Fig. 16.1
Subclinical broad vitreomacular adhesion in a 34-year-old female with pars planitis. Visual acuity was 20/25
Fig. 16.2
Epiretinal membrane in a 56-year-old male with Eales disease treated with pan-retinal photocoagulation. Visual acuity was 20/40
16.2 Uveitic Macular Edema
Morphometric macular changes can be easily observed and analyzed with SS-OCT. More than this, the follow-up of such changes makes it possible to reliably monitor the therapeutic response to any treatment administered with high precision.
Increased macular thickness in patients with uveitis may appear as one of three different patterns in SS-OCT images [6–10].
16.2.1 Diffuse Macular Thickening
Diffuse macular thickening is the most frequent pattern of uveitic macular edema, accounting for 55% of these cases. It is characterized by increased retinal thickness with disturbance of the layered retinal structure, or sponge-like low reflective areas, without intraretinal cystoid cavities, within the thickened area (Fig. 16.3).
Fig. 16.3
Diffuse macular thickening associated with inflammatory juxtapapillary choroidal neovascularization in a 29-year-old female. Visual acuity was 20/30
16.2.2 Cystoid Macular Edema
Cystoid macular edema is present in up to 25% of cases of uveitic macular edema. Although it is usually associated with diffuse macular thickening, the presence of intraretinal cystoid spaces is associated with worse visual prognosis when compared to pure diffuse thickenings (Fig. 16.4). The response to local and systemic therapies of cystoid macular edema is usually good, but recurrences are frequent throughout the follow-up. Although basically any intraocular inflammatory disease may associate cystoid macular edema, this is a typical feature of Birdshot choroidopathy [11, 12] and juvenile idiopathic arthritis [13].
Fig. 16.4
Foveal cystoid macular edema in a 62-year-old female with chronic Birdshot choroidopathy. Visual acuity was 20/40
16.2.3 Subretinal Fluid
The presence of fluid between the photoreceptors and the retinal pigment epithelium is infrequent in patients with uveitis, accounting for 6% of all cases. However, the detection of subretinal fluid has a relevant prognostic impact, as it is the macular edema pattern associated with the worst visual outcome; therefore, therapeutic interventions should be considered immediately after diagnosing its presence (Fig. 16.5). Vogt-Koyanagi-Harada disease is characterized by a particular appearance of large subretinal fluid spaces fenestrated by fibrinous tissue associated with a significant increase of choroidal thickness; both findings respond to systemic steroid-intensive therapy. Other entities that may exhibit subretinal fluid in the SS-OCT images are posterior scleritis [14], sympathetic ophthalmia [15], and neuroretinitis, among others [16].
Fig. 16.5
Subfoveal fluid associated with cystoid macular edema in a 38-year-old patient with posterior scleritis. Visual acuity was 20/6
In addition, choroidal involvement by granulomatous diseases (Fig. 16.6) or lymphoproliferative disorders may also induce serous retinal detachment (Figs. 16.7 and 16.8).
Fig. 16.6
Subretinal fluid secondary to tuberculous choroidal granuloma in a 27-year-old male with miliary tuberculosis. Visual acuity was 20/20
Fig. 16.7
Focal choroidal lesion in a 62-year-old male with systemic follicular lymphoma. Visual acuity was 20/20
Fig. 16.8
Subretinal fluid and severe choroidal involvement with the typical seasick appearance in a patient with extranodal marginal zone MALT lymphoma. Visual acuity was 20/200
16.3 Inflammatory Choroidal Neovascularization
Choroidal neovascularization (CNV) is present in several intraocular inflammatory diseases (Fig. 16.9). The main uveitis associated with inflammatory CNV are multifocal choroiditis (30%), punctate inner choroidopathy (70%), and presumed ocular histoplasmosis syndrome (30%) [17–19].
Fig. 16.9
Illustrative cases of choroidal neovascularization (CNV) in patients with multifocal choroiditis. Top: Active CNV with ill-defined neovascular complex and cystoid macular edema (visual acuity 20/50); Middle: Inactive CNV with outer retinal tubulations and degenerative pseudocysts (visual acuity 20/30); Bottom: Consolidated and healed CNV with complete retinal pigment epithelium envelopment of the CNV and no evidence of neovascular activity (visual acuity 20/20)
16.4 Other Retinal Changes in Patients with Uveitis
16.4.1 Topographic Characterization of Chorioretinal Inflammation
The cautious observation of SS-OCT scans is useful in order to determine the exact composition of inflammatory lesions, thus making possible the differentiation between retinitis (hyperreflective lesions within the neurosensory retina), choroiditis (increased choroidal thickness with hyperreflective foci at the level of the choriocapillaris), and chorioretinitis (combination of the aforementioned lesions) [20].
Also, there are some typical tomographic signs highly suggestive of particular entities: hyperreflective evanescent lesions on top of the retinal pigment epithelium (RPE), eventually in a columnar disposition, in patients with multiple evanescent white dots syndrome [21]; hyperreflective banded lesions from the inner plexiform layer to the outer nuclear layer in patients with acute macular neuroretinopathy [22].
16.4.2 Retinal Pigment Epithelium Atrophy
Chorioretinitis may lead to widespread punched-out lesions at the level of the retinal pigment epithelium that can be identified and evaluated by SS-OCT (Fig. 16.10). These are typical of multifocal choroiditis, punctate inner choroidopathy, and presumed ocular histoplasmosis syndrome [23, 24]. Also, zonal atrophic lesions of the RPE may be observed in acute multifocal placoid pigment epitheliopathy (APMPPE) [25], acute zonal occult outer retinopathy (AZOOR) [26], and serpiginoid syndromes (serpiginous choroiditis, ampiginous chorioretinopathy) [27].
Fig. 16.10
Atrophic changes at the level of the outer retinal layers, retinal pigment epithelium (RPE) and choroid in a 47-year-old patient with relentless placoid chorioretinitis (ampiginous choroiditis). Visual acuity was 20/25
16.4.3 Retinal Atrophic Changes
Retinal atrophy may develop secondary to vascular ischemia or to progressive atrophy of the choroid and the RPE. In cases secondary to retinal ischemia, the area of thinning usually follows the involved vessels, making it easy to recognize the underlying process (Fig. 16.11). On the other hand, zonal atrophic areas correspond to the retina overlying atrophic choroid and/or RPE regions (Fig. 16.10) [28–30].
Fig. 16.11
Zonal retinal atrophy secondary to vascular ischemia due to thrombophlebitis secondary to Behçet disease in a 48-year-old female. The atrophic changes are clearly visible rastering the superior temporal macular area (bottom image). Visual acuity was 20/80
16.5 Assessment of the Choroid in Uveitis
Among the several goals of using imaging techniques in uveitis, one of the most important is to achieve a precise characterization of the pathologic processes that happen in the choroid. Angiographic techniques have traditionally been the only way to explore the choroid. Fluorescein angiography is especially useful for retinal pathology, though signs of choroidal abnormalities may also be observed. Indocyanine green angiography reveals predominantly pathology of the choroid and has been shown to provide valuable data regarding pathogenesis and the monitoring of patients with uveitis. However, some caveats include that this technique is invasive, time-consuming, and difficult to perform repeatedly during the patient’s follow-up. Moreover, it does not provide sufficient information regarding cross-sectional imaging of the choroid, and it does not provide quantitative data. Choroidal structure can be easily observed and analyzed by SS-OCT. Moreover, measurement of its thickness can be performed. Hence, OCT is an excellent tool for both detection of inflammation and monitoring therapeutic response, as it has been shown in several publications. Kim et al. [31] found greater choroidal thickness in patients with Behçet’s disease in active disease as compared to quiescent phase. Ishikawa et al. [32] assessed the effect of treatment with Infliximab in patients with Behçet’s uveitis by measuring changes in choroidal thickness. This treatment reduced the choroidal thickness from week two after the first infusion and the reduced choroidal thickness was maintained thereafter. Zarranz-Ventura et al. [33] showed, in a large series of patients with presumably inactive punctate inner choroiditis, that one-fifth of the lesions analyzed by OCT revealed signs of activity (retinal pigment epithelium elevation with underlying hyporeflective space). Sakata et al. [34] described a new OCT finding that may indicate ongoing inflammation in patients with Vogt-Koyanagi-Harada (VKH) disease in the chronic stage consisting of a localized choroidal thickening or bulging. Sequelae of choroidal chronic inflammation has also been assessed by OCT. Patients with ocular sarcoidosis present thinner choroids in the quiescent stage [35]. Patients with longstanding VKH disease also have thinner choroids [36].
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