Is it necessary to damage the second eye? Methodology for the formation of an experimental model of subretinal neovascular membrane (SNM) in animals. Risk factors for AMD

Myopic choroidal neovascularization may also be referred to as: “subretinal neovascularization in pathological myopia”, “Fuchs spot”, “retinal Foster-Fuchs spot”, “disciform degeneration in pathological myopia”.

Myopic choroidal neovascularization is the most common sight-threatening complication of myopic disease. The visual prognosis is better in younger patients, with a smaller focal size of choroidal neovascularization, higher initial visual acuity, and juxtafoveolar localization of choroidal neovascularization.

Pathogenesis. The exact pathogenesis remains unknown. There are several theories about the pathogenesis of myopic choroidal neovascularization, incl. mechanical theory. Degenerative changes in myopic disease are considered secondary. Excessive elongation of the anteroposterior axis leads to mechanical tension of tissues and the appearance of breaks in the pigment epithelium - Bruch's membrane - choriocapillaris complex, which stimulates the secretion of VEGF by the pigment epithelium with the subsequent development of pathological neovascularization.

Symptoms of myopic choroidal neovascularization

Patients with myopic choroidal neovascularization may experience the following symptoms:

• decreased vision;
• metamorphopsia;
• scotomas;
• flashes of light or floaters in the field of vision.

Typical changes in the posterior pole of the eye in pathological myopia include "parquet" fundus, "lacquer fissures", patchy or diffuse atrophy of the PE, choroidal neovascularization, macular atrophy, posterior staphyloma, straightened and distended vessels, peripapillary atrophy in the temporal region, hemorrhages and changes DZN.

A “parquet” (or “mosaic”) fundus is observed when, due to hypopigmentation or hypoplasia of the RPE, the choroidal vessels become visible through the retina. “Lac cracks” are ruptures of the elastic plate of Bruch’s membrane.

Diagnosis of myopic choroidal neovascularization

Main diagnostic methods: fundus examination, OCT, fluorescein angiography. Autofluorescence and indocyanine green angiography are also used. Diagnostic and differential diagnostic criteria for myopic choroidal neovascularization.

• Ophthalmoscopic signs: changes in the fundus of the eye, characteristic of myopic disease. The subretinal neovascular membrane (SNM) is local and small in size (no more than one diameter of the optic disc), occurring predominantly at the edge of foci of atrophy or “lacquer cracks”; localization is predominantly subfoveal or juxtafoveolar. Hemorrhages are not pronounced and are localized around the SNM.
• OCT: the appearance of specific choroidal neovascularization type 2 in the form of SNM, which is located under the retinal neuroepithelium. Retinal edema is minimal and is often detected only on OCT. RPE detachment. not registered. Retinal neuroepithelial detachment is not pronounced and is located perifocally around the SNM or (less often) above it.

Choroidal neovascularization is newly formed vessels in the fundus area. It often develops with eye diseases and leads to a persistent decrease in visual function, being one of the causes of disability in patients. CNV occurs against the background of various eye pathologies: age-related macular degeneration, severe myopia, pseudohistoplasmosis syndrome, ocular histoplasmosis, retinal angioid stripes. Neovascularization often complicates the course of the postoperative period during laser coagulation of the retina or hyperthermia.

Due to the fact that during photodynamic therapy there is a selective effect on the endothelial cells of pathological newly formed vessels and there is practically no thermal effect, this method of treatment is used in ophthalmological practice to treat patients with subretinal neovascular membrane. The effectiveness of PDT in this disease largely depends on the specific photosensitizer and its distribution in the cell. This property of a photoactive substance is determined by its physicochemical as well as biochemical properties.

Depending on which part of the cell the photosensitizer accumulates, the mechanism of death and the amount of damage to the cellular structure changes. If there is a connection with the cytoplasmic membrane and lysosomes, the cell dies by apoptosis and necrosis. To create a photosensitizer that accumulates in a large number of cellular organelles, scientists synthesize various chemical compounds.

After the photosensitizer has accumulated in the cells, they are irradiated with a laser or other light source. In this case, the wavelength of light coincides with the absorption peak of the photosensitizer. After a molecule of a substance absorbs light particles, excitation occurs and it transitions to the triplet state. At this stage, a photochemical reaction is started.

After this, the reaction proceeds in two ways:

• The triplet photosensitizer molecule reacts directly with the cellular substrate, which leads to oxidation of cell structures.
• A triplet photosensitizer molecule reacts with an oxygen molecule, resulting in the formation of singlet oxygen. Next, the internal structures of the cell are oxidized by active oxygen.

Cell death during photodynamic therapy most often occurs through lipid peroxidation, which is activated with the participation of excited oxygen molecules.

PDT affects pathological newly formed vessels and leads to inhibition of their growth. As a result, the amount of blood in their lumen is significantly reduced, and the exudative process in the fundus of the eye slows down. Subsequently, visual acuity increases.

The drug Visudin is used to treat patients with neovascularization for a long time, and the follow-up period after PDT exceeds five years. Studies provide encouraging results in patients with subretinal neovascularization against the background of age-related macular degeneration and complicated myopia.

Moreover, the effectiveness of treatment depended on the patient’s age and the timing of neovascularization formation. In patients with AMD, stabilization of the process was observed in 30% of cases.

When studying the long-term results of treatment of patients with subretinal neovascular membrane, it was found that:

• Repeated courses of photodynamic therapy should be carried out every 3-6 months.
• A significant complication of PDT with Visudin is the development of atrophy of the pigment epithelium.
• The result should be considered positive if vision has stabilized within three lines.
• Most often, PDT can only stabilize the pathological process, and in 13% of cases there is an improvement in visual function.

Recently, drugs that inhibit the VEGF protein have been developed to treat patients with neovascular membrane. These include:

• Macugen, which is an oligonucleotide. It is administered intravitreally at a dose of 0.3 mg. The frequency of administration is once every six weeks. Clinical studies have established that the effectiveness of Macugen is comparable to the effectiveness of PDT, that is, visual function continues to fade, but at a slower rate.
• Lucentis is an antibody fragment that has inhibitory activity against VEGF. It is also administered intravitreally at a dose of 0.05 ml once a month. To date, large clinical trials of Lucentis have been completed, including in combination treatment (together with PDT). It was found that one year after the start of therapy in the group of patients with isolated photodynamic therapy, visual acuity decreased in 67.9% of cases, and increased in 5.4% of cases. If combined treatment (Lucentis + PDT) was used, an improvement in visual acuity (more than 15 letters) was achieved in 23.8% of patients. In addition, combined treatment was able to significantly reduce the number of photodynamic therapy sessions.
• Avastin is a recombinant human monoclonal antibody and is administered intravitreally at a dose of 1.25 mg every four weeks.

If a combined approach (PDT and anti-VEGCF) is used to treat patients with subretinal neovascular membrane, the number of sessions of photodynamic therapy and intravitreal injections can be reduced, as well as the risk of possible iatrogenic complications. Against this background, the quality of life of patients increases and the risk of recurrent neovascularization decreases.

Another analogue of combination treatment is the combined use of PDT with Visudin and intravitreal injections of Lucentis. In a large study, Lucentis was administered at a dose of 0.5 mg monthly, and PDT was performed seven days before the intended injection of the drug. After this, PDT sessions were repeated every three months. In the control group, patients underwent photodynamic therapy only without Lucentis administration. Over the course of a year, 67.9% of patients from the control group and 90.5% of patients from the main group showed stabilization of visual acuity (decrease of less than 15 letters). This allowed us to conclude that the combined treatment is highly effective, but there are also disadvantages of the technique:

• Frequent intravitreal injections often lead to the development of complications, including various inflammatory reactions, including endophthalmitis.
• A recurrence of the subretinal neovascular membrane may develop, which will lead to a decrease in the patient's visual acuity.

14.08.2013

Subretinal neovascularization (SNV) has a highly variable appearance on optical tomograms. Most often it appears as thickening and is often accompanied by intra- or subretinal cavities for fluid accumulation. Classic SNM appears as an optically dense hyperreflective formation under the retinal neuroepithelium with clear boundaries. Hidden SUI is not visualized due to the shielding properties of the pigment epithelium. However, it is often accompanied by detachment of the RPE, intra- and subretinal accumulation of fluid.

The terminal stage of AMD is characterized by the formation of hemorrhagic detachments of the RPE and a disciform scar. Hemorrhagic detachment of the RPE on tomograms is quite difficult to differentiate from choroidal tumors, since all of this is characterized by hyper-reflectivity of the surface. A disciform scar looks like a homogeneous, highly reflective lesion that involves all layers of the retina. The retina above it is thinned.

In the so-called pseudotumorous form, a dome-shaped detachment of the neuroepithelium appears over a homogeneous, highly reflective lesion that involves the outer layers of the retina (subretinal fibrosis).

A characteristic feature of classical SUI is the appearance of hyperfluorescence with clear boundaries in the early phase (starting from the choroidal phase), followed by an increase in fluorescence until later phases, while the clarity of the boundaries of the neovascular complex decreases.

A characteristic sign of latent SUI is the appearance of hyperfluorescence with unclear blurred boundaries in the late phases. The flow of fluorescein is usually not accurately determined. In the early phases, hyperfluorescence is absent due to the shielding properties of the retinal pigment epithelium layer.

In the early phases, in the area of ​​detachment of the pigment epithelium, a focus of hyperfluorescence with clear boundaries is detected. The intensity of hyperfluorescence increases in the later phases of the study. However, the shape and extent of the focus of hyperfluorescence do not change.

When a sheet of retinal pigment epithelium is torn off, the defect is visualized as an area of ​​hyperfluorescence, and the zone of duplication of the pigment epithelium is hypofluorescent in all phases of the angiographic study.

In the zone of neuroepithelial detachment on the angiogram, hyperfluorescence with unclear contours is formed in the early phase with an increase in the focus of hyperfluorescence in the later phases. In contrast to the detachment of the pigment epithelium, with the detachment of the neuroepithelium, the limits of the fluorescence focus are blurred.

With subretinal fibrosis, multiple zones of hyper- and hypofluorescence are visible in all phases of fluorescein angiography; with a hyperfluorescent focus, detachment of the neuroepithelium is visible in the recirculation phase.
With multifocal ERG, a pronounced decrease in amplitude and latency is determined. This form of macular degeneration on the electroretinogram is characterized by a significant decrease in cone and rod activity in the macular area.

Differential diagnosis includes rupture of a macroaneurysm, choroidal tumors, and central serous chorioretinopathy.

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In the exudative form of age-related macular degeneration (AMD), the patient may initially complain of acute sensitivity to light, decreased contrast sensitivity, impaired color vision, photopsia, and blurred vision.

As the pathology progresses, a person notices a decrease in visual acuity, the appearance of metamorphopsia (curvature of straight lines, image distortion, “jumping” letters when reading).

The disease progresses rapidly, and loss of central vision is possible within 6 months. The patient may lose the ability to read and write. Patients with unilateral development of the exudative form of age-related macular degeneration are at risk of developing choroidal neovascularization in the other eye within 3-5 years.

Ophthalmoscopy may reveal soft confluent drusen, local detachment of the retinal neuroepithelium, and accumulations of hard exudates around the subretinal neovascular complex. Rupture of newly formed vessels in this form can lead to hemorrhage into the subretinal space or into the vitreous body (rarely).
Ophthalmoscopically, predominantly classic SUI is visualized as a gray-green lesion, which is localized under the retinal neuroepithelium.

The main ophthalmoscopic signs at this stage of the existence of a subretinal neovascular complex are characterized by the presence of a disc-shaped gray or white lesion with clear contours, pigment deposition, and the possible presence of choreretinal shunts and anastomoses.

Subretinal neovascularization

Subretinal neovascular membrane (SNM) is a fairly common exacerbation of various fundus anomalies, primarily UMD complicated by myopia, retinal angioid stripes, and central chorioretinitis.
CHM, associated with high myopia and especially age-related macular degeneration, is a pathology with a burdened prognosis. The pathogenesis of this process is completely unknown; therapeutic options are very limited. The main diagnostic methods are biomicroscopy and fluorescein angiography, additional ones are optical coherence tomography and angiography with indocyanine green, long-wave fundusgraphy. The fluorescein-angiographic picture in the initial phases looks like lace, in the advanced phases - continuous hyperfluorescence, which merges, this is determined by the extravasal escape of fluorescein through the wall of the newly formed vessels. On optical coherence tomography, SNM appears as a subretinal optically dense formation with the presence of detachment of the retinal neuroepithelium and/or retinal pigment epithelium.

SNM, taking into account its anatomical localization in the foveoli, is divided into three main groups:
- Extrafoveal - the boundaries of the SNM are removed from the geometric center of the foveal avascular zone;
- Juxtafoveal - the boundaries of the SNM are removed from the center;
- Subfoveal - located under the geometric center of the FAZ.

Based on fluorescein angiography data, two main components of SUI are distinguished - classic and hidden (occult). The classic component of SUI is determined in the early phases of FA and is characterized by clearly defined boundaries of the neovascular complex. Late-stage images show progressive leakage of dye into the surrounding subneuroepithelial space.

The latent component of SUI is characterized by a neovascular complex that does not correspond to the angiographic picture of classical SUI. The category of latent SUI includes fibrovascular detachment and late progression from an unknown source, with the appearance of hyperfluorescence in the late phases of FA; The extent of occult SUI is difficult to determine because it lies beneath the retinal pigment epithelium.

These angiographic differences are important in establishing which group of patients may benefit from laser coagulation or photodynamic therapy.
More often, SUI in AMD is of a mixed nature, when the classical (mostly classical) or hidden (minimally classical) component predominates. Some authors identify a special form of exudative AMD - retinal angiomatous proliferation - the formation of anastomoses between the retinal and choroidal circulation, as well as polypoid choriovasculopathy.

It has long been known that to maintain the protective function of the macula, it is important to maintain the macular pigment - xanthophyll, which suffers in AMD. The three carotenoids we get from food - lutein, zeaxanthin and mesozeaxanthin - accumulate in the macula and together contribute to the creation of macular pigment. The importance of macular pigment is due to its antioxidant activity and ability to block the blue spectrum of light, protecting the macula. To preserve the protective function of the macula and maintain macular pigment, preparations containing lutein and zeaxanthin, for example lutein forte, are recommended.

Laser treatment

In the world, there are two fundamental approaches to the preventive treatment of age-related maculopathy: direct and indirect coagulation of drusen. Direct laser coagulation (DL) involves direct damage to drusen by laser radiation. Indirect laser coagulation is carried out indirectly in nearby undamaged areas of the retina.

Considering the great importance of early treatment of AMD, a new method of indirect selective LC was created for the treatment of patients with age-related maculopathy. Indirect selective laser therapy was performed using a specific laser with a radiation wavelength of 532 nm. The technique is that coagulates are applied in a series of pulses in an amount from 8 to 12 in each series in 4 rows in the form of concentric circles along the macular area at a distance of 750 μm from the center of the fovea. Beam diameter - 50 microns, exposure - 0.01 s, power - from 0.04 to 0.09 W. The pulse energy is selected for each patient individually.

The indication for indirect selective laser coagulation is the beginning of the drainage of soft drusen. OCT reveals how drusen change the relief of the inner layers of the retina. In patients with this, visual acuity is more than 0.7.

The effectiveness of treatment was determined based on functional indicators of the visual analyzer, OCT, and the frequency of formation of subretinal neovascular membranes.

It all started when she read the doctor’s diagnosis on the cover of the patient’s chart in her clinic:

in/in o/uGl.IIa, MVS, PES, PVKhRD.

Teek,” she scratched the back of her head, “perhaps it’s time.”

The funny thing is that in this diagnosis only the first two letters are not clear: “IV”, because the word “intravenous” suggests itself, but in fact this is the first diagnosed open-angle glaucoma of the second “a” stage, high myopia, pseudoexfoliation syndrome, peripheral vitreo-chorio-retinal dystrophy.

Therefore, she decided to put together the first abbreviations that came to mind, maybe they would later be supplemented with a few more and get something convenient for a beginner: a dictionary.

Those interested are welcome. I will be glad to add additions and comments.

Alt (alternatio) - alternates (not constantly)
BCVA - best corrected visual acuity (best corrected visual acuity)
CLR - clear lens replacement - replacement of a transparent lens
Conv (Convergens) - convergence (convergence)
Dev. (Deviatio) - deviation (for example, Dev = 0 or Dev = 10 conv alt)
Div (Divergens) - divergence (divergence)
Gl. - glaucoma
ML - macula lutea - macula lutea, central region of the retina
MZ - macular zone of the retina
OD - right eye (oculus dexter)
OS - left eye (oculus sinister)
OU - both eyes (oculi utriusque)
UCVA - uncorrected visual acuity (visual acuity without correction)
Vis - (from Visus) - vision - visual acuity
AGO - anti-glaucoma surgery
IOP - intraocular pressure
GAO - hydroactivation of outflow (antiglaucoma procedure)
ONH - optic disc
DR - diabetic retinopathy
ZPH - replacement of a transparent lens
IOL - intraocular lens
IRT - acupuncture
LASEK - laser subepithelial keratomileusis
LASIK - laser in situ keratomileusis
LIE - laser iridectomy (anti-glaucoma procedure - hole in the iris)
LTP - laser trabeculoplasty
LCC - laser cyclocoagulation (against glaucoma)
NGSE - non-penetrating deep sclerectomy
OS - retinal detachment
OUG - open-angle glaucoma
PVHRD - peripheral vitreochorioretinal dystrophy
PIN - anterior ischemic neuropathy
POAG - primary open angle glaucoma
PTS - empty sella syndrome (or vehicle passport:)
PES - pseudoexfoliation syndrome
RK - radial keratotomy (Fedorov incisions)
ROZ - retinal visual acuity
STE - sinustrabeculectomy
USDG - Doppler ultrasound
UPK - anterior chamber angle
Phaco - phacoemulsification of cataracts
PRK - photorefractive keratectomy
FEC - phacoemulsification of cataracts
Color Doppler mapping
CRPDS - chorioretinal pigmentary dystrophy of the retina
CCRD - central chorioretinal dystrophy
PAS - partial optic nerve atrophy
ED - excavation of the optic disc
EEC - extracapsular cataract extraction
IV - intravenously
IM - intramuscular
v/o - with glasses
z/a - accommodation reserve
s/c - subconjunctival
s/k - with correction
n/a - does not correct
o/u glaucoma - open-angle glaucoma
p/b - parabulbar
r/b - retrobulbar