Drusen Deposit Accumulation
Drusen form beneath the RPE as early debris deposits.
- Soft: Drusen type (confluent, poorly demarcated)
- Sub-RPE: Location (between RPE and Bruch membrane)
- Age: Risk factor (most common after 60)
- Fundus exam: Visibility (yellow deposits seen)
Drusen formation basics
Placeholder: lipid and protein debris accumulate under the retina.
Early Dry AMD
Mild pigment changes accompany scattered drusen deposits.
- Early: AREDS category (mild risk classification)
- Minimal: Symptom level (often asymptomatic)
- Mottling: Pigment change (RPE hyper/hypo-pigmentation)
- Low-Med: Progression risk (depends on drusen burden)
Early-stage findings
Placeholder: subtle pigmentary irregularity marks early disease.
RPE Atrophy Onset
Focal RPE cell loss creates the first atrophic spots.
- Focal: Atrophy onset (small isolated spots)
- Coupled: Photoreceptor loss (follows RPE death)
- OCT/FAF: Imaging tool (detects early atrophy)
- None: Reversibility (atrophy is permanent)
Onset mechanism
Placeholder: RPE cells die off, exposing underlying tissue.
Geographic Atrophy Expansion
Atrophic patches enlarge and coalesce across the macula.
- ~1.7 mm²/yr: Growth rate (average GA enlargement)
- Coalescent: Pattern (patches merge over time)
- Exposed: Choroid (visible through atrophy)
- Complement inhibitors: Treatment (slow progression)
Expansion pattern
Placeholder: atrophic area grows outward from the fovea region.
Central Vision Loss Assessment
Amsler grid testing reveals the growing central scotoma.
- Amsler grid: Test used (central field screening)
- Scotoma: Symptom (central blind spot)
- Severe: Acuity impact (if fovea involved)
- Preserved: Peripheral vision (usually unaffected)
Functional testing
Placeholder: grid distortion and blind spots map vision loss.
Clinical implication
Placeholder: central loss impairs reading, faces, and driving.
Placeholder: early detection helps preserve remaining central vision.