The concentration of bromide in serum, the clinical response and the therapeutic effect of administration of the product may vary between individuals.
The presence of cluster seizures/status epilepticus, due to the severity of the seizure activity, is often associated with poor response to anti-epileptic treatment. In these cases, remission (seizure freedom) may be difficult to achieve. For dogs with normal hepatic function, phenobarbital is generally considered the first choice antiepileptic drug. However, potassium bromide can be recommended as alternative, especially in dogs with hepatic dysfunction or in dogs with concurrent disorders requiring life-long administration of potentially hepatotoxic medications, since potassium bromide is not metabolised in the liver.
A high chloride intake can increase the elimination of bromide. An increase in the dog’s salt intake may require an adjustment in bromide dose. The salt content of a dog’s diet during the treatment period should be maintained at a stable level. It is advisable not to change the dog’s diet during therapy.
Potassium bromide is a halide anticonvulsant. Bromide replaces chloride in all body fluids. It competes with chloride transport across nerve cell membranes and inhibits sodium transport and so causes membrane hyperpolarisation. This hyperpolarisation raises the seizure threshold and prevents the spread of epileptic discharges. Bromide has effects on active transport across ganglial cell membranes and affects passive movements of ions by competition with chloride for anion channels in post-synaptic membranes that are activated by inhibitory neurotransmitters. This potentiates the effect of GABA which results in a synergistic activity of bromide with other drugs that have GABA-ergic activity, such as phenobarbital.
After oral administration, the potassium bromide salt dissociates and bromide ions are absorbed passively by the gastrointestinal tract. After absorption, the bromide ion rapidly and widely distributes, as does chloride, throughout the extra-cellular space and into cells. As the bromide level is increased in the body, the concentration of chloride is decreased in direct proportion to the increase in bromide. The half-life can vary significantly with dietary chloride content, from approximately 14 days to more than 40 days. Due to this extremely long half-life, it can take several weeks / months to achieve steady state serum concentrations. Bromide ions are excreted unchanged as the monovalent anion. Excretion of bromide is mainly via glomerular filtrations in the kidneys. The rate of elimination of bromide ions increases with chloride intake, as bromide competes with chloride for tubular reabsorption.