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age-related macular degeneration

progressive degeneration of the macula causing central visual loss — classified as dry (atrophic) or wet (neovascular), with wet amd being a sight-threatening emergency

ophthalmologycommonchronic

About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

The Bottom Line

  • Leading cause of irreversible central visual loss in the UK in people over 50
  • Dry AMD (~90%): drusen, RPE changes, geographic atrophy — gradual progression, no specific treatment
  • Wet AMD (~10%): choroidal neovascularisation — rapid central vision loss, needs URGENT anti-VEGF treatment
  • NICE NG82: wet AMD must be treated within 14 days of referral — intravitreal anti-VEGF (ranibizumab, aflibercept)
  • Amsler grid for self-monitoring — new distortion in dry AMD may indicate conversion to wet

Overview

Age-related macular degeneration (AMD) is a degenerative condition affecting the macula, the central part of the retina responsible for detailed vision. Early AMD is characterised by drusen (yellow deposits beneath the retinal pigment epithelium) and pigmentary changes. Late AMD has two forms: dry (geographic atrophy with progressive RPE and photoreceptor loss) and wet (neovascular, with choroidal new vessel growth that leaks fluid and blood under the retina). Wet AMD accounts for only ~10% of AMD cases but ~90% of AMD-related severe visual loss.

Epidemiology

AMD is the leading cause of sight loss in people over 50 in developed countries. In the UK, approximately 600,000 people have some degree of AMD. Major risk factors include age (exponentially increasing after 55), smoking (2–4 times increased risk and the most important modifiable risk factor), positive family history, female sex, and Caucasian ethnicity. Other associations include cardiovascular disease, hypertension, and high BMI.

Clinical Features

Symptoms
Gradual painless loss of central vision (dry AMD — progressive over months to years)
Sudden or rapid-onset central visual distortion (metamorphopsia) — may indicate wet AMD
Central scotoma (dark or missing area in central vision)
Difficulty reading, recognising faces, and performing fine detail tasks
Straight lines appearing wavy or bent (positive Amsler grid test)
Reduced colour perception and contrast sensitivity
Charles Bonnet syndrome: visual hallucinations in patients with significant visual loss
Signs
Drusen visible on fundoscopy — small hard drusen (low risk) vs large soft drusen (high risk)
RPE pigmentary changes and atrophy in dry AMD
Geographic atrophy — well-demarcated areas of RPE and photoreceptor loss in late dry AMD
Subretinal fluid, haemorrhage, or hard exudates — hallmarks of wet AMD
Disciform scar — end-stage fibrotic lesion in untreated wet AMD

Investigations

First-line
Visual acuity (LogMAR)Quantifies central visual function
Slit-lamp biomicroscopic fundus examinationIdentifies drusen, RPE changes, haemorrhage, fluid, atrophy
Amsler gridSelf-monitoring for metamorphopsia — new distortion suggests wet AMD conversion
Second-line
Optical coherence tomography (OCT)Key investigation for wet AMD — detects subretinal/intraretinal fluid, RPE detachment
Fundus autofluorescence (FAF)Maps areas of RPE atrophy in dry AMD
Specialist
Fluorescein angiography (FFA)Demonstrates choroidal neovascularisation and leakage in wet AMD
OCT angiography (OCTA)Non-invasive imaging of choroidal neovascular membranes
1
Dry AMD
  • No proven pharmacological treatment to halt progression
  • Smoking cessation — most important modifiable risk factor
  • Amsler grid self-monitoring — present urgently if new distortion develops
  • AREDS2 supplements (lutein, zeaxanthin, zinc, vitamins C and E) may slow progression in intermediate AMD
  • Low-vision aids and support: Macular Society, ECLO (Eye Clinic Liaison Officer)
2
Wet AMD — URGENT treatment
  • NICE NG82: start anti-VEGF treatment within 14 days of referral
  • Intravitreal anti-VEGF injection: ranibizumab, aflibercept, or bevacizumab (off-label)
  • Loading phase: typically 3 monthly injections, then individualised retreatment
  • Monitor with OCT at each visit — retreat if subretinal/intraretinal fluid recurs
  • NICE recommends treatment if BCVA is between 6/12 and 6/96 in the affected eye
3
Late dry AMD (geographic atrophy)
  • Low-vision rehabilitation and support
  • Register as sight impaired or severely sight impaired if appropriate
  • Counsel about Charles Bonnet syndrome (visual hallucinations — not psychiatric illness)

Complications

  • Severe bilateral central visual loss: Leading to loss of independence, inability to drive or read
  • Charles Bonnet syndrome: Complex visual hallucinations in patients with significant visual loss — benign but distressing
  • Disciform scar: End-stage wet AMD — fibrotic macular scar causing permanent central scotoma
  • Anti-VEGF treatment risks: Endophthalmitis (0.02–0.09% per injection), retinal detachment, raised IOP
UKMLA Exam Tips
  • 1Dry AMD = drusen + atrophy = gradual central loss = NO specific treatment. Wet AMD = new vessels + fluid/blood = RAPID loss = URGENT anti-VEGF
  • 2Metamorphopsia (distortion on Amsler grid) in known dry AMD = suspect conversion to wet AMD → urgent referral
  • 3Anti-VEGF targets VEGF which drives choroidal neovascularisation
  • 4Peripheral vision is preserved in AMD — distinguishes from glaucoma (peripheral vision first)
  • 5Smoking is the single most important MODIFIABLE risk factor
  • 6Charles Bonnet syndrome = visual hallucinations with visual loss — NOT psychiatric, does NOT need antipsychotics
  • 7Do NOT confuse late dry AMD (geographic atrophy) with inactive wet AMD — NICE specifically warns against this
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Verified Sources & References

NICE NG82 — Age-related macular degeneration
RCOphth AMD Commissioning Guidelines