Vision is a precious gift, but like everything else in our bodies, it declines with age. Unfortunately, age-related macular degeneration affects many people as they age, impairing vision, and even causing central blindness. Progressive vision loss is a frightening prospect, but the good news is that modern medicine now employs an arsenal of treatments that can help protect and slow vision loss progression in eyes with macular degeneration.
Macular degeneration, oftentimes called age-related macular degeneration (AMD), is a progressive disease of the retina that slowly reduces central vision. AMD is so common that it is known to be the leading cause of vision loss in adults aged 50 and older. Macular degeneration cannot be cured, but the condition can be managed, allowing many patients to avoid legal blindness.
The macula is a tiny, bowl-shaped area in the center of the retina, and is responsible for all of our central vision, the majority of our color vision, and the fine detail of what we see. The center of the image that passes through the lens of the eye focuses into this bowl, which is rich in millions of colors and light-detecting cells. When the macula is functioning properly, it collects detailed images at the center of the field of vision and sends them to the optic nerve then on to the brain, which interprets them as light. When the macula is not functioning properly, these images are not received correctly. Macular vision, as opposed to peripheral vision, allows us to read, drive, perform detailed work, and recognize faces.
There are two broad types of macular degeneration: “dry” and “wet.” The vast majority of macular degeneration patients have the “dry”, also known as atrophic, type—about 90 percent. The remaining 10 percent of patients have the “wet”, sometimes referred to as “exudative” or “neovascular”, type of macular degeneration.
Dry macular degeneration can further be described by stage; early, intermediate, or late. In early AMD, people generally do not experience any vision loss, in intermediate stages, people may have some vision loss but which may not yet be noticeable, while in late stages vision loss has become noticeable. Wet AMD can progress quickly and therefore commonly presents in the late stage with vision loss already apparent.
In dry, or atrophic, macular degeneration, fatty and protein rich deposits build up under the retina and macula, between a very special layer of cells called the retinal pigment epithelium (RPE) and Bruch’s membrane. The RPE helps maintain the light-sensing cells that make up the majority of the retina—known as photoreceptors—by allowing the movement of nutrients and waste between these photoreceptors and the blood vessels which supply them. Called drusen, these deposits clog up the transport system that allows the retina and macula to get rid of waste products and to receive oxygen-rich nutrients. This, in turn, can cause cells in the macula to become damaged, which causes colors to be less vivid, detailed vision to become blurry, and/or central vision to become cloudy or lost. Dry AMD tends to progress gradually, as the number or size of drusen increases.
In wet, or exudative, macular degeneration, abnormal blood vessels begin to grow in the tissues, called the choroid, below the retina. This condition is called choroidal neovascularization, or CNV. Blood leaks out of these abnormal blood vessels and fills the tissue under the macula, distorting and eventually eliminating vision on that part of the macula. As the condition progresses, the blind spot in the center of the visual field grows larger until only peripheral vision remains. Wet AMD is characterized by more abrupt central vision loss than dry AMD, sometimes over days to weeks. Only 10 to 15 percent of patients with intermediate-stage dry AMD will develop wet AMD, but this stage accounts for 90 percent of the blindness attributable to AMD.
According to the American Academy of Ophthalmology about 6% of the American population has large macular drusen deposits in at least one eye and about 1.5% have advanced macular degeneration. AMD is an age-related condition and can occur as early as a person’s forties, but it is more common in people at an advanced age. AMD symptoms appear in only 6% of seniors between the ages of 65 and 74, but this increases to 20% of seniors over the age of 75.
Macular degeneration is often first identified by an optometrist during a routine eye exam, but the diagnosis will be made by an ophthalmologist or eye doctor.
Any change in vision, however, should prompt a visit to an optometrist or physician. While declining vision is normal as people age, the early stage of macular degeneration has unique, identifiable symptoms:
Blurred central vision
Distorted vision, such as straight lines seeming bent
Difficulty reading, recognizing faces, or doing detail work
Increasing difficulty seeing in low-light conditions
As the name suggests, advanced age is the single most important risk factor for age-related macular degeneration. Other risk factors include
Smoking
Excess weight
Uncontrolled high blood pressure
High cholesterol
Family history of AMD
Gender
Race
To diagnose age-related macular degeneration, an ophthalmologist will rely on
A retinal exam. With pupil-dilating eye drops, drusen will appear as yellowish spots on the retina and are clearly visible. For wet AMD, new blood vessels or even shallow pools of blood may be visible.
A vision test. The ophthalmologist will use a special vision test, called the Amsler grid, to identify unique vision problems caused by macular degeneration that will cause straight lines in the grid to appear wavy.
Fluorescein angiography. An ophthalmologist will inject fluorescein sodium into the bloodstream that will make blood vessels in the retina glow, allowing the doctor to see abnormal blood vessels in the eye with the use of a specialized camera.
Optical coherence tomography (OCT). An OCT test creates a cross-sectional image of the retina and the macula. OCT is a valuable tool for monitoring the progress of AMD.
There is no cure for macular degeneration, and there is no treatment for dry macular degeneration which makes prevention and slowing of progression the cornerstone of management. Several treatment options for wet AMD exist using laser light, normal light, medications, and surgical implants that can slow the progress of the condition and even improve vision.
Scientists do not understand precisely what causes drusen deposits in the retina, so the only treatment for dry AMD is to monitor the retina and take steps to prevent the condition from worsening. Monitoring helps to spot wet AMD early so that treatment can immediately begin to slow the disease and preserve vision. Risk factors should be managed during the dry stages of AMD, as well. Quitting smoking, losing weight, and taking special dietary supplements rich in antioxidants can help reduce the risk of further vision impairment.
In advanced macular degeneration, a laser can block new, abnormal blood vessels in the tissues below the macular retina. The ophthalmologist uses a laser to burn spots on these new blood vessels. The small blood vessels form scars and the blood within them coagulates, blocking blood flow and so preventing the blood leakage that causes vision loss. The procedure is painless and is done on an outpatient basis.
Laser treatment is only used when the new blood vessels are clearly visible, but sometimes they’re not. Standard laser treatment may also produce some loss of vision, and recurrence of the abnormal blood vessel growth is common. Transpupillary thermotherapy uses a lower-powered laser to heat the retinal tissues. This produces blood clots that block the new blood vessels, again, preventing the leakage that causes blindness. Unlike laser photocoagulation, TTT preserves vision. TTT is also painless and performed on an outpatient basis.
Photodynamic therapy is the preferred method employed to block the abnormal blood vessels in advanced AMD. The ophthalmologist first injects a “photosensitizing agent,” verteporfin, into the bloodstream. Verteporfin selectively attaches to the walls of newly formed blood vessels and is harmless until “activated” by light. The ophthalmologist then shines a focused red light on the center of the retina with the assistance of placement with a special contact lens. The verteporfin activates, kills off new blood vessel tissues, and the blood vessel becomes blocked with blood clots and scar tissue. PDT preserves vision and blocks both visible and hidden abnormal blood vessels. Patients must avoid sunlight or intense light for five days, however, to avoid burning the skin or retina.
All treatments for wet age-related macular degeneration prevent the further progress of the disease. The only restorative treatment for advanced wet AMD affecting both eyes is to replace the lens in one eye with a miniature telescope. About the size of a pea, this artificial lens doubles or nearly triples the size of the image hitting the retina. As a result, most of the image that would focus only on the macula falls on the peripheral vision part of the retina. The center of the image is still blacked out, but the patient can see most of the central field using peripheral vision. The telescopic lens is placed in one eye, which the patient uses for reading and detail work. The patient uses the other eye for peripheral vision. IMT does successfully allow patients with advanced AMD to avoid legal blindness.
In the last 20 years, treatment for wet age-related macular degeneration has advanced dramatically. Because science understands the basic process of how the body makes new blood vessels, an entire arsenal of medications that block this process is used to preserve vision in patients with advanced wet AMD.
The growth of blood vessels is stimulated by proteins called vascular endothelial growth factors, or VEGF for short. VEGF also makes blood vessels more permeable and vulnerable to leakage, which is not optimal in the setting of macular health. Medicines that block these proteins are called vascular endothelial growth factor antagonists, or, more simply anti-VEGF drugs. They can be short bits of nucleic acid, such as pegaptanib (Macugen), antibodies, such as ranibizumab (Lucentis), brolucizumab (BEOVU), or off-label bevacizumab (Avastin, an anti-cancer drug), or proteins, such as aflibercept (Eylea). These drugs are injected directly into the eye after a local anesthetic has been applied to the eye’s surface.
Verteporfin is the photosensitizing agent used in photodynamic therapy to eliminate the new blood vessels in advanced macular degeneration. Injected directly into the bloodstream, verteporfin selectively binds to the inner lining of newly-formed blood vessels. When a red light is directed to the injured macula, verteporfin activates and destroys the blood vessels, causing scarring and blood clots that block the new blood vessel.
The Age-Related Eye Disease Study 2 (AREDS2) demonstrated a reduced progression of AMD in patients with intermediate AMD in one or both eyes or advanced AMD in one eye by 25% with supplements which include carotenoids (beta-carotene or lutein with zeaxanthin) and antioxidants (vitamin C, vitamin E, zinc and copper. The AREDS 2 formula, which includes lutein with zeaxanthin and not beta-carotene, can be purchased as an over-the-counter dietary supplement.
Macular degeneration medications only treat advanced-stage “wet” macular degeneration, a condition in which abnormal blood vessels form in the central retina and leak into the lower layers of the retina. There is no “best” medication for inhibiting the growth of retina blood vessels since no agent has shown to be superior to others. A physician will make a decision on which therapy best addresses the unique aspects of a particular case.
| Drug name | Learn more | See SingleCare price |
|---|---|---|
| Lucentis | lucentis details | Get free coupon |
| Avastin | avastin details | Get free coupon |
| Bevacizumab | bevacizumab details | Get free coupon |
| Eylea | eylea details | Get free coupon |
| Visudyne | visudyne details | Get free coupon |
| Preservision Areds | preservision-areds details | Get free coupon |
Different classes of medications have different side effects. However, this is not a complete list, and you should consult with a healthcare professional for possible side effects and drug interactions based on your specific situation.
The most common side effects of VEGF antagonists are temporary reactions to the injection, such as eye pain, bloodshot eyes, eyelid swelling, dry eyes, blurred vision, and bleeding. The most serious side effects include blood clots, vitreous detachment, and cataract formation.
Side effects of verteporfin can occur throughout the body. The most common side effects are eye irritation, dry eyes, vision changes, headache, and flu-like symptoms. Because light activates verteporfin, exposure to sunlight or intense light could cause rapid sunburn and retinal damage. Patients must stay out of intense light or sunlight for five days after the injection.
Dietary supplements typically cause few and only minor side effects. The most common side effect of dietary supplements high in carotenoids is to change the skin to a yellow or orange. The most serious side effects are allergic reactions to the active or inactive ingredients in the supplement.
There is no medical or natural cure for macular degeneration. The progress of the condition can be slowed and the risk of vision loss reduced by making dietary and lifestyle changes.
Antioxidants are key to slowing the progress of dry AMD. A diet high in leafy and green vegetables as well as foods containing zinc, such as cheese, whole grains, and meat will slow the progress.
It’s always a good idea to lose excess weight or quit smoking. Additionally, conditions such as hypertension and diabetes can damage retinal blood vessels and cause vision loss, so it’s a good idea to keep the conditions under control.
Macular degeneration cannot be cured. Dry macular degeneration can be slowed by eating a nutritious diet and managing risk factors. In wet macular degeneration, vision loss can be preserved with medications, laser or light surgery, or implants.
There is no pill for macular degeneration.
Early AMD can be managed through diet and lifestyle changes.
The progress of dry macular degeneration can be slowed by eating a nutritious diet high in antioxidants, quitting smoking, losing weight, and managing other conditions that can cause vision loss, such as diabetes or high blood pressure. Wet macular degeneration can be slowed by medications, laser surgery, or light surgery.
The Age-Related Eye Disease Study 2 (AREDS2) demonstrated that a formula of antioxidant vitamins (vitamin C, vitamin E, zinc, and copper) and carotenoids (beta carotene orzeaxanthin with lutein) reduced the risk of AMD progression by 25 percent. The AREDS2 dietary supplement can be purchased over-the-counter as PreserVision.
The key to avoiding or managing macular degeneration is to eat a diet high in antioxidants and carotenoids. Omega-3 fatty acids are often advised to help slow the progress of the condition, but the evidence doesn’t seem to support this conclusion. In general, a nutritious diet that is low in certain types of fat is the best choice for managing macular degeneration.
New treatments for macular degeneration are on the horizon and some are in clinical trials. Currently, dry macular degeneration is not treatable, so researchers are focusing on using existing drugs, such as sirolimus or statins, or creating new drugs to slow the progress of the disease. Stem-cell therapy is being explored as a means of restoring sight by replacing damaged or dead photoreceptors in the retina.
Most patients with dry macular degeneration will experience vision impairment, but only a small percentage will lose central vision. For people who progress to an advanced stage of dry AMD, the average length of time between diagnosis and legal blindness is 10 years according to the American Optometric Association. About 10 to 15 percent of patients with intermediate dry macular degeneration develop wet macular degeneration, which is the type that produces rapid central vision loss.
Marissa Walsh, Pharm.D., BCPS-AQ ID, graduated with her Doctor of Pharmacy degree from the University of Rhode Island in 2009, then went on to complete a PGY1 Pharmacy Practice Residency at Charleston Area Medical Center in Charleston, West Virginia, and a PGY2 Infectious Diseases Pharmacy Residency at Maine Medical Center in Portland, Maine. Dr. Walsh has worked as a clinical pharmacy specialist in Infectious Diseases in Portland, Maine, and Miami, Florida, prior to setting into her current role in Buffalo, New York, where she continues to work as an Infectious Diseases Pharmacist in a hematology/oncology population.
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