Age-Related Macular Degeneration

Key clinical points

• Dry AMD is far more common; wet AMD accounts for most severe, rapid vision loss.
• Drusen and pigmentary changes define early and intermediate disease.
• AREDS2 supplementation reduces progression risk in intermediate and advanced disease.
• Anti-VEGF injections are the mainstay for neovascular AMD, with newer agents extending treatment intervals.
• Complement inhibitors are now available to slow the growth of geographic atrophy.

Classification and staging

AMD is staged from early (medium drusen) to intermediate (large drusen and/or pigmentary changes) to advanced disease. Advanced AMD takes two forms: geographic atrophy, a well-demarcated loss of the retinal pigment epithelium and photoreceptors, and neovascular AMD, in which abnormal choroidal vessels leak or bleed beneath and within the retina.

OCT is the workhorse for detecting fluid and monitoring therapy, while OCT angiography and fluorescein angiography characterize neovascular membranes.

Risk factors and prevention

Age, smoking, family history, and genetic factors are the strongest risks; smoking cessation is the most impactful modifiable intervention. The AREDS2 formulation of antioxidant vitamins, zinc, lutein, and zeaxanthin reduces the risk of progression to advanced disease in patients with intermediate or advanced AMD in one eye.

Home monitoring for new distortion and prompt evaluation of sudden central visual changes support early detection of conversion to wet disease.

Treatment

Neovascular AMD is treated with intravitreal anti-VEGF agents, which stabilize and often improve vision. Newer higher-durability agents and treat-and-extend regimens reduce injection burden. Geographic atrophy, historically untreatable, can now be slowed with intravitreal complement inhibitors, though these do not restore lost vision.

Low-vision rehabilitation is an essential component of care for patients with established central vision loss.

Recognizing early and intermediate AMD

Early AMD is often asymptomatic and defined by medium-sized drusen without pigmentary change; intermediate AMD shows large drusen and/or retinal pigment epithelium abnormalities and may bring subtle difficulty reading in dim light or slowed dark adaptation. Because vision can be normal at these stages, detection depends on dilated examination and OCT rather than on patient complaints, which makes routine surveillance the main opportunity to intervene.

Risk stratification guides follow-up: patients with intermediate disease, or advanced AMD in one eye, are counseled on AREDS2 supplementation, smoking cessation, and home monitoring with an Amsler grid or a monitoring app, and are told to seek prompt evaluation for any new distortion or central blur that could signal conversion to neovascular disease.