Age-related macular degeneration of the retina. Age-related macular degeneration. Why Lucentis and Eylea are effective

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Maintaining good vision into old age is very difficult. Often, in old age, the ability to see is gradually lost. This is due to the fact that all human organs begin to “wear out” over time. One of the first tissues to suffer is the eye tissue. It is believed that vision deteriorates from the age of 40-45. This happens even in cases where a person has not previously had problems with vision during his life. Vision deterioration occurs gradually. Most people are concerned about “farsightedness,” that is, the inability to see objects that are close. Sometimes, more serious problems develop. These include pathologies such as cataracts, glaucoma, etc. Another common disease is age-related macular degeneration. This disease is dangerous because it can lead to loss of vision.

Age-related macular degeneration (AMD) is a pathology that develops due to degenerative processes in the retina of the eye. This area is directly connected to the brain (it is a peripheral analyzer). With the help of the retina, the perception of information and its transformation into visual images is formed. On the surface of the peripheral analyzer there is a zone that contains many receptors - rods and cones. It is called the macula (yellow spot). The receptors that make up the center of the retina provide color vision in humans. In addition, it is in the macula that light is focused. Thanks to this function, human vision is sharp and clear. Age-related macular degeneration of the retina leads to degeneration of the macular tissue. Not only the pigment layer undergoes changes, but also the vessels feeding this area. Although the disease is called “age-related macular degeneration,” it does not only affect older people. Often, the first symptoms of pathological changes in the eye begin to be felt by the age of 55. In old age and old age, the disease progresses to such an extent that a person may completely lose the ability to see.

Age-related macular degeneration of the retina is a common disease. Often this pathology becomes the cause of loss of ability to work and disability. It is widespread in America, Asia and Europe. Unfortunately, the disease is often diagnosed in late stages. In these cases, it is necessary to resort to surgical treatment. However, with timely therapeutic treatment, as well as the implementation of preventive measures, it is possible to avoid surgical intervention and complications of pathology (blindness).

Like all degenerative processes, this disease tends to be slow and progressive. The causes of dystrophic changes in the macula of the retina can be different. The main one is considered to be the involution of eye tissue. However, in some people, dystrophic changes occur more quickly, while in others, more slowly. Therefore, there is an opinion that age-related macular degeneration is inherited (genetically), and also predominates in people of European nationality. Other risk factors include: smoking, arterial hypertension, frequent exposure to the sun. Based on this, the causes of macular degeneration can be identified. These include:

1. Vascular lesions. Atherosclerosis of small arteries is considered one of the risk factors. Impaired oxygen delivery to eye tissues is one of the main mechanisms for the development of degeneration.
2. Excess body weight.
3. Lack of vitamins and some microelements. Among the substances necessary to maintain retinal tissue are lutein and zeaxanthin.
4. The presence of a large number of “free radicals”. They increase the risk of developing organ degeneration several times.
5. Ethnic characteristics. The disease is more common in people with light-colored eyes. The fact is that representatives of the Caucasian race have a low density of pigment contained in the retina. For this reason, degenerative processes develop faster, as do the symptoms of the disease.
6. Poor nutrition.
7. Exposure to direct sunlight without protective glasses.

Pathology often develops in people with a burdened hereditary history (presence of the disease in parents or grandmothers). In most cases, the disease is diagnosed in the female population.

Like all degenerative changes, this disease has a complex development mechanism. In addition, the pathogenesis of dystrophic processes still cannot be fully studied. It is known that under the influence of unfavorable factors, the macula tissue is subject to irreversible damage. Most often, pathology begins to develop in people suffering from vascular diseases (atherosclerosis, diabetes mellitus) and obesity. Also, the disease is almost always found among the smoking population. Due to blockage of the vascular bed and insufficient nutrition of eye tissue, age-related macular degeneration develops. The pathogenesis of the disease is based on a violation of the redox balance. Free radicals play the main role in this process. These substances are formed in the macula for several reasons. First, the macula of the retina is constantly exposed to oxygen and light. In addition, in this area there is an accumulation of fatty acids that tend to oxidize. Another factor in the pathogenesis of the development of pathology is the origin of the retina. After all, this shell of the eye is considered a peripheral analyzer and is directly connected to the brain. Therefore, it is especially sensitive to “oxygen starvation.”

All of these factors predispose the macula tissue to gradually become thinner. As a result of exposure to radicals, cell membranes are destroyed. The retina becomes even more sensitive to light. Under the influence of ultraviolet and infrared radiation, AMD develops even faster. All these processes lead to the fact that the macular epithelium begins to “lose” pigment receptors and undergoes atrophy. If the destruction of the macula is not stopped in time, tissue detachment occurs. The final stage is the appearance of scars and the development of blindness.

There are 3 forms of macular degeneration. This classification is based on the morphological changes occurring in the retinal tissue. This division is necessary to determine the tactics of treating the disease.

Morphological types of the disease:

1. Age-related macular degeneration - wet form: characterized by the presence of exudate. This option is rare, occurring in 20% of cases. It has a rapidly progressive course. If a person’s vision rapidly deteriorates (within a few days), then it is worth suspecting a disease such as age-related macular degeneration. The wet form develops due to neovascularization, that is, the appearance of a large number of new vessels on the retina. Given the damage in cell membranes, their permeability increases. As a result, swelling and hemorrhage develops.
2. Age-related macular degeneration - dry form: characterized by a slow progression. In another way, this type of pathology is called atrophy. Dry age-related macular degeneration develops in 90% of patients. On examination, drusen are noted - light foci of atrophy, insufficiency of the pigment layer, and defects in the epithelium.
3. Scar form of macular degeneration. It is considered the final stage of AMD. It is characterized by epithelial detachment and the formation of connective tissue (scar). In this case, there is a complete loss of vision.

In some cases, the dry form of AMD turns into an exudative version of the disease. Most often this occurs with vascular lesions, and in particular diabetic retinopathy. Such changes indicate a worsening prognosis and are a signal for urgent measures.

Depending on the form of AMD, symptoms of the disease can develop either slowly or quickly. Often, long-term macular degeneration does not make itself felt for several years. In the dry form of AMD, drusen appear on the surface of the retina - areas of atrophy. As a result, vision gradually deteriorates. The pigment layer suffers to a greater extent, which is why the brightness of the colors is somewhat lost. Visual acuity may change, but only slightly. The wet form of macular degeneration develops quickly. Within a few days, vision can deteriorate significantly, leading to complete blindness. Due to edema and increased membrane permeability, hemorrhages may occur, which are visible to the naked eye. Symptoms observed with AMD:

1. Change the contrast and brightness of the image.
2. Decreased visual acuity.
3. Curvature, distortion of objects.
4. Image blurred.
5. The appearance of loss of visual fields.
6. Inability to read despite wearing glasses.

With the gradual development of pathology, signs of the disease may be absent for a long time. Then there is a gradual deterioration of central vision. When looking forward, most of the image becomes blurred. However, peripheral (side) vision is preserved. Gradually the affected area increases.

In the wet and scar form of AMD, blindness occurs quickly. Unlike the dry type of degeneration, peripheral vision can rarely be preserved. With timely treatment of AMD, the development of blindness can be stopped.

Age-related macular degeneration can be diagnosed in its early stages. Therefore, people suffering from vascular lesions need to be examined by an ophthalmologist 1-2 times a year. Diagnosis of AMD is based on medical history and special examination. Elderly people most often complain of the appearance of a “spot” in front of their eyes, reminiscent of fog. The diagnosis of “macular degeneration” is most often made when vision deteriorates in women, especially if there is a history of type 2 diabetes mellitus or vascular atherosclerosis. In addition to the survey, a number of ophthalmological examinations are performed. Among them are measurement of visual acuity, perimetry, stereoscopic biomicroscopy.

To assess the condition of the vessels, fluorescein angiography of the fundus is performed. Thanks to this study, it is possible to detect areas of epithelial detachment, atrophic drusen, and neovascularization. However, this method of instrumental diagnostics has contraindications and risks. Therefore, before deciding to undergo an examination, it is worth visiting an ophthalmologist and getting his advice.

Once the diagnosis is confirmed, it is necessary to immediately begin treatment for age-related macular degeneration. The dry form of the disease is less aggressive, so it is amenable to drug therapy. This will not help get rid of the pathology completely, but it will stop (slow down) the process for several months or years. First of all, with AMD, you need to follow a diet. Considering that atrophic processes develop due to a lack of carotenoids and blockage of the fundus vessels, the patient should exclude animal fats. To prevent atherosclerotic changes in the small arteries of the retina, you should eat large amounts of fruits, herbs, and vegetables. In addition, such a diet will help compensate for the lack of vitamins and microelements.

To combat free radicals, it is recommended to spend less time in the sun. Patients should also consume antioxidants. These include vitamin E and C. To improve blood supply to the fundus of the eye, it is recommended to use antiplatelet agents and vasodilators.

For the wet form of macular degeneration, not only drug therapy is carried out, but also surgical treatment. Drugs that restore the pigment layer of the retina include the medications “Lutein” and “Zeaxanthin”. These drugs belong to the group of antioxidants. In addition, it is recommended to eat foods containing zinc. If the disease has developed as a result of diabetic retinopathy, it is necessary to carry out glucose-lowering therapy under the control of the glycemic profile.

Drug therapy alone is not enough if the patient is diagnosed with age-related macular degeneration. Treatment of the pathology must be combined with surgical correction. This is especially true for the wet form of AMD. Currently, almost every ophthalmology clinic provides laser treatment for macular degeneration. It may vary. The choice of method depends on the stage of AMD and the manifestations of the pathology. The following methods of surgical correction are distinguished:

1. Laser coagulation of neovascular membrane.
2. Photodynamic therapy with Visudin.
3. Transpupillary laser thermal correction.

If possible and there are no contraindications, pigment epithelium transplantation and vitrectomy (in case of hemorrhage into the vitreous body of the eye) are performed.

Preventive measures include: dieting, weight loss. In case of vascular lesions, smoking cessation is recommended. People with light-colored eyes should also avoid direct exposure to sunlight. In addition, prevention includes the use of vitamins to strengthen vision and microelements.

Time cannot be stopped, just as aging of the human body cannot be avoided. As you age, many problems begin to arise. Including vision problems.

Let's remember a little about the structure of our eye. The macula has a second name - the yellow spot. This is the very center of the retina where the beam of light is focused. It provides central vision as well as color perception of the visual image. Damage to the macula that occurs in patients of the older age group indicates the onset of a pathology such as age-related macular degeneration (abbreviated as AMD).

With macular degeneration, the diameter of the blood vessels supplying the retina decreases. As a result, its tissues cease to fully receive the necessary substances. Dystrophic changes develop in one or both (left and right) eyes. AMD is often the cause of disability and disability.

Of course, when we talk about age-related macular degeneration, we understand that the main cause of this disease is precisely age-related degenerative changes in the retina. But in some patients the disease develops, while in others it does not; in some it progresses rapidly, while in others it progresses extremely slowly. The reasons for this situation have not been fully studied, but histology helps to understand the mechanism of development of the pathological process and identify a number of risk factors:

• Genetic predisposition and heredity (inheritance occurs as an autosomal dominant, an autosomal recessive, or by linkage to the X chromosome).
• Smoking. It significantly increases the risk of developing AMD.
• Arterial hypertension.
• Diabetes.
• Myopia or farsightedness.
• Prolonged exposure to sunlight on eyes not protected by sunglasses.
• Excess body weight. Scientific research points to a link between obesity and the progression of AMD.
• Poor nutrition, as a result of which the patient’s body does not receive enough nutrients necessary for the proper functioning of the visual apparatus (in particular carotenoids).
• Race. Age-related vision changes are more common in whites than in African Americans.
• Vegetative-vascular dystonia or, in short, VSD.
• It should also be noted gender – in the fairer sex this disease is diagnosed more often.
• Eye pathologies. For example, chronic blepharitis or endocrine ophthalmopathy (pseudotumorous or thyrotoxic form).
• Previous eye injuries.

Age-related macular degeneration is more often diagnosed in women and whites.

Classification of macular degeneration

Ophthalmologists classify pathology according to the forms of AMD:

1. Dry (other names - non-exudative, atrophic). Develops slowly.
2. Wet (other names - exudative, neovascular). It is developing rapidly.
3. Scar. The last stage of AMD. It is developing rapidly.

The dry form of AMD is observed in 85% of cases than other forms of pathology. As a person ages, metabolism changes. This results in yellowish spots called drusen in the macula area. These are the foci of atrophy. Drusen are divided into hard and soft. Hard – small and clearly defined; soft - large, with blurry edges, can merge with each other. The patient loses visual acuity gradually. This is one of the differences between this form of pathology and others. Cases have been recorded in which the dry form gradually passed into the final, scarring stage.

The dry form of AMD is also called non-exudative or atrophic.

Neovascular form

Ophthalmologists diagnose this type of pathology in only 10-15% of cases. The wet form of AMD is the result of progression of the atrophic form. The disease develops rapidly. In most cases, central vision is almost completely lost. As drusen (arising in the dry form) increase in size and thicken, the process of formation of new vessels develops on the retina. It is this process, also called neoangiogenesis, that distinguishes the wet form. As a result, the body tries to mistakenly compensate for insufficient nutrition of the retina by sending additional oxygen and substances necessary for functioning.

As the pathology progresses, blood cells and fluid penetrate through the walls of new vessels, accumulating in the area under the retina. Swelling develops and hemorrhages appear. As a result, retinal cells that are particularly sensitive to light are constantly damaged and die. This creates blind spots in central vision.

Classified into:

1. Classic, affecting the subretinal neovascular membrane (SNM).
2. Hidden, also called occult.
3. Mixed.

The wet form is also called exudative or neovascular.

Scar form

When vessels grow under the pigment epithelium, retinal detachment is possible, followed by detachment of the neuroepithelium and the formation of scar tissue (transition to the scar stage).

This is the final stage of age-related macular degeneration. Vision loss is irreversible.

Symptoms directly indicate the form of the disease. In most cases, the disease is asymptomatic.

Symptoms:

1. As a result of the gradual appearance and further increase of drusen, vision deteriorates. In the dry form it is insignificant and gradual, and in the wet and cicatricial form it is rapid.
2. Floaters begin to flash before the eyes (especially typical for the dry form).
3. The pigment layer suffers the most, which is why the perception of the shades and brightness of the picture and its contrast decreases.
4. Hemorrhages arising from edema, which are noticeable to others, indicate the wet form of the disease.
5. Fields of vision disappear.
6. The picture we see becomes blurred.
7. Surrounding objects are distorted, straight lines are bent.

The development of the dry form is asymptomatic at first.

Development of the dry form:

1. In the initial stages there are no symptoms.
2. Central vision gradually deteriorates.
3. Then most of the image becomes cloudy.
4. Over time, the affected area enlarges and darkens, resulting in the formation of a scotoma.
5. Peripheral vision remains intact.

The special features of the second and third forms are as follows:

1. 100% vision loss occurs quickly.
2. It is possible to preserve peripheral vision in very rare cases.

In the final cicatricial form of AMD, the degree of vision loss reaches 100%.

Despite the possibility of long-term asymptomatic progression of the disease, age-related macular degeneration can be diagnosed thanks to modern eye examinations. People over 50 years of age should have regular eye exams. This will identify pathology at an early stage and prevent vision loss.

The dry form can smoothly transform into the most dangerous form - the scar form. Therefore, you need to visit the ophthalmologist regularly.

With a long process of development of pathology, patients coming to the ophthalmologist most often complain of the appearance of a “spot” in front of the eyes, reminiscent of fog. Gradually the defect increases in size.

Diagnostic methods:

• taking anamnesis;
• visometry;
• ophthalmoscopy (examining the fundus of the eye);
• optical coherence retinotomography;
• visocontrastometry;
• fluorescein angiography;
• computer perimetry;
• color stereo photography.

These methods allow for timely and high-quality diagnosis of the macular region of the retina.

Based on the diagnostic results obtained, a course of treatment is prescribed.

When AMD of the eye is detected, the doctor must explain to the patient what it is, prescribe a course of treatment and teach self-diagnosis (relevant for the dry form of the pathology).

For those patients who have already been diagnosed with age-related macular degeneration of the retina, a good method for diagnosing the progression of the disease is the Amsler grid test. This method allows you to determine even the initial signs of macular edema due to the formation of new vessels on the retina.

The Amsler grid is a 40 x 40 cm grid with square cells with a dot in the middle. When diagnosing, the test distance to the Amlser grid is about 50 cm. One eye must be covered with the palm of your hand, and the other eye must be looked at the grid.

If pathology is present, the patient may see non-existent “holes” or “dark spots”, or distortions in the mesh. With this development of events, it is necessary to urgently undergo examination by an ophthalmologist.

Self-examination using the Amsler grid can be performed even every day.

Self-diagnosis allows you to monitor the development of AMD.

Treatment of eye AMD

Treatment of dry form

The dry form is more treatable than the wet form. It has a more favorable course.

Damage in this form of the disease is irreversible. Reducing the risk of transition to the wet form is achieved through drug therapy, which includes taking:

1. Antioxidants.
2. Vitamin and mineral complexes.
3. Taurina.
4. Lutein/beto-carotene/vitamin A/zeaxanthin (one of the drugs or their complex is prescribed depending on the clinical picture of the disease) in the amount of 10 mg/15 mg/28000 IU/2 mg.
5. Anthocyanosides.
6. Vitamins C and E in the amount of 500 mg and 400 IU, respectively, daily.
7. Copper and zinc in the amount of 2 mg and 80 mg, respectively.
8. Selenium and other trace elements.
9. Gingko biloba.

You should visit your doctor regularly to monitor the progress of the disease.

For dry AMD, treatment is based on taking vitamin complexes.

To improve blood circulation in the retina, patients are recommended to take antiplatelet agents and vasodilators.

It is worth noting that conservative medicine, which consists of prescribing dedystrophic drugs, immunomodulators and antioxidants (tablets, injections or drops), is ineffective. When taking these drugs, patients most often ignore the need to visit an ophthalmologist for monitoring. In this regard, the risk of the disease progressing to a more severe stage increases.

Not so long ago, the only effective method of treating the wet form of AMD was laser coagulation - destruction (destruction) of newly formed vessels using a laser. However, this method did not eliminate the cause of the formation of new vessels. In addition, healthy tissue can also be damaged during this procedure.

A less aggressive version of wet laser therapy is photodynamic therapy using the drug Visudin. It is administered intravenously and the retina is irradiated with a laser. The drug has a tropism only for pathological vessels of the retina, is able to accumulate in them and be activated when exposed to a laser beam. Blood clots form in bleeding pathological vessels, and the vessels become “sealed.” With this procedure, there is virtually no risk of damage to healthy tissue.

Visudin is used to treat wet AMD with photodynamic therapy.

But today, VEGF therapy, developed in the early 2000s, is considered a more progressive method. The second name is “Targeted Therapy”. Treatment of eye AMD in this case allows not only to stop the progression of the process, but also to partially restore the patient’s vision. However, this statement is only true if irreversible scar changes have not yet begun.

With VEGF therapy, special drugs are injected into the vitreous body of the eye to stop the formation of blood vessels. The drugs used for these injections are Lucentis, Macugen, Avastin and Eylea.

The following risks are possible with this type of therapy: increased intraocular pressure, retinal detachment, eye infection, temporary visual impairment, hemorrhage.

Among the surgical methods for treating AMD, the following types of operations should be noted:

• pigment epithelium transplantation;
• removal of subretinal neovascular membranes with the formation of scleral folds;
• removal of subretinal hemorrhages.

Lucentis is used to treat wet AMD with VEGF therapy.

Additional measures

For patients who have lost visual acuity, glasses are prescribed. Plus lenses are installed for nearsighted people, and minus lenses for farsighted people. It is recommended to have an anti-reflective coating to protect your eyes from negative effects such as glare from a monitor or TV, or increased eye strain when reading or other work.

It is permissible to use one or another traditional treatment method only after consultation with your doctor. Unfortunately, traditional medicine cannot cure AMD, but it can improve well-being, prevent the development of the disease and relieve symptoms.

1. Soak washed oat grains in a half-liter jar for 4 hours. Drain the water and pour the oats into the pan. Pour in 3 liters of water and cook over medium heat after boiling for 30 minutes. The resulting broth is filtered and stored in the refrigerator. Take warmed up to 5 times a day in a glass. It is recommended to add ground currants, blueberries, chokeberries and honey to the decoction.
2. 1 tablespoon of pharmaceutical calendula is poured into a glass of boiling water and left for 15 minutes. Let it stand. Then strain and take 3 times a day, ¼ cup. You can also apply this infusion to your eyes, 2 drops per eye. Take up to 6 months. Then take a break.
3. Everyone knows about the benefits of aloe and mumiyo. They can also help with AMD. You need to dissolve 50 g of mumiyo in 100 ml of aloe juice. Insist. There are two options for using this infusion. The first is to drink 10 ml 2 times a day. The second is to use as eye drops: 1k. in each eye. After 10 days of taking it, take a break.
4. Onion peels (2 parts), rose hips (2 parts) and pine needles (5 parts) need to be chopped. Pour 1 tablespoon of the mixture into 1 liter of water and boil for 2-3 minutes. Take 1.5 liters daily.
5. A tablespoon of cumin is poured into 250 ml of water. Boil over low heat for 2-3 minutes. Add 1 tsp. cornflower flowers, mix and set aside for 5 minutes. Use 1-2 drops in each eye 2 times a day.
6. Grind the celandine. 1 tsp pour 100 ml of water. Heat on fire for 10 seconds. Let it brew. The infusion is filtered and stored in the refrigerator. Apply 3 drops in each eye 3 times. in a day. Course – 1 month.
7. Take 1 part goat milk and 1 part boiled water. Use the resulting mixture as drops - 1 drop in each eye. After instillation, you need to cover your eyes with a dark bandage or special glasses and lie down for 30 minutes. Course – 1 week.
8. Add 1 tsp to 1/3 cup of chopped nettle. chopped lilies of the valley and add ½ tsp. soda Mix. Place in a dark and dry place for 9 hours. Make compresses from the resulting mass.
9. Treatment with leeches is a separate but very useful area of ​​traditional medicine.

Traditional medicine can be used as an addition to basic treatment.

It is necessary to consume a sufficient amount of foods rich in carotenoids, fresh vegetables, fruits, and herbs.

You should also limit the intake of animal fats from food, which provoke atherosclerotic changes in the retina.

Foods rich in carotenoids:

• carrot;
• pumpkin;
• potato;
• melon;
• spinach;
• cabbage;
• zucchini;
• citrus;
• tomatoes;
• Bell pepper;
• corn;
• apricots;
• peaches;
• persimmon.

Foods with antioxidants:

• Red Ribes;
• blueberry;
• cranberry.

Measures to prevent senile disease - AMD include:

• diet (limiting animal fats; sufficient amounts of fresh vegetables and fruits);
• weight loss;
• blood pressure control;
• wearing sunglasses (especially for patients with light eyes);
• giving up bad habits (smoking);
• taking vitamin complexes;
• playing sports; but from professional sports; for example, triathlon, you will have to refuse.

And, of course, regular examination by an ophthalmologist is necessary.

Nov 28, 2017Anastasia Tabalina

Age-related macular degeneration is a deterioration of vision, up to blindness, in people after 40 years of age. As a rule, the retina begins to atrophy and change. In other words, this disease is called macular degeneration. This pathology is considered chronic because the macular zone of the retina is irreversibly affected. If disturbances are observed in one organ, then after a certain period of time, another will be involved. In this case, the degree of damage can be different, that is, degeneration occurs asymmetrically.

Age-related macular degeneration of the retina is characterized by a progressive course, which begins to develop gradually at first, but then takes on a rapid form. For many years a person may not know about the existence of pathology, but when it reaches a certain degree, it begins to progress.

Ophthalmologists are sounding the alarm: “The best-selling vision aid in Europe was hidden from us. To fully restore your eyes you need...” »

The main symptoms of the disease are the inability to see an object at any distance. Sometimes in life it happens that a familiar person passes by and at the same time makes eye contact, but does not even say hello. In fact, the reason is not that he doesn't want to see you, but that he can't.

While watching TV, the patient also cannot distinguish the image and, even more so, cannot read. The fact is that the picture in the patient’s eyes seems blurry, and the color is incomprehensible. For example, if a person looks at a straight line, he will definitely see a wave. In addition, quite often the patient sees a translucent spot, which is fixed in one place. The disease can be of two forms: dry and wet. Each of them has its own characteristics.

Age-related macular degeneration of the dry form is considered simpler and is observed in the majority of patients. As a rule, it is asymptomatic for many years, with only some signs of farsightedness present. This is poor vision of objects at close range. But distant images look clear and peripheral vision is preserved. With this form of pathology, there is a deterioration in the absorption of nutrients by the cones responsible for this. This happens due to the accumulation of drusen, that is, products of metabolic processes.

The wet form of pathology is quite rare, only in ten cases out of a hundred. It is considered dangerous because it always develops rapidly. If the wet type of age-related macular degeneration is not detected in a timely manner, it can lead to complete blindness. Consequently, to disability. This form is characterized by the ingrowth of eye vessels into the retina, as a result of which blood fluid seeps into the thickness of the organ. Due to this, severe swelling develops, which weakens the functions of the visual apparatus.

Progressive deterioration of vision over time can lead to dire consequences - from the development of local pathologies up to complete blindness. People, taught by bitter experience, use a proven remedy that was previously unknown and popular to restore their vision... Read more"

People with the following disorders can be included in the risk group:

1. Age-related changes after 50 years.
2. Hereditary factor.
3. Female.
4. Diabetes.
5. Smoking and drinking alcoholic beverages.
6. Excessively frequent visits to the solarium and prolonged exposure to the sun.
7. Obesity.
8. Poor nutrition.
9. Vascular diseases.
10. Heart pathologies.
11. Hypertension.

If a decrease in visual acuity is detected, you should immediately go to an ophthalmologist, especially since the symptoms may indicate the presence of other pathologies.

After a thorough eye examination, each patient should have their vision monitored at all times. This is necessary to clarify the rate of progression. This can be done using an image that a person encounters every day. Looking, for example, at your favorite painting (each time from the same distance), you can understand how unclear the image is.

There is also a special control technique: the Amsler grid, which allows you to assess the state of vision. Testing should be carried out exclusively in daylight. The grid must be placed at a distance of 30 cm from your own eyes. Please note that you need to view the image in its usual state. For example, if you always wear glasses, then the test is carried out in them. So, to conduct a vision assessment, you need to cover one eye and look carefully at the point located in the center with the other. If everything is in order with vision, then all the lines and the point will be viewed without distortion.

This is what the mesh will look like for a mild form of the disease:

As you can see, the central part has a slight distortion. The point becomes blurry and the lines become more rounded. The following figure indicates a severe form of pathology.

In this case, the image is distorted even more: the lines take on a wavy shape, and the point appears to be a solid spot.

It is much easier to cure the dry form of the disease, which cannot be said about the wet form. So, age-related macular degeneration wet form treatment:

It is important to know! An effective way to effectively restore vision, recommended by the country's leading ophthalmologists! …

1. Surgical intervention.
2. Treatment with laser.
3. Drug therapy.

Only the attending physician can prescribe a course of treatment, based on the characteristics of the disease. As a rule, in severe cases of pathology, an intravial method of administering drugs is prescribed, or a network by injection into the oral cavity. But, each patient must adhere to a certain diet. Alcohol, smoking, animal fats, fast food and other unhealthy foods are excluded. But it is necessary to use, as with any disease of the visual system, fresh vitamins. They are found in carrots, bell peppers, pumpkin, legumes and grains, eggs, liver, spinach, and broccoli. Eating dark berries, grapes, and blueberries will also not be harmful.

How to restore vision without surgery

We all know what poor vision is. Myopia and farsightedness seriously spoil life by limiting ordinary activities - it is impossible to read something, see loved ones without glasses and contacts. These problems begin to manifest themselves especially strongly after 45 years. When you are face to face with physical weakness, panic sets in and it is hellishly unpleasant. But there is no need to be afraid of this - you need to act! What means should be used and why is described..."

The invention relates to medicine, in particular to ophthalmology, and concerns the treatment of the wet form of age-related macular degeneration (AMD). To do this, Lucentis is first administered as an injection into the vitreous body at a dose of 0.5 mg once a month. Then alpha-fetoprotein is administered parabulbarly in 1.5 ml of isotonic solution at a dose of 0.0075 mg in the evening and glutathione-S-transferase at a dose of 0.0000005 g in the morning. The injection is carried out into each eye daily until the retina with newly formed vessels around the macula is visualized. Next, laser coagulation of the vessels is performed without damaging the macula. Then, a suspension of autologous bone marrow mononuclear cells is transplanted parabulbarly and retrobulbarly, closer to the macula area. The number of mononuclear cells is 5-40 million. In this case, the suspension is administered per 1.5 ml of “NCTF-135”. Administration is carried out 2-4 times with an interval of 2 months. The method allows you to stop neoangiogenesis, weaken the autoimmune process in the eye tissue, i.e. lead to blockade of the pathogenetic mechanisms of AMD development, which eliminates the recurrence of the disease while creating conditions for organotypic regeneration of the retina and a pronounced improvement in visual function. 1 ave.

The invention relates to medicine, in particular to ophthalmology, and can be used to treat the wet form of age-related macular degeneration (AMD).

The incidence of AMD in Russia is more than 15 per 1000 population, and this eye pathology is one of the main reasons leading to decreased vision, blindness, disability and deterioration in the quality of life in older people. Age-related macular degeneration of the retina is a chronic progressive disease, a degenerative (dystrophic) process leading to damage to pigment epithelial cells, photoreceptors, intercellular substance, Bruch's membrane and choriocapillaris layer, resulting in impaired visual function of the eye. The leading role in the pathogenesis of AMD is played by hemodynamic disturbances in the choriocapillaris of the eye.

The purpose of the invention is to reduce blindness and low vision in age-related macular degeneration of the retina.

Drug treatment is used to treat the wet form of age-related macular degeneration of the retina. Angiogenesis inhibitor drugs (Macugen, Lucentis and Avastin), crystalline glucocorticoids are administered intravitreally. A peptide bioregulator obtained from the retina of livestock eyes, retinalamin, is administered subconjunctivally. Laser coagulation and transpupillary thermotherapy, photodynamic therapy with verteporphyrin are also performed. Such treatment is aimed at stabilizing the pathological process; as a rule, it is not possible to improve the acuity and quality of vision.

As a prototype, a method was chosen for the treatment of the wet form of age-related macular degeneration of the retina, including the administration of Lucentis as an injection into the vitreous body at a dose of 0.5 mg once a month (Egorov E.A. et al. Ranibizumab (Lucentis) in the treatment of patients with " “wet" form of age-related macular degeneration. RZhM, 2010, No. 2, 4 p.). The disadvantages of this method are relapses of the disease, the need for repeated injections of this expensive drug and a gradual (with each subsequent administration) weakening of its effectiveness.

The technical result of the invention is the reduction of blindness and low vision in the wet form of age-related macular degeneration of the retina by improving blood circulation, normalizing the microenvironment of retinal cells, stimulating intracellular regeneration of the eye and reversibility of dystrophic changes. Transplanted autologous bone marrow cells induce organotypic regeneration of pathologically altered eye tissues. Normalization of the microenvironment is achieved through the use of the drug α-fetoprotein - Profetal in complex treatment, which improves intravascular and tissue hemoperfusion and stimulates the production of endogenous prostaglandins E1 and E2, which relieve vascular spasms and block the development of autoimmune reactions; α-fetoprotein is a transport protein and replaces the lack of transport protein transthyretin, the synthesis of which decreases with dystrophy of the pigment epithelium. The external introduction of a transport protein facilitates the removal from the retinal area of ​​the eye of accumulated deposited metabolic products, including drusen, and other high-molecular substances that are not normally characteristic of the retina. With increased excretion of decay products in the degeneration zone, the composition of the intercellular environment in the area of ​​the posterior pole of the eyeball is normalized, swelling is eliminated, osmotic pressure and acid-base balance in the tissue environment of the posterior pole are normalized, which creates conditions for the reversibility of dystrophic changes primarily in the retinal pigment epithelium. Not only intracellular and tissue regeneration of the epithelium is initiated, but its function of maintaining the difference in osmotic pressure in the subretinal space and choroid is also restored. As the edema decreases, newly formed vessels are visualized and subjected to laser coagulation. Then autologous bone marrow cells are introduced, which significantly improves blood circulation and tissue trophism in the orbital area, ensures the synthesis of the necessary levels of cytokines that regulate recovery processes, they are also a source of regeneration for the vessels and connective tissue of the eye and retrobulbar fiber. Parabulbar administration of the antioxidant glutathione S-transferase at a dose of 0.000005 grams per every other day significantly reduces damage associated with photo-oxidative stress. As a result, the pathogenetic mechanisms of AMD development are blocked, which eliminates the recurrence of the disease, and atypical neoangiogenesis, which is, in fact, the body’s response to ischemia of eye tissue, stops.

The method is carried out in four stages.

First stage. Use of Lucentis as an injection into the vitreous body at a dose of 0.5 mg (0.05 ml) 1 time/month, once. Lucentis (Ranibizumab) is a human monoclonal antibody fragment to endothelial growth factor A (VEGF-A) and is expressed by a recombinant strain of Escherichia coli. Ranibizumab selectively binds to isoforms of the vascular endothelial growth factor, VEGF-A (VEGF110, VEGF121, VEGF165) and prevents the interaction of VEGF-A with its receptors on the surface of endothelial cells (VEGR1 and VEGR2), which leads to the suppression of neovascularization and vascular proliferation. By inhibiting the growth of newly formed choroidal vessels into the retina, ranibizumab stops the progression of the exudative-hemorrhagic form (wet) of age-related macular degeneration (AMD).

Second phase. Daily parabulbar administration of drugs until visualization of the retina with newly formed vessels around the macula. The antioxidant glutathione-S-transferase is administered in a dose of 0.0000005 grams per injection into each eye per 1 ml of isotonic solution in the morning.

Profetal® is injected into 1.5 ml of isotonic aqueous solution at a dose of 75 mcg per 1 injection into each eye in the evening.

Third stage. Laser coagulation of newly formed vessels (if necessary).

Fourth stage. From the patient's wing of the ilium under local anesthesia, bone marrow is collected in an amount of 10-60 ml on an outpatient basis under aseptic conditions. The bone marrow aspirate with anticoagulant is sent to the cell technology laboratory. In the laboratory, under aseptic conditions, a cell transplant is prepared from the bone marrow in the form of a suspension of bone marrow mononuclear cells per 1.5 ml of NCTF (“NCTF - 135” is a complex biological preparation containing vitamins, minerals, amino acids, nucleic acids and antioxidants, “Laboratoires Filorga” made in France). Some of the cells are frozen in liquid nitrogen and transferred to a cryobank for possible subsequent use. Cell suspension in the amount of 5-40 million autologous bone marrow mononuclear cells per 1.5 ml of NCTF solution. The introduction of cellular material is carried out 2-4 times with an interval of 2 months.

Bone marrow stem cells with this method of transplantation exhibit known properties, namely, they activate organotypic angiogenesis, increasing blood circulation in the vessels of the retina and optic nerve of the eye, and improve the trophism of orbital tissue, which makes it possible to effectively restore impaired visual function.

Clinical examples.

Patient V.M., 78 years old.

Diagnosis: Age-related macular degeneration of the retina of both eyes (wet form). Examination of the fundus revealed many dystrophic lesions in the central region of the retina of both eyes, a large amount of pigment, and retinal edema.

Before treatment: visual acuity of the right eye - 0.05; visual acuity of the left eye - 0.07. Correction is not possible in both eyes. A patient with low vision - a significant decrease in central vision. The process of visual perception is difficult and slow. The patient notes severe blurred vision, significant difficulties in reading and recognizing faces.

Treatment. First, Lucentis was administered as an injection into the vitreous body at a dose of 0.5 mg (0.05 ml) once, then parabulbarly in 1.5 ml of an isotonic solution, alpha-fetoprotein, at a dose of 75 mcg, 12 days in the evening, glutathione-S-transferase, at a dose of 0. 0000005 g 12 days in the morning, in each eye daily until visualization of the retina with newly formed vessels around the macula, then laser coagulation of the newly formed vessels was performed (without damaging the macula), then a suspension of autologous bone marrow mononuclear cells was transplanted parabulbar and retrobulbar, closer to the macula area. Three microsurgical cell transplantations of autologous bone marrow cells were performed with an interval of 60 days.

After treatment: vision of the left and right eyes - 0.2 (without correction). An examination of the fundus revealed that the area of ​​dystrophic lesions and drusen had become significantly smaller, the amount of pigment had decreased, and there was no swelling.

A method for treating the wet form of age-related macular degeneration of the retina, including the introduction of Lucentis as an injection into the vitreous body at a dose of 0.5 mg once a month, characterized in that Lucentis is first administered, then alpha-fetoprotein is injected parabulbarly into 1.5 ml of isotonic solution in a dose 0.0075 mg in the evening, glutathione-S-transferase at a dose of 0.0000005 g in the morning in each eye daily until visualization of the retina with newly formed vessels around the macula, then, if necessary, laser coagulation is carried out (without damaging the macula), then a suspension of autologous bone mononuclear cells is transplanted brain parabulbar and retrobulbar, closer to the macula, using a 1.5 ml suspension of “NCTF-135”, the number of mononuclear cells is 5-40 million, and they are administered 2-4 times with an interval of 2 months.

9-04-2012, 14:04

Description

- a progressive disease characterized by damage to the macular zone (the central zone of the retina in the posterior pole of the eyeball). Other terms are used to refer to this pathology: involutional central chorioretinal dystrophy, sclerotic macular degeneration, age-related macular degeneration, senile macular degeneration, age-related maculopathy, age-related macular degeneration, etc.

ICD-10:

H35.3 Macular and posterior pole degeneration.

Abbreviations: AMD - age-related macular degeneration, RPE - retinal pigment epithelium, SLO - scanning laser ophthalmoscope, TTT - transpupillary thermotherapy. FA - fluorescein angiography, PDT - photodynamic therapy, ERG - electroretinography. ETDRS - Early Treatment Diabetic Retinopathy Study Research Group.

Epidemiology

In Russia, the incidence of age-related macular degeneration (AMD) is more than 15 per 1000 population.

According to WHO, by 2050 the number of people over 60 years of age worldwide will approximately triple (in 2000 - approximately 606 million people). The share of the population of the older age group in economically developed countries is currently about 20%, and by 2050 it will probably increase to 33%. Accordingly, a significant increase in patients with AMD is expected.

? Total affected population this pathology increases with age:

Early manifestations of AMD occur in 15% of people aged 65-74 years, 25% - aged 75-84 years, 30% - aged 85 years and older;

Late manifestations of AMD occur in 1% of people aged 65-74 years, 5% - aged 75-84 years, 13% - aged 85 years and older.

AMD is more common in people over 65 years of age. The predominant gender is female, and in women over the age of 75, AMD occurs 2 times more often.

AMD can lead to a marked decrease in visual acuity and loss of central parts of the visual field. The most significant functional impairments are characteristic of sub-retinal neovascularization followed by atrophy of the RPE, especially if the pathological process involves the fovea.

If there are manifestations of late-stage AMD in one eye, the risk of significant pathological changes in the other eye ranges from 4 to 15%.

Risk factors

There is a clear connection between arterial hypertension and AMD, atherosclerotic vascular lesions (especially the carotid arteries), blood cholesterol levels, diabetes, and excess body weight.

There is a direct relationship between smoking and AMD.

There are indications of a possible link between excess sunlight exposure and age-related macular damage.

The predominant lesion in postmenopausal women is explained by the loss of the protective effect of estrogens against widespread atherosclerosis. However, there was no evidence of the beneficial effects of hormone replacement therapy.

Currently, research into the genetic predisposition to the development of AMD is ongoing (in particular, the responsible genes ARMD1, FBLN6, ARMD3 have been identified).

Prevention. Patients with AMD should be advised to stop smoking, fatty foods, and expose themselves less to direct sunlight. If there is concomitant vascular pathology, measures aimed at its correction are necessary. Issues of vitamin therapy and recommended doses of microelements will be discussed below. In recent years, preventive laser coagulation of the retina in the presence of multiple drusen has been discussed.

Screening

AMD should be suspected in an elderly patient if there are complaints of decreased visual acuity and difficulty reading, especially in low light conditions. Sometimes patients notice loss of individual letters during fluent reading, metamorphopsia. Complaints of changes in color perception and deterioration of twilight vision are much less common. The examination includes determining visual acuity, biomicroscopy (which can reveal other possible causes of symptoms - for example, the presence of age-related cataracts), ophthalmoscopy (including a slit lamp using aspheric lenses) and perimetry. We can also recommend a study of color perception (monocularly), the Amsler test.

It is necessary to remember the likelihood of AMD in patients in whom, after uncomplicated cataract extraction, it is not possible to achieve high visual acuity.

Patients over 55 years of age should have the macular area of ​​the retina examined during routine medical examinations (that is, include wide-pupil ophthalmoscopy in the examination plan).

Diagnosis

The diagnosis of AMD is established if the following symptoms are present(one or more): the presence of hard drusen; presence of soft drusen; strengthening or weakening of RPE pigmentation; atrophic lesions in the macula (geographic atrophy); neovascular macular degeneration - neovascularization of the choroid, serous or hemorrhagic detachment of the RPE and subsequent formation of scar lesions in the macular zone.

? Druze- extracellular deposits of eosinophilic material between the inner layer of Bruch's membrane and the basement membrane of the RPE. This material is a metabolic product of the RPE cells. The presence of drusen may indicate the likelihood of developing more severe AMD in the future. As a rule, patients who do not have other manifestations of AMD do not notice a decrease in central vision. Drusen are divided into hard, soft and confluent.

? Hard drusen usually do not exceed 50 microns in diameter; in the fundus are visible as small, yellowish, clearly defined foci. Biomicroscopy reveals the hyaline structure of drusen. Hard drusen are considered a relatively favorable manifestation of the process, but (if we consider the possibility of progression over a period of up to 10 years), the presence of a large number of hard drusen (more than 8) may predispose to the appearance of soft drusen and more severe manifestations of AMD.

? Soft drusen larger in size, their boundaries are unclear. The risk of their progression is much higher. They can merge and cause detachment of the RPE. If drusen disappear, this most often indicates the development of atrophy of the outer layers of the retina (including the RPE) and the choriocapillaris layer in this area. If soft drusen is detected, the ophthalmologist should recommend that the patient self-monitor using the Amsler grid and contact an ophthalmologist if any new symptoms appear, since this type of drusen is accompanied by a high risk of vision loss (due to the possibility of developing geographic atrophy or choroidal neovascular membrane).

? Drain druses most likely to lead to RPE detachment and atrophic changes or predispose to the development of subretinal neovascularization.

? Drusen dynamics may undergo the following changes::

Hard drusen can increase in size and turn into soft ones; soft drusen may also enlarge and form confluent drusen; Calcifications may form inside the drusen (they look like shiny crystals during ophthalmoscopy); Spontaneous regression of drusen is possible, although drusen are more likely to progress.

? Pigment redistribution. The appearance of areas of hyperpigmentation in the macular zone is associated with changes occurring in the RPE: cell proliferation, accumulation of melanin in them, or migration of melanin-containing cells into the subretinal space. Focal hyperpigmentation is considered one of the factors predisposing to the appearance of subretinal neovascularization. Local hypopigmentation often corresponds to the location of drusen (the RPE layer above them becomes thinner), but can be determined by drusen-independent atrophy of RPE cells or reduced melanin content in them.

? Geographic atrophy of the RPE- an advanced form of dry sclerotic macular degeneration. In the fundus, foci of geographic atrophy are revealed in the form of clearly defined zones of depigmentation with clearly visible large choroidal vessels. In this case, not only the RPE is affected, but also the outer layers of the retina and the choriocapillaris layer in this area. Geographic atrophy can not only be an independent manifestation of AMD, but also occur as a consequence of the disappearance of soft drusen, flattening of the RPE detachment, and even regression of the focus of choroidal neovascularization.

? Exudative (serous) detachment of the RPE- accumulation of fluid between Bruch's membrane and the RPE - is more often detected in the presence of drusen and other manifestations of AMD. The detachment can have different sizes. In contrast to serous detachment of the sensory part of the retina, detachment of the RPE is a local formation with clear contours, round, dome-shaped. Visual acuity may remain quite high, but there is a shift in refraction towards hypermetropia.

Serous detachment of the neuroepithelium is often combined with detachment of the RPE. In this case, there is a greater prominence of the focus; it has a disc-shaped shape and less clear boundaries.

Flattening of the lesion may occur with the formation of local atrophy of the RPE, or rupture of the RPE may occur with the formation of a subretinal neovascular membrane.

Hemorrhagic detachment of the RPE or neuroepithelium is usually a manifestation of choroidal neovascularization. It can be combined with serous detachment.

? Choroidal neovascularization characterized by the ingrowth of newly formed vessels through defects in Bruch’s membrane under the RPE or under the neuroepithelium. Pathological permeability of newly formed vessels leads to fluid sweating, its accumulation in the subretinal spaces and the formation of retinal edema. Newly formed vessels can lead to the appearance of subretinal hemorrhages, hemorrhages into the retinal tissue, sometimes breaking into the vitreous body. This may cause significant functional impairment.

Risk factors for the development of subretinal neovascularization are considered confluent soft drusen, foci of hyperpigmentation, and the presence of extrafoveal geographic atrophy of the RPE.

Suspicion for the presence of subretinal neovascularization should be raised by the following: ophthalmoscopic manifestations: retinal edema in the macular area, the presence of hard exudates, RPE detachment, subretinal hemorrhages and/or hemorrhages into the retinal tissue. Hard exudates are rare and usually indicate that the subretinal neovascularization is relatively old.

Identification of such signs should serve as an indication for fluorescein angiography.

? Disc-shaped scar lesion- the final stage of development of subretinal neovascularization. Ophthalmoscopically in such cases, a disc-shaped lesion of gray-white color is determined, often with pigment deposition. The size of the lesion can vary - from small (less than 1 diameter of the optic disc) to large lesions that can exceed the area of ​​the entire macular zone. The size and location of the lesion are of fundamental importance for the preservation of visual functions.

Classification

? Forms of AMD. In practical ophthalmology, the terms “dry” (non-exudative, atrophic) form and “wet” (exudative, neovascular) form of AMD are used.

? "Dry" form characterized primarily by slowly progressive atrophy of the RPE in the macular zone and the underlying choroid, which leads to local secondary atrophy of the photoreceptor layer of the retina. In other words, the non-exudative form is characterized by drusen in the macular zone of the retina, RPE defects, pigment redistribution, atrophy of the RPE and choriocapillaris layer.

? "Wet" form: germination of newly formed vessels originating in the inner layers of the choroid through Bruch’s membrane into the normally absent space between the RPE and the retina. Angiogenesis is accompanied by exudation into the subretinal space, retinal edema and hemorrhages. Thus, the exudative form is characterized by the following stages: exudative detachment of the RPE, exudative detachment of the retinal neuroepithelium, neovascularization (under the RPE and under the retinal neuroepithelium), exudative-hemorrhagic detachment of the RPE and/or retinal neuroepithelium, scarring stage.

? Early stage. Focal drusen and uneven pigmentation of the RPE are characteristic.

? Late stage. Characteristic features include RPE detachment, RPE rupture, choroidal neovascularization, discoid (fibrovascular) scar, and geographic atrophy of the RPE.

? Choroidal neovascularization. In clinical studies, to determine the prognosis and treatment tactics in the presence of choroidal neovascularization and based on the fluorescein angiographic picture, classic, hidden and mixed forms are distinguished.

? Classical choroidal neovascularization in AMD. It is the easiest to recognize and occurs in approximately 20% of patients. This form is clinically identified as a pigmented or reddish structure under the RPE, and subretinal hemorrhages are common. With FA, the structure fills up early, quickly begins to glow brightly, and then produces increasing sweating.

? Hidden Choroidal neovascularization may be suspected during ophthalmoscopy in the presence of focal dispersion of pigment with simultaneous thickening of the retina, which does not have clear boundaries. Such neovascularization is characterized in FA by late-phase sweating, the source of which cannot be determined.

? Mixed choroidal neovascularization. There are the following options: “predominantly classic” (when the “classic” lesion in area is at least 50% of the entire lesion) and “minimally classic” (in which the “classical” lesion is also present, but makes up less than 50% of the entire lesion).

? Treatment method. When choosing a treatment method, it is necessary to apply the classification of choroidal neovascularization in accordance with its location in the macular zone:

? subfoveal- the choroidal neovascular membrane is located under the center of the foveal avascular zone;

? juxtafoveal- the edge of the choroidal neovascular membrane, the zone of fluorescence blockade by pigment and/or hemorrhage, is within 1-199 μm from the center of the foveal avascular zone;

? extrafoveal- the edge of the choroidal neovascular membrane, the area of ​​fluorescence blockade by pigment and/or hemorrhage, is located at a distance of 200 μm or more from the center of the foveal avascular zone.

Anamnesis

Complaints of decreased visual acuity, the presence of a “spot” in front of the eye, metamorphopsia. Most often, patients with choroidal neovascularization complain of an acute decrease in visual acuity and metamorphopsia.

? Disease history. Patients may not notice a decrease in vision for a long time in the eye that is involved in the process first, or if the decrease in vision develops slowly.

General diseases (especially arterial hypertension, cerebral atherosclerosis).

Family history of AMD.

Familiarization with available medical documentation, including previous entries in the patient’s outpatient record, certificates of hospitalizations, etc. (course of the disease).

Familiarization with the influence of the state of visual functions on the quality of life.

Survey

Determination of visual acuity with optimal correction.

Evaluation of the central visual field.

Assessment of color perception using the Yustova or Rabkin tables.

Biomicroscopy of the anterior part of the eyeball, IOP measurement.

Ophthalmoscopic assessment of the condition of the fundus, including the macular zone of the retina (after pupil dilation with short-acting mydriatics).

Document the condition of the macula, preferably using color stereo fundus photography.

Perform fluorescein angiography and/or indocyanine green angiography.

If retinal edema is suspected, it is recommended to perform optical coherence tomography or macular examination using the Heidelberg Retinal Tomograph (HRT II).

Electrophysiological studies (ganzfeld ERG, rhythmic ERG, pattern ERG, multifocal ERG).

Assessment of visual acuity and refraction

Best-corrected visual acuity should be assessed at each visit. The conditions under which the research is conducted must be standard.

When examining in a clinic or hospital, they usually use Sivtsev tables or test sign projectors. Considering the effect of “recognition” of letter symbols, it is advisable to use Landolt rings in this case.

It is advisable to also note near visual acuity with appropriate correction at each examination.

If refraction changes (shift towards hypermetropia), retinal edema should be suspected (this is possible, for example, with RPE detachment).

Central visual field assessment

Evaluation of the central visual field using the Amsler grid is the simplest and fastest, but extremely subjective study, allowing assessment up to 20° from the point of fixation.

In an ophthalmology office, it is advisable to use standard, printed images Amsler grids. It is advisable to attach the results of the test performed by the patient to the primary documentation: this will allow you to clearly monitor the dynamics of changes.

? Amsler test can be recommended to patients for daily self-monitoring to facilitate the early detection of metamorphopsia or scotoma. The patient should be instructed in detail about the rules of the test (the most important thing is to teach patients to check each eye separately, closing the other eye) and recommend that if any new changes are detected, contact an ophthalmologist as an emergency. Assessment of the state of the visual field. It is preferable to carry it out using computer static perimetry with the inclusion of an assessment of the foveal photosensitivity threshold in the testing strategy. However, with low visual acuity, computer perimetry may not be feasible. In such cases, conventional kinetic perimetry is used, but with an appropriate choice of object size and brightness.

Color perception is assessed using the Yustova or Rabkin tables using standard methods.

Ophthalmoscopic assessment of the condition of the fundus

Ophthalmoscopic assessment of the condition of the fundus of the eye, including the macular zone of the retina, is performed after dilation of the pupil with short-acting mydriatics. To achieve good mydriasis, a combination of drugs is sometimes used, for example, tropicamide 0.5% and phenylephrine 10%. (It is necessary to remember the possibility of systemic side effects of adrenergic mydriatics!)

To examine the central zone of the retina and identify possible edema in the macular zone, fundus biomicroscopy using aspherical lenses 60 and/or 90 diopters, as well as Gruby lenses and various contact lenses (Goldmann lenses, Meinster lenses, etc.). The most commonly used is the three-mirror Goldmann lens.

You can also use direct ophthalmoscopy, but keep in mind that the lack of binocularity may interfere with the detection of macular edema.

Documenting the condition of the macula can be carried out in various ways, ranging from simple sketching of changes and ending with the most preferable color stereo photography of the fundus. Currently existing digital photography systems make it possible not only to avoid the problems of “aging” of prints (for example, previously performed by Polaroid systems), but also to edit the resulting images, superimpose them on each other, store and transmit information in digital form. It is necessary to take fundus photographs of both eyes, since AMD is often bilateral, even if there is decreased visual acuity and other functional manifestations in only one eye.

Fluorescein angiography

In many cases, the diagnosis of AMD can be made based on clinical examination. However, fluorescein angiography (FA) is an extremely valuable additional diagnostic method for this disease, as it allows more accurately determining structural changes and assessing the dynamics of the pathological process. In particular, it is of decisive importance when deciding on treatment tactics. It is advisable to complete it within 3 days after the first examination of a patient with suspected subretinal neovascularization, since many membranes increase in area quite quickly (sometimes by 5-10 µm per day). Considering the possibility of the transition of the “dry” form to the “wet” one, during the dynamic monitoring of patients with drusen (especially in the presence of “soft” drusen), FA is recommended to be performed at 6-month intervals.

? FAG plan. Before the study, the patient is explained the purpose of fundus angiography, the procedure, possible side effects (nausea in 5% of patients during the study, yellow discoloration of the skin and urine during the next day), and the allergy history is specified.

The patient signs the informed consent.

An intradermal fluorescein test is performed.

Currently, in most ophthalmology centers, FA is performed using fundus cameras with digital recording of information. However, it is also possible to use conventional photographic fundus cameras and a scanning laser ophthalmoscope.

Before the study, color photographs of the fundus are taken, and then, in some cases, photography is taken in red-free light (with a green filter).

5 ml of 10% fluorescein solution is administered intravenously.

Photographing is carried out according to generally accepted methods.

If there are signs of subretinal neovascularization in one eye, mid- and late-phase photographs of the other eye should also be taken to identify possible neovascularization (even if its presence is not suspected based on the clinical picture).

? Evaluation of fluorescein angiography results

Druze

Hard drusen are usually punctate, give early hyperfluorescence, fill simultaneously, and the fluorescence stops late. There is no sweating from the druzes.

Soft drusen also show early accumulation of fluorescein in the absence of sweating, but can also be hypofluorescent due to the accumulation of lipids and neutral fats.

Fluorescein is absorbed by drusen from the choriocapillaris.

? Geographic atrophy of the RPE. On FAG, atrophy zones give a defect in the form of a “window”. Choroidal fluorescence is clearly visible already in the early phase due to the absence of pigment in the corresponding areas of the RPE. Since there are no structures that can retain fluorescein, the window defect fades along with background choroidal fluorescence in the late phase. As with drusen, fluorescein does not accumulate here during the study and does not extend beyond the edges of the atrophic focus.

RPE detachment. It is characterized by rapid and uniform accumulation of fluorescein in well-defined local rounded dome-shaped formations, usually occurring in the early (arterial) phase. Fluorescein is retained in the lesions during the late phases and in the recycling phase. There is no leakage of dye into the surrounding retina.

? Subretinal neovascularization

For the fluorescein angiographic appearance of classic choroidal neovascular membrane the following is typical:

The newly formed subretinal vessels fill earlier than the retinal vessels (in the prearterial phase). These vessels quickly begin to glow brightly and look like a network in the form of a “lace” or “cart wheel”. It should be taken into account that if hemorrhages are present, they may partially mask subretinal neovascularization.

Fluorescein leakage from newly formed vessels may increase as the study progresses.

In late stages of FA, fluorescein usually accumulates within the serous retinal detachment located above the choroidal neovascularization.

With hidden choroidal neovascularization, gradually, 2-5 minutes after fluorescein injection, “speckled” fluorescence becomes visible. Hyperfluorescence becomes more significant with the addition of sweating; even accumulations of dye are noted in the subretinal space, without clear boundaries. Repeated assessment of the same area of ​​the fundus in the early phases of FA does not allow finding the source of sweating.

Angiography with indocyanine green gained popularity after the introduction of digital fundus cameras. Indocyanine green has absorption and fluorescence peaks near the red spectrum. It absorbs light at 766 nm and emits at 826 nm (sodium fluorescein absorbs light at 485 nm and emits at 520 nm). Longer wavelengths when using indocyanine green penetrate better into the RPE or subretinal blood or serous fluid. Therefore, choroidal vessels are better visible when studied with indocyanine green than with fluorescein. In addition, unlike fluorescein, indocyanine green is almost completely protein bound and therefore does not cause leakage from normal choroidal vessels and choroidal neovascularization. The dye remains in the subretinal neovascularization for a long time. The lesions are often visible as localized areas of hyperfluorescence in a hypofluorescent background. Angiography with indocyanine green useful for identifying subretinal neovascularization in the presence of RPE detachment, opaque subretinal fluid or hemorrhages. Unfortunately, indocyanine green has not yet been registered with the Ministry of Health and Social Development of Russia and does not have permission for legal use in our country. It should be noted that in cases where there is no hope of preserving vision with any of the therapeutic interventions (for example, in the presence of a fibrovascular scar in the fovea), angiography is not indicated.

Differential diagnosis

Differential diagnosis is carried out:

? In the “dry form” AMD with peripherally located drusen, as well as with degeneration in high complicated myopia. In the latter case, in addition to changes in the macula, characteristic atrophic changes around the optic disc are noted, and drusen are absent.

? In “wet form”

With high complicated myopia (significant refractive error, varnish cracks in the posterior pole, myopic changes in the optic disc);

With a traumatic retinal rupture (usually in one eye; a history of eye trauma, most often concentric to the optic disc);

With angioid stripes, in which, in both eyes, curved lines of red-brown or gray color diverge subretinal from the optic disc;

With the syndrome of presumed ocular histoplasmosis, in which small yellowish-white chorioretinal scars are detected in the middle periphery and in the posterior pole of the retina, as well as foci of scarring in the optic disc;

And also with drusen of the optic disc; choroidal tumors; scar areas after laser coagulation; with inflammatory chorioretinal pathology.

Treatment

Laser surgery

Purpose of laser treatment- reduce the risk of a further decrease in visual acuity below that which the patient already has. To do this, the subretinal neovascular membrane is completely destroyed within healthy tissues, applying intense confluent coagulates. It is recommended to use an argon laser with wavelengths in the green part of the spectrum for coagulation of lesions located extrafoveally, and krypton red for those located juxtafoveally.

? Patient preparation. Before starting laser treatment, it is necessary to have a conversation with the patient (informed consent for laser intervention).

Talk about the likely course of the disease, prognosis, goals of interventions, advantages and risks of alternative treatment methods.

If the patient has an indication for laser coagulation, then he should be explained that from the point of view of long-term prognosis, this intervention is more favorable than simply observation or other methods of treatment.

It should be explained to the patient that it is likely that he will retain peripheral vision, and it should be emphasized that many patients with severe loss of central vision in both eyes can independently cope with many tasks of daily activity.

Warn that visual acuity often deteriorates after laser treatment, that the risk of recurrence of subretinal neovascularization is high (30-40%) and that additional treatment may be required.

In the coming days after the intervention, the patient should be sent to an institution dealing with the problems of helping the visually impaired; It may be necessary to recommend a medical labor examination to establish a disability group.

Usually, the results of the examination on the second day after the intervention are considered fundamentally important, when swelling and decreased vision as a result of treatment are maximum. Patients should be told that visual acuity will not decrease after the second day. If vision deteriorates and distortions increase, the patient should immediately consult an ophthalmologist.

? Indications. Laser treatment reduces the risk of severe vision loss compared with observation in the following groups of patients.

Patients with extrafoveal choroidal neovascularization (200 µm or more from the geometric center of the foveal avascular zone).

Patients with juxtafoveolar choroidal neovascularization (closer to 200 µm, but not under the center of the foveal avascular zone).

Patients with fresh subfoveal choroidal neovascularization under the center of the fovea (no previous laser treatment) or recurrent subfoveal choroidal neovascularization (previous laser treatment, recurrence under the center of the fovea). (In the latter cases, photodynamic therapy, rather than laser coagulation, is currently recommended.)

? Stages of intervention. The most important provisions that must be observed when performing laser intervention:

1. Retrobulbar anesthesia is performed to ensure the eye remains still during the procedure.

2. Immediately before the intervention, the surgeon examines the FA again and accurately determines the boundaries of the intervention.

3. The entire area of ​​choroidal neovascularization is covered with intensive coagulates.

4. The boundaries of the effect carried out are compared with the guidelines on the FA. If the intervention performed appears inadequate, it can be supplemented immediately.

5. Fundus photographs are then taken.

6. A bandage is applied to the eye, and patients are advised to remove the bandage after 4 hours or later, depending on the duration of the anesthetic used.

? Complications. The most common complication of laser treatment is hemorrhage from either the subretinal neovascular membrane or perforation of Bruch's membrane. If hemorrhage occurs during exposure, you need to press the lens onto the eye to increase the IOP and immediately stop the bleeding. It is best to continue applying pressure to the eye with the lens for 15-30 seconds after the bleeding has stopped. If bleeding occurs, it is important not to interrupt treatment. After the bleeding stops, the laser power is reduced and treatment is continued.

? Postoperative follow-up

For early detection of persistent or recurrent subretinal neovascular membranes, control fluorescein angiography should be performed 2 weeks after laser coagulation.

Examinations in the postoperative period continue after this at 1.5, 3 and 6 months from the moment of intervention, and then once every 6 months.

If a recurrence of subretinal neovascular membrane is suspected.

? Relapse. If FA reveals residual activity of the choroidal neovascular membrane, for example, early fluorescence with late sweating in the center or at the edges of the lesion, repeat laser photocoagulation should be performed. Risk factors for recurrence of subretinal neovascularization: arterial hypertension, smoking, the presence of choriodal neovascularization or a disc-shaped scar in the other eye, the presence of soft drusen and pigment accumulations.

Laser coagulation for prophylactic purposes for soft drusen

Laser coagulation around the fovea, performed as a “grid” using low-energy exposure, leads to the disappearance of drusen. A beneficial effect was shown not only in terms of the disappearance of drusen, but also in terms of a greater likelihood of maintaining visual acuity throughout the year. However, during the first years after exposure, the number of cases of development of subretinal neovascular membranes in the affected areas increased. Therefore, the method requires further study and development of criteria and parameters of laser exposure.

Photodynamic therapy

An alternative to laser coagulation has emerged in recent years. photodynamic therapy(PDT). The treatment uses a benzoporphyrin derivative - verteporfin (visudine) - a photosensitive (that is, light-activated) substance with a light energy absorption peak between 680 and 695 nm. Verteporfin, when administered intravenously, quickly reaches the lesion and is selectively captured by the endothelium of newly formed vessels. Irradiation of the focus of neovascularization is carried out using a diode laser with a wavelength of 689 nm, which allows laser energy to freely pass through blood, melanin and fibrous tissue. This makes it possible to selectively act on the target tissue without exposing surrounding tissue to adverse effects. When exposed to non-thermal laser radiation, verteporfin generates free radicals that damage the endothelium of newly formed vessels. As a result, thrombosis and obliteration of subretinal neovascularization vessels occur.

results

The therapeutic effect should be carried out within a week after fluorescein angiography was performed, after which a decision was made about the need for intervention.

When comparing the group in which treatment was carried out according to the standard method (verteporfin), with patients receiving placebo, it was found that a significant decrease in visual acuity after 12 months was absent in the first group in 45-67% of cases, and in the second - in 32-39 %. After another 1 year, the same trend continued.

Since recanalization can occur after vascular occlusion, patients required an average of 5-6 PDT sessions (more than half of them were performed within the first year after the start of treatment). First re-examination An angiographic examination is usually performed after 3 months. If sweating is detected, repeat intervention is performed. If the ophthalmoscopic picture and angiography result remain the same, and there is no sweating, then you should limit yourself to dynamic observation, scheduling a repeat examination after another 3 months.

Subfoveally located classic subretinal neovascular membrane, with visual acuity of 0.1 or higher (such patients account for no more than 20% of all patients suffering from AMD);

AMD with “predominantly classic” (when the “classic” lesion makes up more than 50% of the entire lesion) or with “hidden” subfoveal choroidal neovascularization;

Juxtafoveal lesion located in such a way that when performing laser coagulation the center of the foveal avascular zone would necessarily be affected;

? “hidden” choroidal neovascularization when the lesion size is more than 4 areas of the optic disc; photodynamic therapy is recommended only for very low visual acuity (if the diameter of the lesion exceeds 5400 µm, the patient should be explained that the goal of treatment is only to preserve the visual field);

If the lesion is expected to progress rapidly or if visual acuity without treatment may soon decrease below “useful” (that is, allowing the patient to do without assistance).

Adverse reactions associated mainly with improper administration of drugs (up to tissue necrosis). Approximately 3% of patients experienced a decrease in visual acuity within a week after exposure. To avoid phototoxic reactions, patients are advised not to be exposed to direct sunlight or bright lights and to wear dark glasses.

Efficiency. As a result of assessing the effectiveness of photodynamic therapy, it turned out that this method is one of the most effective: out of 3.6% of treated patients, one was able to prevent a pronounced decrease in visual acuity. However, treatment has a high cost.

PDT and corticosteroids. Recently, there have been reports of better treatment results with a combination of two methods - PDT and intravitreal injection of a corticosteroid (triamcinolone). However, the benefits of this technique have not yet been confirmed by large clinical studies. In addition, in Russia there are no GCS approved for injection into the vitreous body yet.

Transpupillary thermotherapy

Proposed in the early 90s for the treatment of choroidal melanomas transpupillary thermotherapy(TTT) - laser coagulation, in which the energy of waves of the infrared part of the spectrum (810 nm) is delivered to the target tissue through the pupil using a diode laser. Exposure parameters: power 262-267 mW/mm2, exposure 60-90 s, spot diameter 500-3000 microns. Thermal radiation is perceived mainly by the melanin of the RPE and choroid. The exact mechanism of action in AMD remains unclear. There may be an effect on choroidal blood flow. The method is easy to use and relatively cheap.

Indications: occult choroidal neovascularization or occult subretinal neovascular membranes with minimal classic component. Thus, TTT can be used in patients who have virtually no positive effect from PDT. The results of pilot studies are encouraging (the deterioration of the condition was reduced by more than 2 times).

Complications are associated primarily with an overdose of laser energy (normally, the effect should be subthreshold): infarctions in the macular zone, occlusion of retinal vessels, ruptures of the RPE, subretinal hemorrhages and atrophic foci in the choroid are described. The development of cataracts and the formation of posterior synechiae were also noted.

Surgical treatment of age-related macular degeneration

Removal of subretinal neovascular membranes

The indication for surgery is the presence of classic choroidal neovascularization with clear boundaries.

? First, a vitrectomy is performed according to the standard method, then paramacular, from the temporal side, retinotomy is performed. A balanced saline solution is injected through the retinotomy hole to detach the retina. After this, the membrane is mobilized using a horizontally curved peak, and the membrane is removed using horizontally curved tweezers. The resulting bleeding is stopped by lifting the bottle with the infusion solution and thereby increasing the IOP. The liquid is partially replaced with air. In the postoperative period, the patient must maintain a forced position face down until the air bubble is completely resolved.

? Possible complications during and after the intervention: subretinal hemorrhage (from minimal to more massive, requiring mechanical removal); iatrogenic retinal tears at its periphery; formation of the macular hole;

Formation of the preretinal membrane; unresolved or recurrent subretinal neovascularization.

Such interventions help reduce metamorphopsia, provide more constant eccentric fixation, which is often regarded by patients as a subjective improvement in vision. At the same time, even fairly large membranes can be removed through a small retinotomy hole. The main disadvantage is the lack of improvement in visual acuity as a result of the intervention (in most cases it does not exceed 0.1).

Removal of massive subretinal hemorrhages. Massive subretinal hemorrhages can be evacuated through retinotomy holes. In case of formed clots, it is recommended to administer subretinal recombinant tissue plasminogen activator (tPA) during the intervention. If it is necessary to displace hemorrhages from the macular zone, subretinal administration of tPA is successfully combined with the introduction of gas (C3F8) into the vitreous cavity. In the postoperative period, the patient maintains a forced position face down.

Pigment epithelial cell transplantation. Experimental studies on transplantation of pigment epithelial cells are being conducted. At the same time, issues of tissue compatibility still remain unresolved.

Macular translocation

Macular translocation - possible alternative to photodynamic therapy or laser coagulation regarding subfoveal neovascular membranes. In pilot studies, in approximately 1/3 of cases it was possible to achieve not only stabilization, but also some improvement in visual acuity. The main idea of ​​such an intervention is to shift the neuroepithelium of the foveal zone of the retina located above the choroidal neovascular membrane so that the unchanged RPE and choriocapillaris layer are located under it in a new position.

? First, subtotal vitrectomy is performed., and then completely or partially detach the retina. The operation can be performed by performing a retinotomy along the entire circumference (360°), followed by rotation or displacement of the retina, as well as by forming folds (i.e. shortening) of the sclera. The retina is then “fixed” in its new position using an endolaser, and the neovascular membrane is destroyed using laser coagulation. Pneumoretinopexy is performed, after which the patient must remain in a forced position for 24 hours.

? Possible complications: proliferative vitreoretinopathy (in 19% of cases), retinal detachment (12-23%), formation of a macular hole (9%), as well as complications encountered during vitrectomy for other indications. In this case, loss of not only central but also peripheral vision may occur.

Radiation therapy. Despite successful experimental studies, radiation therapy has not yet received widespread clinical use. Clinical studies have not demonstrated benefit from transcutaneous teletherapy (possibly due to the low doses of radiation used).

Drug therapy

Currently there are no therapeutic effects with proven effectiveness in AMD. In the “dry form,” drug therapy is aimed at preventing the formation of drusen and lipofuscin deposits, and in the exudative form, it is intended to prevent pathological angiogenesis.

Antioxidants

It is believed that exposure to sunlight promotes the appearance of free radicals, polyunsaturated fatty acids in the outer layers of the retina, in the RPE and Bruch's membrane. In this regard, attempts were made by introducing into the diet of patients substances with antioxidant effects reduce the effects of oxidative stress. The most well-studied antioxidants include vitamins C and E, betacarotene, flavonoids, and polyphenols. The attention of specialists was also attracted by zinc, which is a coenzyme of carbonic anhydrase, alcohol dehydrogenase and many lysosomal enzymes (including in the RPE).

Patients took high doses of antioxidant vitamins(vitamin C - 500 mg; betacarotene - 15 mg; vitamin E - 400 IU) and zinc (80 mg zinc combined with 2 mg copper). It turned out that the use of supplements did not reveal any positive effect on the course of AMD.

It is believed that taking antioxidant vitamins, lutein, zeaxanthin and zinc can prevent the development and/or progression of AMD. An example of such a complex drug is Okuwait Lutein, containing 6 mg lutein, 0.5 mg zeaxanthin, 60 mg vitamin C, 8.8 mg vitamin E, 20 mcg selenium, 5 mg zinc. It is prescribed 1 tablet 2 times a day in courses of 1 month. The drug does not contain β-carotene.

? Lutein complex contains not only lutein, zinc, copper, vitamins E and C, selenium, but also blueberry extract, vitamin A, β-carotene, taurine. It is prescribed 1-3 tablets per day for 2 months in courses. Considering that the drug contains β-carotene, it should not be prescribed to smoking patients.

Preparations containing blueberry extract(“Myrtilene forte”).

Angiogenesis inhibitors

Experimental and clinical studies have proven that the greatest role in the development of neovascularization in AMD plays endothelial growth factor VEGF (vascular endothelial growth factor). To date, pegaptanib and ranibizumab, which have anti-VEGF activity, have been proposed for clinical practice.

? Pegaptanib (Macuten). By binding to VEGF, pegaptanib prevents the growth of newly formed vessels and increased permeability of the vascular wall - two main manifestations of the exudative form of AMD. The drug is intended for intravitreal administration. The study used pegaptanib at varying doses (0.3, 1.0, and 3.0 mg) every 6 weeks for 48 weeks. Preliminary results: Significant loss of visual acuity is less likely to occur with Macouten treatment (compared to the control group).

? Ranibizumab (RhuFabV2)- a monoclonal antibody that selectively blocks all VEGF isoforms. Intravitreal injections of drugs are performed once every 4 weeks. A phase III clinical trial is currently underway.

Corticosteroids

? Anekortav(Retaane from Alcon) - a suspension that creates a depot; it is administered retrobulbarly using a special curved cannula once every 6 months. Anecortave at a dose of 15 mg is most effective in terms of stabilizing visual acuity and inhibiting the growth of newly formed vessels. In patients receiving anecortave, preservation of visual acuity was achieved in 84% of cases (in the control group - in 50%).

? Triamcinolone- another depot-creating corticosteroid - administered intravitreally at a dose of 4 mg. It has been shown that a single intravitreal injection of this corticosteroid leads to a reduction in the size of the lesion, but does not affect the likelihood of significant vision loss.

Combined approaches

Much more attention is now being paid combined treatment- PDT in combination with intravitreal administration of triamcinolone. However, the effectiveness of such treatment still needs to be confirmed by appropriate clinical studies.

To date, there are two proven effective methods for treating subretinal neovascular membrane, which is the main manifestation of the exudative form of AMD. These are laser coagulation and photodynamic therapy using verteporfin.

Suggested approaches

Research is ongoing to find appropriate interventions for all forms of AMD. And phase III clinical studies that have already been completed allow us to develop new algorithms of effects. Thus, many authors believe that:

In the presence of a subfoveal lesion with “predominant classical” choroidal neovascularization or in case of hidden neovascularization and the size of the lesion is no more than 4 areas of the optic nerve head, photodynamic therapy is recommended;

In the presence of a subfoveal lesion with “minimally classic” choroidal neovascularization, PDT or the angiogenesis inhibitor pegaptanib may be used;

For juxtafoveal lesions located in such a way that laser photocoagulation will necessarily affect the center of the foveal avascular zone, PDT can also be used;

For any other localization (juxtafoveal or extra-foveal), laser coagulation is indicated (however, the number of such patients is no more than 13%).

? To prevent the development of exudative form of AMD use complex nutritional supplements (for example, Okuwait Lutein or Lutein-complex).

Retinalamin (cattle retinal polypeptides) is recommended for use in the form of subconjunctival injections (5 mg 1 time/day, diluted in 0.5 ml of 0.5% procaine, course of 10 injections).

Traditional symptomatic therapy

As for traditionally used drugs to improve regional blood circulation, their use is currently relegated to the background.

For the “dry” form of AMD, you can use vinpocetine 5 mg 3 times a day orally for 2 months or pentoxifylline 100 mg 3 times a day orally for 1-2 months.

Also used as stimulant therapy Ginkgo biloba leaf extract 1 tablet 3 times a day orally in courses of 2 months; blueberry extract (for example, strix, myrtilene forte) 1 tablet 2 times a day orally for 2-3 weeks, algae extract Spirulina platensis 2 tablets 3 times a day orally for 1 month.

In the “wet” form of AMD, you can use dexametazo n 0.5 ml in the form of subconjunctival injections (10 injections); acetazolamide 250 mg 1 time per day in the morning half an hour before meals for 3 days (in combination with potassium supplements), then after a three-day break the course can be repeated. This treatment can be used before laser coagulation. In addition, patients are prescribed ethamsylate 12.5% ​​2 ml IM 1 time per day 10 injections (or in the form of tablets orally 250 mg 3 times a day for 15-20 days) and ascorbic acid + rutoside (1 tablet 3 times a day per within 15-20 days).

The feasibility of using this drug therapy has not yet been confirmed by large clinical randomized placebo-controlled studies.

Further management

Patients with AMD should be under the supervision of a physician, as they more often suffer from arterial hypertension, atherosclerosis of the coronary and carotid arteries, and obesity.

For patients with low visual acuity, we can recommend the so-called aids for the visually impaired. These are devices that magnify images in various ways and enhance the illumination of objects. Among such devices can be named special magnifying glasses, magnifying glasses with various types of mounting, closed-circuit television systems, various digital cameras with image projection on the screen.

Forecast

In patients without therapy, a significant decrease in visual acuity within a period of 6 months to 5 years can be expected in 60-65% of cases. Often the lesion is bilateral and can lead to visual impairment.

The goal of therapeutic interventions for AMD in the presence of choroidal neovascular membranes is achieving stabilization of the pathological process, not improving vision!

Laser coagulation and transpupillary thermotherapy help reduce the incidence of severe vision loss I up to 23-46% of cases (depending on the localization of the process), photodynamic therapy with verteporfin - on average up to 40%, submacular surgery - up to 19%.

Macular degeneration of the retina is one of the causes of irreversible loss of central vision in people over 55-60 years of age. In 2007, age-related macular degeneration was responsible for 8.7% of all cases of blindness on the planet. According to the current trend, this number of cases is expected to double by 2020.

The reason for the decline of visual functions is degeneration of the macula - the most significant part of the retina, responsible for the acuity, sharpness and level of central object vision required for visual work or reading text at close range or driving a vehicle, while peripheral vision in patients such as usually does not suffer at all.

Macular degeneration leads to loss of objective vision, a decrease in overall performance and subsequent disability of the patient, which determines the high socio-medical significance of the disease. At the same time, macular degeneration of the retina can provoke both a slow gradual decrease in vision over several years, and rapid, within just a few months, loss of vision, which depends on the form of age-related macular degeneration and the severity of the disease.

What is the essence of age-related retinal degeneration?

To understand the essence of the pathological process, it is necessary to navigate the structure of the light-sensitive part of the eyeball - the retina. The retina is located at the back of the organ of vision and consists of two main layers. The inner layer is made of special light-sensitive cells - rods and cones. These cells act as receptors - they react to the light signal entering the retina and transmit data about it to the optic nerve. Cones help you see objects in daylight and also form color vision. The rods, in turn, are responsible for twilight vision. The outer layer of retinal cells is made of retinal pigment epithelium, which performs a protective function and is involved in the nutrition of light-sensitive receptors.

The macula or macula is a small part of the retina that is responsible for the formation of central vision. The macular region has the highest density of photoreceptors. In the very center there is a special depression - the fovea or fovea, made only by cones. It is the central fovea that is the main point responsible for human object vision.

Age-related macular degeneration of the retina affects this particular area, which is accompanied by a decrease in central object vision, up to irreversible blindness. Age-related macular degeneration is characterized by the deposition of cellular breakdown products between the retina and the choroid (choroid). This process is also associated simultaneously with morphologically determined hyper- and hypopigmentation of the retina. Such initial changes do not yet cause deterioration and reduction in visual acuity. However, further progression of the disease determines clinically significant changes. There are two forms of age-related macular degeneration of the retina, which will be discussed in detail below.

Forms of age-related retinal degeneration

Age-related macular degeneration, depending on pathophysiological changes, can be represented by two types, which are different in pathogenesis and their manifestations, variants of the development of degenerative changes in the macula and the posterior pole of the eye.

Dry form of macular degeneration

Atrophic or dry age-related macular degeneration accounts for about 85%-90% of cases of this disease and occurs with equal frequency among male and female patients.

This form of the disease is characterized by the deposition of cellular breakdown products, so-called drusen, between pigment epithelial cells and Bruch's membrane. Bruch's membrane is an acellular formation consisting of 5 layers and acts as a barrier between the retina and the choroid. Nutrients and oxygen necessary for normal functioning diffuse through Bruch's membrane to the pigment epithelium and photosensitive receptors of the retina. Metabolic products, on the contrary, are transported from the retina to the choroid.

With age, Bruch's membrane undergoes significant morphological changes, which include thickening, calcification, and degeneration of collagen and elastin fibers. Incomplete elimination and accumulation of metabolic products of lipid nature also occur. Deposits of metabolic products consisting of lipofuscin are called drusen. Drusen are the earliest indicator of macular degeneration of the retina and come in two varieties - soft and hard.

Hard drusen are small, round deposits with well-defined boundaries. They are often a sign of age-related changes in the retina, but do not cause clinically significant visual impairment. As macular degeneration of the eye progresses, small single deposits accumulate into larger formations - soft drusen.

The appearance of soft confluent drusen is associated with an unfavorable prognosis for maintaining high visual vision. There is a disconnection between the retina and the choroid, which disrupts the nutrition of all cellular layers of the retina, causes degradation of photoreceptors and gradual replacement of damaged retinal cells with scar connective tissue.

Geographic atrophy is the final stage of dry macular degeneration, in which large areas of atrophy and death of the retinal pigment epithelium and proliferation of connective tissue are visualized. Such processes lead to significant loss of central vision, which can progress over years. Slow decay of visual functions and a decrease in central vision significantly reduce the patient’s ability to visually work, but not as pronounced as with the wet form of macular degeneration.

Neovascular or wet age-related degeneration of the macula and posterior pole of the eye is an alternative pathway for the development of a pathological process in which the separation of the retinal pigment epithelium and choroid is accompanied by an increase in the concentration of vascular endothelial growth factor. This biologically active substance stimulates angiogenesis, that is, the ingrowth of newly formed vessels under the retina in the projection of the central macular zone.

Neovascularization processes are accompanied by vasodilation, impaired vascular permeability and migration of endothelial cells. Newly formed vessels, penetrating into the subretinal space, destroy the anatomical barrier in the form of Bruch's membrane between the choroid and the retina and form a kind of vascular network, called the “subretinal neovascular membrane”. The wall of the newly formed vessels is functionally defective, which leads to leakage of fluid, plasma and blood cells under the central zone of the retina and is accompanied by subretinal hemorrhages of varying volumes into the macula.

The constant presence of blood and fluid under the retina ultimately leads to the separation of Bruch's membrane, pigment epithelium and the photosensitive layer of the retina from each other, with subsequent disruption of the structure and function of photoreceptors, their degenerative degeneration, fibroglial transformation of tissue in the macular zone into a single scar conglomerate. Over time, a specific ridge forms in the area of ​​the macula, surrounded by scar tissue and small hemorrhages.

Clinically, the processes described above are manifested by disturbances in central vision and the appearance of dark spots (scotomas) before the eyes. Thus, choroidal subretinal neovascularization, being a reparative reaction of the body aimed at improving the trophism of the central retina, increasing the supply of oxygen and nutrients to the macula, leads to the progression of the disease and the inevitable loss of objective vision.

The wet form of age-related macular degeneration of the retina often develops in a short time - the disease can greatly impair the patient's quality of life in a few months or even weeks.

Causes of development of age-related macular degeneration

Until now, scientists have not been able to identify the only reliable cause of age-related macular degeneration of the eyes. However, age-related macular degeneration is believed to have a direct correlation with the age of the patients. Thus, in patients of the middle age group, the disease occurs in only 2% of cases; at the age of 65-75 years, the disease is detected in 20% of patients. And when people reach the 75-year barrier, the risk of developing the disease increases by 35%, that is, age-related macular degeneration of the retina is diagnosed in every third person. That is why, according to most researchers, the main reason for the development of the disease is age.

However, there are a lot of predisposing factors that, when combined with hereditary predisposition, determine the high risks of this pathology. Some of them will be listed below:

• The risk of vision loss associated with macular degeneration in smokers is twice as high as in people without this bad habit.
• Arterial hypertension, various cardiac pathologies, alcohol abuse, obesity, and Alzheimer's disease increase the likelihood of developing degenerative changes in the retina.
• Hereditary predisposition, especially in combination with smoking, should increase suspicion for age-related macular degeneration of the retina.

All these factors cannot directly influence the condition of the retina. However, the biochemical reactions induced by them are the basis of macular degeneration of the eyes.

The retina is thought to be particularly susceptible to oxidative stress due to chronic exposure to visible light and high oxygen concentrations. The discovery of the role of oxidative stress in the development of macular degeneration determined the possibilities of preventive treatment with antioxidants of individuals with an increased risk of age-related macular degeneration of the retina. This issue will be discussed in more detail in the section on therapeutic options.

Symptoms of age-related macular degeneration

The initial stages of age-related macular degeneration, especially if only one eye is involved in the pathological process, are most often asymptomatic. There are also no pain sensations that could cause discomfort and prompt a person to visit an ophthalmologist. Age-related macular degeneration of the retina has many symptoms that affect the daily life of patients, the main ones are the following:

• Reduction in varying degrees, up to complete loss, of object vision with the formation of a spot or spots of gray or black colors in the central field of vision. Distortion of the image in the form of metamorphopsia - the objects in question have an elongated shape, a larger or smaller size than they actually are, broken straight lines. These symptoms are the most common and characteristic of pathology of the macular zone.
• Cloudy and defective central vision causes problems with reading, writing, driving, watching TV, and recognizing faces.

	Vision of a patient with retinal degeneration

• Impaired contrast sensitivity. It becomes difficult for patients to distinguish the textures of environmental objects and their changes. For example, such people may not notice small changes under their feet in the form of a drop in the sidewalk or a step. This increases the risk of falls and injury. Difficulties arise in differentiating colors that are similar in color range.
• Poor tolerance to changes in light levels. Difficulties are caused by walking or driving a car at sunset or dawn, as well as moving from a well-lit room to a darker one.
• Need for more lighting. Patients with age-related macular degeneration need brighter light for reading, cooking, and performing daily tasks.
• Impaired perception of distances. People cannot adequately estimate the distance between objects, skipping steps or tripping over a threshold when walking.

Dry macular degeneration, as a rule, is characterized by a slow decrease in object vision, a gradual increase in symptoms and the development of blurred images when viewing objects both near and from afar. Over time, central vision becomes increasingly blurred, and this area increases in size as the disease progresses.

Wet age-related macular degeneration is characterized by a sharp increase in disease symptoms and causes much more rapid vision loss, sometimes even within a few weeks.

Modern methods of diagnosing the disease

The examination always begins with a conversation, clarifying the details of the disease and complaints of patients who are suspected of age-related macular degeneration of the retina. The symptoms presented by the patient are quite characteristic and typical, which allows one to assume the nature of the pathology, which is subsequently confirmed by standard ophthalmological examinations and instrumental diagnostic methods.

• First of all, a fundus examination or fundoscopy is performed. During visual assessment, characteristic drusen are clearly visible in the form of pale yellow dots. In the wet form of the pathology, abnormal choroidal vessels, as well as foci of local hemorrhage, are well differentiated.

• Amsler grid. The Amsler test is the simplest and most functional test for diagnosing the condition of the central visual field, and is often used for self-monitoring. If a patient has macular degeneration, the visible lines appear broken and wavy, and there are gray or dark spots in the field of vision.

Normal vision	Dry macular degeneration	Wet retinal degeneration

• Fluorescein angiography is performed if choroidal neovascularization is suspected. Hypofluorescent changes are usually associated with hemorrhages and pigmentary hyperplasia. The causes of hyperfluorescent changes are more numerous and include soft and hard drusen, a network of newly formed vessels, atrophy of the pigment epithelium, and subretinal fibrosis.

• Optical coherence tomography is a highly effective non-invasive diagnostic method that allows you to detect the presence of intra- and subretinal fluid, as well as evaluate the effect of the treatment.

Optical coherence tomography of the macula of a healthy eye

Optical coherence tomography for age-related macular degeneration of the retina

Age-related degeneration of the macula and posterior pole requires constant monitoring in order to timely identify the progression of the disease or the transition of the disease from a dry form to a more aggressive wet one.

Dynamic instrumental observation 2-3 times a year in patients suffering from age-related macular degeneration of the retina can significantly improve the prognosis and promptly stop the irreversible decline in central object vision.

If the patient has a complicated medical history, but in the absence of clinical signs of the disease, control examinations of the fundus and dynamic monitoring of the results of instrumental examination for early detection of hard or soft drusen 1-2 times a year are usually recommended.

Age-related macular degeneration. Treatment

Despite the significant achievements of modern methods of diagnostic examination and the early access to a doctor of patients who have been diagnosed with age-related macular degeneration, its treatment is still a difficult task to solve.

How to treat dry macular degeneration?

Unfortunately, there is no therapeutic intervention that would be able to stop the progression or cure patients with dry macular degeneration of the eyes. Taking into account the theory of oxidative stress, patients with a large number of drusen, pigmentary changes or geographic atrophy are advised to take antioxidants according to various regimens.

The goal of this treatment for age-related macular degeneration of the retina is to neutralize oxygen free radicals that provoke pathological reactions. Dosages and individual dosage regimens are determined by the doctor. The main components of such therapeutic regimens are vitamin C, vitamin E, zinc oxide, lutein, beta-carotene, vitamin A, copper oxide. Patients are also usually advised to stop smoking and eat foods rich in polyunsaturated omega-3 fatty acids.

Macular degeneration - wet form: treatment of pathology

Treatment of the wet form of age-related macular degeneration of the retina is aimed at inhibiting the processes of subretinal neovascularization, preventing and treating complications.

Angiogenesis inhibitors

Inhibition of angiogenesis is currently one of the most effective treatments for wet macular degeneration of the retina. The basis of the therapeutic effect is the intravitreal administration of antiangiogenic drugs, that is, drugs that block vascular growth factor and, accordingly, suppress the process of subretinal neovascularization.

The most commonly used in practice are Pegaptanib (Macugen), Bevacizumab (Avastin), Ranibizumab (Lucentis) and Aflibercept (Aylia). The use of drugs in this group for age-related macular degeneration helps stop the growth of pathological blood vessels, thereby reducing the risk of vision loss. Over the past decade, numerous clinical studies have confirmed their high effectiveness in patients diagnosed with wet age-related macular degeneration.

Treatment with angiogenesis inhibitors allowed them not only to stabilize, but also to improve visual function. Significant disadvantages of this type of treatment are the invasive nature of the intervention, a decrease in the effect of treatment if it is abandoned, and the significant cost of treatment, especially taking into account the need for a course of intravitreal injections to achieve a clinically significant result.

Laser coagulation for macular and posterior pole degeneration

Laser treatment methods are indicated for the presence of subretinal neovascular membrane in patients who have been diagnosed with age-related macular degeneration. Treatment consists of laser coagulation of the neovascular membrane located extrafoveolar to the central fovea of ​​the retina.

The purpose of laser coagulation is to stop blood flow in newly formed vessels due to the coagulating effect of laser radiation on their wall. The main disadvantage of this treatment for macular degeneration is the presence of an undesirable damaging effect on the photoreceptors of the retina, which significantly limits the indications for the use of laser treatment, both in terms of the localization of the pathological process and the magnitude of object vision.

Photodynamic therapy

When treating the wet form of age-related macular degeneration of the retina, photodynamic therapy is a worthy alternative to laser treatment. Often, photodynamic therapy is an even more effective way to combat the phenomena of wet degeneration of the macula and posterior pole of the eye compared to the above treatment methods.

The clinical result of treatment is due to the laser effect on newly formed vessels and blocking blood flow in them. The light-sensitive drug Visudin used in photodynamic therapy accumulates only in areas of neovascularization. Laser irradiation of "Visudin" accumulated in newly formed vessels leads to the formation of a blood clot in them and obliteration of the lumen, as a result of which blood flow in the neovascular vascular network completely stops.

The undoubted advantage of photodynamic therapy compared to laser treatment is its exclusive effect only on newly formed vessels without damaging the photoreceptor cells of the retina. It is also necessary to note the possibility of combined use of photodynamic therapy in combination with other methods of treating the wet form of age-related macular degeneration of the retina.

Transpupillary thermotherapy

Transpupillary thermotherapy is one of the safe and effective methods of treating age-related macular degeneration of the retina, which has proven itself in the wet form of macular degeneration with the presence of hidden choroidal neovascularization of any type, including subfoveal localization.

Carrying out transpupillary thermotherapy in the macular region of the retina does not lead to coagulation and photochemical damage to photoreceptor cells, since the main objective of the method is to reduce blood flow in the choroid as a result of irradiation with an infrared laser.

Transpupillary thermotherapy, as a rule, is an alternative to photodynamic therapy when there is no positive therapeutic effect of the latter.

Surgical treatment of macular degeneration

Surgical treatment of age-related macular degeneration of the retina is carried out to improve central vision in advanced stages of the disease when other less invasive treatment methods are ineffective or futile. In some cases, the indication for surgery is the presence of hemorrhagic complications in the form of massive subretinal hemorrhages in the wet form of macular degeneration. Surgical treatment is performed in the form of subtotal vitrectomy, during which the vitreous body is excised and access to the retina and subretinal space is provided.

All types of surgical treatment of retinal degeneration can be divided into three groups: removal (exeresis) of the subretinal membrane and drainage of subretinal hemorrhages, macular translocation and transplantation of pigment epithelial cells.

Removal of the subretinal membrane	Macular translocation

Unfortunately, advanced stages of macular degeneration, in which surgical intervention is indicated, are accompanied by pronounced morphological changes in the retina and underlying intraocular structures, which does not allow for a significant increase in visual acuity after surgery.

However, surgical treatment of retinal degeneration provides the patient with a subjective improvement in vision due to the formation of stable eccentric fixation and a reduction in the phenomena of metamorphopsia.

Forecast of visual functions

Age-related macular degeneration is an irreversible disease that is difficult to treat. This is why periodic preventive visits to an ophthalmologist are necessary for older people. This will help to identify the pathology in time and prevent its pronounced progression.

If there are symptoms and clinical data of macular retinal degeneration in one eye, the frequency of manifestation of the disease in the fellow eye, according to various researchers, is in the range of 5-15%. Over the next year, approximately 25% of these patients completely lose object vision.

At the same time, timely diagnostic examinations and adequate appropriate treatment of retinal degeneration can significantly reduce the number of episodes of severe loss of visual function.

Age-related macular degeneration (dystrophy), or AMD for short, is the most dangerous eye disease for older people, since AMD most often leads to blindness in people over 50 years of age. There are more than 45 million AMD patients worldwide.

“- this phrase very clearly characterizes this disease.

« Age“means that advanced age is a decisive risk factor for AMD, and the older a person is, the more susceptible he is to this disease. For example, for middle-aged people the risk of AMD is 2%, but for those over 75 years old, this figure increases to 30%!

« Macular“means that AMD affects the macula (or macula), the most sensitive area of ​​the retina that provides a person with central vision. It is thanks to central vision that a person is able to distinguish small objects and their details. The insidiousness of this disease lies in the fact that it is painless and patients usually turn to doctors in the later stages of AMD, when vision has already noticeably deteriorated.

« Degeneration“implies the gradual destruction of light-receiving cells of the retina (photoreceptors) due to disruption of their nutrition due to atherosclerotic changes in the blood vessels of the eye. As the disease progresses, a person's vision deteriorates in a manner similar to what is shown in this animated graphic:

If you suddenly suspect that your vision deterioration is due to AMD, you can do a self-diagnosis on.

AMD is explained in a very accessible and clear way in this 7-minute video:

As you probably understood from the video, there are two forms of AMD - dry and wet. Each of them has its own characteristics of course and treatment. Let's look at them in more detail.

Dry form of AMD

This is the most common form of AMD, occurring in 90% of cases. Due to age-related changes in metabolism, non-degradable polymer structures called drusen are formed in the retina (including the macula). The layers of the retina adjacent to these drusen experience an acute lack of nutrients and oxygen, which is why they degenerate (atrophy) with the loss of a large number of photoreceptors.

The fewer intact light-sensitive cells left in the macula, the more noticeable the loss of central vision. At first, a person feels the need for stronger lighting for reading and other visual work. Then patients notice the appearance and growth of a cloudy spot in the center of the field of vision. Over time, this spot increases in size and becomes darker. Because of this, difficulties begin when reading or recognizing faces even at a short distance.

Wet form of AMD

This is a more rapidly developing (and therefore more dangerous!) form of age-related macular degeneration, occurring in 10% of patients with AMD. In this case, the lack of retinal nutrition is compensated by the growth of new, but very fragile capillaries that allow blood and fluid to pass through. Macular swelling occurs.

In places of leakage, photoreceptors die and the photosensitive layer swells. The result is a sharp decrease in vision and the appearance of a distortion effect in the visible image:

Prevention and treatment of AMD

As you already understand, the risk of developing age-related macular degeneration is directly related to the condition of the blood vessels of the eyes. Unhealthy lifestyle (physical inactivity, unhealthy diet, obesity, hypertension, diabetes mellitus), bad habits () - all these factors contribute to the deposition of cholesterol plaques on the walls of blood vessels and deterioration of blood supply to the retina of the eyes.

It's never too late to give up bad habits, increase physical activity, start eating right and enrich your food. Regular (at least once every six months) visits to an ophthalmologist to examine the fundus of the eye will help identify AMD at the initial stage, when treatment is most effective and the risk of vision loss is minimal.

Otherwise, in the later stages of AMD (when the photoreceptors of the macula have already died), it will be impossible to restore vision, unfortunately.

Ophthalmologists recommend that patients with AMD protect their eyes from direct exposure to sunlight, but, in my opinion, this recommendation only worsens the course of the disease. If you constantly hide your eyes from the sun, increased photosensitivity (photophobia) will be added to the symptoms of AMD, which will further worsen the patient’s condition.

It is well known that on a bright sunny day a person (including those suffering from AMD) sees much better than usual. But if bright light causes your eyes to reflexively close and water, then you simply won't be able to take advantage of the chance to see more clearly.

Another famous doctor, William Horatio Bates, proved in practice the benefits of sunlight for the eyes. With the help of a special exercise to irradiate the eyes with sunlight, you can not only get rid of photophobia, but also improve the condition of the retina due to the activation of metabolic processes in it under the influence of light. And this is exactly what AMD patients need.

An indispensable condition for effective prevention and treatment of early stages of AMD is antioxidant protection of the macula by taking carotenoids (lutein and zeaxanthin) - red, yellow or orange pigments found in plant and animal tissues, as well as the minerals zinc, selenium, vitamins C, E and anthocyanosides. "" is one of the most famous lutein-containing drugs that doctors recommend for AMD.

Lutein and zeaxanthin are the main pigments of the macula and provide natural optical protection to visual cells. Natural sources of lutein and zeaxanthin include egg yolks, broccoli, beans, peas, cabbage, spinach, lettuce, kiwi, etc. Lutein and zeaxanthin are also found in nettles, seaweeds and the petals of many yellow flowers.

For dry AMD, treatment is usually limited to taking vitamins and the antioxidants mentioned above. Much less commonly used low-intensity (threshold) laser therapy to destroy drusen (yellowish deposits on the retina) using moderate doses of laser radiation.

Laser therapy is also used to treat wet AMD. One of the types of such therapy is laser photocoagulation– involves the destruction of bleeding defective retinal vessels by a laser beam. However, there is a high risk of destruction of surrounding healthy tissue. Therefore, such laser surgery is more effective outside the macula, where the death of light-sensitive cells is not so critical for vision.

There is a more “gentle” option for laser therapy for wet AMD - photodynamic therapy. The patient is injected intravenously with a special drug (“Visudin”), which tends to attach to the inner surface of blood vessels. After this, the retina of the diseased eye is irradiated with cold laser light, which activates this drug in the pathological capillaries that have grown into the retina. A chemical reaction occurs and the bleeding capillaries are destroyed, which slows down the rate of development of AMD. At the same time, the surrounding healthy tissue is not damaged.

But in first place in the treatment of wet AMD is the so-called anti-VEGF therapy, blocking the action of specific growth factor (VEGF) of defective capillaries. One of the following drugs is injected into the eyeball using a special needle: Bevacizumab (Avastin), Ranibizumab (Lucentis), Pegaptanib (Macugen), Aflibercept (Eylea).

With this method of administration, the drug quickly penetrates all layers of the retina and begins its action aimed at reducing macular edema and preventing new hemorrhages. Some patients experience a positive effect within a week after the injection, but usually 3 injections are needed at an interval of 1 month to achieve maximum results.

Here is a video that explains this method of treating wet AMD in more detail:

Unfortunately, the AMD treatment methods described above are not able to completely cure this disease. Yes, besides, they are not without negative side effects (infection of the eye, increased intraocular pressure, retinal detachment, temporary blurred vision, pain in the eye, etc.).

At best, patients experience some improvement in vision. But usually treatment is considered successful when vision at least stops deteriorating. But this is provided that the patient regularly visits the doctor and undergoes repeated treatment procedures if necessary.

“The best treatment is prevention!” This saying is more appropriate than anywhere else in the case of age-related macular degeneration. If you lead a healthy lifestyle and regularly visit your ophthalmologist, your chance of maintaining your vision into old age increases significantly.

Good vision to you at any age!

And pigment epithelium. AMD in ophthalmology at different periods was designated by different terms: central involutional macular degeneration, senile, Kunta-Junius dystrophy, age-related maculopathy and others. Currently, a consensus has emerged that these are manifestations of the same pathology.

Age-related macular degeneration is the main cause of poor vision and blindness in patients over 50 years of age in Europe and the United States, and in Southeast Asia. The number of people losing their sight increases with age. In our country, this pathology occurs in 15 people out of 1000. Moreover, the average age of patients ranges from 55-80 years.

Age-related macular degeneration (AMD) is characterized by bilateral lesions, central localization of the pathological process, long-term slow course, and steady progression. The disease can be asymptomatic for a long time; patients seek qualified help late, which leads to loss of vision and disability. In the structure of disability due to AMD, 21% are people of working age.

Risk factors for AMD

• Age (over 50 years);
• ethnicity and race;
• heredity;
• white skin color;
• arterial hypertension;
• smoking;
• oxidative stress;
• low content of carotenoids in the macula;
• lack of antioxidants, vitamins, microelements;
• high level of solar radiation.

Diabetes mellitus, atherosclerosis of the carotid arteries, poor nutrition, excess body weight, and impaired carbohydrate and lipid metabolism are also clearly associated with the development of age-related macular degeneration. Women over 60 years of age suffer from this pathology twice as often as men.

Types of Age-Related Macular Degeneration

There are “dry” and “wet” forms of this disease, which depend on the stage of the disease.

“Dry” AMD, or non-exudative, accounts for about 90% of cases and is characterized by slow progression. The “wet” or exudative form occurs in 10% of cases and is accompanied by the development of choroidal neovascularization and rapid loss of vision.

In the development of AMD, the ischemic factor (trophic disorders) is of decisive importance. The disease can develop in two ways:

• The first option is characterized by drusen formation. Drusen are defined symmetrically in both eyes as yellowish thickenings located under the retinal pigment epithelium. Their size, shape and number, as well as the degree of prominence and combination with other changes in the pigment epithelium vary. With significant sizes and an increase in the number of drusen, choroidal neovascularization develops. Characterized by active production of vascular endothelial growth factor, which is a powerful stimulator of angiogenesis. Newly formed vessels can spread under the pigment epithelium, causing retinal lesions. Next, perforation of the pigment epithelium and detachment of the neuroepithelium occurs. A choroidal neovascular membrane is formed, followed by a fibrous scar.
• The second variant is characterized by extensive geographic atrophy of the macular pigment epithelium, with choroidal neovascularization developing only in late stages.

Symptoms of age-related macular degeneration (AMD)

The “dry” form of AMD, in which hard and soft drusen form, is usually accompanied by minor functional impairment. Visual acuity in patients usually remains quite high. In this case, the presence of drusen is considered as a risk factor for the development of neovascularization.

The “wet” form of AMD is characterized by rapid progression and almost always occurs in patients with an existing “dry” form. Symptoms of the “wet” form are as follows:

• a sharp decrease in visual acuity;
• blurred vision;
• weakening of image contrast;
• difficulty reading due to ineffective glasses correction;
• curvature of lines when reading or loss of individual letters;
• metamorphopsia (distortion of objects);
• (appearance of dark spots before the eyes).

More than 90% of all cases of complete loss of vision in AMD are associated with the exudative (“wet”) form of the disease, which is characterized by abnormal growth of newly formed vessels originating in the choroid and growing through defects in Bruch’s membrane under the layer of retinal pigment epithelium, neuroepithelium. This situation is defined in ophthalmology as the formation of a neovascular membrane.

Blood plasma leaks through the wall of new vessels, and deposits of cholesterol and lipids accumulate under the retina. Rupture of newly formed vessels can lead to hemorrhages, which can reach significant volumes. All this leads to disruption of retinal trophism and the development of fibrosis. The retina above the area of ​​fibrosis (scar) undergoes gross changes and is no longer able to perform its functions.

AMD never leads to complete blindness. Initially, it is lost, and an absolute scotoma (dark spot) appears in the central part of the visual field. Since the pathological process affects the macula (the central part of the retina), it remains preserved. As a result of the process, visual acuity is most often no more than 0.1, and the patient sees only with lateral vision.

The disease progresses individually in all patients, but when a neovascular chorioretinal membrane is formed, the time factor plays a key role. Early diagnosis and initiation of treatment during this period allows one to avoid vision loss and achieve stable remission.

Diagnosis of AMD

Macular degeneration can be detected even before clinical symptoms develop. Only timely ophthalmological examination allows timely diagnosis of pathology. To determine the disease, both traditional diagnostic methods (,) and computerized and automated ones are used - computer, visocontrastometry, fluorescence, color stereo photography, which make it possible to qualitatively diagnose macular pathology. With an already verified diagnosis of AMD, patient self-monitoring using the Amsler grid is highly informative. This test can detect symptoms of macular edema due to choroidal neovascularization.

Treatment of age-related macular degeneration (AMD)

In the treatment of AMD, the main principles are timely onset, pathogenetic approach, differentiation depending on the stage of the pathology, duration (sometimes treatment is carried out throughout life), complexity (drug, surgical, laser treatment).

Drug therapy for AMD includes the use of antioxidant drugs, vitamin-mineral complexes, which include zeaxanthin, lutein, anthocyanins, vitamins A, C, E, selenium, zinc, copper and other necessary components, as well as angiogenesis inhibitors and peptide bioregulators.

Laser treatment of AMD involves laser coagulation and photodynamic therapy. Surgical treatment of AMD includes methods such as retinal pigment epithelium, with removal of SNM.

The method of intravitreal administration of Kenalog has become very widespread due to its simplicity and accessibility, which is carried out for macular edema of various etiologies, including “wet” AMD. This method is highly effective, significantly reduces the edematous component, but is associated with a risk of complications.

In recent years, a new progressive method of treating AMD has been practiced - the use of drugs that inhibit the production of vascular endothelial growth factor. These drugs show the best results in terms of vision preservation and are the method of choice.

Video about the disease

Prevention of AMD

All patients with a history of AMD, as well as those from risk groups, should undergo a comprehensive ophthalmological examination every 2-4 years. If complaints characteristic of this pathology appear (decreased visual acuity, loss of letters, metamorphopsia, etc.), you should immediately contact an ophthalmologist.

Moscow clinics

Below are the TOP 3 ophthalmological clinics in Moscow, where you can undergo diagnosis and treatment of age-related macular degeneration.