A chronic, usually age-related condition affecting the macula (central part of the retina).

Leads to loss of central vision (reading, recognising faces, driving), but side/peripheral vision is usually preserved.

The most common cause of visual loss in older adults in the UK.

Types of AMD

Type Pathology Onset Progression Key Features

Dry (atrophic, non-neovascular) Gradual thinning of macula; accumulation of drusen (yellow deposits) Insidious Slowly progressive (years) Blurred central vision, difficulty reading, colours appear faded

Wet (neovascular, exudative) Abnormal choroidal neovascularisation → leakage, haemorrhage, scarring Often sudden Rapid vision loss (days–weeks)

Distorted or wavy vision (metamorphopsia), central dark spot (scotoma), often unilateral at onset

Dry AMD is much more common (~80–90%), but Wet AMD accounts for most severe vision loss.

Symptoms

Blurred or fuzzy central vision

Needing brighter light for reading

Colours appearing duller

Metamorphopsia: straight lines appear wavy or bent (especially in Wet AMD)

Central scotoma: dark, empty, or blurred patch in centre of vision

Difficulty recognising faces

Visual hallucinations (Charles Bonnet syndrome) in some patients with severe sight loss

Tip: Patients with sudden distortion or central dark spots should be referred urgently (within 1–2 weeks) for Wet AMD.

Diagnosis

Visual acuity testing

Amsler grid (patients can use at home for self-monitoring)

Fundoscopy / slit-lamp exam: drusen in Dry AMD; haemorrhage or exudates in Wet AMD

Optical coherence tomography (OCT): key imaging tool

Fluorescein angiography: to confirm neovascular membranes in Wet AMD
Treatment

1. Dry AMD

No cure yet, treatment is mainly supportive:
Lifestyle: stop smoking, maintain healthy weight, good blood pressure and cardiovascular risk control
Nutrition: Age-Related Eye Disease Study 2 (AREDS2) supplements
Vitamin C, Vitamin E, zinc, copper, lutein, zeaxanthin
Shown to slow progression in intermediate/severe Dry AMD
Low-vision aids, magnifiers, good lighting
Clinical trials ongoing for emerging therapies (complement inhibitors)

2. Wet AMD

Early detection is critical
Intravitreal anti-VEGF therapy (first-line):
e.g., ranibizumab, aflibercept, brolucizumab, faricimab
Given as intravitreal injections, typically monthly for 3–4 doses, then less often depending on response
Stabilises or improves vision in most patients
Photodynamic therapy with verteporfin – rarely used now
Laser therapy – rarely used except for well-demarcated extrafoveal lesions
Regular OCT monitoring to guide further injections

Referral

Urgent ophthalmology referral for suspected Wet AMD (within 2 weeks).
Routine referral for Dry AMD unless diagnostic uncertainty or sudden change.

Patient Support

Amsler grid for home monitoring: any new distortion or blank spot warrants prompt review.
Register as sight-impaired if criteria met → access to support services, low-vision clinics, social support.
Advice on driving: DVLA notification required if vision falls below legal standard.

Key Take-Home Messages

Dry AMD: slow, progressive → lifestyle, AREDS2 supplements, visual aids.
Wet AMD: acute, treatable → urgent referral for anti-VEGF injections.
Regular monitoring (self and clinical) is essential.

References

NICE Guideline NG82: Age-related macular degeneration (2018, updated 2023).
Royal College of Ophthalmologists. AMD Clinical Guidelines (2023).
Age-Related Eye Disease Study 2 (AREDS2): JAMA. 2013;309(19):2005-2015.
Brown DM et al. Ranibizumab versus Verteporfin for Neovascular AMD (NEJM, 2006).
Heier JS et al. Aflibercept for Neovascular AMD (Ophthalmology, 2012).
Schmidt-Erfurth U et al. Guidelines for the Management of Neovascular AMD (Progress in Retinal and Eye Research, 2014).
Public Health England / NHS: Living with Age-related Macular Degeneration.

Dr Geranmayeh