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The human retina is made up of layers of cells that line the entire inside of the globe of the eye. The macula is the most sensitive part of the retina, located in the center. The macula is about the size of the head of a straight pin, and contains millions of light-sensing cells that provide sharp, detailed, “straight-ahead” central vision. When light strikes the back of the eye, the cells of the macula and the rest of the retina send electrical signals to the brain through the optic nerve. The brain translates the electrical signals into the images we see.  When macula cells are damaged or destroyed, the images received by the brain are distorted.

  • Age-related macular degeneration (AMD) is a progressive eye condition affecting as many as 15 million Americans and millions more around the world. There is no cure for AMD, which destroys the clear central vision necessary for reading, driving, identifying faces, watching television, safely navigating stairs and performing other daily tasks we take for granted. It can make it more difficult to see contrast and can change the way color is seen. Peripheral vision may not be affected, and it is possible to see “out of the corner of your eye.”
  • AMD is the number one cause of severe vision loss and legal blindness in adults over 60 in the U.S. It escalates with age.  More than one senior in three over the age of 75 is likely to develop signs of AMD, with over 200,000 new cases diagnosed every year.
  • There are two types of AMD – atrophic or “dry AMD" and neovascular or “wet AMD”.  All AMD starts in the dry form. There are treatments available for wet AMD to stop disease progression, and research is underway to find an effective treatment to limit the vision loss that occurs with dry AMD. Even with vision loss resulting from AMD, training and special devices can promote independence and a return to favorite activities.

There are some things you can do to reduce the risk of AMD. Research with large populations around the world has revealed a list of lifestyle factors that can be changed. Other things that contribute to AMD include your family history and age. While you can’t control these risk factors, it’s important to know about them.  

Things You Can’t Change

  • Age – AMD signs are present in about 14% of people 55–64; 20% of those age 65–75; and up to 40% of individuals over age 75.
  • Gender – AMD is more common in women than in men.
  • Race – AMD is more common in Caucasians than other races, but it exists in every ethnicity.
  • Eye Color – AMD is more common in people with blue eyes.
  • AMD in One Eye – If you have AMD in one eye, your chance of developing it in the other eye is higher. Dry AMD in one eye may predispose you to wet AMD in the other eye.
  • Genetics – If others in your family have AMD, you have a greater risk of developing it.

Risk Factors You Can Change

  • Smoking – Smoking increases your risk, especially if AMD runs in your family.
  • Diet – A poor diet, low in antioxidants and high in saturated fats and processed foods may increase your risk of developing AMD.
  • Obesity – People who are very overweight have a higher risk of AMD.
  • Exercise – A sedentary lifestyle contributes to AMD.
  • Cholesterol – High cholesterol is bad for your eyes and your heart.
  • Blood Pressure – High blood pressure may be involved in AMD.
  • Sun Exposure – Ultraviolet and blue light from the sun and electronics can damage the retina.

Dry age-related macular degeneration

Dry AMD is the most common type of macular degeneration and affects 85-90% of people who have the condition. In the dry form, there is a breakdown or thinning of the layer of retinal pigment epithelium (RPE) in the macula. These RPE cells support the light-sensitive photoreceptor cells that are critical to vision. When we look at something, photoreceptor cells (rods and cones) in the retina gather the images and send them to the brain, where vision information is processed.

Dry AMD is characterized by the presence of drusen and thinning of the macula. Dry AMD reduces central vision and can affect color perception. Generally, the damage caused by the dry form is not as rapid as that of wet AMD. However, over time, it can cause profound vision loss. The degeneration or death of these cells is called atrophy. Hence, dry AMD is often referred to as atrophic AMD. The more advanced stage of dry AMD is called geographic atrophy, where entire patches of photoreceptor cells die leaving dark grayish patches in the central vision.

Wet age-related macular degeneration

Wet or exudative AMD, like advanced dry AMD, is also an advanced stage of the disease. Wet AMD, however, has therapeutic options which can preserve and sometimes restore vision.

In wet AMD new blood vessels grow underneath and in the retina. These blood vessels are unhealthy and can leak and bleed causing vision loss. If this happens, then your doctor can offer treatments that try to make the new blood vessels go away.

Patients with wet AMD are monitored closely and may need to visit their doctor and receive treatment every month until the disease is controlled. These treatments are usually injections into the vitreous cavity of the eye or occasionally a laser treatment. Oftentimes with wet AMD, your doctor will perform a fluorescein angiogram of your eyes in the office by injecting a plant-based dye in your vein and taking pictures of your retina over the course of several minutes. This can help your doctor see how the blood vessels are working in your eye. In addition, just like with dry AMD, a retinal scan called Optical Coherence Tomography (OCT) will be performed on your eyes very often, as this allows your doctor to see microscopic changes in your eyes with a non-invasive test.

Diabetic retinopathy is defined as damage to the blood vessels of the retina of the eye and is associated with long-term diabetes. Diabetic retinopathy can be prevented if blood sugar, blood pressure and cholesterol are controlled correctly. Unfortunately, symptoms of diabetic retinopathy usually are not noticed until the eye damage is severe. Some symptoms include blurry vision, gradual vision loss, floaters, problems seeing at night and areas of shadows obscuring vision.

There are two types of diabetic retinopathy: non-proliferative and proliferative.

Non-proliferative diabetic retinopathy begins when the blood vessels in the retina change shape (microaneurysms), become blocked and function abnormally. This can lead to poor oxygen supply to the retina, and fluid leaking from blood vessels into the retina.

Treatment: Not all people with non-proliferative diabetic retinopathy need active treatment, but their eyes need to be monitored closely. If patients develop leaking fluid in the retina which causes vision loss, then they may benefit from treatments to make the blood vessels function more normally. This includes injections of steroids or anti-VEGF (Eylea, Lucentis or Avastin) medications into the eye, or lasers precisely aimed on unhealthy blood vessels.

Proliferative diabetic retinopathy is a more advanced and severe condition. New blood vessels begin to develop and grow in the eye, but because they are fragile they can rupture and hemorrhage easily leading to scarring on the retina and on other parts of the eye.

Treatment: Nearly every patient who develops proliferative diabetic retinopathy will need treatment to try and make the abnormal new blood vessels go away. If new blood vessels begin to grow in the retina, (known as neovascularization) or if the retina swells (macular edema), then injections and laser treatment may be needed to restore or preserve vision.

Central retinal artery occlusion is defined as blockage of the blood supply in the central artery of the retina (the main trunk of the artery). Retinal arteries may become blocked by a blood clot or substances (such as fat or plaque) that get stuck in the arteries. These blockages may occur due to hardening of the arteries in the eye. Also, clots may travel from other parts of the body and block an artery in the retina. A common source of a clot would be from the carotid artery in the neck or from the heart lining. Most clots are caused by conditions such as diabetes, carotid artery disease, high cholesterol, or certain heart rhythm problems like atrial fibrillation.

microscopic view of Central Retinal Artery Occlusion (CRAO)

People with retinal arterial occlusion, whether it is temporary or permanent, have a risk of stroke because clots may also move to the brain. Retinal vessel occlusion more often affects older people. Risk factors are related to the disorders that cause the blockage. The symptom is a sudden blurring or loss of vision in the eye. Breathing in (inhaling) a carbon dioxide-oxygen mixture has been used to treat blockages in the arteries. This treatment causes the arteries of the retina to widen (dilate). It may allow the clot to move down the artery and sometimes break up, which reduces the area of the retina that is affected. The use of the clot-busting drug, tissue plasminogen activator (tPA), within a few hours of retinal artery occlusion may be helpful. Unfortunately, there is no treatment that can consistently restore vision lost from an artery occlusion. However, if it is caught within the first hour and treatment is initiated immediately, recovery is possible in rare cases.

Measures used to prevent other blood vessel (vascular) diseases, such as coronary artery disease, may decrease the risk of retinal artery occlusion. These include: eating a low-fat diet, exercising, stopping smoking, and losing weight if you are overweight. Aspirin is commonly used to prevent the artery from becoming blocked again. It is also helpful to control atrial fibrillation.

The central retinal artery enters the eye through the optic nerve and divides into multiple branches to perfuse the inner layers of the retina. A branch retinal artery occlusion (BRAO) occurs when one of these branches of the arterial supply to the retina becomes occluded. Most commonly, a branch retinal artery occlusion occurs secondary to an embolus. Emboli typically originate within vessels upstream where they dislodge and travel within the circulatory system to ultimately become lodged downstream in a smaller vessel. The most common include cholesterol emboli from carotid atheromatous plaques, platelet-fibrin emboli from thrombotic disease, and calcific emboli from cardiac valvular disease.

Patients with BRAO typically present with sudden, unilateral, painless, partial visual loss. Risk factors for BRAO include high blood pressure, high cholesterol, diabetes, coronary artery disease, or history of stroke.

As the central retinal artery enters the eye through the optic nerve, a central vein, leaves the eye through the same area, and can be occluded too. Veins of the retina can become blocked by a blood clot. Retinal vein occlusion also can occur when the retinal arteries put pressure on the retinal vein. This is usually caused by a condition such as blood clot, diabetes, glaucoma, hardening of the arteries (atherosclerosis), and high blood pressure. Painless visual loss is usually sudden, but it can also occur gradually over a period of days to weeks.

Due to the lack of oxygen in the retina, there is a risk to develop new vessels (neovascularization) and then this new vessels creates an occlusion on the drainage of the aqueous humor that develop in high pressures in the eye (neovascular glaucoma) or they can leak into the gel inside the eye (vitreous hemorrhage.) There is no generally accepted medical therapy for occlusion itself. However, if neovascularization develops, laser treatment of the retina (pan retinal photocoagulation) should be initiated because it may decrease vitreous hemorrhages and prevent neovascular glaucoma.

Patients with a diagnosis of CRVO should be advised to optimize systemic disease control.

Blockage of one of the venous branches in the retina is called a branch retinal vein occlusion (BRVO), and may cause vision loss and other complications. Males and females are, in general, affected equally. Most retinal vein occlusions occur after the age of 50, although younger patients are sometimes seen with this disorder. A major risk factor for branch retinal vein occlusion is atherosclerosis. Other risk factors include history of stroke, coronary artery disease, aging, hypertension, elevated blood lipids, smoking, and glaucoma. Other less common risk factors include blood clotting abnormalities, infectious diseases, and inflammatory disorders. The symptoms of a branch retinal vein occlusion depend on which venous branch is involved. Common symptoms include blurred vision or changes in a portion of the visual field (peripheral vision). Occasionally the branch retinal vein occlusion will affect a vein draining a portion of the retina away from the central vision and will not cause any symptoms. The complications and treatment are the same as in the Central Retinal Vein Occlusion.

A floater is a dark spot, line, or shape that moves or drifts throughout the field of vision. Most people have some floaters and are able to ignore them unless they are numerous or become more prominent. Floaters are caused when the vitreous begins to shrink and becomes cobweb-like or stringy, causing shadows to reflect against the retina.

Floaters develop as a patient ages and usually are merely annoying. However, floaters can be symptoms of more serious vision issues such as retinal tears, eye injury, infection, hemorrhaging, and inflammation. It is important to be seen by an eye care professional if there are drastic changes with regard to floaters, like a shower of new floaters.

If floaters begin to drastically affect vision, a vitrectomy may be recommended. During this surgical procedure, the vitreous of the eye and the floaters are removed and replaced with a salt solution. Note, most surgeons are hesitant to recommend this procedure because it poses certain risks to the patient’s sight, including such complications as retinal detachment, retinal tears, and cataracts.

Flashes are bursts, showers, spots, or arcs of light in a patient’s visual field. Flashes can be associated with floaters. If a patient experiences flashes and a sudden shower of floaters, then immediate medical attention is needed.

The flashes could be caused by the vitreous of the eye pulling away from the retina or the retina becoming detached from the back of the eye. Flashes could be short bursts or happen continually until the retina is repaired. Because visual flashes may be signs of retinal detachment and can lead to vision loss, immediate medical care is essential. Flashes and floaters also may indicate vitreous detachment and other vision issues.

Flashes also can occur after a patient receives a blow to the head and is sometimes referred to as "seeing stars." Some patients see flashes of light that look like jagged lines or waves and last approximately 10 to 20 minutes. These flashes are typically caused by blood vessel spasm in the brain, which are also called migraines. When a headache follows these visual flashes, it is a migraine. If no headache develops, the flashes are called an ophthalmic or ocular migraine.

About 75 percent of patients over the age of 65 experience a posterior vitreous detachment, or PVD. The condition happens as the vitreous changes and begins to pull away from the retina. Symptoms include floaters and flashes of light in vision.

There are no treatments for posterior vitreous detachment. Patients find that the floaters and flashes subside in about six months. Over time, they adapt to having floaters in their field of vision and overall visual acuity remains the same. Very few patients with posterior vitreous detachment develop the much rarer retinal tearing or detachment conditions.

A retinal tear happens when the retina is damaged. The retina can then detach from the back wall of the eye. If the retina becomes partially detached, then blood supply to the retina is reduced and the ability to process light rays is affected. If the retina is totally detached then the images can no longer be transmitted between the eye and brain and blindness results. When retinal detachment has occurred, a patient’s vision may seem watery, wavy, shadowed, or distorted. In some cases, vision may be totally lost.

Normally, as people age the vitreous, a clear gel-like fluid that fills the inner cavity of the eye, begins to decrease and pull away from the retina. This typically is not harmful to the eye. In some cases, the vitreous material stays attached to the retina. This typically is not harmful to the eye. In some cases, the vitreous material stays attached to the retina, causing small tears as it shrinks. These peripheral retina tears do not affect vision but if left untreated, then fluid can seep under the retina leading to a retinal detachment. Retinal detachments also can be caused by posterior vitreous detachment, a related disorder, as well as trauma, diabetes, or inflammatory disorders.

Symptoms of retinal tears vary and may not be noticeable. As the vitreous gel shrinks and pulls away from the retina, flashes of light may appear in the patient’s vision. 

Immediate treatment is needed for retinal tears to prevent the retina from detaching and a loss of vision. Surgical treatments focus on creating a scar that helps to bond the retina to the back of the eye. These treatments are done with laser light or freezing methods. More than 90% of retina detachments can be repaired, preventing further loss of sight and possibly restoring sight.

Cystoid macular edema, commonly called CME, is a painless disorder, which affects the central retina or macula.  When CME is present, multiple cyst-like (cystoid) areas of fluid appear in the macula and cause retinal swelling or edema. This swelling in the retina in turn can cause decreased vision.

Some causes of CME include:

  • Eye surgery, including cataract surgery
  • Diabetes
  • A stroke in the eye causing blockage in the small arteries or veins of the retina (branch or central retinal vein occlusion)
  • Inflammation of the eye
  • Eye trauma

The first symptom of CME is blurry or "wavy" vision in the center of your visual field. Your eye physician can make this diagnosis by carefully examining the eye and also doing a special scan of the back of the eye, called an Ocular Coherence Tomography (or OCT). An OCT is a non-invasive imaging test. OCT uses light waves to take cross-section pictures of your retina. With an OCT, your ophthalmologist can see each of the retina’s distinctive layers. This allows your ophthalmologist to map and measure their thickness. These measurements help with the diagnosis and provide treatment guidance. 

Only your ophthalmologist can recommend the right treatment for CME. Treatment options vary depending on the degree of retinal swelling, but some options include: eye drops, injections of steroids or other medications inside or around the eye, and possibly surgery. No matter what the cause of the CME, it usually takes several months for it to go away. The patient should not get discouraged. It is important that you keep following your ophthalmologist's recommendations.

Hypertensive retinopathy is damage to the retina from high blood pressure. High blood pressure can damage blood vessels in the retina. The higher the blood pressure and the longer it has been high, the more severe the damage is likely to be. When you have diabetes, high cholesterol levels, or you smoke, you have a higher risk of damage and vision loss. Most people with hypertensive retinopathy do not have symptoms until late in the disease. Malignant hypertension may cause the following sudden symptoms, and should be considered a medical emergency. The symptoms include double vision or dim vision, headaches, and/or visual disturbances and sometimes sudden vision loss.

The degree of retina damage (retinopathy) is graded on a scale of 1 to 4:

  • At grade 1, you may not have symptoms.
  • In between grades 1 and 4, there are a number of changes in the blood vessels, areas where blood vessels have leaked, and other parts of the retina.
  • Grade 4 hypertensive retinopathy includes swelling of the optic nerve and of the visual center of the retina (macula). This swelling can cause decreased vision.

Controlling high blood pressure (hypertension) is the only treatment for hypertensive retinopathy. Patients with grade 4 (severe hypertensive retinopathy) often have heart and kidney complications from high blood pressure. They are also at higher risk for stroke. The retina will generally recover if the blood pressure is controlled. However, some patients with grade 4 hypertensive retinopathy will have permanent damage to the optic nerve or macula.

Controlling high blood pressure prevents changes in the blood vessels of the eye, as well as in other organs like the heart, kidneys, and brain.

Macular pucker or epiretinal membrane, or ERM, is a translucent or semitranslucent fibrocellular tissue formed on the surface of the retina in response to changes in the vitreous. It is also called cellophane maculopathy. It can be associated with a wide variety of conditions, including retinal vascular occlusions, uveitis, trauma, intraocular surgery, and retinal breaks. In the majority of cases, there is no known cause. Both sexes are equally affected.

Contracture of ERMs produces distortion and wrinkling of the inner surface of the retina. Affected patients may be asymptomatic, or they may present with symptoms of distortion, decreased image size from the affected eye causing double vision, or swelling of the macula causing decreased vision.

The definite treatment for severe cases of ERMs is vitrectomy with membrane peel. Surgery is not usually recommended unless the distortions or decreased vision are severe enough to interfere with daily living, since there are the usual hazards of surgery, infections, and a possibility of retinal detachment.

A macular hole is defined as a small hole in the macula, the area of the eye that is responsible for the sharp, detailed vision needed for reading, driving and small detail work. This condition is more common in patients ages 60 and older.

Symptoms of a macular hole include problems with the central area of vision. For example, straight lines may appear wavy and reading may be difficult. In later stages, there may be small blank areas in the central vision.

In some cases, macular holes close up by themselves. Other cases require a vitrectomy, a surgical procedure to remove some of the vitreous gel from the interior of the eye to prevent pulling on the retina. The removed gel is replaced with a bubble containing a combination of air and gas. This bubble acts as an internal bandage as the macular hole heals and reseals itself.

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