Purpose: The purpose of this paper is to provide a meaningful literature review about the epidemiology, pathogenesis, clinical signs, imaging and treatment of ocular siderosis (OS).Methods: A computerized search from inception up to March 2020 of the online electronic database PubMed was performed using the following search strings: “ocular siderosis” and “siderosis bulbi”. The reference list in each article was analysed for additional relevant publications.Results: OS is an uncommon cause of visual loss due to a retained ferrous intraocular foreign body (IOFB). It may develop from 18 days to years after a penetrating trauma that usually occurs during hammering. On average, patients are 22–25 years old, and the vast majority are male. The most common cause of OS development is delayed presentation by the patient or missed diagnosis of IOFB after trauma. The pathophysiology is not fully understood; nevertheless, iron deposition causes hydroxyl radical formation, which damages photoreceptors and retinal pigment epithelium. Moreover, iron damages retinal vessels with consequent inner retinal layers degeneration. The most frequent signs are iris heterochromia, pupillary mydriasis, cataract development and retinal arteriolar narrowing with pigmentary retinal degeneration. Electroretinogram signs, in particular,b-wave amplitude reduction, arise earlier than clinical signs. Orbital CT scans and ultrasonography play an essential role in detecting IOFBs. Treatment depends on the IOFB location and OS development. However, it is crucial to remove the IOFB after OS development because visual acuity and clinical signs may improve. Anterior segment IOFBs can be dislodged using an intraocular magnet (IOM) or forceps through limbal paracentesis. In contrast, posterior segment IOFBs require a pars plana vitrectomy and IOM or forceps to be removed through an enlarged sclerotomy or the limbus.Conclusion: Recommending the usage of protective glasses and spreading knowledge about OS may further benefit patient care.

Purpose: To determine whether surgical manipulation steps of the internal limiting membrane (ILM) flap, such as ILM trimmed, ILM tuck inside the hole, ILM massage, are mandatory to obtain satisfactory outcomes for the repair of large stage IV idiopathic macular hole using the inverted ILM flap technique. Methods: In this interventional comparative prospective single-masked study, 81 eyes were randomized into 2 treatments groups. In Group 1 (41 eyes), the classic inverted ILM flap technique was performed. In Group 2 (40 eyes), a modified procedure was used: after ILM peeling, no extra flap manipulation was performed. The macular hole was covered by the inverted ILM flap because of the air pressure at the time of the fluid–air exchange. Results: At 12 months, macular hole closure was observed in 40 eyes (97.6%) in Group 1 and in 39 eyes in Group 2 (97.5%). U-shape closure rate, ellipsoid zone defects, and external limiting membrane defects were similar in both groups. The results indicate no statistical difference in anatomical and functional success between both groups. Conclusion: The macular hole closure rate, improved visual acuity, and no extra complications indicate noninferiority of the modified inverted ILM technique. Internal limiting membrane finishing, tucking, and massage may not be required to obtain surgical success.

Introduction: The purpose of this study was to evaluate choroidal vascular changes in patients with neovascular age-related macular degeneration (nAMD) treated with aflibercept injection over a 3-month period. Methods: Enhanced depth imaging optical coherence tomography scans of 60 eyes with treatment-naïve nAMD and 60 unaffected fellow eyes were retrospectively analyzed. Data was collected at baseline and after 3 monthly intravitreal injections of aflibercept. The ImageJ software was used to binarize OCT scans and measure total choroid area (TCA), luminal area (LA), and stromal area (SA). Choroidal vascularity index (CVI) was defined as the ratio of LA to TCA. Results: After treatment, subfoveal choroidal thickness (CT) in nAMD eyes significantly decreased from 210. 6 ± 61.6 to 194.6 ± 58.7 μm (P < 0.001), TCA from 1.620 ± 0.502 to 1.500 ± 0.451 mm² (P < 0.001), LA from 1.075 ± 0.335 to 0.985 ± 0.307 mm² (P < 0.001), SA from 0.545 ± 0.176 to 0.516 ± 0.153 mm² (P = 0.005), and CVI from 66.36 ± 2.89 to 65.46 ± 2.87% (P = 0.009). The decrease of CVI after treatment was significantly correlated with baseline CVI (Rs = 0.466, P < 0.001), but not with the change in BCVA and presence of dry macula after treatment (always P > 0.05). Conclusion: Choroidal thickness and vascularity significantly decreased after treatment with aflibercept in nAMD eyes. Besides the pharmacologic effect on the neovascular lesion, aflibercept may induce vascular changes also on the underlying choroid.