A review: Diabetic retinopathy—pathophysiologic and therapeutic approaches

Of the five million known diabetics in the United States, 5,000 become blind each year because of diabetic retinopathy. While the pathologic changes in the retina are well defined, the pathogenetic and pathophysiologic factors are not clear, and therapeutic approaches are empirical. The disease may be classified clinically and pathologically into four stages:(1) preretinopathy, characterized by disruption of the blood‐retinal barrier; (2) background retinopathy, exhibiting typical microangiopathic changes; (3) diabetic macular edema, resulting in gradual loss of central vision; (4) proliferative retinopathy, ending in retinal detachment and blindness. Many associated pathophysiologic factors have been described, but the critical pathogenetic mechanisms have not been established. The contributing factors include: (1) hyperglycemia and insulin control; (2) disruption of the blood‐retinal barrier; (3) retinal microangiopathy, including changes of pericyte and endothelial cell basement membrane; (4) formation of microaneurysms; (5) systemic diseases, including hypertension, blood alteration, hormonal changes, and genetic abnormalities; (6) ocular disorders such as optic atrophy, alteration in intraocular pressure, and eye surgery; and (7) retinal and vitreal neovascularization. A number of therapeutic approaches are being actively tested. Treatment with panretinal photocoagulation has been helpful to some patients, and the control of contributing systemic factors may delay progression of the disease. Vitrectomy with or without endoscopic panretinal photocoagulation has been useful in some advanced cases. Pituitary ablation has been effective for treatment of severe diabetic retinopathy, but severe complications have forced its abandonment. Aldose reductase inhibitors and other medications are currently being tested.