Will my vision survive? What is retinal pigmentary degeneration and its treatment. Retinal dystrophy Retinal dystrophy ICD code 10

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, age-related macular degeneration, etc.

DEFINITION

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

ICD-10 CODE

H35.3 Degeneration of the macula and posterior pole.

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

EPIDEMIOLOGY

AMD most often develops in patients over 65 years of age. The overall prevalence 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 aged 65-74 years is 1%; at the age of 75-84 years - 5%; aged 85 years and older - 13%. The predominant gender of patients is female, and in women over 75 years of age 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 recommended stop smoking, fatty foods, and be less exposed to direct sunlight. If there is concomitant vascular pathology, measures aimed at its correction are necessary. Recommended vitamin therapy and treatment with microelements will be discussed below. The question of the advisability of preventive laser coagulation of the retina in the presence of multiple drusen has not yet been resolved.

SCREENING

No screening is carried out. However, in patients over 55 years of age, during routine medical examinations it is necessary to examine the macular zone of the retina, especially if there are characteristic complaints. If patients cannot achieve high visual acuity after uncomplicated cataract extraction, one must remember the likelihood of AMD.

The examination includes determining visual acuity, performing biomicroscopy (to identify other possible reasons the appearance of symptoms, for example, the presence of age-related cataracts), ophthalmoscopy (including a slit lamp using aspheric lenses) and perimetry. We can also recommend a study of color perception (monocularly), the Amsler test.

CLASSIFICATION

When defining 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.

Thus, The “dry” (non-exudative) form is characterized by:

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

The exudative form is characterized by the following stages:

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

The early stage is characterized by:

• local drusen;
• uneven pigmentation of the RPE.

• RPE detachment; RPE rupture;
• disc-shaped (fibrovascular) scar;
• geographic atrophy of the RPE.

ETIOLOGY

The etiology is not determined.

PATHOGENESIS

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

All RPE cells accumulate lipofuscin with age in the form of round yellowish granules with a brown tint, surrounded by lipid membranes and possessing 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. The “yellow” macular pigment plays the role of natural sunglasses: it absorbs the short-wavelength part of blue light, thus participating in the antioxidant protection of the macula. This pigment, consisting of lutein and zeaxanthin, is located in the inner layers of the retina.

During a cascade of biochemical processes under the influence 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 cell enzymes pigment epithelium, do not disintegrate 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. Increased lipid deposits reduce the concentration of growth factors necessary to maintain normal choriocapillaris structure. The density of the choriocapillaris network decreases, and the supply of oxygen to RPE cells deteriorates. Such changes lead to increased production of growth factors and matrix metalloproteinases. Growth factors promote the growth of newly formed vessels, and metalloproteinases cause defects in Bruch's membrane.

Thus, AMD begins with the “dry” form, that is, with changes in the RPE and with the appearance of hard drusen. On later stage soft drusen appear, then they turn into confluent drusen. Progressive damage to the pigment epithelium leads to atrophic changes in the retinal neuroepithelium and choriocapillaris. When defects appear in 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 into the retinal tissue. Sometimes a breakthrough hemorrhage occurs in the CT. The final stage of the development of the process is the formation of a subretinal disc-shaped fibrous scar in the central part of the retina and a significant loss of visual functions.

CLINICAL PICTURE

Clinical manifestations of AMD:

• hard drusen;
• soft drusen;
• strengthening or weakening of RPE pigmentation:
• atrophic lesions in the macula (geographic atrophy);
• choroidal neovascularization;
• serous or hemorrhagic detachment of the RPE;
• scar lesions in the macular area.

Druze

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

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

Soft drusen They are large in size and usually have unclear boundaries. They have a granular structure that can be detected histologically. With FA, early accumulation of fluorescein is determined in the absence of sweating, but they can also be hypofluorescent due to the accumulation of lipids and neutral fats. The risk of disease progression to an advanced stage is significantly higher. Soft drusen may coalesce and cause detachment of the RPE.

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

In dynamics, drusen may undergo the following changes:

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

Redistribution of pigment in the macula

The appearance of areas of hyperpigmentation is associated with changes occurring in the 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.

Localized hypopigmentation often corresponds to the location of the drusen, as the RPE layer overlying them becomes thinner. However, local hypopigmentation can also be determined by atrophy of RPE cells, independent of drusen, or a decrease in the content of melanin in cells.

Geographic atrophy of the retinal pigment epithelium

Geographic atrophy of the RPE- an advanced form of dry AMD. Foci of geographic atrophy are detected in the fundus in the form of clearly defined zones of depigmentation with clearly visible large choroidal vessels. With geographic atrophy, not only the RPE is affected, but also the outer layers of the retina and the choriocapillaris layer in this area. With FA, atrophy zones form a “window” type defect. 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 extend beyond the edges of the atrophic lesion. Geographic atrophy can be not only an independent manifestation of AMD, but also a consequence of the disappearance of soft drusen, flattening of the focus of RPE detachment, and can even occur as a result of regression of the CNV focus.

Serous (exudative) detachment of the retinal pigment epithelium

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

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

During development pathological process Flattening of the lesion may occur with the formation of local atrophy of the RPE or rupture of the RPE with the formation of a subretinal neovascular membrane.

Hemorrhagic detachment of the pigment epithelium or neuroepithelium

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

Choroidal (subretinal) neovascularization

It is typical for CNV ingrowth of newly formed vessels through defects in Bruch’s membrane under the RPE or under the neuroepithelium. Pathological permeability of newly formed vessels leads to fluid sweating, its accumulation in the subretinal spaces and the formation of retinal edema. Neovascularization can lead to the appearance of subretinal hemorrhages, hemorrhages into the retinal tissue, sometimes breaking into the CT. This may cause significant functional impairment.

Risk factors for the development of subretinal neovascularization are:

• confluent soft drusen;
• areas of hyperpigmentation;
• the presence of extrafoveal geographic atrophy of the RPE.

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

CNV, based on FA data, is divided into:

• classical;
• hidden:
• mixed.

Hidden CNV suspected when ophthalmoscopy reveals focal dispersion of pigment with simultaneous thickening of the retina, which does not have clear boundaries. Gradually, 2-5 minutes after fluorescein injection, “speckled” fluorescence becomes visible. The degree of hyperfluorescence increases with the addition of sweating; even accumulations of dye in the subretinal space are noted that do not have clear boundaries. Repeated assessment of the same area in the early phases of FA does not allow finding the source of sweating.

Mixed CNV in research recent years divided into:


When choosing a treatment method, it is necessary to apply a 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 area of ​​fluorescence blockade by pigment and/or hemorrhage, is within 1-199 μm from the center of the foveal avascular zone;
• extrafoveal- the edge of the choroidal neovascular membrane, the area of ​​fluorescence blockade by pigment and/or hemorrhage, is 200 μm or more from the center of the foveal avascular zone.

Formation of a disc-shaped scar

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

DIAGNOSTICS

Anamnesis

When collecting anamnesis, it is necessary to consider:

• patient complaints of decreased visual acuity, difficulty reading, especially in low light conditions: sometimes patients notice the loss of individual letters when reading fluently, metamorphopsia;
• duration of symptoms;
• unilateral or bilateral nature of the lesion;
• the presence of concomitant cardiovascular pathology vascular system(in particular, arterial hypertension, atherosclerotic vascular lesions), lipid metabolism disorders, diabetes, excess body weight;
• smoking;
• heredity.

Physical examination

Physical examination includes:

• Determination of visual acuity with optimal correction:
• Amsler test;
• assessment of color perception using the Yustova or Rabkin tables (monocular);
• biomicroscopy (to identify other possible causes of symptoms, for example, age-related cataracts);
• biomicroscopy of the retina using aspherical lenses 60 and/or 90D, as well as Gruby lenses and various CLs (Goldmann lenses, Meinster lenses, etc.), after pupil dilation with short-term mydriatics.

Laboratory research

Instrumental studies

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

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

Differential diagnosis

In 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 noted, but drusen are absent; a pronounced refractive error is observed).

• high complicated myopia (significant refractive error, varnish cracks in the posterior pole, myopic changes in the optic disc);
• traumatic retinal rupture (usually in one eye; a history of eye trauma, most often the rupture occurs concentrically with the optic disc);
• angioid stripes, when in both eyes curved lines of red-brown or gray color diverge subretinal from the optic disc;
• syndrome of presumed ocular histoplasmosis, when small yellowish-white chorioretinal scars are detected in the middle periphery and in the posterior pole of the retina, as well as foci of scarring in the optic disc;
• drusen optic nerve disc;
• choroidal tumors;
• scar areas after laser coagulation;
• inflammatory chorioretinal pathology.

Indications for consultation with other specialists

• cardiologist/therapist- in the presence of arterial hypertension and other diseases of the cardiovascular system;
• neurologist- in the presence of severe atherosclerosis cerebral vessels;
• endocrinologist- in the presence of uncompensated diabetes.

An example of a diagnosis formulation

Right eye- age-related macular degeneration, “wet” form (classical subretinal neovascularization).

Left eye- age-related macular degeneration, “dry” form.

TREATMENT

Treatment Goals

• Achieving stabilization of the pathological process, rather than improving vision, in the presence of choroidal neovascular membranes.
• Prevention of complications (in the “dry” form - the appearance of subretinal neovascularization, in the “wet” form - the occurrence of hemorrhages of various localizations, increased retinal edema, etc.).
• Prevention of severe vision loss leading to disability.
• Preservation of visual acuity, allowing the patient to care for himself independently - in case of advanced pathology.

Indications for hospitalization

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

Drug treatment

General principles

In the “dry” form In order to prevent the progression of the disease, it is recommended to take biologically active food supplements containing vitamins, lutein, and zinc.

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

Pegaptanib (Macugen)- a small RNA-like molecule with high affinity for the vascular endothelial growth factor VEGF (vascular endothelial growth factor). By selectively binding isoform 165 of this growth factor, pegaptanib prevents the growth of newly formed vessels and increased permeability of the vascular wall - two main manifestations of the exudative form of AMD. The drug is intended for intravitreal administration. The results of one clinical trial show that there is probably no significant loss of visual acuity during treatment with pegaptanib, compared with the control group. In this study, pegaptanib was administered intraviterally at various doses (0.3, 1.0, and 3.0 mg) every 6 weeks for 54 weeks; the effect of stabilizing visual acuity was achieved in a large percentage of cases even with the minimum dose 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 growth factor VEGF. Intravitreal injections of the drug are performed once every 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 world 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 for the treatment of colorectal cancer. Currently, in addition to debates about the ethics of treating patients with a drug that was not developed for the treatment of ophthalmopathology, various attempts are being made to compare the effectiveness and safety of ranibizumab and bevacizumab.

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

Much more attention today given to 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.

When triamcinolone is administered, there is a fairly high probability side effects, primarily, ocular hypertension (about 40% of cases), cataracts. In addition, the relatively low and temporary effect in improving visual acuity has led to the fact that today more attention is paid to angiogenesis inhibitors in the world. 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 traditional therapy used in our country for AMD, but such treatment requires additional large clinical studies.

• 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, stimulant therapy is also used.
• In the “wet” form of AMD, subconjunctival injections of glucocorticoids and oral acetazolamide can be used to reduce swelling. This treatment can be used before laser coagulation.
• The use of drugs with a different mechanism of action, for example, peptide bioregulators, and in particular polypeptides from the retina of livestock eyes (retinalamine), also seems promising.

Biologically active food additives

Okuwait 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. For preventive purposes, they are used in courses of 2 months, 2 times a year. This is the only drug whose effectiveness is on early stages AMD to prevent 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 can be increased to 3 tablets per day). Considering 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 (in the form of copper sulfate) - 1 mg, zinc (in form of zinc oxide) - 5 mg) - 1 tablet 2 times a day. This drug, unlike others, is registered in our country as a drug. Many other drugs of similar composition are also used.

It is important to remember that drugs containing beta-carotene should not be prescribed to smokers due to the risk 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 leaf extract 1 tablet 3 times a day orally, in courses of 2 months.

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

• dexamethasone 0.5 ml in the form of subconjunctival injections (10 injections);
• acetezolamide 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.

Laser treatment

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

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

Visudin (vertenorphine) is 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 with pathological myopia.

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

Effect of the drug based on the fact that it contains a photosensitive (that is, light-activated) substance whose light energy absorption peak is between 680 and 695 nm. Verteporfin is a liposomal form; when administered intravenously, it quickly reaches the lesion and is selectively captured by the endothelium of 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 blood, melanin and fibrous tissue. Thus, it is possible to selectively target target tissue without adversely affecting surrounding tissue. Under the influence 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 performing FA, 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 of 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, repeat intervention is performed. If the ophthalmoscopic picture and the result of FA remain the same, there is no sweating, then you should limit yourself to dynamic observation, scheduling a re-examination after another 3 months.

The results of the studies showed that such treatment can be recommended in the following cases:

• with subfoveal classic subretinal neovascular membrane, with visual acuity of 0.1 or higher (such patients account for no more than 20% of all patients suffering from AMD);
• with “predominantly classic” 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;
• for “hidden” CNV with a lesion size greater than 4 areas of the optic disc, photodynamic therapy: only with very low visual acuity (in addition, if the diameter of the lesion exceeds 5400 µm, the patient should be explained that the goal of treatment is to stabilize visual functions);
• when rapid progression of the lesion is expected or in cases where visual acuity without treatment may soon fall below “useful” (that is, allowing the patient to do without assistance).

In order to reduce the risk of phototoxic reactions, patients are advised to avoid exposure to direct sun rays and bright light, wear dark glasses.

IN Lately Photodynamic therapy is used less frequently in countries where intravitreal administration of an angiogenesis inhibitor is permitted.

Application transpupillary thermotherapy was proposed in the early 90s for the treatment of choroidal melanomas. The method is based on laser coagulation, in which wave energy in 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 choroid. The exact mechanism of the beneficial effects in the treatment of AMD remains unclear. Perhaps there is a certain effect on 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 experience virtually no 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, ruptures of the RPE, subretinal hemorrhages and atrophic foci in the choroid are described. Cataracts and the formation of posterior synechiae were also noted. Perhaps this is why the method has not become widespread.

Surgery

Removal of subretinal neovascular membranes

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

Basic possible complications during and after the intervention:

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

Methods have been developed for the removal of massive subretinal hemorrhages through their evacuation through retinotomy holes. In case of formed clots, it is recommended to administer subretinal recombinant tissue plasminogen activator during the intervention. If it is necessary to shift hemorrhages from the macular zone, subretinal administration of tissue plasminogen activator is successfully combined with the introduction of gas (perfluoroorganic compound) into the CT cavity. In the postoperative period, the patient maintains a forced position face down.

In addition, the decision to perform vitrectomy can be made in case of massive non-resorbable hemorrhage in the CT resulting from breakthrough of subretinal hemorrhage.

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

Also perform surgical interventions for macular translocation. The main idea of ​​such an intervention is to displace the neuroepithelium of the foveal retina, located above the choroidal neovascular membrane, so that the unchanged RPE and choriocapillaris layer are located under it in a new position. To do this, first perform a subtotal vitrectomy, and then completely or partially detach the retina. The operation can be performed by performing a retinotomy along the entire circumference (360°), followed by rotation or displacement of the retina, as well as by forming folds (i.e. shortening) of the sclera. The retina is then “fixed” in its new position using an endolaser, and the neovascular membrane is destroyed using laser coagulation. Pneumoretinopexy is performed, after which the patient must remain in a forced position for 24 hours. During interventions for macular translocation, a number of complications are possible: proliferative vitreoretinopathy (PVR) (in 19% of cases), retinal detachment (in 12-23%), formation of a macular hole (9%), as well as complications encountered during vitrectomy for other types of surgery. indications. In this case, loss of not only central but also peripheral vision may occur. Currently wide application I didn't find this method.

Approximate periods of incapacity for work

The duration of incapacity for work is determined by the severity of the process. In some cases, the issue of the visual disability group should be addressed.

Further management

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

The patient should be advised to healthy image life. Quitting smoking, a diet rich in vitamins and microelements, and limiting the consumption of fatty foods are especially important. Excessive sun exposure should be avoided; it is recommended to wear dark glasses. The patient should be advised of the need to take dietary supplements with antioxidant vitamins, lutein and zinc.

If soft drusen is detected, the ophthalmologist should recommend that the patient perform daily self-monitoring using the Amsler grid and contact an ophthalmologist if any new symptoms appear, since this type of drusen is accompanied by high risk decreased vision.

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 visual organ, 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 central vision loss in both eyes can independently cope with many of their daily activities, especially with the use of assistive devices, and still have a good quality of life.

Sick with low visual acuity We can recommend so-called aids for the visually impaired. These are devices different ways enlarging images and enhancing illumination of objects. Among such devices can be named special magnifying glasses, magnifying glasses with various types of mounting, closed-circuit television systems, various digital cameras with image projection on the screen. Low vision aids are especially important for patients with low visual acuity in both eyes.

FORECAST

If there are manifestations of late-stage AMD in one eye, the risk of minor pathological changes in the other eye is, according to various estimates, from 4 to 15%. Moreover, in approximately 1/4 of such patients, visual acuity in the absence of treatment 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 - on average up to 40%, submacular surgery - up to 19% (it must be taken into account that the treatment was applied to patients with different characteristics of the pathological process, so the comparison is very conditional).

Article from the book: .

Angioid stripes of the macula

Drusen (degenerative) macula

Age-related macular degeneration (atrophic) (exudative)

Retinal degeneration:

• lattice
• microcystic
• palisade
• reminiscent of appearance cobblestone street
• reticular

Excludes: with retinal tear (H33.3)

Dystrophy:

• retinal (albipunctate) (pigmented) (yolk-like)
• taperetinal
• vitreoretinal

Central serous chorioretinopathy

Detachment of the retinal pigment epithelium

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document to record morbidity, reasons for the population’s visits to medical institutions of all departments, causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Retinal diseases - classification according to ICD-10 (codes)

According to the ICD, there are several categories of retinal diseases.

Chorioretinal inflammation (H30)

Chorioretinal inflammation includes the following specific nosologies:

• Focal chorioretinal inflammation (H30.0);
• Disseminated chorioretinal inflammation (H30.1);
• Posterior cyclitis (H30.2);
• Chorioretinal inflammation of other etiology (H30.8);
• Unspecified type of chorioretinal inflammation (H30.9).

Diseases of the choroid of the eyeball, not included in other sections (H31)

This section of the ICD includes:

• Chorioretinal scars (H31.0);
• Degenerative changes choroid(H31.1);
• Dystrophic processes in the choroid of a hereditary nature (H31.2);
• Ruptures of the choroid, hemorrhages in this area of ​​the eye (H31.3);
• Choroidal detachment (H31.4);
• Other pathologies of the choroid (H31.8);
• Unspecified diseases of the choroid (H31.9).

Secondary chorioretinal changes (H32)

Such pathologies include:

This pathology combines:

• Retinal detachment accompanied by a rupture (H33.0);
• Retinal cysts, retinoschisis (H33.1);
• Serous retinal detachment (H33.2);
• Retinal tear not accompanied by detachment (H33.3);
• Ordinary retinal detachment (H33.4);
• Other forms of retinal detachment (H33.5).

Retinal vascular occlusion (H34)

Occlusion of retinal vessels can be of the following types:

• Transient occlusion of the retinal arteries (H34.0);
• Central retinal artery occlusion (H34.1);
• Occlusion of other retinal arteries (H34.2);
• Other types of retinal vascular occlusions (H34.8);
• Unspecified type of retinal vascular occlusion (H34.9).

Other retinal pathologies (H35)

Other retinal diseases include:

• Background retinopathy or retinal vascular pathologies (H35.0);
• Preretinopathy (H35.1);
• The remaining pretinopathy is of the proliferative type (H35.2);
• Degenerative changes in the macula or posterior pole (H35.3);
• Degeneration of the peripheral retina (H35.4);
• Hereditary retinal dystrophy (H35.5);
• Hemorrhage into the retinal substance (H35.6);
• Splitting of cell layers in the retina (H35.7);
• Other specified disorders of the retina (H35.8);
• Unspecified diseases of the retina (H35.9).

Secondary retinal lesions (H36)

Retinal diseases can occur with other pathologies:

• Diabetic retinopathy (H36.0);
• Other disorders in the retina (H36.8).

Eye diseases. Classification according to ICD-10.

H00-H59 DISEASES OF THE EYE AND ITS ACCIDENTAL APPARATUS

diseases of the endocrine system, nutritional disorders and metabolic disorders (E00-E90),

congenital anomalies, deformations and chromosomal disorders (Q00-Q99),

neoplasms (C00-D48), complications of pregnancy, childbirth and postpartum period(O00-O99),

certain conditions arising in the perinatal period (P00-P96),

symptoms, signs and abnormalities identified during clinical and laboratory research, not classified elsewhere (R00-R99),

injuries, poisoning and some other consequences of external causes (S00-T98)

H00.0 Hordeolum and other deep inflammations of the eyelids

H01 Other inflammations of the eyelids

Excludes: blepharoconjunctivitis (H10.5)

H01.1 Non-infectious dermatoses of the eyelid

H01.8 Other specified inflammations of the eyelid

H01.9 Inflammation of eyelid, unspecified

H02 Other eyelid diseases

Excludes: congenital malformations of the eyelid (Q10.0-Q10.3)

H02.0 Entropion and trichiasis of the eyelid

H02.1 Ectropion of the century

H02.5 Other diseases affecting the function of the eyelid

Excludes: blepharospasm (G24.5), tic (psychogenic) (F95.-)

H02.6 Xanthelasma of the eyelid

H02.7 Other degenerative diseases of the eyelid and periocular area

H02.8 Other specified diseases of the eyelid

H02.9 Disease of the eyelid, unspecified

H03* Lesions of the eyelid in diseases classified elsewhere

H03.1* Lesions of the eyelid in other infectious diseases classified elsewhere

H03.8* Lesions of the eyelid in other diseases classified elsewhere

H04 Diseases of the lacrimal apparatus

Excludes: congenital malformations of the lacrimal apparatus (Q10.4-Q10.6)

H04.1 Other diseases of the lacrimal gland

H04.3 Acute and unspecified inflammation of the lacrimal ducts

Excludes: dacryocystitis of the newborn (P39.1)

H04.4 Chronic inflammation of the tear ducts

H04.5 Stenosis and insufficiency of the lacrimal ducts

H04.6 Other changes in the tear ducts

H04.8 Other diseases of the lacrimal apparatus

H04.9 Disease of the lacrimal apparatus, unspecified

H05 Diseases of the orbit

Excludes: congenital malformations of the orbit (Q10.7)

H05.0 Acute inflammation of the orbit

H05.1 Chronic inflammatory diseases of the orbit

H05.2 Exophthalmic conditions

H05.3 Orbital deformity

H05.5 Unremoved, long ago in the orbit, foreign body due to penetrating injury to the orbit

H05.8 Other diseases of the orbit

H05.9 Disease of the orbit, unspecified

H06* Lesions of the lacrimal apparatus and orbit in diseases classified elsewhere

H06.0* Lesions of the lacrimal apparatus in diseases classified elsewhere

H06.2* Exophthalmos due to dysfunction of the thyroid gland (E05.-+)

H06.3* Other disorders of the orbit, in diseases classified elsewhere

H10.0 Mucopurulent conjunctivitis

H10.1 Acute atopic conjunctivitis

H10.2 Other acute conjunctivitis

H10.3 Acute conjunctivitis, unspecified

Excludes: ophthalmia of the newborn NOS (P39.1)

H10.4 Chronic conjunctivitis

H10.8 Other conjunctivitis

H10.9 Conjunctivitis, unspecified

H11 Other diseases of the conjunctiva

Excludes: keratoconjunctivitis (H16.2)

Deleted: pseudopterygium (H11.8)

H11.1 Conjunctival degeneration and deposits

H11.2 Conjunctival scars

H11.3 Conjunctival hemorrhage

H11.4 Other conjunctival vascular diseases and cysts

H11.8 Other specified diseases of the conjunctiva

H11.9 Disease of the conjunctiva, unspecified

H13* Lesions of the conjunctiva in diseases classified elsewhere

H13.0* Filarial infestation of the conjunctiva (B74.-+)

H13.1* Acute conjunctivitis in diseases classified elsewhere

H13.2* Conjunctivitis in diseases classified elsewhere

H13.3* Ocular pemphigoid (L12.-+)

H13.8* Other lesions of the conjunctiva in diseases classified elsewhere

H15.8 Other scleral lesions

Excludes: degenerative myopia (H44.2)

H15.9 Disease of the sclera, unspecified

H16.0 Corneal ulcer

H16.1 Other superficial keratitis without conjunctivitis

H16.3 Interstitial (stromal) and deep keratitis

H16.4 Corneal neovascularization

H16.8 Other forms of keratitis

H16.9 Keratitis, unspecified

H17 Scars and corneal opacities

H17.0 Adhesive leukoma

H17.1 Other central corneal opacities

H17.8 Other corneal scars and opacities

H17.9 Corneal scars and opacities, unspecified

H18 Other corneal diseases

H18.0 Pigmentation and deposits in the cornea

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

H18.1 Bullous keratopathy

H18.2 Other corneal edema

H18.3 Changes in corneal membranes

H18.4 Corneal degeneration

Excludes: Moray ulcer (H16.0)

H18.5 Hereditary corneal dystrophies

H18.7 Other deformities of the cornea

Excludes: congenital malformations of the cornea (Q13.3-Q13.4)

H18.8 Other specified diseases of the cornea

H18.9 Disease of the cornea, unspecified

H19* Lesions of the sclera and cornea in diseases classified elsewhere

H19.0* Scleritis and episcleritis in diseases classified elsewhere

H19.1* Herpes simplex virus keratitis and keratoconjunctivitis (B00.5+)

H19.2* Keratitis and keratoconjunctivitis in other infectious and

H19.3* Keratitis and keratoconjunctivitis in diseases classified elsewhere

H19.8* Other lesions of the sclera and cornea in diseases classified elsewhere

H20.0 Acute and subacute iridocyclitis

H20.1 Chronic iridocyclitis

H20.2 Iridocyclitis caused by lenses

H20.8 Other iridocyclitis

H20.9 Iridocyclitis, unspecified

H21 Other diseases of the iris and ciliary body

Excludes: sympathetic uveitis (H44.1)

Excludes: traumatic hyphema (S05.1)

H21.1 Other vascular diseases of the iris and ciliary body

H21.2 Degeneration of the iris and ciliary body

H21.3 Cyst of the iris, ciliary body and anterior chamber of the eye

Excludes: miotic cyst of the pupil (H21.2)

H21.4 Pupillary membranes

H21.5 Other types of adhesions and tears of the iris and ciliary body

Excludes: corectopia (Q13.2)

H21.8 Other specified diseases of the iris and ciliary body

H21.9 Disease of the iris and ciliary body, unspecified

H22* Lesions of the iris and ciliary body in diseases classified elsewhere

H22.0* Iridocyclitis in infectious diseases classified elsewhere

H22.1* Iridocyclitis in diseases classified elsewhere

H22.8* Other lesions of the iris and ciliary body in diseases classified elsewhere

Excludes: capsular glaucoma with false lens detachment (H40.1)

H25.0 Initial senile cataract

H25.1 Senile nuclear cataract

H25.2 Senile Morgani cataract

H25.8 Other senile cataracts

H25.9 Senile cataract, unspecified

H26 Other cataracts

Excludes: congenital cataract (Q12.0)

H26.0 Childhood, juvenile and presenile cataract

H26.1 Traumatic cataract

If it is necessary to identify the cause, use an additional external cause code (class XX).

H26.2 Complicated cataract

H26.3 Drug-induced cataracts

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

H26.4 Secondary cataract

H26.8 Other specified cataracts

H26.9 Cataract, unspecified

H27 Other lens diseases

Excludes: congenital lens defects (Q12.-), mechanical complications associated with implanted lens (T85.2)

H27.1 Lens luxation

H27.8 Other specified diseases of the lens

H27.9 Lens disease, unspecified

H28* Cataracts and other lesions of the lens in diseases classified elsewhere

H28.0* Diabetic cataract (E10-E14+ with common fourth digit.3)

H28.1* Cataracts in other diseases of the endocrine system, nutritional disorders and metabolic disorders classified elsewhere

H28.2* Cataract in other diseases classified elsewhere

H28.8* Other lesions of the lens in diseases classified elsewhere

H30.0 Focal chorioretinal inflammation

H30.1 Disseminated chorioretinal inflammation

Excludes: exudative retinopathy (H35.0)

H30.2 Posterior cyclitis

H30.8 Other chorioretinal inflammations

H30.9 Chorioretinal inflammation, unspecified

H31 Other diseases of the uvea

H31.0 Chorioretinal scars

H31.1 Uveal degeneration

Excludes: angioid streaks (H35.3)

H31.2 Hereditary dystrophy of the choroid

Excludes: ornithinemia (E72.4)

H31.3 Hemorrhage and rupture of the choroid

H31.4 Choroidal detachment

H31.8 Other specified diseases of the uvea

H31.9 Choroid disease, unspecified

H32* Chorioretinal disorders in diseases classified elsewhere

H32.8* Other chorioretinal disorders in diseases classified elsewhere

H33 Retinal detachment and tears

Excludes: retinal pigment epithelial detachment (H35.7)

H33.0 Retinal detachment with retinal break

H33.1 Retinoschisis and retinal cysts

Excludes: congenital retinoschisis (Q14.1), microcystic retinal degeneration (H35.4)

H33.2 Serous retinal detachment

Excludes: central serous chorioretinopathy (H35.7)

H33.3 Retinal tears without retinal detachment

Excludes: peripheral retinal degeneration without break (H35.4), chorioretinal scars after surgery for retinal detachment (H59.8)

H33.4 Tractional retinal detachment

H33.5 Other forms of retinal detachment

H34 Retinal vascular occlusions

H34.0 Transient retinal arterial occlusion

H34.1 Central retinal arterial occlusion

H34.2 Other retinal arterial occlusions

H34.8 Other retinal vascular occlusions

H34.9 Retinal vascular occlusion, unspecified

H35 Other retinal diseases

H35.0 Background retinopathy and retinal vascular changes

H35.2 Other proliferative retinopathy

H35.3 Macular and posterior pole degeneration

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

H35.4 Peripheral retinal degenerations

Excludes: with retinal tear (H33.3)

H35.5 Hereditary retinal dystrophies

H35.6 Retinal hemorrhage

H35.7 Retinal layer splitting

H35.8 Other specified retinal disorders

H35.9 Retinal disease, unspecified

H36* Retinal lesions in diseases classified elsewhere

H36.0* Diabetic retinopathy (E10-E14+ with common fourth digit.3)

H36.8* Other retinal disorders in diseases classified elsewhere

Excludes: absolute glaucoma (H44.5), birth glaucoma (Q15.0), traumatic glaucoma due to birth injury (P15.3)

H40.0 Suspicion of glaucoma

H40.1 Primary open-angle glaucoma

H40.2 Primary angle-closure glaucoma

H40.3 Glaucoma secondary post-traumatic

H40.4 Glaucoma secondary to inflammatory disease of the eye

H40.5 Glaucoma secondary to other eye diseases

H40.6 Glaucoma, secondary, drug-induced

H40.8 Other glaucoma

H40.9 Glaucoma, unspecified

H42* Glaucoma in diseases classified elsewhere

H42.0* Glaucoma in diseases of the endocrine system, nutritional disorders and metabolic disorders

H42.8* Glaucoma in other diseases classified elsewhere

H43.0 Vitreous loss (prolapse)

Excludes: vitreous syndrome after cataract surgery (H59.0)

H43.1 Hemorrhage into vitreous

H43.2 Crystalline deposits in the vitreous

H43.3 Other vitreous opacities

H43.8 Other diseases of the vitreous

Excludes: proliferative vitreoretinopathy with retinal detachment (H33.4)

H43.9 Vitreous disease, unspecified

H44 Diseases of the eyeball

Includes: disorders affecting multiple structures of the eye

H44.0 Purulent endophthalmitis

H44.1 Other endophthalmitis

H44.2 Degenerative myopia

H44.3 Other degenerative diseases of the eyeball

H44.4 Hypotony of the eye

H44.5 Degenerative conditions of the eyeball

H44.6 Unremoved (long-standing in the eye) magnetic foreign body

H44.7 Unremoved (long-term in the eye) non-magnetic foreign body

H44.8 Other diseases of the eyeball

H44.9 Disease of the eyeball, unspecified

H45* Lesions of the vitreous body and eyeball in diseases classified elsewhere

H45.0* Vitreous hemorrhage in diseases classified elsewhere

H45.1* Endophthalmitis in diseases classified elsewhere

H45.8* Other lesions of the vitreous body and eyeball in diseases classified elsewhere

Excludes: ischemic optic neuropathy (H47.0), optic neuromyelitis [Devic's disease] (G36.0)

H47 Other diseases of the optic nerve and visual pathways

H47.0 Diseases of the optic nerve, not elsewhere classified

H47.1 Papilledema, unspecified

H47.2 Optic atrophy

H47.3 Other optic disc diseases

H47.4 Optic chiasm lesions

H47.5 Lesions of other parts of the visual pathways

H47.6 Lesions of visual cortex

H47.7 Diseases of the visual pathways, unspecified

H48* Disorders of the optic nerve and visual pathways in diseases classified elsewhere

H48.0* Optic nerve atrophy in diseases classified elsewhere

H48.1* Retrobulbar neuritis in diseases classified elsewhere

H48.8* Other lesions of the optic nerve and visual pathways in diseases classified elsewhere

Supranuclear progressive (G23.1)

H49.0 3rd [oculomotor] nerve palsy

H49.1 4th [trochlear] nerve palsy

H49.2 6th [abducens] nerve palsy

H49.3 Complete (external) ophthalmoplegia

H49.4 Progressive external ophthalmoplegia

H49.8 Other paralytic strabismus

H49.9 Paralytic strabismus, unspecified

H50 Other forms of strabismus

H50.0 Convergent concomitant strabismus

H50.1 Concomitant divergent strabismus

H50.2 Vertical strabismus

H50.3 Intermittent heterotropia

H50.4 Other and unspecified heterotropies

H50.6 Mechanical strabismus

H50.8 Other specified types of strabismus

H50.9 Strabismus, unspecified

H51 Other concomitant eye movement disorders

H51.0 Gaze paralysis

H51.1 Convergence insufficiency [insufficient and excessive convergence]

H51.2 Intranuclear ophthalmoplegia

H51.8 Other specified disorders of conjugal eye movement

H51.9 Concomitant eye movement disorder, unspecified

H52 Impairments of refraction and accommodation

Excludes: malignant myopia (H44.2)

H52.3 Anisometropia and aniseikonia

H52.5 Accommodation disorders

H52.6 Other refractive errors

H52.7 Refractive error, unspecified

H53.0 Amblyopia due to anopsia

H53.1 Subjective visual disturbances

Excludes: visual hallucinations (R44.1)

H53.3 Other disorders binocular vision

H53.4 Visual field defects

H53.5 Color vision abnormalities

Excludes: day blindness (H53.1)

H53.6 Night blindness

Excluded: due to vitamin A deficiency (E50.5)

H53.8 Other visual disturbances

H53.9 Visual impairment, unspecified

H54 Blindness and decreased vision

Excludes: transient blindness (G45.3)

H54.0 Blindness in both eyes

H54.1 Blindness in one eye, reduced vision in the other eye

H54.2 Reduced vision in both eyes

H54.3 Unspecified loss of vision in both eyes

H54.4 Blindness in one eye

H54.5 Reduced vision in one eye

H54.6 Unspecified loss of vision in one eye

H54.7 Unspecified vision loss

H57 Other diseases of the eye and its adnexa

H57.0 Abnormalities of pupillary function

H57.1 Eye pain

H57.8 Other unspecified diseases of the eye and adnexa

H57.9 Disorder of the eye and adnexa, unspecified

H58* Other lesions of the eye and its adnexa in diseases

nyakhs classified in other headings

H58.0* Abnormalities of pupillary function in diseases classified elsewhere

H58.1* Visual impairment in diseases classified elsewhere

H58.8* Other disorders of the eye and its adnexa in diseases classified elsewhere

H59 Lesions of the eye and its adnexa after medical procedures

Excluded: mechanical complication from:

Intraocular lens (T85.2)

Other ocular prosthetic devices, implant and graft (T85.3)

H59.0 Vitreous syndrome after cataract surgery

H59.8 Other lesions of the eye and adnexa following medical procedures

H59.9 Damage to the eye and its adnexa following medical procedures, unspecified

What is retinal angiopathy, and what is the disease code according to ICD 10,

Angiopathy is a change in the condition of the vessels of the retina, which can lead to the development of dystrophic changes (retinal dystrophy), myopia, optic nerve atrophy, etc.

Retinal vascular angiopathy is not a disease and ophthalmologists often focus on this, but a condition that can occur against the background of other diseases. Pathological changes in blood vessels appear during injuries and damage, and are also observed in diabetes mellitus.

ICD-10 code

Angiopathy does not have a code according to the international classification, since it is not considered an independent disease. The code is assigned to the disease that led to the development of the pathological condition.

This is what retinal angiopathy looks like

Causes and classification

Angiopathy has several causes. The names in the vessels appear against the background of:

1. Traumatic injuries chest or cervical spine spine. Which leads to impaired blood flow and hypoxia.
2. Arterial hypertension is, simply put, high blood pressure. When blood pressure levels increase, the small capillaries of the retina cannot withstand the load and burst. Hemorrhages occur, which can lead to a decrease in visual acuity, changes in the vessels and their course.
3. Arterial hypotension is low blood pressure that occurs against the background of significant dilation of veins and large vessels, leading to the formation of blood clots in the vessels of the retina.
4. Cervical osteochondrosis is a disease that leads to impaired blood flow to the brain, increased intracranial pressure.
5. Diabetes mellitus is a pathology of the endocrine system, characterized by increased blood sugar levels. In the absence of adequate therapy, diabetes mellitus leads to thickening of the membrane walls and affects the condition of the retinal vascular network.
6. Traumatic brain injury - leads to disruption of brain function, increased intracranial pressure, and the development of hypoxia. In this case, angiopathy occurs as a consequence of the injury.
7. Pregnancy and childbirth - changes in blood vessels can appear during pregnancy or occur after a difficult birth. In this case, the condition is subject to correction, but only if the cause of the pathology has been established.
8. Autoimmune diseases and diseases of the hematopoietic system are nonspecific causes. Against the background of such diseases, changes in the retinal vessels occur quite rarely.

But this information will help you understand what presbyopia and retinal angiopathy is and how it is treated.

The video shows a description of the disease:

There are several types of angiopathy, it happens:

• hypertensive - occurs when blood pressure or intracranial pressure increases;
• hypotonic – develops against the background of low blood pressure and the formation of blood clots;
• diabetic - the main cause is diabetes mellitus or an increase in blood sugar levels (can be diagnosed in children of the first year of life or newborns);
• background – occurs against the background of changes in the condition of the vessels of the retina of the eyes, with a long course it is dangerous for complications;
• traumatic – a consequence of injuries suffered, injuries that occur when blood flow to the brain is disrupted;
• juvenile - appears in children during puberty. The exact cause has not been established. It manifests itself as a sharp loss of visual acuity, develops quickly and can cause glaucoma or retinal dystrophy.

Angiopathy of both eyes is diagnosed more often. But there are cases when the vessels change in only one eyeball. This may indicate a slow progression of the pathology.

Description of symptoms

Angiopathy has a number of specific signs that a person can notice, but leave without proper attention. Attributing the condition to stress or fatigue.

In most cases, patients complain:

1. For the appearance of “flies” in the eyes.
2. To reduce visual acuity.
3. The appearance of flashes or fog before the eyes.
4. For pain or colic in the eyeball area.
5. For rapid fatigue of the visual organs.
6. For the appearance of pinpoint hemorrhages or burst red blood vessels in the area of ​​proteins.

It is necessary to pay attention to decreased visual acuity, the appearance of floaters or lightning before the eyes. Temporary, but complete or partial loss of vision. When, when getting out of bed or during heavy physical exertion, there is a sharp clouding in the eyes, an acute attack of dizziness.

This indicates that the person has problems with blood circulation in the brain, hypoxia or high intracranial pressure. Against the background of these pathologies, retinal angiopathy develops.

Symptoms may change and occur periodically (only when blood pressure levels increase), but these signs should not be ignored. If alarming symptoms appear, you should consult a doctor as soon as possible.

Diagnostics

It is not particularly complicated; you just need to contact an ophthalmologist. The doctor will examine the vessels of the fundus.

To detect changes, it is enough to conduct only one examination, but if necessary, the doctor may recommend an ultrasound of the eyes. Intraocular pressure is also measured, which helps eliminate the possibility of developing glaucoma. But this information will help you understand how retinal angiopathy is diagnosed in a child.

Treatment

Therapy is aimed at eliminating the root cause of the pathological condition. If angiopathy occurs against the background of arterial hypertension, the doctor writes a referral to a cardiologist. The doctor prescribes medications that can stabilize blood pressure levels and reduce the risk of bleeding in the retinal vessels and small capillaries.

If angiopathy is associated with diabetes mellitus, then the underlying disease is treated and attempts are made to prevent the development of complications.

So, what medications can an ophthalmologist prescribe:

• vasodilators (Cinnarizine, Vinpocetine, etc.);

Cinnarizine

Retinal dystrophy includes a number of diseases in which the functioning of this part of the visual organs is disrupted. They are characterized by tissue death and vascular defects. The retina is like a radio receiver. Only it does not catch sound, but light pulses that allow it to project an image. If this part of the eye is affected by disease, its functionality is lost and vision begins to deteriorate. The characteristics of the disease correspond to the following description:

Retinal dystrophy code according to ICD-10

It does not have an ICD-10 code, but it can be included in the list of retinal diseases listed under number H35.

Classification of retinal dystrophy

Retinal dystrophy is divided into two large types. These are hereditary and acquired forms of the disease. If we talk about hereditary dystrophies, then destruction occurs at the level of receptors that allow vision in the twilight. The following types of hereditary lesions are distinguished::

• Generalized - degeneration of the pigment type, congenital blindness or lack of night vision, impaired or absent color perception.
• Peripheral - retinal separation due to the characteristics of chromosomes, damage to connective tissue, dysfunction of the rod and cone systems.
• Central - hereditary macular degeneration with the appearance of spots or yellow lesions, dystrophy against the background of age-related changes.

If we talk about the secondary (acquired) form of retinal dystrophy, it is also divided into peripheral and central. The disease of the central type is in turn divided into wet and dry manifestations of dystrophy. In the first case, the formation of new vessels is observed in the affected area. They are very fragile, so elements contained in the blood leak through them. As a result, edema forms and the light-sensitive elements of the visual organs are damaged. This disease is severe, so increased attention is paid to its treatment.

Dry central retinal dystrophy occurs in 90% of cases. It becomes the result of a metabolic disorder. In this case, accumulations of products involved in metabolism form between the retina and the vessels.

Peripheral dystrophy

This manifestation is typical for myopic people and very often leads to retinal detachment. There are two types of peripheral dystrophy: chorioretinal and vitreoretinal. Peripheral chorioretinal dystrophy (PCRD) affects the membranes of blood vessels. Peripheral vitreochorioretinal dystrophy (PVCRD) affects the condition of the cornea. In addition, peripheral dystrophy can be cystic, frost-like and lattice.

Causes of retinal dystrophy

The causes of dystrophic changes in the retina can be the following factors::

• Scar formation as a result of disruption of the vascular system or decreased local immunity.
• Non-compliance with diet and consumption of unhealthy or low-quality food.
• Bad habits, in particular smoking and excessive consumption of alcoholic beverages.
• Negligence in the treatment of infectious diseases.
• Availability chronic diseases. This could be diabetes, blood pressure surges, diseases of the cardiovascular and endocrine systems.
• Eye surgeries.
• Obesity as a result of metabolic disorders.

These manifestations worsen the condition of the circulatory system and slow down metabolic processes. Because of this, the retina is affected. Here's what they say about the causes of retinal dystrophy on the Internet:

Symptoms of retinal dystrophy

Common signs for all types of retinal dystrophy are the following manifestations::

• Absence or decreased color perception.
• The appearance of image defects (floaters, lightning, flashes, fog).
• Loss of central vision.
• Perception of objects located to the side as a fuzzy picture.
• Decreased visual acuity.
• Loss of sense of movement. An object at rest is difficult to distinguish from one that is moving.
• Need for excessive light while writing or reading.

If we talk about individual forms of the disease, peripheral dystrophy is expressed by the appearance of flashes and dots before the eyes. Damage to the macula is accompanied by curvature of the visible lines. Dry retinal dystrophy distorts visual images. The patient cannot work with small objects and fonts. He has difficulty seeing in the dark and distinguishing faces.

Here is one example of the development of retinal dystrophy and its treatment:

In most cases, the manifestation of symptoms is characteristic of one eye. In addition, the initial stages of retinal dystrophy occur unnoticed. Having discovered the first signs indicating the onset of the disease, you should immediately consult a doctor.

Retinal dystrophy during pregnancy

During pregnancy, retinal dystrophy occurs due to decreased blood flow to the eyes as a result of low blood pressure. If the development of the disease is not stopped in time, it can lead to retinal rupture or detachment. To avoid such consequences, a planned caesarean section or laser coagulation procedure is performed. Laser coagulation is prescribed before the 35th week of pregnancy. The procedure involves creating a reliable connection between the choroid and the retina. The result of such an intervention is to reduce the risk of complications on the visual organs during natural childbirth.

Diagnosis of the disease

Identifying dystrophy and making a correct diagnosis involves conducting the following studies:

• Checking visual acuity (visometry).
• Identification of the visual field (perimetry).
• Check for distortion of visible lines - Amsler test.
• Detection of abnormal deviations in the refraction of light rays (refractometry).
• Biomicroscopy.
• Ophthalmoscopy.
• Determination of the degree of color perception.
• Electroretinography.
• Determination of the degree of adaptation of visual functions in the dark (adaptometry).
• Finding affected areas.
• Retino- and coherent tomography.
• Ultrasonography.
• Collection of analyses.

Depending on the clinical picture The patient is prescribed a consultation with doctors of other specialties.

Treatment of retinal dystrophy

The standard treatment regimen for dystrophy using medication looks like this::

1. Drugs that strengthen and dilate blood vessels. The dosage of Complamin, Noshpa, Papaverine or Ascorutin is selected individually for each patient.
2. Medicines to prevent blood clots. This may be Aspirin, Ticlodipine or Clopidogrel.
3. Vitamin B, administered intramuscularly, and a complex of other vitamins in tablet form.
4. Medicines that prevent the formation of new painful blood vessels (Lucentis).
5. Cholesterol-lowering drugs.
6. Means for improving metabolism inside the eye. Injected intravenously or directly into the structure of the visual organs.
7. Retinalamin, injected into the lower eyelid or eye shell for 10 days.
8. Eye drops that speed up the healing process and metabolism.

Conservative treatment is complemented by physiotherapy. The patient is prescribed procedures such as photo- and electrical stimulation, electrophoresis, and magnetic therapy. If we talk about the use of small doses of laser radiation, they are used to influence the retina and blood.

Laser treatment

The laser beam extends its effect directly to the affected areas of the visual organs. They are exposed to irradiation in order to stimulate and start the metabolic process. The laser is able to strengthen blood vessels through their coagulation and separate affected areas from healthy ones, thereby stopping the spread of the disease. This process involves soldering defective tissues.

Surgery

If conservative and laser methods treatments have not helped to cope with retinal dystrophy, the doctor decides to prescribe surgery. Depending on the complexity of each case, such surgical interventions are performed:

• Revascularization – restoration of blood vessels.
• Vasoconstruction is a narrowing of the spaces between blood vessels.
• Vitretomy is complete or partial removal of the vitreous.

After surgery, it is necessary to take measures to help quickly restore visual functions. You need to make sure that your eyes are not overstrained, wear sunglasses outside, and take vitamins. In addition, it is necessary to stop smoking and overuse alcohol.

Traditional methods of treating retinal dystrophy

Traditional medicine recipes for dystrophy should be used in conjunction with the main treatment regimen prescribed by the doctor. Such means have a good effect:

• Goat milk diluted with boiled water in equal proportions. Within a week, the resulting solution is dripped into the eyes, then covering them with a dark cloth. As a result, the process of retinal detachment will stop.
• For a month, drink half a liter of decoction per day. To prepare it, take 5 parts of pine needles, 2 parts of rose hips and onion peels. They are poured with boiling water and cooked for 10 minutes.
• A decoction of cumin and cornflower flowers is instilled into the eyes 2 times a day.
• For a month, a decoction of celandine is instilled into the eyes 3 times a day.
• Tinctures of birch, horsetail, lingonberry, and mustard are taken orally.
• Wheat grains are left to germinate in a warm place. The embryos grind and eat the resulting mixture.
• For 9 days, a decoction of mumiyo and aloe juice, boiled in proportions of 5:1, is dripped into the eyes.

Before using folk remedies, you need to consult a doctor and make sure that the components of the decoctions do not cause allergic reactions.

Note:If, when a disease is detected, you refuse the help of a doctor and self-medicate, the disease can develop to a severe stage. It can lead to complete loss of vision, which is characterized by the irreversibility of the process.

Prevention of retinal dystrophy

In order to reduce the risk of developing retinal dystrophy, you must follow these rules::

1. Make sure that workplace was properly lit.
2. Any load on the visual organs should be accompanied by periodic rest.
3. It is necessary to visit an ophthalmologist once a year.
4. The diet should consist of foods containing vitamins and microelements necessary for normal metabolism.
5. You need to give up bad habits (alcohol, smoking).

Massage and exercises strengthen the visual organs and normalize blood flow to them. Watch your health. Contact your doctor at the first signs of the disease to begin treatment on time.

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

The disease is caused by disturbances in the vascular system of the eye, and then a scar is formed, the central zone of the retina completely falls out, leaving only peripheral vision. A person distinguishes day from night, sees fuzzy outlines of objects with peripheral vision, but there is no image in the center - it’s as if it’s hanging in front of the eye. black spot.

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

The 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, as well as changes in the internal environments of the body.

This disease is becoming widespread and is 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 a large group of diseases in which the “dying away” of this membrane is observed, that is, its progressive degeneration, leading to deterioration of the patient’s vision.

Etiology and pathogenesis

Most often, the disease is caused by metabolic breakdown products that accumulate with age. A significant place is occupied by infections, intoxication and disruption of the blood supply to the inner membrane.

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

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

As the eye ages, waste products from cell metabolism accumulate, forming so-called “drusen” - yellowish thickenings under the retinal pigment epithelium.

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

As drusen accumulate, they can cause inflammation by triggering the release of vascular endothelial growth factor, a protein that promotes the growth of new blood vessels in the eye. New pathological blood vessels begin to grow, a process called angiogenesis.

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

From this moment, AMD begins to progress, turning into another, more aggressive form - “wet”. Fluid accumulates between Bruch's membrane and the photoreceptor layer, affecting the vulnerable nerves that provide healthy vision.

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

Causes

Often the disease is caused by metabolic breakdown products accumulated with age. Problems of blood supply to the inner membrane, intoxication, and infection play a significant role.

This disease can 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 due to bruises, blows, etc.
• Genetic predisposition to dystrophy.
• Various systemic diseases(diabetes, hypertension, problems with the thyroid gland and kidneys, 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 excess body weight and bad habits have a high likelihood of developing retinal dystrophy.

Low blood pressure during the second trimester of pregnancy leads to poor circulation 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 enveloping the eyeball - mainly 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 developing inside the eye. Defects are divided according to the localization of the lesion: sometimes central and sometimes peripheral vision is affected.

Domestic

Internal reasons:

• aging of the body;
• heredity;
• vascular diseases;
• hypertension;
• farsightedness and myopia;
• increased level cholesterol;
• visual injuries;
• eye surgeries;
• prolonged local inflammation.

High risks of developing degeneration are also observed in people with very white skin and Blue eyes. Patients with such anatomical features acquire diseases more quickly, especially when influenced external factors.

External

TO external reasons relate:

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

Age

In people of retirement age - from 55 years old - a macular form is diagnosed, in which the retina changes due to the 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.

Causes of 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 lining of the eye are diagnosed much more often.

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

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

They can be congenital or secondary (acquired), central in localization (located in the macular region) or peripheral.

Vision in AMD

The etiology of dystrophic processes in the retina is diverse. Retinal dystrophy diagnosed in children in the vast majority of cases is caused by heredity.

Dystrophy can be provoked by any factors that lead to disorders of metabolic processes. In older people, these factors are accompanied by any vascular pathologies, which disrupt the normal supply of oxygen and nutrients to the eye.

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

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

There are more common reasons diseases that 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;
• pathologies of the thyroid gland;
• severe intoxication with various substances;
• severe vitamin deficiency or lack of minerals and other nutrients;
• long-term periodic irradiation of the eyes with ultraviolet radiation.

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

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

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

• Stressful situations.
• Vitamin deficiencies and lack of nutrients in the diet.

• Swelling, inflammation and retinal dystrophy, circulatory disorders and damage to the optic nerve, as well as skull injuries;
• 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 from 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 excess body weight and bad habits have a high likelihood of developing retinal dystrophy. Low blood pressure during the second trimester of pregnancy leads to poor circulation and poor nutrition of the retina. Therefore, pregnant women are also at risk.

The causes of retinal dystrophy during pregnancy may be general diseases:

• Diabetes
• Hypertension
• Vegetovascular dystonia
• Kidney diseases
• Consequences of traumatic brain injuries
• Disorders of the thyroid glands

Classification

There are central as well as peripheral dystrophy of the retina. Central retinal dystrophy occurs in the area that has the clearest vision (the macula area). As mentioned earlier, the disease can be triggered by age-related changes, which is the most common cause. After all, due to age, the blood vessels of the eyes undergo changes.

The progression of the disease gradually reduces visual acuity. Blindness, as a rule, does not occur provided that the peripheral areas of the retina are not involved. Central retinal dystrophy is easy to recognize; it is characterized by curvatures, bifurcation and fractures of the images.

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

This is characterized by a slow decline in vision. The second is different 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 quite quickly, which is characteristic of this form of macular degeneration of the retina. Treatment is required in a qualified and timely manner, 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 man’s age, 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 and metabolism, and as a result, dystrophy develops. Effusion provokes a gradual detachment of the retina, which leads to serious consequences affecting the ability to see.

The onset of complete blindness is possible. Symptoms of chorioretinal dystrophy include blurred vision and distorted images.

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

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

Congenital

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

Based on the localization of pathological changes, the described disease can be divided into three types: peripheral forms, in which the edges of the retina are affected; central chorioretinal dystrophy of the retina, affecting only the center of the specified ocular 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 condition.

For example, central retinal dystrophy is often called age-related, synonyms of which are senile, involutional dystrophy; Sometimes 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 (macula) is 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. Congenital forms are more difficult to treat than acquired forms.

Hereditary generalized forms of dystrophy include:

• Tapetoretinal (also called pigmentary).

• Congenital impairment of night vision.
• Cone dysfunction syndrome. There are two possible manifestations - impaired color vision or blindness.
• Leber's amaurosis.

Peripheral retinal dystrophy in congenital forms is divided into:

• Goldmann-Favre pathology.
• Retinoschisis.

With central retinal dystrophy the following is diagnosed:

• Macular degeneration.
• Stargardt and Best disease.

Central dystrophy is also called macular dystrophy (since the macular region of the retina is affected).

Acquired retinal dystrophies do not have such a complex classification.

A special 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 retinal lesion, the types of disease are distinguished: central and peripheral.

Central retinal dystrophy 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. Compliant initial stage diseases. 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 blood 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:

• decreased central vision (distortion of the contours of objects and lines occurs);
• sensitivity to bright light;
• formation of a dark spot that makes reading and driving difficult vehicle and working with small objects;
• distorted perception of colors.

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Peripheral retinal dystrophy

All dystrophies can be divided into two large groups: acquired (secondary) and congenital (primary). In turn, secondary ones are divided into three more groups depending on the location of the 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 retinal dystrophy remains within normal limits.

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

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

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

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

Retinal pigmentary dystrophy is the rarest anomaly caused by hereditary factors. It is caused by disturbances in the functioning of the retinal photoreceptors, which are responsible for either twilight black-and-white or daytime color vision.

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

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

Degrees of disability

According to ICD-10, severity

I degree

(minor degree of visual impairment) - minor functional impairment;

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

IV degree

(practical or absolute blindness) significant functional impairment.

The criteria for assessing impairment of basic visual functions when determining disability are given in Table. 1.

Assessment of disability has its own characteristics for each category of life activity, but there are also basic (common to most categories) characteristics. All disabilities

Depending on the severity, they are divided into three degrees.

Restrictions of the first degree occur when the patient is able to independently carry out one or another type of life activity, but with certain difficulties (longer time, reduced volume, fragmentation of performance, etc.) and, if necessary, with the use of auxiliary means in connection with moderate persistent impairments functions.

Persistent disability with farsightedness and astigmatism is observed
in very rare cases. It may be associated with the appearance of asthenic complaints
due to decreased vision. In these cases, work with small parts and
requiring visual strain.

Transfer to another job with lower qualifications due to farsightedness
high degree, may be the reason for establishing disability group III.

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 Northwestern and Ural to 2.8 per 10,000 children and the Southern), 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 a dominant pattern. The development of central dystrophy in this case occurs at high speed. The disease develops in both eyes; a characteristic symptom is a violation of color perception.

In children, in addition to retinal dystrophy, strabismus and 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. Vascular pathology in the macula area manifests itself in several anomalies. For example, Stargardt disease, which has an autosomal recessive inheritance principle (both parents of the child have a “sick” gene in their set of chromosomes).

The disease affects both eyes and 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 visual acuity.

Juvenile retinoschisis is an X-linked disease characterized by dystrophic 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 that is a combination of several hereditary diseases. Peak progression occurs at the age of ten.

Classification of the disease, symptoms in children and adults

Negative dynamics of the main indicators of disability in 2000 - 2005 was established. with an increase in the number of people newly recognized as disabled from 39,000 to 66,700 people per year and an increase in the level of primary disability 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 Eastern - 4.5, in the Southern - 6.0, in the North-Western - 4.2, in the Ural - 5.3 , in Siberian 5.1 per 10,000 adult population) and constituent entities of the Russian Federation, where it varies from 1.5 in Moscow to 20.5 in the Republic of Kalmykia per 10,000 adult population.

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

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

Of course, there are contraindications and restrictions to natural childbirth due to eye conditions, 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 cesarean section.

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

Myopia in itself, even 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 to deliver is the condition of the retina.

It is important to know that the degree of myopia does not matter when there is a threat of complications from the retina. According to the literature and from personal experience, most often degenerative 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 ophthalmologist twice during pregnancy: when registering at 12–14 weeks, and then at 32–36 weeks. All patients without exception should visit an ophthalmologist.

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 they reach reproductive age, up to 30% of women suffer from the history, and about a quarter of them have high myopia.

Features of the course of myopia during pregnancy

1. blurred vision, distorted perception of objects (curved, twisted), 2. flashing “spots” and flashes before the eyes - in this case, you need to measure your blood pressure yourself and call an ambulance.

Diagnostics

- examination of the fundus by an ophthalmologist - to exclude severe concomitant pathologies: CBC (hemoglobin, platelets), TAM (protein!), BAC (total protein, ALT, AST, creatinine, urea, sugar, fibrinogen), coagulogram, blood pressure measurement and pulse.

Treatment

Hypermetropia or farsightedness is a vision pathology in which visual acuity in relation to nearby objects is reduced. Objects located in the distance are perceived as clearer. Farsightedness itself is not a contraindication to pregnancy and spontaneous childbirth.

Farsightedness, to a lesser extent than myopia, is dangerous due to degenerative changes in the fundus, but there is such a possibility. As planned, you will be examined by an ophthalmologist and, if necessary, referred for a fundus examination (usually highly qualified studies are carried out in eye microsurgery centers, laser correction laboratories, and so on).

In case of 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, the baby does not require additional examination.

You should know that hypermetropia, like myopia, can have a hereditary predisposition. It is possible to reliably assess a child’s vision only after the age of 2–3 years, since infants may have transient congenital hypermetropia that does not require treatment or correction.

Glaucoma is a disease of the eye system, which is accompanied by increased 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 female body, an increase in progesterone levels and changes in the elasticity and extensibility of many tissue structures, the course of glaucoma during pregnancy, as a rule, improves. Exacerbations are rare, especially if you regularly use the prescribed drops.

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

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

During pregnancy planning, visit an ophthalmologist and consult about changing the drug. Glaucoma is not inherited, so 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 ophthalmological pathologies before conception. In such cases, pregnancy management with the participation of an ophthalmologist is necessary. Natural delivery requires the approval of the treating ophthalmologist.

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

In the second trimester, blood pressure levels decrease 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 may become more complicated, leading to complete detachment or rupture of the retina. This is why it is so important to visit an ophthalmologist during pregnancy.

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

A repeat examination is scheduled between the 32nd and 36th weeks. However, if retinal dystrophy is diagnosed, you must visit an ophthalmologist once a month.

As for childbirth, the choice between a natural birth and a cesarean section is influenced by several factors: the age of the woman in labor, the degree of the disease, the general health of the woman. Doctors often practice cesarean section in order to maximize the safety of the birth process for both the mother and her baby .

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

During laser exposure, 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 chloramphenicol be used for conjunctivitis in children? You will find the answer in this article.

During pregnancy, hormonal levels change and metabolism increases. Blood circulation in all organs and tissues first increases and then decreases.

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

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 your own, they resort to artificial birth, that is, a caesarean section.

A pregnant woman must attend consultations with an ophthalmologist. The first visit usually occurs at the very beginning of pregnancy, when future mom becomes registered.

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

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

If a woman is myopic, then she is examined by an ophthalmologist at least once a month.

If a pregnant woman has retinal dystrophy, then childbirth must be carried out by cesarean section.

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

In the third trimester of pregnancy, a physiological decrease in blood pressure occurs due to hormonal changes and the body’s preparation for childbirth. As a result of decreased blood flow, the amount of nutrients delivered to the retina is reduced. This factor can also provoke the development of dystrophic processes.

Considering 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 eyes, and decreased vision clarity. These phenomena are explained by a spasm of accommodation and may disappear after the birth of the child, or intensify and lead to myopia.

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

• Flashing flies, flashes, lightning before the eyes
• Deterioration of distance vision
• Vague images
• Loss of areas of the visible picture

Pregnant women with severe myopia (more than 5-6 diopters) are at risk. Under the influence of estrogen, the elasticity of 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 doctor’s final decision on the possibility of delivery without risk to vision largely depends on the ophthalmologist’s opinion.

Symptoms

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

Changes become noticeable when the retina is torn or detached. In addition, there is a sharp decrease in visual acuity, and there are flashes and spots in the eyes. If you do not consult a specialist after such symptoms, you can permanently lose your vision. Preosbyopia of both eyes most often occurs in people over 50 years of age.

The disease is dangerous because it develops almost asymptomatically. Very often it is found by chance during examination. The first symptoms begin to appear, as a rule, with retinal tears. These are, first of all, floating “spots” in front of the eyes, flashes.

For a long time, damage to the retina 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 floaters before the eyes or visual field defects in the form of scotomas. 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 the 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 irreversible vision loss. In rare cases, vision loss can be severe.

As the disease progresses, a person suffering from age-related macular degeneration begins to complain of decreased visual acuity and difficulty reading, especially in low light conditions. Patients may also notice the loss of individual letters during fluent reading, and distortion of the shape of the objects in question.

The complaint of changes in color perception is much less common. Unfortunately, more than half of patients do not notice 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 no longer effective.

Early signs of vision loss from AMD include:

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

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

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

In retinal pigmentary degeneration, the pigment epithelium and photoreceptor cells are affected. The first signs appear in early childhood. Characteristic specific symptoms: pigmented lesions (bone bodies), atrophic optic disc and narrowed arterioles.

Pigmentary degeneration

With Leber congenital amaurosis, blindness is observed from birth or children lose vision before age 10. Features: lack of central vision, nystagmus, keratoconus, strabismus, etc. Various degenerative foci are identified throughout the fundus (white and pigmented salt and pepper type, bone bodies), the optic disc is pale, the vessels are narrowed.

X-chromosomal juvenile retinoschisis refers to hereditary vitreochorioretinal dystrophies. In this case, retinal dissection occurs, cysts form on the periphery, into which hemorrhages can occur. In the vitreous body there is hemophthalmos, strands that can lead to retinal detachment.

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

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

Characteristic sign on the fundus there is a “bull’s eye” in the central zone, that is, a dark area with a light ring, surrounded by rounded hyperemia. Symptoms include decreased visual acuity by age 20, impaired color vision and spatial contrast sensitivity.

Stargardt disease

Best's yolk dystrophy - a yellowish lesion resembling the yolk of an egg forms in the macular area. At the age of approximately 10-15 years, decreased vision, distortion of the shape of objects, and “fog” before the eyes appear. Both eyes are affected to varying degrees.

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

Age-related macular degeneration

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

Drusen are located under the pigment epithelium and have a yellowish-white color; they may proliferate into the vitreous body. There are soft (with unclear boundaries), hard (with 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. Quickly leads to blindness.

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

In the early stages, retinal dystrophy is practically asymptomatic, which makes it difficult to diagnose at the very beginning of the process. When dystrophy has already progressed, the following symptoms can be identified in all types of the disease:

• decreased quality of vision;
• increasing limitation of the field of vision;
• loss of image areas, appearance of scotomas;
• perception of images with distorted contours and shapes of objects;
• significant loss of vision in low light;
• color vision disorder;
• changes in the perception of distances to observed objects and incorrect assessment of their sizes;
• the appearance of black dots, colored spots, sparkles, and flickering before the eyes.

Such symptoms are a reason to immediately contact an ophthalmologist, even if only one or several of them appear.

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

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

Leber 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 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-chromosomal retinoschisis is a chorioretinal dystrophy. Its peculiarity is that there is a gradual dissection of the retina and the formation of cystic formations on its periphery.

Over time, chorioretinal dystrophy can lead to hemorrhages 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. Thus, the clinical picture of myopia and pigmentary dystrophy appears simultaneously. In addition, preretinal membranes appear against the background of intact vitreous.

Goldman-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 age 5 years.

Stargardt disease is characterized by localization of the lesion in the macular region. Changes are observed in the fundus of the eye, which are called the “bull’s eye” symptom. The disease is characterized by loss of vision up to 20 years, which is preceded by impaired color perception and decreased visual acuity.

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

If you have these symptoms, you must contact an ophthalmologist as soon as possible, otherwise you may lose your vision.

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

To the primary signs of atrophy optic nerves include:

If any of the above symptoms are detected, you must consult an ophthalmologist to preserve your vision and stop the development of the disease.

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

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

Symptoms of dystrophy depend on its type. Thus, peripheral retinal dystrophy can occur without any symptoms for a long time, so it is usually diagnosed completely by accident. The first signs (“floaters” and flashes) appear only when ruptures appear.

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

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

Symptoms of retinal dystrophy are the following:

• floating “spots” before the eyes;
• flashes of light;
• distortion of straight lines in chorioretinal retinal dystrophy;
• loss of areas of the visual field;
• decreased visual acuity;
• blurred vision;
• change in color perception;
• twilight vision impairment.

If you experience similar symptoms, be sure to consult a specialist. Preventing a disease is much easier than dealing with the consequences.

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

Patients with symptoms of retinal dystrophy often complain of double vision 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 instrument can allow you to examine areas that are inaccessible to an 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 practically painless, but unpleasant for the patient.

Upper eyelid ptosis can be corrected with surgery.

When initial changes are detected, the patient should be constantly monitored by an ophthalmologist and photographs of the fundus should be taken with a photoslit lamp.

Modern medicine has the ability to diagnose the disease using special digital equipment, which allows you to obtain a three-dimensional digital image of the eyeball area. If using this method it is possible to identify areas susceptible to dystrophy, the specialist clearly assesses the size of the problem area in proportion to the total area of ​​the eyeball.

How to treat eyelid xalthesma can be found here.

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

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

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

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.

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

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

The 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 type of AMD and treatment method.

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 are mandatory.

At the same time, its structure and thickness can be assessed and observed over time during treatment. And fluorescein angiography allows you to assess the condition of the retinal vessels, the prevalence and activity of the dystrophic process and determine indications or contraindications for treatment.

These studies are the gold standard in diagnosing 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 tests are performed.

• 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.
• To study the width of the field of view and identify outlier areas in it, the perimetry method is used.
• Refractometry is used to measure the refractive index.
• Fundus examination (ophthalmoscopy) is performed under medicinal mydriasis.
• To identify eye pathologies, biomicroscopy is performed.
• To assess the bioelectrical activity of the layers of the retina, electroretinography is performed.
• To assess the condition of the retinal vessels and register hemorrhages, fluorescein angiography is performed.
• Ultrasound examination of the eye and tomography of the retina may also be performed.

Retinal dystrophy requires examinations such as:

A simple vision test can help identify the disease.

To diagnose retinal dystrophy, the following examinations are necessary:

1. Visual field examination;
2. Study of color perception;
3. Visual acuity testing;
4. Fundus examination using a Goldmann lens;
5. Fluorescein angiography (examination of eye vessels);
6. Ultrasound and electrophysiological examination of the eyes;
7. Tests to determine the state of the body's metabolism.

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

• get examined by an ophthalmologist;
• determine visual acuity;
• evaluate color perception;
• dilate the pupil and examine the fundus using a three-mirror Goldmann lens;
• perform coherent tomography of the eye;
• 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 computer perimetry, and fluorescein angiography of the blood vessels of the fundus. 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.

Assessing the capabilities of the visual analyzer

Visual impairment has an adverse impact on the usefulness of almost all categories of life, but the degree of this impact varies.

A person’s ability to move, self-care, orientation, and communicate mainly depends on the state of basic visual functions—acuity and field of vision. In progress medical and social examination visual functions are determined by mono- and binocular presentation of test tests, but the degree of their impairment, which influences the determination of the presence and severity of disability, is assessed primarily by the state of the functions of the better-seeing or only eye under conditions of tolerable (optimal) correction.

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

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

Treatment

Today, 3 treatment methods 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.

At initial signs 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 drugs to strengthen and expand the blood vessels of the eye and regulate the metabolic process;
• vasodilators;
• retrobulbar corticosteroids;
• diuretics;
• biogenic stimulants;

There are also physical methods therapy:

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

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

In the wet form of PCRD, surgery is performed to remove accumulated fluid in the retina. The last stage is the implantation of “energy” magnet implants into the area 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 lasecoagulation. Using a laser, the damaged retina is cauterized to the tissue connections of the eye in the required location and to the required depth. The laser action occurs in a targeted and selective manner, without damaging healthy tissue around the resulting dystrophy.

In order to identify retinal dystrophy, the treatment of which absolutely cannot be delayed, it is necessary to perform ophthalmological 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 full information about the condition of the retina and optic nerve. Carrying out the necessary laboratory tests will tell you how metabolic processes occur.

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

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

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

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

Laser therapy involves cauterizing pathological vessels. The method prevents the spread of this disease, but under the influence of the laser a burn is formed that forms a scar. The area affected by the laser loses vision.

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

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

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

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

An infusion of Sophora japonica fruits is used as a traditional medicine. The medicinal liquid is infused for at least three months. To prepare the infusion, you need 0.5 liters of vodka, which is mixed with 50 g of Japanese sophora. Use one teaspoon of infusion per glass of water three times a day.

Having discovered 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 the wrong time when qualified help is not available.

Therefore, it is much better to avoid such a development of events.

Retinal detachment is one of the leading causes of 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 of the eye to function as expected, lutein is needed. Human body does not produce it on its own, which indicates the need to compensate for its deficiency from food. Green foods are rich in lutein: peppers, spinach, etc.

Lutein is an excellent natural antioxidant that prevents the process of retinal destruction. 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.

Administration of injections

Intraocular injection of a medicinal substance is a method that helps slow down the wet form of the disease. Medicines belong to the group of intravetreal drugs necessary for anti-VEGF therapy, which is aimed at suppressing the activity of a certain protein. Administration 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, degenerative 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 stretches, which leads to dystrophy.

Modern treatment This 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.

AMD cannot be completely cured. However, the progression of the disease can be slowed down, stopped, and sometimes even improved.

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

The following vegetables and fruits are key to eye health: carrots, pumpkin, zucchini, squash, 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 sufficient in omega-3 fatty acids and lutein.

Large-scale studies have found that a healthy diet and 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 because smoking increases your risk of developing AMD. Fight excess weight and high blood pressure. Enlarge 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 laser photocoagulation of the retina, photodynamic therapy and injections of drugs into the eye.

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

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

AMD is characterized by progressive deterioration of central vision and irreversible damage to the macular area. 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 can begin to develop after 5-8 years.

Often, the patient does not immediately notice problems with vision, since at the initial stage the better seeing eye takes on all the visual load.

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

If vision loss is caused by age-related macular degeneration, then glasses, unfortunately, will not help. Here we can compare the eye to the system of a film camera. In this case, glasses will act as a lens, and the retina will act as a light-sensitive film.

Defects and damage to the film will not allow you to get high-quality photographs, no matter how strong the lenses are. It’s the same 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 type of dystrophy, treatment is prescribed. Treatment is almost always symptomatic, since all degenerations, except secondary ones, are hereditary or predisposed.

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

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

Dosages and regimens for using 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, and vitamin complexes to improve eye nutrition may also be prescribed.

Local treatment is carried out using 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 necessarily prescribed 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, Dicoin);
• drops for the treatment of cataracts containing vitamins and other nutrients (Taufon, Quinax, Oftan-katachrome).

Physiotherapeutic methods are quite effective in combination with the use of medications. Most often, medicinal electrophoresis, phototherapy, electrotherapy, laser therapy, magnetic therapy, and venous blood irradiation with laser are prescribed.

Also used effectively surgery to eliminate the consequences of the degenerative process. According to 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 disappointing. In other cases, predicting 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, as well as the individual characteristics of the patient: the state of his vascular system, the speed of metabolic processes, and others.

Treatment with folk remedies is possible only with the approval of the attending physician, and is only an addition to the main therapy. Treatment at home is carried out using various herbal decoctions to strengthen blood vessels and provide better nutrition eyes, improving blood properties and the condition 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 a 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 issues.

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

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

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

Clopidogrel, Aspirin and other antiplatelet agents help reduce intravascular thrombus formation.

Vasodilating agents and angioprotective substances, such as No-shpa, Papaverine or Ascorutin, taken orally or injected into a vein, dilate and strengthen blood vessels.

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

Drugs that help improve microcirculation can also be used for treatment. A prominent representative of them is Pentoxifylline. It and other drugs from this group are usually injected directly into the ocular structures.

Retinolamine and other polypeptides obtained from the retina of animals (in particular cattle) can also be used in the treatment of dystrophy.

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 prescribed per year.

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

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

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

In relation to such a variant of the pathology as retinal pigmentary dystrophy, surgical treatment, as a rule, consists of a procedure for transplanting fibers of the eye muscles (namely the oblique and external rectus muscles) into the so-called suprachoroidal space. This helps to normalize the blood supply to the retina.

Currently, patients diagnosed with retinal pigmentary dystrophy can also be treated by installing specially designed retinal replacement implants.

Depending on the cause, form and severity of the disease, you can use conservative treatment, 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 to improve microcirculation. These medicines 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 appear in the retinal vessels can significantly aggravate the patient’s condition and also complicate treatment.
• Vasodilators. These drugs act on the vasomotor center or directly on the walls of blood vessels. They expand their lumen, as a result of which blood flow normalizes. It is not advisable to use drops that have a local effect.
• Parabulbar injections of polypeptides, which are made from bovine retina. These drugs improve the regenerative function of retinal cells, which significantly inhibits the development of the pathological process. The pigmented form responds well to this treatment.

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

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

Surgical treatment can be based on classical types of surgery or carried out using innovative technologies. Most effective method treatment is to use 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 eliminated.

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 carry out a full diagnosis to identify the cause of the pathology. After receiving the examination results, the doctor will prescribe the appropriate comprehensive treatment.

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

• improve blood circulation in blood vessels;
• increase restoration and metabolic processes in tissues;
• speed up cupping inflammatory process
• will improve the stability of the central nervous system.

Take medications strictly as prescribed, and do not self-medicate under any circumstances. Getting carried away alternative medicine, you are losing precious time when your vision can still be saved, especially since in this case traditional methods are completely useless.

Therapy is usually symptomatic and can halt the progression 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 dystrophy has already worsened. In this case, treatment is aimed at slowing the progression of dystrophy, strengthening the blood vessels and muscles of the eyes, and restoring metabolism in the eye tissues.

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

• Antioxidants;
• Angioprotectors;
• Corticosteroids;
• Vitamin preparations;
• Lutein-containing drugs;
• Vasodilator and vascular wall strengthening drugs.

You need to know that these drugs can only be effective in the early stages of retinal dystrophy.

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

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

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

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

Complications

Retinal dystrophy during pregnancy is treated with laser coagulation 4-5 weeks before the expected date of birth. The laser “cauterizes” the affected areas and blocks tears. Timely surgery to strengthen the retina 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 of the retina in the most vulnerable places, resulting in its strengthening; the procedure is bloodless, practically painless, but not entirely comfortable for the patient);
• photodynamic therapy;
• Anti-VEGF injections (a drug that inhibits the development of the degenerative process);
• vitamin therapy;
• physiotherapeutic procedures;
• vasoreconstructive surgery, which is aimed at restoring blood supply to the retina.

In any case, after an 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 chorioretinal retinal dystrophy, methods of photodynamic therapy, laser photocoagulation, and 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 intravenous administration photosensitizer substances. They are able to bind proteins of pathological vessels and stop the development of dystrophy. The photodynamic treatment regimen for retinal dystrophy is set individually, depending on the patient’s sensitivity to this type of therapy.

Laser treatment of retinal dystrophy is based on the technique 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 makes it possible to prevent the further spread of the process of retinal dystrophy.

In the treatment of retinal pigmentary dystrophy, mainly physiotherapeutic techniques are used: magnetic and electrical stimulation of eye tissue. Unfortunately, their effectiveness is not high. Vaso-reconstructive surgeries 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 method for treating retinal dystrophy avoids surgical opening of the eyeball. The procedure is performed on an outpatient basis and requires virtually no recovery period.

Diet and vitamin therapy are used as an auxiliary treatment for retinal dystrophy of all types.

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, increased nutrition is necessary, as well as wearing dark glasses. It is recommended to drink 3 times a day fish fat, eat liver in all forms - boiled, fried, even raw, and consume those foods that contain 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 the cooked liver is removed from the heat, the patient should lean over the pan.

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

In addition to heating, 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, detachment and retinal dystrophy3. High myopia (- 6.

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

Loss of visual fields6. Cumulative indications (in combination with developed preeclampsia, a combination of myopia and neurological pathology, and many others, 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 childbirth.

If a cesarean section is indicated for you, this means that there is a real threat of loss or significant deterioration of vision with an unknown prognosis for its recovery. Ask your doctor any questions you have and take care of yourself.

Be healthy.

Doctor Petrova A.V.

Risk groups and disease prevention

Most often, peripheral retinal dystrophy occurs in myopic people. This is explained by the increased length of the eye in myopic people, which entails tension on the retina and its thinning. Elderly people (65 and older) are also at risk.

Often it is peripheral retinal dystrophy that is the cause of decreased vision in old age. This group should also include people with the following diseases: diabetes mellitus, hypertension, atherosclerosis and some others.

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

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

Doctors identify several groups of people who are in a dangerous zone for 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 light colored irises (with a blue tint);
• Smoking;
• 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 inspection should be carried out once every two or three years.

It is important to completely give up 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 general health of the entire body.

Prevention

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

All vision problems can be solved with timely consultation with an ophthalmologist. A 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 are indicated for people who have a genetic predisposition to the disease and myopia.

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

When talking about prevention, we primarily mean the prevention of retinal ruptures and detachments. The main way to prevent these complications is timely diagnosis of peripheral retinal dystrophy in patients at risk, followed by regular monitoring.

Prevention of serious 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 see 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 tears of the retina, preventive laser coagulation of the retina is mandatory.

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

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

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

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

There is no prevention of congenital forms of dystrophy. 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, you need to eliminate the impact of negative factors on a pregnant woman, and also provide her with a complete diet that will contain everything necessary substances for her normal life and fetal development.

But you can avoid the age-related form of retinal dystrophy. To do this, you need to take all measures to prevent exposure to harmful radiation on the eyes, eliminate injuries and promptly treat diseases of other localizations. A special place is occupied by the treatment of those diseases that impair the patency of blood vessels.

Retinal dystrophy is a serious 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 varied, which determines the wide age range that is susceptible to this disease. The basis for success and a favorable outcome is timely diagnosis and early initiation of treatment.

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

There are several simple rules that must be followed if you want to quickly overcome pathology and restore the health of your visual organs.

• Regularly visit an ophthalmologist and oncologist;
• Treat infectious diseases in a timely manner;
• Stop smoking and drinking alcoholic beverages;
• Try to protect yourself from eye or head injuries;
• Monitor your blood pressure;
• In case of profuse bleeding, it is necessary to undergo a repeated blood transfusion procedure.

Preventive treatment includes taking the following medications:

• Antioxidants. These include vitamins C, E, beta-carotene, zinc. Long courses of these drugs are recommended.
• Rheology improving agents and angioprotectors.
• Angiogenesis inhibitors (Lucentis).

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

There are no treatments that can improve vision in dystrophy, but patients can benefit from low vision devices and timely prevention.

Prevention of retinal dystrophy includes:

• regular examinations by an ophthalmologist;
• undergoing examinations using professional ophthalmological equipment;
• regular visits to a specialist, especially for older people (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 a diagnosis of retinal dystrophy

Prognosis for treatment of retinal degeneration:

1. Dry form. The slow-onset form - up to several years - provides a delay for choosing effective treatment and preventing the development of severe complications. Danger: Moderate risk of retinal detachment. In 10-20%, the dry form turns into a wet form.
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 vision loss. The likelihood of retinal detachment is highest due to the accumulation of excess fluid, causing separation of the inner membrane.

When diagnosed with retinal dystrophy, making a prognosis regarding the preservation of visual function can be difficult. Due to the fact that this pathology is characterized by a progressive course, the prognosis in the event of its development cannot be considered favorable.

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

It should also be taken into account that, despite successful therapy, retinal macular degeneration may begin to progress again over time.

Peripheral taperetinal dystrophies.
The earliest change in the retina is the destruction of neuroepithelial cells, and primarily rods, until their disappearance. Changes that occur first in the peripheral part of the retina then spread to the central part. In rare cases, the central part of the retina is predominantly affected (central form of retinal pigmentary dystrophy) or a limited sector-shaped area of ​​the retina (sectoral form). Against the background of the disappearance of neuroepithelial cells, the number of glial cells and fibers increases, which fill the vacated space. Phagosomes disappear in pigment epithelial cells. Pigment cells migrate to the inner layers of the retina. Due to the proliferation of glial tissue and migration of pigment cells, blood circulation in the capillary network is disrupted.
Typically, both eyes are affected. The first symptom of retinal pigmentary dystrophy is decreased vision in the dark (hemeralopia), later visual field defects appear, visual acuity decreases, and the fundus of the eye changes. A characteristic visual field defect is a ring-shaped scotoma, which, as the disease progresses, spreads both to the center and to the periphery and leads to a concentric narrowing of the visual field (tubular visual field). Moreover, despite relatively high central vision, which can persist for many years, a sharp disturbance in orientation leads to disability. In the case of central and sectoral forms of retinal pigmentary dystrophy, a central and sectoral scotoma is identified, respectively.
Pigment deposits, narrowing of retinal arterioles, waxy atrophy of the optic disc are usually found in the fundus. Pigment deposits are located, as a rule, on the periphery of the retina (often around the veins) and have the appearance of typical pigment foci (the so-called bone bodies) or lumps, mosaics, spots. In the central form of pigmentary dystrophy, they are localized mainly in the central part of the retina, in the sectoral form, a sector-shaped arrangement of pigment in the fundus is noted. In rare cases, pigment deposits in the retina may be absent (retinitis pigmentosa without pigment). In the late stage of the disease, areas of choriocapillary atrophy are identified layer of the choroid proper of the eyeball. In some cases, retinal pigmentary dystrophy is accompanied by the development of complicated posterior cortical cataracts, glaucoma, myopia. The disease slowly progresses, ending in blindness in most cases.
Yellow-spotted fundus is a disease with an unknown type of inheritance that manifests itself at the age of 10-25 years. In the deep layers of the retina in the region of the posterior pole of the eyeball, yellow or yellowish-white spots are formed, usually discovered by chance during examination of the fundus. Visual functions are usually not impaired, except in cases of damage to the macular region of the retina, when visual acuity decreases and the ERG is not changed. Treatment is the same as for retinal pigmentary dystrophy.
Congenital stationary night blindness is inherited in an autosomal dominant, autosomal recessive manner, and can be sex-linked. Often combined with myopia. The main symptom is poor orientation in the dark. Visual acuity remains normal or decreases (0.7-0.4). The field of view is often unchanged, in some cases slightly narrowed. The fundus of the eye, as a rule, is without pathology; only when combined with myopia, the foveal reflex is absent and slight depigmentation of the retina is noted. Treatment is the same as for retinal pigmentary dystrophy.
Central taperetinal dystrophies are characterized by pathological changes in the central part of the fundus (2), a progressive decrease in visual acuity, and in the late stage the appearance of a central scotoma. With Best's dystrophy, visual acuity, despite gross changes in the macular area, can remain high for a long time and decreases only with the formation of an atrophic focus in the area of ​​the macula. Central T. Lead to decreased central vision. Peripheral vision and dark adaptation with central T. are not impaired. Treatment is the same as for peripheral tapetoretinal dystrophies.