Treatment of Intraocular Inflammation
Many infectious and noninfectious diseases cause intraocular inflammation. Unless inflammation is controlled early, irreversible damage and blindness may result. Topical and systemic corticosteroids and NSAIDs are used to control inflammation, depending on the cause. Care should be taken when using longterm treatment. Adrenocortical suppression can develop, and animals must be weaned off treatment slowly after the inflammation has resolved. In all species, control of noninfectious intraocular inflammation involves use of high initial doses of systemic corticosteroids (prednisone 1–2 mg/kg) in combination with topical corticosteroids (0.5% or 1% 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 started at the same time as systemic antibiotic therapy. If the cause of intraocular inflammation is unknown, a combination of topical corticosteroids and systemic NSAIDs is also appropriate. Use of H2-blockers or proton pump inhibitors should be considered when starting therapy; GI, liver, and renal parameters should be routinely monitored.
Immune-mediated ocular disease is not uncommon in dogs. This can include episcleritis, nodular granulomatous episclerokeratitis (often seen in Collies as a raised granulomatous lesion involving the episclera and third eyelid and infiltrating into the cornea), and extraocular muscle myositis. 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.
These diseases can be treated with either combined topical and oral corticosteroids (prednisone, 0.5–1 mg/kg, bid) or a lower corticosteroid dose in combination with another immunosuppressive drug. This could be oral azathioprine (1.5–2 mg/kg/day, reducing the dose after 3–5 days), mycophenolate mofetil (7–20 mg/kg, bid for 3–4 wk, then reducing the dose to 10 mg/kg/day), or cyclosporine (5 mg/kg, bid for 2 wk, decreasing to daily if clinical improvement). An alternative treatment for episcleritis in dogs >10 kg is niacinamide (500 mg, PO) and tetracycline (500 mg, PO), tid, decreasing to once to twice daily once improvement occurs.
Many cases of immune-mediated ocular disease can be kept in remission with either azathioprine, 1–2 mg/kg, PO, every 3–7 days for 1–8 mo; mycophenolate mofetil, 10 mg/kg every day or every other day; or cyclosporine 5 mg/kg daily, every other day, or once weekly with or without concurrent low-dose prednisone or prednisolone. Adverse effects of azathioprine include pancreatitis, liver disease, and bone marrow suppression. Frequent hematology and serum biochemistry monitoring is recommended. There are fewer adverse effects with mycophenolate and cyclosporine. These are mainly related to the GI tract and include anorexia, vomiting, and diarrhea. 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.
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. Prognosis depends on the degree of damage.
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 NSAIDs (flunixin meglumine, 0.25–1 mg/kg, IV or PO, bid) are used in conjunction with topical and/or subconjunctival 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 NSAIDs for longer than label recommendations (often 7–10 days); once the uveitis is controlled, the dose is slowly tapered over 2–3 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/day, PO) 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 help prevent recurrence in horses diagnosed with equine recurrent uveitis. Suprachoroidal cyclosporine implants are now more commonly used for longterm management (up to 3 yr).
Trauma to the poll in horses associated with rearing and hitting objects or falling over backward 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 NSAIDs at higher dosages (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 daily for 3 days, then every other day for 6 days) can be used. When given IV, DMSO can cause hemolysis and hemoglobinuria. Prognosis is poor for any return of vision if there has been no improvement after 72 hr.