These proceedings cause the RPE to degenerate, resulting in photoreceptor loss. As the photoreceptors disintegrate, the inner nuclear layer collapses and contacts Bruch's membrane, initializing the degeneration of the outer retinal layers. Some theorize that the mechanism of damage may be through ultraviolet radiation-induced oxidation and free radical formation within these structures. The disease is more common in individuals who have a family history of AMD, are of light complexion, in those who have a cardiovascular history, history of previous lung infection, hyperopia or decreased hand grip strength. It is typically more progressive in males.
Smoking is a significant risk factor.
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. 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. The treatment for symptomatic wet AMD begins with a referral to the vitreoretinal specialist for intravenous fluorescein angiography. Laser photocoagulation reduces the risk of severe vision loss in patients with definable subretinal choroidal neovascular membranes.