Animal Health Solutions

41 Q2 2022 | Animal Health Solutions rectally, but this dosing route may result in diarrhea. Serum levels are recommended at the first steady state period (three months), and every 12 months thereafter. Potassium bromide does not cause metabolic problems such as nephropathies or hepatopathies, and if routine levels are not possible (finances of owner, etc.), bromide may be a better choice than something like phenobarbital. The therapeutic range has been reported to be 810-2400 ug/mL when both phenobarbital and bromide are used, and 880- 3000 ug/mL when bromide is used as a monotherapy. 3 As a monotherapy, bromide has been shown to reduce seizure frequency more than 50% in 73.9% of cases, and lead to a seizure-free state in 52% of cases. 4 As an add-on therapy, bromide has been shown to reduce seizure frequency by at least 50% in 65-72% of cases, and lead to a seizure-free state in 21-72% of cases. 1,3,5 Side effects typically involve sedation, ataxia, and weakness. These side effects, like many caused by anticonvulsants, are most common for several weeks after initiating bromide or following a dose increase. If these side effects do not improve with time (2-4 weeks), a dose adjustment may be indicated. Polydipsia, polyuria, and polyphagia may also be seen. Gastrointestinal upset may result due to irritation of the gastric lining by the drug itself or related to pancreatitis. Large doses may be better tolerated if divided into two daily doses instead of one, and bromide is better tolerated with food in the stomach. A potential association between the use of phenobarbital, potassium bromide, or both and the development of pancreatitis has been noted. In one study 6.8% of patients receiving one or both drugs had an elevated cPLI. 6 However, only 0.6% of dogs in that same study had evidence of clinical pancreatitis and the link is therefore not definitive. Nevertheless, epileptics taking bromide and presenting with signs of pancreatitis should at least be considered to have drug-induced pancreatitis. Bromism is a term used to describe severe adverse effects related to bromide use, and may include symptoms such as changes in mentation, ataxia, and paresis (both upper motor and lower motor neuron). One paper showed that the main variable associated with bromism is the daily dose of bromide, and those dogs that presented with bromism tended to have less-than-ideal drug level monitoring. 7 Treatment of bromism involves diuresis with 0.9% NaCl. While monitoring serum levels is one way to prevent bromism, keeping the diet similar and avoiding large fluctuations in salt content (chloride) is also recommended. 8 The author tends to use bromide in otherwise healthy suspect idiopathic epileptic patients that are not showing a significant and adequate response to monotherapy (usually phenobarbital). However, some patients are not good candidates for phenobarbital monotherapy (pre- existing hepatopathy, owners cannot commit to routine laboratory analysis of blood, once-daily dosing is required) and bromide may be a better first line monotherapy in certain circumstances. In older patients, or patients already showing significant paresis/ataxia, other anticonvulsants (levetiracetam, zonisamide, etc.) may be considered as monotherapies or add-on therapies. Patients with structural encephalopathies may be more likely to experience unacceptable side effects from drugs like phenobarbital and bromide, and in these patients levetiracetam or zonisamide might be better options. Bromide should be used cautiously or not at all in cats as a severe allergic pneumonitis has been reported. 9 Bromide has been shown to be a safe, effective, convenient, and a reliable therapy for dogs suffering from idiopathic epilepsy. 1,2,3,4,5 This author uses it frequently and believes strongly that it forms a core part of available therapeutic options for canine idiopathic epileptics. About the author Dr. Adam E. Moeser is a veterinary neurologist (DACVIM) with MedVet in Commerce, MI. Dr. Moeser completed his Doctor of Veterinary Medicine at the University of Wisconsin School of Veterinary Medicine, followed by a one-year rotating internship at the VCA Aurora and Berwyn hospitals in Illinois. He then completed a three- year neurology and neurosurgery residency at the University of Pennsylvania, and has practiced in Commerce, MI ever since. Areas of interest include canine and feline epilepsy, canine meningoencephalitides, and neurosurgery. 1) Podell M, Fenner W. Bromide therapy in refractory canine idiopathic epilepsy. J Vet Intern Med 7:318-327, 1993. 2) Podell M, Volk HA, Berendt M, et al. 2015 ACVIM consensus statement on seizure management in dogs. J Vet Intern Med 30:477-490, 2015. 3) Trepanier L, Van Schoick A, Schwark WS, et al. Therapeutic serum drug concentrations in epileptic dogs treated with potassium bromide alone or in combination with other anticonvulsants: 122 cases (1992-1996). J Am Vet Assoc. 213: 1449-1453, 1998. 4) Boothe DM, Dewey C. Comparison of phenobarbital with bromide as a first-choice antiepileptic drug for the treatment of epilepsy in dogs. J Am Vet Assoc. 240: 1073- 1083. 5) Schwartz-Porsche D, Jürgens U. Effectiveness of bromide in therapy resistant epilepsy of dogs. Tierarztl Prax. 19:395-401, 1991. 6) Albarracín V, Teles M, Meléndez-Lazo A, et al. Canine pancreas-specific lipase and c-reactive protein in dogs treated with anticonvulsants (phenobarbital and potassium bromide). Topics in Compan An Med. 30:57-61, 2015. 7) Rossmeisl Jr JH, Inzana KD. Clinical signs, risk factors, and outcomes associated with bromide toxicosis (bromism) in dogs with idiopathic epilepsy. J Am Vet Assoc. 234:1425-1431, 2009. 8) Trepanier, LA, Babish JG. Effect of dietary chloride content on the elimination of bromide by dogs. Res Vet Sci. 58:252-255, 1995. 9) Boothe DM, George KL. Disposition and clinical use of bromide in cats. 221: 1131- 1135, 2002.

• Cover