A 16-year-old woman with mild myopia complained of blurred vision and photopsia of the right eye for 1 month. The patient had no particular medical or ocular histories.\nHer BCVA was 1.2 OU. Relative afferent pupillary defect was negative. Left eye was normal. Slit-lamp examination revealed no cells in the anterior chamber, but mild anterior vitreous cells OD. Funduscopic examination showed multiple, faint, small, subretinal white dots at the posterior pole to the midperiphery (, arrowheads), macular granularity, and retinal vascular sheathing at superotemporal midperiphery (, arrows). On FA, the hyperfluorescence was seen from the initial phase corresponding to the white dots (, arrowhead), with the staining of the optic disk and vascular leakages corresponding to the retinal vascular sheathing on the late phase (, arrow). On late-phase indocyanine green angiography, multiple spots of hypofluorescence were observed at the wider area despite no initial abnormal findings (, arrowheads). EDI-OCT revealed segmental loss of the ellipsoid zone at areas of the white dots (, arrows), and the SCT was 341 µm. Goldmann perimetry showed a mild blind spot enlargement of 5×10 degree OD and no abnormality OS. On Humphrey perimetry, MD value was −5.47 dB OD, and OS was unmeasured. In mfERG, entirely decreased amplitude except central normal amplitude was present OD, and the result was normal OS. Systemic screening, similar to what was done for Case 1, showed negative results. She was diagnosed as having MEWDS OD and was followed up with no treatment. One month later, white dots and retinal vasculitis spontaneously disappeared. Three months after the initial visit, the ellipsoid zone at the macula restored and the SCT decreased to 319 µm (). The BCVA remained unchanged. Twelve months after the initial visit, the MD value improved to −0.24 dB OD. Thereafter, there were no recurrences of MEWDS during follow up.
A 48-year-old female presented to us with blurring and distortion of vision in OS since 2 weeks. Her BCVA was 6/6; N6 in OD and 6/24;N10 in OS at presentation. Fundus examination showed an extrafoveal CNVM. Based on multimodal imaging including SD-OCT and FFA, patient was diagnosed to have type-2 CNVM with subfoveal choroidal thickness of 505 μm. She was also treated with antiVEGF monotherapy on pro re nata (PRN) basis and had multiple recurrences over 5 years. Interestingly, she developed FCE at the site of resolved CNVM scar, during 23 months of treatment, which progressively increased from 85 μm to 154 μm in depth over the subsequent follow-ups. We report this as a case of acquired FCE secondary to CNVM [].