Abstract: To describe the current aging population in China and globally, especially as it applies to age-related macular degeneration (AMD). To review the current standards of care for treating both wet (exudative) eAMD and dry (atrophic) aAMD. And to introduce a model for experimentation that is based on the Age-Related Eye Disease Study (AREDS) using eye bank tissue. A literature search that outlines current aging populations, standards of clinical treatment as defined by large, multicenter, randomized clinical trials that present level-I data with a low risk for bias. An experimental model system of AMD is presented that enables scientific analysis of AMD pathogenesis by applying grading criteria from the AREDS to human eye bank eyes. Analysis includes proteomic, cellular, and functional genomics. The standard of care for the treatment of eAMD is currently defined by the use of several anti-vascular endothelial growth (anti-VEGF) agents alone or in combination with photodynamic therapy. Monotherapy treatment intervals may be monthly, as needed, or by using a treat-and-extend (TAE) protocol. There are no proven therapies for aAMD. AMD that is phenotypically defined at AREDS level 3, should be managed with the use of anti-oxidant vitamins, lutein/zeaxanthin and zinc (AREDS-2 formulation). By understanding the multiple etiologies in the pathogenesis of AMD (i.e., oxidative stress, inflammation, and genetics), the use of human eye bank tissues graded according to the Minnesota Grading System (MGS) will enable future insights into the pathogenesis of AMD. Initial AMD management is with lifestyle modification such as avoiding smoking, eating a healthy diet and using appropriate vitamin supplements (AREDS-2). For eAMD, anti-VEGF therapies using either pro re nata (PRN) or TAE protocols are recommended, with photodynamic therapy in appropriate cases. New cellular information will direct future, potential therapies and these will originate from experimental models, such as the proposed eye bank model using the MGS, that leverages the prospective AREDS database.

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.

Background: To measure the anterior and posterior segment structural features of acute primary angle-closure (APAC) eyes.

Methods: A total of 36 subjects with unilateral APAC were recruited in this study. The ocular biometric characteristics were measured by anterior segment optical coherence tomography (AS-OCT) and swept source optical coherence tomography (SS-OCT), respectively at baseline, 2 weeks, and 1 month after surgical intervention.

Results: At baseline, when compared with the fellow eyes, APAC-affected eyes showed significantly greater corneal thickness (P=0.004), shallower anterior chamber depth (ACD) (P<0.001), smaller anterior chamber area (ACA) (P=0.013), angle opening distance at 750 μm from the scleral spur (AOD750) (P=0.002), trabecular–iris space area at 750 μm from the scleral spur (TISA750) (P=0.033), angle recess area (ARA) (P=0.014), and iris area (IARE) (P=0.003), less iris curvature (ICURVE) (P=0.003), and larger lens vault (LV) (P=0.030). After intervention, the corneal thickness was significantly decreased at 1 month (P<0.001), while ACD, ACA, and AOD750 were significantly increased at 2 weeks and 1 month (all P<0.017). Changes in ACD were correlated with decreasing LV (P<0.05). The posterior segment parameters did not change over the 4-week period.

Conclusions: When compared with the fellow eyes, APAC-affected eyes had greater corneal thickness, shallower anterior chamber, narrower angle, less ICURVE, and larger LV. After intervention, the corneal thickness was decreased, while the shallower anterior chamber was relieved to some extent.

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: Acute retinal necrosis (ARN) is a devastating syndrome characterized by panuveitis, retinal necrosis, and a high rate of retinal detachment that may result in poor visual outcomes if not promptly diagnosed and treated. ARN is most commonly caused by viruses within the herpesvirus family. Etiologies include varicella-zoster virus, herpes simplex virus, and cytomegalovirus, and may be promptly diagnosed by polymerase chain reaction testing of aqueous or vitreous fluid. The true incidence of ARN is not known due to its rarity; as a result, clinical treatment is often guided by retrospective case series, case reports, and expert opinion. Standard of care has evolved over time but currently includes a combination of systemic and intravitreal antiviral in conjunction with topical or oral steroids and surgical therapy as needed. Combination therapy may reduce the rate of severe vision loss and increase the rate of visual acuity gain, although further studies are needed in this area. In particular for patients with mild to moderate disease, combination therapy may reduce the rate of retinal detachment. Adjunctive therapies including oral corticosteroid and prophylactic laser barricade are incompletely studied, but corticosteroid in particular, may reduce inflammation, which also is involved in the severe disease pathogenesis observed in ARN. This review discusses the advances in diagnosis and treatment of ARN, including management with combination antiviral medication and surgical interventions.

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.