Iris bombing: causes, symptoms, treatment. Poor preparation of jars and lids

13-12-2012, 22:30

Description

The incidence of the population of the European part of our country with primary angle-closure glaucoma is 2-2.5 times lower than OAG. At the same time, women get sick 2 times more often than men. ZUG, like OGG, refers to age-related diseases, developing more often after 50 years. According to S. Duke-Elder (1955), AG occurs on average 10 years earlier than AG. According to our data, for initial stage disease, this difference was only 5 years. In addition, LUG in most cases is diagnosed immediately after the onset, and OAG - after a few months or years. As a result, the actual age difference between the two forms of primary glaucoma is negligible.

Pathogenesis

Anterior chamber angle block . The main link in the pathogenesis of primary angle-closure glaucoma is the internal block of the drainage system of the eye, i.e. blockade of the angle of the anterior chamber by the root of the iris. Three mechanisms of such blockade are described.

1. In eyes with relative pupillary block, the angle of the anterior chamber may be obscured by an anteriorly protruding iris root. With the expansion of the pupil, bombardment of the iris is combined with the formation of a basal fold.
2. The basal fold of the iris, formed during pupil dilation, closes the filtration zone of the anterior chamber angle. Such a mechanism of the internal block is possible with a narrow angle, its sharp top and the rear position of the Schlemm canal.
3. Anterior displacement of the vitreous body as a result of fluid accumulation in the posterior part of the eye can lead to anterior vitreal and lens blocks. In this case, the root of the iris is pressed against the trabecula by the lens and vitreous body.

The first type of blockade is the most common mechanism for angle-closure glaucoma. The disease in the initial stage has an intermittent course. The occurrence of seizures is associated with an increase in the severity of the relative pupillary block. Iridectomy, eliminating the pupillary block, in most cases prevents further development diseases, if organic changes have not yet developed in the angle of the anterior chamber and the drainage system of the eye. However, mild attacks of glaucoma are also possible after iridectomy with pupil dilation. This indicates a combined mechanism of angle blockade in these patients. Operation Eliminates only one part of this mechanism.

Acute attack of glaucoma has a complex cyclic flow, which can be divided into several phases. The transition from one phase to another is associated with the inclusion of a new pathophysiological mechanism [Nesterov A.P., 1973]. We highlight:

• starting phase,
• reactive phase,
• phase of vascular strangulation and inflammation,
• regression phase.

An attack of glaucoma does not necessarily go through all phases; one or more intermediate phases may fall out. This is usually observed in those cases when, in the first phase of the attack, the blockade of the angle of the anterior chamber is incomplete. Such incomplete attacks are called subacute. Goniosynechia and damage to the trabecular apparatus and Schlemm's canal during an attack can lead to the development of chronic angle-closure glaucoma.

Significantly less common glaucoma attack without pupillary block. In this case, the iris is not protruding, flat, the anterior chamber is of medium depth, the angle of the chamber is narrow or closed (during an attack). The narrowness of the angle is due to excessive anterior attachment of the iris to the ciliary body. An attack of glaucoma develops due to the blockade of the angle of the anterior chamber of the fold of the iris with the expansion of the pupil.

In another, relatively rare, but especially malignant variant of the pathogenesis of angle-closure glaucoma, the decisive role is played by posterior vitreal block. At the same time, vitreal fluid accumulates in the posterior region. eyeball, resulting in a lens block, often combined with an anterior vitreal block.

Secondary organic changes . During an acute attack of glaucoma intraocular pressure reaches a high level, and the root of the iris is pressed against the anterior wall of the APC with great force. Irritation of pain receptors leads to a further reactive increase in intraocular pressure, vasodilation and an increase in their permeability. As a result of damage to the tissue of the iris and strangulation of individual vessels, necrotic and inflammatory processes develop with the formation of goniosynechia and synechia along the edge of the pupil, atrophy of the iris of the segmental and diffuse type, and small subcapsular opacities of the lens.

Less well understood are the secondary changes seen in creeping glaucoma. In such eyes, the angle of the anterior chamber is gradually obliterated, starting from its apex. As a result of this, planar goniosynechia is formed, capturing an entire segment of the angle or even its entire circumference (Fig. 47).

Rice. 47. Obliteration of the CPC in the eye with "creeping" ZUG. SW. 48.

Blockade of the anterior chamber angle leads to a sharp decrease in pressure in the Schlemm's canal and trabecular meshwork. As a result, first functional, and over time, organic blockade of the sinus and trabecular fissures develops for the second time.

Etiology

Allocate three etiological factors, causing the occurrence of blockade of the APC: anatomical predisposition, age-related changes in the eye and an unknown factor of a functional nature, which is commonly called a trigger (trigger) mechanism.

Anatomical features, predisposing to the development of angle-closure glaucoma, are divided into constitutional and acquired. The first include the small size of the eyeball and cornea, the large size of the lens, its more anterior position and the smaller radius of curvature of the anterior surface, the anterior attachment of the iris to the ciliary body. According to our data, in patients with angle-closure glaucoma, the sharp apex of the angle and the posterior position of the Schlemm's canal are most often observed (Fig. 48).

Rice. 48. A section of the drainage zone of the eye, excised during trabeculectomy in a patient with UG. Characteristic posterior position of Schlemm's canal (arrows) and anterior position of the ciliary body. SW. 63.

have a certain significance and structural features of the ciliary body. The massive ciliary body, especially having a triangular configuration in the section, occupies an anterior position and is combined with a narrow angle of the anterior chamber and the posterior position of the Schlemm's canal. With this form of the ciliary body, both the blockade of the angle of the anterior chamber and the cyclocrystalline block occur more easily. There is a certain relationship between the degree of development of the ciliary crown and ciliary processes. This suggests that the level of secretion in eyes with a massive ciliary body is increased. Studies conducted by G. A. Shilkin (1971) really showed that the minute volume of aqueous humor in patients with angle-closure glaucoma is often increased.

To acquired anatomical features, contributing to the development of the internal block, include the continuous growth of the lens during life, thickening peripheral departments lenses, senile flattening of the cornea, atrophy of the iris in the root area, accumulation of fluid in the posterior vitreous.

Both constitutional and acquired anatomical features act in one direction: they reduce the depth of the anterior chamber, narrow its angle, create conditions for the occurrence of a relative pupillary block, and in some cases also for the lens and anterior vitreal blocks.

Clinically, the predisposition of the eye to the development of angle-closure glaucoma is judged by the depth of the anterior chamber, the width of its angle and the position of the iris. The anterior chamber in patients with UG is on average 1 mm (35%) smaller than in healthy individuals of the same age.

According to V. Rosengren (1950), with a chamber depth of more than 2.5 mm, the incidence of angle-closure glaucoma is 1:32,573, and with a depth of less than 2.5 - 1:152, i.e., 214 times more. R. Tornquist (1956) gives the following figures: with an anterior chamber depth of 2-2.5 mm, the incidence is 1:180 (0.55%), 1.5-2 mm - 1:9 (10%), 1-1 .5mm - 52:1 (98%). Thus, with a decrease in the depth of the anterior chamber by 1 mm, the probability of the disease increases by 177 times.

The significance of heredity in the etiology of primary MG insufficiently studied. The literature describes cases of familial glaucoma of this type [Broshevsky TI et al., 1967; Khasanova N. X., 1967], but they are rare. It has been established that the depth of the anterior chamber is genetically determined and is transmitted by the dominant type. Among relatives of patients with USG, a small anterior chamber is often combined with a narrow AUC, but the disease rarely occurs. This can be explained by the complex multifactorial nature of the etiology of CUG.

plays a significant role in the development of primary eye refraction. It is known that hyperopic eyes are distinguished by a small size of the eyeball, a relatively large lens, a massive ciliary body, and a relatively anterior position of the latter and the iris. It is not surprising that ZUG develops especially often in hypermetropic eyes, much less often in emmetropic eyes, and only as an exception in myopes. According to R. Mapstone (1985), to etiological factors LAG can also include diabetes (especially type II) and autonomic neuropathy.

trigger mechanisms . In intermittent angle-closure glaucoma in the interictal period, the angle of the anterior chamber is narrow, but usually open. The trigger mechanism that causes angle block followed by an attack of glaucoma in the "predisposed" eye is not the same in different cases. The change in pupil width is essential. With a sharp expansion of the pupil, as a result of a decrease in the tone of the sphincter, the stroma of the iris shifts to the periphery, forming a large fold, which can block the angle of the anterior chamber. With a moderate expansion of the pupil, its rigidity decreases, and the degree of protrusion with a relative pupillary block increases. The contraction of the dilator does not lead to a displacement of the stroma of the iris to the periphery, but increases the density of contact of the iris with the lens, thereby strengthening the pupillary block. A sharp constriction of the pupil caused by potent miotics can provoke an acute attack of glaucoma. This is due to the expansion of the vessels of the iris and ciliary body, as well as an increase in the density of the pupillary edge of the iris to the anterior surface of the lens.

Among other causes of acute and subacute attacks of glaucoma indicate vascular instability and pronounced fluctuations in the rate of formation of aqueous humor [Shilkina G. A., 1971]. Increased blood supply to the choroid and ciliary body, an increase in the influx of moisture into the posterior chamber of the eye can lead to an attack of glaucoma in eyes with a narrow APC.

Clinic of angle-closure glaucoma with pupillary block

This form of the disease is observed in 70-80% of patients with angle-closure glaucoma. Predominantly women are ill (66%). The age of the patients under our supervision ranged from 40 to 76 years, averaging 59 years. The average age of patients with glaucoma in the initial stage was 56 years, in the advanced stage - 58, in the advanced stage - 63, in almost absolute and absolute - 64 years. The difference in the age of patients with the initial and absolute stages of the disease is worst eye was 8 years old.

Course of the disease undulating with attacks and interictal periods. In the mechanism of the onset of an attack, the anterior displacement of the iridolenticular diaphragm and the formation of a basal fold of the iris during pupil dilation are important. However leading role play a functional pupillary block and the bombardment of the iris caused by it. They are permanent in nature, but immediately before the attack and during it intensify.

The immediate cause of an attack of glaucoma is often emotional arousal. An attack can also be caused by pupil dilation, visual work in a poorly lit room, prolonged work with the head tilted, reception a large number liquids or stimulants medicines, cooling. Sometimes an attack occurs without any apparent reason. At the same time, attempts to artificially induce an attack (for diagnostic purposes) using a combination of various stress tests are far from always successful.

An attack of glaucoma almost never occurs during sleep, when the tone of the parasympathetic nervous system dominates and the pupil is constricted. More often the attack develops in the afternoon and evening. Perhaps this is due to neuropsychic fatigue, increased excitability of the nervous system, as well as a decrease in illumination and pupil dilation. There are acute and subacute attacks of angle-closure glaucoma.

Acute attack of glaucoma . An acute attack has a complex cyclic course, which can be divided into several phases. The transition from one phase to another is associated with the inclusion of a new mechanism. Thus, the clinical picture and the course of acute glaucoma depend on the action of not one, as is commonly believed, but several sequentially activated mechanisms. We highlight:

• starting phase,
• phase of compression of the root zone of the iris,
• reactive phase,
• strangulation and inflammatory phase,
• phase of lowering intraocular pressure.

First phase caused by triggers that lead to blockade of the entrance to the angle of the anterior chamber by the root of the iris. Clinical symptoms during this period are very poor. It can only be noted a decrease in the depth of the anterior chamber and an increase in bombardment of the iris, with gonioscopy - the closure of the angle of the anterior chamber in those segments where it was previously open.

Compression phase characterized by pressing the root of the iris to the corneoscleral region. The compression is due to the fact that the moisture of the anterior chamber cannot penetrate into the corner bay. The liquid flows out of the bay through the Schlemm channel, as a result of which the pressure there drops. The root of the iris, as it were, sticks to the corneoscleral binding. Ophthalmotonus begins to increase rapidly, and the pressure in the Schlemm's canal decreases. The trabecula is displaced and blocks the lumen of the canal. The root of the iris is pressed against the limbal zone of the sclera with increasing force. The total force that presses on the iris root zone up to 1.5 mm wide is 50 g with an ophthalmotonus of 60 mm Hg. Art., and 80 g at 100 mm Hg. Art.

In the iris compression phase patients complain pain in the eye, brow ridge and in the entire half of the head, blurred vision and the appearance of iridescent circles when looking at the light. When examining the eye, dilation of the vessels on the anterior surface of the eyeball, edema of the stroma and epithelium of the cornea, a decrease in its sensitivity, a shallow anterior chamber, protruding anteriorly of the iris, an enlarged pupil and a closed angle of the anterior chamber during gonioscopy are noted. Ophthalmotonus increases during this period.

The appearance of pain in the eye and a decrease in the sensitivity of the cornea are explained compression of nerve branches and endings in the root of the iris and the limbal zone of the sclera. Blurred vision and the appearance of iridescent circles when looking at the light are caused by corneal edema, which in turn occurs as a result of a rapid increase in ophthalmotonus and decompensation of the corneal endothelium. Pupil dilation can be associated with paresis of the sphincter, which occurs with a rapid increase in intraocular pressure, and with compression of the parasympathetic nerve fibers at the root of the iris. Dilation of the anterior ciliary arteries is caused by a sudden increase in resistance to blood flow through the eye due to a rapid increase in ophthalmotonus.

Reactive phase of an acute attack of glaucoma caused by strong pain receptor stimulation trigeminal nerve in the compressed part of the iris. Irritation of the iris receptors leads to the development of reactive phenomena in the eye: the release of histamine, serotonin and prostaglandins into the moisture of the anterior chamber, the expansion of the vessels of the anterior eye, an increase in pressure in them, a sharp increase in vascular permeability and a rapid increase in the minute volume of aqueous humor.

Clinically, there is an increase in the severity of those symptoms that appeared in the second phase of the disease. Pain radiates along the trigeminal nerve to the forehead and temple, the sensitivity of this zone decreases. Excitation spreads along the parasympathetic nervous system causing slow heart rate, nausea, and vomiting. Expand not only the anterior ciliary arteries and their branches, but the entire vascular network on the surface of the eyeball. The moisture of the anterior chamber is opalescent, because due to the increase in vascular permeability, significant amount squirrel. Due to vascular hyperemia and edema, the iris becomes dull, its pattern is smoothed out. During this period, ophthalmotonus reaches its maximum value.

Reactive hypertension in the experiment it is accompanied by pupillary constriction, but it is not observed during an attack of glaucoma. We explain this by the fact that reactive phenomena develop against the background of high intraocular pressure, which already in the previous phase led to paresis of the sphincter of the pupil. In the lens, peculiar opacities are sometimes formed, which E. Vogt (1930) called disseminated subcapsular cataract. The opacities look like white spots located directly under the anterior lens capsule. Their occurrence is associated with microscopic ruptures of the lens capsule. If it is possible to examine the fundus, then the pronounced swelling of the disc attracts attention optic nerve. The retinal veins are dilated, the borders of the disc are blurred.

In the reactive phase of the attack, the root of the iris is pressed against the sclera with such force that the individual radial vessels of the iris are strangulated. As a result acute violation blood circulation in the corresponding sector of the iris develop phenomena of necrosis and aseptic inflammation. Another reason for the development of inflammation in the eye is direct mechanical damage tissues of the iris and trabeculae, especially the endothelium, in the compression zone. The phase of vascular strangulation and inflammation of the iris is clinically manifested by the formation of posterior synechia along the edge of the pupil, destruction and dispersion of the pigment epithelium, the appearance of goniosinechia, diffuse atrophy of the iris in the root zone, the appearance of focal atrophy, more pronounced in the pupillary zone, deformation and displacement of the pupil (Fig. 49 ).

Rice. 49. Segmental iris atrophy and pupillary deformity after an acute attack of glaucoma.

segmental atrophy somewhat more often develops in the upper half of the iris. The pupil also shifts upward or upward and to the side. Displacement of the pupil is caused by the formation of rough goniosinechia, as a result of which the iris seems to be shortened, and sphincter necrosis. Primary localization pathological changes in the upper half of the iris, apparently due to the fact that the angle of the anterior chamber is narrower above than below.

In some cases, inflammatory changes are especially pronounced and are accompanied by the appearance of fibrinous exudate in the anterior chamber and pupil area, significant deposits of corneal precipitates. In such cases differential diagnosis an acute attack of glaucoma and iridocyclitis with hypertension is especially difficult.

The phase of the reverse development of an attack starts with paresis secretory function ciliary body. The suppression of secretion is caused high level ophthalmotonus, inflammatory and degenerative changes in the ciliary body. We also attach a certain importance to reactive phenomena. Reactive hypertension of the eye is replaced by hypotension caused by paralysis of aqueous humor secretion.

Inhibition of secretion of aqueous humor leads to a decrease in pressure only in the posterior part of the eye. The fluid from the anterior chamber cannot pass into the posterior chamber, since the pupil passes moisture in only one direction. Pressure equalization occurs by shifting the diaphragm of the eye posteriorly and reducing the bombardment of the iris. As a result, the chamber angle is partially or completely opened. This is facilitated by the elasticity of the iris, which seeks to restore its original position.

It should be noted that the decrease in ophthalmotonus only at the final stage is associated with the opening of the anterior chamber angle. We have repeatedly observed patients in whom an acute attack stopped, and ophthalmotonus was kept at a low level with a gonioscopically completely closed angle of the anterior chamber. Thus, the process of reducing ophthalmotonus can be divided into two periods: first, fluid secretion is inhibited, and then its outflow is restored to one degree or another. Restoration of the secretory function of the ciliary body occurs within a few days or even a few weeks.

Goniosinechia, segmental and diffuse atrophy of the iris, displacement and deformation of the pupil stay forever. They influence the further course of the glaucomatous process. Goniosynechia and damage to the trabecular apparatus and Schlemm's canal during an attack lead to the development of chronic angle-closure glaucoma. Due to diffuse atrophy of the root of the iris, the resistance of its tissue decreases. As a result, the bombardment of the iris increases, which facilitates the occurrence of a new attack of glaucoma. Atrophy of the processes of the ciliary body leads to a persistent decrease in its secretory function. This in one way or another compensates for the deterioration of the outflow from the eye and reduces the possibility of developing new attacks and their intensity. A pronounced displacement of the pupil in some cases gives the same effect as iridectomy, eliminating the relative pupillary block.

Subacute attack of glaucoma . An attack of glaucoma does not necessarily go through all the phases that are described above. This is usually observed in cases where the internal block in the first phase of the attack is incomplete: the angle of the anterior chamber does not close all the way or is not tight enough. One or more intermediate phases may fall out.

In the simplest case, an attack from the first phase immediately passes into the last. Actually, there is no attack in the full sense of the word with such a course of the disease, since subjective symptoms do not develop at all, and objective ones are very scarce and can only be detected with the help of gonioscopy and tonography. We described such an attack in 1971 and then repeatedly observed it in patients with initial angle-closure glaucoma. With repeated gonioscopy, temporary closure of the angle over a considerable extent and a simultaneous deterioration in the outflow of fluid from the eye are noted.

Subacute seizures are called, during which vascular strangulation and an inflammatory reaction from the iris do not develop, the reactive phase is often absent. Sometimes such attacks are called prodromal. It is impossible to agree with this term, since subacute attacks can be observed at any stage of glaucoma.

Clinical picture attack depends on the degree of blockade of the angle of the anterior chamber. In mild cases, patients complain of blurred vision and the appearance of iridescent circles when looking at the light. On examination, an expansion of large vessels on the surface of the eyeball, a slight swelling of the cornea, and an unsharply pronounced dilation of the pupil are found. Gonioscopy shows blockade of the anterior chamber angle, but the angle is not always closed from below. Ophthalmotonus rises at the height of the attack to 30-35 mm Hg. Art., the coefficient of ease of outflow is reduced to pathological values.

In more severe cases, all symptoms are more pronounced, there is pain in the eye and superciliary arch, ophthalmotonus rises to 35-45 mm Hg. Art. Pain in the eye and a significant expansion of blood vessels on the anterior surface of the eyeball indicate the development of a reactive phase, but it is not pronounced and does not last long, so the next, inflammatory, phase does not occur.

After a subacute attack, there is no deformation and displacement of the pupil, segmental atrophy of the iris, gross goniosinechia. Therefore, a subacute attack leaves no visible consequences.

The course of angle-closure glaucoma with pupillary block. Glaucoma with pupillary block begins with an acute or subacute attack. Even before the onset of the disease, when examining the eye, a shallow anterior chamber, bombardment of the iris, and a narrow entrance to the CPC are noted. The latter is often closed in some areas.

AT early stage disease, ophthalmotonus rises only during an attack. In the interictal period, intraocular pressure and indicators characterizing the hydrodynamics of the eye are within the normal range. For a disease with frequently recurring subacute attacks, E. Lowe (1967) proposed a new name - “ intermittent angle-closure glaucoma". Sometimes the disease immediately begins with an acute attack.

Chronic angle-closure glaucoma . Chronic UG with relative pupillary block occurs after repeated acute attacks as a result of the formation of goniosynechia, damage and degenerative changes in the trabecular apparatus and Schlemm's canal. In such patients, ophthalmotonus remains elevated even in the interictal period, the ease of outflow is steadily reduced, the chamber angle is permanently closed in some areas, and goniosinechia are visible in the open sections of the angle.

The course of chronic angle-closure glaucoma has much in common with the course of simple glaucoma: the outflow of fluid from the eye also progressively worsens, ophthalmotonus increases, glaucomatous atrophy and excavation of the optic disc develop, and visual functions eyes. Changes in the visual field have the same character in closed-angle and open-angle glaucoma.

Division of angle-closure glaucoma into acute, subacute and chronic is conditional. Glaucoma is essentially always chronic illness. However, such a division is rational clinical point vision. In acute and subacute glaucoma, the drainage system of the eye is not damaged. The hydrodynamics of the eye is disturbed only during an attack and returns to normal after it. Thus, glaucoma during this period has an undulating course and is caused by functional disorders in the eye anatomically predisposed to the onset of an attack.

The most effective treatment for acute and subacute glaucoma is iridectomy. It allows you to eliminate the pupillary block that plays important role in the genesis of an attack of glaucoma.

Chronic glaucoma acquires as a result of the damaging effect on the tissues of glaucoma attacks. It is more correct to consider it as secondary glaucoma, which is superimposed on primary angle-closure glaucoma. It is caused by goniosynechia and gross organic changes in the drainage system of the eye. Iridectomy cannot eliminate these changes.

"Crawling" glaucoma

G. Gorin (1960) described a peculiar form of glaucoma, in which there is a gradual fusion of the root of the iris with the anterior wall of the APC. The fusion starts from the very top and gradually spreads anteriorly to the scleral spur and trabecula. R. Lowe (1964) suggested calling this form of the disease primary angle-closure creeping glaucoma. According to him, "creeping" glaucoma is observed in 7% of patients with glaucoma.

According to our data, this form of glaucoma occurs mainly in women. The disease was often asymptomatic, but some patients experienced subacute seizures. The anterior chamber was of medium depth or shallow, the iris was slightly protruded anteriorly, the APC was shortened along the entire circumference or in separate segments. The degree of shortening of the angle varied not only in different patients, but also in different segments of the same eye. At the same time, the iris did not depart from the ciliary body, but from the scleral spur or trabecula at its various levels up to the Schwalbe ring. At a cursory examination, the APC seems open and one can see the transition of the focal light line through its top. However, upon closer examination, it is found that the apex of the angle is not the ciliary body, but the place of fusion of its anterior wall with the iris.

At a narrow angle, its shortening can be diagnosed by observing the course of the focal light line (Fig. 50).

Rice. fifty. The course of the focal light line during gonioscopy. a - in the eye with an open but narrow APC; b - in the eye with "creeping" glaucoma.

With "creeping" glaucoma, this line passes from the scleral surface to the iris without shifting. In normal USG, eyes with a very narrow anterior chamber angle always show a break and a shift in the focal line.

The most effective treatment for creeping glaucoma is iridocycloretraction in different variants. Iridectomy stops the progression of the creeping process in the APC only in some patients.

Angle-closure glaucoma with flat iris

Flat iris glaucoma(Plateau iris glaucoma) occurs infrequently, according to our data, in 5% of cases of UG. The age of the patients observed by us varied from 30 to 62 years. In all patients, the anterior chamber was of medium depth, the iris was flat, without bombage. Along with the absence of signs of pupillary block, the well-developed, relatively thick stroma of the iris attracted attention. On gonioscopy performed in the quiet period, we observed a very narrow (sometimes closed in places) entrance to the APC due to the coracoid configuration of the periphery of the anterior chamber and the thick peripheral fold of the iris stroma (Fuchs' fold). At the height of the attack, after the removal of edema by instillation of glycerol, the APC was closed on the entire or most of its circumference. According to M. Wand et al. (1977), an attack occurs when the pupil is dilated in the dark or under the influence of mydriatics (especially cycloplegic action).

For the relief of an attack, conventional methods of treatment are used. Often enough to drip pilocarpine several times. Conventional peripheral iridectomy is ineffective. A positive result can wide basal iridectomy with the removal of the root of the iris for some length. The systematic use of miotics prevents new attacks. Of the operations, iridocycloretraction is theoretically especially shown. However, there are no sufficiently definitive data in the literature on the effectiveness of this operation for USG with a flat iris.

Angle-closure glaucoma with vitreocrystalline block

This a rare form of primary UG occurs in anatomically predisposed eyes (reduced size of the eyeball, large lens, massive ciliary body) due to the accumulation of vitreal fluid in the posterior part of the eye. In this case, the vitreous body and the lens are displaced anteriorly and, together with the iris, block the APC. Clinical picture resembles the acute attack of glaucoma described above with the same pain syndrome and congestive injection of the eyeball. Attention is drawn to the slit-like anterior chamber and the tight fit of the iris to the lens over its entire anterior surface. Protrusion of the root of the iris, in contrast to the usual attack of ZUG, does not occur.

Conventional treatments for an acute attack of UG are ineffective. Miotics not only do not improve the condition of the eye, but even aggravate the course of the disease. Other antihypertensive drugs reduce IOP, but the attack is not completely stopped. In many cases, significantly more effective than cycloplegic mydriatics, especially atropine. Atropine instillations lead to tension of the zonium ligaments, deepening of the anterior chamber, and opening of the APC.

Article from the book: .

Iris bombing may occur against the background of uveitis. With the progression of this pathology, the functioning of the chambers of the eye is disrupted. Bombing is dangerous because it can lead to loss of vision.

Causes of the disease

Synechia is a predisposing factor. There are cases when bombardment occurs when the pupillary membrane is damaged, due to which a pupillary block is formed. The pupillary membrane can displace the processes of the ciliary body.

If iradocyclitis is observed, the edge of the pupil is fused with part of the lens. In the absence of the lens, a certain part of the pupil is fused with the vitreous body. Bombing can lead to complete closure of the pupil.

As a result, serious ophthalmic problems will arise. Unlike other pathologies that have similar symptoms, bombing is characterized by a sharp increase in intraocular pressure.

Peripheral anterior synechia is formed when the iris fuses with the cornea or trabecular meshwork. The formation of anterior synechia disrupts the outflow of intraocular fluid. The outflow of intraocular fluid may stop completely.

Peripheral anterior synechia often occurs against the background of uveitis. They also appear in people who have a narrow anterior chamber angle. Posterior synechiae are formed by the fusion of the dorsal portion of the iris and the lens shell.

Repeated uveitis increases the likelihood of developing synechiae. Pupillary block is a pathological formation that affects the outflow of intraocular fluid.

This block disrupts the functioning of the organs of vision, in particular, this is due to the formation of posterior synechia. Due to the fact that the volume of intraocular fluid increases and intraocular pressure rises, bombardment of the iris occurs.

With a rapid increase in intraocular pressure, the iris begins to bend into the region of the anterior chamber. Inflammatory reactions cause the corner of the eye to close. As a result of such a problem, peripheral synechiae are formed.

Against the background of uveitis, large adhesions are formed. The iris fuses significantly with part of the lens. The peripheral region of the iris sags, resulting in serious ophthalmic problems.

Diagnosis and conservative treatment

Iris bombing requires complex diagnostics. A patient suffering from uveitis should be observed by a doctor. An ophthalmological examination is necessary to diagnose bombing.

The doctor prescribes isometry, biomicroscopy and tonometry. To identify the disease, a serological test for syphilis, the detection of antibodies to hepatitis B, urine and blood tests are required. It is important to tell your doctor about illnesses that could aggravate the course of uveitis.

If the ophthalmologist detects bombing, conservative or surgical treatment is prescribed. Depending on the features visual organs means are selected: the medicine Diakarb in tablets can be prescribed.

Sodium chloride is prescribed for intravenous administration. A good result is given by drops with adrenaline and atropine. In the fight against the disease, corticosteroids are effective. The goal of medical treatment is to restore intraocular pressure, eliminate the pupillary block.

Other Therapies

Depending on the degree of eye damage, the doctor may prescribe an iridectomy. Surgical manipulation is indicated if the cornea is transparent and the eyeball is not too inflamed. Laser iridectomy is recommended for patients with pseudophakic eyes. Other types of operations are performed on phakic eyes.

A popular surgical procedure is laser iridectomy. Thanks to its capabilities, it is possible to restore the functioning of the eye chambers. The result of the procedure is the elimination of the pupillary block.

To carry out this operation, you need to make several holes on the surface of the eyes. After the procedure, the patient is observed by a doctor. Throughout the entire period, you need to control vision. Surgical iridectomy is performed when laser treatment is not possible.

The patient is also seen by a doctor. If there are no inflammatory reactions, then the operation gave a good result. To evaluate the effectiveness of the procedure, you need to observe the patient for 7 days.

There are situations when the lens is damaged during the intervention. If the operation gives any complications, the patient goes on sick leave, which lasts 1 month. After that, you need to get registered with an ophthalmologist.

Iris bombing often occurs with eye pathology. To avoid this disease, it is necessary to treat other ophthalmic diseases in a timely manner.

Video

Normally, intraocular fluid flows freely from the posterior chamber of the eye to the anterior chamber through an opening in the iris - the pupil. In inflammatory diseases of the choroid, circular adhesions develop between the iris and the lens or vitreous body.

As a result, fluid cannot enter the anterior chamber. The accumulation of fluid leads to an increase in intraocular pressure in rear camera. The iris protrudes into the anterior chamber. This condition of the iris is called iris bombardment.

Causes of iris bombing

Inflammatory diseases of the choroid of the eye

During inflammation, fibrin and protein compounds are produced inside the eye. This stimulates the formation of adhesions between the iris and the lens or vitreous.

Tumors of the choroid

The presence of a tumor in choroid eyes activate weak inflammatory process. This leads to the formation of adhesions between the internal structures of the eye.

eye injury

When should you urgently see a doctor?

• Sudden and severe pain in the eye
• Pain caused by blunt and penetrating trauma to the eyeball
• Pain accompanied by loss of vision
• The pain appeared during the treatment of inflammatory diseases of the eye

Iris bombing symptoms

• Strong pain
• Decreased vision
• Eye redness
• Blepharospasm
• Photophobia (photophobia)
• Tearing, eye irritation

How to Treat Iris Bombing

Iris bombing is a medical emergency. Therapeutic measures suggest:

• 1) decrease in intraocular pressure;
• 2) anti-inflammatory and resolving therapy;
• 3) the formation of an additional message between the posterior and anterior chambers of the eye through a surgical operation - iridectomy.

Laser iridectomy

The laser machine creates a small hole in the iris. This opening allows intraocular fluid to flow from the posterior chamber of the eye into the anterior chamber. Thus, the operation removes the pupillary block and normalizes the intraocular pressure.

Surgical iridectomy

The hole in the iris is formed intraoperatively with a special tool.

Prevention of iris bombing

In the event of inflammatory diseases and eye injuries, immediately seek qualified medical help. Proper treatment will prevent the adhesive process inside the eye and the development of bombing of the iris.

Iris adhesions occur when the iris grows together with synechiae with the cornea (anterior) or with the lens (posterior). Adhesions are formed as a result of eye injury, inflammatory diseases (iridocyclitis, uveitis). Synechia can lead to the development of intraocular hypertension and glaucoma. Synechiae can sometimes be visualized on ophthalmological examination, but are best viewed with a slit lamp and ophthalmoscope.

Anterior adhesions can cause angle-closure glaucoma, as in this case the iris creates an obstacle to the outflow of aqueous humor from the anterior chamber. At the same time, intraocular hypertension increases. If against the background of the anterior synechia there is increased pressure inside the eyeball, then it is necessary to perform cyclodialysis.

With posterior synechia, glaucoma can also occur, but the mechanism for increasing pressure in this case is different. The iris, growing together with the lens, disrupts the outflow of intraocular moisture from the posterior chamber to the anterior region. This block leads to an increase in intraocular pressure.

With posterior adhesions, synechia can be isolated or form a continuous ribbon between the edge of the iris and the lens. In the case of secondary changes in the exudate in the pupil area, a complete closure of the hole may occur. The prelens membrane (circular fusion) causes complete separation of the chambers (anterior and posterior) of the eyeball, resulting in intraocular hypertension. With sufficient accumulation of aqueous humor in the posterior caper, the iris begins to bulge into the anterior chamber under pressure, that is, the so-called bombardment of the iris occurs. With the formation of an annular synechia between the iris and the lens (its anterior capsule), complete occlusion of the pupillary opening may occur.

Interestingly, synechia can form both with the natural lens and after IOL transplantation. The degree of adhesions varies depending on the severity and duration of the inflammatory disease.

At the beginning of the formation of adhesions, various proteolytic enzymes can be effective, which include fibrinolysin, chymotrypsin, lecozyme, trypsin, streptodecase and collalisin. At the same time, it is not so much the proteolytic effect of the drug that is important, but rather the increase in tissue permeability for nutrient compounds, as well as inhibition of the formation of connective tissue cells in the area of ​​inflammation.

In the treatment of synechia, lidase is used, which leads to an improvement in flow properties. hyaluronic acid. In addition, it increases the permeability of tissues for interstitial fluid. As a result, the latter accumulates in a smaller amount in this area.

Used for enzyme therapy traditional methods(instillation of drops, introduction of the parabulbar region or under the conjunctiva) or physiotherapeutic methods (phonophoresis, electrophoresis). Additionally, local or systemic administration of angioprotectors is used.

Cytoplegic drugs (mydriatics), which include homatropin (the action is similar to atropine) are used for posterior synechia. These means keep the pupil in a dilated state, as a result of which it is at some distance from the lens capsule. In this way, fusion is prevented. In the presence of synechia, the introduction of atropine-like drugs leads to a change in the shape of the pupillary opening. It doesn't become round. The prognosis of the disease is determined by the degree of opening of the hole under the influence of drugs. In the case of full opening, the prognosis is favorable, that is, the adhesions are reversible.

For the purpose of anti-inflammatory therapy, corticosteroids are prescribed. With an increase in intraocular pressure, antiglaucoma drugs (fotil, travatan) are added to therapy.

Surgical dissection of adhesions with a scalpel, spatula, scissors is resorted to in more serious cases. In order to prevent the development of glaucoma, such a manipulation can be performed as an independent intervention. Sometimes it is part of other surgeries (cataract repair, iris surgery, anterior eyeball reconstruction).

In the presence of dense and massive adhesions, it is necessary to use Vannas scissors and iris scissors. They penetrate into the anterior chamber of the eye through a small incision in the limbus, which is worn with a special keratome. The incision should be in close proximity to the synechia, but not opposite them. If vessels pass inside the synechia, that is, it is vascularized, then a hyphema may form during dissection.

If the posterior adhesions are located behind an intact iris, then it is worth dissecting them very carefully so as not to damage the lens capsule.