LEARNING OUTCOMES

State the causes of gradual progressive

painless diminution of vision
Summarise the risk factors, types, symptoms,
signs and treatment of age related macular
degeneration

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GRADUAL PROGRESSIVE PAINLESS

DIMINUTION OF VISION
Conjunctiva: Progressive pterygium encroaching
pupillary area
Cornea: Corneal degenerations and corneal
dystrophies
Primary open angle glaucoma
Lens : Cataract
Retina :
A. Macular degeneration and macular
dystrophies
B. Diabetic retinopathy and other retinopathies
C. Chorioretinal degenerations and dystrophies
Optic nerve: Hereditary optic atrophies, drug
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induced optic neuropathies
and toxic amblyopia 2

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AGE RELATED MACULAR

DEGENERATION

Normal Vision

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Age Related Macular

Degeneration

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 The macula is defined

clinically by the area
within the major
temporal vascular
arcades and provides
our sharp,
discriminating vision.

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WHAT IS AGE RELATED MACULAR

DEGENERATION?
Leading cause of significant, irreversible central
visual loss in the Western world.
Characterised by age-dependent alterations in
the sensory retina, retinal pigment epithelium
and choriocapillaris
Incidence is age dependent
Prevalence steadily increases past age 55
Common international classification exists, but
most clinicians still divide AMD into
exudative(dry) and nonexudative(wet) forms

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WHO DEVELOPS AGE-RELATED

MACULAR DEGENERATION?
Anyone can.
Greater incidence of disease in women over men.
Skin pigmentation plays an important role in
exudative disease

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DEFINITION
Age-related macular degeneration (AMD) is a
more advanced, sight-threatening stage of ARM
characterized by one or more of the following:
Geographic atrophy of the RPE with visible
underlying choroidal vessels.
Pigment epithelial detachment (PED) with or
without neurosensory detachment.
Subretinal or sub-RPE choroidal
neovascularization (CNV).
Fibroglial scar tissue, haemorrhage and exudates.

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ETIOLOGY

Exact cause is not known

Multifactorial
Smoking is a consistent risk predictor
Family history of AMD 5X increased risk of
developing AMD themselves
Race more prevalent in Caucasians
ARM(Age Related Maculopathy) particularly when
associated with soft drusen
Cataract, particularly nuclear opacity.
Biomarkers of cardiovascular disease such as
obesity and hypertension

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EPIDEMIOLOGY
WHO estimated in 2002 that 8.7% of the worlds
blindness was due to AMD
14 million persons worldwide blind or severely visual
impaired from AMD
In general, advanced AMD is rare before the age of 55
and more common in persons 75 years of age or older
Advanced AMD can be classified broadly into two
types: dry and wet
Dry AMD accounts for majority of all diagnosed cases
Wet AMD is responsible for majority of severe vision
loss and usually occurs over weeks to months

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PATHOGENESIS
Loss of visual activity typically results from progressive
degeneration of the choriocapillaris, retinal pigment
epithelium, and photoreceptors
Earliest manifestation of the disease appears to be the
abnormalities within Bruchs membrane
Loss of central vision in AMD is the result of changes that
occur in response to deposition of abnormal material
in Bruch membrane.
This material is derived from the RPE and its
accumulation is thought to result from failure to clear the
debris discharged into this region.
Drusen consist of discrete deposits of the abnormal
material located between the basal lamina of the RPE
and the inner collagenous layer of Bruch membrane
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 Concomitant thickening of the collagenous layers within

Burchs membrane, degeneration of elastin and collagen
within Burchs membrane, increased AGED and
accumulation of lipids as well as exogenous proteins
Hydrophobic barrier that impede passage of fluid and
nutrients between the choroid and outer retina resulting
in relative ischemia
Resulting in decreased nutrient delivery to RPE cells and
secondary metabolic stress.
Ischemia of the RPE may lead to increased production of
vascular endothelial growth factor by RPE cells, which is
the major stimulus for neovascularisation of the
choriocapillaris.
Subsequent neovascularization may occur through
fracture in Burchs membrane leading to subretinal and
intraretinal fluid accumulation.

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HISTOPATHOLOGY
Early in the disease process, lipids are deposited
in Bruchs membrane , possibly from failure of
RPE to process cellular debris
Only later in disease process are drusen visible
Appearance of drusen is the earliest visible
clinical sign of AMD
Drusen appear as round yellow deposits
located between RPE and Bruchs membrane
Vary in size, shape and location

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DRUSEN
Small drusen (<63 m) are extremely common,
80% of the general population older than 30
years manifesting at least one
Hallmark of AMD is the appearance of soft or
indistinct (>63 m) drusen
Analysis of drusen reveals that they contain
lipofuscin, amyloid, complement factors, and
additional cellular components.

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CLASSIFICATION

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OCULAR MANIFESTATIONS
Affected individuals are asymptomatic in the early
stages of the disease
Onset is subacute for dry AMD, but as the disease
progresses they report blurred vision or
metamorphopsia in one or both eyes
Decreased reading ability, especially in dim light,
difficulty with glare, and difficulty with dark and
light adaption
May go undetected until abrupt visual loss is
noted
Wet AMD shows a rapid progression of visual acuity
loss relative to its non-neovascular part
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DRY AMD
Drusen appear as focal, whitish yellow
excrescences deep to retina
Cluster in posterior pole but can occur anywhere
on the fundus
Drusen in extra macular location are of no known
visual consequence
20-200m in diameter
Drusen alone does not cause severe visual acuity
loss, but can be associated with mild
metamorphopsia , loss of reading speed, and
impaired contrast sensitivity
Represent significant risk factor for subsequent
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geographical atrophy
and neovascularisation
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HARD AND SOFT DRUSENS

Categorised into HARD and SOFT varieties
Hard drusen
Round, discrete, yellow-white deposits measuring
less than 63m .
Not age related
Do not carry an increased risk for neovascularisation
Soft drusen
Ill defined, with non discrete borders, measuring
63m or more .
Age related
Associated with development of neovascularisation
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Drusen are the by-product of retinal metabolism and

manifest as focal yellow-white deposits deep to the retinal
pigment epithelium. They serve as markers of nonexudative
age-related macular degeneration.

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 Soft drusen may coalesce with neighbouring

drusen
Frequently associated with overlying pigmentary
changes either from photoreceptor dysfunction or
from retinal pigment epithelial demise.
Progressive retinal pigment epithelial disruption
eventually causes loss of overlying sensory retina
and underlying choriocapillaris.
Such developments result in localized atrophic
regions that extend and coalesce around the
fovea, eventually involving the fovea itself.
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GEOGRAPHIC ATROPHY
Visual acuity loss from dry AMD is generally due
to geographic atrophy of foveal region
Seen as one or more well delineated areas of
hypopigmentation or depigmentation due to
absence /severe attenuation of RPE
Larger, deep choroidal vessels are more readily
visualised through the atrophic patches
If the foveal centre is spared, good visual acuity
maybe preserved

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WET AMD
Hallmark is presence of neovascularisation within
the macula
These vessels commonly originate from the normal
choriocapillaris and enter the subretinal space through
defects in the Bruchs membrane, a collagenous layer
separating the choroidal circulation from the retina
May arise from retina known as retinal angiomatous
proliferation
Pigment epithelial detachments are dome-shaped
clear, turbid, or blood-filled elevations of the retinal
pigment epithelium; they may or may not be
associated with choroidal neovascular ingrowth.
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 Clinical manifestations of neovascular AMD can

include the following
a) Subretinal edema
b) Macular edema
c) Retinal,subretinal, or sub-RPE hemorrhage
d) Retinal or subretinal lipid exudates
e) RPE detachment
f) RPE tear
g) Subretinal fibrosis/disciform scar

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PROPHYLACTIC TREATMENT
Use of high dose multivitamins and antioxidants
on a regular basis can decrease the risk of
progression of ARM in those with high risk
characteristics.
These high risk features include visual loss in the
contralateral eye from pre-existing AMI and
confluent soft drusen even in the absence of
visual loss.
Supplements did not provide benefit for those
with early AMD.
The exact compounds used in the AREDS study
were:
500mg of vitamin C
400lU of vitamin E
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TREATMENT OF DRY AMD

Supportive : counselling and linking to support
group/social services
Refraction: with increased near-add; low-vision
assessment
Amsler grid
Lifestyle changes
Vitamin supplementation

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TREATMENT FOR WET AMD

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