The AMDF is a 501(c)(3) non-profit, publicly supported organization. Contributions are tax deductible.

American Macular Degeneration Foundation - Saving sight through research and education
About Us
Latest News
Help & Advice
How to Donate
AMDF Newsletter
Video Presentations
AMDF Bulletin Board
Care & Services Directory
What is Macular Degeneration?
What is Macular Degeneration?

Dry AMD

Wet AMD

Stargardt's

Examinations

Site Map

Home

"WET" MACULAR DEGENERATION

There are two basic types of macular degeneration: "wet" and "dry." Approximately 10-15% of the cases of macular degeneration are the "wet" (exudative) type.

In the "wet" type of macular degeneration, abnormal blood vessels (known as choroidal neovascularization) grow under the retina and macula. These new blood vessels may then bleed and leak fluid, causing the macula to bulge or lift up, thus distorting or destroying central vision. Under these circumstances, vision loss may be rapid and severe.

What the Patient may see—

Photo of seascape showing central vision loss with wet type macular degeneration.

With the "wet" type, the patient may see a dark spot (or spots) in the center of their vision due to blood or fluid under the macula. Straight lines may look wavy because the macula is no longer smooth. Side or "peripheral" vision is rarely affected. However, some patients do not notice any such changes, despite the onset of neovascularization.(1.) Therefore periodic eye examinations are still very important for patients at high risk.

For a video presentation describing what a person with macular degenration sees, click here (This video presentation requires Quicktime.)

Choroidal Neovascularization

There are two forms of choroidal neovascularization (CNV) that have been identified, "classic" and "occult." The classic form is well-defined and usually results in vision that is between 20/250 and 20/400, but it may be worse than 20/800. For eyes with the occult form, the average visual acuity is somewhat better, between 20/80 and 20/200. Occult lesions are not well-delineated and they have less leakage.(2.)

Once CNV has developed in one eye, whether there is a visual loss or not, the other eye is at relatively high risk for the same change. When all four risk factors—more than five drusen, large drusen, pigmental clumping and systemic hypertension—are present, the five-year risk of CNV in the second eye is 87%, whereas if none of these risk factors are present, the risk is 7%.(3.)

In addition, CNV may progress rapidly and any sudden change in central vision therefore requires a prompt examination after dilation of the eyes. The purpose of this exam is to find out whether the sudden loss of vision is due to leakage of blood vessels and which treatment may be appropriate.


Time-Lapse Animation of "wet" Macular Degeneration

Time-lapse animation showing development wet type macular degeneration.

Normal macula. Normal macula.
Abnormal new blood vessels grow under the macula. Abnormal new blood vessels grow under the macula.
The abnormal blood vessels bleed. The abnormal blood vessels bleed. As a result of the bleeding, the macula bulges. The damage to the macula causes central vision to be distorted or destroyed. Vision loss may be rapid and severe.



Until recently the only available treatment to seal these leaking vessels was with a laser. The earliest treatment was Laser Photocoagulation. This was followed by Photodynamic Therapy (PDT) with VisudyneŽ (a drug injected intravenously and used to help direct the laser to the affected area) and was not suitable for all types of lesions. The cost of one treatment averages about $3,000. The blood vessels may again begin to leak and further treatment may be required. The laser treatment itself may cause scarring. Researchers and physicians have looked for a follow-up to this treatment that might maintain vision for a longer period of time without repeated laser use. They are also looking for new therapies which would be effective for all types of wet AMD.

One line of thought stems from work done into cancer research and the causes of angiogenesis—the growth of new blood vessels. It was discovered that there is a protein in the eye which encourages the development of blood vessels called "vascular endothelial growth factor" (VEGF) and drugs are being developed to inhibit VEGF by trapping it or preventing it from binding with elements which will stimulate growth. Chemically synthesized short strands of RNA (nucleic acid) called "aptamers" prevent the binding of VEGF to its receptor.

Presently three types of VEGF inhibitors are in use: Lucentis, Macugen and Avastin. All are given by intraocular injection. A number of injections must be given over an extended period of time. If treatment commences early in the development of the disease, positive results have been shown in slowing progression and in some cases, improving visual acuity. Side effects of intravetreal injections may include:

  • Serious eye infection that may include eye pain, light sensitivity, vision changes.
  • Increased eye pressure
  • Retinal detachment
  • Vitreous floaters
  • Consult with your retinal specialist to make certain you understand what all the side effects might be.

Photodynamic Therapy with VisudyneTM

During April 2000, the FDA approved a new treatment, Photodynamic Laser Therapy, which uses a light-activated drug called VisudyneTM. This treatment for "wet" macular degeneration works through a non-thermal process which results in a selective destruction of the unwanted leaking vessels.(4.) The procedure seals off leaking vessels while leaving healthy ones intact and is believed to be a major improvement over previous laser treatments. In one large clinical trial, photodynamic therapy with VisudyneTM photosensitizer delayed or prevented loss of vision during at least one year follow up in patients with predominantly classic CNV lesions.(5.) Unfortunately, even the most successful treatments do not preclude reoccurrence, making multiple treatments likely. However, the rate of vision loss may be slowed down and some sight may be preserved.

Laser Photocoagulation

Between 1979 and 1994, the Macular Photocoagulation Study Group conducted a number of clinical trials that enrolled patients with CNV lesions in one or both eyes. Each affected eye was randomly assigned to either laser treatment or observation. For eligible eyes with CNV in extrafoveal, juxtafoveal and subfoveal locations, laser treatment reduced the risk of severe visual loss.(6.-8.)

There are three major limitations of laser photocoagulation treatments. First, not more than 10-15% of CNV lesions are small enough and sufficiently delineated by fluorescent angiography to be eligible for laser treatment. Second, even if laser treatment is initially successful, there is at least 50% chance that leakage will recur during the next two years. Many such recurrences are amenable to additional treatment if detected early, which means that patients need careful monitoring after the first treatment. Finally, at least half of patients post-treatment with sufficiently well-circumscribed CNV lesions still have some leakage beneath the center of the fovea. Laser treatment leads to immediate reduction in central vision in these patients with leakages, but with sufficient follow up, the extent of visual loss is less in laser treated eyes than in untreated eyes.(8.-9.) These existing laser therapies are limited in their effectiveness and may also lead to scarring of the macula and additional vision loss.

For a video presentation illustrating the development of macular degenration, click here (This video presentation requires Quicktime.)

References

1. AM Fine, Earliest symptoms caused by neovascular membranes in the macular. Arch Ophthal. 1986;104:513-4.

2. MG Maguire, Natural history. JW Burger, SL Fine, MG Maguire, eds. Age-related Macular Degeneration. St. Louis: Mosby: 1999;17-30.

3. Macular Photocoagulation Study Group. Risk factors for choroidal neovascularization in the second eye of patients with juxtafoveal or subfoveal choroidal neovascularization secondary to age-related macular degeneration. Arch Ophthal. 1997;115:741-7.

4. Miller, JW. Photodynamic therapy of experimental choroidal neovascularization using lipoprotein-delivered benzoporphyrin. Arch Ophthal. 1995;113:810-18.

5. Treatment of age-related macular degeneration with photodynamic therapy [TAP Study Group]. Photodynamic therapy of subfoveal choroidal neovascularization in age-related macular degeneration with verteporfin; One-year results of two randomized clinical trials-TAP Report. Arch Ophthal. 1999;117:1329-45.

6. Argon laser photocoagulation for neovascular maculopathy; 5 year results from randomized clinical trials. Arch Ophthal. 1991;109:1109-14.

7. Laser photocoagulation for juxtafoveal chorodial neovascularization; 5-year results from randomized clinical trials. Arch Ophthal. 1994;112:500-9.

8. Laser photocoagulation for subfoveal neovascular lesions of age-related macular degeneration; Updated findings from 2 clinical trials. Arch Ophthal. 1993;111:1200-9.

9. Visual outcome after laser photocoagulation for subfoveal choroidal neovascularization secondary to age-related macular degeneration: The influence of initial lesion size and initial visual acuity. Arch Ophthal. 1994;112:480-8.

American Macular Degeneration Foundation
P.O. Box 515
Northampton, MA 01061-0515
(413) 268-7660

Email
Privacy Policy