Age-Related Macular Degeneration (AMD)
Age-related macular degeneration (AMD) is a potentially progressive degenerative disorder of the macula that typically affects people aged over 50 years. It is a common cause of irreversible central visual loss and is the leading cause of severe irreversible visual impairment in older adults in the developed world. AMD is broadly classified into dry AMD and wet AMD.
This updated UKMLA guide to AMD is based on NICE NG82 and NICE CKS, which covers classification, risk factors, symptoms, diagnosis, and management.
Classification
There are 2 main traditional types of AMD:
| Dry AMD (atrophic) | Wet AMD (neovascular / exudative) | |
|---|---|---|
| Prevalence | ~90% of AMD cases | ~10% of AMD cases |
| Pathophysiology | Gradual atrophy of retinal pigment epithelium and photoreceptors | Choroidal neovascularisation → leakage, haemorrhage, fibrosis |
Disclaimer:
AMD is traditionally divided into dry AMD and wet AMD, which is the most useful classification for exam and non-specialist levels.
NICE uses a more detailed classification system to describe disease stage and activity, but this level of detail is mainly relevant to ophthalmology.
NICE Classification
| AMD classification | Definition |
|---|---|
| Normal eyes |
|
| Early AMD | Low risk of progression:
Medium risk of progression:
High risk of progression:
|
| Late AMD (indeterminate) |
|
| Late AMD (wet active) |
|
| Late AMD (dry) | Geographic atrophy (in the absence of neovascular AMD)
Significant visual loss (6/18 or worse) associated with:
|
| Late AMD (wet inactive) |
Note that eyes may still develop or have a recurrence of late AMD (wet active) |
Causes and Risk Factors
Smoking is the main modifiable risk factor
- Dose-response relationship
- Stopping smoking reduces the risk of AMD
Other risk factors:
- AMD in the other eye
- Advancing age
- Females
- Family history
- Certain diet patterns
- Low in omega-3 and 6
- Low in vitamins A, C and E
- Low in carotenoids (e.g. lutein) and minerals (e.g. zinc)
- High glycaemic index
- High in saturated fat and cholesterol
- Hypertension and history of cardiovascular disease
- Physical inactivity
Diagnosis
Disclaimer:
This article summarises AMD for educational and exam-focused learning, focusing on the core principles most relevant to a non-specialist level.
As explained above, the traditional dry vs wet AMD classification is more appropriate for non-specialist learning. Therefore, the investigation, diagnosis and management sections have been simplified and adapted around this distinction, rather than following NICE’s full detailed classification system.
Clinical Features
Typically presents as a >50 y/o with:
- Blurring of vision
- Scotoma – mainly affecting the central vision
- Metamorphopsia (straight lines appear bent / wavy / crooked)
Wet AMD presents with rapidly progressing visual deterioration.
Other symptoms:
- Light glare
- Loss of or decreased contrast sensitivity (the ability to discern between different shades)
- Size or colour of objects appears different with each eye
- Abnormal dark adaptation (difficulty adjusting from bright to dim lighting)
- Photopsia (perception of flickering or flashing light)
Advanced AMD can cause Charles Bonnet syndrome (visual hallucinations secondary to visual impairment, despite having intact insight and no underlying psychosis, delirium, or dementia)
Investigation and Diagnosis
Primary Care
| Test | Findings suggestive of AMD |
|---|---|
| Amsler grid |
|
| Fundoscopy | Dry AMD:
Wet AMD is indicated by signs of choroidal neovascularisation, in addition to dry AMD findings
|
If AMD is suspected, refer urgently to ophthalmology
Secondary Care
Initial investigation: slit lamp fundus examination (findings are similar to those of fundoscopy)
- Dry AMD:
- Drusen – main finding
- Changes to the macula (pigmentary / exudative / haemorrhagic / atrophic changes)
- Wet AMD is indicated by signs of choroidal neovascularisation, in addition to dry AMD findings
- Subretinal / intraretinal fluid
- Subretinal haemorrhage
- Retinal pigment epithelial detachment
Dry AMD can usually be diagnosed by slit-lamp fundus examination alone, with no further imaging required
Further imaging is necessary to diagnose wet AMD:
- 1st line: OCT – to detect neovascularisation and subretinal / intraretinal fluid
- 2nd line: fundus fluorescein angiography (FFA) – to confirm neovascularisation if OCT is inconclusive / cannot exclude it
Management
Dry AMD
There are no pharmacological treatments for dry AMD
Mainstay of management is active observation and conservative management:
- Smoking cessation (to reduce risk of progression – see the Smoking Cessation article for more information)
- Consider antioxidant vitamin and mineral supplementation (AREDS2 formula: vitamin C, vitamin E, zinc, copper, lutein, and zeaxanthin)
- Advise on a healthy, balanced diet (low glycaemic index, rich in fruits, green leafy vegetables and fish high in omega-3 fatty acids)
Wet AMD
Mainstay of management: intravitreal anti-VEGF therapy (e.g. ranibizumab, aflibercept, bevacizumab)
Laser photocoagulation is NOT routinely used in wet AMD. It is generally reserved for rare cases of extrafoveal choroidal neovascularisation where anti-VEGF therapy is not feasible or effective.
Do NOT offer photodynamic therapy and intravitreal corticosteroids as an adjunct to anti-VEGF therapy.
References