Diagnostic Ophthalmology

History and clinical signs

A 21-year-old castrated male warmblood horse was examined by the ophthalmology service at the Western College of Veterinary Medicine for evaluation of bilateral corneal opacity, serous ocular discharge, and reduced vision. The left menace response was absent. The pupils were dilated, and direct and consensual pupillary light reflexes were slow and incomplete bilaterally. Palpebral and occulocephalic reflexes were present bilaterally. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were 26 and 30 mm/min in the right and left eyes, respectively. Following sedation with 0.2 mg/kg xylazine IV (Rompun; Bayer, Toronto, Ontario), auriculopalpebral nerve blocks were completed using 2 mL of 2% lidocaine (Bimeda-MTC Animal Health, Cambridge, Ontario). The intraocular pressures were estimated with a rebound tonometer (Tonvet; Tiolat, Helsinki, Finland) and were 65 and 60 mmHg in the right and left eyes, respectively. Fluorescein staining (Fluorets; Bausch & Lomb Canada, Markham, Ontario) was negative bilaterally. On direct examination there were episcleral congestion, buphthalmos, and blepharospasm bilaterally. There was mild diffuse corneal opacity and several well-demarcated, linear, branching, corneal opacities in both eyes. Biomicroscopic examination (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) revealed the diffuse opacity to be associated with thickened corneal stroma consistent with corneal edema. The linear opacities were associated with breaks in Descemet’s membrane (Haab’s Striae). An incipient posterior cortical cataract was noted in the right lens. Following application of 0.5% tropicamide (Mydriacyl; Alcon Canada, Mississauga, Ontario), indirect ophthalmoscopic (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) examinations were completed bilaterally and optic nerve pallor was noted. A photograph of the right eye at presentation is provided for your assessment (Figure 1).

Figure 1.

Photograph of the right eye of a 21-year-old warmblood gelding. The left eye had a similar appearance.

What are your clinical diagnosis, differential diagnoses, therapeutic plan, and prognosis?

Discussion

Our clinical diagnosis was bilateral primary glaucoma. Glaucoma occurs due to a disruption in aqueous humor outflow such that the intraocular pressure (IOP) increases above what is compatible with normal retina and optic nerve function. Glaucoma may be classified as primary, secondary, and congenital. Congenital glaucoma is associated with anterior segment dysgenesis and presents in neonatal and young animals (1,2). Clinical manifestations of congenital glaucoma include intraocular abnormalities consistent with maldevelopment of the anterior segment including uveal hypoplasia, elongated ciliary processes, lenticular colobomata, and microphakia (1,2). Additionally, animals with congenital glaucoma demonstrate marked buphthalmos due to the elastic nature of the young sclera. Secondary glaucoma has an identifiable underlying ocular condition such as chronic uveitis, neoplasia, or lens luxation (3–5). Equine recurrent uveitis (ERU) is the most common cause of glaucoma in the horse (2,6). Glaucoma secondary to ERU may manifest with diffuse corneal edema and signs of chronic or ongoing intraocular inflammation such as a miotic pupil, aqueous flare, posterior synechia, cataract formation, vitritis, and lens subluxation or luxation (2,4). In contrast, primary glaucoma is not associated with antecedent ocular disease. Primary glaucoma is rare in the horse and occurs more commonly in older animals (6,7). The term “primary” implies bilateral potential and heritability. Heritability has not been proven in the horse and some prefer the term “idiopathic” for this form of glaucoma (8). The clinical manifestations of primary glaucoma may be subtle in early stages of disease and include partial or diffuse corneal edema with or without a dilated pupil. With chronicity, eyes develop corneal striae, pupil dilation, and reduced vision. Buphthalmos, lens subluxation, and optic nerve and retinal degeneration occur in the end stages of disease (3–5). In this case, no predisposing ocular disease was identified, and the clinical manifestations were most consistent with chronic primary or idiopathic glaucoma.

Diagnosis of glaucoma in the horse is based on measurement of an elevated IOP and the presence of clinical manifestations of glaucoma. The normal equine IOP ranges from 15 to 30 mmHg and an IOP > 35 mmHg is consistent with glaucoma (9). There is wide variation and large diurnal fluctuations of IOP in the horse, thus, repeated IOP measurements may be required to confirm glaucoma in some horses (3). Applanation tonometry using the Tonopen (Medtronic, Jacksonville, Florida) or rebound tonometry using the Tonovet are utilized to measure IOP in the horse. Auriculopalpebral nerve blocks should be performed before tonometry as eyelid tension can artificially elevate the IOP (10). A complete ocular examination is conducted to evaluate for underlying ocular disease such as ERU or intraocular neoplasia. Potential for vision is assessed through the neuroophthalmic examination; in a globe with a fixed and dilated pupil due to elevated IOP, there is potential for vision if a dazzle reflex and the consensual pupillary light reflex to the contralateral eye are present.

Medical therapy for equine glaucoma is aimed at reduction of the IOP to a level compatible with maintenance of retina and optic nerve health. The most effective drugs for reduction of IOP in the horse are topical carbonic anhydrase inhibitors (CAI) such as 2% dorzolamide hydrochloride alone or in combination with beta-adrenergic blockers such as timolol maleate 0.5% administered every 8 to 12 h (11). Topical prostaglandin analogs such as Latanaprost 0.005%, are potent anti-glaucoma medications used to treat canine glaucoma. These medications, however, do not have as marked effect on reduction of IOP in horses and can exacerbate glaucoma secondary to uveitis, and are therefore rarely used (12). Anti-inflammatory therapy consisting of topical corticosteroid or non-steroidal medications and systemic non-steroidal anti-inflammatory medications are beneficial in control of uveitis and are required if glaucoma is secondary to uveitis.

If there is poor response to topical medications and potential for vision exists, transscleral laser cyclophotocoagulation (TSCP) to cause destruction of the aqueous humor producing cells in the ciliary body may be indicated. This procedure can be successful in reducing intraocular pressure and maintaining vision; however, ongoing use of topical medications is required in most horses, and regeneration of the ciliary body over time means that the procedure may need to be repeated in 6 to 12 mo (11,13). Recently, anterior chamber shunt placement was reported as a potential therapy for refractory equine glaucoma (14).

Glaucoma is a painful condition and end-stage eyes that are blind should be enucleated or referred for evisceration and intrascleral prosthesis placement. In this case topical therapy was initiated with dorzolamide 2%/timolol maleate 0.5% (Cosopt; Merk Frosst Canada, Kirkland, Quebec) every 8 h. As the eyes had potential for vision based on the presence of pupillary light reflexes, TSCP was advised. The owner elected not to proceed with this surgery and ultimately, the horse was euthanized due to his vision deficits.

Prognosis for glaucoma in horses is guarded and depends on the underlying cause. Congenital glaucomas have a poor prognosis as affected eyes are usually blind at presentation with multiple anomalies. Glaucoma secondary to ERU represents the end-stage of that condition and eyes are usually blind and painful when glaucoma develops. Horses with primary glaucoma may maintain vision later in the disease process compared with dogs and humans; however, the long-term prognosis for maintaining vision with medical therapy alone is guarded (3,4). Early detection requires an index of suspicion when subtle signs of corneal edema are manifested, and repeated measurement of IOP to confirm the diagnosis may be needed. Topical therapy may control IOP in the short-term and laser TSCP can be useful for long-term maintenance of vision and IOP control.