Age-Related Macular Disease

Fitriani Umi Hasanah

201820401011121
Pembimbing:
dr. Fatin Hamamah, Sp.M
Definition
• ARMD is a degenerative disease of the central part of the retina—
known as the macula—that results in a loss of central vision, which is
essential for most daily activities
• It is characterized by a loss of visual acuity caused by degeneration of
the choriocapillaris, retinal pigment epithelium (RPE), and
photoreceptors, usually beginning with drusen and pigmentary
changes in Bruch's membrane
Prevalency
• The condition, which affects 30 million to 50 million people
worldwide, is the leading cause of irreversible blindness in developed
countries in people aged 50 years and older
• The prevalence of ARMD increases exponentially every decade after
age 50
Etiology
• genetic,
• environmental,
• metabolic, and
• functional factors; including aging, family history, smoking, high blood
pressure, obesity, hypercholesterolemia, and arteriosclerosis, sun
exposure, atherosclerosis, hypertension, diabetes, polypharmacy,
alcohol, ethnicity, hypothyroidism, and C-reactive protein
Patophysiology
Stages of ARMD
• Early stages of ARMD are characterized by a macula that has
yellowish subretinal deposits (drusen) and/or increased pigment
• Patients with early ARMD have stable visual acuity for many years,
and loss of vision is gradual
 American Academy of Ophtalmology
Retina/Vitreous Panel. Preferred Practice
AREDS Classification of ARMD Pattern Guidelines. Age-Related Macular
Degeneration. San Fransisco, CA: American
Academy of Ophtalmology; 2014

Category Designation Description

No ARMDNo or few small drusen
1
(<63 μm in diameter)
Multiple small drusen (<20), a few
2 Early intermediate drusen (63–124 μm in
diameter), or RPE abnormalities
Extensive intermediate drusen, ≥1
large drusen (125 μm in diameter),
3 Intermediate
or geographic atrophy not involving
center of fovea
Geographic atrophy or neovascular
4 Advanced
maculopathy
AREDS: Age-Related Eye Disease Study; ARMD: age-related macular degeneration; RPE: retinal pigment
epithelium.
• Early AMD. Early AMD is diagnosed by the presence of medium-sized drusen, which are
about the width of an average human hair. People with early AMD typically do not have
vision loss.
• Intermediate AMD. People with intermediate AMD typically have large drusen, pigment
changes in the retina, or both. Again, these changes can only be detected during an eye
exam. Intermediate AMD may cause some vision loss, but most people will not
experience any symptoms.
• Late AMD. In addition to drusen, people with late AMD have vision loss from damage to
the macula. There are two types of late AMD:
• In geographic atrophy (also called dry AMD), there is a gradual breakdown of the light-sensitive
cells in the macula that convey visual information to the brain, and of the supporting tissue
beneath the macula. These changes cause vision loss.
• In neovascular AMD (also called wet AMD), abnormal blood vessels grow underneath the retina.
(“Neovascular” literally means “new vessels.”) These vessels can leak fluid and blood, which may
lead to swelling and damage of the macula. The damage may be rapid and severe, unlike the more
gradual course of geographic atrophy. It is possible to have both geographic atrophy and
neovascular AMD in the same eye, and either condition can appear first.
1. DRY ARMD
• is also known as nonexudative, nonneovascular, or atrophic ARMD
• more common form of ARMD, seen in about 90% of cases
• Vision loss in dry ARMD is gradual and usually is associated with
moderate visual impairment, as well as functional limitations
including fluctuating vision, difficulty reading, and limited vision at
night or under conditions of reduced illumination
• Upon examination, the macula shows areas of depigmentation
• Early to intermediate nonexudative AMD: Significant for the presence
of multiple drusen for early AMD. For intermediate AMD, drusen may
appear confluent with significant pigment changes and pigment
accumulation in the posterior pole. In addition, the retinal pigment
epithelium (RPE) often appears atrophic, with easier visualization of
the underlying choroid vascular plexus
• Difficulty with night vision and with changing light conditions
(specifically, changes in Amsler grid self-evaluation and trouble with
reading)
• Visual fluctuation (ie, some days, vision is poor; other days, vision
appears improved)
• Difficulty with reading and making out faces
• Metamorphopsia (distortion of visual images): Not a major patient
complaint for dry AMD, but it may be present as the atrophy slowly
progresses.
Management dry AMD
• Antioxidant vitamin and mineral supplements (vitamin A, vitamin E,
zinc, and lutein)
• Screening for impaired visual acuity
• Wraparound shades (eg, orange-tinted, blue blocker lenses): Effective
solution for delayed dark adaptation and to protect eyes from direct
sunlight
• Avoidance/cessation of tobacco use
• Frequent follow-up for risk assessment of conversion to exudative
AMD
2. WET ARMD
• also referred to as exudative or neovascular ARMD, accounts for
about 10% of cases
• its presence usually indicates a more advanced disease state, and it is
associated with rapid distortion and a sudden loss of central vision
over a period of weeks to months
• he eyes have two times the expected prevalence of vitreomacular
adhesion and are less likely to have a posterior vitreous detachment.
• Fluid and exudate may accumulate underneath the retina in patients
with neovascular ARMD, resulting in severe macular edema
Diagnosis WET AMD
After a thorough dilated examination of the fundus with slit lamp
biomicroscopy, the following imaging studies are frequently performed
on many patients with signs and symptoms of exudative AMD:
• Color photography of the fundus
• Fluorescein angiography (FA) - Helps to identify and confirm the
source of CNV
• Optical coherence tomography (OCT) - Can identify soft drusen, RPE
detachments, subretinal and intraretinal fluid, CNV, and cystoid
macular edema; can accurately measure foveal and macular
thickness; and can demonstrate the integrity of the photoreceptor
and RPE layers
Management WET AMD
1. Antiangiogenic agents
Animal and clinical studies have established vascular endothelial growth
factor (VEGF) as a key mediator in ocular angiogenesis.Therefore, particular
attention has been focused on the development of pharmaceutical agents to
block or neutralize VEGF expression. The following agents, delivered via
intravitreal injection, have been proven effective in clinical trials:
• Pegaptanib sodium
• Ranibizumab
• Bevacizumab
• Aflibercept
2. Laser treatments
• Laser treatments include the following:
• Thermal laser photocoagulation - Until the advent of anti-VEGF
agents, ophthalmologists traditionally used thermal laser destruction
of CNV as the primary treatment of exudative AMD.
• Photodynamic therapy with verteporfin (PDT) - To avoid creating a
central, blinding scotoma when treating subfoveal CNV with thermal
lasers, clinicians turned to PDT; effective in some forms of CNV,
although its use is sometimes limited by cost.
• If left untreated, the neovascular membrane forms a big scar in the
macular area, resulting in a sudden decrease in central vision
• Choroidal neovascularization (CNV) is an advanced stage of wet
ARMD that can lead to the development of polypoidal choroidal
vasculopathy
• he condition progresses from drusen to the development of CNV,
whereby the choriocapillaries cross Bruch's membrane and spread
laterally within the planes of these lesions
Drusen
• Drusen are focal deposits of extracellular debris that typically form
between the basal lamina of the RPE and the inner collagenous layer
of Bruch's membrane
• generally round and yellowish in color
• These lesions, which are considered the hallmark of ARMD and are
characteristic of the aging eye and age-related maculopathy, can be
detected through various assays
• Drusen are classified as hard or soft, depending upon their borders
and the level of risk they confer on progression of ARMD
• Soft drusen are more commonly found in the macula and pose a
higher risk of ARMD development
• They are slightly larger than hard drusen and do not have well-
defined margins
• Hard drusen tend to be smaller and well defined. The distinct features
of the druse may give an indication of the stage of ARMD
• Drusen are known to contain lipids, carbohydrates, zinc, and at least
129 different proteins, including extracellular matrix
• The molecules trapped in drusen have varying roles, including the
processing of extracellular enzymes, the stigmata of formative
processes (e.g., extrusion or secretion of cellular materials), and
cellular invasion
• Charles Bonnet syndrome is a common side effect of vision loss in
people with AMD. However, it often goes away a year to 18 months
after it begins. In the meantime, there are things you can do to
reduce hallucinations. Many people find the hallucinations occur
more frequently in evening or dim light. Turning on a light or
television may help. It may also help to blink, close your eyes, or focus
on a real object for a few moments
Prognosis
• Prognosis dari degenerasi makula dengan tipe eksudat lebih buruk di
banding dengan degenerasi makula tipe non eksudat. Prognosis dapat
didasarkan pada terapi, tetapi belum ada terapi yang bernilai efektif
sehingga kemungkinan untuk sembuh total sangat kecil