Congenital glaucoma. Retinal dystrophy, glaucoma, blepharospasm, detachment disease: Medical blog of an ambulance doctor Treatment of congenital glaucoma

1. Sections of the eye involved in the formation of intraocular fluid. Ciliary body, iris.

2. Three main ways of outflow of intraocular fluid: 1) anterior chamber angle; 2) perivascular spaces; 3) perineural spaces.

3. Two leading factors that ensure the constancy of ophthalmotonus. Production and outflow of intraocular fluid.

4. The minimum and maximum norm of intraocular pressure in children and adults. 16-27mmHg Art.

5. Permissible daily fluctuations in ophthalmotonus. 5mmHg Art.

6. Factors affecting the body of a pregnant woman, contributing to the violation of the development of outflow pathways of intraocular fluid in the fetus. Viral diseases, hyperthermia, trauma, ionizing radiation, hyper- and hypovitaminosis, metabolic disorders, alcoholism, psychoemotional stress.

7. The age at which congenital glaucoma is more often detected. More often in the first hours - days - weeks of a child's life.

8. Four possible changes in the corner of the anterior chamber in congenital glaucoma: 1) remnants of non-absorbed embryonic tissue (mesoderm) in the corner of the anterior chamber; 2) recession of the anterior chamber angle; 3) atresia of Schlemm's canal; 4) the absence of a suprachoroidal space.

9. Method of detecting changes in the corner of the anterior chamber. Biogoniomicroscopy.

10. Fundamental differences in the etiology of primary and congenital glaucoma. Primary glaucoma occurs mainly in connection with a violation of the links of the neurovascular apparatus that regulates ophthalmotonus, congenital glaucoma is caused by an anomaly in the embryonic development of the anterior chamber angle.

11. Systemic diseases in which hydrophthalmos can be observed. Angiomatosis, neurofibromatosis.

12. Cardinal signs of congenital glaucoma: 1) stagnant injection; 2) an increase in the size of the cornea, eyes; 3) a wide pupil; 4) deep anterior chamber; 5) atrophic excavation of the optic nerve head; 6) high intraocular pressure; 7) decreased visual function.

13. Possible causes of corneal opacity in congenital glaucoma: 1) edema, tears and folds of the Descemet's membrane; 2) corneal dystrophy; 3) physiological opalescence.

14. Method of distinguishing edema from persistent corneal opacities. Instillation of a hypertonic solution (40% glucose solution, glycerin) leads to the disappearance of edema and does not affect stable corneal opacities and temporary opalescence.

15. The main differences between megalocornea and hydrophthalmos. With megalocornea, a large and transparent cornea, the eyeball is not enlarged, intraocular pressure is normal.

16. The reason for the change in the depth of the anterior chamber in congenital glaucoma. Overflow of the chamber with intraocular fluid, due to the difficulty of its outflow.

17. Typical clinical refraction in congenital glaucoma and the factors causing it. Slight myopia develops due to an increase in the sagittal size of the eye.

18. Reasons for the enlargement of the eyeball in congenital glaucoma. Difficulty (closure) of the outflow of intraocular fluid in combination with the high elasticity of the children's eye capsule leads to stretching of the eye.

19. The most frequent signs of congenital glaucoma in children after 2 months of life: 1) photophobia, blepharospasm and restless behavior of the child; 2) enlargement of the cornea and eye; 3) increased intraocular pressure; 4) decreased vision; 5) stagnant

injection; 6) atrophic pathological excavation of the optic nerve head.

20. The criteria that are the basis for the classification of congenital glaucoma: 1) origin; 2) form; 3) stage of the process; 4) the degree of compensation; 5) dynamics (flow) of the process.

21. Two types of congenital glaucoma by origin: 1) hereditary; 2) intrauterine.

22. Three forms of congenital glaucoma: 1) simple; 2) complicated; 3) with accompanying changes.

23. Signs characteristic of a simple form of congenital glaucoma. Presence of only undissolved embryonic tissue in the corner of the anterior chamber and in the iris.

24. Signs characteristic of complicated congenital glaucoma. The presence of phakomatoses (angio- and neurofibromatosis).

25. Signs characteristic of congenital glaucoma with concomitant changes. Syndromes of Marfan and Markezani, macrocornea, microphthalmos, aniridia, coloboma of the choroid, etc.

26. Two types of congenital glaucoma according to the dynamics of the process: 1) stable; 2) progressive.

27. Signs characteristic of stable congenital glaucoma. Stopping the stretching of the eye and the fall of visual functions at normal values \u200b\u200bof the ophthalmotonus.

28. Signs characteristic of progressive congenital glaucoma. Progressive stretching of the eye and a decline in visual functions with normal or increased ophthalmotonus.

29. Criteria for determining the stage of congenital glaucoma: 1) eye parameters (sagittal size of the eye, corneal diameter, limbus width, anterior chamber depth, pupil width); 2) the condition of the optic nerve; 3) visual functions of the eye.

30. Names of the stage of congenital glaucoma: 1) initial; 2) developed; 3) distant; 4) almost absolute; 5) absolute.

31. The main external signs that determine the initial stage of congenital glaucoma according to age: 1) the diameter of the cornea is increased by 2 mm; 2) the anterior chamber is I-2 mm deeper; 3) the pupil diameter is 1-2 mm wider. 32. The main signs of congenital advanced glaucoma:

1) the diameter of the cornea is increased by 3 mm; 2) the anterior chamber is 3 mm deeper; 3) the diameter of the pupil is wider by 3 mm; 4) partial atrophic excavation of the optic nerve head; 5) decrease in visual functions up to 50%.

33. The main signs of advanced congenital glaucoma. Increase in the size of the cornea, anterior chamber, pupil by 4 mm. Severe atrophic excavation of the optic nerve head. Decrease in visual functions up to 1% (99%).

34. The main signs of almost absolute congenital glaucoma. A sharp increase in the size of the eye and the internal structures of the eye. Residual vision in the form of light perception with incorrect projection.

35. The main signs of absolute congenital glaucoma. Gross irreversible changes in the size and structure of the eye. Complete absolute irreversible blindness.

36. Three types of degree of compensation of congenital glaucoma: 1) compensated; 2) uncompensated; 3) decommissioned.

37. Signs of different degrees of compensation for the initial stage of congenital glaucoma: 1) compensated (pressure up to 27 mm Hg); 2) uncompensated (28 mm and more, “cobra” symptom); 3) decompensated (28 mm and more, edema of the cornea and other tissues of the eye, “cobra” symptom).

38. Signs of different degrees of compensation in pronounced, distant, almost absolute and absolute stages of congenital glaucoma: 1) compensated (pressure up to 25 mm Hg); 2) uncompensated (25 mm Hg and higher, “cobra” symptom); 3) decompensated (pressure 25 mm Hg and higher, edema of the cornea and other tissues of the eye, symptoms of "cobra" and "jellyfish head").

39. Method of research of ophthalmotonus: 1) palpation; 2) tonometric; 3) tonographic.

40. The list of studies that determine the dynamics of glaucoma: 1) echobiometry; 2) keratometry; 3) measuring the width of the pupil; 4) biomicroscopy; 5) ophthalmoscopy; 6) ophthalmometry.

41. A fundamental difference in the treatment of patients with congenital and primary glaucoma. Patients with congenital glaucoma are treated surgically, with primary glaucoma - conservatively and, if necessary, surgically.

42. Terms of operations for children with congenital glaucoma. Immediately after diagnosis.

43. Indications for surgical treatment of primary glaucoma. Ineffectiveness of drug treatment.

44. The list of medicines used to reduce intraocular pressure. Solutions of pilocarpine, carbocholine, aceclidine, fu-ramon, eserin, phosphacol, fosarbin, armin, timolol, etc.; diuretics - fonurite, urea, glycerol, etc.

45. Operations aimed at restoring the outflow tract in the initial and advanced stages of congenital glaucoma: 1) goniopuncture; 2) sinusotomy; 3) trabeculectomy.

26. Antiglaucomatous operations aimed at creating additional outflow pathways in the case of advanced and more pronounced stages of the process: 1) goniotomy with goniopuncture; 2) iridenkleisis;

3) cyclodialysis; 4) basal iridectomy; 5) scleroiridectomy.

47. Antiglaucomatous operations aimed at reducing the production of intraocular fluid: 1) cyclodiathermocoagulation; 2) angiodiathermocoagulation.

48. Consequences of untreated congenital glaucoma. Irreversible absolute blindness in the first years of life.

49. Specialists, examining the child, and the timing of examinations to detect congenital glaucoma: 1) micro-pediatrician of the children's room of the maternity hospital; 2) a district pediatrician when receiving a child from a maternity hospital; 3) an ophthalmologist during the first 2 months of a child's life and thereafter.

50. Principle, place and duration of observation and treatment of children with congenital glaucoma: 1) dispensary; 2) in an eye hospital; 3) every 6 months; 4) prior to transfer to an adult network.

51. Percentage of favorable outcomes with timely detection and correct treatment of congenital glaucoma. Process stabilization in 75% of cases.

Glaucoma is a chronic disease of the eye that results in permanent loss of visual function.

Glaucoma affects up to 105 million people in the world; 5.2 million people have blindness in both eyes, 1 patient goes blind every minute, and every 10 minutes - 1 child. In Russia, glaucoma is the main cause of vision disability (28%).

Today in Russia there are more than 850,000 glaucoma patients. Every year, 1 in 1000 people get glaucoma again. The general burden of the population increases with age: among people over 40 it is 1.5%, and over 80 years old - 14%. More than 15% of the blind have lost their sight as a result of glaucoma.

The concept of "glaucoma" unites a large group of eye diseases of various etiology. All of these diseases include:

■ an increase in intraocular pressure above the tolerant level for the optic nerve (TVHD);

■ the development of glaucomatous optic neuropathy with subsequent atrophy (with excavation) of the optic nerve head (Fig. 119, see inset);

■ the occurrence of typical visual field defects.

In the pathogenesis of glaucoma, the violation of the hydrodynamics of the eye, the ratio of production and outflow of intraocular fluid is of great importance.

Intraocular fluid is produced in the posterior chamber of the eye by the processes of the ciliary body, and then enters the anterior chamber of the eye through the opening of the pupil. Previously, moisture passes through the structures of the vitreous body, which thus carries out trophic and metabolic functions.

In the anterior chamber, intraocular fluid is directed to the corner of the anterior chamber of the eye, where the anterior and posterior outflow tracts are located (Fig. 120, see inset).

Intraocular fluid from the posterior chamber through the opening of the pupil enters the corner of the anterior chamber, then flows out, overcoming the resistance of the trabecular tissue, through the cavity of the scleral sinus, collector canals, intrascleral plexus, flowing into the water veins.

Intraocular fluid from the posterior chamber through the opening of the pupil enters the corner of the anterior chamber, then flows along the fibers of the ciliary muscle into the suprauveal and suprachoroidal spaces and further through the sclera to the outside (Fig. 121, see inset).

In recent years, new data on the pathogenesis and clinic of glaucoma have been obtained, which required changes to the existing classification of the disease.

Below is the classification of glaucoma, developed by A.P. Nesterov and E.A. Egorov (2001).

Glaukoma is divided into:

■ by origin - primary, secondary and associated with defects in the development of the eye and other structures of the body;

■ by the age of the patient - for congenital, infantile, juvenile and adult glaucoma;

■ by the mechanism of increasing intraocular pressure - open-angle, closed-angle, with dysgenesis of the anterior chamber angle, with pretrabecular block and with peripheral block;

■ by the level of intraocular pressure - on hypertensive and normotensive;

■ according to the degree of damage to the optic nerve head - on the initial, developed, advanced and terminal;

■ downstream - stable and unstable.

In primary glaucoma, pathogenic processes that occur in the CPC, the drainage system of the eye or in the head of the optic nerve, preceding the onset of the disease, have no independent meaning. They are the initial stages of glaucoma pathogenesis.

In secondary glaucoma, the mechanisms of glaucoma development are caused by independent diseases and cause glaucoma not always, but only in a number of cases. Secondary glaucoma is a possible complication of other diseases.

Glaucoma stages

The division of the continuous glaucoma process is arbitrary. When determining the stage of glaucoma, the state of the visual field and the optic nerve head is taken into account.

Stage I (initial) - the boundaries of the visual field are normal, but there are changes in the paracentral parts of the visual field (individual scotomas in the 5-20 ° zone, Bjerum's arched scotoma, blind spot enlargement). Excavation of the optic nerve head is widened, but does not reach its edge.

Stage II (advanced) - pronounced changes in the visual field in the paracentral region in combination with a narrowing of its boundaries by more than 10 ° in the superior and / or inferior nasal segment, marginal excavation of the optic nerve head.

Stage III (far-reaching) - the borderline of polarisation is concentrically narrowed and in one segment or more is located less than 15 ° from the fixation point, marginal subtotal excavation of the optic nerve head.

Stage IV (terminal) - complete loss of vision or preservation of light perception with incorrect light projection. Sometimes there is a small island of the visual field in the temporal sector.

Intraocular pressure level

When making a diagnosis, intraocular pressure means:

■ the letter "a" - within normal values

(P 0 below 22 mm Hg);

■ the letter "b" - moderately increased intraocular pressure

(R 0 is below 33 mm Hg. Art.);

■ letter "c" - high pressure (P 0 is equal to or higher than 33 mm Hg).

Dynamics of the glaucomatous process

Distinguish between stable and unstable glaucoma. With a stable course of the disease with prolonged observation (at least 6 months), the condition of the visual field and the optic nerve head does not deteriorate. In the case of an unstable flow, such changes are detected upon repeated treatment. When assessing the dynamics of the glaucomatous process, the IOP level corresponds to the target pressure.

SCHEDULE FOR DIAGNOSTICS

■Daily tonometrywithin (3-4 days)

■Biomicroscopy(water veins, anterior chamber depth, angle profile, iris atrophy, pseudoexfoliation, pigment dispersion)

■Defining boundariesvisual fields (perimetry)

■Direct ophthalmoscopy(condition of the optic nerve disc and retina)

There are 5 main groups:

■ congenital primary glaucoma

■ congenital glaucoma combined with other developmental defects

■ primary open-angle glaucoma (POAG)

■ primary angle-closure glaucoma (PZUG)

■ secondary glaucoma

Congenital primary glaucoma

Glaucoma symptoms may appear immediately after the baby is born or over time. Depending on the age at which the disease begins, congenital, infantile and juvenile glaucoma are distinguished.

Primary congenital glaucoma (hydrophthalmos) manifests itself up to 3 years of a child's life. The disease is inherited in a recessive manner, although sporadic cases are possible.

The pathogenesis of this type of glaucoma is associated with dysgenesis of the anterior chamber angle, which is the cause of impaired outflow of aqueous humor and increased intraocular pressure.

The clinical picture includes photophobia, lacrimation, blepharospasm, enlargement of the eyeball, enlargement and edema of the cornea, excavation of the optic nerve head, conjunctival hyperemia.

The stage of the glaucomatous process is determined by the degree of increase in the diameter of the cornea, expansion of the excavation of the optic nerve head and decrease in visual function (Table 4).

Table 4.Stages of glaucomatous process in primary congenital

glaucoma

Diagnostic methods:

■ tonometry (in children under 3 years of age, normal P 0 \u003d 14-15 mm Hg. In primary congenital glaucoma, P 0 exceeds 20 mm Hg or asymmetry of more than 5 mm Hg is detected);

■ measurement of the diameter of the cornea (normally in a newborn the diameter is 10 mm, by 1 year it increases to 11.5 mm, by 2 years - up to 12 mm. year of life);

■ biomicroscopy (edema and opacity of the cornea, tears of the decmethous membrane, deepening of the anterior chamber, atrophy of the iris stroma with exposure of its radial vessels);

■ ophthalmoscopy (normally, the fundus of a newborn is pale, the optic nerve head is paler than that of an adult, physiological excavation is absent or weak. In primary congenital glaucoma, excavation progresses rapidly, but in the early stages, with a decrease in intraocular pressure, excavation is reversible. , knowing that an increase in the diameter of the cornea by 0.5 mm corresponds to an increase in excavation by 0.2);

■ gonioscopy

Differential diagnosis should be carried out with megalocornea, traumatic corneal lesions, congenital dacryocystitis, congenital congenital glaucoma (Peters, Marfan, sclerocornea syndromes, etc.) (Table 5).

General principles of therapy. Medical treatment of primary congenital glaucoma is ineffective and is used only before surgery. For this purpose, drugs are prescribed that inhibit the production of aqueous humor: beta-blockers, 0.25-0.5% solution of timolol maleate 2 times a day by drop, local carbonic anhydrase inhibitors, 2% solution of dorzolamide 3 times a day topically, 1% solution brinzolamide 2 times a day. According to indications, systemic use of carbonic anhydrase inhibitors and osmotic diuretics is possible.

The choice of the type of surgical intervention depends on the stage of the disease and the structural features of the CPC. In the early stages, a goniotomy or trabeculotomy is performed; in the later stages, fistulizing operations and destructive interventions on the ciliary body are more effective.

achieved in 85% of cases. If the operation is performed in the early stages, then in 75% of patients it is possible to maintain visual functions throughout their lives. If the operation was performed at a later date, then vision is preserved only in 15-20% of patients.

Primary infantile glaucoma occurs in children aged 3 to 10 years. Inheritance and pathogenetic mechanisms are the same as in primary congenital glaucoma. However, in contrast to primary congenital glaucoma, the cornea and eyeball are not enlarged. The principles of therapy are similar to those for primary congenital glaucoma.

Primary juvenile glaucomaoccurs between the ages of 11 and 35. Inheritance is associated with abnormalities in chromosome 1 and TIGR. The mechanisms of impaired outflow of intraocular fluid and an increase in intraocular pressure are associated with the occurrence of trabeculopathy and / or goniodysgenesis. An increase in intraocular pressure and progressive glaucomatous atrophy of the optic nerve head are noted. Changes in visual functions occur according to glaucoma

type. The principles of therapy are similar to those for primary congenital glaucoma.

Primary open-angle glaucoma

This group includes several nosological forms of primary glaucoma. The mechanism of disturbance of the outflow of aqueous humor is common for all forms of primary open-angle glaucoma and is associated with the development of trabeculopathy and functional canalicular block. The development of trabeculopathy is due to age-related changes and / or (pseudo) exfoliative syndrome or pigment dispersion syndrome. A change in the hydrodynamics of the eye leads to an increase in intraocular pressure above the tolerant level and the development of atrophy of the optic nerve head in the glaucoma type.

Various types of open-angle glaucoma have some features of the pathogenesis.

Simple primary open-angle glaucoma (POAG) occurs at the age of over 35, pathogenesis is associated with the development of trabeculopathy and the functional block of the Schlemm's canal. According to A.P. Nesterov (1995), a certain role in the development of this type of glaucoma is played by the features of the anatomical structure of the eye: poor development of the scleral spur and ciliary muscle, the posterior attachment of the fibers of this muscle to the sclera, the anterior position of the Schlemm's canal, and a small angle of its inclination to the anterior chamber.

Risk factors in the development of POAG:

■ level of intraocular pressure;

■ age;

■ violation of hemodynamics;

■ metabolic disorders;

■ cytotoxic effects;

■ violation of the extracellular matrix.

The clinical picture.The course of the disease is usually asymptomatic with progressive decline in visual function. Rarely can one find complaints about the periodic appearance of rainbow circles before the eyes, asthenopic complaints. With tonometry, intraocular pressure is higher than the statistical norm in one or two eyes, the difference in intraocular pressure in two eyes is more than 5 mm Hg. Art., the difference between the level of IOP during morning and evening measurements is more than 5 mm Hg. Art. It is advisable to carry out tonometry in a sitting and lying position. Biomicroscopy in the anterior part of the eye reveals microvascular changes in the conjunctiva and episclera

(uneven narrowing of arterioles, expansion of venules, the formation of microaneurysms, small hemorrhages, granular blood flow, "cobra symptom"), diffuse atrophy of the pupillary girdle of the iris and destruction of the pigment border. Gonioscopy reveals symptoms of compaction of the trabecula zone, exogenous pigmentation, filling of the Schlemm's canal with blood). With ophthalmoscopy, thinning and smoothing of the layer of nerve fibers in the peripapillary zone, the development of GON, banded hemorrhages on the optic nerve head or near it) are observed.

Tonography reveals a decrease in the outflow lightness coefficient to 0.1-0.2 mm3 / min per 1 mm Hg. Art.).

When examining the visual field, paracentral scotomas are determined in the Bjerum zone, the narrowing of the boundaries is mainly in the upper and / or lower nasal segments.

Differential diagnosis is performed with normal pressure glaucoma and ophthalmic hypertension.

Exfoliative open-angle glaucomatied with (pseudo) exfoliative syndrome. Develops in old or old age. It is manifested by the deposition of exfoliative material in the anterior segment of the eye and the development of trabeculopathy and the functional block of the Schlemm's canal. Development of pseudoexfoliative syndrome without glaucoma is possible. Exfoliative open-angle glaucoma is more severe than POAG.

The clinical picture. The disease occurs in people over 50 years of age. One eye may be affected at first. Then, after a while, the disease develops in the other eye. Unilateral damage is rarely possible. Biomicroscopy reveals the deposition of exfoliative material (in the form of small grayish scales) along the edge of the pupil, which leads to the gradual disappearance of the pigment border on the anterior lens capsule, the posterior surface of the cornea. With gonioscopy, exfoliative material is found in the trabecular zone.

Pigment glaucomadevelops at a young and middle age in persons with pigment dispersion syndrome. Can be combined with a simple form of POAG. There is spontaneous stabilization of the glaucoma process. Possible development of pigment dispersion syndrome without glaucoma.

The clinical picture. Mostly men (77-90%) at the age from 15 to 68 years get sick. The average age of disease onset for men is 34 years, for women is 49 years. More often there are complaints about the appearance of rainbow circles, blurred vision.

Biomicroscopy reveals iris depigmentation and pigment deposition on different structures of the anterior part of the eye.

Normal pressure glaucoma (glaucoma of pseudo-normal pressure according to V.V. Volkov). This form of glaucoma has traditionally been called low pressure glaucoma. Recently, however, the term "normal pressure glaucoma" is more commonly used to refer to this type of glaucoma.

Worldwide data on the prevalence of normal blood pressure glaucoma vary considerably. The majority of ophthalmologists denied the existence of such glaucoma; diagnostic difficulties still persist. However, recent studies show that glaucoma with normal pressure accounts for 40% (in European countries), and according to some reports, 60% (in Japan) of all cases of POAG.

The clinical picture. The disease occurs over the age of 35 years. However, the onset of the disease usually occurs 10 years later than with POAG. More often, the disease develops in women. First, the disease usually occurs in the left eye, and then signs of pathology are detected in the right eye. Intraocular pressure with traditional measurement methods is within the statistical norm. However, in patients with this form of glaucoma, increases in ophthalmotonus are possible during the day, which are not recorded with traditional daily tonometry. The pressure can change dramatically with changes in body position. A history of ophthalmotonus rises can be detected, and with further observation, intraocular pressure may be within normal limits. In addition, a number of patients with this type of glaucoma have a low tolerance of the optic nerve to increases in intraocular pressure or a low individual rate of ophthalmotonus.

Acute hemodynamic disturbances in the body as a whole (bleeding, hypodynamic crises) or in the optic nerve head (optic nerve infarction).

Chronic disorders of general and local hemodynamics.

Cerebrospinal fluid pressure disorder.

Glaucomatous changes in the optic nerve head (for glaucoma with normal pressure, the appearance of hemorrhages in the optic head area is more characteristic) and visual field.

When diagnosing glaucoma with normal pressure, it is necessary to determine:

■ vascular status (study of the rheological properties of blood, Doppler ultrasonography of the vessels of the brain and ocular artery, calibrometry of the vessels of the retina, etc.);

■ the functional state of the optic nerve and retina (two-variable quantum perimetry, study of the central visual field, electrophysiological study);

■ topography of the optic nerve head (scanning laser ophthalmoscopy and other methods);

■ the dynamics of intraocular pressure during the day, with a change in body position, etc .;

■ functional tests on water veins, etc.

Differential diagnosis in glaucoma with normal pressure is carried out with POAG with increased intraocular pressure, other diseases of the optic nerve that can lead to its atrophy (myopia, ischemic neuropathy, etc.)

General principles of therapy for primary open-angle glaucoma

The mechanisms of glaucoma development have two points of application - the UPC, the damage to the structures of which leads to an increase in intraocular pressure, and the posterior segment of the eyeball, changes in which lead to glaucoma, optic neuropathy and a decrease in visual function. In the treatment of POAG, antihypertensive therapy is distinguished, which includes drug, laser and surgical effects, and neuroprotective therapy.

General principles of antihypertensive therapy. The goal of antihypertensive therapy is to achieve “target pressure”. However, today there are no simple and effective ways to determine target pressure. When prescribing antihypertensive therapy, consider:

■ the patient's age;

■ condition of the optic nerve head (size and depth of excavation, breaks to the edge, color of the neural ring);

■ the state of the peripapillary zone (glaucomatous peripapillary atrophy, peripapillary sclerosis of the choroidal vessels, banded hemorrhages);

■ the state of the visual field;

■ burdened heredity

■ systemic hypotension or a tendency to hypotonic crises, especially nocturnal;

■ tendency to vasospasm and migraines;

■ cardiovascular diseases with disorders of central hemodynamics;

■ violation of hemodynamics in the basin of the internal carotid artery;

■ tendency to hyperglycemia;

■ violation of the rheological properties of blood;

■ moderate and high myopia.

There are 3 groups of patients with different severity of the glaucoma process and different "target pressure":

■ young patients with the initial stage of POAG without pronounced changes in the optic nerve head and peripapillary area, without hereditary burden and concomitant pathology. Target pressure corresponds to 21-23 mm Hg. Art. (tonometric pressure), which should correspond to a decrease in eye pressure by at least 20% of the initial value;

■ patients of various ages with advanced or advanced stages of glaucoma without pronounced concomitant diseases and hereditary burden, as well as patients with initial changes in the visual field, but pronounced changes in the optic nerve head or peripapillary zone, with significant concomitant pathology and hereditary burden. Target pressure corresponds to 17-20 mm Hg. Art. (tonometric pressure), which should correspond to a decrease in intraocular pressure by at least 30% of the initial value;

■ patients with advanced and advanced glaucoma with pronounced changes in the optic nerve head or the peripapillary zone, as well as significant concomitant pathology and hereditary burden. Target pressure corresponds to 16 mm Hg. Art. and below (tonometric pressure), which should correspond to a decrease in intraocular pressure by at least 35-40% of the initial value.

The antihypertensive effect involves:

■ the most effective drug therapy;

■ laser exposure;

■ laser exposure and drug therapy;

■ non-penetrating operation;

■ non-penetrating surgery and drug therapy;

■ traditional penetrating fistulizing surgery;

■ Penetrating fistulizing surgery and drug therapy.

The transition from one type of treatment to another is carried out when the therapy is ineffective. In some cases, already at the beginning of therapy, it is necessary to resort to a more significant effect (in the case of non-compliance of the patient, intolerance to drug therapy, high intraocular pressure, etc.). Therefore, the choice of drug exposure should be carried out taking into account all the characteristics of each individual person.

General principles of antihypertensive drug therapy

■ One of the first-line drugs is prescribed first. If ineffective, it is replaced with another drug of the first choice or combination therapy is prescribed (with the drug of the first and second choice or with two drugs of the first choice).

■ In case of intolerance or contraindications to therapy with drugs of the first choice, treatment begins with drugs of the second choice.

■ As part of combination therapy, do not prescribe more than two drugs at the same time. It is better to choose combined dosage forms.

■ Drugs with the same pharmacological effect should not be used in combination therapy.

First choice drugs:

■ latanoprost, travoprost;

■ timolol;

■ pilocarpine. Second-choice drugs:

■ betaxolol;

■ proxodolol;

■ brinzolamide;

■ clonidine.

When carrying out drug therapy 2-3 times a year for 1-2 months, the therapy is changed. One should not only use a drug of another pharmacological group, but also change the type of effect on the hydrodynamics of the eye.

General principles of POAG neuroprotective therapy

Neuroprotective therapy is effective only if the target pressure is achieved.

E.A. Egorov and V.N. Alekseev (2001) divide neuroprotection into direct, when drugs directly protect the retinal ganglia and optic nerve axons, and indirectly, when

the neuroprotective effect is associated with the effect of drugs on risk factors that accelerate the death of nerve cells.

Direct neuroprotectors include betaxolol, enzymatic antioxidants (superoxide dismutase), peptide bioregulators (retinalamin). Drugs that have an indirect neuroprotective effect can be divided into drugs of the first and second choice. Indirect neuroprotectors include antispasmodics, angioprotectors, calcium antagonists, nootropic drugs, antihypoxants (cytochrome C), non-enzymatic (vitamins C, E, PP, succinic acid, emoxipin, histochrome) antioxidants.

The drugs of the first choice are always indicated for all patients, since they affect the main links of pathogenesis: reduced adaptation, intraocular microcirculation disorders, impaired rheological properties of blood, changes in the vascular wall, including atherosclerosis and metabolic disorders.

Second-choice drugs correct other risk factors for glaucoma, depending on their severity and significance.

Primary angle-closure glaucoma

Primary angle-closure glaucoma with pupillary block - the most common type of this pathology (70-80%), occurs in middle-aged and elderly people. Causes acute and subacute attacks. In the future, due to the formation of goniosinechia, it becomes chronic.

Risk factors: hyperopia, small anterior chamber, narrow angle of the anterior chamber, large lens, thin root of the iris, posterior position of Schlemm's canal.

Pathogenesis is associated with the development of pupillary block with moderate dilation of the pupil, which leads to protrusion of the iris root and blockade of the CPC. Iridectomy stops the attack, prevents the development of new attacks and the transition to a chronic form.

The clinical picture of an acute attack:

■ pain in the eye and its surrounding area with irradiation along the trigeminal nerve (forehead, temple, zygomatic region);

■ bradycardia, nausea, vomiting;

■ decreased vision, the appearance of rainbow circles before the eyes. Survey data:

■ mixed stagnant injection;

■ corneal edema;

■ shallow or slit anterior chamber;

■ with prolonged existence of an attack for several days, opalescence of moisture in the anterior chamber may appear;

■ there is a protrusion anteriorly of the iris, edema of its stroma, segmental atrophy;

■ mydriasis, there is no pupil photoreaction to light;

■ a sharp increase in intraocular pressure.

The clinical picture of a subacute attack:a slight decrease in vision, the appearance of rainbow circles before the eyes;

Survey data:

■ light mixed injection of the eyeball;

■ mild corneal edema;

■ mild pupil dilation;

■ increased intraocular pressure up to 30-35 mm Hg. Art .;

■ during gonioscopy - the CPC is not blocked throughout;

■ during tonography, there is a sharp decrease in the coefficient of ease of outflow.

Differential diagnosis should be carried out with acute iridocyclitis, ophthalmic hypertension, various types of secondary glaucoma associated with a pupillary block (phakomorphic glaucoma, bombing of the iris during its overgrowth, phakotopic glaucoma with an entrapment of the lens in the pupil) or UPC block (neoplastic, phakotopic glaucoma with anterior dislocation camera). In addition, it is necessary to differentiate an acute attack of glaucoma with the syndrome of glaucocyclitic crisis (Posner-Schlossmann syndrome), diseases accompanied by the syndrome of "red eye", trauma to the organ of vision, hypertensive crisis.

Treatment of an acute attack of angle-closure glaucoma.Drug therapy.

During the first 2 hours, 1 drop of 1% pilocarpine solution is instilled every 15 minutes, during the next 2 hours, the drug is instilled every 30 minutes, during the next 2 hours, the drug is instilled 1 time per hour. Further, the drug is used 3-6 times a day, depending on the decrease in intraocular pressure;

0.5% timolol solution is instilled in 1 drop 2 times a day. Inside appoint acetazolamide 0.25-0.5 g 2-3 times a day.

In addition to systemic carbonic anhydrase inhibitors, you can use a 1% suspension of brinzolamide 2 times a day topically;

Osmotic diuretics are used orally or parenterally (most often a 50% glycerol solution is given orally at the rate of 1-2 g per kg of weight).

With an insufficient decrease in intraocular pressure, loop diuretics (furosemide at a dose of 20-40 mg) can be administered intramuscularly or intravenously

If the intraocular pressure does not decrease, despite the therapy, a lytic mixture is injected intramuscularly: 1-2 ml of a 2.5% chlorpromazine solution; 1 ml of 2% diphenhydramine solution; 1 ml of a 2% solution of promedol. After the introduction of the mixture, the patient must comply with bed rest for 3-4 hours due to the possibility of the development of orthostatic collapse.

To stop an attack and prevent the development of repeated attacks, laser iridectomy is required in both eyes.

If the attack could not be stopped within 12-24 hours, then surgical treatment is indicated.

Treatment of a subacute attack depends on the severity of the disturbance in hydrodynamics. Usually 3-4 instillations of 1% pilocarpine solution are sufficient for several hours. A 0.5% solution of timolol is instilled 2 times a day, 0.25 g of acetazolamide is prescribed internally 1-3 times a day. To stop an attack and prevent the development of repeated attacks, laser iridectomy is required in both eyes.

Treatment of chronic angle-closure glaucoma.

The drugs of the first choice are miotics (1-2% pilocarpine solution is used 1-4 times a day). If monotherapy with miotics is ineffective, drugs from other groups are additionally prescribed (non-selective sympathomimetics cannot be used, since they have a mydriatic effect). In this case, it is better to use combined dosage forms (fotil, fotil-forte, normoglaucon, proxacarpine).

In the absence of a sufficient hypotensive effect, they switch to surgical treatment. It is advisable to use neuroprotective therapy.

Ophthalmic hypertension

All cases of non-glaucoma increase in intraocular pressure can be divided into:

■ pseudohypertension,which is associated with an involuntary short-term increase in intraocular pressure when the tonometer approaches the eye. When re-measured after calming the patient, intraocular pressure is within normal limits;

■ symptomatic ophthalmic hypertensionas a symptom of an eye (iridocyclitis, glaucocyclitic crisis, reactive uveal syndrome) or a general disease (Itsenko-Cushing's syndrome, hypothyroidism, diencephalic disorders, pathological menopause), poisoning or side effects of drugs (glucocorticosteroids);

- more often a hereditary disease, accompanied by a gradual increase in intraocular pressure and associated visual disturbances caused by this. The main symptoms of this pathology include an increase in the size of the eyes (in infants), soreness, which leads to anxiety and tearfulness of the child, photophobia, myopia or astigmatism. Diagnosis of congenital glaucoma is made on the basis of ophthalmological examination data, study of the patient's hereditary history and the course of pregnancy, genetic studies. Treatment is only surgical, and it should be performed as early as possible before the development of irreversible secondary disorders in the organ of vision.

ICD-10

Q15.0

General information

Diagnosis of congenital glaucoma

Detection of congenital glaucoma is carried out by an ophthalmologist based on examination data, ophthalmological examinations (tonometry, gonioscopy, keratometry, biomicroscopy, ophthalmoscopy, ultrasound biometry). Also, genetic studies, the study of hereditary history and the course of pregnancy play an important role in the diagnosis of this condition. On examination, enlarged (with an early form) or normal size of the eyes are found, edema of the tissues surrounding the eyeball may also be observed. The horizontal diameter of the cornea is increased, micro-ruptures and turbidity are possible on it, the sclera is thinned and has a bluish tinge, the iris is affected in congenital glaucoma - atrophic processes appear in it, the pupil sluggishly reacts to light stimuli. The anterior chamber of the eye is deepened (1.5-2 times the age norm).

For a long time, no pathological changes occur in the fundus, since by increasing the size of the eyeball, the intraocular pressure does not initially reach significant values. But then the excavation of the optic nerve head develops rather quickly, however, with a decrease in pressure, the severity of this phenomenon also decreases. Due to the increase in the size of the eyes in congenital glaucoma, thinning of the retina occurs, which, if untreated, can lead to its rupture and rhegmatogenous detachment. Often against the background of such changes, myopia is found. Tonometry shows a slight increase in intraocular pressure, but this indicator should be compared with the anteroposterior size of the eye, since stretching of the sclera smoothes the IOP indicators.

The study of the hereditary history can reveal similar changes in the patient's relatives, while it is often possible to determine the autosomal recessive type of inheritance - this is evidence in favor of primary congenital glaucoma. The presence of infectious diseases of the mother, injuries, exposure to teratogenic factors during pregnancy indicates the possibility of developing a secondary form of the disease. Genetic diagnostics is carried out through direct sequencing of the CYP1B1 gene sequence, which makes it possible to identify its mutations. Thus, only a geneticist can unequivocally prove the presence of primary congenital glaucoma. In addition, in the presence of such a condition in one of the parents or their relatives, it is possible to search for the pathological form of the gene before conception or prenatal diagnosis by amniocentesis or other techniques.

Treatment and prognosis of congenital glaucoma

Treatment of congenital glaucoma is only surgical, it is possible to use modern laser technologies. Conservative therapy using traditional means (pilocarpine drops, clonidine, epinephrine, dorzolamide) is auxiliary and can be used for some time while waiting for the operation. Surgical intervention is reduced to the formation of a pathway for the outflow of aqueous humor, which reduces intraocular pressure and eliminates congenital glaucoma. The method and scheme of the operation is selected in each case strictly individually. Depending on the clinical picture and structural features of the eyeball, goniotomy, sinustrabeculectomy, drainage operations, laser cyclophotocoagulation or cyclo-cryocoagulation can be performed.

The prognosis of congenital glaucoma with timely diagnosis and operation is most often favorable, but if the treatment is performed with a delay, visual impairments of various severity are possible. After elimination of glaucoma, at least three months of dispensary observation by an ophthalmologist are required.

The questions asked during the next "direct line" of the newspaper "Zvyazda" in January 2011 were answered by Associate Professor of the Department of Ophthalmology of the Belarusian Medical Academy of Postgraduate Education, Candidate of Medical Sciences Galina SEMAK.

RETINAL DYSTROPHY

- Kletsk, Irina Ivanovna. I have retinal pigmentary dystrophy. What can be the treatment?
- Treatment can only be symptomatic, aimed at helping the eyes a little, maintaining vision, improving the metabolic processes in the eye. There are no radical methods, since retinal pigmentary degeneration is a congenital pathology.
- But after all, even in my school years, when my eyesight was checked, such a pathology was not found ...
- This means that the manifestations of pathology were very weak. But I want to draw your attention to the fact that since retinal pigmentary dystrophy is inherited, your children must be examined and observed.
- Can I get my glasses?
- Dystrophy means that the nerve cells of the retina have died. Of course, they can no longer work. Therefore, no glasses can restore their function. At least some pieces of glass may help you. You have to work with your ophthalmologist and be constantly monitored. Perhaps you can pick up something.

- Stolbtsovsky district, Stepan Ivanovich. Diagnosis - retinal degeneration of the right eye. I received treatment but did not feel any improvement. Is it possible to correct my vision, where can it be done?
- In your case, it is very difficult to improve your eyesight, since vision is an indicator of a person's health in general. The cause of retinal dystrophy of the right eye, most likely, may be high blood pressure, possibly diabetes mellitus or thyroid disease. In other words, general pathology is very often the cause of a decrease in visual acuity. Therefore, you need to be examined by a therapist, cardiologist, endocrinologist and bring all examination data to an ophthalmologist who will draw the correct conclusions. If there are any doubts, then you can seek advice from the Republican Ophthalmological Center of the 10th Clinical Hospital in Minsk.

- Baranovichi, Tatyana Petrovna. I have hypertension, initial cataract, they are referred for a consultation for laser coagulation of the retina. And the question is: does such a drug as Ocuwaite Lutein help in the initial stages of cataracts? Or is it just prevention?
- You must understand that Ocuwaite Lutein is needed not for the treatment of cataracts, but for your retina. This drug was specially developed by a number of leading countries in the world for the elderly. It is after 40 years that the retina often suffers against the background of arterial hypertension, and in order to preserve its pigment, Okuwait Lutein is prescribed. The drug is good and necessary.
You have been appointed for a consultation so that laser surgeons see whether a specific intervention is necessary, to what extent it is necessary ... After 40 years, half of the adult population has an initial cataract. Therefore, there is no need to be upset here, you should drip multivitamin drops and be observed by an ophthalmologist to monitor whether the cataract is progressing. Cataract is not treated conservatively - only surgically, but surgery is resorted to when the disease interferes with vision, worsens the quality of human life. Therefore, drive up to the laser center and treat the retina.

- Kletsk district, Zinaida Ilyinichna. 72 years old. Vision has dropped and continues to fall, eyes hurt.
- What is your blood pressure?
- Increased.
- Does it surprise you that you turned to me as an ophthalmologist, and I ask you about blood pressure? You must clearly understand that visual acuity is an indicator of the health of the body as a whole. If you have high blood pressure, it means that it is high in all organs and tissues, including the eyes. Therefore, the first thing to do is to correct blood pressure. I have to go to a cardiologist and a therapist. Did the ophthalmologist examine you?
- He said that a cataract is developing. The drops were prescribed ...
- Cataracts are the result of high blood pressure, because the metabolic processes in the eye do not occur correctly ... Drops can and should be dripped, but you shouldn't expect them to improve vision. Please deal with your pressure.
The Minsk Regional Hospital now has an excellent ophthalmology department. Ask your local doctor to be referred there or to our 10th hospital in Minsk. You need to be examined.

GLAUCOMA

- Berezinsky district, Natalia. Eye pressure figures - 22 mm Hg. Can glaucoma begin to develop in such a situation? How to determine for yourself what exactly is she? They showed on television how to do it yourself, how to measure the angle of view ...
- You can notice glaucoma using different methods, but what's the point of diagnosing yourself? I have to go to the doctor. Glaucoma does not affect central vision, peripheral vision suffers. There are several methods for measuring intraocular pressure. If the pressure 22 was shown by a non-contact tonometer, then this is not at all the same as on the contact one, according to Maklakov. However, it must be borne in mind that there is also such a phenomenon as low-pressure glaucoma, when the pathological process occurs against the background of low pressure figures. For the investigation in such situations, there are glaucoma rooms today, where the ophthalmologist sends after he has performed visometry, perimetry, tonometry.

- Pruzhany, Zoya Ivanovna. My husband is 58 years old, he has glaucoma of the right eye. We drip cymalon and tramadol. Are we doing it right?
- These are very strong drugs that are used with the maximum treatment regimen. I believe that you need laser or surgical treatment in order not to drip such a large amount of drugs, especially since they also affect the body as a whole. Solve this issue with your ophthalmologist.
- Is there a laser in Brest?
- It should be. If not, you will be referred to us.

BLEFAROSPASM

- Dzerzhinsk, Sophia. What should I do with an ailment like blepharospasm?
- It is very important to find out the etiology of blepharospasm. Very often it occurs if a person has chronic conjunctivitis, keratitis, if the eyes hurt and the eye is, as it were, protected from sunlight, squinting. And then, even in calm eyes, this blepharospasm remains. It is also possible that this is an increased sensitivity of the cornea to light. In this case, sunglasses are often helpful. In this case, you need to find out what is the origin of blepharospasm. Perhaps neurologists can help in the sense of improving the conduction of nerve tissue and eliminating this increased sensitivity to light.

REMOVAL DISEASE

- Grodno, Elena Mikhailovna. My brother has a detachment disease. I lost my eyesight because of this. He recently underwent surgery on his left eye - the retina was sutured. How to preserve the retina and the left eye?
- Where does your brother live?
- In the Vitebsk region.
- Hard physical work with a torso is contraindicated for your brother in the first place.
- He works as a teacher.
- Good, but you need to remember about weights. It is imperative to check the fundus and fundus lens once a year. If he notices that his vision is decreasing, some changes, distortions appear, it is necessary to urgently go to a specialist.
- After cauterization of the retina, my brother began to see worse, a hematoma formed. Why did the blood get under the retina or on the retina?
- This is how the disease proceeds. The retina ruptures, the vessels suffer. That is why I say that it is necessary to monitor all this and further treat with the help of a laser, surgical intervention.
- Maybe he needs to take any vitamins?
- There is a large arsenal of vitamin complexes. If there are no specialists at the place of residence with whom it would be possible to discuss such issues, it is necessary to drive up to Vitebsk, and it is best of all to be observed by one doctor.
- Can he be given a second vision group? Now he has a third ...
- Recommendations regarding this are clearly spelled out, and experts of a different kind should consider such issues.

Itching eyelid

- Minsk, Irina Nikolaevna. The eyelids around the eyes become inflamed - itch, peel off, even cracks appear. I feel irritation around the eyelashes, it itches a little. And this has been observed for several years.
- What did you do?
- I smeared with hydrocortisone, sinaflan ... I constantly use cosmetics. If I don't use it on weekends, for example, it seems to be a little better, but during the week the situation worsens.
- Did you manage not to use cosmetics for a longer time?
- Unfortunately no.
- Firstly, it is impossible to exclude the allergic component. You need to contact an allergist and be tested for allergens. There is an allergy center in Hospital 10, where a therapist will refer you. The second direction of your examinations is an examination by an ophthalmologist, who will look for such phenomena as blepharitis, dry eye. Finally, you yourself perfectly understand that you need to remove the annoying factor. Find yourself a chic frame. We must somehow adapt.
- What if the eyelashes fall out?
- It is necessary to hand over eyelashes for examination under a microscope for demodicosis. Often a tick lives on the eyelashes, and then they fall out, since the follicles from which they grow are affected. The study can be done in the skin and venereal clinic - on Prilukskaya or Smolyachkov.
- Can't you strengthen your eyelashes with oils - castor oils, for example?
- All this can be done when the inflammatory process is over. And while there is a reaction, there is no need to strengthen it.
- Once they told me about the possibility of an allergic reaction, but at the same time they prescribed drugs that improve digestion.
- It is right. You need to know the golden rule for treating allergies: "Cold, hunger, and peace." And, of course, allergens must be removed from use. If you add paint to your face, then immediately maintain a diseased condition.

Svetlana BORISENKO, Olga SHEVKO, newspaper "Zvyazda", January-February 2011.
Original in Belarusian:
http://zvyazda.minsk.by/ru/archive/article.php?id\u003d73437
http://zvyazda.minsk.by/ru/archive/article.php?id\u003d73504
http://zvyazda.minsk.by/ru/archive/article.php?id\u003d73605&idate\u003d2011-02-01
http://zvyazda.minsk.by/ru/archive/article.php?id\u003d73668&idate\u003d2011-02-02

What is called "glaucoma" today? Glaucoma (from the Greek - the color of sea water, azure) is a serious disease of the organ of vision, named after the greenish color, which acquires a dilated and immobile pupil at the stage of the highest development of the painful process - an acute attack of glaucoma. From here comes the second name of this disease - "green water" or "green cataract" (from German "Grun Star").

Congenital glaucoma is a genetic (sometimes acquired) pathology, expressed in the insufficient development of the angle of the eye chamber (anterior) in conjunction with the trabecular network system. This pathology leads to a sharp increase in intraocular pressure in the eye chamber.

This pathology is very rare and does not occur often in ophthalmology, on the order of one case per ten thousand births. Despite the known figures, many experts argue that it is impossible to calculate statistics, since often the congenital form of glaucoma manifests itself already in adulthood and these patients make up completely different statistics.

The disease is inherited in an autosomal recessive mode of inheritance. However, it was estimated that boys prevail among the cases (approximately 3: 2 is the sex distribution).

Also, there are several age periods for the development of this pathology. The main danger of this pathology is the fact that a child can go blind in the absence of treatment for glaucoma after 4-5 years.

Congenital glaucoma - causes.

As mentioned earlier, congenital glaucoma is a pathology of a genetic nature, where about 80% of clinical cases of congenital glaucoma are accompanied by a mutated genome. In this case, the CYP1B1 gene located on the 2nd chromosome has been mutated.

This gene is responsible for the cytochrome P4501B1 protein, which has not yet been reliably studied. However, it is known that cytochromes of the P450 group are involved in energy metabolism within the cell.

There is a hypothesis that this protein is also responsible for the synthesis and destruction of trabecular molecules, the violation of which leads to irreversible consequences of the trabecular network and the manifestation of glaucoma.

To date, geneticists know about a hundred different mutations of this gene, but it was not possible to identify their connection with the manifestation of glaucoma in a child. What can be said about other mutations, the information has not yet been reliably studied.

Presumably, the MYOC gene is located on the 1st chromosome, the defect of which also manifests itself in the form of congenital glaucoma. The MYOC gene encodes a protein called myocellin, which is essential for the formation of the trabecular network of the eye.

It was previously known that this particular gene was the cause of open-angle glaucoma. It has now become known that the combined disruption of these two genes simultaneously causes congenital glaucoma, despite this conclusion, certain geneticists believe that the MYOC gene mutation does not affect the manifestations of glaucoma and lead it to a simple coincidence.

The basis for the manifestation of congenital glaucoma is still considered to be the cumulative defeat of these genes.

Causes and mechanisms of glaucoma development

The pathogenesis of congenital glaucoma is diverse, however, the basis for the increase in IOP is underdevelopment or improper development of the drainage system of the eye. The most common causes of blockage of the trabecula and Schlemm's canal area are undissolved embryonic mesoderm tissue, poor differentiation of angular structures, anterior iris root attachment, and a combination of various anomalies. The severity of the process and the rate of its development depend on the degree of the defect in the outflow tract of the intraocular fluid: the more it is expressed, the earlier the disease manifests itself clinically.

Causes of congenital glaucoma

Intrauterine glaucoma is the result of various pathological factors affecting the fetal eye, which can lead to abnormalities in the anterior part of the eye. An increase in IOP occurs when the outflow of IOP is impaired as a result of the fact that the non-absorbed embryonic mesoderm tissue closes the iris-corneal angle of the anterior chamber.

Less commonly, intrascleral changes or anterior iris attachment are the cause of the formation of a blockage (rejection) of aqueous humor.

The underlying disease is underdevelopment or abnormal development of the drainage system of the eyes.

Heredity plays a significant role in the development of pathology. The predisposition to this type of glaucoma is transmitted mainly in an autosomal recessive manner. Factors that can lead to the development of congenital glaucoma also include:

• infectious diseases transferred by the mother during pregnancy;
• endocrine system disorders;
• hypovitaminosis;
• exposure to ionizing radiation.

Classification of congenital glaucoma

Congenital glaucoma includes several types: congenital glaucoma, or hydrophthalmos (symptoms of the disease appear in the first year of life); infantile, or delayed, congenital glaucoma (aged 3-10 years); juvenile glaucoma (11-35 years old); glaucoma combined with other developmental defects.

Such a significant spread in the age of congenital glaucoma development is directly related to the degree of underdevelopment of the trabecular network of the eye. The more pronounced the violations in these structures, the earlier the accumulation of aqueous humor begins with an increase in intraocular pressure.

If the underdevelopment of the angle of the anterior chamber of the eye does not reach significant values, then in the first years of the child's life, the outflow occurs quite normally, and the disorders develop much later. Attempts to associate certain clinical forms of congenital glaucoma with specific types of mutations in the CYP1B1 gene have so far not been successful, and the mechanisms of development of this or that type of disease are still unknown.

Distinguish between congenital glaucoma. juvenile glaucoma (juvenile glaucoma. or glaucoma of young age), primary glaucoma in adults and secondary glaucoma.

Congenital glaucoma can be genetically determined (predetermined) or caused by diseases and injuries to the fetus during embryonic development or during childbirth. This type of glaucoma occurs in the first weeks and months of life, and sometimes several years after birth. This is a rather rare disease (1 case per 10-20 thousand newborns).

This disease has several varieties. We list them:

• hydrophthalmos (manifests itself in the 1 year of a child's life);
• delayed (infantile) glaucoma (observed at the age of 3 to 10 years);
• juvenile glaucoma (manifests itself after 11 years).

A special form of pathology is combined glaucoma, which is accompanied by anomalies in the development of other organs. Specialists also use the classification of the disease by degrees (there are three degrees of pathology).

Another way to classify congenital glaucoma is according to the characteristics of the course of the disease:

• typical - the clinical picture becomes vivid when the child reaches the age of 3-4 months;
• benign - the clinical picture becomes clear by the second year of life, the eye increases in size slightly;
• malignant - pronounced signs of glaucoma are recorded at the birth of a baby, or in the first months of his life, often a bilateral process, the eyeball is greatly enlarged, the cornea is cloudy
• abortive - intraocular pressure returns to normal, the disease does not progress.

Appointment to a pediatric ophthalmologist (ophthalmologist)

Dear patients, We provide the opportunity to make an appointment directly with the doctor to whom you want to get a consultation. Call the number listed at the top of the site, you will receive answers to all questions. Beforehand, we recommend that you study the About Us section.

How to make an appointment with a doctor?

1) Call 8-863-322-03-16.

Request a call

Call a doctor

2) The doctor on duty will answer you.

3) Tell us about your concerns. Be prepared that the doctor will ask you to tell as much as possible about your complaints in order to determine the specialist required for consultation. Keep all available analyzes at hand, especially those recently done!

4) You will be connected to your future treating doctor (professor, doctor, candidate of medical sciences). Further, directly with him you will discuss the place and date of the consultation - with the person who will treat you.

OPT.OK. 30.04.2017

Glaucoma symptoms. Signs of eye glaucoma

Open-angle glaucoma is the most common form of this disease, in which the angle of the anterior chamber is open, but the outflow of intraocular fluid is impeded due to disturbances in the vascular and drainage systems of the eye.

As a rule, the disease is more severe if it manifests itself at a very early age. Initial symptoms of hydrophthalmos:

• enlargement of the cornea;
• corneal edema;
• cracks in the Descemet shell.

With the progression of the disease, the cornea stretches, and the sclera becomes thinner, acquiring a bluish tint (the choroid begins to shine through it). The limbus (the border of the sclera and the cornea) expands, the anterior chamber of the eye becomes deeper.

Dystrophy of the iris occurs, the pupil reacts worse to light. The size of the lens does not change, but it flattens, over time it can become cloudy (cataract, read about this disease http: // www.

okomed / cataracta. html).

A significant increase in the size of the eyeball can be accompanied by rupture of the ciliary ligaments, subluxation or even dislocation of the lens. With the development of the disease, there is a gradual death of the optic nerve fibers. The retina of the eye is stretched, which can lead to degeneration and detachment.

Diagnosis of congenital glaucoma

Early recognition of congenital glaucoma takes place only if a thorough examination of the newborn's eyes is carried out. Attention should be paid to the size of the eye and cornea. If, during a simple examination by a specialist, a clouding of the cornea, an increase in its size, expansion of the pupils and a deepening of the anterior chamber were noticed, then this should immediately suggest the possibility of a pathology.

In such cases, it is necessary to consult an ophthalmologist and be sure to undergo a study to determine the IOP. Intraocular pressure of children under 2 years of age and in newborns should not be performed by palpation, but exclusively with the help of a tonometer under conditions of physiological sleep, which can be increased with the help of relatively weak hypnotics and tranquilizers (triosin, luminal), and in some cases - and under general anesthesia.

The more accurately and earlier the diagnosis is made, the less traumatic and more effective the prescribed treatment will be, in particular, antiglaucomatous operations. This is what will allow you to get a greater number of chances for maintaining vision in children.

Congenital glaucoma treatment

Medical treatment is ineffective and, as a rule, serves as an adjunct to surgery. It includes the use of miotics, prostaglandin analogs, beta-blockers, carbonic anhydrase inhibitors. Also shown is general strengthening and desensitizing therapy. The basis of surgical treatment is based on two principles: timeliness and pathogenetic orientation. The operation should be carried out as soon as possible, almost immediately after the diagnosis. The choice of the type of operation is based on the results of gonioscopy. Since all congenital glaucomas are angle-closure, the main principle is to improve the outflow of intraocular fluid. In the presence of embryonic mesodermal tissue in the corner of the anterior chamber, a goniotomy is performed. The essence of the operation is the destruction of embryonic tissue using a special tool. Goniotomy is recommended in the initial stage of the disease with normal or slightly elevated IOP. In the advanced stage, goniotomy is combined with goniopuncture, which allows you to create an additional passage for subconjunctival fluid filtration; in some cases, mesodermal tissue is removed by internal and external trabeculotomy. In an advanced stage, they resort to fistulizing operations - sinusotrabeculectomy. In the terminal stage of the disease, operations aimed at reducing the production of intraocular fluid are performed - transscleral diathermo-, cryo- or photocoagulation of the ciliary body.

For foreign patients, the cost of ophthalmic treatment in Germany is strictly regulated according to the Healthcare Price List (GOÄ). Doctors in Germany cannot claim self-determined fees for medical services. They are legally required to adhere to the GOÄ value.

Eye diseases are diseases of the lacrimal glands, the skin around the eyes (including the eyelid), the lens, the optic nerve, the eye muscles, and the orbit (orbit). An estimated 15-20 million people in Germany suffer from eye diseases.

The most common pathology is ametropia (farsightedness or myopia), caused by abnormal refraction of light in the eye through the cornea or lens. 63.5% of the German population aged 16 and over wear glasses.

The most common diseases other than ametropia are age-related retinal diseases, conjunctivitis, glaucoma, and cataracts. In addition, other diseases in the body affect vision (diabetes, multiple sclerosis, Parkinson's disease, Graves disease).

Nearsightedness, hyperopia and presbyopia

Distinguish between myopia (myopia) and hyperopia (farsightedness), which are caused by an incorrect ratio of the length of the eye and the refractive power of the lens. As a result, light rays entering the eye are not focused on the retina, but before or after it. First of all, farsightedness is a natural sign of aging.

If the refractive power of the cornea changes (astigmatism), then we speak of astigmatism, in which light rays are refracted in different directions. This creates a projection onto the retina that does not look like a normal point, but looks like a rod.

Laser correction of ametropia

In addition to correcting ametropia with glasses and contact lenses, laser surgery has been used to treat eyes for almost 20 years. The laser correction procedure has evolved over time. Today, both laser and surgical methods are safe and patient-friendly. Currently, the following laser procedures prevail for the correction of ametropia:

• LASIK
• Femto-LASIK
• ReLEx® smile

Implantable contact lenses for the correction of hyperopia, myopia and astigmatism

Not every patient can undergo vision correction surgery. It depends on the severity of the ametropia. This is where implantable contact lenses come in, offering a good alternative to sight without glasses. There are two types of intraocular lenses:

• Anterior chamber lenses
• Posterior chamber lenses

What type of lenses is the most optimal option in each case is determined by a detailed preliminary examination by an ophthalmologist.

Age-related retinal diseases (retinal detachment)

Treatment of congenital glaucoma is only surgical, it is possible to use modern laser technologies. Conservative therapy using traditional means (pilocarpine drops, clonidine, epinephrine, dorzolamide) is auxiliary and can be used for some time while waiting for the operation.

Surgical intervention is reduced to the formation of a pathway for the outflow of aqueous humor, which reduces intraocular pressure and eliminates congenital glaucoma. The method and scheme of the operation is selected in each case strictly individually.

Depending on the clinical picture and structural features of the eyeball, goniotomy and sinustrabeculectomy can be performed. drainage operations, laser cyclophotocoagulation or cyclo-cryocoagulation.

The prognosis of congenital glaucoma with timely diagnosis and operation is most often favorable, but if the treatment is performed with a delay, visual impairments of various severity are possible. After elimination of glaucoma, at least three months of dispensary observation by an ophthalmologist are required.

With congenital glaucoma in a child, when collecting an anamnesis from the mother, it is necessary to find out how anxious the child is, whether he sleeps well, takes the breast, and often regurgitates food. It is necessary to find out the impact of teratogenic factors (viral diseases, trauma, ionizing radiation, hyper- and hypovitaminosis, congenital and hereditary factors) on the mother's body during pregnancy.

The child's visual acuity is determined in accordance with age. An examination is carried out by the method of lateral illumination, transmitted light, intraocular pressure is determined by palpation.

It is necessary to know that with a careful examination of the condition of the eyes in newborns, even without special ophthalmic devices, it is possible to accurately diagnose in 90% of cases. With the help of a millimeter ruler, applied in the right direction to the edges of the orbit, the size of the cornea is measured (9 mm - in newborns, 10 mm - in children one year old and 11 mm - in children over 3 years old).

a) photophobia, blepharospasm;

b) restless behavior of the child;

c) slight turbidity (dullness, corneal swelling);

d) deep anterior chamber (over 2 mm);

e) dilated pupil. Over 2 mm with a delayed reaction to light.

The main sign of congenital glaucoma is a combination of one of the above signs with increased intraocular pressure.

The diagnosis is made on the basis of the origin, form, dynamics of the process, stage of the process, degree of compensation.

a) expansion and tortuosity of the anterior ciliary vessels in the scleral region ("medusa's head", "cobra's head", emissary symptom);

b) stretching the entire anterior segment of the eye;

c) pronounced edema and opacity of the cornea;

d) trembling of the iris (iridodonesis);

f) the appearance of axial myopia.

Differential diagnosis of congenital glaucoma is carried out from megalocornea - a large cornea (there are no other symptoms of the disease) and parenchymal keratitis. With the latter, there are characteristic changes in the cornea in the absence of other signs of the disease.

1. In the prevention of blindness from congenital glaucoma, the main role belongs to the early detection and surgical treatment of the disease in children already in the first year of life. Therefore, a pediatrician of any profile should pay attention to the early signs of congenital glaucoma.

2. When making a diagnosis of congenital glaucoma

first medical aid is provided in the form of immediate prescription of conservative therapy (cholinomimetics, sympathomimetics, beta-blockers and prostaglandins.)

3. During the first month after diagnosis, surgical treatment is performed. At the initial stages, goniotomy or goniopuncture is performed, and at later stages, combined operations are used

An ailment such as glaucoma is considered to be a large group of eye diseases, which are characterized by a periodic or constant increase in intraocular pressure (IOP), which is characterized by atrophy of the optic nerve, a gradual decrease in vision and the development of visual field defects.

It is customary to distinguish between two main types of glaucoma: open-angle and closed-angle glaucoma, also primary, secondary and congenital glaucoma. The congenital form of this pathological condition is hereditary (about 15% of cases), as well as intrauterine (85% of cases).

In the presence of secondary glaucoma, an increase in IOP is a consequence of damage to the eye, another eye disease, or the whole body.

This article will focus on congenital glaucoma in children.

Treatment for congenital glaucoma should be determined depending on the severity of the disease. In the presence of a moderately pronounced course of glaucoma, therapy can be started with the appointment of eye drops to lower intraocular pressure.

But on its own, this type of treatment is ineffective and ineffective.

Surgical intervention is considered the most effective method for lowering IOP. Only with surgical methods is it possible to eliminate obstacles to the outflow of high-blood fluid, which are caused by structural defects of the drainage zone.

Medical treatment of congenital glaucoma is recognized as insufficiently effective, therefore, such treatment is used only as an adjunct to surgical treatment. Drug therapy includes the use of beta-blockers, miotics, prostaglandins, carbonic anhydrase inhibitors. Desensitizing and restorative therapy is also used.

The principles of timeliness and pathogenetic orientation lie at the foundation of modern surgical treatment of congenital glaucoma. As a rule, the operation is prescribed immediately after the diagnosis is made, the purpose of which is to ensure the normal outflow of intraocular fluid.

Depending on the pathogenesis, this can be: goniotomy, during which the adhesions are cut, goniotomy in combination with goniopuncura (creation of additional channels for fluid outflow), trabeculotomy or sinusotrabeculotomy, to reduce the production of intraocular fluid, transscleral cryo-, thermo- ciliary photocoagulation can be performed body.