R E T I N A H E A L T H S E R I E S | Facts from the ASRS The Foundation

American Society of Retina Specialists

Committed to improving
the quality of life of all people
with retinal disease.

Age-Related Macular Degeneration SYMPTOMS

(AMD) is a deterioration of the retina and choroid that leads
to a substantial loss in visual acuity (sharpness of vision). In early stages, AMD may have no
AMD is the leading cause of significant visual acuity loss in symptoms at all. When the disease
progresses, the symptoms are:
people over age 50 in developed countries.
•D
 istortion (warping) of
Causes: The exact cause of AMD is unknown, but the condition develops as straight lines
the eye ages. There are 2 types of AMD: non-neovascular or dry AMD; and •A
 decrease in the intensity
neovascular or wet AMD. or brightness of colors
In early stages of dry AMD, the hallmark is drusen—pale yellow lesions As the macular degeneration
formed beneath the retina (Figure 1A). Drusen are usually harmless, but as they progresses, AMD symptoms include:
accumulate, dry AMD can progress. Atrophic areas (areas of atrophy or wasting) •A
 gradual or sudden loss of
in the retina also may develop; if the atrophic area is significant and with sharp central vision, or
borders, it is termed geographic atrophy (GA) (Figure 1B). •D
 ark, blurry areas in the center
of vision 
A B

W H AT I S T H E R E T I N A?

Figure 1
Dry AMD. A. Drusen (indicated by arrow). B. Geographic atrophy
Photo courtesy Anat Loewenstein, MD

T H E R E T I N A is a thin layer of
GA is the advanced
light-sensitive nerve tissue that lines
form of dry AMD,
the back of the eye (or vitreous)
which is frequently
cavity. When light enters the eye, it
associated with loss
passes through the iris to the retina
of central vision.
where images are focused and
In wet AMD, there is
converted to electrical impulses that
a sudden or gradual
are carried by the optic nerve to the
decrease in visual acuity,
brain resulting in sight.
blind spots in the center
of vision, and distortion
of straight lines. The
hallmark of wet AMD is
choroidal neovascular-
ization (CNV) (Figure 2).
CNV occurs when Figure 2
Wet AMD. Choroidal neovascularization (indicated by arrow).
abnormal blood vessels Photo courtesy Anat Loewenstein, MD
grow beneath the retina;
these can bleed or leak
and cause a distortion of
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AMD continued from previous page

the retina’s structure. Ultimately, the CNV can turn into a disciform scar that T H A N K YO U TO T H E
replaces the normal architecture of the outer retina and leads to permanent loss R E T I N A H E A LT H S E R I E S
of central vision. AUTHORS

Sophie J. Bakri, MD
Possible Risk Factors: Audina Berrocal, MD
• Age—the strongest risk factor • Family history of AMD Antonio Capone, Jr., MD
• Caucasian race • Cigarette smoking Netan Choudhry, MD, FRCS-C
Thomas Ciulla, MD, MBA
Possible risk factors: Pravin U. Dugel, MD
• Female gender • High blood pressure Geoffrey G. Emerson, MD, PhD
• Higher level of education • High cholesterol Roger A. Goldberg, MD, MBA
Darin R. Goldman, MD
• Light iris color • Sunlight exposure
Dilraj Grewal, MD
• Far-sightedness • Low dietary fish intake
Larry Halperin, MD
• Cardiovascular (heart) disease Vincent S. Hau, MD, PhD
Suber S. Huang, MD, MBA
Diagnostic Testing: Disease features related to AMD may be found in the Mark S. Humayun, MD, PhD
retina and in the layers beneath it. According to these abnormal findings, Peter K. Kaiser, MD
AMD is classified as dry or wet. M. Ali Khan, MD
Anat Loewenstein, MD
An AMD diagnosis is made by a clinical examination with a slit lamp and
Mathew J. MacCumber, MD, PhD
by using several types of imaging, including: Maya Maloney, MD
• Fluorescein angiography (FA) Hossein Nazari, MD
• Indocyanine green angiography (ICGA) Oded Ohana, MD, MBA
• Optical coherence tomography (OCT) George Parlitsis, MD
Jonathan L. Prenner, MD
Treatment and Prognosis: Wet-AMD treatment has been revolutionized in Gilad Rabina, MD
Carl D. Regillo, MD, FACS
recent years after the discovery of vascular endothelial growth factor (VEGF),
Andrew P. Schachat, MD
a family of compounds in the body. VEGF regulates the growth of abnormal
Michael Seider, MD
new blood vessels in the eye—known as neovascularization—that can lead to Eduardo Uchiyama, MD
wet AMD. Allen Z. Verne, MD
Anti-VEGF drugs have been developed to help stop neovascularization and Yoshihiro Yonekawa, MD
preserve vision for AMD patients. There are currently 3 anti-VEGF drugs:
EDITOR
• Avastin® (bevacizumab®) John T. Thompson, MD
• Lucentis® (ranibizumab®)
M E D I C A L I L L U S T R AT O R
• Eylea® (aflibercept®)
Tim Hengst
Wet AMD cannot be cured, but its progression may be blocked with the use
of intravitreal (in-the-eye) anti-VEGF injections. Local anesthetic eye drops
are given before the injections to numb the eye and minimize discomfort.
There are 3 anti-VEGF treatment regimens:
1. Pro re nata (PRN) or “treat and observe”—patients are treated with
three initial monthly injections, followed by treatment as needed.
2. “Treat and extend”—after 3 initial monthly injections, the time between
treatments is gradually increased until wet AMD is stabilized.
3. Monthly injections.

Before the first anti-VEGF drugs were introduced, wet-AMD patients were
treated with laser photocoagulation or photodynamic therapy (PDT).
Anti-VEGF drugs have greatly improved wet-AMD treatment since 2005;
patients today have a much better chance of maintaining their central vision
so they can read, drive, recognize faces, and live normal lives.
No treatment can prevent visual loss for patients with GA (the advanced
form of dry AMD). However, the Age-Related Eye Disease Studies (AREDS),
conducted by the National Eye Institute, have found that a nutritional supplement
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AMD continued from previous page

formula may delay and prevent intermediate dry AMD from moving to the
advanced form.
The AREDS supplement formula, which is widely available over the
counter, contains:
• Vitamin C • Lutein
• Vitamin E • Zeaxanthin
• Zinc

Although patients with either form of AMD can experience a severe decrease
in visual acuity, they will almost never be completely blind. 

Clinical Terms (appearing green within fact sheet text)

Choroid (pronounced CORE oid): The layer of blood vessels and connective tissue
between the retina and the white of the eye, also known as the sclera.
Choroidal Neovascularization (CNV): Growth of abnormal new blood vessels in the
choroid layer of the eye that grow under the retina and macula and disrupt vision.
Disciform scar: A scar that develops in the macula area of the retina resulting from
leakage and bleeding from abnormal blood vessels (neovascularization) in the eye.
Fluorescein angiography (FA): An imaging technique where a yellow dye called sodium
fluorescein is injected into a vein in the arm, allowing a special camera to record
circulation in the retina and choroid in the back of the eye. This test can be very useful
in diagnosing a number of retinal disorders.
Indocyanine green angiography (ICGA): A diagnostic procedure that uses a green dye
to illuminate blood flow in the choroid, which is a layer of blood vessels located between
the white of the eye (sclera) and the retina that supplies nutrients to the inner eye.
Laser photocoagulation: A surgical technique that uses a highly targeted laser light to
seal blood vessels and coagulate (clot) tissue.
Optical coherence tomography (OCT): A non-invasive imaging technique that uses light
to create a 3-dimensional image of your eye for physician evaluation.
Photodynamic therapy (PDT): A treatment for macular degeneration in which a
light-activated medicine (verteporfin) is injected into the bloodstream followed by
application of a cold laser which targets abnormal blood vessels growing in the macula
at the center of the retina.
Slit lamp: An instrument that combines a high-intensity light source with a microscope to
examine the external and internal structures of the eye, including the optic nerve and retina.

Copyright 2016 The Foundation of the American Society of Retina Specialists. All rights reserved.savingvision.org I 20 North Wacker Drive, Suite 2030, Chicago, IL 60606 | (312) 578-8760