Treating Vision Loss
How to spot and treat vision loss from diabetic retinopathy
The eyes may be windows to the soul, but for people with diabetes, peering deep into the retina may also reveal diabetes-related eye disease.
“Vision loss is one of the most common complications of diabetes,” says Raj Maturi, MD, associate professor of clinical ophthalmology at Indiana University School of Medicine and partner at the Midwest Eye Institute in Indianapolis. Two of the most likely culprits in vision loss spurred by high blood glucose are diabetic macular edema and proliferative diabetic retinopathy. Both fall under the umbrella of diabetic retinopathy, which refers to any retinal changes from diabetes.
The good news: Advances in screening are catching problems before serious retinal changes occur—an important step because eye damage may have no symptoms at first. And if you already have a diabetes-related eye disease, the latest eye treatments may save your vision.
The eye is a lot like a camera. “It’s lined by tissue that is light sensitive, just like the sensitive back part of a camera,” says Neil Bressler, MD, professor of ophthalmology and chief of the Retina Division at Johns Hopkins University School of Medicine. Light goes through the transparent front lens, like passing through the lenses of a camera, until it gets to the back wall of the eye. This wall contains a very thin piece of light-sensitive tissue: the retina.
“Just like you can damage the blood vessels that nourish your toes, kidneys, or heart, the tiny blood vessels that nourish the retina could be damaged by diabetes,” he says.
From there, one of two things can happen. The damage may cause the blood vessels to become leaky, much like a hose developing holes. The fluid leaks out of the blood vessels and into the retinal tissue. “[It] swells up like a dried sponge filling with water,” says Bressler. This causes the retina to become thickened, which creates blurry vision. Diabetes-related swelling in the macula, the central part of the eye responsible for straight-ahead vision, is called diabetic macular edema.
In the second process harmful to vision, blood vessels damaged by high blood glucose levels close off, kicking off a cascade of events. The starving retinal tissue produces growth factors, causing new blood vessels to form on the surface of the retina. This process is referred to as proliferative retinopathy.
But these blood vessels are weak and can easily break and bleed. That leads to scar tissue, which can accumulate on the back wall of the eye. Built-up scar tissue can tug on the retina, eventually detaching it from the back of the eye. “[The process is] just like peeling wall paper off of a wall,” says Bressler. The resulting condition is known as retinal detachment.
Both of these problems can start without any vision loss, he says. You may have 20/20 vision and still have macular edema or proliferative diabetic retinopathy, which is why regular dilated eye exams—at least annually in most people with diabetes—are so important.
If you’re put off by the idea of a stranger getting up close and personal with your peepers, take heart. The exam itself is pretty straightforward. Here’s what to expect: Your eye doctor will first check whether there is a change in your eyeglass or contact lens prescription. (People with macular edema, diabetic retinopathy, and other eye diseases can still wear contacts, says Maturi.)
Next, the doctor will drip a few drops in your eyes (full disclosure: it may sting briefly) to dilate the pupils and examine the retina. Twenty to 30 minutes later, your eyes will be fully dilated and, using special lenses and lights, the doctor will visually examine the retina in great detail.
To detect retinopathy, the doctor looks at all of the retinal tissue. “Sometimes you can see diabetic retinopathy only in the far peripheral parts of the eye,” says Maturi.
For signs of macular edema, the doctor looks directly at the macula—but that may not be enough for a diagnosis. Your doctor may perform an optical coherence tomography, a laser-based scan of the back of the eye that measures the retina to detect macular edema. Even though the retina is wafer thin, the test is able to measure retinal thickening as slight as a thousandth of a millimeter, says Bressler.
A fluorescein angiogram is another test that can detect diabetic retinopathy. During the test, a dye is injected into the arm. Within 45 seconds, the dye reaches the back of the eye. Just as blood leaks from the weak blood vessels, so does the dye. “[It] shows exactly where the abnormal blood vessels are located,” Maturi says. Pictures are taken to document the results.
If you have diabetes and go to your doctor with blurry vision, you can expect some or all of these tests to take place. In addition, your doctor will look for cataracts (clouding of the lens in the eye) and glaucoma (high pressure in the eye), which are both more common in people with diabetes. Glaucoma may develop when abnormal blood vessels grow on the iris, the colored part of the eye, due to proliferative retinopathy.
If diabetic retinopathy is mild and stable, treatment is not immediately necessary. Regular dilated eye exams are used to keep track of the progression of the disease, and blood glucose control can keep it from worsening. The treatments for macular edema and proliferative retinopathy differ. Each can prevent vision loss and potentially restore lost vision. Here’s what to expect:
The treatment of diabetes-related vision problems is under rapid change. The FDA recently cleared Lucentis and Eylea for the treatment of proliferative diabetic retinopathy in people who also have diabetic macular edema, and researchers are working on a study to learn whether anti-VEGF agents might have any benefit compared with lasers for proliferative retinopathy. Long-acting anti-VEFG agents are also on the horizon, says Maturi. Instead of just working for a month or two, as the current agents do, these new drugs can potentially work three to six months at a time. Finally, a new drug that works by a new mechanism is being studied and tested for future use.
It may have taken 25 years to improve on lasers, but Bressler’s hoping updates to today’s
treatments come a bit faster. “Hopefully there will always be innovation,” he says.
Disclosures: Raj Maturi, MD, conducts research for Genentech (Avastin, Lucentis), KalVista, and Regeneron (Eylea), and serves as a consultant and researcher for Allergan (Ozurdex). Neil Bressler, MD, has no direct financial disclosures, but works as a researcher for Bayer (Eylea), Genentech, Novartis (Lucentis), and Regeneron through Johns Hopkins University.