Introduction: Epiretinal membrane is one post-operative complication of vitrectomy that can lead to decrease visual acuity. Epiretinal membrane is the early step of proliferative vitreoretinopathy caused by inflammation. Steroid has been used in the treatment of intraocular inflammation. The aim of this study is to compare oral methylprednisolone and placebo toward incidence and severity of epiretinal membrane post pars plana vitrectomy in rhegmatogenous retinal detachment. Methods: This was prospective, double blind, randomized clinical trial. Fourty six eyes who met inclusion criteria were randomized into 2 groups: 26 patients received oral methylprednisolone 0.8 mg /kgBW/day for 6 days, 0.4 mg/kg BW/day for 4 days, and 0.2 mg/kg BW/days for 4 days. The control group of 26 patients received placebo in a comparable manner. Result: Four weeks after vitrectomy incidences of epiretinal membrane were 47.6 % and 58.8 % in methylprednisolone group and placebo group, respectively. Eight weeks post vitrectomy incidences of epiretinal membrane was 47.6 % and 56.2 % in methylprednisolone group and placebo group, respectively. At 4 weeks the severity of epiretinal membrane in methylprednisolone group was 60%; 0%; 40% in grade 0, 1, and 2, respectively. Meanwhile, in placebo group were 60%; 10%; 30% in grade 0, 1, and 2,respectively. Eight weeks post vitrectomy the severity of epiretinal membrane in methylprednisolone group were 40%; 0 %; 60% in grade 0, 1, and 2, respectively. Meanwhile, at placebo group were 55.6 %; 11.1 %; and 33.3 % in grade 0, 1, and 2, respectively. Conclusion: There were no significant differences in incidence and severity of epiretinal membrane at 4 and 8 weeks among 2 groups. Oral methylprednisolone had a tendency to lower incidence of epiretinal membrane compared to placebo.
Introduction: Dapsone has been widely used as a part of multidrug therapy for leprosy patients. Ocular side effects are rare. Ocular toxicity manifestations include retinal necrosis, optic atrophy, macular infarction, bilateral exudative retinal detachment, and choroidal detachment. We reported a rare case of dapsone-induced toxic maculopathy in a leprosy patient. Case Report: A 32-year-old male complained of blurred vision and a gray spot in central vision in the left eye (LE) for one month prior to admission. He had been treated with multidrug therapy (MDT) for leprosy for seven months. The MDT consists of dapsone, clofazimine, and rifampicin. The best-corrected visual acuity (BCVA) of the right eye (RE) and the LE were 6/6 and 6/12, respectively. A funduscopy of the LE showed decreased macular reflex. A color vision defect following the tritan axis was found in the LE. The Humphrey visual field (HVF) test of the LE revealed a central scotoma. Macular optical coherence tomography (OCT) showed intraretinal hyperreflectivity and subretinal fluid. Dapsone was then stopped in collaboration with a dermatologist. Two months after the discontinuation of Dapsone, the BCVA of the LE improved to 6/7.5, then 6/6 three months later. Color vision, macular OCT, and HVF tests revealed improvements. Multifocal ERG of both eyes (BE) also showed improvement in N1 and P1 wave amplitude in both eyes on 9-month follow-up after dapsone discontinuation. Discussion: Instead of direct drug toxicity, the mechanism of ocular side effects is thought to be ischemia caused by two distinct mechanisms. Macular ischemia is caused by acute, severe peripheral hypoxia and the physical effect of red cell fragmentation due to the hemolytic process. After discontinuation of dapsone, this case showed improvement in visual function and macular structure. Conclusion: Toxic maculopathy may be present in leprosy patients receiving dapsone treatment, although it is uncommon. Regular follow-up and evaluation of visual function and macular involvement are essential. Early detection of dapsone-induced toxic maculopathy and prompt discontinuation of dapsone may result in an improvement of visual functions.
Introduction: Non-arteritic Ischemic Optic Neuropathy is the most common type of ischemic optic neuropathy. Nearly half of NAION patients presented with 20/30 or better visual acuity. Central vision is often preserved relative to the visual field loss. Macular edema in NAION patient is rare, and its occurrence may confuse to other disease and lead to unnecessary treatment. Case Report: We identified three NAION patients presented with macular edema. The patients' age was above 40 and had diabetes mellitus (DM). Our patients had clinical findings consistent with NAION with poor visual acuity at the early presentation. Optical coherence tomography examination was performed, and all patients had prominent subretinal fluid. Intravitreal anti-VEGF injection was done on our first patient and no treatment was given to our second and third patient. All patients showed a significant improvement of macular edema. Discussion: Macular edema is a rare clinical manifestation that may contribute a visual deterioration in NAION. The incidence of macular edema in NAION patients is difficult to measure since OCT of macula is not routinely performed. In our report, we encountered three cases of NAION complicated by macular edema that underwent a different approach in therapy. Spontaneous regression of subretinal fluid was seen during observation without any treatment given. Our patients achieved a stable visual acuity and visual field defect. This finding is under the literature that spontaneous recovery will be observed during the natural course of acute NAION. Conclusion: Macular edema is an unusual but self-limiting presentation of NAION. Therefore, a comprehensive examination is needed to prevent any unnecessary treatment.
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