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 55-year-old man (subject 1) presented with bilateral metamorphopsia, with decimal visual acuity being 0.8 in the right eye and 1.2 in the left. The clinical diagnosis of VKH was made based on bilateral panuveitis and multifocal exudative retinal detachments at the posterior poles (). High-dose corticosteroid therapy with gradual tapering was initiated 3 days after presentation. The serous detachments entirely resolved within 9 weeks and visual acuity in the right eye improved to 1.2.\nSerial spectral-domain OCT (SD-OCT) images obtained at the preuveitic, uveitic, and posttreatment phase are shown in . SD-OCT obtained 1 year before the onset of VKH due to symptoms of a floater and visual disturbance demonstrated a dome-shaped posterior protrusion of the RPE and outer retinal layers into the choroidal cavity (ie, conforming FCE) at the fovea in the right eye. SD-OCT at the uveitic phase identified multiple bilateral sensory retinal detachments, with the FCE now involving only the RPE (ie, nonconforming FCE). Nine weeks after the treatment, the nonconforming FCE returned into a conforming pattern.\nThe FCE pattern and its alteration during treatment of the case with VKH were compared to those of four subjects with FCE associated with other chorioretinal conditions (). This comparison group consisted of two patients with age-related macular degeneration (AMD; subjects 2 and 3), one subject with a macular hole (MH; subject 4), and one asymptomatic individual (subject 5). Treatment with intravitreal ranibizumab injections and vitrectomy had been performed in the patients with AMD and MH, respectively. A conforming FCE was observed in three patients (subjects 2, 3, and 5) and pattern alteration from nonconforming to conforming FCE was found after treatment in one subject (subject 4). In the two subjects with AMD, a hyperreflective material around the FCE was absorbed, resulting in a well-demarcated conforming FCE after treatment.