective as a single agent. Because of the risk of hepatotoxicity with
phenobarbital, bromide may be preferable as a first line agent, with smaller
doses of phenobarbital added later if additional seizure control is needed.
Only further experience with clarify this issue.”
WHAT'S THE BEST STARTING DOSE FOR POTASSIUM BROMIDE?
Based on clinical experience, the recommended starting dose for bromide in dogs
is 20-30 mg per kilogram (to determine your dogs kilograms, divide the weight in
pounds by 2.2). KBr is given once or twice daily in either capsule or liquid
form. I’ve found the liquid to be more manageable and easier to dose than the
capsules (the liquid also seems to be a bit more inexpensive). The liquid is
also available in several different flavors which can be easily
dispensed on food and your dog often never knows it’s there!
Remember, that blood levels of KBr should be monitored 1-2 months after
treatment has begun, after any changes in dose or 1 month after stating thyroid
medication. Thereafter, 6-month monitoring is recommended.
IS A LOADING DOSE NECESSARY FOR YOUR DOG?
A loading dose of KBr may be necessary for dogs with frequent or severe seizures
or for dogs who don’t respond to Pb therapy. Since KBr
normally takes longer to reach therapeutic levels (sometimes up to 2 to 3
months), a loading dose can achieve therapeutic levels in most dogs in 4-5 days.
This is a serious question which I had to consider since my Missy was not
responding to increasing doses of phenobarbital and her cluster seizures were
very
severe and frequent. A loading dose of 600 mg/kg was recommended for her, and I
rather reluctantly took the plunge.....it was a very long 5 days, but her
cluster pattern WAS broken!!! Her seizures immediately became less frequent and
severe. Last year, she even enjoyed 8 months seizure-free!!!
PLEASE remember, you must consult with a veterinarian who has some experience in
this area because close monitoring is imperative when a loading dose is
recommended.
WHAT ARE THE POSSIBLE SIDE EFFECTS OF POTASSIUM BROMIDE?
Lethargy, sedation, ataxia (loss of coordination) are quite common side effects
of KBr, along with an increase in thirst and hunger. Although these behaviors
can cause concern, they will usually subside in a relatively short
period of time. For Missy, it seemed to take longer than normal to see
improvement in her severe ataxia and lethargy, so be aware that every dog is
different when it comes to side effects. Please keep in mind if these
behaviors, especially ataxia, do not improve in a few days or weeks, serum
bromide levels should be checked. It’s possible that a slight reduction in the
bromide dose should be considered.
For some dogs, KBr can also cause stomach upset and/or vomiting. I found that
giving KBr with meals, when possible, is a definite plus in avoiding an upset
tummy. Another option to consider is switching to sodium bromide which has all
of the anticonvulsant properties, but does not seem to cause gastrointestinal
problems.
Restlessness and agitation can also be caused by KBr and/or Pb
therapy. This is not a side effect for all dogs and often a small dose of
Melatonin is very effective, especially at night.

REFERENCES:
Dayrell-Hart B, Steinberg SA, VanWinkle TJ, Farnbach GC. Hepatotoxicity of
phenobarbital in dogs: 18 cases (1985-1989). JAVMA 1991; 199: 1060-1066.
Podell M, Fenner WR. Bromide therapy in refractory canine idiopathic epilepsy. J
Vet Intern Med 1993; 7: 318-327.
Trepanier LA. Use of bromide as an anticonvulsant for dogs with epilepsy. JAVMA
1995; 207: 163-166.
Trepanier LA, Van Schoick A, Schwark WS, Carrillo J. Therapeutic serum drug
concentrations in epileptic dogs treated with potassium bromide alone or in
combination with other anticonvulsants. JAVMA 1998; 213: 1449-53.
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