Unilateral invasive intraocular melanoma with choroidal and optic nerve involvement resulting in bilateral vision loss in a Labrador Retriever.

A 10-year-old male castrated Labrador Retriever cross was referred for evaluation of acute vision loss. Ophthalmic examination revealed mild left sided exophthalmos, bilateral resting mydriasis, an absent direct and reduced consensual PLR in the left eye and reduced direct and absent consensual PLR in the right eye. Examination of the cornea and anterior segment with slit lamp biomicroscopy was unremarkable. Indirect fundoscopy revealed a left optic nerve head obscured by a darkly pigmented lesion. Fundic examination in the right eye was unremarkable. Magnetic resonance imaging revealed a smoothly marginated, lobulated cone to irregularly shaped, strongly T1 hyperintense, T2 and T2 fluid-attenuated inversion recovery hypointense, strongly contrast enhancing mass closely associated with the entire left optic nerve, extending across the optic chiasm and into the right optic nerve ventrally. Full clinical staging revealed no evidence of metastasis. Exenteration of the left eye was performed. Histopathology revealed an unencapsulated, poorly demarcated, multilobulated and infiltrative pigmented mass that was effacing the posterior choroid and optic nerve. The mass was composed of a moderately pleomorphic population of heavily pigmented polygonal cells arranged in sheets and clusters, displaying moderate anisocytosis and anisokaryosis. The population of cells contained moderate amounts of abundant brown-black granular pigment consistent with melanin within the cytoplasm. Mitotic figures averaged approximately three per ten 400× fields (2.37 mm2 ). This is the first report of a melanocytic tumor invading along the optic nerve and tract to result in contralateral vision loss.

CSF from a puppy with a cerebral vascular hamartoma.

A 9-week-old puppy with refractory seizures and a dome-shaped head presented to the Mississippi State College of Veterinary Medicine Specialty Center for suspected hydrocephalus. Computerized tomography (CT) findings included transtentorial herniation and an intra-axial mass with dystrophic mineralization. Cerebrospinal fluid analysis revealed an increased nucleated cell count of 1100/µl (RI < 5/µl), erythrocyte count of 2.2 × 106 /µl, and markedly increased microprotein of 1939 mg/dl (RI < 30 mg/dl). On cytologic examination of the CSF, numerous erythrophagocytic, and hemosiderin-laden macrophages were observed, which indicated chronic active hemorrhage. Many neutrophils, macrophages, and lymphocytes that contained numerous intracytoplasmic, pleomorphic, bright yellow crystals were observed. Considering the ongoing hemorrhage, the crystals were presumed to be hematoidin. A biopsy with histopathology was performed on the intra-axial mass, and the results were consistent with a vascular hamartoma. We speculate that the formation of these crystals was related to the ongoing hemorrhage associated with the vascular hamartoma. Identification of these crystals may be useful to aid in the identification of chronic hemorrhage associated with vascular malformations or lesions within the central nervous system.