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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.
  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 can stop or slow choroidal neovascularization. Several small studies have demonstrated some beneficial effects of radiation while other trials have shown no benefit.
   
  Implantable Miniature Telescope (IMT)
  The implantable miniature telescope is a surgical device currently in late stage trials. It magnifies the central visual images on a larger retinal area than normal to improve vision and the quality of life for patients who have lost significant vision. After surgical implantation, patients undergo a visual rehabilitation program.
  Implantable Miniature Telescope allows central vision to be projected on the central and peripheral retina.
 
  With the IMT, central vision is projected on the central and peripheral retina.
  RPE Transplantation
  In many cases of macular degeneration, it appears that the retinal pigment epithelium, or RPE layer, is the first component of the retina to fail. RPE transplantation attempts to replace diseased RPE tissues with healthy RPE cells.
  First, a vitrectomy is performed to remove the vitreous gel from the eye. Then, a small incision is made in the retina to gain access to the sub–retinal space. At this point, RPE cells are injected under the retina.
RPE Transplantation, shown here, are injected under the retina to replace atrophied or diseased RPE tissue.
  As time passes and the retina heals, it is hoped that these transplanted RPE cells will arrange themselves properly to replace lost or diseased RPE.
  This technique is still highly experimental. Although RPE cells can be implanted successfully, the cells may not form the necessary connections with their neighboring cells and tissues. Additionally, rejection of these cells by the body is possible.
   
  Macular Translocation Surgery
  Macular translocation is an experimental surgical technique. This technique aims to move the macula when it overlies diseased sub–retinal tissues.
  First, a vitrectomy is performed to remove the vitreous gel from the eye. Then, a flap of retina is detached from the underlying tissues, cut, and rotated into a new position. The rotated retina is reattached to an area of healthier sub–retinal tissue.
  At this time, this experimental technique is associated with a high percentage of serious complications.
   
  Laser Treatment of Drusen
  Most people with macular degeneration have some drusen, yellow deposits underneath the retina. Some studies have found that low intensity laser treatment causes drusen to shrink and even disappear in some people.
  Although this low intensity laser treatment can make the drusen disappear, there is no scientific proof so far that this treatment is beneficial.
  These experimental treatments are being studied by numerous researchers around the world. It is hoped that some of these procedures will lead to more effective treatment of macular degeneration in the near future.
  Low level laser energy has been found to shrink spots of drusen in some people.
 
  Low level laser energy has been found to shrink spots of drusen in some people. Studies are being conducted to determine if this procedure might stabilize or improve vision.
  Artificial Vision
  Because macular degeneration results in impaired functioning of the retina, researchers are attempting to bypass the retina using electronics or silicon chips to send signals to the brain to improve vision. Typically, surgery is required to implant the device into position. This type of technology is many years away from helping people with macular degeneration, but it may offer hope for improved visual function in the future.
   
  Health & Nutrition & PREVENTION
   
  Risk Factors
  A number of factors are known to increase the risk of developing macular degeneration. Some of these factors are within an individual’s control and can be modified through changes in behavior.
  The following factors may increase your risk for developing age–related macular degeneration:
 
  • age
  • family history of the disease
  • smoking
  • high blood pressure
  • history of cardiovascular disease
  • elevated serum lipids
  • complement factor H
  • excessive exposure to bright sunlight
  The rate of macular degeneration in the population clearly increases with age. By age 75, the odds of having this condition are greater than 1 in 3.
  If your parent or sibling has macular degeneration, you have an increased risk of developing the disease yourself.
  Smoking has been identified as a strong risk factor for macular degeneration in many studies. Smoking will triple the risk of developing macular degeneration. Even secondhand smoking doubles the risk of macular degeneration compared with the general population. It is good to know that stopping smoking will reduce the risks, and after 20 years of not smoking the risks are no different from non–smokers.
  It is particularly important for people with macular degeneration to try to stop smoking in order to protect their vision and to improve their overall health.
  Hypertension (high blood pressure) and cardiovascular disease may place additional stress on the blood vessels of the eye which could accelerate the development of macular degeneration and visual loss.
  Elevated serum lipids (cholesterol and triglycerides) have been associated with an increased risk of macular degeneration. If you have either of these conditions, it is important to follow your doctors’ recommendations for diet and medication.
Try using sunglasses and hats to protect yourself from overexposure to sunlight.
  Complement factor H is a marker of inflammation. Abnormalities in this gene have been linked with macular degeneration. Ongoing research may lead to new insights, diagnostic testing, or treatments.
  Excessive exposure of the eyes to sunlight, particularly the blue and ultraviolet wavelengths, is considered to be a risk factor for both macular degeneration and cataract formation. Try using sunglasses and hats to protect yourself from overexposure to sunlight.
 
  Sun Glasses
 
  Antioxidant Supplements
  Certain antioxidant supplements may prevent or slow the progression of macular degeneration in some people.
  The role of nutrition in the development of macular degeneration is of great interest to patients and researchers. Many studies have been conducted over the past several years to see if antioxidant supplements can prevent or slow the progression of macular degeneration.
  An important research study, the Age–Related Eye Disease Study (AREDS) , showed that one group of macular degeneration patients—those who are at high risk for developing advanced AMD — may be helped by taking supplements containing antioxidants and zinc. In this study, patients in this high–risk group lowered their risk by about 25 percent when treated with high–doses of both zinc and antioxidants.
  Supplements Used in the AREDS Study:
 
  • Vitamin C 500 mg
  • Vitamin E 400 IU
  • Vitamin A as 15 mg beta–carotene ˜25,000 IU
  • Zinc 80 mg as zinc oxide
  • Copper 2 mg as cupric oxide
  The AREDS supplements benefited patients with either form of AMD (wet or dry). In general, the supplements appeared safe when taken for the duration of the study. Patients with AMD should consult with their eye doctor to discuss how the study findings apply to their specific situation.
  The National Institutes of Health is currently sponsoring the AREDS 2, which will evaluate the benefits of oral supplementation with lutein (10 mg/day), zeaxanthin (2 mg/day), and omega-3 long-chain polyunsaturated fatty acids (1 gram/day).
  Smokers or those who quit within 5 years should not take the Vitamin A or beta-carotene.
   
  Nutrition & Diet
  Research has shown that patients who eat diets high in spinach or collard greens are less likely to develop macular degeneration. These and other green leafy vegetables such as: kale, mustard greens, turnip greens, and romaine lettuce, are good sources of two important macular pigments: lutein and zeaxanthin. These recommended nutrients are also found in: orange peppers, yellow corn, broccoli, avocados, oranges, and egg yolks.
Lutein and zeaxanthin are important nutrients found in kale, mustard greens, turnip greens, romaine lettuce, orange peppers, yellow corn, broccoli, avocados, oranges, and egg yolks.
 
  Lutein and zeaxanthin supplements were not available at the time of the Age–Related Eye Disease Study and therefore could not be tested. Many physicians may recommend supplement formulations containing lutein and zeaxanthin.
  Some people with macular degeneration have diets deficient in the mineral zinc. Zinc is found naturally in shellfish, fish, meat, oats, beans, and peas.
  The mineral zinc is found in shellfish, fish, meat, oats, beans, and peas.
 
  Research has shown that patients who eat diets high in omega–3 fatty acids are less likely to develop macular degeneration. Omega–3 fatty acids may also have a protective role against ongoing retinal damage.
 
  Good dietary sources of omega–3 fatty acids are: oily fish (salmon, sardines, tuna), fish oils, walnuts, and some plant oils (flaxseed, canola)
  For macular health, it is recommended to eat a wellbalanced diet with plenty of fruit, being careful to avoid excessive saturated fats and cholesterol. You should talk with your doctor about taking a daily multivitamin or an antioxidant supplement
  Several substances such as bilberry, ginkgo biloba, bioflavinoids, and shark cartilage have received attention in the popular media. There is no good scientific evidence regarding the safety or effectiveness of these preparations in preventing or treating macular degeneration.
   
 

MACULAR HOLE
  Unlike a camera, the image obtained by the retina is not of uniform clarity or sharpness. Only the central portion of the retina, the macula, is sensitive enough to provide high quality vision for tasks such as reading, watching television, or driving. The macula is a very small area, with the central portion being only about the size of the head of a pin. It is only this specialized area of the retina, the macula, that is capable of the detailed vision necessary for many daily tasks.
  In order to maintain its round structure, the central portion of the eye is filled with a jelly–like substance known as the vitreous. The hole is thought to be caused by the vitreous pulling on the central macula, creating a central defect in the retinal tissue. It usually occurs for no obvious reason (idiopathic), although a macular hole can also be caused by trauma or retinal detachment. Macular holes are most common in women in their 60's and are not associated with any systemic medical problems. Approximately 10% of patients with a macular hole in one eye will eventually develop a macular hole in the other eye.. This process results in a defect or dark spot in the central vision with distortion and central vision loss resulting.
 
  Clinical photo of a macular hole
  Symptoms of a macular hole are common to most conditions affecting the central part of the retina. They include: decreased central vision for both distance and reading activities, distortion in central vision, a small defect in the central vision where small letters may disappear. The diagnosis of a macular hole is made a dilated retinal examination and examines the back of the eye. A fluorescein angiogram (injection of a dye into the vein with photographs taken of the back of the eye) may be recommended to evaluate the situation and ensure that the macular hole is due to the vitreous traction as described above, and not secondary to other rare conditions in the back of the eye. OCT testing is probably the simplest test to diagnose and evaluate a macular hole as it will show a hole in the central macula.
 
  OCT of a macular hole
  What treatments are available for macular holes?
   
  1) Observation.
  Treatment for many patients with a macular hole is often not necessary, since many remain asymptomatic. Surgery should be considered, however, for those people with a relatively new macular hole whose distortion, vision loss, or difficulty with depth perception make their daily activities such as reading and driving difficult.
  2) Vitrectomy surgery. 
  Until recently, very little could be done to correct the visual deficit resulting from macular holes. As a result of the introduction of microsurgical techniques, it is now possible to offer a surgical procedure with the potential for some visual improvement. This procedure is known as a vitrectomy, and involves the microscopic surgical removal of the vitreous jell within the center of the eye. Particular attention is paid to removing any of the vitreous attachments from the macula, thus releasing the traction or pulling on the retina which caused the macular hole initially. This permits settling of the retina against the wall of the eye.
  In order to completely close the macular hole, and to have its maximal effect, the gas bubble must apply continued upward pressure against the retinal surface in the area of the macula. Because the macula is located in the back part of the eye, a patient’s head must remain in a “face–down” orientation to allow the air bubble to rise toward the back of the eye and exert this pressure. Patients must maintain this face–down position for approximately 2 weeks after surgery in order to achieve successful closure of the macular hole and maximize the chances for vision improvement. This face–down positioning is the single most critical portion of the procedure for closing macular holes. As a result, emphasis must be placed on the patient’s ability to cooperate with strict face–down positioning at all times for a period of approximately two to three weeks after surgery in order to achieve a successful outcome.
 
Patient positioned face–up. Patient positioned face–down.
  In order to increase the patient’s ability to comply with these instructions, numerous devices have been developed that assist the patient in maintaining this face–down position throughout the day and at night as well. Devices can be purchased or rented from a variety of companies that permit more comfortable positioning during sleep as well as allowing the patient to maintain a face–down position while eating and reading.
  At the end of the 2–3 week period of strict face–down positioning, the patient is then permitted to resume a more normal upright posture. The gas bubble itself, however, may take anywhere from 6–8 weeks following surgery to completely disappear. The air bubble is gradually resorbed by the body, and the vitreous cavity is then filled with liquid produced by cells in the front of the eye. Importantly, patients who have a gas bubble in their eye cannot fly in an airplane and must stay at sea level. This is because at high altitudes the gas can expand and cause the eye pressure to go up to dangerous levels.
  The surgical procedure itself is performed typically under local anesthesia and patients go home that same day. A postoperative examination within 24 hours of surgery is required in all cases. Regular follow–up examinations are performed during the first three weeks of recovery, to monitor for successful closure of the hole, observe for any potential complications, and to reinforce the importance of face–down positioning. Patients typically utilize several eye drops applied to the operated eye over the course of several weeks following the surgical procedure.
 
  Optical Coherence Tomography (OCT) after surgical repair of a macular hole
  Approximately 6–8 weeks after surgery, when the bubble has completely resorbed, the patient is measured for glasses. Full visual recovery may not occur until as late as three months after the surgical procedure.
  Vitrectomy successfully flattens the macular hole in over 75-90% of cases. With successful surgery visual acuity usually improves by about 50% although it may take several years for maximal vision to return.
As with all surgical procedures, there are potential complications or side–effects associated with the repair of the macula hole. These include a small percentage of patients who develop retinal tears or detachments during the surgical procedure itself, or in the immediate postoperative period. These problems are usually repairable.
  In patients who have not already undergone cataract surgery, the development of a cataract occurs in almost all individuals within six months to two years. Surgical removal of the cataract and placement of an intraocular lens is then required.
   
 

EPIRETINAL MEMBRANE(MACULAR PUCKER)
  Epi-retinal membrane (ERM) or macular pucker is a cellophane-like membrane that forms over the macula. It is typically a slow-progressing problem that affects the central vision by causing blur and distortion. As it progresses, the traction of the membrane on the macula may cause swelling. ERM is seen most often in people over 75 years of age. It usually occurs for unknown reasons, but may be associated with certain eye problems such as: diabetic retinopathy, posterior vitreous detachment, retinal detachment, trauma, and many others.
  Macular pucker usually occurs following separation of the vitreous from the surface of the retina (posterior vitreous detachment). Macular pucker can also occur following retinal tear or detachment, trauma, various eye inflammatory diseases, or as an isolated finding (idiopathic). It is not usually associated with medical conditions outside the eye.
 
  This thin layer of scar tissue is known as a macular pucker. Macular pucker is known by a variety of names, including epiretinal membrane, surface wrinkling retinopathy, cellophane retinopathy, and internal limiting membrane disease. All of these names relate to the fact that there is a layer of thin scar tissue on the surface of the macula which resulting in mechanical wrinkling and distortion of the retina.
 
  Clinical photo of a macular pucker. (Click image for full size image.)
  In most cases, the healing response is mild, and results in a very thin layer of cells lying on the surface of the retina. These cells may be clear and may produce no significant visual disturbance. In other cases, this healing process may progress, with an overabundance of cells being produced, forming a thicker, more opaque membrane or layer of scar tissue on the surface of the macula.
  In most patients, even with the formation of a significant macular pucker or epiretinal membrane, there is very slow growth that takes place, and eventually the scar tissue stops proliferating or extending. With time, contraction or pulling of the cells may take place, causing a wrinkled or rippled appearance to this scar tissue. Since the scar cells are attached to the retina, the retina itself becomes wrinkled in association with the progression of the scar. When this occurs in the central, critical portion of vision, the macula, visual symptoms may result.
  The symptoms of a macular pucker are common to many conditions affecting the central part of the retina. These include: distortion in lines or letters while reading, a decrease in central vision for distance and reading activities, and blurring or distortion of images when looking at television or in the theater. The diagnosis of a macular pucker is made when an ophthalmologist performs a dilated retinal examination and examines the back of the eye. A fluorescein angiogram (injection of a dye into the vein, with photographs taken of the back of the eye) may be recommended to evaluate the situation and determine if leakage or swelling of the retina is taking place as a result of the scar tissue being present on the surface of the macula. OCT testing can easily demonstrate the macular pucker on the surface of the retina.
  In most cases, no treatment is recommended for macular pucker. This is due to the fact that the visual distortion and decreased reading and distance vision is minimal in the majority of patients. Although some mild visual problems are noted, these are usually easily adjusted to and pose no limitation on full activity. In some instances, however, the distortion and vision loss may be significant. There may be an inability to perform certain daily tasks such as reading or driving. It is at this point, that consideration for surgical repair would be entertained. Surgery would also be considered if vision loss is moderate, but there is evidence on the fluorescein angiogram of significant leakage posing a threat to permanent damage to central vision in those individuals.
  Repair of a macular pucker or epiretinal membrane is accomplished through use of vitreoretinal surgery. Using microsurgical instruments, a procedure known as a vitrectomy, the microscopic removal of vitreous jell from the center of the eye, is performed. Particular attention is paid from moving any vitreous attachment from the central macular region. Specialized microsurgical instruments are then used to gently peal and remove the scar tissue from the surface of the retina, relieving the traction and reducing the distortion to the retinal surface. During the course of the surgical procedure, a fluid which is chemically similar to the fluid naturally produced by cells inside of the eye is used to replace the vitreous. As part of the procedure, careful inspection for retinal tear or detachment formation is performed, which can occur in association with the development of a macular pucker or occur as a rare complication of the surgical procedure itself. If a tear or break is found, laser treatment may be applied to these areas. Unlike macular hole surgery, macular pucker surgery does not typically involve the use of an intraocular air bubble. As a result, no specialized positioning in the postoperative period is required. However, in rare instances where retinal tears or detachments occur at the time of surgery, air bubbles and special positioning may be required.
  The surgical procedure itself is typically performed under local anesthesia and a patient may remain in the hospital overnight or may be scheduled for ambulatory surgery, able to return home by the end of the day of the surgical procedure itself. A postoperative examination within 24 hours of surgery is required in all cases. Regular follow–up examinations are performed during the first six weeks of recovery, and then at regular intervals after that. Patients typically utilize several eye drops applied to the operated eye over the course of several weeks following the surgical procedure.  
  Approximately 10–12 weeks after surgery, when the eye has recovered from the surgery and the macula has had a chance to return to a more normal configuration, the patient is measured for glasses. Full visual recovery may not occur for at least 3–4 months following the procedure.
  As with all surgical procedures, there are potential complications and side–effects associated with repair of macular pucker. As mentioned, these include a small percentage of patients that develop retinal tears or detachments during the procedure or in the immediate postoperative period. These problems are usually easily repairable. In patients who have not already undergone cataract surgery, development of a cataract may occur more rapidly following vitrectomy surgery. Surgical removal of the cataract and placement of an intraocular lens is then required.
   
 

CENTRAL SEROUS CHORIORETINOPATHY
  Central serous chorioretinopathy is a retinal disorder which affects the macula. Essentially, it is an “idiopathic disorder” which means that the precise cause is unknown. Central serous is associated with an elevation (detachment) of the macula due to leakage of fluid from the circulation behind it (choroidal circulation). The leakage occurs through a defect in the tissue layer known as the retinal pigment epithelium. The retinal pigment epithelium is a single–celled layer that lies between the retina and the choroid . This tissue layer normally serves to prevent fluid from the choroidal circulation from leaking under the retina. In central serous, fluid equilibrium is disturbed leading to leakage beneath the retina which elevates it to produce a macular detachment which distorts vision.
 
  Cross section of the eye wall
  Clinical Features and Demographics
  The syndrome is much more common in men who represent 85–90% of the cases. The onset is usually between the ages of 25 and 45, although, occasionally, a younger patient may be diagnosed with this disease. Older patients will continue to have signs of central serous when they developed it as a younger person, but some of the classic or typical features will be modified by age–related changes.
  Central serous patients in general tend to be slightly hyperopic (far–sighted) but not to have other eye disease. The condition is more common in Caucasians, Hispanics and Asians than in African–Americans who get this condition only rarely.
  There has always been an impression that patients with central serous exhibit a characteristic personality. Patients have been observed to be energetic, dynamic, harried, pressured, and emotionally stressed. One of our earlier reports has identified the Type A Behavioral Pattern as a risk factor for the disease.
   
  Clinical Findings
 
Normal macula       demonstrating a serous neurosensory detachment (red arrow).
 
  Clinical photo of a patient with central serous chorioretinopathy (CSC)
  Patients usually present with a disturbance in central vision, either a gray zone or a blind spot in the central field or metamorphopsia which is waviness or undulation in the central portion of the vision. On clinical examination, the ophthalmologist may find one or more small blister–like elevations to the retinal pigment epithelium. In the acute stages, there is an overlying elevation of the neurosensory retina. Occasionally, patients who have detachments of the retina are asymptomatic, simply because the bubble of fluid does not involve the center of the macula or the foveal region. Signs of previous detachments of the retina can often be detected by the clinician. These are atrophic and pigmentary degenerative zones in the retina. When the neurosensory retina is elevated, it is displaced from its normal source of nutrition, the choroidal circulation. In time, the outer retina may become degenerated. Even when the macula resolves and is no longer detached, it does not function because of the degenerative change. (Thus, there is a rationale for reattaching the macula, if possible, see treatment, below.)
  An important part of the diagnosis of central serous relies on the fluorescein angiogram. In the typical case, a leak can be demonstrated at the level of the retinal pigment epithelium as the fluorescein dye gradually passes into the subneurosensory retinal space. This is the hallmark angiographic feature of the disorder in its classic form. The leaks will vary, depending on the duration of the detachment and the nature of the fluid.
 
Early-phase fluorescein angiogram showing two small leaks (arrows). Fluorescein dye progressively leaks beneath the retina causing central visual distortion and blurriness.
  Some severe variants of the disease are seen in patients who have certain systemic diseases such as severe hypertension, collagen vascular disorders, blood dyscrasias, and organ transplant. The use of corticosteroids may also be a risk factor for central serous
   
  What treatments are available for central serous chorioretinopathy?
  1) Observation.
  Treatment for most patients with CSC is usually not necessary since most cases resolve spontaneously within 3 to 4 months. Early treatment should be considered, however, for those people whose distortion, vision loss, and difficulty with depth perception make their daily activities such as reading and driving difficult. Treatment is also considered if visual symptoms remain for persistent central blisters.
   
  2) Laser photocoagulation surgery.
  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.
  Photocoagulation decreases the duration of CSC by several months, although it appears to have little effect on the final vision or recurrence rate.
 
Preoperative CSC.    Postoperative CSC.
  3) Photodynamic surgery.
  Photodynamic therapy, traditionally used for treating macular bleeding (choroidal neovascularization) in age-related macular degeneration and ocular histoplasmosis, has emerged as an effective treatment for some eyes with CSC. The outpatient procedure is painless and performed in our office. A special photodynamic dye is injected into an arm vein. Fifteen minutes later, a "cold" laser light is aimed at the choroidal neovascularization which selectively absorbs the dye. The laser light activates the dye, causing the production of a very active form of oxygen (singlet oxygen) that seals the leak. Patients can go home immediately following photodynamic therapy but must avoid direct sunlight for 2 days following treatment to avoid skin burns from the dye.
  Prognosis
  The prognosis for visual recovery in central serous is generally good. Usually, the pigment epithelial leaks closes spontaneously and the detachment resolves over a period of weeks to months. Most patients (greater than 90%) will retain vision of 20/30 or better in the affected eye. Although many patients may manifest subtle clinical findings in the opposite eye, most patients (greater than 80%) do not develop bilateral symptoms. Despite good acuity, some of these patients may still note some mild permanent abnormalities in the vision of the affected eye such as decreased contrast, mild distortion and decreased night vision. Reported recurrence rates are 20–30% although we have observed a higher rate among the patients referred to our group (perhaps a more severely affected group since we tend to be referred challenging cases). Weeks, months or even years later, new detachments may evolve. Each detachment runs the risk of further pigment epithelial and retinal damage. Some patients will experience progressive atrophy of the pigment epithelium and severe vision loss, which is permanent. Other patients may develop expanding detachments of the retina as fluid gravitates to detach the inferior retina.
   
 

RETINAL VEIN OCCLUSIVE DISEASE
  Retinal vein occlusion is an eye condition commonly seen by retinal specialists. It is second only to diabetic retinopathy as a cause of visual loss due to retinal vascular disease. There are two forms of retinal vein occlusion, branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO). While there are similarities in the pathogenesis and clinical nature of these two events, each has unique etiologies, differential diagnosis, management and prognosis.
 
  Color photograph showing segmental intraretinal hemorrhage of a branch retinal vein occlusion.
  A branch retinal vein occlusion is essentially a blockage of the portion of the circulation that drains the retina of blood. The arteries deliver blood to the retina. The red blood cells and plasma then course through the capillaries and eventually into the venous system, beginning with small veins and ending with larger ones, and eventually reaching the central retinal vein. With blockage of any vein, there is back–up pressure in the capillaries, which leads to hemorrhages and also to leakage of fluid and other constituents of blood. Usually, the occlusion occurs at a site where an artery and vein cross. The occlusion site determines the extent or distribution of the hemorrhage, ranging from a small vein branch to a quadrantic occlusion involving one fourth of the retina to a hemispheric (hemi–retinal) occlusion involving one half of the retina to an occlusion of the central retinal vein, which involves the entire retina (when the central vein is involved, this is called a central retinal vein occlusion which is discussed below).
  Branch retinal vein occlusions are by far the most common cause of retinal vascular occlusive disease. Males and females are affected equally. Most occlusions occur after age 50, although younger patients are sometimes seen with this disorder (in this age group it is often called papillophlebitis). The highest rate of occurrence is in individuals in their 60’s and 70’s. The risk factors for this disorder are similar to those for vascular occlusive disease elsewhere in the body such as stroke and coronary artery disease. Specifically, aging, high blood pressure, diabetes, and smoking are all risk factors. Glaucoma has also been identified as a risk factor in some studies. There are less common conditions which may put a patient at risk for developing a vein occlusion including blood clotting abnormalities such as hyperhomocysteinemia, activated protein C resistance (Factor V Leiden), protein C and S deficiency, anti–phospholipid antibodies and diseases which cause sludging of the circulation or so–called hyperviscosity. Inflammatory and infectious conditions which cause vasculitis such as sarcoidosis and tuberculosis are also risk factors for vein occlusion. In general, unless there is a reason to suspect these less common conditions (such as young age, history of previous thrombophilia, or history suggestive of inflammation or infection), exhaustive laboratory testing is usually not indicated. Most patients are referred to their internist for the appropriate medical evaluations.
  The diagnosis of a retinal branch vein occlusion poses little difficulty to an ophthalmologist who will detect dilated blood vessels, hemorrhages, and swelling (edema) in the distribution of the vein. It appears that the more complete the blockage, the more intense the hemorrhages and the edema. In fact, the blockage may be so dramatic that the involved capillaries cease to function and close off (ischemia or capillary non–perfusion). About 10% of patients suffering from a branch vein occlusion will experience a branch or a central vein occlusion in the fellow eye in the future.
  There are three complications of branch retinal vein occlusion which threaten vision: macular edema, macular ischemia (non–perfusion) and neovacularization (growth of new abnormal blood vessels).
  When the distribution of the vein involves the center of the retina (macula), bleeding and exudation or leakage occurs there, producing symptoms. Leakage in the macula causes macular edema in which a patient will have blurred vision and loss of portions of the field of vision (corresponding to the distribution of the obstructed vein). Basically, the edema damages the architecture of the retina, causing these symptoms. These visual changes can be monitored with an Amsler grid. A fluorescein angiogram and OCT may be useful in evaluating macular edema and determining whether treatments with laser or pharmacological therapies are necessary (see below).
 
  OCT showing macular edema from a branch vein occlusion
  In the first three to six months after the occurrence of the branch vein occlusion, there is often significant intraretinal hemorrhage that involves the macula, making it difficult to predict the clinical course and visual outcome. After the first few months, it may be useful to do a fluorescein angiogram and OCT. Fluorescein angiography is helpful in analyzing the retinal circulation, particularly the capillaries which may manifest abnormalities such as leakage or macular ischemia (non–perfusion: closure of blood vessels which supply the retina with oxygen and other nutrients). OCT is useful for detecting retinal swelling (edema).
  If the fluorescein angiogram indicates that capillary non–perfusion is the cause of the vision loss, it is unlikely that the vision will improve significantly over time. However, if the poor vision is due to edema or swelling, laser photocoagulation or pharmacological therapies, such as steroids or anti–vasogenic drugs (eg. Avastin), may be useful in sealing leaking capillaries to enhance resolution of the edema for stabilization and improvement of the vision. Intraocular steroids, which are commonly used as a treatment for macular edema, increase the chance of cataract formation and elevation of intraocular pressure (steroid–induced glaucoma).
  Sometimes in venous occlusive disease, scar tissue can form on the surface of the retina. This condition, which is called a macular pucker or an epiretinal membrane may result in distorted vision (metamorphopsia) which is not improved with laser or pharmacologic treatment. Vitrectomy surgery may be indicated for the removal of a macular pucker.
  The most devastating potential problem in a vein occlusion is that of neovascularization. The neovascularization may develop in 40% of those cases where branch vein occlusions produce large areas of capillary non–perfusion. This retinal neovascularization generally develops in the first 6 to 12 months after the occlusion. Unless laser treatment is performed, at least 60% of the patients with neovascularization will experience episodes of vitreous hemorrhage. In severe cases of neovascularization, retinal detachment can occur from pulling by these vessels and associated scar tissue on the retina (traction detachment).
  Laser photocoagulation treatment is a proven therapy for neovascularization in vein occlusions. Indeed, laser treatment can cause stabilization or, at times, regression of the vascular growth. This treatment, while important in helping to prevent further visual loss, is not usually associated with improvement in vision. As vein occlusions evolve, some normal vessels may dilate to compensate for the obstructed vein. Sometimes, these collateral vessels may be difficult to distinguish from neovascularization on clinical examination. A fluorescein angiogram may be useful in this determination.
  Recently, the intraocular injection of anti–vasogenic drugs, that tell blood vessels to stop growing, has shown promising results in the control of retinal neovascularization. These treatments have not yet been assessed in prospective clinical trials but may be used on an off–label basis. One particular medication that has been increasingly utilized for this purpose is Avastin, 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. Avastin lasts about 6 weeks in the eye after a single injection and may need to be repeated if the disease reactivates. Although an injection into the eye sounds painful, it is simple to perform, relatively painless, and very well tolerated by patients.
  There is no known medical treatment for retinal branch vein occlusion. Anti–coagulants such as heparin, coumadin and aspirin have not been shown to be of value in preventing branch vein occlusion or managing its complications. Because anti–coagulants may be associated with systemic complications, they are prescribed only in specific clinical circumstances, for example for patients with known clotting abnormalities.
   
 

CENTRAL RETINAL VEIN OCCLUSION
 
  This is a color photograph showing diffuse intraretinal hemorrhage of a central retinal vein occlusion.
  Central retinal vein occlusion is closure of the final retinal vein (located at the optic nerve) which collects all of the blood after it passes through the capillaries. The systemic risk factors for branch retinal vein occlusion mentioned above are also risk factors for central retinal vein occlusion.
  Central retinal vein occlusion is generally categorized into two forms: non–ischemic and ischemic. This means that some central retinal vein occlusions are associated with a significant obstruction of capillaries or non–perfusion. This predisposes to a peculiar type of neovascularization that occurs in front of the eye on the iris (rubeosis irides). These eyes may develop a very high pressure known as neovascular glaucoma due to obstruction of the fluid outflow channels. This is a very serious complication which is associated with severe vision loss and may cause pain and loss of the eye itself. Laser photocoagulation treatment is very useful in managing rubeosis irides. If performed early in the course (when iris neovascularization is first detected), it may help prevent these complications. Patients with recent central retinal vein occlusions must be followed frequently in order to detect this complication in a timely manner.
  Less frequently than in branch vein occlusion, patients with central retinal vein occlusion, may also develop neovascularization in the back of the eye, causing vitreous hemorrhage and retinal detachment. Laser treatment may be useful in managing these complications.
  As with branch retinal vein occlusion, macular edema and non–perfusion are also frequently seen with central retinal vein occlusion. Macular edema, even without significant macular ischemia, is not treated routinely with laser photocoagulation. This is because a recent study failed to show a benefit for patients with central retinal vein occlusion, particularly for those who are elderly. (In contrast, laser treatment has been shown to be effective for patients with branch retinal vein occlusion). It is possible, but not proven, that some young patients with central vein occlusion of the non–ischemic type may benefit from localized laser treatment for macular edema.
 
  Optical Coherence Tomography showing macular edema from a central vein occlusion
  Some patients with macular edema from central vein occlusions may respond to the off–label intraocular injection of steroids (triamcinolone) or anti–vasogenic drugs (Avastin). These pharmacologic agents wear off over a period of approximately two months and may need to be re–injected if the edema returns. Optical Coherence Tomography (OCT) is a useful test for the detection of macular edema in CRVO and for following the response to treatment.
  If the fluorescein angiogram indicates that capillary non–perfusion is the cause of the vision loss, it is unlikely that the vision will improve significantly over time regardless of any treatment.
  If a patient develops an occlusion of the central vein in both eyes, there is a greater possibility of an underlying systemic cause. It is recommended (by our group) that such patients have a thorough medical work–up as outlined previously.
  Sometimes in venous occlusive disease, scar tissue can form on the surface of the retina. This condition, which is called a macular pucker or an epiretinal membrane may result in distorted vision (metamorphopsia) which is not improved with laser or pharmacologic treatment. Vitrectomy surgery may be indicated for the removal of a macular pucker.
  The most devastating potential problem in a vein occlusion is that of neovascularization. The neovascularization may develop in 40% of those cases where branch vein occlusions produce large areas of capillary non–perfusion. This retinal neovascularization generally develops in the first 6 to 12 months after the occlusion. Unless laser treatment is performed, at least 60% of the patients with neovascularization will experience episodes of vitreous hemorrhage. In severe cases of neovascularization, retinal detachment can occur from pulling by these vessels and associated scar tissue on the retina (traction detachment).
  Laser photocoagulation treatment is a proven therapy for neovascularization in vein occlusions. Indeed, laser treatment can cause stabilization or, at times, regression of the vascular growth. This treatment, while important in helping to prevent further visual loss, is not usually associated with improvement in vision. As vein occlusions evolve, some normal vessels may dilate to compensate for the obstructed vein. Sometimes, these collateral vessels may be difficult to distinguish from neovascularization on clinical examination. A fluorescein angiogram may be useful in this determination.
  Recently, the intraocular injection of anti–vasogenic drugs, that tell blood vessels to stop growing, has shown promising results in the control of retinal neovascularization. These treatments have not yet been assessed in prospective clinical trials but may be used on an off–label basis. One particular medication that has been increasingly utilized for this purpose is Avastin, 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. Avastin lasts about 6 weeks in the eye after a single injection and may need to be repeated if the disease reactivates. Although an injection into the eye sounds painful, it is simple to perform, relatively painless, and very well tolerated by patients.
  In summary, retinal vein occlusions develop from obstruction of the venous outflow from the eye. The blockage may vary in size and location, accounting for a wide range of retinal outcomes. Some of the complications of retinal vein occlusion may be appropriately managed with laser treatment. It is hoped that through further research, even better strategies for prevention and management will be developed.
 

OTHER RETINAL CONDITIONS
 
  • Retinal Artery Occlusion
  • Choroidal Nevus
  • Choroidal Neovascular Membrane (CNVM)
  • Cystoid Macular Edema
  • Ocular Histoplasmosis Syndrome
  • Retinitis Pigmentosa
  • Stargardt’s Disease
  • Temporal Arteritis (Giant Cell Arteritis)
  • Uveitis
   
  Retinal Artery Occlusion
  A retinal artery occlusion occurs when the central retinal artery or one of the arteries that branch off of it becomes blocked. This blockage is usually caused by a tiny embolus (blood clot) in the blood stream. The occlusion decreases the oxygen supply to the area of the retina (i.e., a retinal "stroke") nourished by the affected artery, resulting in permanent vision loss.
  The following conditions increase your risk of retinal artery occlusion:
 
  • High cholesterol
  • Heart disease
  • Arteriosclerosis
  • Hypertension
  • Diabetes
  • Glaucoma
   
  Signs and Symptoms
  * Sudden, painless, loss of vision in one eye (complete loss of vision for central artery occlusion, partial loss of vision for branch artery occlusion)
 
  Treatment
  Unfortunately, there is no treatment that can consistently restore vision lost from an artery occlusion. However, if the problem is caught within the first hour and treatment begins immediately, partial recovery may be occasionally possible.
   
  Choroidal Nevus
  A nevus is a flat, benign, pigmented area that may appear inside the eye or on its surface. Nevi commonly appear on the choroid, the iris, and the conjunctiva. They are similar to freckles and don’t typically change shape or grow.
  Signs and Symptoms
 
  • Brownish, freckle-like spot
  • Usually flat
  Treatment
  Though most nevi are harmless, they should be monitored for changes. Your doctor may take photos or use ultrasound to document the size, shape, and other characteristics of the nevus. In rare cases, the nevus may be biopsied and examined for melanoma (cancer) cells.
   
  Cystoid Macular Edema
  Cystoid macular edema (CME), or swelling of the macula, can occur as a result of disease, injury, or, occasionally, eye surgery. With CME, fluid collects within the layers of the macula, causing blurred, distorted central vision. Though this eye condition rarely causes a permanent loss of vision, recovery is often a slow, gradual process. Most patients recover in two to 15 months.
  Signs and Symptoms
 
  • Blurred central vision
  • Distorted vision (straight lines may appear wavy)
  • Vision is tinted pink
  • Light sensitivity
 
  CME Treatment
  Many cases of CME can be treated with anti-inflammatory drops. Occasionally, medication is injected near the back of the eye for a more concentrated effect. Oral medications are sometimes prescribed to reduce swelling.
   
  Ocular Histoplasmosis Syndrome
  Histoplasmosis is caused by a fungus commonly found in the dust and soil of the Mississippi-Ohio River Valley region. About 62 percent of all adults living in this region are carriers of the syndrome. Men and women are equally affected.
  Histoplasmosis is contracted by inhaling dust that carries the fungal spores. The effect of the syndrome on the body varies greatly from one person to another. Many carriers have no symptoms at all, while others experience flu-like symptoms and mild respiratory infections. People who already have a weakened immune system are more likely to be seriously effected by histoplasmosis.
  The fungus can affect the eye by causing small areas of inflammation and scarring of the retina. These are called “histo spots” and can occur in both eyes. The affect of histo spots on vision depends on their location. Spots in the peripheral area of the retina may have little or no impact on vision, while those located in the center of the macula may cause prominent blind spots.
  Most people with histo spots in the retina are completely unaware of their presence unless the central vision is affected. Studies indicate that only about 5 percent of people with histo spots are at risk of losing vision.
  Signs and Symptoms
  Many patients with histo spots have no symptoms. Others may experience the following:
 
  • Distorted vision
  • Blind spots
  • Scars in the retina, ranging in severity
 
  Histoplasmosis Treatment
  Often, ocular histoplasmosis does not require any treatment. If you are diagnosed with this condition, your doctor will probably recommend that you closely monitor your central vision with an Amsler grid. When the condition causes abnormal blood vessels to develop in the central retina, laser treatment may be used. In some cases, surgical removal of the tiny, abnormal vessels has been successful.
   
  Retinitis Pigmentosa
  Retinitis pigmentosa (RP) is a rare, hereditary disease that causes the rod photoreceptors in the retina to gradually deteriorate. The rods are located at the edge of the retina and are responsible for peripheral and night vision.
  People with RP usually first notice difficulty seeing in dim lighting and gradually lose peripheral vision. The effect this disease has on vision can range from mild problems to blindness.
  RP affects males more than females. Though it is frequently diagnosed during childhood, some people do not have noticeable symptoms until later in life.
 
  Signs and Symptoms
 
  • Difficulty seeing in dim lighting
  • Tendency to trip easily or bump into objects when in poor lighting
  • Gradual loss of peripheral vision
  • Glare
  • Loss of contrast sensitivity
  • Eye fatigue (from straining to see)
  Retinitis Pigmentosa Treatment
  Currently, there is no standard retinitis pigmentosa treatment or therapy available to patients at our practice. However, Vitamin A palmitate have been found to slow down progression, and researchers are studying possible treatment options such as retinal implants and drug therapy. Work is also being done to isolate the genes that are responsible for the disease.
 
  Stargardt's Disease
  Stargardt's disease (also known as fundus flavimaculatus) is a type of macular degeneration that typically surfaces before the age of 20. This disease is an inherited disorder that causes a progressive loss of central vision of both eyes, but does not affect peripheral vision.
  Signs and Symptoms
  Stargardt's is a progressive disease. Symptoms may be mild at first, but will usually worsen over time. Early symptoms include:
 
  • Blurred vision not correctable with glasses or contact lenses (this is one of the earliest symptoms)
  • Difficulty adapting from bright sunlight to a dimmer room
  • Later symptoms
  • Progressive deterioration of central vision
  • Missing areas of central vision
  • Central blind spot
  • Diminishing ability to perceive colors
  Treatment for Stargardt’s
  Unfortunately, there is no known cure for Stargardt's.
 
  Temporal Arteritis (Giant Cell Arteritis)
  Temporal arteritis, also known as giant cell arteritis, is an inflammatory condition that affects the medium-sized blood vessels that supply the head, eyes, and optic nerves. Patients with temporal arteritis experience swelling and tenderness in the blood vessel of the temple and scalp. The disease is most common in people over age 60 and affects women about four times more than it affects men.
  If allowed to progress, temporal arteritis can be sight threatening. Vision loss occurs when the inflamed arteries obstruct blood flow to the eyes and optic nerves. Temporal arteritis may also start to affect arteries in other areas of the body.  Prompt treatment of this condition is essential to prevent permanent vision loss and other health problems.
  Signs and Symptoms
  Patients with temporal arteritis usually notice visual symptoms in one eye at first, but many notice symptoms in the fellow eye within days if the condition is untreated. The following are some of the most common warning signs of the condition:
 
  • Headache
  • Tenderness of scalp (combing hair may be painful)
  • Pain in temple area (may be excruciating)
  • Transient blurred vision
  • Loss of appetite
  • Fever
  • Fatigue
  • Depression
  • Drooping lid
  • Double vision
  • Sore neck
  • Jaw soreness, especially when chewing food
  Treatment
  The ophthalmologist often works in conjunction with the patient's internist to treat this disease. The primary treatment is oral steroid medication to reduce inflammation. Most patients notice an improvement in their symptoms within several days of receiving treatment. In some cases, long-term steroid use is necessary.
 
  Uveitis
  Uveitis is a general term that refers to inflammation or swelling of the structures of the eye that are responsible for its blood supply. These structures are collectively known as the uveal tract, and include the iris, ciliary body, and choroid. Uveitis is often caused by infection or underlying disease, but sometimes the cause is unknown. The condition usually affects people between 20 and 50 years of age.
  Forms of Uveitis
  There are four main categories of uveitis:
 
  • Anterior Uveitis (also known as Iritis) - involves the iris and ciliary body and is the most common type
  • Intermediate Uveitis - affects the ciliary body, vitreous, and retina
  • Posterior Uveitis - involves the retina, choroid, and optic nerve
  • Diffuse Uveitis - affects structures both in the front and back of the eye
  Signs and Symptoms
  Anterior
 
  • Light sensitivity
  • Blurred vision
  • Redness around the iris
  • Pain that may range from aching or soreness to intense discomfort
  • Small pupil
  • Tearing
  • Elevated intraocular pressure
  Intermediate
 
  • Often affects both eyes
  • Floaters
  • Blurred vision
  Posterior
 
  • Blurred vision
  • Pain (if the optic nerve is involved)
  Diffuse
 
  • Combination of symptoms from anterior, intermediate, and posterior uveitis
  Uveitis Treatment
  The appropriate treatment for uveitis is dependent on the severity of the disease and the ocular structures involved. Topical eye drops and/or oral medications may be prescribed to reduce inflammation. In some cases, medication is required to reduce intraocular pressure.
  After inflammation has subsided, treatment may be required for secondary conditions such as cataracts, glaucoma, or the presence of scar tissue.
 
 

AMSLER GRID
 
 
  This test is designed to find abnormalities in the macula, the reading area of the eye.  It helps to find many problems early, when they may still be treatable. Ideally the Amsler grid should be examined daily.  It is often easier to remember to look at the grid if it is placed where you are sure to see it, such as on the refrigerator or the bathroom mirror.
  The grid consists of a pattern of vertical and horizontal lines with a dot in the center.  Test each eye separately, covering the other eye.  Glasses should be worn if they are normally needed for reading, hold the grid at approximately 18 inches from your face .  You should look only at the central dot and while doing this, notice whether all of the lines are present.
  You should also look for any areas where the lines are wavy or distorted.  Any areas where the grid is missing, wavy, or distorted, that are significantly different from your baseline should be reported to your eye doctor immediately.
 
   
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