The vascular tract of the eye consists of. Vascular tract, its three sections, functions
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 along its entire length. It consists of branching vessels of various calibers, forming tissue whose structure resembles cavernous tissue.
Anterior part of the vascular tract is Iris. It is visible through the transparent cornea, painted in one color or another, which indicates the color of the eyes (gray, blue, brown). In the center of the iris there is a 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 by the sympathetic nerve, penetrating from the plexus caroticus.
Ciliary body inaccessible to inspection with the naked eye, unlike the iris. Only with gonioscopy, at the apex 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. In a 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 includes smooth ciliary or accommodative muscle. The inside of 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 limiting membrane to which the fibers of the ligament of zinn 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, and 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, motor and trophic nerves are better developed than sensory nerves, 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 itself or choroid extends from the dentate line to the optic nerve foramen. In these places it is tightly connected to the sclera, and throughout the rest of its length it is adjacent to the sclera, separated from it by the suprachoroidal space where ciliary vessels and nerves pass. Microscopically, several layers are distinguished in the choroid: suprachoroid, layer of large vessels, layer of medium vessels, choriocapillary layer with an unusual width of the lumen of the capillaries and narrow intercapillary lumens.
The choriocapillaris 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 that are rarely found in newborns include aniridia, coloboma of the iris, ciliary body and choroid proper, polycoria, corectopia, “freckles”, aplasia, albinism.AniridiaThis is the absence of the iris. In this case, behind the cornea there is a picture of a maximally dilated pupil, i.e. blackness. Already with side lighting, the contours of the lens and ciliary band are visible. Sometimes a rim is visible - a remnant (rudiment) of the iris root and ciliary processes. The most clear picture of aniridia is given by biomicroscopy and examination in transmitted light, while a red reflex from the fundus of the eye is determined according to the diameter of the cornea. Coloboma of the iris, ciliary body and choroid - the absence of part of the department.Coloboma– the general name for some types of congenital, less commonly acquired, defects of eye tissue (the edge of the eyelid, iris, choroid itself, retina, optic disc, lens). A congenital or acquired defect of the eye, leading to various anomalies: from the appearance of a slight depression of the edge of the eyelid or the lower part of the iris, resulting in a pupil resembling a pear, to defects of the fundus. An enlarged pupil causes symptoms of blindness in a person. Coloboma of the eyelid 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 completely round, and the reaction to light is sluggish. Naturally, with this condition of the iris there is pronounced visual discomfort and decreased visual acuity.
Corectopia Characterized by an eccentric location of the pupil. If there is a shift to the nasal, i.e., optical, zone, then a sharp decrease in visual acuity is possible and, as a consequence, 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, usually fixed to the iris and 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 choroiditis, iridocyclochoroiditis, panuveitis, generalized uveitis. The infection occurs through exogenous or endogenous routes.
Iritis- 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 lining the outside of the retina).
Iridocyclitis- acute inflammation of the iris and ciliary body, or anterior uveitis.
Tumors of the vascular tract- benign formations include neurofibromas, neurinomas, leiomyomas, nevi, and cysts. You can notice changes in the eye if they are localized in the anterior segment. They manifest themselves to one degree or another in changes in the structure and color of the iris. Nevi and cysts look most obvious
Melanoma- a malignant pigmented tumor that can occur in the iris, ciliary body, or choroid. Choroidal melanoma is the most common tumor of the uveal tract, characterized by rapid growth and metastasis.
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Description
Inflammatory diseases of the vascular tract account for 7 to 30% of all eye diseases. There are 0.3-0.5 cases of the disease per 1000 population. In 10% of cases of particularly severe uveitis, blindness develops in both eyes and approximately 30% of patients experience visual impairment.
About 40% of cases of uveitis occur against the background of a systemic disease. In anterior uveitis associated with the presence of HLA-B27 Ag in the blood, men predominate (2.5:1).
The social significance of uveitis is also due to the fact that diseases of the vascular tract most often occur in people of young, working age and can lead to a sharp decrease in visual acuity and blindness.
Changes in intrauterine eye pathology in children are especially severe. As a rule, they sharply reduce vision and make it impossible to study in general schools. Similar outcomes have been established in 75-80% of such children.
Features of the anatomy of the vascular tract
The structure of each of the three sections of the vascular tract - the iris, ciliary body and choroid - has its own characteristics, which determines their function under normal and pathological conditions. Common to all sections are abundant vascularization and the presence of pigment (melanin).
The anterior and posterior sections of the choroid have separate blood supply. The blood supply to the iris and ciliary body (anterior section) comes from the posterior long and anterior ciliary arteries; choroid (posterior) - from the posterior short ciliary arteries. All this creates conditions for isolated damage to parts of the vascular tract.
The selectivity of damage to the choroid is associated with circulatory conditions (anatomical structure of the uveal tract). Thus, blood enters the vascular tract through a few thin stems of the anterior and posterior ciliary arteries, which break up into a vascular network with a significantly larger total lumen of blood vessels. This leads to a sharp slowdown in blood flow. Intraocular pressure also prevents rapid evacuation of blood.
For these reasons, the vascular tract serves as a kind of “settlement pool” for pathogens and their waste products. These can be live or killed bacteria, viruses, fungi, helminths, protozoa and products of their breakdown and metabolism. They can also become allergens.
The third feature is the different innervation. The iris and ciliary body are innervated from the first branch of the trigeminal nerve, and there is no sensory innervation in the choroid.
Classification of uveitis
Uveitis can be divided according to etiology, localization, process activity and course. Be sure to evaluate the localization of the process.
Anterior uveitis includes iritis - inflammation of the iris and cyclitis - inflammation of the ciliary body, which mainly occur together as iridocyclitis.
Posterior uveitis includes inflammation of the choroid itself - choroiditis. Inflammation of all parts of the vascular tract is called panuveitis.
According to the etiology, uveitis is divided into endogenous and exogenous, according to the clinical course - into acute and chronic, according to the morphological picture - into granulomatous (metastatic hematogenous, focal) and non-granulomatous (toxic-allergic, diffuse).
Anterior uveitis is divided according to the nature of inflammation into serous, exudative, fibrinous-plastic and hemorrhagic. Posterior uveitis, or choroiditis, is classified according to the localization of the process into central, paracentral, equatorial and peripheral uveitis or parsplanitis. The process of uveitis is divided into limited and disseminated.
Pathogenesis of uveitis
When introducing infectious agents or exposure to other damaging factors, the reactions of specific cellular and humoral immunity are of great importance. The immune response to foreign substances is expressed in the rapid action of nonspecific factors, interferon and an inflammatory reaction.
In the immune body, specific reactions of antigens with antibodies and sensitized lymphocytes play an active role. They are aimed at localizing and neutralizing the antigen, as well as at its destruction, involving the lymphoid cells of the eye in the process. The choroid, according to scientists involved in these problems, is a target for immune reactions, a kind of lymph node in the eye, and recurrent uveitis can be considered a kind of lymphadenitis. A large concentration of mast cells in the choroid and their release of immune factors contribute to the entry into the depot and the exit of T lymphocytes from this depot. The cause of relapse may be an antigen circulating in the blood. Important factors in the development of chronic uveitis are disruption of the blood-ophthalmic barrier that retains antigens. These are the vascular endothelium, pigment epithelium, and ciliary body epithelium.
In some cases, the emerging disease is associated with cross-reacting antigens of the vascular endothelium with antigens of the uveal tract, retina, optic nerve, lens capsule, conjunctiva, renal glomeruli, synovial tissue and joint tendons. This explains the occurrence of syndromic eye lesions in diseases of the joints, kidneys, etc.
In addition, a number of microorganisms are neurotropic (Toxoplasma and many viruses of the herpetic group). The inflammatory processes they cause occur in the form of retinitis with subsequent damage to the choroid.
Clinic of iridocyclitis
The clinical picture of iridocyclitis is manifested primarily by sharp pain in the eye and the corresponding half of the head, worsening at night. The appearance of pain is associated with irritation of the ciliary nerves. Increased ciliary pain at night can be explained by an increase in the tone of the parasympathetic division of the autonomic nervous system at night and the switching off of external stimuli, which fixes the patient’s attention on pain. The pain reaction is most pronounced in iridocyclitis of herpetic etiology and in secondary glaucoma. Pain in the ciliary body area increases sharply when palpating the eye through the eyelids.
Irritation of the ciliary nerves by reflex causes the appearance of photophobia (blepharospasm and lacrimation). Maybe visual impairment, although at the beginning of the disease vision may be normal.
With developed iridocyclitis iris color changes. Thus, the blue and gray irises acquire greenish tints, and the brown iris looks rusty due to an increase in the permeability of the dilated vessels of the iris and the entry of red blood cells into the tissue, which are destroyed; hemoglobin at one of the stages of decay turns into hemosiderin, which has a greenish color. This, as well as infiltration of the iris, explains two other symptoms - blurred pattern irises and miosis- constriction of the pupil.
In addition, with iridocyclitis there appears pericorneal injection, which often becomes mixed due to the active reaction of the entire system of anterior ciliary arteries. In acute cases, petechial hemorrhages may be observed.
The pain reaction to light intensifies at the moment of accommodation and convergence. To determine this symptom, the patient must look into the distance, and then quickly at the tip of his nose; this causes sharp pain. In unclear cases, this factor, in addition to other signs, contributes to the differential diagnosis with conjunctivitis.
Almost always with iridocyclitis, precipitates, settling on the posterior surface of the cornea in the lower half in the form of a triangle with the apex upward. They are lumps of exudate containing lymphocytes, plasma cells, and macrophages. At the beginning of the process, the precipitates are grayish-white, then become pigmented and lose their round shape.
The formation of precipitates is explained by the fact that blood elements, due to increased vascular permeability, enter the posterior chamber, and due to the very slow flow of fluid from it into the anterior chamber and from the pupil to the posterior surface of the cornea, blood cells manage to stick together with fibrin into conglomerates, which settle on the endothelium cornea due to a violation of its integrity. Precipitates come in different sizes (small pinpoints and large fatty or greasy ones) and different saturations (light or dark gray, pigmented).
Precipitates on the corneal endothelium (Ehrlich-Türk line)
Frequent signs of iridocyclitis are clouding of the moisture of the anterior chamber - Tyndall's symptom of varying severity (depending on the number of cells in the field of view in the anterior chamber), as well as the appearance of hypopyon, which is sterile pus. The formation of hypopyon is caused by the penetration of blood cells (lymphocytes, macrophages, etc.), protein, and sometimes pigment into the anterior chamber. The type of exudate (serous, fibrinous, purulent, hemorrhagic) and its amount depend on the severity and etiology of the process. With hemorrhagic iridocyclitis, blood may appear in the anterior chamber - hyphemas.
The next important symptom of iridocyclitis is the formation posterior synechiae- adhesions of the iris and anterior lens capsule. The swollen, inactive iris is in close contact with the anterior surface of the lens capsule, so a small amount of exudate, especially fibrinous, is sufficient for fusion.
If the pupil is completely closed (circular synechia), the outflow of moisture from the posterior chamber to the anterior chamber is blocked. Intraocular fluid, accumulating in the posterior chamber, protrudes the iris anteriorly. This condition is called bombed iris. The depth of the anterior chamber becomes uneven (the chamber is deep in the center and shallow along the periphery), due to a violation of the outflow of intraocular fluid, the development of secondary glaucoma is possible.
When measuring intraocular pressure, normo- or hypotension is determined (in the absence of secondary glaucoma). A reactive increase in intraocular pressure is possible.
The last constant symptom of iridocyclitis is the appearance exudate in the vitreous, causing diffuse or flocculent floaters.
Thus, the general signs of all iridocyclitis include the appearance of sharp ciliary pain in the eye, pericorneal injection, change in the color of the iris, blurring of its pattern, constriction of the pupil, hypopyon, formation of posterior synechiae, precipitates, exudate in the vitreous body.
Differential diagnosis
Acute iridocyclitis should be differentiated primarily from an acute attack of angle-closure glaucoma and acute conjunctivitis. The main parameters of differential diagnosis are given in table. 2.
Table. Differential diagnosis of iridocyclitis
The angle of the anterior chamber gradually becomes obliterated, secondary glaucoma, complicated cataracts, vitreal vitreous cords, and tractional retinal detachment develop.
For etiological diagnosis in the case of rheumatoid arthritis, it is important to detect general systemic disorders through careful questioning of the patient. Morning stiffness, hyperemia, and joint inflammation are detected.
Laboratory diagnostics include determination of rheumatoid factor, beta lipoproteins, complement titer, determination of urinary excretion of glycosaminoglycans and hydroxyproline as the main component found during the breakdown of collagen.
Tuberculous uveitis
A common cause of uveitis is tuberculosis.
The diseases are accompanied by chronic proliferation without strong inflammatory phenomena (tuberculomas form in the iris and ciliary body). The diseases have signs of an allergic reaction and are accompanied by active inflammation with pronounced exudation.
When determining the tuberculous genesis of uveitis, it is necessary to take into account:
Contact with a patient with tuberculosis;
Previous tuberculosis disease of other organs (lungs, glands, skin, joints);
Data from X-ray and tomographic studies of the lungs and other organs;
Detection of antibodies to tuberculin in the blood serum of patients;
Increased cutaneous and intradermal tuberculin reactions during exacerbation of the ocular process;
Focal reactions to intradermal injection and electrophoresis of tuberculin, results of express diagnostics;
Decrease in antibody titers of lymphocyte sensitization during treatment.
Toxoplasmosis uveitis
Focal chorioretinitis occurs, usually bilateral; more often central, sometimes - peridiscal localization. The disease recurs.
When taking a medical history, it is important to look for exposure to animals, consumption of raw meat, or improper handling of raw meat.
In addition to the above causes of uveitis, it is necessary to note viral lesions of the vascular tract, syphilis, gonorrhea, leprosy, brucellosis, listeriosis, diabetes, AIDS, etc.
Treatment of uveitis
Treatment goals: suppression of infectious etiological factor; blocking or regulating local and systemic autoimmune reactions; replenishment of local (in the eye) and general deficiency of glucocorticosteroids.
To achieve these goals, conservative therapy is used with the mandatory use of glucocorticosteroids and extracorporeal methods (hemosorption, plasmapheresis, quantum autohemotherapy).
General principles of pharmacotherapy for uveitis:
Anti-inflammatory therapy;
The most effective drugs are glucocorticosteroids. For the treatment of anterior uveitis, GCS are used mainly locally or in the form of subconjunctival injections; in the treatment of posterior uveitis, parabulbar injections are used. In severe processes, GCS is used systemically;
GCS is instilled into the conjunctival sac 4-6 times a day, and ointment is applied at night. The most commonly used solution is 0.1% dexamethasone [INN] (Maxidex eye drops and ointment);
Subconjunctivally or parabulbarly, 0.3-0.5 ml of a solution containing 4 mg/ml dexamethasone [INN] (Dexamethasone injection solution) is injected. In addition, prolonged forms of GCS are used: triamcinolone [INN] is administered once every 7-14 days (injection solution 10 mg/ml Kenalog), a complex of disodium phosphate and betamethasone dipropionate [INN] is administered once every 15-30 days ( diprospan injection solution);
In especially severe cases, systemic therapy with GCS is prescribed. For systemic therapy, the daily dose of the drug should be administered between 6 and 8 a.m. before breakfast.
There are continuous therapy of GCS- prednisolone orally 1 mg/kg/day in the morning (on average 40-60 mg), the dose is gradually reduced every 5-7 days by 2.5-5 mg (prednisolone tablets 1 and 5 mg) or IM prolonged forms GCS (kenalog) 80 mg (if necessary, the dose can be increased to 100-120 mg) 2 times with an interval of 5-10 days, then 40 mg is administered 2 times with an interval of 5-10 days, the maintenance dose is 40 mg with at intervals of 12-14 days for 2 months.
When carrying out intermittent therapy, GCS is administered in a 48-hour dose simultaneously, every other day (alternating therapy) or the drug is used for 3-4 days, then a break is taken for 3-4 days (intermittent therapy). A type of intermittent therapy is pulse therapy: intravenous drip methylprednisolone is administered at a dose of 250-500 mg 3 times a week every other day, then the dose is reduced to 125-250 mg, which is administered first 3 times a week, then 2 times a week;
For moderately severe inflammatory processes, NSAIDs are used topically in the form of installations 3-4 times a day - 0.1% solution of diclofenac sodium [INN] (naklof eye drops). Local use of NSAIDs is combined with their use orally or parenterally - indomethacin [INN] orally 50 mg 3 times a day after meals or rectally 50-100 mg 2 times a day. At the beginning of therapy, to more quickly relieve the inflammatory process, use 60 mg intramuscularly 1-2 times a day for 7-10 days, then proceed to using the drug orally or rectally;
If anti-inflammatory therapy is ineffective in a severe process, immunosuppressive therapy is carried out:
Cyclosporine [INN] (tablets of 25, 50 and 100 mg sandimmuneoral) orally 5 mg/kg/day for 6 weeks, if ineffective the dose is increased to 7 mg/kg/day, the drug is used for another 4 weeks. When stopping the inflammatory process, the maintenance dose is 3-4 mg/kg/day for 5-8 months;
The combined use of cyclosporine with prednisolone is possible: cyclosporine 5 mg/kg/day and prednisolone 0.2-0.4 mg/kg/day for 4 weeks, or cyclosporine 5 mg/kg/day and prednisolone 0.6 mg/kg/day for 3 weeks, or cyclosporine 7 mg/kg/day and prednisolone 0.2-0.4 mg/kg/day for 3 weeks, or cyclosporine 7 mg/kg/day and prednisolone 0.6 mg/kg/day for no more than 3 weeks. Maintenance dose of cyclosporine 3-4 mg/kg/day;
Azothioprine [INN] orally 1.5-2 mg/kg/;
Methotrexate [INN] orally 7.5-15 mg/week - in the treatment of anterior uveitis, mydriatics are prescribed, which are installed in the conjunctival sac 2-3 times a day and/or administered subconjunctivally at 0.3 ml: atropine [INN] (1 % eye drops and 0.1% injection solution), phenylephrine [INN] (2.5 and 10% irifrin eye drops or 1% mesaton injection solution);
To reduce the phenomena of fibrinoid syndrome, fibrinolytic drugs are used;
Urokinase [INN] is administered under the conjunctiva at 1250 IE (in 0.5 ml) once a day, lyophilized powder to prepare a solution of 100,000 IU. For subconjunctival administration, the contents of the vial are dissolved ex tempore in 40 ml of solvent;
Recombinant prourokinase [INN] is injected subconjunctivally and parabulbarly at 5000 IU/ml (hemase). For an injection solution, the contents of the ampoule are dissolved ex tempore in 1 ml of physiological solution;
Collalysin [INN] is injected under the conjunctiva at 30 IU. For an injection solution, the contents of the ampoule are dissolved ex tempore in 10 ml of a 0.5% solution of novocaine (collalysin lyophilized powder, 500 IU in ampoules);
Histochrome [INN] 0.2% solution is administered subconjunctivally or parabulbarly;
Lidase is administered at 32 units in the form of electrophoresis;
Wobenzym 8-10 tablets 3 times a day for 2 weeks, then 2-3 weeks 7 tablets 3 times a day, then 5 tablets 3 times a day for 2-4 weeks, then 3 tablets for 6 -8 weeks;
Flogenzym 2 tablets 3 times a day for several months. Take the pills 30-60 minutes before meals with plenty of water.
Protease inhibitors are also used to reduce the effects of fibrinoid syndrome:
Aprotinin [INN] is administered subconjunctivally and parabulbarly: gordox in ampoules of 100,000 KIU (for subconjunctival administration, the contents of the ampoule are diluted in 50 ml of saline, 900-1500 KIU are injected under the conjunctiva);
Contrical lyophilized solution of 10,000 KIU in bottles (for subconjunctival administration, the contents of the bottle are diluted in 10 ml of physiological solution, 300-500 KIU are injected under the conjunctiva; for parabulbar administration, the contents of the bottle are diluted in 2.5 ml of physiological solution, 4,000 KIU are injected under the conjunctiva);
Detoxification therapy: intravenous drip “hemodez” 200-400 ml, 5-10% glucose solution 400 ml with ascorbic acid 2.0 ml;
Desensitizing drugs: intravenous 10% calcium chloride solution, loratadine [INN] for adults and children over 12 years of age, 10 mg orally once a day, for children 2-12 years of age, 5 mg once a day - Claritin;
Etiological antimicrobial therapy depends on the cause of the disease.
Syphilitic uveitis: benzathine benzylpenicillin (retarpen) IM 2.4 million units 1 time in 7 days for 3 injections, benzylpenicillin novocaine salt IM 600,000 units 2 times a day for 20 days, benzylpenicillin sodium salt 1 million every 6 hours within 28 days. If benzylpenicillin is intolerant, doxycycline 100 mg orally 2 times a day for 30 days, tetracycline 500 mg 4 times a day for 30 days, erythromycin at the same dose, ceftriaxone intramuscularly 500 mg/day for 10 days are used. , ampicillin or oxacillin IM 1 g 4 times a day for 28 days.
Toxoplasmosis uveitis: a combination of pyrimethamine [INN] (chloridine) orally 25 mg 2-3 times a day and sulfadimezine 1 g 2-4 times a day is used. 2-3 courses are carried out for 7-10 days with breaks of 10 days. It is possible to use the combination drug Fansidar (F. Hoffmann La Roche), which contains 25 mg of pyrimethamine and 500 mg of sulfodoxine). This drug is taken orally, 1 tablet. 2 times a day every 2 days for 15 days or 1 tablet. 2 times a day 2 times a week for 3-6 weeks. With intramuscular administration, 5 ml of the drug is administered 1-2 times a day every 2 days for 15 days. Pyrimethamine is used in conjunction with folic acid preparations (5 mg 2-3 times a week) and vitamin B12. Instead of pyrimethamine, you can use aminoquinol orally 0.1-0.15 g 3 times a day.
Antibiotics of the lincosamine group (lincomycin and clindamycin) and macrolides (spiramycin) are used. Lincomycin [INN] is used subconjunctivally or parabulbarly at 150-200 mg, intramuscularly at 300-600 mg 2 times a day or orally at 500 mg 3-4 times a day for 7-10 days. Clindamycin [INN] is used subconjunctivally or parabulbarly at 50 mg daily for 5 days, then 2 times a week for 3 weeks, intramuscularly at 300-700 mg 4 times a day or orally at 150-400 mg 4 times a day for 7-10 days. Spiramycin [INN] slow intravenous drips of 1.5 million IU 3 times a day or orally 6-9 million IU 2 times a day for 7-10 days.
Tuberculous uveitis: for severe active uveitis, a combination of isoniazid [INN] is used for the first 2-3 months (orally 300 mg 2-3 times a day, intramuscularly 5-12 mg/kg/day in 1-2 injections, subconjunctival and parabulbar a 3% solution is administered) and rifampicin [INN] (orally 450-600 mg once a day, IM or IV 0.25-0.5 g per day), then a combined therapy with isoniazid and ethionamide [INN] (orally 0.5-1 g per day in 2-3 doses).
In primary uveitis of moderate severity during the first 1-2 months, a combination of isoniazid and rifampicin is used, then for 6 months, a combination of isoniazid and ethionamide or streptomycin [INN] is used (0.5 g orally 2 times a day in the first 3-5 days, and then 1 .0 g once a day, a solution containing 50,000 units/ml is administered subconjunctivally or parabulbarly).
For chronic uveitis a combination of isoniazid with rifampicin or ethionamide, streptomycin, kanamycin and glucocorticosteroids is used.
Viral uveitis: for infections caused by the herpes simplex virus, use acyclovir [INN] orally 200 mg 5 times a day for 5 days or valacyclovir [INN] orally 500 mg 2 times a day for 5-10 days. For infections caused by the Herpes zoster virus, use acyclovir [INN] orally 800 mg 5 times a day for 7 days or valacyclovir [INN] 1 g 3 times a day for 7 days. For severe herpetic infection, acyclovir is used intravenously in a slow drip of 5-10 mg/kg every 8 hours for 711 days or intravitreally at a dose of 10-40 mcg/ml.
For infections caused by cytomegalovirus, ganciclovir [INN] is used intravenously in slow drips at 5 mg/kg every 12 hours for 14-21 days, followed by maintenance therapy with ganciclovir intravenously at 5 mg/ml daily for a week or 6 mg/ml 5 days a week or orally 500 mg 5 times a day or 1 g 3 times a day.
Rheumatic uveitis: phenoxymethylpenicillin [INN] 3 million units/day in 4-6 administrations for 7-10 days.
Uveitis with Reiter's syndrome: There are several ways to use antibiotics:
1. Reception for 1, 3 or 5 days.
2. Reception within 7-14 days.
3. Continuous use for 21-28 days.
4. Pulse therapy - 3 cycles of antibiotic therapy are carried out for 7-10 days with breaks of 7-10 days.
It is most advisable to use the following antibiotics:
Clarithromycin [INN] (orally 500 mg/day in 2 divided doses for 21-28 days;
Azithromycin [INN] - orally 1 g/day once;
Doxycycline [INN] - taken orally 200 mg/day in 2 divided doses for 7 days. It is not recommended for children under 12 years of age;
Roxithromycin [INN] - orally 0.3 g/day in 1-2 doses, course of treatment 10-14 days;
Ofloxacin [INN] - adults 200 mg orally once a day for 3 days. Not recommended for children;
Ciprofloxacin [INN] - adults, 0.5 g/day orally on the first day, and then 0.25 g/day in 2 divided doses for 7 days. Not recommended for children.
Tumors of the vascular tract
Among malignant tumors of the vascular tract, melanoma or melanoblastoma is more common.
Melanoma arises mainly from pigmented spots - nevi. Tumor growth is activated during puberty, pregnancy or old age. It is believed that melanoma is caused by trauma. Melanoblastoma is a tumor of neuroectodermal origin. Tumor cells develop from melanocytes, Schwann cells of the cutaneous nerve sheaths, capable of producing melanin.
The iris is affected in 3-6% of cases of vascular melanoma; ciliary body - in 9-12% and choroid - in 85% of cases.
Iris melanoma
It most often develops in the lower parts of the iris, but is also possible in any other part of it. There are nodular, planar and diffuse forms. In most cases, the tumor is pigmented, dark brown in color; the nodular form of the tumor in the form of a dark, clearly defined spongy mass is more common. The surface of the tumor is uneven, protrudes into the anterior chamber, and can displace the pupil.
Treatment: if the tumor has spread to no more than 1/4 of the iris, its partial removal (iridectomy) is indicated; if there are initial signs of tumor growth in the root of the iris, iridocyclectomy should be performed. A small localized melanoma of the iris can be destroyed by photo- or laser coagulation.
Melanoma of the ciliary body
The initial growth of the tumor is asymptomatic. As melanoma grows, changes appear associated with the mechanical effect of the tumor on adjacent tissues.
Early symptom is a congestive injection in the system of the anterior ciliary vessels; in a limited area, closure of the anterior chamber angle in a certain area is gonioscopically detected.
Paresis of the iris and contact opacification of the lens are noted. Sometimes melanoma is found in the angle of the anterior chamber as a dark formation on the surface of the iris.
IN diagnostics Gonioscopy, biomicroscopy, diaphanoscopy, echoophthalmoscopy (B-method), MRI help.
Treatment: Small, localized tumors of the ciliary body can be excised within healthy tissue, preserving the eyeball. For large tumors, enucleation of the eye is indicated.
Choroidal melanoma
Most often occurs between the ages of 50-70 years. There are nodular - the most common and planar forms of the tumor. The color of choroidal melanoma is black, dark or light brown, sometimes pinkish (the most malignant).
In the clinical picture of choroidal melanoma, 4 stages are distinguished: I - initial, non-reactive; II - development of complications (glaucoma or inflammatory process); III - tumor growth beyond the outer capsule of the eye; IV - generalization of the process with the development of distant metastases (liver, lungs, bones).
Clinic of the disease depends on the location of the tumor. Melanoma of the macular region early manifests itself as visual disturbances (metamorphopsia, photopsia, decreased visual acuity). If melanoma is located outside the macula, it remains asymptomatic for a long time. Then the patient complains of a dark spot in the field of vision.
Perimetry reveals a scotoma corresponding to the location of the tumor. With ophthalmoscopy, a tumor with sharp boundaries is visible in the fundus, protruding into the vitreous body. The color of melanoma ranges from grayish-brown to gray.
In stage I of the disease, the retina tightly fits the melanoma without the formation of folds; There is no retinal detachment yet. Over time, secondary retinal detachment occurs, which masks the tumor. The appearance of stagnant injection and pain indicates the transition of the disease to stage II, i.e., secondary glaucoma begins to develop. A sudden subsidence of pain with a simultaneous decrease in intraocular pressure indicates that the process has gone beyond the eyeball (stage III). Metastases indicate the transition of the tumor to stage IV.
Treatment: enucleation; in case of melanoma germination - exenteration with radiotherapy. If the tumor size is no more than 4-6 optic disc diameters and the distance is no more than 1.5 mm, transpupillary photo- or laser coagulation can be used. For post-equatorial tumors measuring no more than 12 mm and prominence up to 4 mm, transpupillary thermotherapy (use of high temperature) with an infrared laser with a wavelength of 810 nm is used.
Thermotherapy can be combined with brachytherapy. Transscleral brachytherapy (suturing an applicator with strontium or ruthenium radionuclides that produce pure β-radiation) is carried out with a maximum diameter of no more than 14 mm and a tumor thickness of no more than 5 mm. In some cases, cryotherapy is used.
Article from the book:
A) Anatomy of the uveal tract (choroid) of the eye. The uveal tract is formed by the iris, ciliary body and choroid. The iris stroma is formed by pigmented and non-pigmented cells, collagen fibers and a matrix consisting of hyaluronic acid. Crypts vary in size, shape and depth; their surface is covered with a heterogeneous layer of connective tissue cells fused with the ciliary body.
The different colors are determined by the pigmentation of the anterior border layer and deep stroma: the stroma of blue irises is much less pigmented than that of brown irises.
The ciliary body performs the functions of producing aqueous humor, accommodating the lens, and forming the trabecular and uveoscleral outflow tracts. It extends 6 mm from the root of the iris to the anterior zone of the choroid, the anterior section (2 mm) bears the ciliary processes, the flatter and more even posterior part (4 mm) is the pars plana. The ciliary body is covered with an outer pigmented and inner non-pigmented epithelial layer.
The ciliary muscle consists of longitudinal, radial and circular portions. The ciliary processes are formed mainly from coarsely fenestrated capillaries through which fluorescein leaks and veins that drain into the vorticose veins.
The choroid lies between the retina and sclera. It is formed by blood vessels and is bounded internally by Bruch's membrane and the avascular suprachoroidal space externally. It has a thickness of 0.25 mm and consists of three vascular layers receiving blood supply from the short and long posterior and anterior ciliary arteries. The choriocapillaris layer is the innermost layer, the middle layer is the layer of small vessels, the outer layer is the layer of large vessels. The vessels of the middle and outer layers of the choroid are not fenestrated.
The choriocapillary layer is a continuous layer of large capillaries, it lies under the retinal pigment epithelium and nourishes the outer parts of the retina; The capillary endothelium is fenestrated and fluorescein leaks through it. Bruch's membrane consists of three layers: the outer elastic layer, the middle collagen layer, and the inner circular layer, the latter being the basement membrane of the retinal pigment epithelium. The choroid is tightly fixed to the edges, extends forward to the dentate line and connects with the ciliary body.
b) Embryology of the uveal tract. The uveal tract develops from neuroectoderm, neural crest and mesoderm. The sphincter, dilator and posterior epithelium of the iris develop from the neuroectoderm. Pigment differentiation and migration continues in the second and third trimester. The smooth muscles of the iris, choroidal stroma, and ciliary body develop from the neural crest. The formation of the iris begins with the closure of the fetal cleft on the 35th day of gestation. The sphincter muscle appears at the edge of the optic cup at the tenth week of gestation, myofibrils are formed at 10-12 weeks.
The dilator is formed at 24 weeks of gestation. The neuroectoderm differentiates into both pigmented and non-pigmented epithelium of the ciliary body at 10-12 weeks of gestation. Smooth muscle of the ciliary body is already present in the fourth month of gestation even before the formation of the iris stroma; it joins the ciliary groove in the fifth month. The formation of choroidal pigment cells from neural crest cells is completed at birth. Blood vessels develop from the mesoderm and neural crest. The choroidal vasculature differentiates from mesenchymal elements in the second week of gestation and develops over the next 3-4 months.
The pupillary membrane disappears shortly before term birth. At birth the pupil is narrow, but as the dilator muscle develops, it widens. The role of the ciliary muscle in accommodation increases between the third and sixth months of life. By the age of two years, the length of the ciliary body reaches three quarters of the length of the adult ciliary body. In representatives of all races, pigmentation is complete by the age of one; During the first year of life, the irises become darker, and never lighter.
(A) Structure of a normal eye. Please note that the surface of the iris is very prominent due to crypts and folds.(B) Diagram of the normal flow of aqueous humor. The aqueous humor formed in the posterior chamber flows through the pupil into the anterior chamber.
The main route of outflow of aqueous humor is through the trabecular meshwork into Schlemm's canal.
Only a small amount of aqueous humor flows through additional pathways (uveoscleral and through the iris - both not shown).
(A) Formation of the optic vesicle on the lateral wall of the diencephalon. The optic stalk connects the optic vesicle with the forebrain. (9.5 days of mouse gestation, equivalent to 26 days of human gestation). (B) Invagination of the optic vesicle and formation of the lens vesicle (onset at 10.5 days of mouse gestation, corresponding to 28 days of human gestation).
(B) Invagination of the lens fossa, formation of a two-layer optic cup from the invaginated optic vesicle (end of 10.5 days of mouse gestation, corresponds to 32 days of human gestation).
(D) Closure of the embryonic choroidal fissure, formation of the lens vesicle and primary vitreous body (12.5 days of mouse gestation, corresponding to 44 days of human gestation).
(E) Formation of the nerve fiber layer, migration of neural crest cells, and formation of the nuclear belt of the lens (14.5 days of mouse gestation, corresponding to 56-60 days of human gestation).
(E) Eye at the end of the organogenesis stage. The cornea, the iris beginning to form, the rudiments of the extraocular muscles and the lacrimal gland are clearly visible.
Arrows indicate the pupillary membrane (16.5 days of mouse gestation corresponds to >60 days of human gestation).
