Age-related macular degeneration (AMD), also known as age-related macular degeneration, is a pathologic aging change in the structure of the macula. The macula has the most specialized structure and function in the entire retina, and is where vision is most acute. In the early stage, due to the decreased phagocytosis and removal of retinal pigment epithelial cells (RPE), the residual vesicles of retinal pigment epithelial membranes that have not been completely digested and removed are retained in the cytoplasm of the basal cells and are discharged out of the cells and accumulate in the Bruch’s membrane, resulting in the formation of vitreous warts. These changes are most obvious in the macula, and vitreous warts can also be seen in elderly people with normal vision. However, in the middle and late stages of the disease, when the pathologic changes continue to worsen, Bruch’s membrane ruptures, and choroidal capillaries pass through the ruptured Bruch’s membrane to enter the sub-RPE or subretinal neuroepithelium, forming choroidal neovascularization (CNV), which is the most direct factor affecting visual acuity. Due to the structural abnormality of the wall of the neovascularization, leakage and hemorrhage of the vessels often occur, which in turn leads to hemorrhage and edema in the macula and triggers a series of changes that aggravate the loss of vision or even a sudden and significant loss of vision.AMD occurs mostly over the age of 50 years old, and its prevalence increases with age, making it an important cause of blindness in the elderly. Patients often have symptoms such as fixed dark shadows in front of their eyes, slow or sudden loss of vision, and distorted vision. Elderly people often think it is cataract, or people are getting old, vision slowly decreases and do not care, and even miss a good time for treatment. Therefore, once these symptoms should be seen as soon as possible. Etiology: The cause of the disease has not yet been determined. It is believed to be the result of a combination of factors, which may be related to heredity, chronic light damage, nutritional disorders, poisoning, immune diseases and other systemic diseases. Clinical manifestations: the disease is divided into dry and wet two types: 1, dry age-related macular degeneration, both eyes can develop at the same time, and the development is synchronized. This type is characterized by vitreous warts and progressive RPE atrophy: in the early stages, vision is mildly impaired and even remains normal or near normal for a long time. With time, vision slowly decreases, and small dense or fused yellow vitreous membrane warts are seen in the fundus, or there are atrophic areas of flaky gray retina. The atrophic areas are well defined, with scattered pigmented patches within them, and gold-foil-like reflections may also be seen. In general, atrophic degeneration is slow to develop and has a long course. There is a gradual migration between early and late stages, with variable time from early to late stages. Patients in this stage need regular follow-up and attention to protection from direct sunlight. 2.Wet age-related macular degeneration This type is characterized by the formation of choroidal neovascularization (CNV), causing a series of retinal exudation, hemorrhage, scarring and other changes. The patient suddenly has a significant loss of central vision, the degree of which varies greatly depending on the distance from the macular central concavity. In later stages, retinal exudates and hemorrhages are gradually absorbed and replaced by scar tissue, at which point the patient’s vision further decreases. Fundus examination reveals clumps or irregular pigmented plaques. In some cases, when the hemorrhage and exudate are replaced by scar tissue, the lesion does not end there, and new lesions will appear at the edge of the scar, and the process of retinal exudate, hemorrhage, resorption, and scarring occurs again. As this happens repeatedly, the scar tissue expands further and vision is greatly damaged. Therefore, it is essential for AMD patients to have long-term review and follow-up observation even during the stable period after treatment. Examination: Visual acuity, fundus photography, OCT, fluorescein fundus angiography, indocyanine green choroidography, OCTA and other ophthalmologic specialties. Treatment: 1. Oral antioxidant or herbal medicine Oral vitamin C, vitamin E, Zn, lutein, zeaxanthin can partially prevent free radical damage to cells. Once the lesion occurs, according to the patient’s disease dialectical treatment, taking auxiliary blood activation and other traditional Chinese medicines can help accelerate the absorption of retinal hemorrhage. 2.Anti-VEGF therapy Vascular endothelial cell factor (VEGF) plays a key role in the development of choroidal neovascularization (CNV). Anti-VEGF drugs, which bind VEGF isoforms, reduce vascular permeability and inhibit CNV formation. Anti-VEGF drugs are injected into the vitreous cavity under sterile conditions. At present, this treatment is the best first choice for the treatment of CNV caused by AMD at home and abroad. 3.Photodynamic therapy (PDT) is to inject a specific photosensitizer into the patient’s blood, when the drug circulates to the retina, 689nm laser irradiation is used to stimulate the photosensitizer, thus destroying the abnormal neovascularization, while there is no damage to the normal retinal tissue. It is somewhat effective, but there may be some loss of vision. It is often an option for combined treatment. In addition, in order to better cooperate with the treatment should also pay attention to:Control blood pressure, blood sugar, blood fat. Wear dark-colored glasses to reduce light damage. Prohibit smoking and minimize alcohol consumption. In order to reduce the possible risk factors of age-related macular degeneration in patients.