The prevalence of diabetic retinopathy (DR) continues to increase in pregnant females; these individuals are also at a higher risk of disease progression. The lack of evidence regarding the safety and efficacy of current treatment options in pregnancy makes disease management particularly challenging.All pregnant women with diabetes should have a prenatal DR screening, as well as receive counseling regarding the progression and management of DR during pregnancy. Optimal blood glucose and blood pressure control should be encouraged. For patients with proliferative diabetic retinopathy (PDR) in the absence of visually significant diabetic macular edema (DME), panretinal photocoagulation (PRP) remains a safe and effective treatment option. Visually significant DME can be treated with focal laser if areas of focal leakage are identified in the macula on fluorescein angiogram, intravitreal steroids or anti-vascular endothelial growth factor (VEGF) agents, The theoretical risk of anti-VEGF agents to the fetus should be considered and the patients should be extensively counselled regarding the risks and benefits of initiating anti-VEGF therapy before initiating treatment. When the decision is made to treat with anti-VEGF agents, Ranibizumab should be the agent of choice. In conclusion, ophthalmologists should make treatment decisions in pregnant patients with DR on a case-by-case basis taking into consideration disease severity, risk of permanent threat to vision, gestational age, and patient preferences.
Abstract: Encapsulated-cell therapy (ECT) is an attractive approach for continuously delivering freshly synthesized therapeutics to treat sight-threatening posterior eye diseases, circumventing repeated invasive intravitreal injections and improving local drug availability clinically. Composite collagen-alginate (CAC) scaffold in ECT contains an interpenetrating network that integrates the physical and biological merits of its constituents, including biocompatibility, mild gelling properties and availability. An injectable CAC system that supported the growth of HEK293 cells with sustainable glial-derived neurotrophic factor (GDNF) delivery has been developed. Continuous GDNF delivery was detected in culture and in healthy rat eyes for at least 14 days. The gels were well tolerated with no host tissue attachment and contained living cell colonies. Most importantly, gel implantation in dystrophic Royal College of Surgeons rat eyes for 28 days retained photoreceptors while those gels containing higher initial cell number yielded better photoreceptor rescue effect. This rescue effect is clinically relevant as photoreceptor death is a common pathology in many retinal diseases. Moreover, since cells including autologous cells can be genetically engineered to secrete various therapeutic agents, CAC gel offers a flexible system design and is a potential treatment option for other chronic neurodegenerative diseases.
Abstract: Diabetic retinopathy (DR) is the most common microvascular complication in patients with diabetes mellitus (DM), and remains the single greatest cause of blindness in working age adults around the world. In this article, we review the evolution of pharmacotherapies for both diabetic macular edema (DME) and DR such as anti-vascular endothelial growth factor inhibitors and various steroid formulations, as well as other emerging pharmacotherapies currently in late stage clinical testing for this disease.
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: A smooth and timely fitting of a visually appealing, custom-made eye prosthesis after the loss of an eye is not only essential from a cosmetic point of view but above all facilitates good social and psychological rehabilitation. Cryolite glass prostheses must be replaced at least once a year, PMMA prostheses polished once a year and renewed every five years. In children, especially in growth phases, the fit of the prosthesis should be checked at least every six months and adjusted, if necessary. Ocularists and ophthalmologists should determine an individual cleaning procedure together with the patient, which depends on both the prosthesis material and external factors. Complications such as allergic, giant papillary, viral, and bacterial conjunctivitis or even blepharoconjunctivitis sicca must be detected and treated at an early stage to avoid discomfort and to maintain the ability of prosthesis wear. In the case of inflammation-induced shrinkage of the conjunctival fornices or post-enucleation socket syndrome, surgical interventions are necessary. In summary, an early supply with an eye prosthesis, adequate treatment of complications, and attention to psychological aspects, form the basis for a successful long-term rehabilitation of anophthalmic patients.
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.
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)].
