Age-Related Macular Degeneration
The leading cause of visual loss in the United States' senior population is age-related macular degeneration. This condition causes deterioration and possible eventual loss of central vision. There are several risk factors for macular degeneration. Some of these risk factors cannot be modified, such as age or genetics. Other risk factors can be reduced, such as smoking, poor diet, and sunlight exposure.
The most common type of macular degeneration is the "dry" form. In this type of macular degeneration, there is progressive thinning (atrophy) and deposition of waste products (drusen) in the retina. Although vision loss can occur, it is usually minimal and only slowly progressive.
The "wet" form of macular degeneration is fortunately only responsible for 10% of macular degeneration cases. In this condition, abnormal blood vessels are stimulated to grow beneath the retina. Leakage and bleeding from these abnormal vessels can destroy central vision.
Because the wet form of macular degeneration is often devastating, we are searching for ways to prevent it from occurring. The Complications of Age-Related Macular Degeneration Prevention Trial (CAPT) is a National Institutes of Health multicenter study addressing the question of whether or not low energy laser treatment (laser treatment of drusen) to patients with certain forms of asymptomatic dry macular degeneration will prevent visual loss and/or the emergence of the wet form of macular degeneration. The Retina-Vitreous Center is one of only 20 retinal practices nationwide able to enroll patients into this important study.
The Retina-Vitreous Center is also enrolling patients with a particular form of macular degeneration characterized by basal laminar drusen into a study sponsored by the National Eye Institute. This is a natural history study designed to learn more about the prognosis of patients with this condition.
The Age Related Eye Disease Study (AREDS) has now shown that vitamin supplementation is important in slowing the progression of macular degeneration in patients with moderate dry macular degeneration or patients with more advanced disease in one eye only. The most benefit was derived from a combination of antioxidants and zinc, in the following daily doses:
Beta Carotene 15 mg Vitamin C 500 mg Vitamin E 400 IU Zinc 80 mg (as zinc oxide) Copper 2 mg (as cupric oxide)
Consult with your physician, however, before taking such supplements.
Metamorphopsia (distortion) is the usual presenting first symptom when wet macular degeneration begins and thus this symptom should be evaluated promptly. Fluorescein or ICG angiography is used to identify the presence and location of any abnormal new blood vessels. Based on this information, laser treatment is often used to eliminate them.
When treatment is necessary, there are various types of laser photocoagulation which might be used:
- Conventional ("hot") laser treatment coagulates blood vessel membranes. The vision in the area of treatment is permanently affected, and recurrences are common
- Photodynamic Therapy (PDT, or "cold" laser) involves the intravenous injection of a drug, Visudyne, which accumulates in the blood vessel membranes. A low-intensity laser is then used to activate the drug and close the blood vessel membrane. There is no significant damage to normal tissue, but the blood vessels tend to re-open, and repeated treatments are often necessary
- Transpupillary Thermotherapy (TTT, or "warm" laser) uses a laser to warm the abnormal blood vessel membrane. This may cause the membrane to regress
Surgery is also recommended in some cases of macular degeneration. Patients with significant hemorrhage beneath the retina may require surgery to displace or remove the blood. Submacular surgery (surgery to remove blood vessels beneath the retina) and macular translocation (surgery to move the macula to a more healthy location) are sometimes performed in patients with blood vessel growth beneath the center of the macula.
A new treatment for wet macular degeneration involves the injection of Macugen, a medication recently approved by the FDA, through the eye wall into the vitreous cavity. Macugen is injected at 6 weeks intervals and has been shown to reduce the risk of visual loss for all forms of choroidal neovascularization. There are certain risks associated with the intraocular injections, such as infection, but the rate of major complications is low and the injections are generally well tolerated. A similar drug, Lucentis, is currently undergoing phase 3 testing in a multicenter clinical trial, in which The Retina-Vitreous Center is involved. These medications inhibit the growth factors which cause choroidal neovascularization.
Other novel medications are also being investigated for the treatment of wet macular degeneration. Cand5, produced by Acuity Pharmaceuticals, is in Phase II clinical testing at just a few locations nationwide, and the Retina Vitreous Center is actively recruiting patients for this trial. This drug also inhibits the main growth factor involved in choroidal neovascularization, VEGF, but through a unique intracellular mechanism that theoretically might prove more effective that competitive inhibition. The drug is delivered via intraocular injection. Genaera Pharmaceuticals has produced yet another investigative drug, squalamine, which is delivered intravenously and systemically rather than through a local injection in the eye. First discovered in sharks, squalamine has been found to inhibit new blood vessel growth in tumors, and may inhibit choroidal neovascualrization as well. The Retina Vitreous Center is a participating study center in the squalamine trial.
Steroids injected into the eye may also have an inhibitory effect on choroidal neovascularization, and are recommended in certain situations. While intravitreal Kenalog (triamcinolone) is essentially an investigational treatment option, the results of this treatment so far are encouraging. The Retina Vitreous Center is also enrolling patients for the multicenter VISTA trial, which evaluates the efficacy of Visudyne photodynamic therapy with versus without intraocular steroid injection. Our physicians were involved in a Phase III study of Retaane (anecortave acetate), a steroid compound which significantly inhibits neovascularization. The trial has been completed, but the results proved somewhat disappointing. Anecortave acetate is injected beneath the tissues surrounding the eye, but not into the eye itself. The trial compared anecortave acetate to conventional photodynamic therapy and did not prove that anecortave was as effective as photodynamic therapy. Future study results may still demonstrate a role for this drug; in particular, perhaps, in patients with dry macular degeneration in an effort to prevent the development of choroidal neovascularization in the first place.
Another clinical trial in which we are presently treating subjects involves the use of photodynamic therapy (PDT) with Visudyne for occult subfoveal choroidal neovascularization (the VIO Study). PDT is presently only approved by the FDA for use in patients with so-called "classic" choroidal neovascularization, but preliminary studies of this treatment suggest that it is also beneficial for "occult" disease. This study aims to gather more data in an effort to clarify this benefit.
Despite our best efforts, many patients with macular degeneration and other retinal diseases are left with poor vision. For those patients, our Low Vision Center (located at the New Brunswick office) can be utilized. Special lenses and optical devices can be adapted to enable the patient to optimize their visual abilities.
Macular Hole
Macular hole is an abnormal defect in the central part of the retina. Unlike retinal tears which occur in the peripheral retina, macular holes are usually not precursors to retinal detachment. A macular hole looks like a round punched-out defect. Because of its location, this type of retinal hole can cause severe central vision loss. The normal retinal tissue which should fill the hole is usually not missing, though; it is merely spread out to the edge of the hole. Surgery can close the hole, and allow that tissue to return to a normal position, improving vision. Imagine pushing a pencil through a screen; the wires making up the screen are pushed aside, not punched out. The wires may be pushed back into their normal position to repair the screen. Although trauma or disease can cause macular holes, they are usually seen as an age-related manifestation of an abnormality of the vitreous-retinal interface. For unknown reasons, they occur more frequently in women than in men.
Surgery is necessary for the treatment of most macular holes. Macular hole surgery consists of a vitrectomy (removal of the vitreous gel) and filling of the vitreous cavity with a mixture of air and gas. The patient is then asked to remain in a face-down position for 1-2 weeks following this surgery, to allow maximum air/gas contact with the macula. Usually, the intravitreal air/gas spontaneously absorbs from the eye within 6-8 weeks following the operation. In most cases, a macular hole can be closed in this fashion with at least partial restoration of central vision
Macular Pucker
Macular Pucker
Macular pucker is caused by a transparent membrane of scar tissue that grows over the surface of the central retina. The eventual contraction and shrinkage of this membrane can wrinkle and distort the underlying macula, impairing central vision. Macular puckers usually arise from age-related changes in the vitreous gel but can result from any type of eye injury, inflammation, disease, or surgery.
Treatment is not necessary if symptoms are mild. However, if there is significant metamorphopsia or visual loss, vitrectomy may be performed. During this procedure, after the vitreous gel is removed, the membranous tissue that is causing the macular distortion is peeled off the retinal surface and removed from the eye.
