A 5-year-old male Maltese dog was presented with generalized tonic seizures and hypermetria. Multiple nodular subcortical cerebellar enhancements and meningeal enhancement were observed on magnetic resonance imaging. Fluorodeoxyglucose-positron emission tomography/computed tomography was performed due to suspicion of neoplastic disease, and no fluorodeoxyglucose uptake was observed in the intracranial structures. In PET images of this dog, absent fluorodeoxyglucose uptake was identified in the brain indicating no cerebral metabolism, strongly suggested brain death. The dog had no spontaneous breathing and no brainstem reflexes for more than 24 h after the termination of anesthesia. Through these results, this dog was diagnosed with unexpected brain death, and it is presumed that the cause was anesthesia. We report herein a case of brain death in a dog diagnosed using fluorodeoxyglucose-positron emission tomography/computed tomography.
There is only one previous report of canine goitrous hypothyroidism caused by iodine deficiency from 1986. The present case report describes the novel diagnostic methods and long-term outcomes of a dog diagnosed with goitrous hypothyroidism caused by iodine deficiency. A 4-year-old neutered, female Pomeranian dog presented with a cervical mass, lethargy, and inactivity. The dog had a history of eating home-cooked diets sold by a private seller for 1 year. The physical examination and ultrasonography showed two bilaterally symmetric masses in the mid-cervical area (left, 1.8 × 1.4 cm; right, 2.3 × 1.8 cm), and they were suspected to be the thyroid glands. To identify the function of the thyroid gland, the basal concentrations of thyroid hormones [total T4 (tT4) and thyroid-stimulating hormone (TSH)] were measured and a TSH stimulation test was performed: baseline tT4, 0.5 μg/dL (reference interval, 1–4 μg/dL), baseline TSH, 0.81 μg/dL (reference interval, 0.05–0.42 μg/dL), and post-tT4, 1 μg/dL (6 h after the injection of TSH). The values indicated primary hypothyroidism. The urinary iodine concentration was 302 μg/L, which was markedly lower than that of normal dogs (1,289 μg/L). Thyroid scintigraphy with technetium-99m pertechnetate was also performed to quantify the activity of the thyroid gland, and the thyroid-to-salivary ratio was 3.35. Based on the results of these examinations and patient history, the dog was diagnosed with diet-induced (iodine deficiency) goitrous hypothyroidism. The dog was treated with iodine (62.5 μg/day). At 31 days after treatment, clinical signs and thyroid hormones were normalized (tT4, 1.3 μg/dL; TSH, 0.24 μg/dL). One year after treatment, the dog was well with normal concentrations of thyroid hormones (tT4, 1.8 μg/dL; TSH, 0.27 μg/dL) and a partially reduced goiter (left, 1.6 × 1.1 cm; right, 1.2 × 0.9 cm). This is the first case to describe novel diagnostic methods and long-term outcomes of a dog diagnosed with goitrous hypothyroidism caused by iodine deficiency.
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