Inflammation of the choroid. What is ocular uveitis and how to treat it? Symptoms and diagnosis

The most common cause of uveitis is infection. Inflammation develops due to the penetration of streptococci, toxoplasma, mycobacterium tuberculosis, treponema pallidum, herpes viruses, cytomegalovirus, and fungi into the choroid. Pathogenic microbes get there from foci of chronic infection in the body.

Other causes of uveitis:

• reaction to taking certain medications;
• administration of vaccines or serums;
• allergic reaction to external irritants;
• hormonal disorders (diabetes mellitus, menopause);
• eye diseases (keratitis, blepharitis, corneal ulcer);
• systemic autoimmune diseases (rheumatoid arthritis, sarcoidosis, glomerulonephritis, rheumatism, colitis, autoimmune thyroiditis, Crohn's disease, etc.).

Uveitis can occur after injuries, contusions, chemical or thermal burns, or foreign bodies entering the eye. In this case, the cause of the development of the inflammatory process is the introduction of infection from the external environment.

Classification

Uveitis can be acute, chronic and chronic recurrent. The first develops very quickly, over several days or even hours. Usually it causes a lot of suffering to the patient. Fortunately, acute uveitis is easy to diagnose and responds well to treatment. With adequate and timely treatment, the disease goes away without any consequences.

Chronic uveitis has a sluggish course with scanty symptoms. A person may suffer from the disease for many years. Such uveitis often recurs, that is, it worsens. During a relapse, the patient develops severe symptoms of the disease.

Depending on the location, there are:

• Anterior uveitis (iridocyclitis). Affects the iris and ciliary body of the eye. Iridocyclitis is characterized by pathological immobility of the pupil, changes in the color of the iris, and the appearance of precipitates on the inner surface of the cornea. All these signs can be identified by an ophthalmologist during an examination of the patient.
• Posterior uveitis (choroiditis). Characterized by inflammation of the posterior portion of the choroid. The pathological process involves the choroid, which lines the cavity of the eyeball from the inside. In this case, signs of inflammation can only be seen by ophthalmoscopy.
• Peripheral uveitis. It affects the flat part of the ciliary body and the peripheral part of the choroid along with the adjacent retina. Pathology is rare, only in 8-10%. The inflammatory process usually affects both eyes. The difficulty in diagnosing the disease lies in the fact that it is very difficult for a doctor to identify pathological foci. He cannot see them during biomicroscopy and ophthalmoscopy.

Depending on the cause and mechanism of development of uveitis, they are divided into exogenous and endogenous. The former occur under the influence of environmental factors (trauma, infections, burns). The latter are the result of chronic diseases (tuberculosis, syphilis, rheumatoid arthritis, etc.).

Symptoms

The severity of uveitis symptoms directly depends on the activity of inflammatory processes. The acute form of the disease has a clear clinical picture, which allows it to be quickly diagnosed. But chronic, indolent uveitis can be practically asymptomatic for a long time.

Signs of anterior uveitis:

• severe pain and cutting;
• feeling of a foreign body in the eye;
• intolerance to bright light;
• lacrimation;
• redness of the eye;
• decreased visual acuity;
• the appearance of a veil before the eyes;
• lack of pupil reaction to light.

Posterior uveitis, unlike anterior uveitis, does not cause pain. This is explained by the fact that the choroid is completely devoid of sensory nerve endings. Due to the lack of painful sensations, a person may not go to the hospital for a long time.

Symptoms of posterior uveitis:

• flickering flies in the field of view;
• light flashes before the eyes;
• color vision disturbance;
• distortion and decreased visual acuity.

It should be noted that chorioretinitis is rarely isolated. Usually, not only the vascular, but also the retina of the eye is involved in the inflammatory process. Consequently, the patient also develops symptoms indicating retinitis.

Which doctor treats uveitis?

An ophthalmologist is involved in the diagnosis and treatment of uveitis. If necessary, an immunologist, dermatovenerologist, phthisiatrician, allergist, infectious disease specialist or other specialist is involved in the treatment process.

Diagnostics

Pathology can be suspected by the presence of characteristic symptoms in a person. However, to confirm the diagnosis, a thorough examination by a doctor and a full examination are required. The patient may be tested not only in the ophthalmology clinic, but also referred for consultations to other specialists.

Methods for diagnosing uveitis

Method	Description	results
Visiometry	The doctor sits the patient at a distance of 5 meters from Sivtsev’s table and asks him to read its different rows in turn. Thus, it determines the visual acuity of both eyes	With uveitis, patients often experience visual impairment that cannot be corrected with plus and minus lenses
Perimetry	An ophthalmologist determines visual fields manually or using a special device	Allows you to identify defects in the visual field, indicating the presence of inflammatory foci in the fundus
Biomicroscopy	Involves examining the external structures of the eye using a slit lamp.	During the examination, a specialist can identify characteristic signs of inflammation of the iris and ciliary body
Ophthalmoscopy	A method used to examine the fundus of the eye. During the examination, the ophthalmologist uses a direct or indirect ophthalmoscope	Ophthalmoscopy is indispensable in the diagnosis of posterior uveitis. With its help, the doctor can see inflammatory foci in the fundus

If necessary, the patient undergoes optical coherence tomography, angiography, electroretinography and rheoophthalmography. To clarify the cause of uveitis, you may need an x-ray of the lungs, a Mantoux test, allergy tests, CT or MRI of the brain, tests, etc.

Treatment

Treatment of ocular uveitis is carried out in an ophthalmological hospital, where the patient is required to be hospitalized. The treatment regimen is selected individually, taking into account the cause of inflammation.

The following drugs are used to treat uveitis:

• Corticosteroids (Dexamethasone, Betamethasone, Prednisolone). Steroid hormones are used topically. They are prescribed in the form of drops, subconjunctival, parabulbar and even intravitreal injections. Medicines have a powerful anti-inflammatory effect, thereby accelerating recovery.
• Midriatics (Atropine, Tropicamide, Cyclomed). The drugs in this group have the ability to dilate the pupil. They are prescribed to prevent the formation of posterior synechiae - adhesions between the iris and the anterior lens capsule. If the pupil has already become infected, mydriatics can help you cope with the problem.
• Broad-spectrum antibiotics (fluoroquinolones, cephalosporins, macrolides). Used for uveitis caused by bacterial infection. Antibacterial agents can be administered locally (injections) or systemically, in the form of tablets or intramuscular injections.
• Immunosuppressants (Methotrexate, Cyclosporine). They are used to treat autoimmune uveitis.
• Antiviral agents (Ophthalmoferon, Zovirax, Acyclovir). Used to combat uveitis of viral etiology. Kill the infection that caused the development of inflammation.
• Antihistamines (Suprastin, Claritin, Allergodil). Needed for uveitis of an allergic nature. Medicines inhibit the release of allergy mediators, thereby helping to get rid of inflammation and unpleasant symptoms.

The patient may also be prescribed vitamins, electro- or phonophoresis with proteolytic enzymes. In severe cases of the disease and the development of complications, the patient may need surgery (removal of adhesions, vitrectomy). Fortunately, the need for surgery is extremely rare.

Prevention

There is no specific prevention of uveitis. However, the development of the disease can be avoided through timely treatment of tuberculosis, syphilis, toxoplasmosis, rheumatoid arthritis and other systemic diseases.

If signs of acute uveitis appear, you should immediately consult a doctor. With adequate treatment, the disease will go away without any consequences within 3-6 weeks. If the necessary measures are not taken in time, the inflammatory process will become chronic. Naturally, dealing with chronic uveitis is much more difficult.

Uveitis is an inflammatory lesion of the choroid of the eye. The disease may be infectious, traumatic, allergic or autoimmune in nature. To treat uveitis, mydriatics, corticosteroids, antimicrobial and antiviral drugs are used. The treatment regimen is always selected on an individual basis.

Useful video about uveitis

Anatomy of the choroid

Vascular tract (uvea) consists of three sections: the iris ( iris), ciliary or ciliary body ( corpus ciliare) and the choroid itself ( chorioidea).

Iris– the anterior, visible part of the choroid has an extensive network of sensitive innervation from n. ophthalmicus(first branch of the trigeminal nerve). The vascular network of the iris is formed by the anterior ciliary and posterior long ciliary arteries. The iris is divided into anterior (mesodermal) and posterior (ectodermal) sections. The mesodermal layer consists of the outer boundary layer, which is covered with endothelium, and the stroma of the iris. The ectodermal layer consists of muscle, internal boundary and pigment layers. There are two muscles in the iris - the dilator and the pupillary sphincter. The first is innervated by the sympathetic nerve, the second by the oculomotor nerve. The color of the iris depends on its pigment layer and the presence of pigment cells in the stroma.

The function of the iris is to regulate the amount of light entering the retina by changing the size of the pupil, that is, the function of the diaphragm. It also, together with the lens, differentiates the anterior and posterior sections of the eye, and together with the ciliary body produces intraocular fluid. Through the pupil there is an outflow of aqueous humor from the posterior chamber to the anterior chamber.

Ciliary body not available for inspection. Its soreness is examined by palpation; with gonioscopy, a small area of ​​its surface is partially visible, passing into the root of the iris. The ciliary body is a ring about 6-7 mm wide. Its anterior part has about 70 processes, it is called the ciliary crown ( corona ciliaris). The back part is flat, called the ciliary circle, the flat part ( orbіculus cilіaris or pars plana). The ligaments of Zinn are attached to the lateral surfaces of the ciliary processes, which hold the lens.

As in the iris, in the ciliary body there is a mesodermal part, which consists of 4 layers (suprachoroid, muscular layer, vascular layer, basal lamina) and an ectodermal part, which is represented by two layers of epithelium: the outer pigmented and the inner non-pigmented.

In the thickness of the ciliary body there is an accommodative muscle, which has double innervation: parasympathetic ( n. oculomotorius) and sympathetic. Sensory innervation is carried out n. ophthalmicus.

The accommodative muscle consists of three parts: meridian (Brücke's muscle), circular (Müller's muscle) and radial (Ivanov's muscle).

There are many vessels in the ciliary body - branched anterior ciliary and posterior long ciliary arteries and veins of the same name.

Function of the ciliary body: accommodation and production of intraocular fluid.

Choroid- the posterior part of the vascular tract, lining the fundus of the eye, visible through the transparent retina. Consists of 5 layers: suprachoroidal, layer of large vessels, layer of medium vessels, choriocapillaris layer, basal lamina (vitreous membrane of Bruch). The choriocapillary layer is closely connected with the retinal pigment epithelium, therefore, in diseases of the choroid, the retina is involved in the process.

The blood supply to the choroid is carried out by the posterior short ciliary arteries, the outflow of blood occurs through the vorticose veins, which pass through the sclera at the equator. Has no sensory innervation. Function: retinal trophism.

Thus, the iris and ciliary body have a common blood supply and innervation, and therefore are usually affected simultaneously. The peculiarities of the blood supply to the choroid determine the isolation of its lesions. However, all three sections of the choroid are anatomically closely connected; there are anastomoses between the systems of the anterior and posterior ciliary vessels, so the pathological process can involve the entire uveal tract.

Diseases of the choroid

The following types of pathological conditions of the choroid are distinguished:

1) developmental anomalies;

2) inflammatory diseases (uveitis);

3) dystrophic diseases (uveopathy);

4) neoplasms.

Developmental anomalies

Albinism complete absence of pigment in the skin, hair, eyebrows, eyelashes. The iris is very light, visible through red light, sometimes the sclera is visible through. The fundus is light, the choroidal vessels are visible. Low vision, photophobia, and nystagmus are noted.

Treatment: correction of refractive errors, pleoptics.

Aniridia absence of iris. Complaints of low vision, photophobia.

Treatment: contact lenses, surgery - iridoprosthetics.

Polycoria the presence of several pupils. Complaints of low vision, monocular diplopia.

Correctopia change in pupil position .

Treatment: contact lenses, surgery - closed iridoplasty.

Coloboma of the iris defect of the iris, always located below, the pupillary border and sphincter of the pupil are preserved.

Treatment: surgery - closed iridoplasty, contact lenses.

Coloboma of the choroid localized in the lower part of the fundus of the eye, in this area the retina is underdeveloped or absent.

Treatments No.

Residual pupillary membrane in the area of ​​the pupil there are white opaque threads that start not from the edge of the pupil, but from the projection of the small arterial circle of the iris.

Treatment: removed only when vision decreases.

Inflammatory diseases of the vascular tract (uveitis)

There are anterior uveitis (iritis, cyclitis, iridocyclitis), posterior uveitis (choroiditis) and panuveitis, depending on which part of the vascular tract is affected.

Iridocyclitis. The inflammatory process in the anterior part of the vascular tract can begin from the iris (iritis) or from the ciliary body (cyclitis). But due to the common blood supply and innervation of these parts, the disease quickly moves from the iris to the ciliary body or vice versa, and iridocyclitis develops. There are acute and chronic forms of the disease. The patient complains of photophobia, lacrimation, eye pain and decreased vision.

Clinical signs:

- pericorneal or mixed injection;

- pain on palpation of the eye (ciliary pain) and decreased accommodation;

- swelling and hyperemia of the iris, heterochromia;

 the pupil is constricted, poorly responsive to light;

- posterior synechiae - fusion of the iris with the anterior surface of the lens;

- vitreous opacification;

- presence of precipitates on the corneal endothelium.

In severe cases, purulent exudate may appear in the anterior chamber of the eye (hypopyon) or blood (hyphema). After using mydriatics, the pupillary margin may acquire jagged contours as a result of the presence of posterior synechiae. If mydriatics are not used, a circular synechia may form, and then a film that can completely close the lumen of the pupil.

Complications. If posterior synechiae form along the entire pupillary edge of the iris, aqueous humor, which is secreted by the ciliary body, cannot enter the anterior chamber from the posterior chamber, and bombardment (protrusion into the anterior chamber) of the iris occurs. The root of the iris also moves forward, adhesions arise between the anterior surface of the iris and the posterior surface of the cornea (anterior synechiae), which block the angle of the anterior chamber, where the drainage zone of the eye is located. All this leads to increased intraocular pressure and the development of secondary glaucoma). In addition to secondary glaucoma, complications of anterior uveitis can be: band-shaped corneal degeneration, complicated uveal cataract, hypotony, eye subatrophy).

Differential diagnosis carried out with an acute attack of angle-closure glaucoma, acute conjunctivitis (Table 3).

Table 3. Differential diagnosis of acute iridocyclitis with an acute attack of glaucoma and acute conjunctivitis

Signs	Acute attack of glaucoma	Acute iridocyclitis	Acute conjunctivitis
Clinical course, complaints	Sudden onset, severe pain in the eye with irradiation to the temporal region, jaw; headache, nausea, vomiting	Gradual onset, constant aching pain in the eye, photophobia	Gradual onset, foreign body sensation under the eyelids
Visual acuity	Significantly reduced		Normal
Intraocular pressure		Normal or slightly reduced	Normal
Vascular injection	Stagnant	Pericorneal or mixed	Conjunctival
Cornea		Precipitates	Not changed
Anterior chamber of the eye		Normal depth	Normal depth
Reaction to light, pupil size	Absent, wide pupil	Decreased, pupil narrow	Saved, normal
	Sometimes swollen	The pattern is smoothed, swelling	Not changed

Choroiditis (posterior uveitis) - inflammation of the choroid itself, which is usually combined with inflammation of the retina and is called chorioretinitis.

Due to the lack of sensitive innervation, there are no complaints of pain in the eye, photophobia, or lacrimation in choroiditis that are characteristic of anterior uveitis. When examined, the eye is calm. Depending on the localization of the process, patient complaints vary. With central localization, closer to the posterior pole, patients complain of a significant decrease in visual acuity, flashes and blinking in front of the eye (photopsia), as well as metamorphopsia (curvature of objects and lines). These complaints indicate that the retina is involved in the process. Diagnosis is carried out using the ophthalmoscopy method. In the case of peripheral forms of inflammation, depending on the size of the lesions, patients may complain of photopsia and impaired twilight vision (hemeralopia), and in the presence of small and single lesions there are no functional subjective sensations. Inflammation can be focal (isolated) or disseminated. Fresh choroidal lesions are a yellowish-gray cellular infiltrate with unclear boundaries. The retina above the infiltrate is edematous, so the course of the vessels is not ophthalmoscopically visible in some places.

Opacification develops in the posterior parts of the vitreous, and sometimes precipitates are visible on the posterior limiting membrane of the vitreous.

As the inflammatory process subsides, the lesion acquires a whitish-gray color with clear boundaries. In the focal area, the stroma of the choroid atrophies, and a dark brown pigment appears at the site of infiltration. In the chronic course of the process, gray-green granulomas with prominence can sometimes form, which can be the cause of exudative retinal detachment. In this case, it is necessary to carry out a differential diagnosis with a choroidal neoplasm.

Etiology and pathogenesis of uveitis. The mechanisms of development of uveitis are predetermined by the action of infectious, toxic, allergic and autoimmune factors. Most often these are endogenous factors: infection from other foci of inflammation in the body, as well as in systemic diseases: collagenosis, especially juvenile rheumatoid arthritis, ankylosing spondylitis, Reiter's disease; tuberculosis, secondary syphilis, sarcoidosis, Behçet's disease (hypopyon-iridocyclitis, aphthous stomatitis, damage to the mucous membrane of the external genital organs), brucellosis, toxoplasmosis, herpes, etc. Exogenous factors also play a significant role in the etiology of iridocyclitis: the consequences of penetrating eye injuries, chemical burns, perforation of corneal ulcers, etc.

Treatment. In order to identify and sanitize possible foci of infection and other etiological factors, it is necessary to conduct a complete examination of the body. Cycloplegics and mydriatics are used for anterior uveitis to reduce pain and prevent the formation of posterior synechiae. Antibiotics, sulfa drugs, corticosteroids are prescribed locally, parabulbarly, intramuscularly, non-steroidal anti-inflammatory drugs, desensitizing drugs, immunomodulators. If an etiological factor is established, appropriate specific therapy is prescribed. Physiotherapeutic methods of treatment (magnetic therapy, laser irradiation, electrophoresis) must be used.

The choroid of the eye has a complex structure and consists of three sections: the iris, the ciliary (ciliary) body and the choroid itself (choroid). Each of these sections, as already indicated in the lecture on the anatomy of the eye and its age-related characteristics, has its own unique structure and functions. The most important thing in the anatomy of the iris is the presence in it of a muscle that constricts the pupil and a muscle that dilates it, the first is innervated by the oculomotor parasympathetic nerve, and the second by the sympathetic nerve. Sensory nerve endings are “representatives” of the trigeminal nerve; Due to the anterior ciliary vessels, anastomosing with the posterior long ciliary vessels of the ciliary body, its blood supply is carried out. The function of the iris is to regulate the amount of light entering the eye thanks to the “automatic” diaphragm of the pupil depending on the level of illumination. The more light, the narrower the pupil, and vice versa. The iris is involved in ultrafiltration and outflow of aqueous fluid, in thermoregulation, in maintaining ophthalmotonus and in the act of accommodation.

The ciliary body is like a gland of intraocular secretion and is involved in the outflow of aqueous humor. It provides the act of accommodation due to the weaving of fibers of the ligament of zinn into it, and is involved in the regulation of ophthalmotonus and thermoregulation. All these functions are due to the complexity of its glandular and muscular structure. It is innervated by parasympathetic, sympathetic, and sensory nerve endings, and vascularization is provided by the posterior long cylindrical vessels, which have return arteries (anastomoses) both to the iris, as already noted, and to the choroid. Each of the 70 processes of the glandular section of the ciliary body has its own nerve branches and its own vessels.

Thanks to the activity of the ciliary body, continuous nutrition of the avascular structures of the eye (cornea, lens, vitreous) is ensured.

Particular attention should be paid to the fact that the choroid is richly vascularized due to the many branches of the posterior short arteries located in its choriocapillaris layer, which is adjacent to the pigment layer on the outside and the retina on the inside. The choroid is involved in the nutrition of the retinal neuroepithelium, in the outflow of intraocular fluid, in thermoregulation, in the regulation of ophthalmotonus, in the act of accommodation. The choroidal vessels anastomose with the posterior long ciliary vessels of the ciliary body. Thus, all three sections of the choroid have a vascular relationship, and the iris and ciliary body also have innervation. The choroid is very poorly innervated and essentially has only sympathetic nerve endings.

The rich sensory innervation of the iris and ciliary body causes their severe pain during inflammation and damage.

Inflammation of the choroid of the eye

Inflammation of the choroid accounts for about 5% of cases among all eye pathologies. Inflammation of the choroid of the eye can occur in the form of keratoiritis, which was discussed in relation to keratitis.

Iritis, iridocyclitis (these are anterior uveitis), posterior cyclitis (hypercyclitic crises), cyclochoroiditis, choroiditis, chorioretinitis, chorioneuroretinitis (these are posterior uveitis) can occur independently (isolated) or in combination.

In addition, in some cases, inflammation can be total in nature - these are panuveitis.

There are also so-called peripheral uveitis, although they can be classified as posterior cyclitis or cyclochoroiditis.

Uveitis

Before presenting information about some features of the clinical picture of various uveitis, it is appropriate to point out that uveitis in children, regardless of their nature, has a certain uniqueness. Thus, they often have an inconspicuous onset, a subacute course, the symptoms are mildly expressed, the corneal syndrome is weak, the pain is slight, the precipitates are polymorphic, the exudate is often serous, the posterior synechiae are relatively weak and thin, the lens and vitreous body are often involved in the process (opacities), reactive papillitis weakly expressed, frequent relapses, short remissions, no complaints of decreased vision, although it is reduced, the process is often bilateral. However, all parts of the choroid are often involved in the inflammatory process.

As for the clinical picture of uveitis in adults, the disease is more severe than in children, and there are many complaints of significant discomfort in the eye(s).

Types of uveitis

By its nature, uveitis, regardless of its location, can be congenital and acquired, exogenous and endogenous, toxic-allergic and metastatic, granulomatous and non-granulomatous, generalized and local, long-term and abortive, single and recurrent, acute, subacute and chronic, with concomitant general pathology and without it, with reverse development and with complications.

According to the nature of exudation (transudation), uveitis can be serous, fibrinous, purulent, hemorrhagic, plastic and mixed.

To make the correct clinical diagnosis of uveitis, you should begin examining the patient with a brief, focused history of the disease. Then it is necessary to sequentially check visual functions, examine each eye visually and with the help of instruments, examine other organs and systems (by palpation, auscultation, using thermography, tonometry, etc.).

Next, a set of targeted clinical and laboratory studies (x-ray, bacteriological, serological, immunological, virological, etc.) is prescribed. The main attention should be paid to identifying as many symptoms of the disease as possible, keeping in mind that the start of treatment is always symptomatic.

Anterior uveitis

What are the possible symptoms of anterior uveitis (iritis, iridocyclitis)? The first sign of inflammation of the choroid, which may attract attention, is a small and sometimes pronounced corneal syndrome, i.e. photophobia, lacrimation, blepharospasm, redness of the eye with a purple tint (pericorneal injection).

By immediately checking the patient’s vision, you can make sure that it is somewhat reduced and does not improve with the use of weak positive or negative glasses. During an eye examination with lateral illumination or biomicroscopy, one can detect “fogging” (dullness) of the corneal endothelium, as well as precipitates varying in number, size, shape, tone (color), and exudate in the aqueous humor of the anterior chamber, varying in type and quantity ( serous, purulent, etc.).

The iris can be discolored, full-blooded (edematous, hyperemic) with newly formed vessels, lumpy (granulomas).

The pupil may be constricted and its reaction to light may be slow. During the “play” of the pupil during lighting and darkening, and later during its expansion with mydriatics, posterior synechiae (adhesions of the pupillary edge of the iris with the anterior lens capsule) and exudate deposits on the lens can be detected.

Finally, light palpation of the eyeball reveals its soreness. In addition, there may be a general depressed, restless, uncomfortable state of the patient.

All these symptoms indicate inflammation of the choroid. But to determine whether it is anterior uveitis or more widespread, ophthalmoscopy is performed. If the vitreous body is transparent and there are no changes in the fundus, then the diagnosis of anterior uveitis is beyond doubt.

Diagnosis of posterior uveitis

It should immediately be noted that the diagnosis of isolated posterior uveitis, in contrast to the diagnosis of anterior uveitis, can be difficult based on external signs and suspicion of the presence of posterior uveitis arises from such indirect symptoms as impaired visual function in the form of decreased visual acuity, defects in the visual field (microscotomas, photopsia and etc.). In this case, the anterior segment, as a rule, is not changed.

Signs of inflammation of the posterior part of the choroid are detected only ophthalmoscopically and biomicrocycloscopically, when inflammatory foci are detected, varying in type, size, number and location. Having assessed the variety of these foci, i.e., the picture of the fundus, we can assume the possible etiology and activity (severity) of the inflammatory process in the choroid.

The cardinal signs of panuveitis include all of the listed possible symptoms characteristic of anterior and posterior uveitis; diagnosis of panuveitis is relatively easy. With this disease, as a rule, changes are observed in all parts of the choroid, as well as in the lens, vitreous body, retina and optic nerve. Dysregulation of ophthalmotonus (hypotension, hypertension) is also often observed.

Rheumatic uveitis

The most common rheumatic uveitis is characterized by the fact that it occurs against the background of an acute course (attack) of rheumatism.

Rheumatic uveitis is manifested by severe corneal syndrome and pain in the eye area. Mixed injection of the eye is expressed. On the endothelium of the cornea there are multiple gray small precipitates, in the moisture of the anterior chamber there is abundant gelatinous exudate, the iris is full-blooded, its vessels are dilated, multiple thin pigmented posterior synechiae rupture relatively easily after instillation of mydriatics (scopolamine, but not atropine). The lens and vitreous body are practically intact. In the fundus, more or less pronounced vasculitis is detected in the form of grayish “couplings” on the vessels.

All changes undergo reverse development with effective treatment and stabilization of rheumatism, the process recurs against the background of the next attack of the disease.

Treatment of this type of uveitis is local, symptomatic.

Tuberculous uveitis

Tuberculous uveitis occurs more often against the background of active intrathoracic (pulmonary) or mesenteric, sometimes bone tuberculosis, and often against the background of a chronic course of the disease or remission.

The process in the choroid can first of all be suspected by decreased vision and corneal syndrome. Inflammation most often occurs in one eye. Hyperemia of the eye in the form of a mixed injection is slightly expressed, corneal syndrome is hardly noticeable. Very characteristic of tuberculous uveitis are “greasy” large precipitates on the endothelium of the cornea.

In addition, there are pathognomonic grayish-pinkish nodules (granulomas-tuberculomas) surrounded by vessels (similar to infiltrates in tuberculous keratitis) in the iris and “guns” (snowflake-like deposits) on the pupillary edge of the iris. The synechiae in this process are wide, powerful, planar, and difficult to tear under the influence of mydriatics. A yellowish exudate is often found in the anterior chamber of the eye. New vessels form in the iris.

Exudate can often be deposited on the anterior capsule of the lens, sprout with newly formed vessels and connective tissue degenerate (organize). Exudation can spread into the posterior chamber of the eye and into the vitreous body, and as a result, opacities of the posterior capsule of the lens and vitreous body (golden shower) occur. Posterior sequential cataract disrupts the nutrition of the lens, and its inner layers gradually become cloudy.

In the fundus of the eye, tuberculous foci of various sizes can be found in different parts, without distinct contours, yellowish in color, extending from the choroid into the retina. These lesions do not merge and pigment is deposited on their periphery, and in the center they acquire a grayish tint. Naturally, the retina is also involved in the process, as a result of which visual functions (visual acuity, changes in the visual field, as well as color vision) suffer to varying degrees (depending on the location and size of the lesions). This picture of tuberculous uveitis indicates that it is developing according to the type of panuveitis, but there are often cases when it is characterized by signs of anterior uveitis (iridocyclitis) or posterior uveitis (choroiditis).

Syphilitic uveitis

Syphilitic uveitis can occur with congenital and acquired syphilis. With congenital syphilis, inflammation of the choroid, as well as the cornea, may appear in utero, which is detected in a newborn child.

Uveitis in acquired syphilis is characterized by moderate corneal syndrome, mixed injection, serous exudate in the anterior chamber of the eye and multiple polymorphic small precipitates.

In the altered iris, yellowish-reddish nodules-papules are revealed, to which newly formed vessels approach. The posterior synechiae are massive, wide, rupture after instillation of mydriatics, and in their place, pigmented polymorphic lumps remain on the anterior capsule of the lens. Small punctate floating brownish opacities are possible in the vitreous body. Possible post-inflammatory changes in the fundus, reminiscent of “scattered salt and pepper.” This picture is characteristic only of syphilis. Changes in the anterior and posterior parts of the eye with syphilitic uveitis can be observed both in combination and in isolation. In cases where uveitis occurs in the form of choroiditis, its diagnosis in childhood is difficult, since the process is not accompanied by changes in the anterior part of the eye. Choroiditis is manifested only by disturbances in the visual field (discomfort), and children, as is known, do not pay attention to this and do not make any complaints. Inflammation of the posterior part of the eye is discovered either accidentally, for example, due to eye injuries, or in connection with other manifestations of syphilis. As a rule, this pathology is bilateral.

Collagenous uveitis

Collagenous uveitis most often occurs against the background of nonspecific, so-called rheumatoid polyarthritis, which appears and uncontrollably progresses mainly in children of preschool and school age. However, there are not isolated cases when uveitis appears long before the development of polyarthritis.

The eyes are affected by collagenosis in approximately 15% of cases. The eye disease begins gradually and, as a rule, on one eye, and then after various times on the other eye. Uveitis occurs predominantly in the form of iridocyclitis, i.e. anterior uveitis. It is characteristic that most often, although not always, the eye during a normal visual examination is calm and there is no suspicion of an inflammatory process in it. This is especially dangerous in cases where there are no signs of polyarthritis that could “give a signal” for an eye examination. Meanwhile, inflammation progresses almost “asymptomatically”, and its initial stage is missed.

Early signs of uveitis can only be detected in cases where the disease has already been detected (albeit late) in one eye, while the other eye was still healthy. One of the first signs of collagenous uveitis is a gentle hyperemia of the iris and a slower reaction of the pupils to light. A more thorough biomicroscopic examination reveals gray precipitates of various sizes on the posterior surface of the cornea, mainly in its lower segment. After instillation of mydriatics, the pupil dilates slowly and insufficiently, but its shape is round, i.e. there are no posterior synechiae at this time. After weeks or months, the iris becomes pale, grayish, with clearly visible vessels and alternating distinct lacunae and crypts, which indicates dystrophic changes in the structures of the iris.

The continuation of the inflammation process is evidenced by the appearance of posterior synechiae, which, when the pupil dilates, appear massive (wide) planar, almost unbreakable after installations of strong mydriatics (scopolamine + dimexide + cocaine) and subsequent applications or subconjunctival injections of a 0.1% adrenaline solution. In this case, the pupil takes on an irregular star-shaped shape. Gradually, synechiae completely “block” the connection between the anterior chamber and the posterior chamber. The pupillary edge and iris tissue are completely fused with the anterior capsule of the lens.

The inflammatory process in the eye proceeds according to the proliferative type; as a result of exudation, formed cellular elements are deposited in the pupillary zone, they are degenerated connectively, grow into newly formed vessels of the iris and, thus, not only the fusion of the iris with the anterior capsule of the lens occurs, but also complete fusion of the pupil with the connective tissue cloth. As a result of this, the anterior chamber first becomes uneven, and then, due to the lack of outflow of intraocular fluid from the posterior chamber into the anterior iris, it becomes funnel-shaped. In this case, the angle of the anterior chamber closes to a significant extent, and as a result of deterioration in the outflow of intraocular fluid, hypertension can occur, and then secondary glaucoma, which occurs in some protracted untreated cases.

As is clear from the picture drawn, collagenous anterior uveitis is characterized by great originality and severity of the course.

But, as studies show, the matter is not limited only to damage to the anterior and middle parts of the choroid. Simultaneously or some time after the onset of uveitis symptoms, polymorphic small inclusions such as calcifications are found in the conjunctiva of the eyeball. Next, biomicroscopically, crescent-shaped grayish-whitish opacities are revealed in the superficial layers at the border of the limbus and cornea in the 3 and 9 o’clock zones. Gradually, these opacities spread over the surface of the cornea in the area of ​​the open palpebral fissure in the form of a ribbon with “coves of clearing.”

Thus, with collagenous uveitis, the inflammatory-dystrophic proliferative process is localized not only in the anterior part of the choroid, but also spreads to the lens, cornea and conjunctiva. This picture of eye changes is usually called the ocular triad of Still's disease - a combination of uveitis, sequential cataracts, and band-shaped corneal dystrophy. As a rule, in both the initial and advanced stages of collagenous uveitis, no pronounced pathology occurs in the choroid and other parts of the fundus.

Uveitis in other diseases

Uveitis can and practically (in 10-15% of cases) occurs in almost all bacterial, viral, adenoviral and many systemic diseases. Therefore, in essence, in case of any general infectious and systemic disease, there should be a rigorous and urgent vision test, followed by a careful examination of the eyeball and its auxiliary apparatus.

So, for example, the eyes of a patient with influenza, chickenpox, herpes, Behcet's disease (ophthalmostomatogenital syndrome), cytomegaly, Reiter's disease (urethro-oculosynovial syndrome), Besnier-Beck-Schaumann disease (sarcoidosis), cannot fail to be examined. for toxoplasmosis and many other diseases and syndromes. With all these diseases there can be keratitis and, more dangerously, uveitis, since both keratitis and uveitis almost always result in a decrease in visual function.

Hypercyclical crisis

Particularly, in just a few words, it is necessary to say about the so-called hypercyclical crises. Hypercyclic crises usually occur in young and middle-aged women. These conditions appear unexpectedly during the daytime and manifest themselves in the form of sharp pain in one eye, nausea, vomiting, headache, and even fainting. The pulse increases significantly, blood pressure rises, and palpitations appear. The eye is almost calm at this time, but there is a short-term decrease in visual functions. On palpation the eye is painful and hard (T+2). The attack lasts from several hours to 1-2 days and, as it appeared, suddenly disappears without any residual effects.

However, other local manifestations of this pathology are also possible. Thus, against the background of a general serious condition, a predominantly stagnant injection may appear in the eye, the cornea swells, large gray precipitates are deposited on the endothelium of the cornea, the iris swells sharply, but the pupil does not dilate (as in glaucoma), vision drops sharply. This picture of a crisis resembles an acute attack of primary glaucoma. The hypercyclic crisis continues for hours (days).

Similar attacks may be repeated. The etiology of this process has not yet been established.

Treatment during an attack is symptomatic and consists of taking antispasmodics and analgesics. Intravenous infusion of 5-10 ml of a 0.25% solution of novocaine in isotonic sodium chloride solution works well (administer very slowly). Local anesthetics (novocaine, trimecaine, pyromecaine), corticosteroids, dibazole, glucose, taufon, amidopyrine, adrenaline are prescribed hourly in usual pharmacological dosages.

Treatment of uveitis

Due to the fact that the symptoms of uveitis, different in both etiology and course, have many similarities, their treatment, especially until the etiology is clarified and specific drugs are prescribed, should be, as has already been repeatedly indicated, symptomatic in nature.

Treatment of uveitis should include the use of the following medications:

1. anesthetics (novocaine, pyromecaine, trimecaine, dimexide, etc.);
2. antihistamines (diphenhydramine, suprastin, pipolfen, tavegil, diazolin, etc.), calcium preparations;
3. nonspecific anti-inflammatory drugs (amidopyrine and other salicylates, corticosteroids, etc.);
4. vascular strengtheners (rutin, ascorbic acid, etc.);
5. antimicrobial agents (antibiotics, sulfonamides, etc.);
6. antiviral drugs (keretsid, florenal, banafton, poludanum, etc.);
7. neurotropic drugs (dibazol, taufon, B vitamins, etc.);
8. absorbable drugs (potassium iodide, ethylmorphine hydrochloride, lekozim, etc.);
9. cycloplegics (scopolamine, homatropine hydrobromide, mezaton, etc.);
10. specific drugs.

In addition, physioreflexotherapy, laser treatment, and surgical methods are used. Drug treatment of uveitis should be hourly (except for mydriatics, ethylmorphine hydrochloride, etc.).

All patients suspected of having uveitis or diagnosed with uveitis are subject to treatment in the appropriate hospital departments (dispensaries) and specialized sanatoriums.

Persons who have had uveitis are subject to clinical care for at least 2 years after undergoing a treated local or general process.

2-02-2015, 00:38

Description

Inflammation of the choroid- uveitis is one of the common causes of low vision and blindness (25%). The share of endogenous uveitis is 5-12% of cases of eye pathology in children and 5-7% among hospital patients.

Uveitis in children have a variety of clinical manifestations and a multiplicity of options, which makes diagnosis difficult, especially in the initial stage and with atypical development.

The frequency of uveitis is explained by the multitude of vessels that branch into capillaries and repeatedly anastomose with each other in the choroid, which sharply slows down the blood flow and creates conditions for the sedimentation and fixation of bacterial, viral and toxic agents

Separate blood supply to the anterior (iris and ciliary body) and posterior (choroid itself or choroid) sections, as well as anastomoses between all sections of the choroid lead to the occurrence of anterior uveitis (iritis, iridocyclitis) and posterior uveitis (choroiditis), inflammation of the entire choroid ( panuveitis).

Cycloscopy allows you to identify inflammation of the flat part of the ciliary body (posterior cyclitis) and the extreme periphery of the choroid itself (peripheral uveitis). With uveitis, the retina and optic nerve are involved in the process, and neurochorioretinitis occurs.

Poor disease outcomes and insufficient effectiveness of therapy are associated with the etiological and pathogenetic features of uveitis. These are a genetic predisposition to immune disorders, acute and chronic infections with disruption of protective mechanisms, chemical and physical effects leading to the formation of foreign antigens, impaired immunity, neurohormonal regulation and permeability of the blood-ophthalmic barrier.

In patients with uveitis, the body is depleted of protective factors, there is a pronounced accumulation of inducers of the inflammatory reaction, the activity of biogenic amines increases, and the autoimmune process is pronounced, associated with the accumulation of antigens not so much in the vascular membrane as in the retina; there is a significant activation of lipid peroxidation processes. Violation of the physiological insulation of eye tissues and increased permeability of the blood-ophthalmic barrier contribute to the transition of uveitis to a recurrent form.

Uveitis is divided into serous, fibrous (plastic), purulent, hemorrhagic, mixed

The course of uveitis can be acute, subacute, chronic and recurrent. The process can be endogenous and exogenous. Endogenous uveitis can be either metastatic (when the pathogen enters the vascular bed) or toxic-allergic (when the body and eye tissues are sensitized). Exogenous uveitis occurs with penetrating wounds of the eyeball, after surgery, corneal ulcers and other corneal diseases.

Over the past 20 years, the incidence of endogenous uveitis has increased 5 times. Uveitis occurs most often in schoolchildren (68%). Viral uveitis predominates (25%), streptococcal and staphylococcal, toxic-allergic, associated with chronic foci of infection (25%).

The number of uveitis of tuberculous etiology (24%) and bacterial-viral (27%) has increased. There has been a tendency towards a decrease in the frequency of rheumatoid uveitis from 24% in the 70s to 9% in recent years, which is associated with early diagnosis of this disease and timely complex therapy.
At an early age, viral and bacterial-viral uveitis predominate.

The leading form of uveitis is iridocyclitis (up to 58%); peripheral uveitis is detected in 21-47% of patients.
The etiological diagnosis of childhood uveitis is difficult; the detected causative agents often turn out to be only resolving, provoking ones. In order to detect the disease in the early stages and begin treatment in a timely manner, the ophthalmologist must examine the eyes and check visual acuity for any disease of the child.

Diagnosis of uveitis is based on anamnesis, clinical picture, taking into account the general condition of the body, and the results of clinical and laboratory studies.

Scheme of examination of patients with uveitis

1. History of life and illness.
2. Examination of the visual organ: visual acuity without correction and with correction, peri- and campimetry, color vision, anterior and posterior biomicroscopy, gonioscopy, reverse and direct ophthalmoscopy, tonometry, cycloscopy.
3. Additional research methods: X-ray examination of the chest organs, paranasal sinuses, consultation of specialists (therapist, otolaryngologist, phthisiatrician, neurologist, dentist, etc.); ECG.
4. Clinical and laboratory tests: general blood test: content of protein fractions, determination of C-reactive protein. DFA, blood culture for sterility; general urine analysis; urine and blood sugar test; stool analysis for worm eggs.
5. Immunological studies: - study of the reaction of humoral immunity - Wasserman reaction or microreaction to syphilis with cardiolipin antigen, Wright-Huddleson reaction for suspected brucellosis: complement fixation reaction; passive hemagglutination: neutralization, fluorescent antibodies, etc.; Wanye microprecipitation with a set of antigens (strepto- and staphylococcus, tuberculin, tissue antigens), Boyden's reaction with the antigen of the choroid, lens, retina, etc.;
   - cellular immune response:
   A) reaction of blast transformation of peripheral blood lymphocytes, inhibition of microphage migration, leukocytolysis, etc. with strepto- and staphylococcus antigens, tuberculin, toxoplasmin, antigens of herpes simplex virus, cytomegalovirus, tissue antigens;

   b) study of the content of immunoglobulins in blood serum;
   V) intradermal tests with various antigens, taking into account the focal reaction of the eye in the form of exacerbation of the inflammatory process or its subsidence;
   G) study of antibodies to DNA.

6. Isolation of viruses and detection of viral antigens in eye tissues using the fluorescent antibody method.
7. Biochemical research methods: blood and urine testing for acid glycosaminoglycans, urine testing for hydroxyproline, the content of 17-hydroxycorticosteroids, biogenic amines (serotonin, adrenaline) in the blood.

A reliable method of etiological diagnosis remains the focal reaction of the eye to the intradermal injection of tuberculin, toxoplasmin, bacterial allergens (streptococcal, E. coli, Proteus, Neisseria allergens), etc.

Anterior uveitis(iritis, iridocyclitis, cyclitis) are accompanied by pericorneal injection associated with dilatation of the scleral vessels; changes in the color and pattern of the iris due to vasodilation, inflammatory edema and exudation, constriction of the pupil and its sluggish reaction to light due to swelling of the iris and reflex contraction of the sphincter of the pupil; irregular shape of the pupil, since exudation from the vessels of the iris onto the anterior surface of the lens leads to the formation of adhesions (posterior synechiae).

Posterior synechiae can be separate or form fusions of the entire pupillary edge of the iris with the lens. When exudate forms in the pupil area, a fusion occurs. Circular synechia and prelenticular membrane lead to separation of the anterior and posterior chambers of the eye, thereby causing an increase in intraocular pressure. Due to the accumulation of fluid in the posterior chamber, the iris bulges into the anterior chamber (iris bombardment).

The moisture of the anterior chamber becomes cloudy due to serous, fibrinous, hemorrhagic, purulent, mixed exudation. In the anterior chamber, the exudate settles in the lower sections in the form of a horizontal level. Purulent exudate in the anterior chamber is called hypopyon, hemorrhage in the anterior chamber is called hyphema.

Various-sized, polymorphic precipitates are detected on the posterior surface of the cornea. Precipitates consist of lymphocytes, plasma cells, macrophages, pigment particles and other elements that indicate increased vascular permeability of the ciliary body.
A common sign of cyclitis is a decrease in intraocular pressure.

There may be complaints of pain in the eye and pain on palpation of the eyeball. Changes in the composition of the intraocular fluid lead to disruption of the nutrition of the lens and the development of cataracts. Severe and prolonged cyclitis disrupts the transparency of the vitreous body due to exudation and mooring. All these changes cause visual discomfort and decreased vision.

In young children, the pain syndrome is usually mild or completely absent and there are no complaints about decreased vision. There may be no corneal syndrome. pericorneal injection.

Peripheral uveitis(posterior cyclitis, basal uvearetinitis, parsplanitis) are characterized by inflammatory changes in the extreme periphery of the fundus. The predominantly flat part of the ciliary body is affected, but its ciliary part, peripheral parts of the choroid, and retinal vessels may also be involved in the process.
The disease is often bilateral (up to 80%), affecting young people and children; Children aged 2-7 years are most often affected.

In pathogenesis, the main place is given to immune factors, the role of herpetic infection is discussed.
There are various types of nonspecific uveitis. The process in children is more difficult than in adults.
In acute uveitis, exudative foci appear on the extreme periphery of the fundus, more often in the lower outer parts or concentrically around the entire circumference.

In severe cases of the disease, exudate becomes visible behind the lens. Often, exudate appears in the area of ​​the anterior chamber angle, forming trabecular precipitates and goniosynechia.
Due to the spread of exudate through the vitreous canals to the posterior parts of the eye, destruction and increased permeability of the prepapillary and premacular membranes occur, which causes pronounced reactive edema in the peripapillary and macutary zones (possibly as an autoimmune reaction).

The progression of inflammation may be accompanied by exudative retinal detachment in the periphery
In the stage of reverse development, opacities of the vitreous body of varying severity and extent are formed, causing a sharp decrease in vision.

At the extreme periphery of the retina, atrophic chorioretinal lesions, semi-empty retinal vessels, retinoschisis of varying degrees, and dystrophic changes in the macular area can be identified

One of the complications is the development of complicated cataracts, which form starting from the posterior pole of the lens.

Gyniosynechia and the organization of exudate in the trabecutaneous zone can lead to secondary glaucoma. However, hypotension is more common in peripheral uveitis in children.

The phenomena of eye irritation and changes in the anterior segment are extremely scarce, there may be no decrease in vision in the acute phase of the disease, therefore, peripheral uveitis is often detected late, with the progression and dissemination of the process or in the stage of reverse development.

To avoid diagnostic errors, peripheral uveitis should be suspected in case of various vitreous opacities of unknown origin, macular edema or dystrophic changes in the macula, or posterior cortical cataracts.

To specifically identify peripheral uveitis, the extreme periphery of the fundus is examined using indirect (mono- and binocular) ophthalmoscopy with scleral indentation using three-mirror lenses. For changes in the macular area and retinal vessels, fluorescein angiography is indicated.

Posterior uveitis(choroiditis) often have a sluggish, areactive, inconspicuous course and do not cause complaints in children, especially young ones. With posterior uveitis, single or multiple foci of various shapes and contours, sizes and colors may be visible with symptoms of perifocal inflammation (edema) in the choroid.

Often, in accordance with these focal changes, the retina (retinitis) and often the optic disc (papillitis) are also involved in the inflammatory process. In the adjacent layers of the vitreous body, opacification is detected.

Choroiditis always affects the state of the visual field, since, according to focal processes, loss of vision occurs (micro- and macroscotomas). If inflammatory foci are located in the center of the pelvic floor, then visual acuity decreases down to light perception, central absolute and relative scotomas appear, and color perception changes.

Older children and adults may complain of distorted images of objects and changes in their size (metamorphopsia). flashes of light, flickering (photopsia), sometimes a sharp deterioration of vision at dusk (night blindness, hemeralopia). Complaints are caused by changes in the receptor elements of the retina due to disruption of their location due to exudation in the area of ​​inflammation and loss of intimate contact of the choroid with the outer layers of the retina.

Hemeratopia occurs with extensive lesions of the periphery of the choroid and retina of both eyes, for example, with diffuse chorioretinitis.

There is no pain in the eye with choroiditis. The anterior segment of the eye is not changed, the eyes are calm, the ophthalmotonus is not disturbed.
In non-granulomatous (toxic-allergic) uveitis, choroidal infiltration is diffuse. The optic nerve is often involved in the process, which is manifested by hyperemia, blurring of its boundaries, and functional disorders. Foci of exudation are sometimes large, their boundaries are blurred.

Perivasculitis and retinitis are observed, accompanied by exudative effusion, while the retinal vessels are covered with exudate, like a cover. As a result of the process, as a rule, extensive light atrophic foci of the choroid with pigment deposition are formed. Old lesions look white, since the sclera is visible through the transparent retina and the atrophied choroid

The lesions are flat, with more or less brown pigment migrating from the surrounding areas of the choroid.

Panuveitis- damage to all three parts of the choroid. Its symptoms are characteristic of inflammation of each part of the choroid. G).

Basic principles of general and local etiotropic and symptomatic treatment of uveitis. Treatment of patients with endogenous uveitis, regardless of their etiology, is aimed at eliminating signs of inflammation, maintaining or restoring visual functions and, if possible, preventing relapses of the disease.
With endogenous uveitis, the timing of clinical and true recovery does not coincide

The pathogenesis of uveitis is based on a variety of factors, therefore, in the treatment of this complex disease, it is necessary to take into account the etiology and immune status, activity and stage of the process. The impact is aimed at the main components of inflammation - increasing the permeability of the vascular walls of the blood-ophthalmic barrier, exudation into the eye tissue with subsequent destruction and excessive fibrosis against the background of a violation of the general immunobiological state.

After a diagnosis of uveitis is made, as a rule, anesthetics, mydriatic agents, antibiotics, and non-steroidal anti-inflammatory drugs are first prescribed. Local use of steroid drugs is more effective in acute uveitis.

The use of short-acting medications (antibiotics, sulfonamides, corticosteroids, vitamins, enzymes, anesthetics, salicylates, etc.) in an acute process should be frequent in the form of forced installations (each drop is instilled into the conjunctival cavity after 3-5 minutes for an hour 3 times per day with a 1-2 hour break between hour courses; course 3-5 days).

General treatment includes sanitation of foci of infection, the use of antibiotics, nonspecific anti-inflammatory, antiviral, antituberculosis, antitoxoplasmosis, desensitizing therapy and vitamin therapy.

General corticosteroid therapy should be long-term, taking into account the hormonal background of the body (the presence of free and protein-bound hydrocortisone and corticosterone in the blood serum), while keeping in mind its inability to prevent the chronic and recurrent course of uveitis.

It is important to know and prevent serious complications of treatment with corticosteroid drugs (Cushing's syndrome, developmental delay in children, osteoporosis, cortisone psychoses, adrenal insufficiency).

When the body's defenses decrease with a decrease in the content of gamma globulins and immunoglobulins in the blood serum, in some cases it is necessary to use immunostimulants (thymalin, T-activin, poludan, delargin), vaccination, introduction into the body of immunocompetent cells, hyperimmune globulin, levamisole, prodishosan (according to 50-75 mcg intramuscularly 2 times a week; 7-10 injections per course).

To inhibit the biosynthesis of prostaglandins, indomethacin is used, as well as acetylsalicylic acid in age-related doses.

In order to reduce the permeability of vascular walls and restore the vascular endothelium, dicinone is prescribed in age-specific doses in repeated courses of 1.5 months once a quarter, as well as stugeron and prodectin.

When prescribing dicinone, one takes into account its angioprotective effect, which is associated not only with the effect on the endothelium of capillaries and the ground substance of interendothelial spaces, but also with pronounced antioxidant activity (600 times higher than that of ascorbic acid) and an inhibitory effect on the activity of the blood kinin system. This drug, which improves microcirculation and gives a hemostatic effect, is used for severe exudation and hemorrhages. retinovasculitis.

Among the antihistamines prescribed to patients with uveitis, the first place is occupied by phenothiazine derivatives, since they also have high antioxidant activity (150 times higher than that of ascorbic acid), pipolfen, diprazine, etc.

Prescribing glucocorticosteroids(glucocortisone, dexazone and dexamethasone, metypred, medrol, etc.), take into account their antioxidant effect, ability to reduce the production of antibodies, and delay the breakdown of acid glycosaminoglycans. These drugs have a pronounced anti-inflammatory effect, reduce capillary permeability and reduce autoimmune reactions.

Along with these drugs, to improve microcirculation, normalize metabolism in the vascular wall, in the tissue of the choroid, in the retina, to reduce tissue hypoxia, relieve edema, normalize permeability both in acute uveitis and in remission, to prevent relapses, angioprotectors are used doxium, anginin, prodectin, parmedin (taking into account their ability to reduce the activity of bradicycline). For capillary protective action, vitamin P, ascorbic acid, and non-steroidal anti-inflammatory drugs are widely used.

Nonsteroidal anti-inflammatory drugs occupy a leading place in the treatment of uveitis, as they affect different parts of the pathogenesis of the inflammatory process.

Salicylates. pyrazolone derivatives (butadione, reopirin), ortofen, voltaren have pronounced antihyaluronidase, antiprostaglandin, antioxidant, antikinin activity and many other qualities that help inhibit the activity of inflammatory mediators. The drugs are used as part of local and general therapy for uveitis.

At the height of inflammation in the choroid of the eye, the kinin system is activated. The effect of proteolysis inhibitors is especially pronounced in the initial stages of the inflammatory process, therefore it is advisable to block the formation and launch of functional biochemical systems involved in the development of uveitis with the kallikrein-trypsin inhibitor gordox.

The drug inactivates a number of enzymes (plasmin, kallidinogenase, etc.) and prevents the release of kinins, preventing excessive release of fibrin from the bloodstream, which remains one of the many links in the pathophysiological mechanism of inflammation.

Gordox is used by phonophoresis (25,000 KU per 100 ml of isotonic sodium chloride solution; 10-15 procedures per course), in the form of forced installations of Gordox solution into the conjunctival cavity for an hour 2-3 times a day. Patients with severe exudation, retinovasculitis, acute uveitis and a tendency to fibrinous exudate are administered 0.5 ml (5000 KU) of gordox in alternation with dexazone and dicinone.

To improve metabolism in eye tissues, carbogen is used as an antihypoxant in complex therapy. Inhalation of oxygen with small concentrations of carbon dioxide leads to improved microcirculation in the retina and choroid in the affected area and improved tissue metabolism.

When the acute inflammatory phenomena of uveitis subside in the early stages, in order to prevent complications, neurotrophic therapy is started, which is especially necessary for retinal edema, papillitis, and the development of dystrophic foci in the fundus. To improve the trophism of the eye, a 4% solution of taufon is used intramuscularly and in eye drops, sermion, cerebrolysin, semax, cytochrome C, trental, cavinton, stugeron, vitamins, etc.

It is preferable to use local medications, the choice of which depends on the location of the inflammation and the age of the child. Electro-, phono-, magnetophoresis, endonasal electrophoresis, parabulbar injections, administration of drugs through the irrigation system retrobulbar and into Tenon's space (5-6 times a day for 7-15 days) are widely used, which provides a long-term high concentration of the drug and leads to good results.

Proteolytic enzymes (trypsin, chymotrypsin, fibrinolysin, lekozyme, streptodecase, collalizin, etc.) are used to resolve exudate, hemorrhages, synechiae, and molars. It is important not only the fibrinolytic effect of the enzyme, but also improving tissue permeability and inhibiting the development of young connective tissue

Lidase is widely used, the effect of which is associated with a decrease in the viscosity of hyaluronic acid, an increase in tissue permeability and facilitating the movement of fluid in the interstitial spaces.

Enzyme therapy is carried out using electro-, phonophoresis, drop installation, injections under the conjunctiva and parabulbar against the background of general and local therapy with angioprotective drugs

For newly formed vessels in the vascular tract and retina, photo- and laser coagulation is used, as well as cryocoagulation of the zones of newly formed vessels. Vitreotomy is used for opacities and moorings in the vitreous body.

Patients with uveitis in remission are examined by an ophthalmologist at least once a quarter. In spring and autumn, it is advisable to carry out anti-relapse courses of treatment with antiprostaglandin drugs (3 weeks) and angioprotectors Prodectin or Stuteron. dicinone (1.5 months). This tactic makes it possible to reduce the frequency of disease relapses to 6% and has a positive effect in more than a third of patients.

Uveitis is a group of eye diseases associated with inflammation in the choroid of the eye (another name is the uveal tract).

The choroid or uvea is represented by three components: the iris (in Latin iris), the ciliary body or ciliary body (in Latin corpus ciliare) and the choroid proper (in Latin chorioidea).

Depending on the location of inflammation, the following forms of uveitis are distinguished: cyclitis, iritis, iridocyclitis, chorioretinitis, choroiditis, etc. The main danger of this group of diseases is possible consequences in the form of blindness or low vision.

The occurrence of this disease is facilitated by the fact that the vascular network of the eye is very widespread, and blood flow in the uveal tract is slow, which can lead to the retention of microorganisms in the choroid.

Under certain conditions, these microorganisms can lead to inflammation. The occurrence and development of inflammation is also influenced by other features of the choroid, in particular, different blood supply and innervation of its different structures:

• the anterior section (iris and ciliary body) is supplied with blood through the anterior ciliary and posterior long arteries, and is innervated by the ciliary fibers of the first branch of the trigeminal nerve;
• the posterior section (choroid) is supplied with blood by the posterior short ciliary arteries and is characterized by the absence of sensory innervation.

These features determine separate lesions of the anterior and posterior parts of the uveal tract. Either one department or the other may suffer.

Types of disease

1. According to the anatomical principle, uveitis is divided into anterior, intermediate (or median, peripheral), posterior and generalized forms.

• Anterior uveitis: iritis, anterior cyclitis, iridocyclitis. Inflammation occurs in the iris and vitreous body. This localization of inflammation is more common than all others.
• Median uveitis: posterior cyclitis, pars planitis. The ciliary body, retina, choroid and vitreous body are affected.
• Posterior uveitis: choroiditis, chorioretinitis, retinitis, neurouveitis. The choroid, retina and optic nerve are affected.
• Generalized uveitis – panuveitis. This type of disease develops if all parts of the choroid are affected.

Uveitis is characterized by a different nature of the inflammatory process, and therefore the following forms are distinguished:

• serous,
• purulent,
• fibrinous-plastic,
• hemorrhagic,
• mixed uveitis.

Based on the causes of occurrence, uveitis is divided into endogenous (the infection is located and spreads inside the body) and exogenous (the infection is introduced from the outside as a result of injuries, burns, operations). There are also primary (when the disease is not preceded by another eye disease) and secondary uveitis (occurs as a complication after other eye diseases, for example, scleritis or corneal ulcers).

Based on morphological features, granulomatous (focal metastatic inflammation) and non-granulomatous uveitis (diffuse infectious-allergic inflammation) are distinguished.

Depending on the course of the disease, there are acute (lasting no more than three months), chronic (do not go away for a long time, lasting more than three months) and recurrent uveitis (after recovery, inflammation occurs again).

Causes of the disease

Uveitis can occur due to infections, allergic reactions, metabolic disorders, hypothermia, decreased immunity, injuries, and general diseases of the body.

The most common (almost half of the cases) are infectious uveitis. The infection can be caused by mycobacterium tuberculosis, toxoplasma, streptococci, treponema, herpes virus, and fungi. Infection in the choroid can come from any source due to viral diseases, tuberculosis, syphilis, dental caries, tonsillitis, etc.

Allergic uveitis occurs against the background of food and drug allergies.

Uveitis can occur in the presence of the following diseases of the body: rheumatoid arthritis, rheumatism, psoriasis, ulcerative colitis, multiple sclerosis, glomerulonephritis, etc.

Uveitis of a traumatic nature may occur due to eye burns, penetrating injuries to the eye, or the entry of a foreign body into it.

Uveitis may develop against the background of hormonal dysfunction and metabolic disorders (menopause, diabetes, etc.), blood diseases, diseases of the organs of vision (scleritis, blepharitis, keratitis, conjunctivitis, retinal detachment, etc.).

Symptoms of the disease

The symptoms of each form of uveitis are different.

Anterior uveitis is characterized by the following symptoms:

• photophobia,
• decreased visual acuity,
• chronic lacrimation,
• constriction of the pupil,
• soreness,

In the chronic course of anterior uveitis, symptoms occur rarely or are mild: only slight redness and floating spots before the eyes.

Peripheral uveitis occurs with the following symptoms:

• often both eyes are affected symmetrically,
• deterioration of visual acuity.

Posterior uveitis is characterized by late onset of symptoms. They are characterized by:

• blurred vision,
• distortion of objects,
• floating spots before the eyes,
• decreased visual acuity.

Diagnosis of the disease

Timely diagnosis of uveitis is very important, because If left untreated, dangerous eye pathologies can develop, which can lead to complete blindness.

An ophthalmological examination for suspected uveitis may include:

• normal external examination
• visual acuity test,
• determination of fields of view,
• tonometry (a method of measuring intraocular pressure),
• study of pupillary reaction,
• biomicroscopy (examination using a special slit lamp),
• gonioscopy (to study the angle of the anterior chamber of the eye),
• ophthalmoscopy (examination of the fundus of the eye),
• Ultrasound of the eye,
• angiography of retinal vessels,
• tomography of various structures of the eye (including the structure of the optic nerve head),
• rheoophthalmography (measurement of blood flow velocity in the eye vessels).

If the causes of uveitis are other diseases of the body, it is necessary to simultaneously carry out laboratory and functional diagnostics and treatment of these diseases.

Treatment of the disease

The ophthalmologist prescribes treatment for uveitis depending on the type and cause of the disease. Therapy in this case is aimed at preventing complications that can lead to vision loss.

To treat uveitis use:

• mydriatics (atropine, cyclopentol, etc.) eliminate spasm of the ciliary muscle, prevent the appearance of or break existing adhesions.
• use of steroids locally (ointments, injections) and systemically. For this purpose betamethasone, dexamethasone, prednisolone are used. If steroids do not help, immunosuppressive drugs are prescribed.
• eye drops to reduce high intraocular pressure,
• antihistamines for allergies,
• antiviral and antimicrobial agents in the presence of infections.

With timely treatment, mild forms of uveitis disappear within 3-6 weeks.

In severe cases, with significant destruction of the vitreous body, surgical treatment of uveitis is required. In case of iridocyclochoroiditis (or panuveitis), vitreectomy (surgical removal of the vitreous body) can be performed, and if the eye cannot be saved, evisceration of the eyeball is performed (all internal structures of the eyeball are removed).

Treatment of the disease with traditional methods

When treating uveitis, you can use some traditional medicine methods, after discussing the possibility of such treatment with your doctor:

• A decoction of chamomile, rose hips, calendula or sage helps with uveitis. To prepare it, you need 3 tablespoons of herbs and a glass of boiling water. The mixture should infuse for about an hour. Then you should strain it and rinse your eyes with this decoction.
• Aloe can also help. You can use aloe juice for eye drops, diluting it in cold boiling water in a ratio of 1 to 10. You can make an infusion from dry aloe leaves.
• You can use crushed marshmallow root. To do this, you need to pour 3-4 tablespoons of marshmallow root into a glass of water at room temperature. You need to infuse it for 8 hours and then use it for lotions.

Disease prevention

To prevent diseases, you should maintain eye hygiene, avoid hypothermia, eye injuries, overwork, and the development of allergies, and promptly treat various diseases of the body. If any eye disease occurs, treatment should be started immediately so as not to provoke the emergence of more serious diseases.