The retina is the tissue paper thin membrane in the back of the eye that acts like the “film” in a camera. The retina collects information from the images projected upon it from the lens and sends it along the optic nerve to the brain, where it is interpreted and experienced as sight. 1. Diabetes 2. Macular Diseases 3. Retinal Detachment
Diabetes and Your Eyes Diabetes is the leading cause of visual impairment in the United States among patients below the age of 50. Many of the patients who suffer a loss in vision first present for eye examination when, unknown to the patient, the eye disease is already advanced. A few others lose vision despite meticulous eye care. With proper and timely treatment the likelihood of losing vision as a result of diabetic eye disease is much less than in the past. Diabetes is primarily a disease of tiny blood vessels, called capillaries, the thin vessels that connect veins and arteries and act in the circulatory system as the loading docks for nutrients, oxygen, carbon dioxide, and waste products. The damage to the capillaries is cumulative and, as we currently understand it, dependent upon the total time and amount that the blood sugar is above normal. In insulin-dependent diabetes where the onset is often very abrupt, this accumulation of the effects of abnormal blood sugar usually does not show up as any sort of visual problem until at least five years after the initial diagnosis. In the adult onset non-insulin-dependent type of diabetes, eye disease can show up considerably earlier for the simple reason that the diabetes may have been smoldering at a very low level for a number of years prior to the time that the diagnosis is actually made.
The long-term damage to capillaries in the eye manifests itself especially in the retina, resulting in diabetic retinopathy. In the early stages, only tiny dots of red cells that have escaped from damaged capillaries into the retinal tissue (dot hemorrhages) and outpouchings of the walls of tiny blood vessels (microaneurysms) can be seen. This is referred to as background diabetic retinopathy. Damage to blood vessels can then proceed down two paths with two different visual results and two different treatments. One problem, macular swelling (macular edema) results from damaged capillary walls becoming abnormally permeable. The other problem, the growth of new blood vessels (proliferative diabetic retinopathy) results from the complete clogging of large beds of capillaries. Sometimes these problems develop separately and sometimes together.
Diabetic Macular Edema
Patches of capillaries damaged by high blood sugar may leak serum, including fat and protein, into the adjacent retinal tissue. This tissue swelling causes the retina in that area to malfunction. If the affected area involves the center of the retina, gradually developing blurry vision results. The location of the leaks can be demonstrated by a test called fluorescein angiography. This is a test done in the office using a fluorescent dye injected into the large vein in the crook of the patient’s arm. Photographs are taken of the back of the eye with ordinary light, not x-rays. The leakage characteristics of the dye define the areas of damage to the capillaries. Using the fluorescein angiogram as a sort of road map, a laser can be used with an extremely fine light beam to focally cauterize the leaky spots, often resulting in the drying up of the swollen tissue. A very careful clinical study about 10 years ago demonstrated that when such treatment was properly applied, treated eyes were on the average seeing better at three years after the treatment than eyes that were not treated. (It should be noted that some eyes lose substantial amounts of central vision even with optimal laser treatment due to progression of the underlying diabetic disease). In general, the treatment helps the eye to preserve the vision that it has rather than producing visual improvement. The treatment is very minor from the patient’s perspective. Many patients have noted that the treatment is less of a nuisance than the fluorescein angiogram necessary to perform it. The reduction in macular swelling accomplished by the laser develops only gradually over the next two to four months. Usually, if further treatment is necessary or desirable, it is not performed on the same eye until about four months have passed. For several months following the laser treatment, some patients are aware of some tiny blank spots in the vision near the center which corresponds to the actual locations of the laser burns. This perception tends to gradually fade, but the fading occurs very slowly.
Proliferative Diabetic Retinopathy
When whole beds of capillaries close off and fail to carry the necessary oxygen and nutrients, the tissue begins to starve. Starving retinal tissue sends out a chemical message, which asks for new blood vessels to grow. Unfortunately, because of the structure of the eye the resulting new blood vessels grow in the wrong place, usually off the surface of the retina into the vitreous in the interior of the eye. In that location, they are subject to being tugged upon by the shrinking vitreous jelly. This tugging often produces bleeding in the eye, which the patient sees as strings and specks that usually develop very suddenly, often over night. Each of the spots where new blood vessels grow also tacks the vitreous to the retina, establishing a point at which the retina can be elevated or torn by later contraction of the vitreous. Before the laser treatment for this condition became available in the late 1960’s, ophthalmologists knew that a diabetic eye that presented with vitreous hemorrhage had a 50 percent chance of going on to become stone blind within three years. With timely treatment today, only 1 or 2 percent of such eyes will ultimately become completely blind. The laser treatment for proliferative diabetic retinopathy is more involved than that for macular edema. Ultimately somewhere between 700 and 2000 burn spots are made in the peripheral retina. This substantial cauterization destroys much of the starving retinal tissue. Dead retinal tissue no longer asks for new blood vessels to grow, resulting in cessation of growth and often shrinkage of the new blood vessels observed. Because this does not happen instantaneously, it is possible to perform a laser treatment and to have further vitreous hemorrhage occur after the treatment. Although this is a major nuisance, the natural history of vitreous hemorrhage is to gradually clear. Unfortunately, such clearance can take several to many months. If laser treatment has been placed before the hemorrhage, the new blood vessels that caused it are likely to be withering rather than growing. Therefore, the ultimate visual outcome is expected to be substantially better in those eyes with prior treatment. Unlike the treatment for macular edema, the laser treatment for proliferative diabetic retinopathy is usually done with placement of a local anesthetic. Bupivacaine, lidocaine, or a combination of the two is injected not into the eye itself but into the tissue near the eye with a long thin needle. With this the eye goes either partially or completely “to sleep,” so that the treatment can be performed entirely painlessly. The anesthetic sometimes produces temporary double vision, which is best relieved by patching one eye for a number of hours. When the eye wakes up, there is sometimes a headache or brow ache which usually is relieved quite well with acetominophen, or in the unusually severe case with crushed ice in a baggy wrapped in a washcloth held over the closed eye. Head elevation and avoidance of heavy lifting and strenuous exercise can also be helpful during the early period following the treatment. The eye may be quite light sensitive. Sunglasses help. Vision is often quite blurry for a few days and moderately blurry for as long as a few months. Initially, there are many shimmering specks in the peripheral part of the vision corresponding to the areas of laser treatment. This gradually fades over a period of months. Surprisingly, despite the dramatic appearance of the peripheral retina after one of these treatments, central and peripheral vision are often very good. A few eyes lose some of the sharpness of the central vision around the time of such treatment. It is impossible to know whether this is because of progression of the smouldering diabetic retinopathy or if it is actually a direct consequence of treatment. In any case, because of that small chance of vision not improving, our tendency is to wait to perform treatment until it is very clear that the small risks of treatment substantially outweigh the risk of continued observation.
Successful treatment of diabetic retinopathy not only depends on early detection with monitoring and treatment by a doctor, but also on the patient’s attitude and care of their own health. It is proved conclusively that the better the blood sugar control, the less the severity and progression of diabetic retinopathy. You can help save your vision, heart, kidneys, and feet by working with your regular medical doctor to control your blood sugar as closely as possible. You cannot benefit from preventive treatment unless you know that you have a need for it. Examination by an eye physician who is aware you are diabetic and examines you with that in mind is essential. In the complete absence of retinopathy, re-examination should occur on a yearly basis or, under certain circumstances and at the direction of your eye doctor.
What is the Macula? The macula is the most central portion of the retina, directly opposite the lens. It is where the greatest number of light sensitive cells, called cones, are located. Cones are the cells which allow us to see color and fine detail. The high concentration of cones in the macula gives people extremely detailed and rich central vision.
What is Macular Degeneration?
When the light sensing cells (cones) in the macula gradually stop working and eventually die, it is called macular degeneration. This disease occurs most often in people over the age of 60, in which case it is called age related macular degeneration (ARMD). Less common are several hereditary forms of macular degeneration which affect children or teen-agers. Macular degeneration alone does not result in total blindness. While some activities like reading and driving a car become difficult and nearly impossible, there is no need to fear descending into complete darkness, tripping over furniture, running into walls, or needing to carry a white cane. Most patients continue to have some useful vision and are able to carry on many of their usual everyday activities.
What are the Symptoms of Macular Degeneration?
The principal symptom of macular degeneration is a reduction or loss of central vision, with retention of peripheral vision. Macular degeneration makes close and detailed work, like reading or threading a needle, difficult. In some cases, colors will begin to look dim, straight lines will appear to be distorted, and a dark or empty area appears in the center of vision.
What Causes Macular Degeneration?
Many older people develop macular degeneration as part of the body’s natural aging process. The two most common types of age-related macular degeneration are ”dry” (atrophic) and ”wet” (exudative).Most people (between 85 and 90%) of patients have ”dry” macular degeneration. It is caused by aging and thinning of the tissues of the macula. Vision loss is usually gradual. The remainder of cases of macular degeneration are ”wet”, so called because of leakage of blood and fluids into the retina from newly formed blood vessels in the area behind the retina. Usually, blood vessels behind the retina carry nutrients to, and waste products from the retina. Sometimes, though, these fine blood cells begin to proliferate or multiply in a process called neovascularization. The newly created blood vessels then begin to leak into the retina, damaging and killing the cells of the macula. The cause of the sudden proliferation of these vessels is currently unknown.
Treatment of Macular Degeneration
While there is not yet a way to prevent or reverse the effects of macular degeneration, there are some things that can slow the progress of macular degeneration, and some things that can help the patient deal with their slowly degrading eye sight. Treatment of the more common ”dry” macular degeneration focuses mainly on helping the patient to find ways of coping with visual impairment. Since a patient’s peripheral vision is unaffected by macular degeneration, the remaining sight can be used to good advantage. Low vision devices, like magnifying devices, closed-circuit television, large-print reading materials, and talking or computerized devices, can help people to continue with many of their favorite activities. In the case of ”wet” macular degeneration, it is sometimes possible for the doctor to treat the problem in its early stages with laser surgery. The doctor uses a highly focused beam of light to seal the leaking blood vessels that damage the macula. This procedure can slow the rate of vision loss, but cannot halt macular degeneration. Laser surgery also leaves a small, permanently dark ”blind spot” at the point of each laser contact. Overall, the procedure can preserve more sight than it damages, and can slow the progress of macular degeneration, but is not a cure. Some doctors believe a special diet may slow macular degeneration. Although no conclusive scientific evidence has shown this belief to be true, a slightly modified diet, including a greater intake of dark green, leafy vegetables like spinach, collard greens, and kale, can hardly hurt. There has been a great deal of discussion among doctors about the role of vitamins and minerals in the treatment of age related macular degeneration. Many believe that the daily use of a combination of antioxidant vitamins and zinc will reduce the likelihood of progression of macular degeneration in an eye that starts out only mildly affected. Despite the lack of any convincing proof of effectiveness, taking vitamins after receiving the news that you have the early stages of macular degeneration is unlikely to do any harm.
The retina is a thin membrane which is held to the inside back portion of the eye by a kind of suction force. In the front part of the eye the retina is firmly attached at a ring just behind the lens called the pars plana. In the back part of the eye, the retina is continuous with the optic nerve which carries 3 million nerve fibers back to the brain. In between the pars plana and the optic nerve the retina is attached only by suction. The interior portion of the eye is filled with a material called vitreous, which is like a thin bag of jelly. As one gets older the vitreous tends to shrink, a process which is accelerated by prior cataract extraction or being greatly nearsighted. The bag of vitreous is also attached firmly in the front part of the eye at the pars plana. However, as the vitreous shrinks, it ultimately strips itself free from the surface of the retina in the back of the eye and begins to bobble around in the fluid. If it happens that the vitreous was glued on too tightly at a single point or several points just behind its firm attachment in the front part of the eye, the bobbling of the vitreous jelly bag can tear the retina at these points. Such a tear potentially breaks the suction holding the retina on. Depending upon the strength of the suction force that holds the retina on, the size of the tear, and the continued traction of the vitreous on the tip of the tear, the retina may detach.
Fixing Retinal Detachments
Retinal detachments are, in principle, fixed by finding all of the tears and adequately closing them. It is both that simple and that complex. Methods:
The Bubble Procedure
In the bubble procedure, an injection of an expanding gas is made into the back of the eye with a short, very skinny needle. The patient is then asked to position themselves over the next 7-10 days in such a manner that the bubble, rising in the fluid in the back of the eye, plugs the tear(s). This reestablishes the suction, the fluid underneath the retina reabsorbs, and the retina reattaches. After that, the bubble is used like a splint. You can readily see that if the tear that needs to be closed is in the lower portion of the eye or if there are several tears widely spaced, this procedure cannot be effective and is therefore not offered. When the eye wakes up, the bubble is seen as a shimmering surface which is distinguishable from the retinal detachment by the fact that it is always seen as being on the floor no matter which way the head is moved. The bubble is reabsorbed by the blood stream and expelled through the lungs as a natural process over the next 7-10 days. Advantages and Disadvantages The bubble procedure has the advantage that it produces only minimal discomfort and the vision that will return tends to return quickly over a matter of days or weeks. It has two disadvantages. The first disadvantage is the need for positioning, which is mentioned above. Depending on the location of the tear, this can be anything from a minor nuisance to a major problem. Physical inability to maintain the position is one contraindication to doing this procedure. Secondly, if one takes all eyes to which the bubble is applicable, the procedure works only 7 or 8 out of 10 times. This does not mean that the other 2 or 3 out of 10 eyes go blind. It usually means that these eyes will later need scleral buckling, the other, more extensive procedure. Usually, the need for scleral buckling is obvious within the first few days.
The Scleral Buckle
The buckle begins, like the bubble, with anesthetic and freezing treatment. The tissues around the eye are then opened using scissors so that access can be gained to the side of the eyeball, on a spot or spots on the outside of the eye corresponding to where the tears are on the inside. A piece of silicone rubber is then sewn in such a way that when the sutures are tightened, the silicone indents the eye wall, making a hill on the inside of the eye for the tear to rest upon. Often, some of the fluid under the retina is drained out of the eye using a fine needle while the process is carefully monitored using the indirect ophthalmoscope. The drainage and the indentation from the buckle usually close the breaks. Advantages and Disadvantages This procedure has the advantage that it works 9 or 9.5 times out of 10 as a first procedure. The major advantage is that the ”buckle” typically does not require any special positioning. Furthermore, this procedure can be used to repair retinal detachments to which the bubble procedure cannot be usefully applied. It has the disadvantage that it typically hurts considerably more, at least for the following day or two, than does the bubble procedure. The vision that will return does so more slowly, typically over time measured in weeks or months, rather than days or weeks.
Once the retina is successfully reattached, the process of visual improvement begins. In the case where the center of the retina has not detached, the visual results are usually quite good. When the center of the retina has been detached, the visual results are less impressive, only rarely as good as the vision prior to the detachment, but sometimes close to it.
As stated above, the most common problem with each of these procedures is the possibility that the retina may not be attached in one operation. A subsequent attempt at repair can be entertained using a combination of these procedures or other available techniques not covered here (e.g., vitrectomy). About 7 in 100 eyes develop some generalized scarring referred to as PVR (proliferative vitreoretinopathy) which shortens the retina, makes it less elastic, and sometimes holds the breaks open despite efforts to close them. Usually, some combination of techniques can be used to repair retinas that develop this problem, but sometimes, even with the best efforts, PVR results in blindness. Other risks involved in these procedures include infection, perforation of the eye with the anesthetic needle, bleeding, double vision, glaucoma, and acceleration of cataract formation. All of these complications are quite uncommon.