PMC7094199_01
Bilateral presentation of fundus examination. Color fundus photography images show multiple bilateral yellow-white placoid lesions, at the level of external retina, posterior to the equator, and a slight fade of the edges of the optic nerve.
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Dilated fundus examination exhibited a hyperemic optic disc, peripapillary edema, and multiple yellowish-white placoid lesions in the posterior pole, some involving the foveal area, bilaterally (Figure 1).
Bilateral fundus autofluorescence. Images show hypoautoflourescence corresponding to the placoid lesions, with a hyperautofluorescent edge.
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Fundus autofluorescence (FAF) showed hypoautofluorescent lesions with an area of relative hyperautofluorescence along their edge (Figure 2).
Representative fluorescein angiography (FA) images. FA typically showing early hypofluorescent placoid lesions (a) that become hyperfluorescent in the mid and late phases of the angiogram (b).
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Hypofluorescence at the placoid lesions in the early phase that changed to hyperfluorescence at the late phases was evident on fluorescein angiography (FA) (Figures 3(a) and 3(b)).
Representative indocyanine green angiography (ICGA) images. ICGA evidences hypofluorescence through the entire angiogram, corresponding to the placoid lesions.
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Indocyanine green angiography (ICGA) evidenced hypofluorescence of placoid lesions from early to late phases (Figures 4 and 5(a)).
Multimodal evaluation of placoid lesions. (a) Indocyanine green angiography (ICGA) shows hypofluorescence corresponding to the placoid lesions; (b) optical coherence tomography (OCT) angiography demonstrates choriocapillaris ischemia in the corresponding lesions seen on ICGA; (c) OCT exhibiting hyperreflectivity from the outer plexiform layer to the RPE with normal retinal thickness.
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Indocyanine green angiography (ICGA) evidenced hypofluorescence of placoid lesions from early to late phases (Figures 4 and 5(a)). OCT (Avanti RTVue-XR 100, Optovue Inc., Fremont, CA) demonstrated bilateral focal areas of disruption of the ellipsoid layer and hyperreflectivity in the outer retina, primarily localizing to the outer nuclear layer (ONL) but also being seen at the level of the outer plexiform layer (Figure 5(c)). OCTA revealed significant hypoperfusion at the level of the choriocapillaris in the active lesions bilaterally (Figure 5(b)).
Bilateral presentation of fundus examination, after two weeks of follow-up. Color fundus photography images show the placoid lesions in resolution.
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Slit-lamp examination remained unremarkable, and at dilated fundus examination, it was possible to note placoid macular lesions in resolution (Figure 6).
Optical coherence tomography of the right (a) and left (b) eyes after two weeks of follow-up. OCT demonstrated resolution of macular edema and focal atrophy of outer retinal layers, from the outer plexiform layer to the retinal pigmented epithelium, corresponding to the previous hyperreflective areas.
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SD-OCT demonstrated resolution of macular edema and focal atrophy of outer retinal layers corresponding to the previous hyperreflective areas (Figure 7).
Optical coherence tomography angiography (OCTA) images at the level of choriocapillaris revealing focal areas of hypoperfusion in the right (A1 and A2) and left (B1 and B2) eyes. After two weeks, the area of hypoperfusion at the level of the choriocapillaris improved and the thinning of the outer retina in spectral domain optical coherence tomography persisted.
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OCTA showed reperfusion of the choriocapillaris in the affected placoid areas, in both eyes (Figure 8).