A 19- –year-old female was referred for visual loss and superior field defect in her left eye. Best corrected visual acuity (BCVA) was 20/20 in the right eye (RE) and 20/400 in the left eye (LE). Anterior segment examination was within normal limits except Shaffer sign in the LE. In fundus exam, macula off inferior longstanding rhegmatogenous retinal detachment (RRD) and three hours of proliferative vitreoretinopathy (PVR), retinal break and lattice degeneration were found. SB with 360 degrees encircling silicone band (silicone band type 240, FCI Inc., Paris, France) and inferior segmental silicone tire (asymmetrical silicone tire type 276, FCI Inc., Paris, France) with one spot cryo-retinopexy at the break site and subretinal fluid drainage due to chronicity of the RRD were performed. One week after operation, BCVA was improved to 20/80 and retina was totally attached.
Six weeks later, patient came back with severe visual loss in both eyes, since two days before. In examination, BCVA of both eyes were measured as counting finger at one meter and anterior segment was within normal limits, except 1 + anterior chamber. Anterior vitreous cells in both eyes and also bilateral multifocal serous retinal detachment were obvious (Fig. 1). In enhanced depth imaging optical coherent tomography (EDI-OCT) (Spectralis HRA + OCT, Heidelberg Engineering, Heidelberg, Germany) multi-lobular serous retinal detachment, septated subretinal spaces, hyperreflective dot reflexes in subretinal fluid, choroidal thickening and undulation of retinal pigment epithelium (RPE) (Fig. 1).Regarding to the examination and imaging, the diagnosis of SO following SB surgery was presumed. Therefore, the patient was admitted and treated for five days with high dose (1 g/day) intravenous infusion of methyl prednisolone followed by oral prednisolone 1 mg/kg. The inflammation was controlled and serous detachment resolved significantly after five days’ pulse therapy (Fig. 2). All of the systemic work-ups for common causes of choriditis including sarcoidosis, tuberculosis, syphilis and autoimmunity markers were inconclusive. Also familial, drug and past medical history were unremarkable. After pulse therapy, oral prednisolone and mycofenolate mofetil 2 gr/day was initiated .On the fourth day, fluorescein angiography (FA) was performed and showed no significant dye pooling except for mild leakage and mixed hypo and hyper-fluorescent dots scattered at the posterior poles presumably due to choroidal hypoperfusion and abnormal leakage (Fig. 2). Because of unavailability of indocyanine green dye at that time, indocyanine green angiography (ICGA) was not performed at the first presentation of SO.
After 3 months of immunosuppressive treatment, ICGA disclosed (Fig. 3) only a few hypofluorescent dark dots in the both eyes and mild background hyperflorescence at the posterior pole indicating response to treatment with mild subclinical inflammation of choroidal stroma. Because of increased blood glucose, prednisolone tapered rapidly and subtenon triamcinolone acetonide 40 mg/1 cc was injected bilaterally. Induced diabetes was controlled with oral medication which was ceased after one month. Prednisolone was reached to 5 mg/d at the end of second month with continuing of MMF 2 gr/d. Blood glucose was checked frequently and it was in normal limit during the follow-up, and was not relapsed during six months follow-ups. Following one year treatment with MMF 2gr/d and prednisolone 5 mg/d inflammation was in complete remission with complete attached retina in both eyes. Final BCVA was 20/20 and 20/50 in the right and left eyes, respectively. The patient had not any symptom or sign of systemic disease with similar ocular manifestations, especially Vogt-Koyanagi-Harada (VKH) .