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 50-year-old female patient presented to the Ophthalmology Department of the İstanbul University İstanbul Faculty of Medicine with an approximately 2-year history of gradual vision loss in her left eye. Despite progressively decreasing vision in her left eye over the course of 2 years, she had not previously consulted any doctor about the problem. There was nothing extraordinary in the patient’s medical or family history. Her vision was 1.0 (decimal) in the right eye and 0.05 in the left eye. Anterior segment examination was normal and intraocular pressure was 15 mmHg in the right eye and 16 mmHg in the left eye. Pigment epithelium changes were observed in both the right and left macula on fundoscopy (). OCT examination revealed extrafoveal inferonasal choroidal excavation in the right eye (), while in the left eye subfoveal focal choroidal excavation was observed, as well as separation of the retinal pigment epithelium (RPE) photoreceptor layer and subretinal fluid in the same area (). Central foveal thickness was 245 µm in the left eye. Fundus fluorescein angiography (FFA) and indocyanine green angiography (ICGA) revealed hyperfluorescence consistent with pigment epithelium window defect in the macula and temporal quadrant of the right eye, and hyperfluorescence starting in the early phase and increasing in the late phases in the left macula (). The patient was diagnosed with chronic CSCR and her left eye was treated with low-fluence photodynamic therapy (PDT) (25 j/cm2, 300 mW/cm2). The spot size was adjusted targeting the area of choroidal vascular hyperpermeability observed in the ICGA mid-phase from which the subretinal fluid originated.\nAt 1 month after PDT, the subretinal fluid had resolved and visual acuity was 0.3. After 18 months of follow-up, no changes were observed in the lesions in the right eye, visual acuity in the left eye as maintained and there was no recurrence of subretinal fluid. OCT at the final examination showed continuity of the RPE and photoreceptor layer in the area of focal choroidal excavation, and no subretinal fluid was observed (). On FFA, the hyperfluorescence due to RPE window defect was not evident () and there was no active leakage apparent on ICGA ().