ABSTRACT:
This abstract focuses specifically on the ocular consequences of chronic hyperglycemia, shifting the lens from general diabetes to the specific microvascular breakdown within the eye. Abstract Diabetic Retinopathy (DR) remains the leading cause of preventable blindness in the working-age population worldwide. This paper examines the clinical progression and underlying pathophysiology of DR, primarily driven by chronic hyperglycemia-induced microvascular damage. We analyze the transition from Non-Proliferative Diabetic Retinopathy (NPDR)—characterized by microaneurysms, hemorrhages, and cotton-wool spots—to the more severe Proliferative Diabetic Retinopathy (PDR), where the expression of Vascular Endothelial Growth Factor (VEGF) triggers pathological neovascularization. Furthermore, the role of Diabetic Macular Edema (DME) is explored as a primary driver of central vision loss due to increased vascular permeability and fluid accumulation. By reviewing the molecular mechanisms of oxidative stress and the polyol pathway, this paper highlights the critical window for intervention. We conclude that while advancements in anti-VEGF therapy and laser photocoagulation have revolutionized treatment, rigorous glycemic control and regular fundoscopic screening remain the gold standards for preventing irreversible visual impairment.