Age-Related Macular Degeneration: Basics
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Direct answer
Age-related macular degeneration (ARMD) is degeneration of the macula after the age of fifty. The dry form — about 85 to 90 per cent of cases — progresses slowly through drusen and retinal pigment epithelial disturbance to geographic atrophy; the wet form, only 10 to 15 per cent of cases, causes the great majority of severe ARMD blindness through choroidal neovascularisation growing beneath the retina. Wet ARMD presents with sudden distortion of straight lines (metamorphopsia), a central grey patch and rapid central vision loss — the Amsler grid shows wavy or missing lines. Diagnosis rests on optical coherence tomography with fluorescein angiography, and treatment is intravitreal anti-VEGF injection, which preserves or improves vision in most eyes when given before the membrane scars.
What you must remember
- Dry ARMD: hard and soft drusen (hyaline deposits between Bruch membrane and the retinal pigment epithelium), pigment mottling and gradual central fading; geographic atrophy is the advanced, sight-threatening endpoint.
- Wet ARMD: choroidal neovascularisation through a damaged Bruch membrane; sudden metamorphopsia, central scotoma, and on examination subretinal fluid, haemorrhage or a grey-green membrane; untreated it ends in a disciform scar.
- Amsler grid: one eye at a time with reading glasses; wavy lines, blurred patches or missing corners in a previously normal grid demand same-week review — the self-test every dry ARMD patient is taught.
- Imaging: optical coherence tomography shows intraretinal or subretinal fluid and pigment epithelial detachment; fluorescein angiography classifies the membrane as classic or occult, once central to choosing therapy.
- Anti-VEGF therapy: intravitreal ranibizumab 0.5 mg, aflibercept 2 mg or off-label bevacizumab 1.25 mg — commonly three monthly loading injections followed by treat-and-extend or as-needed retreatment; the CATT trial showed bevacizumab equivalent to ranibizumab for most outcomes, which matters for Indian practice on cost.
- AREDS2 supplement for intermediate disease: lutein 10 mg with zeaxanthin 2 mg (beta-carotene removed after it raised lung cancer risk in smokers), vitamin C 500 mg, vitamin E 400 IU, zinc with copper — it slows progression to advanced disease, it does not restore vision.
- Risk factors: age, smoking (the strongest modifiable factor), family history, hypertension and lighter iris; cataract surgery does not clearly worsen it.
- ARMD spares the peripheral field — patients never go completely blind from it, though they lose reading and face recognition; low-vision aids and registration support matter.
- Differential of choroidal neovascularisation: pathological myopia, presumed ocular histoplasmosis, polypoidal choroidal vasculopathy — the treatment logic is shared.
Dry to wet: what changes, and how fast to act
Picture a 68-year-old monitored for drusen and pigment clumping, vision 6/9, dry disease on optical coherence tomography — annual review would suit her, plus an Amsler grid on her fridge and a firm smoking cessation conversation. One morning the door frame looks bent in the right eye. That single symptom converts the timeline: she is seen within days, the grid shows wavy lines near fixation, and tomography now shows subretinal fluid with a pigment epithelial detachment — a choroidal neovascular membrane. Fluorescein angiography confirms leakage. She begins anti-VEGF injections the same week, three monthly doses then a treat-and-extend schedule, because every month of untreated membrane growth is photoreceptor loss; after the disciform scar forms, injections recover little. Contrast the counterfactual in which she waited a year: a haemorrhagic elevation becomes a pale scar, reading vision is gone permanently, and care shifts to low-vision aids and the healthy eye's monitoring. The dry-to-wet conversion is the moment ophthalmology can change this disease's history.
Where students slip
The percentage trap is classic: students quote dry ARMD as benign and forget that the minority wet form causes most severe vision loss, and that new distortion is the symptom that separates the two. Expect a stem describing "straight lines bent while reading" with the answer metamorphopsia and the Amsler grid. Examiners also test the AREDS2 change — beta-carotene out, lutein and zeaxanthin in — and the reassurance point that ARMD never causes total blindness because the periphery survives.
Frequently asked questions
How do dry and wet ARMD differ?
Dry ARMD shows drusen and gradual pigmentary change with slow central visual decline; wet ARMD shows choroidal neovascularisation with sudden distortion, fluid or haemorrhage and rapid loss — and causes most severe ARMD blindness.
What is metamorphopsia and which bedside tool detects it?
Distortion of straight lines, the hallmark symptom of macular disease; the Amsler grid, checked one eye at a time, shows wavy or missing lines and is the self-monitoring tool taught to every ARMD patient.
What does the AREDS2 supplement contain?
Lutein 10 mg and zeaxanthin 2 mg with vitamins C and E, zinc and copper — beta-carotene was removed after it increased lung cancer risk in smokers; the aim is slowing progression, not improving vision.
What is the treatment of wet ARMD?
Intravitreal anti-VEGF injections — ranibizumab, aflibercept or off-label bevacizumab — as a loading course followed by treat-and-extend, started urgently before scarring.
Which form causes most severe vision loss in ARMD?
The wet neovascular form, roughly 10–15 per cent of cases but responsible for the large majority of ARMD-related severe vision loss.
Does ARMD lead to complete blindness?
No — central reading vision is lost but peripheral navigation vision is retained; low-vision aids, eccentric viewing training and magnifiers keep patients independent.