Uveitic macular edema

Abstract

Macular edema (ME) may complicate anterior, intermediate, and posterior uveitis, which may be because of various infectious, neoplastic or autoimmune etiologies. BRB breakdown is involved in the pathogenesis of Uveitic ME (UME). Optical coherence tomography has become a standard tool to confirm the diagnosis of macular thickening, due to its non-invasive, reproducible, and sensitive features. Retinal fluorescein and indocyanine green angiography is helpful to study the macula and screen for associated vasculitis, detect ischemic areas and preretinal, prepapillary or choroidal neovascular complications, and it may provide information about the etiology and be needed to assess the therapeutic response. UME due to an infection or neoplastic infiltration may require a specific treatment. If it remains persistent or occurs in other etiologies, immunomodulatory treatments may be needed. Intravitreal, subconjunctival, or subtenon corticosteroids are widely used. Their local use is contraindicated in glaucoma patients and limited by their short-lasting action. In case of bilateral sight-threatening chronic posterior uveitis, systemic treatments are usually needed, and corticosteroids are used as the standard first-line therapy. In order to reduce the daily steroid dose, immunosuppressive or immunomodulatory agents may be added, some of them being now available intravitreally. Ongoing prospective studies are assessing biotherapies and immunomodulators to determine their safety and efficacy in this indication.

Figure 1

Thirty-eight-year old woman with spondyloarthropathy HLA B27 positive, showing severe anterior uveitis associated with UME. (a): posterior synechiae and fibrinous deposit in the anterior chamber; (b): horizontal central OCT scan showing UME.

Figure 2

Sixty-year old woman with sarcoidosis (a): retinal photography showing candle wax drippings; (b): late phase of fluorescein angiography showing pooling and leakage; (c): OCT showing intra-retinal and sub-retinal fluid accumulation.

Figure 3

Fifty-eight-year old woman with Birdshot retinochoriopathy showing mainly outer retinal ME.

Figure 4

Twenty-three-year old woman with Vogt–Koyanagi–Harada disease. (a): ME retinal photography; (b): ME due to subretinal fluid accumulation.

Figure 5

Eleven-year old girl with Bartonellosis infection showing a swelling optic nerve head, hyperreflective dots and macular edema.

Figure 6

Thirty-year old man with Toxocarosis infection. (a): vitreous inflammation and fuzzy retinal photography; (b): focal retinitis in retinal periphery; (c): epiretinal membrane and ME.

Figure 7

Fifty-one-year old woman with zoster virus retinitis. (a): whitish vitreo-retinal adherence; (b): OCT showing tractional ME.

Figure 8

Twenty-year old woman with inflammatory choroidal neovascularization (a): whitish edematous focal deep macular lesion; (b): OCT showing hyper-reflective pre-epithelial focal lesions corresponding to choroidal neovascularization; (c): multiple hyper-reflective dots corresponding to inflammatory intra-retinal deposits.

Figure 9

Treatment algorithm.