Diabetic Retinopathy

Overview

According to the Centers for Disease Control (CDC), we are now in the midst of an unfolding epidemic of diabetes. The number of Americans with diabetes has increased 33% from 1990 to 1998. The most dramatic increase has been among people in their 30s- up about 70% over the same period of time. The primary reason for this dramatic increase is obesity- which now affects nearly one in every five Americans.

Diabetic retinopathy refers to the damage that occurs to the retina as a result of diabetes and is the leading cause of new cases of legal blindness in working-age Americans. The risk of developing diabetic retinopathy increases with the duration of the disease. After 20 years, more than 90% of diabetics will have some degree of retinopathy, especially those with insulin-dependent diabetes mellitus (IDDM). The changes that occur within the retina are divided into two categories based on their severity- non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR).

Non-Proliferative Diabetic Retinopathy (NPDR)

The precise mechanism whereby elevated blood sugar causes diabetic retinopathy in unknown. The initial damage that occurs is to the supporting cells of the retinal blood vessels. As these cells are lost, these small blood vessels develop outpouchings called microaneurysms. The damaged blood vessels may then begin to leak, allowing blood and fluid to seep into the retina.

Initially, even with the development of leakage and ischemia, the patient may have no symptoms. However, if fluid leaks into the central portion of the retina called the macula, then vision will usually decrease. This is called diabetic macular edema and is a major cause of reduced vision in patients with diabetes.

Proliferative Diabetic Retinopathy (PDR)

As diabetic retinopathy progresses, the blood vessels may close, leading to a lack of oxygen and nourishment to the retina ("ischemia"), and further compromising the retina's ability to function properly. When the retina does not get enough oxygen, it sends out a chemical signal that causes new blood vessels to grow. These blood vessels, however, are not normal. They grow on the surface of the retina and are fragile. This is called proliferative diabetic retinopathy. These fragile blood vessels tend to break and bleed into the vitreous cavity of the eye (vitreous hemorrhage) , often resulting in a sudden and profound loss of vision. Scar tissue may accompany the growth of the abnormal blood vessels. As the scar tissue contracts, it can pull on the retina and cause a retinal detachment and possible blindness. If the abnormal blood vessels grow on the iris in the front of the eye, they may close off the area where fluid drains from the eye, leading to an elevation of the intraocular pressure called neovascular glaucoma.

Treatment

The key to the treatment of diabetes and the prevention of its complications is strict control of blood sugars. The Diabetic Control and Complications Trial (DCCT) was an excellent study that compared conventional therapy in insulin-dependent diabetic patients (i.e. 1-2 shots of insulin a day and infrequent blood sugar checks) with intensive treatment (i.e. multiple insulin shots, insulin pumps and frequent blood sugar checks) over 6.5 years. Patients who had no diabetic retinopathy at the start of the study and received intensive treatment were 76% less likely to develop any retinopathy than the conventional treatment group. For patients who already had a mild degree of retinopathy at the start of the study, the risk of progression was lowered by 54% and the development of proliferative retinopathy was lowered by 47% in the intensive group as compared with the conventional group.

Once retinopathy has developed, laser treatment (photocoagulation) is the primary form of therapy. Before laser treatment, a fluorescein angiogram may be obtained to help guide treatment. This is a test in which a dye is injected into a vein in the arm, and photographs are taken as the dye travels through the retinal blood vessels. The laser photocoagulation is performed as an outpatient office procedure. A contact lens is placed on the surface of the eye after instilling a drop of topical anesthetic, and the laser light is focused on the retina. Occasionally, an injection of an anesthetic around the eye is required if a significant amount of treatment is necessary and the patient finds the treatment uncomfortable.

The specific form of laser treatment depends on which of the complications of diabetic retinopathy is being addressed. In treating diabetic macular edema, the goal is to help stabilize vision by attempting to stop the damaged blood vessels from leaking fluid into the retina. A national study known as the Early Treatment Diabetic Retinopathy Study (ETDRS) clearly showed that there was a great benefit in performing laser photocoagulation when certain parameters were present. It is important to restate that this treatment is performed to keep vision from further declining, but does not usually result in an improvement in vision already lost.

During the treatment, laser burns are placed in either a focal pattern if there are specific areas of leakage to be treated, or in a diffuse pattern if there is a large area of fluid present. After treatment, patients may notice small spots in their vision where laser burns were created; these tend to become less noticeable over time. Success is usually determined several months after the procedure. If the fluid is still present, additional laser photocoagulation may be performed.

For proliferative diabetic retinopathy, another study called the Diabetic Retinopathy Study (DRS) showed that panretinal laser photocoagulation (PRP) reduced the rate of severe visual loss by 60% in patients with specific parameters of PDR. It also reduced the rate of progression of the disease. Once again, it is important to realize that laser treatment is not expected to result in an improvement in vision.

PRP consists of applying numerous (usually greater than 1000) laser burns to the retina. Because so much treatment is needed, it is typically divided into several sessions. Side effects include loss of some peripheral vision, a decrease in night (low light) vision, occasionally some loss of central vision (10% of cases), and possible mild enlargement of the pupil. It is important to realize that when PRP is required, the risks of not treating are much higher than the risk of being treated.

When PRP is unsuccessful in stopping the progression of the proliferative retinopathy, when a vitreous hemorrhage occurs and does not clear on its own, or when a retinal detachment develops, then a vitrectomy is often helpful. A vitrectomy involves inserting instruments into the eye, and removing the vitreous gel, any blood present in the vitreous cavity, and removing the scar tissue that has grown on the surface of the retina.

Future Treatment

As we gain a better understanding of what is occurring on a cellular and molecular level in diabetic retinopathy, new medical therapies are expected to become available. Current and future avenues of exploration include the use of intraocular steroids, growth factor inhibitors, protein kinase C inhibitors, antioxidant vitamins, and antiproliferative agents of the substances that are felt to cause the growth of the new, abnormal blood vessels.