Age-Related Macular Degeneration (AMD): Clinical Teaching Handout
1) Overview
AMD is a chronic degenerative disease affecting the photoreceptor–RPE–Bruch’s membrane–choriocapillaris unit.
It presents in two major forms:
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Dry (atrophic) AMD → slow, progressive central vision loss; may progress to Geographic Atrophy (GA)
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Wet (neovascular) AMD → new, fragile blood vessels cause leakage/bleeding → potentially rapid vision loss
2) Key Risk Factors
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Age > 60
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Family history / complement gene variants
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Smoking (↑ oxidative stress)
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Low intake of leafy greens & carotenoids
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Cardiometabolic disease: HTN, dyslipidemia
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Presence of reticular pseudodrusen = higher progression risk
3) Early Functional Symptoms
| Symptom | Clinical Clue |
|---|---|
| Difficulty in dim light | early rod dysfunction precedes acuity loss |
| Delayed dark adaptation | sensitive indicator of progression |
| Metamorphopsia (wavy lines) | consider conversion to wet AMD |
| Central blur / reduced contrast | early RPE + photoreceptor stress |
4) Structural Biomarkers (OCT-based)
| Feature | Interpretation | Risk Implication |
|---|---|---|
| Soft drusen | Extracellular lipid & complement deposits | Moderate progression risk |
| Subretinal drusenoid deposits (RPD/SDD) | Deposits above RPE; thin choroid | High GA progression risk |
| Hyperreflective foci | Migrating RPE / microglia | Predicts faster degeneration |
| Ellipsoid zone disruption | Photoreceptor loss | Correlates with decreased sensitivity |
5) Pathogenesis (Simplified)
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Oxidative stress → mitochondrial damage in RPE
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Autophagy impairment → lipofuscin & drusen accumulation
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Complement overactivation → chronic para-inflammation
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Choroidal ischemia + rod susceptibility → early functional decline
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Microglia + Müller glia activation sustain degeneration
6) Management Principles
Dry / GA
| Intervention | Notes |
|---|---|
| AREDS2 supplementation | For intermediate AMD (not early or GA) |
| Mediterranean-style diet | Improves oxidative & inflammatory balance |
| Smoking cessation | Strongest modifiable factor |
| Monitor with OCT + dark adaptation tools | Detect progression early |
| C3/C5 complement inhibitors | Slow GA lesion growth (not restorative) |
Wet AMD
| Treatment | Key Clinical Points |
|---|---|
| Anti-VEGF intravitreal therapy | First-line; urgent if new fluid/hemorrhage |
| Treat-and-extend regimen | Maintains control while reducing visits |
| Evaluate for fibrosis/EMT over time | Explains plateaued visual gains |
7) When to Refer Urgently
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New metamorphopsia
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Sudden unilateral central blur
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OCT showing new subretinal/intraretinal fluid or hemorrhage
Urgency: Treatment delay in wet AMD directly correlates with worse final vision.
8) Patient Counseling Phrases
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“AMD is treatable, but early detection protects vision.”
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“Continue check-ups even when vision seems stable.”
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“Lifestyle changes do matter—particularly smoking and diet.”
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“Report any new distortion immediately.”
9) One-Sentence Core Clinical Pearl
The earliest functional sign of AMD progression is impaired rod-mediated dark adaptation — not decreased visual acuity.
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