Age-related macular degeneration, also known as “age-related macular degeneration,” is a multifactorial fundus disease associated with aging. The older you are, the higher the prevalence. It does not usually cause pain in the eye, but the dramatic loss of central vision caused by it can be serious to the patient’s daily life and can eventually lead to blindness.
Age-related macular degeneration is one of the leading causes of severe vision loss in people aged 50 and older, and is one of the leading diseases causing blindness in adults worldwide. According to a study by the World Health Organization, age-related macular degeneration accounts for about 8.7% of the world’s blind, and about 500,000 people go blind every year due to age-related macular degeneration. The results of a survey conducted by Zou Haidong and others in China showed that the prevalence of age-related macular degeneration in people over 50 years old was 15.5%. Among them, wet age-related macular degeneration accounts for 11.9%. According to the population data of the United Nations, the number of people over 50 years old in China was close to 300 million in 2005, according to this ratio, the total number of patients with age-related macular degeneration over 50 years old in China should be close to 40 million. Thus, with the aging of the population, the prevalence of age-related macular degeneration will increase year by year, and the consequent public health problems cannot be ignored.
Pathogenesis
The real cause of this disease is still unclear, but the more recognized mechanism is due to the macular choroidal capillary ischemia, vitreous membrane degeneration rupture, pigment epithelium to the metabolic products of the optic cells (outer segment disc membrane) nibble digestion ability decreased, so that the disc membrane residual vesicles deposited to form vitreous warts. In addition, choroidal neovascularization enters the subretina and exudation and hemorrhage occurs.
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, causing proliferation and migration of vascular endothelial cells.
Susceptible population
AMD occurs in middle-aged and elderly people over 50 years of age, and its risk increases with age. The risk of AMD is higher in women than in 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; people with a family history of AMD have a higher risk of developing the disease.
Classification
AMD is divided into two types: non-neovascular (dry) and neovascular, i.e. choroidal neovascularization (wet). Dry AMD, which accounts for about 80%-85% of patients, generally does not result in significant vision loss, with mild blurring of vision as a common symptom. Wet AMD, which accounts for about 15% of patients, is characterized by a dramatic loss of central vision and blurred vision. It is possible to have vision loss below 0.1 within three or two years. It accounts for 90 percent of cases of complete loss of vision.
Dry age-related macular degeneration can progress and cause loss of vision without turning into wet age-related macular degeneration. Of course, dry age-related macular degeneration can suddenly become wet age-related macular degeneration, even in early age-related macular degeneration. There is no way to know if or when dry age-related macular degeneration will become wet age-related macular degeneration.
Clinical manifestations
1, early visual deformation, vision loss, late severe visual impairment;
2, fundus manifestation: dry: central reflection is unclear, scattered yellow dotted vitreous warts (druson), macular pigment disorder, like pretzel-like or gold foil-like appearance; wet: in addition to 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 pigmented mass or residual part of the hemorrhage.
3, fundus fluorescence angiography: window-like defect 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 membrane warts or residual fluorescence of late contrast.
Diagnosis
1, mostly in older people over 50 years of age, 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.
Treatment
Before 2006, the treatment of wet age-related macular degeneration was almost helpless worldwide, 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 treatment for age-related macular degeneration, which can not only stop the progression of the disease, but also improve the vision.
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.