PurposeTo ascertain the anatomic factors that help achieve non-surgical sealing in full thickness macular hole (FTMH).MethodsRetrospective collaborative study of FTMH that closed without surgical intervention.ResultsA total of 78 patients (mean age 57.9 years) included 18 patients with blunt ocular trauma, 18 patients that received topical or intravitreal therapies and 42 patients with idiopathic FTMH. Mean±SD of the initial corrected visual acuity (VA) in logMAR improved from 0.65±0.54 to 0.34±0.45 (p<0.001) at a mean follow-up of 33.8±37.1 months. FTMH reopened in seven eyes (9.0%) after a mean of 8.6 months. Vitreomacular traction was noted in 12 eyes (15.8%), perifoveal posterior vitreous detachment in 42 (53.8%), foveal epiretinal membrane in 10 (12.8%), cystoid macular oedema (CME) in 49 (62.8%) and subretinal fluid (SRF) in 20 (25.6%). By multivariate analysis, initial VA correlated to the height (p<0.001) and narrowest diameter of the hole (p<0.001) while final VA correlated to the basal diameter (p<0.001). Time for closure of FTMH (median 2.8 months) correlated to the narrowest diameter (p<0.001) and the presence of SRF (p=0.001). Mean time for closure (in months) was 1.6 for eyes with trauma, 4.3 for eyes without trauma but with therapy for CME, 4.4 for eyes without trauma and without therapy in less than 200 µm in size and 24.7 for more than 200 µm.ConclusionOur data suggest an observation period in new onset FTMH for non-surgical closure, in the setting of trauma, treatment of CME and size <200 µm.

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Background: To study the visual outcomes of neovascular AMD (nAMD) treated with anti-vascular endothelial growth factor (VEGF) drugs at national level.Methods: Multicenter national database of nAMD eyes treated with anti-VEGF intravitreal injections (ranibizumab, aflibercept, bevacizumab) in fixed bimonthly (FB) or treat-and-extend (TAE) regimens. Demographics, visual acuity (VA) in logarithm of the minimum angle of resolution (logMAR) ETDRS letters at baseline and subsequent visits, number of injections and visits data were collected using a validated web-based tool (Fight Retinal Blindness!). Results: 1273 eyes (1014 patients) were included, 971 treatment naïve (TN) and 302 previously treated (PT). Baseline VA (mean ± SD) was 57.5 (±19.5) and 62.2 (±17) (p > 0.001), and 24 months final VA was 60.4 (±21.2) and 58.8 (±21.1) (p = 0.326), respectively. Mean VA change at 12/24 months was +4.2/+2.9 letters in TN eyes and +0.1/À3.4 letters in PT eyes (p < 0.001/p < 0.001). The percentage of ≥15 letters gainers/losers at 24 months was 24.8%/14.5% in TN, and 10.3%/15.7% in PT eyes. The median number of injections/visits at 12 months was 7/9 in TN and 6/8 in PT (p = 0.002/p < 0.001) and at 24 months was 11/16 in TN and 11/14 in PT (p = 0.329/p < 0.001). Study drugs included ranibizumab (39.5%), aflibercept (41.2%) and bevacizumab (19.3%).

PurposeTo describe a case of interlamellar keratitis induced by elevated intraocular pressure (IOP) in a patient with a history of LASIK surgery and the importance of having a strong diagnostic suspicion for establishing adequate treatment.MethodsIntraocular pressure‐induced interlamellar keratitis is one of the potential complications of LASIK refractive surgery. The cases described generally occur a few months after surgery although there are some cases that have been described several years after surgery, usually in a context of uveitis and corticosteroid treatment or silent glaucoma. We present a case of 43‐year‐old woman who came to the emergency room with visual acuity (VA) impairment in the left eye in the setting of elevated intraocular pressure‐induced interlamellar keratitis secondary to the intravitreal corticosteroid implant in her left eye due to a diabetic retinopathy. She underwent LASIK surgery 14 years ago.ResultsThe treatment was based on lowering the intraocular pressure. Oral acetazolamide and topical timolol, bimatoprost and brinzolamide were used. The patient recovered her baseline VA and the IOP were properly controlled posteriorly.ConclusionsThis case shows the importance of considering this diagnosis in patients with corneal haze, elevated intraocular pressure and a history of LASIK surgery to establish an adequate treatment. A full recovery is expected.Bibliography1. Galal A, Artola A, Belda J, (2006) Interface corneal edema secondary to steroid‐induced elevation of intraocular pressure simulating diffuse lamellar keratitis. Journal of refractive surgery.2. Lee V, Sulewski M, Zaidi A (2010) Elevated Intraocular Pressure–Induced Interlamellar Stromal Keratitis Occurring 9 Years After Laser In Situ Keratomileusis. Corneal Journal.3. Lyle W, Jin G, Jin Y (2003) Interface fluid after laser in situ keratomileusis. Journal of refractive surgery.4. Tourtas T, Kopsachilis N, Meiller R, et al. (2010). Pressure‐Induced Interlamellar Stromal Keratitis After Laser In Situ Keratomileusis. Corneal Journal.

Purpose: To present a case of persistent corneal edema after endothelial disease of unknown cause and with a severe decrease in the endothelial count and clinical improvement after DWEK (descemetorhexis without endothelial keratoplasty). Methods: A 61‐year‐old immunocompetent male patient, with no relevant ophthalmological or systemic history, who after multiple episodes of subacute endotheliitis with retrokeratic precipitates and diffuse iridian atrophy in his right eye, showed central persistent corneal edema, secondary to a marked decrease in endothelial count and severe decrease in best‐corrected visual acuity (0.2) after several months of inflammatory stability. Results: During flare‐ups of inflammation, treatment with corticosteroids, topical ganciclovir and oral acyclovir was prescribed, with a good clinical response. Aqueous humour samples were taken during the outbreaks without yielding results for herpesviruses. The endothelial count remained low at the central level several months later, although the peripheral count was good. The fellow eye showed a normal count. It was decided to perform DWEK in the endothelial zone of retrokeratic precipitates as a diagnostic measure. The analyses of the endothelial sample FOR THE HERPESVIRIDAE FAMILY do not show results, however, a progressive improvement in corneal edema and visual acuity was observed from the first month after DWEK. He is currently stable, with mild paracentral edema and a best‐corrected visual acuity of 0.7. Conclusions: DWEK is reserved for cases of slightly advanced endothelial dystrophy, in which the central endothelial denudation causes a centripetal migration of the peripheral endothelial reserve. In this case, the clinical findings suggest a viral aetiology of the endothelial loss, therefore, DWEK was considered as a diagnostic procedure, to obtain samples for PCR and as a first step prior to DMEK. The improvement after DWEK in the area of retrokeratic precipitates without the need for a subsequent transplant suggests localized endothelial involvement in cases of endothelial loss associated with localized inflammatory precipitates.