AGE-RELATED MACULAR DEGENRATION
ARMD is a retinal condition where the light-sensing cells in the macula malfunction and over time, cease to work. According to the American Academy of Ophthalmology, it is the leading cause of central vision loss (blindness) in the United States today for those over the age of 50.
ARMD is divided into a "dry" or nonexudative form and a "wet" or exudative form. Eighty-five to ninety percent of cases are categorized as "dry" macular degeneration where deposits known as drusen, slowly build up behind the retina. Dry macular degeneration tends to progress slowly and most patients will maintain reading vision in at least one eye. Ten to fifteen percent of cases involve the growth of abnormal blood vessels under the retina. These cases are called "wet" macular degeneration due to the leakage of blood and other fluid into the retina. Wet macular degeneration usually begins as the dry form and is responsible for 90% of severe visual loss in macular degeneration. If allowed to continue without treatment, it can damage the macula, resulting in missing or blurred vision in the central reading vision. The outer peripheral part of the vision remains intact.
For many years, laser photocoagulation was the only treatment for the leakage and bleeding associated with wet macular degeneration. Unfortunately it left secondary scarring, which in many cases prevented any improvement in vision. Approximately ten years ago, laser treatment was mostly replaced with photodynamic therapy, although improvement in vision was still rare. In photodynamic therapy, an inactive medication (Visudyne) is given intravenously and is carried by the normal circulation to the leaking blood vessels. The medication is then activated with a “cold” laser which does not leave scarring, and the activated medication then constricts the abnormal vessels.
In recent years, newer medications such as Lucentis and Avastin have significantly improved the visual results compared with earlier treatments. These medications are injected directly into the eye and counteract vascular endothelial growth factor (VEGF), which is thought to stimulate the growth of the abnormal blood vessel seen in macular degeneration. With this treatment, 90% of patients have stabilization of their vision and 30% can show a significant improvement. Unfortunately, the treatment is not a cure and similar to other conditions such as high blood pressure, continued treatment is usually necessary to maintain maximum benefit.
Aging: Approximately 10% of patients 66 to 74 years of age will have findings of macular degeneration. The prevalence increases to 30% in patients 75 to 85 years of age.
Smoking: The only environmental exposure clearly associated with macular degeneration is tobacco smoking.
Family History: The lifetime risk of developing late-stage macular degeneration is 50% for people who have a relative with macular degeneration versus 12% for people who do not have relatives with macular degeneration.
Macular Degeneration Gene: Complement factor H (CFH) and complement factor B (CFB) genes have been determined to be strongly associated with a person's risk for developing macular degeneration. It is not yet clear what initiates the immune response against the retina, although this might involve a humoral immune response.
Hypertension: Also known as high blood pressure.
Cardiovascular Risk Factors: High cholesterol, obesity.
High fat intake: High fat intake is associated with an increased risk of macular degeneration in both women and men. Fat provides about 42% of the calories in the average American diet. A diet that derives closer to 20-25% of total calories from fat is probably healthier. Reducing fat intake to this level means cutting down greatly on consumption of red meats and dairy products such as milk, cheese, and butter. Eating more cold water fish (at least twice weekly), rather than red meats and eating any type of nuts may help macular degeneration patients.
Oxidative stress: It has been proposed that age-related accumulation of low molecular weight, phototoxic, pro-oxidant melanin oligomers within lysosomes in the retinal pigment epithelium (RPE) may be partly responsible for decreasing the digestive rate of photoreceptor outer rod segments (POS) by the RPE. A decrease in the digestive rate of POS has been shown to be associated with lipofuscin formation This is a classic sign associated with macular degeneration.
Race: Macular degeneration is more likely to be found in whites than in blacks.
Exposure to sunlight: There is conflicting evidence as to whether exposure to sunlight (especially blue light) contributes to the development of macular degeneration. A recent study in the British Journal of Ophthalmology on 446 subjects found that it does not. High-energy visible light (HEV) has been implicated as a cause of age-related macular degeneration.
- Pigmentary alterations
- Exudative changes: hemorrhages, hard exudates, subretinal/sub-RPE/intraretinal fluid
- Atrophy: incipient and geographic
- Visual acuity drastically decreasing (two levels or more) ex: 20/20 to 20/80
- Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss.
- Central scotomas: Shadows or missing areas of vision.
- Distorted vision (i.e. metamorphopsia): A grid of straight lines appears wavy and parts of the grid may appear blank.
- Trouble discerning colors
- Slow visual function recovery: Especially after exposure to bright light.