Diabetic Retinopathy Clinical Presentation
- Author: Abdhish R Bhavsar, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more...
In the initial stages of diabetic retinopathy, patients are generally asymptomatic; in the more advanced stages of the disease, however, patients may experience symptoms that include floaters, blurred vision, distortion, and progressive visual acuity loss.
The mainstay of diagnosing diabetic retinopathy is a complete ophthalmic examination and dilated retinal examination by an ophthalmologist or retina specialist or retina surgeon.
Outreach screening has the potential to increase screening coverage of high-risk patients with diabetic retinopathy in remote and resource-poor settings or in areas in which no ophthalmologist or retina specialist is available, without the risk of missing diabetic retinopathy and the opportunity to prevent vision loss.
Microaneurysms are the earliest clinical sign of diabetic retinopathy and occur secondary to capillary wall outpouching due to pericyte loss. They appear as small red dots in the superficial retinal layers, and there is fibrin and red blood cell accumulation in the microaneurysm lumen. A rupture produces blot/flame hemorrhages. Affected areas may appear yellowish in time, as endothelial cells proliferate and produce basement membrane.
Dot and blot hemorrhages
Dot and blot hemorrhages occur as microaneurysms rupture in the deeper layers of the retina, such as the inner nuclear and outer plexiform layers. These appear similar to microaneurysms if they are small; fluorescein angiography may be needed to distinguish between the two.
Flame-shaped hemorrhages are splinter hemorrhages that occur in the more superficial nerve fiber layer.
Retinal edema and hard exudates
Retinal edema and hard exudates are caused by the breakdown of the blood-retina barrier, allowing leakage of serum proteins, lipids, and protein from the vessels.
Cotton-wool spots are nerve fiber layer infarctions from occlusion of precapillary arterioles. With the use of fluorescein angiography, there is no capillary perfusion. These are frequently bordered by microaneurysms and vascular hyperpermeability.
Venous loops and venous beading
Venous loops and venous beading frequently occur adjacent to areas of nonperfusion and reflect increasing retinal ischemia. Their occurrence is the most significant predictor of progression to proliferative diabetic retinopathy.
Intraretinal microvascular abnormalities
Intraretinal microvascular abnormalities are remodeled capillary beds without proliferative changes. These collateral vessels do not leak on fluorescein angiography and can usually be found on the borders of the nonperfused retina.
Macular edema is the leading cause of visual impairment in patients with diabetes. A reported 75,000 new cases of macular edema are diagnosed annually. This may be due to functional damage and necrosis of retinal capillaries.
Clinically significant macular edema is defined as any of the following:
Retinal thickening located 500 μm or less from the center of the foveal avascular zone (FAZ)
Hard exudates with retinal thickening 500 µm or less from the center of the FAZ
Retinal thickening 1 disc area or larger in size located within 1 disc diameter of the FAZ
Nonproliferative diabetic retinopathy
Mild nonproliferative diabetic retinopathy (NPDR) is indicated by the presence of at least 1 microaneurysm. Mild NPDR reflects structural changes in the retina caused by the physiological and anatomical effects of diabetes.
More advanced stages of NPDR reflect the increasing retinal ischemia, setting the stage for proliferative changes.
Moderate nonproliferative diabetic retinopathy includes the presence of hemorrhages, microaneurysms, and hard exudates. With this condition, soft exudates, venous beading, and intraretinal microvascular abnormalities (IRMA) occur less frequently than with severe NPDR.
Severe NPDR (4-2-1) is characterized by hemorrhages and microaneurysms in 4 quadrants, with venous beading in at least 2 quadrants and IRMA in at least 1 quadrant.
Proliferative diabetic retinopathy
Neovascularization is the hallmark of PDR. It most often occurs near the optic disc (neovascularization of the disc [NVD]) or within 3 disc diameters of the major retinal vessels (neovascularization elsewhere [NVE]). (See the image below.)
Preretinal hemorrhages appear as pockets of blood within the potential space between the retina and the posterior hyaloid face. As blood pools within this space, they may appear boat shaped. (See the image below.)
Hemorrhage into the vitreous may appear as a diffuse haze or as clumps of blood clots within the gel.
Fibrovascular tissue proliferation is usually seen associated with the neovascular complex and also may appear avascular when the vessels have already regressed. (See the images below.)
Traction retinal detachments usually appear tented up, immobile, and concave, as compared to rhegmatogenous retinal detachments, which are bullous, mobile, and convex. A combination of both mechanisms is not an uncommon finding, however.
Macular edema is the leading cause of visual impairment in patients with diabetes. It may result from functional damage and necrosis of retinal capillaries. In cases of PDR, edema also may be caused by retinal traction if the retina is sufficiently elevated away from the retinal pigment epithelium.
Proliferative diabetic retinopathy is classified as early or high risk. In early PDR, new vessels are present, but they do not meet the criteria for high-risk PDR. In high-risk PDR, NVD is one-third to one-half, or greater, of the disc area (DA); there may be any amount of NVD with vitreous or preretinal hemorrhage; and NVE is one-half or greater of the DA, with preretinal or vitreous hemorrhage.
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