Many infectious and noninfectious diseases cause intraocular inflammation. Unless inflammation is controlled early, irreversible damage and blindness may result. Topical and systemic corticosteroids and NSAID are used to control inflammation, depending on the cause. Care should be taken when using longterm treatment. Adrenocortical suppression can develop and, following resolution of inflammation, animals must be weaned off treatment slowly. In all species, control of noninfectious intraocular inflammation involves the use of high initial doses of systemic corticosteroids (1–2 mg/kg prednisone) in combination with topical corticosteroids (0.5% or 1.0% prednisolone acetate or 0.1% dexamethasone alcohol, tid-qid). Some cases of infectious disease (eg, rickettsial infections) can be treated with low doses of systemic corticosteroids, but only after antibiotic therapy has been started for 24–48 hr. Topical steroids can be initiated at the same time as systemic antibiotic therapy. If the cause of intraocular inflammation is unknown, a combination of topical corticosteroids and systemic NSAID is also appropriate. Use of H₂-blockers or proton pump inhibitors should be considered when starting therapy; GI and renal parameters should be routinely monitored.

Canine Immune-mediated Disease

Nodular granulomatous episclerokeratitis (NGE) is often seen in Collies as a raised granulomatous lesion involving the episclera and third eyelid and infiltrating into the cornea. In addition to infectious anterior and posterior uveitis, immune-mediated uveitis (uveodermatologic syndrome) associated with an immune reaction to melanin is seen in a number of breeds, more commonly those of Arctic origin. Both are treated with either combined topical and oral corticosteroids (prednisone, 0.5–1 mg/kg, bid) or a lower corticosteroid dose in combination with oral azathioprine (1.5–2 mg/kg, sid, reducing the dose after 3–5 days). Some cases of NGE can be kept in remission with azathioprine, 1–2 mg/kg, PO, every 3–7 days for 1–8 mo. An alternative treatment for dogs >10 kg is administration PO of 500 mg niacinamide and 500 mg tetracycline, tid, decreasing to sid or bid once improvement occurs. Adverse effects of azathioprine include pancreatitis, liver disease, and bone marrow suppression. Frequent hematology and serum biochemistry monitoring is recommended. In uveodermatologic syndrome, recurrence is common and prognosis for longterm control is only fair. Many animals become blind from secondary glaucoma associated with the chronic uveitis and/or retinal detachment and degeneration.

Canine Optic Neuritis

Inflammation of the optic nerve is more common in dogs than in other species. It can be caused by infection (eg, distemper, systemic mycoses), neoplasia, contiguous inflammation, or granulomatous infiltration (reticulosis/ granulomatous encephalomyelitis). Systemic corticosteroids (prednisone, 1–2 mg/kg, PO) for extended periods (often weeks) are used in an attempt to retain vision. Granulomatous encephalomyelitis is responsive to early treatment with systemic corticosteroids.

Damage to the optic nerve as a result of trauma is treated with systemic corticosteroids at similar dose rates as above. The prognosis depends on the degree of damage.

Equine Uveitis

The principles of anti-inflammatory treatment for equine uveitis (see Equine Recurrent Uveitis) are very similar regardless of the initiating cause. In acute uveitis, systemic NSAID (flunixin meg-lumine, 0.25–1.0 mg/kg, IV or PO, bid) are used in conjunction with topical corticosteroids to control the intraocular inflammation. Phenylbutazone does not seem to be as effective in the initial treatment of equine uveitis. Horses are often treated with high doses of NSAID for longer than label recommendations (often 7–10 days); once the uveitis is controlled, the dose is slowly tapered down over 1–2 wk. Concurrent gastric protection with either an H₂-blocker (ranitidine, 6.6 mg/kg, PO, tid or 1 mg/kg, IV, tid, or famotidine, 0.23–0.35 mg/kg, IV, bid-tid or 1.88–2.8 mg/kg, PO, bid-tid) or a proton pump inhibitor (omeprazole, 4 mg/kg, PO, sid) is recommended. Renal function should be monitored and extreme care taken if the horse is also being treated with gentamicin. Oral aspirin (25 mg/kg/day) has been used longterm to prevent recurrence in horses diagnosed with equine recurrent uveitis.

Equine Optic Neuritis

Trauma to the equine poll associated with rearing and hitting objects or falling over backwards can result in sudden blindness. This is associated with overextension or shearing of the optic nerve within the optic canal secondary to movement of the brain in the skull. Treatment is systemic anti-inflammatory agents, usually NSAID at higher dose rates (flunixin meglumine, 0.5–1.1 mg/kg, IV or PO) and for longer than label recommendations. Prophylactic use of H₂-blockers or a proton pump inhibitor is recommended. In addition, dimethyl sulfoxide (DMSO; 1 g/kg, IV as a 20% solution in saline or 5% dextrose in water given sid for 3 days, then every other day for 6 days) can be used. When given IV, DMSO can cause hemolysis and hemoglobinuria. No return of vision after 72 hr indicates a poor prognosis for any vision return.

Last full review/revision March 2012 by Nick Whelan, BSc, BVSc, MVSc, MACVSc, DACVCP, DACVO