Dry AMD is slow; wet AMD is fast. Both forms share the same risk factors but need very different management. Any new distortion of straight lines or sudden central blur in someone over 50 is a wet AMD red flag — it needs same-week ophthalmology assessment, not a routine optician appointment in six months.
Fast answer: dry vs wet AMD at a glance
Dry AMD is drusen and atrophy, with slow loss of central vision over years, managed with AREDS2 supplements, lifestyle change and Amsler grid monitoring. Wet AMD is abnormal new blood vessels and leakage, causing distortion and central blur over weeks, treated with anti-VEGF injections every 4 to 16 weeks for life. Around 10 to 15% of dry AMD eyes convert to wet AMD over 5 to 10 years.
Honest one-liner: any new distortion of straight lines or sudden central blur in someone over 50 is a wet AMD red flag — it needs same-week assessment, not a routine optician appointment in six months.
What is age-related macular degeneration?
The macula is the central 5 mm of the retina, packed with cone photoreceptors and responsible for sharp central vision, reading, fine detail, colour and face recognition. Age-related macular degeneration is a progressive disease of the macular retinal pigment epithelium (RPE), Bruch’s membrane and choriocapillaris driven by ageing, oxidative stress and complement-mediated inflammation.
Lipoprotein and cellular debris accumulates as drusen beneath the RPE. Over years RPE function fails, photoreceptors atrophy and central vision gradually deteriorates — this is the dry pathway. In a subset of patients the choroid grows new, abnormal blood vessels through Bruch’s membrane (choroidal neovascularisation) which leak fluid and blood beneath or within the retina — this is the wet pathway and can cause rapid sight loss within weeks if untreated.
AMD never affects peripheral vision, so total blindness from AMD does not occur. The worst-case scenario is severe loss of central reading vision in both eyes.
Dry vs wet AMD: head-to-head comparison
| Feature | Dry AMD | Wet AMD |
|---|---|---|
| Proportion of cases | ~85% | ~15% |
| Pathology | Drusen, RPE atrophy, photoreceptor loss | Choroidal neovascularisation, leakage, haemorrhage |
| Speed of vision loss | Years | Days to weeks if untreated |
| Hallmark symptom | Gradual central blur | Sudden distortion of straight lines |
| OCT finding | Drusen, RPE atrophy, geographic atrophy in late disease | Subretinal / intraretinal fluid, PED, choroidal neovascularisation |
| Treatment | AREDS2 + lifestyle; complement inhibitors for GA (US) | Anti-VEGF intravitreal injections |
| Frequency of visits | Annual | Every 4–16 weeks |
| Risk of conversion | 10–15% dry → wet over 5–10 years | N/A |
Both can coexist: a single eye can have dry AMD with superimposed wet AMD, and the two eyes can be at different stages. Each eye is assessed individually.
Symptoms: when to suspect AMD — and when to act fast
Symptom timing is the single most useful clinical clue. Slow change favours dry AMD; sudden change favours wet AMD or another emergency.
Dry AMD — gradual: slow blur of central reading vision over years, need for stronger reading lights, difficulty recognising faces from a distance, reduced contrast and colour vibrancy, and a central area appearing slightly faded or smudged.
Wet AMD — sudden / rapid: sudden distortion of straight lines (door frames, lined paper), a central grey or blurred patch (scotoma), words missing in the middle of a sentence, a rapid drop in reading vision over days to weeks, and object size appearing different in the two eyes.
Red flags for same-week ophthalmology referral: any new distortion of straight lines, central scotoma, sudden blur, words missing on the page, or any acute change in vision in someone over 50. Use a simple Amsler grid at home, one eye at a time, weekly, with reading glasses if you wear them — any new distortion or missing area should be reported the same day.
How AMD is diagnosed in 2026
A consultant ophthalmologist (medical retina subspecialist) confirms AMD and its subtype with a focused history and a panel of standard imaging tests:
- History & symptom timing — gradual vs sudden, monocular vs binocular.
- Visual acuity — Snellen and ETDRS letter scores; reading speed.
- Amsler grid — in clinic and at home for ongoing monitoring.
- Slit-lamp biomicroscopy — dilated examination of the macula.
- Optical coherence tomography (OCT) — the gold-standard test; identifies drusen, atrophy, intraretinal / subretinal fluid and pigment epithelial detachment (PED).
- OCT angiography (OCTA) — visualises choroidal neovascularisation without dye injection.
- Fundus autofluorescence — maps geographic atrophy and at-risk RPE areas.
- Fluorescein angiography — reserved for atypical or polypoidal lesions.
In clinically suspected wet AMD the goal is to start anti-VEGF treatment at the same visit (one-stop service) or within 1 to 2 weeks — speed of treatment determines visual outcome.
New distortion or sudden central blur? A same-week consultant macula assessment includes OCT and a definitive diagnosis the same day.
Book an AMD assessmentTreatment options: dry vs wet AMD in 2026
Dry AMD is managed without injections in most cases:
- AREDS2 supplements — vitamin C 500 mg, vitamin E 400 IU, lutein 10 mg, zeaxanthin 2 mg, zinc oxide 80 mg (or 25 mg low-zinc), cupric oxide 2 mg. Reduces 5-year risk of progression to advanced AMD by ~25% in eligible intermediate-stage patients. Not licensed for prevention.
- Strict smoking cessation — smoking is the single biggest modifiable risk factor and continued smoking accelerates progression to advanced AMD.
- Cardiovascular risk control — blood pressure, cholesterol, glucose, weight.
- Mediterranean-style diet — oily fish twice weekly, dark green leafy vegetables, nuts, olive oil; reduce ultra-processed foods.
- UV and blue-light protection — wraparound sunglasses on bright days.
- Amsler grid monitoring — weekly, each eye independently.
- Low-vision support — magnifiers, large-print, screen readers, certified visual impairment registration where appropriate.
Wet AMD is treated by intravitreal injection of an anti-VEGF agent that blocks the vascular endothelial growth factor signal driving abnormal blood vessel growth and leakage:
| Drug | Brand(s) | UK status 2026 | Typical maintenance interval |
|---|---|---|---|
| Aflibercept 2 mg | Eylea | NHS & private (NICE TA294) | 8–12 weeks |
| Aflibercept 8 mg | Eylea HD | NHS & private (NICE TA924) | 12–16 weeks |
| Ranibizumab 0.5 mg | Lucentis (and biosimilars) | NHS & private | 4–8 weeks |
| Faricimab 6 mg | Vabysmo | NHS & private (NICE TA800) | 12–16 weeks |
| Brolucizumab 6 mg | Beovu | Private (selected NHS use) | 8–12 weeks |
Standard regimens start with three monthly loading injections, then move to a treat-and-extend protocol where the interval between injections is extended in 2-week steps as long as the OCT macula remains dry. Most UK 2026 patients receive 6 to 8 injections in year 1 and 4 to 6 injections per year thereafter. Treatment is generally lifelong.
Geographic atrophy and the new complement inhibitors
Late-stage dry AMD with geographic atrophy (GA) — sharply demarcated patches of RPE and outer-retinal loss — was untreatable until recently. In 2023 to 2024 the FDA approved two intravitreal complement inhibitors that slow GA growth:
- Pegcetacoplan (Syfovre) — complement C3 inhibitor, monthly or every-other-month intravitreal injection.
- Avacincaptad pegol (Izervay) — complement C5 inhibitor, monthly intravitreal injection.
Both drugs slow but do not reverse GA growth, with reductions in lesion expansion of approximately 15 to 25% in pivotal trials. Risks include a small increased rate of conversion to wet AMD and intraocular inflammation. UK NICE evaluation is ongoing in 2026 and these agents are not yet routinely available on the NHS; selected private use is offered on a named-patient basis at major UK medical retina centres. Early dry AMD does not currently require any injection therapy — complement inhibitors are reserved for selected patients with documented expanding geographic atrophy threatening the central fovea.
Lifestyle, supplements and self-monitoring — what works
Strong evidence: AREDS2 supplements (intermediate AMD), strict smoking cessation, a Mediterranean-style diet, oily fish twice weekly (omega-3), dark green leafy vegetables and blood pressure control.
Probable benefit: daily exercise (30 minutes), weight reduction if BMI over 30, cholesterol management, diabetes control and wraparound UV-blocking sunglasses outdoors.
Not recommended: beta-carotene supplements in current or former smokers (lung cancer risk), high-dose unspecified multivitamins as a substitute for AREDS2, unregulated “eye health” supplements without published trial evidence, and blue-light blocking glasses for indoor screen use (no proven AMD benefit).
For how vision changes after cataract surgery and how to distinguish AMD from cataract, see why does my vision get cloudy years after cataract surgery?
UK 2026 AMD treatment cost: NHS vs private
| Pathway | Cost | Typical wait | Notes |
|---|---|---|---|
| NHS wet AMD pathway | Free at point of care | Same week (urgent) | Macula clinic; choice of drug per local formulary |
| Private wet AMD injection | £650–£1,250 per injection | Same week | Choice of drug; OCT included |
| Private medical insurance | Usually covered subject to excess | Same week | Pre-authorisation required; lifetime cap on some policies |
| AREDS2 supplements | £15–£30 per month | Over-the-counter | Look for the verified AREDS2 formulation |
For the private cataract pathway and how it interacts with macular disease, see can my optician refer me for private cataract surgery in the UK?
FAQs: wet vs dry AMD (UK 2026)
What is the difference between wet and dry AMD?
What are the symptoms of wet AMD?
What are the symptoms of dry AMD?
How is wet AMD treated in the UK in 2026?
How is dry AMD treated in the UK in 2026?
How often do wet AMD injections need to be given?
Is dry AMD likely to turn into wet AMD?
Are anti-VEGF injections painful?
How much do private wet AMD injections cost in the UK in 2026?
Will I go blind from AMD?
Sources and methodology
- Clinical guidance: NICE TA294 (aflibercept), TA800 (faricimab), TA924 (aflibercept 8 mg), TA446 (ranibizumab biosimilars); Royal College of Ophthalmologists clinical guidelines for AMD.
- Trial evidence: AREDS2 trial; VIEW, HAWK, HARRIER, TENAYA, LUCERNE and PULSAR pivotal trials; OAKS / DERBY (pegcetacoplan); GATHER1 / GATHER2 (avacincaptad pegol).
- UK service data: RCOphth medical retina service standards; UK macula service activity data 2024–2026.
- Editorial review: reviewed by a UK GMC-registered consultant medical retina specialist before publication.
Independent sources we reference: NICE TA294, NICE TA800, Royal College of Ophthalmologists, Macular Society and NHS overview of AMD.
Editorial information · not a substitute for personalised medical advice. Treatment suitability is confirmed by a UK GMC-registered consultant ophthalmologist at consultation.