Age-Related Macular Degeneration
Age-related macular degeneration causes painless, progressive loss of central vision in older adults; the boards test distinguishing gradual dry AMD (drusen, managed with AREDS2 vitamins and smoking cessation) from acute wet AMD (choroidal neovascularization with metamorphopsia, treated urgently with intravitreal anti-VEGF).
Overview
Age-related macular degeneration (AMD) is the leading cause of irreversible central vision loss in adults over 50 in the developed world. It targets the macula — the cone-rich center of the retina responsible for sharp, detailed vision — so patients lose central acuity (reading, recognizing faces) while peripheral vision is preserved; they rarely go completely blind. Vision loss is painless and the eye looks white and quiet.
Two forms exist:
- Dry (non-exudative / atrophic) — ~85–90% of cases; slowly progressive.
- Wet (exudative / neovascular) — ~10–15%; less common but responsible for most severe, rapid vision loss.
The strongest overall risk factor is age; the strongest modifiable factor is smoking. Others: family history, white race, and hypertension / cardiovascular disease.
- Leading cause of irreversible central vision loss in patients >50; peripheral vision spared
- Dry (85–90%): drusen (yellow deposits between the RPE and Bruch membrane) → gradual central blur; geographic atrophy = advanced form
- Wet (10–15%): choroidal neovascularization (CNV) leaks/bleeds → acute vision loss + metamorphopsia (straight lines look wavy); accounts for most severe vision loss in AMD
- Painless, white eye — no redness or pain
- Biggest risk factor = age; biggest modifiable = smoking
- Amsler grid = detection and home monitoring (central scotoma, line distortion)
- OCT = best test to detect sub-/intraretinal fluid; monitors anti-VEGF response
- Fluorescein angiography = confirms leaking CNV in wet AMD
Dry vs. Wet AMD
| Feature | Dry (non-exudative) | Wet (neovascular) |
|---|---|---|
| Frequency | ~85–90% | ~10–15% |
| Hallmark | Drusen, geographic atrophy | Choroidal neovascularization |
| Onset | Gradual, slow | Acute / rapid |
| Key symptom | Slow central blur | Metamorphopsia, acute loss |
| Fundus | Drusen, RPE pigment change | Subretinal fluid, hemorrhage, exudate |
| Treatment | AREDS2 vitamins, stop smoking | Intravitreal anti-VEGF |
| Severity | Milder, slower | Worse — most severe vision loss |
Vignette: A 72-year-old man reports that over 3 days the straight edges of his door frames and bathroom tiles look wavy and bent, with a gray blur in the center of his right eye. The eye is white and painless. Amsler grid shows distortion; fundus exam reveals subretinal fluid and a small macular hemorrhage.
- Diagnosis: Wet (neovascular) AMD from choroidal neovascularization
- Next best step: OCT (± fluorescein angiography) to confirm CNV, then urgent referral for intravitreal anti-VEGF (bevacizumab, ranibizumab, or aflibercept)
- Pearl: Acute metamorphopsia in an older adult = wet AMD until proven otherwise; treat fast to preserve vision.
Vignette: An 80-year-old woman with a 40-pack-year smoking history has 2 years of slowly worsening trouble reading fine print. The eye is painless with no redness. Fundus shows numerous drusen and pigmentary (RPE) changes — no hemorrhage or fluid. She asks how to protect her better eye.
- Diagnosis: Dry (non-exudative) AMD, intermediate stage
- Next best step: AREDS2 supplements to slow progression + smoking cessation + Amsler-grid home monitoring
- Pearl: Because she smokes, use AREDS2 (lutein/zeaxanthin) — beta-carotene is avoided in smokers (↑ lung cancer risk). AREDS2 slows progression but does not reverse vision loss or help early/no AMD.
Dry = Drusen — both start with "Dr-"; Dry is the Dominant type (~85–90%) and develops slowly.
Wet is Worse — Wavy lines (metamorphopsia), rapid loss, and it needs anti-VEGF.
AREDS2 → beta-carotene Banned in smokers (lung cancer) → swapped for lutein / zeaxanthin.
- Dry AMD: no cure; AREDS2 (vitamins C & E, zinc, copper, lutein, zeaxanthin) slows progression in intermediate AMD or advanced AMD in one eye only — not preventive, not for early AMD
- Smokers: give AREDS2 (lutein/zeaxanthin), never original AREDS beta-carotene (↑ lung cancer)
- Wet AMD: first-line = intravitreal anti-VEGF; laser photocoagulation / photodynamic therapy are older second-line options
- All patients: smoking cessation (biggest modifiable factor), Amsler-grid monitoring, low-vision aids
- Don't confuse with other painless acute vision loss: CRAO (cherry-red spot), retinal detachment ("curtain," flashes/floaters), vitreous hemorrhage
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