DIAGNOSTIC OPHTHALMOLOGY

History and clinical signs

An 8-year-old, Thoroughbred mare was referred to the Western College of Veterinary Medicine because she was blind. The blindness had developed suddenly one evening, approximately 1 y previously. The owners had noted bilateral mydriasis. Previous examinations by several veterinarians had confirmed blindness and focal papillary hemorrhages.

Physical examination revealed that abnormalities were present in both eyes. The palpebral and oculocephalic reflexes were present. The pupils were fixed and dilated, and the menace responses were negative. Schirmer tear tests (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were 13 mm/min in both eyes. The intraocular pressures were estimated with an applanation tonometer (Tonopen XL; Biorad Ophthalmic Division, Santa Clara, California, USA) and were 19 mmHg and 13 mmHg in the right and left eye, respectively. Biomicroscopic (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) examination failed to reveal anterior segment abnormalities. Indirect ophthalmoscopy (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) was completed. Posterior segment abnormalities were similar in both eyes. A photograph of the right fundus is provided for your assessment (Figure 1). What are your diagnoses? What etiologies have been reported for this condition?

Figure 1. A photograph of the right fundus of a blind 8-year-old Thoroughbred mare. The left fundus was similar in appearance. Note the multifocal areas of peripapillary and nontapetal depigmentation, optic nerve pallor, and lack of retinal blood vessels.

Discussion

Our diagnoses were blindness, optic nerve degeneration, peripapillary retinal degeneration (lack of retinal blood vessels), and focal choroidal degeneration (focal grey patches medial, lateral and ventral to the optic disc). The horse failed to navigate photopic and scotopic maze tests. Given the chronicity (> 1 y), the characteristic symmetrical optic disc degeneration with loss of retinal vessels, the fixed and dilated pupils, and the normal physical examination, we did not advise further diagnostic tests.

Fixed and dilated pupils and blindness are consistent with afferent pupillary defects. The history that accompanied this case included an acute onset of mydriasis and blindness, detected by the owner. The horse was maintained in a small paddock, was fed timothy brome hay, and received oats once daily. The horse was healthy and abnormalities were limited to blindness and mydriasis, when the referring veterinarian examined the horse within 24 h. No treatment was initiated after the horse became blind.

Optic nerve and retinal degeneration in the horse has been reported to develop secondary to equine recurrent uveitis (1), glaucoma (2,3), blood loss (4,5), exposure to toxins, trauma (6,7), progressive retinal atrophy (PRA) (8), and carotid artery ligation (9). Equine recurrent uveitis was excluded as an etiology in this horse, based on the lack of characteristic clinical manifestations, including hyalitis, aqueous flare, miosis, posterior synechia, and subcapsular cataracts. Similarly, glaucoma was excluded on the basis of normal intraocular pressures and a lack of buphthalmos, corneal striae and edema, and optic disc cupping. When the blindness developed, there was no history of acute blood loss or severe anemia, which excluded these etiologies. Similarly, there was no historic evidence of exposure to toxins, or cervical or cranial surgery. Progressive retinal atrophy is a rare condition in the horse (1); however, it has been described in Thoroughbreds (8). The clinical manifestations are unique and include nyctalopia and progressive vision loss over several months (1,8). The sudden vision loss in this patient was not consistent with PRA. Traumatic optic neuropathy was the most likely etiology for this condition, based on the history, and physical and ophthalmic examination findings.

Traumatic optic neuropathy develops secondary to severe blunt trauma. The optic nerves in horses are tethered between the eyes and the optic chiasma, within the bony optic canal and meninges. Blunt head trauma may result in optic nerve concussion, stretching, or avulsions and may result in blindness (1,6,7). The optic nerve will atrophy a few weeks later and will manifest as a pale yellow disc with diminished peripapillary retinal vessels, as seen in this horse. Nonsteroidal anti-inflammatories or steroids administered systemically at the time of the trauma may decrease the swelling and inflammation in these nerves (1). The prognosis for vision is guarded.