A 28-year-old female patient presented with metamorphopsia in her left eye starting 2 days earlier. There was nothing of note in her medical or family history, and her visual acuity was 1.0 in the right eye and 0.8 with -5.0 D refraction in the left eye. Anterior segment examination was normal. Fundus examination was normal in the right eye, but macular pigmentary alterations were observed in the left eye (). On FFA there was hyperfluorescence beginning in the early phases and increasing in the late phase, which was more suggestive of choroidal neovascular membrane (CNVM) than CSCR (). Although it is recommended for a definitive diagnosis, ICGA was not done. Despite smooth foveal contours in the left eye on OCT, an area of subfoveal focal choroidal excavation and overlying hyporeflective subretinal fluid were detected (). The lesion in the patient’s left eye was accepted as CNVM and an intravitreal bevacizumab injection was administered. At follow-up 1 month later, the patient’s symptoms had improved, vision in her left eye improved to 0.9 and the hyporeflective area evident on OCT had decreased in size. At 2-year follow-up, visual acuity in the left eye was 0.8 and persistent RPE changes were observed on fundoscopy (). Hyperfluorescence which increased slightly in the late phases was observed on FFA of the left eye (). On OCT, the focal choroidal excavation remained unchanged, the overlying hyporeflective area had resolved and the photoreceptor layer appeared continuous ().
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 [].