AGE-RELATED MACULAR

DEGENERATION (AMD)

MARLIYANTI N. AKIB
DEPT. OF OPHTHALMOLOGY
FAC. OF MEDICINE
HASANUDDIN UNIVERSITY
INTRODUCTION

• AMD : MACULAR DEGENERATIO DUE

TO SENILITY
• PATHOGENESIS : STILL UNCLEAR
• HISTOPHATOLOGIC FINDING:
IMPAIRED OF RETINAL PIGMENT
EPITHELIAL AND BRUCH
MEMBRANE
• Many elderly adults experience attenuation
in their ability to function effectively
• and independently. Such a decline is
multifactorial and includes impairment of
vision.
• Nearly every assessment of visual function
has been shown to diminish later in life.
• Decreased visual acuity, visual field,
contrast sensitivity, motion perception, and
dark adaptation
• are all recognized deficits found in elderly
patients
Stratifikasi lapisan retina

5
• Retinal ganglion cells accumulate lipofuscin
with aging; there is evidence for up to 25%
loss in ganglion cell, number in certain
retinal locations. There is preferential loss
of rods in the retina with aging, but with
progressive aging cone numbers eventually
decline. shows thickening and decreased
permeability with age.
• RPE cells show numerous aging changes
including accumulation of lipofuscin,
alterations in cell shape, density,
• pigmentation, lysosomal activity, and
extracellular matrix formation. Bruch’s
membrane
• Arteriosclerotic aging changes occur
• in the retinal vessels while the macular
choriocapillaris shows a decrease in total
capillary number with age.
• Age-related macular degeneration (AMD) is
common among the elderly, and its
incidence increases progressively with
advancing age.

• According to the Beaver Dam Eye Study,

11% of the population are affected by AMD
at age 65–74, and this number increases to
28% after age 74.
Retinal pigment epithelial

• visual pigment regeneration

•Transport of necessary nutrients/ ions to photoreceptors
cells and removal the waste products from photoreceptors
• Absorb light
• Maintains the subretinal space
• Phagocytoses rod and cone outer segments
• Participates in retinal and polyunsaturated fatty acid
metabolism
• Forms the outer blood-ocular barrier
• Heals and forms scar tissue
 AGE-RELATED MACULAR
DEGENERATION (AMD)

1. Drusen

2. Drusen and AMD

3. Atrophic AMD

4. Exudative AMD
• Pigment epithelial detachment (PED)
• Choroidal neovascularization (CNV)
 classification
• 1. Non-exudative or atrophic ARMD. It is
also called dry or geographic ARMD and is
responsible for 90 percent cases.
• It typically causes mild to moderate,
• gradual loss of vision.
• Patients may complain of distorted vision,
difficulty in reading due to central
shadowing
Pathologic changes :

Affect the outer retina, RPE, Bruch’s membrane and

choriocapillaris
• photoreceptors are reduced indensity and distribution
• Ultrastructural aging changes occur in th epigment
epithelium,
• including Loss of melanin granules, formation of
lipofuscin granules, and accumulation of residual bodies
Basal laminar deposit accumulate, consist of granular
lipid-rich material and collagen fibers collecting
between the basal lamina (plasma membrane) of the
RPE cell and the inner aspect of basement membrane

Progressive involutional changes in the

choriocapillaries
Risk factors:

• Include positive family history

• Cigarette smoking
• Hyperopia
• Light iris color
• Hypertension
• Hyperchlesterolemia
• Female gender
• Cardiovascular disease
 Drusen
Histopathology

Hard Soft

• Small well-defined • Larger, ill-defined spots

spots • May enlarge and coalesce
• Usually innocuous
• Increased risk of AMD
 FA of drusen
``

Degree of hyperfluorescence depends on:

• Extent of overlying RPE atrophy (window defect)

• Amount of staining

• Lipid content
Drusen and AMD - progression

Atrophic AMD Exudative AMD

 Atrophic AMD
Progression

Initially drusen and non-specific RPE changes

Late RPE (geographic) atrophy

 Atrophic AMD

Fluorescein angiogram Management

Hyperfluorescence from RPE window defect Low-vision aids if appropriate

 Signs of Pigment epithelial detachment

Circumscribed, dome-shaped elevation Sub-RPE fluid may be clear or turbid

 FA of pigment epithelial detachment

Early, well-defined Progressive increase in No increase in size of lesion

hyperfluorescence hyperfluorescence
 ICG angiogram of pigment
epithelial detachment

Early, well-defined Later, thin surrounding No increase in size of lesion

hypofluorescence hyperfluorescent ring
Possible subsequent course of PED

Spontaneous resolution Geographic atrophy

CNV RPE rip

 Choroidal neovascularization (CNV)
• Less common than atrophic AMD but more serious
• Metamorphopsia is initial symptom
• Most lesions are not visible clinically
Suspicious clinical signs

Pinkish-yellow subretinal lesion Subretinal blood or lipid

with fluid
 Angiographic classification of CNV
Well-defined (classical) Occult

• Extrafoveal > 200 m from centre of • Poorly defined

FAZ
• Juxtafoveal < 200 m from centre of
FAZ • Obscured by PED, blood or exudate
• Subfoveal - involving centre of FAZ
 FA of classical CNV

Very early ‘lacy’ filling Leakage into subretinal Late staining

pattern space and around CNV
ICG angiogram in PED with occult CNV

PED is hypofluorescent CNV is hyperfluorescent (hot spot)

Possible subsequent course of CNV

Haemorrhagic sensory and Subretinal (disciform) scarring

RPE detachment

Massive subretinal exudation Exudative retinal detachment

Potential indications for laser treatment of CNV
• Classic extrafoveal CNV on FA
• Occult extrafoveal CNV on ICG

Pre-treatment FA of classic CNV

 Technique of laser photocoagulation of CNV
• Perimeter is treated with overlapping 200 m (0.2-0.5 sec) burns
• Entire area is covered with high energy burns

Late staining around

Lack of leakage following successful treatment margin is normal
Results of laser photocoagulation of CNV
• Initial risk of severe visual loss reduced by over 50%
• Frequent subsequent recurrence with subfoveal involvement

Recurrence of CNV several months after initially successful treatment

• Treatment
• Laser photocoagulation
• PDT Photodynamic therapy
• Anti VEGF intravitreal
• . Ophthalmoscopically
• it is characterised by occurrence of drusens
(colloid bodies), pale areas of RPE
• atrophy and irregular or clustered
pigmentation.
• Drusens appear as small discrete, yellowish-
white, slightly elevated spots.
• In later stages, there occurs enlargement of
the atrophic areas become
• (geographic atrophy).
• 2. Exudative ARMD.
• It is also called wet or neovascular ARMD.
It is responsible for only 10 percent cases
• associated with comparatively rapidly
progressive marked loss of vision.
• Typically, the course of exudative ARMD
• rapidly passes through many stages. These
include:
• Stage of drusen formation,
• Stage of RPE detachment,
• Stage of choroidal neovascularisation
CNV,
• Stage of haemorrhagic detachment of RPE,
• Stage of haemorrhagic detachment of
• Stage of haemorrhagic detachment of
• neurosensory retina, and
• Stage of disciform (scarring) macular
degeneration.
• Treatment
• There is no effective treatment for non-
exudative ARMD.
• However, some treatment options are
• available for exudative ARMD.
• Role of dietary supplements and
antioxidants in prevention or treatment of
ARMD. The age-related eye disease study
(AREDS) has suggested that use of certain
specific antioxidants, vitamins sted that use
• of certain specific antioxidants, vitamins
• vitamin C and E, beta carotene, zinc and
copper) could possibly prevent or delay the
progression of ARMD.
• Treatment modalities available to treat
exudative
• (neovascular) ARMD are:
• Argon green-laser photocoagulation is the
• treatment of choice for extrafoveal
choroidal neovascular membrane (CNVM).
• Photodynamic therapy (PDT) is the
treatment of choice for subfoveal and
juxtafoveal classic CNVM.
• In PDT, vertiporfin, a photosensitizer or
• light activated dye is injected intravenously.
diode laser source at a wavelength (689 nm)
occult CNVM. PDT is definitely better than
TTT
• Transpupillary thermotherapy (TTT) with
a diode
• laser (810 nm) may be considered for
subfoveal
• Surgical treatment in the form of
submacular surgery
• to remove CNVM and macular
translocation surgery are being evaluated.
•
• Pharmacologic modulation with
antiangiogenic
• agent like interferon alfa-29, and inhibitor
of vascular endothelial growth factor
(VEGF).