Age-Related Macular Degeneration
By Connie Goldsmith, RN, BSN, MPA

Changes in vision occur throughout our lives. Some young people need glasses for driving or watching movies.
Others wbo enjoy perfect vision until they reach middle age discover they require reading glasses. Many people must wear bifocals or trifocals to obtain the best vision at every distance. However, these problems are minor irritations compared to the loss of vision caused by a common agerelated disorder.
Painlessly and insidiously, age-related macular degeneration (AMD) affects an estimated 10 million Americans.' It's the most common cause of vision loss and blindness in people over 65, and it can affect people at younger ages as well.'
The risk of developing AMD steadily increases with age.
People in their 50s bave about a 2% chance of developing it, while the risk rises to nearly 30% in those over age 75.^ Every three minutes, another case of AMD is diagnosed in the US.^
Each year, 200,000 people with AMD lose all central vision in one or both eyes.' More people than ever before will be forced to live with AMD as the baby boomer generation continues to grow older.
This article reviews the anatomy and function of the normal retina. It also identifies tbe risk factors for AMD and its causes, as well as its diagnosis and treatment. A diagnosis of AMD means a significant decrease in vision, and, in some cases, complete blindness. Because patients face important concerns related to their everyday activities, methods of addressing those issues will be discussed.

Normal Vision
For a person to see properly, light must pass through the cornea, pupil, and the lens. Then it must be focused onto the retina, the innermost layer of tissue at the back of the eye.
The surface of the retina must he flat and smooth to produce a good visual image. The retina contains two types of lightsensing photoreceptot cells called rods and cones. Rods, concentrated at the periphery of the retina, allow us to see objects in dim light and provide our peripheral vision. Cones are responsible for sharp, centra! vision in bright light, as well as color perception.
At the center of the retina lies the macula. It's 5-6 mm in diameter, with a small depressed area in the center called the fovea, which is the site of sharpest vision. During activities that require good vision—for example, reading and driv-

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ing—the lens focuses incoming light onto the macula, where millions of cells change it into nerve impulses that travel through the optic nerve to the part of the brain that interprets what the eye sees. Below the retina is a region of tiny blood vessels called the choroid. Between tbe retina and the choroid is an extremely thin layer of tissue called the retinal pigment epithelium (RPE). Oxygen and nutrients pass from the choroid through the RPE to nourish the retina.

Risk Factors and Causes of AMD
Although the exact cause of AMD is unknown, important risk factors have been identified, including aging, gender (more common in women), cigarette smoking (decreases blood flow to retinal vessels,) race (most common in whites), family history (certain genes increase the risk for
AMD by 30%), antioxidant deficiency, elevated cholesterol, hypertension, increased exposure to sunlight or ultraviolet light, hliie or green eyes (less protective pigmentation), and severe farsightedness. In most cases, a combination of environmental and genetic factors is likely present.^''
Age-related macular degeneration is caused by two different disease processes, both of which can lead to significant loss of central vision. About 8 5 % of people are affected by the less virulent condition called dry or nonexudativc
AMD.^ Drusen, a yellowish-white material formed of amorphous debris, is deposited in the macula below the RPE, causing its detachtnetit atid scarring the mactila. The pigmentation and the cone cells break down, adding to the debris. Nearly everyone over age 50 has small, bard drusen in at least one eye, although most people will not progress to
AMD.'' Those with larger, soft drusen, or many drusen, are much more likely to develop it.'' People with dry AMD experience a gradual loss of central vision over several years.*
About 15% of people with AMD develop the more serious form, called wet or exudative AMD, and it accounts for most of the blindness and severe loss of vision associated with AMD.^ Wet AMD damages tbe macula more quickly, sometimes in just weeks or months. It begins when abnormal blood vessels grow in the choroid, a process called choroidal neovasculadzation (CNV). Tbe new vessels are fragile and often leak serum and blood into tbe RPE layer under the macula; sometimes the abnormal vessels hemorrhage into retinal tissue. Photoreceptors are rapidly

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destroyed and central vision loss can be profound. The damaged area contracts, leaving an elevated scar on the macula. It often

both eyes 6.7

On the left: as seen with normal vision. On the right: as seen by a person with macular degeneration. Source: National Eye Institute, Nationai Institutes of Heaith.

Symptoms and Diagnosis of AMD
The onset of AMD may not be recognized by some patients because it doesn't cause pain. Also, the braiti learns to compensate by supplying missing pieces of visual information, leaving some patients unaware of symptoms until the disease has progressed. If only one eye is affected, people often continue to drive, read, and perform other close work using tbe unaffected eye.

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Inevitably, the disease progresses and symptoms do develop. One of the most common is that straight lines begin to
On the ieft: as seen with normai vision. On the right: as seen by a person with appear wavy. Other symptoms may include macuiar degeneration. Source: Nationai Eye Institute, Nationai institutes of Health. decreased color perception, sensitivity to glare, problems with depth perception, and a dark blur or "white-out area" in the central vision. As time passes, deterioration of the central vision becomes impossible to ignore. Macular degeneration may be discovered durTreatment for AMD ing a routine vision exam, or tbe patient may present with vision problems suggesting the presence of AMD.''^'^
Tbere is no standard treatment currently available for
Common diagnostic exams include the following.^
• A visual acuity examination using the Snellen eye chart, whicb can measure vision at various distances.
• Ophtbalmologic examination after dilation ot pupils by medications, which may reveal the presence of drusen or signs of hemorrhage in the macula.
• T h e Amsler Grid, a standardized pattern of straight lines like a checkerboard, whicb can detect early
AMD. The patient focuses on a black dot on the grid.
People without AMD will see straight lines; people with it may see wavy, distorted lines.
• Wet AMD will be diagno.sed by angiography, a procedure in which dye is injected into a peripheral vein, while photographs of the macula are taken with a special camera. If AMD is present, the dye seeps into retinal tissue, highlighting broken or leaking vessels.

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dry AMD, aithotigh intake of certain dietary supplements looks promising. A study by the National Eye Institute
(NEI) demonstrated that antioxidants (500 mg vitamin C,
400 ID vitamin E, and I 5 mg beta-carotene) and 80 mg zinc taken daily, reduced the risk of developing advanced AMD by 25%, and vision loss by 19%.^ Other researchers reported that a daily intake of about 6 mg of the carotenoids lutein and zeaxanthin (found in deep green, yellow, and orange fruits and vegetables), reduced the risk of AMD by 56%.*
Fortunately, dry AMD develops very slowly, and many people can continue to lead normal lives, especially if it affects only one eye.^
Becau.se the damage done by wet AMD is irreversible, the treatment goal is to preserve current vision. Laser photocoagulation is the only proven long-term treatment. In this procedure, pulses of precisely controlled light are aimed at the choroidal neovascularization beneath the retina. The lasers

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Wet AMD - Subfoveal Occult CNV

Healihy Fo\ca

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' New vessels leak Ruid into sub-RPE space (exudation)

Cross-section of a healthy macula. Used with permission from Index Corporation.

Cross-section of a macula with wet AMD showing choroidal neovascularization. Used with permission from Iridex Corporation.

heat destroys the GNV, while the patient experiences only mild discomfort because the eyes are anesthetized. While scarring from the treatment leaves a permanent blind spot, progression of the disease is temporarily halted.
Unfortunately, about 50% of patients will develop new leakage of vessels within three years and may require additional surgery.^''' angiography to detect recurrent CNV. Patients with wet
AMD may consider using the Amsler Grid daily or weekly to monitor their vision, because early treatment may be able to prevent further vision loss.

The United States Food and Drug Administration approved a promising new treatment for wet AMD three years ago. In this procedure, called phntodj'namic therapy, a light-sensitive dye is injected into a peripheral vein. When the dye reaches the eye, it concentrates in the area of abnormal blood vessel growth. When low-intensity laser energy is directed into the eye, the dye absorbs it, destroying tlie blood vessels. The retina remains undamaged, unlike treatment with photocoagulation.^'''''
Success in treatment of wet AMD is measured in lines of vision gained, retained, or lost on standard vision charts.
Two years after photodynamic therapy, an average of 53% of treated patients had lost fewer than three lines of vision, compared to about 37% of untreated patients.' Because this treatment has only been used for three years, its long-term effectiveness is unknown, although as with photocoagulation, it's likely that more than one treatment will be required. Because the light-sensitive drug remains in the patient's system for days, photodynamic therapy carries the possibility of unusual complications. Both the eyes and skin may be badly burned if exposed to stmlight, halogen light, and even notmal bright indoor lighting, such as found in a dental office. Sunscreen offers no protection. Patients must cover their skin with clothing and wear sunglasses that block up to 90% of visible light for at least five days. Other potential adverse effects include flu syndrome, headache, cardiac arrhythmias, and eczema.'"
Patients should understand that regardless of which procedure is used, the ophthalmologist will need to follow their AMD with periodic eye exams, including fluorescein

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What's on the Horizon?
Many investigational studies are underway to develop more effective treatments for both forms of AMD:
• A^e-Related Eye Disease Study (AREDS)— randomized clinical trials to evaluate the effects of pharmacologic doses of antioxidants and zinc on the progression of A M D . "
• Complications of Age-Related Macular Degeneration
Prevention Trial (CAPT)— use of low-intensity laser in eyes with macular drusen in an attempt to prevent later complications of AMD and preserve visual funaion.
Study subjects must have bilateral drusen; only one eye will be treated, leaving the other as die control."
• Submacular Surgery Trials (SST)—surgical removal of CNV and areas of hemorrhage in an attempt co improve or maintain vision of patients with wet
AMD, especially in those who are unresponsive or unsuitable for laser treatment."
• Transpupiliary thetmotherapy (TTT)—-use of laser photocoagulation to create a prolonged, but moderate, temperature increase in the retina and abnormal
CNV. This process causes less damage to the retina than standard laser therapy.^
" Transplantation ofphotoreceptorand retinal pigmentation cells from non-damaged areas to damaged areas. These cells may be injected tmder the retina.^
•Thalidomide is being evaluated as a treatment for wet
AMD becau.se of its ability to inhibit aiigiogenesis (the formation of new abnormal blood vessels) in the eyes. A small clinical triaJ of about 75 patients is underway.^

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Retina with dry AMD. Used with permission from
Iridex Corporation.

Retina with wet AMD showing a disciform scar.
Used with permission from Iridex Corporation.

Considerations for Health Care Providers

decreased self-confidence, social isolation, and impairment in performing many activities of daily living. Patients may experience a period of grief and mourning over their vision loss, similar to the process that comes with death—denial, anger, depression, and finally, acceptance.'^
Ideally, a person witb AMD will comply with necessary follow-up care, learn how to safely use low-vision aids, regain self-conftdence, perform normal self-care activities such as bathing and dressing, and return to the The ability to cope witti normal pattern of socialization. AMD depends on iiow
Some patients are reluctant to tell much visiop is lost, how family and friends about their decreased vision for fear of becom- sudden or gradual the ing a burden. The ability to cope change is, the padeut's with AMD depends on how much pre-illness coping style, vision is lost, how sudden or gradual the change is, the patient's pre- and, especially, the illness coping style, and, especially, patient's support system. the patients support system.'^

Blindness is one of the most feared disabilities, and people diagnosed with AMD are certain to be anxious about their future. Patients should understand that they may retain good peripheral vision and some usefiil color vision.
They'll likely be able to move about tbeir homes and perform some tasks independently, even though they may be defined as legally blind (a visual acuity of 20/200 or less in the best eye with corrective lenses). It's more accurate to refer to patients with AMD as having low vision, rather than as blind.
Dental hygienists may discover that some of tbeir patients have AMD, atid it's important to utilize communication skills appropriate for low-vision individuals:'^
• Identify yourself when entering the room.
• Describe wbat you're doing, step by step.
• Turn on ligbts and open curtains to provide as much light as possible.
• Tell tbe patient when you leave the room.
" When escorting a visually impaired patient to treatment areas, allow the patient to hold your arm, rather than the other way around.
• Describe the surroundings during tbe walk.
• Be careful about labeling a low-vision patient as confused; he or she may be maldng mistakes simply because of vision problems.
• Make sure that the treatment facility is prepared to accommodate guide animals.
• Enlarge written materials as much as possible for reading ease.
• Include significant others when instructing patients about oral care so that they may assist \i necessary.
Patients with impaired vision may be subject to sensory and perceptual alterations related to decreased vision, anxiety due to fear of blindness and increased dependence.

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Many resources are available to individuals with low vision. Patients should be encouraged to participate in local support groups in order to share problems atid sokitions with otbers, like how to modify the home to provide a safe and .secure environment. Health care providers can refer patients to low-vision specialists for training in the devices they need. Utility companies may offer discounts or special services such as free directory assistance. Legal blindness entides people to claim an additional tax deduction on their federal income tax return. Talking books and tape players are available through public libraries and the U.S. Library of Congress. The U.S. Department of
Health and Human Services may provide rehabilitative counseling. Health care providers can help educate the public about age-related macular degeneration. People should be encouraged to follow a healthy lifestyle, including eating a low-fat diet high in leafy green vegetables, smoking cessa-

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Assistive Devices fer People with Lew Visien
• Mognifying devices (TV screens and tabletop magnifiers)
• Large print devices (books, cards magazines, clocks, and watches)
• Reading machines
• Large button telephones
• Taiking books and timepieces
• Special high intensity iighting
• Hand-heid telescopes
• Spectacle mounted telescopic ienses for distance vision
• Spectacie mounted microscopic lenses for close vision
• Reading aids such as angied book stands, book racks, and prismatic glasses 6. Gottlieb Jl; Age-related macular degeneration. Journal of the American Medical Association 2002:288(18);22332236.
7. Fine SL Berger JW, Maguire MG, Ho AC: Age-reiated macuior degeneration. The New Engiahd Joumai of
Medicine 200G;342(7):483-492,
8. Suppiements siov^^ tiie course of maouior degeneration.
Harvard Women's Health Watch 2001:iXC5):l-2.
9. Henney JE; New theropy for macuiar degeneration. The
Journal of the American Medioa! Association 2000;283
C21);2779.
10. Ricin D, Lane AM. Milier JW; Photodynamic therapy; The nurse's role. Insight: the Journal of the American Society of Ophthalmic Registered Nurses2(Xl^: 26C2):44-48.
11. Nationai Eye institute, 2003; Clinical Studies supported by the NEi. Availabie at http;//wvi/v^^.nei.nih.gov/neitrials/ toc-researcharea.asp. Accessed 2/13/03.
12. Lueokenotte AG; Sensory function. In Gerontologic
Nursing. 2nd ed. St. Louis, Mosby, 2000, pp. 695-707.
Connie Goldsmith, RN, BSN, MPA, is a freelance writer who lives in
Sacramento, CA. Her clinical experience includes 12 years in cardiac and neurologic critical care. She writes for adult and children's magazines, as well as protessionci health journals, and has published two nonfictian books for older children.
^

Sourc0: listed references

tion, and use of good-quality sunglasses co protect eyes from ultraviolet iight. In addition, everyone over 60 years old should have an annual eye examination through dilated pupils. While there is not yet a cure for AMD, effective treatments are available and more are on the way. The earlier
AMD can be detected, the earlier it can be treated, and the greater the potential for avoiding fijture vision loss.

For further infoimation
Americon Foundation for the Blind
800/232-5463; www.afb.org
Macuiar Degeneration Foundation, inc.
888/633-3937; www.eyesight.org

References
1. Age-related maouiar degeneration {JAMA Patient
Page). Journal of the American Medioai Association
2002, 288(18);2358.
2. Nationai Eye Institute, 2002: Facts abaut age-related macuiar degeneration. Avaiiabie at http://www.nei. nih.gov/heaith/maoulardegen/armd_facts.htm. Accessed 1 /26/03.
3. Macuiar Degeneration Foundation, 2001; Aduit macuiar degeneration. Avaiiabie at wv/w.eyesight,org/Aduit/ aduit.html. Accessed 2/26/02.
4. Riordan-Eva P; Eye. in Current Medicai Diagnosis and
Treatment 2000. 41st ed.. New York, Lange Medioai
Books, MoGraw-Hiil, 2002. pp, 210-211.
5. iHyman L, Sohachat AP, He Q, Leske MC; Hypertension, cardiovascular disease, and age-reiated macuiar degeneration Archives of Optittialmology 2000,118(3):
351-358.

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Notionai Eye institute
301/496-5248; www.nei.nih.gov
Nationai Federation of the Biind
410/659-9314; www.nfb.org

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