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Introduction/Background: Idiopathic uveal effusion syndrome (IUES) is caused by a histochemical disorder in the sclera that produces a malfunction in the ocular venous drainage, this leads to disorders in nearly every ocular structure. The presumption diagnosis is clinical and the treatment options are limited with few described successful cases and a controverted management. Methods: Case report. Patient monitored with optical coherence tomography and ocular B-scan ultrasound imaging. Treated with scleral surgery. Results: A 50 year-old male, with chronic bronchitis, came to ophthalmology emergency room with red right eye (OD) and visual acuity (VA) 0.3 logMAR. In the biomicroscopy of OD there was dilated episcleral veins, narrow anterior chamber, intraocular pressure of 32 mm Hg, papilla edema and 360° serous peripheral retinal detachment (RD) that partially affected the macula with cystic macular edema. There was not any other remarkable finding. The left eye was normal. The B-scan ultrasonography showed a 360° ciliary body detachment. The axial length was normal. Orbital nuclear magnetic resonance and angio-computed tomography was performed and an arterio-venous fistula or any other compressive mass was ruled out; an OD little thickened sclera was described. The corticosteroid treatment worsened the serous RD and the VA diminished. We opted for surgical treatment (4 rectangular scleral flaps of 6 x 4 mm of 2/3 thickness, anterior to the equator) to improve the vortex vein drainage with little success. Conclusions: IUES results in a challenging diagnosis and treatment. In our case, corticosteroids worsened the symptoms and signs, and the surgery was insufficient. Other publications describe more aggressive treatments (4 scleral flap of 2/3 thickness 4x5 mm with scleral excision of 3x4 mm exposing the choroid, Ex-PRESS shunt inserted obliquely in the sclerotomy), some with better success. More publications and new therapeutic strategies addressed to increase the venous drainage would be necessary to reach an IUES management consensus. [ABSTRACT FROM AUTHOR]

Introduction/Background: The presence of perfluorocarbon into the anterior chamber can produce endothelial damage and increased intraocular pressure. An unusual approach is presented for removal of the perfluorocarbon migrated to the anterior chamber in an aphakic patient, which remained after the refloat of the complex bag-IOL dislocated in the vitreous chamber. Methods: Case report. Results: A myopic magna patient underwent surgery for dislocation of the complex capsular bag-intraocular lens on the right eye. Pars plana vitrectomy was performed with 23 G and refloating of the complex capsular bag-lens dislocated with perfluorocarbon. A month after the surgery procedure, a level of 1.5 mm of perfluorocarbon was noted in the anterior chamber. To remove it, in the operating room, the patient was positioned semi-sitting, in a 45 degrees angle to the horizontal. The knees were flexed and the feet rested on the ground. The surgeon with the microscope was placed in front of the patient to perform the procedure: a main incision was done at IV and another accessory incision at VIII, viscoelastic was injected into the anterior chamber and the perfluorcarbon was completely removed with manual irrigation-aspiration. Finally, saline solution was used to hydrate the corneal incisions. Conclusions: The semi-sitting position of the patient is a useful way to reach the perfluorocarbon located in the bottom of the anterior chamber, otherwise the supine position cause its displacement to the posterior chamber. Thus, we think it's a good option to manage this vitreorretinal surgery complication allowing the complete perfluorocarbon removal with a simple surgery. Acknowledgements: None. [ABSTRACT FROM AUTHOR]

Introduction/Background: Hallervorden-Spatz syndrome is an autosomal recessive neurodegenerative disorder with brain iron accumulation. The classical form has a progressive early onset in infancy that results in the presence of extrapyramidal symptoms and retinitis pigmentosa (RP). The clinical symptoms and signs in RP include nyctalopia and peripheral visual field reduction. Cystoid macular oedema (CMO) can occasionally occur in RP. Pathogenesis of CMO remains unclear and no gold-standard treatments or protocols have established yet. Methods: Case report. Patient monitored with OCT imaging and treated with topic brinzolamide 10 mg/ml and topical nepafenac 1 mg/ml. Results: A 10 year-old female, diagnosed with Hallervorden- Spatz disease, was derived to the Ophthalmology service from Paediatrics with a progressive vision loss. During exploration, bestcorrected visual acuity (BCVA) was 0.2 in both eyes. Macular OCT was performed and a bilateral CMO was found. Bone spicule pigmentation was observed in periphery without further pathological findings. She was diagnosed with RP. Topic brinzolamide was prescribed and there was vision improvement with bilateral reduction of the CMO. Two months later, BCVA deteriorated although CMO diminished; treatment with brinzolamide was maintained and a topical non-steroidal anti-inflammatory (nepafenac) was added. After three months of double therapy, her BCVA was 0.9 in both eyes and the CMO had considerably reduced. Two months later, the CMO was prominent again and her BCVA had decreased again. Due to the evolution with topical treatment, the patient was finally derived to a children's referral hospital where she can be treated more aggressively (intravitreal and/or subtenon triamcinolone acetonide injection, intravitreal dexamethasone implant or intravitreal anti-VEGF injection). Conclusions: There is no specific treatment to arrest or reverse the photoreceptor degeneration, but complications can be managed in diverse ways. Since a protocol to treat CMO in RP is lacking, a gradually aggressive treatment steps should be followed. Acknowledgements: To Ana Montoliu Antón, Francisco Ramos Martí, Soledad Peña, María Redón Soriano and especially Luis León Ibáñez. [ABSTRACT FROM AUTHOR]

Introduction/Background: Spontaneous closure of idiopathic macular holes (MH) has been documented with imaging techniques, but the pathogenesis of the formation and the closure remains unclear although there are some hypotheses. The aim of our case report, monitored with OCT imaging, is to add further support to one of these hypotheses: the closure by a retinal tissue bridge over the MH, and to stress the importance of a short period of observation. Methods: Observational case report. OCT imaging was used to monitor the formation and resolution of a case of an idiopathic stage III macular hole. Results: A 77 year-old woman with an ocular history of a retinal detachment in the right eye 20 years ago with a poor outcome and a mild diabetic retinopathy, came to the emergency room with blurred vision of 3 days of evolution in the left eye. During exploration, the best-corrected visual acuity (BCVA) was 0.5 LOGMAR in the left eye. On OCT, a lamellar hole and a subclinical posterior vitreous detachment were diagnosed and follow-up visits were programmed. Six months later, BCVA was 0.2 and a full-thickness MH was diagnosed; surgery was proposed, but the patient denied. Ten months after the initial examination, the BCVA was 0.6 and the full-thickness MH was covered by a retinal bridge. Five months later, there was a complete resolution of the MH with normal foveal contour that stabilised in the following months and remains unchanged until now. Conclusions: Observation of MH during the first months is advised, especially when the diameter is small. We also want to draw attention to the potential mechanism through which a MH with no vitreomacular traction can resolve. It has been proposed the implication of Müller cells in forming a bridge of retinal tissue, but further investigations need to be done in this direction. Acknowledgements: To Elena Sorlí Clemente, Francisco Ramos Martí, and especially Ana Montoliu Antón and Soledad Peña. [ABSTRACT FROM AUTHOR]

Introduction/Background: The intraretinal hemorrhage, as it is presented in this case report, can be manifested as a retinal rapidly growing mass and simulate a tumoral lesion. Methods: Case report. Results: The diabetic 53 year-old patient presented was treated with bilateral panphotocoagulation and vitrectomy for proliferative diabetic retinopathy in his right eye. In a successive control visit, he reported that his visual acuity gradually decreased in the right eye. In the fundus, there was an intraretinal solid lesion at the proximal third of the superior temporal arcade with rapidly growing in three months without inflammatory or infectious signs associated. In order to discard tumors or aggressive infectious processes, imagining and, serological and biochemical studies were performed without outstanding results. Over the days, the lesion regressed slowly and intraretinal hemorrhage appeared in areas where there was the mass. The process resolved without sequelae in about a year. Conclusions: In the management of a rapidly growing lesion in the posterior pole is a priority rule to discard poor prognosis lesions such as melanoma, lymphoma or choroidal metastases but without forgetting in the differential diagnosis other processes such as intraretinal hemorrhage, where only the natural evolution of the process with the reabsorption of the bleeding will give us the diagnosis. Acknowledgements: None. [ABSTRACT FROM AUTHOR]