Background
Pituitary-dependent hyperadrenocorticism (PDH) is a common cause of hypercortisolism in dogs and is frequently associated with functional pituitary tumors.
Objectives
This report describes the clinical and multimodal imaging findings in a dog with presumptive pituitary-dependent hyperadrenocorticism and a large pituitary-region mass associated with acute blindness. Bilateral temporal bone defects provided an acoustic window for transcranial ultrasonography.
Methods
A 10-year-old, 7-kg, spayed female Pomeranian dog presented with generalized seizures and acute blindness. Brain and abdominal computed tomography (CT) were performed without general anesthesia, with intravenous administration of iohexol (320 mg I/mL) at a dose of 1.5 mL/kg. Transcranial ultrasonography was subsequently performed through the bilateral presumed congenital temporal bone defects. Endocrine evaluation included low-dose dexamethasone suppression and adrenocorticotropic hormone stimulation tests.
Results
Brain CT revealed a 1.94 × 2.0 × 1.48 cm hyperattenuating, well-marginated, homogeneous mass centered in the hypophyseal fossa and extending into the suprasellar region, with marked mass effect in the region of the optic chiasm. Bilateral adrenal enlargement was also identified. Endocrine findings supported hyperadrenocorticism, and the combination of endocrine findings, bilateral adrenal enlargement, and the pituitary-region mass supported a presumptive diagnosis of PDH. Transcranial ultrasonography allowed visualization of the mass through the temporal bone defects and showed a broadly similar well-defined and homogeneous appearance. Medical management with trilostane was initiated. At the 6-month follow-up, systemic signs and seizure activity remained clinically stable, whereas the visual deficit persisted. No follow-up CT or MRI was performed.
Conclusions
This case highlights the diagnostic challenges associated with large pituitary-region masses in dogs when histopathological confirmation is unavailable. The combination of clinical, endocrine, and imaging findings supported a presumptive diagnosis of PDH associated with a pituitary-region macrotumor. The bilateral temporal bone defects provided an unusual acoustic window through which the intracranial lesion could be visualized by ultrasonography. Although this finding suggests a potential adjunctive role for transcranial ultrasonography in selected cases, its diagnostic equivalence or reliability for longitudinal monitoring cannot be established from a single examination. Trilostane provided clinical control of the systemic manifestations of hypercortisolism but should not be interpreted as treatment of the intracranial mass effect.