Central retinal degeneration — dry (atrophic) and wet (neovascular) forms; leading cause of central vision loss in older adults.
Also known as: AMD, age-related macular degeneration, dry AMD, wet AMD, neovascular AMD, geographic atrophy, ARMD
Overview
Progressive degenerative disease of the macula characterized by drusen, retinal pigment epithelial (RPE) changes, and ultimately loss of photoreceptors and central vision. Dry (non-exudative, atrophic) AMD comprises ~85-90% of cases; wet (neovascular, exudative) AMD is defined by choroidal neovascularization (CNV) and accounts for most severe vision loss.
Epidemiology
Leading cause of irreversible central vision loss in adults >50 in industrialized countries. Prevalence rises sharply with age — ~10% by 60, ~30% by 75. Whites of European ancestry are most affected.
Try two board-style Age-Related Macular Degeneration questions
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Question 1EENTMedium
A 70-year-old male with progressive vision loss over 2 years has central scotoma and difficulty reading. Funduscopy shows drusen deposits, geographic atrophy of the retinal pigment epithelium (RPE), and pigmentary changes in the macula bilaterally. Visual acuity is 20/200 right and 20/80 left. Which of the following is the most likely diagnosis?
ADry age-related macular degeneration
BHydroxychloroquine retinopathy
CAge-related cataracts
DDiabetic macular edema
EWet age-related macular degeneration
Reveal answer & full explanation
Correct answer: A — Dry age-related macular degeneration
ADry age-related macular degeneration✓
BHydroxychloroquine retinopathy
CAge-related cataracts
DDiabetic macular edema
EWet age-related macular degeneration
Why Dry age-related macular degeneration is correct
Dry (non-neovascular) age-related macular degeneration (AMD) is the most common form (85-90%)
Characterized by drusen (extracellular deposits between the retinal pigment epithelium and Bruch membrane), RPE atrophy (geographic atrophy), and pigmentary changes
Causes gradual central vision loss (scotoma) because the macula is affected
Why the others are wrong
Diabetic macular edema — related to diabetes, not drusen or geographic atrophy (anchoring on retinal pathology)
Wet age-related macular degeneration — involves choroidal neovascularization with rapid central vision loss and metamorphopsia, treated with anti-VEGF injections; the slow course with drusen and geographic atrophy points to the dry form (right-disease-wrong-subtype)
Age-related cataracts — cause gradual blurry vision but not central scotoma or drusen on funduscopy (confused-with lens opacity)
Hydroxychloroquine retinopathy — tempting because hydroxychloroquine toxicity also causes gradual, bilateral paracentral or central vision loss with pigmentary changes of the macular RPE, but it requires prolonged hydroxychloroquine exposure, usually 5 or more years, and its classic (late) fundus sign is a bull's-eye ring of parafoveal RPE depigmentation that spares the fovea, not drusen; drusen with geographic atrophy are the hallmark of dry AMD (confused-with toxic maculopathy)
Additional high-yield points
Treatment: (1) AREDS2 formula (vitamins C 500mg, E 400 IU, zinc 80mg, copper 2mg, lutein 10mg, zeaxanthin 2mg) reduces progression to advanced AMD by ~25% in intermediate AMD or advanced AMD in one eye; not for early AMD; (2) no anti-VEGF injections (only for wet AMD); (3) low vision aids, magnification devices, eccentric viewing training; (4) smoking cessation (smoking doubles AMD risk)
Question 2EENTMedium
A 70-year-old woman presents with 2 weeks of painless central vision loss with metamorphopsia (straight lines appear wavy) in her right eye. Fundoscopic exam of the right eye shows drusen deposits and subretinal hemorrhage. Amsler grid testing shows distortion. What is the most likely diagnosis?
Why wet (neovascular) age-related macular degeneration is correct
Subretinal hemorrhage confirmed on fundoscopy distinguishes wet AMD from dry AMD
Wet (neovascular) AMD involves choroidal neovascularization causing vision loss over days to weeks, usually in one eye at a time, with subretinal hemorrhage and metamorphopsia
Dry age-related macular degeneration — presents with drusen deposits and gradual central vision loss over years with geographic atrophy, but without subretinal hemorrhage; treated with Age-Related Eye Disease Study 2 (AREDS2) supplements (vitamins C, E, zinc, copper, lutein, zeaxanthin) to slow progression
Diabetic macular edema — also causes central vision loss but arises from retinal thickening with microaneurysms and hard exudates in a diabetic, not drusen with subretinal hemorrhage
Open-angle glaucoma — is likewise painless but produces gradual peripheral field loss over years with an increased cup-to-disc ratio, sparing central acuity until late and never causing metamorphopsia
Central retinal vein occlusion — also causes painless monocular vision loss with retinal hemorrhage in older adults, but its onset is usually sudden and the hemorrhages are diffuse intraretinal flame and blot hemorrhages throughout the retina with dilated, tortuous veins and disc swelling, not drusen with a subretinal hemorrhage at the macula
Additional high-yield points
Age-related macular degeneration (AMD) is the leading cause of blindness in patients over 65
Amsler grid testing reveals distortion (metamorphopsia) in macular disease
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Accumulation of extracellular debris (drusen — lipid- and protein-rich material) between RPE and Bruch membrane impairs metabolic exchange of photoreceptors. Oxidative stress, complement dysregulation (CFH variants), and mitochondrial dysfunction drive RPE loss and photoreceptor degeneration → geographic atrophy in late dry AMD. In wet AMD, choroidal vessels proliferate through Bruch membrane in response to VEGF, forming choroidal neovascularization that leaks fluid and blood beneath the retina → subretinal fluid, hemorrhage, and ultimately disciform scar.
Clinical presentation
Symptoms
Dry AMD: gradual painless central blurring, difficulty reading, central scotomas; often asymptomatic early
Wet AMD: SUDDEN-onset central distortion (metamorphopsia — straight lines look wavy), central scotoma, or decline in vision over days to weeks
Patients describe missing letters in words or distortion seen on Amsler grid testing
Peripheral vision is preserved
Signs / physical exam
Drusen on dilated fundus exam — hard (small, discrete) or soft (large, confluent, indistinct borders)
UV protection with sunglasses is reasonable but unproven (evidence linking sunlight to AMD is inconsistent)
Amsler grid self-monitoring for new distortion → urgent ophthalmology if change
AREDS2 supplementation for intermediate AMD, or advanced AMD (geographic atrophy or neovascular) in one eye to protect the fellow eye: vitamin C 500 mg, vitamin E 400 IU, zinc 80 mg (or lower 25 mg formulation), copper 2 mg, lutein 10 mg, zeaxanthin 2 mg — replaces beta-carotene from original AREDS (lung cancer risk in smokers)
Do NOT use AREDS2 in early AMD (no benefit) and avoid beta-carotene formulation in smokers
Second-line / adjunct
Wet AMD — intravitreal anti-VEGF — ranibizumab, bevacizumab (off-label, equivalent efficacy per CATT/IVAN), aflibercept, brolucizumab, faricimab — typically monthly loading then treat-and-extend; mainstay of therapy
Photodynamic therapy with verteporfin — rarely used today, reserved for polypoidal CNV
Thermal laser photocoagulation — only for select extrafoveal CNV; largely supplanted by anti-VEGF
Geographic atrophy (late dry AMD) — complement inhibitors approved by FDA: intravitreal pegcetacoplan (C3 inhibitor) and avacincaptad pegol (C5 inhibitor) slow progression of GA
Implantable telescope or augmented-reality devices in selected end-stage cases
Complications
Irreversible central vision loss; legal blindness if bilateral
Conversion of dry to wet AMD (Amsler grid surveillance is for this)
Disciform scar — end-stage wet AMD with severe permanent central scotoma
Fall risk, loss of independence, depression
Endophthalmitis (~1 per 2,000-5,000) and intraocular pressure spikes from intravitreal injections
PANCE pearls
Dry AMD = drusen + RPE changes ± geographic atrophy; wet AMD = choroidal neovascularization with fluid, hemorrhage, or exudates.
SUDDEN metamorphopsia in an older patient with AMD = wet AMD until proven otherwise — urgent referral for anti-VEGF.
AREDS2 is for INTERMEDIATE AMD or ADVANCED AMD (dry or wet) in one eye, not early AMD; replaces beta-carotene because of lung cancer risk in smokers (CARET trial).
Hand Amsler grids to AMD patients and instruct to check each eye daily and report new distortion or scotoma.
Newer complement inhibitors (pegcetacoplan, avacincaptad) slow geographic atrophy progression but do not restore vision.
References
AAO 2024 — American Academy of Ophthalmology (Vemulakonda GA et al.). Age-Related Macular Degeneration Preferred Practice Pattern. Ophthalmology 2025;132(4):P1-P74
AREDS — AREDS Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration. Arch Ophthalmol 2001;119(10):1417-1436
AREDS2 — AREDS2 Research Group. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration. JAMA 2013;309(19):2005-2015
CATT — CATT Research Group. Ranibizumab and bevacizumab for neovascular age-related macular degeneration. NEJM 2011;364(20):1897-1908
IVAN — Chakravarthy U et al (IVAN Study Investigators). Alternative treatments to inhibit VEGF in age-related choroidal neovascularisation: 2-year findings of the IVAN randomised controlled trial. Lancet 2013;382(9900):1258-1267
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