The retinal lesions of diabetes, known as diabetic retinopathy,are theleading cause of blindness in working age population. It is estimated thatmore than 8000diabetic patients become blind every year from retinal complications.Much of this blindness can be prevented if the retinopathy is detectedearly enough for treatment with laser photocoagulation. The aim of lasersurgery is to prevent visual loss; thus, the optimal time for treatmentis before the patient experiences visual symptoms.
Unforunately, because visual loss is often a late symptom of advanceddiabetic retinopathy, many patients remain undiagnosed even as their diseaseis causing severe retinal damage. As a result, many patients are examinedonly after the optimal time for treatment has passed.
Providing timely laser surgery depends on improving the diagnosis ofthe asymptomatic diabetic patient through careful examination of the retina.
To understand the management of diabetic retinopathy, it is necessaryto comprehend first its pathogenesis and clinical appearance. Normal retinavessels, including the capillaries, are impermeable to large molecules.By contrast, in the diabetical retina, the capillaries leak proteins, complexcarbohydrates, and lipids. What causes the initial changes in the diabeticretina is unclear, although the effect of elevated sugar levels on theretinal capillaries may be important.
The effects of diabetes on the retina are reflected in progressive stagesthat are defined by ophtalmoscopic criteria. In the first stage, termednonproliferative diabetic retinopathy (NPDR), retinal blood vessels leak.If there is enough leakage into the macula,visual acuity is reduced. INthe second stage, called proliferative diabetic retinopathy(PDR), progressiveretinal ischemia promotes the grouth of fragile new blood vessels thatbleed. This neovascularization, accompained by fibrous proliferation, growsinto the posterior surface of the vitreous. Eventually, bleeding and tractioncause retinal detachment and blindness.
In early nonproliferative retinopathy, direct ophtalmoscopy revealsmicroaneurisms, hard exudates, and intraretinial hemorrages. Each of theseabnormalities may occur in isolation or in combination. Microaneurismsare usually the erliest visible manifestations of diabetic retinopathy.They appear as tiny red dots scattered in the retina posteriorly. Sometimesthey are surrounded by a ring of yellow lipid, or hard, exudate. Intraretinalhemorrages appear either as small red dots or blots indistinguishable frommicroaneurysms or as larger flameshaped hemorrages.
These nonproliferative changes produce no symptoms unless they involvethe macula. The prevalence of diabetic macular edema is strongly relatedto the duration of diabetes.
Nonproliferative retinopathy may progress to include abnormalities thathave been associated with a high risk for imminent proliferative retinopathy.Although no treatment may be necessary at this stage, the patient mustunderstand that reevaluation within the next few months is critical.
The most easily recognized abnormalities of advanced nonproliferativeretinopathy are cotton-wool spots. These are areas of capillary closureand resultant ischemia or infarction of the nerve fiber layer of the retina.Cotton-woolspots appear in the fundus as discrete white spots with featheryedges.
More closely related to the risk of progression to proliferative retinopathyare irregular dilations of retinal veins, called venous beading ;dilated,tortuous intraretinal vessels;and extensive retinal hemorrages. Once thissigns have appeared, approximately 50% of patients willdevelop proliferativeretinopathy within 1 year.
Proliferative retinopathy is responsable for most of the devasting visualloss in diabetes. The ophtalmoscopic changes of proliferative diabeticretinopathy are new retinal blood vessels, or neovascularization, sometimesleading to vitreous hemorrhage and fibrous proliferation. all of the nonproliferativefindings, including macular edema, may also be present.
The delicate new vessels that form on the surface of the retina resemblea tangle of hair of a fishnet. As these fragile new vessels grow, theymay bleed into the vitreous cavity, a condition called vitreous hemorrhage.It may be very mild, perceived by the patient as a sudden showerof darkdots or floaters, or more severe, filling the vitreouswith blood and decreasingthe patient’s visual acuity to light perception. Retinal detachmant mayalso occur.
Neovalcularization in diabetes is not always confined to the retina.The retinal ischemia may cause new vessels to grow on the surface of theiris as well. Iris neovascularization is sometimes referred to as rubeosisiridis because of the reddish color change. These vessels may cause adhesionbetween the iris peripherally and the trabecular meshwork. The adhesioninterferes with the normal drainage of aqueous fluidfrom the eye and maylead to glaucoma.
Fibrous proliferation generally accompaines neovascularization. Becausethe proliferating fibrocytes contain contractile proteins, the fibrovascularstalk shrinks, sometimes causing tearing or detachment of the retina.Evenif the retina does not detach, the fibrovascular membrane may wrinkle anddistort the retina, causing visual loss.
Diabetic Retinopathy A slide sript program American Academy of Ophthalmology
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