Age-Related Macular Degeneration (AMD): Causes and Treatment

Age-related macular degeneration (AMD) is a progressive disease of the macula — the central, highest-resolution region of the retina responsible for detailed central vision, reading, recognising faces, and driving. AMD is the leading cause of severe, irreversible visual impairment and legal blindness in adults over 50 in developed countries, affecting approximately 200 million people worldwide, a figure projected to reach 300 million by 2040.

AMD does not cause complete blindness — peripheral vision is preserved — but the loss of central vision is profoundly disabling. Patients describe not being able to read, recognise faces, or perform fine manual tasks, even while remaining mobile and independent.

The Macula — Why It Matters

The macula occupies the central 5–6 mm of the retina, housing the fovea at its centre — a tiny pit densely packed with cone photoreceptors that enable high-acuity, colour vision. This tiny region is responsible for the central 5–10° of visual field, yet this is the part of the visual field used for virtually all critical tasks.

The macula is supported by the retinal pigment epithelium (RPE) — a monolayer of cells beneath the photoreceptors that recycles visual pigments, supports photoreceptor health, and disposes of metabolic waste by transporting it to the choroid (the vascular layer beneath the RPE).

In AMD, this support system fails — waste accumulates, RPE cells degenerate, and photoreceptors die.

Types of AMD

AMD is classified into early/intermediate and late AMD. Late AMD takes two forms: dry (geographic atrophy) and wet (neovascular AMD).

Early and Intermediate AMD

Drusen — extracellular deposits of lipids, proteins, and debris that accumulate between the RPE and Bruch's membrane (the supporting layer beneath the RPE) — are the hallmark early finding. Visible on fundoscopy and OCT as yellow-white spots beneath the retina.

• Small, hard drusen: associated with normal ageing; low risk of progression
• Medium drusen: early AMD; 5-year progression risk to late AMD approximately 12%
• Large drusen (>125 μm): high risk of progression; 5-year risk of late AMD in the worse eye approximately 45% if large drusen are present bilaterally with pigmentary changes

Most patients with early AMD have no or minimal visual symptoms. Some may notice mild difficulty with dark adaptation.

Late Dry AMD — Geographic Atrophy (GA)

In geographic atrophy, patches of RPE and overlying photoreceptors irreversibly degenerate, creating sharply demarcated areas of atrophy that expand slowly (approximately 1.7 mm²/year on average) until they encroach on the fovea, causing central scotoma (blind spot in central vision).

GA is bilateral in the majority of patients and progresses over years. Until 2023, no approved treatment existed. Two complement inhibitors — pegcetacoplan (Syfovre) and avacincaptad pegol (Izervay) — are now FDA-approved for GA, slowing area growth by approximately 20–30% with monthly or bimonthly intravitreal injections.

Late Wet AMD — Neovascular AMD (nAMD)

In neovascular AMD, choroidal neovascularisation (CNV) occurs — abnormal new blood vessels grow from the choroid through Bruch's membrane and beneath or into the RPE, driven by vascular endothelial growth factor (VEGF). These vessels are fragile and leak fluid and blood into and beneath the retina, causing:

• Rapid, often sudden distortion of central vision (metamorphopsia) — straight lines appear wavy or bent
• Central blurring or grey area (scotoma)
• Reduction in reading vision

Wet AMD progresses rapidly — without treatment, severe vision loss occurs in 90% of patients within 2 years. However, wet AMD is now highly treatable with anti-VEGF therapy.

Risk Factors

Risk Factor	Impact
Age	Prevalence increases dramatically with age: <1% at 55–64; 10–12% at 75–84; >30% at 85+
Smoking	2–3× increased risk; dose-dependent; the most modifiable risk factor
Family history / genetics	Strong genetic component: ARMS2/HTRA1 and CFH gene variants confer 3–7× increased risk
Cardiovascular risk factors	Hypertension, obesity, dyslipidaemia independently associated
White/European ethnicity	Higher prevalence than East Asian or African populations
Female sex	Slight excess, partially explained by longer lifespan

Dietary factors: High dietary lutein and zeaxanthin (leafy green vegetables) and omega-3 fatty acids are associated with reduced risk. The AREDS and AREDS2 supplements (vitamins C, E, zinc, copper, lutein, zeaxanthin) reduce progression from intermediate to advanced AMD by approximately 25%.

Diagnosis

Fundoscopy

Dilated fundoscopy by an ophthalmologist visualises drusen, RPE changes, areas of atrophy, and signs of neovascularisation (subretinal haemorrhage, grey-green CNV membrane beneath the retina).

Optical Coherence Tomography (OCT)

The essential investigation for AMD — provides cross-sectional, high-resolution images of retinal layers:

• Identifies drusen location and size
• Detects subretinal and intraretinal fluid (hallmarks of active wet AMD)
• Measures central retinal thickness and RPE integrity
• Monitors treatment response (fluid resolution with anti-VEGF)

OCT Angiography (OCTA) — non-invasive, dye-free imaging of retinal and choroidal blood flow; identifies CNV networks without fluorescein injection.

Fluorescein Angiography (FFA)

Intravenous fluorescein dye with retinal photography; maps choroidal neovascularisation (classic vs occult CNV), areas of leakage, and guides photodynamic therapy decisions. Less commonly needed since OCT and OCTA advances.

Amsler Grid

A simple home-monitoring tool — a grid of horizontal and vertical lines with a central dot. Patients check daily whether lines appear wavy, distorted, or missing (metamorphopsia) — early warning sign of new wet AMD activation requiring urgent ophthalmology review.

Treatment

Wet AMD — Anti-VEGF Injections

Anti-VEGF therapy has transformed wet AMD from a rapidly blinding condition to one that can be stabilised, with many patients gaining vision. VEGF inhibitors block the neovascular growth signal, cause regression of the abnormal vessels, and reduce fluid leakage.

Available anti-VEGF agents:

Drug	Approval	Frequency	Notes
Ranibizumab (Lucentis)	2006	Monthly or PRN	Original approved agent; gold standard
Aflibercept (Eylea)	2011	Every 8 weeks (after loading)	Binds VEGF-A, VEGF-B, and PIGF; extended dosing
Faricimab (Vabysmo)	2022	Up to every 16 weeks	Dual target: VEGF-A and Ang-2; longest approved interval
Bevacizumab (Avastin)	Off-label	Monthly	Full-length anti-VEGF; comparable efficacy at lower cost

Treatment protocol: 3 monthly loading injections, then treat-and-extend or pro-re-nata (treat-as-needed) based on OCT monitoring.

Intravitreal injection is performed as an outpatient procedure under topical anaesthesia — the eye is anaesthetised with drops, disinfected with povidone-iodine, and the drug injected through the vitreous into the posterior segment. The procedure takes 5 minutes. Most patients find it manageable.

Outcomes: approximately 90–95% of patients with wet AMD treated with anti-VEGF maintain or improve vision; 30–40% gain 3 or more lines on the Snellen chart. Treatment is ongoing — stopping therapy is associated with recurrence.

Dry AMD — Supplements and Emerging Treatments

AREDS2 supplementation (vitamins C and E, zinc, copper, lutein and zeaxanthin) — reduces the risk of progression from intermediate to advanced AMD by 25%. Recommended for patients with bilateral large drusen or unilateral late AMD in the fellow eye.

Geographic atrophy: pegcetacoplan (Syfovre) and avacincaptad pegol (Izervay) — complement inhibitors that slow GA growth; intravitreal injections every 1–2 months; approved 2023.

Lifestyle Modifications

• Smoking cessation — the most impactful modifiable intervention
• Mediterranean diet rich in leafy greens, fish, and olive oil
• Daily Amsler grid monitoring to detect wet AMD conversion early
• Protection from UV light (sunglasses)

AMD Care in China

China's retinal specialists and ophthalmology centres offer:

• AMD assessment: OCT, OCTA, fundoscopy, and visual acuity assessment
• Anti-VEGF injection clinic: ranibizumab, aflibercept, and faricimab available; injection clinic scheduling confirmed with the hospital
• Treat-and-extend protocols: structured monitoring with OCT-guided dosing to minimise injection frequency while maintaining vision
• Cost: care in China is generally less expensive than UK private treatment, but the hospital prices each case individually — ask us for the written quote before you commit.
• Comprehensive low vision rehabilitation: magnification devices, eccentric viewing training, and assistive technology for advanced AMD
• Full English care navigation from assessment through ongoing monitoring and injection therapy

Contact a ChinaMedicalTour care navigator to arrange a macular assessment, AMD evaluation, or anti-VEGF injection consultation.

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Medical content based on MSD Manuals and international AMD treatment guidelines. Evidence reviewed 2025.

Frequently Asked Questions

Can international patients schedule comprehensive eye examinations and specialist consultations in China?

Yes. Comprehensive ophthalmic evaluations including optical coherence tomography (OCT), visual field testing, corneal topography, and fundus photography are coordinated at specialized eye hospitals.

What specialized ophthalmic treatments and laser therapies are evaluated in China?

Tertiary ophthalmology centers offer micro-incision cataract surgery, anti-VEGF intravitreal injections, retinal photocoagulation, and minimally invasive glaucoma procedures tailored to individual eye pathology.

How is post-treatment follow-up handled for traveling eye patients?

Follow-up visual checks, eye drop regimens, and detailed bilingual ophthalmic clinical notes are provided upon discharge to ensure seamless continuation with domestic eye care providers.