Diabetic retinopathy is a diabetes complication that damages the small blood vessels of the retina and is a leading cause of blindness in working age adults worldwide. Chronic high blood sugar, high blood pressure and abnormal blood lipids drive progressive injury to retinal capillaries. Early stages feature microaneurysms, small hemorrhages and leakage of fluid and lipids, which can cause diabetic macular edema when they affect the central retina. As damage advances, widespread capillary closure leads to retinal ischemia and the release of vascular endothelial growth factor, stimulating fragile new vessels in proliferative diabetic retinopathy. These vessels are prone to bleeding, scar formation, traction on the retina and ultimately retinal detachment.

Research emphasizes early detection and tight metabolic control to delay onset and progression. Modern imaging techniques such as optical coherence tomography and wide field retinal photography allow detection of subtle edema, microvascular changes and areas of nonperfusion before vision loss occurs. Studies show that intensive glucose and blood pressure control significantly reduce retinopathy risk, but long term follow up indicates that many patients still develop disease, highlighting the role of additional factors such as inflammation, oxidative stress and genetic susceptibility.

Current treatments target advanced stages. Intravitreal injections of anti VEGF agents reduce macular edema and neovascularization and are now first line therapies. Focal and panretinal laser photocoagulation remain important to reduce ischemic drive and prevent complications. Vitrectomy surgery is used for non clearing vitreous hemorrhage and tractional retinal detachment. Ongoing research explores neuroprotective agents, combination therapies, biomarkers for individualized risk prediction and artificial intelligence systems to automate large scale screening and grading of disease severity.