Diabetic Retinopathy | Retina Eye Center | Augusta & Aiken
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Diabetic Retinopathy

Diabetic retinopathy is the most common cause of blindness in individuals between 20 and 74 years old. Elevated blood glucose for prolonged periods of time causes damage to the retinal blood vessels (along with the kidneys and nerves). Such damage to the blood supply of the retina can result in abnormal bleeding, swelling of the retina, poor blood flow to the retina, and/or scarring of the retina.


Approximately 10 million new cases of diabetes are diagnosed every year. It affects approximately 6% of individuals between 45 and 64 years old, and 11% of individuals over 65. Diabetic retinopathy of some degree is present in approximately 90% of type 1 (juvenile) diabetic individuals after 10 to 15 years; the most severe form occurs in approximately 25% during this time. For type 2 (adult-onset) diabetics, 84% of individuals taking insulin and 53% not taking insulin will develop retinopathy between 15 to 20 years; 25% will develop the most severe form after 25 years. Macular edema (swelling of the central retina) affects about 20% of diabetics and is a common cause of visual loss.

Clinical Appearance & Symptoms

Diabetic retinopathy is subdivided into two forms: non-proliferative diabetic retinopathy (NPDR) and a more severe form, proliferative diabetic retinopathy (PDR).

NPDR starts with damage to the retinal blood vessels from a prolonged elevation of blood glucose. The blood vessels develop tiny weak areas called microaneurysms. Over time, these microaneurysms can rupture and leak. This can result in retinal bleeding or hemorrhage. Fluid from the bloodstream can also leak into the retina and cause swelling, a condition called macular edema. Fats and proteins from the bloodstream may leak into the retina as well and are referred to as hard exudates. Macular edema tends to cause central blurring of vision and/or distortion. Over time, the poor blood supply can result in the death of nerve cells responsible for fine vision (a process called macular ischemia); this can lead to a permanent central blind spot with corresponding untreatable decreased central vision. (Figure 1, 2)

After prolonged poor blood flow, the retina produces substances that promote the growth of new, abnormal blood vessels (a process called retinal neovascularization). Retinal neovascularization marks the shift from non-proliferative to proliferative diabetic retinopathy (PDR) and is a very serious condition. This development of new blood vessels may appear logical, as the old, original blood vessels are often permanently damaged and poorly functioning. However, the retinal neovascularization process tends to do more harm than good over the long term. The new blood vessels are fragile and tend to bleed into the vitreous cavity, a condition termed vitreous hemorrhage. A vitreous hemorrhage can cause significant floaters in the vision (from floating blood cells) and may cause transient near-total blindness if the hemorrhage is particularly dense. The new blood vessels may also grow along the surface of the retina, scar, and contract; this can pull on the retina and cause a very serious condition called traction retinal detachment.


When diabetic retinopathy is identified, your retinal specialist may perform additional testing to further evaluate the condition. The purpose is usually to identify areas of macular edema, macular ischemia, and retinal neovascularization (see above)

Fluorescein angiography may be employed in the diagnosis of retinal vein occlusion. In this procedure, a dye is injected into an arm vein and travels through the circulatory system to the eye. The dye acts as a tracer and is photographed as it passes through the ocular circulation. Sites of leakage can be identified that correspond to areas of macular edema or retinal neovascularization. Areas of compromised circulation can also be localized in evaluating macular ischemia and general retinal ischemia. (Figure 3, 4)

Optical coherence tomography (OCT) is commonly used to obtain a high-resolution image of the retina and any associated macular edema (Figure 5). This technique is very valuable in quantifying the degree of fluid and monitoring response to potential treatment (Figure 6). It can also very effectively show any traction on the surface of the retinal tissue.

B-scan ultrasonography is used to evaluate the retina when the view is blocked by hemorrhage (bleeding) in the vitreous cavity. The sound waves of the ultrasound can penetrate the bloody vitreous and depict the anatomic status of the underlying retina.


The most important aspect in the treatment of diabetic retinopathy is the long-term control of blood glucose. Patients should monitor their glucose daily and follow their hemoglobin A1c level with their diabetes doctor. They should also control any coexisting conditions that can worsen retinopathy; these include hypertension and elevated cholesterol/lipids.

Retinal intervention is generally aimed toward preventing visual loss from macular edema and complications of proliferative diabetic retinopathy.

Macular Edema:

Macular edema is frequently treated with laser. Research studies have shown that laser treatment results in 1 the rate of significant visual loss when compared to those who did not receive laser. Unfortunately, most patients treated with laser do not gain significant vision. In an attempt to improve visual outcomes, retinal specialists have been injecting experimental medications into the vitreous cavity to target macular edema. These medications are currently offered on an off-label basis to patients who may be good candidates after an extensive discussion of risks and potential benefits. Currently, these medications include Kenalog (a corticosteroid) and Avastin (an anti-neovascular agent). In certain cases, vitrectomy surgery may be recommended to treat specific causes of macular edema.

Proliferative Diabetic Retinopathy:

Complications of proliferative diabetic retinopathy result from retinal neovascularization, so this process is the target of most treatments. Untreated retinal neovascularization may result in vitreous hemorrhage and/or traction retinal detachment. The main procedure for attempting to control retinal neovascularization involves the use of a laser; this treatment is called panretinal photocoagulation. The peripheral retina is treated extensively with a laser to target abnormal blood vessels and prevent complications. Research has shown that an individual with specific characteristics warranting laser will have 1 the risk of significant visual loss compared to those not undergoing laser treatment. Unfortunately, individuals do not typically gain vision after this type of laser treatment.

Vitreous Hemorrhage:

When a vitreous hemorrhage develops, the patient usually experiences significant floaters or diffuse blurring (blindness) in one eye. The hemorrhage will often clear on its own over several weeks, so immediate intervention is often unnecessary. However, there are often times when the hemorrhage is slow to clear or new hemorrhages continue to occur. In these cases, vitrectomy surgery is often recommended (see the section on Treatment/Vitrectomy). In this procedure, the vitreous gel is removed along with the blood that fills the vitreous cavity. At the time of surgery, a laser is usually applied to treat the retinal neovascularization that is suspected to be the source of bleeding. Traction Retinal Detachment:

With traction retinal detachment (Figure 7), vitrectomy surgery is often performed to relieve the traction on the retinal surface caused by scar tissue and allow the retina to lay flat on the back wall of the eye (Figure 8) after vitrectomy surgery). The procedure involves peeling of the scar tissue, or membranes, from the retinal surface using microscopic instruments such as forceps, scissors, and pics.

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