Age-related macular degeneration. Age-related macular degeneration (AMD). Types of Age-Related Macular Degeneration

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The retina is a specific structural and functional unit of the eyeball, necessary for capturing the image of the surrounding space and transmitting it to the brain. From an anatomical point of view, the retina is a thin layer of nerve cells thanks to which a person sees, since it is on them that the image is projected and transmitted along the optic nerve to the brain, where the “picture” is processed. The retina of the eye is formed by light-sensitive cells, which are called photoreceptors, since they are able to capture all the details of the surrounding “picture” that appears in the field of vision.

Depending on which area of ​​the retina is affected, they are divided into three large groups:
1. Generalized retinal dystrophies;
2. Central retinal dystrophies;
3. Peripheral retinal dystrophies.

With central dystrophy, only the central part of the entire retina of the eye is affected. Since this central part of the retina is called macula, then the term is often used to denote dystrophy of the corresponding localization macular. Therefore, a synonym for the term “central retinal dystrophy” is the concept of “macular retinal dystrophy”.

In peripheral dystrophy, the edges of the retina are affected, while the central areas remain undamaged. With generalized retinal dystrophy, all parts of the retina are affected - both central and peripheral. A special case is age-related (senile) retinal dystrophy, which develops against the background of senile changes in the structure of microvessels. According to the location of the lesion, senile retinal dystrophy is central (macular).

Depending on the characteristics of tissue damage and the characteristics of the course of the disease, central, peripheral and generalized retinal dystrophies are divided into numerous varieties, which will be discussed separately.

Central retinal dystrophy - classification and brief description of varieties

• Stargardt's macular dystrophy;
• Yellow-spotted fundus (Franceschetti's disease);
• Best's vitelline (vitelliform) macular degeneration;
• Congenital cone retinal dystrophy;
• Colloid retinal dystrophy Doina;
• Age-related retinal degeneration (dry or wet macular degeneration);
• Central serous choriopathy.

Central chorioretinal retinal dystrophy

Due to the presence of subretinal effusion characteristic symptom This dystrophy is a decrease in visual acuity and the appearance of wave-like curvatures of the image, as if a person is looking through a layer of water.

Macular (age-related) retinal degeneration

Both forms of macular degeneration of the retina develop in people over 50–60 years of age against the background of senile changes in the structure of the walls of microvessels. Against the background of age-related dystrophy, damage occurs to the vessels of the central part of the retina, the so-called macula, which provides high resolution, that is, allows a person to see and distinguish the most small parts objects and surroundings at close range. However, even with severe age-related dystrophy, complete blindness occurs extremely rarely, since the peripheral parts of the retina remain intact and allow a person to partially see. Preserved peripheral parts of the retina allow a person to navigate normally in his usual environment. In the most severe course of age-related retinal dystrophy, a person loses the ability to read and write.

Dry (non-exudative) age-related macular degeneration The retina is characterized by the accumulation of waste products of cells between the blood vessels and the retina itself. These waste products are not removed in a timely manner due to disruption of the structure and function of the microvessels of the eye. Waste products are chemical substances, which are deposited in the tissues under the retina and look like small tubercles yellow color. These yellow tubercles are called Druze.

Dry retinal dystrophy accounts for up to 90% of cases of all macular degeneration and is a relatively benign form, since its course is slow, and therefore the decrease in visual acuity is also gradual. Non-exudative macular degeneration usually occurs in three successive stages:
1. The early stage of dry age-related macular degeneration of the retina is characterized by the presence of drusen small size. At this stage, the person still sees well and is not bothered by any visual impairment;
2. The intermediate stage is characterized by the presence of either one large drusen or several small ones localized in the central part of the retina. These drusen reduce a person's field of vision, as a result of which he sometimes sees a spot in front of his eyes. The only symptom at this stage of age-related macular degeneration is the need for bright light for reading or writing;
3. The pronounced stage is characterized by the appearance of a spot in the field of vision, which is dark in color and big size. This spot does not allow a person to see most of the surrounding picture.

Wet macular degeneration of the retina occurs in 10% of cases and has an unfavorable prognosis, since against its background, firstly, there is a very high risk of developing retinal detachment, and secondly, vision loss occurs very quickly. With this form of dystrophy, new blood vessels, which are normally absent, begin to actively grow under the retina of the eye. These vessels have a structure that is not typical for the eye, and therefore their membrane is easily damaged, and fluid and blood begin to leak through it, accumulating under the retina. This effusion is called exudate. As a result, exudate accumulates under the retina, which puts pressure on it and gradually peels off. That is why wet macular degeneration is dangerous due to retinal detachment.

With wet macular degeneration of the retina, a sharp and unexpected decrease in visual acuity occurs. If treatment is not started immediately, complete blindness may occur due to retinal detachment.

Peripheral retinal dystrophy - classification and general characteristics of types

Peripheral retinal dystrophies are often caused by changes in the length of the eye against the background of progressive myopia and deterioration of blood circulation in this area. As peripheral dystrophies progress, the retina becomes thinner, resulting in the formation of so-called tractions (areas of excessive tension). These tractions, when present for a long time, create the preconditions for a tear in the retina, through which the liquid part vitreous seeps under it, lifts it up and gradually peels off.

Depending on the degree of danger of retinal detachment, as well as on the type of morphological changes, peripheral dystrophies are divided into the following types:

• Lattice retinal dystrophy;
• Retinal degeneration of the “snail traces” type;
• Frost-like degeneration of the retina;
• Cobblestone retinal degeneration;
• Small cystic degeneration of Blessin-Ivanov;
• Retinal pigmentary dystrophy;
• Pediatric Leber's taperetinal amaurosis;
• X-chromosomal juvenile retinoschisis.

Lattice retinal dystrophy

Most often (in 2/3 of cases) lattice retinal dystrophy is detected in men over 20 years of age, which indicates its hereditary nature. Lattice dystrophy affects one or both eyes with approximately equal frequency and then progresses slowly and gradually throughout a person's life.

With lattice dystrophy, white, narrow, wavy stripes are visible on the fundus, forming lattices or rope ladders. These stripes are formed by collapsed and hyaline-filled blood vessels. Between the collapsed vessels, areas of thinning of the retina are formed, which have the characteristic appearance of pinkish or red lesions. In these areas of the thinned retina, cysts or tears can form, leading to detachment. The vitreous body in the area adjacent to the area of ​​the retina with dystrophic changes is liquefied. And at the edges of the area of ​​dystrophy, the vitreous body, on the contrary, is very tightly fused to the retina. Because of this, areas of excessive tension on the retina (traction) arise, where small tears are formed that look like valves. It is through these valves that the liquid part of the vitreous penetrates under the retina and provokes its detachment.

Peripheral retinal dystrophy of the “snail traces” type

Frost-like retinal dystrophy

Retinal dystrophy "cobblestone"

Small cystic retinal dystrophy Blessin–Ivanov

Retinal pigmentary dystrophy

Pediatric Leber's taperetinal amaurosis

X-chromosomal juvenile retinoschisis

Congenital retinal dystrophy

• Pigmentary dystrophy;
• Leber's amaurosis;
• Nyctalopia (lack of night vision);
• Cone dysfunction syndrome, in which color perception is impaired or complete color blindness is present (a person sees everything as gray or black and white).

• Stargardt's disease;
• Best's disease;
• Age-related macular degeneration.

• X-chromosomal juvenile retinoschisis;
• Wagner's disease;
• Goldman-Favre disease.

Retinal dystrophy during pregnancy

If a woman had any eye diseases before pregnancy, for example, myopia, hemeralopia and others, this significantly increases the risk of developing retinal dystrophy during pregnancy. Since various eye diseases are widespread in the population, the development of retinal dystrophy in pregnant women is not uncommon. It is precisely because of the risk of dystrophy with subsequent retinal detachment that gynecologists refer pregnant women for consultation with an ophthalmologist. And for the same reason, women suffering from myopia need permission from an ophthalmologist to give birth naturally. If the ophthalmologist considers the risk of fulminant dystrophy and retinal detachment during childbirth to be too high, he will recommend a cesarean section.

Retinal dystrophy - causes

Local causative factors of retinal dystrophy include the following:

• Hereditary predisposition;
• Myopia of any severity;
• Inflammatory eye diseases;
• Previous eye surgeries.

• Hypertonic disease;
• Diabetes;
• Past viral infections;
• Intoxication of any nature (poisoning with poisons, alcohol, tobacco, bacterial toxins, etc.);
• Increased blood cholesterol levels;
• Deficiency of vitamins and minerals entering the body with food;
• Chronic diseases (heart, thyroid, etc.);
• Age-related changes in the structure of blood vessels;
• Frequent exposure to direct sun rays on the eyes;
• White skin and blue eyes.

Retinal dystrophy - symptoms and signs

• Decreased visual acuity in one or both eyes (the need for bright light for reading or writing is also a sign of decreased visual acuity);
• Narrowing of the field of view;
• The appearance of scotoma (a spot or sensation of a curtain, fog or obstruction in front of the eyes);
• A distorted, wave-like image before the eyes, as if a person is looking through a layer of water;
• Poor vision in darkness or twilight (nyctalopia);
• Impaired color discrimination (colors are perceived as different, not corresponding to reality, for example, blue is seen as green, etc.);
• Periodic appearance of “floaters” or flashes before the eyes;
• Metamorphopsia (incorrect perception of everything related to the shape, color and location in space of a real object);
• Inability to correctly distinguish a moving object from a stationary one.

In addition to the listed clinical symptoms, retinal dystrophy is characterized by the following signs, identified during objective examinations and various tests:
1. Distortion of lines on Amsler test. This test consists in the fact that a person alternately looks with each eye at a point located in the center of a grid drawn on a sheet of paper. First, the paper is placed at a distance arm's length away from the eye and then slowly brought closer. If the lines are distorted, this is a sign of macular degeneration of the retina (see Figure 1);


Figure 1 – Amsler test. At the top right is a picture seen by a person with normal vision. At the top and bottom left is the image that a person sees with retinal dystrophy.
2. Characteristic changes in the fundus (for example, drusen, cysts, etc.).
3. Reduced electroretinography readings.

Retinal dystrophy - photo

This photograph shows retinal dystrophy of the “cobblestone” type.

This photograph shows dry age-related macular degeneration of the retina.

Retinal dystrophy - treatment

General principles of treatment of various types of retinal dystrophy

Drug therapy for retinal dystrophy involves the use of the following groups of drugs:
1. Antiplatelet agents– drugs that reduce thrombus formation in blood vessels (for example, Ticlopidine, Clopidogrel, acetylsalicylic acid). These drugs are taken orally in tablet form or administered intravenously;
2. Vasodilators And angioprotectors – drugs that dilate and strengthen blood vessels (for example, No-shpa, Papaverine, Ascorutin, Complamin, etc.). The drugs are taken orally or administered intravenously;
3. Lipid-lowering drugs – drugs that lower blood cholesterol levels, for example, Methionine, Simvastatin, Atorvastatin, etc. The drugs are used only in people suffering from atherosclerosis;
4. Vitamin complexes , which contain elements important for the normal functioning of the eyes, for example, Okyuvit-lutein, Blueberry-forte, etc.;
5. B vitamins ;
6. Drugs that improve microcirculation , for example, Pentoxifylline. Typically, drugs are injected directly into the structures of the eye;
7. Polypeptides, obtained from the retina of cattle (the drug Retinolamine). The drug is injected into the structures of the eye;
8. Eye drops containing vitamins and biological substances, promoting repair and improvement of metabolism, for example, Taufon, Emoxipin, Ophthalm-Katachrome, etc.;
9. Lucentis– a remedy that prevents the growth of pathological blood vessels. Used for the treatment of age-related macular degeneration of the retina.

The medications listed above are taken in courses, several times (at least twice) throughout the year.

In addition, for wet macular degeneration, Dexamethasone is injected into the eye, and Furosemide is administered intravenously. When hemorrhages develop in the eye, heparin, Etamsylate, aminocaproic acid or Prourokinase are administered intravenously in order to quickly resolve and stop it. To relieve swelling in any form of retinal dystrophy, Triamcinolone is injected directly into the eye.

The following physiotherapy methods are also used in courses for the treatment of retinal dystrophies:

• Electrophoresis with heparin, No-shpa and nicotinic acid;
• Photostimulation of the retina;
• Stimulation of the retina with low-energy laser radiation;
• Electrical stimulation of the retina;
• Intravenous laser blood irradiation (ILBI).

• Laser coagulation of the retina;
• Vitrectomy;
• Vaso-reconstructive operations (crossing the superficial temporal artery);
• Revascularization operations.

Approaches to the treatment of macular degeneration of the retina

If macular degeneration is in a more severe stage, then along with drug treatment, physiotherapy methods are used, such as:

• Magnetic stimulation of the retina;
• Retinal photostimulation;
• Laser stimulation of the retina;
• Electrical stimulation of the retina;
• Intravenous laser blood irradiation (ILBI);
• Surgeries to restore normal blood flow in the retina.

If a person has wet dystrophy, then first of all laser coagulation of sprouting, abnormal vessels is performed. During this procedure, a laser beam is directed to the affected areas of the retina, and under the influence of its powerful energy, blood vessels are sealed. As a result, fluid and blood stop sweating under the retina and peeling it off, which stops the progression of the disease. Laser coagulation of blood vessels is short in duration and completely painless procedure, which can be performed in a clinic setting.

After laser coagulation, it is necessary to take drugs from the group of angiogenesis inhibitors, for example, Lucentis, which will inhibit active growth new, abnormal vessels, thereby stopping the progression of wet retinal macular degeneration. Lucentis should be taken continuously, and other medications should be taken in courses several times a year, as with dry macular degeneration.

Principles of treatment of peripheral retinal dystrophy

Retinal dystrophy - laser treatment

Examples of therapeutic treatment of dystrophy with a laser are retinal stimulation, during which the affected areas are irradiated in order to activate metabolic processes in them. Laser stimulation of the retina in most cases gives an excellent effect and allows you to stop the progression of the disease for a long time. An example of surgical laser treatment for dystrophy is coagulation of blood vessels or delimitation of the affected area of ​​the retina. IN in this case The laser beam is directed to the affected areas of the retina and, under the influence of the released thermal energy, literally glues and seals the tissue and, thereby, delimits the treated area. As a result, the area of ​​the retina affected by dystrophy is isolated from other parts, which also makes it possible to stop the progression of the disease.

Retinal dystrophy - surgical treatment (operation)

Vitamins for retinal dystrophy

Vitamins for retinal dystrophy must be taken in two forms - in special tablets or multivitamin complexes, as well as in the form of food products rich in them. Richest in vitamins A, E and group B fresh vegetables and fruits, grains, nuts, etc. Therefore, these products must be consumed by people suffering from retinal dystrophy, since they are sources of vitamins that improve the nutrition and functioning of the eyes.

Prevention of retinal dystrophy

• Do not overstrain your eyes, always give them rest;
• Do not work without eye protection from various harmful radiation;
• Do eye exercises;
• Eat well, including fresh vegetables and fruits in your diet, as they contain large amounts of vitamins and microelements necessary for the normal functioning of the eye;
• Take vitamins A, E and group B;
• Take biologically active additives with zinc.

Retinal dystrophy - folk remedies

IN last years statistics ophthalmological diseases noted an increase in AMD (age-related macular degeneration). She also revealed the genetic nature of AMD. According to her calculations, only 5-5.5% of older people suffer from AMD, regardless of genetic failure.

Causes of AMD

But not only genetic changes influence the degree of development of AMD, but also external factors are a significant link in the appearance and intensification of AMD symptoms. For example, this bad habit, how smoking increases the likelihood of developing AMD from 12% to 38-40%.

Based on this, we can say that eliminating risk factors, that is, wearing sunglasses, correct balanced diet, plus appropriate drug treatment significantly reduces the possibility of developing AMD. As for not exudative form AMD, the method of its treatment is still ambiguous. Domestic medicine is quite successful in treating AMD through “anti-dystrophic” therapy, during which they use periocular injections and specially targeted drugs. But this option therapy has not been confirmed. Therefore, it is not used in Europe and America.

In order to prove the effectiveness of a particular method, it is necessary:

1. Carefully plan and monitor the treatment process in detail, thanks to meta-analyses and systematic reviews;
2. Collect all available test results, or base the study on a single case;
3. Conduct clinical studies on a certain number of patients, or develop an agreement on this problem thanks to experts.

Macular degeneration and the influence of minerals and antioxidants on the process of its treatment and prevention

For many years medicinal and preventive value antioxidants, and these are beta-carotene, vitamins C and E, selenium, manganese, zinc minerals, was based only on a theoretical basis. Later it was believed that taking dietary antioxidants prevents the development of AMD, but are they a means of prevention? age retinal changes were not clear.

Only in the 90s of the 20th century was the importance of taking vitamins A, C and E, zinc, selenium and beta-carotene confirmed. High doses of antioxidants really affect visual acuity and progressionAMD.

But subsequently, another study showed that large doses of antioxidants and minerals have their own side effects.

For example, beta-carotene in smokers can be a trigger for lung cancer. And an excess of beta-kerotene in the body of any person, on the contrary, leads to the development of neovascular AMD. And this fact does not depend on harmful factors environment and genetic characteristics.

A large amount of vitamin E for a person often ends in a heart attack in people suffering from diabetes. An excess of zinc can lead to hospitalization for those who suffer from diseases of the genitourinary system.

Also, the effect of taking beta-carotene, vitamins A, C and E, alpha-carotene, beta-cryptoxanthin and lycopene was not observed in the initial stages of AMD.

A little about carotenoids

Carotenoids are natural pigments of organic origin that are produced by bacteria, algae, fungi, plants and corals. They are what give the orange color to the vast majority of fruits and vegetables. Of the 600 carotenoids existing in nature, 34 are found in the human body. For the eyes, they perform the function of sunglasses (located in the retina). But only two carotenoids are involved in the organ of vision. These are zeaxanthin and lutein. Zeaxanthin has the ability to be formed from lutein. As for lutein, it is not produced human body and must come from outside. But for both zeaxanthin and lutein, the main vehicle is food, or rather fruits and vegetables.

And the fact that a decrease in the amount of lutein and zeaxanthin in the blood leads to an increase in the incidence of AMD has been repeatedly confirmed by collected clinical data. The results are truly amazing, since the percentage of risk in case of a lack of lutein and zeaxanthin reaches and even goes beyond fifty.

Recent studies have confirmed the effectiveness of taking 10 mg of lutein and 2 mg of zeaxanthin per day. At the same time, they created another option prophylactic drug, which is suitable for smokers, by replacing beta-carotene in it with carotenoids that are safe for this group of patients. Scientists have also identified a safe preventive dose of zinc, reducing it from 80 mg per day to 25. It is this dose that is most absorbed by the body and does not lead to side effects.

PUFAs, or polyunsaturated fatty acids

Age macular degeneration unites people at risk for developing myocardial infarction. It's no secret today that excessive consumption of fatty foods can cause problems with the cardiovascular system. And since the symptoms of age macular degeneration and are similar to each other, we can conclude that rational nutrition is both preventive and therapeutic in nature for this category of disease.

Polyunsaturated omega-3 fatty acids include: alpha-linoic acid, eicosapentaenoic fatty acid, docosahexaenoic fatty acid. When examined, they can be found in the outer segments of rods and cones. They have anti-inflammatory properties, prevent cell apoptosis and pathological angiogenesis, and are directly involved in changes in rhodopsin. In addition, these acids prevent the accumulation of lipofuscin in the retina (its pigment epithelium) and lipids in Bruch's membrane.

After analysis, epidemiologists confirmed the fact that excessive consumption of animal fats actually increases the risk of developing severe stages of AMD. But fish, consumed at least once a week, is a good preventive product for neovascular AMD, and in addition helps to transform bilateral drusen into geographic atrophy of the pigment epithelium and choriocapillaris layer.

What are the therapeutic prospects for dry AMD?

Treatment of age-related macular degeneration with conservative methods is not limited to taking antioxidants and minerals. Also good for prevention biological supplements. Vitamin therapy, which includes: vitamin D, vitamin A, vitamin B12 and vitamin B6; undoubtedly, it is also not unimportant in the treatment of AMD. Bioflavonoids and anthocyanosides help eliminate capillary fragility and improve the condition of connective tissue. In the future, therapy is expected to benefit from enzymes (wobenzym) and peptide regulators (cortexin and retinalamine). But today the results from taking this category of drugs are very doubtful. The same can be said about aspirin therapy.

According to World Organization Health care, age-related macular degeneration is one of the most common causes of blindness and low vision in older age groups. Age-related macular degeneration is a chronic degenerative disorder that most often affects people over 50 years of age. According to official materials from the WHO Center for the Prevention of Avoidable Blindness, the prevalence of this pathology in terms of appeal in the world is 300 per 100 thousand population. In economically developed countries of the world, AMD as a cause of low vision ranks third in the structure of eye pathology after glaucoma and diabetic retinopathy. In the US, 10% of people aged 65 to 75 years and 30% over 75 years old have loss central vision due to AMD. End-stage AMD (blindness) occurs in 1.7% of the total population over 50 years of age and about 18% of the population over 85 years of age. In Russia, the incidence of AMD is 15 per 1000 population.

AMD is characterized by progressive deterioration of central vision and irreversible damage to the macular area. Macular degeneration is a bilateral disease (in approximately 60% of cases, both eyes are affected), however, as a rule, the lesion is more pronounced and develops faster in one eye; in the other eye, AMD can begin to develop after 5-8 years. Often, the patient does not immediately notice problems with vision, since at the initial stage the better seeing eye takes on all the visual load.

IMPORTANT! When visual acuity decreases both at distance and at close range; difficulties encountered when reading and writing; the need for stronger lighting; If a translucent fixed spot appears before the eye, as well as distortion of the contours of objects, their color and contrast, you should immediately consult an ophthalmologist. The diagnosis of macular degeneration can only be made by a medical specialist. However, self-control is highly informative visual functions each eye separately using the Amsler test.

Mechanism of development and forms of age-related macular degeneration (AMD)

• The macula is made up of several layers of special cells. A layer of photoreceptors is located above the layer of retinal pigment epithelial cells, and below is a thin Bruch's membrane, separating the upper layers from the network of blood vessels (choriocapillaris), which provide the macula with oxygen and nutrients.

• As the eye ages, waste products from cell metabolism accumulate, forming so-called “drusen” - yellowish thickenings under the retinal pigment epithelium. The presence of many small drusen or one (or several) large drusen is considered the first sign of an early stage "dry" forms of AMD. The “dry” (non-exudative) form is the most common (in approximately 90% of cases).

• As drusen accumulate, they can cause inflammation by triggering the release of Vascular Endothelial Growth Factor (VEGF), a protein that promotes the growth of new blood vessels in the eye. The growth of new pathological blood vessels begins, this process is called angiogenesis.

• New blood vessels grow through Bruch's membrane. Since newly formed vessels are pathological in nature, blood plasma and even blood pass through their walls and enter the layers of the macula.

• From this moment on, AMD begins to progress, moving into another, more aggressive form - "wet".Fluid accumulates between Bruch's membrane and the photoreceptor layer, affecting the vulnerable nerves that provide healthy vision. If this process is not stopped, hemorrhages will lead to detachments and the formation of scar tissue, which threatens irreparable loss of central vision.
  The “wet” (exudative) form is much less common than the “dry” form (in approximately one or two cases out of 10), but is more dangerous - rapid progression occurs and vision deteriorates very quickly.

Symptoms of the “wet” form of AMD

• A sharp decrease in visual acuity, inability to improve vision with glasses correction.
• Blurred vision, decreased contrast sensitivity.
• Dropout of individual letters or crooked lines when reading.
• Distortion of objects (metamorphopsia).
• The appearance of a dark spot in front of the eye (scotoma).

Decreased visual acuity	Reduced contrast sensitivity
Central scotoma	Metamorphopsia - perception of objects in a distorted form

Goal of treatment for age-related macular degeneration

Age-related macular degeneration is treatable. However, not so long ago there was only one way to stop the “leaking” of blood vessels in wet AMD - laser coagulation. But this method did not eliminate the cause of the appearance of pathological vessels, and was only a temporary measure.

In the early 2000s, more than effective treatment called targeted therapy. This method is based on the impact of special substances specifically on the VEGF protein.

Currently, so-called anti-VEGF therapy has completely changed approaches to the treatment of AMD, allowing one to preserve vision and maintain the quality of life of millions of people around the world. Anti-VEGF therapy can not only reduce the progression of AMD, but in some cases even improve vision. Treatment is effective, but only if it is carried out before scar tissue forms and permanent vision loss occurs.

Intravitreal injections of drugs - Anti-VEGF therapy

In order for drugs that counteract the development of new blood vessels to effectively act on the macula, it is necessary to inject directly into the vitreous body of the eye. The procedure is performed in a sterile operating room by a qualified ophthalmologist.

The drug administration procedure takes only a few minutes and does not cause any pain. As the anti-VEGF drug penetrates the macula tissue, it reduces the level of activity of the protein, which stops the growth of abnormal blood vessels, after which these vessels begin to disintegrate and regress, and with continued treatment, the abnormal fluid also resolves.

Controlling angiogenesis and associated swelling stabilizes visual function and prevents further damage to the macula. According to clinical studies, approximately 30% of patients receiving anti-VEGF therapy for wet AMD recover some of the vision lost due to this disease.

Drugs for the treatment of age-related macular degeneration - LUCENTIS and Eylea

The first drug for anti-VEGF therapy in the form of intravitreal injections, certified in Russia for use in ophthalmology, was LUCENTIS, which has made a real revolution in the treatment of AMD and has become the “gold standard”. In June 2006, it was approved by the American Drug Control Agency (FDA) as unique remedy for the treatment of age-related macular degeneration, and in 2008 it was registered in Russia. Since 2009, EXCIMER ophthalmological clinics have been using the drug LUCENTIS in clinical practice.

Scientists continued their research to create a drug with a more prolonged action, not inferior in quality results to LUCENTIS. In November 2011, it was approved in the United States for the treatment of wet age-related macular degeneration of the retina. new drug EILEA. Since March 2016, the drug has been registered in Russia and began to be used in ophthalmological clinics Excimer.

Why are LUCENTIS AND EYLEA effective?

Before the advent of these drugs, anti-VEGF therapy used drugs designed to treat oncological diseases. LUCENTIS (and subsequently EYLEA) were specifically developed for use in ophthalmology, which ensures their higher effectiveness and safety.

The composition of the drug LUCENTIS molecules included active substance— ranibizumab, which reduces excessive stimulation of angiogenesis (growth of pathological vessels) in age-related macular degeneration and normalizes retinal thickness. LUCENTIS quickly and completely penetrates all layers of the retina, reduces macular edema and prevents an increase in the size of the lesion, the progression of the formation and sprouting of blood vessels and new hemorrhages.

EILEA- a drug containing the active substance - aflibercept, the molecules of which act as a “trap”, merging with the molecules of not only vascular endothelial growth factor (VEGF), but also placental growth factor (PIFG). EYLEA is characterized by a longer intraocular effect, which allows injections to be performed less frequently. In addition, this drug can be used not only for the “wet” form of age-related macular degeneration, but also in cases of visual impairment caused by diabetic macular edema and macular edema due to retinal vein occlusion.

What does scientific research show?

The clinical activity and safety of the drugs have been proven in a number of large international tests. The results are truly impressive - the majority of patients not only stopped the progression of the disease and maintained visual acuity, but this indicator significantly improved.

Central retinal thickness before and after treatment

• In comparison with laser treatment (photodynamic therapy), anti-VEGF therapy drugs significantly surpassed the results in terms of visual acuity obtained: by 6 months of treatment, injection therapy gave ~8.5-11.4 letters (on the ETDRS scale), while in the laser treatment group - 2.5 letters. By week 52, the anti-VEGF groups had gained 9.7–13.1 letters, whereas the laser group had lost 1 letter.
• After 52 weeks of treatment, the proportions of patients maintaining visual acuity in the LUCENTIS and EYLEA groups were 94.4% and 95.3%, respectively.
• The proportions of patients with an increase in visual acuity of ≥15 letters on the ETDRS scale - with EYLEA - 30.6%, with LUCENTIS - 30.9%, and the average value of improvement in visual acuity was 7.9 letters and 8.1 letters when treated with EYLEA and LUCENTIS.
• The average change in the thickness of the central zone of the retina: -128.5 µm (EYLEA) and -116.8 µm (LUCENTIS).

Frequency of administration and dosage

A drug LUCENTIS is injected into the vitreous body in a dose of 0.5 mg (0.05 ml). First, 3 consecutive monthly injections of Lucentis are carried out (the “stabilization” phase), then the number of injections is recommended by the doctor depending on the state of visual functions and the degree of the disease (the “maintenance” phase). The interval between doses is at least 1 month. After the stabilization phase, treatment with the drug is suspended, but 2-3 times a year patients need to be screened for the condition of the visual system.

Treatment with the drug EILEA start with three consecutive injections into the vitreous at a dose of 2 mg, then perform one injection every 2 months, with no additional follow-up examinations between injections required. After reaching the “stabilization” phase, the interval between injections can be increased by the attending physician based on the results of changes in visual acuity and anatomical parameters.

Cost of basic services

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Macular degeneration is a term that combines a group of retinal diseases in which central vision is impaired.

The reason for this lies in retinal ischemia (insufficient blood supply), which develops due to various factors.

The lack of comprehensive treatment almost always leads to blindness.

The second name of the disease is age-related macular degeneration of the retina, since it usually develops over the age of 45-50 years. Most often, both eyes are involved in the pathological process.

Causes of the occurrence and development of the disease

It has not yet been established exactly what causes age-related macular degeneration of the retina. To date, scientists have put forward a number of hypotheses on this issue, but none of them reliably explains the problem.

One of the theories is an insufficient intake of minerals and vitamins into the body: carotene, lutein, ascorbic acid, zinc and tocopherol. You can read more about vitamins in foods.

The next hypothesis is based on eating disorders. A number of studies have found that eating saturated fat accelerates the process of macular degeneration.

Not on last place costs of smoking. If you believe the statistics, then In smokers, macular degeneration progresses several times faster than among non-smokers. This fact is explained by the fact that nicotine reduces normal blood flow in all organs and systems, including the retina.

More than 20% of cases of macular degeneration are genetic in nature

The most widespread theory is that of hereditary predisposition. During the research, scientists discovered that more than 20% of cases of macular degeneration are genetic in nature and are inherited from one generation to another.

Suggestions have been made about the possible role of cytomegalovirus and herpes simplex virus in the occurrence of the disease.

Risk factors:

• Increased cholesterol levels in the blood serum;
• Age: starting from 40-45 years old, people get sick more often;
• Gender: women suffer from macular degeneration three times more often than men;
• Hereditary predisposition;
• Poor nutrition with a predominance of animal fats;
• The presence of cardiovascular diseases such as cerebral atherosclerosis and arterial hypertension;
• Smoking;
• Chronic stress;
• Overweight and obesity;
• Prolonged exposure of the eye to ultraviolet light;
• Flaw vitamin substances and antioxidants;
• Unfavorable environmental conditions.

Types of macular degeneration

It is customary to divide macular degeneration into two types:

• Dry macular degeneration, or non-exudative;
• Wet macular degeneration, or exudative.

Dry form

This type of dystrophy occurs in no more than 10% of cases. It is based on violations of the pigment layer of the epithelium, as well as the formation of limited areas of retinal atrophy.

Formation mechanism

The pathogenesis of the dry form of macular degeneration has not yet been precisely studied, but scientists have been able to more or less reliably describe the mechanism of formation of this pathology.

Most often, retinal dystrophy is preceded by it.

In this case, drusen (small flocculent formations) grow on the surface of the vitreous plate, which compress the retinal pigment epithelium. In these places, the amount of pigment decreases and then disappears altogether.

At the same time, in the drusen area, thinning of Bruch’s membrane occurs (this is the most inner layer choroid), which in in some cases accompanied by calcification.

Clinical manifestations

Typically, the non-exudative form of the disease resolves with minor functional changes. Visual acuity remains at 50% or more.

On initial stage the ophthalmologist may notice drusen and minor defects in pigmented epithelium. Then single oval or round foci of macular atrophy appear. In some cases, they merge and become similar to a geographical map.

At the same time, people notice that scotomas appear in their field of vision - these are the so-called blind spots. Their number and size may vary.

Wet form of macular degeneration

The wet form of macular degeneration is characterized by the appearance of more severe changes in the fundus, which are caused by small hemorrhages and fibrosis.

Formation mechanism

Many questions related to the mechanism of formation of the wet form of macular degeneration of the retina still remain unclear.

It is known that at some point a colloidal or granular substance is formed between the retinal pigment epithelium and Bruch's membrane.

Its formation is due to the fact that as a result of increased permeability of the vessels of the retina and choroid, blood plasma leaks out and accumulates under the layer of pigment epithelium.

Over time, the exudate “thickens” and turns into a colloid, which is facilitated by lipids and cholesterol present in the blood plasma. As a result, neuroepithelial detachment occurs, which disrupts the blood supply to the retina.

At this stage, compensatory mechanisms begin to be launched, aimed at the growth of new retinal vessels. The newly formed vessels form a kind of membrane on the surface of the retina, which subsequently becomes the cause of hemorrhages and its detachment. All this leads to the development of macular degeneration.

Diagnostics

In most cases, diagnosing age-related macular degeneration is not difficult. Ophthalmoscopy and fluorescein angiography of the fundus vessels are used.

Amsler test

Mandatory research is carried out with a grid. It helps determine whether the patient's central vision is impaired.

Procedure for performing the Amsler test:

1. Wear glasses or contacts (if you usually wear them).
2. Sit comfortably and place the net 30 centimeters in front of your eyes.
3. Cover one eye with a shield.
4. Focus your gaze on the central point, and, without looking away from it, evaluate the rest of the grid. Check to see if all the squares are the same size, if there are any curved lines or hazy areas, etc.
5. Repeat the procedure with the second eye.

How to evaluate the result

Normally, if the patient’s central vision is not impaired, he sees the image clearly. There are no distortions or hard-to-see spots on the grid, and all squares are the same size.

The results look like this:

How a healthy person sees the grid / How a person with impaired central vision sees the grid

The Amsler test should become a mandatory test for all patients over 45 years of age.

Clinical manifestations

Main symptoms:

Symptoms of the disease long time may be absent or disappear spontaneously. The most common complaint that patients make is the appearance of visual effects before the eyes. These can be flashes, lightning, floating spots and others.

It must be said that macular degeneration rarely leads to total blindness. Due to the fact that the pathological process affects only the central part of the retina, peripheral vision is always preserved. Thus, a person will have only peripheral vision.

Treatment of macular degeneration of the retina

To date, there are no treatments for age-related retinal macular degeneration with 100% effectiveness. There are three main areas of therapy:

1. Laser treatment;
2. Conservative treatment;
3. Surgical methods of correction.

The ophthalmologist's tactics will depend on how long the disease has existed.

Conservative therapy

For the treatment of dry form of macular degeneration recommended to take medicines, which normalize the metabolic processes of the retina.

These include vitamin preparations with selenium and zinc (for example, adruzene), as well as antioxidants (tocopherol, ).

Beneficial influence Preparations based on blueberries are also provided: difrarel, blueberry forte, myrtilen forte and others.

To improve blood flow in the macula area(macular area), must be used vasodilators. They have the following effects:

• Reduce the permeability of blood vessel walls;
• Increase local blood flow;
• Reduces blood viscosity;
• Inhibit the aggregation (gluing) of blood cells, which improves microcirculation;
• Increase the flow of oxygen to tissues;
• Accelerate the absorption of glucose necessary to maintain energy metabolism.

Medicines that meet all of the above requirements: Cavinton, Stugeron, Tanakan, Trental, Picamilon and others.

In recent years, pharmaceutical market There are drugs that inhibit (slow down) the growth of new vessels in the retina. These are Lucentis and Avastin. Let's look at them in more detail.

. This drug inhibits the growth of new blood vessels on the retinal surface. Just one injection of Avastin often helps achieve the desired result.

It was found that the use of this medicine is associated with more than 50% of cases of restoration of visual acuity.

Lucentis. The molecules of this product have a very low mass, which allows them to penetrate through all retinal layers and reach the target.

In 2006, Lucentis was approved in the United States of America as the drug of choice for the treatment of the exudative form of age-related macular degeneration. The drug appeared on the territory of the Russian Federation two years later.

The purpose of using this medication is stop the progression of vision loss. However, the medicine cannot restore those areas of the retina that have died from dystrophy. Meanwhile, some patients note that Lucentis to some extent helped them restore their vision.

This direction of therapy began to be used in ophthalmological practice in the mid-seventies of the last century.

The laser beam enhances the antioxidant activity of the retina, stimulates microcirculation, and also promotes the elimination (removal) of decay products.

Laser treatment of the retina is indicated in the case of non-exudative type of macular degeneration without the formation of large retinal drusen.

However, the laser has the best effect on exudative and exudative-hemorrhagic dystrophies. In this case, there is a decrease in swelling in the area of ​​the macula and destruction of the membrane formed by new vessels.

In practice, krypton, argon or diode lasers are used. Many experts prefer the krypton red ray, as it is believed that it has minimal damaging effects.

Surgical methods of treatment

Surgical treatment of retinal macular degeneration is carried out using the following techniques:

• Standard vitrectomy;
• Retinotomy in the posterior pole area;
• Change in position of the macula.

Vitrectomy– partial or complete removal vitreous body in order to gain rapid access to the retina. Here the doctor removes the subretinal membranes that cause visual impairment. Subsequently, the removed vitreous tissue is replaced with a specialized liquid or gas.

Retinotomy is performed to remove subretinal hemorrhages. During the operation, the doctor makes an incision in the retina, through which the blood that has leaked under the retina is removed. It is impossible to remove blood clots, so drugs are injected into the area where they are located to promote spontaneous resorption of the hematoma.

The position of the macula is changed by subtotal vitrectomy and a circular incision in the retina. Afterwards, the retina is peeled off and shifted in the desired direction. As an option for surgery, the position of the retina can be changed by forming folds on it. In this case, a circumferential cut is not made.

Folk remedies for the treatment of macular degeneration

Often patients independently use the following folk remedies to treat macular degeneration of the retina:

I would like to note that before using these methods, you should definitely consult with your doctor.

Lifestyle with macular degeneration

The initial stages of macular degeneration do not lead to a noticeable change in the patient’s lifestyle. In some cases, there is a need for better lighting to perform work that previously did not require it.

As the disease progresses, the patient's vision deteriorates significantly. Distortions of visible reality occur, and a dark spot appears in the field of vision.

All this puts a person in front of the need to give up driving a car, reading, performing actions that require high precision and good vision. In general, the presence of macular degeneration makes the patient's lifestyle passive.

Prevention

According to the latest data, age-related macular degeneration of the retina tends to “rejuvenate”, that is, it begins to manifest itself at an older age. early age. That is why disease prevention plays a very important role.

• Quit smoking forever;
• Always protect your eyes from ultraviolet exposure (wear sunglasses, hats, etc.);
• Do not start treatment for hypertension if you have it;
• Visit your ophthalmologist regularly (at least once a year);
• Minimize cholesterol and all foods containing excess animal fats in your diet;
• If you have a hereditary predisposition to the disease, take vitamins with zeaxanthin and lutein. By the way, these elements are found in beans, spinach, egg yolks, kiwi, lettuce, peas, as well as in seaweed (for example, kelp).

What is AMD?

Age-related macular degeneration (AMD), or macular degeneration, is a disease that affects the central, most important area of ​​the retina - the macula, which plays a key role in vision.

Age-related macular degeneration is the leading cause of irreversible vision loss and blindness among people aged 50 years and older in the developed world. Because people in this group represent a growing proportion of the population, vision loss from macular degeneration is a growing problem.

According to WHO, the share of the population of the older age group in economically developed countries is about 20%, and by 2050. will probably increase to 33%. Accordingly, due to the expected increase in life expectancy, the steady increase in atherosclerosis and concomitant pathologies, the problem of AMD remains the most pressing. In addition, in recent years there has been a clear trend toward “rejuvenation” of this disease.

The cause of decreased vision is degeneration of the macula, the most important area of ​​the retina, responsible for the sharpness and acuity of central vision necessary for reading or driving a car, while peripheral vision is practically unaffected. The socio-medical significance of this disease is due precisely quick loss central vision and loss of general performance. The severity of the process and loss of central vision depends on the form of AMD.

Dry and wet forms of AMD

Intense metabolism in the retina leads to the formation of free radicals and other active forms oxygen, which can cause the development of degenerative processes due to insufficient functioning of the antioxidant system (AOS). Then, in the retina, especially in the macula and paramacular region, under the influence of oxygen and light, non-cleavable polymer structures are formed - drusen, the main component of which is lipofuscin.

With the deposition of drusen, atrophy of the adjacent layers of the retina occurs and the growth of pathological newly formed vessels in the retinal pigment epithelium is noted. Subsequently, scarring processes occur, accompanied by loss of large quantity retinal photoreceptors.

Ophthalmologists distinguish two variants of the course of this disease - dry (non-exudative, atrophic) and wet (exudative, neovascular) forms of AMD.

The dry form of AMD is more common than the wet form and is detected in 85% of all cases of AMD. Yellowish spots known as drusen are diagnosed in the macular area. The gradual loss of central vision limits patients' ability to see fine details, but it is not as severe as in the wet form. However, the dry form of AMD may slowly progress over several years to late stage geographic atrophy (GA) is the gradual degradation of retinal cells, which can also lead to severe vision loss.

Doesn't exist today radical treatment dry form of AMD, although some are now in clinical trials. A huge number of clinical studies have proven that certain nutrients such as beta-carotene (vitamin A), vitamins C and E can help prevent or slow the progression of dry macular degeneration. Research shows that taking large doses of some food additives and eye vitamins can reduce the risk of developing early-stage AMD by 25%. Eye doctors also recommend that patients with dry AMD wear sunglasses with UV protection.

The wet form of AMD is present in approximately 10-15% of cases. The disease develops quickly and often leads to significant loss central vision., dry AMD progresses to more advanced and damaging forms of the eye disease. In wet AMD, the process of new blood vessels growing (neovascularization) begins. The wall of such vessels is defective and allows blood cells and fluid to pass through, which accumulate in the space under the retina. This leakage causes permanent damage to the light-sensitive cells in the retina, which die and create blind spots in central vision.

Choroidal neovascularization (CNV) underlies the development of wet AMD. Abnormal vascular growth is the body's faulty way of creating a new network of blood vessels to ensure supply. required quantity nutrients and oxygen to the retina. Instead of this process, scarring occurs, resulting in severe loss of central vision.

Causes and risk factors for developing AMD

Despite numerous studies on AMD, the causes of this disease remain unclear to date. AMD is a multifactorial disease.

Age is the main reason. The incidence increases sharply with age. Among middle-aged people, this disease occurs in 2%, at the age of 65 to 75 years it is diagnosed in 20%, and in the group from 75 to 84 years old, signs of AMD are found in every third person. A significant portion of the population has a congenital predisposition to AMD, but there are a number of factors that either contribute to the onset of the disease or prevent it.

A number of risk factors have been proven that negatively affect natural protective mechanisms and therefore contribute to the development of AMD, the most significant are:

• Race - the highest prevalence of AMD is observed in Caucasians
• Heredity - family history is an important risk factor in 20% of patients with AMD. A threefold increase in the risk of developing AMD has been established if the disease occurs in relatives in the first generation
• Cardiovascular diseases play a significant role in the development of AMD. It has been established that with atherosclerosis, the risk of damage to the macular area increases 3 times, and in the presence hypertension– 7 times.
• Cigarette smoking is the only risk factor whose significance was confirmed in all studies. Quitting smoking reduces the risk of developing AMD.
• Direct exposure to sunlight
• Nutrition - AMD risk higher in people who eat more saturated fat and cholesterol and who are overweight.
• Light iris
• Cataracts, especially nuclear ones, are a risk factor for the development of AMD. Cataract surgery may contribute to the progression of the disease in patients with existing changes in the macular area.

Symptoms of AMD

Age-related macular degeneration usually causes slow, painless, and irreversible vision loss. In rare cases, vision loss can be severe.

Early signs of vision loss from AMD include:

• appearance of dark spots in central vision
• blurred image
• distortion of objects
• deterioration in color perception
• sharp deterioration of vision in poor lighting and darkness

The most basic test for determining the manifestations of AMD is the Amsler test. The Amsler grid consists of intersecting straight lines with a central black dot in the middle. Patients with symptoms of AMD may see that some lines appear blurred or wavy, and dark spots appear in the field of vision.

An ophthalmologist can distinguish the manifestations of this disease even before changes in the patient’s vision develop and refer him for additional examinations.

Diagnosis of AMD

Diagnosis of AMD is based on medical history, patient complaints, assessment of visual functions and data from examination of the retina using various methods. Currently, fundus fluorescein angiography (FAGD) is recognized as one of the most informative methods for detecting retinal pathology. To conduct FAHD, various models of cameras and special contrast agents - fluorescein or indocyanine green - are used, which are injected into the patient’s vein, and then a series of fundus photographs are taken.

Stereoscopic images can also be used as a baseline for dynamic monitoring of a number of patients with severe dry AMD and patients during treatment.

For a fine assessment of changes in the retina and macula, OCT (optical coherence tomography) is used, which makes it possible to detect structural changes at the most early stages retinal degeneration.

Treatment of dry and wet forms of AMD

Despite enormous strides in improving diagnostic methods for AMD, its treatment remains limited. complex problem. In the treatment of dry forms of AMD and with a high risk of developing the disease, courses of antioxidant therapy are recommended in order to normalize metabolic processes in the retina.

According to the AREDS study, beneficial effect benefit from antioxidant supplementation was achieved in those participants who had intermediate or late stage AMD in at least one eye. Combination therapy with antioxidants, zinc and copper over 5 years reduced the incidence of late-stage AMD by 25%, and the risk of loss of visual acuity of 3 or more lines by 19%.

It should be remembered that replacement therapy for the prevention and treatment of the dry form of AMD cannot be a course course; its use is possible only on an ongoing basis. It should be used in persons over 50 years of age, and in the presence of risk factors (smoking, overweight, complicated medical history, cataract extraction), and earlier.

Treatment of wet AMD is aimed at suppressing the growth of abnormal blood vessels. Today, there are a number of drugs and techniques registered in Russia that can stop or reduce the manifestations of abnormal neovascularization, which has improved vision in a significant number of people with wet form AMD.

For getting additional information, read our article “Treatment of age-related maular degeneration.”

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