Diagnostic Ophthalmology

History and clinical signs

A 6-year-old neutered male miniature schnauzer dog was referred to the ophthalmology service at the Western College of Veterinary Medicine for an evaluation of a sudden onset of blindness. Vaccinations for distemper, parvo, and rabies viruses were current and the dog had recently been dewormed. Our neuro-ophthalmic examination revealed that the pupillary responses were very sluggish and the pupils in photopic conditions were dilated. The menace responses were absent. The palpebral, and oculocephalic reflexes were present bilaterally. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were approximately 22 mm/min bilaterally. The intraocular pressures were estimated with a rebound tonometer (Tonovet; Tiolat Oy, Helsinki, Finland) and they were 18 mmHg bilaterally. Biomicroscopic (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) and indirect ophthalmoscopic (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) examinations were completed. Abnormalities were not detected with either biomicroscopic and indirect ophthalmoscopic examinations (Figure 1). Scotopic and photopic maze testing confirmed a lack of functional vision. The owner had noted that the vision loss developed acutely approximately 1 wk earlier. We advised and completed a photopic electroretinogram which revealed 40 microvolt a-waves and 110 microvolt b-waves. These were considered to be within normal reference ranges for a dog of this age. A physical examination, complete blood cell count, serum biochemical profile, and urinalysis were done; however, no significant abnormalities were noted. A routine sedation, general anesthesia, and a contrast-enhanced cranial computerized tomography (CT) (Figure 2).

Figure 1.

Photograph of the fundus of the right eye.

Figure 2.

Computed tomographic scan of the optic chiasma of a 6-year-old miniature schnauzer dog.

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Discussion

Our clinical diagnoses were blindness with afferent pupillary defects due most likely to optic neuritis, a neoplastic invasion, or compression of the optic chaisma. Contrast enhanced cranial CT scans confirmed the diagnosis of bilateral optic neuritis. Note the contrast enhanced optic nerves that extend to the chiasm in Figure 2. A central spinal fluid examination was recommended but not completed. This dog was medicated with 1 mg/kg of prednisone given orally twice daily. Vision returned within 12 h of therapy and the medication was continued at 2 mg/kg per day for 3 wk after which the dosage was reduced by approximately 1/2 for 3 wk, and then to 1 mg/kg once per day. Vision has been maintained and the corticosteroid therapy will be further reduced to alternative day therapy provided no vision loss is noted. A follow-up examination by the ophthalmologist at approximately 4 mo confirmed that photopic and scotopic vision were present and no additional abnormalities were noted on ophthalmologic or physical examination. Oral prednisone therapy was continued indefinitely at 1 mg/kg once per day.

Optic neuritis is an uncommon cause of acute blindness in middle-aged to older dogs in our referral service. The most common eitology for sudden vision loss in dogs with normal to near normal ophthalmoscopic examination is sudden acquired retinal degeneration (SARD) which accounts for in excess of 95% of our etiologic diagnoses of acute blindness in dogs in our practice. An idiopathic acute retinal degeneration, SARD is characterized histologically by generalized photoreceptor apoptosis which progresses to pan-retinal degeneration within weeks (1). The diagnosis is confirmed by a lack of electrical responses on an electroretinogram (2). Unfortunately, there is no effective therapy for SARD in dogs. The presence of electrical responses in the dog herein precludes the diagnosis of SARD and warrants a complete systemic evaluation, and most importantly, sectional imaging of the optic nerves and chiasma.

In our practice, optic chiasmal neoplasia is the second most common etiologic diagnosis in these acutely blind dogs. The most common neoplasms are meningiomas (3) and lymphosarcomas. These optic nerve and chiasmal tumors are diagnosed with sectional imaging [magnetic resonance imaging (MRI) or CT scans]. Varied therapies exist for optic nerve and chiasmal neoplasms including external beam radiation and surgical removal. Unfortunately, vision loss is usually permanent although neoplastic growth can be substantially inhibited.

Optic neuritis, although relatively uncommon, is an important etiologic diagnosis of acute blindness in dogs as this disorder can often be effectively treated and vision restored. Optic neuritis in dogs is usually a manifestation of granulomatous meningoencephalitis (4). This is an immune-mediated disorder of the central nervous system (CNS) that most commonly affects small to mid-sized dogs. The clinical manifestations are usually limited to acute vision loss and afferent pupillary defects. The diagnosis should be achieved quickly to ensure minimal permanent optic nerve damage. The essential diagnostic evaluations include a complete ophthalmoscopic examination, an electroretinogram, and sectional imaging with the CT or MRI. In our experience, vision returns within days of instituting immuno-suppressive corticosteroid therapy. Vision can often be maintained provided that continued, albeit reduced, systemic corticosteroid therapy is maintained for life. Optic neurititis may progress to granulomatous meningoencephalitis and manifest with seizures and depression. However, in our experience this seems to be less common with effective therapy. The etiology for this disorder remains unknown.