SIGNS AND SYMPTOMS
Age-related macular degeneration (AMD) is the leading cause of legal blindness in the United States of America for persons over the age of 65. AMD is present in approximately 10 percent of the population over the age of 52 and in up to 33 percent of individuals older than 75. AMD is an extension of abnormalities that begin and progress through Bruch’s membrane, involving the retinal pigment epithelium (RPE) and photoreceptors. The earliest clinical manifestation of AMD are drusen and macular pigmentary atrophy. The presence of drusen does not indicate AMD. However, it serves as precursor, warning that there is the potential for progression and visual loss. AMD is bilateral in 55 percent of cases.

The visual symptoms associated with AMD depend on its severity and type. In general, the “dry” form (no subretinal choriodal neovascularization, exudation or hemorrhage) is less severe, producing a gradual, painless distortion or loss of central vision. Some patients complain of color distortion. “Wet” AMD (subretinal choriodal neovascularization, exudation and or hemorrhage) often produces severe central visual loss. Visual loss produced by wet AMD is often rapidly progressive.

Some of the clinical retinal signs of dry AMD include drusen of the posterior pole, granular clumping and disorganization of the RPE in the macular area, macular RPE hyperplasia and degeneration of the outer retinal layers with circumscribed areas of geographic atrophy of the RPE.

Some of the clinical retinal signs associated with wet AMD include hard and soft drusen, subretinal thickening secondary to classic or occult choroidal neovascularization (producing a grayish-green subretinal hue), subretinal, intraretinal or vitreous hemorrhage, subretinal and intraretinal exudation with serosanguinous fluid accumulation and fibrovascular scar formation (disciform scarring).

PATHOPHYSIOLOGY
All forms of AMD possess initial, common changes within the macular RPE. While the mechanisms and processes are poorly understood, some postulate these changes are initiated by isolated regions of choriocapillaris vascular failure. These proceedings cause the RPE to degenerate, resulting in photoreceptor loss. As the photoreceptors disintegrate, the inner nuclear layer collapses and contacts Bruch’s membrane, initializing the degeneration of the outer retinal layers. Some theorize that the mechanism of damage may be through ultraviolet radiation-induced oxidation and free radical formation within these structures.

Wet AMD results when the macular RPE/Bruch’s barrier is compromised by new, weak and leaky blood vessels that grow upward into the retina from the choriocapillaris. These occult (poorly defined) or classic (more easily defined) subretinal choroidal neovascular membranes may leak serosanguinous fluid causing RPE detachment, sensory retinal detachment, subretinal or intraretinal bleeding or fibrovascular, disciform scarring.

MANAGEMENT
Begin managing patients with potential or diagnosed AMD by recognizing the associated risk factors and providing patient education. The disease is more common in individuals who have a family history of AMD, are of light complexion, in those who have a cardiovascular history, history of previous lung infection, hyperopia or decreased hand grip strength. It is typically more progressive in males. Smoking is a significant risk factor.

The management of patients with dry AMD begins with biannual eye examination, with dilated funduscopy. Home therapy, aimed at early detection, using a home Amsler grid may work to monitor the stability of suspicious or involved maculae. The elimination of potentially harmful ultraviolet light using UV coatings on spectacles and sunglasses may also reduce the risk of photochemical /oxidative damage to the retina for all patients.

Researchers have indicated that oral antioxidants like vitamins C and E and oral zinc may play a role in reducing retinal damage by terminating the chemical reactions initiated by free radicals, created by retinal metabolism. Multiple vitamins, oral zinc or products specifically designed for this purpose, such as Ocuvite and ICaps, are useful as a tool for slowing the progression of AMD.

The treatment for symptomatic wet AMD begins with a referral to the vitreoretinal specialist for intravenous fluorescein angiography. The Macular Photocoagulation Study (MPS) examined the efficacy of treating subretinal, extrafoveal (200 to 2,500 µm from the center of the foveal avascular zone, juxtafoveal (1 to 200 µm from the center) and subfoveal choroidal neovascular membranes with laser photocoagulation. Laser photocoagulation reduces the risk of severe vision loss in patients with definable subretinal choroidal neovascular membranes.

In cases where hemorrhage and exudate obscures the angiogram or the neovascular membrane is poorly defined by fluorescein angiography, indocyanine green angiography may offer an additional modality to determine if treatment is feasible. Unfortunately, the recurrence rate following treatment is approximately 50 percent. Most recurrences develop within the first year, making a three-month follow up schedule critical. The efficacy and effectiveness of surgical procedures for the removal of subretinal neovascular membranes are currently under investigation.

In cases where bilateral central visual acuity has been lost, low vision and vision rehabilitation specialists may be able to offer training or optical devices which improve patients’ quality of life. Macular translocation surgery has been performed with significant success and restored usable vision to patients with wet ARMD.

CLINICAL PEARLS

• In general, the risk to patients with dry AMD for progression to wet AMD, over any given five-year period, is approximately 14 to 20 percent.

• In patients who have already lost one eye to wet AMD, over the course of five years, the risk of developing wet stage disease in the fellow eye is 10 percent for patients whose fellow eye has neither large drusen or pigment clumps, 30 percent for fellow eyes containing either large drusen or pigment clumps and 50 percent for fellow eyes with both pigment clumps and large drusen present.

Other reports in this section

• Posterior Vitreous Detachment
• Tractional Retinal Tears
• Epiretinal Membrane
• Diabetic Retinopathy
• Lattice Degeneration
• Retinal Vein Occlusion
• Retinal Artery Occlusion
• Macular Degeneration
• Toxoplasmosis
• Choroidal Melanoma
• Acquired Retinoschisis
• Hollenhorst Plaque
• Idiopathic Central Serous Chorioretinopathy
• Macular Hole
• Presumed Ocular Histoplasmosis Syndrome
• Retinal Macroaneursym
• Retinitis Pigmentosa
• Retinal Detachment
• Hypertensive Retinopathy
• Retinal Pigment Epithelium (RPE) Detachment
• Papillophlebitis
• Ocular Ischemic Syndrome
• Coats’ Disease and Leber’s Miliary Aneurysm