Retina Disease Treatment and Surgery

We treat a variety of retina diseases and perform all major retinal surgeries. These surgeries may involve lasers and/or incisions. In addition we also treat / perform surgery for diabetic retinopathy, hypertensive retinopathy, retinal detachments, retinal holes and tears, macular degeneration, retinal membranes, infections, hereditary conditions and optic nerve diseases.

HOW THE EYE WORKS

The human eye is like a camera where outside images are focused onto a piece of film

The cornea and crystalline lens are the lenses that focus the picture onto the eye's film, the retina.
The iris is the colored circle in the front of the eye.
The black , in the center of the iris, enlarges and contracts to regulate the amount of light entering the eye.
The vitreous is a transparent jelly filling the inside of the eye.
The choroid is a system of blood vessels which covers the outer retinal surface, providing it with oxygen and nourishment.
The sclera, or white of the eye, is a tough protective outer shell that corresponds to the body of a camera.
The optic nerve carries the light images to the brain.
The retina is a very thin layer of tissue that lines the inner part of the back of the eye and is continuous with the optic nerve. It contains photoreceptor cells (rods and cones), which capture the light rays that enter the eye. These light impulses are then sent to the brain for processing via the optic nerve.



	Diagram of the normal retina and macula.	Photograph of the macular region

The macula is a specialized area of the retina that allows us to see detailed, central vision. This makes it possible for us to read, watch television, and recognize faces. The retina reacts to light through a chemical process which then sends nerve impulses directly to the brain where the "picture" is processed.

Unlike a camera, the image obtained by the retina is not of uniform clarity or sharpness. Only the macula is sensitive enough to provide high quality central vision. Any disease that affects the macula, such as diabetes, macular degeneration, macular hole, macular pucker, ocular histoplasmosis, retinal detachment, or retinal vein occlusions can cause symptoms such as central blurriness or distortion.

Vitreous and Retina Problems

The following are some major and common vitreous and retina problems:

Diabetic Retinopathy: This is a serious problem that affects Diabetics. Early signs include blurred vision, floaters, and sudden or progressive vision loss.
Macular Degeneration: A condition of the macula, the part of the retina that allows us to see objects with great detail. Age-related macular degeneration is the most common cause of vision loss in the U.S. for people 50 and older.
Retinal Detachment: This condition occurs when the retina’s sensory and pigment layers separate. If left untreated, it can be extremely detrimental to vision.
Macular Holes: Usually a result of the normal aging process, a macular hole can cause wavy, distorted, or blurred vision. In some cases, it can even cause a complete loss of central vision.

RETINAL DIAGNOSTIC TESTING

RETINAL ANGIOGRAPHY

Ophthalmic Fluorescein & Indocyanine Green Angiography

What Is Eye Angiography?

Fluorescein and indocyanine green (ICG) angiography are diagnostic tests which use special cameras to photograph the structures in the back of the eye. These tests are very useful for finding leakage or damage to the blood vessels which nourish the retina (light sensitive tissue). In both tests, a colored dye is injected into a vein in the arm of the patient. The dye travels through the circulatory system and reaches the vessels in the retina and those of a deeper tissue layer called the choroid (see Figure below). Neither test involves the use of X–rays or harmful forms of radiation.

Fluorescein is a yellow dye which glows in visible light. Indocyanine is a green dye which fluoresces with invisible infrared light; it requires a special digital camera sensitive to these light rays. Schematic drawing illustrating a cross–section of the back of the eye with indocyanine green dye in the both the retinal blood vessels and the deeper choroidal vessels.

Why Is Eye Angiography Performed?

Both tests can help retina specialists diagnose and evaluate specific eye diseases. Fluorescein dye is best for studying the retinal circulation while indocyanine green is often better for studying the deeper choroidal blood vessel layer .Certain eye disorders, such as diabetic retinopathy and retinal vascular occlusive disease affect primarily the retinal circulation and are usually imaged with fluorescein dye. In other disorders, such as age–related macular degeneration, where leakage is from the deeper choroidal vessels, both tests may be useful. Indocyanine green angiography is especially helpful when there is leakage of blood which may make interpretation of fluorescein studies difficult.

This fluorescein study shows fluid leakage in a patient with the “wet” form of age–related macular degeneration. The retinal blood vessels are easily seen.

When abnormal vessels or leakage is identified with an angiogram, laser treatment or pharmacological therapies may be indicated to prevent vision loss. The tests can also be useful for following the course of disease or response to treatment.

Fluorescein and ICG angiography are universally employed throughout the world as diagnostic tests.

What Are The Risks Of Eye Angiography?

Both fluorescein angiography and indocyanine green angiography are considered very safe and serious side–effects from these tests are uncommon. However, there is the possibility that a patient may have a reaction to the dyes. While fluorescein contains no iodine and is safe in patients known to be allergic, indocyanine green is currently formulated with iodine and should not be used in these individuals. Some people may experience slight nausea after dye injection that usually passes quickly. Patients who are allergic to the dye can develop itching and a skin rash. These symptoms generally respond quickly to oral medications such as anti–histamines or steroids. Very rarely, a sudden life–threatening allergic reaction called anaphylaxis can occur. This condition requires medical treatment. There is also a possibility of an infiltrate of the dye into the skin at the injection site; this would cause some discomfort or discoloring of the skin for several days. Fluorescein dye will also turn a patient’s urine orange and may slightly discolor the skin as well for a brief period. For special patient populations there may be individual risks of these procedures which your physician will specify for you.

OPTICAL COHERENCE TOMOGRAPHY(OCT)

Optical Coherence Tomography (OCT) is a diagnostic test that allows for the imaging and measurement of retinal thickness. OCT is very useful in detecting retinal swelling or fluid accumulation secondary to a variety of retinal conditions. It provides very valuable information and is also useful for following the response to a treatment. OCT testing has become a standard of care for the assessment and treatment of most retinal conditions. OCT uses rays of light to measure retinal thickness and can be performed in a few minutes. No radiation or x–rays are used in this test.


Optical Coherence Tomography (OCT) demonstrating normal retinal architecture.	Abnormal Optical Coherence Tomography demonstrating retinal swelling

ULTRASOUND(B-Scan)

Ultrasound is a test that uses sound waves to assess ocular and retinal conditions. If your doctor cannot view the retina because of some opacity that blocks the view, they may use an ultrasound to determine the general status of the retina. Ultrasound is commonly used to assess the retina in patients with a dense cataract or vitreous hemorrhage. Ultrasound is simple to perform, painless, and does not involve any radiation

DIABETIC RETINOPATHY

What You Should Know About Diabetic Retinopathy

If you have been diagnosed with diabetes and are afraid of losing your vision, you are not alone. Diabetes has many faces—it affects people of all ages, races and nationalities. Of the almost 20 million people in the United States with diabetes, almost half of those will eventually develop some sort of diabetic eye disease. Diabetic retinopathy is the leading cause of new cases of legal blindness among working–age Americans.

Typically, changes begin to take place in the retina after a patient has been living with diabetes for 10 to 15 years.

Diabetes primarily affects the blood vessels in the retina, the light sensing tissue at the back of the eye. These vessels work like tubes, bringing oxygen and other nutrients into and out of the eye. Damage to these vessels is called diabetic retinopathy. Diabetic retinopathy develops gradually and painlessly.

Although good control of your blood sugar and blood pressure can help prevent diabetic eye disease, significant problems can still occur. Regular dilated eye examinations are therefore the only way to diagnose problems early, before vision loss occurs.

Diabetic vision loss is often preventable with early detection and treatment. At the Eye Center of Texas we specialize in all aspects of diabetic eye disease. The advanced diagnostic and treatment techniques we use often keep you seeing normally, allowing you to enjoy life to its fullest.

What is diabetes?

Diabetes mellitus is a disease causing the blood sugar (glucose) to become elevated. There are two basic kinds of diabetes. Type 1 diabetes is diagnosed early in life and requires insulin to bring the glucose level down to normal. Type 2 diabetes occurs later in life, and can be controlled with diet, pills, or insulin, depending on its severity. Approximately 18 million Americans have diabetes, with over one-third of those affected being undiagnosed.

How does diabetes affect the eye?

Over time, diabetes primarily affects the blood vessels that nourish the retina. In the earliest phase of the disease, known as background or nonproliferative diabetic retinopathy, The retinal vessels work like a garden hose, bringing oxygen and other nutrients into and out of the eye. Diabetes causes them to sprout tiny leaks, or microaneurysms the arteries in the retina become weakened and leak, forming small, dot-like hemorrhages. These leaking vessels often lead to swelling or edema in the retina, which may result in decreased vision. Central vision can become blurred, just as a water droplet placed on a photograph will cause the picture to blister and become distorted.

Macular Edema

In some cases of non–proliferative diabetic retinopathy, enough leakage may occur in the retina to cause it to become swollen with fluid. This condition is called diabetic macular edema. Macular edema is the most common cause of vision loss in patients with diabetes, occurring in upwards of 10% of all diabetic patients. Patients with diabetic macular edema experience reduced vision in the form of blurring, darkening or distorted images. Often the amount of retinal and macular edema, and associated symptoms, will be unequal between the two eyes.


(diabetic macular edema)	Nonproliferative diabetic retinopathy


Color retinal photograph demonstrating diabetic macular edema. The image is centered on the macula with the optic nerve seen on the right of the photo (right eye). The macula is swollen with fluid. There are white fatty deposits in the retina (exudates) which are frequently seen in such cases.


Fluorescein angiogram of the same patient illustrated above. The test pinpoints the areas of leakage and helps determine its severity. Fluorescein angiography helps the ophthalmologist determine whether laser treatment is indicated. It also helps in targeting the proper areas for treatment.

OCT scan (bottom) of normal macula compared to OCT image of diabetic macular edema (bottom).


The next stage is known as proliferative diabetic retinopathy. In this stage, circulation problems lead to oxygen-deprivation in some areas of the retina. New, fragile, blood vessels develop as the circulatory system attempts to maintain adequate oxygen levels within the retina. This is called neovascularization. These new vessels do not help the eye, however. They are fragile and can cause blindness by hemorrhaging or retinal detachment

Who gets diabetic retinopathy?

Diabetic retinopathy develops gradually over many years. People with Type I diabetes, those requiring insulin to control their blood sugar, and patients with diabetes for many years are at an increased risk for developing retinal problems. Poor control of the blood glucose, pregnancy, uncontrolled high blood pressure, and smoking also aggravate diabetic retinopathy.

Approximately 50% of diabetics (about 5 million Americans) will develop some form of diabetic retinopathy. Diabetic retinopathy is the leading cause of vision loss and new-onset blindnesss in the United States in those 20 to 74 years of age, with new cases of blindness developing in 12,000 to 24,000 persons annually. Remarkably, much of this vision loss is preventable with more timely diagnosis and treatment.

Signs and Symptoms:

The effect of diabetic retinopathy on vision varies widely, depending on the stage of the disease. Some common symptoms of the disease are listed below:

Blurred vision - often linked to blood sugar levels
Floaters and flashes
Sudden loss of vision

Though the symptoms listed above can signal diabetic retinopathy, diabetes can cause various other eye symptoms as well. If you are diabetic and experiencing any type of vision problem, you should seek treatment from a doctor immediately. Many diabetic retinopathy patients are examined by an internist, endocrinologist or optometrist before they are referred to our retina specialists for treatment.

How is diabetic retinopathy diagnosed?

You can't diagnose diabetic retinopathy by looking in the mirror since your eye will usually look and feel normal. Vision is also often normal despite the presence of potentially blinding eye conditions. Only a thorough retinal examination through a dilated pupil or in many instances through Optos screening camera can detect these problems. Properly timed laser treatment can effectively stabilize vision although it is less likely to improve it. The key to maintaining good eyesight, therefore, is early diagnosis and treatment before symptoms occur. Most diabetic patients need dilated eye examinations at least once a year throughout their lifetime. Further testing, including photography and fluorescein angiography, may be done to assist in the diagnosis and treatment of any changes thought to cause visual loss.


Normal Vision.	Diabetic Retinopathy.

What treatments are available for diabetic retinopathy?

1) Medical.

Good control of your blood sugar can significantly decrease the chances of diabetic retinopathy developing or progressing. However, there are some people who, despite eating right and controlling their diabetes as best as possible, will still get significant eye disease. Adequate blood pressure, and dyslipidemia (“ high cholesterol’) control also contribute to the severity of the retinal condition.

2) Laser surgery.

a) Introduction.

Laser photocoagulation is one of the main ways that diabetic retinopathy is treated. A laser is an instrument that produces a pure, high-intensity beam of light energy. The laser light can be focused onto the retina, selectively treating the desired area while leaving the surrounding tissues untouched. The absorbed energy heats, or photocoagulates, the retina, creating a microscopic spot.

Laser surgery is performed in our office while you are awake and comfortable. The laser treatment usually takes less than 30 minutes to complete and you can go home immediately following surgery. Arrangements for transportation should be made in advance since you may not be able to drive right away.

It will take several weeks to months before we can tell whether the laser surgery has been successful. Since diabetes is a progressive disease, many patients need more than one treatment to control their eye problem and prevent further loss of vision.

b) Macular edema.

The laser is used to seal the leaking vessels causing macular edema (focal or grid photocoagulation). In the Early Treatment Diabetic Retinopathy Study, photocoagulation decreased the risks of persistent macular edema and significant visual loss by about 50%, regardless of the baseline vision. Significant visual loss occurred in 5% of treated eyes compared to 8% of untreated eyes at 1 year, 7% of treated eyes compared to 16% of untreated eyes at 2 years, and 12% of treated eyes compared to 24% of untreated eyes at 3 years of follow-up. Photocoagulation was shown not to be of benefit for eyes without clinically significant macular edema, as the risk of significant visual loss with or without treatment was small.


Central diabetic macular edema with yellow, fatty lipid threatening the macular center.	Excellent response following laser photocoagulation.

c) Proliferative diabetic retinopathy.

To treat the abnormal growth of tiny blood vessels and bleeding that often result from diabetic retinopathy, we frequently use a type of laser surgery called pan retinal photocoagulation (PRP). When performing this diabetic retinopathy treatment, the surgeon uses a laser to destroy oxygen-deprived retinal tissue outside of a patient’s central vision. This prevents further growth of fragile blood vessels and seals leaking ones, helping to stop the disease from progressing. Some patients will experience some generalized blurring of vision which is usually transient but may persist indefinitely. Since there are these side effects, panretinal photocoagulation should be performed only for specific indications which have been well established through clinical trials. Despite these side effects, when indicated, panretinal photocoagulation has been clearly shown to reduce the risk of severe visual loss in proliferative diabetic retinopathy. The tradeoff of this treatment is that it creates some blind spots in the patient’s peripheral vision, and difficulty in night vision.

Panretinal photocoagulation (PRP) consists of yellow laser spots placed outside the optic nerve and macula.

In the Diabetic Retinopathy Study, the overall risk of severe visual loss with proliferative diabetic retinopathy at the 2-year follow-up examination was 16% in the control eyes compared to 6% in the treated eyes. With Diabetic Retinopathy Study high-risk characteristics, this risk increased to 26% of the control eyes and 11% of the treated eyes.

3) Intraocular steroids, and other medications.

Although laser photocoagulation was the only treatment available for diabetic macular edema since the 1970's, the recent advent of intraocular steroids has added another successful treatment for this disease. Injection of anti-inflammatory steroid medication (Kenalog) into the eye (a painless in-office procedure) appears to rapidly improve macular edema and vision loss, often more successfully than laser. However, the injections often have to be repeated every 4-6 months, and the long-term visual results remain to be determined. Temporarily increased eye pressure (glaucoma) and cataract are the most common and treatable side-effects. Pending ongoing studies, the role of laser photocoagulation versus intraocular steroids is still unclear. Studies are also ongoing evaluating devices that will allow for a long-term, sustained release of steroids into the eye.

Other Off–label Medications

Recently, the intraocular injection of anti–vasogenic drugs, that tell blood vessels to stop growing and leaking, has shown promising results in the control of retinal neovascularization and retinal edema. These treatments have not yet been assessed in prospective clinical trials for diabetic retinopathy but may be used on an off–label, non–approved basis.

One particular medication that has been increasingly utilized for this purpose is Avastin (bevacizumab), a drug that is approved for the intravenous treatment of colon cancer. Intraocular injections of Avastin have shown promising early results, and an excellent safety profile, in the control of retinal swelling and neovascularization due to a variety of retinal conditions including diabetes. Avastin lasts about 6 weeks in the eye after a single injection and the injection may need to be repeated if the disease reactivates.

4) vitrectomy surgery.

Some patients with severe proliferative retinopathy will develop extensive bleeding or retinal detachment that can cause blindness. Vitrectomy surgery is done in the operating room, usually on an outpatient basis. These advanced microsurgical techniques often allow us to restore vision by removing the hemorrhage and bleeding tissues. Vitrectomy is also used for some eyes with macular edema that fail to respond to laser photocoagulation or intraocular steroids.



Yellowish neovascular tissue is detaching the macula.	The retina reattached following vitrectomy surgery.

A vitrectomy is a common retinal surgery in which the vitreous gel is removed with the aid of tiny surgical instruments in the operating room. If scar tissue has accumulated on the retina small instruments are used to peel the scar tissue off of the surface of the retina to relieve the traction. Once the blood is removed, laser is usually added to the side part of the retina during the surgery. The goal of surgery for a traction retinal detachment is to try to stabilize the vision and decrease the chance of the vision worsening.

A vitrectomy is performed in the operating room while you are in a semi–sleep state and your eye is numb. The surgery takes about one to two hours and patients go home that night. The surgeon may place a gas bubble in the eye at the end of surgery to act as a splint to keep things in place as they heal. The gas bubble will be slowly absorbed by your body over several weeks. It is important to note that if a gas bubble is left in the eye patients cannot fly and must stay at sea level until the gas disappears.

MAINTAINING EYE HEALTH

To minimize vision problems associated with diabetes, patients should:

Maintain appropriate blood sugar levels when possible
Follow a healthy diet
Get sufficient amounts of exercise
Schedule routine examinations with an ophthalmologist so problems can be caught early
Lose weight when indicated, as per your primary care physician's direction

FLASHES AND FLOATERS

What You Should Know About Flashes & Floaters

Floaters are seen as clouds, or lines that seem to float in your field of vision. Flashes, which may be associated with floaters, appear as flickers of light.

Although flashes and floaters are usually common and harmless, their sudden appearance can be a symptom of an eye hemorrhage or a retinal detachment. Early detection is critical in successfully treating these conditions. You should therefore have an emergency eye examination for sudden floaters or flashes in one eye.

What are floaters?

Floaters are usually caused by condensations of the vitreous, the clear jelly-like fluid that fills the inside of your eye. Shrinking of the vitreous causes the gel to pull off of the eye wall, causing a posterior vitreous detachment (PVD). This is commonly age related, but is also more common with nearsightedness, following trauma or surgery, or with inflammation inside the eye. Floaters can also be caused by bleeding into the vitreous (as in proliferative diabetic retinopathy and retinal vein occlusions) or with eye inflammations.

Although they appear to be in front of your eye, they are actually floating within the vitreous inside your eye. You may sometimes see small specks or clouds moving in your field of vision. They may have variable shapes, including small dots, cobwebs, clouds, or lines. They are often most noticeable when looking at a plain blue background, such as a computer screen or blue sky.

What are flashes?

Flashes are often caused by the vitreous pulling on the retina during a posterior vitreous detachment or with the development of a retinal break or detachment. The flashes often develop just before floaters are seen. They usually are bright light-colored, occur in only one eye, and are without shape.

Migraines are another common cause of flashing lights. Some people experience flashes of light that appear as jagged, often colored, lines or "heat waves" in both eyes, often lasting 10-20 minutes. If a headache follows the flashes, it is called a migraine headache. However, jagged lines or "heat waves" can occur without a headache as part of an ophthalmic migraine. Migraines are often associated with light sensitivity, nausea, and tiredness.

Can flashes or floaters cause vision loss?

Sudden flashes or floaters can signify a retinal break or detachment which can cause blindness if left untreated. You should have an emergency eye examination for sudden floaters or flashes in one eye. However for most, these symptoms are temporary, and not associated with any serious eye problems or permanent vision loss.

Although floaters are usually frightening and annoying when they first develop, they usually become much less noticeable within several weeks to months. The floaters can often be moved out of the way by moving your eyes around. Rarely, some will require vitrectomy, a relatively painless outpatient surgery, to remove the vitreous for visually disabling floaters.

Occasionally, floaters and flashes can be an indication of a more serious problem than PVD. Other possible causes include: retinal tears, retinal detachment, infection, inflammation, hemorrhage, and eye injury. Occasionally, flashes of light are caused by migraine headaches. When related to a headache, they usually appear in both eyes and last for 20-30 minutes before the headache starts.

Signs and Symptoms

Black spots or “spider webs” that seem to float in a cluster or alone
Spots that move or remain suspended in one place
Flickering or flashing lights that are most prominent when looking at a bright background like a clear, blue sky

Symptoms that may indicate a more serious problem

Sudden decrease of vision along with flashes and floaters
Veil or curtain that obstructs part or all of the vision
Sudden increase in the number of floaters

Treatment:

Surgery is not necessary for most patients with floaters or flashes. Often, floaters become less noticeable over time as they settle below the line of sight. If flashes and floaters are related to a problem other than a PVD, another form of surgery may be required.

RETINAL TEARS AND DETACHMENT

What You Should Know About Retinal Detachment

The retina is the neurosensory tissue that lines the back wall of the eye. Like the film in a camera, the retina is responsible for creating the images that one sees. The center of the retina is called the macula and is the only part capable of fine detailed vision, i.e. reading vision, recognizing faces, etc. The remainder of the retina , the peripheral retina, is for side vision. The retina outside the center of the macula, which makes up more than 95% of the retina, is not capable of the fine detailed vision.

When the retina detaches, it separates from the back wall of the eye and is removed from its blood supply and source of nutrition. The retina will degenerate and lose its ability to function if it remains detached. Central vision will be lost if the macula remains detached.

What are the common symptoms of retinal detachment?

Painless:

Light flashes
“Wavy” or “watery” vision
Veil or curtain obstructing vision
Shower of floaters that resemble spots, bugs, or spider webs
Sudden decrease of vision

Vision loss can progress rapidly. Untreated, retinal detachment usually causes permanent blindness.
If you are experiencing symptoms of a detached retina, contact Eye Center of Texas right away. Receiving immediate treatment increases the chance that you may regain lost vision and/or limit further loss.

What causes a retinal detachment?

Breaks in the retinal tissue (retinal holes and retinal tears) are normally found in approximately 10% of people. In a small minority of persons with retinal breaks, liquid vitreous leaks beneath the retina, separating it from the eye-wall and causing a retinal detachment. A sudden separation of the vitreous from the retina (posterior vitreous detachment) is often the inciting event causing a retinal break or detachment. Macular pucker can also develop following a vitreous detachment.

Types of Retinal Detachment

There are three types of retinal detachments:

The most common type occurs when there is a break in the sensory layer of the retina and fluid seeps underneath, causing the layers of the retina to separate. Nearsighted people are more susceptible to this type of detachment because their eyes are longer than average from front to back, causing the retina to be thinner and more fragile. Patients who have undergone eye surgery or have experienced a serious eye injury are also at greater risk for this type of detachment.
The second most common type occurs when strands of vitreous or scar tissue create traction on the retina, pulling it loose. Patients with diabetes are more likely to experience this type.
The third type of detachment happens when abnormal excess of fluid collects underneath the layers of the retina, causing it to separate from the back wall of the eye. This type usually occurs in conjunction with another disease affecting the eye that causes swelling or bleeding.

Who gets retinal detachment?

Retinal detachment develops in approximately 1 in 10,000 people per year. Certain conditions increase the likelihood of retinal detachment, including acute symptomatic retinal breaks, acute posterior vitreous detachment, nearsightedness, eye injury, eye surgery, or a history of retinal detachment in family members. If a person has a retinal detachment in one eye, there is a 10% chance of eventually developing a detachment in their other eye.

How is a retinal detachment diagnosed?

Anyone who has sudden flashes, floaters, or peripheral vision loss needs an urgent examination by an eye doctor familiar with retinal diseases. A careful dilated retinal examination is necessary to diagnose retinal breaks or detachment.



A billowing retinal detachment surrounds the macula.	The retinal tear (arrow) causing this detachment is seen in the inferior retinal periphery.

Ultrasound imaging of the eye is also very useful for the doctor to see additional detail of the condition of the retina from several angles.

How are retinal breaks and detachment treated?

1) RETINAL BREAKS.

Asymptomatic retinal breaks in low risk eyes do not require treatment. Eyes with symptomatic breaks need preventive treatment. High-risk eyes with asymptomatic breaks are often treated as well. "Gluing" the surrounding retina with heat (laser photocoagulation) or cold (cryotherapy) usually prevents retinal detachment from developing.

White laser photocoagulation spots surround a retinal tear (arrow).

2) RETINAL DETACHMENT.

Once the retina separates from the eye-wall it must be surgically pushed back into place; the causative retinal breaks are then "glued" with laser photocoagulation or cryotherapy. There are several surgical options available for repairing retinal detachment. Scleral buckling pushes the "wall against the wallpaper" whereas pneumatic retinopexy and vitrectomy push the "wallpaper against the wall." Surgery is usually performed within a day or two of diagnosis, particularly if the macula and central vision are not yet affected.

Scleral buckle.

This surgical procedure has been in use for more than 40 years, and, until approximately 25 years ago, was the only procedure available. It is still commonly used for rhegmatogenous retinal detachments, especially when there are no complicating factors. The procedure involves localizing the position of all the retinal breaks, treating all retinal breaks with the cryoprobe and supporting all the retinal breaks with a scleral buckle. The buckle is usually a piece of silicone sponge or solid silicone. The type and shape of the buckle varies depending on the location and number of retinal breaks. The buckle is sewn onto the outer wall of the eyeball (sclera) to create an indentation or buckle effect inside the eye. The buckle is positioned so that it pushes in on the retinal break and effectively closes the break. Once the break is closed, the fluid under the retina (subretinal fluid) will usually spontaneously resolve over 1–2 days. Sometimes the surgeon elects to drain the subretinal fluid at the time of surgery. Most often, a scleral buckle procedure can be done with local anesthesia and as same day surgery (in and out of the hospital on the same day). Postoperatively, there are usually no positioning requirements and one can resume most activities within several days (except for anything that would jar the head).

Scleral buckling is an outpatient procedure performed in the operating room under local anesthesia. A piece of silicone rubber is permanently sewn to the outside of the eye, pushing (or "buckling") the eye-wall (sclera) against the retinal breaks. The eye looks and feels normal following surgery. Scleral buckling successfully re-attaches in the retina in over 90% of eyes with one operation.

Pneumatic retinopexy.

Since the 1980’s this has been a popular way to repair a straight–forward rhegmatogenous retinal detachment, especially if there is a single break located in the superior portion of the retina. This procedure involves injecting a gas bubble into the middle part of the eye (vitreous cavity). It is then critical to position oneself so that the gas bubble covers the retinal break. If the break can be covered by the bubble, the subretinal fluid will usually resolve within 1–2 days. The retinal tear is either treated with cryopexy before the bubble is injected or with laser after the retina has flattened. The main advantages of this approach are that it can be done in the office, thus avoiding hospitalization and that it avoids some of the complications of scleral buckling surgery, although it has its own set of complications. The main disadvantages are the requirement for precise head positioning for up to 7–10 days following the procedure and a slightly lower initial success rate as compared to a scleral buckle or TPPV. If the retina is not reattached by a pneumatic retinopexy procedure, a scleral buckle and/or TPPV can be done at that point.

In this procedure, the retina surgeon numbs the eye with local anesthesia and injects a small gas bubble into the eye’s cavity. The bubble facilitates the repositioning of the retina back into its normal location, and keeps the two detached layers up against each other. Because the gas rises, this treatment works best for detachments in the upper portion of the eye.

After a gas bubble is injected into the eye, the patient positions their head so the bubble floats up against the retinal detachment. Once the retina re-attaches, usually within several days, the causative retinal breaks are surrounded with laser photocoagulation or cryotherapy. The cryopexy can be performed before the injection of the gas bubble in many case. Over a period of one to two weeks, the eye gradually absorbs the gas bubble.

Pneumatic retinopexy has a 75% success rate following placement of the initial bubble. Initial failures are primarily due to poor patient compliance with head positioning or the development of new retinal breaks. Subsequent surgery (i.e. scleral buckling or vitrectomy) is usually successful in re-attaching the retina.

Vitrectomy.

Usually referred to as a Trans Pars Plana Vitrectomy (TPPV), this procedure was first used ˜25 years ago and has been continuously refined and improved since then. Over the last 5–10 years a TPPV procedure has become the initial surgery of choice for repair of many retinal detachments. The procedure involves making small incisions into the wall of the eye to allow the introduction of instruments into the vitreous cavity (the middle of the eyeball). The first part of the procedure usually is the removal of the vitreous using a vitreous cutter. Then, depending on the type and cause of the detachment, a variety of instruments (scissors, forceps, pics, lasers, etc…) and techniques (excision of tractional bands, air–fluid exchange, silicone oil fill, etc…) are used to reattach the retina. A TPPV can also usually be done as same day surgery and with local anesthesia. It is sometimes important to maintain a specific head position after surgery to keep the retina attached. More information regarding vitrectomy surgery can be found on the vitrectomy page.

Vitrectomy is an outpatient surgery performed in the operating room under local anesthesia. The vitreous is removed, directly eliminating the retinal traction on the causative retinal breaks. Scar tissue growing over the retinal surface can be removed as well. The eye is then filled with a gas bubble. This mechanically pushes the retina back against the eye-wall. Laser photocoagulation or cryotherapy are then used to seal the retinal breaks. Vitrectomy surgery has a variable success rate (often over 90%), depending on the severity of the retinal detachment.

In rare cases where other types of retinal detachment surgeries are either inappropriate or unsuccessful, silicone oil may be used to reattach the retina. The vitreous gel is removed and replaced with silicone oil, which presses the retina into place. While the oil is inside the eye, the vision is extremely poor. After the retina has resealed itself against the back of the eye, a second procedure may be performed to remove the oil.

Surgical Results

Approximately 90% of rhegmatogenous detachments can be initially repaired with one or a combination of these procedures. Sometimes, a scleral buckle is combined with a TPPV. If the retina does not reattach or detaches again after initial reattachment, it is usually due to the development of scar tissue on the surface of the retina and tractional forces within the vitreous cavity. If this happens following a scleral buckle procedure, it is often necessary to do a TPPV to repair the detachment. Sometimes, an intraocular gas bubble can be injected and the retina reattached following positioning. If a TPPV was done initially, it is often necessary to go back and do another TPPV to remove the new scar tissue and/or perform a scleral buckle. If a pneumatic retinopexy was the initial procedure, another pneumatic can be done or a scleral buckle or TPPV can be performed. As one can tell, there is no set way to repair a detachment and all the available procedures can be used in different combinations and sequences depending on the specific situation.

Visual Results

The visual prognosis depends mainly on the pre-existing status of the retina before it detached. If the macula has not detached, the pre–existing vision will usually be retained following successful repair. However if the macula is detached and central vision is impaired by the detachment, there may be permanent loss of central vision even if the retina is successfully repaired. The longer the macula is detached, the more likely there will be loss of vision due to irreversible damage to the photoreceptor cells. In general, if the center of the macula is detached for more than 4–5 days, there may be significant loss of central vision following surgical reattachment.

Will my vision improve after retinal reattachment surgery?

The most important factor predicting final eyesight is the vision immediately before surgery. If the vision is initially good, successful surgery generally yields good sight. However, if the central vision is poor pre-operatively, final vision is often decreased even with successful retinal reattachment.

Patients usually need to have their glasses changed several months after retinal reattachment surgery, particularly following scleral buckling. Final vision may also be decreased by the later development of a cataract, which often follows vitrectomy surgery. Cataract surgery is often successful in restoring vision in such cases.

What you can do...

Early detection is key in successfully treating retinal detachments and tears. Awareness of the quality of your vision in each eye is extremely important, especially if you are in a higher-risk group such as those who are nearsighted or diabetic. Compare the vision of your eyes daily by looking straight ahead and covering one eye and then the other.

Notify your doctor immediately if you notice any of the following:

An obstruction of your peripheral vision (veil, shadow, or curtain)
Sudden shower of floaters
Light flashes
Spider webs

MACULAR DEGENERATION

Macular degeneration is the most common cause of severe visual loss in people over the age of 50. Over 8 million people in the US alone have some form of this disease.

The term “macular degeneration” includes many different eye diseases, all of which affect central, or detail vision. Age–related macular degeneration is the most common of these disorders, mainly affecting people over the age of 60.

Age–related macular degeneration is an eye disease that primarily affects the central portion of the retina known as the macula. The risk for developing macular degeneration increases with age and is in excess of 30% by age 75. Other risk factors include: a family history of the disease, cigarette smoking, diet, excessive sunlight exposure, hypertension and cardiovascular disease.

This photograph shows a normal, healthy retina as viewed by an eye doctor during an examination.

This photograph shows a normal, healthy retina as viewed by an eye doctor during an examination. The ophthalmologist will pay careful attention to the appearance of the macula and fovea when examining the retina.

AMD is classified as either wet (neovascular) or dry (non-neovascular). About 10% of patients who suffer from macular degeneration have wet AMD

DRY MACULAR DEGENERATION

The majority of people with macular degeneration have an early form of the condition and experience minimal visual loss. For many of these people, macular degeneration will not progress to a more serious condition.

In the early stages of macular degeneration, the transport of nutrients and wastes by the RPE slows down. As waste products accumulate under the retina, they form yellowish deposits called drusen.

In the healthy retina, a layer of cells called the retinal pigment epithelium (RPE) supplies the photoreceptors with nutrients and pumps out the waste products created as the photoreceptors convert light into nerve signals.

An eye doctor examining a patient at this stage may note the presence of these drusen, even though most people have no symptoms. When drusen have been noted on examination, monitoring will be needed over time, although most patients will not progress to develop visual loss. Many people over the age of 60 will have some drusen.

A portion of people with drusen may begin to experience mild visual loss. At this point, macular degeneration may progress in one of two ways. These two types of degeneration are known as the dry (atrophic) and the wet (exudative) forms of the disease.

This retinal photograph shows numerous yellow drusen in and around the macular region of the retina.

Eyes with geographic atrophy, a variant of dry macular degeneration, develop a wearing away of the macular pigmented tissues. The atrophy causes discrete islands of blind spots. Vision is good unless the atrophy extends into the macular center.



Geographic atrophy just spares the macular center.	The atrophy gradually enlarged, causing loss of central vision.

Wet (Exudative) Macular Degeneration

For reasons that are not fully understood, a minority of people with macular degeneration develop a more serious form of the disease. People with large “soft” drusen (drusen with indistinct borders), many drusen that run together, or focal pigmentation are at greater risk for developing the wet (exudative) form of the disease.

In the wet form of macular degeneration, new blood vessels begin to grow underneath the retina. The proliferation of these new blood vessels is called choroidal neovascularization, or CNV.

In a variant form of the disease, the new blood vessels may begin within the retina and grow toward the choroid layer. This form is called retinal angiomatous proliferation, or RAP. Another variant is called polypoidal choroidal vasculopathy, or “polypoidal.” The polypoidal vessels in this condition tend to cause extensive bleeding under the retina.

In wet macular degeneration, new blood vessels grow underneath the retina in a process called choroidal neovascularization, or CNV.

It is believed that the diseased retina stimulates the production of these new blood vessels in response to a decreased supply of nutrients and slow transport of wastes. Unfortunately, new blood vessels do not improve the health of the retina. Instead, they often leak blood or fluid into the retina.

This retinal photograph shows fluid and blood beneath the retina which suggests the presence of choroidal neovascularization (CNV)

As CNV continues, the new vessels may leak blood or fluid under the retina, causing the retinal surface to become uneven. As a result, objects in that portion of your visual field may appear wavy or distorted. The neovascularization may even break through some of the retinal layers. Blind spots may appear in your vision if portions of the retina become damaged by the CNV.

Often the first sign of fluid under the retina is distortion of straight lines. Just as in a camera, if the film is not lying flat, images will be distorted. Since these changes can be subtle, regular testing with the Amsler grid in this booklet can be helpful in the early detection of problems.

[Blind spots like those shown here may appear as the condition worsens.]

As the surface of the retina becomes uneven, objects in your vision may appear blurred, wavy, or distorted. As the condition progresses, blind spots may appear.

Any change in the appearance of the grid may be a sign of choroidal neovascularization and should prompt a visit to the eye doctor. If caught early enough, the CNV might be treatable before it causes too much damage.

[The amsler grid test, shown here, is an important tool for the early detection of any changes in your vision.]

The first indication of fluid under the retina may be a distortion of straight lines. The Amsler grid test is an important tool for the early detection of any changes in your vision.

Eventually, areas of neovascularization and leakage can lead to the death of the overlying photoreceptors and scarring of the macula. Scarring is the final stage of macular degeneration, and it frequently results in significant visual loss.

It is important to realize that this entire process occurs only in the macula, and affects only central, or detail vision. Peripheral, or side vision is rarely affected by macular degeneration. While macular degeneration is the leading cause of legal blindness, it rarely leads to total blindness.

This retinal photograph shows a large yellow scar in the macular region resulting from advanced CNV. A person with this type of scarring would experience a significant loss of vision in that eye.

Legal blindness means the vision is 20/200 or worse in the better eye even with corrective lenses or that the peripheral visual field is restricted sufficiently to cause tunnel vision.

Examination & Diagnosis

A thorough examination by an eye doctor is the best way to determine if you have macular degeneration or if you are at risk for developing the condition.

The exam begins by testing your visual acuity or the sharpness of your vision. There are several different tests for visual acuity. The most familiar one has lines of black letters on a white chart.

Next, your eyes may be tested with an Amsler grid. This test helps your doctor determine if you are experiencing areas of distorted or reduced vision, both common symptoms of macular degeneration. If you do have macular degeneration, your doctor will use the Amsler grid to determine if your vision has changed.

After these visual tests, the front part of your eyes will be examined to determine if everything is healthy. Your doctor may put anesthetic drops in your eyes before measuring the pressure in each eye.

Then, drops are administered which cause your pupils to dilate. This will allow your doctor to examine the retina through the enlarged pupil. The drops typically take between 20 and 45 minutes to work, and will wear off in about 4 hours. While the pupils are dilated, it is usually difficult to read, and bright lights may be uncomfortable. Some patients use sunglasses after dilation to reduce light sensitivity.

After the dilating drops are administered and allowed time to work, the eye doctor will seat the patient at a device called a slit lamp. The slit lamp is a special microscope that enables the doctor to examine the different parts of the eye under magnification. When used with handheld lenses or special contact lenses, the slit lamp gives the examiner a highly magnified view of the retina.

[The slit lamp is a microscope that gives the examiner a magnified view of the retina.]

The slit lamp is a microscope that gives the examiner a magnified view of the retina. Your doctor will look for drusen and other areas of the retina that appear suspicious or abnormal.

The examiner will look for drusen and other areas of the retina that might appear suspicious or abnormal. Since choroidal neovascularization (the new blood vessel growth found in the “wet” form of macular degeneration) occurs beneath the retina, the blood vessels themselves are not usually visible. But the examination can reveal clues such as: bleeding, elevation of the retina, or fluid behind the retina, that suggest the presence of choroidal neovascularization (CNV). In these cases, further testing may be necessary.

This retinal photograph shows many drusen and fluid under the retina, suggestive of choroidal neovascularization.

Additional testing will be required for complete diagnosis and treatment.

Angiography

A technique called angiography is the most useful test for determining the presence of choroidal neovascularization (CNV). The procedure is painless and very safe. The patient will be seated at a fundus camera, which takes pictures of the retina. A small IV catheter is inserted into a large vein, usually in the arm. Several pictures are taken at this time.

The fundus camera takes pictures of the fundus, or retina. A small IV catheter is inserted into a vein for the injection of fluorescein or ICG dye.

Then, a dye is injected into the vein. The dye circulates throughout the blood vessels of the body. As the dye enters the blood vessels of the eye, a series of photographs is taken of the retina. Special filters make the dye stand out against the background of the retina.

By looking at the pattern of the blood vessels and observing whether dye leaks from any of the vessels as time passes, your ophthalmologist can locate sites of choroidal neovascularization if they are present.

Two dyes are commonly used in ophthalmology: an orange dye called fluorescein and a green dye called indocyanine green. These dyes are different than those used for angiograms of the heart or brain. Unlike in angiography used in other parts of the body, X-rays are not used in this procedure since the examiner can look through the pupil and see the blood vessels directly.

This fluorescein angiogram shows choroidal neovascularization (CNV) in the macula. The bright area indicates dye leaking from the neovascular vessels.

The majority of treatable CNV can be seen with fluorescein dye. Fluorescein angiography is an extremely safe procedure, and it has been performed in millions of patients for over 25 years. The overwhelming majority of patients experience no symptoms when the dye is injected. A small minority may feel flushed or briefly nauseated. Rarely, someone has an allergy to fluorescein and may experience itching or other symptoms that require treatment.

Sometimes, an area of CNV is not clearly defined, or it may be obscured by overlying fluid or blood. In these cases, it is sometimes helpful to perform the angiography using a different dye called indocyanine green.

Optical Coherence Tomography

An OCT device is used to map the anatomy of the retina.

Optical Coherence Tomography (OCT) is a new technique for imaging the retina. It is a non–invasive test which records the features of the retina and displays this information as cross-sectional views, or optical ‘slices.’ For this procedure, the patient is seated at the OCT device.

Laser light is used to map the anatomy of the retina, and the resulting computer images are saved for analysis. OCT evaluations are not a replacement for angiography, rather they are complementary techniques.

This is an OCT image of the macula of a normal, healthy eye. The depression in the center is the fovea. The colors in the OCT image represent the different layers of the retina. Note how smooth and even the layers are.

This is an OCT image of the macula in an eye with wet macular degeneration. The affected tissue layers beneath the retina are no longer smooth and flat.

Treatment & Research

PHARMACOLOGIC(Drug)THERAPY

Lucentis

Lucentis is another drug that blocks VEGF. It was in the late stages of testing in 2005 and will likely be available for the treatment of patients in 2006.

Like Macugen, treatment with Lucentis involves injecting the drug into the vitreous body of the eye. As it diffuses throughout the back of the eye, the drug comes in contact with VEGF proteins in the damaged area of the retina and choroid. Lucentis binds to the VEGF proteins, preventing them from stimulating further blood vessel growth and leakage.

In the early stages of treatment, injections are repeated every 4 weeks. The optimal timing of subsequent treatments is still under investigation. Lucentis is the first drug to offer hope of improvement in vision for some patients while stabilizing vision in the majority of patients.

Other drugs which target the production of VEGF, the circulation of VEGF, or the receptor for VEGF are currently under investigation in preliminary clinical trials. Research is also underway to develop better methods of delivering drugs to the eye to reduce the need for frequent injections.

Lucentis and Avastin

Before the approval of Lucentis, retinal specialists had started using a related drug called Avastin (bevacizumab) which was not approved for ocular use but was available for cancer treatment and was chemically related to Lucentis (both drugs are made by the same company Genentech). The results that retinal specialists have seen with Avastin (which is now in use worldwide for AMD) appear to be similar to the results seen with Lucentis. There has been a great deal of media attention to both of these drugs because although they may both help in AMD, they have very different costs. Lucentis is expensive and Avastin is very inexpensive. Both drugs are now covered by insurance plans for the treatment of wet AMD. However, only Lucentis has been approved for use in this indication (so far). The National Eye Institute has initiated a study which will compare these two drugs to each other which should help retinal specialists advise patients in an informed way.

There are potential risks and benefits of these varied drug options which a retinal specialist would discuss with an AMD patient before helping him or her to decide which treatment is best for his condition.

This is an exciting and hopeful time for patients and their doctors. Macular degeneration is now receiving the attention it has long–deserved. With a vast amount of ongoing research, we expect to see continued progress in treating this disease in coming years.

www.Lucentis.com

Macugen

After preparation, the eyelids are pulled back and Macugen is injected into the vitreous body of the eye.

Macugen is the first drug therapy for wet macular degeneration, approved late in 2004. Treatment with Macugen aims to block the stimulus of blood vessel growth in order to stabilize vision.

In wet macular degeneration, new blood vessels grow in the choroid layer underneath the retina. Growth of these new, leaky vessels is stimulated by proteins known as Vascular Endothelial Growth Factor, or VEGF.

To control the growth of the leaky blood vessels, a drug called Macugen is injected directly into the vitreous body of the eye. The drug then diffuses throughout the retina and choroid. Your ophthalmologist will take precautions to minimize the risks of injection.

Inside the eye, Macugen binds strongly to the abnormal VEGF proteins it comes in contact with. This prevents the VEGF molecules from stimulating further blood vessel growth and leakage.

Over a period of weeks, Macugen is slowly absorbed into the circulatory system, and excreted from the body. In order to keep an adequate amount of medicine in the eye, injections are repeated every 6 weeks. Initial studies show that a course of therapy of one or two years may be necessary to stabilize vision in most patients.

Macugen attaches to VEGF molecules in the retina and choroid, preventing them from stimulating more abnormal vascularization.

www.Macugen.com

Visudyne Photodynamic Therapy

Since the year 2000, photodynamic therapy has been used to treat some forms of wet macular degeneration. This treatment couples a laser with a light–sensitive drug to destroy leaking blood vessels in the retina.

To begin the treatment, a special light–sensitive drug is infused into a vein in the arm and allowed to circulate throughout the body. In the bloodstream, the drug attaches itself to molecules of low–density lipoprotein, or LDL.

Photodynamic therapy is an experimental treatment that combines low–level laser treatment with a lightsensitive drug. The drug is infused into the arm much like the dyes used in angiography.

Inside the retina, the abnormal blood vessels attract and absorb LDL. Since the drug is attached to the LDLs, it also accumulates inside the abnormal vessels. With time, the drug is cleared from the normal nearby blood vessels.

The injected drug accumulates in the abnormal blood vessels.

Next, eye drops will be used to numb the eye, and a special contact lens is placed on the eye to focus the laser. At this point, low intensity laser energy is directed through the contact lens, onto the area of choroidal neovascularization (CNV).

Low intensity laser energy is applied to the area of CNV. The laser destroys the abnormal vessels where the lightsensitive dye is concentrated, sparing the overlying retina.

Low intensity laser energy is applied to the area of CNV. The laser destroys the abnormal vessels where the lightsensitive dye is concentrated, sparing the overlying retina.

The laser energy activates the drug concentrated in the abnormal blood vessels, causing them to close and stop growing. Using this low–intensity laser spares the overlying retina from damage. In some cases your ophthalmologist may also inject a steroid into the treated eye. The steroid reduces inflammation and swelling.

Usually, the whole procedure takes less than 30 minutes. When you go home afterwards, and for the next 5 days, you do have to be careful not to expose yourself to direct sunlight or other bright lights as the drug is cleared from your system.

Several sessions of photodynamic therapy are typically required to control the neovascular growth. It is common for patients to have three or four treatments in the first year and two treatments the second year. Your ophthalmologist will use angiograms and/or OCT imaging of your retina to determine if additional treatments might be beneficial. The goal of treatment is to stabilize your vision. Your ophthalmologist will discuss the risks, benefits, limitations and alternatives for your particular case.

www.Visudyne.com

Laser Treatment

Thermal laser used in surgery emits a series of precisely controlled beams of light energy.

The thermal laser used for this surgery emits a series of precisely controlled beams of light energy. Only minimal discomfort is felt as several pulses of laser light are directed at the CNV.

The laser light (shown in green) passes through the tissues of the retina. In the area of CNV, the laser energy is converted into heat (white spot). This heat burns the CNV and some of the surrounding retinal tissues.

One treatment for wet macular degeneration uses a thermal laser to coagulate the CNV and stop it from spreading. In some cases, the area of involvement may be too extensive to treat. Your doctor will discuss with you the risks, benefits, limitations and alternatives in your particular case.

Laser treatment for wet macular degeneration is done on an outpatient basis with local anesthesia (eye drops). To begin the procedure, the patient is seated at a special slit lamp. A lens is placed on the eye to give your ophthalmologist a magnified view of the retina. Next, your ophthalmologist will aim the laser directly at the CNV beneath your retina. Only minimal discomfort is felt as several small pulses of laser light are directed at the CNV.

The laser light passes through the tissues of the retina where the light is absorbed by the CNV and pigmented tissues beneath the retina (RPE and choroid). The absorption of laser energy produces heat which burns the CNV and some of the surrounding retinal tissues, causing a small scar to form. After treatment, the scarred area will appear as a permanent blind spot in your vision.
Green laser

It is important to realize that laser treatment generally doesn’t improve your vision. Laser treatment is a compromise: a small portion of retina is sacrificed in order to prevent damage to a much larger area which would occur if the CNV were allowed to continue growing. When laser treatment is successful, the scar produced by the laser is smaller than the scar that would have resulted if the CNV had been left untreated.

This is an image of a fluorescein angiogram before treatment.

Before treatment. This fluorescein angiogram shows a well–defined area of choroidal neovascularization (CNV) underneath the macula.

Even if successful, laser treatment treats the CNV but not the underlying disease process of macular degeneration. It is not uncommon for CNV to come back in the future. Following laser treatment, is often necessary to use angiography to detect any recurrences of CNV. If new CNV is found, your eye doctor may recommend additional treatment to preserve your remaining vision.

This is an image of a fluorescein angiogram after treatment.

After treatment. This fluorescein angiogram shows the same eye after laser treatment. The CNV beneath the macula has been successfully treated.

Experimental Treatments

Although there are now effective treatments for macular degeneration, there is no cure for the chronic disease process. For this reason and for the hope of better visual results for the patient, many new methods of treatment are being developed and tested. A wide variety of therapies are being considered, including:

off–label drugs
rheopheresis
low dose radiation therapy
submacular surgery
RPE transplantation
macular translocation surgery
laser treatment of drusen
artificial vision

We will briefly discuss each of these experimental treatments.

Off–Label Drugs

The term “off–label” means using drugs for a purpose for which they were not originally approved. For example, aspirin is used to prevent heart attacks and for blood thinning even though the FDA label did not initially list these specific reasons. Now these reasons have been added to the list of indications.

Physicians may use any available drug to treat macular degeneration, including drugs approved for other reasons. Steroids injected into the eye and Avastin injected into the eye are examples of offlabel uses of medications. Your doctor may discuss these drugs as part of treatment.

The initial results of steroids used in combination with photodynamic therapy showed better visual results than would be expected from PDT alone. Several larger trials are underway to confirm these findings.

Avastin is a drug which is related to Lucentis and acts in the same fashion. Avastin was developed to block new blood vessel growth to tumors in patients with cancer. Several reports with a limited number of patients have been published. Your doctor may consider if Avastin might be right for you.

Rheopheresis

Rheopheresis attempts to remove abnormal circulating proteins from the bloodstream. In this procedure, blood is removed from the veins in the arm and filtered with a machine to remove heavy proteins. The rest of the blood is returned to the bloodstream. This treatment is under investigation in a number of research centers. A small study has indicated there may be some beneficial effects. Larger, controlled trials are ongoing.

Low Dose Radiation Therapy

Radiation therapy for wet macular degeneration is under investigation in a number of research centers. Because growing blood vessels are sensitive to radiation, it has been suggested that radiation may stop or slow choroidal neovascularization.

Low dose radition in some studies have shown some beneficial effects.

It is not yet known if low dose radiation ca