Diagnostic Ophthalmology

History and clinical signs

A 13-year-old, spayed, female cocker spaniel crossbreed was examined at the ophthalmology service at the Western College of Veterinary Medicine. She had had a 2-month history of a red right eye. The menace responses and the pupillary light, palpebral, and oculocephalic reflexes were present in both eyes. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were 17 and 19 mm/min in the left and right eye, respectively. The intraocular pressures, estimated with a rebound tonometer (Tonvet; Tiolat, Helsinki, Finland), were 10 mmHg bilaterally. The pupils were dilated with tropicamide (Mydriacyl; Alcon Canada, Mississauga, Ontario) and a biomicroscopic examination (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) and an indirect ophthalmoscopic examination (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) were completed. Abnormalities noted upon direct examination were limited to the right eye and included conjunctival hyperemia, and congestion and thickening of the episclera, extending from the 5 o’clock to 9 o’clock region, with adjacent superficial stromal corneal vascularization and corneal edema. The right eye was photographed; it is provided for your assessment (Figure 1).

Figure 1.

Photograph of the right eye of a 13-year-old cocker spaniel crossbreed.

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Discussion

Our clinical diagnosis was diffuse episcleritis of the right eye. Differential diagnoses for episcleral inflammation include primary episcleritis; episcleritis occurring secondary to other ocular disease, such as uveitis, glaucoma, keratitis, or orbital disease; and infiltrative neoplasia (1). Episcleritis secondary to other ocular disease was ruled out, based on a complete ophthalmic examination. The dog was placed under general anesthesia and the episclera was biopsied to allow us to differentiate primary episcleritis from neoplasia. Light microscopic evaluation of the biopsy revealed a mixed population of inflammatory cells, primarily consisting of lymphocytes, plasma cells, and macrophages. No infectious agents or foreign material was present. These findings were consistent with a diagnosis of primary episcleritis. Treatment was initiated with neomycin/ polymyxin B/dexamethasone (Maxitrol; Alcon Canada, Mississauga, Ontario) q6h. This antibiotic and steroid combination was used to prevent bacterial infection of the biopsy site and to address the inflammatory process. Reevaluation was completed 4 wk following initiation of therapy, at which time the episcleral and corneal changes had resolved. The biopsy site had healed; therefore, a topical antibiotic was no longer necessary and therapy was changed to only topical dexamethasone (Maxidex, Alcon Canada). The frequency of administration was gradually tapered; q8h for 4 wk, followed by q12h for 4 wk, then q24h for 4 wk, then q48h. The dog remains in remission with q48h therapy.

Primary episcleritis may be diffuse or nodular. Cocker spaniels and golden retrievers are predisposed to diffuse episcleritis (2). Diffuse episcleritis may also be called simple episcleritis; it may be unilateral or bilateral. It usually manifests clinically as an elevated sector lesion, posterior to the limbus, with episcleral and conjunctival vascular congestion. The perilimbal cornea adjacent to the inflammation is usually edematous and may be vascularized (1,2). The nodular form is most commonly diagnosed in collie breeds and is commonly referred to as nodular granulomatous episclerokeratitis (NGE), although alternative nomenclature includes nodular fasciitis, fibrous histiocytoma, proliferative conjunctivitis, pseudotumor, and collie granuloma (2,3). Nodular granulomatous episclerokeratitis is usually bilateral and manifests clinically as a raised pink mass affecting the temporal limbus, cornea, and the nictitating membrane. Diffuse and nodular episcleritis are similar histologically and consist of a cellular infiltrate dominated by lymphocytes, plasma cells, and macrophages (2–5).

The etiology of primary canine episcleritis is presumed to be immune-mediated (1–5). Investigations have failed to find any association with a local infectious process or systemic immune-mediated disease (2–4). Medical therapy consisting of topical corticosteroids is usually successful in bringing about remission of clinical signs. The steroid preparation should consist of 1% prednisolone acetate or 0.1% dexamethasone; an initial treatment frequency of q6h for several weeks is usually required. In some cases, systemic corticosteroids or other immunomodulators, such as azathioprine, may be necessary to bring about remission (3). Once remission is achieved, the frequency of administration can be gradually tapered. Although some cases may resolve completely without recurrence after withdrawal of therapy, most will require long-term maintenance therapy to maintain remission (2,5).