Dominant retinal drusen - causes and treatment. Age-related macular degeneration Echographic signs of the optic nerve drusen

The appearance of soft druses 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 pigment epithelium retina. With long-term 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 resorption of drusen. Subsequently, this was repeatedly confirmed. To find out whether laser coagulation of drusen improves visual function of patients and can prevent further development CNV and geographic atrophy, The Choroidal Neovascelarization Prevention Trail Research Group (CNPT) and The Complications of Age-Related Macular Degeneration Prevention Trial Research Group (CAPT) were conducted in the United States. It was concluded that laser coagulation does not reduce the risk of developing CNV and geographic atrophy, nor does it lead to an 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 of \u200b\u200bdrusen injury. Microperimetry, being more accurate than visometry, is a method of dynamic observation of functional state retina with "dry" form of AMD, revealed a decrease in the light sensitivity of the retina over the area of \u200b\u200bsoft macular drusen. Using these techniques in last years reports of effectiveness began to appear in the literature laser treatment soft macular druses with a positive functional result.

Our previous studies have shown that laser coagulation of soft macular druses leads to their regression, but does not improve visual functions, including the photosensitivity of the retina. However, when coagulating druses are very big size we noticed that their fit leads to an improvement in functional performance.

purpose

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

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 drainage drusen in the second eye, 10 patients had a “wet” AMD form, 1 patient had an atrophic form, 1 patient had CVS thrombosis, and 2 patients had cataracts. ... The initial diameter of the OPE-like druses varied from 800 to 2500 μm, the height - from 130 to 380 μm. 23 eyes were included in the study group, where threshold laser coagulation of druses was performed. Of these, 11 eyes underwent direct LC, applying laser exposure directly to the drusen area. In 8 eyes, indirect LC was performed, when coagulates were applied between druses. Mixed LK was performed in 4 eyes, when laser exposure was carried out both directly on the druses and between them. The control group included 16 eyes, where the natural course of the disease was observed. The observation period ranged from 6 months. up to 1 year. In some patients, the follow-up period was up to 2-3 years. Control examinations were carried out after 3, 6 and 12 months. after treatment.

For treatment, we used an Nd: YAG laser coagulator with frequency doubling manufactured by Alcon (USA). Radiation parameters: wavelength - 532 nm, pulse duration - 0.1 s, radiation power - 80-100 mW, spot diameter - 100 μm. The radiation power was selected individually at a remote site from the center of the macula until the appearance of barely distinguishable coagulates.

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

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

When performing microperimetry, we used the research protocol "Macula 20 ° 0dB" and recorded the average value of the retinal light sensitivity at all 76 points measured during this protocol, and additionally measured the average retinal light sensitivity at the central 28 and 12 points (Fig. 1).

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

Results and discussion

In the treatment group, starting from 3 months. of observation there was a partial regression of drusen in most cases (81%), while in the control group, druses did not change in 81.3% (Fig. 2). By the follow-up period of 1 year, in the treatment group in 88.9% there was a complete regression of macular druses, 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. The differences between the groups turned out to be statistically significant (рo<0,05).

The frequency and timing of drusen regression were the same when performing different laser coagulation techniques. However, almost all patients who underwent laser coagulation using an indirect technique, in the first month after treatment, complained of the appearance of multiple relative cattle in the field of vision, which gradually decreased by 2-3 months. observation. In our opinion, this is due to the fact that with the indirect technique, laser coagulates are applied between druses along the healthy retina, where photosensitivity is preserved, and its damage leads to temporary functional losses. With the direct technique, laser coagulates are applied directly over the area of \u200b\u200bthe drusen, where the retinal light sensitivity has already been reduced, so patients subjectively do not notice the consequences of laser exposure. That is why we consider direct laser coagulation of druses to be the most preferable.

The mean values \u200b\u200bof the volume and thickness of the retina in the macular region, the values \u200b\u200bof the thickness of the retina in the center of the macula (in the 1 mm zone), measured by the device automatically, did not differ statistically significantly between the two groups, as well as within each group by the observation period of 6 months. (po\u003e 0.05). Initially, the thickness of the neurosensory retina over the 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. After observation, 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 \u003d 0.03) (Fig. 3). Compared with the control group by 6 months. observation, the thickness of the sensorineural retina was greater (Fig. 4).

By the follow-up period of 1 year in the treatment group, in one case, there was a development of geographic atrophy in the foveola after adherence of soft macular druses. There were no cases of choroidal neovascularization in the treated patients, and in the control group, a “wet” form of AMD developed in one eye.

There was no statistically significant difference between the mean values \u200b\u200bof distance, near, and ETDRS visual acuity when comparing between the two groups, as well as within each group at all follow-up periods (рo<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 mean photosensitivity of the retina at 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 at the central 12 points above the macular drusen area (8.4 ± 1.3 dB in the main group and 6.8 ± 1.1 dB in the control). When comparing two groups, already starting from 3 months. observation, microperimetry showed that the light sensitivity of the retina in the central 12 points increased statistically significantly in the treatment group compared with the control group (Fig. 6). It should be noted that in the absence of improvement in visual acuity, but with an increase in retinal photosensitivity, 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 druses 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 patient's visual acuity. Ophthalmoscopically, against the background of the yellowish material of soft macular druses, it is not always possible to note the presence of pre-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 druses with their gradual complete regression and with a good functional result, which lasts for two years. The initial visual acuity in this patient was high (vis \u003d 0.9), which indicates that 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 direct technique for 6 months. there was a complete regression of the druses. By the follow-up period of 1 year, visual acuity remained 0.9 as before, but the light sensitivity of the retina at the central 12 points increased to 13.5 dB. The patient noted the complete disappearance of metamorphoses and an improvement in the quality of vision. 2 years after treatment, visual acuity of 1.0 was recorded and the light sensitivity of the retina in the central 12 points was 15.3 dB.

Figure 8 shows an example of complete regression of large OPE-like druses, however, with a significantly worse functional result, since at the time of initiation of treatment the drusen had existed under the retina for a long time, and atrophy of the pigment epithelium in the foveola had already formed. This is evidenced by the patient's initially lower visual acuity (vis \u003d 0.4), as well as the characteristic signals on optical coherence tomography both before and after treatment. Already by 3 months. follow-up, complete regression of OPE-like druses occurred. By 6 months. observation, the visual acuity remained at the same 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 druses, the already formed atrophy of the pigment epithelium gradually increases and geographic atrophy is formed in the foveola, which is best seen on the infrared image of the fundus (Fig.8e).

findings

1. Threshold laser coagulation of large soft macular druses 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. An early start of treatment leads to better functional results.

Friends of the optic nerve

Drusen of the optic nerve head, or hyaline bodies,ophthalmoscopically look like foci 1-2 diameter veins with white or yellowish-pinkish opalescence. Later, they may undergo calcification. Druses more often appear along the periphery of the disc, but they also occur in its center, and are also located in groups away from the blood vessels. Druses are superficial and deep. Deep drusen are better defined with side illumination and may resemble papilledema. Surrounding the optic nerve head, they usually do not go beyond it by more than 1/2 DD and never become pigmented. Disc drusen do not match with Bruch membrane drusen. Changes can be unilateral and bilateral, sometimes the paired eye is affected after several years. Visual functions are not reduced or slightly reduced.

Histologically, drusen are deposits of hyaline and are more often localized in front of the ethmoid plate, but they can also be located behind it.

FAGD plays an important role in the diagnosis of drusen of the optic nerve head, especially in the differential diagnosis of drusen and edema of the optic nerve head. With drusen, a scalloped edge hyperfluorescence of the disc is noted on the fluorescent angiogram, there is no contrasting of tissues outside of it, there are no changes in retinal and papillary vessels, as is the case with edema (Fig. 9-1-9-4).

Drusen pressure on the optic disc tissue can lead to atrophy of nerve fibers and cause the blind spot to expand. In some cases, there are retinal and vitreous hemorrhages.

They can also be seen in Grenblad-Strandberg syndrome, retinal pigment abiotrophy, and tuberous sclerosis.

Literature

Seitz R .:Die intraokularen Drusen. Klin. WE. Augenheilk 152 .-- 1968. - P. 203-211.

Anterior ischemic neuropathy

Epidemiology

The disease is an ocular symptom of various systemic processes. The average age of patients is 50-60 years.

Etiology and pathogenesis

The disease is polietiologic. In particular, the role of hypertension, generalized atherosclerosis, diabetes mellitus, rheumatism, temporal arteritis is noted. In isolated cases, anterior ischemic neuropathy can develop after significant blood loss, anesthesia, surgical interventions, sometimes it is observed against the background of druses of the optic nerve head, after cataract extraction. The disease usually develops in one eye, but involvement of the paired eye is possible at various intervals, up to 10 years.

In the pathogenesis of anterior ischemic neuropathy, the leading role belongs to circulatory disorders in the posterior short ciliary arteries.

Clinic

Anterior ischemic neuropathy develops acutely, more often in the morning after sleep, less often after heavy lifting and hot baths. Harbingers of the disease: slight periodic blurred vision, severe headache, pain behind the eye. Anterior ischemic neuropathy can also develop without prior symptoms. Visual acuity is reduced. Defects in the lower half of the visual field are often found, in addition, the temporal and nasal half of the visual field may fall out. Ophthalmoscopic

the picture is varied. In the acute period, the optic disc is edematous, its boundaries are not differentiated, hemorrhages may appear on its surface and in the peripapillary zone. Sometimes a soft exudate forms on the surface of the optic nerve head. In some cases, occlusion of the cilioretinal artery or the central retinal artery occurs simultaneously with anterior ischemic neuropathy.

FAGD at an early stage in the acute phase of the process: the optic disc in the ischemic zone is not contrasted. The capillaries of its intact part are ectasized, their walls are highly permeable, which leads to hyperfluorescence of the healthy part of the disc at the late stage of FAGD. Concomitant changes in FAGD include uneven caliber of arteries, unevenness of their contours (atherosclerotic changes in blood vessels) (Fig. 9-5-9-8).

Treatment

Topically applied corticosteroids. Conduct dehydration therapy, prescribe vasodilators, disaggregation drugs and fibrinolytics. Shows the installation of b-blockers at night to increase the perfusion pressure in the eye.

Literature

1.

2. Hayreh S.Anterior ischemic optic neuropathy. - Berlin-Heidelberg-New-York. - 1975 .-- 145 p.

CONSTANT DISC OF THE OPTICAL NERVE

The stagnant disc of the optic nerve is an edema of non-inflammatory origin and in most cases is caused by an increase in intracranial pressure.

Etiology

Diseases of the central nervous system, general diseases, diseases of the eyeball and orbit, deformation of the skull.

Among diseases of the central nervous system, the most common cause of the development of stagnant disc (64% of cases) is tumors

brain. The disease, as a rule, is bilateral, unilateral stagnant disc occurs with tumors of the orbit and traumatic hypotension of the eyeball.

Diagnostics

Anamnesis, visual field examination, ophthalmoscopy, and FAGD are important in the diagnosis of stagnant optic nerve head.

Classification

The classification is based on the stages of development of the process:

1. Initial stagnant optic disc.

2. Expressed congestive optic nerve head.

3. Pronounced stagnant optic nerve head.

4. Congestive disc atrophy.

5. Atrophy of the optic nerve after stagnation.

Clinic

At the initial stages, the optic disc is hyperemic, its borders are blurred, the veins are dilated, but not tortuous. Hemorrhages at this stage, as a rule, are not observed. Then the edema captures the entire optic nerve head, its increase is noted. The veins are not only dilated, but also twisted, the arteries are somewhat narrowed. At this stage, the vascular funnel is still preserved.

With pronounced congestive discs, hyperemia, an increase in the optic nerve head, and blurred boundaries are observed. Veins are dilated, twisted, hemorrhages appear, white foci.

At the stage of a pronounced stagnant disc, the ophthalmoscopic picture consists of the same details as in the previous stage, but due to an increase in edema, the optic nerve head will more penetrate into the vitreous body. With the prolonged existence of a stagnant disc, atrophy gradually begins to develop, a grayish tint appears against the background of disc hyperemia, which further increases as the edema decreases. With the development of atrophy, the disc becomes a dirty gray color (Fig. 9-9-9-12).

With a stagnant disc, normal, visual functions persist for a long time. With a sufficiently long existence of stagnation as a result of the death of peripheral fibers of the optic

the ditch narrows the boundaries of the field of view. With the onset of atrophy of the optic nerve head, the narrowing of the field progresses rapidly. Various forms of hemianoptic visual field defects indicate the impact of the main pathological process on a particular part of the visual pathway. A decrease in visual acuity often occurs in parallel with a narrowing of the field of view.

Treatment

Treatment consists in eliminating the cause of the stagnation of the optic nerve head.

Literature

Throne E. Zh.Diseases of the visual pathway. - L .: Medgiz, 1955 .-- S. 35-108.

OPTICAL NEBIT

Optic neuritis is an inflammatory process in the optic nerve. In most cases, the disease involves both the trunk and the sheath of the nerve.

Etiology

The etiological factors are numerous. They are grouped into 5 main groups:

1. Inflammatory diseases of the brain.

2. Acute and chronic infections.

3. Local foci of inflammation.

4. Diseases of internal organs of non-infectious origin (diabetes mellitus, blood diseases).

5. Inflammatory diseases of the eyeball and orbit.

The most common causes of optic neuritis are diseases of the brain and kidneys.

Pathogenesis

The mechanism of development of pathological changes in the fundus in optic neuritis is due to the inflammatory process. Hyperemia of the optic nerve head is caused by vasodilation; hemorrhage and exudation are associated with increased permeability of the vascular wall. Exudation leads to inflammatory edema of the optic nerve head tissue and causes blurring of its boundaries.

Diagnostics

Diagnosis is based on the results of ophthalmoscopy, visual field examination

and FAGD.

Clinic

The course of optic neuritis is diverse and is determined by both the severity and the causes of the inflammatory process. With mild inflammation, the optic nerve head is hyperemic, its borders are blurred, papillary arteries and veins are dilated.

With a more intense inflammatory process, all of the listed changes increase, hemorrhages and exudate deposits appear.

With pronounced neuritis, disc hyperemia and blurring of its boundaries are so significant that it merges with the surrounding retina. On the surface of the optic nerve head, as well as in the area of \u200b\u200bthe peripapillary retina, there are many hemorrhages and white foci of exudate. In most cases, neuritis is not characterized by the standing of the optic nerve head above the level of the retina.

Typically early visual impairment in parallel with the development of the ophthalmoscopic picture. This is observed in terms of both acuity and field of view. The severity of a decrease in visual functions correlates with the intensity of the inflammatory process and mainly depends on the degree of damage to the papillomacular bundle.

Changes in the visual field are more often manifested by a narrowing of its boundaries, while the deeper the inflammation penetrates into the optic nerve trunk, the more pronounced the narrowing of the boundaries of the visual field. If the inflammatory process involves nerve fibers running in the center of the optic nerve trunk, a central scotoma is observed. With the transition of neuritis to optic nerve atrophy, first of all, hyperemia decreases and at first a weak, and then more intense blanching of the optic nerve head develops. Over time, a typical picture of secondary atrophy forms. The vessels become narrow, hemorrhages and exudate dissolve.

With FAGD at the onset of the disease, there is intense hyperfluorescence of the visual disc.

of the body nerve, increasing in the late phases of FAGD (Fig. 9-13).

At the final stage of the process, with the development of optic nerve atrophy, persistent disc hypofluorescence is observed on the fluorescent angiogram.

Treatment

Treatment is most effective when the etiology of the disease is clarified and should be etiotropic. Prescribing antibiotics is mandatory. Corticosteroids are also used topically and internally, vitamins of group B.

Literature

1. Throne E.Zh.Diseases of the visual pathway. - L .: Medgiz, 1955 .-- S. 109-124.

2. Spar T., Rockwell D.Treatment of optic neuritis with intrevenous megadose corticosteroids: a consecutive series / Ophthalmol. - Vol. 95. - 1988. - P. 131-134.

PITS OF THE VISUAL DISC

NERVE

The pits of the optic nerve head are rare congenital diseases, manifested at the age of 20 to 40 years by a decrease in vision caused by serous macular detachment.

Diagnostics

The main diagnostic methods are ophthalmoscopy and FAGD.

Clinic

Oval depressions of a grayish-white color, ranging in size from 1/8 to 1/2 DD, in the temporal sector of the optic nerve head are determined. In the macular region, there is edema (neuroepithelial detachment), sometimes cystic degeneration of the retina. On FAGD, late fluorescence of the pits of the optic nerve head is determined. Detachment of neuroepithelium in the macular region with this pathology does not contrast in the early and late phases of FAGD (Fig. 9-17-9-24).

Treatment

Laser coagulation along the edge of the optic nerve head and barrier laser coagulation, delimiting the zone of neuroepithelial detachment.

Literature

1. Katsnelson L.A., Forofonova T.I., Bunin A. Ya.Vascular diseases of the eyes. - M .: Medicine, 1990 .-- S. 217-226.

2. Gass J. D.Stereoscopic atlas of macular diseases. - St. Louis, etc .: CV Mosby Co., 1977. P. 368-410.

Figure: 9-1.Superficial drusen of the optic nerve head.

Figure: 9-2.Deep drusen of the optic nerve head.

Figure: 9-3.Drusen of the optic nerve head. Irregular scalloped hyperfluorescence of the optic nerve head. FAGD. Arterio-venous phase.

Figure: 9-4.Drusen of the optic nerve head. FAGD. Late phase. More intense hyperfluorescence of the optic nerve head, scalloped coloration of its borders is preserved.

Figure: 9-5.Anterior ischemic neuropathy. Ischemic edema of the optic nerve head with isolated hemorrhages.

Figure: 9-6.Anterior ischemic neuropathy. Sectoral hyperfluorescence of the inner half of the optic nerve head (from ectazed papillary capillaries). FAGD. Late phase.

Figure: 9-7.Atrophy of the optic nerve head after suffering anterior ischemic neuropathy.

Figure: 9-8.Hypofluorescence of the optic nerve head after anterior ischemic neuropathy. FAGD. Arterio-venous phase.

Figure: 9-9.Congestive optic disc. Edema of the optic nerve head and peripapillary retina, dilated veins, deposits of solid exudate and hemorrhages in the peripapillary region.

Figure: 9-10.Congestive optic disc. FAGD. Late phase, sharply dilated, convoluted veins. Hyperfluorescence of the optic nerve head.

Figure: 9-11.FAGD of a patient with congestive optic nerve head. Arterial phase. Sharply dilated veins, extravasal hyperfluorescence from dilated papillary and peripapillary vessels.

Figure: 9-12.Congestive optic disc. Sharply dilated convoluted retinal veins and vessels of the papillary and peripapillary regions. The caliber of the retinal arteries is not changed. The disc tissue is edematous, its borders are not clearly contoured.

Figure: 9-13.Optic neuritis. Hyperfluorescence of the optic nerve head as a result of increased permeability of papillary vessels. FAGD. Late phase.

Figure: 9-14.Optic neuritis. The optic disc is hyperemic, its borders are blurred. Retinal veins and papillary vessels are dilated.

Figure: 9-15.Optic neuritis with initial atrophy of nerve fibers.

Figure: 9-16.Small fossa in the form of a round grayish depression in the temporal half of the optic nerve.

Figure: 9-17.FAGD. Arterio-venous phase. Hyperfluorescence of the fossa of the optic nerve head without secondary focal changes in the center.

Figure: 9-18.The fossa of the optic nerve head, occupying 1/4 of the DD.

Figure: 9-19.Large fossa of the optic nerve head.

Figure: 9-20.Non-fluorescent fossa of the optic nerve head. Hyperfluorescence in the central zone of the fundus in the form of small foci as a result of disorganization of the pigment epithelium. FAGD. Arterio-venous phase.

Figure: 9-21.FAGD of the same patient as in Fig. 9-20. Late phase. Bright hyperfluorescence of the fossa of the optic nerve head with secondary changes in the center.

Figure: 9-22.Glaucomatous excavation in differential diagnosis with a large fossa of the optic nerve head.

Figure: 9-23.A unique case is a foreign body on the optic nerve head that mimics the fossa of the optic nerve head.

Drusen of the optic nerve head (optic nerve disc) - This is a common structural anomaly. It is often confused with stagnant optic nerve disc, which appears in very serious brain diseases and other pathologies.

Druzy of the optic nerve disc is an anomaly in which the optic nerve head has fuzzy boundaries and slightly dominates. The anomaly can be unilateral and bilateral, sometimes the paired eye is affected after several years.

Druses are hyaline-like, opalescent material with calcium inclusions. The pathogenesis of drusen remains unclear. It is believed that drusen arise from the products of axonal degeneration due to their calcification. Ophthalmoscopy reveals a prominant pink optic disc with faded borders, little or no physiological excavation. Druses, localized in the marginal areas, look scalloped and indistinct. Most often, drusen are located in the nasal half of the disc. Drusen become more visible with age. Sometimes minor hemorrhages are detected due to mechanical damage to the walls of small vessels upon contact with drusen, ischemic disorders caused by vascular compression. Hemorrhages resolve spontaneously within 1-2 months. It is possible a combination with anomalies of blood vessels, which begin to divide earlier and more often than usual, as well as their tortuosity and bending through the neuroretinal edge. The superficial vessels are not hidden, despite the disc stagnation, which is characteristic of a stagnant disc. Deep drusen (difficult to diagnose because they lie deeper than the surface of the disc), better defined with lateral illumination, more reminiscent of the optic disc edema. Superficial druses are like wax pearl-like irregularities. Drusen usually do not go beyond ½ DD and are never pigmented.

Clinical picture

• Visual acuity varies from 1.0 to 0.1;
• Depression of color sensitivity to a red stimulus is possible, which indicates the presence of ischemic changes.
• A spontaneous venous pulse may be present in 80% of cases.
• With perimetry in 66-81% of the eyes, enlargement of the blind spot, central or centrocecal scotomas, peripheral defects are revealed.
• Defects in the visual field often do not correspond to the apparent location of druses.
• Progression of all the listed signs is possible!

Tactics

• Visometry, perimetry, OCT, photo registration, CT, ultrasound, PAH, possibly EFI are required.
• Long-term follow-up with a neuro-ophthalmological examination at each visit is necessary to exclude diagnostic errors in the timely identification of possible complications.
• Consultation with a neurologist, therapist, pediatrician.

findings

• Druze of the optic nerve disc is not so simple and harmless;
• Long-term follow-up is necessary with a neuro-ophthalmological examination at each visit.
• We can offer part of the research and dynamic observation in our center.

8290 0

Age-related macular degeneration (AMD) is a common degenerative retinal disease in which central debate is impaired. By definition, this disease occurs in people 50 years of age and older, and the incidence increases with age. According to experts, the rate of detection of AMD in people over 50 years old is approximately 10-35%. Allocate "dry", or nonexudative, and "wet", or exudative form of AMD.

"Dry" or non-exudative age-related macular degeneration. Definition

The most typical manifestation of "dry" AMD are drusen. They are deposits between the basement membrane of the retinal pigment epithelium and Bruch's membrane (Fig. 1-1, 1-2). Various types of drusen are described, in particular large drusen (64 μm or more); small drusen ( 63 μm or less), calcified drusen, which are characterized by splash and yellow color, and basal laminar drusen - small, rounded, diffusely located, more noticeable on fluorescent angiograms than in clinical examination of the fundus (Fig. 1-1-1 -3).

Figure: 1-1. Large (large) druses. Fundus photographs show mainly large drusen, some of which merge with each other (enlarged image). Visual acuity 20/25 (0.8).

Figure: 1-2. Drained druses. The fundus photograph shows multiple, large, mostly drained drusen. The fusion is more pronounced on the temporal side of the central fossa. Drained drusen is a risk factor for the development of exudative age-related macular degeneration.

Figure: 1-3. Basal laminar drusen. The fundus photograph shows numerous small, rounded, diffuse drusen (enlarged image) with extensive fusion areas at the posterior pole and in the middle periphery of the retina. Basal laminar drusen are better seen with fluorescein angiography than with clinical examination.

Figure: 1-4. Solid druses. Hard drusen (enlarged image) are small (63 microns or less) and are not a risk factor for the development of more severe forms of age-related macular degeneration.

Figure: 1-5. Focal hyperpigmentation. The fundus photograph shows multiple drusen and changes in the retinal pigment epithelium (enlarged image). Focal hyperpigmentation is localized in the fossa region and directly on the nasal side of it. Focal hyperpigmentation is a risk factor for disease progression and transition to more severe forms of age-related macular degeneration, which leads to loss of visual acuity.

Figure: 1-6. Non-geographic atrophy.
A. Multiple large drusen and areas of damage to the retinal pigment epithelium. Two zones of non-geographic atrophy surround the fovea region from above and from the temporal side. Thinning of the retinal pigment epithelium is noted, however, the boundaries of the atrophy area are indistinct, and the underlying large vessels of the choroid are not visible.
B. Fluorescent angiogram. Translucent hyperfluorescence is visible in the area of \u200b\u200bnon-geographic atrophy; later photographs show no fluid seepage.

Figure: 1-7. The final stage of geographic atrophy. An extensive area of \u200b\u200bgeographic atrophy with involvement of the central fossa. The underlying large vessels of the choroid are translucent. Visual acuity - counting the fingers on the face.

Multiple large drusen are diffuse thickenings of Bruch's membrane. Large drusen, also known as soft drusen, are a risk factor for more severe AMD and vision loss. Small drusen (known as hard druses) do not by themselves increase the risk of progression AMD (Fig. 1-4).

Other ophthalmoscopic features of dry macular degeneration are changes in the pigment epithelium, such as non-geographic atrophy, focal hyperpigmentation, and true geographic atrophy (Figure 1-5). The granularity of the retinal pigment epithelium can be an early symptom of retinal pigment epithelium lesions in AMD.

This process can progress with the formation of zones of non-geographic atrophy (Fig. 1-6), in which the amount of pigment in the pigment epithelium of the retina decreases (at the same time, this does not lead to a complete absence of pigment, therefore, the underlying vessels of the choroid are not visible).

With geographic atrophy, separate areas of "baldness" of the retinal pigment epithelium appear, with a minimum diameter of 250 µm, accompanied by the loss of underlying pigment in the stroma of the retinal vascular membrane, while large vessels of the chornoid are clearly visible (Fig. 1-7).

S.E. Avetisov, V.K. Sealing wax

Drusen are very small yellow or white spots that appear in Brujah's membrane (one of the layers of the retina).

They are globules of mucoproteins and mucopolysaccharides that gradually calcify the optic disc. Retinal pigment epithelial cells accumulate damaged cells.

The remaining damaged cells (called lipofuscin) from the oxidative process accumulate in Bruch's membrane and create hyaline bodies (drusen), which are the earliest visible signs of dry macular degeneration... It is a cluster of proteins and oxidized lipids that are not destroyed.

The color is white or yellowish pink. Over time, they calcify.

Symptoms:

• swelling of the optic nerve head;
• blurred disc boundaries.

During diagnostics, shiny particles are found on the optic disc surface. These are the Druses.

They have a pathological effect on the nervous tissue, which is characterized by a deterioration in visual acuity... Over time, the field of vision narrows, the boundaries of the blind spot expand and arched scotomas appear.

Globules of mucoproteins and mucopolysaccharides are located deeply, simulating stagnation and edema of the optic disc. Therefore, the diagnosis is often made incorrectly.

Changes occur in one or both eyes. Often, the second visual organ is affected several years after the diagnosis of the disease.

Druses are of several types:

• hard - round, have clear edges, small and scattered at a great distance from each other;
• soft - large, close, blurred edges.

Soft hyaline bodies can disrupt the layers of the retina and lead to detachment of the pigment epithelium.

Causes

Druses of the optic nerve disc and retina appear due to the effects of such factors:

• chronic bacterial infection;
• diabetes;
• eclampsia during childbirth;
• trauma;
• prolonged inflammatory processes of the visual analyzer;
• intrauterine infections.

Today, drusen are considered as polyetiological pathology with an incomprehensible mechanism of development.

Diagnostics

It is easy to diagnose drusen if they are located on the surface of the optic nerve.FAGD plays an important role in diagnostics. Fundus fluorescence angiography does not require special preparation.

The examination takes no more than 2 minutes for each organ... For diagnostics, a dye is used, which is easily washed off with cold water. The dye does not penetrate beyond the vessels into the surrounding tissues. It starts to fluoresce when the excitation light source is turned on.

FAGD shows scalloped marginal hyperfluorescence of the disc; tissue contrast does not occur outside of it.

In some cases, in the process of diagnosis, hemorrhage in the retina and vitreous body is found.

Additionally, ultrasound and ophthalmoscopic examination are performed. If the hyaline bodies have time to calcify, computed tomography is prescribed.

Visual fields are also determined to identify defects in peripheral vision.

Treatment

There is no proven and standard therapy. The number of friends will gradually increase, they will increase in size.

You can improve visual perception with spectacles or contact lenses.

To prevent the growth of abnormal blood vessels, you should have regular check-ups with an ophthalmologist. This anomaly requires surgery to prevent bleeding.

Regular examinations are necessary to study the dynamics of the progression of the loss of the peripheral visual field.

It is impossible to prevent a worsening of the condition, since doctors do not know the exact mechanism of the development of pathology, as well as methods of prevention.

Complications

Anterior ischemic neuroopticopathy is considered the main complication of the pathological condition.... It leads to a rapid and sudden loss of visual perception in one or both organs of vision.

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Vision is restored up to 90%

Poor eyesight significantly impairs the quality of life, makes it impossible to see the world as it is. Not to mention the progression of pathologies and complete blindness.