9-06-2012, 06:46

Description

SYNONYMS

Age-related macular degeneration, sclerotic macular degeneration, involutional central chorioretinal dystrophy, AMD, age-related maculopathy, age-related macular degeneration, senile macular degeneration, etc.

DEFINITION

AMD- a progressive disease characterized by damage to the macular zone (the central zone of the retina and the posterior pole eyeball). AMD can lead to a pronounced decrease in visual acuity and loss of the central portions of the visual field. The most significant functional disorders are characteristic of subretinal neovascularization with subsequent RPE atrophy, especially if the pathological process captures the central fovea (fovea).

ICD-10 CODE

H35.3 Macular and posterior pole degeneration.

If necessary, to identify the drug that caused the lesion, use an additional code of external causes (class XX).

EPIDEMIOLOGY

Most often, AMD develops in patients over 65 years of age. The overall incidence of the population increases with age: if the proportion of people with early manifestations of this pathology at the age of 65-74 years is 15%, then at the age of 75-84 years it is already 25%, and at the age of 85 years and older - 30%. Accordingly, the proportion of people with late manifestations of AMD at the age of 65-74 years is 1%; at the age of 75-84 years - 5%; aged 85 years and older - 13%. The predominant sex of patients is female, and in women over 75 years old, this pathology is noted 2 times more often. In Russia, the incidence of AMD is more than 15 per 1000 population.

PREVENTION

Patients with AMD are advised give up smoking, fatty foods, less direct sunlight. In the presence of concomitant vascular pathology, measures aimed at its correction are necessary. Recommended vitamin therapy and treatment with trace elements will be discussed below. The question of the advisability of prophylactic laser coagulation of the retina in the presence of multiple drusen has not yet been resolved.

SCREENING

Screening is not performed. However, in patients over 55 years of age, during routine medical examinations, it is necessary to examine the macular area of ​​the retina, especially in the presence of characteristic complaints. If patients fail to achieve high visual acuity after uncomplicated cataract extraction, AMD must be considered.

The examination includes the determination of visual acuity, biomicroscopy (to identify other possible causes symptomatology, such as the presence of age-related cataracts), ophthalmoscopy (including slit lamp using aspherical lenses) and perimetry. We can also recommend a study of color perception (monocularly), the Amsler test.

CLASSIFICATION

When determining the main clinical forms of AMD, the following terms are most often used in practical ophthalmology:

• "dry" (or non-exudative, or atrophic) form;
• "wet" (or exudative, or neovascular) form.

For the "dry" form characterized primarily by slowly progressive atrophy of the RPE in the macular zone and the choroid located under it, which leads to local secondary atrophy of the photoreceptor layer of the retina. In addition, drusen are present in this zone (Fig. 31-49).

In this way, The "dry" (non-exudative) form is characterized by:

• drusen in the macular zone of the retina;
• PES defects;
• redistribution of pigment;
• atrophy of RPE and choriocapillary layer.

Under the "wet" form understand, as a rule, the germination of newly formed vessels, originating in the inner layers of the choroid, through the Bruch's membrane into the resulting (normally absent) space between the pigment epithelium and the retina. Neovascularization is accompanied by exudation into the subretinal space, retinal edema, and hemorrhages.

The following stages are characteristic of the exudative form:

• exudative detachment of PES;
• exudative detachment of the retinal neuroepithelium;
• neovascularization (under the pigment epithelium and under the retinal neuroepithelium);
• exudative-hemorrhagic detachment of RPE and/or retinal neuroepithelium;
• scarring stage.

Sometimes there are early and late stages of AMD. This is argued by the fact that the terms "exudative form" and "non-exudative form" do not characterize the severity of the process: for example, both drusen and geographic atrophy can be attributed to the "dry" form.

The early stage is characterized by:

• local Druse;
• uneven pigmentation of RPE.

The late stage is characterized by:

• detachment of PES; rupture of PES;
• discoid (fibrovascular) scar;
• geographic atrophy of PES.

ETIOLOGY

The etiology has not been determined.

PATHOGENESIS

AMD- chronic degenerative (dystrophic) process in RPE, Bruch's membrane and choriocapillary layer (J.D.M. Gass, 1977). RPE is involved in vitamin A metabolism, melanin synthesis, production of the basal and apical extracellular matrix, and in the transport of various substances between photoreceptors. One of the most important functions of PES is the constant participation in phagocytosis and the removal of thousands of discarded distal segments (disks) of photoreceptors. The decay products pass through the Bruch's membrane and are removed by the choriocapillaries.

All RPE cells accumulate lipofuscin with age in the form of rounded yellowish granules with a brown tint, surrounded by lipid membranes and having autofluorescence. Lipofuscin is considered a marker of aging; with age, it accumulates not only in the pigment epithelium, but also in other tissues.

The retina is very sensitive to damage associated with oxidation processes, which is due to the constant high tissue demand for oxygen, the presence of polyunsaturated fatty acids, and exposure to light. "Yellow" macular pigment plays the role of natural sunglasses: it absorbs the short-wavelength part of blue light, thus participating in the antioxidant defense of the macula. This pigment, composed of lutein and zeaxanthin, is located in the inner layers of the retina.

In the course of a cascade of biochemical processes under the action of oxygen, free radicals are formed, which play an important role in the development of AMD. Lipid peroxidation leads to the formation of large molecular chains that are not recognized by the enzymes of the pigment epithelium cells, do not break down and accumulate with age, forming drusen.

Besides, Bruch's membrane thickness increases with age its permeability to blood serum proteins and lipids (phospholipids and neutral fats) decreases. An increase in lipid deposits reduces the concentration of growth factors necessary to maintain the normal structure of the choriocapillaries. The density of the choriocapillary network decreases, the supply of RPE cells with oxygen worsens. Such changes lead to an increase in the production of growth factors and matrix metalloproteinases. Growth factors promote the growth of newly formed vessels, and metalloproteinases cause defects in the Bruch's membrane.

In this way, AMD begins with a "dry" form, that is, from changes in RPE and from the appearance of solid drusen. On the later stage soft drusen appear, then they turn into confluent ones. Progressive damage to the pigment epithelium leads to atrophic changes in the retinal neuroepithelium and choriocapillaries. With the appearance of defects in the Bruch's membrane, CNV spreads under the pigment epithelium and neurosensory retina. As a rule, this is accompanied by retinal edema, fluid accumulation in the subretinal space, subretinal hemorrhages and hemorrhages in the retinal tissue. Sometimes there is a breakthrough hemorrhage in the ST. The final stage in the development of the process is the formation of a subretinal discoid fibrous scar in central department retina and significant loss of visual function.

CLINICAL PICTURE

Clinical manifestations of AMD:

• solid drusen;
• soft drusen;
• increase or decrease in RPE pigmentation:
• atrophic foci in the macula (geographic atrophy);
• neovascularization of the choroid;
• serous or hemorrhagic detachment of PES;
• cicatricial foci in the macular zone.

Druze

Druze- extracellular deposits of eosinophilic material between the inner collagen layer of Bruch's membrane and the basement membrane of the RPE. The drusen material is the products of RPE cell metabolism. The presence of drusen indicates the likelihood of developing a more pronounced macular degeneration. As a rule, patients who do not have other manifestations of this pathology do not notice a deterioration in central vision. Among the drusen, hard, soft and drain are distinguished (Fig. 31-49).

Solid Druse noticeable in the fundus as small, clearly defined foci of yellowish color; their diameter usually does not exceed 50 microns. Biomicroscopy reveals the hyaline structure of drusen. With FA, a characteristic early hyperfluorescence is detected, the drusen are filled at the same time, the glow stops late. There is no sweating from the druze. They are considered a relatively favorable manifestation of the process, however, if we consider the possibility of progression of the disease for up to 10 years, the presence of a large number of hard drusen (> 8) may predispose to the appearance of soft drusen and more severe manifestations of macular degeneration.

Soft Druse are large and usually have indistinct borders. They have a granular structure that can be detected histologically. In FAH, early accumulation of fluorescein is determined in the absence of its sweating, but it can also be hypofluorescent due to the accumulation of lipids and neutral fats. The risk of disease progression to a late stage is much higher. Soft drusen can coalesce and cause RPE detachment.

Drain Druse can lead to RPE detachment; to atrophic changes in the retina or to the development of subretinal neovascularization.

In dynamics, druze can undergo the following changes:

• hard drusen can increase in size and turn into soft ones;
• soft drusen can also enlarge, form confluent drusen, which can lead to RPE detachment;
• inside the drusen, calcifications can form, which look like shiny crystals during ophthalmoscopy;
• spontaneous regression of drusen is also possible, although most often they are prone to progression.

Redistribution of pigment in the macula

The appearance of areas of hyperpigmentation is associated with changes occurring in RPE: proliferation of cells in this layer, 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 the drusen, as the layer of RPE over them becomes thinner. However, local hypopigmentation can also be determined by atrophy of RPE cells, which does not depend on drusen, or a decrease in the content of melanin in cells.

Geographic atrophy of the retinal pigment epithelium

Geographic atrophy of RPE- advanced form of dry AMD. Foci of geographic atrophy are detected in the fundus in the form of clearly defined areas of depigmentation with well-defined large choroidal vessels. With geographic atrophy, not only RPE suffers, but also the outer layers of the retina and the choriocapillary layer in this zone. With FA, atrophy zones form a defect of the “window” type. Already in the early phase, choroidal fluorescence is clearly visible, since there is no pigment in the corresponding zones of the pigment epithelium. Fluorescein does not accumulate and does not go beyond the edges of the atrophic focus. Geographic atrophy can be not only an independent manifestation of AMD, but also a consequence of the disappearance of soft drusen, flattening of the RPE detachment focus, and may even occur as a result of regression of the CNV focus.

Serous (exudative) detachment of the retinal pigment epithelium

Serous detachment of RPE- fluid accumulation between Bruch's membrane and RPE. Most often, detachment is detected in the presence of drusen and other manifestations of AMD (including CNV). The size of the detachment can be different. In contrast to the serous detachment of the sensory part of the retina, detachment of the RPE is a rounded dome-shaped local formation with clear contours. Visual acuity can remain quite high, but there is a shift in refraction towards hypermetropia. In FA, detachment is characterized by a rapid and uniform accumulation of fluorescein, usually occurring in the early (arterial) phase. The dye is retained in the foci during the late phases and during the recirculation phase, there is no leakage into the surrounding retina.

With detachment of the pigment epithelium, serous detachment of the neuroepithelium is often combined. At the same time, a greater prominence of the focus, which has a disc-shaped shape and less clear boundaries, is noted.

In the course of development pathological process flattening of the focus with the formation of local RPE atrophy or RPE rupture with the formation of a subretinal neovascular membrane may occur.

Hemorrhagic detachment of the pigment epithelium or neuroepithelium

Hemorrhagic detachment of the pigment epithelium or neuroepithelium, usually a manifestation of CNV. It can be combined with serous detachment.

Choroidal (subretinal) neovascularization

CVD is characterized ingrowth of newly formed vessels through defects in the Bruch's membrane under the RPE or under the neuroepithelium. Pathological permeability of newly formed vessels leads to fluid leakage, its accumulation in the subretinal spaces and to the formation of retinal edema. Neovascularization can lead to the appearance of subretinal hemorrhages, hemorrhages in the retinal tissue, sometimes breaking through into the ST. In this case, significant functional impairment may occur.

Risk factors for the development of subretinal neovascularization are:

• drain soft drusen;
• foci of hyperpigmentation;
• presence of extrafoveal geographic atrophy of RPE.

Suspicion of the presence of subretinal neovascularization should cause the following ophthalmoscopic manifestations:

• retinal edema in the macular area:
• detachment of PES;
• accumulation of pigment in the form of a ring or plaque;
• subretinal hemorrhages and / or hemorrhages in the retinal tissue:
• the presence of hard exudates.

Hemorrhages may be small. Hard exudates are rare and usually indicate that the subretinal neovascularization has formed relatively long ago.

CNV, based on FAG data, is divided into:

• classical;
• hidden:
• mixed.

Classic CNV found in approximately 20% of patients. A pigmented or reddish structure under RPE is usually clinically detected, and subretinal hemorrhages are often encountered. In FA, newly formed subretinal vessels fill earlier than retinal vessels (in the pre-arterial phase). These vessels quickly begin to glow brightly and look like a network in the form of lace or a cartwheel. Bleeding, if present, may partially mask subretinal neovascularization. There may be leakage of fluorescein from the newly formed vessels, increasing in the course of the study. In the late phases of FAH, the dye usually accumulates within a serous retinal detachment located above the choroidal neovascular membrane.

Hidden HNV suspected in the case when ophthalmoscopy reveals focal dispersion of the pigment with simultaneous thickening of the retina, which does not have clear boundaries. Gradually, 2-5 minutes after the injection of fluorescein, "mottled" fluorescence becomes visible. The degree of hyperfluorescence increases with the addition of perspiration, even dye accumulations in the subretinal space are noted, which do not have clear boundaries. Re-evaluation of the same site in the early phases of FAH does not reveal the source of the sweat.

Mixed CNV in recent studies are subdivided into:


When choosing a treatment method, it is necessary to apply the classification of CNV, based on the type of location of CNV 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 blockade of fluorescence by pigment and/or hemorrhage is within 1-199 microns from the center of the foveal avascular zone;
• extrafoveal- the edge of the choroidal neovascular membrane, the zone of fluorescence blockade by pigment and/or hemorrhage is located at a distance of 200 microns or more from the center of the foveal avascular zone.

Formation of a discoid scar

discoid scar- the final stage of development of subretinal neovascularization. Ophthalmoscopically in such cases, a gray-white discoid focus is determined, often with pigment deposition (Fig. 31-51). The size and localization of the focus are of fundamental importance for the preservation of visual functions.

DIAGNOSTICS

Anamnesis

When taking anamnesis, consider:

• patient complaints of decreased visual acuity, difficulty in reading, especially in low light conditions: sometimes patients notice the loss of individual letters during fluent reading, metamorphopsia;
• the duration of symptoms;
• unilateral or bilateral nature of the lesion;
• the presence of comorbidities cordially- vascular system(in particular, arterial hypertension, atherosclerotic vascular lesions), lipid metabolism disorders, diabetes, overweight;
• smoking;
• heredity.

It is desirable to evaluate the impact of visual impairment on the patient's quality of life.

Physical examination

Physical examination includes:

• determination of visual acuity with optimal correction:
• Amsler test;
• assessment of color perception using Yustova or Rabkin tables (monocularly);
• biomicroscopy (to identify other possible causes of symptoms, such as age-related cataracts);
• retinal biomicroscopy using aspherical lenses 60 and / or 90D, as well as Gruby lenses and various CLs (Goldmann lenses, Mainster lenses, etc.), after pupil dilation with short-acting mydriatics.

Laboratory research

Instrumental Research

For assessment of the functional state of the organ of vision use:

• perimetry, especially computer static perimetry, in particular the macular test and the determination of foveal sensitivity (for low visual acuity, conventional kinetic perimetry is used, with an appropriate choice of size and brightness of the object);
• electrophysiological studies (ganzfeld ERG, rhythmic ERG, pattern ERG, macular ERG, multifocal ERG).

For detection and documentation of anatomical changes in the macula apply the following methods.

Differential Diagnosis

With the "dry" form of AMD, differential diagnosis is carried out with:

• peripherally located drusen;
• degeneration with high complicated myopia (with it, in addition to changes in the macula, characteristic atrophic changes around the optic disc are also noted, but there are no drusen; a pronounced refractive error is observed).

With the "wet" form of AMD, differential diagnosis is carried out with:

• high complicated myopia (significant refractive error, varnish cracks in the posterior pole, myopic changes in the optic disc);
• traumatic rupture of the retina (usually in one eye; a history of eye injury, most often the rupture is concentric to the optic disc);
• angioid stripes, when curved lines of red-brown or gray color subretinally diverge from the optic disc in both eyes;
• a syndrome of supposed histoplasmosis of the eyes, when small yellowish-white chorioretinal scars are detected on the middle periphery and in the posterior pole of the retina, as well as foci of scarring in the optic disc;
• friends of the optic nerve disc;
• tumors of the choroid;
• cicatricial foci after laser coagulation;
• inflammatory chorioretinal pathology.

Indications for consulting other specialists

• cardiologist/therapist- in the presence of arterial hypertension, other diseases of the cardiovascular system;
• neuropathologist- in the presence of severe atherosclerosis of cerebral vessels;
• endocrinologist- in the presence of uncompensated DM.

Diagnosis example

Right eye- age-related macular degeneration, "wet" form (classic subretinal neovascularization).

left eye- age-related macular degeneration, "dry" form.

TREATMENT

Treatment Goals

• Achieving stabilization of the pathological process, and not improving vision - in the presence of choroidal neovascular membranes.
• Prevention of complications (with a "dry" form - the appearance of subretinal neovascularization, with a "wet" form - the occurrence of hemorrhages different localization, increased retinal edema, etc.).
• Prevention of severe vision loss leading to disability.
• Preservation of visual acuity, allowing the patient to serve himself independently, in case of advanced pathology.

Indications for hospitalization

In the vast majority of cases, patients with AMD can be examined and treated on an outpatient basis. In those countries where the intravitreal use of angiogenesis inhibitors is allowed, injections into the CT are also performed for patients without hospitalization (naturally, such an injection is performed under aseptic and antiseptic conditions).

Medical treatment

General principles

In the "dry" form in order to prevent the progression of the disease, it is recommended to take biologically active additives to food containing vitamins, lutein, zinc.

In the "wet" form possible intravitreal administration of angiogenesis inhibitors. The main advantage of this approach is that these drugs are effective in all types of subretinal neovascular membranes. Accordingly, the decision on intervention can be made even without a preliminary angiographic study. There are currently no registered medicines from this group, pegaptanib (Makugen) and ranibizumab (Lucentis) are being prepared for registration. In some countries, these drugs are already being used to treat patients with retinal neovascularization.

Pegaptanib (macugen)- a small RNA-like molecule with a high affinity for vascular endothelial growth factor VEGF (vascular endothelial growth factor). By selectively binding the 165 isoform of this growth factor, pegaptanib prevents the growth of newly formed vessels and increased vascular wall permeability, two main manifestations of the exudative form of AMD. The drug is intended for intravitreal administration. The results of one of clinical research- show that there is probably no significant loss of visual acuity with pegaptanib treatment compared with the control group. In the study described, pegaptanib was administered intraviterally at various doses (0.3, 1.0, and 3.0 mg) every 6 weeks for 54 weeks; the effect of stabilization of visual acuity was achieved in a large percentage of cases already at the minimum of the doses used.

For the same purpose - to inhibit angiogenesis - another drug is used - ranibizumab (lucentis). Ranibizumab is a monoclonal antibody that blocks all isoforms of the VEGF growth factor. Intravitreal injections of the drug are performed 1 time in 4 weeks. In randomized clinical trials (ANCHOR and MARINA), ranibizumab was administered intravitreally at a dose of 0.3 and 0.5 mg. In most cases, not only stabilization was noted, but also some improvement in visual acuity.

In addition, in the world of ophthalmology there is a tendency to prefer more cheap drug, related to ranibizumab, is bevacizumab (Avastin). This antibody with anti-VEGF activity was initially used intravenously to treat colorectal cancer. Currently, in addition to disputes about the ethics of treating patients with a drug that was not developed for the treatment of ophthalmic pathology, various attempts are being made to compare the efficacy and safety of ranibizumab and bevacizumab.

Another direction of treatment with the help of blockade of angiogenesis continues to develop - intravitreal administration of crystalline glucocorticoids. At present, injections of triamcinolone (kenalog-40) have begun to be used quite actively. Despite the fact that this drug is used intravitreally “off-label” (that is, without official authorization) all over the world, such treatment has become widespread. The drug is administered intravitreally, most often at a dose of 4 mg. One pilot study showed that a single intravitreal injection of this glucocorticoid resulted in a reduction in the size of the lesion, but did not affect the likelihood of a significant reduction in vision.

Much more attention today give combined treatment: photodynamic therapy in combination with intravitreal administration of triamcinolone. However, the effectiveness of such treatment still needs to be confirmed by appropriate clinical studies.

With the introduction of triamcinolone, the probability is quite high side effects, first of all, ophthalmohypertension (about 40% of cases), cataracts. In addition, the relatively low and temporary effect in terms of improving visual acuity has led to the fact that today in the world more attention is paid to angiogenesis inhibitors. It is possible that over time, schemes for the sequential use of intravitreal injections of glucocorticoids and angiogenesis inhibitors will be developed.

There is also a traditional therapy used in our country for AMD, but such treatment requires additional large clinical trials.

• In the "dry" form of AMD, drugs are used to improve regional blood circulation, but today their use fades into the background, since many authors question the theory of circulatory failure as the main etiopathogenetic factor in the development of AMD. In this form of AMD, stimulation therapy is also used.
• In the "wet" form of AMD, subconjunctival injections of glucocorticoids and oral acetazolamide can be used to reduce swelling. Such treatment can be used before laser coagulation.
• It also seems promising to use drugs with a different mechanism of action, for example, peptide bioregulators, and in particular polypeptides of the retina of cattle (retinalamine).

Biologically active food supplements

Okuvayt Lutein(contains lutein - 6 mg, zeaxanthin - 0.5 mg, vitamin C - 60 mg, vitamin E - 8.8 mg, selenium - 20 mcg, zinc - 5 mg) 1 tablet 2 times a day. FROM preventive purpose apply courses for 2 months 2 times a year. This is the only drug whose effectiveness in the early stages of AMD to prevent the progression of the process has been confirmed by extensive multicenter studies.

Lutein complex(contains lutein - 2 mg, standardized blueberry extract - 130 mg, vitamin C - 100 mg, vitamin E - 15 mg, vitamin A - 1100 IU, beta-carotene - 1.3 mg, zinc - 5 mg, copper - 0, 5 mg, selenium - 15 mg, taurine - 50 mg).

The usual prophylactic dose is 1 tablet 1 time per day (as directed by the doctor, the dose may be increased to 3 tablets per day). Given that the drug contains beta-carotene, it should not be prescribed to smokers. For preventive purposes, it is used in courses of 2 months 2 times a year.

Vitrum Vision forte(contains vitamin C - 225 mg, vitamin E - 36 mg, beta-carotene - 1.5 mg, lutein - 2.5 mg, zeaxanthin - 0.5 mg, copper (as copper sulfate) - 1 mg, zinc (in zinc oxide) - 5 mg) - 1 tablet 2 times a day. This drug, unlike others, is registered in our country as a drug. Many other preparations of a similar composition are also used.

It is important to remember that drugs containing beta-carotene should not be prescribed to smokers because of the danger of stimulating the development of lung cancer.

Drugs to improve regional blood circulation:

• vinpocetine 5 mg 3 times a day orally, in courses of 2 months;
• pentoxifylline 100 mg 3 times a day orally, in courses of 1-2 months;
• ginkgo biloba leaves extract 1 tablet 3 times a day orally, in courses of 2 months.

Stimulant drugs:

• preparations with blueberry extract (for example, myrtilene forte) 1 tablet 2 times a day orally, in courses of 2-3 weeks;
• algae extract Spirulina platensis 2 tablets 3 times a day inside, in courses of 1 month.

Drugs to reduce retinal edema:

• dexamethasone 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, then after a three-day break, the course can be repeated.

Peptide bioregulators- cattle retinal polypeptides (retinamine) in the form of subconjunctival injections (5 mg 1 time per day, diluted with 0.5 ml of 0.5% procaine or 0.9% sodium chloride solution, a course of 10 injections).

laser treatment

Purpose of laser treatment- reduce the risk of further deterioration of vision. The subretinal neovascular membrane within the affected tissues is completely destroyed by coagulation with argon green or cryptopin red (wavelength 647 nm) lasers. The Macular Photocoagulation Study (MPS) showed that laser treatment significantly reduced the risk of severe visual loss in patients with extrafoveolar and juxtafoveolar CNV.

Photodynamic therapy has become an alternative to laser coagulation. When using it, they take vertenorphin (vizudin), a benzoporphyrin derivative.

Vizudin (vertenorphin)- the only drug approved for use in Russia for the treatment of patients with choroidal neovascularization (CNV).

Indications for use. Age-related macular degeneration in patients with predominantly classic subfoveal CNV or subfoveal CNV in pathological myopia.

Method of application and dose. PDT with Vizudin is a 2-stage process. Within 10 minutes, Vizudin is administered intravenously. 15 minutes after the start of the injection, Vizudin is activated with a non-thermal laser (689 nm) for 83 seconds.

The action of the drug based on the fact that it contains a photosensitivity (that is, activated by light exposure) substance, the peak absorption of light energy which is between 680 and 695 nm. Verteporfin is a liposomal form; when administered intravenously, it quickly enters the lesion and is selectively captured by the endothelium of the newly formed vessels of the neovascular membrane. 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 the blood, melanin and fibrous tissue. Thus, it is possible to selectively affect the target tissue without adversely affecting the surrounding tissues. Under the action of non-thermal laser radiation, verteporfin generates free radicals that damage the endothelium of newly formed vessels, which leads to thrombosis and obliteration of subretinal neovascularization vessels. The procedure must be carried out within a week after the FAG, after which a decision is made on the need for intervention.

Since recanalization can often occur after vascular occlusion, on average, patients required 5-6 sessions. photodynamic therapy(more than half of them were performed within 1 year after the start of treatment). The first re-examination with FA is usually carried out after 3 months. If sweating is detected, perform re-intervention. If the ophthalmoscopic picture and the result of FA remain the same, there is no sweating, then you should limit yourself to dynamic observation, appointing a second examination after another 3 months.

The results of the conducted studies have shown that such treatment can be recommended in the following cases:

• with subfoveal classic subretinal neovascular membrane, with visual acuity of 0.1 and above (such patients account for no more than 20% of all patients suffering from AMD);
• with "predominantly classical" or "hidden" subfoveal CNV;
• with a juxtafoveal lesion located so that when performing laser coagulation, the center of the foveal avascular zone would necessarily be affected;
• with "hidden" CNV with a focus size of more than 4 areas of the ONH, photodynamic therapy: only with very low visual acuity (in addition, if the focus diameter exceeds 5400 microns, the patient should be explained that the goal of treatment is to stabilize visual functions);
• with the expected rapid progression of the lesion or in cases where visual acuity without treatment may soon fall below "useful" (that is, allowing the patient to do without outside help).

However, approximately 3% of patients experience a decrease in visual acuity within a week after exposure (an average of 4 rows of the ETDRS table).

In order to reduce the risk of phototoxic reactions, patients are advised to avoid direct exposure for 2 days. sun rays and bright light, wear sunglasses.

AT recent times photodynamic therapy is less commonly used in countries where intravitreal administration of an angiogenesis inhibitor is allowed.

Application transpupillary thermotherapy was proposed in the early 90s for the treatment of choroidal melanomas. The method is based on laser coagulation, in which the energy of the infrared part of the spectrum (810 nm) is delivered to the target tissue through the pupil using a diode laser. Thermal radiation is perceived mainly by the melanin of the RPE and the choroid. The exact mechanism of benefit in the treatment of AMD remains unclear. Perhaps there is a certain effect on the choroidal blood flow.

The indication for transpupillary thermotherapy is occult CNV or occult subretinal neovascular membranes with a minimal classical component. Thus, transpupillary thermotherapy can be used in cases where patients practically do not notice a positive effect from photodynamic therapy. The method is easy to use and relatively inexpensive.

However, when using transpupillary thermotherapy, frequent complications are noted, primarily associated with an overdose of laser energy (normally, the effect should be subthreshold): infarctions in the macular zone, occlusion of retinal vessels, RPE ruptures, subretinal hemorrhages and atrophic foci in the choroid are described. Cataracts and the formation of posterior synechia were also noted. Perhaps that is why the method is not widely used.

Surgery

Removal of subretinal neovascular membranes

First, vitrectomy is performed according to the standard technique, then paramacularly, retinotomy is performed from the temporal side. A balanced saline solution is injected through the retinotomy opening to detach the retina. The membrane is then mobilized with a horizontally curved spike, and the membrane is removed by inserting horizontally curved forceps through the retinotomy. The resulting bleeding is stopped by lifting the vial with an infusion solution and thereby increasing IOP. Perform a partial replacement of the liquid with air. In the postoperative period, the patient must observe a forced position face down until the air bubble is completely resorbed.

Main possible complications during and after the intervention:

• subretinal hemorrhage (from minimal to more massive, requiring mechanical removal);
• Iatrogenic retinal breaks in its periphery:
• macular hole formation:
• formation of the preretinal membrane;
• unresolved or recurrent subretinal neovascularization.

Such interventions can reduce metamorphopsia, provide more permanent eccentric fixation, which is often regarded by patients as a subjective improvement in vision. 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 after the intervention).

Techniques have been developed for removing massive subretinal hemorrhages by evacuating them through retinotomy openings. In the case of formed clots, it is recommended to administer subretinally recombinant tissue plasminogen activator during the intervention. If it is necessary to displace hemorrhages from the macular zone, the subretinal injection of tissue plasminogen activator is successfully combined with the injection of gas (perfluoroorganic compound) into the CT cavity. In the postoperative period, the patient observes a forced position face down.

In addition, the decision to vitrectomy can be made in case of massive non-absorbable hemorrhage in the CT, which arose as a result of a breakthrough of subretinal hemorrhage.

Currently, experimental studies are being carried out on RPE cell transplantation, but the issues of tissue compatibility remain unresolved.

Perform also macular translocation surgery. The main idea of ​​such an intervention is to displace the neuroepithelium of the foveal zone of the retina, located above the choroidal neovascular membrane, so that the unchanged RPE and the choriocapillary layer are in a new position under it. To do this, first perform subtotal vitrectomy, and then completely or partially exfoliate the retina. The operation can be performed by performing a retinotomy around the entire circumference (360°) with subsequent rotation or displacement of the retina, as well as by forming folds (that is, shortening) of the sclera. Then the retina is "fixed" in a new position using an endolaser, and the neovascular membrane is destroyed using laser coagulation. Pneumoretinopexy is performed, after which the patient must observe a forced position during the day. A number of complications are possible during macular translocation interventions: proliferative vitreoretinopathy (PVR) (in 19% of cases), retinal detachment (in 12-23%), macular hole formation (9%), as well as complications encountered during vitrectomy for other testimony. In this case, there may be a loss of not only central, but also peripheral vision. At present, this technique has not found wide application.

Approximate periods of incapacity for work

Terms of disability are determined by the severity of the process. In some cases, it is necessary to decide on the group of visual disability.

Further management

After the intervention, patients are advised to monitor their condition daily using the Amsler grid and, if any new symptoms appear, contact an ophthalmologist. For early detection persistent or recurrent subretinal neovascular membranes, a control FAG is performed within the time limits established by the relevant protocols. After that, inspections continue after 1.5; 3 and 6 months from the moment of intervention, and then - at least 1 time in 6 months.

The patient should be advised to lead a healthy lifestyle. Smoking cessation, a diet rich in vitamins and microelements, and limiting the intake of fatty foods are especially important. Excessive insolation should be avoided, it is recommended to wear dark glasses. The patient should be explained the need for taking biological supplements with antioxidant vitamins, lutein and zinc.

If soft drusen are identified, the ophthalmologist should advise the patient to perform daily self-monitoring using the Amsler grating and consult an ophthalmologist if any new symptoms appear, since this type of drusen is accompanied by a high risk of visual impairment.

In the presence of CNV, the patient must strictly adhere to the recommended schedule of repeated examinations, since even with treatment, relapses of the pathological process are not excluded. The patient must understand that the goal of treatment is to stabilize the state of the organ of vision, including visual acuity, and not to improve vision. The patient needs to be explained: most likely, he will retain peripheral vision.

It should be emphasized that many patients with severe loss of central vision in both eyes can cope with many things in their daily activities, especially when using assistive devices, and they still have good quality life.

Sick with low visual acuity we can recommend the so-called aids to the visually impaired. These are devices that magnify images and enhance the illumination of objects in various ways. Among such devices can be named special magnifying glasses, loupes with various types of mounts, closed-loop television systems, and various digital cameras with projection of images on a screen. Assistance to the visually impaired is especially important for patients with poor visual acuity in both eyes.

FORECAST

In the presence of manifestations of the late stage of AMD in one eye, the risk of minor pathological changes in the other eye is, according to various estimates, from 4 to 15%. At the same time, in approximately 1/4 of these patients, visual acuity, if untreated, may decrease to hundredths over the next 12 months.

According to various data, laser coagulation and transpupillary thermotherapy can reduce the number of cases of severe vision loss to 23 - 46% (depending on the localization of the process), photodynamic therapy with verteporfin - up to an average of 40%, submacular surgery - up to 19% (it must be taken into account that treatment was applied to patients with different characteristics of the pathological process, so the comparison is very conditional).

Article from the book: .

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2013

Peripheral retinal degenerations (H35.4)

Ophthalmology

general information

Short description

Approved by the minutes of the meeting
Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan

No. 23 dated 12/12/2013

Peripheral chorioretinal degeneration- chorioretinal changes in the periphery of the fundus, when only the retina and choroid are involved in the process. It can occur both in nearsighted and farsighted people, and in people with emmetropic refraction.

I. INTRODUCTION

Protocol name: Peripheral chorioretinal degeneration

Protocol code:

Code (codes) according to ICD-10:

H35.4 Peripheral chorioretinal degeneration

Abbreviations used in the protocol:

PCRD - peripheral chorioretinal degeneration

optic disc - optic disc

VEP - visual cortical evoked potentials

ELISA - enzyme immunoassay

ECG - electrocardiography

HIV human immunodeficiency virus

ERG - electroretinogram

Protocol development date- 2013

Protocol Users- an ophthalmologist at a polyclinic and a hospital.

Classification

Clinical classification

By type they are divided into:

1. Lattice dystrophy is the most common cause of retinal detachment. A family-hereditary predisposition to this type of dystrophies is assumed with a higher frequency of occurrence in men. As a rule, it is found in both eyes. Most often localized in the upper outer quadrant of the fundus equatorially or anteriorly from the equator of the eye. When examining the fundus of the eye, lattice degeneration looks like a series of narrow white, as it were, fleecy stripes that form figures resembling a lattice or a rope ladder. This is what obliterated retinal vessels look like. Between these altered vessels, pinkish-red foci of retinal thinning, cysts and retinal breaks occur. Characteristic changes in pigmentation in the form of darker or lighter spots, pigmentation along the vessels. The vitreous body is, as it were, fixed to the edges of the dystrophy, i.e. “tractions” are formed - strands that pull the retina and easily lead to breaks.

2. Dystrophy of the "snail track" type. On the retina, whitish, slightly gleaming, streaky inclusions with many small thinnings and perforated defects are found. Degenerative foci merge and form ribbon-like zones, which appearance reminiscent of a snail's footprint. Most often located in the upper outer quadrant. As a result of such dystrophy, large round gaps can form.

3. Hoarfrost dystrophy is an inherited disease of the periphery of the retina. Fundus changes are usually bilateral and symmetrical. On the periphery of the retina there are large yellowish-white inclusions in the form of "snow flakes" that protrude above the surface of the retina and are usually located near thickened partially obliterated vessels, may be dark spots. Hoarfrost degeneration progresses over a long period of time and does not lead to ruptures as often as ethmoid and snail print.

4. Cobblestone degeneration located, as a rule, far on the periphery. Separate white foci are visible, slightly elongated, near which small clumps of pigment are sometimes determined. It is more often found in the lower parts of the fundus, although it can be determined along the entire perimeter.

5. Cystic (small cystic) retinal dystrophy located on the extreme periphery of the fundus. Small cysts can merge to form larger ones. With falls, blunt injuries, ruptures of cysts are possible, which can lead to the formation of perforated ruptures. When examining the fundus of the eye, the cysts look like multiple round or oval bright red formations.

6. Retinoschisis — retinal dissection- Can be congenital or acquired. More often it is a hereditary pathology - a malformation of the retina. Congenital forms of retinoschisis include congenital retinal cysts, X-chromosomal juvenile retinoschisis, when patients, in addition to peripheral changes, often have dystrophic processes in the central zone of the retina, leading to decreased vision.

Acquired dystrophic retinoschisis most often occurs with myopia, as well as in the elderly and senile age.

mixed forms- a combination of different types of degenerations.

Peripheral chorioretinal degenerations can lead to retinal breaks. By appearance, retinal breaks are divided into perforated, valvular and by the type of dialysis.

Perforated breaks most often occur as a result of lattice and cystic dystrophy, the hole in the retina gapes.

A rupture is called valvular when a portion of the retina covers the site of the rupture. Valvular tears are usually the result of vitreoretinal traction, which "pulls" the retina along with it. When the gap is formed, the area of ​​vitreoretinal traction will be the top of the valve.

Dialysis is a linear tear of the retina along the dentate line - the site of attachment of the retina to the choroid. In most cases, dialysis is associated with blunt trauma to the eye.

The gaps in the fundus look like bright red, clearly defined foci of various shapes, through which the pattern of the choroid is visible. Retinal breaks are especially noticeable on a gray background of detachment.

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

The list of mandatory diagnostic measures before planned hospitalization for drug and laser treatment:

1. Consultation with an ophthalmologist

2. Visometry

3. Biomicroscopy

4. Ophthalmoscopy

5. Tonometry

6. Cycloscopy

7. Perimetry

8. Echobiometry

9. Lacrimal lavage

10. ENT, dentist, therapist

11. Consultation of narrow specialists (phthisiatrician, cardiologist, endocrinologist, epidemiological environment, etc.) in the presence of concomitant pathology.

12. Clinical and laboratory studies: general analysis blood, general urinalysis, blood sugar test, fecal test for helminth eggs, fluorography, ECG, coagulogram, blood clotting test, microreaction, HIV blood, biochemical blood test (ALT, AST, electrolytes, bilirubin, creatinine, urea), ELISA of blood for markers of hepatitis.

List of main diagnostic measures:

1. Consultation with an ophthalmologist

2. Visometry

3. Biomicroscopy

4. Ophthalmoscopy

5. Tonometry

6. Cycloscopy

7. Perimetry

8. Echobiometry

9. Keratorefractometry

List of additional diagnostic measures:

1. Doppler ultrasound to detect the degree of blood flow reduction in the vessels of the eye

2. A, B scan to determine the anterior-posterior and transverse size of the eyeball and to exclude retinal detachment

3. Electrophysiological studies - ERG and VEP for differential diagnosis with other diseases

Diagnostic criteria

Complaints and anamnesis

Peripheral chorioretinal degenerations are dangerous because they are practically asymptomatic. Most often they are found by chance during the inspection. In the presence of risk factors, the detection of dystrophy may be the result of a thorough targeted examination. Complaints about the appearance of lightning, flashes, the sudden appearance of more or less floating flies, which may already indicate a retinal tear. Burdened hereditary anamnesis in relation to myopia.

Physical examination

The level of blood pressure (to prevent the occurrence of hemorrhages during laser interventions)

Laboratory research: not informative.

Instrumental research:

Visometry: decreased visual acuity

- Biomicroscopy: destruction of the vitreous body of varying severity

- Ophthalmoscopy: degenerative changes in the retina in the central zone in the presence of various degrees of myopia:

Stage 1: initial changes in the optic disc in the form of a scleral ring, the formation of cones up to ¼ DD, less often large sizes, with a normal ophthalmoscopic picture of the macula in normal and redless light

Stage 2: initial disturbances in the pigmentation of the fundus, changes in the shape and color of the optic disc, cones of various sizes, often up to 1/2 DD, the disappearance of foveolar reflexes. With no red

Ophthalmoscopy yellow spot of orange-yellow color, normal shape, without reflexes.

Stage 3: pronounced violations of the pigmentation of the fundus, an increase in the spaces between the vessels of the choroid, large cones - up to 1.0 DD. In normal light, the macular area is of the "parquet" type or darkly pigmented. In redless light, a deformed yellow spot with light yellow foci or white patches on an orange-yellow background is determined.

Stage 4: depigmentation, cones more than 1 DD, true staphyloma. A yellow spot in ordinary light resembles a tissue eaten by a moth. Atrophic foci outside the macular region are possible. In redless light, the yellow spot is discolored, sharply deformed and resembles a light yellow blot.

Stage 5: extensive cone more than 1 DD, true staphyloma. In the macular region, an atrophic focus, sometimes merging with the cone. In redless light, yellow color is absent or is determined in the form of separate islands. In the absence of myopia, there will be no changes in the central zone.

- Tonometry: increase in IOP above the tolerable level;

- Perimetry: narrowing of the peripheral boundaries of the visual field,

- Cycloscopy:

I. Chorioretinal changes in the equator.

1. Lattice dystrophy.

2. Pathological hyperpigmentation

3. Retinal breaks with valves and caps.

II. Chorioretinal changes in the dentate line

1. Cystic dystrophy

2. Retinoschisis

3. Chorioretinal atrophy

III. mixed forms

Echobiometry: determination of the transverse and longitudinal size of the eye

Indications for expert advice:

In the presence of concomitant general pathology, a conclusion of the relevant specialist is necessary that there are no contraindications to surgical laser treatment. Without fail, the conclusion of an otorhinolaryngologist and a dentist for the absence of chronic foci of infection.

Differential Diagnosis

The differential diagnosis in the presence of myopia is between peripheral chorioretinal degeneration of myopic genesis and peripheral pigmentary degeneration.

Indicators	Complicated myopia	Peripheral pigmentary degeneration
Visual acuity	Vision improves with correction	Vision does not change with correction
line of sight	Slight narrowing around the periphery	concentric narrowing of the visual field
Ocular fundus	Chorioretinal changes in the form of lattice dystrophy, cystic dystrophy, retinoschisis. In the form of mixed forms	Redistribution of pigment in the form of "bone bodies", may be absent

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

Treatment

Treatment Goals

Stabilization degenerative changes on the retina and visual acuity, prevention of retinal detachment

Treatment tactics

Non-drug treatment:
- mode - general,
- diet - table No. 15.10, enriched with vitamins and minerals,
- appointment of light procedures,
- physiotherapy with a helium-neon laser No. 5-7 with a stimulating purpose (according to indications).
- Limitation of physical activity
- Spectacle correction

A) gymnastics according to Avetisov-Mats

C) gymnastics according to Dashevsky

D) electrical stimulation

E) computer programs "Relax", "Eye"

E) Amblyocor

Medical treatment

Mydriatics and cycloplegics:
tropicamide 0.5; 1% - for pupil dilation 2 drops 2 times a day

Atropine sulfate 1% 2 drops x 2 times a day

Trophic therapy:
Sodium chloride - dilution of drugs 200.0 ml.

Vinpocetine - improvement of tissue trophism 1 tab. 3 times a day for 1 month; 2.0 - 4.0 ml. in / in the physical. solution No. 10

Cinnarizine - improvement of tissue trophism 1 tab - 3 times a day for 1 month

Retinoprotectors(mildronate, retinolamine 1 tab. 3 times a day for 1 month; 0.5 p / b No. 10.

Cerebrolysin - lymphotropic drug 2.0 ml. intramuscularly; 0.5 ml. parabulbarno

Emoksipin - antioxidant 0.5 ml. parabulbar; 2.0 intramuscularly No. 10, or drip 1 drop 4 times a day, contact eye films No. 10.

Retinol acetate / palminate + Tocopherol acetate - antioxidant 1 tab. 2 times a day.

Vasodilator drugs:

Angioprotective drugs

Cyanocobalamin - vitamin therapy 1.0 ml. intramuscularly

Pyridoxine hydrochloride - vitamin therapy 1.0 ml. intramuscularly.

Ascorbic acid - vasoconstrictor -5% - 2.0 ml №10 i/m

Taurine 0.5 ml p / b No. 10;

Surgery(on an outpatient basis)

Laser coagulation of zones of peripheral degeneration

Preventive actions

Antibacterial and anti-inflammatory therapy for the prevention of postoperative inflammatory complications

Limitation physical activity

Further management:

Within 7-10 days after laser intervention, instillation of anti-inflammatory and antibacterial drugs

Ophthalmoscopy and cycloscopy 2 times a year

Treatment effectiveness indicators:
- stabilization of visual functions,
- stabilization and delimitation of degenerative foci and retinal breaks.

Hospitalization

Indications for hospitalization
- deterioration of visual functions,
- progression of degenerative conditions on the periphery of the fundus.

Type of hospitalization - planned.

Information

Sources and literature

1. Minutes of the meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2013
   1. 1. Jack J. Kansky [et al.]. Fundus diseases /; ed. S.E. Avetisova. - M.: MED-press-inform, 2008. - 424 p. 2. L.V. Dravica [i dr.]. Condition of the fellow eye in patients with unilateral retinal detachment // Ars Medica. - 2010. - No. 13(33). - S. 162-164. 3. American Academy of Ophthalmology. - 2008. - Mode of access: http://one.aao.org/CE/PracticeGuidelines/PPP.aspx. - Date of access: 08/10/2011. 4. M. Bonnet, P. Aracil, F. Carneau. Nongmatogenous retinal detachment after prophylactic argon laser photocoagulation / / Graefes Arch Clin Exp Ophthalmol. - 1987. - No. 225. - P. 5-8. 5. Brinton, D.A. Retinal Detail: Principles and Practice-3rd edition.- Oxford University Press in cooperation with the American Academy of Ophthalmology, 2009. - 258 p. 6. Byer, N.E. Lattice degeneration of the retina // Surv Ophthalmol. - 1979. - Vol. 23. - No. 4.-P. 213-248. 7. Byer, N.E. Long-term natural history of lattice degeneration of the retina // Ophthalmology. - 1989.-Vol. 96. - No. 9. - P. 1396-1401. 8. Byer, N.E. Natural history of posterior vitreous detachment with early management as the premier line of defense against retinal detachment // Ophthalmology. - 1994. - Vol. 1 0 1 .-No. 9 .-P. 1503-1514. 9. Byer, N.E. The long-term natural history of senile retinoschisis with implications for management / / Ophthalmology. - 1986. - Vol. 93. - No. 9. - P. 1127-1137. 10. Byer, N.E. The natural history of asymptomatic retinal breaks // 10. Ophthalmology. - 1982. - Vol. 89. - No. 9. - P. 1033-1039. 11. Byer, N.E. What happens to untreated asymptomatic retinal breaks, and are they affected by posterior vitreous detachment? / / Ophthalmology. - 1998. - Vol. 105. - No. 6. - P. 1045-1050. 12. M.C. Sharma. Determination of the incidence and clinical characteristics of subsequent retinal tears following treatment of the acute posterior vitreous detachment-related initial retinal tears / / Am J Ophthalmol. - 2004. - No. 138. - C. 280-284. 13.D.S. Chauhan. Failure of prophylactic retinopexy in fellow eyes w ithout a posterior vitreous detachment // Arch Ophthalmol. - 2006. - No. 124. - C. 968-971. 14.M.R. Dayan. Flashes and floaters as predictors of vitreoretinal 15. pathology: is follow-up necessary for posterior vitreous detachment? // eye. - 1996. - No. 10. - C. 456-458. 16.J.C. Folk, E.L. Arrindell. The fellow eye of patients with phakic lattice retinal detachment // Ophthalmology. - 1989. - No. 96. - P. 72-79. 17. R. Sarrafizadeh. Incidence of retinal detachment and visual outcome in eyes presenting with posterior vitreous separation and dense fundus-obscuring vitreous hemorrhage // Ophthalmology. - 2 0 0 1 .-V ol. 108, No. 10. - P. 2273-2278. 18. Kreis, A.. W. Aylward, J. G. Wolfensberger, T. J . Prophylaxis for retinal detachment Evidence or Eminence Based? // Retina. - 2007. - No. 27. - P. 468-472. 19. Lewis, H. Peripheral retinal degenerations and the risk of retinal detachment // Am J. Ophthalmol. - 2003. - No. 136. - P. 155-160. 20. Schroeder W, Baden H. Retinal detachment despite preventive coagulation // Ophthalmologe. - 1996. - No. 93. - P. 144-148. 21. Singh, AJ. Seemongal-Dass R.R. Natural history of posterior vitreous detachment with early management as the premier line of defense against retinal detachment / / Eye. - 2 0 0 1 .-No. 1 5 .-P. 152-154. 22.R.E. coffee. Symptomatic posterior vitreous detachment and the incidence of delayed retinal breaks: case series and meta-analysis // Am J 23. Ophthalmol. - 2007. - No. 144. - C. 409-413. 24. 22. K.A. overdam. Symptoms predictive for the later development of retinal breaks // Arch. Ophthalmol. - 2001.-No. 119.-C. 1483-1486. 25. 23. Williamson, T.N. Vitreoretinal Surgery / T.N. Williamson. - Berlin Heidelberg: Springer-Verlag, 26. 2008. - 227 p.
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Hereditary diseases of the retina and optic nerve- an extensive heterogeneous group of diseases leading to a decrease or complete absence of vision. Depending on the primary lesion of the retina or optic nerve, the following subgroups are distinguished.

Code by international classification ICD-10 diseases:

• G45.3
• H31.2
• H35.5
• H53.5
• H53.6

Congenital amaurosis - inherited abiotrophy of rods and cones of the retina and atrophy of the optic nerves, manifested by the rapid development of bilateral central scotoma. Observed predominantly in men, can develop at any age (many forms are congenital - Leber's congenital amaurosis: . type 1: 204000, GUC2D, GUCSD, LCA1, 600179 [guanylate cyclase 2D], 17p13; . type 2: 204100, RPE65 [pigment protein retinal epithelium], 180069, 1p31). It is characterized by progressive deterioration of vision. It is based on inherited diseases (mutations of the mitochondrial and nuclear genomes). At least 18 mitochondrial DNA mutations and at least 6 nuclear DNA loci are known. The high frequency of the disease in men is explained by the influence of androgens (for example, a case of a sharp loss of vision in patients with the MTND4 * LHON11778A mutation after androgen therapy is described).

Optic nerve atrophy is the end result of dystrophic changes in retinal ganglion neurons. Primary optic nerve atrophy is a genetically determined pathology; a component or a single manifestation in a series hereditary diseases, differing in the timing of the appearance of atrophy, severity, accompanying symptoms and type of inheritance. All major types of inheritance are noted, including mutations in the mitochondrial genome (Leber's optic nerve atrophy, #535000, MTND genes).

Optic nerve atrophy is often a component of hereditary syndromes. optic nerve deafness and distal neurogenic amyotrophy (258650, r) .. Metaphyseal dysplasia, anetoderma (focal skin atrophy) and optic nerve atrophy (250450, r) .. Optic and auditory nerve with dementia (311150, А).

Pigmentary retinal degeneration is a progressive atrophy of the neuroepithelium with atrophy and pigment infiltration of the inner layers of the retina. The often used term "retinitis pigmentosa" does not quite accurately reflect the essence of the process, since there is no inflammatory reaction as such. The main manifestations are due to the loss of retinal rods. It is based on many mutations in a number of loci (for example, the genes of peripherin, rhodopsin, cGMP controlled photoreceptor channel, etc.). Pigmentary retinal degeneration, not associated with other disorders, is most often inherited as r (268000) and less commonly as À recessive (312600) trait. Dominant inheritance is noted in 3-4% of cases. In addition, atypical retinitis pigmentosa has been observed in a variety of other conditions, including recessive disorders such as abetalipoproteinemia (200100), Alstrom syndrome (203800), Refsum syndrome (266500), Bardet-Biedl (209900), Lawrence-Moon (245800), Usher ( 276900), Cockayne (216400), pallidar degeneration (260200).

Colloidal retinal degeneration (Doin's cellular choroiditis, *126600, 2p16, DHRD gene, B). Multiple round whitish lesions located near the optic disc and in the area between the superior and inferior temporal arterioles.

Sorsby fundus dystrophy (#136900, pseudo-inflammatory fundus dystrophy, 22q12.1-q13.2, tissue metalloproteinase inhibitor gene - 3 TIMP3 [*188826], В). Clinically: macular degeneration, fundus, retinal atrophy.

Macular dystrophy, cystic (*153880, 7p21-p15, MDDC gene, B). Clinically: cystic macular edema, whitish punctate vitreous deposits, farsightedness, strabismus, decreased visual acuity, pericentral retinitis pigmentosa.

Rod and cone dystrophy, types and genes: . type 1, 600624, CORD1, CRD1, 18q21.1 q21.3; . type 2, 120970, CRX, CORD2, CRD, 602225, 19q13.3

Retinal pigment epithelium dystrophy, 179605 (mutations in the RDS, RP7 peripherin gene), 6p21.1 cen

Early retinal dystrophy (autosomal recessive): 180069, RPE65 gene, 1p31

Central choroidal dystrophy (215500, CACD gene, 17p)

Diagnostics

Differential diagnosis. Infectious retinopathy - viral (rubella) or bacterial (syphilis). Residual effects of exudative retinal detachment. Secondary toxic retinopathies (chloroquine or phenothiazines). Other pathological conditions (occlusion of the ophthalmic artery, trauma).

Current and forecast. The prognosis is most unfavorable for congenital forms. The course in most cases is chronic, slowly progressive.

ICD-10. H31.2 Hereditary dystrophy of the choroid. H35.5 Hereditary retinal dystrophies. Q14 Congenital malformations [malformations] of the posterior segment of the eye

APPS

Night blindness- a sharp deterioration in vision in low light conditions - occurs with a deficiency of retinol (alimentary hemeralopia, symptomatic hemeralopia [diseases of the retina, choroid, optic nerve, liver damage]), as well as in a number of congenital conditions. Night blindness develops with mutations in the gene a - subunit of rod transducin, b - subunit of cGMP phosphodiesterase, rhodopsin. Ogushi disease (258100, defects specific to visual retina proteins - arrestin (181031) and rhodopsin kinase (180381). Synonyms: hemeralopia, nyctalopia, chicken blindness. ICD-10. H53.6 Night blindness. OMIM. 310500 Stationary congenital night blindness with myopia. 139330 Night blindness congenital stable. 300071 Stationary congenital night blindness, type 2. 163500 Night blindness congenital stationary, type 3. 180380 Night blindness, congenital stationary rhodopsin - associated. 258100 Ogushi disease.

color blindness(achromatopsia) - lack of color vision. The ability to distinguish any colors (trichromasia, the foundations of the theory of color vision was proposed in 1802 by Thomas Young) is determined by the presence of all three visual pigments in the retina (for red, green and blue - primary colors). Dichromasia - defects in color perception (mainly in men; for example, various defects in men make up 8% of the total population) according to one of the primary colors - are divided into protanopia, deutanopia and tritanopia (from the Greek. first, second and third [meaning serial numbers primary colors: respectively red, green, blue]). Protanopia (perception of red suffers, approximately 25% of cases of color blindness). Deitanopia (color blindness in the perception of green, about 75% of all cases). Tritanopia (predominantly the perception of violet color suffers, defective vision in blue and yellow). Color blindness - a violation of color vision - the inability to distinguish between red and green color a. ICD-10. H53.5 Color vision anomalies.

Blindness is transient(amaurosis fugax) - an acute episode of complete or partial loss of vision, usually lasting no more than 10 minutes. The reasons: short-term ischemia in the carotid artery (as a rule, embolism of the retinal arteries). Treatment. Drug therapy.. Antihypertensive agents.. Fibrinolytic agents.. Antiplatelet agents (acetylsalicylic acid, dipyridamole). Surgical: carotid endarterectomy. ICD-10. G45.3 Transient blindness.

Choroideremia X - linked(*303100, CHM gene, Xq21.2; form with deafness and obesity, 303110) - hereditary eye disease, progressive decrease in visual acuity, narrowing of visual fields, hemeralopia and myopia; characteristic changes in the fundus of the eye (almost complete absence vascular pattern, sharp contours and reddish-brown color of the yellow spot, indistinct boundaries of the optic nerve head). Synonym: progressive atrophy of the choroid. ICD-10. H31.2 Hereditary dystrophies of the choroid.

The retina of the eye is responsible for the perception of the image. Retinal dystrophy is a violation of its nutrition.

The disease is caused by disorders in the vascular system of the eye, and then a scar is formed, the central zone of the retina completely falls out, and only peripheral vision remains. A person distinguishes day from night, sees fuzzy contours of objects with peripheral vision, but there is none in the center of the image - a black spot seems to be hanging in front of the eye.

Retinal dystrophy is a group pathological conditions, which have a common manifestation - changes in the tissues of the retina, which lead to its death.

Nerve cells in the retina perceive the refraction of light rays and transmit information to the brain through the optic nerve. This layer is quite thin, which makes it very sensitive to impact. physical factors and changes in the internal environment of the body.

This disease is becoming more common and probable cause complete or partial loss of vision. This pathology is characterized by rapid progression, and the symptoms depend on the cause and localization of the process.

Retinal dystrophy is the name of an extensive group of diseases in which there is a "death" of this membrane, that is, its progressive degeneration, which leads to a deterioration in the patient's vision.

Etiology and pathogenesis

Most often, the disease is caused by metabolic waste products that accumulate with age. A significant place is occupied by infections, intoxications and circulatory disorders of the inner membrane.

Retinal dystrophy can also develop in young people, against the background of pregnancy, cardiovascular diseases and pathologies of the endocrine glands.

The macula is made up of several layers of specialized cells. A layer of photoreceptors is located above the layer of retinal pigment epithelium cells, and below is a thin Bruch's membrane that separates the upper layers from the network of blood vessels (choriocapillaries) that provide the macula with oxygen and nutrients.

As the eye ages, the products of cell metabolism accumulate, forming the so-called "drusen" - yellowish thickenings under the retinal pigment epithelium.

The presence of many small drusen or one (or several) large drusen is considered the first sign of the early stage of the "dry" form of AMD. The "dry" (non-exudative) form is the most common (about 90% of cases).

As they accumulate, drusen can cause inflammation by producing vascular endothelial growth factor, a protein that promotes the growth of new blood vessels in the eye. The growth of new pathological blood vessels begins, this process is called angiogenesis.

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

From this point on, AMD begins to progress, passing into another, more aggressive form - “wet”. Fluid builds up between Bruch's membrane and the photoreceptor layer, affecting vulnerable nerves, resulting in healthy vision.

If this process is not stopped, then hemorrhages will lead to detachments and the formation of scar tissue, which threatens with an irreparable loss of central vision.

The reasons

Often, the disease is caused by metabolic decay products accumulated with age. A significant role is played by the problems of blood supply to the inner membrane, intoxication, and infection.

This disease can also develop at a young age, against the background of pregnancy, pathologies of the endocrine glands and diseases of the cardiovascular system.

The main causes of retinal dystrophy include:

• Various eye diseases and inflammatory processes (myopia, uveitis).
• Infectious diseases and intoxications.
• Eye injuries as a result of bruises, blows and so on.
• Genetic predisposition to dystrophy.
• Various systemic diseases (diabetes, hypertension, thyroid and kidney problems, atherosclerosis, and so on).

All these reasons, except for genetic predisposition, may not always contribute to the appearance of retinal dystrophy, but they are risk factors. Doctors say that people with overweight and bad habits are more likely to develop retinal dystrophy.

Low blood pressure during the second trimester of pregnancy leads to circulatory disorders and poor nutrition of the retina. Therefore, pregnant women are also at risk.

The causes of retinal dystrophy, first of all, lie in age-related changes that occur in the vascular system that envelops the eyeball - mainly this is a circulatory disorder, the cause of which, in turn, is vascular sclerosis.

Negative factors, which can be divided into internal and external, lead to undesirable changes that develop inside the eye. Defects are divided into localization of the lesion: sometimes central, and sometimes peripheral vision suffers.

Internal

Internal reasons:

• body aging;
• heredity;
• vascular diseases;
• hypertension;
• farsightedness and myopia;
• elevated cholesterol levels;
• injuries of the visual organs;
• eye surgery;
• prolonged local inflammation.

Individuals with very white skin and blue eyes are also at high risk of developing degeneration. Patients with such anatomical features acquire diseases faster, especially when influenced by external factors.

External

External causes include:

• prolonged exposure to UV rays on the retina;
• smoking (including passive);
• poisoning (poisons, alcohol).

Age

In persons of retirement age - from the age of 55 - a macular form is diagnosed, in which the retina changes due to aging of the body. In addition to the above reasons, the development of the disease is also influenced by specific factors that appear more often in old age.

Reasons for the development of age-related macular degeneration:

• cataract;
• diabetes;
• atherosclerosis;
• obesity;
• vitamin deficiency;
• increased levels of free radicals.

More often the disease affects the female half of the population, and men suffer from it much less often.

Reference! In representatives of the white race, defects in the inner membrane of the eye are diagnosed much more often.

Despite numerous studies devoted to AMD, the causes of this disease remain to date not fully elucidated. AMD is a multifactorial disease.

Age is the main reason. The incidence increases sharply with age. Among middle-aged people, this disease occurs in 2%, at the age of 65 to 75 years it is diagnosed in 20%, and in the group from 75 to 84 years, signs of AMD are found in every third.

There are congenital or secondary (acquired), localization central (located in the macular region) or peripheral.

Vision with AMD

The etiology of dystrophic processes in the retina is diverse. Diagnosed in children, retinal dystrophy in the vast majority of cases is provoked by heredity.

Provocative for dystrophy can be any factors that lead to disorders of metabolic processes. In older people, these factors are joined by any vascular pathologies, due to which the normal supply of oxygen and nutrients to the eye is disrupted.

Retinal degeneration begins in almost half of patients diagnosed with myopia. The dependence is direct - the more pronounced myopia, the greater the possibility of developing dystrophy. Also in the course of observations, it was noticed that pathology often develops in representatives of the white race with fair skin and eyes.

Local causes of retinal dystrophy also include eye injuries of varying severity, in which the retina was damaged, inflammatory diseases structures of the eye of various etiologies, clouding of the lens. The disease can develop after surgical interventions on the eyes.

There are more general causes of the disease, which are not such in themselves, but with a high degree of probability can provoke a degenerative process. These factors include:

• hypertension;
• endocrine diseases, especially diabetes mellitus;
• thyroid pathology;
• severe intoxication with various substances;
• severe beriberi or lack of minerals and other nutrients;
• long-term periodic exposure of the eyes to ultraviolet light.

Retinal dystrophy has causes that, albeit conditionally, are still divided into two groups.

The mechanism for the development of retinal dystrophy has not been fully studied, but there are factors that significantly increase the likelihood of developing such a condition. There are such causes of the appearance of pathology:

• Diabetes.
• Diseases of the cardiovascular system, which are accompanied by a functional or morphological narrowing of the lumen of the vessels. These are diseases such as atherosclerosis, systemic vasculitis and hypertension.
• Intense exposure to ultraviolet radiation on the unprotected eye.
• bad habits and overweight.
• Heredity.

• stressful situations.
• Avitaminosis and lack of nutrients in the diet.

• Edema, inflammation and retinal dystrophy, circulatory disorders and damage to the optic nerve, as well as trauma to the skull;
• Diseases of the central nervous system such as: brain tumor, meningitis, syphilis, herpes zoster, less often influenza and acute respiratory infections;
• hypertension;
• Atherosclerosis;
• Great loss of blood.

It is almost impossible to independently determine the cause of optic nerve atrophy. This can only be done by a professional ophthalmologist, after a thorough examination of the patient.

30 to 40% of cases of retinal dystrophy develop in people suffering from myopia

It has been proven that 30 to 40% of cases of retinal dystrophy develop in people suffering from

All these reasons, except for genetic predisposition, may not always contribute to the appearance of retinal dystrophy, but they are risk factors.

Doctors say that people with overweight and bad habits are more likely to develop retinal dystrophy. Low blood pressure during the second trimester of pregnancy leads to circulatory disorders and poor nutrition of the retina. Therefore, pregnant women are also at risk.

Causes of retinal dystrophy during pregnancy can be common diseases:

• Diabetes
• Hypertension
• Vegetovascular dystonia
• kidney disease
• Sequelae of traumatic brain injury
• Thyroid disorders

Classification

Distinguish between central and peripheral retinal dystrophy. Central retinal dystrophy occurs in the area with the clearest vision (macula area). As mentioned earlier, the disease can be provoked by age-related changes, which is the most common cause. Indeed, due to age, the blood vessels of the eyes undergo changes.

The development of the disease gradually reduces visual acuity. Blindness, as a rule, does not appear, provided that the peripheral regions of the retina are not involved. Recognizing central retinal dystrophy is simple, it is characterized by curvature, bifurcation and fractures of the images.

Central macular degeneration of the retina can be characterized by two forms of the course of the disease: dry and wet. The first is characterized by tuberous formations of accumulated metabolic products of the retina and choroid.

It is characterized by a slow decline in vision. The second differs in that it has liquid and blood accumulations in the area of ​​the retina, caused by the germination of newly formed vessels.

Visual acuity falls quickly enough, which is typical in this form of macular degeneration of the retina. Treatment requires qualified and timely, regardless of the form of the disease.

Therapy is prescribed based on the results of diagnostics carried out by a medical institution.

Central chorioretinal dystrophy of the retina occurs in the male half of the population, the age of the man, as a rule, exceeds 20 years. The cause of the development of the disease is the accumulation of vascular effusion under the retina.

This interferes with the normal process of nutrition, metabolism, and as a result, dystrophy develops. The effusion provokes a gradual retinal detachment, which leads to serious consequences that affect the ability to see.

It is not excluded the onset of complete blindness. Symptoms of chorioretinal dystrophy are visual impairment and image distortion.

Peripheral retinal dystrophy symptoms may be mild and seem invisible to the patient. Although sometimes spots or light flashes are noted. Peripheral retinal dystrophy is detected using ophthalmoscopy: the eyeball is examined and fluorescent antigraphy is performed.

Dystrophies are divided into congenital and acquired. They are also classified by localization into three types, each of which includes several varieties. According to this classification, degenerations are generalized, in the peripheral region or in the macula (central).

Congenital

Speaking about the types of retinal dystrophy, it should be noted that, according to the causal factor, this pathology is classified into two main groups: congenital forms associated with certain hereditary phenomena, developing in childhood and also called primary, and acquired (they are also secondary), caused by any diseases and / or injuries.

Based on the localization of pathological changes, the described ailment can be divided into three varieties: peripheral forms, in which the edges of the retina are affected; central chorioretinal dystrophy of the retina, affecting only the center of the specified eye structure; generalized forms, characterized by the spread of the pathological process throughout the retina.

It should be noted that in our country there are many problems with the classification of this disease. Many terms can refer to essentially the same state.

For example, central retinal dystrophy is often referred to as age-related, which is synonymous with senile, involutional dystrophy; periodically this disease is called age-related macular degeneration; the disease is also sometimes referred to as central chorioretinitis.

At the same time, Western doctors use only one term - macular degeneration of the retina, which is quite logical, because the macula (yellow spot) is precisely located in the central part of the retina. By the way, this term is also used in domestic medicine in addition to the names listed above.

It is customary to divide dystrophy into congenital and acquired. In addition, according to localization, central and peripheral are distinguished. If retinal dystrophy is combined in the central (macular region) and its peripheral part, then this form is called generalized. It is more difficult to treat congenital forms than acquired ones.

Hereditary generalized forms of dystrophy include:

• Tapetoretinal (it is also called pigmentary).

• Congenital disorders of night vision.
• Cone dysfunction syndrome. Two manifestations are possible - a violation of color perception or blindness.
• Amaurosis Leber.

Peripheral retinal dystrophy in congenital forms is divided into:

• Pathology Goldman-Favre.
• Retinoschisis.

With central retinal dystrophy, the diagnosis is:

• Macular degeneration.
• Stargardt and Best disease.

Central dystrophy is also called macular (because the macular area of ​​the retina is affected).

Acquired retinal dystrophies do not have such a complex classification.

A separate place is occupied by retinal dystrophy during pregnancy. Most often, it develops against the background of preeclampsia or eclampsia.

Depending on the location of the lesion of the retina, the types of the disease are distinguished: central and peripheral.

Central retinal degeneration or macular degeneration

A disease accompanied by damage to central vision. As a rule, it develops in people whose age exceeds 55 years.

There are two forms of macular degeneration:

• dry form. Corresponds to the initial stage of the disease. During this period, visual acuity decreases, however, the patient does not feel it.
• wet form. If the disease was not diagnosed in time, then the dry form of dystrophy is transformed into a wet one. This indicates the development of the disease, the new stage of which is characterized by the fragility of the vessels of the eye and their predisposition to fragility. As a result, hemorrhages occur in the eye.

The main symptoms of central retinal dystrophy include:

• decrease in central vision (there is a distortion of the contours of objects and lines);
• sensitivity to bright light;
• formation of a dark spot that makes it difficult to read, drive vehicle and work with small objects;
• distorted color perception.

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Peripheral retinal dystrophy

All dystrophies can be divided into two large groups: acquired (secondary) and congenital (primary). In turn, the secondary ones are further divided into three groups depending on the localization of defects: central, peripheral and generalized.

Chorioretinal retinal dystrophy, also known as age-related macular degeneration of the retina, is typical for people over 50 years of age. The disease can lead to complete loss of central vision. At the same time, the peripheral vision of a patient with chorioretinal dystrophy of the retina remains within the normal range.

Without central vision, clarity of perception of objects is impossible. People with symptoms of this type of retinal dystrophy are unable to read or drive. The rate of progression of the disease depends on the type and severity of chorioretinal dystrophy of the retina.

The wet form of the disease is considered the most severe, rapid and difficult to treat. However, the most common (in 9 out of 10 cases) is the dry form of chorioretinal retinal dystrophy. With it, the process of gradual destruction of the cells of the central part of the retina (macula) takes several years.

With another type of retinal dystrophy, peripheral dystrophy retina, changes affect the peripheral parts of the fundus. The danger of this disease is that the early stage of development of peripheral retinal dystrophy is almost asymptomatic. The first dystrophic changes can be diagnosed only with the help of special ophthalmic equipment.

However, it is very important to diagnose these changes at an early stage of peripheral retinal dystrophy. Only in this case it is possible to effectively prevent a serious complication of the disease - retinal detachment or rupture. Such pathologies, unlike their root cause, are quite difficult to treat.

Pigmentary retinal dystrophy is the most rare anomaly caused by hereditary factors. It is caused by disturbances in the work of retinal photoreceptors responsible for either twilight black-and-white or daytime color vision.

Pigmentary retinal dystrophy can be transmitted from mother to child in an autosomal recessive or autosomal dominant pattern of inheritance. Most often, men suffer from retinitis pigmentosa. The clinical picture of the disease and the mechanism of development are deeply individual.

With retinitis pigmentosa mild degree there is only a slight decrease in visual acuity in a poorly lit space. In severe cases of retinitis pigmentosa, complete loss of visual function is possible.

Degrees of disability

According to ICD-10, the severity

I degree

(small degree of low vision) - minor dysfunctions;

III degree (high degree of low vision) severe functional impairment;

IV degree

(practical or absolute blindness) significantly pronounced dysfunction.

Criteria for assessing violations of the main visual functions in determining disability are given in Table. one.

Assessment of disability has its own characteristics for each category of life activity, however, there are also basic (typical for most categories) characteristics. All life restrictions

depending on the severity is divided into three degrees.

Restrictions of the first degree take place when the patient is able to independently carry out one or another type of life activity, but with certain difficulties (longer expenditure of time, reduction in volume, fragmentation of performance, etc.) and, if necessary, with the use of aids due to moderate persistent disorders functions.

Persistent disability with farsightedness and astigmatism is observed
in very rare cases. It may be associated with the appearance of asthenotic complaints.
due to decreased vision. In these cases, work with small parts is not available and
requiring eye strain.

Transfer to another, lower qualification job due to farsightedness
high degree, may be the reason for the establishment of III group of disability.

Primary disability of children

Prevalence

primary disability of children

due to visual impairment in the Russian Federation in 2000-2005. amounted to 1.4 per 10,000 children with fluctuations in this indicator both in various federal districts (from 0.8 in the North-Western and Urals to 2.8 per 10,000 children and in the South), and in individual subjects of the Federation (from 0, 1 in the Novosibirsk and Kemerovo regions to 26.4 per 10,000 children in the Chechen Republic and Dagestan).

The disease, also called degeneration, can often be observed in childhood. Macular degeneration is most common among children.

The risk of the disease increases if inheritance occurs according to the dominant pattern. The development of central dystrophy in this case occurs at a high speed. The disease develops in two eyes, a characteristic symptom is a violation of the perception of colors.

In children, in addition to retinal dystrophy, strabismus and a slight twitching of the eyeball are observed. Since the pathology is genetic in nature, there are no effective drugs that can cure the disease completely.

In most cases, degenerative disorders of the visual analyzer in children are hereditary. The pathology of the vessels of the macula is manifested by several anomalies. For example, Stargardt's disease, which has an autosomal recessive inheritance principle (both parents of a child have a “sick” gene in their set of chromosomes).

The disease affects both eyes, begins to progress after the 5th age. The prognosis is unfavorable, since it is impossible to cure such dystrophy, and over time, the optic nerve can completely atrophy.

Best's disease is also a congenital condition. A cystic formation appears in the center of the macula, reducing the level of central vision acuity.

Juvenile retinoschisis is an X-linked disease characterized by degenerative changes followed by degradation of the vitreous body. It affects boys, girls become carriers of the "sick" gene. The clinical picture is manifested by nystagmus (involuntary eye movements) and strabismus.

Retinitis pigmentosa is a severe pathology, which is a combination of several hereditary diseases. The peak of progression occurs at the age of ten.

Classification of the disease, symptoms in children and adults

The negative dynamics of the main indicators of disability in 2000-2005 was established. with an increase in the number of newly recognized disabled people from 39,000 to 66,700 people per year and an increase in the primary disability rate from 3.1 (2000) and 3.5 (2004) to 5.8 (2005) per 10,000 adults.

The prevalence of primary disability is not the same in different federal districts (in the Central - 5.4, in the Volga - 7.9, in the Far East 4.5, in the South 6.0, in the North-West - 4.2, in the Urals - 5.3 , in the Siberian 5.1 per 10,000 adults) and subjects of the Russian Federation, where it varies from 1.5 in Moscow to 20.5 in the Republic of Kalmykia per 10,000 adults.

The highest frequency of primary disability among the population of retirement age (18.2), which is significantly higher than the same indicator for people of middle (3.4) and young (1.0 per 10,000 of the corresponding population) age. Among adults with a newly diagnosed disability, patients of retirement age account for 79.8%, and of working age - 20.2%.

This question worries many expectant mothers who, as a rule, suffer from myopia, less often with eye diseases such as astigmatism, farsightedness, congenital cataracts, as well as those who have undergone eye surgery - scleroplasty, surgery for strabismus, laser vision correction.

Of course, there are contraindications and restrictions to natural childbirth due to the condition of the eyes, but most of them are temporary.

High myopia and natural childbirth.

In obstetrics, for a long time there has been an opinion that high myopia (more than -6.0 diopters) is an indication for caesarean section.

However, modern practice shows that childbirth through the natural birth canal is possible with this pathology.

Myopia, in itself, even if of a high degree, cannot be a limitation, and, moreover, a contraindication to delivery through the natural birth canal. The determining factor that can influence the decision on delivery is the condition of the retina.

It is important to know that the degree of myopia with the threat of complications from the retina does not matter. According to the literature and personal experience, the most common dystrophic changes, and retinal breaks occur with an average degree of myopia from 3 to 6 diopters.

Myopia and pregnancy

All pregnant women should visit an optometrist twice during pregnancy: at registration at 12-14 weeks, and then at 32-36 weeks. The ophthalmologist should be visited by all patients without exception.

This is a planned event aimed at preventing complications from the visual apparatus and one of the factors influencing the choice of the preferred method of delivery.

Myopia or nearsightedness is a very common eye disease. In terms of frequency of occurrence, it ranks second among all eye diseases in women of childbearing age. By the time of reproductive age, up to 30% of women suffer from history, and about a quarter of them have a high degree of myopia.

Features of the course of myopia during pregnancy

1. blurred vision, distorted perception of objects (curved, twisted), 2. flickering of "flies" and flashes before the eyes - in this case, it is necessary to independently measure blood pressure and call an ambulance team.

Diagnostics

– examination of the eye day by an ophthalmologist – to exclude severe concomitant pathology: KLA (hemoglobin, platelets), OAM (protein!), BAC (total protein, AlAT, AsAT, creatinine, urea, sugar, fibrinogen), coagulogram, blood pressure measurement and pulse.

Treatment

Hypermetropia or farsightedness is a visual pathology in which visual acuity is reduced in relation to closely spaced objects. Objects located at a distance are perceived as clearer. By itself, farsightedness is not a contraindication to gestation and independent childbirth.

Hyperopia to a lesser extent than myopia is dangerous with dystrophic changes in the fundus, but there is such a possibility. An ophthalmologist will examine you in a planned manner and, if necessary, send you for an examination of the fundus (usually highly qualified studies are carried out in eye microsurgery centers, laser correction laboratories, and so on).

In the case of the presence of foci of dystrophy, high-tech treatment with laser techniques is indicated.

Consequences for the mother: as a rule, there is no significant change in visual acuity. Consequences for the fetus: not identified, no additional examination is required for the baby.

You should be aware that hypermetropia, as well as myopia, may have a hereditary predisposition. It is possible to reliably assess the vision of a child only at the age of 2-3 years, since infants may have transient congenital hypermetropia that does not require treatment and correction.

Glaucoma is a disease of the eye apparatus, which is accompanied by an increase in intraocular pressure. In women of reproductive age, this disease is much less common than those listed above. Glaucoma happens different types(open-angle, closed-angle), but in itself it is not an obstacle to conceiving and bearing a baby.

Due to hormonal changes in the female body, an increase in progesterone levels and a change in the elasticity and extensibility of many tissue structures, the course of glaucoma during pregnancy usually improves. Exacerbations are rare, especially if the prescribed drops are used regularly.

However, not all eye drops can be used during pregnancy. Despite the apparent scanty dose of the drug entering the mother's body, the consequences can be very sad (intrauterine growth retardation, spontaneous miscarriage, uterine hypertonicity, pathological effects on the development of the central nervous system of the fetus).

1. Carbonic angibrase inhibitors (trusopt, dorzopt)2. Prostaglandins (travatan) 3. Beta blockers (timolol, arutimol, okumed, glautam, okuker)

During the planning of pregnancy, visit an ophthalmologist and consult about the replacement of the drug. Glaucoma is not inherited, so an additional examination of the newborn is not required.

In addition to myopia, there are other eye diseases.

Retinal dystrophy during pregnancy can develop if the expectant mother suffered from myopia or other ophthalmic pathologies before conception. In such cases, it is necessary to conduct pregnancy with the participation of an oculist. Vaginal delivery requires the approval of the attending ophthalmologist.

Ophthalmologists often have to deal with retinal dystrophy in women during pregnancy, when hormonal changes occur in full force in the body, leading to the activation of all metabolic processes, including changes in blood circulation in the eyes.

In the second trimester, the level of blood pressure decreases slightly, which leads to a slowdown in blood flow and, as a result, a decrease in blood in the vessels of the eye. Changes can provoke the development of retinal dystrophy.

During childbirth, the situation can be complicated to complete detachment or rupture of the retina. That is why it is so important to visit an ophthalmologist during pregnancy.

At the doctor's appointment, a standard diagnosis of the state of the visual system, including the fundus, will be carried out.

A re-examination is scheduled in the period from the 32nd to the 36th week. However, in case of diagnosing retinal dystrophy, it is necessary to visit an ophthalmologist once a month.

As for childbirth, several factors influence the choice between natural birth and cesarean section: the age of the woman in labor, the degree of the disease, the general health of the woman. Often, doctors practice cesarean section in order to maximize the safety of the birth process, both for the mother and for her baby .

If it is extremely important for a future mother to give birth to a child on her own, doctors recommend undergoing a procedure for prophylactic peripheral laser coagulation of the retina, which is performed at the 35th week of pregnancy.

In the process of exposure to a laser, it is possible to connect the choroid of the eyeball with the retina by scarring the tissue. In this case, a caesarean section can be avoided.

Treatment of chalazion without surgery is possible in the early stages of the disease. Can levomycetin be used for conjunctivitis in children? You will find the answer in this article.

During pregnancy, the hormonal background changes, metabolism increases. Blood circulation in all organs and tissues first increases and then decreases.

All these changes can negatively affect the retina. At risk are women who were diagnosed with myopia, hemeralopia and other eye diseases before pregnancy.

Due to the high risk of retinal detachment, a woman needs permission from an ophthalmologist before giving birth. If a specialist forbids giving birth on their own, they resort to artificial childbirth, that is, they do a caesarean section.

A pregnant woman must attend consultations with an ophthalmologist without fail. The first visit usually takes place at the very beginning of pregnancy, when the expectant mother becomes registered.

The first visit to the ophthalmologist at the beginning of pregnancy, the second towards the end of pregnancy

During the examination, the doctor carefully examines the vessels of the fundus to detect angiopathy and other pathologies of the retina. The second visit to the optometrist occurs towards the end of pregnancy. Such simple measures can prevent a formidable complication of childbirth - retinal detachment.

If a woman has myopia, then in this case she is examined by an ophthalmologist at least once a month.

If a pregnant woman has retinal dystrophy, then childbirth is necessarily carried out by caesarean section.

This is due to the fact that retinal dystrophy can subsequently cause ruptures and retinal detachment.

In the third trimester of pregnancy comes physiological decline blood pressure, due to hormonal changes and preparation of the body for childbirth. As a result of reduced blood flow, the amount of nutrients delivered to the retina decreases. This factor can also provoke the development of dystrophic processes.

Given all of the above, we can conclude that regular monitoring of the expectant mother by an ophthalmologist is an integral part of pregnancy management.

Pregnant women often feel tired and dry in the eyes, reduced visual clarity. These phenomena are explained by a spasm of accommodation and may disappear after the birth of a child, or intensify and lead to myopia.

Particular attention should be paid to the following symptoms indicating dystrophic changes in the retina:

• Flickering flies, flashes, lightning before the eyes
• Decreased distance vision
• blurry imagery
• Loss of areas of the visible pattern

At risk are pregnant women with severe myopia (more than 5-6 diopters). Under the influence of estrogen, the extensibility of the connective tissue increases, the eyeball stretches, which leads to thinning of the retina and increases the risk of damage.

Developing retinal dystrophy during pregnancy can lead to retinal detachment and loss of vision.

Increased stress on the cardiovascular system can trigger the progression of the disease, so it is important to undergo a preventive examination in the first trimester and after 32 weeks.

The final decision of the doctor on the possibility of delivery without risk to vision largely depends on the conclusion of the ophthalmologist.

Symptoms

Peripheral retinal degeneration of the 1st degree is difficult to detect, especially at an early stage. During this period, there are practically no symptoms, so the diagnosis occurs, alas, in the later stages of the development of the disease. The causes of divergent strabismus in children may be neurological factors or prolonged exposure to the computer.

Changes become noticeable in case of rupture or detachment of the retina. In addition, there is a sharp decrease in visual acuity, and flashes and spots in the eyes. If after such symptoms you do not consult a specialist, you can permanently lose your eyesight. Preosbyopia in both eyes is most common in people over 50 years of age.

The disease is so dangerous that it develops almost asymptomatically. Very often it is found by chance during examination. The first symptoms begin to appear, as a rule, with retinal breaks. These are, first of all, floating "flies" before the eyes, flashes.

long time retinal damage occurs without clinical manifestations. The pathology is characterized by a decrease in peripheral vision, which leads to difficult orientation in space.

In rare cases, patients complain of the appearance of floating flies before the eyes or defects in the visual field in the form of cattle. Symptoms such as "lightning bolts" or flashes of bright light indicate a retinal tear and require immediate attention.

Peripheral dystrophy is characterized by a unilateral course, but with a lattice variant, in most cases, both eyes are affected.

• decreased visual acuity;
• loss of peripheral vision and the ability to navigate in poorly lit spaces.

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

As the disease progresses, a person suffering from age-related macular degeneration complains of decreased visual acuity, difficulty in reading, especially in low light conditions. Also, patients may notice the loss of individual letters during cursory reading, the distortion of the shape of the objects in question.

Much less common is a complaint about a change in color perception. Unfortunately, more than half of patients do not notice a deterioration in vision in one eye until the pathological process affects the fellow eye. As a result, changes are often detected in advanced stages, when treatment is already ineffective.

Early signs of vision loss from AMD are:

• dark spots in central vision
• fuzzy image
• distortion of objects
• deterioration in color perception
• sharp deterioration of vision in low light and in the dark

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

An ophthalmologist can distinguish the manifestations of this disease even before the development of changes in the patient's vision and direct him to additional examinations.

Pigmentary retinal degeneration affects the pigment epithelium and photoreceptor cells. The first signs appear in early childhood. Characteristic specific symptoms: pigmented foci (bone bodies), atrophic optic disc and narrowed arterioles.

Pigmentary degeneration

With Leber's congenital amaurosis, blindness occurs from birth or children lose their sight before the age of 10. Features: lack of central vision, nystagmus, keratoconus, strabismus, etc. Various degenerative foci (white and pigmented such as salt and pepper, bone bodies) are determined throughout the fundus of the eye, the optic disc is pale, the vessels are narrowed.

X-chromosome juvenile retinoschisis refers to hereditary vitreochorioretinal dystrophies. In this case, retinal stratification occurs, cysts are formed on the periphery, into which hemorrhages can occur. In the vitreous body, hemophthalmos, strands that can lead to retinal detachment.

Wagner's disease is manifested by myopia, reshinoschisis, pigmentary dystrophy and preretinal membranes with a transparent vitreous body.

Goldmann-Favre disease - hereditary dystrophy has a progressive course, the main manifestations of which are bone bodies, retinoschisis and vitreous degeneration. Stargardt's disease - affects the macular area.

A characteristic sign in the fundus is a "bull's eye" in the central zone, that is, a dark area with a light ring, surrounded by rounded hyperemia. Symptoms are a decrease in visual acuity by the age of 20, a violation of color perception and spatial contrast sensitivity.

Stargardt disease

Yolk dystrophy of Best - in the macular region a yellowish focus is formed, resembling the yolk of an egg. At the age of about 10-15 years, there is a decrease in vision, a distortion of the shape of objects, a “fog” before the eyes. Both eyes are affected to varying degrees.

Age-related (involutional, senile) central retinal dystrophy is one of the most common causes decreased vision in people over 50 years of age with a hereditary predisposition.

age-related macular degeneration

- non-exudative - characterized by a redistribution of pigment, drusen, areas of retinal dystrophy. The foci can merge, resembling a picture of a "geographic map".

Drusen are located under the pigment epithelium and have a yellowish-white color, their prominence into the vitreous body is possible. There are soft (with fuzzy boundaries), hard (have clear boundaries) and calcified.

The course of the non-exudative form is benign, develops slowly

- exudative - in its development it goes through several stages: exudative detachment of the pigment epithelium, exudative detachment of the neuroepithelium, neovascularization, exudative-hemorrhagic detachment, reparative stage. It quickly leads to blindness.

Risk factors for age-related macular degeneration: blue eyes and white skin, a diet low in vitamins and minerals, high cholesterol, smoking, arterial hypertension, hypermetropia, cataracts, eye surgery.

In the early stages, retinal dystrophy is almost asymptomatic, which makes it difficult to diagnose it at the very beginning of the process. When dystrophy is already progressing, in all varieties of the disease, the following symptoms can be distinguished:

• decreased quality of vision;
• increasing limited field of view;
• loss of areas of the image, the appearance of livestock;
• perception of an image with distorted contours and shapes of objects;
• significant loss of vision in low light;
• color perception disorder;
• changes in the perception of distances to the observed objects and an incorrect assessment of their size;
• the appearance before the eyes of black dots, colored spots, sparks, flickering.

Such symptoms are a reason for an immediate appeal to an ophthalmologist, even if only one or a few of them appear.

Depending on the form of retinal dystrophy, its clinical picture will also differ. Pigmentary degeneration affects the cells that are responsible for the production of pigment and the perception of light.

It manifests itself at an early age and has symptoms such as atrophy of the optic disc, the presence of pigmented lesions, and narrowing of the arterioles. If timely treatment is carried out, then the pigment form has a favorable outcome.

Leber's congenital amaurosis is one of the types of pathology that leads to the fastest loss of vision. Children suffering from this disease go blind before the age of 10, and symptoms appear much earlier. Leber's amaurosis is characterized by damage to the entire area of ​​the retina, that is, there are multiple foci of dystrophy that also affect the optic nerve head.

X-chromosome retinoschisis is chorioretinal dystrophy. Its feature is that there is a gradual separation of the retina and the formation of cystic formations on its periphery.

Over time, chorioretinal dystrophy can lead to bleeding into these cysts, as well as into the vitreous body, which is called hemophthalmos. The chorioretinal form has a severe course, as it is accompanied by hemorrhages.

Wagner's disease has a complex combination of symptoms. So, at the same time there is a clinical picture of myopia and pigmentary dystrophy. In addition, preretinal membranes appear against the background of an intact vitreous body.

Goldmann-Favre disease is considered hereditary. It is characterized by intense progression, which affects not only the retina, but also leads to significant destructive changes in the vitreous body. Symptoms may appear before the age of 5 years.

For Stargardt's disease, localization of the lesion in the macular region is characteristic. In the fundus, there are changes that have a name - a symptom of "bull's eye". The disease is characterized by loss of vision up to 20 years, which is preceded by impaired color perception and a decrease in visual acuity.

• it becomes difficult for a person to distinguish colors;
• flies flash before the eyes or bright flashes appear;
• the forms of the visible object are distorted;
• central vision deteriorates or disappears altogether;
• peripheral vision is impaired;
• the picture before the eyes becomes blurry, wavy;
• need brighter lighting for reading and writing;
• visual acuity is impaired;
• a person cannot distinguish a moving object from a non-moving one;
• vision deteriorates at night;
• veil before the eyes.

If you have these symptoms, you should contact an ophthalmologist as soon as possible, otherwise you can lose your sight.

For patients diagnosed with partial atrophy of the optic nerve, disability is not a sentence. This disease can and should be treated. Obvious symptoms that the patient must pay attention to will help to identify the pathology at an early stage of development.

To the primary signs of atrophy ophthalmic nerves include:

If any of the above symptoms are detected, it is imperative to contact an ophthalmologist to preserve vision and stop the development of the disease.

Since there are a lot of different types of retinal dystrophies, below are descriptions of the most common of them. The symptoms and prognosis of each type of pathology may have both some similarities and significant differences.

The most obvious symptom of any dystrophy is a progressive loss of vision. Other signs of the disease can only be detected by ophthalmologists.

Symptoms of dystrophy depend on its type. So peripheral retinal dystrophy can proceed without any symptoms for a long time, so it is diagnosed, as a rule, quite by accident. The first signs ("flies" and flashes) appear only when gaps appear.

With central dystrophy, a person sees straight lines distorted, parts of the field of vision fall out.

Other symptoms: blurred vision, change in normal perception of colors, blurred vision, distortion of visual fields, impaired twilight vision.

Symptoms of retinal dystrophy are:

• floating "flies" before the eyes;
• flashes of light;
• distortion of straight lines in chorioretinal retinal dystrophy;
• loss of parts of the field of view;
• decreased visual acuity;
• clouding in the eyes;
• change in color perception;
• blurred vision.

If you have similar symptoms, be sure to consult a specialist. It is much easier to prevent a disease than to deal with the consequences.

An early symptom of retinal dystrophy is a gradual decrease in near vision clarity. The disease progresses slowly and eventually leads to the perception of distorted images.

Patients with symptoms of retinal dystrophy often complain of doubling of visually perceived objects, broken lines, and the presence of blind spots in vision. However, complete blindness as a result of retinal dystrophy develops quite rarely.

Diagnostics

PCRD can be diagnosed with a dilated pupil using a three-mirror lens. This tool can allow you to examine those areas that are inaccessible to the ophthalmoscope.

For a detailed examination of the eyes, scleropressure is necessary, which allows you to move the retina to the middle for a more serious examination of the periphery. The procedure is almost painless, but unpleasant for the patient.

Ptosis upper eyelid can be corrected with surgery.

When initial changes are detected, the patient should be constantly observed by an ophthalmologist and take photographs of the fundus with a photo-slit lamp.

modern medicine has the ability to diagnose the disease using special digital equipment that allows you to get a three-dimensional digital image of the eyeball area. If using this method it is possible to determine the zones prone to dystrophy, the specialist clearly assesses the size of the problem area in proportion to the total area of ​​the eyeball.

How to treat xalthesma of the eyelids can be found here.

Diagnosis of AMD is based on anamnesis data, patient complaints, assessment of visual functions and retinal examination data. various methods. Currently, one of the most informative methods for detecting retinal pathology is recognized as fundus fluorescein angiography (FAHD).

For FAHD, various models of cameras and special contrast agents - fluorescein or indocyanine green are used, which are injected into the patient's vein, and then a series of fundus images are taken.

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

OCT (optical coherence tomography) is used to finely assess changes in the retina and macula, which makes it possible to detect structural changes at the earliest stages of retinal degeneration.

Central vision with AMD gradually becomes fuzzy, blurred, dark spots appear in the center of the visual field, straight lines and objects begin to distort, color perception deteriorates. Peripheral vision is preserved.

If you have these symptoms, you should immediately contact an ophthalmologist for examination.

Your doctor will probably perform a fundoscopy (examination of the retina) after dilating your pupils with special eye drops. Several additional diagnostic procedures may be required to determine the form of AMD and the method of treatment.

Obligatory are the determination of visual acuity, examination of the fundus, as well as specialized high-tech techniques: optical coherence tomography of the retina and fluorescein angiography of the fundus.

At the same time, its structure and thickness can be assessed and observed in dynamics, against the background of treatment. And fluorescein angiography allows assessing the state of the retinal vessels, the prevalence and activity of the dystrophic process, and determining indications or contraindications for treatment.

These studies are the gold standard in the diagnosis of age-related macular degeneration worldwide.

To make a diagnosis, various instrumental studies of the structures of the eye are carried out, the condition of the fundus is visually assessed, and general clinical analyzes are carried out.

• One of the methods for determining retinal dystrophy is the Amsler test.
• Color perception is assessed using various tests, for example, Rabkin.
• Visiometry is performed to determine the quality of vision.
• The method of perimetry is used to study the width of the field of view and identify drop-out areas in it.
• Refractometry is used to measure the refractive index.
• The study of the fundus (ophthalmoscopy) is performed under medical mydriasis.
• To identify pathologies of the eye, biomicroscopy is performed.
• To assess the bioelectrical activity of the layers of the retina, electroretinography is performed.
• Fluorescent angiography is performed to assess the state of the retinal vessels and register hemorrhages.
• Can also be carried out ultrasound procedure eyes and retinal tomography.

Retinal dystrophy requires examinations such as:

A banal eye test helps to identify the disease

To diagnose retinal dystrophy, the following examinations are necessary:

1. Study of visual fields;
2. Study of color perception;
3. Checking visual acuity;
4. Examination of the fundus using a Goldman lens;
5. Fluorescent angiography (examination of eye vessels);
6. Ultrasound and electrophysiological examination of the eyes;
7. Analyzes to determine the state of metabolism of the body.

To diagnose the symptoms of retinal dystrophy, you should follow these steps:

• be examined by an ophthalmologist;
• determine visual acuity;
• evaluate color perception;
• dilate the pupil and examine the fundus with a three-mirror Goldman lens;
• perform coherent eye tomography;
• perform an ultrasound of the eye.

The most informative methods for diagnosing retinal dystrophy are laser scanning of the retina using an optical tomograph, central computerized perimetry, and fluorescein angiography of the fundus blood vessels. They allow you to identify the earliest symptoms of retinal dystrophy.

Additionally, at an early stage of diagnosing the disease, tests can also be used to check color perception, visual contrast, and the size of the central and peripheral visual fields.

Assessment of the capabilities of the visual analyzer

Visual impairment has an adverse effect on the usefulness of almost all categories of life, but the degree of this effect is different.

A person's ability to move, self-service, orientation, communication mainly depends on the state of the main visual functions - visual acuity and field of vision. In the process of medical and social examination, visual functions are determined by mono- and binocular presentation of test tests, however, the degree of their violations that affect the establishment of the presence and severity of disability is assessed mainly according to the state of the functions of a person who sees better or single eye under conditions of tolerable (optimal) correction.

The capabilities of the visual analyzer in relation to specific tasks of labor activity and training are more difficult to characterize: in addition to analyzing visual acuity and visual field, it is necessary to evaluate other functions of the visual organ that are significant for performing various types of work (including visual profile work) or vocational training.

These functions include light sensitivity (dark adaptation), color perception, state binocular vision, near visual acuity and accommodation.

Treatment

To date, 3 therapies are used to treat PCRD:

• surgical intervention;
• medication treatment;
• laser therapy.

All three methods are used to stabilize the dystrophic process and prevent rupture of the mesh area, and not to restore visual function.

adults

As with other diseases, in the case of retinal dystrophy, it is necessary to note the causes, forms and stage of the disease. What is macular degeneration of the retina can be found here.

With the initial signs of vitreochorioretinal dystrophy of the retina, in order to delay the progress of the process, it is necessary to carry out therapy with the following medications:

• absorbable preparations for strengthening and expanding the vessels of the eye and regulating the metabolic process;
• vasodilators;
• corticosteroids retrobulbarno;
• diuretics;
• biogenic stimulants;

There are also physical methods therapy:

• phono- and electrophoresis;
• microwave therapy;
• intravenous laser blood irradiation;
• ultrasound.

To improve blood circulation and metabolism, vasoreconstructive surgeries are performed - ligation of the branches of the surfaces of the temporal artery, surgeries on the vorticose veins and the posterior pole of the eye.

In the wet form of PCRD, surgery is performed to remove the accumulated fluid in the retina. The last stage is the implantation of "energy" magnets-implants in the region of the posterior pole of the eye. You can read about the effective treatment of night blindness on our website.

The main method of combating this disease is laser coagulation. With the help of a laser, the damaged retina is cauterized to the tissue connections of the eye in the required place and to the required depth. The action of the laser occurs pointwise and selectively, without damaging healthy tissues around the resulting dystrophy.

In order to identify retinal dystrophy, the treatment of which is absolutely impossible to delay, it is necessary to perform ophthalmic examination procedures, which involve a process that examines the patient's fundus, an electrophysiological examination, and an ultrasound examination.

All this allows you to get complete information about the state of the retina and optic nerve. Carrying out the necessary laboratory tests will tell you how the metabolic processes proceed.

Initially diagnosed retinal dystrophy, treatment involves the use of drugs, the action of which is aimed at strengthening and expanding blood vessels. In addition, recommended means that stimulate the qualitative improvement of metabolism in the body.

As a rule, a complex of vitamins and minerals is prescribed in combination with drugs aimed at improving blood supply.

Methods are used that stimulate metabolic processes, the activity of which has been disturbed by retinal dystrophy. Laser treatment is very effective. The therapy uses methods of laser coagulation and photodynamic therapy.

The basis of photodynamic treatment is the injection of photosensitizers, which prevent the development of the disease by binding the proteins of vessels with pathology.

Laser therapy consists in cauterization of pathological vessels. The method prevents the spread of this disease, but under the influence of a laser, a burn forms, forming a scar. The area affected by the laser loses sight.

In the treatment of pigmentary degeneration, physiotherapeutic methods are usually used: electrical and magnetic stimulation of tissues, however, the effectiveness of such treatment is not very high.

Sometimes a vasoreconstructive operation can be used, which has a positive effect on the blood circulation of the retina. Additionally, diet therapy and complex intake of vitamins can be used.

Often, dystrophy is triggered by myopia, then an argon laser can be used to strengthen the retina.

The laser is a versatile tool that opens up many possibilities in modern ophthalmology. When exposed to it, a sharp increase in temperature occurs and tissue coagulation (coagulation) improves.

As a means traditional medicine use an infusion of Japanese Sophora fruits. The medicinal liquid is infused for at least three months. To prepare the infusion, 0.5 l of vodka is required, which is mixed with 5 g of Japanese sophora. Apply one teaspoon of infusion to a glass of water, three times a day.

Having found a pathology in the retina, it is necessary to carry out procedures aimed at strengthening it. Otherwise, at the moment of tension, there is a risk of detachment.

In turn, detachment requires urgent surgical intervention. It is important that retinal detachment can occur at an inopportune moment, when qualified help is not available.

So it's much better to avoid similar development events.

Retinal detachment occupies one of the first places among the reasons for getting a disability. Approximately 70% of patients affected by this pathology are people of working age.

To slow down the development of the disease and improve metabolic processes in the retina, ophthalmologists advise taking multivitamins in combination with vasodilators.

It is known that in order for the retina to function as expected, lutein is needed. The human body does not produce it on its own, which indicates the need to make up for its deficiency from food. Lutein is rich in green foods: peppers, spinach, etc.

lutein is great natural antioxidant, which has an interfering effect on the process of destruction of the retina. In addition, it counteracts the creation of free radicals.

After diagnosing the eye, the doctor determines the form of degeneration and selects the type of correction that will best stop the progression.

Injection

intraocular injection medicinal substance- a way to help slow down the wet form of the disease. Medications belong to the group of intravenous drugs required for anti-VEGF therapy, which is aimed at suppressing the activity of a certain protein. The introduction is carried out only on an outpatient basis and exclusively by a doctor.

Pharmacological agents:

After the substance enters the vitreous body of the eye, doctors manage to stop the growth of new vessels - they disintegrate, so the patient soon feels the restoration of visual functions. When using anti-VEGF therapy, 1/3 of patients experience improvement in vision.

Very often, dystrophic changes in the retina accompany moderate and high degrees of myopia. The fact is that usually in this case the size of the eyeball increases, and the retina lining its inner surface is stretched, which leads to dystrophy.

Modern treatment such a condition, as well as other types of dystrophies (many inflammatory and vascular diseases of the retina lead to dystrophies), occurs with the help of an argon laser. The main goal of this treatment is to strengthen the retina.

It is impossible to completely cure AMD. However, the development of the disease can be slowed down, suspended, and sometimes even improved.

It is well known that the risk of AMD is reduced by a healthy diet containing fresh fruits rich in vitamins C and E, lutein and zeaxanthin, dark green vegetables and salad.

The following vegetables and fruits are key for eye health: carrots, pumpkin, zucchini, zucchini, green beans, tomatoes, lettuce, spinach, broccoli, cabbage, turnips, melon, kiwi, dark grapes, dried apricots.

According to a number of studies, it is recommended to eat fish (salmon, tuna, mackerel) and nuts, which are rich in omega-3 fatty acids and copper, at least 2-3 times a week. There is evidence that a diet rich in omega-3 fatty acids and lutein.

In large-scale studies, it has been found that a healthy diet and the intake of dietary supplements containing specially selected micronutrients (vitamins, trace elements and antioxidants) can slow the progression of the disease.

In particular, it turned out that the use of sufficiently high doses of certain antioxidants (vitamins C and E, copper, zinc, carotenoids lutein and zeaxanthin *) can reduce the risk of progression of existing dry AMD.

If you smoke, you should stop smoking as smoking increases your risk of developing AMD. Fight overweight and high blood pressure. Increase physical activity.

In the later stages, when a wet form of AMD is detected, the prognosis for maintaining high visual acuity is less favorable, and treatment requires more expensive and complex procedures, including retinal laser photocoagulation, photodynamic therapy, and drug injections into the eye.

According to the World Health Organization, age-related macular degeneration is one of the most common causes of blindness and low vision in older people. Age-related macular degeneration is a chronic degenerative disorder that most often affects people over the age of 50.

According to the official materials of the WHO Center for the Prevention of Avoidable Blindness, the prevalence of this pathology in the world is 300 per 100 thousand of the population. In economically developed countries of the world, AMD, as a cause of low vision, ranks third in the structure of eye pathology after glaucoma and diabetic retinopathy.

AMD is manifested by progressive deterioration of central vision and irreversible damage to the macular zone. Macular degeneration is a bilateral disease, however, as a rule, the lesion is more pronounced and develops faster in one eye, in the other eye AMD may begin to develop after 5-8 years.

Often, the patient does not immediately notice problems with vision, because at the initial stage, the better seeing eye takes over the entire visual load.

Perhaps laser treatment, the possibility of which is determined by the laser surgeon, photodynamic therapy, when a special substance [photosensitizer] is injected intravenously, it lingers in the tissue of the affected retina and does not linger in healthy areas of the retina.

If the vision loss is caused by age-related macular degeneration, then glasses, unfortunately, will not help. Here you can compare the eye with the system of a film camera. Glasses in this case will act as a lens, and the retina will act as a photosensitive film.

Marriage and damage to the film will not allow you to get high-quality photos, no matter how strong the lenses are. So it is in the eye - even with the highest quality glasses, an image focused on a retina damaged by a pathological process cannot be perfectly perceived.

Depending on the clinical picture and the type of dystrophy is prescribed treatment. Almost always, treatment is symptomatic, since all degenerations, except for secondary ones, are hereditary or predisposed.

The following methods of treatment are used: conservative, laser, surgical (vitreoretinal surgery, scleroplasty in case of detachment, etc.)

Conservative treatment of retinal dystrophy is aimed at relieving symptoms. Drug therapy is also carried out to eliminate the provoking factors of the pathological degenerative process. For this, agents are used that improve the condition of the vascular walls, strengthen the smooth muscles of the vessels, and blood circulation.

Dosages and regimens for the use of these drugs are selected individually, depending on the severity of vascular pathologies.

Injections of blood thinners to prevent the development of thrombosis, lipid-lowering drugs to lower cholesterol levels, vitamin complexes to improve eye nutrition.

Local treatment is carried out with the help of polypeptides and drugs to improve microcirculation. These drugs are injected directly into the affected area, that is, injections are made into the eyes.

Eye drops are also required to improve the nutrition of the eye, restore its structures and stimulate metabolism.

For symptomatic treatment drops can be used, which include:

• non-steroidal (Voltaren, Naklof, Indocollir);
• corticosteroid anti-inflammatory substances (Prednisolone, Betamethasone);
• local anesthetics (Tetracaine, Lidocaine, Dikoin);
• drops for the treatment of cataracts, containing vitamins and other nutrients (Taufon, Quinax, Oftan-katahrom).

Quite effective in combination with the use of drugs are physiotherapeutic methods. Most often, drug electrophoresis, phototherapy, electrotherapy, laser therapy, magnetotherapy, venous blood irradiation with a laser are prescribed.

It is also effective surgery to eliminate the consequences of the degenerative process. According to the indications, patients may be recommended to undergo laser coagulation of the retina, vitrectomy (removal and replacement of the lens), revascularization or vasoreconstruction of the eye.

In hereditary forms of retinal dystrophy, the prognosis is usually unfavorable. In other cases, the prediction of the situation depends on the degree and stage of the lesion, the rate of progression of the degenerative process, the type of pathology, the presence and severity of concomitant diseases, and also on individual features patient: the state of his vascular system, the rate of metabolic processes and others.

Treatment folk remedies possible only with the approval of the attending physician, and is only an addition to the main therapy. Treatment at home is carried out with the use of various herbal decoctions to strengthen blood vessels and provide better eye nutrition, improve blood properties and the state of the vascular system.

It is also possible to carry out symptomatic treatment using traditional medicine.

In order to get an answer to the question of how to treat retinal dystrophy, you must first make the correct diagnosis, because, as mentioned above, this pathology has many options. In this regard, the best tactic would be to contact a specialist in these matters.

Due to the fact that the changes that have developed as a result of the described pathology cannot be reversed, in patients with a diagnosis of retinal dystrophy, treatment has as its main goal to stop the further progression of the disease, being, in general, only symptomatic.

To achieve this task, both medicinal and surgical, and physiotherapeutic, including using laser technologies, methods can be used to slow down the development of the disease, reduce the severity of manifestations and thus improve vision, albeit only partially.

With retinal dystrophy, drug treatment is reduced to the use of drugs from various groups.

Clopidogrel, Aspirini and other representatives of antiplatelet agents help to reduce intravascular thrombus formation.

Vasodilators and angioprotective agents, such as No-shpa, Papaverine or Ascorutin, taken by mouth or injected into a vein, dilate and strengthen blood vessels.

Lipid-lowering drugs for retinal dystrophy are used only in patients suffering from atherosclerosis. These medicines lower cholesterol levels. Examples include Methionine and Simvastatin.

For treatment, drugs that improve microcirculation can also be used. Their brightest representative is Pentoxifylline. It and other drugs from this group, as a rule, are injected directly into the eye structures.

In the therapy of dystrophy, Retinolamine and other polypeptides obtained from the retina of animals (in particular, large horned ones) can also be used.

In patients diagnosed with retinal dystrophy, treatment with drugs from the groups listed above is usually carried out in courses. At least two such courses are usually assigned per year.

Among other things, with a wet type of illness against the background of intravenous use of Furosemide (a diuretic drug), a hormonal agent called Dexamethasone is injected into the eye. This is done to relieve swelling.

In retinal dystrophy, treatment with drugs is often supplemented with surgical interventions, which can be carried out in the form of laser coagulation of the retina (in order to prevent its detachment), in the form of vitreectomy, revascularizing or vasoreconstructive operations aimed at improving blood supply and metabolic processes in the retina of the organ of vision.

With the diagnosis of peripheral retinal dystrophy, treatment with laser coagulation gives a good effect. However, after it is carried out, patients are prescribed special medications - angiogenesis inhibitors that prevent the growth of abnormal vessels.

With regard to such a variant of the pathology as retinitis pigmentosa, surgical treatment, as a rule, consists in transplanting eye muscle fibers (namely, oblique and external rectus muscles) into the so-called suprachoroidal space. This contributes to the normalization of the blood supply to the retina.

Currently, patients diagnosed with retinitis pigmentosa can also be treated by placing specially designed retinal implants.

Depending on the cause, form and severity of the disease, conservative treatment can be used, which is based on the use of medications as well as surgical treatment. It is necessary to start treating the disease as early as possible.

Drug therapy for retinal dystrophy is based on the use of the following groups of drugs:

• Preparations for improving microcirculation. These drugs help restore normal capillary blood flow. Thus, the lack of nutrients and oxygen in the retina is eliminated. In addition to parenteral forms, there are also eye drops.

• Blood thinners. Stagnation of blood and impaired microcirculation can cause thrombosis. Blood clots that have appeared in the vessels of the retina can significantly aggravate the patient's condition, and also complicate treatment.
• Vasodilators. These drugs affect the vasomotor center or directly on the walls of blood vessels. They expand their lumen, resulting in normal blood flow. It is not advisable to use drops that have a local effect.
• Parabulbar injections of polypeptides that are made from the retina of cattle. These drugs improve the regenerative function of retinal cells, which significantly slows down the development of the pathological process. The pigmented form lends itself well to such treatment.

• Vitamin complexes for the eyes. These drugs can be taken in the form of tablets or drops. Treatment will be more effective if drops are used, because the active substances will immediately enter the focus of the pathology.

The treatment required by the chorioretinal form should exclude anticoagulants. On the contrary, drugs that have a hemostatic effect to prevent hemorrhages should be involved. You can use drops that have an antibacterial effect to avoid the attachment of an infectious factor.

Surgical treatment can be based on classical types of surgery or carried out using innovative technologies. The most effective method of treatment is the use of a laser to separate the affected areas of the retina from the healthy ones. Thanks to this treatment, further progression of dystrophy is almost completely excluded.

The process of treating dystrophy will be ineffective if the cause that provoked the development of the disease is not eliminated, and the eyes are not provided with the necessary amount of nutrients.

Since eye atrophy in most cases is an investigative disease, and not an independent one, the doctor will first of all conduct a complete diagnosis to identify the cause of the pathology. After receiving the results of the examination, the physician will prescribe the appropriate complex treatment.

To combat pathology, eye drops, injections, tablets and electrophoresis are most often used. Each of these tools together and individually will help:

• improve blood circulation in the vessels;
• increase recovery and metabolic processes in tissues;
• accelerate the relief of the inflammatory process
• improve the stability of the central nervous system.

Take the drugs strictly as directed, and in no case self-medicate. Being carried away by alternative medicine, you lose precious time when your eyesight can still be saved, especially in this case. folk methods completely useless.

Therapy is usually symptomatic and may halt the progress of the disease.

It can take a long time to cure retinal dystrophy. This is quite difficult, and it is not always possible to get a positive result.

It will not be possible to restore vision when an exacerbation of dystrophy has already occurred. In this case, the treatment is aimed at slowing down the progression of dystrophy, strengthening the vessels and muscles of the eyes, and restoring metabolism in the eye tissues.

Treatment with drugs is based on the use of drugs such as:

• Antioxidants;
• Angioprotectors;
• corticosteroids;
• Vitamin preparations ;
• lutein-containing drugs;
• Vasodilating and strengthening the walls of blood vessels.

It is necessary to know that these drugs can be effective only in the early stages of the development of retinal dystrophy.

At the beginning of the disease, physiotherapy gives good results. It is aimed at strengthening the retina and eye muscles. The most commonly used physiotherapy methods are:

• Electro- and phonophoresis;
• Laser irradiation of blood;
• Ultrasound and microwave therapy;

Surgery is performed to improve blood circulation in the vessels of the eyes and metabolic processes in the retina. In the case of wet degeneration, surgery is needed to remove fluid from the retina.

One of modern methods The treatment for retinal dystrophy is laser photocoagulation. It allows you to prevent detachment. During laser coagulation, damaged areas are cauterized to other areas to a certain depth. The laser does not touch healthy areas. Unfortunately, laser photocoagulation cannot restore lost vision, but it can stop further damage to the retina.

Complications

Retinal dystrophy during pregnancy is treated by laser coagulation 4-5 weeks before the expected date of birth. The laser "cauterizes" the affected areas and blocks the gaps. Timely retinal strengthening surgery reduces the risk of detachment and increases the chances of a natural birth.

Treatment of retinal dystrophy involves the following steps:

• laser coagulation of the retina (laser burning the retina in the most vulnerable places, resulting in its strengthening, the procedure is bloodless, almost painless, but not entirely comfortable for the patient);
• photodynamic therapy;
• injections of Anti-VEGF (a drug that inhibits the development of the degenerative process);
• vitamin therapy;
• physiotherapy procedures;
• vasoreconstructive surgery, which is aimed at restoring the blood supply to the retina.

In any case, after the examination, the specialist will determine how to treat retinal dystrophy in order to help the patient as much as possible and protect him from the prospect of extreme vision loss.

In the treatment of retinal dystrophy of the chorioretinal form, methods of photodynamic therapy, laser photocoagulation, as well as injections of Anti-VEGF drugs are used. The latter are a special protein that can stop degenerative processes in the macula of the eye.

Photodynamic treatment of retinal dystrophy involves the intravenous administration of photosensitizer substances. They are able to bind the proteins of pathological vessels and stop the development of dystrophy. The mode of photodynamic treatment of retinal dystrophy is set individually, depending on the sensitivity of the patient to this type of therapy.

The laser treatment of retinal dystrophy is based on the method of cauterization of pathological vessels. At the site of the burn, a scar forms on the tissues of the macula of the eye, and vision in this area of ​​the eye is not restored. But this technique allows you to prevent the further spread of the process of retinal dystrophy.

In the treatment of retinitis pigmentosa, mainly physiotherapeutic methods are used: magnetic and electrical stimulation of eye tissues. Unfortunately, their effectiveness is not high. Vasoreconstructive operations aimed at improving the blood supply to the retina also have a limited effect.

Prevention of retinal detachment in peripheral retinal dystrophy is carried out using laser coagulation. This minimally invasive non-contact technique for the treatment of retinal dystrophy avoids surgical opening of the eyeball. The procedure is performed on an outpatient basis and practically does not require a recovery period.

As ancillary treatment retinal dystrophy of all types, dietary and vitamin therapy is used.

Treatment with folk remedies

The first drug for anti-VEGF therapy in the form of intravitreal injections, certified in Russia for use in ophthalmology, was LUCENTIS, which made a real revolution in the treatment of AMD and became the "gold standard".

Treatment with folk remedies

With retinal dystrophy, enhanced nutrition is necessary, as well as wearing dark glasses. It is recommended to drink fish oil 3 times a day, eat all kinds of liver - boiled, fried, even raw and consume those foods that have a lot of vitamin A: fresh tomatoes, cream, eggs, spinach, millet, green salad.

Boil 0.5 kg of liver (beef or lamb). When the pan with cooked liver is removed from the fire, the patient should bend over the pan.

His head should be covered, for example, with a large thick scarf so that its ends, hanging from the head, cover all sides of the pan. This is necessary so that the steam from the pan does not escape to the sides.

In addition to warming up, you need to eat boiled liver for two weeks.

1. Rapidly progressive myopia (reduction of vision by 1 diopter or more during pregnancy)2.

Pathology of the optic nerve, edema, retinal detachment and dystrophy3. Myopia of a high degree (- 6.

0 or more) single eye4. Glaucoma of any clinical form5.

Loss of visual fields 6. Cumulative indications (in combination with developed preeclampsia, a combination of myopia and neurological pathology, and many others that are identified individually).

Eye diseases are now so common that sometimes they are not given as much attention as they should be. Do not ignore scheduled consultations with an ophthalmologist in the antenatal clinic, do not refuse additional research and listen to the recommendations for delivery.

If you are shown a cesarean section, then this means that there is a real threat of loss or significant deterioration of vision with an unknown prognosis for its restoration. Ask your doctor questions that interest you and take care of yourself.

Be healthy.

Doctor Petrova A.V.

Risk groups and disease prevention

Most often, peripheral retinal dystrophy occurs in nearsighted people. This is due to the increased length of the eye in myopic, which entails tension in the retina and its thinning. The elderly (65 and older) are also at risk.

Often, it is peripheral retinal dystrophy that causes vision loss in old age. Also, this group should include people with the following diseases: diabetes mellitus, hypertension, atherosclerosis and some others.

Patients with myopia (nearsightedness) are most susceptible to the development of peripheral dystrophy. This is due to the fact that with myopia the length of the eye increases, which leads to tension of the retina and its thinning.

In addition, the people most susceptible to this pathology include patients with diabetes, hypertension and atherosclerosis.

Doctors distinguish several groups of people who are in the danger zone of the development of the disease and should be regularly examined by an ophthalmologist.

• Elderly people (over 50 years old);
• People with myopia (nearsightedness);
• Patients with vascular diseases, diabetes, hypertension, cardiovascular system;
• People with a light color of the iris (with a blue tint);
• smokers;
• overweight people;
• Heredity.

Despite the fact that it is no longer possible to stop the process of retinal degeneration, doctors can control the process if the pathology is detected in time.

For people suffering from myopia, visiting an ophthalmologist should not be less than once a year. A preventive examination should be carried out once every two or three years.

It is important to completely abandon bad habits, eat healthy foods, not get carried away with taking medications, and include moderate physical activity in your daily routine.

The main thing to remember is that the condition of the eyes is a reflection of the overall health of the whole organism.

Prevention

1. Prevention is necessary for people who are genetically predisposed to this disease, suffering from myopia and diabetes.
2. For timely detection of the disease, be sure to conduct an annual examination by an ophthalmologist; children and adolescents need such an examination more often - once every six months.
3. PCRD is a disease that can manifest itself in both adults and children.
4. If there is a hereditary genetics, the vision test should be more thorough.
5. Do not endanger the organs of vision, because timely identification of problems will help stop the destructive process and restore vision.
6. A special exercise for the eyes will also be useful.
7. The best prevention PCRD is a complete fortified nutritional complex that provides the body with the supply of essential vitamins and minerals, which improves the functioning and health of the eyeball. Including fresh fruits and vegetables in the regimen, you can minimize the likelihood of retinal dystrophy.
8. If you have problems with the organs of vision, it is better to give up smoking and drinking alcoholic beverages.

All vision problems can be solved with the help of a timely visit to an ophthalmologist. The specialist will help identify the problem and prescribe competent treatment.

Prevention of retinal dystrophy is an ophthalmological examination. First of all, it is necessary for people suffering from atherosclerosis, hypertension and diabetes. Also, preventive diagnostics is indicated for people who have a genetic predisposition to the disease and myopia.

• any time before pregnancy,
• up to the 35th week of pregnancy.

Speaking about prevention, first of all, they mean the prevention of ruptures and retinal detachment. The main way to prevent these complications is the timely diagnosis of peripheral retinal dystrophy in patients at risk, followed by regular follow-up.

Prevention of formidable complications depends entirely on the discipline of patients and attention to their own health. Patients with existing retinal pathology and patients at risk should be examined 1-2 times a year.

During pregnancy, it is necessary to be observed by an ophthalmologist and examine the retina (through a wide pupil) at least twice - at the beginning and at the end of pregnancy. In the presence of thinning or ruptures of the retina, preventive laser coagulation of the retina is mandatory.

Prevention of the dystrophic processes themselves on the periphery of the retina is possible in representatives of the risk group - these are myopic patients, patients with a hereditary predisposition, patients with arterial hypertension, diabetes mellitus, vasculitis and other diseases.

Such people are also recommended regular preventive examinations by an ophthalmologist with an examination of the fundus of the eye under conditions of medical pupil dilation and courses of vascular and vitamin therapy in order to improve peripheral blood circulation and stimulate metabolic processes in the retina.

The main way to prevent this disease is the timely diagnosis and treatment of ruptures and thinning of the retina.

This requires a thorough examination of the fundus after instillation of drops that dilate the pupil, using special equipment. An ophthalmologist examines the retina and prescribes treatment.

Prevention of congenital forms of dystrophy does not exist. Most forms of this disease are formed as a result of anomalies or disorders of intrauterine development.

But you can reduce the likelihood of these problems occurring. To do this, it is necessary to exclude the impact of negative factors on a pregnant woman, as well as provide her complete diet, which will contain all the necessary substances for its normal life and development of the fetus.

But you can avoid the age-related form of retinal dystrophy. To do this, all measures must be taken to prevent the effects of harmful radiation on the eyes, to exclude injuries and to treat diseases of other localization in a timely manner. A special place is occupied by the treatment of those diseases that violate the patency of blood vessels.

Retinal dystrophy is a formidable disease that is highly likely to lead to complete loss of vision. It can appear in young children and the elderly.

The reasons for the development of this disease are diverse, which leads to a wide age range that is susceptible to this disease. The basis for success and a favorable outcome is timely diagnosis and early treatment.

Treatment should include those drugs that are needed to address the underlying cause. It can be drops and parenteral forms.

There are a few simple rules that must be followed if you want to quickly overcome the pathology and restore the health of the organs of vision.

• Systematically visit an ophthalmologist and an oncologist;
• Treat in a timely manner infectious diseases;
• Stop smoking and drinking alcohol;
• Try to protect yourself from eye or head injuries;
• Monitor your blood pressure;
• With profuse bleeding, it is necessary to undergo a second blood transfusion procedure.

Preventive treatment includes taking the following drugs:

• Antioxidants. These include vitamins C, E, beta-carotene, zinc. Long-term courses of these drugs are recommended.
• Means that improve rheology, and angioprotectors.
• Angiogenesis inhibitors (Lucentis).

To stop the progression of the existing pathology, you can use a method such as laser coagulation of the retina. The mechanism of its action consists in the local destruction of the pigment epithelium, followed by hypertrophy of the surrounding cells, which close the formed defect and, due to a more active metabolism, more effectively remove existing deposits.

There are no treatments that can improve vision in dystrophy, however, devices for the visually impaired and timely prevention can help patients.

Prevention of retinal dystrophy includes:

• regular check-ups with an ophthalmologist;
• passing examinations on professional ophthalmic equipment;
• regular visits to a specialist, especially for the elderly (after 60 years - at least once every six months).

This article is posted for educational purposes only and does not constitute scientific material or professional medical advice.

Search for paid ophthalmologists (ophthalmologists) for the treatment and diagnosis of retinal dystrophy in Novosibirsk

Prognosis for the diagnosis of retinal dystrophy

The prognosis of therapy for retinal degeneration:

1. dry form. Slow-flowing form - up to several years - gives a delay for selection effective treatment and avoid the development of severe complications. Danger: moderate risk of retinal detachment. In 10-20%, the dry form turns into a wet one.
2. wet form. The prognosis for this type of disease is unfavorable: changes in the retina occur abruptly (within several months), and possible hemorrhage poses a high risk of loss of vision. The likelihood of retinal detachment is as high as possible due to the accumulation of excess fluid, which provokes the separation of the inner membrane.

When diagnosing retinal dystrophy, it is not easy to make a prediction regarding the preservation of visual function. For the reason that this pathology is characterized by a progressive course, the prognosis in case of its development cannot be considered favorable.

At the same time, according to foreign doctors, specified disease does not by itself cause complete blindness. Almost always, a certain percentage of vision remains, and this is mainly peripheral vision.

At the same time, one should take into account the fact that, despite successful therapy, macular retinal dystrophy may begin to progress again over time.

Such a complex eye disease as retinal angiopathy does not have an ICD-10 code. And this does not mean that this pathology of the organs of vision does not deserve the close attention of ophthalmologists. What are the symptoms of this disease, and how is it treated?

Recall. that ICD-10 is the International (accepted by WHO for physicians of all categories and countries) classification of diseases in the tenth revision.

In medical terms, angiopathy is a vascular disorder of the eye, manifested in a violation of the tone of the vessels of the retina and the capillary bed of the fundus. Against the background of this pathology, there is a decrease in blood flow and nervous regulation. There is no separate classification of this condition in ICD-10, since it is the result of much more serious diseases. Most often, angiopathy occurs against the background of such diseases:

1. intracranial hypertension.
2. Damage to the cervical segments.
3. Osteochondrosis of the cervical spine.
4. Various blood infections.
5. Diabetes.
6. Abuse of smoking and alcoholic beverages.
7. congenital anomalies.

And these are just some of the possible causes of violations of the blood supply to the retina. The danger of this pathology lies in the fact that against the background of angiopathy, more serious pathologies, such as retinal dystrophy and / or myopia, may occur. Moreover, in the absence of timely and adequate treatment, this violation in the trophism of the retina can lead to complete loss of vision.

It is characteristic that angiopathy, including diabetic retinopathy, affects both eyes simultaneously. This serves as a hallmark in the differential diagnosis. Angiopathy is detected during examination of the fundus by an ophthalmologist.

Etiology of the disease and common types of course

There is a vascular pathology of this type in adults and children. Therefore, it is difficult to determine the true cause of occurrence in a particular case. But still, the main provoking factor is considered to be any chronic disease. The main factor causing angiopathy is the general pathology of the vessels of the body, in which there is a violation of the structure of the vascular wall, including in the vascular bed of the retina.

Very often there is such a lesion of the vessels of the retina in the last trimester of pregnancy or after childbirth, which took place with violations. For a child, such angiopathy does not pose any threat, but the mother should immediately begin the treatment prescribed by the ophthalmologist.

The types of flow can be listed as follows:

1. 1. Hypertensive angiopathy of the retina. Starts when it occurs hypertension and its progression. Often under the influence of increased pressure there is a rupture of the capillary and hemorrhage in the retina. But with rapid detection and timely elimination, this does not pose a threat of loss of vision.
2. 2. Hypotonic. The nature of the flow at reduced pressure is opposite to the first type. The danger of this condition lies in the threat of a blood clot in the capillaries and subsequent obstruction of the vessel.
3. 3. Diabetic threatens extensive obstruction of the fundus vessels.
4. 4. Traumatic angiopathy - this condition occurs when a traumatic lesion of the cervical or thoracic spine and subsequent increase in intracranial pressure to critical levels.
5. 5. Juvenile angiopathy is the most poorly studied form of vascular eye disease. This form is accompanied by single or multiple hemorrhages in the vitreous body and/or retina. Often complicated by cataracts, glaucoma, or even complete loss of vision.