A 5-year-old neutered male Cavalier King Charles Spaniel was evaluated for a 3-week history of progressive
paresis. The dog had been receiving
potassium citrate capsules to acidify urine for the past 2 years because of an earlier history of
urolithiasis. Results of neurologic examination, spinal cord radiography, and magnetic resonance imaging of the skull and spinal cord revealed no lesions that could have accounted for the
neurologic signs. The main abnormalities on a clinical chemistry profile were marked hyperchloremia (179 mmol/L, reference interval 108-122 mmol/L) and an anion gap of -50.4 mmol/L (reference interval 16.3-28.6 mmol/L). Because of the severe hyperchloremia, serum
bromide concentration was measured (400 mg/dL; toxic concentration >150 mg/dL; some dogs may tolerate up to 300 mg/dL). Analysis of the
potassium citrate capsules, which had been compounded at a local pharmacy, yielded a mean
bromide concentration of 239 mg/
capsule. Administration of the capsules was discontinued and there was rapid resolution of the dog's
neurologic signs. This case of extreme
bromide toxicity, which apparently resulted from inadvertent use of
bromide instead of
citrate at the pharmacy, illustrates the importance of knowing common interferents with analyte methodologies and of pursing logical additional diagnostic tests based on clinical and laboratory evidence, even when a patient's history appears to rule out a potential etiology.