Macular Degeneration (AMD) — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Age-related macular degeneration (AMD) is a progressive retinal disease affecting the macula — the central 5mm of the retina responsible for high-acuity central vision used for reading, driving, and face recognition. AMD is the leading cause of severe visual impairment and blindness in adults over 50 in high-income countries, affecting approximately 200 million people worldwide, with prevalence projected to rise to 300 million by 2040 as populations age. AMD is classified into two forms: Dry (atrophic) AMD accounts for 85-90% of cases — characterised by drusen (extracellular deposits of lipids and proteins beneath the retinal pigment epithelium), RPE atrophy, and progressive geographic atrophy (GA) of the macula. Wet (neovascular) AMD accounts for 10-15% of cases but causes 90% of severe vision loss — characterised by pathological growth of new abnormal blood vessels (choroidal neovascularisation/CNV) beneath the retina that leak, bleed, and scar, causing rapid central vision loss. Dry AMD can convert to wet AMD; risk is approximately 10-15% per year in advanced dry AMD. AMD causes central vision loss — peripheral vision is preserved, so complete blindness from AMD alone is rare.

AMD results from complex interactions of aging, genetic susceptibility, and environmental factors causing oxidative stress, drusen accumulation, inflammation, and complement dysregulation in the retinal pigment epithelium (RPE) and Bruch's membrane. Non-modifiable risk factors: advancing age (prevalence doubles with each decade over 50 — affects 2% of those aged 65-69 and 30% of those aged 85+); family history (2-4x increased risk in first-degree relatives); female sex (slightly higher risk); Caucasian and Chinese ethnicity. Genetic: complement factor H (CFH Y402H — the most important risk variant — doubles AMD risk per allele); complement component 3 (C3); ARMS2/HTRA1 (chromosome 10q26 locus); CFB and C2 variants are protective. Complement dysregulation drives inflammation and drusen formation in AMD. Modifiable risk factors: smoking is the strongest modifiable risk factor (increases AMD risk 2-4x — current smokers have 3-4x higher risk than never-smokers; risk persists for 20+ years after stopping); cardiovascular risk factors (hypertension, obesity, high dietary fat intake, and low omega-3 consumption increase risk). Sunlight and UV exposure have modest associations. Protective factors: dietary lutein and zeaxanthin (found in leafy green vegetables — spinach, kale), omega-3 fatty acids (oily fish), and antioxidants.

Early dry AMD is often asymptomatic — detected during routine eye examination by the presence of drusen. As AMD progresses: central visual distortion (metamorphopsia — straight lines appearing wavy or bent — the hallmark symptom of wet AMD; detected by Amsler grid test); central blurring or 'blank spot' (scotoma) in the centre of vision; difficulty reading small print; need for increased lighting; difficulty recognising faces; and reduced contrast sensitivity. Peripheral vision remains intact throughout — AMD does not cause complete blindness. Wet AMD presents with more rapid and severe vision loss — often developing over days to weeks — with metamorphopsia and central scotoma. Sudden loss of central vision, new distortion of straight lines, or a dark patch in the central vision requires same-day emergency ophthalmology assessment — wet AMD is treatable but requires urgent intervention to prevent irreversible visual loss. Geographic atrophy (advanced dry AMD) causes gradually enlarging central scotoma over years.

AMD diagnosis is made by ophthalmic examination and imaging. Visual acuity assessment (Snellen chart) and Amsler grid testing (self-monitoring for metamorphopsia — patient views a regular grid for distortion or missing areas). Dilated fundus examination (slit-lamp biomicroscopy): drusen (yellow-white extracellular deposits of varying size — soft drusen above 63 microns are highest risk); RPE changes (pigment mottling, geographic atrophy — areas of RPE loss); subretinal fluid; haemorrhage or exudate (suggest CNV/wet AMD). Optical coherence tomography (OCT): the most important diagnostic and monitoring tool — provides cross-sectional retinal imaging with micron resolution, detecting drusen, intraretinal/subretinal fluid, RPE detachment, and geographic atrophy progression. OCT angiography (OCTA): non-invasive imaging of the retinal vasculature — detects CNV without fluorescein injection. Fluorescein angiography (FFA): IV fluorescein injection with fundal photography — identifies CNV type (classic, occult) and extent; gold standard for wet AMD diagnosis before treatment. AMD Classification (AREDS system): no AMD, early AMD (small-medium drusen), intermediate AMD (large drusen or pigmentary changes), and advanced AMD (GA or neovascular).

Dry AMD: no approved treatment reverses early or intermediate dry AMD. AREDS2 supplements (zinc oxide 80 mg + copper oxide 2 mg + vitamin C 500 mg + vitamin E 400 IU + lutein 10 mg + zeaxanthin 2 mg — daily) reduce the risk of progression to advanced AMD by 25% in intermediate AMD patients and those with advanced AMD in one eye — not beneficial in early AMD. Avoidance of high-dose beta-carotene in smokers and ex-smokers (increases lung cancer risk). Geographic atrophy (advanced dry AMD): pegcetacoplan (Syfovre — complement C3 inhibitor — intravitreal injection monthly or every other month) was FDA-approved in 2023 — reduces GA progression rate by 22% at 12 months. Avacincaptad pegol (Izervay — complement C5 inhibitor) received FDA approval in 2023 with similar efficacy. These represent the first approved treatments for geographic atrophy. Wet AMD: anti-VEGF (vascular endothelial growth factor) intravitreal injections are the standard of care and have transformed the prognosis of wet AMD from inevitable severe vision loss to stabilisation or improvement in approximately 90% of patients. Available agents: ranibizumab (Lucentis); aflibercept (Eylea); bevacizumab (Avastin — off-label, lower cost); brolucizumab (Beovu); faricimab (Vabysmo — dual anti-VEGF/Ang-2 — allows extended dosing intervals of up to 4 months). Treatment regimens: initially monthly injections for 3-6 loading doses, then pro re nata (PRN) or treat-and-extend (T&E) based on disease activity on OCT. Close monitoring every 4-8 weeks is essential — delay in treatment during active CNV causes permanent vision loss. Port delivery system (Susvimo — continuous ranibizumab release) allows 6-monthly clinic visits. Low vision rehabilitation: magnification aids, tinted lenses, electronic reading aids, eccentric viewing training.

Loss of central vision (central scotoma) — the defining complication of advanced AMD — causes inability to read, drive (DVLA standard failure at Snellen below 6/12 in the better eye), recognise faces, or perform fine visual tasks. Legal blindness (visual acuity 6/60 or worse in the better eye) occurs in approximately 15-20% of untreated wet AMD patients. AMD does not cause complete blindness (peripheral vision is preserved), but its impact on independence, employment, and quality of life is profound. Depression and anxiety affect approximately 30-40% of AMD patients with significant central vision loss. Geographic atrophy (advanced dry AMD) causes slowly progressive permanent central vision loss with no reversal possible even with current treatments. Conversion from dry to wet AMD occurs in approximately 10-15% of advanced dry AMD patients per year — typically presenting as sudden visual distortion or blurring requiring urgent anti-VEGF injection. Falls and hip fractures are more frequent in patients with impaired central vision and depth perception from bilateral AMD.

Smoking cessation is the single most impactful modifiable AMD prevention measure — reduces risk by 50-75% and slows progression. Mediterranean dietary pattern (high in leafy green vegetables — lutein and zeaxanthin; oily fish twice weekly — omega-3 fatty acids; olive oil; nuts) is associated with 25-35% reduced AMD risk and slower progression. UV-protective sunglasses with CE UV400 protection reduce cumulative retinal UV exposure. Control cardiovascular risk factors (blood pressure, cholesterol, weight). Annual eye examinations from age 50 in high-risk individuals (family history, smokers, those with early AMD in one eye) — early detection enables preventive supplementation and close monitoring. Home Amsler grid monitoring: all patients with intermediate or unilateral advanced AMD should self-test with an Amsler grid weekly; any new distortion or blind spot requires same-day ophthalmology assessment. AREDS2 supplements are recommended for intermediate AMD and advanced AMD in one eye — begin supplementation as recommended by your ophthalmologist.

Go to an emergency eye unit or ophthalmology clinic same-day for: sudden new onset of central vision distortion (straight lines appearing wavy — Amsler grid distortion); a new dark patch or blank area appearing in the central vision; sudden significant blurring of central vision that was not present yesterday; or any rapid change in vision in a patient with known AMD. Wet AMD can cause irreversible photoreceptor damage within days to weeks of onset if untreated — early anti-VEGF injection preserves vision and reverses fluid. Do not wait for a routine appointment. Contact your ophthalmologist promptly for: worsening Amsler grid distortion on weekly home monitoring; difficulty with familiar tasks (reading, driving, face recognition) that has changed recently; or any new floaters or flashes of light. Annual dilated fundal examinations from age 50 are recommended for everyone, particularly those with family history of AMD or who smoke.