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Diabetic Macular Edema

Diabetic macular edema (DME) is swelling of the macula, or central retina, in patients with diabetes mellitus. The retina is like the film in a camera, and the central part of the retina is the most important for detailed central vision. The retina is fed by a tree of blood vessels. Diabetes affects the blood vessels in the eye and may cause them to leak. When fluid leaks out of the retinal blood vessels, it collects in the retina and causes the retina to swell like a sponge. When the retina is swollen, central vision may be blurred or distorted.

Diabetic Macular Edema

Diabetic macular edema is the leading cause of vision loss in patients with diabetes mellitus. DME is more likely to occur with longer duration of diabetes and poor control of diabetes. High blood pressure also increases the risk of DME.

Vision loss from diabetic macular edema tends to occur gradually over time. Diabetic changes in the retina are almost always visible before diabetic macular edema occurs, which is why regular examination of the retina is important for all diabetic patients. It is easier to maintain good vision by preventing DME in the first place rather than treating it after it occurs.

EVALUATION. Your retinal surgeon may order diagnostic tests in the office to determine the degree of diabetic swelling and damage to the retina. Optical coherence tomography (OCT) is a scan of the retina that locates and measures swelling. Fluorescein angiograph identifies poor blood flow and fluid leakage in the retina.

TREATMENT. Treatment of diabetic macular edema involves good control of blood sugar, good control of blood pressure, and not smoking. Without controlling these, the success rate of any treatment is reduced. Treatments for diabetic macular edema include laser as well as injections. In many cases, treatment involves a combination of these therapies. Your retinal surgeon is trained in the most effective use of these treatments and will tailor the treatment to your individual eyes.

Medications that can be injected into the eye (intravitreal injections) for treatment of diabetic macular edema include bevacizumab (Avastin, which is used off-label for this condition), ranibizumab (Lucentis, which is FDA approved for this condition), aflibercept (Eylea, which is FDA approved for this condition), dexamethasone (Ozurdex, which is FDA approved for this condition) and triamcinolone (a steroid which is used off-label for this condition) which can be injected around the side of the eye.

It is important to understand that the first goal of treatment is the prevention of further vision loss, which is likely to happen without treatment. The second goal of treatment is improvement of the vision. Modern treatments are very effective at both of these goals, particularly when diabetes and high blood pressure are well controlled.

With a combination of the best treatments available, we reduce the risk of further vision loss by at least half. The chance of visual improvement is about 15% with laser treatment. The chance of visual improvement is higher with injections of steroids or Avastin but repeated injections are usually needed to maintain these improvements. The longer the retinal swelling has been present, the harder it is to improve vision, since some degree of vision loss may become permanent over time.


Proliferative Diabetic Retinopathy

Proliferative Diabetic Retinopathy

Proliferative diabetic retinopathy is a serious complication of diabetes mellitus. Damage to the retinal blood vessels causes release of a chemical mediator known as VEGF which causes abnormal new blood vessels to grow and proliferate like weeds. These new blood vessels may leak and bleed, causing vision loss. If these vessels continue to grow, they may cause scar formation and pull the retina off the wall of the eye.

Proliferative Diabetic Retinopathy (PDR) often occurs without any early warning signs, which is why regular retinal examination is critical in patients with diabetes. Bleeding from abnormal blood vessels may be seen as floaters in the vision, or as dramatic vision loss if a large amount of bleeding occurs suddenly. This blood may clear on its own over weeks or months, and sometimes the blood may not clear in which case surgery is required.

Gradual vision loss may occur from scar formation on the retina. The scarring can cause traction on the retina resulting in loss of vision. Surgery may be required to remove the scar tissue.

EVALUATION. Proliferative diabetic retinopathy is generally diagnosed by an eye care professional. Diagnostic imaging is sometimes needed. This testing may include fluorescein angiography (a yellow dye is injected into a vein in your arm and rapid sequence photos are taken of your eye), ocular ultrasound (a probe is placed on your eyelid and reflected sound waves produce images on a screen) and optical coherence tomography (light beams are sent into your eye and the reflected light is then processed by a computer). All of these tests have almost no side effects and are essentially painless.

TREATMENT. There are various methods of treating proliferative diabetic retinopathy. These methods may be employed individually or together.

Laser Treatment: Panretinal photocoagulation (PRP) laser treatment creates hundreds of small laser burns throughout the peripheral retina, thereby improving the flow of oxygen to the central retina, which is most important for everyday vision. The application of laser also decreases the stimulus for new blood vessel growth. This treatment may be done in one or more sessions. This treatment is highly effective and has saved vision in millions of patients.

Micro-incisional sutureless vitrectomy surgery: This procedure is recommended in cases of advanced bleeding or scarring inside the eye. Vitrectomy surgery is performed in an operating room. Tiny needle-sized incisions are made in the eye. The surgeon views the interior of the eye through a microscope while using fine instruments to remove blood, clear out scar tissue, repair the retina and perform laser treatment.

Anti-VEGF therapy: This form of therapy causes stabilization and temporary shrinkage of the new blood vessel formations, thus decreasing the likelihood of bleeding. The medicine is injected into the eye in the office after numbing medicines are given. The anti-VEGF medication has a temporary effect and may need to be repeated periodically depending on the response to treatment. This treatment is sometimes used prior to vitrectomy surgery or in combination with laser.

The development of diabetic retinopathy is related to the severity and length of time with diabetes. Control of blood sugar and blood pressure are of paramount importance in preventing diabetic retinopathy. Additionally, it is extremely important to avoid cigarette smoking. Smoking significantly increases the risk that a diabetic patient will develop diabetic retinopathy. Finally periodic eye exams by an eye care professional are the best way to preserve vision. Early detection of retinopathy followed by appropriate treatment reduces the chance of blindness.


Diabetic Retinopathy: The big picture

Diabetes affects about one fifth of the American adult population, and diabetic retinopathy is the leading cause of legal blindness in this group. Diabetes affects the eyes in the same way that it affects the kidneys and other organs: small blood vessels are damaged and over the years, this can result in permanent tissue damage. Vision loss in diabetes is due primarily to damage in the retina.

The retina is like the film of the camera. Just as focusing the lens of a camera will not create a clear picture if the film is damaged, getting a pair of glasses will not improve the vision if diabetes has damaged the retina.

Diabetes causes even more damage when combined with high blood pressure, so controlling both is important to prevent blindness. Diabetic retinopathy is more common in patients with poorly controlled diabetes and patients with more years of diabetes. Diabetic retinopathy may already be present at the time of diagnosis of adult onset (Type II) diabetes.

Diabetic retinopathy begins long before the vision is affected. Regular examination of the retina is important to identify and treat diabetic retinopathy before vision loss occurs. Once the vision is affected, treatments can often improve the vision, but it may never return to normal even with treatment.

Diabetic retinopathy causes vision loss in three main ways:
Blood vessels begin to leak fluid, like a garden hose with holes in the side. This fluid collects in the retina and causes swelling, called diabetic macular edema. Central vision may be reduced.
Abnormal blood vessels grow out of the retina into the middle of the eye. These blood vessels may break and bleed into the middle of the eye, or they may continue growing and start pulling the retina off the wall of the eye. This is called proliferative diabetic retinopathy.
Blood vessels may become blocked and starve the retina of oxygen. If this process, called ischemic retinopathy, continues long enough, the retina may permanently lose function.

Controlling blood sugars and high blood pressure is critical to the treatment of all forms of diabetic retinopathy. Without good control of blood sugar and blood pressure, all other treatments are less likely to have positive outcomes. Diabetic macular edema is treated with laser or injections of medicine into the eye in order to stop the leakage of fluid. In some cases, surgery may help as well. Proliferative diabetic retinopathy is treated with laser photocoagulation. In some cases, micro-incisional vitrectomy surgery may be required to remove blood in the eye or to remove scar tissue pulling the retina away from the wall of the eye (retinal detachment).


Wet Age-related Macular Degeneration

Age-related macular degeneration (AMD) is a condition that affects the central retina (macula), which is most important for reading vision and daily tasks. Wet AMD is an advanced form of the disease and can cause rapid and severe loss of central vision in one or both eyes. Wet AMD is also known as neovascular AMD or exudative AMD. Until only a few years ago, a diagnosis of wet AMD meant unavoidable loss of vision, but treatments available for the last several years have finally allowed doctors to control the disease and even improve vision in some cases.

Wet AMD

The onset of age-related macular degeneration is determined largely by genetics. However, only a small fraction of individuals with AMD go on to develop the advanced wet form, and this progression cannot be predicted by genetics. Smoking greatly increases the risk of developing wet AMD. There is good scientific evidence that patients with intermediate stage AMD can reduce their chance of developing wet AMD by using a specific vitamin supplement called the AREDS supplement.

In the wet form of AMD, abnormal blood vessels grow behind the retina. These blood vessels can leak fluid or they can break and bleed. When blood and fluid collect behind the central retina, vision can drop dramatically.

EVALUATION. Because several different diseases can produce blood or fluid in the central retina, your retina specialist will usually order tests to confirm the diagnosis of wet AMD and also document a starting point for treatment in order to measure progress over time. Optical coherence tomography (OCT) is a fast, non-invasive laser scan of the retina which measures and locates fluid in and behind in the retina. Fluorescein angiography (FA) identifies leakage of fluid under and within the retina with a series of photographs taken after intravenous injection of fluorescein dye.

TREATMENT. The primary treatment for wet AMD is injection of medication into the eye. The leakage of blood and fluid in wet AMD is caused by a hormone called VEGF (vascular endothelial growth factor). The medicines injected into the eye block this hormone (anti-VEGF medicines). There are three anti-VEGF medicines currently injected into the eye as treatment for wet AMD:

LUCENTIS. Lucentis (ranibizumab) was developed for use in wet AMD and is FDA-approved for this purpose. The medicine is very expensive (approximately $2,000 per injection). In most cases the cost is covered partially or completely by health insurance. The medicine is almost always given repeatedly, at monthly intervals or less frequently, in order to achieve the best effect. Lucentis has been studied extensively in large randomized clinical trials, providing the highest quality evidence for its effectiveness.

AVASTIN. Avastin (bevacizumab) works almost exactly the same way that Lucentis works. Avastin was initially developed for intravenous use in patients with colon cancer and it is FDA-approved for that purpose. For more than 5 years, retina specialists have been injecting Avastin off-label into the eye for treatment of wet AMD. The cost per injection is much lower than Lucentis. Avastin is thought by many retina specialists to work as well as Lucentis. Avastin has been studied carefully, but large randomized clinical trials have not been completed for Avastin use in wet AMD the way they were for Lucentis. A large randomized clinical trial is currently being conducted by the National Institutes for Health directly comparing Lucentis and Avastin, and the results should be available in the near future.

EYLEA. Eylea (aflibercept) is the newest medication FDA-approved for treatment of wet AMD. This medicine costs almost the same as Lucentis and is usually covered partially or completely by health insurance. A large randomized study showed that Eylea is effective when compared to Lucentis and may be used at less frequent treatment intervals in some patients.

It is important to understand that these injections do not cure wet AMD. The injections reduce bleeding and fluid leakage behind the retina but ongoing injections are usually needed to control the disease. Your retina specialist will talk to you about what to expect over the course of treatment.

Photodynamic therapy (PDT) is an additional treatment that is sometimes used for treatment of wet AMD. PDT by itself is not as effective as Lucentis or Avastin, but a number of studies have shown that PDT combined with Lucentis or Avastin in selected cases can provide good results and reduce the number of anti-VEGF treatments needed to control the disease. Photodynamic therapy consists of intravenous injection of a medicine called Verteporfin, followed by a laser treatment that activates the drug in the area of leaking blood vessels behind the retina.


Dry Age-related Macular Degeneration

Dry AMD refers to characteristic changes in the retina, which is the sensory tissue in back of the eye responsible for vision. Some of the earliest changes include small drusen, which are accumulations of cellular and inflammatory waste products underneath the retina, resulting in distortion of the overlying retinal tissue. Additional dry AMD changes include thinning of the retina itself as well as accumulation of pigment within the retina, which can result in gradual central vision loss. These changes can be detected by careful clinical examination as well as high resolution imaging equipment to document and measure these alterations.

Dry AMD

EVALUATION. A test called optical coherence tomography (OCT) is employed to determine exactly where these deposits are located as well as whether there is evidence of fluid or blood that may be hallmarks of progression to the wet form of AMD. Another test called fluorescein angiography can also be used to directly photograph the retinal blood vessels and identify abnormal new blood vessels, which would indicate the development of wet AMD.

AREDS vitamins. While there are currently no FDA-approved therapies to treat or reverse vision loss from dry AMD, a large multi-center prospective clinical trial (The AREDS Study) demonstrated that a specific combination of vitamins A, C, E, zinc and copper can reduce the risk of developing wet AMD by approximately 25%. Special formulations also exist for current or former smokers that eliminate vitamin A and often replace it with lutein. Not all patients with dry AMD were shown to benefit from AREDS vitamins; speak with your retinal specialist to determine whether your specific findings warrant use of these daily non-prescription medications. New treatments for dry AMD are being tested in clinical trials. If you are interested in participating in studies to treat high risk dry AMD, speak with your retinal specialist.

SMOKING. By far the greatest life-style risk factor for vision loss from macular degeneration is smoking. Discontinuing smoking in high risk patients may significantly reduce the risk of vision loss.

AMSLER GRID MONITORING. Because dry AMD can progress to wet AMD in 10-50% of patients depending on clinical findings, patients with dry AMD should carefully monitor their central vision using an Amsler grid. Each eye should be independently tested regularly. If any new visual distortion is noted, this should be immediately reported to your retinal specialist for examination and prompt treatment if needed. This exercise may serve as the most important measure to save your sight, since early treatment provides the best visual outcomes if dry AMD progresses to wet AMD.


Advanced vision loss with AMD: What to expect

Age-related macular degeneration (AMD) can affect your eyes in a variety of ways. The early stages of the disease are visible during retinal examination but do not to cause significant vision loss. The intermediate stage is visible on examination and may cause very mild blurring or distortion of vision. The use of a vitamin supplement may significantly reduce the chance of progressing from this stage to the advanced wet stage, based on the results of a large national scientific study called AREDS. It is also important to monitor the vision with a grid (the Amsler grid) to detect progression of disease early on. In the advanced dry form, tissue in the center of the retina becomes thin and stops functioning, causing gradual, irreversible central vision loss. There is currently no approved treatment for the advanced dry form, but several promising treatments are under development and may be available through clinical trials in the next few years. In the advanced wet form, abnormal blood vessels grow under the center of the retina and leak fluid or blood, causing central vision loss. The advanced wet form is currently treated with injections of medicine into the eye. These treatments can almost always prevent further loss of vision and in many cases can improve vision significantly.

DEPRESSION AND LOSS OF INDEPENDENCE. Older patients with vision loss from AMD are more likely to experience depression than older individuals without AMD. Depression is often related to loss of independence and loss of the ability to perform daily activities such as driving and reading. Patients with vision loss from AMD may not be able to participate in activities they enjoy without help, but they may also resist asking for help because they do not want to burden their family and friends. Talking openly about these issues can be helpful for everybody involved and reduce the emotional toll on both patients and caregivers.

THE CHARLES BONNET SYNDROME. Many patients with central vision loss, particularly when both eyes are affected, will see hallucinations such as familiar faces, repeating patterns (like wallpaper), or objects that are not there. These images tend to be clear, rather than fuzzy like "floaters" in the eye. Other senses such as smell and hearing are not affected, and these hallucinations are not related to dizziness or other symptoms outside of the eye.

Patients with advanced AMD have lost central vision, which means that the brain receives an incomplete picture from the eye. Another name for the Charles Bonnet Syndrome is release phenomena because the brain essentially "releases" images into this missing central space in the picture. This is not a sign of "going crazy" and patients have insight into the fact that the objects or patterns they are seeing are not actually present.

Many patients with the Charles Bonnet Syndrome do not mention their hallucinations to their family, friends or doctors because they are afraid of being diagnosed with mental illness. Family and friends can help by asking about the symptoms described above and providing reassurance that these experiences are "part of the package" of the advanced AMD.

LOW VISION SERVICES. When central vision decreases due to AMD, a number of aids may increase a patient's ability to make the most of the remaining vision. In particular, magnification and good lighting can greatly improve the ability to read and perform daily tasks. A number of devices, both simple and complex, exist to help maximize vision. Seeing a low vision specialist may be helpful in identifying the most appropriate vision aids for your particular needs, ranging from specialized reading glasses to closed circuit magnified television systems. Your retina specialist can provide you with a referral to a low vision specialist.


Branch Retinal Vein Occlusion

The retina is fed by a system of blood vessels (arteries and veins) like a tree, with the trunk in the optic nerve and branches extending to the farthest edges of the retina. A branch retinal vein occlusion (BRVO) is vein blockage along a branch of the tree, usually at a point where an artery crosses over a vein and compresses it. This results in poor blood flow to a section of the retina. Since the retina is like film in a camera, a patient experiences branch retinal vein occlusion as painless vision loss. If the vein occlusion is away from the center or the retina, central vision may be unaffected. If the vein occlusion affects the central retina, vision may be severely limited.

BRVO

Branch retinal vein occlusion occurs most often in patients with high blood pressure, diabetes, high cholesterol , atherosclerosis, or high intraocular pressure (glaucoma). Smoking is also a major risk factor for BRVO. In some cases, no clear cause is found for BRVO, and in some cases BRVO is caused by rare conditions such as blood disorders that cause spontaneous clotting. Your doctor will determine the appropriate workup for underlying causes of BRVO depending on your age and medical history.

EVALUATION. Your retinal surgeon may order diagnostic tests in the office to determine the degree of damage caused by the vein occlusion. Blood flow in the affected area may be permanently reduced. Swelling may occur in the central part of the retina (the macula) resulting in decreased vision. In some cases, the eye may grow abnormal blood vessels. These complications of BRVO can be detected by a combination of clinical examination and imaging tests. Optical coherence tomography (OCT) is a fast, non-invasive scan of the retina which measures and locates swelling in the retina. Fluorescein angiography (FA) evaluates blood flow in the retina with a series of photographs taken after intravenous injection of a dye (fluorescein).

TREATMENT. If swelling (macular edema) is present, your retinal surgeon may recommend one or more treatments including laser or injection of medicine into the eye. If the eye is growing abnormal blood vessels (neovascularization), your surgeon may recommend laser treatment. In some cases, micro-incisional sutureless vitrectomy surgery is recommended. In all cases, treatment of underlying medical conditions such as high blood pressure is critical to preventing another retinal vein occlusion in the future.

Treatments for macular edema associated with branch retinal vein occlusion include laser, intravitreal injection (injection of medicine into the eye), or surgery. Medications which can be injected into the eye in these cases include bevacizumab (Avastin, which is used off-label for this condition), ranibizumab (Lucentis, which is FDA approved for this condition), aflibercept (Eylea, which is FDA approved for this condition), and dexamethasone (Ozurdex steroid implant, which is FDA approved for this condition).


Central Retinal Vein Occlusion

The retina is fed by a system of blood vessels (arteries and veins) like a tree, with the trunk in the optic nerve and branches extending to the farthest edges of the retina. A central retinal vein occlusion (CRVO) is blockage of the large vein in the trunk thereby reducing blood flow to the entire retina. Since the retina is like film in a camera, a patient experiences central retinal vein occlusion as painless vision loss. Vision may be affected to varying degrees, and patients who present with relatively good vision tend to maintain good vision long-term.

CRVO

Central retinal vein occlusion occurs most often in patients with high blood pressure, diabetes, carotid artery disease, or high intraocular pressure (glaucoma). In some cases, no clear cause is found for CRVO, and in some cases CRVO is caused by rare conditions such as blood disorders or medications that cause spontaneous clotting. Your doctor will determine the appropriate medical workup depending on your age and medical history.

EVALUATION. Blood flow in the retina may be damaged permanently to some degree. Swelling may occur in the central part of the retina (macular edema). In some cases, the eye may grow abnormal blood vessels. Abnormal blood vessels in the front of the eye may cause elevated eye pressure, or neovascular glaucoma. Imaging tests may be helpful in identifying these complications of CRVO. Optical coherence tomography (OCT) is a non-invasive scan of the retina which measures and locates swelling in the retina. Fluorescein angiography (FA) evaluates blood flow in the retina with a series of photographs taken after intravenous injection of a dye (fluorescein).

TREATMENT. Treatment of CRVO depends on the findings on examination and diagnostic imaging. If swelling is present in the macula (macular edema), your retinal surgeon may recommend injection of one or more medicines into the eye. If the eye is growing abnormal blood vessels (neovascularization), your surgeon may recommend laser treatment. In some cases, micro-incisional sutureless vitrectomy surgery is recommended to remove blood from the eye or to treat macular edema that has not responded to any other treatments. In all cases, treatment of underlying medical conditions such as high blood pressure or diabetes is critical to preventing another retinal vein occlusion in the future.

Treatments for macular edema associated with central retinal vein occlusion include laser, intravitreal injection (injection of medicine into the eye), or surgery. Medications which can be injected into the eye in these cases include bevacizumab (Avastin, which is used off-label for this condition), ranibizumab (Lucentis, which is FDA approved for this condition), aflibercept (Eylea, which is FDA approved for this condition), and dexamethasone (Ozurdex steroid implant, which is FDA approved for this condition).


Retinal Artery Occlusion

The retina is fed by a system of blood vessels (arteries and veins) like a tree, with the trunk in the optic nerve and branches extending to the farthest edges of the retina. A central retinal artery occlusion (CRAO) is blockage of blood flow to the retina in the main trunk with sudden, severe vision loss throughout the visual field of one eye. A branch retinal artery occlusion (BRAO) is blockage along a branch of the tree. This results in poor blood flow to a section of the retina. A patient experiences branch retinal artery occlusion as sudden, painless loss of a portion of vision. If the artery occlusion is away from the center of the retina, central vision may be unaffected. If the artery occlusion affects the central retina, reading vision may be severely limited. The blockage or occlusion may last only a few seconds, or it may be permanent.

The common associations with retinal arterial occlusion are atherosclerosis, systemic hypertension, and diabetes. An embolus or "floating log jam" such as cholesterol or a detached blood clot may come from the heart or carotid arteries and block a retinal artery. Carotid artery disease occurs in 45% of patients with CRAO. If presenting before age 30, retinal artery occlusion is more often associated with migraine, trauma, and coagulation disorders (blood disorders that cause easy clotting). In elderly patients, a disease called giant cell arteritis can cause inflammation of the central retinal artery, resulting in occlusion.

Retinal Artery Occlusion

EVALUATION. Your retinal surgeon may order diagnostic tests in the office to determine the degree of damage caused by the artery occlusion. Blood flow in the affected area may be permanently reduced. In some cases, the eye may grow abnormal blood vessels. These complications of BRAO or CRAO can be detected by a combination of clinical examination and imaging tests. Fluorescein angiography (FA) evaluates blood flow in the retina with a series of photographs taken after intravenous injection of a synthetic dye (fluorescein) which contains no iodine. Carotid studies, magnetic resonance angiogram, echocardiogram, and blood tests may be ordered to look for medical problems which may be life-threatening if untreated.

While it is important to identify and treat the underlying cause of a retinal arterial occlusion, there are no well-established medical or surgical techniques for treating the actual occlusion. Massage of the eye may be attempted to increase blood flow, decrease eye pressure, and dislodge emboli. Fluid may be taken from the front of the eye to lower eye pressure quickly. Sublingual nitroglycerin (nitroglycerin tablet placed under the tongue) has been tried with variable success.

If new vessels grow in the front of the eye, they may cause glaucoma, sometimes with pain and loss of vision. These abnormal new blood vessels can be treated with laser and injections of medicine into the eye, but these treatments do not restore vision.

In all cases, treatment of underlying medical conditions (such as diabetes or high blood pressure) is critical to prevent stroke or blood vessel blockage elsewhere in the body.


Cystoid Macular Edema

Cystoid macular edema (CME) refers to swelling of the central part of the retina (the macula). The retina is like the film in a camera, and the macula is responsible for detailed central vision. When the macula experiences swelling (edema), central vision is reduced.

CME

CME can occur for a variety reasons. Cystoid macular edema can accompany inflammation in the eye after ocular surgery (such as cataract surgery) or it can occur after blockage of a retinal vein (branch retinal vein occlusion or central retinal vein occlusion). Primary inflammatory disorders of the eye (uveitis) can cause CME. Wet age-related macular degeneration can cause CME, although other findings such as bleeding and fluid under the retina are usually seen as well. Macular edema can occur in diabetic patients due to leaky blood vessels, in which case the term "diabetic macular edema" is used. CME can occur from mechanical traction on the macula, as in the case of an epiretinal membrane. Less common causes of CME include retinitis pigmentosa, cancer in the eye, and radiation. CME is rarely seen as a side effects of medications such as niacin (used to treat high cholesterol).

EVALUATION. Like many conditions, cystoid macular edema can range from mild to severe. In most cases, CME is visible during detailed examination of the macula by an eye specialist. Additional testing is often indicated to determine the cause and severity of CME. Common tests include optical coherence tomography (OCT) and fluorescein angiography (FA). OCT is a laser scan of the retina which measures the degree of swelling and shows your doctor a cross section of the swollen area. Fluorescein angiography involves a small intravenous injection of dye (fluorescein) followed by a series of photographs of the retina. The images show blood flow and any leakage from blood vessels in the retina, and the patterns seen in these images are often necessary to diagnose the cause of cystoid macular edema.

TREATMENT. The treatment of CME depends on the underlying cause. In some cases, such as after cataract surgery, eye drops may be an appropriate first treatment. In many cases, swelling is reduced by an injection of medicine in the eye after the eye is numbed. Several different medicines can be injected into the eye depending on the cause of CME, and your retina specialist will discuss these options in detail if such treatment is deemed appropriate. In some diseases, such as branch retinal vein occlusion or diabetic macular edema, the treatment regimen may include one or more sessions of laser. If an epiretinal membrane is pulling on the retina and causing CME, micro-incisional sutureless vitrectomy surgery may be recommended to remove the membrane. Surgery is sometimes recommended in other conditions as well depending on the response to first line therapies.


Macular Hole

A macular hole is a full thickness defect in the central retina (macula). Since the macula is responsible for reading vision, patients who develop a macular hole complain of distorted vision and loss of central vision in the affected eye. The incidence of macular hole is 3.3 cases per 1000 in the population. The risk for developing a macular hole in the fellow eye is 10% - 15%. Small macular holes occasionally resolve spontaneously but the majority will persist. Once a macular hole develops, vision usually stabilizes at 20/200 if left unrepaired. Changing eyeglasses will not correct the blur and distortion caused by the macular hole.

Macular Hole

The vitreous is the gel that fills the eye. The majority of macular holes are caused by a spontaneous separation of the vitreous overlying the center of the retina (macula). The vitreous has a strong natural adhesion to the macula. Due to age-related changes in the vitreous gel, contraction of the vitreous overlying the macula may pull open a defect in the macula creating a macular hole. Less common causes of a macular hole include blunt trauma to the eye, contraction of a preexisting epiretinal membrane (macular pucker), or extreme near-sightedness (high myopia).

EVALUATION. Macular holes are frequently identified by an eye care professional using a slit lamp biomicroscope. Fluorescein angiography (a dye test to evaluate blood flow) is often performed to evaluate a macular hole and rule out other conditions. Optical coherent tomography (OCT) is a type of imaging test used to produce high resolution cross sectional images of the macula in order to confirm the diagnosis, exclude other conditions, and monitor the macular hole before and after surgical repair.

MICRO-INCISIONAL SUTURELESS SURGERY. Macular holes can be repaired by a surgical procedure called vitrectomy with membrane peeling and fluid gas exchange. This operation is performed in a hospital or surgery center on an outpatient basis. During surgery, the retinal surgeon removes the vitreous gel and then releases all forms of traction by separating the back of the vitreous from the retina and peeling any membranes surrounding the macular hole. The eye is filled with a bubble of sterile air mixed with a long acting gas. After surgery, the patient must stay in a face down position so that the gas bubble is positioned over the macular hole at the back of the eye.

Patients may sit upright for meals and in order to shower and use the bathroom but should otherwise stay and sleep in the face down position for a period of time determined by the surgeon, usually several days to a week. Eighty to ninety percent of macular holes can be successfully repaired with this technique. The majority of patients will enjoy relief of distortion and an improvement of two or more lines of visual acuity. There are no medications that will repair a macular hole. With a gas bubble in the eye, one should never travel to a higher elevation or fly in an airplane until the gas bubble has disappeared. Otherwise, the gas bubble may expand in the eye at the higher altitude causing acute glaucoma and permanent blindness. Rare complications of surgery include bleeding, the development of a retinal tear or detachment, and infection. These complications occur in 1 out of several thousand patients. More commonly, a cataract may develop following macular hole surgery if cataract surgery was not previously performed.


Epiretinal Membrane (Macular Pucker)

Epiretinal membrane (ERM), also known as macular pucker or cellophane maculopathy, is a common disorder of the central retina (macula) which may cause a central blur or distortion in the vision. An ERM is a layer of scar-like tissue on the surface of the retina. Most eyes with ERM are asymptomatic, but ERMs may require intervention if the vision is significantly affected due to distortion or lack of clarity.

In some cases, an epiretinal membrane develops as a response to injury or swelling in the eye. An ERM may form after a retinal tear or detachment, after cataract surgery, or after swelling in the eye from a variety of diseases such as diabetes or uveitis. However, in most cases there is no identifiable cause of the epiretinal membrane.

Epiretinal Membrane

EVALUTION. A visually significant ERM is usually first identified on clinical examination of the eye. An ERM may cause only a slight wrinkle in the retina, or it may pull on the retina and cause swelling or distortion with decreased vision. Imaging tests such as optical coherence tomography (OCT) and fluorescein angiography (FA) can be helpful in demonstrating the degree to which an ERM is distorting or damaging the underlying retina.

MICRO-INCISIONAL SUTURELESS SURGERY. Vitrectomy is the surgical removal of the gel in the eye, or vitreous. Membrane peeling, or removal of the scar tissue, is then performed using microscopic instruments such as picks and forceps. Vitrecomy with membrane peeling is an outpatient procedure that usually takes less than an hour. Surgery is most often performed under local anesthesia, but can be done under general anesthesia as well.

Visual improvement after surgery for epiretinal membrane is gradual, since the retina does not immediately snap back into its normal configuration after surgery. Significant visual improvement is usually seen by 6-8 weeks after surgery, but vision may continue to improve for 6 months or more. Vitrectomy with membrane peeling can lead to visual improvement in 75-90% of eyes with enough distortion and blur to warrant surgery. The average postoperative acuity is half way between preoperative vision and 20/20. It is important to consider that postoperative vision may not be perfect, but most eyes that undergo this surgery have a decrease in distortion. Eyes that have had a prior retinal detachment in the macula are less likely to have return of fine vision. Rare complications after vitrectomy surgery include bleeding, infection, retinal tear and retinal detachment. These complications occur in 1 out of several thousand patients. More commonly, cataract may advance at a faster pace following vitrectomy. Patients who have not previously undergone cataract surgery should expect to need cataract surgery within 1-2 years of vitrectomy surgery.


Central Serous Chorioretinopathy

Central serous chorioretinopathy (CSCR) causes painless blurring of central vision, primarily in young men ages 20-45. Common symptoms include distortion, color vision changes, micropsia (objects look smaller), and a central blind or gray spot. These symptoms are caused by a blister of fluid that collects under the center of the retina. The retina is the "film" of the eye's camera and the symptoms are related to the size and duration of the fluid blister. The fluid collection usually resolves spontaneously but may recur in the same or fellow eye months or year later.

CAUSES OF CSCR. The exact cause of central serous chorioretinopathy is controversial. Fluid appears to leak from the choroid (a layer of tissue behind the retina) into the space under the retina, but it is unclear whether the underlying problem is in the choroid or the retinal pigment epithelium (RPE), a layer that sits between the retina and the choroid.

In most cases, CSCR is not related to an underlying medical condition or use of medications. Stress and "Type A" personality traits have been associated with CSCR. Steroid use is a common trigger for CSCR, regardless of whether the steroids are taken by mouth, by inhaler, or by topical application. Other associations include organ transplantation, Cushing syndrome, hypertension, systemic lupus erythematosus, pregnancy, and use of some medications.

Central Serous Chorioretinopathy

EVALUTION. The blister of fluid under the retina is usually visible on clinical examination by an eye professional, but additional testing is helpful to confirm the diagnosis (other conditions may also cause fluid collections) and monitor change over time. Optical coherence tomography (OCT) is a non-invasive scan of the retina which measures and illustrates the subretinal fluid in cross-section. Fluorescein angiography involves a small intravenous injection of dye (fluorescein) followed by a series of photographs of the retina. The images can differentiate between various causes of subretinal fluid and can also identify the precise source of fluid leakage.

TREATMENT. Initially, the pocket of subretinal fluid in CSCR is measured and usually observed, since the fluid reabsorbs spontaneously in the vast majority of cases. If imaging shows improvement, continued observation is usually most appropriate.

In some cases, particularly those in which the fluid fails to reabsorb within three to six months, treatment may be recommended in order to facilitate resolution of the fluid. Current treatment options include thermal laser, photodynamic therapy and intravitreal injection. Thermal laser treats the source of leakage with a "hot" laser, while photodynamic therapy treats the source of leakage with a "cold" laser after intravenous injection of a medication called Verteporfin. Intravitreal injection involves the injection of a medicine into the eye after numbing drops are given in the office. If treatment is advised, your retina specialist will discuss the various options and make recommendations based on your particular case.

While most cases of CSCR resolve without treatment, and those cases that require treatment tend to resolve as well, it is important to understand that CSCR is often a chronic disease. Repeat episodes are common and may occur in the same eye or the other eye. Even after the fluid reabsorbs, vision may not return to normal due to damage in the retinal tissue. When a trigger such as steroids is identified, avoiding that trigger in the future will help reduce the chance of a recurrence.


Vitreomacular Adhesion

Vitreomacular adhesion refers to an attachment between the vitreous gel which fills the eyeball and the central part of the retina which lines the back of the eye. If the vitreous gel separates from the retina except for a persistent central attachment, then the gel can physically pull on the retina and cause swelling or deformation which results in blurred or distorted vision.

CAUSES OF VITREOMACULAR ADHESION. At birth, the vitreous gel is clear and firm. The surface of the gel is attached to the retina, as shown in the first image below. With age, the gel begins to liquefy and soften. Eventually, in most eyes, the surface of the gel separates cleanly from the retina, creating a posterior vitreous detachment, as shown in the second image below. However, in some eyes the attachment between the gel and the retina is strong enough that the gel separates only partially, leaving a small area of attachment as shown in the third image below. This attachment can pull on the retina cause various deformations.

EVALUTION. Your retinal surgeon may order diagnostic tests in the office to identify and characterize the adhesion between the vitreous gel and the retina. Optical coherence tomography (OCT) is a scan of the retina that measures abnormal retinal contours in very high resolution. In some cases of vitreomacular adhesion, fluorescein angiography imaging is helpful in indentifying blood vessel leakage that may be associated with the traction exerted by the vitreous gel on the retinal surface.

TREATMENT. Treatment is usually warranted only if vitreomacular adhesion is resulting in vitreomacular traction affecting the vision. Treatment options include observation, intravitreal ocriplasmin injection, or micro-incisional surgery.

Observation. Your retinal surgeon may order diagnostic tests in the office to identify and characterize the adhesion between the vitreous gel and the retina. Optical coherence tomography (OCT) is a scan of the retina that measures abnormal retinal contours in very high resolution. In some cases of vitreomacular adhesion, fluorescein angiography imaging is helpful in indentifying blood vessel leakage that may be associated with the traction exerted by the vitreous gel on the retinal surface.

Intravitreal ocriplasmin. Jetra (ocriplasmin) was FDA approved in 2012 for treatment of vitreomacular adhesion. This clear liquid injection is given in the office after the eye is numbed. The odds of resolution with this treatment vary depending on the exact characteristics of the adhesion. If the adhesion does not resolve with ocriplasmin treatment, then vitrectomy surgery is usually required to treat the persistent vitreomacular adhesion.

Micro-incisional surgery. Micro-incisional vitrectomy surgery is performed in the operating room as a same-day procedure. The surgery is able to successfully separate the vitreomacular adhesion more than 90% of the time. In some cases, a gas bubble is placed in the eye and face-down position is required in order to achieve the best visual outcome after surgery.

Visual improvement following treatment depends on several factors. Without physical separation of the adhesion, vision is unlikely to improve. If the adhesion separates (spontaneously or with treatment), the vision is likely but not guaranteed to improve. Visual improvement is less likely if the retinal deformation is very severe or has been present for a long period of time. If the adhesion separates but causes a full thickness macular hole, then vision may actually worsen, and treatment is then required to close the macular hole.


Posterior Vitreous Detachment

Between the lens in the front and the retina in the back of the eye lies a clear gel called the vitreous. A posterior vitreous detachment (PVD) is a separation between the vitreous gel and the retina.

At birth, the vitreous gel is clear and firm, and it is attached to the retina. With age, the vitreous gel becomes liquefied and some of the proteins in the gel clump together—these are the small floaters that most people see. Eventually the back surface of the gel may separate from the retina, beginning near the optic nerve and macula (central retina) and continuing towards the edges of the retina.

The incidence of PVD increases with age. Most of the time, a PVD occurs without any sudden new symptoms. Some of the time, however, a PVD is marked by the sudden onset of new flashes or floaters in the affected eye. Posterior vitreous detachment usually occurs spontaneously, but may occur acutely in the setting of trauma.

Flashes and Floaters. As the separation of the vitreous gel from the retina moves from the center out towards the edges of the retina, the gel may pull on the retina at the leading edge. This traction on the retina may cause retinal neurons to fire, resulting in transient colorless "flashes" in the vision.

Once the gel separates from the retina, clumps of protein on the back surface of the vitreous gel may be seen as large new floaters. Floaters in the setting of a PVD may also represent blood (hemorrhagic PVD) or pigment cells (retinal tear), which are discussed more below.

Hemorrhagic PVD. As the vitreous gel pulls away from the retina, the gel may tear a blood vessel on the retinal surface. A few drops of blood may leak out of the blood vessel into the gel and be seen as new floaters. While these floaters may be annoying, the blood generally does not cause any damage to the eye tissues. Hemorrhagic PVD is concerning because in the presence of blood there is a high likelihood of a retinal tear. If a tear is present, the blood may obscure it, and so frequent careful retinal examinations are appropriate in order to identify a retinal tear as early as possible and prevent a vision-threatening retinal detachment. In cases of dense hemorrhage that does not clear quickly on its own, surgery may be recommended to remove the blood and identify and treat the underlying source of bleeding.

Retinal tear. When a PVD occurs with flashes or floaters, there is about a 10% chance of developing a retinal tear. Most of these tears occur within 6 weeks of the initial symptoms. Tears occur because of the traction at the leading edge of the gel separating from the retina. An untreated retinal tear may lead to retinal detachment with severe vision loss.

What to expect after a PVD occurs. Detailed examination by a retinal specialist may be necessary after a PVD, depending on the findings at the time of examination. The primary purpose of examination is the detection of a retinal tear, which would be treated without delay in order to prevent severe vision loss.

In most cases, the new floaters from a PVD will not go away entirely. However, the brain often learns to ignore the new floaters, and the floaters may become more mobile and move away from the central vision as the vitreous gel continues to liquefy with time. In cases of hemorrhagic PVD, the floaters may decrease over time as the blood breaks down and disappears. Flashes usually decrease and stop as the process of vitreous separation completes itself. This may take days, weeks or even months depending on the characteristics of the gel. If you experience a sudden increase in flashes, the onset of additional new floaters, or a shadow in the vision, contact your eye care provider immediately, as these may be symptoms of a retinal tear or detachment.


Retinal Tear

The eye is like a camera: it has a lens in the front that focuses light and film in the back that captures light. The retina is the "film" inside the human eye and contains over a million neurons as well as a network of blood vessels that keep the tissue healthy. Between the lens in the front and the retina in the back of the eye lies a clear gel called the vitreous.

As the vitreous gel changes with age, it may pull away from the retina in the back of the eye. This process usually starts near the back and continues towards the front of the eye, with traction on the retina at the leading edge. If the retina is unusually thin or damaged, the gel pulling may be enough to cause a full thickness tear in the retina. Retinal tears are more common in patients who are very near-sighted; patients with a family history of retinal tear or retinal detachment; or patients with a prior retinal tear or detachment in the same or other eye. Retinal tears may also occur after trauma or surgery in the eye.

TREATMENT. The goal of treatment is the creation of a controlled scar surrounding the retinal tear. This scar serves to weld the retina and seal it to the underlying tissues, thereby preventing fluid from moving through the retinal tear into the space under the retina (retinal detachment). The scar can be created by either laser treatment or a freezing treatment, depending on the location and characteristics of the tear.

Retinal Tear Laser Retinopexy. Laser treatment is delivered through the front of the eye using either a head-mounted apparatus or a laser apparatus connected to a slit lamp in conjunction with a contact lens. While this treatment is generally not painful, there are sensory nerves that run through the back of the eye which may be stimulated by the treatment. Some patients may have a mild headache after treatment, which is usually easily remedied with over-the-counter acetominophen.

Cryoretinopexy (cryotherapy). Cryotherapy involves the application of a probe to the outer wall of the eye corresponding to the location of the retinal tear. A freeze is created at the tip of the probe, extending inwards to the retina. Cryotherapy is usually experienced as an "ice cream headache" most of which resolves within minutes. Some patients have a headache or eye ache afterwards, which can be treated with over-the-counter acetominophen.

Many patients with retinal tears initially present with symptoms such as flashes of light or new floaters. It is important to understand that treatment is not meant to get rid of these symptoms. The flashes occur because the vitreous gel is pulling on the retina. This process usually resolves spontaneously within days or weeks but in some cases will last much longer. The continuation of intermittent flashes after treatment is usually not concerning unless the flashes increase in frequency or are associated with new floaters or other vision changes.

Floaters in the setting of a retinal tear may occur for two reasons. When the vitreous gel pulls away from the back of the eye (a normal, age-related process), small condensations in the gel will appear as floaters. While these floaters are annoying, they do not cause problems on their own. These floaters will be more noticeable when looking at a clear blue sky or a white wall. In some cases, the floaters are due to blood that was released when the retina tore. This blood eventually breaks down and disappears, but the rate of disappearance is unpredictable and may vary from days to months.


Retinal Detachment

The eye is like a camera: it has a lens in the front that focuses light, and film in the back that captures light. The retina is the "film" inside the human eye and contains over a million neurons as well as a network of blood vessels that keep the tissue healthy. Between the lens in the front and the retina in the back of the eye lies a clear gel called the vitreous.

RRD A retinal detachment occurs when the retina pulls away from the wall of the eye. The retina cannot function normally when it is detached from the wall of the eye, which is why a retinal detachment can limit the vision to varying degrees depending on how much of the retina is detached.

There are different kinds of retinal detachments: rhegmatogenous, tractional, and exudative. The most common kind, a rhegmatogenous retinal detachment, occurs when fluid moves through a retinal hole or tear into the space under the retina, causing the retina to detach. The remainder of this handout deals specifically with rhegmatogenous retinal detachment.

TREATMENT. The goals of treatment are to get the fluid out from under the retina and to seal the tears or holes that caused the problem in the first place. Removing the fluid allows the retina to reposition itself (reattach) against the wall of the eye and thereby regain its nourishing blood supply and restore vision. Sealing the tears or holes in the retina helps make sure that the retina does not re-detach in the future. Fortunately, over eighty to ninety percent of retinal detachments can be repaired with only one procedure. The following are the most commonly used methods to repair a retinal detachment.

SCLERAL BUCKLE. Scleral buckling entails sewing a piece of silicone to the outside wall of the eye. This material may be sewn to a section of the outside eye wall, or it may go around the eye for 360 degrees forming a "belt" around the eye. The silicone material indents the wall of the eye (buckles) and pushes the wall of the eye closer to the retinal tear. The tear is treated with freezing therapy which causes local tissue damage and controlled scarring which seals the tear. The fluid already under the retina is either absorbed by the body or actively drained from under the retina and the retina is thereby reattached.

MICRO-INCISIONAL VITRECTOMY SURGERY. Vitrectomy is a type of surgery that takes place primarily inside the eye. The surgery takes place through three very small openings in the white part of the eye. The surgeon uses fine instruments and an operating microscope to remove the vitreous gel inside the eye and drain the fluid out from under the retina. The surgeon may use a laser to seal the retinal tears or holes. A bubble of gas is commonly placed inside the eye in order to hold the retina in place while it heals. The patient may be asked to maintain a specific head position for several days after surgery in order to position the gas bubble correctly.

PNEUMATIC RETINOPEXY. Unlike scleral buckling and vitrectomy, which are performed in the operating room, pneumatic retinopexy is performed in the office with only local anesthesia. The surgeon will determine whether this is a good option based on the characteristics of the retinal detachment. Pneumatic retinopexy consist of at least three parts. 1. The tear in the retina needs to be sealed to the eye wall. This is usually done with cryotherapy, a freezing treatment applied to the outside of the eye after numbing medications are given. 2. Gas is injected into the back part of the eye (vitreous cavity). When the head is later positioned appropriately, this bubble pushes the fluid out from under the retina and pushes the retinal tear closed. Proper positioning by the patient immediately after this procedure is critical. 3. Fluid is removed from the eye in order to make place for the gas. This can be done before the gas is injected, after the gas is injected, or both before and after.

LASER SURGERY. In certain selected cases it may be advisable to "wall off" the detachment to prevent the retinal detatchment from spreading within the eye. In cases such as these, a barrier of scar tissue forms as a result of laser (or freezing treatment) and the detachment remains fixed in its position. This technique is most often used when the area of detachment is very small and located at the far edge of the retina so that vision is not significantly affected. This technique is also sometimes used for patients who cannot safely undergo any other procedure due to severe medical illness.

RESULTS OF TREATMENT. Results of retinal reattachment surgery are divided into two categories: anatomic results and visual results. The overall anatomic success rate of retinal detachment repair is greater than 90%. This means that the surgeon can successfully put the retina back into place 9 out of 10 times. Sometimes more than one procedure is required to achieve anatomic success. The visual result depends on the patient's pre-operative vision as well as the body's ability to heal. If the center of the retina is attached prior to the surgery, then post-operative vision tends to be similar to pre-operative vision. However, if the central retina is detached prior to the surgery, there may be some degree of permanent vision loss even after successful reattachment. Some procedures will accelerate cataract formation, in which case cataract surgery is needed later in order to achieve the best possible vision.


Lattice Degeneration

Lattice degeneration is a common peripheral retinal degeneration, with oval or linear patches of retinal thinning. Lattice degeneration affects about 10% of the population and is bilateral in 30 to 50% of those patients. It may run in families and it is more common in near-sighted eyes. Patients with lattice degeneration are typically asymptomatic, and the lesions are usually an incidental finding of dilated eye exam. Lattice lesions usually develop during the teenage years and may continue to develop over many years. Lattice degeneration may predispose the retina to tears or atrophic holes which may lead to retinal detachment. For this reason, the acute onset of floaters, flashes of light, peripheral field loss, or central vision loss should be taken seriously and a detailed retinal examination is appropriate.

Lattice

Lattice lesions may be single or multiple and are usually located near the periphery of the retina. The back part of the eye is filled with a gel called the vitreous. Condensed vitreous gel is adherent at the margins of lattice and may pull on the retina. Lattice lesions appear to be caused by loss of peripheral retinal capillaries (fine blood vessels), which leads to thinning of all retinal layers and in some cases a full-thickness retinal hole. Lattice degeneration and associated retinal holes or breaks can be detected by peripheral retinal examination with scleral depression, a technique in which the doctor pushes on the edge of the eye with an instrument in order to clearly visualize the periphery of the retina.

TREATMENT. Mild lattice does not interfere with vision and does not present a high risk for future retinal detachment. Prophylactic treatment is indicated only in specific circumstances. Lattice degeneration complicated by retinal tear or an increasing cuff of fluid under the retina constitutes an urgent indication for treatment with laser retinopexy or cryoretinopexy. Both of these techniques create a controlled scar around the tear in order to seal it and prevent a vision-threatening retinal detachment from occurring. Lattice lesions in fellow eyes of patients who have retinal detachment in the other eye may be treated prophylactically, but there is still a small chance of retinal detachment even after treatment.

Patients with significant lattice lesions may be at slightly increased risk for vision loss due to retinal detachment. These high risk patients should have regular follow-up examinations of the retina. Patients with lattice degeneration should be aware of the signs and symptoms of retinal tear or detachment and seek urgent ophthalmic care when needed.


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