SIGNS AND SYMPTOMS
The visual symptoms associated with AMD depend on its severity and type. In general, the dry form (no subretinal choriodal neovascularization, exudation or hemorrhage) is less severe, producing a gradual, painless distortion or loss of central vision. Some patients complain of color distortion. Wet AMD (subretinal choriodal neovascularization, exudation and or hemorrhage) often produces severe central visual loss. Visual loss produced by wet AMD is often rapidly progressive.
Some of the clinical retinal signs of dry AMD include drusen of the posterior pole, granular clumping and disorganization of the RPE in the macular area, macular RPE hyperplasia and degeneration of the outer retinal layers with circumscribed areas of geographic atrophy of the RPE.
Some of the clinical retinal signs associated with wet AMD include hard and soft drusen, subretinal thickening secondary to classic or occult choroidal neovascularization (producing a grayish-green subretinal hue), subretinal, intraretinal or vitreous hemorrhage, subretinal and intraretinal exudation with serosanguinous fluid accumulation and fibrovascular scar formation (disciform scarring).
Wet AMD results when the macular RPE/Bruchs barrier is compromised by new, weak and leaky blood vessels that grow upward into the retina from the choriocapillaris. These occult (poorly defined) or classic (more easily defined) subretinal choroidal neovascular membranes may leak serosanguinous fluid causing RPE detachment, sensory retinal detachment, subretinal or intraretinal bleeding or fibrovascular, disciform scarring.
The management of patients with dry AMD begins with biannual eye examination, with dilated funduscopy. Home therapy, aimed at early detection, using a home Amsler grid may work to monitor the stability of suspicious or involved maculae. The elimination of potentially harmful ultraviolet light using UV coatings on spectacles and sunglasses may also reduce the risk of photochemical /oxidative damage to the retina for all patients.
Researchers have indicated that oral antioxidants like vitamins C and E and oral zinc may play a role in reducing retinal damage by terminating the chemical reactions initiated by free radicals, created by retinal metabolism. Multiple vitamins, oral zinc or products specifically designed for this purpose, such as Ocuvite and ICaps, are useful as a tool for slowing the progression of AMD.
The treatment for symptomatic wet AMD begins with a referral to the vitreoretinal specialist for intravenous fluorescein angiography. The Macular Photocoagulation Study (MPS) examined the efficacy of treating subretinal, extrafoveal (200 to 2,500 Ám from the center of the foveal avascular zone, juxtafoveal (1 to 200 Ám from the center) and subfoveal choroidal neovascular membranes with laser photocoagulation. Laser photocoagulation reduces the risk of severe vision loss in patients with definable subretinal choroidal neovascular membranes.
In cases where hemorrhage and exudate obscures the angiogram or the neovascular membrane is poorly defined by fluorescein angiography, indocyanine green angiography may offer an additional modality to determine if treatment is feasible. Unfortunately, the recurrence rate following treatment is approximately 50 percent. Most recurrences develop within the first year, making a three-month follow up schedule critical. The efficacy and effectiveness of surgical procedures for the removal of subretinal neovascular membranes are currently under investigation.
In cases where bilateral central visual acuity has been lost, low vision and vision rehabilitation specialists may be able to offer training or optical devices which improve patients quality of life. Macular translocation surgery has been performed with significant success and restored usable vision to patients with wet ARMD.
Other reports in this section
Eyelids & Eyelashes | Conjunctiva & Sclera | Cornea
Uvea | Vitreous & Retina | Optic Nerve & Brain | Oculosystemic Disease
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