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Ophthalmology›Condition·Updated Jul 11, 2026·v1

Age-Related Macular Degeneration

Age-related macular degeneration (AMD) is a progressive retinal disorder causing central vision loss. It is classified into dry (non-neovascular) and wet (neovascular) forms. Anti-VEGF therapy is the mainstay for wet AMD, with treat-and-extend regimens optimizing outcomes. For dry AMD, AREDS2 supplements slow progression in intermediate disease, and complement inhibitors reduce geographic atrophy growth. Prompt diagnosis using OCT is critical. Smoking cessation and cardiovascular health are key preventive measures.

High Evidence572 references·2,977 words·12 min read·v1
Age-Related Macular DegenerationOphthalmologyRetinaAMDNeovascular AMDGeographic AtrophyAnti-VEGFComplement InhibitorsAREDS2

Quick Reference

RxDrug of choiceFor neovascular AMD: ranibizumab, aflibercept, or faricimab. For geographic atrophy: pegcetacoplan or avacincaptad pegol.
AltAlternativesBevacizumab (off-label) for nAMD; brolucizumab for nAMD; photodynamic therapy for PCV.
⊘AvoidAnti-VEGF is contraindicated in active ocular infection; use caution in pregnancy (avoid bevacizumab, aflibercept). Complement inhibitors contraindicated if active neovascularization.
DxTest of choiceOptical coherence tomography (OCT) for initial diagnosis of neovascular AMD; fluorescein angiography for gold standard leakage detection.
ScKey scoreAREDS Simplified Severity Scale (0-4) for 5-year risk of late AMD.
→When to referAny patient with acute metamorphopsia, suspected neovascular AMD, or rapid progression of GA. Also for surgical management of submacular hemorrhage.
AMD is the leading cause of irreversible vision loss in elderly; prompt diagnosis with OCT and anti-VEGF therapy for neovascular disease can preserve vision. For intermediate AMD, AREDS2 supplements reduce progression. For GA, complement inhibitors offer modest benefit.
Age-related macular degeneration (AMD) is a progressive disorder of the macula causing irreversible central vision loss. It is the leading cause of blindness in adults ≥65 years in developed countries. AMD is classified into dry (non-neovascular) and wet (neovascular) forms, with distinct pathogenic pathways and treatment strategies. Early detection and risk stratification are critical for preserving vision.

Overview and Recommendations

Background

  • •Age-related macular degeneration (AMD) is a progressive degenerative disorder of the macula, the central retina responsible for high-acuity vision, and is the leading cause of irreversible blindness in adults ≥65 years in developed countries, affecting 25.3% of Europeans aged ≥60 years (any AMD) and 2.4% with late AMD. By 2040, an estimated 77 million Europeans will have some form of AMD.
  • •AMD is staged along a continuum from early to late disease, defined by fundus features and risk of progression. The AREDS simplified severity scale stratifies 5-year risk of late AMD into levels 0 through 4, with rates ranging from 0.3% to 55.6%; incorporation of reticular pseudodrusen (RPD) approximately doubles the risk at most levels.
  • •The disease is classically divided into dry (non-neovascular) AMD, encompassing early/intermediate disease and geographic atrophy (GA), and wet (neovascular) AMD, defined by macular neovascularization (MNV) with exudation. The distinction is clinically critical: anti-VEGF therapy is effective only for neovascular disease, while AREDS2 nutritional supplementation reduces progression risk only in intermediate dry AMD.
  • •Pathophysiology centers on the retinal pigment epithelium (RPE) with oxidative stress, complement dysregulation (especially alternative pathway, driven by CFH variants), and lipid metabolism defects leading to drusen formation. The angiogenic switch to wet AMD is driven by hypoxia-inducible factor-1α (HIF-1α) upregulating VEGF-A, the master angiogenic cytokine.
  • •Modifiable risk factors include smoking (strongest, 2-4 fold increased risk), low physical activity, heavy alcohol use, and poor diet. The AREDS2 formulation (lutein/zeaxanthin, vitamins C/E, zinc) reduces progression to late AMD in intermediate disease (HR 0.91).
  • •The four pillars of management for neovascular AMD are anti-VEGF agents: ranibizumab, aflibercept, faricimab, and brolucizumab, with treat-and-extend regimens achieving superior outcomes. For GA, complement inhibitors (pegcetacoplan, avacincaptad pegol) are the first disease-modifying therapies, reducing lesion growth by 22-30%.

Evaluation

  • •Suspect AMD in any patient ≥50 years presenting with painless, progressive central vision loss, difficulty reading small print, or noticing distortion (metamorphopsia) or scotomas. Acute onset over days to weeks suggests neovascular conversion.
  • •Ask about onset and duration of symptoms, presence of metamorphopsia, scotoma, photopsia, and risk factors: smoking history, family history of AMD, cardiovascular disease, and current medications (anticoagulants).
  • •Examine visual acuity with ETDRS chart or Snellen equivalent, and test contrast sensitivity if possible. Perform Amsler grid testing (sensitivity ~67% for neovascular AMD, specificity 99%).
  • •Dilated fundus examination with a 90-D lens is essential. Look for drusen (hard, soft, cuticular or reticular pseudodrusen), RPE pigmentary changes, geographic atrophy (sharply demarcated RPE loss with visible choroidal vessels), and signs of neovascular activity: subretinal/intraretinal fluid, hemorrhage, lipid exudates, or grey-green CNV lesion.
  • •Order optical coherence tomography (OCT) as the test of choice for initial diagnosis of neovascular AMD. OCT identifies intraretinal fluid (IRF), subretinal fluid (SRF), pigment epithelial detachment (PED), and hyperreflective foci. IRF is the strongest biomarker of active disease.
  • •Fluorescein angiography (FA) remains the gold standard for detecting active choroidal neovascularization leakage. Indocyanine green angiography (ICGA) is superior for diagnosing polypoidal choroidal vasculopathy (PCV), common in Asian populations.
  • •Diagnostic criteria follow the AREDS simplified severity scale: grade 0 (no large drusen or pigment changes) to 4 (large drusen in both eyes + pigment changes in both eyes). Reticular pseudodrusen double the risk of progression.
  • •Also consider differential diagnoses: diabetic retinopathy, retinal vein occlusion, central serous chorioretinopathy, inherited macular dystrophies (Stargardt disease, Best disease), and age-related choroidal atrophy (ARCA).
  • •In patients with acute vision loss and hemorrhage, rule out giant cell arteritis (headache, jaw claudication, elevated ESR). For bilateral symmetrical GA, consider genetic testing for Stargardt disease.
  • •OCT angiography (OCTA) can detect nonexudative macular neovascularization (neMNV) in fellow eyes, which is a risk factor for future exudation.
  • •Functional testing: microperimetry, low-luminance visual acuity, and rod-mediated dark adaptation are more sensitive to early dysfunction than standard acuity.
  • •Deep learning algorithms on OCT achieve performance comparable to specialists for AMD classification, with sensitivity 0.98 for detecting AMD vs normal.

Management

  • •Initiate anti-VEGF therapy within 7 days of confirmed active neovascular AMD. First-line options: ranibizumab 0.5 mg, aflibercept 2 mg, or faricimab 6 mg intravitreal injection. Bevacizumab 1.25 mg (off-label) is also evidence-based.
  • •Administer a loading phase of 3 monthly injections. After loading, adopt a treat-and-extend (TAE) regimen: extend treatment intervals by 2 weeks up to every 12-16 weeks based on OCT findings. TAE yields mean gains of +8.8 letters at 1 year vs +3.5 for PRN.
  • •For patients with incomplete response after 3 loading doses (persistent IRF, no CST reduction, or VA decline), switch to an alternative anti-VEGF agent. Consider faricimab or aflibercept 8 mg. Switching to faricimab reduced CST by 31.3 μm after first injection.
  • •For geographic atrophy (GA), consider complement inhibitors: pegcetacoplan 15 mg intravitreal monthly or every other month, or avacincaptad pegol 2 mg monthly. These reduce GA growth by 22-30% at 12-18 months but increase risk of neovascular conversion (11.9-20.9%).
  • •For intermediate AMD, prescribe AREDS2 supplements: lutein 10 mg/zeaxanthin 2 mg, vitamin C 500 mg, vitamin E 400 IU, zinc oxide 80 mg, cupric oxide 2 mg. This reduces progression to late AMD by ~25% over 5 years.
  • •Manage submacular hemorrhage: for thick foveal hemorrhage ≤14 days, consider pneumatic displacement with intravitreal tPA 50 μg + SF6 gas, plus anti-VEGF. Post-procedure maintain head-upright face-forward position for 3 days.
  • •Monitor for complications: intraocular inflammation (IOI) occurs in 0.19% of faricimab injections, 3.7% of aflibercept 8 mg in real-world; treat with topical steroids. Endophthalmitis risk is 0.026% per injection; vitreous hemorrhage 0.012% (PDS 5.2%).
  • •Do NOT use anti-VEGF for non-neovascular subretinal fluid (drusenoid PED) - it may resolve spontaneously. Do NOT rechallenge with faricimab after mild IOI - risk of occlusive retinal vasculitis.
  • •For patients with recurrent exudation despite Q8W dosing, escalate to monthly dosing or switch to faricimab. Consider aflibercept 8 mg for extended intervals.
  • •When to refer to a retina specialist: any patient with new-onset metamorphopsia, suspected neovascular AMD, or GA with rapid progression. Also refer for surgical management of submacular hemorrhage or PDS implantation.
  • •Discharge criteria: after stable disease with no exudation for ≥3 consecutive extended intervals, consider extending follow-up to 6 months. However, indefinite monitoring is recommended due to risk of recurrence.
  • •For patients with non-central GA, AREDS2 supplements slow progression toward the fovea (50.7 μm/year vs 72.9 μm/year). Advise on Mediterranean diet and smoking cessation.
  • •In pregnant women requiring treatment, use ranibizumab 0.5 mg due to minimal systemic exposure. Avoid bevacizumab and aflibercept.
  • •In elderly patients with limited life expectancy, use treat-and-extend or PRN with faricimab to reduce visit burden.
  • •Emerging therapies: photobiomodulation (Valeda) may improve BCVA by +5.4 letters in dry AMD, but evidence is low certainty. AI-based screening with fundus photography achieves >98% sensitivity and specificity.

Board Review — High Yield

  • •AREDS Simplified Severity Scale, Stratifies 5-year risk of late AMD from 0.3% (level 0) to 55.6% (level 4); reticular pseudodrusen double the risk.
  • •Anti-VEGF loading dose, Three monthly injections are standard; treat-and-extend regimens achieve better outcomes than PRN.
  • •Intraretinal fluid (IRF) on OCT, Strongest biomarker for active disease; persistent IRF after loading predicts worse visual outcomes.
  • •Subretinal fluid (SRF) on OCT, Associated with better visual outcomes and lower risk of GA progression.
  • •Complement inhibitors for GA, Pegcetacoplan (C3 inhibitor) and avacincaptad pegol (C5 inhibitor) reduce GA growth by 22-30% but increase risk of neovascular conversion.
  • •Smoking cessation, The single most impactful modifiable risk factor; current smokers have 2-4 fold increased risk of late AMD.
  • •AREDS2 supplements, Lutein/zeaxanthin, vitamins C/E, zinc reduce progression to late AMD by ~25% in intermediate disease; beta-carotene should be avoided in smokers.
  • •Polypoidal choroidal vasculopathy (PCV), Common in Asian populations; diagnosed with ICGA; treated with anti-VEGF ± photodynamic therapy.
  • •Port Delivery System (PDS) with ranibizumab, Provides 24-week refill intervals; noninferior to monthly injections but higher ocular adverse events (RR 1.80).
  • •Fibrosis in nAMD, Prevalence 32% at 12 months, 56% at 60 months; approximately 60% of fibrosis burden develops within first year of treatment.

Deep Dive — Evidence Details

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