age-related macular degeneration
TRANSCRIPT
- 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
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- Diameter 5 mm
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- 4 mm temporal, 0.8 inferior to optic disc
- Fovea
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- Depression of ~1 disc diameter (1.5 mm) at centre of macula
4. Anatomy
- Foveola
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- Central point of fovea
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- 0.35 mm in diameter
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- Thinnest part of retina
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- Cones only
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- High levels of visual acuity
5. Anatomy Choroid RPE Foveola 6. Anatomy 7. Definitions
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- Two forms:
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- Non-exudative (dry)
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- Most common (90%)
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- Geographic atrophy
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- Exudative (wet)
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- Neo-vascularisation
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- Causes more devastating and sudden vision affects
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8. Pathophysiology
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- Progressive thickening of Bruchs membrane with age
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- Interferes with RPE - photoreceptor metabolism
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- Metabolites from photoreceptors accumulate on Bruchs membrane
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- Like debris!
9. Pathophysiology
- Drusen (colloid bodies)
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- Earliest clinical sign
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- Lipid or collagen rich deposits (waste)
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- Lie between Bruchs membrane and RPE
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- Further disruption of RPE/photoreceptor metabolism
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- Cause variable amount of depigmentation and eventually atrophy of overlying RPE
10. Pathophysiology Drusen Bruchs Membrane RPE Photoreceptors Choroid 11. Pathophysiology
- Hard Drusen
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- Small localised collection of hyaline material within or on Bruchs membrane
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- Sharp, well demarcated boundaries
- Soft Drusen
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- Involve overlying focal RPE detachment
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- Poorly demarcated boundaries
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- Larger/commonly become confluent
12. Hard Drusen 13. Soft Drusen 14. Pathophysiology
- Drusen
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- Can become calcified (glistening appearance)
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- Can become confluent representing widespread RPE abnormality
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- Increase risk of vision loss!
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- Can be inherited as a dominant trait
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- Hard Drusen
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- No progression / consequence
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15. Confluent Drusen 16. Calcified Drusen 17. Pathophysiology
- RPE degeneration, seen as:
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- Focal areas of hypo- and hyper- pigmentation (stippling)
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- Eventually areas of atrophy of the RPE revealing underlying choriocapillaris
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- Geographic atrophy = end stage
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18. RPE Degeneration 19. RPE Degeneration 20. Summary
- Age-related thickening of Bruchs 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:
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- Slow/progressive atrophy of RPE and photoreceptorsor
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- Collapse of an RPE detachment overlying soft drusen
- Advanced form = Geographic Atrophy
22. Geographic Atrophy (GA)
- Clinical Features:
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- Soft drusen present in early stages (significant risk factor for GA due to RPE detachment)
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- Decreased retinal thickness and increased visualisation of choroidal vessels
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- Sharply demarcated pale area
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- Choroidal vessels sometimes white
23. Geographic Atrophy (GA) 24. Geographic Atrophy (GA) 25. Geographic Atrophy (GA)
- Signs/Symptoms:
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- Marked decrease VA (unless foveal sparing)
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- Central field loss (positive scotoma)
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- Difficulty recognizing faces
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- Difficulty reading if large scotoma
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- Difficulties in dim light / adapting
26. Exudative AMD
- Clinical Features:
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- Choroidal neo-vascularisation
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- Exudative detachment of RPE and/or retina
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- Disciform scar
27. Choroidal Neovascularisation
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- Proliferations of fibrovascular tissue from choriocapillaris through defects in Bruchs membrane
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- Sub-RPE or sub-retinal
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- Membranes have a greyish/green or pinkish/yellow hue in late stages
28. Choroidal Neovascularisation
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- Tendency to leak
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- Serous and blood
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- Distorted or blurred vision
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- Red if sub-retinal, darker if sub-RPE
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- Rarely vitreous haemorrhage
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- Cause RPE and retinal detachments
29. Choroidal Neovascularisation
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- Fibrous tissue proliferation scar development (Disciform scar)
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- Permanent vision loss
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- Further bleeding
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- risk of exudative retinal detachment
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30. Choroidal NeovascularisationRPE BruchsMembrane Photoreceptors Choroid 31. Choroidal Neovascularisation 32. Choroidal Neovascularisation 33. Choroidal Neovascularisation 34. Disciform Scar 35. Investigation
- History
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- Gradual change = non-exudative
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- Sudden change = exudative
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- Difficulties reading/recognising faces
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- Difficulties with changing light / adapting after bright light (remember when assessing!)
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- Distortion = exudative change!
36. Investigation 37. Investigation
- Visual acuity
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- Distance and near
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- No improvement (worse?) with pin-hole
- Amsler-grid
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- Field test for central 20 degrees
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- Show scotoma/distortion
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- Monocular/ correct add for WD!
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- No varifocals/bifocals!!!!
38. Amsler Chart 39. Amsler Chart 40. Amsler Chart 41. Investigation
- Fundus Examination
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- Binocular view detect elevation
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- VOLK or contact lens
42. Management
- Urgent refer any suspected neovascular membrane or sub-retinal fluid
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- Fluorescein angiography
- Absence of previous drusen sub-retinal fluid(?)
- Non-exudative no surgical treatment
43. Mx. Non-exudative
- Advice and support
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- Likely to progress
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- Central vision only
- Advice re. Lighting
- High add or LVAs
44. Mx. Non-exudative
- Amsler Chart self monitoring
- Low Vision referral
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- Daily living skills
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- LVAs
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- Eccentric fixation training?
- Registration
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- Social Service - advice and benefits
45. Mx. Exudative
- Argon laser photocoagulation
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- Extrafoveal/Juxtafoveal CNV
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- Subfoveal?
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- Immediate loss of VA
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- Slow progression NOT improve
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- 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
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- Photosensitizer dye accumulates in proliferating tissues
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- damaged by appropriate wavelength light
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- More specific than laser only destroys tissue with photosensitive dye
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- High cost!!
50. Mx. Exudative
- Radiation Therapy
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- Not conclusive
- Surgical translocation
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- Still experimental
- Membrane removal
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- Suitable for young not old
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- RPE transplantation?
51. Risk Factors
- Fair skin/blue eyes
- Female
- Obesity
- Hypertension
- High-fat diet / High cholesterol
- Long-sighted
52. Risk Factors
- Smoking
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- Accelerate development of wet form - twice the risk
- Sunlight
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- short wavelengths accelerate degeneration
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- History of out-door life
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- Sunglasses/polaroids?
53. Prevention
- Supplements
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- Carotenoid pigments green leafy vegetables
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- Zinc mixed results
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- Anti-oxidants Vit A and C (particularly combined with Zinc)
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- Selenium
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- Problems with side-effects
54. Prevention
- Age-Related Eye Disease Study (AREDS) 2001
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- Vit C 500mg
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- Vit E 400 mg
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- Vit A 15 mg
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- Zinc 80 mg (Copper 2mg)
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- Did not help early stages; reduced risk of progression to advanced forms.
55. PreventionUS$ 68.95 per 500ml bottle 56. References
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- www. rcophth .ac. uk /publications /guidelines/ armd .html
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- Mx, prognosis, aetiology etc
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- Kanski, Clinical Opthalmology
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- Various ophthalmology textbooks or atlases
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- Berger et al. Age-related macular degeneration