Abstract: Advances in intraocular lens (IOL) design have rendered cataract surgery a refractive procedure. Newer IOL types include bifocal, trifocal and extended depth of focus (EDOF) IOLs. Their basic difference nestles in the number of focal points that each lens provides, which in turn leads to different visual outcomes. Familiarity of surgeons with the various characteristics of each lens is of utmost importance for accurate IOL selection to match each patient’s needs. In this review, we aim to compare the clinical outcomes after implantation of multifocal and EDOF IOLs in terms of distance, intermediate and near vision, contrast sensitivity, and reading performance. Finally, we discuss the defocus curve and the optical and photic phenomena associated with each type of IOL.

Abstract: Orbital fractures generally do not cause eyelid malposition. Studies have shown that mostly eyelid malposition is mainly due to the choice of surgical approaches of orbital fracture repair. Approaches are divided into transcutaneous and transconjunctival ones. The application of orbital fracture approaches depends on fractures’ range and the surgeons’ preferences. Eyelid malposition after orbital fracture surgery is not only an aesthetic concern but also a functional complication, which will cause eyes discomfort, such as corneal exposure and ocular irritation. Some patients may have multiple types of eyelid malposition. In this review, we summarized the surgical approaches of orbital fractures and the complications including scar, ectropion, retraction, entropion, flattening, laceration and lacrimal canaliculus avulsion and notch deformity that associated with eyelid, especially the lower eyelid. Reports revealed that the scar usually occurred in infraorbital incisions compared with subtarsal and subciliary incisions, and the transconjunctival approach had a higher incidence of entropion and flattening, and less ectropion than the transcutaneous approach. Meanwhile, pathogenesis of eyelid malposition after orbital fracture surgery are discussed. Furthermore, to prevent eyelid malposition complications, doctors should choose the appropriate orbital fracture approach according to the patient’s needs, and delicate tissue management, technical expertise, and meticulous hemostasis are necessary. Conservative treatment with taping, lubricating ointment, and steroid for eyelid malposition complications should be performed first, and then surgical intervention when the conservative treatment fails.

Abstract: Autoimmune retinopathy (AIR) refers to both paraneoplastic and non-paraneoplastic forms of a rare, acquired retinal degeneration thought to be mediated by the production of antiretinal antibodies. However, the mechanisms underlying AIR pathogenesis are incompletely understood, and it remains a diagnosis of exclusion given the lack of definitive testing as well as its protean clinical presentation. This review summarizes the current literature on the epidemiology, diagnosis, and management of AIR, with a focus on non-paraneoplastic disease and the potential role of immunomodulatory therapy. A recent expert consensus statement on diagnosis and management of non-paraneoplastic AIR served as a framework for interpreting the limited data available, a process that was complicated by the small sample sizes, heterogeneity, and retrospective nature of these studies. Additional work is needed to characterize AIR patients on the basis of cytokine and immunogenetic profiling; to establish the pathogenicity of antiretinal antibodies; and to standardize treatment regimens as well as assessment of clinical outcomes.

Abstract: An intestinal dysbiosis is connected to a number of inflammatory diseases through various mechanisms relating to its effect on immune cell function and differentiation. This is a review of the literature summarizing our current understanding of intestinal microbial contributions to non-infectious uveitis and strategies to target the intestinal microbiome to treat uveitis. Several groups have demonstrated an intestinal dysbiosis associated with certain types of non-infectious uveitis. Additionally, approaches to treat uveitis by modifying the intestinal microbiota, such as oral antibiotics or administration of oral short chain fatty acids (SCFAs), which are intestinal bacterial metabolites produced by fermentation of dietary fiber, can successfully treat uveitis in mouse models. This reduction in severity of ocular inflammation occurs via the following mechanisms: enhancement of regulatory T cells, decreasing intestinal permeability, and/or affecting T cell trafficking between the intestines and the spleen. Other strategies that are directed at the intestinal microbiota that might be effective to treat uveitis include dietary changes, probiotics, or fecal microbial transplantation. The commensal gut bacteria are influential in systemic and intestinal mucosal immunity and thus contribute to the development of extraintestinal inflammation like uveitis. Targeting the intestinal microbiome thus has the potential to be a successful strategy to treat non-infectious uveitis.

Abstract: Inherited retinal diseases (IRD) are a leading cause of blindness in the working age population. The advances in ocular genetics, retinal imaging and molecular biology, have conspired to create the ideal environment for establishing treatments for IRD, with the first approved gene therapy and the commencement of multiple therapy trials. The scope of this review is to familiarize clinicians and scientists with the current landscape of retinal imaging in IRD. Herein we present in a comprehensive and concise manner the imaging findings of: (I) macular dystrophies (MD) [Stargardt disease (ABCA4), X-linked retinoschisis (RS1), Best disease (BEST1), pattern dystrophy (PRPH2), Sorsby fundus dystrophy (TIMP3), and autosomal dominant drusen (EFEMP1)], (II) cone and cone-rod dystrophies (GUCA1A, PRPH2, ABCA4 and RPGR), (III) cone dysfunction syndromes [achromatopsia (CNGA3, CNGB3, PDE6C, PDE6H, GNAT2, ATF6], blue-cone monochromatism (OPN1LW/OPN1MW array), oligocone trichromacy, bradyopsia (RGS9/R9AP) and Bornholm eye disease (OPN1LW/OPN1MW), (IV) Leber congenital amaurosis (GUCY2D, CEP290, CRB1, RDH12, RPE65, TULP1, AIPL1 and NMNAT1), (V) rod-cone dystrophies [retinitis pigmentosa, enhanced S-Cone syndrome (NR2E3), Bietti crystalline corneoretinal dystrophy (CYP4V2)], (VI) rod dysfunction syndromes (congenital stationary night blindness, fundus albipunctatus (RDH5), Oguchi disease (SAG, GRK1), and (VII) chorioretinal dystrophies [choroideremia (CHM), gyrate atrophy (OAT)].