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A 38-year-old man saw a physician for the first time in 10 years after noticing visual loss in his left eye. His history revealed many risk factors for and symptoms of diabetes mellitus (DM). On an undilated funduscopic examination, his physician was able to see some hemorrhages and hard exudates. A fingerstick in the office showed a blood glucose level of 420 mg/dL. He was treated for DM and referred to an ophthalmologist to be evaluated for his diabetic retinopathy (Figure 20-1).
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Diabetic retinopathy (DR) is a leading cause of blindness in the United States. Nonproliferative DR is characterized by microaneurysms, macular edema, cotton-wool spots, superficial (flame) or deep (dot-blot) hemorrhages, and exudates. Proliferative DR also has neovascularization of the retina, optic nerve head, or iris. Because patients may be asymptomatic until vision loss occurs, screening is indicated in all diabetic patients. Excellent glycemic control lowers a patient's risk of developing DR.
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- In developed nations, DR is the leading cause of blindness among people younger than age 40 years.1
- In a community-based study, 29% of adults older than age 40 years with DM had DR. Prevalence in black patients was higher than in white patients (38.8% vs. 26.4%).2
- Twenty-one percent of patients have retinopathy at the time type 2 diabetes is diagnosed.3
- More than 60% of patients with type 2 DM have retinopathy within 20 years of diagnosis.3
- After 40 years of type 1 DM, 84% of patients have retinopathy.4
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- Hyperglycemia results in microvascular complications including retinopathy.
- Several biochemical pathways linking hyperglycemia and retinopathy have been proposed.3
- In nonproliferative retinopathy, microaneurysms weaken vessel walls. Vessels then leak fluid, lipids, and blood resulting in macular edema, exudates, and hemorrhages (Figures 20-1 and 20-2).
- Cotton-wool spots result when small vessel occlusion causes focal ischemia to the superficial nerve fiber layer of the retina.
- In proliferative retinopathy, new blood vessels form in response to ischemia (Figure 20-3).
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