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Age Related Macular
Degeneration
INTRODUCTION
• Degenerative disorder affecting the macula
• Characterized by the presence of specific
clinical findings like drusen and RPE changes in
the absence of another disorder
TYPES
• DRY – non neovascular: includes
- Early
- Intermediate
- Dry type of advanced AMD
• WET – neovascular
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Epidemiology
• The WHO estimated in 2002 that 8.7/ of world
blindness was due to AMD.
• AMD rare before the age of 55 and more
common in person 75 years of age and older.
• The prevalence of advanced AMD increases
with each decade after the age 50.
• Highest prevalence occurring after the age of
80.
RISK FACTORS
• Age-major risk factor
• Gender -Female>Male
• Race -White>Blacks
• Family history
• Light exposure
• Hypertension
• Smoking
• Drugs – Aspirin ,chloroquine and phenothiazine
• Ocular factors - blue coloured iris, hyperopia,
cataract sx.
• Dietary factors -high fat intake and obesity increases
risk .
PATHOPHYSIOLOGY OF ARMD
ARMD is characterized by -
• Drusen formation.
• RPE abnormalities -hyper and hypopigmentation.
• Geographical atrophy of RPE and choriocapillaries.
• Neovascular maculopathy.
Drusen
• The earliest clinically detectable sign
• Drusen are tiny pin point,yellow deposits of
abnormal hyaline material located at interface of
Bruch’s membrane and the RPE.
• Rarely present <45yrs
• On H/P - Drusen are focal areas of the
eosinophilic material between the basement
membrane of RPE & BM.
HISTOLOGICAL LOCATION OF DRUSEN
INL 
ONL
IS
OS
RPE
CC
DRUSEN SIZE
• Small < 63 microns – not a sign of AMD
• Intermediate 63-124 microns
• Large >/=125 micron
• Very large >250 microns
HOW TO MEASURE DRUSEN?????
SMALL OR HARD DRUSEN
• Discrete , well demarcated, yellowish white
• Occur with ageing – alone not enough to
classify as AMD
• FFA- pin point window defect
• Risk of progression to advanced AMD – 1.3%
after 5 years
SOFT DRUSEN
• > 63 microns
• Located b/w RPE basement membrane & inner
collagenous layer of bruchs membrane
• Intermediate 64- 124 microns
• Large drusen > 124 micron
• Very large drusen > 250 micron
• Decreasing density of the drusen from centre to
the margin
• Tendency to cluster and merge with one another
- coalascence
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• There is no increases with age
• May spontaneously regress or disappear over
period of time- leaving RPE atrophy
• Eyes with soft drusen are at an increased risk
of developing RPE abnormality, geographic
atrophy and CNV
SOFT DRUSENS FFA
• FFA- hyperfluorescence early and fade or stain
in late phase
• Persistent staining is due to pooling of dye in
focal detachment of RPE membrane or
staining of diffuse drusen material
• RPE cells over the soft drusen are hypo
pigmented or atrophic
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RISKS OF ADVANCED AMD IN LARGE
DRUSEN
Eyes with B/L large drusen
• Risk of CNV is 18% in atleast 1 eye in 3 years
• Risk of geographic atrophy – 8%
Eyes with large drusen with CNV in one eye
• Large drusen present – 46% risk of CNV in
good eye in 5 yrs
• If no large drusen 10% risk only
SPECIAL TYPES OF DRUSEN
• Cuticular drusen
• Pseudodrusen or subretinal drusen or
subretinal drusenoid deposit
CUTICULAR DRUSEN
• Small( like hard drusen) but are more numerous
than hard drusens and extend beyond arcades
upto mid periphery
• Located betweeen RPE basement membrane and
inner collagenous layer of bruchs membrane
• FFA- starry night appearance due to RPE atrophy
over the drusen
• FAF- Mild decrease in FAF over the drusen
• OCT- triangular or saw tooth appearance
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SUBRETINAL DRUSENOID DEPOSITS
• Pseudo drusens or reticular drusens
• Located internal to the RPE between RPE and
sensory retina
• Composition is like soft drusen
• Appear as white or blue and are better seen with
blue light
(blue light not filtered as they are above the RPE)
• Network like appearance seen- reticular
• More in perifoveal region
Dry AMD
(1)SYMPTOMS:
• Initially none
• Difficulty in dark adaptation
• Decreased vision
(2) SIGNS:
• Intermediate- large soft drusen
• RPE hypo/hyperpigmentation
• Geographic atrophy
• Drusenoid RPE detachment
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(3)OCT FINDINGS:
• Drusens
• Outer retinal tubulations
• Outer retinal corrugations
(4) FA – window defect due to unmasking of
background choroidal fluorescence
CHANGES IN RPE IN NON
NEOVASCULAR AMD
• Pigment mottling
• Stippled hypopigmentation
• Focal hyperpigmentation
• Geographic atrophy
• PIGMENT MOTTLING AND STIPPLED
HYPOPIGMENTATION
- These occur when the neurosensory retina
thins over the abnormal RPE area
- May precede the GA
- RPE overlying the drusens shows
hypopigmentation
• FOCAL HYPERPIGMENTATION
- clinically evident pigment clumping at the
level of outer retina or subretinal space
- Maybe punctate, linear or reticular in shape
- Present in 3-12 % of adults >50 yrs
- Higher risk of CNV if focal hyperpigmentation
and soft drusens are present and if the other
eye has CNV 58-73% within 5 years
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GEOGRAPHIC ATROPHY
• Advanced form of dry AMD when it involves the
fovea
• RPE atrophies in well defined round area with
atrophy of underlying choriocapillaries- so large
choroidal vessels seen easily
• These start as round areas often ringing the fovea
and then coalesce and enlarge and ultimately
involve the fovea
• Upto 20% of cases of legal blindness due to AMD
are caused by geographic atrophy
Contd…
• The area of geographic atrophy has atrophic
RPE and choriocapillaries  atrophy of
photoreceptor layer  scotoma
• If it involves the fovea then V/A can drastically
decrease
• GA then becomes advanced form of AMD
**Risk of developing CNV at the edge of GA**
• FFA – RPE window defect
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HOW DOES GA ARISE?
1. Areas of confluent large drusens may regress
and leave irregular shaped areas of GA
2. Small foci of pigmentory mottling areas may
coalesce and progress to a single area of GA
3. Spontaneous flattening of the RPE
detachment may result in GA
• Thin fovea no rpe choroid hyperrefl
• oct
INVESTIGATIONS
• Amsler grid test:- Assesses distorted &
scotoma , small irregularities in the central
field of vision ( 10degree)
• Ophthalmoscopy:- to detect
drusen,neovascularization
• Fluorescein and ICG angiography:-
Hyperfluorescent lesions:
• Hard and soft drusen
• RPE atrophy
• RPE tear
• CNV
• Serous PED
• Subretinal fibrosis
Hypofluorescent lesion
• Haemorrhage, lipid
MANAGEMENT OF DRY ARMD
• Education and follow up:- Periodic
examinations are advised
• Amsler grid test:- Check for visual changes
regularly
Antioxidants:- use of high dose of multivitamins &
antioxidants decreases the risk of progression of
ARMD in high risk pt.
– Extensive intermediate Drusen
– At least one large Drusen
– non central GA in one or both eyes
– Late AMD in one eye
REDUCES RISK OF PROGRESSION TO ADVANCED AMD BY
25%
Combination of antioxidants vitamins
and minerals-
AREDS1 Formula
• Vitamin E 400IU
• Vitamin C 500mg
• Beta Carotene 15mg ( Vit A 2500IU)
• Zinc 80mg
• Copper (Cupric Oxide) 2mg
AREDS2 Formula
• Vitamin E 400IU
• Vitamin C 500mg
• Leutin 10mg
• Zeaxanthin 2mg
• Zinc 25-80mg
• Copper 2mg
• Lifestyle changes-obesity reduction and
smoking cessation.
• Avoiding UV light
• Low vision aids - E readers,smart phone,tablets
• Piggy back IOL for near vision (Sharioth IOL)
• Laser photocoagulation- for drusen reduction
EXPERIMENTAL SX-
(1) Miniature intraocular telescope implantation
(2) Retinal translocation surgery
• Intravitreal injection of LAMPALIZUMAB(
complement factor d antibody)- FAILED TRIAL
• Intravitreal brimonidine( neuroprotective) and
zimura( inhibits splitting of c5- membrane attacking
complex) under trial
• Visual cycle modulation: ameliorating the formation
of cytotoxic products by reducing the rate of vitamin
A processing. Clinical trials( eg feretinide, emixustat)
underway
• Photocoagulation of drusen leads to a substantial
reduction in their extent, does not reduce the risk of
progression to AMD.
• Saffron(20 md/day)- short term improvement
• Other therapeutic options – subretinal stem cell
transplantation, intravitreal injection of a range of
drugs including ciliary neurotrophic factor
RETINAL PIGMENT EPITHELIUM
DETACHMENT
• Due to disruption of physiological
forces which maintaining adhesion.
• Reduction of hydraulic conductivity of
thickened Bruchs Membrane
• Appear as sharply demarcated, dome
shaped elevations of RPE
Four types of PED
• Serous PED - may or may not overlie CNV
• Fibrovascular PED - is a form of occult CNV
• Drusenoid PED - does not have CNV,large soft
drusen,often bilateral
• Haemorrhagic PED - always have underlying
CNV or PCV
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RPE tear
• Tear occur at junction of attached and
detached RPE
• Crescent shaped pale area of RPE dehiscence
next to darker area due to retracted & folded
flap
• It can occur spontaneously, following laser or
after intravitreal
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Wet AMD
• Break in bruchs membrane is a trigger for
CNV
• Buds of neovascular tissue from
choriocapillaries perforate the outer aspect
of bruchs membrane
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TYPES OF WET AMD(MACULAR
PHOTOCOAGULATION STUDY)
(1) Type I: - occult CNV (80%)
• The fibrovascular complex proliferates betweeen
the bruchs membrane of RPE and inner collagen
layer of Bruch’s membrane
• This FV complex destroys the normal
architecture of choriocapillaries, Bruch’s and
RPE.
• Seen in 2 forms
– PED- fibrovascular pigment epithelium detachment
– Late leakage of an undetermined origin
TYPE 1 CNV IN SUB RPE SPACE
• May leak fluid under the RPE causing its detachment
• Fluid may accumulate below the RPE lifting it up from
Bruch’s membrane
• CNV can bleed causing haemorrhagic RPE detachment
• Fluid may appear in sub retinal space – serous RD
clinical or OCT
• Sub RPE blood may break into subretinal space and
rarely break into vitreous- subhyaloid haemorrhage
and vitreous haemorrhage
• The fibrovascular complex may scar and form disciform
scar
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(2) Type II: Classic CNV (20%)
• It can grow through RPE and reach subretinal space- type II
CNV
• Types
– Subfoveal
– Juxtafoveal
– extrafoveal
• F.A.- Dye fills in a well defined “lacy pattern”
• Subsequent leakage into subretinal space pver 1-2 minutes
• Most CNV – subfoveal
• OCT- Subretinal hyperreflective material
• Present above RPE
armd.pptx
Clinical features
History:-
• Gradual change in non-exudative ARMD
• Sudden change in exudative ARMD
Symptoms:-
• VA reduced for both distance and near; no
improvement with PH
• Metamorphopsia
• Photopsia
• Abnormal dark adaption
SIGNS OF WET AMD
• Presence of SRF- serous retinal detachment in the macula
• Subretinal blood( bright red)
• RPE detachment- hemorrhagic RPE detachment appears
darker
• Subretinal / intraretinal lipids
• Subretinal pigment ring
• Cystoid macular edema
• Subretinal grey white lesion- type 1
• Sea fan pattern of subreinal small vessels- type 2
• RPE rip
• Disciform scar
FFA IN WET AMD
• Earliest frame where leakage starts defines
the CNV lesion
• Classic CNV
–well demarcated area of intense
hypofluorescence
-leakage progresses into late phase and usually
obscures the boundary
CLASSIC CNV - II
• Well demarcated area of intense hyperfluorescence
appearing early and showing progressive leakage
• Fluorescence most intense at the perimeter of the CNV
• Centre may show hypofluorescence
• Leakage progresses into the late phase of the
angiogram and usually obscures the boundary of the
CNV
• Classsic description of visible subretinal vascular
network (lacy) is seen in minority of eyes with AMD
• Many times occult component will also be seen
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CLASSIC CNV (according to location)
• Subfoveal :any part of the lesion is located
below the centre of the fovea
• Juxtafoveal : the edge of the CNV is more than
1 micron from the centre of the FAZ and
within 200 microns
• Extrafoveal : the central border of the CNV is
beyond 200 micron from the centre of FAZ
PED
• Fibrovascular PED
• Irregular elevation of RPE with stippled or
granular irregular fluorescein is seen usually
about 1-2 minutes after dye injection
• Best seen with - stereo angiogram
• Progressive leakage occurs and causes a
stippled hyperfluorescence that is not intense
as cassic
ANGIOGRAPHIC SUBTYPE OF CNV
• In eyes with combination of CNV :
(1) Classic :classic components >50% of total
lesion area
(2) Minimally classic: 1-50% rest occult part
(3) Occult : no classic component
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FACTS ABOUT CNV
• Most lesions are subfoveal and occult
• 20% subfoveal lesions are predominantly
classic
• Approximately half of juxtafoveal and
extrafoveal lesions are predominantly classic
OCT signs of CNV activity
• Intraretinal cyst
• Subretinal cyst
• RPE detachment
• Subretinal blood
• Subretinal tissue
armd.pptx
ICG
• Longer infra red wavelength can penetrate
RPE and choroid
So it is useful in cases of :
• Occult CNV or poorly defined CNV
• CNV with overlying hge or fluid or exudate
• Distinguish serous from vascularized portions
of fibrovascular PED
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Variants of neovascular AMD
Retinal angiomatosis proliferans
• Predominantly intraretinal neovascularization
• Frequently Bilateral & Symmetrical
• K/A Type-III neovascular AMD
armd.pptx
MANAGEMENT OF WET ARMD
A) Anti-VEGF Agents -first line treatment
• Bevacizumab - 1-1.25 mg in0.05ml, repeated 6-8 weekly
• Ranibizumab - First 3 injections of 0.5 mg in 0.05 ml four
weekly and later on physician's assessment
• Aflibercept -2mg in 0.05ml First 3 injections monthly then
every 2 months as maintenance regimen
• Pegatanib - Given 0.3 mg dose six weekly minimum for two
years
• Photodynamic therapy-
• I.v. infusion of photosensitizer drug and
application of continuous nonthermal laser light
directed at CNVM
• Wavelength of light used corresponds to
absorption peak of drug
• Application of verteporfin involves 2 steps:
• a) I.V infusion of drug -6mg/m2 over 10mins.
• b) Activation of drug by 689nm light
• MOA- Endothelium damage of new vessels
,Platelet adhesion and thrombosis
• Main Indication- Subfoveal predominantly Classic
CNV with visual acuity of 6/60 or better
• Contraindication- Porphyria
• Advantages -
– Highly selective tissue necrosis.
– Scarring is unlikely, as collagen & elastin are
unaffected
– Resistance to treatment does not develop with
repeated treatment
Complications-
– photosensitivity
– acute severe vision decrease (loss of 4 lines within a
week)
• Laser Photocoagulation-
• Thermal blue-green Argon laser or diode laser
ablation of CNV
• Modality for juxtafoveal and extrafoveal lesion
• FA should be performed before laser
photocoagulation
Complications are
– Rupture of the pigment epithelium
– Choroidal haemorrhage
– Atrophy of the RPE in the area adjoining
– Accidental treatment of the fovea
SURGICAL OPTIONS
• Submacular excision of CNV-
• Useful in management of large subfoveal
haemorrhage where prompt evacuation of blood
limits toxicity to photoreceptor
Technique –
– after pars plana vitrectomy CNVM is removed from
subretinal space by making retinotomy temporal to
fovea and inducing localized retinal detachment
– Lastly fluid-air exchange is performed at end of
surgery and gas tamponade given
RPE transplantation-
• CNV excision creates localized RPE defects
with BM abnormalties.
• Lack of RPE ingrowth into dissection bed
results in choriocapillaries and photoreceptor
atrophy
• RPE transplantation improve vision by
reestablishing function of photoreceptors
• RPE cells from donor eyes, stem cells or iris
pigment epithelium
Macular translocation-
• Aim -Relocate central neurosensory
retina away from CNV to area of healthier
RPE, bruch membrane and choroid
EMERGING TREATMENTS FOR AMD
• Anecortave acetate
– angiostatic steroid that does not exhibit
glucocorticoid receptor-mediated activity 15 mg
delivered as a posterior juxtascleral depot every 6
months.
• Fluocinolone acetonide
– Synthetic hydrocortisone derivative
– Intra-vitreal implant inside the eye
– Sustained release for up to 36 months
• Squalamine lactate
– MOA -Blocks the action of VEGF and integrin
expression, thereby inhibiting angiogenesis.
– It is Ineffective intravitreally so given I.V.
• VolociximabIt
– inhibits activity of 5ß1 integrin protein found on
endothelial cells so preventing angiogenesis.
• SphingomabIt
– targeted against sphingosine-1-phosphate which is
implicated in angiogenesis, scar formation, and
inflammation
• Sirolimus ( Rapamycin)-
– It Inhibits response of immune system to IL-2 and
blocks T and B-cells activation
– Subconjunctival injection every 2 months for dry
AMD with GA
• Vatalanib
– is a potent inhibitor of all known VEGF receptor
tyrosine kinases, VEGFR1 , VEGFR2 & VEGFR3 .
• Bevasiranib
– silences the genes that lead to the growth of
blood vessels under the retina
• Methotrexate –
– It inhibits dihydrofolate reductase, inhibiting
lymphocyte proliferation.
– It is used for wet AMD
• POT-4-
– It inhibit the complement activation system
– Intravitreal gel sustained release system
– Neutralize early AMD inflammatory component
• Lampalizumab
– Complement inhibiting monoclonal antibiotic injected
intravitreal on monthly basis, reduced progression of
GA by 44%
• Brimonidine
– Highly selective α2 agonist
– It protects retinal ganglion cells, bipolar cells, and
photoreceptors from degeneration after retinal
ischemia and retinal phototoxicity by upregulating
trophic factors.
– Intravitreal implant, which delivers the drug over a 3-
month period.
• Alprostadil –
– Reduction in choroidal blood flow is more
pronounced in patients with AMD These drugs
increase mean choroidal blood flow
Gene therapy
• Insertion of functioning gene into human cells
to correct genetic error or to introduce new
function to already existing cells
Molecules for gene therapy include
• VEGF
• Pigment epithelium derived factor (PEDF)
• matrix metalloproteinase (MMP),
• Tissue inhibitor of metalloproteinase (TIMP)
THANK
YOU

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armd.pptx

  • 2. INTRODUCTION • Degenerative disorder affecting the macula • Characterized by the presence of specific clinical findings like drusen and RPE changes in the absence of another disorder
  • 3. TYPES • DRY – non neovascular: includes - Early - Intermediate - Dry type of advanced AMD • WET – neovascular
  • 7. Epidemiology • The WHO estimated in 2002 that 8.7/ of world blindness was due to AMD. • AMD rare before the age of 55 and more common in person 75 years of age and older. • The prevalence of advanced AMD increases with each decade after the age 50. • Highest prevalence occurring after the age of 80.
  • 8. RISK FACTORS • Age-major risk factor • Gender -Female>Male • Race -White>Blacks • Family history • Light exposure • Hypertension
  • 9. • Smoking • Drugs – Aspirin ,chloroquine and phenothiazine • Ocular factors - blue coloured iris, hyperopia, cataract sx. • Dietary factors -high fat intake and obesity increases risk .
  • 10. PATHOPHYSIOLOGY OF ARMD ARMD is characterized by - • Drusen formation. • RPE abnormalities -hyper and hypopigmentation. • Geographical atrophy of RPE and choriocapillaries. • Neovascular maculopathy.
  • 11. Drusen • The earliest clinically detectable sign • Drusen are tiny pin point,yellow deposits of abnormal hyaline material located at interface of Bruch’s membrane and the RPE. • Rarely present <45yrs • On H/P - Drusen are focal areas of the eosinophilic material between the basement membrane of RPE & BM.
  • 12. HISTOLOGICAL LOCATION OF DRUSEN INL  ONL IS OS RPE CC
  • 13. DRUSEN SIZE • Small < 63 microns – not a sign of AMD • Intermediate 63-124 microns • Large >/=125 micron • Very large >250 microns HOW TO MEASURE DRUSEN?????
  • 14. SMALL OR HARD DRUSEN • Discrete , well demarcated, yellowish white • Occur with ageing – alone not enough to classify as AMD • FFA- pin point window defect • Risk of progression to advanced AMD – 1.3% after 5 years
  • 15. SOFT DRUSEN • > 63 microns • Located b/w RPE basement membrane & inner collagenous layer of bruchs membrane • Intermediate 64- 124 microns • Large drusen > 124 micron • Very large drusen > 250 micron • Decreasing density of the drusen from centre to the margin • Tendency to cluster and merge with one another - coalascence
  • 17. • There is no increases with age • May spontaneously regress or disappear over period of time- leaving RPE atrophy • Eyes with soft drusen are at an increased risk of developing RPE abnormality, geographic atrophy and CNV
  • 18. SOFT DRUSENS FFA • FFA- hyperfluorescence early and fade or stain in late phase • Persistent staining is due to pooling of dye in focal detachment of RPE membrane or staining of diffuse drusen material • RPE cells over the soft drusen are hypo pigmented or atrophic
  • 21. RISKS OF ADVANCED AMD IN LARGE DRUSEN Eyes with B/L large drusen • Risk of CNV is 18% in atleast 1 eye in 3 years • Risk of geographic atrophy – 8% Eyes with large drusen with CNV in one eye • Large drusen present – 46% risk of CNV in good eye in 5 yrs • If no large drusen 10% risk only
  • 22. SPECIAL TYPES OF DRUSEN • Cuticular drusen • Pseudodrusen or subretinal drusen or subretinal drusenoid deposit
  • 23. CUTICULAR DRUSEN • Small( like hard drusen) but are more numerous than hard drusens and extend beyond arcades upto mid periphery • Located betweeen RPE basement membrane and inner collagenous layer of bruchs membrane • FFA- starry night appearance due to RPE atrophy over the drusen • FAF- Mild decrease in FAF over the drusen • OCT- triangular or saw tooth appearance
  • 25. SUBRETINAL DRUSENOID DEPOSITS • Pseudo drusens or reticular drusens • Located internal to the RPE between RPE and sensory retina • Composition is like soft drusen • Appear as white or blue and are better seen with blue light (blue light not filtered as they are above the RPE) • Network like appearance seen- reticular • More in perifoveal region
  • 26. Dry AMD (1)SYMPTOMS: • Initially none • Difficulty in dark adaptation • Decreased vision (2) SIGNS: • Intermediate- large soft drusen • RPE hypo/hyperpigmentation • Geographic atrophy • Drusenoid RPE detachment
  • 28. (3)OCT FINDINGS: • Drusens • Outer retinal tubulations • Outer retinal corrugations (4) FA – window defect due to unmasking of background choroidal fluorescence
  • 29. CHANGES IN RPE IN NON NEOVASCULAR AMD • Pigment mottling • Stippled hypopigmentation • Focal hyperpigmentation • Geographic atrophy
  • 30. • PIGMENT MOTTLING AND STIPPLED HYPOPIGMENTATION - These occur when the neurosensory retina thins over the abnormal RPE area - May precede the GA - RPE overlying the drusens shows hypopigmentation
  • 31. • FOCAL HYPERPIGMENTATION - clinically evident pigment clumping at the level of outer retina or subretinal space - Maybe punctate, linear or reticular in shape - Present in 3-12 % of adults >50 yrs - Higher risk of CNV if focal hyperpigmentation and soft drusens are present and if the other eye has CNV 58-73% within 5 years
  • 33. GEOGRAPHIC ATROPHY • Advanced form of dry AMD when it involves the fovea • RPE atrophies in well defined round area with atrophy of underlying choriocapillaries- so large choroidal vessels seen easily • These start as round areas often ringing the fovea and then coalesce and enlarge and ultimately involve the fovea • Upto 20% of cases of legal blindness due to AMD are caused by geographic atrophy
  • 34. Contd… • The area of geographic atrophy has atrophic RPE and choriocapillaries  atrophy of photoreceptor layer  scotoma • If it involves the fovea then V/A can drastically decrease • GA then becomes advanced form of AMD **Risk of developing CNV at the edge of GA** • FFA – RPE window defect
  • 37. HOW DOES GA ARISE? 1. Areas of confluent large drusens may regress and leave irregular shaped areas of GA 2. Small foci of pigmentory mottling areas may coalesce and progress to a single area of GA 3. Spontaneous flattening of the RPE detachment may result in GA
  • 38. • Thin fovea no rpe choroid hyperrefl • oct
  • 39. INVESTIGATIONS • Amsler grid test:- Assesses distorted & scotoma , small irregularities in the central field of vision ( 10degree) • Ophthalmoscopy:- to detect drusen,neovascularization
  • 40. • Fluorescein and ICG angiography:- Hyperfluorescent lesions: • Hard and soft drusen • RPE atrophy • RPE tear • CNV • Serous PED • Subretinal fibrosis Hypofluorescent lesion • Haemorrhage, lipid
  • 41. MANAGEMENT OF DRY ARMD • Education and follow up:- Periodic examinations are advised • Amsler grid test:- Check for visual changes regularly
  • 42. Antioxidants:- use of high dose of multivitamins & antioxidants decreases the risk of progression of ARMD in high risk pt. – Extensive intermediate Drusen – At least one large Drusen – non central GA in one or both eyes – Late AMD in one eye REDUCES RISK OF PROGRESSION TO ADVANCED AMD BY 25%
  • 43. Combination of antioxidants vitamins and minerals- AREDS1 Formula • Vitamin E 400IU • Vitamin C 500mg • Beta Carotene 15mg ( Vit A 2500IU) • Zinc 80mg • Copper (Cupric Oxide) 2mg
  • 44. AREDS2 Formula • Vitamin E 400IU • Vitamin C 500mg • Leutin 10mg • Zeaxanthin 2mg • Zinc 25-80mg • Copper 2mg
  • 45. • Lifestyle changes-obesity reduction and smoking cessation. • Avoiding UV light • Low vision aids - E readers,smart phone,tablets • Piggy back IOL for near vision (Sharioth IOL) • Laser photocoagulation- for drusen reduction EXPERIMENTAL SX- (1) Miniature intraocular telescope implantation (2) Retinal translocation surgery
  • 46. • Intravitreal injection of LAMPALIZUMAB( complement factor d antibody)- FAILED TRIAL • Intravitreal brimonidine( neuroprotective) and zimura( inhibits splitting of c5- membrane attacking complex) under trial • Visual cycle modulation: ameliorating the formation of cytotoxic products by reducing the rate of vitamin A processing. Clinical trials( eg feretinide, emixustat) underway • Photocoagulation of drusen leads to a substantial reduction in their extent, does not reduce the risk of progression to AMD. • Saffron(20 md/day)- short term improvement • Other therapeutic options – subretinal stem cell transplantation, intravitreal injection of a range of drugs including ciliary neurotrophic factor
  • 47. RETINAL PIGMENT EPITHELIUM DETACHMENT • Due to disruption of physiological forces which maintaining adhesion. • Reduction of hydraulic conductivity of thickened Bruchs Membrane • Appear as sharply demarcated, dome shaped elevations of RPE
  • 48. Four types of PED • Serous PED - may or may not overlie CNV • Fibrovascular PED - is a form of occult CNV • Drusenoid PED - does not have CNV,large soft drusen,often bilateral • Haemorrhagic PED - always have underlying CNV or PCV
  • 51. RPE tear • Tear occur at junction of attached and detached RPE • Crescent shaped pale area of RPE dehiscence next to darker area due to retracted & folded flap • It can occur spontaneously, following laser or after intravitreal
  • 53. Wet AMD • Break in bruchs membrane is a trigger for CNV • Buds of neovascular tissue from choriocapillaries perforate the outer aspect of bruchs membrane
  • 55. TYPES OF WET AMD(MACULAR PHOTOCOAGULATION STUDY) (1) Type I: - occult CNV (80%) • The fibrovascular complex proliferates betweeen the bruchs membrane of RPE and inner collagen layer of Bruch’s membrane • This FV complex destroys the normal architecture of choriocapillaries, Bruch’s and RPE. • Seen in 2 forms – PED- fibrovascular pigment epithelium detachment – Late leakage of an undetermined origin
  • 56. TYPE 1 CNV IN SUB RPE SPACE • May leak fluid under the RPE causing its detachment • Fluid may accumulate below the RPE lifting it up from Bruch’s membrane • CNV can bleed causing haemorrhagic RPE detachment • Fluid may appear in sub retinal space – serous RD clinical or OCT • Sub RPE blood may break into subretinal space and rarely break into vitreous- subhyaloid haemorrhage and vitreous haemorrhage • The fibrovascular complex may scar and form disciform scar
  • 58. (2) Type II: Classic CNV (20%) • It can grow through RPE and reach subretinal space- type II CNV • Types – Subfoveal – Juxtafoveal – extrafoveal • F.A.- Dye fills in a well defined “lacy pattern” • Subsequent leakage into subretinal space pver 1-2 minutes • Most CNV – subfoveal • OCT- Subretinal hyperreflective material • Present above RPE
  • 60. Clinical features History:- • Gradual change in non-exudative ARMD • Sudden change in exudative ARMD Symptoms:- • VA reduced for both distance and near; no improvement with PH • Metamorphopsia • Photopsia • Abnormal dark adaption
  • 61. SIGNS OF WET AMD • Presence of SRF- serous retinal detachment in the macula • Subretinal blood( bright red) • RPE detachment- hemorrhagic RPE detachment appears darker • Subretinal / intraretinal lipids • Subretinal pigment ring • Cystoid macular edema • Subretinal grey white lesion- type 1 • Sea fan pattern of subreinal small vessels- type 2 • RPE rip • Disciform scar
  • 62. FFA IN WET AMD • Earliest frame where leakage starts defines the CNV lesion • Classic CNV –well demarcated area of intense hypofluorescence -leakage progresses into late phase and usually obscures the boundary
  • 63. CLASSIC CNV - II • Well demarcated area of intense hyperfluorescence appearing early and showing progressive leakage • Fluorescence most intense at the perimeter of the CNV • Centre may show hypofluorescence • Leakage progresses into the late phase of the angiogram and usually obscures the boundary of the CNV • Classsic description of visible subretinal vascular network (lacy) is seen in minority of eyes with AMD • Many times occult component will also be seen
  • 65. CLASSIC CNV (according to location) • Subfoveal :any part of the lesion is located below the centre of the fovea • Juxtafoveal : the edge of the CNV is more than 1 micron from the centre of the FAZ and within 200 microns • Extrafoveal : the central border of the CNV is beyond 200 micron from the centre of FAZ
  • 66. PED • Fibrovascular PED • Irregular elevation of RPE with stippled or granular irregular fluorescein is seen usually about 1-2 minutes after dye injection • Best seen with - stereo angiogram • Progressive leakage occurs and causes a stippled hyperfluorescence that is not intense as cassic
  • 67. ANGIOGRAPHIC SUBTYPE OF CNV • In eyes with combination of CNV : (1) Classic :classic components >50% of total lesion area (2) Minimally classic: 1-50% rest occult part (3) Occult : no classic component
  • 69. FACTS ABOUT CNV • Most lesions are subfoveal and occult • 20% subfoveal lesions are predominantly classic • Approximately half of juxtafoveal and extrafoveal lesions are predominantly classic
  • 70. OCT signs of CNV activity • Intraretinal cyst • Subretinal cyst • RPE detachment • Subretinal blood • Subretinal tissue
  • 72. ICG • Longer infra red wavelength can penetrate RPE and choroid So it is useful in cases of : • Occult CNV or poorly defined CNV • CNV with overlying hge or fluid or exudate • Distinguish serous from vascularized portions of fibrovascular PED
  • 74. Variants of neovascular AMD Retinal angiomatosis proliferans • Predominantly intraretinal neovascularization • Frequently Bilateral & Symmetrical • K/A Type-III neovascular AMD
  • 76. MANAGEMENT OF WET ARMD A) Anti-VEGF Agents -first line treatment • Bevacizumab - 1-1.25 mg in0.05ml, repeated 6-8 weekly • Ranibizumab - First 3 injections of 0.5 mg in 0.05 ml four weekly and later on physician's assessment • Aflibercept -2mg in 0.05ml First 3 injections monthly then every 2 months as maintenance regimen • Pegatanib - Given 0.3 mg dose six weekly minimum for two years
  • 77. • Photodynamic therapy- • I.v. infusion of photosensitizer drug and application of continuous nonthermal laser light directed at CNVM • Wavelength of light used corresponds to absorption peak of drug • Application of verteporfin involves 2 steps: • a) I.V infusion of drug -6mg/m2 over 10mins. • b) Activation of drug by 689nm light • MOA- Endothelium damage of new vessels ,Platelet adhesion and thrombosis
  • 78. • Main Indication- Subfoveal predominantly Classic CNV with visual acuity of 6/60 or better • Contraindication- Porphyria • Advantages - – Highly selective tissue necrosis. – Scarring is unlikely, as collagen & elastin are unaffected – Resistance to treatment does not develop with repeated treatment Complications- – photosensitivity – acute severe vision decrease (loss of 4 lines within a week)
  • 79. • Laser Photocoagulation- • Thermal blue-green Argon laser or diode laser ablation of CNV • Modality for juxtafoveal and extrafoveal lesion • FA should be performed before laser photocoagulation Complications are – Rupture of the pigment epithelium – Choroidal haemorrhage – Atrophy of the RPE in the area adjoining – Accidental treatment of the fovea
  • 80. SURGICAL OPTIONS • Submacular excision of CNV- • Useful in management of large subfoveal haemorrhage where prompt evacuation of blood limits toxicity to photoreceptor Technique – – after pars plana vitrectomy CNVM is removed from subretinal space by making retinotomy temporal to fovea and inducing localized retinal detachment – Lastly fluid-air exchange is performed at end of surgery and gas tamponade given
  • 81. RPE transplantation- • CNV excision creates localized RPE defects with BM abnormalties. • Lack of RPE ingrowth into dissection bed results in choriocapillaries and photoreceptor atrophy • RPE transplantation improve vision by reestablishing function of photoreceptors • RPE cells from donor eyes, stem cells or iris pigment epithelium
  • 82. Macular translocation- • Aim -Relocate central neurosensory retina away from CNV to area of healthier RPE, bruch membrane and choroid
  • 83. EMERGING TREATMENTS FOR AMD • Anecortave acetate – angiostatic steroid that does not exhibit glucocorticoid receptor-mediated activity 15 mg delivered as a posterior juxtascleral depot every 6 months. • Fluocinolone acetonide – Synthetic hydrocortisone derivative – Intra-vitreal implant inside the eye – Sustained release for up to 36 months
  • 84. • Squalamine lactate – MOA -Blocks the action of VEGF and integrin expression, thereby inhibiting angiogenesis. – It is Ineffective intravitreally so given I.V. • VolociximabIt – inhibits activity of 5ß1 integrin protein found on endothelial cells so preventing angiogenesis. • SphingomabIt – targeted against sphingosine-1-phosphate which is implicated in angiogenesis, scar formation, and inflammation
  • 85. • Sirolimus ( Rapamycin)- – It Inhibits response of immune system to IL-2 and blocks T and B-cells activation – Subconjunctival injection every 2 months for dry AMD with GA • Vatalanib – is a potent inhibitor of all known VEGF receptor tyrosine kinases, VEGFR1 , VEGFR2 & VEGFR3 . • Bevasiranib – silences the genes that lead to the growth of blood vessels under the retina
  • 86. • Methotrexate – – It inhibits dihydrofolate reductase, inhibiting lymphocyte proliferation. – It is used for wet AMD • POT-4- – It inhibit the complement activation system – Intravitreal gel sustained release system – Neutralize early AMD inflammatory component
  • 87. • Lampalizumab – Complement inhibiting monoclonal antibiotic injected intravitreal on monthly basis, reduced progression of GA by 44% • Brimonidine – Highly selective α2 agonist – It protects retinal ganglion cells, bipolar cells, and photoreceptors from degeneration after retinal ischemia and retinal phototoxicity by upregulating trophic factors. – Intravitreal implant, which delivers the drug over a 3- month period.
  • 88. • Alprostadil – – Reduction in choroidal blood flow is more pronounced in patients with AMD These drugs increase mean choroidal blood flow
  • 89. Gene therapy • Insertion of functioning gene into human cells to correct genetic error or to introduce new function to already existing cells Molecules for gene therapy include • VEGF • Pigment epithelium derived factor (PEDF) • matrix metalloproteinase (MMP), • Tissue inhibitor of metalloproteinase (TIMP)