EENT · PANCE / PANRE

Age-Related Macular Degeneration (AMD)

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.

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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

Feature	Dry (Non-exudative) AMD	Wet (Neovascular) AMD
Prevalence	~85-90% of AMD	~10-15% of AMD; majority of severe vision loss
Onset of vision loss	Gradual over years	Sudden over days to weeks
Hallmark finding	Drusen, RPE changes, geographic atrophy	Choroidal neovascularization with fluid/hemorrhage
Key symptom	Central blurring, scotoma	Metamorphopsia, acute central scotoma
First-line treatment	AREDS2 (if intermediate/advanced), lifestyle, smoking cessation	Intravitreal anti-VEGF (ranibizumab, bevacizumab, aflibercept, faricimab)
Late-stage therapy	Complement inhibitors (pegcetacoplan, avacincaptad) for GA; low-vision aids	Continued 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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