DIABETIC RETINOPATHY Süleyman ÖZEN

Diabetic Retinopathy Diabetic retinopathy is a progressive microangiopathy characterized by small-vessel damage and occlusion

thickening of the capillary endothelial basement membrane reduction of the number of pericytes microaneurysms hemorrhages Diabetic Retinopathy

Risk Factors for Development and Progression of Retinopathy chronic hyperglycemia hypertension hypercholesterolemia smoking Type I DM do not develop retinopathy for at least 3–5 years. Type II DM may have retinopathy at the time of diagnosis, and it may be the presenting manifestation.

Classification nonproliferative retinopathy maculopathy

Nonproliferative Retinopathy Mild nonproliferative retinopathy is characterized by at least one microaneurysm. Moderate nonproliferative retinopathy, there are extensive microaneurysms, intraretinal hemorrhages, venous beading, and/or cotton wool spots. Severe nonproliferative retinopathy is characterized by cotton-wool spots, venous beading, and intraretinal microvascular abnormalities (IRMA). Moderate nonproliferative diabetic retinopathy showing microaneurysms, deep hemorrhages, flame-shaped hemorrhage, exudates, and cotton wool spots.

2.Maculopathy Diabetic maculopathy manifests as focal or diffuse retinal thickening or edema, caused primarily by a breakdown of the inner blood–retinal barrier at the level of the retinal capillary endothelium, which allows leakage of fluid and plasma constituents into the surrounding retina. It is more common in type II diabetes and requires treatment once it becomes clinically significant. Clinically significant macular edema with two circinate rings of exudates.

3. Proliferative Retinopathy The most severe ocular complications of diabetes mellitus are due to proliferative diabetic retinopathy. Progressive retinal ischemia eventually stimulates the formation of delicate new vessels that leak serum proteins . Early proliferative diabetic retinopathy is characterized by the presence of any new vessels on the optic disk (NVD) or elsewhere in the retina (NVE). The fragile new vessels proliferate onto the posterior face of the vitreous If the vessels bleed, massive vitreous hemorrhage may cause sudden visual loss . There is a risk of developing neovascularization and vitreous hemorrhage once a complete posterior vitreous detachment has developed. In eyes with proliferative diabetic retinopathy and persistent vitreoretinal adhesions, elevated neovascular fronds may undergo fibrous change and form tight fibrovascular bands, which cause vitreoretinal traction. This can lead to progressive traction retinal detachment. 3. Proliferative Retinopathy Frond of neovascular tissue (arrows) arising from the superotemporal vascular arcade in proliferative diabetic retinopathy.

Imaging Fluorescein angiography is useful for identifying microvascular abnormalities in diabetic retinopathy . Large filling defects of capillary beds—“capillary nonperfusion”—show the extent of retinal ischemia and are usually most prominent in the midperiphery. The fluorescein leakage associated with retinal edema may assume the petaloid configuration of cystoid macular edema (CME) or may be diffuse. Late-phase fluorescein angiogram shows hyperfluorescence typical of diffuse (noncystoid) diabetic macular edema.

Screening TYPE I DM within 3 years from diagnosis TYPE II DM on diagnosis ANNUALLY Digital fundal photography has been proven to be an effective and sensitive method for screening. Seven-field photography is the gold standard, but two 45° fields, one centered on the macula and the other centered on the disk, are becoming the method of choice in most screening programs.

Treatment Clinically significant macular edema requires focal laser if focal and grid laser if diffuse. Intravitreal injections of triamcinolone or anti-VEGF agents are also effective. Vitrectomy is able to clear vitreous hemorrhage and relieve vitreoretinal traction