Age-related macular degeneration

Introduction to age-related macular degeneration Age-related macular degeneration (ARMD), also known as senile macular degeneration (SMD), is one of the important eye diseases associated with age-related blindness; according to clinical and pathological findings, age-related macular degeneration is divided into 2 Type, atrophic senile macular degeneration and exudative senile macular degeneration. Atrophic age-related macular degeneration is mainly caused by choroidal capillary atrophy, thickening of the glass membrane and atrophy of the retinal pigment epithelium; exudative age-related macular degeneration is mainly caused by the destruction of choroidal blood vessels in the subretinal Blood vessels that cause serous and/or bleeding of the retina and/or pigment epithelium. basic knowledge The proportion of illness: 0.0025% Susceptible people: seen in the elderly Mode of infection: non-infectious Complications: choroidal neovascularization

Causes of age-related macular degeneration

(1) Causes of the disease

The cause of age-related macular degeneration is still unclear, but according to a large number of epidemiological survey data, clinical case analysis over the years, and various animal studies have shown that the factors that may cause age-related macular degeneration are: genetic Factors, environmental effects, congenital defects, posterior pole retinal chronic photodamage, malnutrition, immune or autoimmune diseases, inflammation, metabolic disorders, scleral hardness changes, poisoning, cardiovascular diseases, etc., including the macula Long-term chronic photodamage of the retina may be an important basis for the degeneration of retinal pigment epithelium (RPE) and photoreceptors in the macular area, but so far there is no clear evidence to prove what causes the age directly. Macular degeneration, the disease is likely to be the result of long-term effects of multiple factors.

(two) pathogenesis

Aging and degeneration are important factors in causing age-related macular degeneration. During a lifetime, RPE is responsible for providing nutrients for the outer layer of the retina, maintaining important functions of metabolism, and engulfing and digesting the metabolism of the outer disc membrane of photoreceptors. Complex biochemical function, RPE phagocytose a large number of photoreceptor outer disc membranes, using RPE intracellular mitochondria, lysosome, smooth endoplasmic reticulum, rough endoplasmic reticulum and Golgi body organelles, digestion, and recycling The useful material of the outer disc membrane, while the indigestible material forms some residual body - lipofuscin is stored in the RPE cells. As the age increases, the RPE phagocytizes and digests the photoreceptor outer disc membrane. The function is also gradually declining, resulting in more and more indigestible residual bodies. The lipofuscin in RPE is increasing with age, and the residual metabolites are continuously discharged from the inside of the RPE cells to the bottom.

Slowly accumulate between the RPE and the Bruch membrane, forming a large amount of drusen, which causes the RPE-Bruch membrane-choroidal capillary complex to degenerate, causing the macular and posterior retina choroid to shrink. It can further cause thickening of the collagen layer in the Bruch membrane and rupture of the elastic fiber layer, causing the choroidal capillaries to enter the RPE and the retinal nerve epithelium through the ruptured Bruch membrane to form subretinal neovascularization (SRNV) or choroid Choroidal neovascularization (CNV), once the CNV is formed, due to the poor structure of the new blood vessels, blood vessel leakage and hemorrhage will occur, which will lead to a series of secondary pathological changes accompanied by the entry of new blood vessels. There will be a proliferation of connective tissue at the same time, completely destroying the choroidal tissue of the posterior pole, and eventually a large number of scars in the macular area and the posterior pole.

Age-related macular degeneration prevention

Because there is no special treatment for this disease, it is thought that in the early stage, oral zinc can prevent the progression of macular degeneration, while antioxidants such as vitamins 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.

Age-related macular degeneration complications Complications choroidal neovascularization

1. The result of the development of focal atrophic plaque drusen is that the retinal pigment epithelium disappears, resulting in atrophic zone. At this time, the drusen disappears, and finally leads to atrophy and choroidal capillary dysfunction, which may be the cause of atrophy. Among patients with choroidal neovascularization, 34.8% also had retinal pigment epithelial atrophy.

2. Retinal pigment epithelial detachment Retinal pigment epithelial serous detachment is an exudative complication of macular degeneration. Due to the diffuse thickening of the inner layer Bruch membrane, it is easy to produce fissures. This fissure is actually between the Bruch membranes. Detachment increases the risk of choroidal neovascularization.

3. Choroidal neovascularization forms a soft drusen, which is easy to form choroidal neovascularization. In the eyes of large fusion drusen with progressive leakage during fluorescein angiography, the risk of discoid degeneration is greater and there is a fusion. There is a greater risk of choroidal neovascularization and its complications in focal dysplasia of the drusen and macular area.

4. Disciform scar The discoid scar in the macula is the most important outcome of choroidal neovascularization. The thickened inner layer of Bruch membrane produces fissures, new blood vessels invade, and thin-walled neovascularization often occurs bleeding and exudation. Therefore, the retinal pigment epithelium and the inner layer of Bruch membrane are serous and hemorrhagic, and fibrous tissue proliferation occurs between the two layers of tissue, so that fibrous vascular scar tissue is formed.

5. Other patients with discoid scars may also have other complications, such as extensive exudation in the retina or subretinal (sometimes called the senile Coats response) and serous and adjacent retinal and/or retinal pigment epithelium. (or) hemorrhagic detachment, individual diseases such as slow-developing serous and/or hemorrhagic detachment can spread to the choroidal motion, veins, into the area of the disc-shaped scar.

Symptoms of age-related macular degeneration Common symptoms Fatigue light reflex disappears Retinal hemorrhage Pigment loss Visual distortion

Dry AMD is caused by long-term chronic progressive atrophy of the RPE-Bruch membrane-choroidal capillary complex.

Dry AMD occurs in the elderly over 50 years old, the eyes are symmetrical, the visual acuity is extremely slow and progressive decline, the patient often has symptoms such as visual distortion, the fundus examination of the pigmentation of the macular area of both eyes, the central concave light reflection disappears, the posterior pole Sometimes there are some yellow-white drusen phlegm of different sizes and borders. In some patients in the late stage of the disease, due to the atrophy of RPE and pigment loss, the posterior pole retina has a clearer map-like atrophy area. The choroidal capillaries also shrink, and there are some large choroidal vessels in the atrophy zone.

Wet AMD is caused by damage to the Bruch membrane. The choroidal capillaries grow to the retinal pigment epithelium and retinal neuroepithelial cells through the damage of the Bruch membrane, forming choroidal neovascularization (CNV). Once the CNV is formed, the structure of the neovascular is imperfect. It will cause a series of pathological changes such as exudation, hemorrhage, mechanization, scars, etc., resulting in the loss of central vision loss.

Most of the wet AMD occurs in the elderly over 60 years old. Most of them are first-onset. The contralateral eye may only occur after a long period of time. However, there are also a small number of patients with both eyes at the same time or soon after, according to a large number of foreign statistics. In monocular wet AMD patients, 12% to 15% of the contralateral eye develops wet AMD every year, and about 75% of patients within 5 years may develop symptoms in the lateral eye.

Unlike the progressive decline in dry AMD vision, patients with wet AMD have a rapid decline in visual acuity after onset, often with a significant decrease in the short term. Some patients can even clearly indicate the date of onset, but fundus examination can find the posterior fundus lesion. The scope of the disease has been very extensive, and a wide range of lesions are not formed in a short period of time. Because the lesions occur in the posterior pole, the lesions have not affected the fovea. Therefore, many patients have no symptoms. Once the lesions invade the fovea, the central vision is affected. Loss, the patient will find vision loss.

Wet AMD can be generally divided into three phases according to its course of disease:

1. Early or called pre-exudation fundus examination, there may be yellow-white exudative drusen in the early stage of the pole or macular area, and the boundary is blurred, especially the glass membranes are fused to form a soft glass membrane. This will be a precursor to the occurrence of wet AMD.

2. The lesions in the exudation period develop further, CNV blood vessels begin to leak, serous RPE detachment and serous retinal neuroepithelial detachment can occur in the posterior pole of the fundus, and grayish white CNV can be seen, and sometimes some hard exudation can be seen around the lesion. If there is bleeding in the CNV blood vessels, retinal hemorrhage and subretinal hemorrhage can be seen. The hemorrhage is located in the superficial layer of the retina, and it is bright red. The bleeding is dark red in the deep retina. If the bleeding time is longer, hemoglobin is decomposed and absorbed, and the hemorrhage area It can gradually turn yellow. If the bleeding is located under the retinal pigment epithelium and at the choroid, the bleeding area can be black due to pigmentation of the pigment epithelium and choroid, which is sometimes misdiagnosed as choroidal melanoma.

CNV bleeding can be very extensive, not only limited to the macular area, but also can occupy the entire posterior pole. In more serious cases, it can even extend beyond the equator to form a large range of black bulging lesions, also known as choroidal hematoma, which may often be Misdiagnosed as choroidal melanoma and removed the eyeball, if the amount of bleeding is large, severe cases of bleeding can break through the inner membrane of the retina, into the vitreous to cause vitreous hemorrhage, a large amount of vitreous hemorrhage can even lead to the fundus can not be examined, may also be traction later Retinal detachment, secondary glaucoma, neovascular glaucoma and other more serious complications, clinically, if the elderly suddenly see a large amount of vitreous hemorrhage, the fundus can not be examined, and the contralateral eye macular area has drusen, pigment Disorders or typical dry AMD manifestations should be considered as massive bleeding from wet AMD.

3. After a long course of disease in the scar stage, the subretinal hemorrhage is gradually absorbed, and replaced by fibrous tissue associated with neovascularization and RPE metaplasia. In the late stage of the disease, a large piece of scar is formed in the posterior pole of the fundus, and fundus examination It can be seen that the macular area or the posterior pole has a white mechanical membrane and some pigmentation, and the patient's central vision loss is exhausted.

About 16% of patients can have new CNV around the scar after a period of time, so a new round of exudation, hemorrhage, mechanization, scar and other pathological changes are repeated, resulting in a wider range of lesions.

When patients over the age of 45 complain of visual distortion, dark spots, or recent visual loss, detailed clinical examinations should be performed, including optimal corrected visual acuity and anterior segment examination, visual field examination, and slit lamp microscope with three sides. Mirrors and retinoscopes, as well as indirect ophthalmoscopes to carefully examine the fundus. If necessary, macular stereography can be used. Amsler checklist can detect visual distortion and dark spots. Patients with any central vision should be examined quickly. There are liquid, hemorrhage, yellow exudation, or fatty deposits and gray-green choroidal lesions. Slit lamps or ophthalmoscopes are not certain. Fluorescence angiography should be performed. The choroidal neovascularization is early and there are many opportunities for treatment. Whether it is photocoagulation, a patient with this disease in the macula should check the fundus twice a year, and the choroidal neovascularization that can be treated has time-dependent properties, because the disease can be treated within the first month after the rapid loss of vision. The choroidal neovascularization begins outside the fovea, but soon spreads to the underside of the foveal avascular region, so it should be detected and treated as soon as possible. Treatment.

The late diagnosis of this disease is generally not difficult, the key is early diagnosis, the early symptoms of this disease often have no symptoms, retrospective study of the early symptoms of the disease, followed by blurred vision, visual distortion, reading difficulties, center or side center Dark spots and visual fatigue, Andrew studied the symptoms of 103 choroidal neovascularization in the early stage of the disease. The visual distortion and close reading difficulty are the earliest symptoms of the disease. When the above symptoms occur, the patient should be carefully examined. It is also found that myopia is rarely afflicted with this disease. Most of the patients have refractive changes such as elevation and hyperopia. Therefore, this disease can add attention to fatigue and close reading difficulties. It is easier to detect changes in central vision when examining the near vision of the disease.

Examination of age-related macular degeneration

1. Fundus angiography Fundus angiography, which is commonly used to diagnose fundus diseases, has only been fundus fluorescein angiography (FFA) for many years. In recent years, indocyanine green angiography (ICGA) has been invented. The former is mainly used for the diagnosis of retinal vascular diseases. The diagnosis of choroidal vascular disease is not ideal; the latter is mainly used for the diagnosis of choroidal vascular disease, clinical use of FFA and ICGA combined angiography, greatly improving the diagnosis of fundus diseases.

Dry AMD fundus fluorescein angiography showed that the posterior pole of the angiography showed fluoroscopy due to the atrophy of RPE. Most of the drusen also showed fluorescing fluorescence. A few glass enamels may show fluorescein staining if the posterior pole RPE has a map-like atrophy, and angiography shows a local map-like fluoroscopy. If the choroidal capillaries also shrink in the later stages of the disease, the existing thick choroidal vessels are present on the background of local weak fluorescence.

In the dry AMD indocyanine green choroidal angiography, the drusen of the drusen appears to obscure fluorescence from beginning to end.

Wet AMD fundus fluorescein angiography, in the early stage of angiography, ie, pre-arterial or early arterial, appears lace-like, car-like, velvety or reticular CNV morphology, and soon there is obvious fluorescein leakage, resulting in CNV A strong fluorescence is formed, the surrounding bleeding shows fluorescence shielding, and the late scar formation, fundus fluorescein angiography shows weak fluorescence in the early scar area, but the scar can be stained at the late stage of contrast to form a strong fluorescence.

According to the development of fundus fluorescein angiography CNV, it is clinically divided into two types: typical CNV and occult CNV. The so-called typical CNV refers to the form of CNV which is clear in the early stage of angiography, and soon Fluorescein leakage, a strong fluorescent lesion is formed later, and the so-called occult CNV refers to the thickening of the lesion area, lipid exudation, pigmentation or scarring, and incomplete CNV development in the early stage of angiography. It is only a few mottled fluorescence with unclear borders, and the fluorescence is gradually enhanced in the middle and late stages, and fluorescein leakage appears in the late stage.

In addition, according to the stereoscopic image of the fundus, the presence or absence of RPE ridges and the occult CNV are classified into two types: fibro-vascular pigment epithelial detachment and late leakage of undetermined origin. The former fundus fluorescein angiography showed strong fluorescent spots after 1 to 2 minutes after dye injection, and there was a clear fluorescein leakage zone in the late stage; the latter showed fluorescein leakage only about 2 to 5 minutes after dye injection. Early images showed no abnormal fluorescence, and it was difficult to find the source of leakage. The boundary of late leakage was not clear.

Wet AMD indocyanine green choroidal angiography is often different from FFA, with more changes, can be expressed as hot or abnormally large choroidal vessels, because indocyanine green fluorescence is not affected by retinal and choroidal hemorrhage, sometimes more complete display than FFA The shape and extent of CNV can be observed. Even in the early stage of angiography, CNV nourishing blood vessels with rapid filling and rapid emptying can be observed, but it may also show abnormally strong fluorescence in FFA, but no positive findings in ICGA, so typical The CNV and occult CNV are simple concepts of fundus fluorescein angiography. They are not suitable for the analysis of indocyanine green choroidal angiography. In addition, since the fluorescence intensity of ICGA is lower than that of FFA, the leakage of CNV in ICGA is often different. It is evident in the FFA.

2. Optical coherence tomography The OCT image of dry age-related macular degeneration is mainly characterized by thinning of the retinal neuroepithelial layer in the upper and lower vascular arches, especially in the macular area, and the light reflection intensity of each layer is slightly enhanced or weakened, showing red reflection. The retinal pigment epithelium/choroidal capillary layer of the band presents several or more semi-arc ridges of varying sizes corresponding to the drusen in the fundus image.

The exudation, hemorrhage and scar caused by CNV of wet AMD have the following manifestations in OCT:

(1) CNV:

1 Typical CNV: OCT is characterized by a red reflection band of the retinal pigment epithelium/choroidal capillary layer, which is thickened locally. The smaller CNV usually exhibits a fusiform red reflective group, while the large CNV is a larger range. Irregular thickening, accompanied by deformation of the retinal pigment epithelium / choroidal capillary layer, the boundary is clear, if the CNV breaks through the pigment epithelial layer into the subretinal, OCT appears as a red reflective group under the neuroepithelial space, and the nourishing blood vessels of CNV The retinal pigment epithelium/choroidal capillary layer is interrupted, and the red reflective band extends vertically or obliquely into the neuroepithelial area, and its blood vessel branches are visible.

2 occult CNV: about 85%, OCT performance is similar, only the boundary is unclear.

(2) Hemorrhage and exudation: In the lesions of wet AMD, hemorrhage and exudation often lead to serous and/or hemorrhagic subretinal and/or pigment epithelial detachment, and serous detachment is manifested by the formation of liquid accumulation. Reflective cavity, bleeding in the OCT image is moderately strong reflection, and obscuring the subsequent tissue, hemorrhagic detachment, such as under the retina, the detachment of the neuroepithelial yellow-green light reflection band leading edge is unclear, leaving the zone Irregular high-reflection points or zones can be seen. The pigment epithelial band can be partially or completely obscured. Some patients can form cystoid edema due to massive exudation and hemorrhage.

(3) Scar: OCT is characterized by localized thickening of the retinal pigment epithelium/choroidal capillary layer, clear boundaries, and enhanced reflection, such as pigmentation in the scar, partially blocking the posterior choroidal band, in addition, scar The retinal tissue above is usually thinned by atrophy.

3. Classification of drusen Glass drus is different in terms of quantity, size, shape, distribution, pigmentation and degree of bulging. The following types of drusen have been confirmed by clinical and histopathology:

(1) Hard drusen: Under the ophthalmoscope, this type of drusen is a small, scattered circle. Yellow-white deposits appear in the posterior part of the fundus and may be accompanied by retinal pigment epithelium covering the surface. The lack of pigment and/or the hypertrophy of the surrounding retinal pigment epithelium, which is accompanied by pigmentation changes, helps to find drusen with ophthalmoscopy.

(2) soft [diffuse, confluent, serous] soft dursen: soft glassy enamel is usually a large amorphous yellow deposit with irregular shape , indefinite size, soft appearance, with unclear edges, located in the deep layer of the retina, often tend to fuse, when the soft glass membrane becomes larger and fused, it resembles the retinal pigment epithelial serous detachment, accompanied by this period The pigmentation change (hyperpigmentation, reduction or deficiency) may also be more pronounced, and when the vitreous membrane becomes fused, the risk of vascular invasion and adjacent RPE and photoreceptor cell degeneration is increased.

(3) semi-solid (mixed, serogranular) semisolid drusen: Sark uses a hybrid glass film to describe a glass film with both hard and soft glass film characteristics., ophthalmoscopy This kind of glass film can have a soft edge like a soft glass film, but it shows a fairly flat appearance like a hard glass film. Bressler et al. advocate the use of mixed glass film for hard and soft. The eye of the drusen is described by a semi-solid glass film crucible with a glass film which exhibits a more typical soft glass film, flat and more atrophic.

(4) basement membrane (nodular) basal laminar drusen: it has numerous, small and uniform, scattered round, mildly elevated yellow subretinal lesions, With posterior retroreflective illumination, these drusen are semi-transparent nodular structures, unlike hard, soft or semi-solid drusen, which is found in younger patients with There is a small, yellow exudative detachment that should not be confused with basement membrane deposits.

(5) Calcified drusen: is a hard deposit with a glittering appearance, often surrounded by a regional retinal pigment epithelium atrophy.

Diagnosis and differentiation of age-related macular degeneration

Diagnostic criteria

The disease usually occurs in both eyes, at one glance, the second eye has a high risk of developing the disease, and the color resolution of the unilateral patients, the macular threshold, the dark adaptation test and the Amsler table central visual field examination, 4 examination results All of them showed that when the unilateral side of the disease had a visual acuity of 1.0, there was abnormal visual function, which showed a decrease in tone resolution and retinal light sensitivity, a dark adaptation function and an abnormality in the central field of the Amsler table. Eisner found that the disease was advanced. The normal vision of the two eyes is normal, there is no macular degeneration, but the sensitivity of blue cone cells is reduced and the color vision is changed. The density of visual pigment in the foveal cone is lower than that of the normal eye, so the patient with early disease of the other eye has advanced disease, especially At a glance, there are a large number of fusion drusen, paying attention to early examination and early diagnosis.

Differential diagnosis

Dry AMD should be differentiated from Stargardt's disease and central halo-like retinal choroidal atrophy. Stargardt's disease occurs mostly in adolescence, and the age of onset is more than 10 years old. It has vision loss since childhood, and the fundus is There are elliptical retinal choroidal atrophy lesions in the posterior pole. Many patients are accompanied by retinal yellow-white spots. The majority of the age of central halo-like retinal choroidal atrophy is also in their 10s. Visual acuity has been around for a long time. Fundus examination is often accompanied. There is atrophy of the choroid around the optic disc. The visual acuity of the patients with dry AMD has been normal. The visual acuity is mostly in the elderly, and the onset time is very different from the course of the disease.

Wet AMD should be differentiated from central exudative chorioretinitis, CNV caused by macular degeneration in high myopia, fundus vascular streaks, choroidal melanoma and other diseases. Central exudative chorioretinitis occurs mostly in young women. Single eye disease, the lesion range is very small, usually 1/3 ~ 1/2 optic disc diameter; high myopia patients have a history of high myopia, fundus examination can be seen leopard-like fundus, scleral staphyloma and lacquer-like cracks; fundus vessels The streak can be seen around the optic disc with brownish-black radial streaks, and the streak of the posterior pole of the fundus can produce CNV. The fundus fluorescein angiography can see very striking vascular-like streaks; choroidal melanoma fundus fluorescein Angiography is characterized by obscuration in the early stage of angiography, but there are many small strong fluorescent spots on the edge of the lesion at the end of the angiography. Later, there are fluorescein leakage, and sometimes the blood vessels in the tumor and the retinal blood vessels can be simultaneously developed to form a double circulation phenomenon. , ocular ultrasound can also assist in the diagnosis, careful analysis, combined with fundus fluorescein blood vessels Movies, ultrasound and other means can be identified when the above-mentioned diseases.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.