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What is your diagnosis? Marked hyperchloremia in a dog
Ida Piperisova1, Jennifer A Neel, Mark G Papich
1Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.
Veterinary Clinical Pathology
|April 28, 2009
Summary
A dog experienced severe neurological issues due to bromide toxicity from compounded medication. Discontinuing the medication led to rapid recovery, highlighting the importance of medication accuracy.
Area of Science:
- Veterinary Neurology
- Clinical Toxicology
- Canine Medicine
Background:
- A 5-year-old Cavalier King Charles Spaniel presented with progressive paresis.
- The dog had a history of urolithiasis and was treated with potassium citrate capsules for 2 years.
- Initial diagnostic workup, including advanced imaging, did not reveal the cause of the neurological signs.
Observation:
- Neurologic examination, spinal radiography, and MRI revealed no causative lesions.
- Clinical chemistry showed marked hyperchloremia (179 mmol/L) and a negative anion gap (-50.4 mmol/L).
- Serum bromide concentration was critically elevated at 400 mg/dL.
Findings:
- Analysis of the compounded potassium citrate capsules revealed a mean bromide concentration of 239 mg/capsule.
- The severe hyperchloremia and negative anion gap were attributed to bromide toxicity.
- The toxicity was likely caused by the pharmacy inadvertently using bromide instead of citrate.
Implications:
- This case underscores the critical importance of accurate pharmaceutical compounding and quality control.
- It highlights the need for clinicians to consider medication formulation errors as a cause of unexpected clinical signs.
- Awareness of common laboratory analyte interferences and pursuing logical diagnostic pathways are crucial for accurate diagnosis and treatment, even with seemingly straightforward patient histories.
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