Bromide
is an old anticonvulsant drug. It works by replacing negatively
charged chloride ions through the chloride channels causing neuronal
hyperpolarisation. Bromide has synergistic effect with drugs
that enhance chloride conduction (such as phenobarbitone). Bromide
is usually administered as the potassium salt (KBr) but sodium
salts may be used in patients with adrenal insufficiency and
renal dysfunction.
Bromide
is slowly excreted by the kidneys without the requirement for
hepatic biotransformation. Bromide has a very long half-life
(25 to 46 days) in dogs
so steady state serum concentration is not reached for 3 to 6 months.
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Fact Sheet Bromide |
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Indications
Bromide is commonly used in combination with phenobarbitone in refractory epileptics
or in patients that have suffered liver disease. It should be used with
caution in patients with impaired renal function.
Dose
Recommended oral dosage in dogs is 30 mg/kg once daily. Therapeutic
serum concentrations are 880 to 3000 mg/ml as a solitary agent and 810
to 2400 mg/ml in combination with phenobarbitone.
If
adequate serum concentrations are needed rapidly, a loading dose
of bromide can be used. For a more rapid effect than that obtained
with oral maintenance
dosing regimes, a per rectum loading protocol has been devised. Intrarectal
administration may be preferred in the patient that is heavily sedated from
prior diazepam and phenobarbitone administration. A loading dose for KBr
(600 mg/kg) can be administered over a 24-hour period as 6 per
rectum boluses (100mg/kg,
q 4h). The side-effects seen with the use of this regime may be transient
diarrhoea and sedation.
Side
effects
Tend to be dose-dependent and include: polyuria, polydipsia, polyphagia, transient
sedation or ataxia during the first 2 to 3 weeks (before tolerance develops).
Hyperactivity and pruritus may be seen occasionally. Overdosage may be associated
with ataxia, depression, tremors, neuropathies, stupor or coma (bromism) – sodium
chloride IV or orally accompanied by furosemide may be considered.
Bromide
is a gastric irritant and may cause vomiting – this may
be minimised by administering bromide with or shortly after feeding.
References
Nichols
ES, Trepanier LA, Linn K (1996) Bromide toxicosis secondary
to renal
insufficiency in an epileptic dog. JAVMA 208, 231-233.
- PubMed -
Podell
M, Fenner WR (1993) Bromide therapy in refractory canine
idiopathic epilepsy. JVIM 7, 318-327.
- PubMed -
Shaw
N, Trepanier LA, Center SA et al (1996) High dietary
chloride content associated with loss of
therapeutic serum bromide concentrations in an epileptic dog. JAVMA 208,
234-236. - PubMed -
Yohn
SE, Wallace BM, Sharp PE (1992) Bromide toxicosis (bromism)
in a dog treated with potassium bromide for refractory seizures. JAVMA 201,
468-470. - PubMed -
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