Senile macular degeneration is also called age-related macular degeneration or aging macular degeneration. There is no significant relationship between the onset of the disease and gender and race. Both eyes are affected at the same time or successively, depending on the clinical manifestations, divided into two types: atrophic and exudative, the former is more common and the latter is only 1/10-15 of the former.
What is the cause of age-related macular degeneration?
The cause is not yet determined and may be related to genetic chronic photodamage, nutritional disorders, toxic immune diseases, cardiovascular system, respiratory system and other systemic diseases, or may be the result of a combination of factors.
The main manifestation of this disease is the aging change of macular structure, which is mainly due to the decrease of phagocytosis and digestion ability of retinal pigment epithelial cells to the outer segment of the optic disc membrane. There are four types of vitreous warts: hard, soft, fused, calcified, and vitreous warts are also seen in elderly people with normal vision, but the secondary pathological changes that occur as a result of these changes lead to macular degeneration.
What tests should be done for age-related macular degeneration?
To understand the whole picture of the crystal, the examination should be conducted in a dark room after the pupil is fully dilated as follows.
1.Focal illumination examination method: using direct light to see if there is clouding and dislocation of the crystal.
2.Iris projection method: projecting a thin light at 45º from the pupil margin obliquely to the crystal if the crystal is cloudy at the core and there is a crescent-shaped transparent area between the cloudy area and the pupil margin the heavier the shadow the narrower the shadow if the crystal is all cloudy the crescent-shaped shadow disappears completely.
3.Checking glasses thorough illumination method: put the light into the pupil area when normal, a uniform red shadow such as crystal or refractive interstitial clouding can be seen in the red shadow with black dots or black lumps examination can make the patient turn the eye to see whether the black shadow move or not to understand the site of clouding;.
4, slit lamp examination method: slit lamp for optical section examination from front to back can be seen many light and dark hierarchical structure representing different periods of the lens nucleus each level of transparency is not completely consistent among which the front surface of the adult nucleus of the former capsule and the post-embryonic surface is clearer.
What are the manifestations and how to diagnose age-related macular degeneration?
The disease is divided into two types: atrophic and exudative, as mentioned above, and it has been observed that atrophic can be transformed into exudative, so it is considered necessary to classify the types.
1, atrophic senile macular degeneration (atrophic also known as dry or non-exudative both eyes often develop simultaneously and synchronously with the clinical course and performance of senile hereditary macular degeneration (i.e. Haab disease) whether it is the same disease because both occur in the elderly family survey is difficult to determine. This type is characterized by progressive pigment epithelial atrophy and is clinically divided into two stages.
(1) early stage (preatrophy preatrophic stage): mild impairment of central vision or even remain normal or near normal visual field for a considerable period of time can be detected 5 to 10 º central disc-like darker dots with cyan yellow visual markers more easily detected 180 º line static visual field examination 0 º 5 to 10 º on each side of the visual sensitivity decreased Amsler square check is often positive occasionally with macroglossia or microsopia.
The macula has a relatively dense hard vitreous warts of different sizes, some of which fuse with each other to form small flakes between the vitreous warts, mixed with flaky pigmented depigmented spots with a peppery appearance. The halo (lantern phenomenon) indicates the presence of superficial detachment of the pigment epithelium. The fluorescence spot strengthens in the middle stage and gradually fades in the late stage, indicating that there is no neovascularization under the pigment epithelium or it is not thin enough to be visible (hidden neovascularization).
(2) Late stage (atrophic stage): there is a serious impairment of central vision with a false absolute central dark spot and a dense or fused vitreous warts and a large light gray atrophy area under the examiner’s eye, and the boundaries of the atrophy area become clear.
The fluorescence contrast shows strong fluorescence in the atrophic area early and fades with the background fluorescence. The fluorescence spot does not expand during the whole contrast process, suggesting translucent fluorescence due to pigment epithelial atrophy, but in some cases, the strong fluorescence spot and weak fluorescence spot appear simultaneously in the atrophic area, indicating that there is choroidal capillary atrophy and occlusion in addition to pigment epithelial atrophy.
Atrophic degeneration has a slow onset and long course, and it is difficult to separate the early and late stages of the disease from each other, and because of the individual differences, the time from the early stage to the late stage varies, but the degree of lesions in both eyes is basically symmetrical.
2.Exudative senile macular degeneration (exudative senile macular degeneration) Exudative is also called wet, that is, Kuhnt-Junius called senile disciform macular degeneration (senile disciform macular degeneration) This type is characterized by the presence of active neovascularization under the pigment epithelium. This type is characterized by active neovascularization under the pigment epithelium, which causes a series of exudative hemorrhagic scarring changes clinically in three stages.
(1) Early stage (pre-disciform stage): the central vision is obviously reduced and its degree varies depending on whether the central fossa is involved or not Amsler square is positive and the central dark spot can be detected at the corresponding place of the lesion.
The macula has dense vitreous warts of varying sizes under the examiner’s eye, mainly soft and fused with each other, while pigmented and depigmented spots can be seen from time to time, some pigmented spots surround the vitreous warts in a halo-like pattern, and the central fossa reflection is faint or disappears. The difference between the two is that the fluorescence spot of the former is enlarged during the whole process and the latter is not.
(2) middle stage (evolutionary stage): the main characteristics of this stage are the macula due to neovascular leakage to form the pigment epithelial layer and/or neuroepithelial layer plasma or/and hemorrhagic detachment sharp loss of vision under the examiner’s eye in addition to the aforementioned early changes plus a wider range of dark round or round-like lesions and slightly elevated so that the entire lesion area is grayish mottled some Some cases also murmur with dark red hemorrhagic spots slit lamp microscopy plus anterior microscopy photomicrographic examination reveals subcortical or/and subneuroepithelial plasma exudate on the pigment in the same location as the lesion further development in the deep retinal layers appear yellowish-white exudate exudate either in uniform patches; some in clusters of varying intensity; some within the lesion; some around the edge of the lesion in an irregular ring or brow moon shape (Coats reaction) In severe cases, hemorrhage may lead to subepithelial or neuroepithelial dark red or even gray-brown hematoma; sometimes it may penetrate the inner border membrane into the vitreous and form vitreous hemorrhage fluorescence in the early stage of the lesion, and then lace-shaped or wheel-shaped fluorescence may appear, suggesting the presence of active neovascularization. The fluorescence in the detached cavity is generally uniform and consistent, but when accompanied by pigmentation or hemorrhage, the fluorescence in the corresponding area is obscured by the rupture of the neovascularization, which is severe and results in the formation of a large hematoma as seen under the aforementioned microscope. In the late stage of fluorescence masking imaging, one to two gradually increasing and expanding fluorescent spots (called hot spots) can sometimes appear in the area of such fluorescence masking, proving the existence of subretinal neovascularization.
(3) Late stage (reparative stage): the exudate and hemorrhage are gradually collected and replaced by scar tissue, at which time the visual acuity is further impaired and the fundus examination shows a slightly elevated concordant mass or an irregular white plaque (reddish-yellow in the process of hematoma absorption) located below the retinal vessels. In some cases, when the hemorrhage and exudate are replaced by scar, the lesion does not end there, but new neovascularization appears at the margin of the scar and the scar undergoes the process of exudate and hemorrhage resorption again, and so on, further enlarging the scar. Gradually expanding and enhancing fluorescence spot exudative age-related macular degeneration in both eyes with a time interval of less than five years.
What diseases are easily confused with age-related macular degeneration?
However, in the early stage of the disease, especially in the atrophic type, it is important to distinguish it from the age-related vitreous warts that appear in the eyes with normal vision.
The most reliable way to differentiate the exudative form of hematoma from choroidal melanoma is by fluoroscopy, in which the background fluorescence is obscured and the hematoma appears as a large nonfluorescent area of melanosis due to leakage of neovascularization within the disease.
The exudative type has exudation and hemorrhage in the macula of one eye into the mutation phase, especially in the younger age group, and should be distinguished from central exudative chorioretinitis, in which inflammatory cellular clouding can be seen in the vitreous humor of the posterior part of the eye without vitreous warts.
How should age-related macular degeneration be treated?
Since the cause of this disease is still unclear, there is no effective treatment and fundamental preventive measures. In recent years, most scholars advocate that laser photocoagulation of neovascularization should be performed early for exudative patients to avoid deterioration of the disease. In addition to argon laser, krypton laser, Nd:YAG laser, dye laser, etc. can be selected according to the location of neovascularization near the amount of pigment with or without bleeding cover, etc. Laser photocoagulation is only to close the existing neovascularization and can not prevent the formation of new neovascularization is a symptomatic treatment, while a slight overdose of laser itself can make the choroidal neovascularization must be vigilant.
Anti-aging and circulation improvement herbs have a better effect on the atrophic type of this medicine and have a role in preventing the recurrence of exudative scar repair and the development of the disease in the other eye.
In recent years, the relationship between zinc and retinopathy has been emphasized. Zinc is highly abundant in the eye tissue, especially in the retinal pigment epithelium and choroid, and is involved in many enzymes such as vitamin A1 dehydrogenase peroxidase, etc. Newsonc et al. believe that internal administration of zinc can prevent the development of macular degeneration. The use of vitamin CE as a hydroxyl scavenger to prevent free radical damage to visual cells can also be tried.
How to prevent age-related macular degeneration?
As there is no specific treatment for this disease, some people think that internal zinc can prevent the progression of macular degeneration, while antioxidants such as vitamin CE can prevent the damage of free radicals to the cells and protect the retinal cells as a retinal tissue nutrient.
According to Xinhua News Agency, a professor at the Human Nutrition Research Center in Boston recently gave eight elderly women strawberry and spinach extracts and found that each had a “potent antioxidant activity effect”-they could increase their body’s antioxidant capacity by 20%. This is equivalent to consuming 1250 mg of vitamin C.
Spinach and strawberries are both highly nutritious fruits and vegetables, and are among the top producers of the antioxidants vitamin C and vitamin E. Antioxidant vitamins C and E protect the body’s cell membranes from oxidative damage and scavenge metabolic “waste” such as oxygen free radicals in the body; prevent or reduce degenerative aging of organs due to the deposition of “lipofuscin” in internal organs. In 3.5 ounces (1 ounce equals 28.3 grams) of grass mold pulp contains 1270 mg of vitamin C and is rich in vitamin E.
Strawberries and spinach are also rich in folic acid, which can prevent “nutritional macrocytic anemia” (macrocytic anemia) and itchy or bleeding skin. Spinach contains flavonoids that prevent macular degeneration in the eyes of the elderly, thus slowing down the degeneration and aging of the macula that leads to blindness or vision loss.
In terms of how to eat strawberries and spinach, experts suggest that it is best to reduce the processing. Seniors can make a little strawberry jam and canned strawberries during the peak of the summer season. Put freshly cooked strawberries (more water for canning, less water for sauce) directly into clean, sealed glass jars for long-term storage. Spinach must be cooked before eating, you can make more fried spinach and spinach soup.
Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly in developed countries , and with the accelerating trend of population aging, it has now also become one of the four major blinding diseases in the elderly in China E2].The exact cause of AMD has not been determined yet, and it is likely to be the result of cross-reactivity of multiple factors, such as. genetics, light, social factors, nutritional factors, toxic damage, immune response and smoking . Lutein, as a high-energy blue light filter and antioxidant, may play a role in protecting the macula and retina from photodamage. This article provides a review of lutein and the prevention and treatment of AMD.
Lutein
Chemical properties: Lutein (3,3-dihydroxy-a-carotene) is the predecessor of vitamin A. The molecular formula is C40H5602, and the relative molecular mass is 568.85. Only one isomer exists in nature, namely zeaxanthin (3,3-dihydroxy-B-carotene). Lutein is widely found in various vegetables, fruits and flowers, especially in kiwifruit, yellow corn and egg yolk, and also in some fish and human plasma and milk juice. It can be separated and extracted by membrane separation technology, drying method, high performance liquid chromatography and its modification method, luteolin ester extraction method, etc.
Absorption and metabolism: Mammals cannot synthesize lutein on their own and must obtain it from vegetables and fruits. Fatty diet can stimulate the secretion of bile to emulsify fat and promote the absorption of lutein. Lutein is absorbed from the small intestine and, like lipids, passes through the duodenum in the form of celiac particles and is finally transported to the liver. In the liver, it is either stored or incorporated into very low density lipoproteins in the body plasma. The FDA approved lutein as a food supplement for use in food and beverages as early as 1995 to enrich its nutritional value.
Dietary lutein is rapidly and effectively absorbed by the body. Under normal dietary conditions, the concentration of lutein in human plasma is 0.08-0.35 ug/ml. 16 hours after oral administration of a single preparation of lutein, the plasma concentration of lutein reaches a maximum, and continuous supplementation with 10 mg/d lutein for 18 days will result in a continuous increase in plasma lutein content to 1.4ug/ml. Lutein is absorbed and distributed in many organs of the body to perform its biological functions. The level of lutein in the blood can be used as an indicator of a healthy diet and the absence of inflammation.
Epidemiological studies have found that eating large amounts of carotenoid-rich foods, especially those rich in lutein, can prevent AMD. a clinical study of lutein supplementation in patients aged 60-81 years with age-related retinal macular degeneration at the Centre for Eye and Neuroscience Research, University of Manchester, UK, showed that after l5 weeks of lutein supplementation, the pigment content of the retinal macula increased significantly and The damaged retinal tissue was repaired. This indicates that lutein supplementation has a significant improvement effect on age-related retinal macular lesions, at least early ones.
In many patients with localized retinal atrophy, the central macular recess is well preserved, consistent with the densest macular pigment in that area. weiter studied patients with circumferential macular lesions and found that the extent of uninvaded lesions was consistent with the spatial distribution of macular pigment, inferring that macular pigment helps protect the central macular recess. Autopsy results also confirmed a direct relationship between low lutein content (macular pigment concentration) in the eye and AMD prevalence, with AMD patients having significantly lower levels of lutein in their eyes than non-AMD patients.
Individual differences in lutein are consistent with risk factors for AMD. High macular pigment density is associated with fewer risk factors for the development of AMD, and vice versa for the development of AMD. For example, light iris is a high risk factor for AMD, and light iris patients are usually associated with low macular pigment density. tomany et al. found that brown iris patients were at a lower risk for retinal pigment epithelium (RPE) loss and AMD than blue iris patients. The protective effect of iris color may be that such individuals have more tissue melanin, which prevents exposure of the retina to sunlight and reduces direct photodamage, which in turn reduces the incidence of AMD. This can also be explained by the higher prevalence of AMD in whites than in other people of color. In addition, smoking and heavy beer consumption can increase the prevalence of severe AMD.
There are two main carotenoids in the macula of the retina: lutein and its isomer zeaxanthin. The lutein family is now thought to improve visual acuity and protect the central retina by improving the aberrant effect. This may be based on two roles.
(1) As a high-energy blue light filter, lutein accumulates mainly in the Henle fiber cell layer consisting of many photoreceptor neuronal axons, which overlie the photoreceptors. Lutein weakens blue light before it reaches the photoreceptors and the retinal pigment epithelium and the lower choroidal vascular layer. It is generally believed that reducing the intensity of blue light is effective in reducing oxidative stress in the retina, sometimes by as much as 90%, usually by 40%, thus fully explaining the reduced risk of developing AMD observed in some epidemiological studies.
(2) As an antioxidant, spitting and scavenging light-induced tissue oxygen tension, Kim et al. demonstrated that luteolin can burst single-linear oxygen and reduce the production of the phototoxic metabolite A2E under blue light induction, thus reducing its effect on DNA damage. suggesting that lutein as an antioxidant protects the macula and reduces damage in the short wavelength band of visible light. Bernstein et al, on the other hand, found a significant increase in macular pigment density in AMD patients supplemented with lutein compared to unsupplemented individuals, and no significant difference from age-matched controls.