age-related macular degeneration
Introduction
Introduction to age-related macular degeneration Age-related macular degeneration (age-related macular degeneration) or aging macular degeneration (agingmacular degeneration), mostly originated in the age of 50, the older, the higher the prevalence, the incidence and gender, There is no obvious relationship between races. Both eyes are suffered at the same time or in succession. Due to different clinical manifestations, they are divided into atrophic and exudative types. The former is more common, while the latter is only 1/10 to 15 of the former. basic knowledge Sickness ratio: 0.1% Susceptible people: good for people aged 50 or older Mode of infection: non-infectious Complications: choroidal neovascularization
Cause
Causes of age-related macular degeneration
Age factor (45%):
All studies have shown that age is a major influencing factor. The older the age, the higher the incidence. About 25% of people over the age of 65 have AMD. The cause of age-related macular degeneration is not fully understood. It may be due to the increase in age, the transmission of retinal nutrients and the discharge of waste are all obstacles, and many metabolites are accumulated in the retina.
Genetic factors (10%):
Studies have shown that to a certain extent, the incidence of immediate family members of AMD patients is high. When you have AMD at a glance, the other eye has a 40% chance of developing the disease within 5 years. Some scholars have suggested that the disease may be related to recessive genes on autosomes.
Cardiovascular disease (5%):
Cardiovascular disease may promote the progression of the disease, so it is necessary to strengthen physical exercise and have a strong body to delay the development of the disease.
Nutritional factors (5%):
Studies have shown that the macular degeneration of the fundus is related to the lack of carotene, lutein and vitamin C, E, etc., can eat some corn, kiwi, tomatoes, green vegetables, etc. to supplement the appropriate amount of trace elements. Eat more meats containing more unsaturated fatty acids such as fish to reduce the risk of the disease. As for foods with higher cholesterol, try to eat less.
Other factors (10%):
A study in the United States showed that smoking is twice as likely as normal people to have age-related macular degeneration. Caucasians have a higher risk of having a higher prevalence among women under the age of 75. In addition, chronic glare stimulation can also aggravate the disease.
Prevention
Age-related macular degeneration prevention
Because there is no special treatment for this disease, it is believed that oral administration of zinc can prevent the progression of macular degeneration, while antioxidants such as vitamin C and E can prevent free radical damage to cells, protect visual cells, and retinal tissue. The role of nutrients, most scholars advocate that for exudative type, laser photocoagulation should be performed early to avoid deterioration of the disease.
Complication
Complications of age-related macular degeneration Complications choroidal neovascularization
Abnormal neovascularization grows under the retina of the macula, called choroidal neovascularization (CNV).
Symptom
Symptoms of age-related macular degeneration Common symptoms pigmented pigmentation loss visual impairment senile leukoplakia visual field vision change macular avoidance phenomenon
The disease has atrophic and exudative patterns as described above. It has also been observed that atrophicity can be converted into exudative, so it is considered necessary for typing, but in most cases, clinical manifestations are light and prognosis is excellent. The inferior type is very different.
1. Atrophic senile macular degeneration:
Atrophic, also known as dry or non-exudative, both eyes often develop synchronously and simultaneously, and have the same clinical course and performance as senile hereditary macular degeneration (ie Haab disease), whether they are the same disease, because both Occurred in the elderly, the family is difficult to investigate, it is difficult to determine, this type is characterized by progressive pigment epithelial atrophy, clinically divided into two phases:
(1) Early stage (preatrophic stage of atrophy): The central vision is slightly damaged, even if it is normal or close to normal for a long time, the visual field can detect 5~10o central disc-like dark spots, and it is easier to detect with blue and yellow optotypes. , 180o line static visual field examination 0o on both sides of each 5 ~ 10o visual sensitivity decline, Amsler checklist examination is often positive, occasionally large or small.
Under the ophthalmoscope, the macula has a dense hard glass drusen, and the size of the sputum is different. Some of them are fused into a small piece. Between the drusen, there is a little flaky pigment depigmentation pigmentation, and the appearance is Salt and pepper, the lesion is centered on the center fossa, and gradually examined to the periphery. There is no clear boundary at the edge. In some cases, the whole macular part is dark, and the slit lamp microscope and the front mirror are used for light section inspection, and the microscopic uplift and its surroundings are visible. There is a red halo (lantern phenomenon), which indicates that there is a shallow detachment in the upper layer of the pigment. In this period, the fluorescent spots are quickly strengthened. The intensity is maximum within one minute after the start of the venous phase, and most of them are consistent with the background fluorescence, rapidly weakening and gradually disappearing. In a few cases, when the background fluorescence subsided, the fluorescent mask was still visible. In the case of the pigmented epithelial layer, the round or round-shaped fluorescent spots appeared in the early stage of the angiography, and the middle stage was strengthened, and the late stage gradually subsided, and the fluorescent spots did not expand. There is no neovascularization under the pigment epithelial layer, or it is slender and not sufficient for visualization (hidden neovascularization).
(2) Late stage (atrophic stage): The central vision is seriously damaged, and there is a virtual absolute central dark spot. Under the ophthalmoscope, there is a dense or fused glassy sputum and a large piece of light gray atrophy. The boundary of the atrophy area becomes clear. There are salt and pepper spots scattered on the surface, and there is also a beaten bronze appearance.
Fluorescence angiography showed strong fluorescence in the early atrophy area, and disappeared with the background fluorescence, disappeared and disappeared synchronously. The fluorescence spots did not expand during the whole angiography, suggesting the fluorescence of the pigment epithelium atrophy, but in some cases, in the atrophy zone. Strong fluorescent spots and weak fluorescent spots appear simultaneously, indicating that there is atrophy and occlusion of choroidal capillaries in addition to pigment epithelial atrophy.
Atrophic degeneration is slow, the course is long, and the transition between early and late stages is difficult to separate. In addition, the individual differences are large, so the length of time from early to late is different, but the degree of lesions in both eyes is basically symmetrical.
2, exudative senile macular degeneration (exudative senile macular degeneration):
Exudation, also known as wetness, is known as Kuhnt-Junius's senile disciform macular degeneration. This type is characterized by active neovascularization under the pigment epithelial layer, causing a series of exudations. Bleeding, scar changes, clinically divided into three phases.
(1) Early stage (predisciform stage of discoid degeneration): The central visual acuity decreased significantly, and the degree was different depending on whether the central fossa was involved. The Amsler square table was positive, and the central dark spot was detected corresponding to the lesion.
Under the ophthalmoscope, there are dense, different sizes of drusen in the macula, which are mainly soft and fused together. At the same time, pigment spots and depigment spots are seen from time to time. Some pigment spots surround the glass membrane. Halo, the central fossa is dim or disappears. At this time, fluoroscopy: the early appearance of fluorescence in the drusen and pigmentation, which is enhanced, weakened, disappeared and synchronized with background fluorescence. In some cases, it remains strong after the background fluorescence disappears. Fluorescent spots indicate that there are two cases: one is the staining of the drusen; the other is the presence of new blood vessels under the pigment epithelial layer. The distinction between the two is that the former enlarges the fluorescent spot during the whole process, and vice versa.
(2) Metaphase (evolutionary stage): The main feature of this period is the formation of pigment epithelial layer and/or neuroepithelial serous or/and hemorrhagic detachment due to neovascular leakage, and the visual acuity drops sharply. In addition to the change, plus a wide range, the color of the round or round lesions, and slightly raised, so that the entire lesion is gray and mottled, and some cases have murmurs with dark red bleeding spots, slit lamp microscope plus The anterior mirror light section examination showed serous exudation under the subcortical or/and neuroepithelial layer on the pigment, and the bleeding position was the same. The lesion developed further, and yellow-white exudation appeared in the deep layer of the retina, and the exudation was uniform. Consistent plaque; some are clustered spots with different shades; some are located in the lesion; some are around the edge of the lesion, showing an irregular ring or eyebrow-like (Coats reaction), when the bleeding is severe, it can lead to pigmentation Subepithelial or neuroepithelial dark red or even gray-brown hematoma; sometimes spread to the nerve fiber layer and see flaming hemorrhage; can also penetrate the internal boundary membrane into the vitreous, forming vitreous hemorrhage, fluoresce In the early stage of photo-angiography, the lesion area showed variegated fluorescence, and lace-like or wheel-like fluorescence appeared immediately, suggesting the presence of active new blood vessels. After that, the fluorescence continued to spread, and until the venous phase or later, the entire detachment cavity was filled. Fluorescence, the contour is clearer, the pigment epithelium is detached; otherwise, the neuroepithelial detachment, the strong fluorescence in the detached cavity persists after the background fluorescence disappears, and the fluorescence in the detached cavity is generally uniform, but when accompanied by When pigment hyperplasia or hemorrhage, there is a corresponding fluorescent mask, the neovascular rupture is severe and the hematoma seen under the aforementioned ophthalmoscope is formed, and a large amount of fluorescent masking occurs. In the late stage of contrast, sometimes such a fluorescent masking area may appear 1 to 2 A fluorescent spot that is gradually enlarged and enlarged (called a hot spot) proves the presence of new blood vessels under the retina.
(3) Late stage (reparative stage): exudation and hemorrhage gradually merged and replaced by scar tissue. At this time, the visual acuity is further damaged. The fundus examination shows a slightly agglomerated block or irregular white patches (hematoma absorption). During the process, it is reddish yellow. The plaque is located under the retinal blood vessels. Hemorrhagic plaques and pigmented spots are often seen on the surface of the plaque or at its edges. In some cases, after the bleeding and exudation are replaced by scars, the lesion does not end. New neovascularization occurs at the edge of the scar, and the process of exudation, hemorrhage, absorption, and scarring is repeated, and the scar is further enlarged. Therefore, long-term follow-up observation of such patients is necessary. It can be seen that the light-colored scar is pseudo-fluorescent; the pigmentation hyperplasia is fluorescently shielded; if there is neovascularization and exudation between the scar edge or the scar, the bleeding is gradually enlarged and enhanced, and the exudative age-related macular degeneration has successively Onset, the interval is usually no more than five years.
Examine
Examination of age-related macular degeneration
Understand the whole picture of the crystal, check it in the dark room after fully diverging, the specific method is as follows:
1. Focus illumination inspection method: direct illumination with light to see if the crystal is turbid and dislocated.
2. Iris projection method: the thin light is projected from the pupil edge obliquely to the crystal at 45o. If the crystal turbidity is located at the core, there is a crescent-shaped transparent area between the turbid area and the pupil edge. The heavier the turbidity, the narrower the shadow, such as When the crystals are completely turbid, the crescent-shaped shadows completely disappear.
3. Ophthalmoscope method: the light is put into the pupil area, and a uniform red shadow can be seen in normal times. If the crystal or the refractive interstitial opacity, there are black spots or black blocks in the red shadow, the patient can be rotated during the examination. Eyeball, see if the shadow moves or not to understand the turbid part.
4. Slit lamp inspection method: The slit lamp is used for optical section inspection. From front to back, there are many layers of light and dark layers, which represent the lens nucleus of different periods. The transparency of each layer is not completely consistent. The former capsule, the adult anterior surface And the surface of the embryo is relatively clear.
Diagnosis
Diagnosis and differential diagnosis of age-related macular degeneration
diagnosis
When the above various clinical manifestations have become obvious, the diagnosis is not difficult, but in the early stage of the disease, especially in the early stage of atrophic type, when it is distinguished from the senile drusen that appears in normal vision, the main difference is that it is excluded. In addition to the function, the former glass film is different in size, quite dense, and the boundary is relatively vague. There are pigment spots such as pigment spots and discoloration spots between the glass membranes, and the latter is sparse, similar in size, and has no pigmentation disorder.
Differential diagnosis
Exudative type should be differentiated from choroid melanin when hematoma occurs under the pigment epithelial layer. The most reliable method is fluorescein angiography. The hematoma is covered by a large fluorescence-free area due to background fluorescence, and the melanin disease appears due to neovascular leakage in the body. More lake-like strong fluorescent spots.
Exudative monocular enters the mutation phase, there is exudation and hemorrhage in the macula, especially in those with younger age of onset, and it is also differentiated from central exudative choroiditis. The latter has no drusen, and the back of the eye Inflammatory cellular opacity can be seen in the vitreous, while the latter is the opposite. In addition, systemic pathogens are also available for reference.
