Diabetic retinopathy affects more than 5.3 million people age 18 years or older in the United States. Most patients who've had diabetes mellitus for 20 years have some degree of diabetic retinopathy.
Diabetic retinopathy is classified into 2 types: nonproliferative and proliferative:
The typical funduscopic findings are microaneurysms and hemorrhages. Retinal hemorrhages, depending on their location, have a dot-blot or flame-shaped appearance. As vascular permeability increases, retinal edema may ensue. Lipoproteins may precipitate out, giving the appearance of hard exudates. Infarctions of the nerve fiber layer also may occur, producing the appearance of cotton-wool spots. As background retinopathy increases in severity, more numerous retinal hemorrhages are seen, along with irregularity of the veins or venous beading.
In patients with background diabetic retinopathy, the leading cause of decreased visual acuity is macular edema. Diabetic macular edema can be categorized as focal or diffuse:
As retinal ischemia increases, vascular endothelial growth factor is upregulated, which promotes retinal neovascularization. Although neovascularization may occur in the iris or the trabecular meshwork and thus result in neovascular glaucoma, the primary location of the neovascularization is on the retinal surface.
The natural history of retinal neovascularization is for continued growth and fibrosis. As the vitreous contracts, it may cause the sites of neovascularization to bleed. Typically, the hemorrhage occurs in the vitreous, causing such symptoms as floaters and the appearance of cobwebs.
As the neovascularization progresses, fibrosis develops. The increasing retinal neovascularization and fibrosis may exert tractional forces on the retina. When this traction overcomes the adhesive force of the retina to the retinal pigment epithelium, a traction retinal detachment occurs. Once the macula is detached, visual acuity is poor.
The mainstay of treatment for diabetic macular edema and proliferative diabetic retinopathy is laser photocoagulation. Prompt treatment is recommended when eyes have high-risk characteristics of proliferative disease. Panretinal photocoagulation in eyes with high-risk characteristics decreases the risk of severe visual loss by approximately 60%.
For an eye that does not have high-risk characteristics, panretinal photocoagulation may still be recommended, depending on the condition of the other eye, as well as the documented progression of the retinopathy. Focal laser photocoagulation for clinically significant diabetic macular edema decreases the risk of moderate visual loss by 50%. Such photocoagulation is most effective in patients with focal or multifocal leakage primarily from microaneurysms.
Diffuse macular edema, due to leaking primarily from parafoveal capillaries, may suggest an underlying systemic condition. Often, patients with this type of edema have hypertension, congestive heart failure, or renal disease as a contributing factor. Normalization of blood pressure or diuresis may improve diabetic macular edema.
There is strong evidence that lowering hemoglobin A1C levels to approximately 7% is advantageous in reducing the onset and progression of diabetic retinopathy. Similarly, research shows that a decrease in systolic or diastolic blood pressure, or both, can help reduce the development and progression of diabetic retinopathy. Aggressive lowering of total cholesterol and triglyceride levels may cause regression of the exudates.
Mayo Clinic ophthalmologists treat thousands of patients with retinal diseases each year.