The back of the vascular tract is called. Vascular tract of the eye

Middle layer of the eye is vascular tract of the eye (uvea), which embryogenetically corresponds to the pia mater and consists of three parts: the choroid itself (choroid), the ciliary body (corpus ciliare) and the iris (iris). The vascular tract is separated from the sclera by the suprachoroidal space and is adjacent to it, but not all the way. It consists of branching vessels of various calibers (from rather large ones with circular muscles to capillaries - simple endothelial tubes), forming a tissue resembling a cavernous one in structure. All intraocular veins do not have valves.

Anterior part of the vascular tract is Iris. It is visible through a transparent cornea, painted in one color or another, which indicates the color of the eyes (gray, blue, brown, etc.). In the center of the iris is the pupil (pupilla), which, thanks to the presence of two muscles (sphincter and dilator), can narrow to 2 mm and expand to 8 mm to regulate the entry of light rays into the eye.

The sphincter (m. sphincter pupillae) is innervated by the parasympathetic oculomotor nerve, the dilator (m. dilatator pupillae) is sympathetic, penetrating from the plexus caroticus. Throughout the edge of the pupil in the form of a pigmented fringe, the posterior pigmentary layer of the iris is visible, which is a continuation of the optically inactive retina and is of ectodermal origin.

The relief of the anterior surface of the iris is extremely peculiar and is due to radially located vessels and connective tissue trabeculae, as well as depressions in the tissue (lacunae or crypts). This anterior part of the iris is called the iris stroma, which is mesodermal in origin. The thickness and density of the stromal layer, the intensity of its pigmentation determines the color of the iris. In the complete absence of pigment in the anterior boundary layer of the iris, it looks blue-blue due to transmission through the colorless stroma of the pigment sheet. There is also almost no pigment in the iris of a newborn, the stromal layer is very loose and thin, so the iris has a bluish-bluish tint.

There are fibers in three directions in the muscle: fibers of the meridian direction, circular direction and radial fibers. The accommodative function of the ciliary body is provided by combined contractions of all these muscle fibers. In the ciliary body, as in the iris, there are: the mesodermal part, consisting of muscle and connective tissue, rich in blood vessels and the neuroectodermal, retinal, consisting of two epithelial sheets.

The vascular layer of the ciliary body consists of a widely branched vascular network and loose fibrous collagen tissue. The vessels penetrate into the ciliary body from the suprachoroidal space (the gap between the sclera and the ciliary body) and at the root of the iris, together with the anterior ciliary artery, forms a large circle of blood circulation of the iris, from which the ciliary body is supplied with arterial branches. The processes of the ciliary body, where the capillaries form a network, are very rich in vessels, are very wide and are located directly under the epithelium.

From the inside, the ciliary body is lined with two layers of epithelium - a continuation of the embryonic retina. On the surface of the epithelium there is a boundary membrane to which the fibers of the zonium ligament are attached. The ciliary body performs a very important function, its processes produce intraocular fluid, which nourishes the avascular parts of the eye - the cornea, lens, vitreous body. The ciliary epithelium has a huge number of nerve endings. In newborns, the ciliary body is underdeveloped. In the first years of life, the motor and trophic nerves are better developed than the sensory ones; therefore, during inflammatory and traumatic processes, the ciliary body is painless. By the age of 7-10 years, the ciliary body is the same as in adults.

The choroid proper or choroid extends from the dentate line to the opening of the optic nerve. In these places it is tightly connected with the sclera, and in the rest of its length it is adjacent to the sclera, separated from it by the suprachoroidal space, where the ciliary vessels and nerves pass. Microscopically, several layers are distinguished in the choroid: the suprachoroid, the layer of large vessels, the layer of medium vessels, the choriocapillary layer with an unusual width of the capillary lumen and narrow intercapillary lumens.

The choriocapillary layer provides nutrition to the outer layers of the retina, i.e. neuroepithelium.

Blood supply: The posterior short and long ciliary arteries depart from the trunk of the ophthalmic artery and in the posterior part of the eyeball, in the circumference of the optic nerve, penetrate the eye through the posterior emissaries. Here, short ciliary arteries (there are 6-12 of them) form the choroid proper. The posterior long ciliary arteries in the form of two trunks pass in the suprachoroidal space from the nasal and temporal sides and go anteriorly. In the region of the anterior surface of the ciliary body, each of the arteries is divided into two branches, which are curved in an arcuate manner and, merging, form a large arterial circle of the iris. The anterior ciliary arteries, which are the terminal branches of the muscular arteries, take part in the formation of the great circle. The branches of the great arterial circle supply blood to the ciliary body with its processes and the iris. In the iris, the branches have a radial direction to the pupillary edge.

From the anterior and long posterior ciliary arteries (even before their confluence), recurrent branches are separated, which are sent posteriorly and anastomose with the branches of the short posterior ciliary arteries. Thus, the choroid receives blood from the posterior short ciliary arteries, and the iris and ciliary body from the anterior and long posterior ciliary arteries.

Different blood circulation in the anterior (iris and ciliary body) and in the posterior (choroid proper) sections of the choroid causes their isolated lesion (iridocyclitis, choroiditis). At the same time, the presence of recurrent branches does not exclude the occurrence of a disease of the entire choroid at the same time (uveitis).

The posterior and anterior arteries take part in the blood supply not only to the vascular tract, but also to the sclera. At the posterior pole of the eye, the branches of the posterior ciliary arteries, anastomosing with each other and with the branches of the central retinal artery, form a corolla around the optic nerve, the branches of which feed the part of the optic nerve adjacent to the eye and the sclera around it.

Research: Iris: color is not changed (the same on both sides); the drawing is clear; the pigment fringe is preserved along the entire circumference.

Ciliary body: painless on palpation.

The vascular tract consists of 3 parts: the iris, the ciliary body, and the choroid itself (choroid). It consists of branching vessels of various calibers (from rather large ones with circular muscles to capillaries - simple endothelial tubes) that form a tissue resembling a cavernous one in structure.

The iris is the anterior part of the choroid, forming a vertical diaphragm with a hole in the center - the pupil, which regulates the amount of light entering the retina.

The iris consists of two sheets - the anterior mesodermal sheet, consisting of the anterior border (accumulation of cells, including the chromatophore) and vascular layer, and the posterior ectodermal - consisting of the posterior border plate and the pigment epithelium layer. The thickness is 0.4 mm, the thinnest iris at the root is 0.2 mm. The iris has a variety of colors - from blue to black, its color is due to the intensity of pigmentation of the anterior boundary layer, as well as the thickness and density of the stroma. There are two muscles in the iris - antagonists. One is placed in the pupillary part, its fibers are located circularly to the pupil (sphincter), with their contraction, the pupil narrows. Another muscle is represented by radially extending muscle fibers in the ciliary part (dilator), with the contraction of which the pupil expands. The function of the iris is to regulate the amount of light entering the eye, due to the reaction of the pupil. The pupil is narrower, the more light, and vice versa. Pupil width from 2 to 8 mm. In newborns, the pupils are narrow - from 2 to 4 mm in diameter. Pupillary reaction to light is alive immediately after birth. When illuminated, the pupils narrow to 1.5 mm and dilate slightly in the dark. This can be explained by the lack of development of cranial nerves and muscles of the iris in newborns.

The iris takes part in ultrafiltration and the outflow of aqueous humor, in thermoregulation, and maintaining ophthalmotonus.

The ciliary body is a closed ring around the entire circumference of the eye, about 6 mm wide. Consists of flat (4 mm) and thickened (crown) parts. The thickened (coronal) part consists of ciliary processes (2 mm), 70-80 of them, height 0.8 mm. Each of them has its own nerve branches and its own vessels. It is innervated by parasympathetic, sympathetic and sensory nerve endings. The ciliary body produces aqueous humor, participates in the outflow of intraocular fluid, in thermoregulation, and provides an act of accommodation.

The ciliary body is supplied with blood by the posterior long ciliary arteries, which have recurrent branches to the iris and choroid.

The choroid itself (choroid) occupies 2/3 of the back of the eyeball, extends from the dentate line to the opening of the optic nerve. The choroid is involved in the nutrition of the retinal neuroepithelium, in the outflow of intraocular fluid, in thermoregulation, and in the regulation of ophthalmotonus.

The choroid is richly vascularized with short posterior ciliary arteries. They anastomose with the posterior long ciliary arteries.

The posterior short ciliary arteries form a network that is located in three layers (according to the anatomical nomenclature - plates): the outermost (supravascular plate), adjacent to the inner surface of the sclera - a layer of large vessels (Haller's layer); layer of medium vessels (vascular plate), (Zatler layer); a layer of small vessels (vascular-capillary plates) facing the retinal neuroepithelium, which is the innermost layer and directly feeds the retinal neuroepithelium. Choriocapillaries are able to pass simultaneously up to 4-5 erythrocytes, which is important for the function that choriocapillaries perform. The choroid itself has the highest perfusion, its venous blood contains a large amount of oxygen, and this is also associated with its function. The choroid has only sympathetic nerve endings.

The thickness of the choroid is from 0.2 to 0.4 mm, on the periphery 0.1-0.15 mm. Microscopically, it has 5 layers: 1) supravascular layer; 2) a layer of large vessels; 3) a layer of small and medium-sized vessels; 4) capillary layer; 5) basal plate (Bruch's membrane).

There may be congenital anomalies, degenerative changes, inflammatory diseases, tumors, and injuries in the vascular tract.

A significant number of congenital anomalies is associated with a violation of the normal and timely closure of the germinal fissure, which is located in the lower inner part of the secondary optic vesicle. Normally, it closes on the 5-6th week of intrauterine life. As a rule, the embryonic fissure begins to close in the middle, where the ciliary body will develop.

Among the most severe anomalies is aniridia- lack of iris. Most often bilateral. It is often combined with congenital glaucoma due to the absence or fusion of intratrabecular spaces and Schlemm's canal, as well as the angle of the anterior chamber with mesenchymal-embryonic tissue. Common symptoms in aniridia are subluxation, rarely dislocation of the lens, microphakia, lens coloboma, cataracts. Aniridia is combined with aplasia or hypoplasia of the fovea of the retina, which lead to a sharp decrease in central vision. The disease is inherited in a dominant manner.

Iris coloboma- a defect in the iris, located downwards. Coloboma can be unilateral or bilateral, complete or partial. It can be combined with coloboma of the choroid and other anomalies in the development of the eye. It has a family-hereditary, often dominant character.

Polycoria- the presence of several pupillary holes in the iris. It is characteristic that they have sphincters if this is true polycoria.

corectopia- displacement of the pupil, often bilateral, symmetrical.

Heterochromia- anomaly of pigmentation of the iris.

Albinism- absence or insufficiency of pigment in the choroid, retinal pigment epithelium, skin, hair, accompanied by nystagmus and low visual acuity.

Congenital cysts of the iris.

Congenital miosis and mydriasis.

Anomalies of the vascular tract can be combined with other malformations, such as cleft lip, cleft palate, etc.

Dystrophy of the iris and ciliary body

1. Fuchs syndrome (1906) - has been described as a unilateral process.

On a calm eye, the iris begins to discolor, multiple gentle precipitates appear on the posterior surface of the cornea, diffuse opacification of the vitreous body, then complicated cataract and quite often secondary glaucoma. Cataract can be without precipitates, it can be bilateral. In any case, it can be complicated by glaucoma. Neurotrophic and neurovascular processes are associated with dysfunction of the autonomic nervous system.

For the differential diagnosis in 1957, the Amsler-Calmette method was proposed - after a puncture of the anterior chamber, after a few seconds, a thin thread of blood emanating from the chamber angle appears on the opposite side. A small hyphema (2-3 mm) is formed, which resolves in a few hours. The resulting hemorrhage is associated with a violation of the sympathetic innervation of the walls of blood vessels, which is manifested by their expansion and increased permeability.

2. Essential mesodermal progressive dystrophy of the iris. Progressive foci of dystrophy of the stroma of the iris appear, in some places the pigment layer shines through. Sometimes holes are formed through which the pigment leaf of the iris protrudes, resembling a tumor. This can lead to diagnostic errors. The pupil is elongated or pear-shaped (ectopic pupil), there is an eversion of the pigment sheet, the regulation of IOP is disturbed. Even in the case of regulation of ophthalmotonus with the help of surgery, the process continues to progress.

However, inflammatory diseases of the vascular tract of the eye are more common.

Among all ocular pathology, inflammation of the choroid is from 5 to 15%, and among patients in hospitals, 5-7%. Uveitis, combined with systemic lesions of the body, according to Katargina L.A., Arkhipova L.T. (2004), have recently increased significantly and range from 25 to 50%.

Term "uveitis" means any inflammatory disease of the choroid of the eye.

Allocate endogenous and exogenous uveitis. The cause of uveitis can be exogenous factors: penetrating eye injuries, surgical interventions, keratitis. In these cases, inflammation of the choroid occurs a second time as a complication of the underlying disease.

The cause of endogenous inflammatory processes of the choroid are: viral diseases, tonsillitis, sepsis, pneumonia, brucellosis, toxoplasmosis, anicteric leptospirosis, oral diseases, gonorrhea, tuberculosis, malaria, relapsing fever. In addition, any inflammatory focus in the body can become a source of inflammation of the choroid; from non-infectious diseases, collagenoses, gout, diabetes can be the cause of inflammation. In some cases, the etiology remains unclear.

A number of classifications have been proposed that involve the division of all endogenous uveitis according to anatomical, etiological and pathogenetic features, in addition to the division of uveitis according to localization into anterior, middle (peripheral), posterior and generalized, as well as the division according to the nature of the course into acute, subacute, chronic and recurrent.

More detailed and in-depth classifications involve taking into account the leading pathogenetic features.

Classification of uveitis To date, there is no generally accepted classification of uveitis. Uveitis can be divided by etiology, localization, process activity and course.

The classification is based on the classification proposed by Zaitseva N.S. (1984):

A. By etiology:

I. Infectious and infectious-allergic uveitis:

1) viral;

2) bacterial;

4) fungal.

II. Allergic non-infectious uveitis:

1) with hereditary allergies to factors of the external and internal environment (atopic);

2) with drug allergies;

3) with food allergies;

4) serum uveitis with the introduction of various vaccines, sera;

5) Fuchs heterochromic cyclite;

6) glaucoma cycle crises.

III. Uveitis in systemic and syndromic diseases:

1) with rheumatism;

2) with rheumatoid arthritis;

3) with Bechterew's disease;

4) with Reiter's syndrome;

5) with Behcet's disease;

6) with Segren's (Sjogren's) syndrome;

7) with multiple sclerosis;

8) with psoriasis;

9) with glomerulonephritis;

10) with ulcerative colitis;

11) with sarcoidosis;

12) with Vogt-Koyanagi-Harada syndrome;

13) with other lesions.

IV. Post-traumatic uveitis:

1) after a penetrating injury to the eye;

2) contusion;

3) postoperative;

4) phacogenic;

5) sympathetic ophthalmia.

V. Uveitis in other pathological conditions of the body:

1) in case of metabolic disorders;

2) in violation of the functions of the neuroendocrine system (with menopause, diabetes);

3) toxic-allergic iridocyclitis (with the collapse of the tumor, blood clots, retinal detachment, blood disease).

VI. Uveitis of unknown etiology.

B. By process localization:

I. Anterior uveitis:

Iridocyclitis;

Cyclite;

Keratouveitis.

II. peripheral uveitis.

III. Posterior uveitis (focal, multifocal, disseminated):

Neurochorioretinitis;

Endophthalmitis.

IV. Panuweit:

Generalized uveitis;

Uveakeratitis;

Panophthalmitis.

B. By process activity:

1. Active.

2. Subactive.

3. Inactive.

G. Downstream:

4. Sharp.

5. Subacute.

6. Chronic (remission, relapse).

Risk factors for uveitis are:

1) genetic predisposition;

2) insufficiency of defense mechanisms and impaired permeability of the hemato-ophthalmic barrier under the influence of adverse factors of endogenous and exogenous nature;

3) the presence of general systemic and syndromic diseases, foci of acute and chronic infection.

In the clinic, the following pathogenetic forms of uveitis can be distinguished:

1) infectious and infectious-allergic uveitis;

2) allergic uveitis with non-infectious allergy-atopy;

3) uveitis in systemic syndromic diseases;

4) posttraumatic (postoperative) uveitis, including phacogenous iridocyclitis and sympathetic ophthalmia;

5) uveitis in other pathological conditions of the body (diabetes, metabolic disorders, tumors, stress).

The pathogenesis of uveitis is as follows:

1. The leading factors determining the preservation of immunological homeostasis in the body are the body's genotype, the state of the thymus gland, adrenal glands, pituitary-adrenal system, the normal functioning of the T- and B-immunity systems, and nonspecific immunity factors.

2. The interaction of these systems carries out and regulates immune responses in the body to the flow of antigens or immune complexes into the eye. The main sources of antigens are extraocular foci of infection or non-infectious sources of sensitization, leading to the circulation of antigens in the blood, sensitization of the body and disruption of the interaction of defense mechanisms.

3. The factors provoking the disease with uveitis are the violation of the hemato-ophthalmological barrier (HOB) of the eye under the influence of exogenous (trauma, hypothermia, overheating, acute infections) or endogenous factors (chronic stress, chronic and other infections), effects that lead to impaired permeability GOB.

4. Antigen-antibody reactions in the tissues of the eye as a clinical syndrome of uveitis are accompanied by inflammation, vasculopathy, and other phenomena of immune cytolysis, dysfermentosis, microcirculation disorders, followed by scarring and dystrophy. The clinic of uveitis is determined by the nature and duration of exposure to the antigen, the state of immunity and the pituitary-adrenal system, as well as the genotype of the organism.

5. In the implementation of immunological damage to eye tissues, pharmacologically active substances (lymphokines, complement, histamine, serotonin, adrenaline, acetylcholine, prostaglandins) play a role in conditions of disruption of the normal interaction of antigens, immunological and biochemical mechanisms.

Through the vascular tract, infections and toxic agents most easily penetrate the eyeball. In the body, it is rare to find such favorable conditions for settling and fixing microorganisms and their toxins. Blood to the eye enters through the anterior and posterior ciliary arteries, the total lumen of which is much less than the total lumen of the vasculature of the iris, ciliary body and choroid. During the transition from the vessels of the uveal tract to those draining blood from it into the vorticose and anterior ciliary veins, the total lumen of the blood bed also sharply narrows. The expansion of the vascular bed in the vascular tract contributes to the slowing down of blood flow. It turns out, as it were, a kind of settling pool, where pathogenic microorganisms and toxins are brought by the blood stream.

The rapid evacuation of blood to some extent also interferes with the constantly acting press - intraocular pressure. What matters is the absence of valves in the veins of the eye.

It has already been noted that the blood supply to the choroid itself comes from the posterior - short ciliary arteries, and the iris and ciliary body - from the anterior and posterior long ciliary arteries. Therefore, there may be separate lesions of the anterior and posterior sections of the vascular tract of the eye. The vessels of the choroid anastomose with the posterior long ciliary vessels of the ciliary body.

Consequently, all three sections of the choroid have a vascular relationship and this can lead to simultaneous inflammation of all sections of the vascular tract of the eye.

The defeat of the anterior section is called iridocyclitis, the defeat of the posterior section is called choroiditis.

The defeat of all parts of the vascular tract is called uveitis, or panuveitis. There are also so-called peripheral uveitis.

The choroid is anatomically and functionally intimately connected with the outer layers of the retina, which is always involved in the process in choroiditis, and inflammatory diseases of the retina, as a rule, are complicated by damage to the choroid. The cause of inflammatory diseases of the vascular tract of the eye can be exogenous and endogenous factors. Uveitis can be congenital or acquired in nature.

Exogenous uveitis is rare, they are secondary - with perforated wounds of the eyeball, after surgery on the eyeball, with corneal ulcers and other diseases.

The first place in the etiology of inflammatory diseases of the vascular tract is occupied by endogenous factors. Uveitis occurs in all countries.

Over the past 20 years, there have been many reports of lesions of the uveal tract, retina, and optic nerve caused by viruses. The most common uveitis, in the etiology of which viruses of the herpes group, influenza, rubella, adenoviruses play a role.

Intrauterine and early acquired viral uveitis in children is usually caused by rubella viruses, cytomegaloviruses, herpes viruses, influenza, varicella, measles, adenoviruses, less often lymphocytic choriomeningitis viruses. Infection with herpes simplex virus No. 1 and No. 2 by the age of 15 is observed in 80-90% of the population, and the manifestation of the disease is in 1% of patients.

Cytomegalovirus (salivary gland virus) belongs to the herpes group, is common in the United States (1% of newborns and 10% of them have CNS lesions). In 50% of healthy children under 3 years of age, the virus is found in the salivary glands.

Rubella, chickenpox, and, in adults, shingles, cause severe eye diseases.

In epidemics of adenoviral keratoconjunctivitis and general respiratory adenoviral infections, adenoviral iritis and iridocyclitis are observed in 7-10% of patients. Uveitis occurs in children suffering from pneumonia, sepsis, and other general diseases against the background of the general respiratory syndrome.

Influenza viruses cause uveitis in 1-11% of patients. Often, influenza or other viral infection is a "trigger" factor for recurrence of uveitis of another etiology.

Over the past 20-30 years, the number of allergic uveitis has increased, as well as those developing against the background of systemic diseases affecting the joints, skin, mucous membranes and other organs, disseminated vasculitis and vasculopathies, i.e. in systemic and syndromic diseases.

Uveitis is not uncommon in onchocerciasis, histoplasmosis, toxoplasmosis, sarcoidosis. In untreated mothers, congenital toxoplasmosis is detected in 36-50% of their children, the eyes and central nervous system are affected. The incidence of tuberculosis varies widely. According to L.A. Katsnelson, tuberculous etiology occurs in 20.5% of patients.

Streptococcal infection is more often detected with rheumatism. The dominant source of streptococcal infection is chronic tonsillitis, less often sinusitis, diseases of the teeth, joints, prostatitis, hepatitis, ulcerative colitis, pneumonia, otitis media and polyarthritis more often in children.

The causative agent of rheumatism is group A β-hemolytic streptococcus, it "starts" the autoimmune process in genetically predisposed people. Emerging immune complexes circulate for a long time and are fixed in organs and tissues. Patho-histological picture: Ashoff-Talalaev (tissue necrosis and proliferation of connective tissue cells). Complications: thromboembolism, septic endocarditis.

The frequency of staphylococcal etiology is 1.3-2%, it can be a complication of pneumonia, sepsis, erysipelas, boils, pyelonephritis, tooth extraction, paranasal sinus disease, after surgery.

Focal infection, according to Katsnelson L.A., is 8.6% (with anterior uveitis - 10.3%, with posterior - 5.9%), brucellosis - from 0.5 to 2%.

A significant place in the structure of uveitis is occupied by uveitis in systemic and syndromic diseases. The most common uveitis in rheumatism, rheumatoid arthritis, sarcoidosis, Reiter's syndrome, Behcet, Vogt-Kayanagi-Harada, systemic lupus erythematosus, scleroderma, Still's disease, Bechterew's disease, polyarteritis nodosa.

Uveitis is observed in different age groups, but more often begins in children and at a young age.

Uveitis in systemic diseases is always the result of a violation of the functions of the immune system and refers to autoimmune diseases. The autoimmune component, as a rule, is involved in the development of uveitis of any infectious and unexplained etiology. Immune reactions cause the migration of T and B - lymphocytes, the release of mediators of immune reactions, biologically and pharmacologically active substances: histamine, serotonin, prostaglandins, a decrease in the activity of glycolysis enzymes and a deficiency of hydrocortisone. Prostaglandins are inflammatory mediators. Prostaglandins stimulate the biological synthesis of steroid hormones.

Early changes in collagenosis are noted in the metabolism of glycosaminoglycans and collagen, which, under the action of glycolytic enzymes, become free forms and appear in the blood and urine of patients in the form of cleavage products - glycosaminoglycans and hydroxyproline (a specific amino acid - a marker of collagen). Their presence in the urine and blood of patients with uveitis in elevated concentrations indicates collagenous damage to the eyes (Katargina L.A., Arkhipova L.T., 2004).

According to the classification of uveitis, granulomatous and non-granulomatous, or toxic-allergic uveitis are distinguished.

Granulomatous are metastatic hematogenous uveitis, in which the primary focus is always in the vascular tract. It has the character of an inflammatory granuloma with perifocal inflammation around. Inflammatory granuloma consists of leukocytes, mononuclear phagocytes, epithelioid and giant cells, sometimes with the presence of the pathogen (tuberculosis, toxoplasma, brucella, leprosy, etc.)

Non-granulomatous, or toxic-allergic, uveitis is caused by physical, chemical, toxic, allergic factors. Here the process is diffuse - the tissue is edematous, the capillaries are dilated, there is cell infiltration by leukocytes, lymphocytes, and plasma cells.

The most important in the genesis of these uveitis is the sensitization of the body and tissues of the eye with the development of a hyperergic reaction in it. The focal process can be localized in different parts of the eye and outside it. Most often, toxic-allergic uveitis occurs on the basis of influenza, rheumatism, nonspecific infectious polyarthritis, Still's disease in children, focal infection (teeth, tonsils, sinuses), metabolic diseases (gout, diabetes), Behçet's disease, etc. There may be transitional and mixed forms.

Tuberculous uveitis can be both granulomatous and toxic-allergic.

With toxic-allergic iridocyclitis, panuveitis and chorioretinitis of various etiologies with a subacute course of the process and a pronounced exudative component, with a recurrent and chronic course, an increase in antioxidant activity is observed, therefore, massive antioxidant therapy is required.

An objective individual indicator of the antioxidant activity of blood serum can be the content of a specific protein in it - ceruloplasmin. The fraction of blood serum that contains ceruloplasmin has a high antioxidant activity. Ceruloplasmin is an inhibitor of peroxidation due to the neutralization of free radicals and the oxidation of iron ions. The content of ceruloplasmin in uveitis is increased.

The clinical picture of anterior uveitis is manifested by pain in the eye, sometimes sharp, especially at night, and pain in the corresponding half of the head. There are also reflex closure of the eyelids (bluff-rospasm), lacrimation and photophobia as a reflex reaction associated with general innervation.

Patients do not complain of decreased vision in the initial period.

If this is inflammation, then there are all signs of inflammation.

Objective signs are: pericorneal or mixed injection of the eyeball, precipitates on the posterior surface of the cornea - lumps of exudate containing lymphocytes, macrophages, plasma cells. They are located mainly in the lower half of the cornea and are often located in the form of a triangle with the top up. Precipitates can be point, small, large sebaceous. In severe and prolonged iridocyclitis, they can be deposited in the angle of the anterior chamber and on the surface of the lens. Precipitates may contain pathogens. The iris changes in color, the blue iris becomes green, gray - dirty green, brown - rusty. The change in color depends on the increase in the blood filling of its vessels, the violation of the permeability of the walls of the vessels, as a result of which the blood cells enter the tissue of the iris, and the blood hemoglobin turns into bilirubin. The color of the iris is also affected by the exudate that fills the crypts of the iris. This also explains the blurring, blurring of her drawing, as well as the narrowing of the pupil. The iris sometimes looks somewhat bumpy due to the formation of granulomas.

The moisture of the anterior chamber may become cloudy due to the presence of exudate, which may be serous, fibrinous, purulent, or hemorrhagic. The type and amount of exudate depend to a certain extent on the etiology of the process and its severity.

Since the iris is inactive and very swollen, it more closely touches the anterior surface of the lens, the exudate is organized and the so-called posterior synechiae are formed. The more fibrin in the exudate, the faster the posterior synechia is formed, the pupil may become irregular in shape. The entire pupillary edge of the iris (seclusio pupillae with the anterior surface of the lens) can be soldered. The exudate can completely close the pupil and so the infection of the pupil (occlusio pupillae) is organized. In such cases, in addition to reducing visual acuity, secondary glaucoma may develop due to a violation of the outflow of intraocular fluid.

The vitreous body becomes cloudy. Due to the appearance of a mooring in it, traction retinal detachment develops.

With iridocyclitis, cataracts can develop, the optic nerve and retina can be involved in the process. There are violations of the regulation of ophthalmotonus (hypotension or hypertension). In acute hypertensive uveitis, an increase in IOP is more often associated with inflammation from the first days of the disease. This is due to an increase in HBV secretion. Edema and diffuse inflammatory infiltration are noted, a large number of dilated full-blooded vessels with extravasates are the cause of hypersecretion. The cause of hypertension may also be the presence of exudate in the angle of the anterior chamber.

In chronic hypertensive uveitis, inflammation is mild, but posterior synechiae, goniosinechia, and gross opacities of the vitreous body appear, due to deterioration of the outflow, but this is already secondary glaucoma.

The course of iridocyclitis is often recurrent. Most often, relapses are observed in patients with rheumatism, rheumatoid arthritis, tuberculosis, focal and viral infections. Most anterior uveitis in children is caused by juvenile rheumatoid arthritis.

The vascular tract is rich in chromophores. They have high antigenic properties, antibodies to the altered uveal tissue appear. Relapses are explained by repeated allergic reactions.

A characteristic feature of uveitis in children is a sluggish chronic course, especially in younger age groups. The disease begins imperceptibly, without pain, depends on the state of the child's body. A focused history is needed.

Uveitis is described in yersiniosis, an acute infectious disease, the causative agent of which is the gram-negative bacterium Yersinia enterocolitica. Yersiniosis can cause damage to the anterior and posterior sections of the eye. Iridocyclitis, as a rule, occurs in the first week of the disease, and the defeat of the posterior section begins from the second week with a change in the fundus. But everything can occur in any period of the disease.

Posterior uveitis

The anterior segment of the eye may not be changed, and ophthalmoscopy in the fundus reveals foci of various types, sizes and quantities. Their localization is different, since the process proceeds in the form of chorioretinitis. Patients complain of decreased vision, the appearance of photopsies, black dots before the eye. The cardinal signs of panuveitis contain symptoms characteristic of anterior and posterior uveitis. Changes in panuveitis are observed in all parts of the choroid, as well as in the lens, vitreous body, retina and optic nerve. In the structure of posterior uveitis, infectious lesions account for a significant proportion. The leading ones are toxoplasmosis (up to 30% of all posterior uveitis), tuberculosis, histoplasmosis, toxocariasis. A significant place is occupied by various idiopathic chorioretinitis and retino-vasculitis. The role of various infectious lesions in immunocompromised patients, with AIDS and other conditions is increasing.

An important place in the structure of posterior uveitis is occupied by non-infectious uveitis associated with systemic and syndromic diseases (L.A. Katargina, L.T. Arkhipova, 2004).

The most difficult form of uveitis to diagnose is peripheral uveitis, since the primary focus is located in an area inaccessible to conventional ophthalmological examination methods. A good effect is the study of the periphery of the fundus using a Goldman lens. Peripheral uveitis affects more often young people (up to 30 years - 87%). In 73% - the process is bilateral. Characteristic for peripheral uveitis are the development of an inflammatory process in the flat part of the ciliary body, the development of edema of the macular zone and the optic disc, followed by the involvement of the peripheral parts of the retina in the process and, in the future, the appearance of a number of complications.

Various terms are often used to refer to inflammation of this area of the eye: pars-planitis, vitriitis, peripheral exudative retinitis, cyclochorioretinitis, chronic posterior cyclitis, peripheral uveoretinitis.

The term "pars-planitis" is used to define one of the varieties of peripheral uveitis with the presence of snow-like exudate in the pars-plan of the ciliary body, which is accompanied by severe vitritis, severe macular edema and poor prognosis (Katargina L.A., Arkhipova L.T., 2004).

With peripheral uveitis, patients complain of "blurred vision", "floating flies" before their eyes, 1/3 of patients complain of decreased vision. At an early stage, the cause of vision loss is macular edema and secondary vitritis. The process is concentrated in the so-called basis of the vitreous body, where it is firmly connected to the membranes of the eye. Here, the cellular structure creates conditions for the retention of exudate.

When the exudate is located in the granular zone of the flat part of the ciliary body, the form of uveitis is called basal and occurs in 25% of cases. If the exudate is localized in front of the anterior hyaloid membrane in the pars plana striatal zone, this form is called prebasal. Happens in 10% of cases. With the current of the intraocular fluid, exudative masses from the prebasal zone are washed out into the posterior and then into the anterior chamber and settle on the trabecular tissue in the form of precipitates. In 65% of cases, both zones are involved in the inflammatory process at the same time.

A contact three-mirror lens allows you to examine the peripheral parts of the retina, but the flat part of the ciliary body and even often the dentate line remain invisible. It can be seen with scleral compression.

Normally, the irido-lenticular space appears dark; in the presence of exudate, it acquires a whitish color.

A more severe course of the process and with more frequent relapses occurs if ½ of the circumference of the flat part of the ciliary body is involved in the pathological process. In 30% of patients, the exudate is not limited to the zone of the flat part of the ciliary body, but descends along the preretinal tract and, as it were, hangs over the peripheral parts of the retina. With involvement in the process of the peripheral parts of the retina, the disease is more severe.

In 83% of patients, accompaniment bands are expressed along the course of peripheral venules. Peripheral phlebitis in 7% of patients is complicated by vascular occlusion, which leads to the appearance of ischemic zones, neovascularization, degenerative changes in the retina, its thinning, and ruptures. From the retina, the newly formed vessels grow into the exudative masses of the flat part of the ciliary body. From the newly formed vessels, hemorrhages occur in the retina and vitreous body (3% of patients). Due to the exudate stretching of the vitreous body fibers, the traction forces are redistributed and edema of the macular zone appears (51% of patients), and in a later period, cysts of the macular zone appear. Edema confirms FAG. Optical disc edema occurs in 21% of patients (Katsnelson L.A., 1999).

Due to the presence of exudate on the periphery of the fundus, all patients have a cellular reaction in the vitreous body, first on the periphery, and as the disease progresses, cells appear in the central parts of the vitreous body.

Complications of peripheral uveitis

Degenerative changes in the macular region (26.4%), posterior vitreous detachment cause splitting of the anterior limiting membrane of the retina. This leads to the fact that the thin inner wall of the cyst can rupture in the macular zone and form a lamellar or even complete retinal tear.

The epiretinal membrane reduces visual acuity. In addition to the formation of episcleral films, the appearance of preretinal membranes is characteristic, due to the resorption of exudative foci or as a volumetric proliferation of glial elements of the retina into the vitreous body.

Exacerbations of the disease are possible, and then new active exudative foci and a picture of “fallen snow on a dense old snow mass” appear next to or above the fibrous exudate.

The formation of rough proliferation in the base of the vitreous has a traction effect on the retina and causes its detachment (3%). In 5% of patients with prebasal and mixed forms, there is an increase in IOP (presence of exudate). A complicated posterior capsular cataract develops (the appearance of antibodies to lens antigens) and biochemical processes associated with inflammation.

There are 4 types of peripheral uveitis:

1. Active peripheral uveitis ending in complete cure (40%).

2. Rarely recurrent (exacerbation once a year or less) occurs in 53% of patients.

3. Often recurrent (2 times a year of exacerbation) - in 35%.

4. Sluggish subacute course of the process (without remissions) - in 7%.

Differentiate with the following pathological conditions:

1. Cystic edema of the macular zone (no snowball-like foci on the periphery of the fundus).

2. Retrolental fibroplasia (early age, premature birth).

3. Familial exudative vitreoretinopathy. Pars plana is free from exudate. Exudate in the form of jelly on the periphery of the retina.

4. Exudative peripheral Coates retinitis (exudate is located subretinally, usually one eye is affected).

5. Fuchs syndrome (iris atrophy, precipitates on the posterior surface of the cornea, no snowy exudate on the periphery of the fundus).

6. Sarcoid uveitis (cotton-like foci located preretinally on the extreme periphery of the retina, pars plana is not involved in the process). This is a polysystemic disease.

The etiology of peripheral uveitis remains unclear. The association with multiple sclerosis and sarcoidosis suggests that in some cases, peripheral uveitis is autoimmune. At the same time, the symptom complex of peripheral uveitis can be a manifestation of a number of infectious diseases - borreliosis, toxoplasmosis, toxocariasis, infection with the herpes simplex virus and Epstein-Barr. It is now believed that peripheral uveitis is a multifactorial disease (Zaitseva N.S. et al., 1986; Slepova O.S., 1988; Katargina L.A. et al., 1997, 2000).

Toxoplasmosis uveitis

More often they proceed according to the type of chorioretinitis and in 75% they have a chronic course. They can be acquired (during life) and congenital (intrauterine infection).

Acquired toxoplasmosis in the vast majority of cases, it proceeds as an asymptomatic carriage. A person infected with toxoplasma is not an epidemiologically significant source of infection. Only with congenital toxoplasmosis, the source of invasion for the child is the mother who gave birth to him. Isolated cases of human infection during transplantation of organs and tissues are described.

With acquired toxoplasmosis, the incubation period lasts from 3 days to several months. In the acute form, general weakness, muscle pain, dyspeptic disorders, malaise, decreased ability to work are detected, ends with recovery with the preservation of Toxoplasma cysts in the tissues and with the outcome of asymptomatic carriage. In some cases, in the acute form of toxoplasmosis, a generalization of the process is observed. Acute can turn into chronic, which is characterized by blurred clinical manifestations.

The most severe is chronic acquired toxoplasmosis with involvement of the brain in the process. There are uveitis, exudate and proliferation of the retina, disseminated chorioretinitis. The most common is central chorioretinitis, which begins with a picture of acute serous retinitis. Near the focus, hemorrhages are visible in the retina. Eye damage in the form of chorioretinitis, uveitis, optic nerve atrophy can sometimes be the only clinical manifestation of chronic acquired toxoplasmosis.

The diagnosis is made on the basis of subfebrile temperature, lymphadenopathy, enlargement of the liver and spleen, eye damage, and the presence of calcifications in the brain.

Congenital toxoplasmosis develops as a result of intrauterine infection of the fetus from a mother with toxoplasmosis. Transmission occurs by the transplacental route. The disease of a woman leads to infection of the fetus at the end of the first and during the second trimester of pregnancy in 40% of cases, in the third trimester in 60% of cases. Toxoplasma circulating in the blood of the fetus is introduced into all organs and tissues.

The defeat of the fetus leads to miscarriages, stillbirths, as well as severe damage to organs that are not compatible with life (anencephaly). With a lesion in the late period of the development of the disease in women, changes are observed both in the eyes and in the central nervous system.

Changes in the eyes - focal infiltration of the membranes of the eye and the development of small areas of necrosis with the subsequent appearance of granulation tissue in the retina and choroid. If intrauterine uveitis is transferred, then corneal opacity, anterior and posterior synechia, atrophy of the iris stroma, lens opacities, changes in the vitreous body are noted.

There are acute, subacute and chronic stages of the disease of congenital toxoplasmosis. In the acute stage, there may be nystagmus, strabismus.

In subacute - clouding of the vitreous body, chorioretinitis, iridocyclitis, uveitis, nystagmus, strabismus. In the chronic phase - microphthalmos, chorioretinitis, optic nerve atrophy.

The most characteristic sign of congenital toxoplasmosis is pseudocoloboma of the macula. This is a huge atrophic focus ranging from ½ to several disc diameters. Against the background of the pseudocoloboma of the macula, well-preserved vessels of the choroid are visible along its entire length. The vessels of the choroid are strongly altered, sclerotic. Chorioretinitis is often bilateral and in congenital toxoplasmosis is one of the most frequent symptoms of the disease. It is characteristic that congenital chorioretinitis of toxoplasmic etiology affects the papillomacular region.

With congenital toxoplasmosis, in addition to the chorioretinal focus, large, rough, sometimes multiple atrophic foci are determined in the macular region, often rounded with clear boundaries and the deposition of a large amount of pigment, mainly along the edge of the focus. Vision in the central localization of the focus is sharply reduced.

With congenital toxoplasmosis, there is a relapse of the disease, in which, along with old changes, fresh foci appear. Fluorescein angiography helps in the diagnosis. Retinitis in congenital toxoplasmosis are rare, but occur with symptoms of severe exudation and even retinal detachment. In this case, they are differentiated from Coats' external exudative retinitis. If the inflammatory focus is located close to the optic nerve head, the picture resembles Jensen's chorioretinitis. Congenital toxoplasmic chorioretinitis is often associated with CNS involvement. These are residual effects of meningoencephalitis, cerebral arachnoiditis. The radiograph shows calcified calcifications.

Congenital toxoplasmosis may be latent for a long time, convulsions and chorioretinitis may appear at the age of 2-7 years.

The diagnosis is made on the basis of the clinical picture, positive serological reactions in the newborn and in the mother. Craniograms may show signs of hydrocephalus and other changes, as well as an anisoorbital syndrome. A combination of toxoplasmosis with bacterial and viral infections is possible.

The scheme of treatment of toxoplasmosis of the eyes

On the first day, 0.1 g of chloridine (0.025 × 4 times a day) and 4 g of sulfadimesine (1 g × 4 times a day).

All other days of treatment - chloridine 0.025 g × 2 times a day and sulfadimezin 0.5 g × 4 times a day. From the first day, you can prescribe folic acid at 0.02 g × 3 times a day. By 5-7 days - a blood and urine test.

Sulfadimezin is recommended to drink a few sips of soda water. From the 5th day of treatment with chloridine and sulfadimezin, prednisolone is prescribed. On the first day 100 mg, on the second day 50 mg, over the next days the daily dose is 30 mg, gradually reduce the drug to 5 mg per day, a total course of 25 days, it is recommended intramuscularly 5% solution of vitamin B 1, 1 ml daily No. 20.

For the prevention of congenital toxoplasmosis, pregnant women are given chloridine in the same doses in combination with sulfadimezine in 3 courses. Each course consists of two cycles of 5 days with intervals between cycles of 1 week, between courses - 1.5-2 months. The first course - between 2-14 weeks, the 2nd course - 14-26 weeks, the 3rd - 26-40 weeks of pregnancy. Between cycles, blood and urine tests are mandatory.

Folic acid is also prescribed, and in the presence of severe hypersensitivity, corticosteroids are prescribed.

There are other treatment regimens, for example, tindurin 1 tablet × 4 times a day for the first three days, in the next - 1 tablet × 2 times a day with simultaneous administration of sulfonamides.

Corticosteroids are administered orally, under the conjunctiva, or retrobulbar. Symptomatic therapy is glyceroascorbate, diacarb inside, lasix intramuscularly, for resorption of hemorrhages in the retina and vitreous - heparin retrobulbar, dicynone intramuscularly and retrobulbar. Desensitizing therapy, laser coagulation aimed at the destruction of cysts in the retina (laser coagulation after preliminary fluorescein angiography).

Tuberculous uveitis may occur against the background of active pulmonary or mesenteric, sometimes bone, tuberculosis, and often against the background of a chronic course of the disease or remission. Tuberculosis of the eye is most common in middle and old (over 60 years) age. With anterior localization - at 40-59 years old, posterior tuberculous uveitis - at 20-39 years old.

Tuberculosis of the eyes of the anterior localization is characterized by a frequently relapsing course with short periods of remission, and the posterior one tends to increase the duration of remission.

Tuberculous lesions of the eyes of the anterior localization are in the form of scleritis, parenchymal and sclerosing keratitis, granulomatous iritis, fibrinous-plastic, serous irido-cyclitis.

Posterior tuberculous uveitis is observed in the form of focal chorioretinitis, peripheral uveitis and Eels periphlebitis.

Tuberculous uveitis often occurs in one eye, mixed injection is slightly pronounced, and a weak corneal syndrome is detected. Large sebaceous precipitates on the posterior surface of the cornea are characteristic. There may be grayish-pink nodules in the iris (granulomas-tuberculomas) surrounded by vessels. Synechia are wide, powerful, planar, poorly torn under the action of mydriatics. There may be newly formed vessels in the iris, yellowish exudate in the anterior chamber. Exudate can be deposited on the anterior lens capsule, organized and germinated by newly formed vessels. Exudation extends into the posterior chamber and into the vitreous body and, as a result, clouding of the posterior lens capsule and vitreous body.

On the fundus, there may be yellowish foci protruding from the choroid into the retina, without distinct contours of different sizes, then in the center the lesion acquires a grayish tint, pigment is deposited along the periphery of the lesion. The retina is usually involved in the process.

The etiology of the disease is established on the basis of anamnesis data, a comprehensive clinical and laboratory examination, an ophthalmological examination, immunological tests, and in some cases, positive ex yuvantibus therapy.

Complications of uveitis - uveal cataract, postveal glaucoma, exudative retinal detachment, marginal corneal ulcers, subretinal neovascular membranes, corneal perforations and rough extensive leukomas in tuberculous keratouveitis.

There were mixed lesions of the eyes of tuberculosis-herpetic and tuberculosis-toxoplasmosis etiology, which are characterized by a long, chronic, recurrent course, focal lesions of the cornea, uveal tract with a pronounced exudative reaction, the development of various complications. Patients with a complicated course of ocular tuberculosis have a deficiency of all classes of immunoglobulins, as a result of which the elimination of antigenic complexes that contribute to the development of complications is disturbed.

Diagnostics. For tuberculosis of various localization, the most highly sensitive test is the detection of specific antibodies by the Mycofot method from Dynagen.

In the diagnosis of anterior localization, the most informative diagnostic RBTL with tuberculin and pric-test Mantoux reaction, and in the case of posterior localization, skin and focal reactions to the introduction of different dilutions of tuberculin are the most informative.

Eye tuberculosis treatment

Systemic and local administration of anti-tuberculosis drugs in combination with desensitizing, symptomatic treatment, vitamin complex and active local use of corticosteroids in exudative form of inflammation. Rifampicin orally at a dose of 0.6 g per day, 2-3 months. Isoniazid inside 0.2-0.3 g × 1 time per day, 2-3 months. Dexamethasone parabulbarno 2 mg × 2 times a day, total No. 10-15. After the end of the course, isoniazid is prescribed orally 0.2-0.3 g × 3 times a day for 2-3 months. With damage to the optic nerve, treatment is carried out with anti-tuberculosis drugs for 9-12 months. To reduce exudation against the background of anti-tuberculosis therapy, dexamethasone is used parabulbarno 3-4 mg × 1 time per day, 10 days. In severe cases, dexamethasone is administered intravenously over 30 minutes, 16-20 mg in 200.0 ml of isotonic sodium chloride solution in the morning 1 time in 2 days (total dose 100-120 mg), 10-12 days. After completion of pulse therapy, oral prednisolone 50-10 mg × 1 time in the morning, 1-2 months, is indicated, followed by its gradual withdrawal.

Regional lymphotropic antibacterial therapy is effective in the productive type of tuberculosis, which is carried out by the introduction of streptomycin sulfate, saluzide in ¼ - ½ daily dose, into the cervical regional lymph nodes daily for 2-3 weeks.

Syphilitic uveitis can be both with congenital and acquired syphilis.

Congenital may appear already in utero and this is detected in a newborn child. The entrance gates for acquired syphilis are the mucous membranes and skin. Infection occurs sexually, including oral-genital and rectal contact, sometimes through kissing or close bodily contact. The greatest danger is posed by untreated patients with skin manifestations of the primary or secondary period of syphilis. In a few hours, spirochetes enter the regional lymph nodes and spread throughout the body, which reacts to this by infiltration of perivascular tissues with lymphocytes, plasmocytes, and later fibroblasts. As a result, the endothelium of small blood vessels proliferates and swells, leading to obliterating endarteritis. Within 5-10 years after infection, the vessels and membranes of the brain are affected - meningovascular neurosyphilis, later - parenchymal neurosyphilis. Involvement in the process of the cortex and membranes of the brain leads to progressive paralysis. Damage to the posterior columns and nodes of the spinal cord causes dorsal tabes.

The incubation period of primary syphilis is from 1 to 13 weeks, usually 3-4 weeks. The primary period of syphilis is a hard chancre without treatment heals within 4-8 weeks.

The secondary period appears 6-12 weeks after infection and reaches its maximum development after 3-4 months. Either it goes away quickly, or it lasts for months. 10% have uveitis, sometimes acute syphilitic meningitis develops with swelling of the optic nerve.

Acquired uveitis is characterized by moderate corneal syndrome, mixed injection, serous exudate in the anterior chamber, and small polymorphic multiple precipitates. In the iris there are yellowish-reddish nodules - papules, to which newly formed vessels approach. Posterior synechiae are wide, but easily torn after instillation of mydriatics. In the vitreous body there may be fine floating opacities.

On the fundus, changes resembling "loose salt and pepper" are possible. If the syphilitic process proceeds according to the type of choroiditis, then in children the diagnosis is difficult. As a rule, this pathology is bilateral.

In the tertiary period, which occurs 3-10 years after infection, this is the gummous period. Gumma can also be in the vascular tract of the eye.

Meningovascular neurosyphilis - a symptom of Argyle-Robertson: the pupil is narrowed and asymmetrical, and there is no reaction to light while maintaining the ability to accommodate. Progressive paralysis in 40-50-year-old patients.

Differentiate with sarcoidosis, toxoplasmosis, tuberculosis, fungal choroiditis, with idiopathic uveitis, choroidal metastases of malignant tumors.

Treatment

Benzylpenicillin i / m 500 thousand units. x 4-6 times a day, 10 days. After completing the course of benzitine - benzylpenicillin / m 600 thousand units. actions x 1 time per day for 3-6 weeks. Dexamethasone parabulbarno 2-3 mg / day. x 5-10 days after completion of the course. Betamethosone parabulbarno 1.0 mg x 1 time per week, 3-6 weeks or methylprednisolone depot parabulbar 40 mg x 1 time per week, 3-6 weeks. There are other treatment regimens.

L.S. Strachunsky et al. 2002 propose such a treatment regimen. Drugs of choice: benzathine, benzylpenicillin 2.4 million IU IM 1 q 7 days for a course of 2-3 injections or bicillin 1-2.4 million IU once every 5 days, 6 injections in total, or benzylpenicillin proxin 1, 2 million IU IM every 12 hours for 20 days or bicillin 3 - 1.8 million IU IM 2 times a week, 10 injections in total

Alternative drugs: doxycillin - 0.1 g orally every 12 hours for 30 days, ceftriaxone - 0.5 g / m daily for 10 days.

Most common, especially in children, are rheumatic uveitis. Uveitis in adults is more severe than in children. It is characteristic that uveitis occurs against the background of an acute course (attack) of rheumatism. But it can be chronic, more often recurrent.

Characteristic for him: pain in the eye, a sharp corneal syndrome, multiple precipitates, tender, abundant gelatinous exudate in the anterior chamber. The vessels of the iris are dilated, full-blooded, give the iris a red color, multiple thin pigmented synechiae are revealed, which are quite easily torn after instillation of mydriatics. In the vitreous body there may be gentle opacities, in children - significant. In the fundus, there are more or less pronounced vasculitis in the form of grayish "couplings" on the vessels. Recurs on the background of another attack. In some cases, there is macular edema, sometimes papillitis. In chronic course, the prognosis is unfavorable. Positive immune responses to C-reactive protein are helpful in making the diagnosis.

Rheumatoid uveitis

Juvenile rheumatoid arthritis (JRA) is one of the most common forms of joint damage in children and adolescents. Allocate: system variant JRA; polyarticular (with positive and negative rheumatoid factor); oligoarticular. In polyarthritis involving five or more joints, the frequency of uveitis increases. First, the joints fall ill, often the knees, then the elbows and small joints of the hands and feet. And uveitis manifests itself in the first 5 years from the onset of the articular process, but may appear much later, which makes it difficult to diagnose uveitis. Girls of the preschool age group are more susceptible to this disease (Katargina L.A., Arkhipova L.T., 2004).

Uveitis with JRA proceeds, as a rule, as chronic iridocyclitis, but can proceed as peripheral or panuveitis.

Small, grayish, dry precipitates are characteristic. Posterior synechiae quickly form. For early childhood, the organization of fibrinous deposits and the infection of the pupil are characteristic. There is a rapid development of diffuse subatrophy of the iris and diffuse clouding of the lens.

One of the classic signs of rheumatic uveitis (RU) is band-like corneal dystrophy, which is a hyaline degeneration of Bowman's membrane and superficial layers of the stroma. IOP in children with RU is normal or low, but in 15-20% of cases glaucoma develops, often many years after the development of uveitis. The disease is bilateral. Exacerbations occur most often in the spring and autumn. Floating and semi-fixed opacities appear in the vitreous body. The posterior segment is involved in the process very rarely, but there may be macular cystic degeneration.

In severe cases, RU is accompanied by the development of traction retinal detachment with the development of subatrophy of the eye.

Differentiate with uveitis occurring with damage to the joints.

The clinical diagnosis of RU is based primarily on the identification of a characteristic complex of articular and ocular changes.

Treatment

Systemic use of corticosteroid drugs, non-steroidal anti-inflammatory drugs and cytostatics in various dosages and combinations. Cyclosporine A is used. In mild forms, diclofenac is administered orally. Locally: instillations of naklof, dexazone, as well as mydriatics. In severe uveitis, corticosteroid drugs are administered parabulbarno. Sometimes there is a need for surgical treatment of cataracts and glaucoma.

Still's disease- a picture of uveitis, as in rheumatoid arthritis, but “calcifications” are deposited in the conjunctiva and grayish-whitish corneal opacities are found in the area of the open palpebral fissure in the form of a ribbon. Still's disease is characterized by a triad: uveitis, complicated by cataracts, and ribbon-like corneal dystrophy. In addition to chronic polyarthritis and eye disease, lymphadenopathy and splenomegaly are noted. A typical disease for girls of preschool age. In younger children - an imperceptible course, in older children - more acute. Sometimes the ocular triad may be the only manifestation of Still's disease.

Reiter's disease(urethro-oculo-synovial syndrome) is characterized by a triad of clinical manifestations: arthritis, urethritis, conjunctivitis.

In most cases, the disease begins with urethritis that occurs after sexual contact, and sometimes with an exacerbation of a chronic urinary tract infection. In scrapings of an epithelium of an urethra chlamydias are most often found. Urethritis can be acute, with profuse purulent discharge. It develops, as a rule, at a young age (20-40 years), mainly in men.

In the pathogenesis of damage to the joints, eyes and other manifestations of Reiter's disease, immune disorders are of great importance. 5-7 days after the onset of the disease, most patients develop bilateral conjunctivitis with scanty discharge, and sometimes with profuse purulent discharge. After 10-14 days, spontaneous recovery occurs.

But xerosis of the conjunctiva and symblepharon can develop. Episcleritis, keratitis, tenonitis, inflammation of the lacrimal gland are possible. Quite often, iridocyclitis occurs, acutely, with plastic exudate, hyphema and hypopyon. It can recur and then it is complicated by cataracts, secondary glaucoma.

Rarely, neuroretinitis, choroiditis, retrobulbar neuritis, retinal hemorrhage occur.

Approximately after 1-4 weeks, arthritis appears, mainly affecting the joints of the lower extremities. One of the most typical signs of Reiter's disease is damage to the skin and mucous membranes. There may be keratoderma, a psoriasis-like rash and changes in the nails, superficial painless erosions on the mucous membranes of the oral cavity, tongue, and glans penis are possible. As the condition improves, changes in the skin and mucous membranes disappear. But atrophy of the muscles adjacent to the affected joints, lymphadenitis of the inguinal glands can develop.

Possible cardiac arrhythmias due to damage to the myocardium, pericardium, kidney damage by type of glomerulonephritis, pyelonephritis, amyloidosis. Polyneuritis, encephalomyelitis, psychosis, bronchitis, enteritis, colitis, vulvitis, orchitis, hepatitis may develop. After 3-6 months, the disease ends in complete recovery.

Differentiate with Stevens-Johnson syndrome, Behcet's disease, Bechterew's disease. The latter disease is characterized by widespread lesions of the spine and a large symmetry of polyarthritis.

The clinical manifestations of Reiter's disease in children, as well as in adults, are diverse, and among the two, three or more symptoms inherent in the disease, articular syndrome usually comes first and it is he who becomes the reason for visiting a doctor. There can be acute, protracted, primary chronic and recurrent forms of the disease. In children, the disease often begins acutely and is accompanied by fever. In half of the patients, the process is localized in one (often in the knee) joint, then in other joints, but the lower limbs are more often affected.

In Reiter's disease in children, the sacroiliac joint is affected. Characterized by early muscle atrophy, which develop early and are symmetrical.

In the primary attack, radiological changes are represented by soft tissue edema, narrowing of the joint space, and osteoporosis. Erosive lesions of the articular surfaces and ankylosis are formed only in patients with chronic and recurrent forms of the disease.

Vivid manifestations of infection of the genitals are dysuric phenomena and severe leukocyturia. In girls, vulvovaginitis and vulvitis, urethritis, cystitis and pyelonephritis are described. Boys have urethritis, sometimes accompanied by balanitis and cystitis.

The detection of cervicitis in girls with Reiter's disease is of great diagnostic value, since cervicitis is considered the main diagnostic criterion for Reiter's disease in adult women.

The most common symptom of eye pathology in children is conjunctivitis, less often - keratoconjunctivitis. The lesion is mostly symmetrical with hyperemia and edema of the conjunctiva, mucous or mucopurulent discharge. Duration from 5 days to 3 weeks.

In some, the course is more severe, with severe edema, damage to the sclera and cornea, photophobia, lacrimation, blepharospasm, with painful enlargement of the parotid lymph nodes.

Uveitis is acute, with pain and redness of the eye, sometimes with small precipitates on the posterior surface of the cornea. There may be synechia in the anterior chamber angle (ACC), which can further lead to an increase in intraocular pressure. Sometimes uveitis develops simultaneously with arthritis. In most patients, the process is bilateral, with a benign course. But some children have a severe course in the form of fibrinous uveitis, clouding of the lens.

The most common in children is damage to the oral mucosa in the form of erythematous spots or superficial erosions that are bright red or pink in color, 0.2-2.0 cm in diameter, rounded or irregularly rounded. Rarely, chlamydia can be detected from erosive surfaces with scrapings.

Equally often in children with Reiter's disease there are circinary balanitis and balanoposthitis.

Treatment

Prescribed drugs that act on chlamydia (tetracycline series), non-steroidal anti-inflammatory drugs and corticosteroids, as well as delagil, plaquenil, gold salts.

Now a complex treatment regimen using new drugs, developed by Professor Yu.F. Maichuk, is being applied. (2000): maxaquin 400 mg × 1 time per day in combination with suprastin for 10 days. For local treatment, okacin 0.3% x 5-6 times a day and eubetal ointment (betamethasone 1 mg, tetracycline 5 mg, chloramphinecone 10 mg) x 4-5 times a day are recommended.

Many people still prescribe tetracycline with nystatin, 100 thousand units. ×4 times a day for 5-7 days with simultaneous application of 1% tetracycline ointment or 1% erythromycin ointment ×2-3 times a day for 2 weeks, then dexamethasone instillations are added.

Treatment in children, as in adults, is difficult. A number of authors have proposed simultaneous treatment of the articular process, immunocorrection, sanitation of foci of infection, and local anti-inflammatory therapy in the foci of the lesion.

Behçet's disease is a multisymptomatic inflammatory chronic disease with a relapsing course. Described in 1937, it is characterized by ulceration of the oral mucosa (aphthous stomatitis), genital ulcers, and uveitis with hypopyon. Eye damage in Behçet's disease is one of the most unfavorable and severe manifestations of the disease.

Uveitis is recurrent, bilateral, proceeds according to the type of anterior and posterior uveitis, as well as panuveitis.

The joints, blood vessels, central nervous system and gastrointestinal tract are affected. Choroiditis, retinal vasculitis, papillitis, skin rashes may occur.

On the skin of the hands and feet, papules, vesicles, pustules often appear, covered with scales and crusts with ulceration in the center. Erosive balanitis is possible, sometimes there is an asymmetric polyarthritis of the interphalangeal joints of the hands and feet.

50% have arthritis involving the knee and other large joints, 25% have migratory thrombophlebitis of the superficial or deep veins, sometimes leading to obstruction of the vena cava. 18% have chronic meningoencephalitis, there may be benign hypertension, or there may be life-threatening changes in the trunk and spinal cord. Gastrointestinal involvement resembles Crohn's disease.

Generalized vasculitis can lead to the development of aneurysms or thrombosis, as well as changes in the kidneys. Less commonly, the lungs are affected with the formation of aneurysms of the pulmonary arteries.

Occurs between 15 and 40 years of age, much more often in men. It rarely starts in childhood.

Morphological changes: chronic non-granulomatous uveitis with pronounced processes of fusion formation, fibrinous exudate under the exfoliated ciliary body, CVA thrombosis, severe destruction of the retina with proliferation of glia. The diagnosis of Behçet's disease is based primarily on clinical findings.

Treatment Behcet's disease broad-spectrum antibiotics, sulfonamides, calcium chloride, single-group blood transfusion, autohemotherapy, dehydration therapy, corticosteroids under the conjunctiva, retrobulbar and inside. Locally - midriatiki. Chlorambucil (leukeran) - 12 mg daily for 2 years. Combinations of prednisolone with immunosuppressants are used.

Levamisole - immunocorrector, restores the functions of phagocytes and lymphocytes - 150 mg per day for 3 days with breaks of 4-11 days (4-8 cycles in total). Mouth aphthae and genital ulcers are treated with various septic solutions.

Some use the following treatment regimen: prednisolone 60-80 mg per day, with posterior uveitis - cyclosporine, first 5 mg kg per day, then up to 10 mg / kg per day. The minimum level of cyclosporine in the blood should be maintained in the range from 50 to 200 mg / ml.

ankylosing spondylitis, or ankylosing spondylitis-Strumpel-Marie&ndash; a systemic inflammatory disease of the connective tissue with a predominant lesion of the articular-ligamentous apparatus of the spine, as well as peripheral joints and involvement of internal organs (heart, aorta, kidneys) in the process.

In the development of the disease, importance is attached to the infectious-allergic factor, heredity, and spinal injury. The onset of the disease is usually observed at the age of 40 years. Often there are eye lesions: uveitis, keratitis. It can lead to clouding of the lens and the development of secondary glaucoma, very rarely - to atrophy of the optic nerve. The precursors of Bechterew's disease are iridocyclitis, iritis, episcleritis, resistant to conventional methods of treatment. In 2-11% of patients, eye symptoms appear several years before the development of the pathological process in the spine and joints.

Iritis and iridocyclitis occur as a bilateral exudative non-granulomatous process. It is characterized by a frequently relapsing course. In an acute process, there is a pronounced pericorneal injection, corneal edema, tender corneal precipitates, exudate is possible in the anterior chamber. The posterior synechiae are very thin.

In the fundus, edema may develop in the macular region, as well as hyperemia of the optic nerve head. One of the important differential diagnostic signs in both children and adults is the carriage of HLA-B27 in most patients (Katargina L.A., Arkhipova L.T., 2004).

Treatment

Mydriatics and corticosteroids. The latter are prescribed in instillations, as well as parabulbar and subconjunctival. Anti-inflammatory drugs are prescribed - indomethacin orally, 50 mg × 3-4 times a day. In severe cases of the process, corticosteroids are administered orally, intramuscularly and even parabulbarno.

Sarcoidosis Besnier-Beck-Schaumann disease is a polysystemic granulomatous disease of unknown etiology.

It occurs between the ages of 20 and 40 (most often). Histologically, there are multiple noncaseating epithelioid granulomas with little or no necrosis, which may resolve or lead to fibrosis. They usually appear in the mediastinal peripheral lymph nodes, lungs, liver, eyes and skin, less often in the spleen, bones, joints, skeletal muscles, heart and central nervous system.

Symptoms of the disease depend on the localization of the process: they may be absent, minor or severe.

The disease begins acutely or proceeds chronically. Characterized by the appearance of fever, erythema nodosum, enlarged mediastinal lymph nodes, arthritis. In the blood, leukopenia, eosinophilia, increased ESR.

If the liver is affected, then the temperature rise is persistent, the patient loses weight. With damage to the lungs - cough and shortness of breath, but may be absent. As a result, pulmonary fibrosis, cystic changes and cor pulmonale may develop.

The chronic form may be asymptomatic, and there may be skin lesions (papules, plaques, subcutaneous nodules). Granulomas in the nasal mucosa and conjunctiva are possible. Myocardial damage leads to angina pectoris and heart failure, conduction disorders with a fatal outcome. Possible acute polyarthritis, damage to the cranial nerves (especially the facial). Diabetes insipidus, kidney stones (hypercalcemia) may develop.

Ocular pathology is manifested by episcleritis, a ribbon-like degeneration of the cornea due to hypercalcemia. There may be dry keratoconjunctivitis with damage to the lacrimal glands.

Granulomatous sarcoidosis uveitis may be anterior or posterior.

Anterior uveitis is more common. It begins imperceptibly, with a slight pain in the eye. On examination - a minor injection.

But it can begin acutely with severe pain and lacrimation, pronounced pericorneal or mixed injection. A small amount of precipitates is detected on the posterior surface of the cornea. Then their number increases. Nodules and multiple posterior synechia appear on the iris at the pupillary edge. Nodules are a collection of epithelioid and phagocytic cells. The number of nodules increases, the number of precipitates increases, the cornea becomes cloudy. Nodules capture the stroma of the iris, vascularization appears, a bombarded iris may develop with the development of secondary glaucoma.

In posterior sarcoidosis uveitis, the vitreous body, retina, choroid, and even the optic nerve head may change. In the vitreous body, the changes look like "snowballs", there are often chains that resemble bundles of pearls.

On the fundus marked periphlebitis, separate areas of retinal edema near the veins. In the chronic course of the process, sarcoid nodules may appear in the retina.

Both in anterior and posterior uveitis, changes in the optic disc are observed - its hyperemia or neuropathy. The appearance of a congestive disc may indicate extraocular sarcoidosis, that is, the localization of granulomas in the orbital, intracranial part of the optic nerve or chiasm. If sarcoidosis of the optic nerve is suspected, computed tomography is used. A biopsy of the lymph nodes, follicles of the conjunctiva, and the lacrimal gland is performed. The Kweili reaction helps in the diagnosis.

The disease is differentiated from non-pigmented malignant melanoma of the iris and ciliary body, primary non-melanoma tumors of the iris, inflammatory pseudotumor, formations in the iris in lymphomas, leukemia, with secondary granuloma in tuberculosis and syphilis, with optic neuritis in multiple sclerosis.

Treatment

For the treatment of uveitis, corticosteroids are prescribed in the form of drops, subconjunctival and retrobulbar injections. At the same time, with low efficiency of topical application, corticosteroids are prescribed orally, intramuscularly and even intravenously. When prescribing corticosteroids, contraindications (diabetes, gastrointestinal ulcers, tuberculosis, mental disorders) should be taken into account. For the relief of severe symptoms (shortness of breath, arthralgia, fever), with liver failure, cardiac arrhythmia, CNS damage, hypercalcemia, corticosteroids are also prescribed orally. If you need a quick therapeutic effect - prednisolone 60 mg per day or methylprednisolone 48 mg per day. It is better to start with 15-20 mg of prednisolone per day and 12-16 mg per day of methylprednisolone. The course of treatment lasts a year or more.

If tolerated doses of corticosteroids do not help, a trial course of chlorambucil 4–8 mg per day or methotrexate 10 mg per week is recommended; hydroxychlorochil 400 mg daily as a palliative for disfiguring skin sarcoidosis. Clinical and laboratory studies are carried out once every 2-3 months.

Geerfordt syndrome- Refers to varieties of sarcoidosis. It was described by a Danish ophthalmologist in 1909. It is characterized by a triad: bilateral chronic parotitis, facial paralysis and uveitis.

Young adults are more likely to get sick, less often children from 5 to 15 years old and more often women.

Iridocyclitis flows chronically, rarely acutely. Accompanied by fatty precipitates, synechia, hypertension, clouding of the vitreous body, rash of nodules - granulomas - in the iris, sometimes hypopyon.

Parotitis proceeds chronically, painlessly, with a strong compaction of the salivary glands, the glands do not suppurate.

In 50% of cases, paralysis of the facial nerve occurs, as a rule, after an increase in the parotid glands. Uveoparotid fever is accompanied by the development of nodules in the skin, adenopathy. There may be meningoencephalitis with neurological disorders.

Treatment corticosteroids, ACTH, local, as in other iridocyclitis, uveitis.

Histoplasmosis is an infectious disease caused by Histoplasma capsulatum. It exists in two forms: in humans - in yeast, in contaminated soil - in the form of mold. It is characterized by a primary lesion of the lungs and sometimes hematogenous dissemination with ulceration of the oropharynx and gastrointestinal tract, enlargement of the liver and spleen, lymphadenopathy and necrosis of the adrenal glands.

The disease is accompanied by multifocal choroiditis, peripapillary scarring and hemorrhage in the area of the macula. Uveitis occurs months or years after the onset of acute acquired histoplasmosis. Infection occurs by inhalation of dust containing spores of the fungus. Severe forms are more common in men. It comes in three forms:

Primary acute;

Progressive disseminated form;

Chronic cavernous form (does not differ from tuberculosis caverns, cough, increasing shortness of breath, progressive respiratory failure).

The diagnosis is made after examination of sputum, biopsies of lymph nodes, bone marrow or liver.

Forecast

The acute form usually has a benign course. Progressive in 90% ends lethally. In chronic cases, death occurs from respiratory failure. Against the background of AIDS, histoplasmosis often quickly leads to the death of the patient.

Treatment

Corticosteroids local and general. Laser photocoagulation in the development of a pathological cystic process in the macular zone.

In the disseminated form - amphotyrecin B.

Birdshot choroidopathy- chronic bilateral, either intermediate or posterior uveitis, which is characterized by diffuse vitreous opacification and multifocal choroiditis. Often the disease is complicated by cystoid macular edema. The cause has not been identified, but 80-90% of patients are carriers of HLA-A29.

The main treatment is systemic or topical corticosteroids.

Toxocariasis described in 1937. It is characterized by fever, bronchitis, hepatosplenomegaly, eosinophilia.

In humans, pulmonary (visceral) and imaginal (intestinal) are distinguished. On the 25-28th day from the beginning of infection, female Toxocara lay eggs, which enter the environment with the feces of animals.

In animals, larvae emerge from swallowed invasive eggs into the intestines, which penetrate into the wall of the small intestine, and then into the vascular bed and through the circulatory system enter the lungs. Some go into the lumen of the trachea and bronchi, then with sputum they are swallowed again and in the intestine they reach puberty. Part of the larvae penetrates into the capillaries of the lungs, with the blood flow they are brought into various organs and tissues and encapsulated in them. Humans become infected by ingestion of infective eggs in food and water, as well as by contact with infested animals. Larval toxocariasis occurs at any age, but more often in children 1-4 years old. With a weak invasion, pruritus, recurrent urticaria, bronchitis and eosinophilia are observed. With massive invasion - fever, hepatosplenomegaly, bronchopneumonia with bouts of coughing, bronchial asthma, skin rashes, the formation of specific granulomas in various organs containing toxocar larvae.

When the process subsides, a light, shiny prominating focus with pigment around the focus and a dark gray formation in its center is visible on the fundus. This formation is a cellular infiltrate with larval remnants. There may be limited retinal detachment with vitreoretinal sutures. Vessels can grow into the focus later. Sometimes preretinal exudate appears on the extreme periphery and in the flat part of the ciliary body, and then the picture resembles peripheral uveitis. In the macular area, there is preretinal fibrosis, pigment redistribution, and sometimes retinal traction. The optic nerve is rarely involved in the process. It can be papillitis, neuroretinitis. Optic neuritis occurs with disc edema and peripapillary hemorrhages, with subretinal exudation.

Generalized uveitis is most common in toxocariasis and is more common in young children. On the posterior surface of the cornea, precipitates are observed, in the moisture of the anterior chamber - a cellular reaction, sometimes even a hypopyon. In the iris, a granulomatous node is determined; on the fundus, on the periphery of the retina, yellowish masses resembling retinoblastoma are visible. In the vitreous body - yellow exudate. The fundus is not visible. Possible exudative retinal detachment.

The process can end with a total clouding of the lens, secondary glaucoma or subatrophy of the eyeball.

In rare cases, a migrating larva is found inside the eye. It can be in the vitreous body, in the retina. Its location can change every 1-2 minutes. The migrating larva may end up in the corner of the anterior chamber after perforation of the iris.

Diagnosis is based on anamnesis, clinical picture and laboratory diagnostics. Of the laboratory tests, the most sensitive and specific is the enzyme immunoassay (ELISA). Of great importance in the diagnosis of the ophthalmic form of toxocariasis is the determination of specific antibodies and eosinophils in the moisture of the anterior chamber and in the vitreous body. Only the results of histological examination are reliable (L.A. Katargina, L.T. Arkhipova, 2004). Differential diagnosis is carried out with retinoblastoma, toxoplasmosis, Coats' external exudative retinitis, sarcoidosis, retrolental fibroplasia, primary persistent vitreous, parsplanitis.

Treatment

Locally: for iritis and iridocyclitis, instillations, subconjunctival and parabulbar injections of corticosteroids. Dexamethasone 0.1% solution 1-2 drops - 3-6 times a day, for 15-20 days. Dexamethasone parabulbarno 3-4 mg × 1 time per day, 10 days. In severe cases, glucocorticosteroids are used systemically, and not locally.

In severe course of the process, prednisolone is prescribed orally at a dose of 0.5-1 mg / kg per day, anthelmintic therapy.

Inside give thiabendazole at a dose of 25-50 mg / kg per day for 7-10 days or mebendazole 100 mg × 2 times a day for 5-7 days.

Of the other anthelmintic drugs, Vermox is recommended at 200-300 mg per day for 1-4 weeks, medamin at a dose of 10 mg/kg per day in repeated cycles of 10-14 days. Albendazole is prescribed at a dose of 10 mg / kg per day in two doses (morning, evening) for 7-14 days.

Be sure to examine the blood during treatment.

Vitrectomy is performed to remove the larva from the vitreous body and prevent the development of endophthalmitis. Perhaps the use of sufficiently intense laser coagulation. Coagulates are applied to the migrating larva to completely destroy it.

Imaginal toxocariasis is rare. Complaints of nausea, abdominal pain, profuse salivation, loss of appetite, dizziness are common. Toxocara eggs are found in feces.

Treatment

Piperazine, colibacterin and decaris. The prognosis is favorable.

Vogt-Koyanagi-Harada Syndrome(uveameningeal syndrome) is a systemic disease characterized by damage to many organs and systems, including the eyes, ears, skin and meninges.

It begins more often at the age of 27-50 years, but children can also get sick. Changes in the skin and hair come to the fore: partial hair loss - alopecia, their local graying - poliosis; focal depigmentation of the skin - vitiligo, etc., as well as mild neurological symptoms (paresthesia, headaches, etc.). Less commonly, the process proceeds as severe uveomeningitis. The disease may be preceded by a prodromal stage with a rise in body temperature, headache, ataxia, pain in the orbit when moving the eyeballs, etc. (Rysaeva A.G., 1982; Katargina L.A., Arkhipova L.T., 2004).

On the part of the eyes, it is a chronic bilateral recurrent granulomatous uveitis or uveoencephalitis, occurring with sebaceous precipitates on the posterior surface of the cornea, the formation of posterior synechia, fusion and infection of the pupil, leading to secondary glaucoma with lens opacity and atrophy of the eyeball.

An objective examination can note not only the formation of nodules in the iris, but also its diffuse thickenings, which contribute to the blockade of the anterior chamber angle and an increase in IOP.

In the vitreous body, pronounced opacities are observed, in the fundus there is swelling of the optic nerve head, which is combined with retinal edema, and in severe cases with its total detachment.

As the process progresses, neovascularization of the retina and optic nerve occurs and rather rapidly increases, which leads to vitreal hemorrhages, as well as the formation of pro-, intra- and subretinal proliferative membranes, and as a result, to a sharp decrease in vision.

Meningeal phenomena can be characterized by signs of increased intraocular pressure, bilateral papillitis, mental disorders with suicidal attempts, changes in the electroencephalogram. The disease can begin with meningeal symptoms, manifested by headache, vomiting, in 50% of patients with temporary hearing loss. In the cerebrospinal fluid - pleocytosis.

They help to diagnose: depigmentation of eyelashes, hair, head, pigmentless spots on the skin of the face and trunk, changes in the central nervous system, changes in EPI, EOG, FAG, immunogenetic studies that reveal a wide range of changes in the eyes.

The etiology is still not exactly clear. Most researchers are inclined to the viral origin of the disease.

Differential diagnosis is carried out with sarcoidosis, posterior placoid multifocal pigment epitheliopathy and a number of white dot syndromes.

Treatment

Corticosteroids, dehydration therapy. Corticosteroids are prescribed in the form of drops, subconjunctival and parabulbar, as well as intramuscularly and intravenously. Maintenance steroid therapy is carried out for 4-6 months. Immunosuppressants are used (cyclophosphamide orally, 100 mg per day, 3000 mg per course), leukeran, orally, 6 mg per day for 20-30 days, metatrexate, 5 mg per day in two doses of 5 days with breaks of 3 days (all th 5-6 cycles). A blood test is required to control the number of leukocytes and platelets.

For side effects in steroid therapy, a combination with cyclosporine is used with a corresponding reduction in the dose of prednisolone. There are indications of the effectiveness of plasmapheresis in the treatment of these patients.

Of the immunostimulants, levomisole is used at 150 mg per day (in 2 divided doses for 3 days). The course of treatment is repeated 3 times in 12-15 days.

Brucellosis- a common infectious disease with a predominant lesion of the musculoskeletal system, nervous, reproductive systems and a tendency to a long relapsing course. Brucellosis is a zoonotic infection. It is especially typical for small and large cattle (goats, sheep, cows, pigs, deer).

Infection of people occurs through the alimentary route (through milk or dairy products), as well as through contact with animals (livestock care, carcass processing, etc.).

Pathogens - Brucella, small (0.3-2.5 microns) immobile bacteria, gram-negative, stable in the external environment. Having entered the human body through the skin or mucous membranes of the digestive tract, less often through the respiratory tract and conjunctiva, Brucella enter the regional lymph nodes, and then into the blood. From the blood, the pathogen is fixed by the organs of the reticuloendothelial system (liver, spleen, bone marrow, lymph nodes), in which secondary foci of infection are formed. They are a source of prolonged bacteremia, resulting in a generalization of the process with the formation of metastases (specific granulomas). Sensitization of the body develops with various organic manifestations.

The duration of the incubation period is from a week to several months.

There are acute brucellosis, acute recurrent, chronic active brucellosis, chronic inactive brucellosis (Yushchuk N.D., Vengerov Yu.Ya., 2004).

The onset of the disease is gradual or subacute, in children it can be acute. Against the background of a slight malaise, a fever appears, the temperature is 39-40 degrees, which lasts from 3 days to 3-4 weeks or more. Chills, pronounced sweating. The skin is pale, micropolyadenopathy is noted, sometimes the liver and spleen are enlarged.

Then it goes into the phase of acute recurrent brucellosis, in which there are repeated febrile attacks of varying duration. During attacks, arthralgia, myalgia, neuralgia, local lesions of the musculoskeletal system, genital organs, nervous and cardiovascular systems are observed. Men can develop orchitis, epididymitis. There is the development of infectious-allergic myocarditis, rarely endocarditis. Increased changes in the nervous system. In severe cases, mental disorders, meningism phenomena are possible. Serous meningitis may develop.

Acute recurrent brucellosis without a clear line turns into chronic active. All changes become more pronounced. After 2-3 years, the disease passes into an inactive phase, but positive serological tests and the Burne test remain.

Brucellosis can clinically cause an inflammatory process in any part of the vascular tract of the eye; the entire uveal membrane can be involved in the process. In the uveal tract, the brucellosis process most often manifests itself in the form of a banal exudative iridocyclitis, which occurs acutely or has a protracted character, with relapses for several years.

In the acute form, pain, pericorneal injection, pupillary constriction, folds of the Descemet's membrane, formed precipitates on the posterior surface of the cornea or lumpy deposits, sometimes hypopyon, are noted.

With a prolonged flow in the iris, a network of newly formed vessels develops, the exudate takes on a plastic character, contributing to the formation of powerful posterior synechiae up to complete fusion and fusion of the pupil. Secondary glaucoma and cataracts develop. The process may end in the death of the eyeball.

But the process can proceed without the presence of granulomas, as an exudative process with clouding of the vitreous body. Sometimes there is a metastatic ophthalmia of brucellosis etiology.

Rarely observed focal, disseminated and central chorioretinitis of brucellosis origin.

Currently, infectious-allergic forms of ophthalmobrucellosis dominate, which differ in pathogenesis, clinic, diagnosis and treatment from systemic brucellosis and from metastatic ophthalmobrucellosis, it is isolated into an independent nosological unit (Dolgatov E.I., 2004). According to him, the most common forms of infectious-allergic ophthalmic brucellosis are also brucellosis limbopathy, edematous-hypertrophic conjunctivitis, marginal sclerosing keratitis, phlyctenular keratoconjunctivitis, scleritis and episcleritis, serous-plastic sluggish anterior uveitis. Rarely there are myositis of the oculomotor muscles, optic neuritis, dacryocystitis, various vascular pathologies of the eyeball, including CVA thrombosis, retinal dystrophy.

Serological and allergological methods are used to diagnose brucellosis. For the diagnosis of the infectious-allergic form of ophthalmobrucellosis, test-tube methods are recommended - the reaction of blastotransformation, inhibition of leukocyte migration, since serological reactions and the Burne test are often negative.

Treatment

Apply tetracycline at a dose of 5 g x 4 times a day or doxycycline 0.1 g x once a day for 3-6 weeks in combination with streptomycin 1.0 x 2 times a day for 2 weeks.

An effective combination of biseptol or its analogues at a dose of 6 tablets per day with rifampicin at a daily dose of 0.9 g for 4 weeks.

Non-steroidal anti-inflammatory drugs (indomethacin, diclofenac), as well as salicylates, delagil, etc. are used.

In some cases, corticosteroids are used (prednisolone 40-60 mg per day with a dose reduction after obtaining a clinical effect). Course - 2-3 weeks. Physiotherapeutic procedures, methods of reflexology, massage, physiotherapy exercises are used. In chronic inactive and residual brucellosis, spa treatment is widely used.

Treatment of infectious-allergic ophthalmobrucellosis is aimed at desensitizing the body, strengthening the vascular wall, improving microcirculation and tissue trophism.

In the presence of systemic manifestations of brucellosis, antibiotic therapy is indicated, that is, general treatment, which is carried out in conjunction with the relevant specialists.

Locally used in the form of subconjunctival injections of 0.8 ml of dexazone, 0.2 ml of 1% mezaton solution and instillation of 0.1% dexamethasone solution. You can use diprospan in instillations, laying eye ointments. For resorption of exudate, enzyme preparations are prescribed: fibrinolysin, lidase.

Physiotherapeutic procedures are also carried out (UHF, diadynamic currents, electrophoresis with medicinal substances and plasmapheresis).

Differentiate with influenza, SARS, typhoid fever, Cooley fever, yersiniosis, ornithosis, leptospirosis, miliary tuberculosis, sepsis, infective endocarditis, and later with rheumatism, rheumatoid arthritis, and other diseases of the musculoskeletal system.

Diagnosis of endogenous uveitis

Analysis of the patient's complaints is the first step in the diagnosis of uveitis.

With anterior and panuveitis, complaints are reduced to redness of the eyes, photophobia, pain in the eye, sometimes there is a decrease or blurred vision, changes in eye color, size and shape of the pupils. Pain is not typical for young children.

Then, an external examination of the eye, biomicroscopy, ophthalmoscopy with a thorough examination of the periphery of the fundus, gonioscopy, and tonometry are performed. On examination, a pericorneal injection is noted.

With biomicroscopy, there is fogging of the endothelium of the cornea, the presence of corneal precipitates from single to multiple, of various sizes (from pulverized to 1 mm in diameter).

Precipitates can be "fat", in which there are clusters of lymphocytes, plasma and giant cells, they can be small whitish, in which there are clusters of neutrophils, lymphocytes. The cornea is carefully examined, the moisture content of the anterior chamber, which may contain exudate (serous, fibrinous, purulent or hemorrhagic), the iris with hyperemia, edema, smoothness of the pattern, the presence of exudative-fibrinous deposits or hemorrhages on its surface. There may be posterior synechiae, nodules along the edge of the pupil (Keppe's nodes) or on the surface of the iris (mesodermal Boussac's nodules). The presence of characteristic nodules in the iris is an important diagnostic feature of ocular sarcoidosis.

When examining the CPC, attention is drawn to the presence of exudate, neovascularization, which lead to an increase in IOP.

When examining the lens, it should be determined whether there is any clouding (complicated cataract), which occurs with uveitis. In the vitreous body, turbidity is detected due to the presence of inflammatory cells and protein substances. Possible posterior vitreous detachment. Fixation of vitreal cords to the retina and ciliary body can lead to ciliary body detachment, retinoschisis, retinal cysts, and retinal detachment. This is followed by reverse and direct ophthalmoscopy, biomicroscopy with a Goldmann lens, and fluorescein angiography.

In the fundus, one can see cystic macular edema, which is the result of cystic accumulation of extracellular intraretinal fluid in the outer plexiform and inner nuclear layers due to a violation of the blood-ophthalmic barrier and which is better detected using fluorescein angiography.

In the fundus, vasculitis, perivasculitis, narrowing and obliteration of blood vessels, hemorrhages, cotton-like foci (a symptom of retinal ischemia) are detected, solid exudate appears, and subretinal neovascular membranes are formed. There may be choroiditis, chorioretinitis.

At the periphery of the fundus, when viewed with a Goldman lens, whitish fibroglial masses can be seen above the zone of the flat part of the ciliary body (snowy exudate), which are a symptom of uveitis. In the periphery, areas of neovascularization may also be detected.

On the part of the optic nerve, there may be its hyperemia, edema or papillitis, glaucomatous excavation, neovascularization, atrophy.

An important role in establishing the diagnosis should be given to the anamnesis and a detailed general somatic examination.

Laboratory diagnostics is also carried out to identify the etiology of uveitis, determine the prognosis and select an adequate treatment strategy.

The method of fluorescent antibodies is used, which is used to analyze scrapings of the conjunctiva and cornea, as well as to study tissue sections obtained during surgery or at autopsy. This technique is available and quickly performed.

Passive hemagglutination reaction (RPHA), neutralization reaction (RN), complement fixation reaction (RCC), indirect immunofluorescence reaction (RNIF), enzyme immunoassay, ELISA, etc. are used.

In addition to the etiological examination, to determine the treatment tactics and predict the course of uveitis, laboratory studies are carried out, the patient's immune status is determined, as well as the study of local and systemic interorgan and organ-specific autoimmune reactions. They determine the number of T- and B-lymphocytes, assess the phagocytic activity of neutrophils, determine the main classes of serum immunoglobulins and complement titer and circulating immune complexes, determine the subpopulation of lymphocytes, set up blastotransformation of lymphocytes, determine specific Ig E, serum thymic activity, cytokines, and other reactions . Various cytokines are detected in blood serum, lacrimal fluid and intraocular fluids.

For diagnosis, fluorescein angiography, ultrasound research methods, electrophysiological studies (EPS), as well as thermographic studies are used.

Glaucomocyclitis crises

In 1929 Terven and in 1936 Kraup described unilateral glaucoma with precipitates and emphasized the difference from secondary "uveal" glaucoma. In 1948-1949. Posner and Schlossman described a similar condition and called it glaucoma-cyclitis crisis. These are repeated unilateral attacks of increased IOP with the appearance of precipitates.

The general condition remains satisfactory, the functions of the eye (visual acuity and field of vision) are not impaired or only slightly impaired. Miotics with dexazone and calcium cut off the attack.

Kraup believed that this was a manifestation of allergy, and Posner and Schlossman believed that this was hypersecretion of chamber moisture due to disorders of the central nervous system and peripheral nervous system. They attached particular importance to the role of the hypothalamus. Some believed that an increase in IOP is a consequence of cyclitis, Theodore called it an intermediate form between primary and secondary glaucoma, and Grefe considered it as one of the forms of serous uveitis, more often of tuberculous etiology, referring to secondary glaucoma.

In the literature there are indications of isolated cases of bilateral glaucoma cyclitis crisis. 24 patients are described. Calm eyes, some have slight corneal edema, precipitates, the pupil of the correct round shape, wide, 6 people have heterochromia. The precipitates disappeared quickly. There were no changes in the fundus. Gonioscopy - the angle of the anterior chamber is open, wide. They believe that this is a peculiar manifestation of secondary glaucoma on the basis of anterior uveitis of an allergic nature.

Treatment of iridocyclitis, uveitis consists of local and general:

Local: 1% atropine solution, 0.25% scopolamine solution, 1% homotropine solution, 1% mezaton solution, 1% midriacil solution - to dilate the pupil, prevent the formation of posterior synechiae, fusion and fusion of the pupil, rupture of posterior synechiae, if they already formed.

If the pupil does not dilate well or the posterior synechia does not rupture from the use of these mydriatics, you can apply 1% atropine ointment, a combination of medriatics, adrenaline wick 1:1000 with cocaine 1-2%, adrenaline 1:1000 0.2 ml under the conjunctiva.

It must be remembered that atropine increases IOP. With frequent and prolonged instillation of atropine, poisoning is possible, the first sign of which is a feeling of dryness in the mouth, nasopharynx. In this case, atropine should be canceled and replaced with another mydriatic.

Corticosteroids are used in the form of instillations, under the conjunctiva and retrobulbar, antimicrobial agents (sulfonamides), antiviral drugs (bonafton, zavirax, poludan, etc.), absorbable drugs (potassium iodide, papain, lycozyme), electrophoresis with mydriatics, antibiotics, calcium chloride, corticosteroids.

Treatment

Anti-infective agents (antibiotics, sulfonamides), anti-inflammatory agents (amidopyrine, reopyrin, butadione, corticosteroids), antihistamines (suprastin, tavegil, diazolin), general strengthening agents (ascorbic acid, rutin, calcium preparations), neurotropic agents (dibazol, B vitamins) are used. etc.), analgesics, perivasal blockades, leeches, repeated blood transfusions in fractional doses, exchange plasmapheresis, which has an immunotropic effect, removes pathogenic factors, antibodies and immune complexes, inflammatory mediators, immune system hormones, toxic products, increases the amount of T-active cells and activates phagocytosis.

Uveitis in systemic diseases is always the result of a violation of the functions of the immune system and refers to autoimmune diseases. The autoimmune component, as a rule, is involved in the development of uveitis of any infectious and unexplained etiology. Immune reactions cause the migration and proliferation of T- and B-lymphocytes, the release of mediators of immune reactions, biochemically and pharmacologically active substances - histamine, serotonin, prostaglandins, a decrease in the activity of glycolysis enzymes and a deficiency of hydrocortisone.

The complex treatment of uveitis should include etiologically directed, pathogenetically substantiated, immunoregulatory and corrective agents, nonspecific and specific hyposensitization, physical, laser and surgical methods. Certainly specific preparations, resort-climatic treatment are used. Sanitation of all foci (teeth, tonsils, paranasal sinuses, deworming). If uveitis is complicated by secondary glaucoma and IOP is high, then surgery is indicated in any period of the disease.

If there is no effect of conservative therapy, there are intense vitreous opacities and intravitreal bands, lens opacities, recurrences of uveitis, leading to a sharp and irreversible decrease in objective vision without exacerbation, a sluggish form of the disease with a steady progression of the inflammatory process, surgical intervention is indicated. The following types of operations are recommended:

1. Isolated closed vitrectomy.

2. Vitrectomy with removal of the exudative pupillary membrane.

3. Vitrectomy with lensectomy.

4. Vitrectomy with extracapsular cataract extraction.

In peripheral uveitis, corticosteroids, broad-spectrum antibiotics, desensitizing agents, and physiotherapeutic methods are also applied topically.

In autoimmune processes, cyclophosphamide (No. 10-15), electrophoresis with corticosteroids are prescribed under the conjunctiva and parabulbarno.

In severe forms, general treatment with corticosteroids, desensitizing therapy (10% calcium chloride intravenously, subcutaneously 0.25% calcium chloride according to the scheme, diphenhydramine, suprastin, pipolfen, tavegil, etc.) are indicated.

With a focal infection, antibiotics are prescribed under the conjunctiva, parabulbar and intramuscularly (the greatest effect: gentamicin 200 mg per course and ampiox 2.0 g per course). Of the enzymes, fibrinolysin, lidase, lekazyme are used in the form of electrophoresis and subconjunctival injections.

In case of hemorrhages in the retina, ascorutin, angioprotectors (dicinone, prodectin) are prescribed in tablets. With macular edema and secondary glaucoma - dehydration therapy. With sluggish processes - vitamins of group B.

In an immunodeficient state, levomisole, sodium nucleinate inside are indicated.

Sometimes aiming and delimiting argon is performed - laser coagulation of peripherally located foci.

With hemorrhages - targeted coagulation of newly formed vessels.

Interferon is used, which affects the synthesis of nucleic acids and proteins. It suppresses the products induced by viruses of enzymes.

Poludan has interferonogenic activity. It is administered at 50-100 IU in 0.5 cm³ of distilled water for 2-3 weeks.

Apply hyperimmune serum, titrated gamma globulins, if necessary - vaccines. Patients resistant to corticosteroid therapy undergo cryopexy of the vitreous base.

Questions

1. What are the structural features of the vascular tract of the eye?

2. Name the main functions of the choroid.

3. How to correctly classify inflammatory processes in the vascular tract?

4. How are uveitis subdivided according to pathogenesis?

5. How are uveitis subdivided according to the localization of the process?

6. What features of the blood supply to the choroid determine the frequency of predominantly isolated lesions of its individual sections?

7. What are the main objective signs of iritis?

8. What methods are used to examine the iris?

9. List the symptoms indicating the presence of an inflammatory process in the ciliary body.

10. List the complications of iridocyclitis.

11. Name the type of injection typical for iridocyclitis.

12. Specify the complaints made by patients with iridocyclitis.

13. List the complaints of patients with chorioretinitis.

14. Name the main objective symptoms of chorioretinitis.

15. What are the features of influenza uveitis?

16. Etiology and clinic of metastatic ophthalmia.

17. List the form of local treatment for uveitis?

18. Name the main drugs for local treatment of iridocyclitis.

19. List the principles of treatment of uveitis.

20. What do you know about pupil dilators and their synergists?

Eye Diseases: Lecture Notes Lev Vadimovich Shilnikov

3. Vascular tract of the eye

The vascular tract, consisting of the iris, ciliary body and choroid, is located medially from the outer shell of the eye. It is separated from the latter by the suprachoroidal space, which is formed in the first months of a child's life.

The iris (anterior part of the vascular tract) forms a vertically standing diaphragm with a hole in the center - the pupil, which regulates the amount of light entering the retina. The vascular network of the iris is formed by branches of the posterior long and anterior ciliary arteries and has two circles of blood circulation.

The iris can have a different color: from blue to black. Its color depends on the amount of melanin pigment contained in it: the more pigment in the stroma, the darker the iris; in the absence or small amount of pigment, this shell has a blue or gray color. In children, there is little pigment in the iris, so in newborns and children of the first year of life, it is bluish-grayish. The color of the iris is formed by the age of ten or twelve. On its front surface, two parts can be distinguished: a narrow one, located near the pupil (the so-called pupillary), and a wide one, bordering on the ciliary body (ciliary). The boundary between them is the pulmonary circulation of the iris. There are two muscles in the iris that are antagonists. One is placed in the pupillary region, its fibers are located concentrically to the pupil, with their contraction the pupil narrows. Another muscle is represented by radially running muscle fibers in the ciliary part, with the contraction of which the pupil expands.

In infants, muscle fibers that dilate the pupil are poorly developed, parasympathetic innervation predominates, so the pupil is narrow (2–2.5 mm), but expands under the action of mydriatics. By the age of one to three years, the pupil acquires the size characteristic of adults (3–3.5 mm).

The ciliary body consists of a flat and thickened coronal parts. The thickened coronal part consists of 70 to 80 ciliary processes, each of which has vessels and nerves. The ciliary, or accommodative, muscle is located in the ciliary body. The ciliary body is dark in color and covered with retinal pigment epithelium. Zinn ligaments of the lens are woven into it in the interprocesses. The ciliary body is involved in the formation of intraocular fluid that nourishes the avascular structures of the eye (cornea, lens, vitreous body), as well as in the outflow of this fluid. In newborns, the ciliary body is underdeveloped, the accommodative muscle is in a spastic state.

The vessels of the ciliary body depart from the large arterial circle of the iris, which is formed from the posterior long and anterior ciliary arteries. Sensitive innervation is carried out by long ciliary fibers, motor - by parasympathetic fibers of the oculomotor nerve and sympathetic branches.

The choroid, or the choroid itself, is composed mainly of short posterior ciliary vessels. In it, with age, the number of pigment cells increases - chromatophores, due to which the choroid forms a dark chamber that prevents the reflection of rays entering through the pupil. The basis of the choroid is a thin connective tissue stroma with elastic fibers. Due to the fact that the choriocapillary layer of the choroid is attached to the retinal pigment epithelium, a photochemical process is carried out in the latter.

From the book Eye Diseases author Lev Vadimovich Shilnikov

From the book Normal Physiology: Lecture Notes author Svetlana Sergeevna Firsova

From the book Homeopathy for General Practitioners author A. A. Krylov

From the book Homeopathy. Part II. Practical recommendations for the choice of drugs by Gerhard Keller

From the book Dietetics: A Guide author Team of authors

From the book Canon of Medicine author Abu Ali ibn Sina

From the book What the tests say. Secrets of medical indicators - for patients author Evgeny Alexandrovich Grin

From the book Homeopathic Handbook author Sergei Alexandrovich Nikitin

From the book Dog Treatment: A Veterinarian's Handbook author Nika Germanovna Arkadieva-Berlin

From the book Exercises for Internal Organs for Various Diseases author Oleg Igorevich Astashenko

7. Samara Clinical Ophthalmological Hospital named after T.I. Eroshevsky, structure, leading scientific and practical areas.

9. Biomicroscopy, its possibilities in the study of the organ of vision.

12. Refraction. Physical and clinical refraction of the eye. Types of clinical refraction.

13. Refractogenesis. What is a further point of clear vision.

14. Myopia.

15. Prevention of myopia and its complications.

16. Hypermetropia, methods of determination.

17. Accommodation, absolute or relative. Definition methods.

18. Physiological changes and pathological disorders of accommodation. Correction of prebiopia taking into account clinical refraction.

19. The cornea, features of its structure and nutrition. Classification of diseases of the cornea.

1. Anomalies of development;

2. Inflammatory (keratitis, scleritis);

3. Dystrophic;

4. Tumors.

20. Keratitis, subjective and objective signs. Classification of keratitis, principles of treatment. Providing first aid for keratitis.

21. Purulent keratitis, etiology, pathogenesis. Purulent ulcer of the cornea. Medical and surgical treatment, taking into account the etiology and severity of the process. Prevention.

22. Herpetic keratitis (primary and secondary). Pathogenesis, clinic, treatment. Prevention.

23. Tuberculous and syphilitic keratitis. Clinic, treatment. Prevention.

24. Consequences of keratitis. Keratoplasty, keratoprosthetics. Ways of conservation of the cornea.

25. Diseases of the sclera. Scleritis, neoplasms, clinic, treatment.

26. Eyelids, anatomy and physiology, blood supply and innervation. Classification of diseases of the eyelids.

27. Inflammatory diseases of the eyelids.

28. Non-inflammatory eyelid diseases: eyelid edema, eyelid neoplasm.

29. Inversion, eversion of the eyelids.

30. Ptosis, lagophthalmos.

31. Lacrimal organs, anatomy and physiology. Classification of diseases of the lacrimal organs.

32. Inflammatory diseases of the lacrimal organs.

33. Conjunctiva, anatomical features of the structure, physiology. Classification of diseases of the conjunctiva.

35. Adenovirus conjunctivitis

36. Diphtheria conjunctivitis

37. Gonococcal conjunctivitis.

38. Trachoma and paratrachoma.

39. Vascular tract, structure, physiology, features of vascularization and innervation. Classification of diseases of the vascular tract.

40. Inflammatory diseases of the anterior vascular tract.

42. Inflammatory diseases of the posterior vascular tract.

41. Chronic iridocyclitis.

45. Eye socket, structural features. Classification of diseases of the eye.

46. Inflammatory diseases of the orbit. Phlegmon of the eye...

47. Non-inflammatory diseases of the orbit. Neoplasms…

53. Cataract, classification, etiology, clinic, principles of treatment.

54. Congenital cataract. Classification, clinic, diagnosis, treatment.

55. Senile cataract, classification, clinic, diagnosis, complications, treatment. Dif. Diagnostics.

56. Complicated and traumatic cataract. Etiology, clinic, diagnosis, treatment.

57. Afakia. Clinic, diagnostics, correction.

58. Anatomical structures of the eyeball, providing normal intraocular pressure. Methods for determining IOP.

59. Glaucoma, definition, classification, early diagnosis, principles of treatment. Prevention of blindness from glaucoma.

60. Congenital glaucoma. Etiology, clinic, diagnosis, treatment.

61. Primary glaucoma. Classification. Clinic of open-angle and closed-angle glaucoma. Dif. Diagnosis, treatment.

62. Secondary glaucoma. Etiology, clinic, diagnosis, treatment.

63. Acute attack of glaucoma (angle-closure and secondary). Clinic, dif. Diagnosis, treatment. Providing first aid.

85. Visual disability. Classification, causes, diagnosis of irreversible and treatment of reversible blindness.

Group I - 4th degree of visual impairment:

86. The main causes of low vision and blindness in the world and in Russia.

87. Provision of medical and social assistance to the blind and visually impaired. All-Russian Society of the Blind and its significance.

88. Simulation of blindness and decreased visual acuity in one and both eyes. Definition methods.

90. Military medical examination. Permissible standards for service in the army of the Russian Federation for visual acuity, color vision, clinical refraction.

77. Classification of injuries of the organ of vision. Superficial mechanical damage to the organ of vision, clinic, treatment. Providing first aid.

78. Blunt injuries of the organ of vision. Clinic, diagnosis, treatment, prevention. Providing first aid.

79. Penetrating wounds of the eyeball. Classification, clinic, diagnostics. Providing first aid and specialized medical care.

80. Early complications of penetrating wounds of the eyeball.

81. Late complications of penetrating wounds of the eyeball. Sympathetic ophthalmia, theory of occurrence, treatment, prevention.

82. Mechanical injuries of the orbit. Clinic, diagnosis, treatment. Syndrome of the superior orbital fissure.

83. Chemical and thermal eye burns. Classification. Providing first aid and specialized medical care.

84. Damage to the organ of vision by ultraviolet and infrared rays, penetrating radiation. Providing first aid for electrophthalmia.

73. Changes in the organ of vision in hypertension, atherosclerosis, chronic nephritis, preeclampsia in pregnant women.

74. Changes in the organ of vision in diabetes mellitus. Clinic. Causes of blindness in diabetes mellitus. Modern methods of treatment.

75. Changes in the organ of vision in thyrotoxicosis. Clinic, treatment. Prevention of keratitis in malignant exophthalmos.

76. Changes in the organ of vision in toxoplasmosis. Clinic, diagnosis, treatment. Prevention.

64. Retina, features of the structure and attachment in the eyeball, vascularization, physiology. Classification of diseases of the retina.

66. Acute obstruction of retinal vessels. Etiology, clinic, differential diagnosis, treatment. Providing first aid.

68. Retinal dystrophies (youthful and senile). Clinic, diagnosis, treatment.

67. Retinal detachment. Etiology, clinic, treatment, prevention.

72. Neoplasms of the retina and optic nerve. Clinic, diagnosis, treatment.

70. Inflammatory diseases of the optic nerve (papillitis, retrobulbar neuritis). Etiology, diagnosis, treatment, prevention.

71. Non-inflammatory diseases of the optic nerve (atrophy, congestive optic nerve papilla). Etiology, clinic, diagnostics, treatment,

69. Optic nerve, structural features, vascularization. Classification of diseases of the optic nerve.

48. Oculomotor muscles, features of attachment and functions, innervation.

49. Binocular vision, the advantages of binocular vision over monocular. Definition methods. Significance in human life.

50. Strabismus: true, imaginary, hidden, methods of determination. Concomitant and paralytic strabismus. differential diagnosis.

51. Dysbinocular amblyopia. Clinic. Principles of treatment of concomitant strabismus (pleopto-orthoptic and surgical).

16. Hypermetropia, methods of determination. Clinic, complications. Modern methods of correction.

39. Vascular tract, structure, physiology, features of vascularization and innervation. Classification of diseases of the vascular tract.

Middle layer of the eye is vascular tract of the eye, which embryogenetically corresponds to the pia mater and consists of three parts: the choroid itself (choroid), the ciliary body and the iris. The vascular tract is separated from the sclera by the suprachoroidal space and is adjacent to it, but not all the way. It consists of branching vessels of various calibers, forming a tissue resembling a cavernous tissue in structure.

Anterior part of the vascular tract is Iris. It is visible through a transparent cornea, painted in one color or another, which indicates the color of the eyes (gray, blue, brown). In the center of the iris is the pupil, which, thanks to the presence of two muscles (sphincter and dilator), can narrow to 2 mm and expand to 8 mm to regulate the entry of light rays into the eye.

The sphincter is innervated by the parasympathetic oculomotor nerve, the dilator is sympathetic, penetrating from the plexus caroticus.

ciliary body inaccessible to inspection with the naked eye, unlike the iris. Only with gonioscopy, at the top of the chamber angle, one can see a small area of the anterior surface of the ciliary body, slightly covered by the delicate fibers of the uveal part of the trabecular apparatus. The ciliary body is a closed ring, about 6 mm wide. On the meridian section, it has the shape of a triangle. In the ciliary body, on its inner surface, there are 70-80 processes. The ciliary body consists of smooth ciliary or accommodative muscle. From the inside, the ciliary body is lined with two layers of epithelium - a continuation of the embryonic retina. On the surface of the epithelium there is a boundary membrane to which the fibers of the zonium ligament are attached. The ciliary body performs a very important function, its processes produce intraocular fluid, which nourishes the avascular parts of the eye - the cornea, lens, vitreous body. The ciliary epithelium has a huge number of nerve endings. In newborns, the ciliary body is underdeveloped. In the first years of life, the motor and trophic nerves are better developed than the sensory ones; therefore, during inflammatory and traumatic processes, the ciliary body is painless. By the age of 7-10 years, the ciliary body is the same as in adults.

The choriocapillary layer provides nutrition to the outer layers of the retina, i.e. neuroepithelium.

Diseases of the choroid include inflammatory diseases of an infectious or toxic-allergic nature ( iritis, iridocyclitis, endophthalmitis, panuveitis), dystrophic processes, tumors and injuries, as well as congenital anomalies

Anomalies of the choroid, which are occasionally found in newborns, include aniridia, coloboma of the iris, ciliary body and choroid proper, polycoria, corectopia, freckles, aplasia, albinism.Aniridiait is the absence of the iris. At the same time, behind the cornea there is a picture of a maximally dilated pupil, that is, blackness. Even with side illumination, the contours of the lens and the ciliary band are visible. Sometimes a rim is visible - the remnant (rudiment) of the iris root and ciliary processes. The most distinct picture of aniridia is given by biomicroscopy and examination in transmitted light, while, according to the diameter of the cornea, a red reflex from the fundus is determined. Coloboma of the iris, ciliary body and choroid - the absence of part of the department.coloboma- the general name of some types of congenital, less often acquired defects in the tissues of the eye (the edge of the eyelid, the iris, the choroid itself, the retina, the optic disc, the lens). A congenital or acquired defect of the eye, leading to various anomalies: from the appearance of a small indentation of the edge of the eyelid or lower part of the iris, as a result of which the pupil resembles a pear, to defects in the fundus. An enlarged pupil leads to the appearance of symptoms of blindness in a person. Eyelid coloboma is a congenital depression at the edge of the eyelid

Polycoria- these are two or more pupils; one of them is larger, and the rest are smaller; the shape of these pupils is not quite round, and the reaction to light is sluggish. Naturally, with this condition of the iris, there is a pronounced visual discomfort and a decrease in visual acuity.

Corectopia Characterized by an eccentric pupil. If there is a shift to the nasal, i.e., to the optical zone, then a sharp decrease in visual acuity is possible and, as a result, the development of amblyopia and strabismus.

Interpupillary membrane is the most harmless anomaly, which is often found in children. It can have a bizarre shape in the form of a web, oscillating in the aqueous humor of the anterior chamber, as a rule, fixed to the iris and the anterior lens capsule. Pronounced and dense membranes in the central zone of the lens can reduce visual acuity.

Inflammatory diseases of the vascular tract: iris - iritis, ciliary body - cyclitis, iridocyclitis or anterior uveitis, damage to the vascular tract - posterior uveitis or choreoiditis, iridocyclochoroiditis, panuveitis, generalized uveitis. The infection enters by exogenous or endogenous routes.

Irit- inflammation of the iris or iris and ciliary body (iridocyclitis).

Uveitis- inflammation of the choroid of the eyeball. Anatomically, the choroid of the eyeball is divided into the iris, the ciliary body and the choroid itself, located behind the ciliary body and making up almost 2/3 of the choroid (actually lines the retina from the outside).

Iridocyclitis- acute inflammation of the iris and ciliary body, or anterior uveitis.

Tumors of the vascular tract- from benign formations there are neurofibromas, neurinomas, leiomyomas, nevi, cysts. You can notice changes in the eye if they are localized in the anterior segment. They are manifested in one way or another in a change in the structure and color of the iris. The most obvious are nevi and cysts

Melanoma- malignant pigment tumor, can occur in the iris, ciliary body, choroid. Choroidal melanoma is the most common tumor of the uveal tract, characterized by rapid growth and metastasis.

Inflammatory diseases of the vascular tract of the eye develop quite often. This is due to the presence of a large number of vessels in various parts of the uveal tract. The vessels branch into capillaries, the latter repeatedly anastomose with each other and form a dense vascular network. Due to the pronounced branching of the vessels in the region of the uveal tract, the rate of blood flow is sharply reduced. The drop in blood flow tension creates conditions for settling and fixing various bacterial and toxic agents in the tissues of the uveal tract. Inflammation of all parts of the vascular tract of the eye - panuveitis - is relatively rare. Much more often there is inflammation of the anterior uveal tract - iridocyclitis, or anterior uvei t. Inflammation of the iris (iritis), isolated from the ciliary body, is rare. This is due to the common blood supply system for the iris and ciliary body. Posterior uveitis is choroiditis.

The ratio of the frequency of various forms of uveitis - anterior, posterior and panuveitis - is defined as 5:2:1, i.e. panuveitis occurs 5 times less often than anterior uveitis or iridocyclitis.

There are primary and secondary, exogenous and endogenous forms of inflammation of the uveal tract. Primary is understood as uveitis arising on the basis of general diseases of the body, and secondary - uveitis that develops with eye diseases (keratitis, scleritis, retinitis, etc.). Exogenous uveitis develops with penetrating wounds of the eyeball, after operations, perforated ulcers of the cornea; endogenous uveitis are in most cases metastatic.

According to the clinical course, uveitis is divided into acute and chronic. However, this distinction is to some extent arbitrary. Acute uveitis can become chronic or chronically recurrent. It is also necessary to distinguish between focal and diffuse uveitis, and according to the morphological picture of inflammation - granulomatous and non-granulomatous. Granulomatous include exclusively metastatic hematogenous uveitis, and non-granulomatous - uveitis caused by toxic or toxic-allergic influences (Woods). As the name suggests, granulomatous uveitis is characterized by the development of an inflammatory granuloma composed of lymphocytes, epithelioid and giant cells. In a non-granulomatous process, inflammation is diffuse hyperergic in nature. Many authors recognize the possibility of transient and mixed forms of uveitis.

Anterior uveitis, or iridocyclitis, is usually classified according to the nature of inflammation: serous, exudative, fibrinous-plastic, purulent, hemorrhagic. Posterior uveitis, or choroiditis, is usually classified according to the localization of the process: central, paracentral, equatorial, peripheral choroiditis. In addition, it is customary to distinguish between limited and disseminated choroiditis.

For practice, the classical division of uveitis into acute and chronic remains important. Acute inflammation corresponds to an exudative-infiltrative process, and chronic inflammation corresponds to an infiltrative-productive process.

Clinic of iritis and iridocyclitis

Despite the fact that the iris is relatively rarely affected in isolation from the ciliary body and, as morphological studies have shown, the process in the iris and ciliary body is always the same, in the clinic it is customary to distinguish between iritis and iridocyclitis for a number of symptoms. The iris is accessible for inspection, all clinical signs of iritis are detected early enough, while signs of cyclitis are detected later. All this rather indicates the severity of the process, rather than its separateness.

The disease begins acutely. Suddenly, without any special prodromal signs, pain occurs in the eye, radiating to the corresponding half of the head. At the same time, photophobia, lacrimation, blepharospasm appear. The pain noticeably intensifies at night, sometimes becoming intolerable. The eye turns red, vision is reduced. Involvement in the process of the ciliary body is accompanied by an increase in edema and redness of the eyelids, pain appears when touching the eyeball in the projection area of the ciliary body. Severe pain is due to the presence in the iris and ciliary body of a large number of sensitive nerve endings from the trigeminal nerve system.

Objective signs. The eyelids are edematous, hyperemic, especially the upper. Pericorneal or mixed injection is expressed on the eyeball.

The tissue of the iris swells due to pronounced edema, the openwork pattern is obscured, as exudate is deposited on the surface of the iris in its crypts. The blue and gray-blue color of the iris becomes dirty green. .The brown iris takes on a rusty hue. This is due to edema and a sharp blood supply, the appearance of exudate with the presence of blood elements. Erythrocytes are destroyed, hemoglobin undergoes stages of decay and turns into hemosiderin, which has a greenish color. All this changes the color tone of the iris.

Edema, blood supply to the vessels of the iris lead to a narrowing of the pupil. Reflex reactions that occur during inflammation increase miosis.

Due to abundant exudation, turbidity appears in the moisture of the anterior chamber. Often, pus (hypopion) settles at the bottom of the chamber in the form of a strip, with hemorrhagic iritis, blood is found - hyphema.

A frequent companion of iritis, especially fibrinous-plastic ones, are adhesions of the iris with the anterior lens capsule - posterior synechia. They are especially distinguishable when the pupil is dilated by mydriatic means.

As a result of insufficient treatment or a severe course of the process, the iris may be soldered to the lens along the entire pupillary edge - pupil fusion (seclusio pupille), and with further deposition of fibrin-rich exudate, pupil infection (occlu-sio pupille) may occur.

Infection of the pupil leads to disruption of communication between the posterior and anterior chambers. The intraocular fluid, accumulating in the posterior chamber of the eye, protrudes the iris anteriorly. This condition is called the bombed iris (iris bombee) l. In this case, the anterior chamber in the place of protrusion of the iris anteriorly is shallow, and in the center, where the pupillary part of the iris is soldered to the lens, it remains deep. Due to impaired outflow, secondary glaucoma may develop.

In severe cases, due to abundant exudation, the iris is soldered to the anterior lens capsule not only by the pupillary edge, but by almost the entire posterior surface ("planar" soldering of the iris). At the same time, signs of secondary glaucoma can also be noted, but unlike the “bombed” iris, the anterior chamber of the eye is deep enough throughout.

Involvement in the inflammatory process of the ciliary body can also be indicated by objective signs - the appearance of precipitates on the posterior surface of the cornea and opacities in the vitreous body. With inflammation of the ciliary body - cyclitis - cellular elements fall into the moisture of the anterior chamber, which stick together with fibrin and gradually settle on the posterior surface of the cornea. This is how precipitates are formed. They can be of various sizes, colors and shapes. Most often, the precipitates are located in the form of a triangle with the apex up, and in its upper part smaller precipitates are visible, and at the bottom - larger, massive, "greasy". The color of precipitates can be white, gray-white and yellow. Fresh precipitates have fairly clear boundaries.

Precipitates gradually disappear due to the processes of resorption and phagocytosis. Sometimes they persist for a long time (months \ even years), having the shape of wedge-shaped flat bodies. In rare cases, precipitates are deposited on the anterior and posterior surfaces of the lens or on the anterior membrane of the vitreous to the hyaloid-capsular ligament. Opacities in the vitreous body are of varying intensity - from a slight diffuse with serous iridocyclitis to coarse flaky, significantly reducing vision - with fibrous-plastic iridocyclitis.

In severe cases, connective tissue moorings are formed in the vitreous body, which can lead to traction detachment of the retina.

Uveopathy. Often there is a peculiar picture of diseases of the iris and ciliary body. It is similar to chronic anterior uveitis (iridocyclitis), but there are no signs typical of a uveal inflammatory process: pericorneal injection, fusion of the pupillary edge of the iris with the anterior lens capsule, iris hyperemia and pupillary constriction, no pain. At the same time, heterochromia, deposition of precipitates, opacities in the vitreous body take place. These signs indicate a change in the function of the ciliary processes, which begin to produce intraocular fluid containing protein and uniform elements.

This picture of the pathological process is called dysfunction of the ciliary body and the iris. Ciliary body dysfunction, Fuchs heterochromia, essential progressive atrophy of the iris and some other diseases are combined into a group of uveopathies. Unlike uveitis, these diseases are not inflammatory, but dystrophic (neuro-dystrophic) in nature.

choroiditis

With posterior uveitis - choroiditis - there are no complaints of pain in the eye, photophobia, lacrimation, since there is no sensory innervation in the choroid. On external examination, the affected eye is calm. Ophthalmoscopy is used to diagnose choroiditis. If the lesion in the choroid is small and is located in the peripheral parts of the fundus, then the disease can be detected only during random or preventive examinations. In the case when the posterior part of the eyeball is affected, in particular the area of the macula, the patient pays attention to a sharp decrease in central vision, flashes and flickering before the eye (photopsia), distortion of the letters and objects under consideration (metamorphopsia). These complaints indicate that the retina is involved in the process. Indeed, in the vast majority of cases, it is not choroiditis, but chorioretinitis. If photopsia and especially metamorphopsia indicate damage to the cone apparatus in the area of the macula, then with a more pronounced lesion of the peripheral parts of the choroid with involvement of the peripheral parts of the retina (rod apparatus), the patient may complain of poor twilight vision (hemeralopia).

Inflammation of the choroid can be focal (isolated) and disseminated. Inflammatory foci in the choroid of various sizes and shapes, but the most typical is a rounded shape. The size of the foci is from half to one and a half diameters of the optic nerve head. Rarely, choroidal lesions are small or very large. Fresh choroidal foci have indistinct borders, yellowish-gray color (Fig. 169, see color insert). An inflammatory focus in the choroid is a cellular infiltrate. Inflammatory infiltration, as well as exudation, spread to the retina. The latter becomes edematous, so that in some places the course of small retinal vessels is invisible. In some cases of acute choroiditis, opacities develop in the posterior vitreous near the retina. As a result, liquefaction of the vitreous body may occur. Sometimes precipitates are visible on the posterior boundary layer of the vitreous body.

With further course, the choroidal focus becomes whitish-gray, acquires clearer boundaries. The pigment epithelium of the retina penetrates into the area of the inflamed area. There is also an increase in choroid chromatophores. All this leads to the accumulation of dark brown pigment in place of the resolving infiltrate of the choroid. The normal red-brown background of the fundus is lost, connective tissue scars and sclerotic blood vessels become visible; the lumen of the latter is greatly reduced or completely closed. The more the tissue atrophies, the more the white sclera is visible.

In rare cases, in the chronic course of the process, inflammatory granulomas of a gray-green hue with a planar distribution and prominence may occur. In this case, exudative retinal detachment may develop. In such cases, there is a need for differential diagnosis with a tumor process in the choroid.

Sometimes with choroiditis, hemorrhages are observed. In the thickness of the choroid, they have a reddish-gray or purple hue, in contrast to retinal hemorrhages, which are more characteristic of a light red color.

Complications of uveitis

Correct and timely treatment of iridocyclitis ends with complete or almost complete recovery. Posterior uveitis can also end relatively well, with the exception of central choroiditis (maculitis), after which visual acuity almost always decreases to one degree or another. Often there are relapses of iridocyclitis, especially toxic-allergic, developing on the basis of collagenoses.

Both anterior and posterior uveitis are often accompanied by complications that can lead to serious consequences, including blindness.

A severe complication of anterior uveitis should be considered band-like corneal degeneration. More often it develops on the basis of chronic long-term uveitis (with Still's disease, sympathetic ophthalmia, etc.).

Opacities in the lens - complicated cataract - a common complication of both anterior and posterior uveitis. The main pathogenetic factors contributing to the development of complicated cataracts in uveitis are malnutrition of the lens, the action of toxins, and changes in the lens epithelium. Opacities usually occur first in the posterior part of the lens. Other sections of the lens gradually become cloudy, so that a complete or almost complete complicated cataract develops.

The most serious complications of anterior uveitis include secondary glaucoma.

The pathogenesis of secondary uveal glaucoma is diverse. In addition to the obvious mechanical factors (pupil infection) leading to an increase in intraocular pressure, other possible causes of secondary glaucoma can be mentioned: an increase in the production of intraocular fluid, difficulty in outflow in the anterior chamber angle due to edema of the corneoscleral trabecula, deposits of exudate and excess pigment, and later the formation of goniosynechia, etc.

With choroiditis, intraocular pressure, as a rule, does not increase. With an unfavorable course of anterior uveitis or panuveitis, in some cases, intraocular pressure decreases, which is especially detrimental to the eye. The cause of intraocular hypotension is considered to be deep dystrophic processes in the ciliary body - inhibition of the function of the ciliary epithelium and, as a result, a decrease in the production of intraocular fluid. In severe cases, hypotension is followed by subatrophy and then atrophy of the eyeball.

Very serious complications can be observed in the retina and optic nerve. More often they develop on the basis of posterior uveitis, but can also be noted with anterior uveitis. In the retina, phenomena of stagnation and exudation, small and larger hemorrhages occur. Inflammatory exudation in the retina can be so significant that a picture of exudative retinal detachment develops.

As for the optic nerve, inflammation of the disc (papillitis) and very rarely retrobulbar neuritis may occur in it on the basis of uveitis. With prolonged hypotension, congestive disc phenomena can be observed without a noticeable decrease in visual functions.

Etiology of uveitis

While the cause of the exogenous uveitis discussed above is clear, the etiology of endogenous uveitis remains unclear in many cases. The appearance of large sebaceous precipitates, several yellowish tubercles in the iris may indicate the tuberculous nature of the process.

Quite characteristic is the clinical picture of currently rare syphilitic uveitis - papular and gummous, as well as syphilitic choroiditis. Yellowish-pink papules are located along the pupillary edge of the iris, and gumma often occurs in the ciliary body and the angle of the anterior chamber, growing into the iris. With syphilitic choroiditis, numerous small dark and gray foci (“salt and pepper”) are visible on the periphery of the fundus.

In most cases, based on the clinical picture of uveitis, it is not possible to judge the etiology of the process. In the pathogenesis of uveitis, infectious, toxic and allergic processes are most likely. In many infectious diseases, both anterior and posterior uveitis may occur.

Currently, among the etiological factors, attention is paid to tuberculosis, toxoplasmosis, onchocerciasis, brucellosis, rheumatism, allergic and autoimmune processes, various autointoxications, focal infection, to a lesser extent - syphilis and other infections.

Bacteriological factors may even play a greater role in the origin of uveitis than previously thought. Viruses, rickettsiae, protozoa, fungi, nematodes, etc. can be named as possible causative agents of uveitis.

In recent years, to establish the etiology of uveitis, puncture of the anterior chamber and a serological study of the moisture of the anterior chamber have been performed. However, even these studies do not always make it possible to identify the pathogen, since it can be fixed in the tissues of the uveal tract. As a result of a thorough comprehensive examination of the patient, the etiology of endogenous uveitis can be established only in 23% of cases. There are indications of a significant role of streptococcal infection in the origin of uveitis (22%).

In the study of allergic factors in the origin of uveitis, ophthalmologists face essentially the same difficulties as in the study of infectious ones. It is often not possible to accurately establish one or another allergen. Autosensitization phenomena have been found in endogenous uveitis, and changes in the structure of organ-specific antigens of the uveal tract may be due to various infectious and autointoxication factors.

Essentially, autoimmune phenomena are responsible for the occurrence of uveitis in collagenoses. Collagenoses are known to be characterized by fibrinoid degeneration of mesenchymal tissue. In the genesis of collagenoses, dysproteinemia matters. Of the collagen diseases, the most common cause of uveitis is rheumatism and primary chronic polyarthritis, including childhood chronic polyarthritis (Still's disease). Quite often, uveitis occurs with ankylosing spondylarthrosis, which is also referred to as a group of collagenoses. In some cases, uveitis is caused by a focal infection: inflammation of the paranasal sinuses, tonsillitis, otitis media, dental disease, adnexitis, cholecystitis, etc. The possibility of a tonsillogenic nature of uveitis should be especially emphasized. In chronic tonsillitis, the spread of focal infection by the hematogenous route is noted. With a focal infection, not only the pathogens themselves, but also their toxins can act as a pathogenetic factor. Finally, relatively rarely, uveitis as one of the symptoms characterizes some syndromic inflammatory diseases of unknown etiology: Reiter's disease (oculo-urethro-synovitis), Behçet's disease (uveo-aphthous syndrome), Vogt-Koyanagi-Harada disease (uveo-cutaneo-meningoencephalitis) and some others.

Treatment of iritis and iridocyclitis

conservative therapy. The appointment of funds that expand the pupil (mydriatics) is the first and most important therapeutic measure. Treatment of anterior uveitis and iridocyclitis with mydriatics creates rest for the iris, reduces hyperemia of the iris, exudation, prevents the formation of posterior synechia and possible infection of the pupil. The main mydriatic agent is a 1% solution of atropine sulfate, which dilates the pupil, causing paresis of the muscle that constricts the pupil. Due to the pronounced plethora of the iris with iridocyclitis, it is often not possible to achieve maximum pupil dilation, so atropine is often prescribed in combination with a 2-3% cocaine solution and a 0.1% adrenaline solution. In addition, distraction therapy is shown (leeches on the temple, hot foot baths). With already existing posterior synechia, the administration of fibrinolysin and a mixture of mydriatics by electrophoresis is often effective. Thermal procedures (hot water bottle, paraffin, diathermy) are used to reduce inflammation.

Mydriatics are prescribed for anterior uveitis, regardless of the etiology of the process. The same applies to strong anti-inflammatory and antiallergic drugs - corticosteroids (instillations of 0.5% cortisone solution daily 5-6 times a day, subbulbar or subconjunctival injections of 2.5% suspension of cortisone or hydrocortisone 0.5-1 ml 2 times a day). week).

As inflammation subsides in uveitis, resolving therapy intensifies (dionin instillations in increasing concentrations - 2-9%, electrophoresis with aloe extract, lidase, thermal procedures). All of the indicated local therapy for uveitis should be carried out against the background of a general process, taking into account the etiology of the process.

Patients with uveitis of tuberculous etiology are prescribed ftivazid, tubazid and other drugs of specific action, intramuscularly streptomycin (at least 20-30 g per course). With iridocyclitis, streptomycin is best administered under the conjunctiva, with choroiditis - subbulbarno. At the same time, vitamins bi, Big and C, desensitizing agents are prescribed (inside suprastin, subcutaneously 0.25% solution of calcium chloride from 0.5 to 4 ml, for a course of up to 15-20 injections). Streptomycin and calcium chloride are useful to administer by electrophoresis.

In brucellosis, along with antibiotics and sulfa drugs, specific vaccine therapy is indicated.

Toxoplasmosis uveitis is treated with chloridine (0.025 g 2 times a day for 5 days) and sulfadimezine (0.5 g 4 times a day for 7 days). After a 10-day break, the course of treatment should be repeated 2-3 times.

Treatment of all infectious uveitis developing after influenza, tonsillitis, as well as with uveitis of unknown origin, but with a suspected infectious process, is carried out with sulfonamides and broad-spectrum antibiotics (bicillin, morphocycline intramuscularly, tetracycline antibiotics inside).

In rheumatic uveitis and uveitis due to other collagen diseases, vigorous antibiotic therapy, oral and parenteral salicylates, topical, oral and parenteral corticosteroids are also indicated.

Vitamin therapy (ascorutin, undevit inside, B vitamins parenterally), osmotherapy (in the form of intravenous infusions of 10% sodium chloride or calcium chloride solution, 40% hexamine solution, glucose, etc.) are prescribed for all types of uveitis of any origin.

With dysfunctions of the ciliary body and iris, desensitizing, resolving therapy and vitamin therapy should prevail.

Surgical treatment of uveitis. Surgical treatment is indicated for secondary glaucoma, which develops as a result of the infection of the pupil and bombardment of the iris. In these cases, iris transfixation may be recommended. Graefe's linear knife is inserted into the limbus, passed through the protruding parts of the "bombed" iris and removed from the eye through the limbus from the opposite side. After a slight "sawing" movement, the knife is removed.

Four holes can form in the iris, but, as a rule, a pronounced coloboma of the iris is obtained in one or two places. Through them, the circulation of intraocular fluid is restored, which leads to a decrease in intraocular pressure. Radial iridectomy or iridotomy may be effective.

To reduce the production of intraocular fluid in secondary uveal hypersecretory glaucoma, non-perforating operations such as diathermo-coagulation or cryoapplication of the sclera in the ciliary body zone can be performed.

Surgical treatment of the consequences of uveitis also includes operations to create an artificial pupil. For this purpose, an iridectomy is performed, and in aphakic eyes, a capsuloiridotomy. Recently, photo- or laser coagulation has been successfully used.

Neoplasms of the uveal tract

Significant difficulties may arise in the diagnosis and treatment of neoplasms of the vascular tract of the eye. It is often difficult to decide whether a neoplasm is benign or malignant. Accurate diagnosis of tumors is possible only with histological examination. Sometimes pseudotumor processes are taken for tumor growth: tuberculomas, syphilomas, retrolental and retrochoroidal hemorrhages, macular degeneration, retinoschis. In the elderly, tumors are similar to exudative arteriosclerotic changes in the fundus.

According to the literature, the percentage of uveal tract tumors found in eyes with absolute glaucoma and cataracts is quite high, especially if the glaucomatous process is unilateral.

Research methods in the diagnosis of neoplasms. A number of methods are used to diagnose neoplasms of the vascular tract of the eye. Neoplasms can be indicated by congestion in the vein system of the conjunctiva and sclera, staphylomas of the sclera, displacement of the pupil, dark tissue nodes detected when examining the anterior part of the eye.

Elements of tumor growth in the region of the root of the iris and in the angle of the anterior chamber can be noted during biomicroscopy and gonioscopy.

Most often, diaphanoscopy is used to diagnose neoplasms of the uveal tract.

Of the latest methods, it is necessary to point to radioisotope diagnostics, research using ultrasound and luminescent analysis.

For radioisotope indication, radioactive phosphorus (P32) is used. The method is based on the fact that tumor tissue retains radioactive phosphorus longer than healthy tissue. With the introduction of about 100 μCi of P32 into the patient's body (inside on an empty stomach or intravenously), a small counter measures the radiation strength. The counter is attached to the sclera, respectively, of the neoplasm and in a similar place in the healthy eye. Calculations are carried out after 1, 24, 48 and 72 hours.

The test is considered positive for benign neoplasms if the counter readings in a place suspected of a neoplasm are 30–40% higher than the control ones (for malignant tumors, this figure should be at least 60%).

Ultrasound examination using echo-ophthalmographs makes it possible to identify plus-tissue and thus make a differential diagnosis between a tumor and an essential retinal detachment. When re-examination using ultrasound devices, it is possible to judge the degree of survival of the tumor and, thereby, the rate of its growth. The most valuable is the use of ultrasound diagnostics in case of suspected neoplasm in the macular region, when diaphanoscopy and radioisotope diagnostics are difficult.

Benign neoplasms of the vascular tract. Benign tumors include neurofibromas, neurinomas, leiomyomas, and some types of melanomas. Together with benign neoplasms, cysts are usually considered, which are not actually tumors.

Neurofibromas and neurinomas are rare neoplasms, these are symptoms of widespread neurofibromatosis (Recklinghausen's disease). At the same time, light yellow or darker nodules are visible in the iris.

Leiomyoma is an even rarer neoplasm that originates from the smooth muscles of the iris or ciliary body.

Leiomyomas, as well as relatively rare benign melanomas, are usually mistaken for malignant melanoblastomas. They are diagnosed by histological examination after enucleation or removal of tumors within healthy tissues.

Uveal tract cysts can be spontaneous (due to disruption of embryogenesis processes). Incomparably more common are traumatic epithelial cysts of the iris that occur after penetrating wounds of the eye or intraocular operations. Cysts develop not only after the penetration of the epithelium into the cavity of the eye after injury or surgery, but also when it grows along the wound channel. Iris cysts are light brown or gray-brown in color, rounded in shape and transparent. With the growth of a cyst, complications such as corneal clouding, complicated cataracts, lens subluxation, and secondary glaucoma may occur. If an iris cyst is found, the operation should not be rushed. Surgical intervention is indicated only when the cyst tends to grow. Cases of reverse development of spontaneous cysts are described.

Attempts to treat cysts with conservative or sparing surgical methods (for example, puncture of the cyst with suction of its contents and injection of iodine or trichloroacetic acid) are often ineffective.

With indications for surgical treatment, one should strive to make a complete removal of the cyst, preferably with iridectomy. An incision along the limbus and isolation of the cyst should be made carefully to avoid opening its walls.

Pigmented tumors of the vascular tract. Of greatest practical importance is the study of malignant neoplasms of various parts of the uveal tract - melanomas, since they are observed most often.

Benign pigmented neoplasms - nevi - can also occur in the iris, ciliary body and choroid. In the iris, they are almost always diagnosed, as they are visible with a simple examination. Choroidal nevi are detected during random or preventive examinations of the fundus. Often, nevi become malignant and are the source of melanomas (in more than half of the cases), but sometimes they remain unchanged for many years. With a tendency to increase (infiltrative growth), iris nevi are removed within healthy tissues, and choroidal nevi are subjected to laser or xenon irradiation (see below).

Iris melanoma has the appearance of a brown or dark brown formation that rises above the level of the iris.

In this case, the pupil is often displaced towards the tumor, and with strong growth, on the contrary, it can be more or less closed by it. A hyphema may occur.

Ciliary body melanoma is recognized when it reaches a significant size and is visible outside the pupil when examined in transmitted light as a dark brown formation. Often there are melanomas of the iridociliary zone.

Choroidal melanoma can develop anywhere in the fundus. Unlike melanoma of the anterior uveal tract, it is not dark brown, but grayish brown. The tumor has the appearance of a prominating rounded formation. With melanoma of the choroid, vision can be sharply reduced if it is located in the macular or paramacular region. In most patients, diagnosis is not difficult. In doubtful cases, when an extensive retinal detachment is visible, diaphanoscopy (including “bloody”), ultrasound, and the use of radioisotopes contribute to accurate diagnosis.

In cases of late diagnosis of choroidal melanoma, secondary glaucoma may develop, and then the tumor grows into the orbit. Subsequently, patients die from metastases in the internal organs.

Significant progress has been made in the surgical treatment of uveal tract melanomas in recent years. Enucleation, which used to be the only operation, is giving way to other operations performed with the preservation of the eyeball, and often high vision. In addition, on a large number of observations, various authors have proved that enucleation cannot be considered a radical measure for the prevention of a tumor process in the body.

Recently, surgeries for the removal of tumors of the iris and iridociliary zone have become widespread. Excision of the tumor is carried out within healthy tissues using demarking diathermocoagulation. When removing tumors of the iridociliary zone, it becomes necessary to cut the sclera and expose the ciliary body (iridocyclectomy operation). Such operations are based on the fact that melanomas of the iris and ciliary body, in contrast to similar tumors of the choroid. although they have infiltrative growth, they rarely metastasize (4-8%). With melanoma of the cilcar body, enucleation should be performed in most patients, however, with such a tumor, one can raise the question of an iridocyclectomy operation with preservation of the eye, especially the only one.

Significant progress has been made in the treatment of choroidal melanomas. They are associated with the use of photocoagulators using the energy of a xenon lamp or an optical quantum generator - a laser. Photocoagulation can be performed if the degree of survival of the tumor does not exceed 2.0-4.0 D, and the diameter is 2 optic discs. Above the tumor, which is planned to be destroyed by the photocoagulator, there should not be retinal detachment or large vessels. Finally, the main condition is that the refractive media must be transparent. Photocoagulation sessions are usually repeated 5-6 times. If these conditions are not met, as well as with pronounced melanoblastomas of the choroid, enucleation is indicated.

The prognosis depends on the cell type of melanoma. Type A spindle cell melanomas with nuclear inclusions, type B without nuclear inclusions, and fascicular melanomas are recognized as the least malignant. More malignant are epithelioid and mixed tumors. The first subgroup of melanomas originates from Schwann cells, and the second - from melanoblasts of the choroidal stroma. Recently, the neurogenic nature of some tumors of the uveal tract has been suggested.

Congenital anomalies of the vascular tract of the eye are most often manifested by its colobomas. Sometimes there is a coloboma of the iris, ciliary body and choroid at the same time. The coloboma, which involves all parts of the vascular tract, corresponds embryologically to the course of the secondary palpebral fissure.

Often there is an isolated coloboma of the iris or choroid. Diagnosis of these anomalies is not difficult. The iris coloboma is located in the midline in the lower section. Rarely, atypical colobomas of the iris in the nasal side are encountered, even more rarely - in the temporal side or up.

Atypical colobomas include macular coloboma in the form of an oval defect in the vascular and retinal membranes. In recent years, pseudocoloboma of the macula on the basis of congenital toxoplasmosis has been diagnosed more often.

A typical coloboma of the choroid is localized in the lower part of the fundus. Often it reaches the nipple of the optic nerve, and sometimes captures it. The white color of the defect depends on the translucence of the sclera, since the chorioidea is completely absent in this case. In colobomas of the choroid, the retina is underdeveloped, and often absent, so many authors interpret this as a coloboma of the choroid and retina.

A serious congenital pathology of the vascular tract of the eye should include aniridia - the absence of the iris. There may be partial or almost complete aniridia. There is no need to talk about complete aniridia, since at least insignificant remnants of the iris root are detected histologically. With aniridia, there are frequent cases of congenital glaucoma with symptoms of eyeball distension (hydrophthalmos), which depend on the infection of the angle of the anterior chamber with embryonic tissue.

Aniridia is sometimes associated with anterior and posterior polar cataracts, lens subluxation, and rarely lens coloboma.

Less common is true and false polycoria, i.e., the formation of several pupils. True polycoria, when several pupils can react to light, depends on a violation of the correct development of the edges of the eyecup. False polycoria occurs when the pupil is partially and unevenly closed by remnants of the embryonic pupillary membrane.