**6. Medical treatment**

Treatment is aimed to control both the uveitis and IOP. The uveitis is treated by topical and/or systemic corticosteroids and/ or immunosuppressive drugs to achieve resolution or remission. Sub-Tenon corticosteroids such as triamcinolone acetonid (Kenalog®) 20-40mg (0.5-1ml) or methylprednisolone acetate (Depo-medrol®) 40-80mg may be given to treat noninfectious uveitis and macular edema. Intravitreal implants such as Ozurdex®, a copoly‐ mer of glycolic and lactic acid with 700µg of dexamethasone may be injected through the pars plana with 22G injector. It dissolves gradually over 6 months to H2O and CO2 and re‐ leases the dexamethasone. However, they all and especially those that cannot be removed (sub-Tenon and intravitreal) should be used cautiously in patients with glaucoma and are contraindicated in steroid responders and steroid-induced glaucoma. In cases of steroid res‐ ponders orcorticosteroid-induced glaucoma, topical corticosteroids may be replaced by IOPsparing corticosteroids such as such as loteprednol etabonate 0.5% (Lotemax®) or rimexolone 1%(Vexol®) but because of low potency, they may be more frequently required. These agents are especially useful for maintenance. Alternatively, topical non-steroidal antiinflammatory (NSAID) such as nepafenac 0.1% (Nevanac®), ketorolac tromethamine 0.5% (Acular® or Tradol®), diclofenac sodium (Voltaren® (0.1%), Solaraze® (3%)) or indometha‐ cin 1% (Indoptic®) may be used. Topical immunosuppressive agent such as cyclosporine A 0.5-2% and systemic immunosuppressive drugs may be alternatives for corticosteroids and NSAID. The dosage of corticosteroids depends on the severity of inflammation and is titrat‐ ed according to the response to treatment. The corticosteroids are gradually tapered accord‐ ing to the response since abrupt discontinuation may cause flare-up. Topical cycloplegic agents such as cyclopentholate HCl 1% (in neonates 0.5%) tid are added to control pain that originates from the ciliary body and to prevent the formation of posterior synechiae.

procedure may be performed with contact lens such as Abraham (+66D), Wise (+103D), CGIor without it. The advantages of a contact lens are additional magnification, focusing the beam, absorbing part of the heat, stabilizing the eye and keeping the eyelids open. Topical apraclonidine (Iopidine®) 0.5%-1.0% or other alpha 2 agonist (e.g., brimonidine tartrate) is administered following the procedure to decrease IOP spikes and corticosteroids such as prednisolone acetate 1% qid are prescribed for a week to decrease intraocular inflammation and risk of synechiae formation. Additional anti-glaucoma medications may be added. This procedure facilitates aqueous flow from the posterior into the anterior chamber and may re‐ sult in deepening of the anterior chamber and lowering the IOP. The major complication is acceleration of cataract. If Nd:YAG laser is unavailable, Argon laser iridotomy may be per‐ formed. The parameters for this procedure depend on the iris pigmentation. For brighter iris, the power is lower than for darker ones. The preparatory stretch burns are of 200-600mW, 0.2-0.6 sec, 200-500 µ m. The penetration burns are of 800-1000mW, 0.2 sec, 50µm. The iridotomy size should be increased to 150-500µm. The position of the Argon iri‐ dotomy in this case is preferably supero-nasal to prevent injury to the macula. Argon laser may increase the intraocular inflammation because it releases pigment due to a different mechanism of action (plasma creation by ionizing in cases of ND:YAG versus coagulation in Argon). The treatment before and after the procedure is identical to Nd:YAG laser iridoto‐ my. Perforation of the iris is confirmed when aqueous mixed with pigment is flowing from the posterior to the anterior chamber through the iridotomy. The lens should be visible through the iridotomy, since positive transillumination is not reliable. When laser iridotomy is not feasible or is impossible to perform, surgical peripheral iridectomy should be per‐ formed. Complications include visual disturbances such as halo and glare, development and progression of cataract, transient corneal burns, temporary increase in IOP, intraocular in‐

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flammation and rarely retinal injury, CME and malignant glaucoma.

obstruction of the open angle by inflammatory products.

**7.2. Surgical treatment**

Argon laser trabeculoplasty has no role in uveitic open-angle glaucoma because of its low success rate. It may increase the intraocular inflammation and alter the angle structure. Some authors found selective (ND:YAG) laser trabeculoplasty to be effective in 20% of the patients, [39] but the follow-up was limited and the effectiveness is expected to decline. Therefore, it is not an ideal solution. The reason is that both procedures do not prevent the

Surgical procedures are reserved for patients who fail to respond to medical treatment. Sur‐ gical intervention is required in 56% of the children and in 35% of the adults with uveitic glaucoma. [6] Any intraocular intervention should be performed on a quiet eye for at least 3 months. Topical corticosteroids or other medications as indicated above should be adminis‐ trated two weeks preoperatively and postoperatively to control the uveitis. Systemic cortico‐ steroids may be added. Any intervention on an inflamed eye may result in exacerbation of the uveitis, failure of the procedure and complications. When increased postoperative intra‐ ocular inflammation is anticipated, enoxaparin (Clexan®) (40mg/500 balanced salt solution (BSS)), a low-weight molecular heparin decreases the intensity of such inflammation in sur‐

The preferred anti-glaucoma medications include topical alpha agonists, carbonic anhydrase inhibitors and beta-blockers. Prostaglandins may be added in a quiet eye but should be avoided in an inflamed eye and herpetic keratouveitis because they may exacerbate the in‐ traocular inflammation and cause CME. [33]- [35] Oral or intravenous carbonic anhydrase inhibitors (acetazolamide 500mg) and hyperosmotic agents (oral glycerol 50% or IV manni‐ tol 20% 1gr/kg) should be added if the reduction in IOP is not to the normal range. The effi‐ cacy of prostaglandins and alpha adrenergic agonists may decrease with concurrent use of topical or systemic NSAID. [36], [37] The glaucoma is controlled by medical treatment in 26% of the children and 24% of the adults. [6] In near future, ocular implants containing slow release IOP sparing corticosteroids may improve the visual outcome of patients with macular edema secondary to uveitis without inducing steroid-induced glaucoma. In future, new drugs such as Rho kinase inhibitors may replace existing medications.
