EENT · PANCE / PANRE

Age-Related Macular Degeneration (AMD)

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

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 1EENTEasy
A 72-year-old woman has painless, progressive blurring of her central vision with difficulty reading and distortion of straight lines on Amsler grid testing. Funduscopy shows drusen and geographic atrophy in the macula. Which of the following is the most likely diagnosis?
  • AAge-related macular degeneration
  • BCentral retinal artery occlusion
  • CProliferative diabetic retinopathy
  • DRhegmatogenous retinal detachment
Reveal answer & full explanation
Correct answer: A — Age-related macular degeneration
  • AAge-related macular degeneration✓
  • BCentral retinal artery occlusion
  • CProliferative diabetic retinopathy
  • DRhegmatogenous retinal detachment

Why Age-related macular degeneration is correct

  • Age-related macular degeneration is the most common cause of irreversible central vision loss in adults over 55
  • Painless progressive central blurring, difficulty reading, and metamorphopsia (distorted straight lines on Amsler grid) localize the problem to the macula
  • Drusen and geographic atrophy on funduscopy are the hallmark of the dry (atrophic) form, which accounts for ~90% of cases
  • Dry AMD is managed with AREDS2 supplementation to slow progression; conversion to wet AMD (choroidal neovascularization) is treated with anti-VEGF injections

Why the others are wrong

  • Central retinal artery occlusion — causes sudden, painless monocular loss with a pale retina and cherry-red spot, not gradual drusen-associated decline; anchoring on "painless vision loss"
  • Proliferative diabetic retinopathy — produces neovascularization and hemorrhage in a patient with diabetes, not drusen and geographic atrophy; buzzword-match without the diabetes history
  • Rhegmatogenous retinal detachment — presents acutely with flashes, floaters, and a curtain over the field, not slow central distortion; premature closure on "older adult with vision change"
Question 2EENTMedium
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
  • BDiabetic macular edema
  • CWet age-related macular degeneration
  • DAge-related cataracts
Reveal answer & full explanation
Correct answer: A — Dry age-related macular degeneration
  • ADry age-related macular degeneration✓
  • BDiabetic macular edema
  • CWet age-related macular degeneration
  • DAge-related cataracts

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)

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)
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Risk factors

  • Age >50 (most important)
  • White (European) ancestry
  • Family history of AMD; CFH and ARMS2 polymorphisms
  • Cigarette smoking — modifiable, dose-dependent
  • Cardiovascular risk factors: hypertension, dyslipidemia, atherosclerosis
  • Obesity
  • Diet low in antioxidants/leafy greens; high in saturated fat
  • Chronic sunlight (UV/blue light) exposure
  • Female sex

Pathophysiology

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)
  • RPE changes — pigmentary mottling, hyperpigmentation, hypopigmentation
  • Geographic atrophy (late dry AMD) — sharply demarcated areas of RPE loss with visible choroidal vessels
  • Wet AMD: subretinal hemorrhage, exudates, subretinal fluid, RPE detachment, gray-green CNV membrane, disciform scar
  • Amsler grid: distortion, missing areas (central scotoma)
  • Reduced visual acuity

Classic findings

Drusen on fundoscopy in dry AMD; sudden metamorphopsia with subretinal fluid and hemorrhage in wet AMD.

Differential diagnosis

  • Diabetic macular edema — Known diabetes, dot-blot hemorrhages, exudates, fluid on OCT; anti-VEGF and/or laser
  • Central serous chorioretinopathy — Younger men, steroid exposure, type A personality; focal serous detachment on OCT
  • Cataract — Generalized blur and glare without metamorphopsia; lens opacity
  • Macular hole — Sudden central scotoma; full-thickness hole on OCT
  • Epiretinal membrane — Distortion; cellophane reflex on macula; OCT confirms
  • Stargardt disease / inherited macular dystrophy — Young onset, family history, electrophysiology
  • Polypoidal choroidal vasculopathy — Asian patients, recurrent serosanguineous detachments; ICG angiography

Diagnostic workup

Labs

  • Not routinely indicated for diagnosis

Imaging

  • Dilated fundus examination
  • Optical coherence tomography (OCT) — primary imaging modality; detects intraretinal/subretinal fluid, drusen, RPE elevation, geographic atrophy
  • OCT angiography (OCTA) — non-invasive detection of CNV
  • Fluorescein angiography — gold standard for CNV; defines lesion type (classic vs occult)
  • Indocyanine green angiography — for polypoidal lesions
  • Amsler grid for monitoring distortion at home
  • Fundus autofluorescence — assesses geographic atrophy

Diagnostic algorithm

FeatureDry (Non-exudative) AMDWet (Neovascular) AMD
Prevalence~85-90% of AMD~10-15% of AMD; majority of severe vision loss
Onset of vision lossGradual over yearsSudden over days to weeks
Hallmark findingDrusen, RPE changes, geographic atrophyChoroidal neovascularization with fluid/hemorrhage
Key symptomCentral blurring, scotomaMetamorphopsia, acute central scotoma
First-line treatmentAREDS2 (if intermediate/advanced), lifestyle, smoking cessationIntravitreal anti-VEGF (ranibizumab, bevacizumab, aflibercept, faricimab)
Late-stage therapyComplement inhibitors (pegcetacoplan, avacincaptad) for GA; low-vision aidsContinued anti-VEGF; low-vision rehabilitation
Dry vs wet AMD — clinical, imaging, and therapeutic distinctions.

Treatment

First-line

  • Smoking cessation — modifiable risk factor with strongest evidence
  • Mediterranean-style diet rich in leafy greens, fish (omega-3), and colored fruits
  • Cardiovascular risk factor management (blood pressure, lipids, weight)
  • UV protection with sunglasses
  • Amsler grid self-monitoring for new distortion → urgent ophthalmology if change
  • AREDS2 supplementation for intermediate or advanced dry AMD in one 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
  • Low-vision rehabilitation — magnifiers, eccentric viewing training, audio resources
  • 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 OR ADVANCED dry AMD in one eye, not early AMD; replaces beta-carotene because of lung cancer risk in smokers (CARET trial).
  • Anti-VEGF (ranibizumab, bevacizumab, aflibercept, faricimab) revolutionized wet AMD — CATT showed bevacizumab equivalent to ranibizumab.
  • 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 2019 — American Academy of Ophthalmology. Age-Related Macular Degeneration Preferred Practice Pattern. Ophthalmology 2020;127(1):P1-P65
  • 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 — IVAN Study Investigators. Ranibizumab versus bevacizumab to treat neovascular AMD: 2-year findings. Lancet 2013;382(9900):1258-1267

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Commonly confused with

vs Diabetic Retinopathy

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Differentials & related conditions

Diabetic Retinopathy

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