Drusen of the optic disc symptoms. Drusen of the retina. Macular degeneration dry form. Prevention and treatment

The occurrence of soft drusen in the macular area is one of the manifestations of the "dry" form of age-related macular degeneration (AMD). Morphologically, soft macular drusen are deposits of amorphous material between the inner collagen layer of Bruch's membrane and the basement membrane of the retinal pigment epithelium. With prolonged existence, drusen can increase in size, begin to resemble large detachments of the retinal pigment epithelium (the so-called OPE-like drusen), which leads to a significant decrease in visual functions. In addition, numerous studies have shown that large soft confluent drusen increase the risk of transition to the "wet" form of AMD, which is characterized by the development of choroidal neovascularization (CNV) .

In 1971 Gass J.M. first reported that the method of laser coagulation (LC) of the retina promotes the resorption of drusen. Subsequently, this was repeatedly confirmed. To find out whether laser coagulation of drusen improves the visual functions of patients and whether it can prevent the development of CNV and geographic atrophy in the future, multicenter randomized controlled trials "The Choroidal Neovascelarization Prevention Trail Research Group" (CNPT) and "The Complications of Age-Atrophy" were conducted in the United States. Related Macular Degeneration Prevention Trial Research Group" (CAPT) . It was concluded that laser coagulation does not reduce the risk of developing CNV and geographic atrophy, and does not lead to improvement in visual function.

With the advent of new diagnostic methods, such as optical coherence tomography, electroretinography and microperimetry, it became possible to assess in more detail the morphological and functional state of the retina directly in the area affected by drusen. Microperimetry, being more accurate than visometry, a method of dynamic monitoring of the functional state of the retina in the "dry" form of AMD, made it possible to identify a decrease in the photosensitivity of the retina over the area of ​​soft macular drusen. With the use of these techniques, in recent years, reports have begun to appear in the literature about the effectiveness of laser treatment of soft macular drusen with a positive functional result.

Our previous studies have shown that laser coagulation of soft macular drusen leads to their regression, but does not improve visual functions, including retinal photosensitivity. However, during coagulation of very large drusen, we noticed that their fit leads to an improvement in functional parameters.

Target

Evaluation of morphological and functional results of threshold laser coagulation of OPE-like soft confluent macular drusen.

Material and methods

The study included 34 patients (39 eyes) with large confluent OPE-like soft macular drusen. 5 patients had bilateral OPE-like drusen, 20 patients had soft confluent drusen in the other eye, 10 patients had wet AMD, 1 patient had an atrophic form, 1 patient had CVD thrombosis, and 2 patients had cataracts. . The initial diameter of OPE-like drusen varied from 800 to 2500 µm, and their height varied from 130 to 380 µm. 23 eyes were included in the main group, where threshold laser coagulation of drusen was performed. Of these, direct LC was performed on 11 eyes, applying laser exposure directly to the drusen area. In 8 eyes, indirect LC was performed when coagulates were applied between the drusen. Mixed LC was performed on 4 eyes, when laser exposure was carried out both directly on the drusen and between them. The control group included 16 eyes, where the natural course of the disease was observed. The follow-up period was 6 months. up to 1 year. In some patients, the follow-up period was up to 2-3 years. Control examinations were performed after 3, 6 and 12 months. after treatment.

For treatment, an Nd:YAG laser coagulator with frequency doubling (Alcon, USA) was used. Radiation parameters: wavelength - 532 nm, pulse duration - 0.1 s, radiation power - 80-100 mW, spot diameter - 100 microns. The radiation power was selected individually in a remote area from the center of the macula until barely visible coagulates appeared.

All patients underwent a complete ophthalmological examination, including visorefractometry, near visual acuity testing, ETDRS visual acuity, tonometry, retinal biomicroscopy, fundus photography, optical coherence tomography (OCT) on a Cirrus tomograph by Carl Zeiss Meditec and microperimetry on the fundus microperimeter "NIDEK MP-1".

On OCT, in addition to the main parameters determined automatically by the device, the thickness of the neurosensory retina was measured over the largest OPE-like drusen. To do this, use the function of the measuring ruler and manually measure the distance from the inner limiting membrane to the retinal pigment epithelium. In addition, using OCT, the condition of macular drusen after laser coagulation was assessed as "complete regression", "partial regression", "no dynamics" or "increase in the size and/or number of drusen".

When performing microperimetry, the Macula 20° 0dB study protocol was used and the average retinal photosensitivity was recorded at all 76 points measured during this protocol, and the average retinal photosensitivity was additionally measured at the central 28 and 12 points (Fig. 1).

Statistical analysis used nonparametric methods of data processing. The Wilcoxon matched group test was used to test the hypothesis about the equality of two average dependent samples, and the Mann-Whitney U test was used for independent samples. When assessing the significance of differences between groups, the indicators of which were presented as a percentage, the agreement criterion?2 was used.

Results and discussion

In the treatment group already starting from 3 months. observations, there was a partial regression of drusen in most cases (81%), while in the control group, drusen in 81.3% did not change (Fig. 2). By the follow-up period of 1 year in the treatment group in 88.9% there was a complete regression of macular drusen, in other cases their partial regression was observed (19%). In the control group, in 50% of cases, drusen remained unchanged, in 20% there was an increase in their number, and partial (20%) or complete (10%) regression was observed. Differences between groups were statistically significant (ro<0,05).

The frequency and timing of regression of drusen were the same when performing various laser coagulation techniques. However, almost all patients who underwent indirect laser coagulation complained in the first month after treatment of the appearance of multiple relative scotomas in the field of vision, which gradually decreased by 2–3 months. observations. In our opinion, this is due to the fact that with the indirect technique, laser coagulation is applied between the drusen along the healthy retina, where light sensitivity is preserved, and its damage leads to temporary functional losses. In the direct technique, laser coagulation is applied directly over the area of ​​the drusen, where the light sensitivity of the retina is already reduced, so patients subjectively do not notice the consequences of laser exposure. That is why we consider direct laser coagulation of drusen to be the most preferable.

The average values ​​of the volume and thickness of the retina in the macular region, the values ​​of the thickness of the retina in the center of the macula (in the 1 mm zone), measured automatically by the device, did not differ statistically significantly between the two groups, as well as within each group by the follow-up period of 6 months. (po>0.05). Initially, the thickness of the neurosensory retina over OPE-like drusen was significantly reduced and averaged 164±10 µm in the main group and 167±12 µm in the control group. By 6 months observations, the average value of the thickness of the neurosensory retina over the largest OPE-like drusen in the main group, where drusen regressed, significantly increased from 164±10 to 225±8 µm (p0=0.03) (Fig. 3). Compared with the control group by 6 months. observations, the thickness of the neurosensory retina was greater (Fig. 4).

By the follow-up period of 1 year, in the treatment group, in one case, the development of geographic atrophy in the foveolus occurred after the attachment of soft macular drusen. There were no cases of development of choroidal neovascularization in treated patients, and in the control group, a "wet" form of AMD developed in one eye.

Statistically significant difference between the average values ​​of visual acuity for distance, near and according to the ETDRS method was not revealed when comparing between the two groups, as well as within each group at all follow-up periods (po<0,05). На рисунке 5 представлена динамика остроты зрения вдаль, на основании которой мы можем говорить лишь о тенденции сохранения или даже небольшого увеличения остроты зрения вдаль после лазеркоагуляции ОПЭ-подобных мягких макулярных друз по сравнению с контрольной группой.

The initial average light sensitivity of the retina in all 76 points was reduced and amounted to 12.7±0.7 dB in the main group and 11.8±0.9 dB in the control group. The lowest numbers were recorded in the central 12 points above the area of ​​macular drusen (8.4±1.3 dB in the main group and 6.8±1.1 dB in the control group). When comparing the two groups, already starting from 3 months. observations, microperimetry showed that the light sensitivity of the retina at the central 12 points increased statistically significantly in the treatment group compared to the control group (Fig. 6). It should be noted that in the absence of improvement in visual acuity, but with an increase in the photosensitivity of the retina, patients noted a positive trend, expressed in a decrease in metamorphopsia and an increase in reading speed.

Our observations have shown that the duration of the existence of OPE-like drusen is very important for predicting the functional outcome of treatment. When the drusen material is under the retina for a long time, atrophy of the pigment epithelium occurs in the central zone, which irreversibly reduces the visual acuity of the patient. Ophthalmoscopically, against the background of yellowish material of soft macular drusen, it is not always possible to note the presence of an already existing atrophy of the pigment epithelium. However, this is indirectly indicated by the initially low visual acuity, the presence of a large number of areas of hyperplasia of the pigment epithelium, as well as the presence of characteristic signals on optical coherence tomography.

Figure 7 shows an example of successful laser coagulation of large OPE-like soft macular drusen with their gradual complete regression and with a good functional result that lasts for two years. The initial visual acuity in this patient was high (vis=0.9), which indicates that the atrophy of the pigment epithelium has not yet formed. Despite the high visual acuity, the light sensitivity of the retina was significantly reduced in the central zone and amounted to 6.4 dB in the central 12 points. After laser coagulation by a direct method for 6 months. there was a complete regression of the friends. By the follow-up period of 1 year, visual acuity remained as before 0.9, but the light sensitivity of the retina at the central 12 points increased to 13.5 dB. The patient noted the complete disappearance of metamorphopsia and improvement in the quality of vision. 2 years after treatment, visual acuity of 1.0 was recorded, and the light sensitivity of the retina at the central 12 points was 15.3 dB.

Figure 8 shows an example of complete regression of large OPE-like drusen, however, with a significantly worse functional result, since at the time of treatment, the drusen existed for a long time under the retina, and atrophy of the pigment epithelium in the foveolus had already formed. This is evidenced by the initially lower visual acuity of the patient (vis=0.4), as well as characteristic signals on optical coherence tomography both before and after treatment. Already by 3 months. observations, there was a complete regression of OPE-like drusen. By 6 months observation, visual acuity remained as before 0.4, but the light sensitivity of the retina in the central 12 points increased from 4.0 to 9.2 dB, and the patient subjectively noted a positive trend. Unfortunately, despite the complete regression of the drusen, the already formed atrophy of the pigment epithelium gradually increases and geographic atrophy forms in the foveolus, which is best seen on the infrared image of the fundus (Fig. 8e).

conclusions

1. Threshold laser coagulation of large soft macular drusen leads to their regression in 88.9% of cases, which is accompanied by an increase in the thickness of the neurosensory retina and an improvement in the photosensitivity of the retina.

2. The most preferred technique is direct laser coagulation, since it does not cause iatrogenic damage to areas of the retina not affected by drusen and complaints of relative scotomas in the first months after treatment.

3. Early treatment leads to better functional outcome.

Drusen of the optic disc occurs as a result of a hereditary anomaly in the genome or the influence of various factors, which contribute to the deposition of protein inclusions in the nerve fibers. In this case, the patient may not feel any manifestations of the disease for a long time, however, in severe cases, loss of visual fields, a violation of color perception and other manifestations appear. There is no specific treatment for this pathology, only supportive therapy is possible.

Pathological inclusions can be detected using ultrasound.

Causes and course of pathology

Drusen of the ONH can result from a genetic abnormality and are inherited in an autosomal dominant manner. That is, the disease is transmitted from a sick parent to all children. Pathology can also be observed as a result of exposure to any pathological factors. Drusen appear in both eyes and this disease mainly affects representatives of the European race. At birth, this anomaly is not visible, and its first signs appear at about 12 years of age. In this case, the optic nerve head changes its appearance and many vessels grow into it, and pathological inclusions also appear. Drusen are protein inclusions in nerve fibers, as a result of which the functional activity of nerve endings is disrupted. Over time, calcium salts are deposited in these foci, which causes systemic eye diseases.

Pathology is most often diagnosed in young people under the age of 30 years.

Drusen on the retina and optic nerve arise as a result of exposure to the human body of such factors:

  • intoxication;
  • the presence of a focus of chronic bacterial infection;
  • diabetes;
  • intrauterine infections;
  • eclampsia during childbirth;
  • intranatal hypoxia;
  • trauma;
  • prolonged inflammation of the eyeball.

Main symptoms

Drusen of the optic disc provokes the development of such characteristic clinical signs in a patient:

  • visual acuity may be normal or slightly reduced;
  • lack of color sensitivity;
  • presence of spontaneous venous pulse;
  • increase in the size of the blind spot;
  • the appearance of livestock;
  • photopsia in the form of a veil and flashes of light;
  • gradual increase in symptoms.

Diagnostic methods


The study is absolutely safe and does not require prior preparation.

It is possible to suspect the presence of optic disc drusen by chance during a routine ophthalmoscopic examination or when a patient develops complaints characteristic of this disease. To confirm the diagnosis, it is recommended to conduct an ultrasound diagnosis of the eyeballs with visualization of the optic nerve. You can also use computed tomography, which will reveal smaller elements of the inclusions. Visiometry and the establishment of visible fields of view are recommended. The delivery of a general and biochemical blood test is shown.

9-04-2012, 14:04

Description

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

ICD-10:

H35.3 Macular and posterior pole degeneration.

Abbreviations: AMD - age-related macular degeneration, RPE - retinal pigment epithelium, SLO - scanning laser ophthalmoscope, TTT - transpupillary thermotherapy. FAG - fluorescein angiography, PDT - photodynamic therapy, ERG - electroretinography. ETDRS - Early Treatment Diabetic Retinopathy Study Research Group (Research group on the study of early treatment of diabetic retinopathy).

Epidemiology

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

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

? General strickenness of the population this pathology increases with age:

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

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

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

AMD can lead to a pronounced decrease in visual acuity and loss of the central portions of the visual field. The most significant functional disorders are characteristic of subretinal neovascularization with subsequent RPE atrophy, especially if the pathological process captures the fovea.

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

Risk factors

There is a clear relationship between arterial hypertension and AMD, atherosclerotic lesions of blood vessels (especially carotid arteries), blood cholesterol levels, diabetes mellitus, overweight.

There is a direct relationship between smoking and AMD.

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

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

At present, studies of the genetic predisposition for the development of AMD are ongoing (in particular, the responsible genes ARMD1 , FBLN6 , ARMD3 have been identified).

Prevention. Patients with AMD should be advised to give up smoking, fatty foods, and less exposure to direct sunlight. In the presence of concomitant vascular pathology, measures aimed at its correction are necessary. Issues of vitamin therapy and recommended doses of trace elements will be discussed below. In recent years, prophylactic laser coagulation of the retina in the presence of multiple drusen has been discussed.

Screening

AMD should be suspected in an elderly patient with complaints of reduced visual acuity, difficulty in reading, especially in low light conditions. Sometimes patients notice loss of individual letters during fluent reading, metamorphopsy. Complaints about changes in color perception, deterioration of twilight vision are much less common. Examination includes visual acuity testing, biomicroscopy (which may reveal other possible causes of symptoms such as age-related cataracts), ophthalmoscopy (including a slit lamp using aspherical lenses), and perimetry. We can also recommend a study of color perception (monocularly), the Amsler test.

It is necessary to be aware of the possibility of AMD in patients who fail to achieve high visual acuity after uncomplicated cataract extraction.

Patients over 55 years of age should have the macular area examined during routine medical examinations (i.e., include ophthalmoscopy with a wide pupil in the examination plan).

Diagnosis

AMD is diagnosed with the following symptoms(one or more): the presence of solid drusen; the presence of soft drusen; strengthening or weakening of RPE pigmentation; atrophic foci in the macula (geographic atrophy); neovascular macular degeneration - neovascularization of the choroid, serous or hemorrhagic detachment of PES and the subsequent formation of cicatricial foci in the macular zone.

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

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

? Soft Druse larger in size, their borders are fuzzy. The risk of their progression is much higher. They can coalesce and cause RPE detachment. If the drusen disappear, this most often indicates the development in this zone of atrophy of the outer layers of the retina (including RPE) and the choriocapillary layer. If soft drusen are identified, the ophthalmologist should recommend that the patient perform self-monitoring using the Amsler grid and consult an ophthalmologist if any new symptoms appear, since this type of drusen is associated with a high risk of visual impairment (due to the possibility of developing geographic atrophy or choroidal neovascular membrane).

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

? Druses in dynamics may undergo the following changes:

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

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

? Geographic atrophy of RPE- advanced form of dry sclerotic macular degeneration. In the fundus of the eye, foci of geographic atrophy are identified as clearly defined areas of depigmentation with well-defined large choroidal vessels. In this case, not only RPE suffers, but also the outer layers of the retina and the choriocapillary layer in this zone. Geographic atrophy can be not only an independent manifestation of AMD, but also occur as a result of the disappearance of soft drusen, flattening of RPE detachment, and even regression of the focus of choroidal neovascularization.

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

Serous neuroepithelial detachment is often combined with RPE detachment. At the same time, there is a greater prominence of the focus, it has a disc-shaped shape and less clear boundaries.

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

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

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

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

Suspicion of the presence of subretinal neovascularization should cause the following ophthalmoscopic manifestations: retinal edema in the macular zone, the presence of solid exudates, RPE detachment, subretinal hemorrhages and / or hemorrhages in the retinal tissue. Hard exudates are rare and usually indicate that the subretinal neovascularization has formed relatively long ago.

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

? Discoid scar focus- the final stage of development of subretinal neovascularization. Ophthalmoscopically in such cases, a gray-white discoid focus is determined, often with pigment deposition. The size of the focus can be different - from small (less than 1 diameter of the optic disk) to large foci, which can exceed the entire macular area in area. The size and localization of the focus are of fundamental importance for the preservation of visual functions.

Classification

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

? "Dry" form It is characterized primarily by slowly progressive atrophy of the RPE in the macular area and the choroid located below it, which leads to local secondary atrophy of the photoreceptor layer of the retina. In other words, the non-exudative form is characterized by drusen in the macular area of ​​the retina, RPE defects, pigment redistribution, atrophy of the RPE and the choriocapillary layer.

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

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

? late stage. RPE detachment, RPE rupture, choroidal neovascularization, discoid (fibrovascular) scar, and RPE geographic atrophy are characteristic.

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

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

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

? mixed choroidal neovascularization. There are such options: “mostly classic” (when the “classic” lesion in area is at least 50% of the entire focus) and “minimal classic” (with it there is also a “classic” lesion, but it is less than 50% of the entire focus).

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

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

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

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

Anamnesis

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

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

General diseases (especially arterial hypertension, atherosclerosis of cerebral vessels).

Burdened heredity for AMD.

Acquaintance with the available medical documentation, including previous entries in the patient's outpatient card, certificates of hospitalizations, etc. (the course of the disease).

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

Survey

Determination of visual acuity with optimal correction.

Assessment of the central field of view.

Assessment of color perception using Yustova's or Rabkin's tables.

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

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

Documentation of the state of the macula, preferably by color stereophotography of the fundus.

Performing fluorescein angiography and/or indocyanine green angiography.

If retinal edema is suspected, an optical coherence tomography or macular examination using a Heidelberg retinal tomograph (HRT II) is recommended.

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

Assessment of visual acuity and refraction

Visual acuity with optimal correction should be assessed at each visit. The conditions under which the study is conducted should be standard.

When examining in a clinic or hospital, they usually use Sivtsev tables or projectors of test marks. Taking into account the effect of "recognition" of alphabetic symbols, it is advisable to use Landolt rings in this case.

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

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

Central visual field assessment

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

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

? Amsler test can be recommended to patients for daily self-monitoring to facilitate early detection of metamorphopsias or scotomas. The patient should be instructed in detail about the rules of the test (most importantly, teach patients to check each eye separately, closing the other eye) and advise him to contact an ophthalmologist if any new changes are detected as a matter of urgency. Assessment of the state of the field of view. It is preferably carried out using computer static perimetry with the inclusion of an assessment of the foveal photosensitivity threshold in the testing strategy. However, with low visual acuity, computerized perimetry may not be feasible. In such cases, the usual kinetic perimetry is used, but with an appropriate choice of the size and brightness of the object.

The evaluation of color perception is carried out using the Yustova or Rabkin tables according to the standard method.

Ophthalmoscopic assessment of the condition of the fundus

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

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

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

Documentation of the condition of the macula can be carried out in various ways, ranging from simple sketching of changes to the most preferred color stereophotography of the fundus. Currently existing digital photography systems allow not only to avoid the problems of "aging" of prints (for example, previously performed by polaroid systems), but also to edit the resulting images, superimpose them on each other, store and transmit information in digital form. Fundus X-rays should be taken in both eyes because AMD is often bilateral, even if visual acuity loss and other functional findings are present in only one eye.

Fluorescein angiography

In many cases, the diagnosis of AMD can be made based on clinical findings. However, fluorescein angiography (FAG) is an extremely valuable additional diagnostic method in this disease, as it allows more accurate determination of structural changes and assessment of the dynamics of the pathological process. In particular, it is of decisive importance in deciding the question of treatment tactics. Preferably done within 3 days. after the first examination of a patient with suspected subretinal neovascularization, since many membranes increase in area quite quickly (sometimes by 5-10 microns per day). Taking into account the possibility of the transition of the "dry" form to the "wet" one, during the dynamic observation of patients with drusen (especially in the presence of "soft" drusen), FAG is recommended to be performed at a 6-month interval.

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

The patient signs the informed consent.

An intradermal test for fluorescein is performed.

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

Before the study, color photographs of the fundus are performed, and then, in some cases, photographing in redless light (with a green light filter).

5 ml of 10% fluorescein solution is injected intravenously.

Photographing is carried out according to the generally accepted method.

If there are signs of subretinal neovascularization in one eye, photographs of the other eye in the middle and late phase should also be taken to identify possible neovascularization (even if there is no suspicion of its presence on the clinical picture).

? Evaluation of the results of fluorescein angiography

Druze

Hard drusen are usually punctate, give early hyperfluorescence, fill at the same time, and fade late. There is no sweating from the druze.

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

Fluorescein is absorbed by drusen from choriocapillaries.

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

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

? Subretinal neovascularization

For fluorescent angiographic picture of classic choroidal neovascular membrane the following:

Newly formed subretinal vessels fill earlier than retinal vessels (in the pre-arterial phase). These vessels quickly begin to glow brightly and look like a network in the form of a "lace" or "cart wheel". It should be borne in mind that if there are hemorrhages, they can partially mask subretinal neovascularization.

Weakening of fluorescein from newly formed vessels may be noted, increasing during the study.

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

With latent choroidal neovascularization, gradually, 2-5 minutes after the injection of fluorescein, "mottled" fluorescence becomes visible. Hyperfluorescence becomes more significant when perspiration is added, even dye accumulations in the subretinal space are noted, which do not have clear boundaries. Re-evaluation of the same area of ​​the fundus in the early phases of FAH does not reveal the source of sweating.

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

Differential Diagnosis

Differential diagnosis is carried out:

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

? In "wet form"

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

With a traumatic rupture of the retina (usually in one eye; a history of eye injury, most often goes concentrically on the optic disc);

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

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

And also with the friends of the optic nerve disc; tumors of the choroid; cicatricial foci after laser coagulation; with inflammatory chorioretinal pathology.

Treatment

Laser surgery

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

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

Tell about the likely course of the disease, prognosis, goals of intervention, advantages and risks of alternative treatments.

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

The patient should be explained that he will most likely retain peripheral vision, emphasizing that many patients with severe loss of central vision in both eyes can independently cope with many tasks of everyday activities.

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

The patient in the next few days after the intervention should be sent to an institution dealing with the problems of helping the visually impaired; it may be necessary to recommend the passage of a medical and labor examination to establish a disability group.

Usually, the results of the examination on the second day after the intervention are considered fundamentally important, when edema and visual impairment as a result of treatment are maximum. Patients should be told that visual acuity will not decrease after the second day. If vision deteriorates and distortions increase, the patient should, without delay, contact an ophthalmologist.

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

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

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

Patients with fresh subfoveolar choroidal neovascularization under the center of the fovea (no previous laser treatment) or recurrent subfoveolar choroidal neovascularization (previous laser treatment, relapse under the center of the fovea). (In the latter cases, photodynamic therapy is currently recommended instead of laser photocoagulation.)

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

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

2. Immediately before the intervention, the surgeon again looks through the FAG, while accurately determining the boundaries of the impact.

3. The entire zone of choroidal neovascularization is covered with intense coagulates.

4. The boundaries of the effected impact are compared with the landmarks on the FAG. If the performed intervention looks inadequate, it can be supplemented immediately.

5. Then photographs of the fundus are taken.

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

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

? Postoperative follow-up

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

Examinations in the postoperative period continue after that after 1.5, 3 and 6 months from the moment of intervention, and then 1 time in 6 months.

If you suspect a recurrence of the subretinal neovascular membrane.

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

Laser coagulation for prophylactic purposes in soft drusen

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

Photodynamic therapy

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

results

Therapeutic effect should be made within a week after performing fluorescein angiography, after which a decision was made on the need for intervention.

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

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

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

AMD with "predominantly classical" (when the "classic" lesion is more than 50% of the entire focus) or with "hidden" subfoveal located choroidal neovascularization;

Juxtafoveal lesion, located so that when performing laser coagulation, the center of the foveal avascular zone would necessarily be affected;

? "hidden" choroidal neovascularization with a focus size of more than 4 areas of the optic disc; photodynamic therapy is recommended only for very low visual acuity (if the diameter of the focus exceeds 5400 microns, the patient should be explained that the goal of treatment is only to preserve the field of view);

If the lesion is expected to progress rapidly, or if visual acuity without treatment may soon fall below "useful" (that is, allowing the patient to do without outside help).

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

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

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

Transpupillary thermotherapy

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

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

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

Surgical treatment of age-related macular degeneration

Removal of subretinal neovascular membranes

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

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

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

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

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

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

Pigment epithelial cell transplantation. Pilot studies are being carried out on the transplantation of pigment epithelium cells. At the same time, issues of tissue compatibility remain unresolved.

Macular translocation

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

? First, a subtotal vitrectomy is performed., and then completely or partially exfoliate the retina. The operation can be performed by performing a retinotomy around the entire circumference (360°) with subsequent rotation or displacement of the retina, as well as by forming folds (that is, shortening) of the sclera. Then the retina is "fixed" in a new position using an endolaser, and the neovascular membrane is destroyed using laser coagulation. Pneumoretinopexy is performed, after which the patient must observe a forced position during the day.

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

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

Medical therapy

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

Antioxidants

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

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

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

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

There are also drugs containing blueberry extract("Mirtilene forte").

Angiogenesis inhibitors

Experimental and clinical studies have shown that the most important factor in the development of neovascularization in AMD is endothelial growth factor VEGF (vascular endothelial growth factor). To date, pegaptanib and ranibitzumab, which have anti-VEGF activity, have been proposed for clinical practice.

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

? Ranibicumab (RhuFabV2) is a monoclonal antibody that selectively blocks all isoforms of VEGF. Intravitreal injections of drugs are made 1 time in 4 weeks. A Phase III clinical trial is currently underway.

Corticosteroids

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

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

Combined approaches

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

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

Suggested Approaches

Research is ongoing to find adequate interventions for all forms of AMD. And already completed phase III clinical trials make it possible to develop new treatment algorithms. Thus, many authors believe that:

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

In the presence of a subfoveal lesion with "minimal-classic" choroidal neovascularization, PDT or the angiogenesis inhibitor pegaptanib may be used;

With a juxtafoveal lesion located in such a way that the center of the foveal avascular zone will necessarily be affected during laser coagulation, PDT can also be used;

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

? To prevent the development of exudative AMD complex nutritional supplements are used (for example, Okuvayt Lutein or Lutein-complex).

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

Traditional symptomatic therapy

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

With the "dry" form of AMD, you can use vinpocetine 5 mg 3 times a day orally in courses of 2 months or pentoxifylline 100 mg 3 times a day orally in courses of 1-2 months.

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

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

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

Further management

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

Patients with low visual acuity can be recommended so-called aids for the visually impaired. These are devices that magnify images and enhance the illumination of objects in various ways. Among such devices can be named special magnifying glasses, loupes with various types of mounts, closed-loop television systems, and various digital cameras with projection of images on a screen.

Forecast

In patients in the absence of therapy, a significant decrease in visual acuity in the period from 6 months to 5 years can be expected in 60-65% of cases. Often the lesion is bilateral and can lead to visual disability.

The goal of therapeutic interventions in AMD in the presence of choroidal neovascular membranes is achieving stabilization of the pathological process rather than improving vision!

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

Central retinal dystrophy is the main cause of visual impairment in a person over forty years of age. As a result, this disease is often called senile dystrophy.

In order to timely treat such a disease as the central type of dystrophy or peripheral retinal dystrophy, it is necessary to remember the first symptoms of the development of the pathological process at the initial stage of its course.

Central dystrophy - is the disease dangerous?

Macular degeneration, or in other words central degeneration, is a dangerous disease. The disease can occur in one eye, but quickly move to the other. Moreover, it can occur both independently and under the influence of other diseases. Loss of vision, if macular degeneration has occurred, can be even at a young age. The first period of the disease may be asymptomatic. Therefore, to prevent the onset of the disease, it is necessary to undergo an examination by an ophthalmologist as often as possible.

The retinal dystrophy that appeared in the patient suggests that in this case there are serious disturbances in the organization of nutrition, as a result of which the retina of the eye suffers. And the definition of "senile" will tell you that peripheral retinal dystrophy, or dystrophy of the central zones, is directly related to the effect of age-related changes in the body, including the human eye. Central dystrophy develops as a result of pathological vascular changes or hypertension, atherosclerosis.

Human eyes are arranged like a camera. The lenses that are in front of the camera transfer the images to the back of the camera. The eyes do the same. The retina of the eye is a visual tissue that contains certain zones: the macular, that is, the central zone, and the periphery zone. The macular area occupies the central area together with the optic nerve. Its minor part, namely the retina, helps us to see.

Types of retinal dystrophy

Retinal dystrophy is conventionally divided into the following categories:

  • congenital, or hereditary (for example, pigmented variety);
  • acquired.

Hereditary dystrophy includes:

  1. Pigmentary dystrophy. The pigmented type of dystrophy is associated with poor performance of the receptors that are responsible for vision at dusk. Pigmentary dystrophy is a fairly rare disease at the present time.
  2. Point white retinal dystrophy, which appears in childhood and progresses seriously as a person grows.

Pigmented and dotted white dystrophy of the eye, as a rule, are age-related, i.e. are caused by aging of the body and appear in combination with cataracts.

Retinal dystrophy is characterized by the possibility of developing such categories as:

  • central dystrophy;
  • peripheral type of disease (otherwise pvhrd).

Peripheral dystrophy often appears with myopia or an eye injury (not including the central region of the retina). In this case, the appearance of specific "flies" in the eyes is possible.

If the patient has a seriously impaired retina, treatment should be carried out after a scrupulous study of the causes of such a disease. The reasons may be:

    1. Low insulin production in the patient's body, high blood pressure, the development of certain kidney diseases.
    2. Patient's nearsightedness.
    3. Received eye injuries (or as a result of tissue degeneration).
  1. congenital predisposition.

Symptoms of the disease: description and features

Central retinal dystrophy can be expressed by the appearance of such a symptom as a feeling of soreness and discomfort when looking "close" and "far". The most alarming outcome of this disease of the retina is the curvature of straight lines, when there is a feeling that the patient seems to be looking through hot air. A dark spot may appear in front of the sore eye, often you can not distinguish, just not see, some letters in the text. Often objects that are at a distance may have a different shade or appear reduced in size when viewed with the affected area of ​​the retina.

If at least one of these alarming bells is present, it is necessary, without delay, to contact an ophthalmologist, undergo a qualitative examination, after which the doctor will be able to prescribe the correct and necessary treatment in each specific case.

It should be noted that you can check your eyesight on your own, for which it is enough to use a simple method using a checkered sheet. The technique is called the "Amsler lattice". This test will allow you to see even small deviations in a person's vision.

An ophthalmologist who examines the fundus at an early stage in the development of a disease may find that the retina of the eye has rather small (yellowish) foci, which, in turn, are called "drusen". They do not harm vision, but need specialist supervision to prevent the occurrence of dry and wet forms of the disease.

Treatment of retinal dystrophy

If retinal dystrophy is detected, the treatment will not be able to fully restore the patient's lost vision. To date, effective ways to eliminate dystrophy have not yet been created. However, regular visits to an ophthalmologist and its proper control prevent the occurrence of severe complications, while preventing the progression of the disease and thereby maintaining visual functions.

If treatment is not started in a timely manner, then dry central dystrophy can gradually flow into a wet form. The drusen, in turn, begin to mix with each other, as a result of which the retina begins to delaminate, and fluid accumulates in the vacated space. If the course of the disease occurs in this way, then the risk of vision loss increases significantly.

Violation of the blood supply occurs due to swelling of the patient's eye, which, as a rule, appears in the central region of the retina. The development of pathological vessels of the circulatory system leads to the fact that the retina rises. As a result, these vessels can bleed or leak fluid, which contributes to further retinal delamination. The longer this disease progresses, the faster the function of the eye decreases, treatment in this situation is simply necessary.

Applied in time, laser therapy significantly stops the loss of vision if the retina is affected, but the treatment does not guarantee its complete safety. The main task of such therapy is to remove the edema that has appeared in a timely manner and at the same time stop the occurrence of pathological vessels.

Retinal laser treatment can help to remove black marks before the eyes. For complex treatment, medications are prescribed that relieve swelling and hemorrhage. However, there is one thing: although the area of ​​the retina is restored, but the vision becomes somewhat worse. The decrease in vision is milder than if no treatment had been given, and the central dystrophy continued to progress.

It should be noted that no matter what form of central dystrophy, it is necessary to register with an ophthalmologist and undergo an examination at least once every six months. Treatment may include the avoidance of physical activity in excess of an acceptable level. A patient with eye dystrophy should:

  • avoid hot baths or showers;
  • be sure to follow a dietary diet;
  • fried and fatty should be avoided;
  • consume the required amount of vegetable oil;
  • limit your intake of salt and sugar;
  • if the day is sunny, it is necessary to use tinted glasses;
  • if the work is associated with eye strain, then it is necessary to apply ten-minute gymnastics for the eyes during breaks, preferably every half hour.

A person who has relatives in the family who have central dystrophy or peripheral dystrophy should be very attentive to the health of their eyes. This disease may be hereditary. If the area of ​​the retina has undergone dystrophic changes, then the reverse process is very difficult to treat (almost impossible). Much depends on the person himself: the sooner you seek help from a doctor if central dystrophy is detected, the sooner treatment will be started, which will help maintain vision and a full life.

Retinal dystrophy - treatment, classification, symptoms

Retinal dystrophy - what is it? This question is asked by every person who has certain pathological disorders in the visual organ. In fact, this disease includes a whole group of pathologies of the retina, which is the functional structure of the eyeball. Retinal dystrophy is characterized by the death of tissues in the retina, that is, the organ begins to rapidly degenerate. The retina is considered the most important element of the visual organ, as it is responsible for visual acuity. After all, it is she who transmits light impulses to the parts of the brain. It consists of the thinnest layer of nerve and photosensitive cells, which are photoreceptors.

Classification features of retinal dystrophy

Dystrophy is congenital and acquired. It is classified as follows:

Symptoms of retinal dystrophy

The main symptoms of retinal dystrophy:

  1. Blurry image of objects and partial loss of color vision.
  2. The presence of dark spots and flies before the eyes.
  3. Deterioration of lateral perception and loss of visual acuity.
  4. The formation of bright flashes and distortion of objects.
  5. Veil before the eyes and the importance of good lighting when reading.
  6. The patient cannot distinguish a moving object from a stationary one.

Reasons for the development of dystrophy in the retina

  1. Pathological changes in the functionality of the circulatory system of the retina, which leads to significant scarring.
  2. Weakened immune system and malnutrition. It turns out that low-quality products can lead to deformation of the retina.
  3. Bad habits: smoking and drinking alcohol.
  4. Viral infection, which was not treated in a timely manner or not qualified.
  5. Diabetes mellitus, heart disease, hypertension, pathology of the endocrine apparatus.
  6. Complication after surgery.
  7. Bad metabolism.

How to treat retinal dystrophy, diagnosis

To make an accurate diagnosis of retinal dystrophy, a hardware examination is prescribed. This may be visiometry, ultrasound examination, perimetry, fluorescein angiography. In addition, analyzes are collected for laboratory study and instrumental examination. Be sure to apply electrophysiological research methods to determine the degree of functioning of visual and nerve cells. Treatment of retinal dystrophy is carried out as comprehensively as possible and, first of all, it is drug therapy, which includes the following:

  1. Vasodilator and angioprotective drugs strengthen and expand the circulatory system, and also eliminate symptoms. These can be drugs such as Askorutin, Papaverine, Complamin. The dosage and duration of the course of treatment is determined solely at the individual level.
  2. Antiplatelet drugs prevent the formation of blood clots. It can be "Acetylsalicylic acid", "Ticlopidine", "Clopidogrel".
  3. Vitamin premixes are required.
  4. To improve microcirculation, "Pentoxifylline" is prescribed.
  5. Lucentis will be able to prevent the growth of capillaries.
  6. Eye drops: "Taufon", "Oftalm-Katahrom", "Emoxilin" and more. These drugs lead to the regeneration of damaged cells and the acceleration of metabolism in the area of ​​the visual organ.
  7. Electrical stimulation of the retina.
  8. Photostimulation of the eye.
  9. Low energy laser radiation.
  10. Magnetotherapy, electrophoresis and so on.

Surgical intervention

In the most complex and neglected forms, surgical intervention is used. These may be the following methods:

  1. Laser coagulation of the retina of the eye can stop the progression of the disease. With the help of a laser installation, point cauterization of damaged tissues is performed.
  2. The operation can be performed by the vasoreconstructive method.
  3. It can also be revascularization.
  4. Vitrectomy involves the removal of damaged areas with aspiration and the installation of an implant.

IMPORTANT! After drug therapy, it is imperative to follow all the doctor's instructions. First of all, it is impossible to expose the eyes to overexertion and exposure to sunlight. It is important to additionally take vitamins and minerals, to give up bad habits.

Similar posts