The prevalence of diabetes mellitus in adults of China has reached 12.8%. Diabetic retinopathy (DR) accounts for approximately 1/4-1/3 of the diabetic population. Several millions of people are estimated suffering the advanced stage of DR, including severe non-proliferative DR (NPDR), proliferative DR (PDR) and diabetic macular edema (DME), which seriously threat to the patients’ vision. On the basis of systematic prevention and control of diabetes and its complications, prevention of the moderate and high-risk NPDR from progressing to the advanced stage is the final efforts to avoid diabetic blindness. The implementation of the DR severity scale is helpful to assess the severity, risk factors for its progression, treatment efficacy and prognosis. In the eyes with vision-threatening DR, early application of biotherapy of anti-vascular endothelial growth factor can improve DR with regression of retinal neovascularization, but whether it is possible to induce capillary re-canalization in the non-perfusion area needs more investigation. Laser photocoagulation remains the mainstay treatment for non-center-involved DME and PDR.
Retinal break is the cause of primary retinal detachment, which remains a main cause for visual loss, and closure of the breaks is the principle of treatment. Currently surgical treatment can successfully reattach the retina in most cases. However, some basic questions still beset treatment of the disease, such as the cause responsible for development of retinal breaks and how to prevent it, and how the visual recovery can be satisfactory after reattachment surgery. Recent research indicates that the development of retinal breaks is associated with the process of vitreous liquefaction, posterior vitreous detachment (PVD) and abnormal vitreoretinal adhesion and traction. The retinal breaks can occur in the posterior margin of the vitreous base in the eye with complete PVD. Partial PVD may cause posterior breaks especially in cases of myopic traction maculopathy associated with schisislike thickening in the outer retina (foveoschisis) and vitreomacular traction. It is known that microstructural changes and atrophy of the macula, and epiretinal membrane formation are the reasons for poor vision after the retina is reattached. Therefore, more attention should be paid to further understand the vitreous pathology and traction mechanism, to research for methods of its clinical evaluation and strategy of prevention and treatment, and to accelerate visual recovery after reattachment surgery, in order to raise the standard of the disease treatment.
Diabetic retinopathy (DR) is the leading cause of visual impairment worldwide. Severe non-proliferative diabetic retinopathy, diabetic macular edema, and proliferative DR (PDR) are defined as vision-threatening DR (VTDR). In the context of managing systemic disease, the primary treatments for VTDR include panretinal photocoagulation (PRP), intravitreal injection of anti-vascular endothelial growth factor (VEGF) drugs or dexamethasone sustained release agents, and microincision vitreous surgery. Although these therapies are already widely used in clinical practice, there is still much debate about the optimal timing and method of their application, especially in the pursuit of optimal efficacy, cost-effectiveness, patient compliance, and the reduction of frequent ongoing treatments. There is no consensus on the best treatment for PDR. Determining the specific criteria for each therapy indication is one of the key considerations. In addition, consideration should be given to the priority between PRP and intravitreal injection, as well as to compare the relative effectiveness of anti-VEGF agents with PRP. Early surgical intervention is not always a necessary option for PDR patients with vitreous hemorrhage and fibrovascular membranes. Combining different therapies to optimize treatment strategies is also an important topic. These issues address several points of contention in best practice guidelines that need to be addressed through more in-depth research to provide better guidance for clinical practice and ultimately improve patient outcomes.
With the tremendous progress in fundus imaging and histopathology over the past decade, the understanding of age-related macular degeneration (AMD) has taken a qualitative leap. AMD is defined as a progressive neurodegenerative disease of photoreceptors and retinal pigment epithelium (RPE) characterized by extracellular deposits under RPE and the retina, including drusen, basal laminar and linear deposits, and subretinal drusenoid deposits, that can evolve to atrophy of the retina, RPE and choroid and neovascularization in the choroid and/or retina. It is the leading cause of blindness and visual impairment in older populations, despite recent advances in treatments. AMD is a multifactorial disease with genetic and environmental factors including advanced age, smoking, high-fat diet, and cardiovascular disorder to enhance the disease susceptibility. The physiopathologic mechanism includes inflammatory processes (complement pathway dysregulation, inflammasome activation), intrinsic (e.g., photo-oxidation) and extrinsic oxidative insult to the retina, age-related metabolic impairment (mitochondrial, autophagic and endoplasmic reticulum stress). Autophagy dysfunction and local inflammation in aged RPE specially result in the extracellular deposits, cell death and AMD. Further investigation of the pathogenesis of AMD will provide with new therapeutic targets and strategy for prevention and treatment of the disease in the early stages.