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Age Related Macular
Degeneration.
Nitin Renge.
DEFINITION:
• A common, chronic, Progressive degenerative disorder of
Macula that affects older individuals and features central
visual loss as a result of abnormalities in Photoreceptor /
Retinal pigment epithelium/ Bruch’s membrane/ Choroidal
complex often resulting in Geographic atrophy &/or
Neovascularization.
Introduction
• Leading cause of irreversible visual loss in Industrialized countries.
• Common in Caucasian populations-54%.
• Key Features:--
Earliest signs rarely visible before 50 years.
Bilateral disease ( 50% bilateral within 5 years of visual loss
in first eye )
Drusen
Hyperpigmentation of RPE
Hypopigmentation of RPE
Geographic Atrophy
Detachment of RPE
Macular choroidal Neovascularization
• Associated Features :---
Subretinal Fluid
Intraretinal Fluid
Subretinal Haemorrhage
Intraretinal or Inner retinal Haemorrhage
Lipid Exudation
Subretinal Fibrosis ( Disciform scarring )
Specific genetic risk allels, particularly in gene
controlling the Complement system.
Anatomy:--
• Macula
Diameter 5.5 mm, at post pole & temporal to optic disc.
• Fovea Centralis
Depression of 1.85 mm diameter & 0.25mm thick.
• Foveola --
Central point of fovea
0.35 mm in diameter
3mm temporal,1mm inferior to optic disc
Thinnest part of retina
Cones only
High levels of visual acuity
Foveola
RPE
Choroid
Foveola
Fovea
MACULA
Para-foveal zone
Peri-foveal zone
MACULA: ANATOMY
Umbo
Classification:---
• Conventionally Two forms:
1) Non-exudative, Non-neovascular (dry)
Most common (90%)
Geographic atrophy advanced stage of dry ARMD
2) Exudative, Neovascular (wet)
Less common (10%)
Associated with more rapid progression to advanced vision loss
Main manifestations are CNV & PED
Clinical Classification:---
Cetegory Defination, based on presence of
lesions within two disc diameters
of the Fovea in either eye
No apparent
ageing
changes
No Drusen, No AMD pigmentary
abnormalities
Normal
ageing
changes
Only Drupelets (drusen < 63 micro m),
No AMD pigmentary abnormalities
Early AMD Medium drusen(>63 micro m & < 125
Micro m) , No AMD pigmentary
abnormalities
Intermediate
AMD
Large drusen (> 125micro m) , Any AMD
pigmentary abnormalities
Late AMD Neovascular AMD &/or Any geographic
atrophy
AMD: STAGING:-
• AREDS Categories:
• No AMD (AREDS category 1)
• No or a few small (<63 micrometres in diameter) drusen.
• Early AMD (AREDS category 2)
• Many small drusen or a few intermediate-sized (63-124 micrometres in diameter)
drusen, or macular pigmentary changes.
• Intermediate AMD (AREDS category 3)
• Extensive intermediate drusen or at least one large (≥125 micrometres) drusen, or
geographic atrophy not involving the foveal centre.
• Advanced AMD (AREDS category 4)
• Geographic atrophy involving the foveal centre (atrophic, or dry, AMD)
• Choroidal neovascularisation (wet AMD)
• evidence for neovascular maculopathy (subretinal haemorrhage, serous retinal or
retinal pigment epithelium detachments, lipid exudates, or fibrovascular scar).
Risk Factors:---
• Age
• Race- Caucasians > African Americans
• Heredity 1) CFH-Bilateral GA 2)HTRA1-risk of bilateral CNV 3)C3- GA>CNV
• Smoking
• Obesity
• Hypertension & other cardiovascular risk factors
• Dietary Factors
• Aspirin- may increase risk of NV-AMD
• Other Factors- Cataract Surgery, Blue iris colour, High sunlight exposure & Female
Gender
Pathogenesis
• Progressive thickening of Bruch’s membrane with age
• Interferes with RPE - photoreceptor metabolism
• Metabolites from photoreceptors accumulate on Bruch’s membrane
• Forms lipid deposits as basal linear & basal laminar deposits
• Later forms Drusens (colloid bodies)
Earliest clinical sign
Lipid or collagen rich deposits (waste)
Also contains Amyloid, Complement factors & additional cellular
components
Lie between Bruch’s membrane and RPE
Further disruption of RPE/photoreceptor metabolism
Cause variable amount of depigmentation and eventually atrophy of
overlying RPE
Drusen
Bruch’s Membrane
RPE
Photoreceptors outer seg
Choroid capillaries
Neuron connected to optic
nerve
Rods & Cones
1)Small Drusen (drupletes) <63 um
Sometimes termed Hard Drusen
Sharp, well demarcated boundaries, White-yellow
Small localised collection of hyaline material within or on Bruch’s
membrane
4)Intermediate Drusen >63 < 125um
Fairly well-defined, Yellow-white, deposits at level of RPE
3)Large Drusen > 125 um ( Soft Drusen )
Less well delineated, Yellow-white
Larger/commonly become confluent
Poorly demarcated boundaries
Involve overlying focal RPE detachment (Drusenoid RPE detachment)
Soft Drusen:
1) Membranous:
63-175 µ
Pale, shallow appearing drusens
2) Granular:
About 250 µ
Solid appearing drusens
3) Serous:
>500 µ
Have pooled serous fluid
blister like appearance
May result in serous PED
Hard drusen
Pigment epithelium
defects
Hard Drusen
Soft Drusen
Confluent Drusen
Representing widespread RPE abnormality
Increase risk of vision loss
Calcified Drusen (glistening appearance)
Dystrophic Calcification may develop
in all type of Drusen
RPE degeneration, seen as:
• Focal areas of hypo- and hyper- pigmentation (‘stippling’)
• Associated with progression to late AMD with Visual loss
• Eventually areas of atrophy of the RPE revealing underlying large &
deep choriodal vessels
‘Geographic atrophy’ = end stage or Late advanced stage of Dry AMD
a) Drusen with Pigmentary abnormality b) Geographic Atrophy
Differential Diagnosis of Drusens
1) Donyne Honeycomb retinal dystrophy (Malattia leventinese,
Autosomal dominant radial drusen)
2) Cuticular Drusen- FA characteristics is ‘Star in the Sky’
appearance
3) Type 2 Membranoproliferative Glomerulonephritis.
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
AMD: SYMPTOMS
Initial symptoms:
• Straight lines appear wavy
• Blurry vision
• Distorted vision
• Objects may appear as the wrong shape or size
• A dark empty area in the centre of vision
• Patient’s ability to perform normal daily tasks such as reading, sewing, telling the
time, driving are greatly impaired.
Non-Exudative AMD
• Symptoms:-
Gradual mild to moderate impairment over months or years
Both eyes usually affected but often asymmetrically
Vision may fluctuate, & is often better in bright light
• Signs:-
Intermediate-large soft drusen may confluent
Focal hyper &/or hypopigmentation of RPE
Slow/progressive atrophy of RPE and photoreceptors
Drusenoid RPE detachment
Advanced form = Geographic Atrophy
• Clinically , dry AMD may manifest:-
Stage of drusen and/or hyperpigmentation
Stage of incipient atrophy (non geographic atrophy)
Stage of geographic atrophy
• Diagnostic criteria:-
Degenerative disorder in persons >50 years, characterized by the
presence of any of the following:
Soft drusen (>63 µ)
RPE abnormalities- areas of hypo/hyperpigmentation
(excluding pigment surrounding small, hard drusen)
Visual acuity (VA) is not a criterion for the diagnosis
DRY AMD: COURSE AND VISUAL PROGNOSIS
• Patients with only drusen not have much loss of vision, but require
additional magnification of the text and more intense lighting to read
small points.
• Presence of large drusen (>63 microns in diameter) is associated with a
risk of the late form of the disease like CNV.
• Geographic atrophy- severest form of the dry AMD, RPE atrophy >175
microns with exposure of the underlying choroidal vessels.
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
•Signs/Symptoms:-
Marked decrease VA (unless foveal sparing)
Central field loss (positive scotoma)
Difficulty recognizing faces
Difficulty reading if large scotoma
Difficulty in dim light/adapting
GEOGRAPHIC ATROPHY
DD’s for dry ARMD
Herediatry Diseases:- Pattern dystrophy, Stargardt disease, Best’s disease, Angioid streaks
Central serous chorioretinopathy
Macular telangiectasia type II
Multifocal choroiditis
Acute posterior multifocal placoid pigment epitheliopathy
Toxic lesions:- Chloroquin, Phenothiazines, Canthaxathin
Cuticular Drusen with or without a vitelliform lesion
Adult vitelliform dystrophy
Exudative AMD
• Clinical Features:-
Choroidal neo-vascularisation
Exudative detachment of RPE, sub-RPE(type1) and/or subretinal (type2)
Disciform scar
• Choroidal Neo-vascularisation:-
Proliferations of fibrovascular tissue from choriocapillaris through defects in
Bruch’s membrane
Sub-RPE or sub-retinal
Membranes have a grey-green or pinkish-yellow hue in late stages
• Tendency to leak:-
Serous and blood
Distorted or painless blurred vision, usually with metamorphopsia
Red if sub-retinal, darker if sub-RPE
Rarely vitreous haemorrhage
WET AMD
Photoreceptors and pigment epithelium send a distress signal to choriocapillaries to make new vessels
New vessels grow behind the macula
Breakdown in the Bruch’s membrane
Blood vessels are fragile
Leak blood and fluid
Scarring of macula
Potential for rapid and severe visual damage
Age related macular degeneration nitin
• Diagnostic criteria
persons >50 years, characterized by the presence of any of the following
choroidal neovascularization
serous retinal pigment epithelial detachment
hemorrhagic retinal pigment epithelial detachment
fibrotic scar in the macula
• The hallmark of neovascular AMD is CNV & potential manifestations
are-
Subretinal fluid
Macular edema
Retinal , subretinal ,or sub-RPE hemorrhage
Retinal or subretinal lipid exudate
Plaque like membrane or grey or yellow green discrete discoloration
RPE detachment
RPE tear
Sub-retinal fibrosis or disciform scar
.
• CNV lesion is well demarcated & its location may be determined by closest point
to the FAZ.
• Lesion location is classified angiograpically as follows:-
1. Subfoveal: under the centre of FAZ
2. Juxtafoveal: 1-199 µm from the centre of FAZ
3. Extrafoveal: >200 µm & <2500 µm from the centre of FAZ
• Types:
• Type I: CNV beneath RPE
• Type II: CNV above RPE
Wet AMD: A Rapid Descent
TIME
Wet AMD
Blindness
Severe Vision Loss
Early Intermediate Advanced
(dry) (dry) (wet)
No Vision Loss
Today: many are
diagnosed after
vision loss
There are no good
predictors for who will
develop Wet AMD or
when
Common Ophthalmic condition associated with CNV
Age-related macular degeneration
Angoid streaks
Best’s disease
Choroidal Osteoma
Fundus Flavimaculatus
Idiopathic Causes
Multifocal Choroiditis
Ocular Histoplasmosis Syndrome
Optic disc drusen
Optic nerve head pits
Pathological ( Progressive ) Myopia
Pattern dystrophies
Photocoagulation
Sarcoidosis
Serpiginous or Geographic Choroiditis
Toxoplasmic Retinochoroiditis
Traumatic Choroidal Rupture
Polypoidal choroidal Vasculopathy
Pattern of CNV Hyper fluorescence on FA
Classic CNV (20%)
-Well demarcated
boundaries (Lacy pattern)
during early transit
-Subsequently leaking into
subretinal space over 1-2
min, with late staining of
fibrous tissue
Occult CNV (80%)
Type 1
-Fibro vascular PED
-Irregular elevation RPE.
-Boundaries may be well
demarcated or poorly
demarcated.
-Persistent staining or
leakage of dye at 10 min
Type 2
-Late leakage of
undetermined of source
(LLUS)
-Boundaries poorly
demarcated
-Source of late leakage
can not be determined
from earlier frames of
angiograms
CLASSIC CNV
OCCULT CNV (TYPE-I)
OCCULT CNV (TYPE-II)
RPE DETACHMENT (PED)
Depending on cause, it is of many types:
• Drusenoid
• Serous
• Fibro vascular
• Hemorrhagic
RPE TEAR
• Spontaneously or on photocoagulation of CNV or
after intravitreal injections.
• Visual acuity abruptly fall with foveal involvement.
• FA shows in late phase hypofluorescence
corresponding to thickened folded RPE with adjacent
hyperfluorescence over the torn area, two area often
separated by a sharply defined border.
DISCIFORM SCAR
VARIATION
• Retinal angiomatosis proliferans-10-20% of Neovascular AMD in
Caucasians.
• Has been termed Type-III CNVM
• Frequently Bilateral & Symmetrical
• Characterized by predominantly intraretinal neovascularization
• 3 Stages:
• Stage 1
• Intraretinal neovascularization
• Stage 2
• Subretinal neovascularization
• Stage 3
• CNV clearly evident clinically/angiographically.
• RCA (retino-choroidal anastamoses)
• A Diciform scar will often form
• Polypoidal Choroidal Vasculopathy
A variant of neovascular AMD
MC in women (5:1) & relatively young , African & East Asian ethnic origin
Often Bilateral & Asymmetrical
Sudden onset of unilateral visual impairment
Causes multiple recurrent serosanguineous retinal & RPE detachments
Typical OCT findings in PCV may reveal a classic hyperreflectivity in the
choroidal layers known as the "double-layer" sign
Investigations
• History:- Gradual change = non-exudative
Sudden change = exudative
• Visual Symptoms:- VA for Distance and near & no improvement with pin-hole
Difficulty in reading/recognising faces, driving
Difficulty with changing light / adapting after bright light
Distortion of images mostly with exudative changes
Less common symptoms include night glare, photopsia (flickering or flashing
lights), visual hallucinations (Charles Bonnet syndrome) & abnormal dark adaptation
• Amsler grid test: Assesses distorted & scotoma , small irregularities in the central field of
vision ( 10degree)
• Ophthalmoscopy: to detect drusen, as well as neovascularization
• Fluorescein and ICG angiography: Determines the presence and location of
neovascularization
• Optical coherence tomography
MANAGEMENT
• Antioxidants: AREDS-1 study & follow-up AREDS-2 Study
use of high dose of multivitamins & antioxidants decreases the risk of progression of ARMD
in those with high risk characteristics as age >55 with one or more of following
Extensive intermediate Drusen
At least one large Drusen
GA in one or both eyes
Late AMD in one eye ( greatest benefit in AREDS1)
Combination of antioxidants vitamins and minerals-
AREDS1 Formula AREDS2 Formula
Vitamin E 400IU Vitamin E 400IU
Vitamin C 500mg Vitamin C 500mg
Beta Carotene 15mg ( Vit A 2500IU) Leutin 10mg
Zinc 80mg Zeaxanthin 2mg
Copper (Cupric Oxide) 2mg Zinc 25-80mg
Copper 2mg
Cont..
• Dry ARMD:- 1) Antioxidant suplimentation & Risk factors modulation
2) Low Vision Aids
3) Anti-inflammatory drugs-
Sirolimus (Rapamycin) antifungal, immunosuppressant & used as SC every 2
months.
Intravitreal Steroids as FA implants (sustain release upto 36 months)
4) Complement Inhibition-
POT-4 neutralize early AMD inflammatory component & it is a Intravitreal gel
sustain release system
ARC1905 a C5 inhibitor Aptamer prevents C5a production
Eculizumab a Antibody against C5, currently approved only for PNH
Lampalizumab a monoclonal antibody, used as intravitreal monthly
5) Neurotrophic Factors-
NT501 a genetically modified RPE intravitreal implant, shown retinal
thickness as early as 4 months.
6) AL-8309A- as topical solution, light induced oxidative damage
Cont..
7) Reduction of Retinal Toxins- In Dry AMD lipofuscin (a waste products)
accumulates at leading edge of lesion
ACU-4429 & Fenretinide (Oral doses) prevents accumulation of
lipofuscin
8) Choroidal Blood Perfusion Enchancers-
MC-1101 as Topical drug, shown to increase mean choroidal
blood flow
9) Other Options
Photocoagulation of Drusen
Saffron (20mg/day) a neuroprotective effect
Intravitreal neuroprotective drug Brimonidine
Surgery like Retinal translocation, Subretinal Stem cell
Transplantation
Wet-ARMD
• Anti-angiogenic Drugs (Anti-VEGFs)-
1) Bevacizumab (Avastin)- Dose- 1-1.25 mg(0.05ml), repeated 6-8
weekly
2) Ranibizumab (Lucentis)- Dose- First 3 injections of 0.5 mg (0.05 mL)
four weekly & further on physician's assessment
3) Pegatanib (Macugen)- Given 0.3 mg dose six weekly minimum for
two years
4) Aflibercept (Eylea)-2mg (0.05ml) First 3 injections monthly then
every 2 months as maintenance regimen
• Photodynamic Therapy (PDT)- was developed in the 1990s
Includes IV Verteporfin & a red diode laser (689 nm wavelength)
Verteporfin (a benzoporphyyrin derivative)- second generation potent
photosensitizer of the tetrapyrrole group
Cont..
Absorbs light at 690 nm, a longer wavelength is important because it allows deep
tissue penetration, through blood, pigments & fluid which could accumulate beneath
the retina
Plasma half-life ranges approximately from 5 to 6 hours & BPD-MA/Verteporfin
is excreted mainly by the bile (90%)
Administered intravenously as a liposomal preparation & partitions into the LDL
phase of the lipoprotein fraction of the blood
Endothelial cells which form the neovessels of tumors & neovascular
membranes have been shown to have increased the population of LDL receptors that
play a major role in the mechanism of the uptake & therefore the selectivity of the
photosensitizer in these cells
MOA- The target cells are light irradiated & the molecules of the dye gain
energy passing from the ground state to an excited, highly reactive, short-lived triplet
state which transfers the excess of energy by two pathways
1) The energy absorbed from the triplet state is transferred to other
molecules leading to the generation of free radicals, which instantaneously oxidize a
wide variety of biomolecules - Type I mechanism
Cont..
2) The energy absorbed from the triplet state is transferred to oxygen
generating high reactive short-lived oxygen - Type II mechanism which appears to
play the major role in the effect seen in PDT
The interactions of these highly reactive compounds cause cellular and
vascular damage
Associated with an immediate induction of acute inflammatory responses
Leading to occlusion of the feeding vessels i.e neovascular capillaries
Main Indication- Subfoveal predominantly Classic CNV with visual acuity of
6/60 or better
The potential advantages of PDT are:-
Scarring is unlikely, as collagen & elastin are unaffected, leaving organs
intact
Highly selective tissue necrosis & Resistance to treatment does not develop
with repeated treatment
• Laser Photocoagulation- Includes Thermal blue-green Argon laser or
diode laser ablation of CNV, now rarely used
Modality for juxtafoveal (well-defined choroidal neovascular lesions
located 1 to 199 µ from the foveal centre, or 200 to 2500 µm from the foveal
centre but showing blood or pigmentation less than 200 microns from the foveal
centre) & extrafoveal (located 200 to 2500 µm from the foveal centre) CNV
associated with AMD
A fluorescein angiography (FA) should be performed 72 to 96 hours before
photocoagulation in order to select treatable cases & to guide the ophthalmologist
during treatment
Patients should undergo treatment as quickly as possible, since
neovascular lesions may grow 10 to 18µ per day
Treatment should be performed so that a white lesion in the retina is
obtained
Cont..
The neovascular lesion should be surrounded by laser marks with a diameter
of 200µ and duration of 0.2 to 0.5 seconds
After surrounding the perimeter of the neovascular lesion, its central part is
covered with 200µ burns; the remaining lesion is covered with 200 to 500µ burns,
with duration of 0.5 to 1.0 seconds
Laser treatment should avoid retinal blood vessels and the optic nerve
(treatment should start 10-200 µm from the optic nerve), as well as preserve at
least 1.5 hours of the papillomacular bundle (no peripapillary treatment)
Follow-up:- it is necessary to perform medical examinations and control FA 2
to 3 weeks, 4 to 6 weeks, 3 to 4 months and 6, 8, 9 and 12 months after treatment
Recurrence is rare after 2 years
The greater risks exist 6 weeks to 12 months after treatment
Cont..
Complications:- 1) Choroidal haemorrhage (rarer if spots ≥ 200 microns and
time intervals ≥ 0.2 seconds are used)
2) Premacular fibrogliosis
3) Accidental treatment of the fovea in extrafoveal or
juxtafoveal lesions
4) Rupture of the pigment epithelium (more frequent in cases
of PED)
5) Atrophy of the RPE in the area adjoining the laser scar
(immediately after treatment or years later)
• Laser photocoagulation remains currently indicated for the treatment of well-
defined extrafoveal choroidal membranes
• For classic juxtafoveal membranes, laser photocoagulation could theoretically be
considered as an option for cases in which the entire neovascular lesion can be
treated without damaging the fovea
• TRANSPUPILLARY THERMOTHERAPY:-
First described by Oosterhuis et al. in 1998 for treatment of choroidal
melanoma
The goal of TTT is to create and maintain tissue hyperthermia
The diode laser (810 nm, near infrared):-
Low absorption in xanthophyll, minimum nerve fibre
layer damage
Poorly absorbed by haemoglobin, allowing treatment
through preretinal and subretinal blood
Mainly absorbed in the choroid, enabling effective
treatment of choroidal lesions
So effectively treat subfoveal occult choroidal
neovascular membranes and preserve vision
Cont..
• TECHNIQUE:- delivered through a slit lamp using an antireflective Goldmann contact
lens & an infrared diode laser at 810 nm, specially modified to give a long pulse
mode
The slit lamp has a special large spot size adapter with an adjustable
beam width of 0.5 mm, 0.8 mm, 1.2 mm, 2.0 mm & 3.0 mm
The treatment is given using one spot that encompasses the entire
lesion
Laser parameters used are duration of 60 seconds, at power settings
between 250 and 1000 mW, depending upon the spot size used
For a 3 mm spot size, the initial power setting is 800 mW by keeping the
power density around 10 W/ sq.cm
The end point is an area of no visible colour change to a light grey
appearance
Full treatment results are usually seen within 2-3 months after the
procedure
• Submacular excision of CNV
• Macular translocation
• Retinal rotation
• Homologous Iris/Retinal pigment epithelium transplantation
• Autologous RPE transplantation
SURGICAL OPTIONS
EMERGING TREATMENTS
• Retaane (Anecortave Acetate)-
modified steroid promising in reducing the risk of vision loss due to the
growth of unhealthy blood vessels in wet AMD
• AdPEDF (Adenovirus based pigment epithelium derived factor)-
a gene that leads to the production of the protein PEDF, which helps
keep photoreceptors healthy, thereby preserving vision
• siRNA (Bevasiranib)-
silences the genes that lead to the growth of unhealthy, vision-robbing
blood vessels under the retina
• ATG3 (mecamylamine)-
a topical formulation that inhibits the nicotinic acetylcholine receptors
• EVIZON (squalamine lactate)-
aminosterol with anti–angiogenic activity
derived from the liver of the dogfish shark, administered intravenously
(no eye injection)
• OT-551 (antioxidant eye drops)-
supplement the eye’s natural defense system against disease & injury
protection against both cataract and dry AMD
• Encapsulated Cell Technology (ECT)-
tiny capsule (6 mm) implanted into the eye, contains retinal cells that
produce a vision-preserving protein ,Ciliary Neurotrophic Factor (CNTF)
keep photoreceptors alive and healthy, preserving vision
THANK
YOU

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Age related macular degeneration nitin

  • 2. DEFINITION: • A common, chronic, Progressive degenerative disorder of Macula that affects older individuals and features central visual loss as a result of abnormalities in Photoreceptor / Retinal pigment epithelium/ Bruch’s membrane/ Choroidal complex often resulting in Geographic atrophy &/or Neovascularization.
  • 3. Introduction • Leading cause of irreversible visual loss in Industrialized countries. • Common in Caucasian populations-54%. • Key Features:-- Earliest signs rarely visible before 50 years. Bilateral disease ( 50% bilateral within 5 years of visual loss in first eye ) Drusen Hyperpigmentation of RPE Hypopigmentation of RPE Geographic Atrophy Detachment of RPE Macular choroidal Neovascularization
  • 4. • Associated Features :--- Subretinal Fluid Intraretinal Fluid Subretinal Haemorrhage Intraretinal or Inner retinal Haemorrhage Lipid Exudation Subretinal Fibrosis ( Disciform scarring ) Specific genetic risk allels, particularly in gene controlling the Complement system.
  • 5. Anatomy:-- • Macula Diameter 5.5 mm, at post pole & temporal to optic disc. • Fovea Centralis Depression of 1.85 mm diameter & 0.25mm thick. • Foveola -- Central point of fovea 0.35 mm in diameter 3mm temporal,1mm inferior to optic disc Thinnest part of retina Cones only High levels of visual acuity Foveola RPE Choroid
  • 7. Classification:--- • Conventionally Two forms: 1) Non-exudative, Non-neovascular (dry) Most common (90%) Geographic atrophy advanced stage of dry ARMD 2) Exudative, Neovascular (wet) Less common (10%) Associated with more rapid progression to advanced vision loss Main manifestations are CNV & PED
  • 8. Clinical Classification:--- Cetegory Defination, based on presence of lesions within two disc diameters of the Fovea in either eye No apparent ageing changes No Drusen, No AMD pigmentary abnormalities Normal ageing changes Only Drupelets (drusen < 63 micro m), No AMD pigmentary abnormalities Early AMD Medium drusen(>63 micro m & < 125 Micro m) , No AMD pigmentary abnormalities Intermediate AMD Large drusen (> 125micro m) , Any AMD pigmentary abnormalities Late AMD Neovascular AMD &/or Any geographic atrophy
  • 9. AMD: STAGING:- • AREDS Categories: • No AMD (AREDS category 1) • No or a few small (<63 micrometres in diameter) drusen. • Early AMD (AREDS category 2) • Many small drusen or a few intermediate-sized (63-124 micrometres in diameter) drusen, or macular pigmentary changes. • Intermediate AMD (AREDS category 3) • Extensive intermediate drusen or at least one large (≥125 micrometres) drusen, or geographic atrophy not involving the foveal centre. • Advanced AMD (AREDS category 4) • Geographic atrophy involving the foveal centre (atrophic, or dry, AMD) • Choroidal neovascularisation (wet AMD) • evidence for neovascular maculopathy (subretinal haemorrhage, serous retinal or retinal pigment epithelium detachments, lipid exudates, or fibrovascular scar).
  • 10. Risk Factors:--- • Age • Race- Caucasians > African Americans • Heredity 1) CFH-Bilateral GA 2)HTRA1-risk of bilateral CNV 3)C3- GA>CNV • Smoking • Obesity • Hypertension & other cardiovascular risk factors • Dietary Factors • Aspirin- may increase risk of NV-AMD • Other Factors- Cataract Surgery, Blue iris colour, High sunlight exposure & Female Gender
  • 11. Pathogenesis • Progressive thickening of Bruch’s membrane with age • Interferes with RPE - photoreceptor metabolism • Metabolites from photoreceptors accumulate on Bruch’s membrane • Forms lipid deposits as basal linear & basal laminar deposits • Later forms Drusens (colloid bodies) Earliest clinical sign Lipid or collagen rich deposits (waste) Also contains Amyloid, Complement factors & additional cellular components Lie between Bruch’s membrane and RPE Further disruption of RPE/photoreceptor metabolism Cause variable amount of depigmentation and eventually atrophy of overlying RPE
  • 12. Drusen Bruch’s Membrane RPE Photoreceptors outer seg Choroid capillaries Neuron connected to optic nerve Rods & Cones
  • 13. 1)Small Drusen (drupletes) <63 um Sometimes termed Hard Drusen Sharp, well demarcated boundaries, White-yellow Small localised collection of hyaline material within or on Bruch’s membrane 4)Intermediate Drusen >63 < 125um Fairly well-defined, Yellow-white, deposits at level of RPE 3)Large Drusen > 125 um ( Soft Drusen ) Less well delineated, Yellow-white Larger/commonly become confluent Poorly demarcated boundaries Involve overlying focal RPE detachment (Drusenoid RPE detachment)
  • 14. Soft Drusen: 1) Membranous: 63-175 µ Pale, shallow appearing drusens 2) Granular: About 250 µ Solid appearing drusens 3) Serous: >500 µ Have pooled serous fluid blister like appearance May result in serous PED
  • 17. Confluent Drusen Representing widespread RPE abnormality Increase risk of vision loss
  • 18. Calcified Drusen (glistening appearance) Dystrophic Calcification may develop in all type of Drusen
  • 19. RPE degeneration, seen as: • Focal areas of hypo- and hyper- pigmentation (‘stippling’) • Associated with progression to late AMD with Visual loss • Eventually areas of atrophy of the RPE revealing underlying large & deep choriodal vessels ‘Geographic atrophy’ = end stage or Late advanced stage of Dry AMD
  • 20. a) Drusen with Pigmentary abnormality b) Geographic Atrophy
  • 21. Differential Diagnosis of Drusens 1) Donyne Honeycomb retinal dystrophy (Malattia leventinese, Autosomal dominant radial drusen) 2) Cuticular Drusen- FA characteristics is ‘Star in the Sky’ appearance 3) Type 2 Membranoproliferative Glomerulonephritis.
  • 22. 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
  • 23. AMD: SYMPTOMS Initial symptoms: • Straight lines appear wavy • Blurry vision • Distorted vision • Objects may appear as the wrong shape or size • A dark empty area in the centre of vision • Patient’s ability to perform normal daily tasks such as reading, sewing, telling the time, driving are greatly impaired.
  • 24. Non-Exudative AMD • Symptoms:- Gradual mild to moderate impairment over months or years Both eyes usually affected but often asymmetrically Vision may fluctuate, & is often better in bright light • Signs:- Intermediate-large soft drusen may confluent Focal hyper &/or hypopigmentation of RPE Slow/progressive atrophy of RPE and photoreceptors Drusenoid RPE detachment Advanced form = Geographic Atrophy
  • 25. • Clinically , dry AMD may manifest:- Stage of drusen and/or hyperpigmentation Stage of incipient atrophy (non geographic atrophy) Stage of geographic atrophy • Diagnostic criteria:- Degenerative disorder in persons >50 years, characterized by the presence of any of the following: Soft drusen (>63 µ) RPE abnormalities- areas of hypo/hyperpigmentation (excluding pigment surrounding small, hard drusen) Visual acuity (VA) is not a criterion for the diagnosis
  • 26. DRY AMD: COURSE AND VISUAL PROGNOSIS • Patients with only drusen not have much loss of vision, but require additional magnification of the text and more intense lighting to read small points. • Presence of large drusen (>63 microns in diameter) is associated with a risk of the late form of the disease like CNV. • Geographic atrophy- severest form of the dry AMD, RPE atrophy >175 microns with exposure of the underlying choroidal vessels.
  • 27. 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 •Signs/Symptoms:- Marked decrease VA (unless foveal sparing) Central field loss (positive scotoma) Difficulty recognizing faces Difficulty reading if large scotoma Difficulty in dim light/adapting
  • 29. DD’s for dry ARMD Herediatry Diseases:- Pattern dystrophy, Stargardt disease, Best’s disease, Angioid streaks Central serous chorioretinopathy Macular telangiectasia type II Multifocal choroiditis Acute posterior multifocal placoid pigment epitheliopathy Toxic lesions:- Chloroquin, Phenothiazines, Canthaxathin Cuticular Drusen with or without a vitelliform lesion Adult vitelliform dystrophy
  • 30. Exudative AMD • Clinical Features:- Choroidal neo-vascularisation Exudative detachment of RPE, sub-RPE(type1) and/or subretinal (type2) Disciform scar • Choroidal Neo-vascularisation:- Proliferations of fibrovascular tissue from choriocapillaris through defects in Bruch’s membrane Sub-RPE or sub-retinal Membranes have a grey-green or pinkish-yellow hue in late stages • Tendency to leak:- Serous and blood Distorted or painless blurred vision, usually with metamorphopsia Red if sub-retinal, darker if sub-RPE Rarely vitreous haemorrhage
  • 31. WET AMD Photoreceptors and pigment epithelium send a distress signal to choriocapillaries to make new vessels New vessels grow behind the macula Breakdown in the Bruch’s membrane Blood vessels are fragile Leak blood and fluid Scarring of macula Potential for rapid and severe visual damage
  • 33. • Diagnostic criteria persons >50 years, characterized by the presence of any of the following choroidal neovascularization serous retinal pigment epithelial detachment hemorrhagic retinal pigment epithelial detachment fibrotic scar in the macula • The hallmark of neovascular AMD is CNV & potential manifestations are- Subretinal fluid Macular edema Retinal , subretinal ,or sub-RPE hemorrhage Retinal or subretinal lipid exudate Plaque like membrane or grey or yellow green discrete discoloration RPE detachment RPE tear Sub-retinal fibrosis or disciform scar .
  • 34. • CNV lesion is well demarcated & its location may be determined by closest point to the FAZ. • Lesion location is classified angiograpically as follows:- 1. Subfoveal: under the centre of FAZ 2. Juxtafoveal: 1-199 µm from the centre of FAZ 3. Extrafoveal: >200 µm & <2500 µm from the centre of FAZ • Types: • Type I: CNV beneath RPE • Type II: CNV above RPE
  • 35. Wet AMD: A Rapid Descent TIME Wet AMD Blindness Severe Vision Loss Early Intermediate Advanced (dry) (dry) (wet) No Vision Loss Today: many are diagnosed after vision loss There are no good predictors for who will develop Wet AMD or when
  • 36. Common Ophthalmic condition associated with CNV Age-related macular degeneration Angoid streaks Best’s disease Choroidal Osteoma Fundus Flavimaculatus Idiopathic Causes Multifocal Choroiditis Ocular Histoplasmosis Syndrome Optic disc drusen Optic nerve head pits Pathological ( Progressive ) Myopia Pattern dystrophies Photocoagulation Sarcoidosis Serpiginous or Geographic Choroiditis Toxoplasmic Retinochoroiditis Traumatic Choroidal Rupture Polypoidal choroidal Vasculopathy
  • 37. Pattern of CNV Hyper fluorescence on FA Classic CNV (20%) -Well demarcated boundaries (Lacy pattern) during early transit -Subsequently leaking into subretinal space over 1-2 min, with late staining of fibrous tissue Occult CNV (80%) Type 1 -Fibro vascular PED -Irregular elevation RPE. -Boundaries may be well demarcated or poorly demarcated. -Persistent staining or leakage of dye at 10 min Type 2 -Late leakage of undetermined of source (LLUS) -Boundaries poorly demarcated -Source of late leakage can not be determined from earlier frames of angiograms
  • 41. RPE DETACHMENT (PED) Depending on cause, it is of many types: • Drusenoid • Serous • Fibro vascular • Hemorrhagic
  • 42. RPE TEAR • Spontaneously or on photocoagulation of CNV or after intravitreal injections. • Visual acuity abruptly fall with foveal involvement. • FA shows in late phase hypofluorescence corresponding to thickened folded RPE with adjacent hyperfluorescence over the torn area, two area often separated by a sharply defined border.
  • 44. VARIATION • Retinal angiomatosis proliferans-10-20% of Neovascular AMD in Caucasians. • Has been termed Type-III CNVM • Frequently Bilateral & Symmetrical • Characterized by predominantly intraretinal neovascularization • 3 Stages: • Stage 1 • Intraretinal neovascularization • Stage 2 • Subretinal neovascularization • Stage 3 • CNV clearly evident clinically/angiographically. • RCA (retino-choroidal anastamoses) • A Diciform scar will often form
  • 45. • Polypoidal Choroidal Vasculopathy A variant of neovascular AMD MC in women (5:1) & relatively young , African & East Asian ethnic origin Often Bilateral & Asymmetrical Sudden onset of unilateral visual impairment Causes multiple recurrent serosanguineous retinal & RPE detachments Typical OCT findings in PCV may reveal a classic hyperreflectivity in the choroidal layers known as the "double-layer" sign
  • 46. Investigations • History:- Gradual change = non-exudative Sudden change = exudative • Visual Symptoms:- VA for Distance and near & no improvement with pin-hole Difficulty in reading/recognising faces, driving Difficulty with changing light / adapting after bright light Distortion of images mostly with exudative changes Less common symptoms include night glare, photopsia (flickering or flashing lights), visual hallucinations (Charles Bonnet syndrome) & abnormal dark adaptation • Amsler grid test: Assesses distorted & scotoma , small irregularities in the central field of vision ( 10degree) • Ophthalmoscopy: to detect drusen, as well as neovascularization • Fluorescein and ICG angiography: Determines the presence and location of neovascularization • Optical coherence tomography
  • 47. MANAGEMENT • Antioxidants: AREDS-1 study & follow-up AREDS-2 Study use of high dose of multivitamins & antioxidants decreases the risk of progression of ARMD in those with high risk characteristics as age >55 with one or more of following Extensive intermediate Drusen At least one large Drusen GA in one or both eyes Late AMD in one eye ( greatest benefit in AREDS1) Combination of antioxidants vitamins and minerals- AREDS1 Formula AREDS2 Formula Vitamin E 400IU Vitamin E 400IU Vitamin C 500mg Vitamin C 500mg Beta Carotene 15mg ( Vit A 2500IU) Leutin 10mg Zinc 80mg Zeaxanthin 2mg Copper (Cupric Oxide) 2mg Zinc 25-80mg Copper 2mg
  • 48. Cont.. • Dry ARMD:- 1) Antioxidant suplimentation & Risk factors modulation 2) Low Vision Aids 3) Anti-inflammatory drugs- Sirolimus (Rapamycin) antifungal, immunosuppressant & used as SC every 2 months. Intravitreal Steroids as FA implants (sustain release upto 36 months) 4) Complement Inhibition- POT-4 neutralize early AMD inflammatory component & it is a Intravitreal gel sustain release system ARC1905 a C5 inhibitor Aptamer prevents C5a production Eculizumab a Antibody against C5, currently approved only for PNH Lampalizumab a monoclonal antibody, used as intravitreal monthly 5) Neurotrophic Factors- NT501 a genetically modified RPE intravitreal implant, shown retinal thickness as early as 4 months. 6) AL-8309A- as topical solution, light induced oxidative damage
  • 49. Cont.. 7) Reduction of Retinal Toxins- In Dry AMD lipofuscin (a waste products) accumulates at leading edge of lesion ACU-4429 & Fenretinide (Oral doses) prevents accumulation of lipofuscin 8) Choroidal Blood Perfusion Enchancers- MC-1101 as Topical drug, shown to increase mean choroidal blood flow 9) Other Options Photocoagulation of Drusen Saffron (20mg/day) a neuroprotective effect Intravitreal neuroprotective drug Brimonidine Surgery like Retinal translocation, Subretinal Stem cell Transplantation
  • 50. Wet-ARMD • Anti-angiogenic Drugs (Anti-VEGFs)- 1) Bevacizumab (Avastin)- Dose- 1-1.25 mg(0.05ml), repeated 6-8 weekly 2) Ranibizumab (Lucentis)- Dose- First 3 injections of 0.5 mg (0.05 mL) four weekly & further on physician's assessment 3) Pegatanib (Macugen)- Given 0.3 mg dose six weekly minimum for two years 4) Aflibercept (Eylea)-2mg (0.05ml) First 3 injections monthly then every 2 months as maintenance regimen • Photodynamic Therapy (PDT)- was developed in the 1990s Includes IV Verteporfin & a red diode laser (689 nm wavelength) Verteporfin (a benzoporphyyrin derivative)- second generation potent photosensitizer of the tetrapyrrole group
  • 51. Cont.. Absorbs light at 690 nm, a longer wavelength is important because it allows deep tissue penetration, through blood, pigments & fluid which could accumulate beneath the retina Plasma half-life ranges approximately from 5 to 6 hours & BPD-MA/Verteporfin is excreted mainly by the bile (90%) Administered intravenously as a liposomal preparation & partitions into the LDL phase of the lipoprotein fraction of the blood Endothelial cells which form the neovessels of tumors & neovascular membranes have been shown to have increased the population of LDL receptors that play a major role in the mechanism of the uptake & therefore the selectivity of the photosensitizer in these cells MOA- The target cells are light irradiated & the molecules of the dye gain energy passing from the ground state to an excited, highly reactive, short-lived triplet state which transfers the excess of energy by two pathways 1) The energy absorbed from the triplet state is transferred to other molecules leading to the generation of free radicals, which instantaneously oxidize a wide variety of biomolecules - Type I mechanism
  • 52. Cont.. 2) The energy absorbed from the triplet state is transferred to oxygen generating high reactive short-lived oxygen - Type II mechanism which appears to play the major role in the effect seen in PDT The interactions of these highly reactive compounds cause cellular and vascular damage Associated with an immediate induction of acute inflammatory responses Leading to occlusion of the feeding vessels i.e neovascular capillaries Main Indication- Subfoveal predominantly Classic CNV with visual acuity of 6/60 or better The potential advantages of PDT are:- Scarring is unlikely, as collagen & elastin are unaffected, leaving organs intact Highly selective tissue necrosis & Resistance to treatment does not develop with repeated treatment
  • 53. • Laser Photocoagulation- Includes Thermal blue-green Argon laser or diode laser ablation of CNV, now rarely used Modality for juxtafoveal (well-defined choroidal neovascular lesions located 1 to 199 µ from the foveal centre, or 200 to 2500 µm from the foveal centre but showing blood or pigmentation less than 200 microns from the foveal centre) & extrafoveal (located 200 to 2500 µm from the foveal centre) CNV associated with AMD A fluorescein angiography (FA) should be performed 72 to 96 hours before photocoagulation in order to select treatable cases & to guide the ophthalmologist during treatment Patients should undergo treatment as quickly as possible, since neovascular lesions may grow 10 to 18µ per day Treatment should be performed so that a white lesion in the retina is obtained
  • 54. Cont.. The neovascular lesion should be surrounded by laser marks with a diameter of 200µ and duration of 0.2 to 0.5 seconds After surrounding the perimeter of the neovascular lesion, its central part is covered with 200µ burns; the remaining lesion is covered with 200 to 500µ burns, with duration of 0.5 to 1.0 seconds Laser treatment should avoid retinal blood vessels and the optic nerve (treatment should start 10-200 µm from the optic nerve), as well as preserve at least 1.5 hours of the papillomacular bundle (no peripapillary treatment) Follow-up:- it is necessary to perform medical examinations and control FA 2 to 3 weeks, 4 to 6 weeks, 3 to 4 months and 6, 8, 9 and 12 months after treatment Recurrence is rare after 2 years The greater risks exist 6 weeks to 12 months after treatment
  • 55. Cont.. Complications:- 1) Choroidal haemorrhage (rarer if spots ≥ 200 microns and time intervals ≥ 0.2 seconds are used) 2) Premacular fibrogliosis 3) Accidental treatment of the fovea in extrafoveal or juxtafoveal lesions 4) Rupture of the pigment epithelium (more frequent in cases of PED) 5) Atrophy of the RPE in the area adjoining the laser scar (immediately after treatment or years later) • Laser photocoagulation remains currently indicated for the treatment of well- defined extrafoveal choroidal membranes • For classic juxtafoveal membranes, laser photocoagulation could theoretically be considered as an option for cases in which the entire neovascular lesion can be treated without damaging the fovea
  • 56. • TRANSPUPILLARY THERMOTHERAPY:- First described by Oosterhuis et al. in 1998 for treatment of choroidal melanoma The goal of TTT is to create and maintain tissue hyperthermia The diode laser (810 nm, near infrared):- Low absorption in xanthophyll, minimum nerve fibre layer damage Poorly absorbed by haemoglobin, allowing treatment through preretinal and subretinal blood Mainly absorbed in the choroid, enabling effective treatment of choroidal lesions So effectively treat subfoveal occult choroidal neovascular membranes and preserve vision
  • 57. Cont.. • TECHNIQUE:- delivered through a slit lamp using an antireflective Goldmann contact lens & an infrared diode laser at 810 nm, specially modified to give a long pulse mode The slit lamp has a special large spot size adapter with an adjustable beam width of 0.5 mm, 0.8 mm, 1.2 mm, 2.0 mm & 3.0 mm The treatment is given using one spot that encompasses the entire lesion Laser parameters used are duration of 60 seconds, at power settings between 250 and 1000 mW, depending upon the spot size used For a 3 mm spot size, the initial power setting is 800 mW by keeping the power density around 10 W/ sq.cm The end point is an area of no visible colour change to a light grey appearance Full treatment results are usually seen within 2-3 months after the procedure
  • 58. • Submacular excision of CNV • Macular translocation • Retinal rotation • Homologous Iris/Retinal pigment epithelium transplantation • Autologous RPE transplantation SURGICAL OPTIONS
  • 59. EMERGING TREATMENTS • Retaane (Anecortave Acetate)- modified steroid promising in reducing the risk of vision loss due to the growth of unhealthy blood vessels in wet AMD • AdPEDF (Adenovirus based pigment epithelium derived factor)- a gene that leads to the production of the protein PEDF, which helps keep photoreceptors healthy, thereby preserving vision • siRNA (Bevasiranib)- silences the genes that lead to the growth of unhealthy, vision-robbing blood vessels under the retina • ATG3 (mecamylamine)- a topical formulation that inhibits the nicotinic acetylcholine receptors
  • 60. • EVIZON (squalamine lactate)- aminosterol with anti–angiogenic activity derived from the liver of the dogfish shark, administered intravenously (no eye injection) • OT-551 (antioxidant eye drops)- supplement the eye’s natural defense system against disease & injury protection against both cataract and dry AMD • Encapsulated Cell Technology (ECT)- tiny capsule (6 mm) implanted into the eye, contains retinal cells that produce a vision-preserving protein ,Ciliary Neurotrophic Factor (CNTF) keep photoreceptors alive and healthy, preserving vision