proliferative diabetic retinopathy

PDR develops as a consequence of prolonged hyperglycemia causing microvascular damage to retinal capillaries, leading to pericyte loss, capillary occlusion, and progressive retinal ischemia. The ischemic retina upregulates vascular endothelial growth factor (VEGF), which drives pathologic neovascularization—the hallmark distinguishing PDR from nonproliferative diabetic retinopathy (NPDR). These new vessels are fragile, growing along the retinal surface and into the vitreous cavity, and can cause vitreous hemorrhage when they rupture. Fibrous tissue often accompanies neovascularization, and subsequent contraction can cause tractional retinal detachment. Neovascularization can also occur at the iris (rubeosis iridis), potentially causing neovascular glaucoma by obstructing aqueous outflow at the angle. Clinically, PDR is diagnosed via fundoscopic exam showing neovascularization of the disc (NVD) or elsewhere (NVE), sometimes with associated hemorrhage or fibrovascular proliferation. Risk factors include duration of diabetes, poor glycemic control (elevated HbA1c), hypertension, and dyslipidemia. Management includes panretinal photocoagulation (PRP) laser therapy to reduce the ischemic drive for VEGF production, intravitreal anti-VEGF agents (e.g., bevacizumab, ranibizumab), and vitrectomy for non-clearing vitreous hemorrhage or tractional detachment. Tight glycemic and blood pressure control are essential in prevention and slowing progression. PDR is a leading cause of blindness in working-age adults and underscores the importance of routine dilated eye exams in diabetic patients.