Macular degeneration

Overview

•Leading cause of irreversible central visual loss in people over 50 in the developed world

•Damages the macula - central vision (reading, face recognition) affected; peripheral vision relatively spared

•Two types: dry (atrophic) - gradual, no neovascularisation; wet (neovascular) - rapid, choroidal neovascularisation (CNV), worst prognosis

•Caucasian ethnicity confers higher risk; no strong sex predisposition

Risk factors

Smoking - most important modifiable risk factor
Age >50 years
Caucasian ethnicity
Family history
Large/confluent drusen
Advanced AMD in one eye

Presentation

•Metamorphopsia - straight lines appear wavy or distorted (hallmark symptom)

•Central scotoma - blurred or grey/black patch in central visual field

•Reduced visual acuity - difficulty reading, recognising faces, discerning colours

•Impaired dark adaptation - difficulty in dim light/night (early dry AMD symptom)

•Fluctuating visual disturbance - day-to-day variation characteristic of dry AMD

•Sudden severe central visual loss - in wet AMD; may follow vitreous haemorrhage or large subretinal bleed

Dry vs wet AMD
FeatureDry AMDWet AMD
PathologyDrusen accumulation, RPE atrophy, geographic atrophyChoroidal neovascularisation (CNV), leakage, haemorrhage
FundoscopyYellow drusen deposits in macular area, pigmentary changesSubretinal haemorrhage, fluid, neovascularisation
Visual lossGradual, fluctuatingRapid, severe - worst prognosis
Key investigationAmsler grid, OCTFluorescein angiography
TreatmentNo curative treatment; antioxidants, smoking cessationIntravitreal anti-VEGF (ranibizumab/aflibercept)

Feature	Dry AMD	Wet AMD
Pathology	Drusen accumulation, RPE atrophy, geographic atrophy	Choroidal neovascularisation (CNV), leakage, haemorrhage
Fundoscopy	Yellow drusen deposits in macular area, pigmentary changes	Subretinal haemorrhage, fluid, neovascularisation
Visual loss	Gradual, fluctuating	Rapid, severe - worst prognosis
Key investigation	Amsler grid, OCT	Fluorescein angiography
Treatment	No curative treatment; antioxidants, smoking cessation	Intravitreal anti-VEGF (ranibizumab/aflibercept)

Investigations

•Amsler grid - detects metamorphopsia; patients see distorted/missing lines; appropriate next step when dry AMD suspected and no neovascularisation

•Fundoscopy - drusen appear as discrete yellow deposits in macula; haemorrhage/fluid in wet AMD

•OCT - detects subretinal fluid, RPE detachment, geographic atrophy; essential in secondary care

•Fluorescein angiography - gold standard when CNV suspected (wet AMD); maps choroidal blood flow, confirms diagnosis, guides anti-VEGF treatment

🎯
Drusen = dry AMD; choroidal neovascularisation = wet AMD. Do not confuse slit-lamp (anterior segment only) or tonometry (intraocular pressure for glaucoma) with AMD investigations.

Management

•Dry AMD - no curative treatment exists

•First-line: antioxidant supplementation (AREDS2: vitamin C, vitamin E, zinc, lutein, zeaxanthin) - reduces progression risk by ~one third in intermediate/advanced AMD; avoid beta-carotene in smokers (lung cancer risk)

•Smoking cessation - most impactful modifiable intervention

•Low vision aids; self-monitoring with Amsler grid; psychosocial support

•Wet AMD - intravitreal anti-VEGF is mainstay

•First-line: ranibizumab (intravitreal) - anti-VEGF monoclonal antibody fragment; NICE-approved; given monthly then as needed

•Alternative: aflibercept (intravitreal) - anti-VEGF fusion protein; NICE-approved; less frequent dosing

•Second-line: photodynamic therapy (PDT) with verteporfin - where anti-VEGF ineffective or contraindicated; laser photocoagulation largely superseded

⚠️
Ranibizumab and photodynamic therapy target abnormal blood vessels of wet AMD - they have no role in dry AMD. If a patient has dry AMD already on antioxidants and vision deteriorates, there are no further medical therapies to offer.