Age-Related Macular Degeneration

1. Age-Related Macular
Degeneration
Dr Charlotte Hazel

2. Introduction
•Leading cause of blindness in the
Western World
•Common in Caucasian populations
•Bilateral disease
•60% bilateral within 5 years of visual
loss in first eye
•Earliest signs rarely visible before 45
years.

3. Anatomy
•Macula
•Diameter 5 mm
•4 mm temporal, 0.8 inferior to optic disc
•Fovea
•Depression of ~1 disc diameter (1.5 mm) at
centre of macula

4. Anatomy
•Foveola
•Central point of fovea
•0.35 mm in diameter
•Thinnest part of retina
•Cones only
•High levels of visual acuity

5. Anatomy
Choroid
RPE
Foveola

6. Anatomy

7. Definitions
•Two forms:
•Non-exudative (dry)
•Most common (90%)
•Geographic atrophy
•Exudative (wet)
•Neo-vascularisation
•Causes more devastating and sudden
vision affects

8. Pathophysiology
•Progressive thickening of Bruch’s
membrane with age
•Interferes with RPE -
photoreceptor metabolism
•Metabolites from photoreceptors
accumulate on Bruch’s membrane
•Like debris!

9. Pathophysiology
•Drusen (colloid bodies)
•Earliest clinical sign
•Lipid or collagen rich deposits (waste)
•Lie between Bruch’s membrane and RPE
•Further disruption of RPE/photoreceptor
metabolism
•Cause variable amount of depigmentation
and eventually atrophy of overlying RPE

10. Pathophysiology
Drusen
Bruch’s Membrane
RPE
Photoreceptors
Choroid

11. Pathophysiology
•Hard Drusen
•Small localised collection of hyaline
material within or on Bruch’s membrane
•Sharp, well demarcated boundaries
•Soft Drusen
•Involve overlying focal RPE detachment
•Poorly demarcated boundaries
•Larger/commonly become confluent

12. Hard Drusen

13. Soft Drusen

14. Pathophysiology
•Drusen
•Can become calcified (glistening
appearance)
•Can become confluent – representing
widespread RPE abnormality
•Increase risk of vision loss!
•Can be inherited as a dominant trait
•Hard Drusen
•No progression / consequence

15. Confluent Drusen

16. Calcified Drusen

17. Pathophysiology
RPE degeneration, seen as:
•Focal areas of hypo- and hyper-
pigmentation (‘stippling’)
•Eventually areas of atrophy of the
RPE revealing underlying
choriocapillaris
‘Geographic atrophy’ = end stage

18. RPE Degeneration

19. RPE Degeneration

20. Summary
Age-related thickening of Bruch’s membrane
Interferes with photoreceptor/RPE metabolism
Causing deposition of metabolites / formation
of drusen
Damage to overlying RPE/photoreceptors and
underlying choriocapillaris

21. Non-Exudative AMD
•Gradual mild to moderate impairment over
months or years
•Cause:
•Slow/progressive atrophy of RPE and
photoreceptors or
•Collapse of an RPE detachment overlying soft
drusen
•Advanced form = Geographic Atrophy

22. Geographic Atrophy (GA)
•Clinical Features:
•Soft drusen present in early stages
(significant risk factor for GA – due to RPE
detachment)
•Decreased retinal thickness and increased
visualisation of choroidal vessels
•Sharply demarcated pale area
•Choroidal vessels sometimes white

23. Geographic Atrophy (GA)

24. Geographic Atrophy (GA)

25. Geographic Atrophy (GA)
•Signs/Symptoms:
•Marked decrease VA (unless foveal
sparing)
•Central field loss (positive scotoma)
•Difficulty recognizing faces
•Difficulty reading if large scotoma
•Difficulties in dim light / adapting

26. Exudative AMD
•Clinical Features:
•Choroidal neo-vascularisation
•Exudative detachment of RPE
and/or retina
•Disciform scar

27. Choroidal Neovascularisation
•Proliferations of fibrovascular
tissue from choriocapillaris
through defects in Bruch’s
membrane
•Sub-RPE or sub-retinal
•Membranes have a
greyish/green or pinkish/yellow
hue in late stages

28. Choroidal Neovascularisation
•Tendency to leak
•Serous and blood
•Distorted or blurred vision
•Red if sub-retinal, darker if sub-
RPE
•Rarely vitreous haemorrhage
•Cause RPE and retinal
detachments

29. Choroidal Neovascularisation
•Fibrous tissue proliferation –
scar development (Disciform
scar)
•Permanent vision loss
•Further bleeding
•risk of exudative retinal detachment

30. Choroidal Neovascularisation
RPE
Bruch’s
Membrane
Photoreceptors
Choroid

31. Choroidal Neovascularisation

32. Choroidal Neovascularisation

33. Choroidal Neovascularisation

34. Disciform Scar

35. Investigation
•History
•Gradual change = non-exudative
•Sudden change = exudative
•Difficulties reading/recognising faces
•Difficulties with changing light /
adapting after bright light (remember
when assessing!)
•Distortion = exudative change!

36. Investigation

37. Investigation
•Visual acuity
•Distance and near
•No improvement (worse?) with pin-hole
•Amsler-grid
•Field test for central 20 degrees
•Show scotoma/distortion
•Monocular/ correct add for WD!
•No varifocals/bifocals!!!!

38. Amsler Chart

39. Amsler Chart

40. Amsler Chart

41. Investigation
•Fundus Examination
•Binocular view – detect elevation
•VOLK or contact lens

42. Management
•Urgent refer any suspected
neovascular membrane or sub-
retinal fluid
•Fluorescein angiography
•Absence of previous drusen – sub-
retinal fluid(?)
•Non-exudative – no surgical
treatment

43. Mx. Non-exudative
•Advice and support
•Likely to progress
•Central vision only
•Advice re. Lighting
•High add or LVA’s

44. Mx. Non-exudative
•Amsler Chart – self monitoring
•Low Vision referral
•Daily living skills
•LVA’s
•Eccentric fixation training?
•Registration
•Social Service - advice and benefits

45. Mx. Exudative
•Argon laser photocoagulation
•Extrafoveal/Juxtafoveal CNV
•Subfoveal?
•Immediate loss of VA
•Slow progression NOT improve
•Possible recurrence (up to 50%)

46. Fluorescein Angiography
CNV Pre- and Post- Laser Tx
CNV Pre-Laser CNV Post-Laser

47. Laser Scars

48. Recurrence

49. Mx. Exudative
•Photodynamic therapy
•Photosensitizer dye accumulates in
proliferating tissues
•damaged by appropriate wavelength light
•More specific than laser – only destroys
tissue with photosensitive dye
•High cost!!

50. Mx. Exudative
•Radiation Therapy
•Not conclusive
•Surgical translocation
•Still experimental
•Membrane removal
•Suitable for young not old
•RPE transplantation?

51. Risk Factors
•Fair skin/blue eyes
•Female
•Obesity
•Hypertension
•High-fat diet / High cholesterol
•Long-sighted

52. Risk Factors
•Smoking
•Accelerate development of ‘wet’ form
- twice the risk
•Sunlight
•short wavelengths accelerate
degeneration
•History of out-door life
•Sunglasses/polaroids?

53. Prevention
•Supplements
•Carotenoid pigments – green leafy
vegetables
•Zinc – mixed results
•Anti-oxidants – Vit A and C
(particularly combined with Zinc)
•Selenium
•Problems with side-effects

54. Prevention
•Age-Related Eye Disease Study
(AREDS) 2001
•Vit C 500mg
•Vit E 400 mg
•Vit A – 15 mg
•Zinc – 80 mg (Copper – 2mg)
•Did not help early stages; reduced risk of
progression to advanced forms.

55. Prevention
US$ 68.95 per
500ml bottle

56. References
•www.rcophth.ac.uk
/publications /guidelines/armd.html
Mx, prognosis, aetiology etc
•Kanski, Clinical Opthalmology
•Various ophthalmology textbooks or
atlases
•Berger et al. Age-related macular
degeneration