What is age-related macular degeneration? Age-related macular degeneration (AMD), also known as age-related macular degeneration (AMD), is a multifactorial eye disease associated with ageing. AMD is one of the major causes of severe vision loss in people aged 50 and older, and its prevalence increases with age. The dramatic loss of central vision caused by AMD can be a serious factor in a patient’s daily life and can eventually lead to blindness. Geriatric macular degeneration causes about 8.7% of the world’s blind people, and about 500,000 people become blind every year due to age-related macular degeneration, which is one of the top diseases causing blindness among adults worldwide and one of the four major blindness-causing diseases in China. With the gradual aging of China’s population structure, the prevalence of age-related macular degeneration will further increase. Therefore, AMD is attracting more and more attention in the world. Wang Hong, Ophthalmology Department, Qilu Hospital of Shandong University, Liangping County People’s Hospital, Deng Zongyong What causes AMD? The real cause of this disease is still unclear. The more recognized mechanism is due to the ischemia of choroidal capillaries in the macula, the rupture of vitreous membrane degeneration, and the decrease of pigment epithelium’s ability to nibble and digest the metabolic products of optic cells (outer segmental disc membrane), so that the residual vesicles of the disc membrane are deposited to form vitreous warts. In addition, choroidal neovascularization enters the subretina and exudation and hemorrhage occur. The inflammatory response to AMD causes cells and growth factors such as vascular endothelial growth factor ( VEGF is a vascular-derived, vasoactive, inflammation-stimulating and neuroprotective growth factor. VEGF bound to cell surface receptors activates a cascade of intracellular signaling systems that cause proliferation and migration of vascular endothelial cells. What are the different types of AMD? AMD is divided into two types: non-neovascular (dry), and neovascularization (choroidal neovascularization, CNV) (wet). Dry AMD accounts for about 80%-85% of patients and generally does not result in significant vision loss, with mild blurred vision as a common symptom. Wet AMD accounts for about 15% of patients and is characterized by neovascularization under the pigment epithelium. The strength of neovascularization is poorer than that of normal vessels, so leakage and bleeding can easily occur, causing recurrent edema and eventually scar formation, resulting in permanent blindness. The main symptoms are a sharp loss of central vision and blurred vision. It is possible that within three or two years, the visual acuity decreases to less than 0.1. It accounts for 90% of cases of complete loss of vision. Therefore, aggressive treatment is advocated for wet AMD. How many stages of wet AMD can be classified? Wet AMD is generally divided into early, intermediate and late stages according to the course of the disease, (1) Early stage (pre-disciform degeneration) with significant loss of central vision, the degree of which varies depending on whether the central fossa is involved. The central comparative dark spot can be detected at the corresponding place with the lesion. (2) Middle stage (mutation stage) The main feature of this stage is the formation of plasma or/and hemorrhagic detachment of the pigment epithelium and/or neuroepithelium due to leakage of neovascularization in the macula. Visual acuity decreases sharply. (3) Late stage (repair stage) The exudate and hemorrhage are gradually absorbed and replaced by scar tissue. Further visual impairment occurs. Funduscopic examination reveals a slightly elevated mass or formation of irregular white plaques (reddish-yellow in the course of hematoma resorption). The plaque is located below the retinal vessels. Hemorrhagic and pigmented spots are often visible on the surface of the plaque or at its edges. In some cases, when the hemorrhage and exudation are replaced by scarring, the lesion does not end there, but new neovascularization appears at the edge of the scar, and the process of exudation, hemorrhage, resorption, and scarring is repeated. This process is repeated, causing the scar to expand further. Who is at risk for AMD? AMD occurs in middle-aged and older people over the age of 50, and its risk increases with age. Women have a higher risk of AMD than men; smokers have a multi-fold increased risk of AMD compared to non-smokers; studies have shown a correlation between obesity and progression from early to mid-stage AMD to advanced AMD; and people with a family history of AMD have a higher risk of developing the disease. What are the manifestations of AMD? 1, early visual deformation, vision loss, late severe visual impairment; 2, fundus manifestation: dry: central reflection is unclear, scattered yellow dotted vitreous warts (druscn), macular area pigment disorder, like pepper salt or gold foil-like appearance; wet: in addition to the atrophy type performance, but also visible exudation, hemorrhage, the formation of yellow-white, gray-black or gray-blue disc-like elevation, the late source of the disease is white mechanized scar and pigment mass or residual partial hemorrhage. 3, fundus fluorescence angiography: window-like defects of pigment epithelial atrophy; exudative type with neovascular membrane under the pigment epithelium and the resulting hemorrhage of obscured fluorescence, strong fluorescence of leakage; translucent fluorescence of vitreous warts or residual fluorescence of late contrast. How to diagnose AMD? 1.Mostly develops in older people over 50 years old, the older the age, the higher the incidence. 2.Deformation of vision, loss of vision or obvious visual impairment occurs successively in both eyes. 3.The fundus examination has more obvious vitreous warts and typical physical signs. 4.Fluorescence angiography of the fundus can make a clear diagnosis. How to treat AMD? Before 2006, the treatment of wet age-related macular degeneration was almost helpless in the world, mainly relying on photodynamic therapy and laser to stabilize the disease, which is difficult to improve vision and easy to recur. However, in recent years, Anti-VEGF therapy has been recommended by several international clinical guidelines as the first line of treatment for age-related macular degeneration, which can not only stop the progression of the disease, but also improve the visual acuity. 1.Non-surgical treatment Laser photocoagulation therapy: The traditional method for wet AMD is laser photocoagulation therapy. The specificity of macular area has great limitation on photocoagulation. Photocoagulation will destroy the healthy tissues around the lesion and aggravate the damage of vision, so it is only suitable for a small proportion of patients whose neovascularization is far from the center of the macula. Photodynamic therapy (PDT): A photosensitizer called vetiporfin is injected intravenously into the neovascularization of the eye, and then a beam of light of a special wavelength is shone into the diseased area of the eye. This light activates the drug in the neovascularization, and the activated drug destroys the neovascularization, thereby delaying vision loss. Photodynamic therapy for AMD is selective and generally does not damage the healthy tissue surrounding the lesion, but it is not significantly effective for microscopic typical CNV where the typical lesion accounts for less than 50% of the lesion area. Photodynamic therapy can control the progression of the lesion and slow down the rate of vision loss, but it cannot completely stop the loss of vision. The disease may recur after treatment, requiring repeat treatment. Intravitreal injection of anti-VEGF therapy is another new treatment for AMD after photodynamic therapy. The representative drug is ranibizumab. This method blocks the action of intraocular vascular endothelial growth factor and promotes the atrophy of subretinal neovascularization. After treatment, macular edema is improved and neovascularization is somewhat controlled. This method usually requires several injections. 2.Surgical treatment When macular hemorrhage is large or vitreous hemorrhage cannot be absorbed, vitrectomy or retinal microsurgery can be performed to remove the accumulated blood. What is the scope of application of vitreous cavity injection of anti-VEGF drugs? (1) Macular edema caused by various reasons (including diabetic macular edema, macular edema caused by various diseases such as post-cataract surgery or post-uveitis;) (2) Choroidal neovascular membrane formation caused by various reasons (including age-related macular degeneration, highly myopic macular degeneration, mid-bleed, etc.); (3) Retinal neovascularization (such as diabetic retinopathy, venous obstruction, retinal perivasculitis, Coat’s disease, choroidal osteoma, choroidal hemangioma, etc.); (4) retinal vein obstruction; (5) neovascular glaucoma and other diseases. What is the safety of vitreous cavity injection of anti-VEGF drugs? Ranibizumab (Lucentis) vitreous injection is relatively safe, but like other intraocular injections, there is a risk of endophthalmitis and retinal detachment and vitreous hemorrhage. Therefore, attention must be paid to the aseptic operation during injection, and the drug should be reviewed in the first week after administration to provide timely treatment in case of serious complications. Local reactions after drug administration mainly include: conjunctival hemorrhage, eye pain, and temporary increase in intraocular pressure. Incidence of serious complications: infectious endophthalmitis (0.7%), severe uveitis and vitreous hemorrhage (0.4%), retinal detachment (0.4%).