Diabetic retinopathy – pathophysiology

Abstract

SummaryDiabetic retinopathy (DR) is a common complication of diabetes and is a leading cause of visual impairment and blindness in many countries. This visual impairment results from long‐term accumulated damage to the small blood vessels in the retina. It takes several years before any clinical symptoms of retinopathy appear in diabetic patients. The definition of diabetic retinopathy is based on observation of vascular changes. The first recognizable vascular abnormalities are microaneurysms and small hemorrhages, followed by signs of vascular leakage, such as hard exudates and larger hemorrhages, vascular dropout, and neovascularizations. A number of hyperglycemia‐induced metabolic stresses have been implicated in the pathophysiology of DR. The microvasculature of the retina responds to hyperglycemia through a number of biochemical changes, including the activation of protein kinase C, increased advanced glycation end‐products formation, polyol pathway and oxidative stress. However, it has been long known that the neuroretina is affected at an early stage by diabetes‐induced metabolic changes. DR is now recognized as a neurovascular complication or sensory neuropathy resulting from disruption of the neurovascular unit.