AGE-RELATED MACULAR
DEGENERATION
MODERATOR- DR SANDEEP SHIVRAN
PRESENTER- DR DEEPAK KUMAR
INTRODUCTION
• Age-related macular degeneration is a
degenerative disorder affecting the macula.
It affects bruchs membrane, retinal pigment
epithelium and photoreceptors.
• ARMD is a leading cause of blindness in
elderly population above the age of 60 yrs.
• It is the most common cause of permanent
bilateral central vision loss in elderly.
PREVALENCE
• ARMD is responsible for 8.7% total blindness
all-over world.
1) The first epidemological study (1976) was the
framingham eye study, shows prevalence of
ARMD with age.
Age b/w 65-74:- 11%
75-85:- 28%
overall 55-85:- 8.8%
2) BLUE MOUNTAIN EYE STUDY(2002)
• provides an accurate estimate for the age specific
prevalence of ARMD.
3) BLUE MOUNTAIN EYE STUDY(1997)
• This study suggests that neovascular ARMD among
women is double that of man
4) THE BEAVER DAM STUDY(1992)
• This study disclose positive relationship b/w ARMD
and smoking
5) ROTTERDAM STUDY(2003)
• Suggest positive co relation B/w high BP and
increased incidence of ARMD
RISK FACTORS
1. age > 55yr ( most important)
2. Smoking
3. Gender (female:male = 1.34: 1)
4. Hyperopia
5. White race
6. Hypertension
7. Genetic susceptibility
8. Beta blockers and Aspirin
TYPES OF ARMD
1) NON EXUDATIVE / DRY / ATROPHIC ARMD
• This is the most common form of ARMD about
90% of all ARMD cases
• It progresses slowly
• severe visual impairment over 5 to 10 yrs
• Geographic atrophy is advance stage of dry
ARMD
• The earliest sign of DRY ARMD => DRUSENS in
macular region.
• DRUSENS are tiny pinpoint ,discrete yellow
deposits , histopathologically accumulation of
abnormal hyaline material located B/w bruchs
membrane and RPE.
• In advance geographical atrophy of macula
there is a large,well demarcated area of atrophy
and it is possible to see clearly the underlying
choroid vessels.
• Drusen classified clinically as follows:
1.Hard drusen: Discrete
Well delineated margin
Size <125um.
2.Soft drusen: Granular/membranous
Poorly defined margin
Size b/w 63-250um
3.Reticular drusen: Diffuse,small,regular deposits
drusen like material in the macula.
4.Calcific drusen: Sharply demarcated, glistening,
refractile lesions
2) EXUDATIVE / WET /NEOVASCULAR ARMD
• WET ARMD is less common only 10 %
• More aggressive in nature than dry ARMD
responsible for 90% of all severe visual loss
• The clinical course more rapid than dry, visual loss
within 3 yrs
• Complications are
Choroidal neovascularisation (CNV),
Pigment epithelial detachment(PED),
Retinal angiomatous proliferation (RAP) and
Polypoidal choroidal vasculopathy (PCV).
• Separation of the RPE and choroid layer
alongside an increase in vascular endothelial
growth factor(VEGF) stimulates angiogenesis
of choroidal blood vessels into the retina
beneath the macula.
• Angiogenesis begins with vasodilatation and
increase in vascular permeability, followed by
activation and proliferation of vascular
endothelial cells.
• Abnormal growth of new blood vessels and
leakage of serous fluid and blood into the
macular region B/w bruchs membrane and
RPE
• Choroidal neovascularisation appears as pale
pink-yellow or grey green elevation at the
macula.
CLINICAL CLASSIFICATION
CARMS STAGING
GRADE NO. OF SIZE OF RPE CHANGES PED
DRUSENS DRUSENS
GRADE 1 Less than 10 Small (<63um) No RPE No PED
changes
GRADE 2 More than 10 Small With or No PED
Less than 15 Intermediate without RPE
(63-125um) changes
GRADE 3 More than 15 Intermediate Pigment Drusenoid PED
More than 1 Large drusen epithelium +/-
(>125um) changes
GRADE 4 Geographic atrophy with involvment of the macular centre or noncentral
geographic atrophy of 350um or more in size
GRADE 5 Exudative AMD including PED , serous or hemorrhagic retinal detachments,
CNVM with subretinal and sub-RPE hemorrhage or fibrosis or scars
CLINICAL FEATURES
SYMPTOMS
• DRY ARMD =>Gradual/progressive diminution
of central vision.
• WET ARMD => Sudden painless loss of vision
• Common visual complaints =>
Distortion of vision
Straight lines as wavy
Central scotomas
CLINICAL FEATURES
SIGNS
EARLY SIGNS
DRUSENS – SMALL
INTERMEDIATE
LARGE
PIGMENTARY ABNORMALITIES –
HYPERPIGMENTATION (due to subretinal pigment )
HYPOPIGMENTATION (due to RPE atrophy)
CLINICAL FEATURES
SIGNS
LATE SIGNS
ATROPHIC/DRY/GEOGRAPHIC ARMD-
Large choroidal vessels underlying area of RPE atrophy
become visible
Pre-existing drusens may disappear.
EXUDATIVE/WET/NEOVASCULAR ARMD
Drusens with RPE detachment (PED)
Choroidal neovascularization
Haemorrhagic detachment of neurosensory retina
INVESTIGATIONS
• Visual acuity
• Pin hole
• Colour vision
• Photostress test
• Two point discrimination test
• Maddox rod test
• Amsler grid charting
• FUNDUS Examinations- direct/indirect ophthalmoscope, slit lamp
biomicroscopy with +90/+78D non contact lens.
• OCT (Optical Coherence Tomography)
• FFA (Fundus Fluorescein Angiography}
• ICG (Indocyanine Green Angiography)
VISION PHOTO
AMSLER GRID CHART
FUNDUS EXAMINATION
Category 5
OCT-Dry ARMD(DRUSEN)
OCT- DRY ARMD(GEOGRAPHIC ATROPHY)
WET OCT
FFA PHOTO
FFA PHOTO
ICG
MANAGEMENT
• LIFE STYLE CHANGES
• ANTIOXIDENT
• ANTI ANGIOGENIC AGENT
• ABLATION
• SURGERY
• STEM CELL TREATMENT
ANTIOXIDANTS
• VIT-C 500 mg
• VIT-E 400 mg
• CAROTENOIDS(LEUTEIN/ZEOXANTHIN)
• ZINC OXIDE 80 mg
• Combination of antioxidants & zinc reduces
risk of advanced ARMD by 25 %
AGENTS WHICH INHIBIT CHOROIDAL
NEOVASCULARIZATION
• BEVACIZUMAB(AVASTIN)
• RANIBIZUMAB(LUCENTIS)
• PEGAPTANIB(MACUGEN)
• AFLIBERCEPT(EYLEA)
ANTI ANGIOGENIC AGENTS
• BEVACIZUMAB
• Full length monoclonal antibody 150 KD
• Bind all isoforms of VEGF
• DOSES – 0.05ml (1.25mg),MONTHLY DOSE
• RANIBIZUMAB
• Recombinant humanized immunoglobulin G1,
Kappa isotype ,Antibody fragment (Fab)(48KD)
• Binds all isoforms of VEGF
• DOSES-3 inj of 0.5mg(0.05ml)
• Every month for 3 months
• PEGAPTANIB
• 28 Base ribonucleotide aptamer
• Binds to heparin-binding domain of VEGF-A
• DOSES- 0.3 mg , 6 weekly for 2 years
• AFLIBERCEPT (VEGF Trap)
• A fusion protein of key binding domains of human
VEGF-1 AND 2 combined with a human IgG Fragment
• Blocks all forms of VEGF-A
• Also blocks placental growth factor 1 & 2
• DOSES- 2 mg (0.05 ml) monthly for 3 months
• Than 2 monthly for 2 months
LASER PHOTOCAUGULATION
Patients with extra foveal choroidal neovascular membrane with distinct margin.
A 532nm frequency doubled YAG laser.
Dis-advantage : Immediate and significant fall in central vision,
Evolution of dense central scotoma
Risk of recurrence is higher
Cannot use at sub-foveolar region
PHOTODYNAMIC THERAPY
• Can be used in sub foveolar region
• because it selectively destroy the neovascular
complex without causing any damage to
retinal tissue.
• Photo sensitizers =>increase lesion targeting.
• To expose the lesion dye is injected prior to
this therapy.
SURGERY
• SUBMACULAR EXCISION OF CNV
• MACULAR ROTATION/TRANSPOSITION SX
• RETINAL ROTATION
• AUTOLOGOUS RPE TRANSPLANTATION
STEM CELL TREATMENT
REHABILATATION
• LOW VISION AIDS-
Individuals who experiences untreatable visual
loss and effects daily life
Simple magnifiers
Reading lamps
Scanning devices
THANK YOU
