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    • Basic and Clinical Science Course - Excerpt
  • 2020–2021 BCSC Basic and Clinical Science Course™

    Go to Academy Store Learn more and Purchase.

    9 Uveitis and Ocular Inflammation

    Chapter 14: Complications of Uveitis

    Uveitic Macular Edema

    Uveitic macular edema is a common cause of vision loss in eyes with uveitis. The edema is usually caused by active intraocular inflammation and appears to be mediated by the proinflammatory cytokines vascular endothelial growth factor (VEGF) and interleukin-6, which cause retinal vascular leakage and retinal pigment endothelium dysfunction. Less commonly, UME may be caused by mechanical vitreomacular traction; the distinction can be differentiated by OCT. It can also be quantitatively evaluated and monitored by serial spectral-domain OCT and fluorescein angiography studies. The severity of UME does not necessarily correspond to the level of inflammatory disease activity; UME is often slow to respond and clear and frequently remains even after visible, active inflammation has resolved. Smoking appears to be associated with a greater prevalence of UME, especially in patients with intermediate uveitis and panuveitis.

    • Lin P, Loh AR, Margolis TP, Acharya NR. Cigarette smoking as a risk factor for uveitis. Ophthalmology. 2010;117(3):585–590.

    • Rothova A. Inflammatory cystoid macular edema. Curr Opin Ophthalmol. 2007;18(6):487–492.

    Treatment

    Treatment of UME must first be directed toward control of intraocular inflammation. If UME persists despite control of inflammation, therapy directed specifically toward the UME is required. This treatment may be regional or systemic. Periocular injections of corticosteroid may be used; a superotemporal posterior sub-Tenon injection of 20–40 mg of triamcinolone acetonide is preferred. Theoretically, this technique delivers juxtascleral corticosteroid closest to the macula. The injections may be repeated monthly. If UME persists, then 2–4 mg of intravitreal preservative-free triamcinolone may be considered. Intravitreal triamcinolone can be highly effective in reducing UME, particularly in non-vitrectomized eyes, but its effect is time limited; the drug is eliminated more quickly from the vitreous cavity of vitrectomized eyes. Visual improvement and reduction of UME after intravitreal triamcinolone injection typically occur within 4 weeks. Eyes with a longer duration of UME and worse vision on presentation tend to show the least amount of vision improvement after treatment with intravitreal triamcinolone. Corticosteroid-induced elevation of IOP may occur in up to 40% of patients, especially in those younger than 40 years.

    Sustained delivery of corticosteroid to the vitreous cavity through the use of implants is also effective. Currently available implants in the United States include the fluocinolone acetonide implant and an intravitreal sustained-release drug-delivery system for dexamethasone (700 μg). The risk of ocular hypertension is lower for the dexamethasone delivery system than for the fluocinolone implant. The VEGF inhibitors can also reduce inflammatory UME, but the action is of short duration and repeat injections are required. Intravitreal methotrexate (400 μg/0.1 mL) has been shown to be effective in reducing UME in a limited number of patients and is under active investigation. See Chapter 5 for additional information on the use of corticosteroids in the treatment of uveitis including UME.

    Topical NSAIDs can be beneficial in treating pseudophakic UME, but their effectiveness in the treatment of UME has not been established. Oral acetazolamide, 500 mg once or twice daily, has also been effective in reducing UME, particularly in patients whose inflammation is well controlled. Systemic interferon therapy has shown efficacy in resolving recalcitrant UME, with complete control in 62.5% of patients in one study. Common adverse effects include flulike symptoms.

    Surgical therapy for UME is still controversial. Pars plana vitrectomy for UME in the presence of hyaloidal traction on the macula (as demonstrated on OCT imaging) may be visually and anatomically beneficial. In the absence of vitreomacular traction, however, the efficacy of pars plana vitrectomy in treating UME is not well understood. There is some suggestion that vitrectomy may be beneficial in managing recalcitrant UME, but this application requires further investigation.

    • Becker M, Davis J. Vitrectomy in the treatment of uveitis. Am J Ophthalmol. 2005;140(6): 1096–1105.

    • Deuter CM, Kötter I, Günaydin I, Stübiger N, Doycheva DG, Zierhut M. Efficacy and tolerability of interferon alpha treatment in patients with chronic cystoid macular oedema due to non-infectious uveitis. Br J Ophthalmol. 2009;93(7):906–913.

    • Jennings T, Rusin MM, Tessler HH, Cunha-Vaz JG. Posterior sub-Tenon’s injections of corticosteroids in uveitis patients with cystoid macular edema. Jpn J Ophthalmol. 1988;32(4): 385–391.

    • Kok H, Lau C, Maycock N, McCluskey P, Lightman S. Outcome of intravitreal triamcinolone in uveitis. Ophthalmology. 2005;112(11):1916.e1–e7.

    • Schilling H, Heiligenhaus A, Laube T, Bornfeld N, Jurklies B. Long-term effect of acetazolamide treatment of patients with uveitic chronic cystoid macular edema is limited by persisting inflammation. Retina. 2005;25(2):182–188.

    • Taylor SR, Habot-Wilner Z, Pacheco P, Lightman SL. Intraocular methotrexate in the treatment of uveitis and uveitic cystoid macular edema. Ophthalmology. 2009;116(4): 797–801.

    • Tran TH, de Smet MD, Bodaghi B, Fardeau C, Cassoux N, Lehoang P. Uveitic macular oedema: correlation between optical coherence tomography patterns with visual acuity and fluorescein angiography. Br J Ophthalmol. 2008;92(7):922–927.

    Excerpted from BCSC 2020-2021 series: Section 9 - Uveitis and Ocular Inflammation. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.

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