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Lecture notes, cheat sheets
Eye diseases. Lecture notes
Directory / Lecture notes, cheat sheets Table of contents
LECTURE No. 1. The structure of the eye (part I) The eye as an integral part of the so-called opto-vegetative (OVS) or photoenergetic (FES) system of the body is involved in the adaptation of the internal environment of the body to external conditions. The vast majority of information about the world around comes to the child through the organ of vision. The eye is in a figurative and literal sense a part of the brain, placed on the periphery. 1. The structure of the orbit When studying the anatomy of a child, it must be remembered that the orbit in children under the age of one year approaches a trihedral prism in shape. Later it takes the form of a truncated tetrahedral pyramid with rounded edges. The base of the pyramid faces outwards and anteriorly, the apex inwards and backwards. In newborns and children of the first year of life, the angle between the axes of the orbits is sharper, which creates the illusion of convergent strabismus. However, this imaginary strabismus gradually disappears, as the angle between the axes of the orbits increases. The upper wall of the orbit borders the cranial cavity and is formed in front by the orbital part of the frontal bone, and behind by the lesser wing of the sphenoid bone. In the outer corner of the wall, a recess for the lacrimal gland is revealed, and at the place where the upper wall passes into the inner wall, a notch (or hole) for the superior orbital vein and artery is determined. There is also a spike block through which the tendon of the superior oblique muscle is thrown. In the process of comparing the orbits in terms of age, it is revealed that in children the upper wall of the orbit is thin, there is no pronounced superciliary tubercle. When studying the outer wall of the orbit, it is noted that it borders on the temporal cranial fossa. The orbital process of the zygomatic bone separates the orbit from the maxillary sinus, and the sphenoid bone of the inner wall separates the contents of the orbit from the ethmoid sinus. The fact that the upper wall of the orbit is simultaneously the lower wall of the frontal sinus, the lower upper wall of the maxillary sinus, and the inner side wall of the ethmoidal labyrinth, explains the relatively unhindered and rapid transition of the disease from the paranasal sinuses to the contents of the orbit and vice versa. At the top of the orbit in the lesser wing of the sphenoid bone, a round opening for the optic nerve and ophthalmic artery is defined. The superior orbital fissure is located outside and below this opening between the large and small wings of the sphenoid bone and connects the orbit with the middle cranial fossa. All the motor branches of the cranial nerves pass through this gap, as well as the superior ophthalmic vein and the first branch of the trigeminal nerve, the ophthalmic nerve. The inferior orbital fissure connects the orbit to the inferior temporal and pterygoid fossae. The maxillary and zygomatic nerves pass through it. The entire orbit is lined with periosteum; in front of the bony edge of the orbit to the cartilage of the eyelids is the tarsoorbital fascia. With closed eyelids, the entrance to the orbit is closed. Tenon's capsule divides the orbit into two sections: the eyeball is located in the anterior section, and the vessels, nerves, muscles, and orbital tissue are located in the posterior section. 2. Muscles and soft tissues of the eye The superior, inferior, external and internal rectus and superior and inferior oblique muscles related to the oculomotor muscles, as well as the muscle that lifts the upper eyelid, and the orbital are located in the orbit. Muscles (except for the inferior oblique and orbital) start from the connective tissue ring that surrounds the visual opening, and the inferior oblique muscle from the inner corner of the orbit. The muscles are separated from the limbus by an average of 5,58,0 mm. In newborns, this value is 4,05,0 mm, and in children aged fourteen years, 5,07,5 mm. The superior and inferior oblique muscles are attached to the sclera 16 mm from the limbus, the external rectus turns the eye outward, the internal inwards, the superior moves upwards and inwards, the inferior downwards and inwards. The eyelids cover the front of the eye socket. The connection of the free edges of the lower and upper eyelids with each other occurs through external and internal adhesions. There is a variation in the width and shape of the palpebral fissure. Normally, the edge of the lower eyelid should be 0,51,0 mm below the corneal limbus, and the edge of the upper eyelid should cover the cornea by 2 mm. In newborns, the palpebral fissure is narrow, its vertical size is 4,0 mm, horizontal 16,5 mm. The skin of the eyelids is thin, delicate, poor in fatty tissue, loosely connected with the underlying parts, the underlying vessels shine through it. The muscles of the eyelids are poorly developed. The muscular layer of the eyelids is represented by a circular muscle, innervated by the facial nerve and providing closure of the eyelids. Under the muscle is cartilage, in the thickness of which the meibomian glands are located, translucent in the form of yellowish radial stripes. The back surface of the eyelids is covered with a connective sheath. On the front edge of the eyelids there are eyelashes, near the root of each eyelash there are sebaceous and modified sweat glands. The lifting of the upper eyelid is carried out with the help of the muscle of the same name, which is innervated by the branches of the oculomotor nerve. The blood supply to the eyelids is carried out by the external branches of the lacrimal artery, the internal arteries of the eyelids and the anterior ethmoid artery. The outflow of blood occurs through the veins of the same name and further into the veins of the face and orbit. Lymphatic vessels located on both sides of the cartilage flow into the anterior and submandibular lymph nodes. Sensitive innervation of the eyelids is carried out by the first and second branches of the trigeminal nerve, motor by the third and seventh pair of cranial nerves and the sympathetic nerve. 3. Connective sheath of the eye The connective sheath, the conjunctiva, covers the eyelids from the inside, passes to the sclera and continues in an altered form to the cornea. There are three sections of the conjunctiva: cartilage (or eyelids), transitional fold (or fornix) and the eyeball. All three sections of the conjunctiva with closed eyelids form a closed slit cavity, the conjunctival sac. The blood supply of the conjunctiva is carried out by the arterial system of the eyelids and the anterior ciliary arteries. The veins of the conjunctiva accompany the arteries, the outflow of blood occurs in the system of facial veins and through the anterior ciliary veins of the orbit. The conjunctiva of the eye has a well-developed lymphatic system. Lymph enters the anterior and submandibular lymph nodes. The conjunctiva receives sensory nerves in large quantities from the first and second branches of the trigeminal nerve. The conjunctiva in young children has a number of features. It is thin and tender, somewhat dry due to insufficient development of the mucous and lacrimal glands, subconjunctival tissue is poorly developed. The sensitivity of the conjunctiva in a child of the first year of life is reduced. The conjunctiva performs mainly protective, nourishing and absorption functions. 4. Lacrimal organs The lacrimal organs consist of a tear-producing and tear-removing apparatus. The tear-producing apparatus includes the lacrimal gland and Krause's glands. The lacrimal gland is located in the bony cavity of the upper outer part of the orbit. Twenty or more (up to thirty) excretory ducts of the gland open into the lateral part of the superior conjunctival fornix. Tear production is carried out mainly from the second month of a child's life. Krause's lacrimal glands are located in the conjunctiva of the upper and lower fornix and secrete tear fluid constantly. The lacrimal ducts include the lacrimal puncta, lacrimal canaliculi, lacrimal sac, and lacrimal canal. The lacrimal openings normally gape, facing the eyeball and immersed in the lacrimal lake. They lead to the superior and inferior lacrimal ducts, which empty into the lacrimal sac. The wall of the lacrimal sac consists of a mucous membrane covered with a bilayer columnar epithelium and submucosal tissue. The lower section of the lacrimal sac passes into the lacrimal canal, which opens under the inferior nasal concha at the border of its anterior and middle thirds. In 5% of cases at birth, the lacrimal canal is closed with a gelatinous film. If it does not resolve, the outflow of tears stops, its stagnation is formed, resulting in dacryocystitis of newborns. LECTURE No. 2. The structure of the eye (part II) 1. The structure of the eyeball The eyeball has an irregular spherical shape. Its anterior section is more convex. The anteroposterior size of the eye is on average 16 mm in a newborn, 19 mm by one year of life, 20 mm by three, 21 mm by seven, 22,5 mm by fifteen, and 23 mm by twenty years. The weight of the eyeball of a newborn is about 3,0 g, and that of an adult is 8,0 g. The eyeball has three shells: outer (represented by the cornea and sclera), middle (represented by the vascular tract) and inner (represented by the retina). Inside the eyeball are aqueous humor, lens, vitreous body, blood vessels. 2. Cornea and sclera The cornea is the anterior transparent part of the capsule of the eye. Its horizontal size in a newborn is 9,0 mm, by one year 10,0 mm, by three years 10,5 mm, by five years 11,0 mm, and by nine years it acquires the same dimensions as in adults, 11,5 .0,5 mm. The vertical dimension of the cornea is 78 mm smaller. The radius of curvature of the cornea is 1,12 mm. The thickness of this shell in the center in a child is 0,8 mm, in an adult 85 mm. The cornea contains up to XNUMX% water. The cornea normally has transparency, specularity, luster, sensitivity, sphericity. The cornea is the strongest refractive medium in the eye (60,0 diopters in newborns and 40,0 diopters in adults). The cornea is nourished by diffusion of nutrients from the marginal looped network and moisture from the anterior chamber. Sensitive innervation of the cornea is carried out by the trigeminal nerve, and trophic innervation is also due to the branches of the facial and sympathetic nerves. The sclera is a dense opaque fibrous membrane, occupies 5/6 of the entire outer shell of the eye and anteriorly passes into the transparent cornea, and the surface layer of the sclera passes into the transparent shell later than the middle and deep ones. Thus, at the transition point, a translucent limbus border is formed. In the posterior pole of the eye, the sclera becomes thinner and has a large number of holes through which the fibers of the optic nerve exit. This area of the sclera is called the lamina cribrosa and is one of its weak points. The plate under the influence of increased pressure can stretch, forming a deep excavation of the optic disc. Outside, the sclera is covered with episclera, which forms the inner wall of Tenon's space. All oculomotor muscles are attached to the sclera. It has openings for the blood vessels and nerves of the eye. In newborns and children of the first years of life, the sclera is thin, elastic, the choroid is visible through it, so the sclera has a bluish tint. With age, it becomes white, and by old age it turns yellow due to the degeneration of its tissue. Thin, elastic sclera in children of the first years of life under the influence of high intraocular pressure can stretch, which leads to an increase in the size of the eye (hydrophthalmos, buphthalmos). The outer shell is the main optical medium, it gives the eye a shape, maintains a constant volume, which is associated with the turgor of the eye, performs the function of protecting the thinner and more delicate inner shells of the eye. 3. Vascular tract of the eye The vascular tract, consisting of the iris, ciliary body and choroid, is located medially from the outer shell of the eye. It is separated from the latter by the suprachoroidal space, which is formed in the first months of a child's life. The iris (anterior part of the vascular tract) forms a vertically standing diaphragm with a hole in the center of the pupil that regulates the amount of light entering the retina. The vascular network of the iris is formed by branches of the posterior long and anterior ciliary arteries and has two circles of blood circulation. The iris can have different colors: from blue to black. Its color depends on the amount of melanin pigment it contains: the more pigment in the stroma, the darker the iris; in the absence or small amount of pigment, this shell has a blue or gray color. Children have little pigment in the iris, so in newborns and children of the first year of life it is bluish-grayish. The color of the iris is formed by the age of ten to twelve. On its anterior surface two parts can be distinguished: narrow, located near the pupil (the so-called pupillary), and wide, bordering the ciliary body (ciliary). The boundary between them is the pulmonary circulation of the iris. There are two muscles in the iris that are antagonists. One is placed in the pupillary area, its fibers are located concentrically with the pupil, and when they contract, the pupil narrows. Another muscle is represented by radially running muscle fibers in the ciliary part, with the contraction of which the pupil dilates. In infants, the muscle fibers that dilate the pupil are poorly developed; parasympathetic innervation predominates, so the pupil is narrow (22,5 mm), but dilates under the influence of mydriatics. By one to three years, the pupil acquires dimensions characteristic of adults (33,5 mm). The ciliary body consists of a flat and thickened coronal parts. The thickened coronal part consists of 70 to 80 ciliary processes, each of which has vessels and nerves. The ciliary, or accommodative, muscle is located in the ciliary body. The ciliary body is dark in color and covered with retinal pigment epithelium. Zinn ligaments of the lens are woven into it in the interprocesses. The ciliary body is involved in the formation of intraocular fluid that nourishes the avascular structures of the eye (cornea, lens, vitreous body), as well as in the outflow of this fluid. In newborns, the ciliary body is underdeveloped, the accommodative muscle is in a spastic state. The vessels of the ciliary body depart from the large arterial circle of the iris, which is formed from the posterior long and anterior ciliary arteries. Sensitive innervation is carried out by long ciliary fibers, motor parasympathetic fibers of the oculomotor nerve and sympathetic branches. The choroid, or the choroid itself, is composed mainly of short posterior ciliary vessels. In it, with age, the number of pigment cells of chromatophores increases, due to which the choroid forms a dark chamber that prevents the reflection of rays entering through the pupil. The basis of the choroid is a thin connective tissue stroma with elastic fibers. Due to the fact that the choriocapillary layer of the choroid is attached to the retinal pigment epithelium, a photochemical process is carried out in the latter. 4. Retina and optic nerve The retina contributes to the lining of the entire inner surface of the vascular tract. It is also a peripheral part of the visual analyzer. Under microscopic examination, ten layers are distinguished in it. At the place corresponding to the transition of the choroid itself into the flat part of the ciliary body (the region of the dentate line), only two layers of epithelial cells are preserved from its ten layers, passing to the ciliary body, and then to the iris. In the region of the dentate line, as well as at the exit of the optic nerve, the retina is tightly fused with the underlying formations. For the rest of its length, it is held in a constant position by the pressure of the vitreous body, as well as the connection between the rods and cones and the retinal pigment epithelium, which is genetically related to the retina, and anatomically closely related to the choroid. There are three types of neurons in the retina: rods and cones, bipolar cells, and multipolar cells. The most important area of the retina is the yellow spot, located at the posterior pole of the eyeball. The macula has a central fossa. In the area of the central fovea of the macula, instead of ten layers, only three or four layers of the retina remain: the outer and inner border plates and the layer of cones and their nuclei located between them. However, newborns have all ten layers in the macula area. This, along with other reasons, explains the child’s low central vision. In the central zone of the retina, predominantly cones are located, and towards the periphery the number of rods increases. Nerve cell fibers (about 100) form the optic nerve, passing through the lamina cribrosa of the sclera. The inner part of the optic nerve is called the disc (nipple). It has a somewhat oval shape, its diameter in newborns is 000 mm, in adults it reaches 0,8 mm. In the center of the disc are the central retinal artery and vein, which branch and participate in feeding the inner layers of the retina. Topographically, in addition to the intraocular one, the intraorbital, intracanalicular and intracranial parts of the optic nerve are distinguished. In the cranial cavity, the optic nerve forms a partial decussation of the nerve fibers of the chiasm. The optic tracts emerge from the chiasm in the form of two separate trunks, ending in the primary visual centers (external geniculate bodies, visual tuberosities). Through the internal capsule in the form of a bundle, the optic fibers go to the cortical visual centers, ending in the occipital lobe, in the region of the avian spur furrow (field seventeen to nineteen according to Brodmann). 5. Lens and vitreous body The transparent contents of the eyeball are represented by aqueous humor, the lens and the vitreous body. Aqueous moisture is contained in the anterior and posterior chambers of the eye. Its quantity in children does not exceed 0,2 cm3, and in adults it reaches 0,45 cm3. The anterior chamber is the space bounded by the posterior surface of the cornea in front, the iris behind, and in the region of the pupil by the lens. The chamber has the greatest depth in the center, to the periphery it gradually decreases. In a newborn, mainly due to the greater sphericity of the lens, the anterior chamber is smaller than 1,5 mm. The place where the cornea passes into the sclera, and the iris into the ciliary body, is called the angle of the anterior chamber of the eye. Through the angle of the anterior chamber, aqueous and anterior ciliary veins, aqueous humor is drained. The posterior chamber is the space bounded anteriorly by the iris and posteriorly by the anterior surface of the lens. Through the region of the pupil, the posterior chamber communicates with the anterior one. The lens is a transparent elastic body, has the shape of a biconvex lens. In newborns, the lens is almost spherical in shape. With age, the lens flattens somewhat, the radius of curvature of the anterior surface increases from 6 to 10 mm, and the posterior surface from 4,5 to 6 mm. The anteroposterior size of the lens of a newborn is 4 mm, and the diameter is 6 mm; the lens of an adult is 44,5 and 10 mm, respectively. The lens has anterior and posterior surfaces, anterior and posterior poles, sagittal axis, and equator. The lens is held in place by the ciliary body by the ligament of zon. The lens contains a capsule and lenticular, or cortical, fibers. In children, the fibers are elastic; with age, the center of the lens becomes denser, and from the age of twenty-five to thirty, a core begins to form, which gradually increases in size. 65% of the lens consists of water. It performs a refractive function; in relation to the average refractive power of the eye, it accounts for up to 40 out of 7780 diopters in newborns, and by the age of fifteen, 20 out of 60 diopters. The vitreous body is the main supporting tissue of the eyeball. Its weight in a newborn is 1,5 g, in an adult 67 g. The vitreous body is a formation of a gelatinous consistency, 98% consisting of water, containing an insignificant amount of protein and salts. In addition, it has a thin connective tissue skeleton, thanks to which it does not blur, even if taken out of the eye. On the anterior surface of the vitreous body there is a recess, the so-called plate-shaped fossa, in which lies the posterior surface of the lens. The vitreous body, being a transparent medium, provides free passage of light rays to the retina, protects the inner membranes (retina, lens, ciliary body) from dislocation. 6. Blood supply and innervation of the eye The blood supply to the eye is provided by the ophthalmic artery, a branch of the internal carotid artery. The outflow of venous blood is carried out by the whirlpool and anterior ciliary, and then by the ophthalmic veins of the upper and lower. The superior vein leaves through the superior orbital fissure and flows into the cavernous sinus, the inferior orbital vein passes through the inferior orbital fissure with its second branch, opens into the deep veins of the face and the venous plexus of the pterygopalatine fossa. The sensory nerves of the eye are mainly branches of the first branch of the trigeminal nerve. The main nerve plexus for the eye is the ciliary ganglion (2 mm). It is adjacent to and external to the optic nerves. The node is formed by a sensitive branch from the nasociliary nerve, parasympathetic from the oculomotor nerve and sympathetic from the plexus of the internal carotid artery. Four to six short ciliary nerves depart from the ciliary ganglion, which penetrate the sclera at the posterior pole and are joined by branches of the sympathetic nerve (which dilates the pupil). Short ciliary nerves provide all tissues of the eye with sensitive, motor and sympathetic innervation. Parasympathetic fibers innervate the sphincter of the pupil and the ciliary muscle. Motor innervation is provided by cranial nerves. LECTURE No. 3. Methodology for examining the condition of the eye (part I) Examination of the organ of vision, regardless of complaints and first impressions, should always be carried out sequentially, according to the principle of the anatomical arrangement of its parts. However, it should be an unshakable rule to start the examination with a check of visual functions, especially visual acuity, since after diagnostic interventions the child will no longer give correct indications about the state of vision. 1. External examination of the eye in natural light The study of the organ of vision begins with an external examination of the eye in natural light. In the region of the orbit, changes can be associated mainly with congenital pathology in the form of dermoid cysts, cerebral hernia or tumors (angiomas, sarcomas, etc.). Pay attention to the condition of the eyelids. In rare cases, there may be a congenital or acquired coloboma of the eyelids, their fusion (ankyloblepharon), congenital or as a result of a gross cicatricial process. It is not uncommon to see congenital drooping of the upper eyelid (ptosis). There may be changes in the skin of the eyelids (hyperemia, subcutaneous hemorrhages, edema, infiltration) and the edges of the eyelids (scales and crusts at the base of the eyelashes, ulceration, cysts, etc.). Usually, the eyelids fit snugly against the eyeball, but sometimes in chronic inflammatory processes of the mucous membrane, an eversion of the lower eyelid may occur, and with cicatricial changes in the mucous membrane and cartilage, eyelid torsion may occur. Sometimes in children in the first month of life, a congenital inversion of the lower eyelid is found, while the eyelashes are turned towards the cornea. With eversion of the lower eyelid, the lacrimal point, usually facing the eyeball and immersed in the lacrimal lake, lags behind somewhat, which leads to lacrimation and lacrimation. On examination, pay attention to the correct growth of eyelashes. With ulcerative blepharitis, trachoma, chronic meibomitis, abnormal growth of eyelashes (trichiasis), baldness of the edges of the eyelids (madarosis) can be observed. The state of the lacrimal ducts should be judged by the severity of the lacrimal puncta, their position, the presence of discharge from them when pressed on the area of the lacrimal canaliculi (canaliculitis) or the lacrimal sac (dacryocystitis). Inspection of the lacrimal gland is carried out by pulling the upper eyelid up, while the subject should look at the tip of his nose. In some acute and chronic inflammatory processes (dacryoadenitis), the gland can be enlarged, sometimes through the mucous membrane you can see its cystic degeneration, abscesses, etc. Pay attention to the position of the eyeballs in the orbit. Anterior displacement of the eye (exophthalmus) is possible, more often observed with retrobulbar hemorrhages, tumors. The value of the protrusion of the eye is determined by the exophthalmometer. The displacement of the eyeball back (enophthalmus) is observed with the degeneration of the bones of the orbit, Horner's syndrome. Most often in children there is a lateral deviation of the eyeball (strabismus). Check the range of motion of the eyeball. To do this, the subject needs to fix the doctor's finger moving in all directions with a fixed head position. This is how paresis of individual oculomotor muscles is detected, nystagmus is detected with extreme abduction of the eyeballs, as well as the predominance of one or another muscle group. In addition, this way they get an idea of the size of the eyeballs (buphthalmos, microphthalmos), the size of the cornea (micro and macrocornea), the depth of the anterior chamber, the size and reaction to light of the pupil, the state of the pupil area (mydriasis, coloboma), etc. 2. Side lighting method The method of lateral, or focal, illumination is used to study the condition of the mucous membrane of the eyelids and the anterior part of the eyeball (the mucous membrane of the eyeball, sclera, cornea, anterior chamber, iris and pupil), as well as the lens. The study is carried out in a darkened room. The lamp is placed to the left and in front of the patient. The doctor illuminates the patient's eyeball, throwing a focused beam of light from the lamp onto its individual sections using a lens of 13,0 or 20,0 diopters. The mucous membrane of the lower eyelid becomes accessible for inspection when the edge of the eyelid is pulled down. This requires the patient to look up. When examining the mucous membrane, attention should be paid to all its parts (cartilage, the region of the transitional fold and the lower half of the eyeball). At the same time, the presence of edema, infiltration, cicatricial changes, foreign bodies, films, discharge, color, surface (follicles, papillae, polyposis growths), mobility, translucence of the ducts of the meibomian glands, etc. are determined. For a thorough examination of the conjunctiva of the upper eyelid, it is necessary to turn it out. At the same time, the patient is asked to look down, and at this time, with the thumb of the left hand, the eyelid is pulled up so that the ciliary edge of the eyelid moves away from the eyeball. With the thumb and forefinger of the right hand, they grab it closer to the base of the eyelashes and try to raise the edge of the eyelid up, while simultaneously pressing the upper edge down with the thumb or forefinger of the left hand. With the thumb of the left hand in this position, the everted eyelid is held until the examination is completed. When examining the mucous membrane of the upper fornix, which remains invisible during normal eversion, it is necessary to additionally slightly press through the lower eyelid on the eyeball. In this case, in the region of the palpebral fissure, there is a protrusion of the upper transitional fold loosely connected with the underlying tissues. For a more thorough examination of the upper fornix, especially if foreign bodies are suspected in this section of the conjunctiva, a double eversion is performed using an eyelid lifter. The mucous membrane of the eyeball is also examined under focal illumination. Fix attention on the state of its vessels, transparency, the presence of changes (inflammation, neoplasms, cicatricial changes, pigmentation, etc.). A white or bluish sclera usually shines through the mucous membrane. With the defeat of the cornea, sclera and choroid of an inflammatory nature, the vessels located in the sclera or in the thickness of the sclera around the limbus expand. Pay attention to the condition of the limb. It can be expanded (with glaucoma), thickened (with spring catarrh), infiltrated (with trachoma). The vessels of the conjunctiva of the eyeball can enter it (with trachoma, scrofula). Especially carefully with the help of focal illumination examine the cornea. Sometimes in children with a sharp blepharospasm (squeezing of the eyelids) or edema (with gonorrhea, diphtheria), it is not possible to push the eyelids apart. In such cases, eyelid lifters must be used to examine the anterior eyeball. The child's mother or nurse tightly hugs the child, clasping his body with one hand with her hands pressed, the other head. The mother clasps the child's legs between her knees. The doctor slightly pulls the upper eyelid and carefully brings the eyelid lifter under it. If the child is very restless, then he is laid on his back, the doctor fixes the child's head between the knees, the mother holds the child's arms and legs. In this case, the hands of the doctor remain free. 3. Combined inspection For a more detailed examination of the organ of vision, a combined research method is also used. It consists in examining the illuminated place through a strong magnifying glass, with side illumination of the eye. Instead of a second loupe, you can use a binocular loupe that gives a magnification of 610 times. It is especially convenient to use this method in an outpatient setting in the absence of a slit lamp. When examining the cornea, attention is paid to its size, shape, transparency, etc. If there are changes, the freshness of inflammatory infiltrates, their shape, depth of location, and areas of ulceration are determined. Pay attention to the ingrowth of superficial and deep vessels into the cornea, smoothness, sphericity and luster of its surface. When examining the cornea, it is always necessary to examine its sensitivity. Most simply, it is determined by a piece of cotton wool with a thinned end, which, when touched to the cornea, causes a protective reflex (closing of the eyelids, withdrawal). To objectify the research, specially made hairs are used, as well as algesimetry. To detect defects in the corneal epithelium, one drop of a 1% fluorescein solution is instilled into the conjunctival sac. After several blinks, the conjunctival cavity is rinsed with saline. The paint, easily washed off from the surface of the cornea, covered with epithelium, colors the eroded areas emerald green. These areas are clearly visible when examined using a combined method. Then they examine the anterior chamber, fix attention on its depth, uniformity, transparency of moisture, the presence of blood, exudate in it, etc. When examining the iris, its color is determined (the presence of heterochromia, areas of excessive pigmentation). The radial pattern of the iris, usually depending on the state of its trabecular tissue, is well expressed in light irises. They also clearly visible pigment fringe along the edge of the pupillary area. Detect congenital and acquired defects of the iris, its fusion with the cornea (synechia anterior), anterior lens capsule (synechia posterior). Unions can be single, along the edge of the pupil, and circular (synechia circularis, seclusio pupillae). They usually occur as a result of an inflammatory process in the vascular tract. In case of damage, detachments of the iris at the root (iridodialisis), tears and ruptures of the sphincter of the pupil are observed. The study of the pupil begins with determining its shape, width, direct and friendly reaction to light. Different width of the pupils of the left and right eyes (anisocoria) is often a pathological phenomenon. The direct reaction of the pupil to light is checked by pointing a beam of light at it with a lens or an ophthalmoscope. In this case, the second eye is tightly closed with the palm of your hand. Pupillary reaction is considered alive if under the influence of light the pupil quickly and distinctly narrows, and sluggish if the pupil reaction is slow and insufficient. A change in the direct pupillary reaction may depend on a violation of the conduction of the motor descending path of the reflex or on disorders in the area of \uXNUMXb\uXNUMXbthe connection of the optical and motor paths. Examining the friendly reaction of the pupils, one eye is illuminated with an ophthalmoscope, following the reaction of the pupil of the other eye. In conclusion, the reaction of the pupils to the installation at a close distance, which takes place with the participation of accommodation and convergence, is checked. For this, the patient is asked to fix the object with his eyes, gradually approaching the eyes, and follow the reaction of the pupils, which are constricted at the same time. With the defeat of the motor pathway of the reflex, the reaction of the pupils is absent. There may be congenital changes such as displacement of the pupil (corectopia) or many pupils (policoria), and with iridodialysis, a change in the shape of the pupil. LECTURE No. 4. Methodology for examining the condition of the eye (part II) 1. Examination of the eye in transmitted light The deep media of the eye (the lens and the vitreous body) are examined in transmitted light using an ophthalmoscope. The light source (matte electric lamp with a power of 60100 W) is placed on the left and behind the patient, the doctor sits opposite. Using an ophthalmic mirror placed in front of the researcher's right eye, a beam of light is directed into the pupil of the examined eye from a distance of 2030 cm. The researcher examines the pupil through the opening of the ophthalmoscope. The rays reflected from the fundus (mainly from the choroid) cause a red glow of the pupil, which is especially clearly observed if it is dilated. In cases where the refractive media of the eye are transparent, the reflex from the fundus is uniformly red. Various obstacles in the way of the passage of the light beam, i.e., turbidity of the media, delay part of the rays reflected from the fundus of the eye. Against the background of a red pupil, these opacities are visible as dark spots of various shapes and sizes. Changes in the cornea can be easily excluded when viewed using lateral illumination. Opacities of the lens and vitreous body are differentiated quite easily. The relative depth of opacities can be determined by inviting the patient to look in different directions. Dark spots against the background of a red pupil, associated with clouding of the lens, move relative to the center of the pupil, naturally, only when the eyeball moves. Those located in the anterior layers of the lens are displaced in the direction of movement of the eye, located in the posterior sections in the opposite direction. Opacities in the anterior parts of the lens are quite clearly visible in side illumination. Vitreous changes look a little different. Most often they resemble dark strands, flakes that continue to move after stopping the gaze. With a significant change in the vitreous body due to inflammation of the vascular tract or hemorrhage, the reflex from the fundus becomes dull or absent. 2. Ophthalmoscopy The fundus of the eye is examined using the ophthalmoscopy method, which is one of the most important methods for studying the organ of vision, allowing one to judge the condition of the retina, its vessels, choroid and optic nerve. The most widely used ophthalmoscopy method is the reverse. The study is carried out in a darkened room. An ophthalmoscopic mirror is placed in front of the right eye of the researcher sitting at a distance of 4050 cm from the subject. The light source is positioned behind and to the left of the patient, as in a transmitted light examination. After obtaining a uniform glow of the pupil, the researcher places a magnifying glass (usually 13,0 diopters) 78 cm in front of the patient’s eye, resting his finger on his forehead. It is necessary to ensure that the researcher’s pupil, the mirror hole, the center of the magnifying glass and the pupil of the subject are on the same line. A true reverse image of the fundus, magnified approximately 5 times, is seen hanging in the air at a distance of about 7 cm in front of the magnifying glass. To examine a larger area of the fundus, if there are no contraindications, the patient’s pupil is first dilated with a 1% solution of homatropine or a 0,25% solution of scopolamine. Examination of the fundus begins with the most visible part of the optic nerve head. Since it is located medially from the posterior pole, during ophthalmoscopy it can be seen only when the eyeball is rotated 1215° to the nose. Against the red background of the fundus, the optic disc appears as a yellowish-pink, slightly oval formation with clear boundaries. In children under one or two years of age, the disc is often grayish. The blood supply to the nasal half is better, so its color is brighter. In the center of the disc, due to some divergence of the fibers, a whitish vascular funnel is formed (physiological excavation). The color, contours and tissue of the optic nerve head change due to inflammatory and congestive phenomena, optic nerve atrophy, damage to the choroid and many general diseases, in particular blood vessels, etc. Pay attention to the condition of the retinal vessels emerging from the middle of the optic nerve head, their caliber, color, width of the reflex strip located along the lumen of larger arteries and eyelids. The caliber of blood vessels (in a healthy child in the first months of life the ratio of the caliber of arteries and veins is 1:2, at an older age 2:3) changes both in a number of eye diseases and in many general diseases, in particular arterial hypertension, endarteritis, kidney diseases, diabetes, etc. Functionally, the most important part of the retina is the macula. It is better to examine it by first dilating the pupil. The patient must look at the ophthalmoscope mirror. During reverse ophthalmoscopy in older children, the macula appears as a dark red oval, surrounded by a shiny stripe of macular reflex, formed due to thickening of the retina along the edge of the macula. In the center of the macula, a shiny light dot is usually visible - a reflex from the central fovea, the foveal reflex. Newborns and children of the first year of life do not have macular and foveal reflexes. In the area of the macula, the retinal vessels are not visible or sometimes extend somewhat to its periphery. The periphery of the fundus up to the dentate line is examined with different directions of the patient's gaze. The pattern and color of the fundus largely depend on the pigment content in the retinal pigment epithelium of the choroid. More often, the fundus is uniformly colored red, and the vessels of the choroid are clearly visible on it. The less pigment in the fundus, the lighter it appears due to the translucency of the sclera. With age, the tone of the fundus of the eye changes from pale pink to dark red. A thorough study of changes in the fundus of the eye is carried out using direct ophthalmoscopy. To do this, they resort to using an electric ophthalmoscope equipped with its own lighting system. The refractive media of the eye of the subject (a magnification of 13-15 times is achieved) serve as a magnifying glass. The device is powered from the mains through a step-down transformer. It is more convenient to conduct an examination with a dilated pupil. Direct ophthalmoscopy allows the researcher to get as close as possible to the patient's eye (by 24 cm), until the fundus becomes visible through the opening of the ophthalmoscope. The ophthalmoscope is held so that the index finger of the researcher lies on the disk with corrective glasses. By rotating the disk, a lens is placed that gives the sharpest image of the fundus. Examination of the right eye of the patient is carried out by the right eye of the oculist, respectively, the examination of the left eye is also carried out. Direct ophthalmoscopy makes it possible to see such subtle changes, the nature of which remains unclear with reverse ophthalmoscopy. Direct ophthalmoscopy makes it possible to see such subtle changes, the nature of which remains unclear with reverse ophthalmoscopy. Due to a significant increase and the existing binocular attachment, it is possible to use it for stereoscopic examination of the fundus, which is especially necessary when differentiating subtle changes in the optic nerve head. To examine the fundus, an ophthalmochromoscope is used, which allows one to examine the fundus in light of different spectral compositions (red, yellow-green, purple, etc.). A polarizing photo-ophthalmoscope makes it possible to examine and photograph the fundus of the eye in polarized light. Registration of changes can be carried out by a photographic camera and an ophthalmic (retino) photo. 3. Biomicroscopy For a detailed study of the transparent structures of the eye and its membranes, the biomicroscopy method is used. It consists in using a narrow, sharply limited homogeneous beam of light, the focus of which can be placed at different depths and in different parts of the eye. Such a beam of light allows you to create a pronounced contrast between the illuminated and unlit areas of the eye, to obtain a thin section of its transparent tissues. The study of the obtained sections is carried out using a binocular microscope. For biomicroscopy, a slit lamp is used, in which a special freely moving illuminator is mounted on a common axis of rotation with the microscope. This device allows you to consider very minor changes in the cornea, lens, vitreous body, in the fundus. Due to the fact that the light beam crosses the transparent tissues from front to back at different angles, it is easy to determine the depth of the changes and their nature. For example, biomicroscopy of the cornea clearly shows even point defects in its epithelium, especially after staining with fluorescein, it is easier to judge the depth of the location of opacities, infiltrates, foreign bodies, we can confidently talk about the superficial or deep nature of vascularization. With the help of a slit lamp, you can see gentle changes in the endothelium of the cornea, its edema, precipitates, consider a suspension of blood cells in the moisture of the anterior chamber, the appearance of the vitreous body (hernia) in it after injury, surgery. No less valuable data is obtained when examining the iris under a microscope. In cases of pathology, it can be seen dilated and newly formed vessels, areas of atrophy, the appearance of tubercles, posterior synechia, etc. The role of biomicroscopy in studying the state of the lens and vitreous body is invaluable. It allows you to determine the severity, localization of lens opacities, to judge the degree of maturity of the cataract, its origin, the state of the capsule. When examining the vitreous body, they judge the nature of the changes in it, the type of destructive disturbances, etc. This method provides great opportunities for studying pathological changes in the retina, choroid, and optic nerve. For example, subtle changes in the macular area in some types of degeneration can only be seen with a slit lamp. At the same time, studies in redless light and in light of various intensities are expedient. Biomicroscopy of the eye in young children is possible only with the help of a manual slit lamp, and sometimes only during drug-induced deep sleep or under anesthesia. LECTURE No. 5. Methodology for examining the condition of the eye (part III) 1. Gonioscopy Gonioscopy (from Latin gonia "angle") is a special method for examining the angle of the anterior chamber. It can only be carried out with the help of optical gonioscopes. The study of the chamber angle is of great importance for the diagnosis, therapy and prognosis of a number of diseases (glaucoma, uveitis, injuries, etc.). The most important outflow pathway for intraocular fluid begins at the camera angle. The angle can be narrowed, obliterated, foreign bodies, a germinating tumor can be found in it. A gonioscope is a tetrahedral glass prism or pyramid with mirrored inner surfaces. The front part of the device is intended for contact with the cornea and has a corresponding curvature. A reflecting mirror stands in the path of the rays emerging from the chamber angle in such a way that the opposite angle is visible in it. Before the examination, drip anesthesia of the eye is performed with a 0,5% solution of dicaine or a 1% solution of lidocaine. The subject is seated in front of a slit lamp and his head is fixed on a facial rig. The combined focuses of the illuminator and microscope are aimed at the cornea. The gonioscope is inserted into the conjunctival cavity, the researcher holds its body with his left hand. An approximate examination of the angle is usually carried out in diffuse light; for long-term gonioscopy, a slit diaphragm is used. In the corner of the anterior chamber one can see Schlemm's canal, corneoscleral trabeculae, and ciliary body. 2. Tonometry This is a method for measuring intraocular pressure. The study is necessary in all cases when the thought arises that a patient has glaucoma, secondary hypertension of the eye or its hypotension, with various general and local diseases. Approximate pressure in the eye can be determined by palpation. In this case, it is necessary that the patient looks down, and the researcher, with index fingers located above the level of the cartilage, presses in turn through the upper eyelid (when looking up through the lower) on the eyeball (similar to the study of abscess fluctuation). When analyzing pressure, it is necessary to compare its value in one and the other eye. If the ophthalmotonus is within the normal range, it is designated as TN if its value is 2835 mm Hg. Art. T + 1, more than 36 mm T + 2, if hypotension of the order of 1522 mm Hg is detected. Art. T 1, less than 12 mm Hg. Art. T 2. For the quantitative determination of ophthalmotonus in Russia, the Maklakov tonometer is most widely used. It is a cylinder weighing 10 g with a base made of matte porcelain plates. Before measuring intraocular pressure, the plates are wiped with cotton wool moistened with alcohol and smeared with a thin layer of paint (collargol, methylene blue). Intraocular pressure is measured in a horizontal position, asking the patient to look at the ceiling or his own finger. The cylinder, held by a special holder, is placed on the center of the cornea, previously anesthetized with a 0,5% solution of dicaine (or 1% solution of lidocaine) (35 minutes after anesthesia). By lowering the holder to approximately 1/3 of the cylinder (in one touch), the weight is allowed to flatten the cornea. The imprint of the flattening circle obtained on the plate is printed on paper slightly moistened with alcohol. Using a special ruler, the diameter of the circle is used to determine the intraocular pressure in millimeters of mercury. The numbers of tonometric pressure (1116 mm Hg) are always higher than the true ones (1826 mm Hg), since the tonometer increases the intraocular pressure at the time of measurement. There are other types of tonometers (for example, Dashevsky), indicators of intraocular pressure during mass examinations. Using tonometers of different weights (5; 7,5; 10 and 15 g) in ascending order, it is possible to determine the reaction of the eye membranes to different weights. The results of these four measurements can be represented as an ascending elastotonometric curve. 3. Tonography This is a method for studying the hydrodynamics of the eye. It allows you to determine the state of the outflow of intraocular fluid and is used mainly in the examination of patients with glaucoma or if it is suspected. During tonography, the tonometer is placed on the cornea of the examined eye and kept on it for 35 minutes. As a result of compression, an increase in ophthalmotonus occurs, the outflow of fluid from the eye increases, which leads to a gradual decrease in intraocular pressure. The degree of reduction is different in healthy individuals and in patients with glaucoma, which is reflected in the nature of the tonographic curve. Graphic registration of changes in ophthalmotonus becomes possible due to the connection of a recording device. The data is recorded on a moving paper tape. The degree of reduction in intraocular pressure during tonography depends on the volume of aqueous humor displaced from the eye, which in turn is associated with the state of the outflow tract. According to the obtained data, using special tables and formulas, it is possible to determine the outflow ease coefficient, which quantitatively characterizes the function of the drainage system of the eye. The outflow easiness coefficient is an important indicator in the diagnosis of glaucoma. A decrease in its value, even with a normal level of ophthalmotonus, may indicate the presence of glaucoma. Tonographic studies are useful for monitoring the effectiveness of medical and surgical treatment of glaucoma. 4. Echoophthalography To study the optical system of the eye, to measure the anteroposterior and other dimensions, the method of ultrasonic echo-ophthalography is used. It consists in the registration of ultrasonic signals reflected from the interfaces between the media and tissues of the eye with different acoustic properties. Research is carried out using a diagnostic echoophthalograph device. Before the examination, 0,25% dicaine or 1% lidocaine and sterile petroleum jelly are instilled into the eye, serving as a contact medium between the eye and the device sensor. The sensor is first placed on the cornea. When in contact with the sclera, it is sequentially placed on various meridians, thereby achieving ultrasound probing of all parts of the eyeball. Reflected ultrasonic vibrations are recorded on the screen in the form of echo signals. With corneal abduction, the anterior wave is determined on the echogram, corresponding to the reflection of ultrasound from the cornea, the second and third waves correspond to reflections from the anterior and posterior surfaces of the lens. The vitreous body is acoustically homogeneous and does not show teeth on the echogram. The posterior complex of teeth corresponds to the reflection of ultrasound from the fundus and retrobulbar tissues. Ultrasound examination is also used to detect foreign bodies in the eye, for the purpose of diagnosing retinal detachments, tumors, etc., especially in cases where examination of the fundus is impossible due to clouding of the transparent media. 5. Exophthalmometry If a patient has exophthalmos or enophthalmos (protrusion or retraction of the eyeball), special devices are used to quantify them and judge the dynamics of the process (orbital tumors, retrobulbar hematoma, orbital bone fractures, etc.). The most common mirror exophthalmometer. It consists of two frames moving along the rod on a sled. The latter are equipped with mirrors intersecting and placed at an angle of 45° to the visual axis of the eye and with a millimeter scale. There are recesses on the edges of the frames, which, during the study, are attached to the outer walls of the orbit of a sick child. The patient should look straight ahead. The top of the cornea is reflected in the mirror of the exophthalmometer; on the millimeter scale of the ruler, one can see the distance between the center of the cornea and the edge of the orbit. This figure indicates the protrusion of the eye. The degree of protrusion of each eye is alternately determined. LECTURE No. 6. Diagnosis, clinic and treatment of inflammatory diseases of the eyelids Signs of diseases of the eyelids are very characteristic. Patients are often concerned about itching and burning in the eyelids, eye fatigue, and there may be a change in the shape and size of the palpebral fissure, the position of the ciliary edge of the eyelids, etc. The pathology of the eyelids, unlike diseases of the eyeball, is quite easy to determine already with an external examination. A sharp swelling and hyperemia of the eyelids may indicate the presence of gonoblenorrhea (in children), diphtheria, as well as an abscess of the eyelids, acute meibomitis, barley. Edema, especially in the outer part of the upper eyelid, is noted in cases of inflammation of the lacrimal gland. Pronounced "cold" edema can be with allergic conditions. When examining the edge of the eyelids, attention is paid to the features of eyelash growth, the presence of skin changes at their base, the condition of the excretory ducts of the meibomian glands. To clarify the diagnosis, carefully examine the eyelids and their position under side lighting and palpation. During the examination, attention is paid to the presence of skin lesions, which can be the entrance gate for infection. 1. Abscess of the century (abscessus palpebrae) On examination, hyperemia of the skin of the eyelids is determined, palpation reveals induration (edema, infiltration) and tissue tension, their soreness. In addition, the anterior lymph nodes may be enlarged and painful. If, along with all these signs, there is local softening and fluctuation, then it is advisable to open the abscess (incision). In the absence of fluctuations, the administration of antibiotics in the form of injections around the abscess and oral administration of antibiotics or sulfonamides and UHF therapy are indicated. 2. Meybomite (meibomitis, hordeolum internum) If, when examining a patient, there is limited infiltration in the eyelid area, the eyelid is painful on palpation, and when everted through the conjunctiva, a translucent yellowish focus in the cartilage is visible, then the diagnosis of meibomitis is undoubted acute purulent inflammation of the meibomian gland. Severely leaking meibomitis can lead to the formation of an extensive abscess of the eyelid. Treatment. Warming procedures, UHF therapy, disinfectants. 3. Chalazion This is a tumor-like, limited, somewhat protruding formation, dense to the touch, painful, soldered to the cartilage. It usually occurs after acute inflammation of the eyelid (meibomitis) and in some cases gradually increases. Treatment of chalazion (hailstones) consists in absorbable drug therapy. However, most often it is ineffective, and then surgical removal of the hailstone in the capsule through an incision in the conjunctiva of the eyelid and cartilage is indicated, followed by treatment of the chalazion bed with an iodine solution. 4. Barley (hordeolum) Barley is a purulent inflammation of the hair follicle or sebaceous gland of the edge of the eyelid, located at the root of the eyelash. The causative agent is most often a representative of the pyogenic flora, mainly staphylococcus aureus. Infection is facilitated by blockage of the excretory duct of the gland with a secret, as well as a decrease in the overall resistance of the body and diabetes mellitus. Clinical picture and diagnosis. It is characterized by the appearance of a circumscribed and sharply painful swelling near the edge of the eyelid, which is accompanied by swelling and redness of its skin and (often) the conjunctiva. The inflammatory formation grows quite quickly, and after two to four days it undergoes purulent melting, which can be determined by the appearance of a yellow head at the top of the stye. On the third or fourth day, its contents (pus, dead tissue) break out, after which the pain immediately decreases and the inflammation subsides. Swelling and redness of the skin disappear around the end of the week. In some cases, the inflammatory formation consists of several closely spaced or merged heads. In such cases, barley can occur against the background of intoxication, high temperature, and regional lymphadenitis. A similar clinical picture is observed in acute purulent inflammation of the meibomian gland, meibomitis, however, the breakthrough of pus usually occurs from the side of the conjunctiva and cartilage, after which granulations (connective tissue) often grow. In persons with reduced body resistance, barley is prone to recurrence and is often combined with furunculosis. Complications of stye can occur due to orbital phlegmon, thrombophlebitis of the orbital veins, purulent meningitis, which is most often associated with attempts to squeeze pus out of it. When examining the eyelids, their hyperemia, swelling, density and pain are revealed, i.e. the picture resembles a limited abscess or acute meibomitis. However, upon closer examination, the inflammatory focus is determined in a limited area of the ciliary edge of the eyelid in the form of swelling and hyperemia at the root of the eyelash. Usually after three to four days the inflammatory focus suppurates and opens. Treatment. Dry heat and UHF are applied locally. A 23% solution of albucid, a 20% solution of erythromycin, and a 1% solution of dexamethasone are instilled into the conjunctival sac 0,1 times a day. The area of infiltration (inflammation) on the skin of the eyelid is lubricated with a 1% alcohol solution of brilliant green. After opening the stye, 2% albucidal ointment (sodium sulfacyl), 20% syntomycin emulsion, 1% tetracycline ointment, 1% hydrocortisone emulsion, 1% yellow mercury ointment are applied to the eyelids 1 times a day. If the disease is accompanied by symptoms of intoxication, sulfanilamide preparations are administered orally 1 g 4 times a day or tetracycline antibiotics (biomycin 100 IU 000 times a day, tetracycline or terramycin 46 g 0,25 times a day). With recurrent barley, the patient is shown a thorough examination (determination of the immune status, glycemia, glucose tolerance, etc.) to identify the cause of the disease. Assign courses of antibiotic therapy, vitamin therapy, sometimes repeated transfusions of canned blood and autohemotherapy (transfusion of one's own blood). 5. Toxicoderma (toxicodermia) eyelid In the practice of a pediatrician, there are often cases of drug intolerance. It must be remembered that this intolerance can occur after topical atropine, quinine, antibiotics and other drugs. At the same time, children go to the doctor with reddening of the skin of the eyelids, vesicles on the eyelids, erosions at the site of the former vesicles, as well as with conjunctivitis. This pathological condition is called eyelid toxicoderma. Treatment. Cancellation of drugs that can cause the disease, and the appointment of desensitizing agents (calcium chloride, diphenhydramine). 6. Eyelid herpes Sometimes, after an infection, a cold, edematous eyelids are observed with the presence of transparent vesicles or crusts that appear after the vesicles dry. The process is accompanied by severe itching and local pain. This is most likely a simple herpes of the eyelids, caused by a filterable virus (herpes symplex). In some cases, on the skin, more often than the upper eyelid, as with herpes simplex, vesicles of large sizes and in greater numbers are found. The transparent contents of the vesicles may become cloudy, become purulent, crusts, ulcers may form. The process is accompanied by severe local and headaches. This is herpes zoster. The basis of the disease is the defeat of the trigeminal nerve, often its first branch. Treatment. Analgesics, B vitamins, brilliant green moxibustions. 7. Vaccine eyelid pustules An external examination reveals cyanotic edges of the eyelids, pustules (cloudy vesicles) and sores with a greasy coating on the skin. The eyelids are painful on palpation, the anterior lymph nodes are enlarged and painful. Most often, from the anamnesis of these patients, it is revealed that they have had chicken pox or they have been vaccinated against smallpox. Treatment is symptomatic. 8. Infectious mollusk (molluscum contagiosum) On the eyelids of children, single and multiple yellowish nodules of various sizes and with a depression in the center are found. This is a typical picture of an infectious mollusk. Its causative agent is a filterable virus. Due to the significant contagiousness of the disease, treatment consists in removing the nodules and treating the bed with iodine (Lugol's solution). 9. Scaly blepharitis (blepharitis squamosa) If the patient complains of itching in the eyelids, eye fatigue, and on examination it is found that the edges of the eyelids are hyperemic, thickened, small grayish scales or yellowish crusts (a frozen secret of the sebaceous glands) are visible at the base of the eyelashes, then this makes it possible to suspect scaly blepharitis. 10. Ulcerative blepharitis (blepharitis ulcerosa) In cases where the edges of the eyelids are sharply hyperemic, thickened, covered with ulcers and yellowish crusts, after which the surface bleeds, one should speak of ulcerative blepharitis. At the same time, hair follicles and sebaceous glands are involved in the process. As a result, scars remain, eyelashes fall out (madarosis), often begin to grow incorrectly. Uncorrected refractive errors, anemia, beriberi, helminthic invasions, diabetes, diseases of the teeth, tonsils, etc. predispose to the occurrence of blepharitis. Treatment of blepharitis is aimed at eliminating its possible cause. In addition, general strengthening agents are prescribed. The edges of the eyelids are degreased with 70% alcohol, treated with disinfectant solutions: calendula, 1% solution of brilliant green, and then lubricated with 1% synthomycin emulsion, 10% sulfacyl ointment, etc. Before starting treatment for ulcerative blepharitis, hair removal must be performed eyelashes 11. Trichiasis Occasionally (especially in children), when examining the intermarginal space, it is possible to detect abnormal growth of trichiasis eyelashes. Separate eyelashes face the eye, irritate the conjunctiva and cornea, causing tearing, pain, contributing to the development of corneal ulcers. Partial trichiasis in children may be due to scarring after ulcerative blepharitis, frequent styes. Treatment. Diathermocoagulation of eyelash bulbs with a needle electrode; with gross changes, plastic surgery is indicated. LECTURE No. 7. Congenital pathologies and neoplasms of the eyelids 1. Ankyloblepharon (ankyloblepharon) When examining newborns, congenital fusion of the eyelids in the form of dense scars or thin bridges is extremely rare. This congenital pathology is called ankyloblepharon and occurs as a result of a violation of the reverse development of eyelid fusion in the fetus in the seventh month of pregnancy. Treatment. Immediate dissection of adhesions and plastic. 2. Eyelid coloboma (coloboma palpebrae) Occasionally, along the edge of the eyelid, more often than the upper one, a congenital defect of various sizes is found in the form of a triangle with the base down (this is the so-called coloboma). Treatment. Plastic replacement of the defect with a free graft or a pedicled flap. 3. Epicanthus (epicanthus) Some children have a wide nose bridge due to the presence of semilunar skin folds located on both sides of the back of the nose and covering the inner canthus of the eye. This congenital anomaly is called the epicanthus. Epicanthus is often combined with ptosis, strabismus. Treatment is operative. 4. Inversion of the eyelids (entropium palpebrarum) Inversion of the eyelid (entropion) is an incorrect position of the eyelid, in which its edge with growing eyelashes is partially or all over turned towards the eyeball. Distinguish torsion of the century cicatricial, spastic and senile. Etiology and pathogenesis. With cicatricial inversion of the eyelid, etiological factors are trachoma and other conjunctival processes leading to the development of scars in the conjunctiva, as well as chemical and thermal burns of the conjunctiva. Cicatricial shortening of the conjunctiva and curvature of the cartilage tighten the edge of the eyelid and deflect it towards the eye. The occurrence of spastic entropion occurs due to spastic contraction of the age-old part of the orbicularis oculi muscle. Chronic inflammatory processes in the conjunctiva, causing irritation of the orbicularis oculi muscle, lead to its convulsive contraction, as a result of which the cartilage of the eyelid can rotate around its length towards the eye. Age volvulus senile occurs in old age due to age-related changes. Age-related accumulation of orbital fat and loss of skin elasticity lead to the fact that the eyelid (usually the lower one), without meeting support from the side of the eye, easily turns inward not only with convulsive, but also with simple closure of the palpebral fissure. The clinical picture. 1. Cicatricial inversion of the eyelid. The eyelid is trough-like curved convexity forward. The posterior edge of the edge of the eyelid is rounded, the entire edge of the eyelid and its skin surface are turned towards the eye, the eyelashes injure the eyeball, causing severe irritation. The disease develops slowly, gradually progressing. Friction of the eyelashes and thickening of the rim of the eyelid contribute to the formation of corneal infiltrates and ulcers. The same long course is observed with cicatricial volvulus caused by burns of the conjunctiva, since the volvulus of the eyelid leads to chronic irritation of the mucous membrane, and then to its inflammatory infiltration. A similar picture is given by trichiasis (a congenital anomaly in the location of the eyelashes). With trachoma, twists are often noted in combination with trichiasis (eyelash growths are directed in different directions). 2. Spastic inversion of the century. The edge of the eyelid with eyelashes and the skin surface of the eyelid are turned towards the eye and irritate it. The absence of scars on the conjunctiva distinguishes this form from cicatricial inversion, and the presence of spasm from senile. 3. Inversion of the eyelid senile. The edge of the eyelid with eyelashes and the skin surface of the eyelid are turned towards the eye and cause irritation. The course is long, chronic, with a tendency to constant progression. Treatment. With cicatricial inversion, treatment is surgical. Prevention is reduced to the treatment of the underlying disease. With spastic volvulus, therapy is reduced to treating the underlying disease and placing disinfectant ointments and drops in the conjunctival sac. Stubborn torsion is often eliminated by simple transection of the outer commissure of the eyelids. With severe irritation that cannot be treated, surgical intervention is performed. In case of accidental twisting, sometimes it is enough to put the eyelid in the correct position and fix it in this position with narrow strips of adhesive tape. Astringents and zinc drops must be injected into the conjunctival sac. With persistent torsion, an operation is indicated. 5. Eversion of the eyelids (ectropium palpebrarum) This is a condition opposite to inversion, i.e., characterized by the distance of the eyelid from the eye and accompanied by lacrimation due to eversion of the lower lacrimal opening. It is often observed due to cicatricial changes after burns and other injuries of the eyelids. Treatment. plastic surgery. 6. Lagophthalmos, or "hare's eye" (lagophthalmus paralyticus) If, when the eyelids close, they partially cover the eyeball, then in the absence of changes in the eyelids, this may indicate the presence of paresis or paralysis of the facial nerve that innervates the circular muscle of the eyelids. Lagophthalmos appears as a result of otitis, purulent mastoiditis and some infectious diseases. The danger of this lesion lies in the fact that the eye, especially at night, remains open. The cornea in the lower segment undergoes drying, becomes cloudy. Treatment. Ointment dressings, temporary stitching of the eyelids in the event of keratitis, plastic surgery. 7. Dermoid cyst In the internal or external adhesion of the eyelids in children, a small neoplasm of a rounded shape is found. It is of an elastic consistency, sometimes dense, not soldered to the skin, but often connected to the periosteum, does not decrease during compression, painless. This is a dermoid cyst of the orbit. It arises from the detached parts of the ectoderm and is located mainly in the area of \uXNUMXb\uXNUMXbbone sutures. Increases in size slowly. Treatment. Surgical removal of the cyst along with the capsule. 8. Eyelid hemangioma Often in children in the first days after birth, a tumor with a reddish or bluish tinge is found on the eyelids. This is a hemangioma. Its shape can be different: capillary, cavernous, recemous, etc. With capillary hemangioma, a flat dark red spot is determined on the eyelid, consisting of dilated superficial vessels. Cavernous hemangioma is more massive, often grows into the thickness of the eyelid, leads to more gross external changes. Hemangiomas have a tendency to rapid expansive growth. Treatment. Rapid surgical removal of hemangioma often with simultaneous skin plasty. Depending on the shape and size of the hemangioma, cryotherapy, sclerotherapy (administration of alcohol, quinineurethane, etc.) and radiotherapy are also indicated. 9. Neurofibromatosis (Recklinghausen's disease) In this systemic disease, there is often a plexiform neurofibroma of the upper eyelid in the form of a diffuse tumor. In the thickness of the eyelid, dense strands along the cutaneous nerves are felt. Persistent symptoms of neurofibromatosis are café-au-lait patches on skin. If, along with the eyelids, neurofibromatosis affects the ciliary nerves, then various changes in the eyes are possible, hydrophthalmos is often observed in children. Treatment of plexiform neurofibroma of the eyelids consists in excision of tumor-like tissues, which, however, does not prevent recurrence and progression of the process. LECTURE No. 8. Diagnosis, clinic and treatment of pathologies of the lacrimal organs 1. General diagnostic questions With the pathology of the lacrimal gland, there may be increased tearing or, conversely, dry eyes. However, pain and size change are more often determined. There are dacryadenitis in the form of sharp inflammatory changes in the eyelids and conjunctiva or cysts of the lacrimal gland, resembling translucent tumors of various sizes. Palpation of the lacrimal gland area is performed through the skin of the upper eyelid, while determining its consistency, size and location. More often, changes are noted in the lacrimal ducts. The study of their condition begins with an examination of the lower lacrimal opening. It usually faces the eyeball and becomes visible if you bend the lower eyelid slightly. Atresia of the lacrimal openings, their dislocation, and narrowing may be detected, which is accompanied by impaired absorption of tears and the appearance of lacrimation. In old age, inversion of the lacrimal punctum is often observed. If there are no changes in the lacrimal opening, then lacrimation may be due to pathology of the lacrimal canaliculi or other parts of the lacrimal ducts. To determine the state of the main function of the lacrimal ducts (the passage of tears through the lacrimal canaliculi and its discharge into the nose), a color test is used. The tubular test is carried out as follows. Drops of a 3% solution of collargol are instilled twice into the conjunctival sac. The patient is asked to make blinking movements. With normal patency of the lacrimal canaliculi and unchanged suction function of the lacrimal sac, the conjunctival cavity is freed from collargol within 30 seconds. Such a tubular test is regarded as positive. But in some cases it may be significantly delayed or become negative. After 23 minutes, if the patency of the nasolacrimal canal is not impaired, collargol appears in the nose, and it can be detected by inserting a cotton swab on a probe under the inferior turbinate. If the collarhead test is delayed or negative, it is necessary to rinse the lacrimal ducts with saline solution. Passing a blunt needle or conical probe into the lacrimal sac before washing it also serves as a diagnostic technique, as it allows one to judge the presence of narrowing of the tubule or obstacles in it. Rinsing is carried out after instillation of a 0,5% solution of dicaine (1% lidocaine) into the conjunctival cavity. With good patency of the lacrimal ducts, liquid flows out of the nose in frequent drops or streams. If there is obstruction, it flows back past the cannula or through the superior lacrimal opening. 2. Acute dacryoadenitis (dacryoadenitis acuta) Dacryoadenitis inflammation of the lacrimal gland. It can be both acute and chronic. It occurs mainly due to endogenous infection with measles, scarlet fever, mumps, typhoid fever, rheumatism, tonsillitis, influenza. The process is often one-sided. If there is edema in the lateral part of the upper eyelid, according to the localization of the lacrimal gland, and the upper eyelid acquires an S-shape, palpation in this area is marked by induration and soreness, when the eyelid is raised, an enlarged palpebral part of the lacrimal gland is visible, swelling of the mucous membrane of the eyeball (chemosis) is noted, sometimes yellowish areas of suppuration of the gland or opened abscesses from the side of the conjunctiva are visible, purulent contents are released into the conjunctival cavity, and the mobility of the eye upwards and outwards is limited, regional lymph nodes are enlarged and painful, this indicates dacryoadenitis. It can occur in children after infectious diseases (mumps, etc.). clinical picture. Sharp swelling, soreness, redness of the outer part of the upper eyelid. The palpebral fissure takes on an altered shape. There is redness and swelling of the conjunctiva of the eyeball in the upper outer section. Downward and inward displacement of the eye and limitation of its mobility can be observed. The anterior regional lymph nodes are enlarged and painful. However, more often the disease proceeds benignly, the infiltrate undergoes regression by the tenth and fifteenth day. Treatment. The goal of treatment is to combat the general disease. In case of an acute process, antibiotics (ampicillin, oletethrin, metacycline in four doses), sulfonamides, and symptomatic drugs are prescribed. Physiotherapy with dry heat, UHF, UV irradiation, iodine electrophoresis, washing of the conjunctival cavity with furatsilin at a dilution of 1: 5000, ointments with sulfonamides and antibiotics (for example, 1% tetracycline ointment) are indicated locally. 3. Canaliculitis (canaliculitis) With canaliculitis, there is a slight swelling in the area corresponding to the lacrimal openings and tubules. In addition, hyperemia of the skin, lacrimation and purulent discharge are revealed, and when pressing on this swelling with a finger or a glass rod, a mucous or purulent plug is released from the lacrimal opening. In some cases, the squeezed out contents of the tubule is a crumbly yellowish secret containing grains of fungal calculus. It is necessary to subject the discharge to bacteriological examination. Treatment. Antibiotics and sulfonamides are used locally; sometimes dissection of the affected tubule is used, scraping out the contents with a sharp spoon, followed by treatment of the cavity with a 12% solution of lapis, iodine tincture. 4. Dacryocystitis (dacryocystitis) Dacryocystitis inflammation of the lacrimal sac. It occurs in acute and chronic form. When examining children in the first weeks of life, a slight lacrimation and lacrimation are sometimes detected, and in some cases a purulent discharge is detected. If, moreover, when pressing on the area of the lacrimal sac, the mucous or purulent contents of the sac are released from the lacrimal puncta into the conjunctival cavity, then the diagnosis of neonatal dacryocystitis becomes obvious. If dacryocystitis exists for a long time, then a strong stretching (dropsy) of the lacrimal sac occurs, swelling is observed, a significant protrusion of tissues in the area of the lacrimal sac. Often, dacryocystitis is complicated by the development of phlegmon of the lacrimal sac. At the same time, pronounced swelling and a sharp painful infiltration of surrounding tissues appear. The palpebral fissure may close completely. Etiology and pathogenesis. The development of chronic dacryocystitis occurs due to stenosis of the nasolacrimal duct, leading to stagnation of tears and discharge from the mucous membrane of the lacrimal sac. There is a gradual stretching of the wall of the bag. The contents that accumulate in it are a favorable environment for the development of pathogenic microflora (streptococcus, pneumococcus, etc.). Conditions are created for the progression of a sluggish inflammatory process. The transparent secretion of the lacrimal sac cavity becomes mucopurulent. The most common damage to lacrimal openings and canaliculi is caused by eyelid injuries. Clinical picture and diagnosis. Complaints of persistent lacrimation, purulent discharge from the eye. There is an excess of tears along the edge of the lower eyelid, a soft protrusion of the skin at the inner edge of the eye. When pressing on the area of the lacrimal sac, mucous or mucopurulent contents flow out abundantly from the lacrimal openings. The lacrimal sac can be stretched so much that the grayish contents can be seen through the thinned skin. This condition is called hydrocele of the lacrimal sac. For diagnosis, biomicroscopy, tubular and nasal samples are used. In case of insufficient clarity of the test results, washing and bougienage of the lacrimal ducts are done, which makes it possible to clarify the level and extent of the lesion. Subsequently, a contrast x-ray of the lacrimal ducts is performed. Treatment. Chronic dacryocystitis is treated only surgically. A dacryocystorhinostomy is necessary to create a direct fistula between the lacrimal sac and the nasal cavity. 5. Dacryocystitis of newborns A complex of factors plays a role in the etiology and pathogenesis of dacryocystitis in children: anatomical and topographical features of the lacrimal ducts, nasal pathology, and impaired nasal breathing. Dacryocystitis is often caused by obstruction of the nasolacrimal duct due to changes in the lacrimal sac, bones or nasal mucosa. Clinical picture, treatment. Mucopurulent discharge, lacrimation, redness of the conjunctiva, swelling in the area of the lacrimal sac. A sign of the disease is the release of mucopurulent contents through the lacrimal openings when pressing on the area of the lacrimal sac. Treatment of dacryocystitis in newborns, even if they have not caused abscesses or cellulitis in the past, consists of acupressure of the lacrimal sac area, followed by washing it with a disinfectant solution containing lidase. However, usually these manipulations do not lead to a cure. Probing should be performed in the first month of the child's life. It is also indicated in children under the age of two or three years, if for some reason it was not carried out earlier. For chronic dacryocystitis in children three years of age and older, if probing does not restore the patency of the nasolacrimal ducts, dacryocystorhinostomy is indicated. It consists of creating an anastomosis between the lacrimal sac and the middle meatus. Before surgery, an X-ray examination of the lacrimal ducts is required. Bismuth nitrate or iodolipol (more often) is used as a contrast agent, injected into the lacrimal sac using a cannula needle. Treatment is carried out in stages and sequentially: 1) massage of the lacrimal sac every two to three weeks; 2) washing the lacrimal ducts in one to two weeks; 3) retrograde probing of the nasolacrimal duct for up to two to three weeks; 4) probing of the nasolacrimal ducts from above for up to two to three weeks; 5) endonasal dacryocystorhinostomy from two to three years. LECTURE No. 9. Diagnosis, clinic and treatment of pathologies of the orbit The main symptom of most diseases of the orbit, both inflammatory and non-inflammatory, is exophthalmos, along with which other symptoms can be noted. The eyeball, depending on the localization of the process in the orbit, can be displaced in one direction or another, its mobility can be limited, diplopia occurs. Sometimes there are changes in the condition of the edges and walls of the orbit. In the presence of dense tissue in the retrobulbar space, the reposition of the eyeball is difficult. In inflammatory diseases of the orbit, eyelids are often involved in the process, possibly a serious general condition of the patient. 1. Phlegmon of the orbit (Phlegmona orbitae) In children of any age, but more often in the first year of life and at school age, among full health, eyelid edema suddenly and quickly appears, sometimes significant, chemosis is possible. Exophthalmos develops rapidly, but there may also be a shift of the eyeball to the side (with ethmoiditis, periostitis). The mobility of the eyeball, as a rule, is limited due to a mechanical obstacle, damage to the muscles and motor nerves. There is a severe general condition, high fever, headaches and pain in the orbit. In infants, general symptoms of the disease often prevail over local ones. In children of the first months of life, except for exophthalmos, it is not possible to identify other signs of the disease. A carefully collected history, consultations of an otolaryngologist, a dentist, and radiography of the paranasal sinuses contribute to the establishment of its cause. In infants, orbital phlegmon is more often associated with inflammatory processes in the upper jaw, umbilical sepsis and dacryocystitis, in schoolchildren with orbital injuries and sinusitis. Treatment. Loading doses of broad-spectrum antibiotics intramuscularly, periorbitally and retrobulbarno. If necessary, the cells of the ethmoid labyrinth are opened, the maxillary sinus is punctured. At the same time, the phlegmon of the orbit is opened with drainage of the wound cavity with turunda soaked in antibiotics. 2. Sarcoma of the orbit On examination, the patient is found to have exophthalmos, displacement of the eyeball, limitation of its mobility, diplopia, a painless tumor-like elastic formation, sometimes soldered to the underlying tissues and skin, is palpated. More often the tumor is localized in the upper half of the orbit. The diagnosis becomes even more likely when indicating the rapid growth (weeks and months) of the tumor. Orbital sarcoma should be differentiated from eosinophilic granuloma, tumor-like forms of leukemia. To clarify the diagnosis, additional research methods are needed: radiography of the orbits, sternal puncture (study of the myelogram), often puncture biopsy. Treatment consists of orbital exenteration followed by x-ray and chemotherapy. 3. Lymphomas of the orbit In some types of leukemia (hemocytoblastosis, etc.), tumor-like infiltration nodes appear on the upper or, less commonly, lower edge of the orbit, developing from the hematopoietic tissue of the flat bones of the orbit. Exophthalmos, displacement of the eyeball are noted. The process is often two-way. To clarify the diagnosis, blood tests and a myelogram are necessary. Treatment is carried out in the hematology department. With the appointment of cytostatic agents, infiltrates may disappear without a trace. LECTURE No. 10. Diagnosis, clinic and treatment of diseases of the conjunctiva 1. General Provisions The most common pathology of the conjunctiva is its inflammation conjunctivitis. Detection in a patient of such signs as swelling and redness of the eyelids and conjunctiva, photophobia, tear or suppuration and blepharospasm, combined with an indication of gluing of the eyelids in the morning and after sleep, pain in the eyes, often help to diagnose conjunctivitis. For the purposes of the etiological and differential diagnosis of conjunctivitis, it is always necessary to pay attention to the intensity of hyperemia, the nature of the follicles or papillae, hemorrhages, films, the color, quantity and consistency of the discharge, changes in the regional lymph nodes (increase and soreness), the presence of headache, high temperature, general ailments, etc. Pronounced lacrimation with photophobia and blepharospasm may indicate involvement of the cornea. To make a diagnosis, it is important to find out how the disease began, how long it lasted, and what the previous treatment was. It is necessary to clarify the general condition of the patient’s body preceding this eye disease, contacts, the presence of the disease in areas adjacent to the eye (mumps, rhinitis, stomatitis, etc.). It must be remembered that the annual development of conjunctivitis during the flowering period of poplar and various flowers, as well as after eating certain berries, citrus fruits, pineapples and other fruits, may indicate the allergic nature of the inflammatory process. Only a clear understanding of the symptoms that are pathognomonic of certain types of conjunctivitis makes it possible to make a correct etiological diagnosis, and, therefore, to promptly resolve the issue of the place, method and duration of treatment, methods and means of prevention, etc. Thus, it is known that pronounced swelling and hyperemia of the eyelids occur with adenoviral conjunctivitis and gonoblenorrhea. Cyanosis and thickening of the eyelids are observed in the initial period of conjunctival diphtheria. The tear-stained appearance of a child in the first ten days of life often accompanies tear pneumococcal conjunctivitis. In young children with epidemic Koch-Wicks conjunctivitis (as a rule) and with adenoviral epidemic keratoconjunctivitis (in most cases), there is an increase in the preauricular and submandibular lymph nodes. Copious, watery, meat-slop-colored or purulent discharge of yellow-green color and creamy consistency, appearing two to three days after birth, is characteristic of the gonococcal process. For conjunctivitis caused by Koch-Wicks bacillus and pneumococcus, purulent discharge is specific in the area of the canthus and along the edge of the eyelids at the root of the eyelashes. Scanty mucous discharge occurs with adenoviral and allergic conjunctivitis. Any inflammatory process of the conjunctiva is primarily accompanied by dilation, tortuosity and hyperemia of the vessels of all its parts. Hyperemia of the conjunctiva of the eyeball is more pronounced at the fornix and decreases towards the limbus, has a bright pink color and moves with displacement of the conjunctiva. Hyperemia of the conjunctiva of the eyelids obscures the normal vascular pattern and characteristic striations, which are normally caused by the transillumination of the meibomian gland ducts. Films on the conjunctiva can be of different colors, thicknesses and sizes. Their formation is due to the ability of some pathogens (adenoviruses, diphtheria bacillus, some strains of pneumococcus) to coagulate tissue proteins. With pneumococcal and adenoviral conjunctivitis, the film is easily removed from the surface of the mucous membrane. If, after removing the film, a bleeding, ulcerated surface remains, this often indicates a diphtheria process. The appearance of follicles and papillae in the mucous membrane indicates the involvement of subconjunctival adenoid tissue in the process; follicles usually appear on the conjunctival cartilage at the corners of the palpebral fissure, as well as on the transitional folds. They may be small and pink in adenoviral keratoconjunctivitis, grayish-pink in pharyngoconjunctival fever. These conjunctivitis is characterized by the development of follicles on the unchanged mucous membrane. With trachoma, follicles develop on the infiltrated mucous membrane, have a grayish-pink color, and are randomly located. Large lumpy papillary growths located on the dull bluish conjunctiva, most often of the upper eyelid, resembling a cobblestone street in appearance, are characteristic of allergic spring conjunctivitis. Hemorrhages may be small and petechial in pneumococcal conjunctivitis caused by Koch-Wicks bacillus. In the study of the conjunctiva by the method of combined examination or in the light of a slit lamp, cicatricial changes are detected. More often they can be noted as radial stripes on the conjunctiva of the upper eyelid or as a linear scar running parallel to the sulcus subtarsalis. The presence of such changes, as a rule, indicates the postponed trachoma. In cases where, along with similar scars, the mucous membrane is infiltrated and there are follicles, there is every reason to diagnose trachoma of the second or third stage. Deep star-shaped scars remain after conjunctival diphtheria. To confirm the etiology of conjunctivitis, in addition to analyzing the corresponding clinical picture, bacteriological studies of discharge from the conjunctiva are carried out while simultaneously identifying the sensitivity of the pathogen to antibiotics and sulfonamides. This allows for etiotropic treatment. The presence of bluish-red areas on the conjunctiva that protrude above its surface, increasing when the child cries and tilts the head, is characteristic of a vascular hemangioma tumor. A small round formation with clear boundaries of a whitish-yellow color, found during a simple examination, most often located in the inferolateral quadrant, may be a dermoid of the conjunctiva. Sometimes on the conjunctiva of the eyeball, more often at three or nine o'clock at the limbus, there is a flat, somewhat raised formation of a yellowish color, in some cases with pigment inclusions. These are nevi, or birthmarks, of the mucous membrane. 2. Conjunctivitis Conjunctivitis is an inflammation of the mucous membrane that lines the back of the eyelids and the eyeball. Etiology. Due to the occurrence, bacterial conjunctivitis (staphylococcal, streptococcal, gonococcal, diphtheria, pneumococcal), viral conjunctivitis (herpetic, adenovirus, epidemic keratoconjunctivitis), chlamydial conjunctivitis (trachoma), allergic and autoimmune conjunctivitis (drug, hay fever, tuberculosis-allergic) are distinguished. According to the nature of the course, conjunctivitis is divided into acute and chronic. Clinical picture. General symptoms characteristic of all conjunctivitis include subjective complaints of the patient and objective signs. Subjective symptoms include a burning sensation and itching in the eye, a feeling of blockage, and photophobia. Objective symptoms include lacrimation, narrowing of the palpebral fissure, redness and swelling of the conjunctiva of the eyelids, due to which it loses its luster and becomes “velvety.” Redness of the eyeball with conjunctivitis is observed in the periphery. Acute infectious conjunctivitis (the most common of all bacterial conjunctivitis) is caused by staphylococci and streptococci. Both eyes are involved in the pathological process, but more often not simultaneously, but sequentially. In addition to the symptoms common to all conjunctivitis, this type is characterized by the presence of a purulent discharge that glues the eyelashes. The disease may be preceded by cooling or overheating, swimming in a polluted reservoir or staying in a dusty room, as well as acute respiratory illness. Objectively pronounced redness of the conjunctiva of the eyelids and eyes. Pneumococcal conjunctivitis develops most often in weakened individuals, the elderly and children. It is characterized by pinpoint hemorrhages in the conjunctiva, swelling of the eyelids and the formation of whitish-gray films. Acute epidemic Koch-Wicks conjunctivitis is highly contagious and is transmitted through contaminated hands, clothing and underwear. The disease begins suddenly with a sharp swelling of the eyelids, redness of the conjunctiva of the eyelids and the eyeball. Among other general symptoms, malaise, fever, runny nose and headaches are often observed. The discharge is initially scanty, then becomes profuse and purulent. The illness lasts five to six days. Sick people must be isolated. Gonococcal conjunctivitis (gonoblenorrhea) is caused by gonococcus and is clinically divided into gonoblennorrhea of newborns, children and adults. Newborns can become infected either by passing through the vaginal birth canal of a mother with gonorrhea or through baby care items. Clinically, gonoblennorrhea manifests itself on the second or third day after birth with pronounced swelling of the eyelids, sharp redness of the conjunctiva with profuse bloody discharge (the color of meat slop), which after three to four days, when the swelling of the eyelids has already decreased, becomes purulent in nature. A complication of gonoblenorrhea is ulceration of the cornea, which can lead to the formation of a thorn, and if the cornea is perforated, infection can penetrate into the deep parts of the eyeball and blindness. Currently, such serious complications are relatively rare. Gonoblenorrhea in adults occurs with severe general symptoms: fever, damage to the joints and the cardiovascular system. In adults, complications of gonococcal conjunctivitis are quite common. Diphtheria conjunctivitis is rare (if the anti-diphtheria vaccination regimen is not followed) and is accompanied by severe intoxication, high body temperature, enlarged lymph nodes and their soreness. Local distinctive signs of diphtheria conjunctivitis are gray filmy deposits on the conjunctiva of the eyelids and eyeball. Their removal is painful and accompanied by bleeding. After one to one and a half weeks, the discharge becomes purulent, the affected areas of the conjunctiva are rejected and heal with a scar within one and a half to two weeks. In this case, the formation of adhesions between the eyeball and the inner surface of the eyelids is possible. The causative agent of herpetic conjunctivitis is the herpes simplex virus. Most often, herpetic conjunctivitis is unilateral and has a long course. There are three forms: catarrhal, follicular and follicular-ulcerative. In the first case, the inflammation is mild, accompanied by the appearance of blisters on the edges of the eyelids and mucous or mucopurulent discharge; in the latter case, erosions and ulcers are formed. Adenovirus conjunctivitis is caused by adenoviruses and is accompanied by fever and pharyngitis. Allergic and autoimmune conjunctivitis develops with increased sensitivity of the body to a wide variety of substances. Drug conjunctivitis occurs with prolonged local treatment with antibiotics, anesthetics and is a special case of allergic conjunctivitis. Treatment. For acute infectious conjunctivitis, antimicrobial drugs are prescribed: 30% sodium sulfacyl solution, antibiotic solutions, furatsilin solution at a dilution of 1: 5000, 24% boric acid solution, 3% collargol solution. On the first day of illness, drops are instilled into the conjunctival sac every hour, in the next three to four days 56 times a day. In case of acute conjunctivitis, a sterile bandage should not be applied to the affected eye so as not to cause stagnation of purulent discharge. Prevention of acute conjunctivitis involves following the rules of personal hygiene. Treatment of gonococcal conjunctivitis includes the use of sulfanilamide drugs and broad-spectrum antibiotics orally and intramuscularly, frequent rinsing of the eyes with a weak solution of potassium permanganate with the instillation of albucid. At night, an ointment containing antibiotics or sulfonamides is applied over the eyelids. Treatment is carried out until complete recovery, which must be confirmed bacteriologically. The prognosis for timely and adequate treatment is favorable. In newborns, mandatory prevention of gonoblennorrhea is carried out: immediately after birth, a 30% solution of sulfacyl sodium is instilled into each eye three times within an hour. Treatment of diphtheria conjunctivitis is carried out in the infectious diseases department using anti-diphtheria serum and antibiotics or albucid and 1% tetracycline ointment locally. Treatment of viral conjunctivitis includes local use of antiviral drugs (0,11,2% oxolinum solution, 0,25% oxolinic ointment), specific antiviral immunotherapy (globulin) and the use of restoratives (vitamins). Treatment of allergic and medicinal conjunctivitis requires immediate discontinuation of the drugs that caused such a reaction, and the use of desensitizing and antihistamine drugs orally, as well as topical glucocorticosteroids (eye drops and ointments). LECTURE No. 11. Clinical features and principles of treatment of some conjunctivitis and tumors of the conjunctiva 1. Acute epidemic conjunctivitis (Koch-Wicks conjunctivitis) In children, mainly toddlers, often in the morning, after sleep, against the background of general symptoms characteristic of conjunctivitis, pronounced swelling (chemosis) of the lower transitional folds, petechial hemorrhages in the conjunctiva of the eyelids and transitional folds can be observed. In older children, against the background of hyperemic mucous membrane of the eyeball, ischemic densified white areas in the form of two triangles are formed, the base facing the cornea. When examining the cornea, infiltrates can be detected. This clinical picture is characteristic of acute epidemic conjunctivitis (Koch-Wicks). Young children may experience general symptoms. Recovery occurs within five to seven days. 2. Pneumococcal conjunctivitis Sometimes, along with the general symptoms of conjunctivitis in children, pinpoint hemorrhages are found in the conjunctiva of the eyeball and transitional folds, and gentle pinpoint infiltrates are visible on the cornea near the limbus. With such changes, one can think of acute pneumococcal conjunctivitis. The presence of delicate gray films on the conjunctiva of the eyelids and vaults, weakly associated with the underlying tissue and, when removed, do not leave bleeding surfaces, will indicate a false-membrane form of pneumococcal conjunctivitis. If conjunctivitis develops at the end of the first week of a child's life, is characterized by lacrimation and a tearful appearance of the child, then there is reason to diagnose lachrymal conjunctivitis of newborns. The illness lasts up to two weeks. 3. Blennorrheal conjunctivitis There is a sharp swelling of both eyes on the second or third day after birth; when the palpebral fissure opens, watery fluid is ejected almost like a fountain from the conjunctival cavity, the conjunctiva is thickened and bleeds slightly. This clinical picture is typical for the initial period of gonoblenorrhea. If the disease lasts more than a week, then a sharp infiltration of the conjunctiva and pyorrhea are observed, swelling and hyperemia of the eyelids decrease at this stage. The discharge is purulent, yellowish-green in color. The conjunctiva of the eyeball is swollen and surrounds the cornea in the form of a shaft. During this period, changes in the cornea are possible due to disruption of its nutrition due to severe infiltration of the eyelids and mucous membrane, as well as as a result of the melting effect of pus on its tissue. In the third or fourth week of the disease, papillary hypertrophy of the conjunctiva may be detected. The eyes are almost calm, the swelling of the eyelids and conjunctiva is slight, and a liquid greenish discharge appears again. Papillae form on the conjunctiva, it becomes uneven and rough. The process can be protracted or chronic. However, usually in the second month the phase of reverse development of all signs of the disease begins, resulting in clinical recovery. 4. Diphtheria conjunctivitis There may be cases when, during an urgent home call or at the time of going to the clinic, a child experiences severe swelling and cyanosis of the eyelids. The eyelids resemble plums in appearance; upon palpation they are dense and painful. The conjunctiva is pale due to compression of the vessels, or there are grayish-yellow films with numerous hemorrhages on it. Removal of films is accompanied by bleeding. When the disease lasts seven to ten days, sloughing films and granulation tissue with a large amount of pus are visible. This is a typical diphtheritic form of conjunctivitis. Subsequently, star-shaped scars form at the site of granulation. Sometimes less pronounced symptoms of eyelid edema, more delicate films on the conjunctival cartilage and scanty discharge are observed. This is how the lobar form of diphtheria conjunctivitis manifests itself. In children under one year of age, diphtheria of the eyes, as a rule, is manifested only by a slight swelling and hyperemia of the conjunctiva with a cyanotic tint, there are almost no films. This is the catarrhal form of diphtheria. 5. Treatment of bacterial conjunctivitis I. Toilet of the eyelids: washing the conjunctival cavity with weak solutions of disinfectants (2% boric acid solution, furatsilin solution at a dilution of 1: 5000, etc.). II. Local effect on the pathogen, taking into account its sensitivity to various drugs. For this, drops and ointments with antibiotics and sulfonamides are prescribed. The frequency of instillations is determined by the severity of the disease. In severe cases, drops are prescribed every hour. The ointment is applied in the morning, afternoon and evening. III. To prevent damage to the cornea, various antibacterial and vitamin ointments are shown. IV. General therapy. 6. Adenopharyngoconjunctival fever (AFCL) At an outpatient appointment, a child may meet with symptoms of conjunctivitis, which, according to the anamnesis, developed against the background of pharyngitis and fever. In this case, photophobia and blepharospasm are sometimes detected. The conjunctiva is hyperemic, edematous, but the discharge is poor, mucous. You should remember about the age-related features of AFCL. Thus, in children one to two years old, edema and hyperemia are moderate, scanty serous mucous discharge is noted, there may be films on the conjunctiva of the eyelids, usually tender, they are easily removed (membranous form). The duration of the illness is about ten days. In schoolchildren, conjunctival hyperemia is combined with the presence on the mucous membrane of the eyelids and transitional folds (usually below) of grayish-pink gelatinous follicles and papillae (follicular form). The follicles disappear without a trace after two weeks. In school-age children, swelling of the eyelids, hyperemia and slight swelling of the conjunctiva with a delicate grayish-bluish coating (catarrhal form) are more often observed. The illness lasts eight to ten days. 7. Epidemic follicular keratoconjunctivitis (EFCC) Acute inflammation of the conjunctiva, sharp hyperemia of the conjunctiva of the eyelids, transitional folds, eyeball, a large number of small grayish-pink follicles and papillae, scanty mucous discharge, enlargement and tenderness of the preauricular and submandibular lymph nodes allow one to suspect an adenoviral disease. These signs may be accompanied by pinpoint or coin-shaped superficial subepithelial infiltrates in the cornea after a week, and sometimes after one to two months. The epithelium over them is often preserved and not stained. The disease lasts from two to seven weeks and is called epidemic follicular keratoconjunctivitis. 8. Treatment of adenovirus conjunctivitis Children with adenoviral conjunctivitis should undergo treatment in boxed hospital departments. They are isolated from children's groups for a period of twenty days. In order to prevent complications and fight secondary infections, tetracycline antibiotics are prescribed in the form of 1% ointments. Instillations of a 0,050,1% solution of deoxyribonuclease are used as a virusostatic agent. In severe cases, globulin is injected locally and intramuscularly. Local and general use of vitamins B, D, C and absorbable drugs is also indicated. 9. Tumors of the conjunctiva Sometimes blurry bluish areas are found on the conjunctiva of the eyelids and the eyeball, somewhat rising above the level of the rest of the conjunctiva, which increase with straining and crying, they grow rapidly in the first year of a child's life. This clinical picture is typical for hemangioma. When examining the conjunctiva of the eyeball at the limbus, transparent, yellowish, slightly raised formations with or without vessels, so-called pigmentless nevi, can be found. If such formations contain inclusions of pigment, and their color varies from light brown to black, and they often tend to grow, then they speak of pigmented nevi. Sometimes, in the inferolateral segment of the eyeball, a round or oval-shaped formation of a whitish-yellow color and dense elastic consistency is detected, on the surface of which there are hairs. Treatment of benign tumors of the mucous membrane consists in their prompt removal. In the treatment of small non-pigmented and especially pigmented nevi in non-limbal localization, photocoagulation is used. LECTURE No. 12. Trachoma Trachoma is a chronic infectious disease of the eyes. The causative agent of the infection is the microorganism chlamydia, which causes damage to the conjunctiva and cornea, resulting in scarring, destruction of the cartilage of the eyelids and complete blindness. The disease has been known since ancient times; trachoma has long been found among the populations of Africa and Asia. The appearance of trachoma in Europe is associated with the campaign of Napoleon Bonaparte’s troops in Egypt in 1798. Currently, in the countries of Africa, Southeast Asia, and South America, there are more than 400 million patients with trachoma, including 200 million cases of complete blindness caused by trachoma . There is no trachoma in Russia, only imported cases occur. Etiology and epidemiology. The causative agent of trachoma was discovered in 1907, it is found in the cells of the epithelium of the conjunctiva and cornea, and in its properties and intracellular development cycle is similar to other chlamydia. Trachoma is an anthroponotic disease (transmitted only from person to person) with an epidemic spread. The living conditions of the population and the level of its sanitary culture play an important role in the spread of trachoma. The transfer of the infectious agent is carried out by direct and indirect means (through hands, clothes, towels). The main sources of infection in the foci of trachoma are patients with active forms of the disease. An essential role in the transmission of the infection also belongs to the carriers of the infectious agent, persons with its unusual localization (for example, in the lacrimal ducts) and an atypical course of the process. The role of flies in the mechanical transfer of the pathogen is not excluded. Susceptibility to trachoma is universal and high. Immunity after the transferred disease is absent. Trachoma is widespread in tropical and subtropical countries. In Russia, this infection has been eliminated. Pathological anatomy. In the initial period of trachoma, diffuse infiltration of neutrophilic leukocytes and histiocytes is determined in the conjunctiva. Starting from the tenth to twelfth day, lymphocytic and plasma cell infiltration develops. In addition to diffuse infiltration, trachoma is characterized by the formation of follicles, which at first are focal accumulations of lymphocytes. The trachomatous process is marked by early onset dystrophic changes and necrosis of the tissues of the conjunctiva, primarily in the area of the follicles. The stroma of the follicles undergoes sclerosis and hyalinosis, but their resorption without scar formation is possible. A fibrous tissue develops around the follicles, forming a capsule, in which cell infiltrates and the infectious agent can remain "immured" for many years. In patients with a severe course of the disease, diffuse-infiltrative processes in the conjunctiva and edema predominate, there is a thickening of the conjunctiva with an increase in the size of the follicles and their noticeable protrusion of the papillary form of trachoma. In the cornea, there is diffuse inflammation of varying intensity with the penetration of newly formed vessels and infiltration into the region of the upper limbus and the formation of trachomatous pannus (clouding of the surface layers of the cornea). In severe cases, follicles appear in the stroma (own substance) of the cornea. In the lacrimal organs there is inflammation with lymphoid plasma infiltration and scarring. Severe cases are characterized by the spread of infiltration into the deep layers of the cartilage of the eyelids. In the meibomian glands, the development of cysts, vacuolization, fatty degeneration, hyalinosis, cartilage amyloidosis are observed. Clinical picture. The incubation period is seven to fourteen days. The onset of the disease is acute, but in many patients it develops gradually, and the course of the infection is chronic. Both eyes are usually affected. The onset of the disease is possible without any sensations. Sometimes there is a slight mucopurulent discharge, a sensation of a foreign body and a burning sensation in the eyes. With the acute onset of the disease, symptoms of acute conjunctivitis are observed (redness of the skin of the eyelids, photophobia, copious mucopurulent discharge, the conjunctiva is swollen and hyperemic). There are four stages during the trachomatous process: 1) development of follicular reaction, lymphoid subconjunctival infiltration, limbitis (inflammation of the limbus) and pannus of the cornea; 2) the appearance of scars replacing follicles; 3) the predominance of scarring of the conjunctiva and cornea; 4) ending scarring, covering the conjunctiva, cornea, cartilage of the eyelids. Depending on the predominance of certain pathological elements in the active period (first-third stages) of trachoma, four forms of the disease are distinguished: 1) follicular, in which predominantly follicles are observed; 2) papillary with a predominance of papillary growths; 3) mixed, when both follicles and papillary growths are found; 4) infiltrative, characterized by predominant infiltration of the conjunctiva and cartilage of the eyelids. The clinical picture of trachoma when infected in early childhood is similar to neonatal blenorrhea. Repeated exacerbations in these patients cause the development of corneal cicatricial changes characteristic of trachoma. The most severe complication of trachoma is a trachomatous corneal ulcer, which is promoted by a secondary bacterial infection. In addition, complications of trachoma include acute and chronic conjunctivitis, progressed due to the addition of a bacterial or viral infection. In trachoma, diseases of the lacrimal ducts are often observed, caused by the causative agent of trachoma in combination with a secondary infection. The consequences of trachoma are due to the process of scarring, which leads to the appearance of adhesions between the conjunctiva of the eyelid and the eyeball. In this case, the conjunctival arches are shortened or disappear altogether. Changes in the cartilage of the upper eyelid in trachoma lead to inversion of the eyelid, abnormal growth of eyelashes. As a consequence of trachoma, drooping of the upper eyelid (ptosis) develops, giving the face a peculiar sleepy expression. As a result of cicatricial changes in the lacrimal gland, lacrimation decreases, drying of the conjunctiva and cornea xerosis occurs. Pronounced scarring of the conjunctiva, combined with trichiasis (improper growth of eyelashes) and inversion of the eyelids, leads to reduced vision, and scarring and clouding of the cornea to partial or complete loss of vision. Diagnostics. The diagnosis of trachoma is established when at least two of the four cardinal signs of the disease are detected, such as follicles on the conjunctiva of the upper eyelid, follicles in the region of the upper limb or their consequences (fossae), typical conjunctival scars, pannus, more pronounced in the upper limbus. In epidemic foci of trachoma, one of these symptoms is sufficient for the diagnosis. The diagnosis is confirmed by a cytological method (detection of cytoplasmic inclusions of the causative agent of Provachek Halberstedter bodies in epithelial cells), detection of chlamydia antigens by immunofluorescent methods in epithelial cells of scrapings from the conjunctiva, isolation of chlamydia from the conjunctiva by cultivation in the gall sac of chicken embryos or in tissue culture, determination of specific antibodies in serum blood. The predominantly sluggish course of inflammation of the mucous membrane, accompanied by diffuse infiltration of the submucosal tissue, the presence of papillae, follicles and whitish scars, swelling in the limbus, infiltration and neoplasm of vessels in the cornea, going mainly from top to bottom (pannus), indicate primarily trachomatous keratoconjunctivitis (trachoma ). Under the conditions of a mass examination in trachomatous foci in the presence of subtle and atypical follicles, minor and uncharacteristic changes in the cornea, negative laboratory results, a diagnosis is made such as suspected trachoma. With mild hyperemia of the conjunctiva of the eyelids and its slight infiltration, the absence of follicles and questionable changes in the cornea, but if there are inclusions in the scraping from the conjunctiva, they speak of pretrachoma. If patients periodically complain about the sensation of a foreign body, heat in the eyes, if discharge is observed, the conjunctiva is hyperemic and sharply infiltrated, and papillae (papillary form) and follicles (follicular form) are visible around the vessels, the number and size of which are varied, then this is trachoma of the first stage , or the initial progressive phase of the disease. All changes, as a rule, develop first in the region of the lower transitional fold, since there is more adenoid tissue, but they are more easily detected on the conjunctiva of the upper eyelid, in the region of the upper transitional fold. First of all, follicles are found in the semilunar fold and on the lacrimal caruncle. It is possible to have both follicles (in children) and papillae (mixed form) on the infiltrated conjunctiva. If inflammation and infiltration of the conjunctiva and adenoid tissue are combined with degeneration, disintegration of follicles and their replacement with connective tissue (scarring), which is detected only using a combined examination method or in the light of a slit lamp (dots and white stripes in transitional folds and on the conjunctiva of the cartilage of the upper eyelid ), and a not very pronounced ptosis is visible, which developed as a result of the spread of infiltration and scarring in the area of the levator tendon and Müller muscle, that is, there is reason to characterize this process as a pronounced regressive (second) stage of trachoma. The third stage of the disease is characterized by a slight inflammation in the form of a gentle infiltration, the presence of single follicles and a large number of white scars in the conjunctiva. The fourth stage of trachoma, or the stage of clinical recovery, is characterized by the presence of cicatricial changes in the mucous membrane of the eyelids and eyes without signs of inflammation. Already in the first stage of trachoma in the cornea, manifestations of pannus limbitis can be detected. The limbus is edematous and cloudy, its vessels are full-blooded and dilated, small gray and gelatinous follicles are observed around the vessels. In the second and third stages of the disease, superficial infiltrates are visible in the cornea on the border with the upper limbus, which, merging, form a diffuse opacification of the cornea. These opacities are penetrated by superficial conjunctival vessels, anastomosing with each other. Depending on the number of conjunctival vessels that have sprouted into the cornea, several types of pannus can be distinguished: micropannus (thin) vessels are few, corneal infiltration is gentle; vascular a large number of vessels grow into the clouded part of the cornea; fleshy (sarcoidosis) significant infiltration and vascularization of the cornea. Complications. Frequent consequences of trachoma are inversion of the eyelids and abnormal growth of eyelashes trichiasis, as a result of which the cornea and conjunctiva are mechanically irritated and injured. Possible posterior simblefaron fusion of the conjunctiva of the eyelids with the conjunctiva of the eyeball. A severe consequence of trachoma, which develops as a result of severe scarring of the conjunctiva and leads to the death of the glandular apparatus, the closure of the ducts of the lacrimal glands and their death, is xerosis, the drying of the mucous membrane and cornea. These changes can be detected in the third stage of trachoma. The fourth stage of trachoma is divided into four groups depending on the degree of visual acuity reduction: 1) zero group without visual impairment; 2) the first group decreased vision to 0,8; 3) the second group decreased vision to 0,4; 4) the third group decreased vision below 0,4. Treatment and prevention. Topically apply 1% ointments or solutions of tetracycline, erythromycin, oletethrin, 10% solutions of sodium sulfapyridazine, 5% ointments or 3050% solutions of etazol 36 times a day. If necessary, one to two weeks after the start of treatment, follicle expression is performed. In cases of severe trachoma, the use of tetracycline, oletethrin, etazol, sulfapyridazine is recommended, and vitamin therapy and the elimination of allergic manifestations are also indicated. In complex therapy, interferon and interferon inducers, immunomodulators are used. At the stage of outcomes and consequences, surgical treatment (corrective and plastic) is carried out. Timely and systematic use of antibiotics and sulfonamides makes it possible to achieve a cure and prevent complications. Drug therapy is combined with mechanical (squeezing (expression) of follicles), which contributes to a more active effect of antibiotics on the flora and gentle scarring. Expression is performed once every two weeks under local anesthesia, after which active drug therapy continues again. Patients who have tender scars are considered cured. For six months they must instill a 30% solution of albucid, and then a commission of ophthalmologists decides on further anti-relapse treatment and its duration. Prevention is reduced to the timely detection of patients, their clinical examination and regular treatment. LECTURE No. 13. Pathology of the oculomotor apparatus (strabismus) Strabismus is the deviation of one or both eyes from a common point of fixation, while normal vision is disturbed (the coordinated work of both eyes). Etiology. Allocate explicit and latent strabismus. Pathology is considered only obvious strabismus, subdivided into paralytic and concomitant. Paralytic strabismus is observed with weakness of the muscular apparatus of the eyeball, which may be due to trauma, tumor, neuroinfections, concomitant strabismus develops in childhood. Clinical picture and diagnosis. Clinically, paralytic strabismus is manifested by the limitation or absence of movements of the squinting eye in the direction of the affected muscle, while there is a feeling of doubling of objects. With a long-term strabismus, a decrease in vision (up to blindness) of the squinting eye is possible. Concomitant strabismus develops in childhood, while the movements of the eyeballs are preserved in full, and there is no doubling. Deviation of the eye to the nose is referred to as convergent strabismus; when the eye deviates to the temple, strabismus is considered divergent. In addition, there are deviations of the eyeball up and down, as well as a combination of horizontal and vertical deviation of the eyes. With a constant deviation of one eye, strabismus is considered one-sided, both eyes are bilateral, alternate deviation of one or the other eye is intermittent. If possible (depending on the age of the child), then before starting the study, it is necessary to get acquainted with the anamnesis, find out at what age the strabismus appeared. Detected from the first days of birth, it may be due to birth trauma, and signs of paresis of the oculomotor muscles may be detected. They find out whether the strabismus arose suddenly or gradually, in which the parents see the reason for its appearance. If the latter is associated with a previous eye disease, then, perhaps, a decrease in vision contributed to its development. Clarify the presence of amblyopia, signs of paralytic strabismus. In all patients with strabismus, both the anterior segment of the eye and the fundus of the eye are carefully examined with a dilated pupil. To decide on treatment methods, it is necessary to find out whether the patient wears glasses, at what age they were prescribed to him, and whether he wears them constantly or periodically. Determine when the last glasses were written out and which ones; Do they correct strabismus, and if so, to what extent? They clarify whether any other treatment was carried out (switching off the eye, exercises on devices, operations, etc.) and what result this gave. After clarifying all these questions, it is necessary to examine the visual acuity of the child, first without correction, then with the existing glasses. If the vision is below 1,0 in glasses, an attempt is made to correct it. If even with correction it was not possible to achieve full vision, this may indicate (in the absence of morphological changes in the eye) a steady decrease in vision without visible organic changes as a result of the existing strabismus of dysbinocular amblyopia. The most convenient division of amblyopia according to severity based on the possibility of studying at school and serving in the army: 1) light 0,80,5; 2) average 0,40,3; 3) severe 0,20,05; 4) very severe 0,04 and below. Then the nature of fixation is determined. This means that non-central fixation is accompanied by very low visual acuity. In all patients with strabismus, in order to decide whether they need to wear glasses, clinical refraction is examined by skiascopy or refractometry 6080-1 minutes after two or three times instillation of a 0,25% solution of homatropine (0,1% solution of scopolamine in combination) into the eye followed by instillation of XNUMX% adrenaline). It should be remembered that instillation of cycloplegics deprives farsighted patients of the opportunity to accommodate excessively, therefore, in a number of patients with hypermetropia who did not wear glasses, in whom strabismus arose due to a violation of the relationship between accommodation and convergence, after turning off accommodation, the deviation of the eye disappears. In this case, this type of strabismus can be considered accommodative. Consequently, spectacle correction of ametropia (farsightedness with convergent strabismus and myopia with divergent strabismus) relieves the patient from accommodative strabismus. In cases where the correction of ametropia does not completely eliminate the deviation of the eye, the strabismus should be considered partially accommodative. If the strabismus does not decrease under the influence of correction, therefore, it is of a non-accommodative nature. When examining a child, the type of strabismus is established. The eye can be deflected inward convergent strabismus (strabismus convergens), as well as outward divergent strabismus (strabismus divergens). Sometimes, along with a horizontal deviation, there is a deviation of the eye upward (strabismus sursum vergens) or downward (strabismus deorsum vergens). Vertical deviation of the eye usually indicates the presence of muscle paresis. The next step in the study is the determination of the angle of strabismus. It is determined by various methods, the simplest of which is the Hirshberg method. In this study, the angle of deviation is judged by the position of the point reflex from the light source on the cornea of the squinting eye. To obtain a reflex, an ophthalmoscope mirror is used, which is attached to the lower edge of the orbit. The patient is asked to look in a mirror. A point reflex appears on the cornea of the patient's fixing eye, respectively, in the center or almost in the center of the pupil. On the squinting eye, the light reflex is detected asymmetrically to the reflex of the fixing eye (primary deflection angle). With convergent strabismus, the reflex is shifted outward from the center of the cornea, with divergent inward. Its location along the edge of the narrow pupil indicates an angle of 15°, in the center of the iris at 2530°, at the limbus 45°. To determine the angle of the secondary deviation (the deviation of the fixing eye is more often observed), cover the fixing eye with the hand, forcing the patient to look at the ophthalmoscope mirror more often with the deviating eye. With concomitant strabismus (strabismus concomitans), the primary and secondary deviation angles are equal. The big difference in their size comes to light at paralytic strabismus (strabismus paraliticus). A somewhat more accurate study of the angle of deviation on the perimeter. To do this, in a slightly darkened room, it is necessary to seat a sick child behind the perimeter, setting his chin in the middle of the stand. A candle is placed in the center of the horizontal arc of the perimeter, which the patient must fix with his gaze. The second candle is moved along the perimeter until its image on the cornea of the squinting eye takes a position symmetrical to the image of the candle on the fixing eye. The position of the candle on the perimeter arc determines the degree of deviation of the eye; work is facilitated on the electrical perimeter. The angle of strabismus can be determined on the syneptophore according to the scale of the device according to the position of the visual lines. The angle of strabismus is determined both without glasses and with glasses. In children with strabismus, vision is usually monocular, rarely simultaneous. The next step in examining a child with strabismus is to determine the functional state of the oculomotor muscles. You can judge the mobility of the eyes by asking the patient to follow the researcher's finger moving in different directions. In this study, muscle dysfunctions, mainly of horizontal action, are more clearly revealed. If the internal rectus muscle functions normally, then when the eyeball is rotated, the inner edge of the pupil reaches the level of the lacrimal openings. For convergent strabismus, due to the training of this muscle in farsighted people, as a rule, hyperfunction of the adductor is characteristic. Divergent strabismus, on the contrary, due to the weakness of the internal rectus muscle, is accompanied by some restriction of the movement of the eye inwards. When the eyeball is retracted, the outer limbus should normally reach the outer commissure of the eyelids. An important sign of paralytic strabismus is the limitation of the movement of the eyeball towards the paralyzed muscle. After obtaining information about the state of the sensory and motor apparatus in a patient with strabismus, as well as examining all the environments of the eye, visual acuity and visual field, a clinical diagnosis is made, for example: concomitant convergent strabismus of the right eye, non-accommodative, moderate amblyopia, far-sighted astigmatism. According to the diagnosis, treatment is prescribed. In some cases, due to the fact that there is a significant discrepancy between the visual line and the optical axis of the eye (angle r), a false impression of convergent or divergent strabismus is created. This condition is called imaginary strabismus. With it, binocular vision is not impaired, it is not subject to treatment. Often in children with refractive errors, latent strabismus (heterophoria) can be detected, a disorder of muscle balance, which is hidden due to the presence of binocular vision. Hidden strabismus can be detected if the urge to merge is eliminated. To do this, asking the child to fix an object located at a distance of 2530 cm from him, cover one eye with his palm. An obstruction to binocular vision is created. Under the palm of the eye deviates inward or outward, depending on the type of heterophoria. If you quickly remove your hand, then due to the desire to merge deviations of the eye, it makes an adjusting movement. If a child has a violation of binocular vision, heterophoria is a factor conducive to the appearance of visible strabismus. One of the types of disorders of the oculomotor apparatus is nystagmus (nystagmus). Nystagmus is called spontaneous oscillatory movements of the eyeballs. In the direction of oscillatory movements, it can be horizontal, vertical and rotatory. The range of oscillations and their frequency can be varied. With nystagmus, as a rule, visual function is significantly impaired. Nystagmus can be labyrinthine or central. In children, ocular, or fixation, nystagmus is most often observed, due to a sharp decrease in vision due to various ocular pathologies. Differential diagnosis of concomitant and paralytic strabismus does not present significant difficulties and is carried out in the process of a thorough study of the motor function of the eyes. Treatment and prevention. Treatment of paralytic strabismus includes the elimination of the cause that caused paresis of the oculomotor muscle, and local effects (physiotherapy). To correct double vision, prismatic glasses are prescribed. Surgical treatment consists in strengthening the affected muscles and is used when conservative therapy is ineffective. Treatment of concomitant strabismus includes a conservative stage (pre and postoperative) and surgical. Conservative treatment consists in restoring the normal relationship between accommodation and convergence, retinocortical connections, as well as in an attempt to improve visual acuity, the development of eye mobility. With strabismus, if the patient has a refractive error and in the past glasses were not prescribed or do not correspond to refraction, glasses are first prescribed. When wearing correctly prescribed glasses, eye deviation disappears in 2135% of patients. With accommodative strabismus, only spectacle correction of ametropia and anisometropia is usually sufficient. In isolated cases, with accommodative strabismus, after a short wearing of glasses, binocular vision appears, but more often vision remains monocular, therefore, orthooptic treatment is necessary, which consists in joint exercise of both eyes until binocular vision appears. If the patient, despite wearing glasses, has low vision, i.e., there is amblyopia, it is necessary to conduct a course of pleoptic treatment aimed at eliminating amblyopia before the operation. The vision of the amblyopic eye should be at least 0,3 in order to be able to start orthooptic exercises in the postoperative period. With lower visual acuity, these exercises are usually not very effective. In young children (up to five years of age), for the treatment of amblyopia, regardless of the type of fixation, the method of direct gluing (occlusion) is used, that is, turning off the better seeing eye. Fixation disorder at this age is usually unstable. A well-seeing eye, after covering it with a sterile napkin, is sealed with a plaster. You can close the glass in glasses with dark paper and plaster, but it is best to use a special soft occluder that is fixed in glasses. In order to train the amblyopic eye, exercises with increased visual load are simultaneously prescribed. Every three days it is necessary to remove the occluder (sticker) and inject disinfectant drops into the conjunctival sac. Once every two weeks, visual acuity of both eyes is checked. Usually, vision in the amblyopic eye improves rapidly in the first two weeks after the start of treatment. If the vision of the better seeing eye decreases to 0,6, the occlusion time must be reduced by 12 hours. Subsequently, the issue of the duration of daytime occlusion is decided depending on the dynamics of vision in both eyes. Usually direct occlusion lasts for several months. When the vision of the amblyopic eye equals that of the better seeing eye, the occlusion is stopped. Gradually, they begin to open their eyes, increasing the sticking time every day in order to prevent a sudden drop in vision to the original numbers. The restored vision of the amblyopic eye is often accompanied by the transition of monolateral strabismus to alternating (intermittent), which further prevents the recurrence of amblyopia. In children over five to six years of age, if the amblyopic eye is incorrectly fixed, switching off the better seeing eye is not recommended, as this leads to strengthening of the incorrect fixation. Sometimes in such cases the amblyopic eye is switched off (this is the so-called reverse occlusion) for a month and a half. During this period, in some cases, correct fixation is restored. In school-age children, both with central and with incorrect fixation, treatment is carried out according to the method of E. S. Avetisov, which consists in irritating the central fossa of the retina with the light of a flash lamp inserted into the optical system of a large ophthalmoscope. The course of treatment is 2530 lessons. Surgical treatment is carried out taking into account the functional ability of the oculomotor muscles. With convergent strabismus with a large deviation of the eye, Kovalevsky tenomyoplasty is preferable in order to lengthen the muscle, with smaller angles of recession of the internal rectus muscle. In the presence of alternating strabismus, the same type of operation should be performed simultaneously on both eyes. If the operation on the internal rectus muscles is not very effective, intervention on the external resection (tenorrhaphy), prorraphy is possible. With divergent strabismus, due to weakness of the internal rectus muscle, as a rule, tenorrhaphy of the internal rectus muscle or a dosed partial resection of it with transplantation closer to the limbus is performed. In the postoperative period, the entire complex of treatment is again carried out, aimed at improving vision, eliminating residual deviation, restoring normal retinal correspondence, and developing fusion (image fusion). With normal retinal correspondence, classes to develop binocular vision are carried out at home using a mirror stereoscope. Treatment should be long-term and regular (one to two years) until binocular vision appears and evidence of the patient’s recovery. If, during the examination, clear signs of paralysis or paresis of one of the muscles are detected in the patient (limited mobility of the eyeball, diplopia), it is necessary to subject him to a thorough neurological examination. The question of surgical intervention is raised in such cases only after long-term treatment of the underlying disease and is agreed upon with a neurologist. Treatment of strabismus begins at three to four years of age and should end in preschool age. Prevention of strabismus consists of early determination of clinical refraction (up to one or two years), checking visual acuity and spectacle correction of ametropia, observing sanitary and hygienic conditions for visual work, and eliminating pathological changes in the eye. LECTURE No. 14. General issues of the pathology of the vascular tract 1. Questioning the patient Having come into contact with the patient, one should briefly find out the timing and alleged causes of the disease, the nature of its course, the treatment performed, its effectiveness, etc. There are slight transient pains in the eye, redness of the eye, and sometimes a decrease in vision. Pain in the eye with iridocyclitis in children, unlike adults, is very weak and intermittent, so seeking medical attention is often belated. If the history reveals that the eye disease arose after or against the background of some general changes in the child’s condition, then it should be borne in mind that most often iridocyclitis in children develops with influenza, tuberculosis, rheumatism, diseases of the paranasal sinuses, teeth, and toxoplasmosis , childhood infections, etc. Anomalies and tumors are predominantly congenital in nature. 2. External examination of the eye and examination of the cornea Examination of the patient should begin with checking the field acuity and color vision. Next, a general external examination of the face and eyes is performed. Pay attention to the position of the eyes and their appendages, their mobility and comparative sizes. With the help of lateral illumination, the nature of the injection of the vessels of the eyeball is determined. A mixed injection of the eyeball may be indicative of iridocyclitis. To make sure that there is a mixed injection, an adrenaline test is performed. Pericorneal injection for anterior uveitis is the same as for patients with keratitis. In young children, the injection of the eyeball is slightly expressed. After determining the nature of hyperemia of the eyeball using lateral illumination, the state of the cornea is examined using a combined method. As a rule, in side lighting it appears normal. However, when examined by a combined method, especially in the light of a slit lamp, peculiar deposits are often found on the corneal endothelium. These are precipitates, glued lumps of pigment, lymphocytes, macrophages, plasma cells, sometimes fibrin, etc. In the process of their study, attention is paid to the size, shape and color (small, medium and large, gray, yellowish, "fat", etc.) , since these signs can suggest one or another nature of the pathological process. Be sure to determine the state of the depth of the anterior chamber (it may be uneven due to a change in the position of the iris), the presence of its adhesions to the cornea (anterior synechiae) or to the anterior lens capsule (posterior synechiae). Particular attention is paid to the contents of the anterior chamber, since with iridocyclitis the moisture may become cloudy, and depending on the etiology and severity of the process, hyphema, hypopyon, gelatinous or serous exudate may appear. 3. Examination of the iris of the pupil and lens When examining the iris of a diseased eye, it should be compared with the iris of a healthy eye. At the same time, it is possible to detect a change in its color (gray, brownish, yellowish, reddish, etc.), blurring of the pattern (smoothness of crypts and lacunae), the presence of separate dilated and newly formed vessels. By changing the color of the iris, we can conclude that the expansion of its vessels, the appearance of transudate and exudate in it. A very important diagnostic sign of iritis is the condition of the pupil. It is almost always narrowed, reacts sluggishly to light, and often has an irregular shape due to the formation of posterior synechiae. Changes in the pupil area are especially clearly visible after instillation of mydriatics (scopolamine, homatropine, etc.) into the conjunctival sac. It should be remembered that in cases where there is fusion and infection of the pupil and there is no outflow of moisture from the posterior chamber to the anterior chamber, the iris protrudes (bombing), the anterior chamber becomes small and uneven, and an increase in ophthalmotonus is observed. When examining the lens on its anterior capsule, it is often possible to detect brown clumps of remnants of the pigment epithelium after rupture of the posterior synechiae, but gray, yellowish, crumbly or membranous deposits of exudate can be detected, the type and severity of which depend on the nature of the process. To clarify their location, to identify the type and nature of the exudate, an examination with a slit lamp is necessary. 4. Fundus examination and ophthalmoscopy The eye is examined in transmitted light, attention is paid to the nature of the reflex from the fundus. If there are precipitates on the posterior surface of the cornea, sweating of the endothelium, exudate deposits on the anterior and posterior capsules of the lens, the moisture of the anterior chamber is turbid, or opacities in the vitreous body are determined, then the reflex from the fundus will be unevenly pink. In cases where there are opacities of the vitreous body, they are detected by shadows that have a different shape, size, intensity and mobility. These opacities are due to the presence of transudate or exudate. Next, ophthalmoscopy is performed and the state of the retinal vessels (expansion, narrowing, uneven caliber, etc.), the optic nerve head (size, color, clarity of contours), the central zone and periphery of the retina (foci of various sizes, shapes, colors and localizations) are ascertained . After examining the fundus, be sure to palpate the eye. If the child pulls his head back, this indicates the appearance of pain in the ciliary body. At the same time, intraocular pressure is palpated, which is often below normal, however, as already mentioned, in the presence of posterior and anterior synechia, intraocular pressure can be increased as a result of a violation of the outflow of intraocular fluid. 5. Identification of inflammatory processes Thus, if a child has a mixed or pericorneal injection of the eyeball, clouding of the moisture of the anterior chamber, precipitates, changed color and pattern of the iris, the shape and size of the pupil, posterior synechia and opacities in the vitreous body, and some pain in the eye during palpation and reduced ophthalmotonus, there is every reason to diagnose iridocyclitis (anterior uveitis). However, not always all of the above symptoms are expressed in iridocyclitis. Sometimes such a characteristic symptom as the presence of precipitates is enough to diagnose iridocyclitis. In contrast to the indicated ophthalmological picture, which is characteristic of inflammation of the iris and ciliary body, with an inflammatory process in the choroid itself (choroiditis, posterior uveitis), the eye is usually calm and there are no changes in its anterior section. Depending on the localization of the process, patients may present various complaints. Sometimes they complain about the curvature of straight lines (metamorphopsia), flashes before the eye (photopsia), the surrounding objects seem to them either small (with micropsia) or large (with macropsia), there is a loss of visual field (central scotomas, absolute and relative). These complaints are characteristic of central posterior uveitis maculitis. There may be complaints of poor twilight vision (this is how night blindness, or hemeralopia, manifests itself) with many lesions in the periphery. Ophthalmologically, inflammatory foci are detected in the fundus. If the lesion is fresh, then it has a grayish or yellowish-white color, its boundaries are not too distinct, and there is no pigment in the lesion around it. Patients should be examined using an electric ophthalmoscope and a slit lamp. Biomicroscopy allows you to detect a variety of changes in the vitreous body, different in shape, intensity and color of cloudiness. Patients with posterior uveitis, in addition to visual acuity, should check the field of view, determine the nature of the cattle and examine the color perception. In cases where changes characteristic of iridocyclitis (anterior uveitis) and choroiditis (posterior uveitis) are found in the eye, we can talk about the presence of panuveitis (iridocyclochoroiditis). If the process captures only the iris, it is iritis, if the ciliary body is cyclitis. Sometimes, with ophthalmoscopy, focal changes are detected in the fundus: it is seen that the retinal vessels pass through the focus, bending along its edge, there is an accumulation of pigment along the retinal vessels, in front of them and in the focus area. All this is a sign of chorioretinitis. According to the nature of the ophthalmological picture, focal and diffuse forms of choroiditis are distinguished. Focal changes in the fundus, combined with changes in the optic nerve head, which are manifested in its hyperemia, blurred borders, vein dilation, are characteristic of neurochorioretinitis, most often observed in tuberculosis, lues (syphilis), sympathetic ophthalmia. In such patients, there is an increase in the blind spot. In the clinical course of uveitis in different age groups, a number of features are noted. The phenomena of eye irritation are expressed the weaker, the younger the child. In children under four years of age, the precipitates are small and occur in small numbers. Exudate in the anterior chamber, fusion and infection of the pupil, sequential cataracts and secondary glaucoma are more common in children under five years of age. In children of toddler and preschool age, there is a tendency to generalize the process with spread to all parts of the vascular tract and the absence of characteristic clinical symptoms that help to identify the etiology of the disease. In this regard, laboratory tests and immunological tests are very important to clarify the cause of the disease. So, to make a final clinical diagnosis, not only data on the onset of the disease, the nature of the course of the process, the features of the clinical picture (the nature of precipitates, exudate, posterior synechia), its connection with other diseases, but also laboratory data (bacteriological, virological, immunological, etc.) .) analyzes. The diagnosis of iritis and iridocyclitis is by no means difficult. However, in the initial stages, when pericorneal injection is mild, iritis must be differentiated from conjunctivitis. If a gentle turbidity of the anterior chamber moisture is detected, then an illusion of corneal edema is created, and this, in turn, can lead to a more gross diagnostic error: iritis can be mistaken for glaucoma. An error in diagnosis can lead to undesirable consequences, since with iridocyclitis, atropine should be instilled to dilate the pupil, and with glaucoma, atropine will aggravate the severity of the process. If you skip the onset of the disease, mistaking it for conjunctivitis, and do not prescribe mydriatics, then posterior synechia may form, which subsequently cannot be broken. 6. Detection of congenital anomalies and neoplasms Congenital pathology of the vascular tract is usually associated with various kinds of pathological effects on the organ of vision during the second critical period of intrauterine development. Therefore, it is important to clarify how the pregnancy of the mother of the child being examined proceeded, whether there were any harmful effects on the mother’s body (viral diseases, toxoplasmosis, X-ray exposure, drug therapy, etc.). In the practice of a pediatrician, cases of congenital anomalies of the vascular tract, especially the iris, are possible. In this regard, when examining a child, it is imperative to pay attention to the eyes, since anomalies of the vascular tract can be combined with other malformations, such as cleft lip, cleft palate, microcornea, microphthalmos, etc. With the help of lateral illumination, the anterior part of the eye is examined , pay attention to the pattern and color of the iris, the size, position and shape of the pupil. With such an examination, the following anomalies can be detected: 1) congenital coloboma of the iris; 2) aniridia; 3) polycoria; 4) corectopia; 5) age spots of the iris. To determine the coloboma of the choroid, it is necessary to perform ophthalmoscopy. Patients should determine visual acuity and visual field, which can be impaired to varying degrees. When diagnosing neoplasms in the vascular tract, attention should be paid to the position of the eyes (sometimes a deviation of the eyeball can be detected, which is a sign of a decrease in visual acuity). The eyeball may be enlarged, which indicates a complication of the tumor - secondary glaucoma. Neoplasms of the anterior vascular tract are detected when viewed with side lighting and with a slit lamp. In this case, the following changes in the iris can be detected: 1) cysts; 2) angiomas; 3) neurofibromas; 4) melanomas. Pay attention to the color and pattern of the iris, the displacement of its pupillary edge, which can be observed with a tumor of the ciliary body. Neoplasms of the ciliary body are determined by ophthalmoscopy and gonioscopy. At the beginning of the disease, patients do not complain. Diagnosis is aided by radioisotope studies and luminescent biomicroscopy. LECTURE No. 15. Iridocyclitis Iridocyclitis is an inflammation of the anterior choroid (iris and ciliary body). Etiology and pathogenesis. The causes of the disease are general diseases of the body, often of an infectious nature, viral infections, rheumatism, tuberculosis, focal infections, eye injuries, syphilis, toxoplasmosis, diabetes, gout, gonorrhea, brucellosis. The disease occurs as a result of the introduction with blood into the tissue of the iris and ciliary body of pathogens of various infections and their toxins or various toxic-allergic reactions to various inflammatory processes, as well as a complication of inflammatory diseases of the cornea or penetrating damage to the eyeball. clinical picture. There are two forms of iridocyclitis acute and chronic. Acute iridocyclitis Acute iridocyclitis is the cause of severe pain in the eye, photophobia, lacrimation, blepharospasm, and headache. Diffuse hyperemia of the sclera around the cornea with a purple tint (pericorneal injection), discoloration and blurring of the iris pattern, narrowing and deformation of the pupil, and its poor reaction to light are characteristic. When the pupil is dilated (with a 1% solution of platiphylline, a 1% solution of homatropine, a 0,25% solution of scopolamine or a 1% solution of atropine), as a result of adhesions of the iris to the anterior surface of the lens, the pupil takes on an irregular stellate shape. The moisture in the anterior chamber becomes cloudy, and a gelatinous exudate forms in the area of the pupil. So-called grayish-white precipitates, round-shaped deposits of exudate, appear on the posterior surface of the cornea. In severe cases, purulent exudate is visible and clouding is detected in the vitreous body. The disease is long-term, with relapses. Influenza iridocyclitis occurs and proceeds acutely, the pain syndrome is expressed slightly. The pathological process is manifested in a sharp pericorneal reaction, the appearance of serous exudate, the deposition of precipitates in the form of small dots on the posterior surface of the cornea. Often there are fusions of the pupillary edge of the iris with the anterior capsule of the lens in the form of separate thin pigmented posterior synechiae. Over time, as a result of increased permeability of the vessels of the ciliary body, a gentle opacification forms in the vitreous body. The outcome of the process is favorable, but relapses are possible. One eye is most commonly affected. Rheumatic iridocyclitis begins acutely and proceeds rapidly. Hemorrhage is observed in the anterior chamber, as well as under the conjunctiva, there is a sharp mixed injection of the eyeball. Exudation has a gelatinous character, insignificant, but there are numerous pigmented posterior synechia. The vitreous body is rarely involved in the pathological process. Both eyes are affected. The disease occurs in autumn and spring, coincides with relapses of rheumatism. Iridocyclitis in collagen diseases. The most studied is iridocyclitis in infectious nonspecific polyarthritis. Eye damage occurs suddenly, its course is sluggish. The earliest signs are small precipitates on the posterior surface of the cornea near the inner and outer limbus. Later, ribbon-like and multiple dry precipitates appear on the cornea on the posterior surface of the cornea, as well as delicate ribbon-like opacities in the deep layers of the cornea near the inner and outer limbus. Later, on the cornea, ribbon-like and multiple opacities become coarse, capture the cornea throughout the entire palpebral fissure, vessels from the limbus, as a rule, are not suitable for opacities. The stroma of the iris is atrophic, vessels are visible, new vessels are formed, multiple posterior synechiae, and sometimes adhesions, pupillary infection and vitreous clouding are possible. Then a secondary cataract develops. Both eyes are most commonly affected. Chronic iridocyclitis The course of chronic iridocyclitis is sluggish, sometimes with slight pain, moderate hyperemia, but exudation often occurs, which leads to the formation of coarse adhesions of the iris with the lens, the deposition of exudate in the vitreous body, and atrophy of the eyeball. An important role in the development of chronic iridocyclitis is played by the herpes simplex virus, tuberculosis, penetrating wounds of the eye. Tuberculous iridocyclitis has a sluggish course, occurs gradually, is characterized by the appearance of new vessels in the iris, which sometimes fit and surround single or multiple tuberculomas. There may be flying nodules along the edge of the pupil. The precipitates are large, have a greasy appearance, contain a lot of exudate. Synechiae are wide, relatively often they lead to complete fusion and infection of the pupil, there are opacities in the vitreous body. The cornea and sclera may be affected. One eye is most commonly affected. Complications. Secondary cataract, fusion of the pupil, fusion of the pupillary edge of the iris throughout with the anterior capsule of the lens, which is accompanied by a violation of the outflow of intraocular fluid, resulting in secondary glaucoma. Treatment of complications is carried out in accordance with the clinical picture and treatment of the underlying disease. Treatment and prevention. Treatment of iridocyclitis is reduced to the treatment of the underlying disease and special ophthalmic treatment. The latter includes dilation of the pupil with mydriatics. With the formation of posterior adhesions, the introduction of fibrinolysin and a mixture of mydriatics by electrophoresis is recommended. Anti-inflammatory and antiallergic drugs are prescribed: corticosteroids in the form of instillations of a 5% cortisol solution 56 times a day or subconjunctival injections. When the process subsides, resorption therapy is indicated: instillation of ethylmorphine, electrophoresis with aloe extracts, lidase, thermal procedures. Prevention is based on the timely treatment of the underlying disease and the elimination of chronic foci of infection. LECTURE No. 16. Clinic and treatment of iritis and hemeralopia 1. Irit Iritis is an inflammatory process in the iris. Etiology and pathogenesis. The introduction of infection into the eye during injuries, various diseases (flu, diseases of the teeth and tonsils, tuberculosis, rheumatism, brucellosis, etc.). The introduction of pathogens or their toxins into the choroid occurs through the system of ciliary vessels. clinical picture. The inflammatory process in the iris begins with aching pains in the eye, which subsequently spread to the temporal region. At the same time, photophobia, lacrimation, blepharospasm appear, vision deteriorates. On examination, there is dilation of the passing vessels and pericorneal injection. In this case, a pinkish-violet corolla appears around the cornea. The conjunctival cavity remains clean and the cornea is shiny and transparent. A characteristic sign of iritis is a change in the color of the iris. To get a clear idea of this change, it is recommended to examine the iris in natural light, comparing the color in one and the other eye. Gray and blue irises turn green or rusty, brown turns yellow. Changing color, the iris becomes cloudy and loses the characteristic pattern of depressions (iris crypts). Hyperemia of the vessels in iritis causes a narrowing of the pupil, which can be easily seen by comparing the diseased eye with a healthy one. In order to correctly diagnose the disease, it is necessary to know the characteristic differences between iritis and an attack of glaucoma. With iritis, the pupil of the diseased eye is much smaller and does not react as quickly to light as the pupil of a healthy eye; on palpation, the diseased eye seems softer than the healthy one. With glaucoma, the pupil of the diseased eye is wider than the pupil of the healthy one, and does not narrow when the eye is illuminated; on palpation, the diseased eye seems much harder than the healthy one. A characteristic feature of iritis are the so-called adhesions (synechia). The adhesions of the iris to the anterior surface of the lens are called posterior iris commissures. They can be detected when mydriatics are instilled into the eye (1% solution of platyphylline, 1% solution of homatropine hydrobromide or 1% solution of atropine). Under their influence, the pupil dilates unevenly, its shape becomes irregular. When mydriatics are instilled into a healthy eye, the pupil, expanding unevenly, retains its regular round shape. Posterior adhesions pose a certain danger in iritis, since their large accumulation can serve as an obstacle to the penetration of intraocular fluid through the pupil into the anterior chamber, which leads to the formation of excess fluid and, consequently, to an increase in intraocular pressure. If it is not reduced, blindness may occur. Complications of iritis are decreased visual acuity, cataracts, secondary glaucoma. Treatment. Emergency care in the treatment of the inflammatory process of the choroid consists primarily of preventing the formation of posterior adhesions of the iris or their ruptures, if they have already appeared. For this purpose, repeated instillation of mydriatics is used. It should be remembered that mydriatics can only be used when intraocular pressure is low (if intraocular pressure is elevated, it is better to use a 0,1% solution of adrenaline or a 1% solution of mesatone instead of these drugs). A swab moistened with one of these solutions is placed behind the lower eyelid. Then, repeated instillations of a solution of ofthandexamethasone or a 12% suspension of hydrocortisone are performed. At the same time, antibiotics are required. Treatment depends on the etiology of the disease, with appropriate antibiotic therapy and topical corticosteroids. Be sure to prescribe vitamin therapy. With already formed posterior adhesions, the introduction of fibrinolysin, papain and a mixture of mydriatics by electrophoresis is recommended. When the inflammatory process subsides, resolving therapy, electrophoresis with aloe extract, lidase, and thermal procedures are indicated. 2. Hemeralopia Hemeralopia (night blindness, night blindness) is a violation of twilight vision. Etiology and pathogenesis. The causes of congenital hemeralopia have not been studied. Hemeralopia can be essential (of unknown etiology), beriberi or hypovitaminosis A, as well as beriberi B and PP can act as contributing factors. The appearance of symptomatic hemeralopia occurs with diseases of the retina and optic nerve. In the pathogenesis of the disease, the process of restoration of visual purpura plays a role. clinical picture. Weakening of vision and spatial orientation at dusk. Decrease in light sensitivity, changes in electroretinogram, violation of the process of dark adaptation, narrowing of visual fields, especially in colors. The grounds for the diagnosis are complaints, the clinical picture, dark adaptation studies and electroretinography. In the case of congenital hemeralopia, a persistent decrease in vision occurs. A favorable prognosis is noted for essential hemeralopia, in the case of symptomatic hemeralopia it depends on the course and outcome of the underlying disease. Treatment and prevention. Congenital hemeralopia cannot be treated. With symptomatic hemeralopia, it is necessary to treat the underlying disease. With essential hemeralopia, the appointment of vitamin A inside is indicated: for adults, 50 IU / day, for children from 000100 to 000 IU / day. At the same time, riboflavin is prescribed (up to 1000 g / day). Prevention of essential hemeralopia is adequate intake of vitamin A. LECTURE No. 17. Uveitis Uveitis is inflammation of the choroid (uveal tract) of the eye. Distinguish between the anterior and posterior sections of the eyeball. Iridocyclitis, or anterior uveitis, is inflammation of the anterior iris and ciliary body, and choroiditis, or posterior uveitis, is inflammation of the posterior, or choroid. Inflammation of the entire vascular tract of the eye is called iridocyclochoroiditis, or panuveitis. Etiology and pathogenesis. The main cause of the disease is infection. The infection penetrates from the external environment with eye injuries and perforated corneal ulcers and from internal foci with general diseases. In the mechanism of development of uveitis, the protective forces of the human body play an important role. Depending on the reaction of the choroid, atopic uveitis associated with the action of environmental allergens (pollen, food, etc.) is distinguished; anaphylactic uveitis caused by the development of an allergic reaction to the introduction of immune serum into the body; autoallergic uveitis, in which the allergen is the choroid pigment or lens protein; microbial-allergic uveitis, which develops in the presence of a focal infection in the body. clinical picture. The most severe form of uveitis is panuveitis (iridocyclochoroiditis). It can occur in acute and chronic forms. Acute panuveitis develops due to the entry of microbes into the capillary network of the choroid or retina and is manifested by sharp pains in the eye, as well as decreased vision. The process involves the iris and ciliary body, and sometimes the vitreous body and all the shells of the eyeball. Chronic panuveitis develops as a result of exposure to brucellosis and tuberculosis infection or the herpetic virus, occurs in sarcoidosis and Vogt-Koyanagi syndrome. The disease proceeds for a long time, with frequent exacerbations. Most often, both eyes are affected, resulting in reduced vision. When uveitis is combined with sarcoidosis, lymphadenitis of the cervical, axillary and inguinal lymphatic glands is observed, and the respiratory mucosa is affected. Peripheral uveitis affects people twenty to thirty-five years of age, and the lesions are usually bilateral. The disease begins with decreased vision and photophobia. Subsequently, due to clouding of the vitreous body and its peeling, a sharp decrease in vision is noted. With peripheral uveitis, the following complications are possible: cataract, secondary glaucoma, secondary retinal dystrophy in the macular region, swelling of the optic nerve head. The basis for the diagnosis of uveitis and its complications is eye biomicroscopy. Conventional research methods are also used. Treatment. For the treatment of acute uveitis, it is necessary to administer antibiotics: intramuscularly, under the conjunctiva, retrobulbar, into the anterior chamber of the eye and vitreous body. Provide rest to the organ and put a bandage on the eye. In chronic uveitis, along with specific therapy, hyposensitizing drugs and immunosuppressants are prescribed, and, according to indications, vitreous body moorings (adhesions) are excised. The treatment of peripheral uveitis is no different from the treatment of other forms of uveitis. 1. Influenza uveitis Influenza uveitis is characterized by an acute onset during and after influenza. Serous exudate is detected in the anterior chamber, posterior synechiae are easily ruptured when mydriatics are instilled, the precipitates are usually small. The disease lasts two to three weeks and, with timely treatment, usually ends safely. In children, it is often accompanied by symptoms of reactive papillitis. General treatment: oral durable (long-acting) preparations of broad-spectrum antibiotics (tetracyclines) and sulfonamides in age-appropriate doses, as well as antibiotics and sulfonamides, to which the conjunctival bacterial flora is sensitive, aspirin; intravenous 40% solution of methenamine; local mydriatics and vitamins. 2. Rheumatic uveitis It begins acutely, often against the background of a rheumatic attack; its seasonality is very characteristic. In children, a subacute course of the process is observed. Both eyes are often affected. A jelly-like exudate and a lot of easily ruptured posterior synechiae are found in the anterior chamber. In children, significant clouding of the vitreous body is observed. The disease lasts five to six weeks, and there is a tendency to relapse. Positive immune reactions to CRP, high titers of ASG and ASLO, a positive DFA test, and a positive skin allergy test with fibroallergenstreptococcus help in making a diagnosis. Treatment is general: inside aspirin (pyramidone, salicylic sodium, butadione), prednisolone, injections of cortisone, ACTH (intramuscularly), penicillin durant preparations. Doses are determined according to age. A diet rich in calcium and potassium salts, restriction of sodium chloride and liquid are recommended, mydriatics, vitamins, corticosteroids, sulfonamides, iontophoresis with pyramidon are locally prescribed. 3. Uveitis with focal infection Uveitis with focal infection is characterized by the presence of an inflammatory focus in the body (in the paranasal sinuses, tonsils, teeth, etc.), various-sized precipitates, and flaky opacities in the vitreous body. Treatment. It is necessary first of all to act on the root cause to remove carious teeth and roots, especially granulomas with cysts. Operations are performed on the paranasal sinuses against the background of the use of antibiotics and local therapy. 4. Uveitis in tuberculosis infection With tuberculosis infection, various forms of damage to the vascular tract are observed, depending on the state of the reactivity of the organism, the massiveness and virulence of the infection. Tuberculous lesions of the vascular tract are characterized by an inconspicuous onset, a sluggish course, the presence of "sebaceous" precipitates, "guns" along the pupillary edge of the iris, tuberculous tubercles, powerful, difficult to tear posterior synechiae. Sometimes the cornea is involved in the process. Sequential (complicated) cataracts often appear in early childhood. Additional research methods clarify the diagnosis: Pirquet, Mantoux tests, detection of focal reactions to tuberculin tests, biochemical studies of blood protein fractions before and after tuberculin tests, examination of sputum, washings of gastric contents for tuberculosis pathologies, tomographic examination of the lungs. Treatment. Complex therapy, specific antibacterial agents. First-line drugs (streptomycin, ftivazid, saluzide, tubazid) and second-line drugs (cycloserine, tibon, ethoxide, etc.) are used. Antibiotic treatment should be combined with PAS, but PAS should be used with caution in hemorrhagic forms. All drugs are prescribed according to the scheme according to age. Desensitizing and deallergizing agents are shown (diphenhydramine, diprazine, cortisone, calcium chloride, fish oil), vitamin therapy (vitamins D, A, B2, B1, rutin or vitamin P), diet therapy (food rich in fats, but with restriction of carbohydrates and sodium chloride ), climatotherapy. It is recommended to stay outdoors for a long time, observing the regime of work and rest. In the treatment of granulomatous tuberculous uveitis, PAS in the form of drops should be prescribed locally, as well as subconjunctival injections of a freshly prepared 2,8% PAS solution, alternating with subconjunctival administration of oxygen, iontophoresis with calcium chloride, streptomycin, saluzide under the conjunctiva, etc. Mydriatics are also indicated and corticosteroids. 5. Uveitis in nonspecific infectious polyarthritis It should be remembered that with this systemic disease caused by damage to connective tissue, the eyes can also be affected. The disease most often occurs in children aged three to four years. Characterized by acute or subacute onset, joint pain, and swollen lymph nodes. There is a lesion of connective tissue elements in the stroma of the cornea, conjunctiva, sclera, uveal tract, which is expressed in dry keratoconjunctivitis, corneal dystrophy, scleritis and episcleritis. First of all, the vascular tract is affected. The first signs of eye involvement in the pathological process are dry gray precipitates of various sizes on the posterior surface of the cornea. Chronic plastic iridocyclitis gradually develops with the formation of coarse stromal posterior synechia, leading to fusion and fusion of the pupil. The latter cause an increase in intraocular pressure. Further, dystrophic changes occur in the cornea near the limbus, respectively, at three and nine o'clock. Subsequently, the turbidity takes a ribbon-like form. Gradually, clouding of the lens develops, usually from the anterior layers. Thus, the presence of nonspecific polyarthritis, band-like corneal degeneration, chronic iridocyclitis, and sequential cataracts are characteristic features of Still's disease. However, there are cases when changes of this kind are not accompanied by infectarthritis for a long time and, therefore, are the earliest, and sometimes the only signs of this type of collagenosis. Treatment is comprehensive, restorative: intravenous 40% glucose solution, blood transfusions, physical therapy, joint exercises, electrophoresis of the joint area with calcium chloride, antiallergic and anti-inflammatory treatment (calcium gluconate, aspirin, butadione, chloroquine, delagil, corticosteroids, etc.). Vitamin therapy: vitamins B1, B12, B6 are prescribed intramuscularly; inside vitamins A, E, B1, B2, C. Absorption therapy: dionin, oxygen, ultrasound. Surgical treatment: partial layered keratectomy, iridectomy, cataract extraction in remission. 6. Toxoplasmosis uveitis The ophthalmic form of toxoplasmosis occurs as a sluggish serous iridocyclitis with significant clouding of the vitreous body. The central or peripheral exudative chorioretinitis is more often observed. Central chorioretinitis is manifested by a sharp decrease in visual acuity. Ophthalmoscopy reveals large white chorioretinal lesions with pigment in the central zone of the retina. Diagnostic positive serological reactions (RSK with the patient's blood serum) and a skin test with toxoplasmin help. In addition, with congenital toxoplasmosis, defects in the overall development of the child, hydro or microcephaly in combination with mental retardation can be observed. Radiological foci of calcification in the brain can be determined. Treatment. According to the scheme, in a certain dosage, depending on age, chloridine is prescribed in combination with sulfa drugs and cortisone. Local symptomatic therapy. 7. Principles of local treatment of uveitis of various etiologies Uveitis requires both general and local treatment. Local treatment is aimed at preventing the development of adhesions of the iris with the lens capsule, creating peace of the iris and ciliary body, for which it is necessary to achieve maximum pupil dilation using drugs that paralyze the sphincter (1% solution of atropine sulfate, 0,25% solution of scopolamine) and stimulating dilator (0,1% solution of hydrochloric adrenaline). To relieve pain, novocaine blockade and leeches on the skin of the temple are indicated. As anti-inflammatory drugs, injections under the conjunctiva of a 2% solution of pyramidon or a 0,51% solution of cortisone, electrophoresis with calcium chloride are used. 8. Metastatic ophthalmia The disease develops when the infection penetrates endogenously, as a result of the pathogen entering the eye with blood flow in pneumonia, cerebral meningitis, endocarditis, sepsis, etc., more often in young children, weakened, against the background of a very serious general condition. Usually one eye is affected. The process develops like endo or panophthalmitis. There is a rapid decline in visual acuity. With endophthalmitis, a mixed injection of the eye occurs; in transmitted light, a yellowish focus of various sizes is visible in the vitreous body. Panophthalmitis is characterized by severe swelling of the conjunctiva, chemosis, and massive mixed injection of the eyeball. The moisture in the anterior chamber becomes cloudy, the iris becomes yellow-brown, purulent yellow exudate is detected in the vitreous body, the general condition of the patient is serious. With a high virulence of the infection and a sharp weakening of the body, purulent melting of the eye tissue may occur, leading to its death. Sometimes the process ends with atrophy of the eyeball. Treatment. They act on the main cause of the disease, prescribe antibacterial and desensitizing therapy, antibiotics intramuscularly, intravenously, intraarterially and under the conjunctiva of the eyeball, sulfonamides, atropine, dry heat, UHF therapy are indicated locally. If the course of the process is unfavorable and the eyeball is atrophied, enucleation is performed. LECTURE No. 18. Choroiditis Choroiditis is an inflammation of the choroid itself. Etiology and pathogenesis. The cause of the inflammatory process of the choroid is an infection (tuberculous, streptococcal, staphylococcal, viral, syphilitic, brucellosis). The structure and functions of the choroid are such that they contribute to the retention of bacteria, viruses, protozoa, helminths and other pathogens brought in with the blood or lymph flow. The mechanism of development of choroiditis is based on immune reactions. The changes that determine the clinical picture of choroiditis are the result of antigens and immune complexes entering the eye. Extraocular foci of infection serve as sources of antigens. The occurrence of choroiditis can provoke hypothermia, acute and chronic infectious diseases, eye injury. Of particular importance is microbial allergy, manifested by hyperergic inflammation (hyperergy, increased reactivity). In this case, microbes can play the role of a trigger, and the inflammatory reaction develops as an autoimmune process. Choroiditis can be endogenous and exogenous. Endogenous are caused by tubercle bacillus, viruses, the causative agent of toxoplasmosis, streptococcus, brucellosis infection, etc. The occurrence of exogenous choroiditis occurs as a result of involvement in the inflammatory process of the choroid in traumatic iridocyclitis and diseases of the cornea. Choroiditis is divided into focal and diffuse. In the case of focal choroiditis, foci of inflammation can be single (isolated) and multiple (with scattered, disseminated choroiditis). Depending on the localization of the inflammatory formation, choroiditis is divided into central (with a focus in the central region of the fundus), peripapillary (with a focus around the optic nerve head), equatorial (with a focus in the equatorial zone of the eye) and peripheral, in which the inflammatory formation is localized in the peripheral regions. fundus near the dentate line. Pathological anatomy. With focal choroiditis, a limited infiltrate (a focus of inflammation with an increased volume and increased density) from lymphoid elements located around the dilated vessels throughout its entire thickness is found in the choroid. In diffuse choroiditis, the components of the infiltrate are lymphocytes, epithelioid and sometimes giant cells. The infiltrate compresses blood vessels and disrupts the blood supply to tissues. Inflammation of the choroid causes changes in the retina due to the destruction of the pigment epithelium layer, as well as the development of edema and hemorrhage. In the course of treatment, the infiltrate in the choroid can resolve. Then the cellular elements of the infiltrate are replaced by connective tissue, forming a scar. The retinal pigment epithelium grows along the periphery of the scar. With tuberculous choroiditis, cellular changes depend on the stage of development of the tuberculous process. In primary tuberculosis, inflammation in the choroid proceeds according to the exudative type. Diffuse infiltration includes epithelioid cells and Pirogov-Langhans giant cells. In secondary tuberculosis, granulomas are formed with caseous (curdled) necrosis and subsequent formation of tuberculomas. clinical picture. Patients with choroiditis do not have eye pain and visual disturbances. Therefore, it is detected only with ophthalmoscopy. When involved in the process of adjacent parts of the retina (chorioretinitis), visual impairment occurs. When the chorioretinal focus is located in the central parts of the fundus, there is a sharp decrease in vision and distortion of the objects in question, and the patient notes a sensation of flashes and flicker (photopsia). With damage to the peripheral parts of the fundus, twilight vision decreases, sometimes "flying flies" are observed before the eyes. Limited defects are revealed in the field of view of the scotoma, corresponding to the location of the foci. With inflammation in the fundus, grayish or yellowish foci with fuzzy contours are visible, protruding into the vitreous body; retinal vessels are located above them, without interruption. During this period, hemorrhages in the choroid, retina and vitreous body are possible. The progression of the disease leads to clouding of the retina in the focus area. Under the influence of the treatment process, the chorioretinal focus flattens, becomes transparent, acquires clearer contours, the choroid becomes thinner, and the sclera shines through it. With ophthalmoscopy, a white focus with large vessels of the choroid and pigment lumps is visible against the red background of the fundus, which indicates the onset of the stage of choroidal atrophy. When the chorioretinal focus is located near the optic nerve head, inflammation may spread to the optic nerve. A characteristic scotoma appears in the field of view, merging with the physiological one; with ophthalmoscopy, blurring of the boundaries of the optic nerve is determined. Peripapillary choreoretinitis develops, or Jensen's parapapillary neuroretinitis. With tuberculous lesions of the choroid, such clinical forms as miliary, disseminated, focal (with central and peripapillary localization of the focus) choroiditis, choroidal tuberculoma, and diffuse choroiditis are more common. The latter is more often observed at a young age against the background of chronically current primary tuberculosis. The inflammatory process in the choroid is accompanied by a pronounced reaction of the retina and vitreous body and ends with atrophy of the choroid. With toxoplasmosis, focal choroiditis develops, with congenital toxoplasmosis, central focal choroiditis. With acquired syphilis, diffuse choroiditis occurs. The course of choroiditis is often chronic, with relapses. Complications of choroiditis can be secondary retinal dystrophy, exudative retinal detachment, neuritis with transition to secondary optic nerve atrophy, extensive hemorrhages in the vitreous body with subsequent mooring. Hemorrhages in the choroid and retina can lead to the formation of rough connective tissue scars and the formation of a neovascular membrane, which is accompanied by a sharp decrease in visual functions. Diagnosis and differential diagnosis. The diagnosis is made on the basis of the results of direct and reverse ophthalmoscopy, fluorescein angiography of the fundus. These methods allow you to establish the stage of the disease, which is of great importance for the treatment and outcome of the disease. In 1/3 of cases, the etiology remains unclear, which requires a comprehensive examination of the patient. Currently, immunological diagnostic methods are widely used, which include serological reactions, detection of sensitivity to various antigens, determination of immunoglobulins (antibodies) in blood serum, tears and intraocular fluid, detection of a focal reaction in the eye in response to the introduction of allergens. Differential diagnosis is carried out with external exudative retinopathy, nevus (pigment tumor) and the initial stage of choroidal melanoma. Ultrasound and radioisotope research methods are necessary to clarify the diagnosis. Treatment and prevention. Treatment is aimed at eliminating the underlying disease. The treatment complex includes pathogenetic, specific and non-specific hyposensitizing agents, physiotherapeutic and physical methods of influence (laser coagulation, cryocoagulation). Specific hyposensitization is carried out in order to reduce the sensitivity of sensitized eye tissues in tuberculosis, toxoplasmosis, viral, staphylococcal and streptococcal choroiditis. The antigen is administered in small doses repeatedly. Specific hyposensitization is a promising method of treatment that excludes relapses. Nonspecific hyposensitization is indicated for chorioretinitis at all stages of treatment: during the period of active inflammation, with relapses, and also for the prevention of exacerbation. For this, antihistamines are used (diphenhydramine, suprastin, tavegil, pipolfen, diazolin, etc.). An important role in the treatment of choroiditis is played by antibacterial therapy, which is used in accordance with the nature of the process and for the sanitation of foci of infection. With an unknown etiology (cause) of choroiditis, broad-spectrum antibiotics are used. Corticosteroids are prescribed along with other drugs, immunosuppressive drugs (mercaptopurine, imuran, metatrexate, fluorouracil, cyclophosphamide, etc.). Antibiotics, corticosteroids, cytostatics are administered intramuscularly, orally, retrobulbarno (behind the eyeball), suprachoroidally and by electrophoresis. The arsenal of therapeutic agents includes vitamins C, B1, B6, B12. For resorption of exudate and hemorrhages in the choroid, retina, vitreous body, enzymes are used (trypsin, fibrinolysin, lidase, papain, lecozyme, streptodecase), which are administered intramuscularly, retrobulbar and by electrophoresis. Cryocoagulation of the choroid is indicated for secondary dystrophies after suffering choroiditis to prevent retinal detachment. For the same purposes, with hemorrhagic chorioretinitis, laser coagulation is used. Prevention of choroiditis is reduced to the timely diagnosis and treatment of acute and chronic infectious diseases. LECTURE No. 19. Tumors of the choroid and anomalies of the vascular tract 1. Cysts of the iris In the iris, single thin-walled or multiple blisters of various shapes and sizes are determined, which grow and can cause secondary glaucoma. If the cysts have a yellowish tint, they are called pearl cysts. They can occur in the iris due to the germination of the corneal epithelium into it after perforated wounds or surgical interventions. 2. Cysts of the ciliary body Determined by cycloscopy and gonioscopy. At the extreme periphery, at the dentate line, yellow-gray bubbles are visible, protruding into the vitreous body. Ciliary body cysts should be differentiated from retinal detachment, which is characterized by the presence of light gray or pink blisters, retinal swelling, and changes in the course and color of blood vessels. Cysts often cause secondary glaucoma. Treatment is carried out, as a rule, in the event of secondary glaucoma and consists in diathermocoagulation of the ciliary body, sometimes in excision of the cyst. Iris cysts are treated with diathermo or photocoagulation and excision. 3. Angioma of the choroid Angiomas are more often localized in the paracentral parts of the fundus, have a round shape, a yellowish-cherry color, and their borders are unclear. According to the location of the angiomas, a defect in the field of view is observed. If angioma of the vascular tract does not grow, it cannot be treated. When angioma grows, it should be differentiated from melanoblastoma. Diagnosis is aided by radioisotope studies and angiography. It should be taken into account that melanoblastoma occurs mainly in adults and elderly people. 4. Pigment tumors These benign melanomas in children can be localized in different parts of the vascular tract. Benign melanomas ("birthmarks") of the iris are of different sizes, slightly rise above its surface and have a dark color of varying intensity. They usually don't grow. Melanomas of the ciliary body are almost never detected in vivo and do not cause noticeable changes in the functions of the eye. Choroidal melanomas are often discovered incidentally during ophthalmoscopy. They look like spots of varying sizes and localization, dark with a gray tint, round in shape, with fairly clear boundaries. The retina under these spots is not changed or, due to the pronounced thickness of the melanoma, is somewhat protruded into the vitreous body. The state of eye function depends on the severity and location of melanomas. Children with melanomas of the vascular tract are subject to dispensary observation. At the slightest increase in the size of melanoma, radioisotope diagnostics and other additional studies are indicated. Melanoblastoma of the vascular tract in children is almost never registered. It is more common in people over thirty years of age. Treatment. Surgical intervention, diathermo, photo or laser coagulation. 5. Neurofibromatosis If, during examination using lateral illumination and biomicroscopy, the unevenness of the anterior chamber is determined, multiple nodules of a brownish-yellowish round shape with clear boundaries are found in the iris, slightly rising above the surrounding unchanged tissue of the iris, you should find out whether the patient has changes on the skin (pigment spots café-au-lait color, tumors along the skin nerves), which is characteristic of neurofibromatosis, or Recklinghausen's disease. It must be remembered that in such a patient, an increase in intraocular pressure is possible. Sometimes, in the absence of common clear manifestations of neurofibromatosis, the detection of changes in the organ of vision is of great diagnostic value. 6. Anomalies of the vascular tract Congenital coloboma of the iris (coloboma iridis congenitum) is the result of non-closure of the slit of the eye cup. The downward direction of the coloboma, the preservation of the sphincter of the pupil and its reaction to light, and sometimes the symmetry of the lesion of both eyes are characteristic. Sometimes it is combined with coloboma of the choroid itself and other malformations. With ophthalmoscopy, the coloboma of the choroid itself appears as a varied shape and size of a white sector with clear edges, over which the retinal vessels pass without change. Choroid coloboma, depending on its location, can cause a decrease in visual functions. Polycoria (polycoria) multiple pupils. Corectopia (corectopia) displacement of the pupil. Both of these anomalies may be accompanied by a decrease in vision. Aniridia (aniridia congenita) absence of the iris. In transmitted light, a bright red reflex is recorded. Visual functions are sharply reduced. May be associated with glaucoma. In such cases, surgical treatment of glaucoma is indicated. Heterochromia is the difference in the color of the irises in the right and left eyes. Albinism (albinismus) is the absence or deficiency of pigment in the choroid, retinal pigment epithelium, skin, and hair. Often such individuals have pronounced nystagmus and poor vision due to excessive light in the eyes. Wearing smoky glasses is shown. The residual pupillary membrane (membrana pupillarus perseverans) is the remnants of a film that closes the pupil, which dissolves by the end of uterine life. It has the appearance of thin threads starting from the small arterial circle of the iris or from its surface and attached to the anterior lens capsule. Sometimes, crossing the pupil, the membrane goes to the small arterial circle on the opposite side. Occasionally, the remnants of the pupillary membrane are an accumulation on the anterior capsule of the lens of small pigment clumps, shaped like asterisks. LECTURE No. 20. Pathologies of the fundus (part I) 1. General diagnostic questions If patients complain of deterioration in visual acuity, changes in peripheral vision, loss in visual fields (scotomas), blurred vision at dusk (hemeralopia, or night blindness), impaired color perception, then pathology of the retina can be assumed. When clarifying the data on the picture of the fundus in children and adults, it should be borne in mind that in newborns the fundus is light, the optic nerve head is grayish-pink, its boundaries are not entirely clear, there may be pigment deposits at the optic nerve head, the macular reflex is absent, the ratio the caliber of arteries and veins is 1:2. In pathological conditions of the retina, due to various reasons, a variety of changes can be observed in the fundus: 1) edema and retinal detachment; 2) clouding and ischemia; 3) atrophic foci; 4) tumor formations; 5) change in the caliber of vessels; 6) preretinal, retinal and subretinal hemorrhages. To judge the location in the retina of foci of hemorrhages, one should be guided by their shape, size, color, location in relation to the vessels of the retina. The lesions located in the layer of nerve fibers have the appearance of streaks or an oblong (linear) shape. In the area of the macula, in the layer of Henle, the lesions are located radially, form a “star” pattern, and have a yellowish-white color. In the middle layers of the retina, lesions are round or irregular in shape and have a yellowish or bluish tint. If the lesion is located in such a way that it covers the retinal vessels, then it is located in the inner layer of the retina. In cases where the lesion is located behind the retinal vessels, it is located in the middle or outer layers of it. The presence of pigment in the focus speaks in favor of damage to the neuroepithelial layer and choroid. The defeat of the inner layers of the retina is accompanied by swelling of the optic disc, its hyperemia. At the same time, the disk tissue is opaque, its borders are blurred, the retina in the peripapillary zone is opaque. Retinal hemorrhages have the form of lines, strokes located radially around the optic nerve head. Larger hemorrhages are triangular in shape with the apex facing the optic nerve head. Point hemorrhages of a rounded and oval shape are located in the middle and outer layers of the retina. Hemorrhages in the region of the optic disc or in the area of the macula, which are ovoid, dark in color, or bowl-shaped with a dark lower half and a lighter upper layer, are characteristic of preretinal localization. Subretinal hemorrhages have the appearance of a blurry red spot behind the retinal vessels. The ischemic retina is dull white, without a sharp border. The edematous retina looks dull, cloudy, the retinal vessels are not clearly visible. For a detailed examination of the fundus, patients should dilate the pupils with mydriatics. 2. Pigmentary degeneration (degeneration) of the retina (retinitis pigmentosa) From the anamnesis of patients with retinitis pigmentosa, characteristic complaints of poor vision at dusk are revealed. Objectively determined concentric narrowing of the field of view, impaired dark adaptation. The optic disc is waxy, the retinal vessels, especially the arteries, are constricted. On the periphery of the fundus, there is an accumulation of pigment in the form of "bone bodies". The field of view gradually narrows to a tubular one, the process always ends in blindness due to the death of photoreceptors and atrophy of the optic nerve. The disease is often bilateral and may present in early childhood; in half of the cases is hereditary. The presence of non-pigmented foci in the fundus is characteristic of non-pigmented retinal degeneration. Functional disorders in patients are the same as in retinitis pigmentosa. 3. Macular degeneration of the retina (degeneratio maculae luteae) Patients complain of a decrease in visual acuity, they note that they are better oriented in the evening than in the afternoon. With ophthalmoscopy in the area of the macula, pigmented and yellowish dotted foci, blanching of the optic nerve head from the temporal side are determined. When examining the visual field, a relative central scotoma is determined, as well as a violation of color perception for red and green colors. The disease is bilateral and often has a family-hereditary nature. 4. Macular Degeneration in Tay Sachs Disease This systemic disease, which is detected in children four to six months old, is manifested by mental retardation, seizures, muscle weakness due to fatty degeneration of ganglion cells of the retina and brain. In the area of the macula in such children, a degenerative white lesion with a bright red round spot in the center is detected. The child, as a rule, goes blind and dies before reaching the age of two. Treatment. Due to the fact that the etiological factors in the development of retinal dystrophies are not yet known, treatment is aimed at improving retinal trophism. It consists mainly in the appointment of vasodilators, vitamins of groups B, A, E, C, PP, intermidin, pilocarpine, cysteine, heparin, glucose, etc. 5. Retrolental fibroplasia Every premature newborn, especially if he was in an oxygen tent, should be examined by an optometrist. These children may develop retrolental fibroplasia of retinopathy of prematurity. It occurs in both eyes of children in incubators already in the second to fifth week after birth. There are three periods of the course of the disease. The first period (the acute phase lasting from three to five months) is characterized by the presence of retinal edema, vasodilation, and gentle diffuse opacification of the vitreous body on the periphery of the fundus. The second period (regression period) is characterized by the spread of newly formed vessels with their supporting tissue from the area of retinal changes into the vitreous body, the appearance of hemorrhages, and retinal detachment. In the third period (scar phase), a significant mass of opaque tissue and foci of proliferation are detected in the vitreous body, covering most of the retina. Fibrous masses gradually fill the entire vitreous body up to the lens. The anterior chamber becomes shallow, posterior synechiae appear due to developing iridocyclitis, then complicated cataracts, secondary glaucoma, and microphthalmos occur. Often eye changes are accompanied by microcephaly, hydrocephalus, tissue hypoplasia of the hemispheres, cerebellum, leading to mental retardation. Symptomatic treatment: absorbable therapy, corticosteroids. 6. External exudative hemorrhagic retinitis, or Coates' disease (retinitis exsudativa haemorrhagica externa) The disease is characterized by varicose veins in the central zone of the fundus. Exudative and hemorrhagic foci of white, gray or yellowish (golden) color with fuzzy contours, bumpy or smooth surface are found near the optic nerve head. The retina prominates in these places. The vessels “climb” onto the lesions, make bends, form loops, aneurysms, resembling the picture of angiomatosis. Exudation can be so pronounced that it appears as if there is a retinal detachment, as in retinoblastoma. Exudate accumulates between the choroid and the retina and penetrates the vitreous body. The fundus becomes poorly visible due to exudate and repeated hemorrhages. Gradually, the vitreous body takes on the appearance of a homogeneous grayish mass with hemorrhagic inclusions. Over time, the exudate is replaced by connective tissue, powerful moorings are formed that extend from the retina into the vitreous body and lead to retinal detachment. Gradually, starting from the posterior sections, the lens becomes cloudy. Visual functions decrease depending on the severity of the process. In the later stages, when there is retinal detachment, diaphanoscopy, radioisotope studies and echography help to exclude retinoblastoma. Treatment. The etiology of the disease is not yet known, so treatment is usually ineffective. Given the similarity of the process with retinal tuberculosis, specific anti-tuberculosis therapy is often used in combination with non-specific anti-inflammatory and resolving agents (corticosteroids and enzymes). 7. Acute obstruction of the central retinal artery (embolia s. thrombosis arteriae centralis retinae) Patients complain of a sudden sharp deterioration in vision, a typical picture is determined in the fundus: against the background of an ischemic milky-white retina, the central fovea stands out in the form of a cherry-red spot (the “cherry pit” symptom), the arteries are sharply narrowed, intermittency of blood flow is determined in narrow retinal arteries. Gradually, the optic disc becomes pale and atrophies, and the patient becomes blind. In children, embolism is rare, but sometimes spasm or embolism occurs in the presence of autonomic vascular disorders or rheumatic endocarditis. In adults, the causes of embolism are hypertension, rheumatism, endarteritis. 8. Thrombosis of the central retinal vein (thrombosis venae centralis retinae) The disease develops more often in older people on the basis of sclerotic changes, vascular changes in hypertension, in children with blood diseases. Patients complain of a rapid decrease in vision in one eye, the appearance of fiery flashes, fog before the eyes. The picture of the fundus: the optic disc and retina are edematous, the size of the disc is enlarged, it is red, protrudes into the vitreous body, the vessels are lost in the edematous tissue, the veins are dilated, tortuous, reminiscent of leeches. Throughout the fundus of the eye, especially in the area of the disk, there are various sizes and forms of hemorrhage. Treatment of acute obstruction of the central retinal artery, as well as thrombosis of the central retinal vein: therapy of the main suffering, the appointment of heparin, fibrinolysin, antispasmodics and vasodilators, and later absorbable drugs, physiotherapy. For the prevention of secondary glaucoma with thrombosis of the central retinal vein, instillations of pilocarpine are indicated. LECTURE No. 21. Pathologies of the fundus (part II) 1. Retinoblastoma Retinoblastoma is a malignant neoplasm that develops in the retina of the eye. It belongs to congenital tumors. It is detected in children aged two to four years. Retinoblastoma can be either unilateral or bilateral. The disease is detected more often in the first year of life. In approximately 30% of cases, the process is bilateral, often of a family-hereditary nature. Etiology, pathogenesis and pathological anatomy. The etiology has not been reliably established. A possible cause is considered to be a mutation of the chromosomes of germ cells due to internal and external factors. Retinoblastoma consists of neuroglia, that is, it is a glioma in its structure. Glia develops from the ectoderm and has great energy to reproduce and form new elements. Glial tissue permeates all layers of the retina and optic nerve. There are differentiated and undifferentiated forms of the tumor. The specific structures of differentiated retinoblastoma are true rosettes, which consist of a cylindrical form of embryonic-type neuroepithelial cells, sometimes there are abortive forms of the outer segment of photoreceptors. In undifferentiated forms, small cells with a large nucleus and a narrow rim of the cytoplasm are found, located diffusely or forming pseudorosettes around the vessels, surrounded by a zone of necrosis and calcifications. Mitoses are often noted in the tumor, dissemination to the vitreous body and the anterior chamber of the eyeball develops. Forms and stages of retinoblastoma. There are five stages of tumor development: 1) latent; 2) primary; 3) developed; 4) far gone; 5) terminal. The latent stage of retinoblastoma is characterized by such early indirect signs as unilateral pupil dilation, slowing or lack of its reaction to light. More pronounced is not a direct, but a friendly pupillary reflex. The depth of the anterior chamber may be reduced. These signs can be combined with slight changes in the fundus. The initial stage is characterized by the fact that ophthalmoscopy reveals a yellowish-white lesion with unclear contours in the fundus, often covered with retinal vessels. Small satellite lesions are observed around the lesion. Tumor growth leads to amaurosis (blindness). The tumor can spread into the vitreous body in the form of grayish-white, sometimes yellowish or greenish masses with blurred boundaries, on the surface of which hemorrhages are visible. Retinoblastoma is detected in lateral lighting and with the naked eye by the yellow glow of the pupil area. It is the last symptom that usually forces parents to show the child to an ophthalmologist. The process can spread across the retina (exophytic growth) and towards the vitreous body (endophytic growth). The appearance of retinal detachment makes diagnosis difficult. The advanced stage (glaucoma stage) is characterized by tumor growth and an increase in the volume of the contents of the eye, which often leads to an increase in intraocular pressure. In this case, pain in the eye, congestive injection, corneal edema, a decrease in depth and clouding of the moisture of the anterior chamber (pseudohypopion) are possible due to the fact that individual particles of the tumor come off and disperse inside the eye. The pupil is dilated and does not react to light. In some cases, implantation nodules resembling tuberculous ones are found in the iris. Advanced stage (germination stage). This stage of retinoblastoma is characterized by tumor growth beyond the eyeball, more often through the sclera, along the vessels, through the sheaths of the optic nerve, etc. Posterior growth of the tumor is manifested by exophthalmos with limited eye mobility, the spread of the process into the cranial cavity causes an expansion of the optic nerve canal, which is detected on radiograph. In the terminal stage (stage of metastases), enlarged cervical, submandibular lymph nodes are determined, further gross changes are observed from the side of the eye, up to the collapse of the membrane and the sharpest exophthalmos (the eye is dislocated). Tumor-like formations in the bones of the skull are revealed, and tuberosities of the liver, spleen, kidneys and other organs are enlarged. The process is accompanied by pain, the onset of cachexia, changes in the blood picture. Clinical picture. Retinoblastoma can be unilateral or bilateral. Bilateral tumors are often combined with microcephaly, cleft palate and other embryonic developmental defects. The onset of the disease usually goes unnoticed. The first clinical symptom may be decreased visual acuity. Sometimes an early clinical sign of a unilateral lesion may be strabismus. Then there will be a change in eye color (yellowish reflex), observed in the depths of the eyeball and visible through the pupil (the so-called amaurotic cat's eye). This phenomenon occurs due to the presence of gliomatous nodes on the retina and forces the child’s parents to consult a doctor. The tumor is characterized by slow growth. In the clinic of retinoblastoma, with an objective examination of the fundus, four stages are distinguished. At the first stage, retinal whitish-pink lesions with smooth or uneven relief, newly formed vessels and gray areas of calcifications are visible. Their dimensions do not exceed one quadrant of the fundus, the surrounding tissues are not changed. In the second stage, intraocular dissemination occurs. Whitish inclusions of various sizes are already observed in the vitreous body, precipitate-like deposits are noted in the angle of the anterior chamber of the eyeball and on the posterior surface of the cornea. Secondary glaucoma, buphthalmos (hydrophthalmos) appear. When a tumor grows into the retina, the accumulation of exudate under it leads to retinal detachment. Vision is reduced to complete blindness. The third stage is characterized by extraocular spread of the tumor. Accompanied by exophthalmos, tumor growth into the cranial cavity, most often along the optic nerve, gives symptoms of brain damage (headache, nausea, vomiting). Germination of retinoblastoma in the choroid leads to hematogenous dissemination and an unfavorable outcome. As a result of tumor necrosis, toxic uveitis may develop. In the fourth stage, symptoms due to metastasis join the eye symptoms. Metastasis occurs to lymph nodes, bones, brain, liver and other organs. Complications and diagnosis. A complication of retinoblastoma with a favorable outcome may be loss of vision in one or both eyes. A possible complication is the development of retinoblastoma into sarcoma (rhabdomyosarcoma), leukemia. The diagnostic criterion for retinoblastoma at the first stage of the disease is the detection of an amaurotic cat's eye. To objectively confirm the diagnosis, they resort to ophthalmoscopy, radiography, ultrasound examination of the eyeball and skull. Retinoblastoma should be differentiated from pseudoglioma, which occurs as a result of an inflammatory process, and it must also be distinguished from organized hemorrhage, proliferating retinitis, retinal detachment, Coates' disease, cysticercosis, tuberculosis, etc. Anamnesis (past infectious diseases) is important for making a diagnosis, the presence in some cases on the radiographs of the orbit of foci of calcification. Diaphanoscopy and echographic studies help in the diagnosis. Treatment and prevention. At the first and second stages of the disease, organ-preserving cryoapplication is possible. At later stages, treatment consists in the timely surgical removal of the tumor (enucleation of the affected eye in a unilateral process or both eyes in a bilateral process). Enucleation of the eyeball is performed with resection of the optic nerve at a distance of 1015 cm from the posterior pole of the eyeball. In the future, radiation therapy is carried out in combination with chemotherapy or alone. Photocoagulation may also be performed. Cyclophosphamide, prospedin, methotrexatebeve are used as antitumor drugs. Prevention of retinoblastoma consists in the timely genetic examination of those families whose relatives have been treated for retinoblastoma in the past. 2. Retinal anomalies Patients do not complain. Ophthalmoscopy at the optic disc reveals white, shiny, with a silver tint smears, radially arranged, resembling white flames, somewhat passing to the optic disc. These are myelin fibers. When examining the functions of vision, no pathological changes were noted. There is an increase in the blind spot. LECTURE No. 22. Diagnosis, clinic and treatment of pathologies of the optic nerve 1. General diagnostic questions If the patient complains of a deterioration in visual acuity, changes in the field of vision, a violation of color perception, these are signs of a pathology of the optic nerve. In such cases, it is necessary to check visual acuity, the field of view for white, red and especially green colors, to do a campimetric study, to check color perception according to Rabkin's tables. Depending on the nature of the damage to the optic nerve, visual functions change to some extent, the blind spot increases, color perception and dark adaptation are disturbed. The optic disc may be enlarged, hyperemic or pale, its color, shape and borders are changed, prominence into the vitreous body or excavation is noted. The combination of certain signs may give rise to a diagnosis of neuritis, stagnation or atrophy of the optic nerve. In the diagnosis of diseases of the optic nerve, a decisive role belongs to functional studies, which also make it possible to judge the dynamics of the process. In addition to functional studies, X-ray of the skull, lumbar puncture, consultations of a neuropathologist, otolaryngologist and other specialists are of great help. For effective treatment, it is important to establish an etiological diagnosis, to find out the cause of the disease. 2. Neuritis of the optic nerve (neuritus nervi optici) The most common causes of optic neuritis in children are infectious diseases, arachnoiditis, sinusitis, multiple sclerosis, etc. Lesions of the optic nerve are observed in the intraocular part of it (papillitis), behind the eye (retrobulbar neuritis) and in the intracranial region (opticochiasmatic arachnoiditis). With papillitis, patients complain of a rapid drop in visual acuity, which is also established during the examination. Disturbances in color perception, changes in the field of vision, an increase in the blind spot are determined, and in the fundus there is hyperemia of the disc, blurring of its borders, vasodilation, deposition of exudate along the vessels and in the vascular funnel, as well as hemorrhages in the tissue and retina. Such changes may be absent at the beginning of retrobulbar neuritis, then visual acuity suffers first of all. There may be pain when moving the eyeball. With retrobulbar neuritis, the papillomacular bundle is more often affected, which is then manifested by blanching of the temporal half of the disc. After retrobulbar neuritis, descending atrophy of the optic nerve develops. Characteristic of damage to the optic nerve in its intracranial part (opticochiasmal arachnoiditis) are complaints of a decrease in visual acuity (which is confirmed during examination), a change in the visual field of the chiasmatic type, manifested in the loss simultaneously in both eyes of the corresponding or opposite parts of the visual field (hemianopsia) . On the fundus of the pathology is not detected. The disease is usually bilateral, prolonged, and may be accompanied by headache. With the development of the process in the fundus, there may subsequently be phenomena of stagnation of the optic nerve head and its atrophy. Pneumoencephalography, lumbar puncture help the diagnosis. Treatment of neuritis etiological. It is necessary to prescribe antibiotics in combination with B vitamins, urotropin, glucose infusions, tissue therapy, nicotinic acid, angiotrophin, dibazol, aloe, FIBS. Treatment should be long, repeated courses, since part of the visual fibers may be functionally inhibited or be in a state of parabiosis, i.e., have the ability to recover. If a patient has optic-chiasmatic arachnoiditis, the intervention of a neurosurgeon is possible. The operation is indicated for persistent progressive loss of vision, as well as an increase in the central scotoma, and consists in dissecting the moorings around the optic nerve and chiasm. 3. Congestive nipple (disk) of the optic nerve (papillitis oedematosa s. oedema papillae n. optici) Causes of a congestive disc are volumetric processes in the brain that lead to an increase in intracranial pressure: tumors, brain abscesses, gummas, tuberculomas, cysticercosis, meningiomas, hydrocephalus, injuries of the skull and orbits. Diagnosis is aided by targeted examinations. Attention should be paid to the data of the anamnesis indicating hypertension syndrome, x-ray of the skull, diagnostic lumbar puncture, bilateral process in the fundus. Changes in the fundus, characteristic of a congestive nipple, vary depending on the stage of the process. Initially, the patient does not complain, visual acuity is not changed. In the fundus, congestive hyperemia of the disc, blurring of its borders due to retinal edema, which spreads along the vessels and increases it in the upper and lower sections, are noted. As a result, an increase in the blind spot is determined, which is of great importance for diagnosis. Subsequently, the optic nerve disk increases in size, its marginal edema increases, the disk protrudes into the vitreous body, the veins expand, and the arteries narrow, the vessels sink in the edematous retina, hemorrhages appear from the dilated veins on the disk, and white foci of transudate are determined near the disk. Visual acuity gradually decreases, the blind spot increases even more. In the future, a significant increase and blanching of the optic nerve is determined in the fundus, which mushroom-like protrudes above the level of the retina by 23 mm, which is determined using direct ophthalmoscopy. In the macular area, a "star" pattern may be observed. Patients complain of a significant decrease in vision. Vision changes depend on the localization of the pathological process in the brain. Bitemporal and binasal hemianopsia are observed when the process is localized in the chiasm region, for example, with pituitary tumors, craniopharyngiomas. Homonymous hemianopsia is a consequence of the impact of the pathological focus on the visual tracts. With a long-term congestive disc, the edema gradually decreases, the disc becomes grayish, its contours are indistinct, the caliber of the veins normalizes, and the arteries remain narrow. Subatrophy of the optic disc develops. Visual functions are still partially preserved. If the process progresses, secondary atrophy of the optic nerve develops, which is expressed in the fact that the disc becomes white, its boundaries are fuzzy, the vessels narrow, especially the arteries, and the patient goes blind. 4. Atrophy of the optic nerve (atrophia nervi optici) The disease occurs as a result of an inflammatory or congestive process in the optic nerve, accompanied by a progressive decrease in visual acuity and a characteristic picture of the fundus (blanching of the optic nerve head, vasoconstriction). With primary atrophy of the optic nerve, the borders of the disc are clear, and with secondary indistinct. Secondary atrophy of the optic nerve is observed after papillitis or congestive nipple, primary after retrobulbar neuritis, optochiasmal arachnoiditis, with spinal tabes. In addition, secondary atrophy of the optic nerve can occur as a result of many diseases of the retina of an inflammatory, dystrophic and post-traumatic nature, as well as angiocirculatory disorders. Possible congenital atrophy of the optic nerve. Treatment. Means aimed at improving blood circulation and stimulating the remaining depressed nerve fibers (nicotinic acid injections, oxygen under the conjunctiva, vitamins B1, B12, B6, tissue therapy, intravenous glucose, glutamic acid, ultrasound treatment, cysteine iontophoresis, etc.). 5. Glioma of the optic nerve (glioma nervi optici) Glioma is a primary tumor of the optic nerve. It occurs rarely and only in preschool children. The disease is characterized by three main features: 1) slowly increasing unilateral exophthalmos; 2) decreased visual acuity; 3) a picture of a stagnant disc in the fundus. The leading symptom is an irreducible (not decreasing with pressure on the eyeball) exophthalmos, which does not change with head tilt, tension, crying. The protrusion of the eye is, as a rule, straight forward, and only sometimes there is a slight outward deviation, which is due to the localization of the tumor of the optic nerve in the region of the muscular funnel. The tumor may spread along the optic nerve into the skull, and then there may be no exophthalmos. In such cases, X-ray examination helps to diagnose. Glioma should be differentiated from exophthalmos in thyrotoxicosis, orbital angioma, and cerebral hernia. The diagnosis is helped by such studies as radiography of the orbit, skull, optic nerve canal, angiography. Radioisotope diagnostics helps to exclude a malignant process in the orbit. LECTURE No. 23. Injuries of the eye 1. Perforated wounds of the eyes Due to the nature of the injuring objects (such as, for example, wooden sticks, glass fragments, metal particles), injuries are more often infected and are always severe. Corneal perforation wounds are characterized by the presence of a wound that passes through all layers of the cornea. The anterior chamber is small, but with good adaptation of the wound edges, especially with stab wounds, it can recover by the time of examination by an ophthalmologist. Ophthalmotonus is reduced. In connection with damage to the intraocular vessels, hyphema can be observed. If there is damage to the anterior capsule of the lens, then a cataract appears. Scleral perforated wounds are often not visible and are indirectly manifested by a deep anterior chamber and hypotension of the eye. The lens is damaged less frequently than with corneal injuries. Simultaneously with the injury of the sclera, the choroid and retina are injured. In the fundus, retinal ruptures and hemorrhages can be determined, respectively, at the site of injury to the sclera. Corneoscleral wounds can combine in their clinical picture signs of corneal and scleral wounds. With penetrating wounds of the eyeball, along with the inlet in the cornea or sclera, there may also be an outlet. It is diagnosed more often with ophthalmoscopy by the presence of retinal rupture and hemorrhages in the direction opposite to the inlet. In addition, in some cases, there is hemorrhage in the retrobulbar space, manifested by exophthalmos, soreness, and limited mobility of the eyeball. According to the scheme proposed by E. I. Kovalevsky in 1969, according to severity, it is advisable to divide perforated wounds into simple, complex and complicated. For simple perforated wounds of various localization, adapted edges are characteristic without loss of the internal contents of the eye; for complex (more common in children) prolapse and infringement of the membrane. Complications of penetrating wounds are manifested in the form of metallosis (siderosis, chalcosis, etc.), purulent and non-purulent inflammation, as well as sympathetic ophthalmia. Treatment. For cut or puncture wounds with adapted edges no longer than 2 mm, surgical treatment is not performed. Antibiotics are prescribed intramuscularly or orally, instillation of a 30% solution of sulfacyl into the conjunctival sac. When the wound is localized in the center of the cornea, mydriatics are indicated, while myotics are indicated in the periphery or in the limbus region. A sterile bandage is applied to the eye. Bed rest is observed for four to five days. The administration of tetanus toxoid is mandatory. For more extensive and especially complicated wounds, surgery is performed under anesthesia. Before the operation, a culture of the conjunctiva is taken to determine the flora and its sensitivity to antibiotics. In the postoperative period, conservative treatment is carried out using antibiotics, corticosteroids, vitamin absorption therapy according to indications (oxygen under the conjunctiva, ultrasound). Once their location has been established, intraocular magnetic foreign bodies are removed using an electromagnet. If the foreign body is located in the anterior chamber or iris, it is removed through the corneal wound, in other cases diascleral, along the shortest path, followed by suturing the scleral wound and diathermocoagulation around it. Unremoved metallic magnetic and amagnetic foreign bodies cause metallosis, which is accompanied by inflammatory and degenerative changes in the vascular tract, retina, as well as clouding of the optical media of the eye with a gradual decline in vision up to blindness. Operated patients should be on strict bed rest for five to twelve days, depending on the location of the wound, and receive conservative therapy. With sluggish, non-treatable iridocyclitis, which is more common with corneoscleral injuries with damage to the ciliary body, there is a risk of sympathetic inflammation in a healthy eye. Sympathetic inflammation (ophthalmia) can occur within a period of two weeks to several years from the moment the other eye is injured. The disease occurs as serous or plastic sluggish uveitis, as well as in the form of neuroretinitis or a mixed form of the disease. The process is manifested by moderate pericorneal injection of the eyeball, dust-like precipitates on the posterior surface of the cornea, posterior synechiae, and occurs with multiple relapses, most often in the form of plastic uveitis with fusion and fusion of the pupil. The outcome of the disease is a sharp decrease in vision, and often blindness. Almost the only preventive measure is timely (up to ten days) removal of the damaged eye to preserve vision in the undamaged eye. When sympathetic ophthalmia begins, it is necessary to urgently inject 23 ml of a 0,50,1% hydrocortisone solution under the conjunctiva daily or 1 times a week, prescribe prednisolone (dexamethasone) orally according to the age-specific dosage regimen and broad-spectrum antibiotics in combination with B vitamins . 2. Contusion of the eye Based on clinical, morphological and functional data, blunt injuries are divided into four degrees of severity (according to V. V. Mishustin). Blunt injuries of the first degree are characterized by reversible damage to the appendages and the anterior part of the eye, visual acuity and field of vision are completely restored. With blunt injuries of the second degree, damage to the appendages, anterior and posterior parts of the eyeball is observed, mild residual effects are possible, visual acuity is restored to at least 0,5, the boundaries of the visual field can be narrowed by 10-20°. With blunt injuries of the third degree, more pronounced residual effects are possible, a persistent drop in visual acuity within 0,40,05, narrowing of the visual field boundaries by more than 20 °. Blunt injuries of the fourth degree are characterized by irreversible violations of the integrity of the membranes of the eye, hemophthalmos, damage to the optic nerve. Visual functions are almost completely lost. Treatment. For intraocular hemorrhages, oral administration of rutin (vitamin P), ascorbic acid, and calcium chloride is indicated; in case of retinal concussion, dehydrating agents are prescribed (25% solution of magnesium sulfate intramuscularly, 40% solution of glucose intravenously, etc.), vitamin therapy (orally and parenterally, especially B vitamins). After a few days, oxygen injections under the conjunctiva of the eyeball, ionogalvanization with dionine or potassium iodide, and ultrasound are prescribed to resolve the hemorrhages. With dislocation and subluxation of the lens, accompanied by constant irritation of the eye or hypertension, its prompt removal is indicated, with retinal detachment, diathermo, cryo or photocoagulation with shortening (filling, depression, corrugation) of the sclera. With subconjunctival ruptures of the sclera, the wound is sutured, followed by conservative therapy with antibiotics and corticosteroids. A metallic magnetic foreign body is removed from the cornea with a magnet. If the foreign body in the cornea is amagnetic, then under local anesthesia with a 1% solution of dicaine (lidocaine), they are removed using a spear-shaped needle, and disinfectants are prescribed (30% sulfacyl solution, 1% synthomycin emulsion). Multiple small foreign bodies in the conjunctiva of the eyeball must be removed only if the eye is irritated. Large foreign bodies are removed with a lance-shaped needle in the same way as corneal foreign bodies, after instillation of a 1% dicaine solution. Orbital injuries can be the result of blunt trauma and wounds. In some cases, they are accompanied by subcutaneous emphysema, which most often occurs when the lower inner wall is damaged and is characterized by crepitus, bone defects detected on the radiograph, impaired skin sensitivity along the first and second branches of the trigeminal nerve, superior orbital fissure syndrome (ptosis, external and internal ophthalmoplegia, violation of the sensitivity of the cornea), exophthalmos due to retrobulbar hematoma or displacement of fragments into the orbital cavity or enophthalmos with divergence of fragments and an increase in the cavity of the orbit, rupture and separation of the optic nerve, ruptures of the choroid and retina. Fractures of the outer wall of the orbit may be accompanied by ruptures of the outer parts of the eyelids, hemosinus of the maxillary sinus, lockjaw. With fractures of the inner wall, various changes are observed in the lacrimal ducts, tears of the inner corner of the eyelids and severe damage to the eyeball. Injuries to the lower wall are complicated by hemosinus and fractures of the zygomatic bone. With fractures of the upper wall, cerebral phenomena are possible. Orbital injury is usually treated surgically. Foreign bodies present in the orbit are removed if they cause an inflammatory process or compression of soft tissues, the optic nerve or blood vessels. Bone fragments are also removed. Assign conservative treatment. 3. Eye burns The most common thermal burns in children are burns caused by lime, potassium permanganate crystals, and office glue. Due to an oversight by medical personnel during the prevention of gonoblennorrhea according to Matveev Kreda, newborns sometimes suffer burns from a concentrated (1030%) solution of silver nitrate. In children, burns are more severe than in adults. Particularly severe damage (colliquation necrosis) occurs with chemical burns, mainly with alkalis. Acid burns, especially sulfuric acid, are also very severe, but the acid does not penetrate deep into the tissue (coagulative necrosis). According to severity, burns are divided into four degrees, taking into account their localization, size and condition (hyperemia, bladder, necrosis) of burned tissues. First-degree burns are characterized by edema and hyperemia of tissues, second-degree burns are blisters, erosions, and superficial, easily removable necrotic films. The burn of the third degree is characterized by necrosis, which captures the thickness of tissues with the formation of a grayish folded scab, and the fourth degree by necrotic changes in almost all membranes of the eye. Third- and fourth-degree burns can be complicated by aseptic uveitis and endophthalmitis and result in eye atrophy. Another serious complication of these burns is perforation of the necrotic capsule of the eye with loss of membranes and subsequent death of the entire eye. The consequences of damage to the skin and conjunctiva are cicatricial eversion and inversion of the eyelids, their shortening, leading to non-closure of the palpebral fissure and the formation of adhesions between the conjunctiva of the eyelids and the eyeball, symblepharon, which, unlike trachomatous, is anterior. A burn can be caused by a chemical substance and hot foreign bodies that have entered the eye, as well as exposure to radiant energy, electric welding without goggles, and prolonged exposure to snow. Bright sunlight causes ultraviolet burns of the cornea and conjunctiva. There is a sharp photophobia, lacrimation, blepharospasm, edema and hyperemia of the mucous membrane. Biomicroscopy shows vesicles and erosions in the corneal epithelium. Watching a solar eclipse or molten glass or metal without protective goggles can cause infrared burns. The patient complains of the appearance of a dark spot before the eye. Ophthalmoscopy shows retinal edema in the macular region. After a few days, pigment mottling (dystrophy) may appear. The preservation of central vision depends on the degree of damage to the retina. Treatment. First aid for chemical burns of the eyes consists of abundant and prolonged rinsing of the burn surface of the conjunctival cavity with water, removing particles of the substance that have entered the eye. Further treatment is aimed at fighting the infection (local disinfectants are prescribed), improving the trophism of the cornea (subconjunctival injections of autologous blood with penicillin, vitamin drops and ointments, oxygen injections, intravenous 40% glucose solution, injections under the conjunctiva of riboflavin, fibrin film are indicated), reduction of corneal edema (instillation of glycerin and oral fonurite are recommended). Due to insufficient oxygenation of the cornea, unithiol and cysteine are indicated. In order to prevent adhesions in severe burns, a daily massage of the conjunctival fornix with a glass rod is performed after dicaine anesthesia. For third and fourth degree burns, urgent hospitalization in an eye hospital is indicated, and plastic surgery is often recommended. In cases of aniline burns, frequent rinsing with a 3% tannin solution should be prescribed; for lime burns, instillation of a 4% solution of disodium salt of ethylenediaminetetraacetic acid (EDTA) is indicated; for burns with potassium permanganate, a 5% solution of ascorbic acid is indicated. 4. Frostbite of the eyes Frostbite of the eyeball is extremely rare, since the protective apparatus protects the eye from exposure to low temperatures. However, under unfavorable conditions (workers of Arctic expeditions, pilots, athletes, etc.), as a result of the absence of cold receptors in the cornea, cases of frostbite of the cornea are possible. Subjective sensations during frostbite are manifested in the feeling of a foreign body under the eyelids. Since in such cases, medical workers do not detect foreign bodies, anesthesin (dicaine, lidocaine) is instilled as first aid. This, in turn, aggravates the conditions of frostbite, since the eye loses all sensitivity, and the protective reflex of closing the eyelids and moistening the cornea stops. Objectively, during frostbite, tender subepithelial vesicles appear in the cornea, on the site of which erosions subsequently form: eye irritation is absent at first and occurs only 68 hours after frostbite (like ultraviolet burns). According to the severity of frostbite are divided in the same way as burns. Treatment. Instillation of miotics, vitamin drops, application of 1% synthomycin emulsion or sulfacyl ointment. 5. Combat damage to the organ of vision Combat injuries of the organ of vision have a number of significant features compared to peacetime injuries. Unlike household injuries, all combat injuries are gunshot wounds. More often, eye injuries are caused by shrapnel, bullet wounds are rare. Wounds, as a rule, are multiple and are combined with powder gas burns. A characteristic feature of combat injuries is a high percentage of perforated wounds and severe concussions of the eye, damage to the orbit, combined wounds, combined with wounds of the skull and brain. The main principle of treatment is the phasing with the evacuation of the patient as directed. First aid (the application of a bandage from an individual package) is provided to the wounded on the battlefield by a comrade or medical personnel. The first medical (eye) aid (dressing and drug treatment) is provided on the day of injury in the SME or on the PHC. On the same day, the wounded is sent to the PPG, GLR or evacuation hospital, where he is assisted by an ophthalmologist. The first ophthalmic care unit is the Army Ophthalmic Reinforcement Group, part of the ORMU. These groups, together with groups in other specialties, are transferred to the KhPPG, where wounds are treated for the wounded. Slightly wounded soldiers finish treatment in these hospitals and return to the front. Seriously wounded soldiers are sent to the evacuation hospital of the first and second echelons of the GBF. They provide full-scale ophthalmosurgical care. The wounded, who need long-term treatment, are evacuated from the GBF to the evacuation hospitals of the inner region. Children often experience damage to the eye, similar to combat: when launching rockets, explosions of capsules, cartridges, which are produced without adult control. LECTURE No. 24. Myopia and astigmatism 1. Myopia Myopia (myopia) is one of the variants of the refractive power (clinical refraction) of the eye, which is formed simultaneously with a decrease in distance vision due to a mismatch in the position of the back main focus in relation to the central zone of the retina. Myopia is congenital (hereditary, intrauterine origin), with age it progresses and can be malignant. Acquired myopia is a type of clinical refraction. Often, with age, it increases slightly and is not accompanied by noticeable morphological changes in the eyes. This process of refractogenesis is considered as a biological option. But under certain conditions, the frequency of both congenital and acquired myopic refraction is pathological: the so-called progressive myopia is developing. Such myopia progresses in most children in the early school years, so it is often called "school", although this is not entirely correct, since myopia can progress at a more mature age. Causes of myopia Myopia usually appears in childhood, progressing with age. The following factors are of great importance in the development of myopia: 1) genetic, in which myopic parents often have myopic children. Factors such as weakness of the accommodative muscle, weakness of the connective tissue (the sclera becomes extensible, resulting in an increase in the length of the eyeball) can be inherited; 2) adverse environmental conditions, especially during prolonged work at a close distance from the eye. This is a professional, school myopia, easily developing with an incomplete development of the organism; 3) weakness of accommodation, leading to an increase in the length of the eyeball, or, on the contrary, tension of accommodation (inability of the lens to relax), which leads to spasm of accommodation. In contrast to true myopia, with false myopia, vision is restored to normal with drug treatment (i.e., seven-day instillation of a 1% atropine solution). This requires careful observation and skiascopy with the participation of an ophthalmologist. Spasm of accommodation can be eliminated with the help of special therapeutic exercises for the eyes. The initial signs of false myopia, or spasm of accommodation, a person may suspect in himself: 1) during visual work at close range, rapid eye fatigue, pain in the eyes, in the forehead, in the temples may occur; 2) near visual work can often be facilitated by using weak plus lenses (in this case, this does not mean that a person has farsightedness); 3) it may be difficult or slow to "set" the eyes to different distances, especially when looking from a close object to a distant one; 4) distance vision deteriorates. Spasm of accommodation, if left untreated, becomes persistent over time, difficult to treat and can lead to true myopia. Progressive myopia Progressive myopia is any type of myopia manifested by deterioration of distance vision. There is information about the antecedent of false myopia to true, i.e., this is a condition in which there is a more or less rapid and pronounced drop in distance visual acuity due to spasm, or tension, accommodation. However, after eliminating the spasm with the help of cycloplegic drugs (atropine, scopolamine, homatropine), vision is restored to normal, and refractometry reveals emmetropia or even farsightedness. In recent decades, myopia (myopia) more often began to develop in preschoolers who, during their upbringing, had a high visual load in combination with a sedentary lifestyle, poor nutrition and weakening of the body due to frequent illnesses (tonsillitis, dental caries, rheumatism, etc.). Among students in first and second grades, myopia occurs in 36%, in third and fourth grades in 6%, in seventh and eighth grades in 16%, in ninth and tenth grades in more than 20%. Severe (high, advanced) myopia causes over 30% of low vision and blindness from all eye diseases; it is an obstacle to the choice of many professions. The mechanism of development of myopia that occurs during childhood consists of three main links, such as: 1) visual work at close range (weak accommodation); 2) burdened heredity; 3) weakening of the sclera, violation of trophism (intraocular pressure). Consequently, according to the predominance of certain causes of development, myopia can be conditionally divided into accommodative, hereditary and scleral. The development of each of these forms of myopia over time leads to irreversible morphological changes in the eyes and a pronounced decrease in visual acuity, which often does not improve much or does not improve at all under the influence of optical correction. The main reason for this is a significant elongation of the axis of the eye: instead of 2223 mm, it reaches 3032 mm or more, which is determined using an echo-ophthalmograph. If myopia progresses within a year by less than 1,0 diopters, then it is conditionally considered benign, and if the increase is 1,0 diopters. and more malignant. However, the matter is not only in progression, but also in the size and changes in the intraocular structures (vitreous body, choroid, retina, optic nerve). A large stretching of the eyes during myopia leads to an expansion of the palpebral fissure, as a result of which a kind of bulging is created. The sclera becomes thinner, especially in the area of attachment of the lateral muscles and near the edge of the cornea. This can be determined with the naked eye by the bluish tint of the cornea due to translucence of the choroid, and sometimes by the presence of anterior staphylomas of the sclera. The cornea also stretches and thins. The anterior chamber of the eye deepens. Mild iridodonesis (trembling of the iris), destruction or liquefaction of the vitreous body may occur. Depending on the genesis and magnitude of myopia, changes in the fundus occur. It is necessary to distinguish between such changes as: 1) near-disk light reflexes; 2) myopic cones; 3) true staphylomas; 4) changes in the area of the retinal spot; 5) cystic retinal degeneration; 6) retinal detachment. Stretching of the sclera and atrophy of the pigment epithelium layer near the disc often lead to the appearance of myopic cones. Signs of a high amount of myopia are usually staphylomas, or true protrusions of the posterior sclera. In the area of the retinal spot, the most formidable changes of a degenerative and atrophic nature occur with high myopia. The formation of cracks in the choroid in the form of yellowish or whitish stripes, and then the appearance of white polymorphic, often merging foci with scattered clumps and accumulations of pigment, are the consequences of stretching the posterior segment of the eyeball. With the development of pathological changes in the area of the retinal spot, patients develop metamorphopsias (distortion of the shape and size of visible objects), weakening of vision, which eventually leads to a strong decrease, and sometimes to an almost complete loss of central vision. Progressive myopia occurs simultaneously with pathological changes in the extreme periphery of the fundus in the form of racemose retinal degeneration, and then multiple small retinal defects of slit-like, oval or round shape. Additional possibilities for the occurrence of retinal detachment explain the changes in the vitreous body. High myopia can sometimes appear in children in the first months of life, which suggests that such myopia is either hereditary or congenital. The latter develops as a result of diseases or underdevelopment in the antenatal period and is more common in children who have had a mild form of retrolental fibroplasia. Usually this myopia does not lend itself well to optical correction. Prevention and treatment of myopia. To prevent progressive myopia, the following is necessary: 1) preventing the development of myopia among the younger generation (primary prevention); 2) delay in the progression of already existing myopia (secondary prevention). The beginning of the prevention of myopia or its development should occur with the clarification of heredity and the determination of clinical refraction in children under one year old, but not later than 12 years of age. At the same time, there should be a differentiated attitude to the upbringing of the child, taking into account the state of his heredity and refraction. To do this, divide the children into two groups: 1) children with heredity aggravated by myopia, regardless of the detected size and type of refraction, with congenital myopia, with emmetropia; 2) children with farsighted refraction without heredity burdened by myopia. These are the so-called prevention groups (risk groups). Ophthalmologists must transmit lists of these groups to kindergartens and schools annually in July-August. Treatment of myopia can be conservative and surgical. Conservative treatment begins with vision correction with glasses or contact lenses. It is necessary to have the convenience of glasses and their compliance with the configuration and size of the face, ensuring visual acuity in both eyes within 0,91,0-2,03,0 and the presence of stable binocular vision. Glasses should be used constantly. In cases of moderate or high myopia, bifocal glasses can be used in such a way that the lower hemisphere of the lens is weaker than the upper one by an average of 3,0 diopters. With high myopia and anisometropia (more than XNUMX diopters), correction with hard or soft contact lenses is recommended. Treatment of rapidly progressive and severe myopia is a serious and often difficult task. The development of changes in the area of the retinal spot, the appearance of recurrent hemorrhages in the retina and vitreous body require the cessation of visual work, the creation of rest for the eyes, protection from harsh light and vigorous treatment. Both local and general treatment with calcium chloride, cysteine, preparations of Chinese magnolia vine, ginseng, mezaton, ethylmorphine hydrochloride (dionine), as well as subconjunctival oxygen injections, reflex therapy are recommended. It is necessary to prescribe rutin with ascorbic acid, riboflavin, thiamine, vitamin E, intermedin, adenosine triphosphoric acid, taufon, etc. If correction with glasses or contact lenses, conservative treatment methods, as well as reflexology do not stop or significantly reduce the rate of progression of the process, then surgical treatment is indicated. The decision on the timing and method of surgery is made depending on a number of factors. The younger the child, the faster the annual (over two to three years) progression of myopia (more than 1,0 diopters per year), the more significant the increase in the sagittal size of the eye, the greater the indications for strengthening the eye capsule with scleroplasty. The choice of scleroplasty technique is made in accordance with the stage of myopia, i.e., the location and magnitude of morphological changes. It is necessary to take into account that the less myopia, the more effective scleroplasty. Prevention of rapid progression of myopia through scleroplasty is effective in almost 90% of cases. Within two to three years after surgery, myopia often increases by 1,0 diopters. versus 3,04,0 diopters. with a conservative method of treatment. If myopia is stable for two to three years, but the child who has reached adulthood does not want to wear glasses and contact lenses or if it is impossible to ensure high visual acuity with their help, a keratotomy can be performed, i.e., non-through incisions on the cornea, due to which reduces its refractive power by a given amount. Keratotomy is most effective for low and moderate myopia, and for high myopia, keratomileusis is possible. Treatment of accommodative false myopia primarily requires limiting visual work at close range, correct correction of existing ametropia and anisometropia. The main methods of treatment are various training exercises for the ciliary muscle, instillation of drugs prescribed by an ophthalmologist, as well as reflexology. 2. Astigmatism Astigmatism is a refractive error in which different types of ametropia or different degrees of one type of ametropia are combined in one eye. Etiopathogenesis of astigmatism and its forms. The development of astigmatism is based on the unequal refraction of light rays in different meridians of the eye, which is associated with differences in the radius of curvature of the cornea (less often the lens). On the two main mutually perpendicular meridians, the strongest and weakest refractive power is observed. As a result of this feature, the image on the retina always turns out to be fuzzy, distorted. As a rule, the cause is an anomaly in the structure of the eye. However, such changes can occur after operations, eye injuries, diseases of the cornea. There is a simple astigmatism, in which emmetropia is noted in one of the main meridians, and ametropia (myopia or hypermetropia) in the other; complex astigmatism, when ametropia of the same type, but of varying degrees, is noted in both main meridians of the eye; mixed astigmatism, in which myopia is noted in one of the main meridians, and hypermetropia in the other. In astigmatic eyes, there are main meridians with the strongest and weakest refractive power. If the refractive power is the same throughout the meridian, then astigmatism is called correct, if different, incorrect. With direct astigmatism, the vertical main meridian has the strongest refraction, with the reverse horizontal. When the main meridians pass in an oblique direction, one speaks of astigmatism with oblique axes. Correct direct astigmatism with a difference in refractive power in the main meridians of 0,5 diopters. considered physiological, not causing subjective complaints. Clinical picture and diagnosis of astigmatism. Patients complain of a decrease in visual acuity, rapid eye fatigue during work, headache, and sometimes vision of objects twisted. Spherical convex and concave glasses do not improve vision. The study of refraction reveals the difference in the refractive power of the eye in different meridians. The basis of the diagnosis is to determine the refraction in the main refractive meridians. Treatment of astigmatism. Spectacles with cylindrical or spherical-cylindrical lenses (astigmatic lenses) are prescribed. The constant wearing of such glasses maintains high visual acuity and good performance. LECTURE No. 25. Primary glaucoma Glaucoma is a chronic eye disease that manifests itself as a constant or periodic increase in intraocular pressure, a special form of optic nerve atrophy, and significant changes in the visual field. Etiopathogenesis and classification. There are primary, secondary and congenital glaucoma. The development of primary glaucoma is influenced by both local and general factors. Local factors include changes in the drainage system and microvessels of the eye, general hereditary predisposition, neuroendocrine and hemodynamic disorders. Before an increase in intraocular pressure, trophic changes occur in the drainage system of the eye, which causes a violation of the circulation of aqueous humor and an increase in ophthalmotonus. Classifying primary glaucoma, it is necessary to take into account the form and stage of the disease, the level of intraocular pressure and the dynamics of visual functions. The state of the iridocorneal angle of the anterior chamber and the site of violation of the main resistance to the outflow of aqueous humor determines the form of glaucoma. There are open-angle and closed-angle forms of glaucoma. With open-angle glaucoma, dystrophic changes in the trabecular tissue and intratrabecular canals of varying severity, as well as blockade of the Schlemm's canal, occur. Types of open-angle glaucoma include pigmentary, pseudoexfoliative and low intraocular pressure glaucoma. In pigmentary open-angle glaucoma, the pigment completely covers the trabecular zone, which leads to a violation of the outflow of aqueous humor and an increase in intraocular pressure. Pseudoexfoliative glaucoma leads to the deposition of pseudoexfoliation on the posterior surface of the cornea, iris, ciliary body, and in the iris-corneal angle of the anterior chamber. Pseudoexfoliative glaucoma often coexists with cataracts. Glaucoma with low intraocular pressure is characterized by typical symptoms of primary glaucoma: visual field changes and partial atrophy of the optic nerve with glaucomatous excavation of the optic disc. With damage to the optic nerve is often associated with its low tolerance to ophthalmotonus, as well as severe sclerosis of the vessels that feed the optic nerve. Often there is a combination of glaucoma with low intraocular pressure and persistent vegetative-vascular dystonia, proceeding according to the hypotensive type. Angle-closure glaucoma is characterized by blockade of the iris angle of the anterior chamber by the root of the iris, as well as the development of goniosynechia. Glaucoma occurs with pupillary block, shortening of the iris angle of the anterior chamber, flat iris, and vitreocrystalline block. In mixed form of glaucoma, the signs of open-angle and closed-angle glaucoma are combined. There are four stages of the disease: initial, advanced, advanced and terminal, and at the same time an acute attack of angle-closure glaucoma. The designation of each stage is carried out by a Roman numeral for a brief record of the diagnosis. The staging of glaucoma is determined by the state of the visual field and the optic disc. The initial stage is characterized by the absence of marginal disc excavation and changes in the peripheral boundaries of the visual field. The advanced and advanced stage of glaucoma is characterized by the presence of marginal excavation, narrowing of the peripheral boundaries of the visual field, and the appearance of central and paracentral scotomas. At the advanced stage of the disease, the visual fields are narrowed by at least 5° from the inside, at a far advanced stage, the field of vision is narrowed at least in one meridian and does not go beyond 15° from the fixation point. According to the state of ophthalmotonus, normal, moderately elevated and high intraocular pressure are distinguished. clinical picture. Open-angle glaucoma usually occurs after the age of forty. The onset of the disease is often asymptomatic. 1520% of patients complain about the appearance of iridescent circles around the light source, periodic blurred vision. Often there is an early, age-inappropriate weakening of accommodation. There are minor changes in the anterior part of the eye. Sometimes there is an expansion of the ciliary arteries and episcleral veins. The depth of the anterior chamber in the case of open-angle glaucoma is usually not changed. Characteristic is the early appearance of changes in the iris in the form of segmental atrophy of the ciliary zone or diffuse atrophy of the pupillary zone with destruction of its pigment border. The clinical picture of open-angle glaucoma is characterized by the development of glaucomatous atrophy of the optic nerve in the form of marginal excavation. In this case, a whitish or yellowish ring (halo) may appear near the optic nerve head. In gonioscopic examination, the iris angle of the anterior chamber is always open, and is usually quite wide and only in rare cases somewhat narrowed. Corneoscleral trabeculae are sclerotic. There is exogenous pigmentation of the iris angle of the anterior chamber. With open-angle glaucoma, there is a slow and gradual increase in intraocular pressure as resistance to the outflow of aqueous humor increases. There are the following average figures for the ease of outflow, which correspond to the stages of development of open-angle glaucoma: in the initial stage 0,14, in advanced and advanced 0,08, in the terminal 0,04 mm3 / min per 1 mm Hg. Art. The deterioration of visual functions may be a consequence of the growing phenomena of glaucomatous atrophy of the optic nerve head. Early changes in the visual field are characterized by the expansion of the blind spot and the appearance of small scotomas in the paracentral region, later turning into Bjerrum's arc scotoma. Further development of the glaucomatous process characterizes the detection of defects in the peripheral visual field. The narrowing of the visual field occurs mainly on the nasal side (in the upper nasal sector). The late stages of the disease are characterized by concentric narrowing of the visual field and a decrease in visual acuity. Primary open-angle glaucoma is typical for middle-aged and elderly people. Changes occurring in the body are characteristic of this age group. A number of negative factors such as low blood pressure, the presence of cervical osteochondrosis, sclerotic changes in extracranial vessels affect the course and prognosis of primary open-angle glaucoma. All these factors lead to a deterioration in the blood supply to the brain and eyes. This leads to a disruption of normal metabolism in the tissues of the eye and optic nerve, a decrease in visual functions. Local factors negatively affecting the course and prognosis of open-angle glaucoma include a decrease in the resistance of the optic nerve head to compression, deterioration in tonographic parameters, unstable intraocular pressure (above 28 mm Hg with tonometry with a load of 10 g), an increasing ratio of excavation diameters and optic disc. Angle-closure glaucoma accounts for 20% of primary glaucoma cases. It usually progresses over the age of forty. It most often manifests itself in individuals with hypermetropia, since the anatomical features of eyes with such refraction (small anterior chamber and large lens) are predisposed to its development. The course of angle-closure glaucoma is characterized by periods of exacerbations and remissions. There are two main factors influencing the mechanism of increasing intraocular pressure: the advancement of the iris lens diaphragm (or the formation of an iris fold at its root during pupil dilation) and a functional pupillary block. In this case, the iris takes on a bulging configuration (bombing) and causes blockade of the anterior chamber angle. The course of the disease occurs in waves: with increases in intraocular pressure (attacks) and interictal periods. An acute attack of angle-closure glaucoma is provoked by emotional arousal, pupil dilation, copious fluid intake, overeating, cooling, body position that causes venous congestion in the eye area (with prolonged head tilt down, neck compression, etc.), drinking in a significant amount. Patients have pain in the eye, radiating along the trigeminal nerve to the forehead and temples, blurred vision, the appearance of iridescent circles when looking at a light source. Characterized by a slow pulse, nausea, and sometimes vomiting. The listed symptoms are observed either simultaneously, or each separately. An acute attack of glaucoma is always characterized by a decrease in visual acuity. There is an expansion of the anterior episcleral vessels (congestive injection), clouding of the cornea as a result of edema of its epithelium and stroma, a shallow anterior chamber, pupil dilation with a sharply reduced reaction to light. Sometimes the moisture of the anterior chamber becomes cloudy due to an increase in the protein content in it. The iris is hyperemic, its tissue is swollen. Opacities are often noted in the lens in the form of white spots located subcapsularly (disseminated subcapsular Vogt cataract). Corneal edema makes it difficult to examine the fundus. If it is possible to reduce the swelling of the cornea, then it becomes clear that the optic disc is swollen, and the retinal veins are dilated. In an acute attack of glaucoma, intraocular pressure is maximal, the iris angle of the anterior chamber is completely closed. There is a rapid increase in ophthalmotonus and a decrease in pressure in the Schlemm's canal. The root of the iris is often pressed against the corneoscleral zone with such force that it compresses the vessels of the iris. This causes an acute local circulatory disorder and focal necrosis of the iris, and then there are zones of its atrophy and deformation of the pupil. All this is a consequence of the development of aseptic inflammation, the appearance of posterior synechia and spraying of iris pigment epithelium cells, goniosynechia and subcapsular cataracts. This can adversely affect the optic nerve. Subacute attack of angle-closure glaucoma is milder. In this case, the angle of the anterior chamber of the eye does not close all the way or is not tight enough, which determines the clinical picture of the disease. Mild cases are characterized by blurred vision and the appearance of iridescent circles when looking at a light source. There is an expansion of the superficial vessels of the eyeball, slight swelling of the cornea, a slight dilation of the pupil. When gonioscopy marked blockade of the angle of the anterior chamber of the eye, especially below. Characterized by an increase in intraocular pressure up to 40 mm Hg. Art., a significant decrease in the coefficient of ease of outflow. With an increase in intraocular pressure up to 60 mm Hg. Art. symptoms are more pronounced: pain in the eye and superciliary arch and all of the above signs appear. The result of a subacute attack, in contrast to an acute one, is characterized by the absence of deformation and displacement of the pupil, segmental atrophy and gross goniosinechia. Diagnostics. Early diagnosis of primary glaucoma is extremely important. It is based on the patient's complaints, the history of the disease, the clinical picture, the results of the study of the functions of the eye, especially the central region of the visual field, the state of intraocular pressure and tonography data. Tonometry is the main method for determining intraocular pressure. The pressure is measured in the supine position of the patient with a tonometer with a load of 10 g, while the tonometric pressure is determined, which normally should not exceed 27 mm Hg. Art. Intraocular pressure in the right and left eyes normally differ by about 5 mm Hg. Art. Daily tonometry is considered very important for the diagnosis of glaucoma. Measurement of intraocular pressure is usually made at 68 o'clock in the morning and at 68 o'clock in the evening, it is desirable to measure it in the middle of the day. Determination of daily changes in ophthalmotonus occurs in a hospital or in a glaucoma dispensary: morning measurement of intraocular pressure is carried out in a patient still in bed. The normal study duration is 710 days, with a minimum of 34 days. There is a calculation of the average morning and evening indicators of the level of intraocular pressure and the amplitude of the ophthalmotonus. The optimal range of ophthalmotonus fluctuations during the day should not be higher than 5 mm Hg. Art. The difference in fluctuations exceeding 5 mm Hg. Art., is the reason for suspicion of glaucoma. Of great importance is the absolute value of the rise in ophthalmotonus (more than 27 mm Hg). If they occur repeatedly, then this is a reliable sign of glaucoma. Elastotonometry is a method for determining ophthalmotonus in the case of measuring intraocular pressure with tonometers of various masses. With elastotonometry, it is necessary to use a set of Maklakov tonometers weighing 5, 7,5, 10 and 15 g, with the help of which, in ascending order of their mass, intraocular pressure is measured 4 times. The readings of tonometers of different masses are plotted on a graph: the mass of tonometers in grams is plotted on the abscissa axis, and the values of tonometric intraocular pressure are plotted on the ordinate axis. The grounds for suspicion of glaucoma are the high onset of the elastocurve (intraocular pressure more than 21 mm Hg with tonometry with a load of 5 g), a shortened or elongated type of elastocurve (span less than 7 and more than 12 mm Hg). More accurate data on the hydrodynamics of the eye are obtained using electronic tonographs. Tonography is a method for studying the dynamics of aqueous humor with graphic recording of intraocular pressure. The method essentially consists in prolonged tonometry with further calculation of the main indicators of the hydrodynamics of the eye, the coefficient of ease of outflow and the minute volume of aqueous humor. Electronic tonographs help to conduct tonographic studies. The nature of the state of the outflow tracts of aqueous humor from the eye as a whole is determined by the coefficient of ease of outflow. In addition, it can be used to calculate the minute volume of aqueous humor. A guaranteed confirmation of the diagnosis is a combination of the results of tonography, daily tonometry and perimetry of the central part of the visual field. The diagnosis of glaucoma is not in doubt if the outflow easiness coefficient is less than 0,15, and the diurnal curve is pathological, in addition, scotomas are noted in the central part of the visual field. Glaucoma is suspected in the following cases: intraocular pressure equal to 27 mm Hg. Art. and higher; complaints characteristic of glaucoma; shallow anterior chamber; blanching of the optic disc (or part of it) or the beginning development of glaucomatous excavation; asymmetry in the condition of the two eyes (differences in the level of intraocular pressure, the depth of the anterior chamber, the condition of the optic discs); the presence of small paracentral relative and absolute scotomas in the field of view. If during the first measurement of intraocular pressure according to Maklakov (with a load of 10 g), the tonometric pressure is equal to 27 mm Hg. Art. and above, it is necessary to repeat the measurement after 2030-XNUMX minutes (strictly observing the rules of tonometry) to make sure that there is an increased intraocular pressure, eliminating the measurement error. Differential diagnosis of glaucoma is carried out with ophthalmohypertension. Treatment. Currently, there are three main areas of drug treatment of glaucoma: ophthalmohypotensive therapy (local and general) in order to normalize intraocular pressure; therapy that improves the blood supply to the inner membranes of the eye and the intraocular part of the optic nerve; therapy aimed at normalizing metabolism in the tissues of the eye in order to influence the degenerative processes characteristic of glaucoma. The selection of local antihypertensive drugs for the treatment of patients with primary glaucoma is carried out taking into account the following circumstances. Intraocular pressure usually decreases after a single instillation. This is the basis for conducting a drug test before the systematic administration of the drug. With subsequent instillations, the hypotensive effect is regularly repeated. Nevertheless, the manifestation of the antihypertensive effect of the drug does not occur immediately, at first it may be mild and intensify in subsequent days of treatment. The hypotensive effect in the case of prolonged use decreases until complete resistance to this drug. With long-term treatment of a patient with glaucoma, this is the reason for the expedient replacement of one drug with another. Often there is resistance to the drug from the very beginning (this drug does not help reduce intraocular pressure, therefore, its administration is impractical). In some cases, after the instillation of the drug, an increase in intraocular pressure occurs (a paradoxical effect). In this case, the appointment of this tool is contraindicated. In the case of developing a drug treatment regimen for a patient with glaucoma, an observation period is established (at least two to three weeks), after which it is necessary to use the drug. In the future, the effectiveness of treatment is monitored once every 1 months. Treatment of patients with primary glaucoma usually begins with the administration of instillations of solutions of cholinomimetic drugs, most often a 1% solution of pilocarpine hydrochloride 23 times a day. Pilocarpine helps improve the outflow of aqueous humor from the eye, which is a consequence of lowering intraocular pressure. If normalization of intraocular pressure is not observed after treatment with a 1% solution of pilocarpine hydrochloride, instillation of a 2% solution of pilocarpine 3 times a day is prescribed. If three-time instillations are insufficient, long-acting solutions of pilocarpine are used. These drugs are used 3 times a day. In the ophthalmic medicinal film, pilocarpine hydrochloride is also prescribed 12 times a day and 2% pilocarpine ointment at night. Other cholinomimetic agents (13% solutions of carbacholine or 25% solutions of aceclidine) are used much less frequently. If cholinomimetic drugs are insufficiently effective, one of the miotic agents with anticholinesterase action (prozerin, phosphakol, armin, tosmilen) is additionally prescribed. The frequency of instillation of these drugs is no more than twice a day. Their action is also aimed at improving the outflow of aqueous humor from the eye. For patients with open-angle glaucoma with low or normal blood pressure, with insufficient effectiveness of pilocarpine hydrochloride, instillations are added 1 2% solutions of adrenaline hydrotartrate, dipivalyl epinephrine, isoptoepinal, or adrenopilocarpine is prescribed 2 3 times a day. The decrease in the production of aqueous humor and partly the improvement in its outflow are explained by the hypotensive effect of adrenaline. When treating patients with open-angle glaucoma, along with pilocarpine, it is necessary to use 3% and 5% solutions of fethanol. Adrenaline differs from fethanol in that the latter has a longer and milder effect on blood vessels, therefore it is indicated for patients with glaucoma combined with the initial stage of hypertension. The hypotensive effect of fethanol is mainly due to a decrease in the secretion of aqueous humor. It is possible to use instillations of a 0,5% solution of clonidine (hemitone). The hypotensive effect of clonidine leads to inhibition of aqueous humor secretion, as well as improvement of its outflow. The effectiveness of treatment is monitored 23 times a month. They are also used in the form of eye drops/adrenergic blocking agents (1% anaprilin, 1% propranolol, 0,250,5% optimol). The decrease in the secretion of aqueous humor is explained by the hypotensive effect of these drugs. They do not change the size of the pupil and do not affect blood pressure. In the case of insufficient effectiveness of local antihypertensive therapy for open-angle glaucoma, it is supplemented with a short-term appointment of antihypertensive drugs of general action: carbonic anhydrase inhibitors (diamox, diacarb), osmotic (glycerol) and neuroleptic drugs (chlorpromazine). Carbonic anhydrase inhibitors reduce the production of intraocular fluid, which leads to a decrease in intraocular pressure. These drugs are especially effective in hypersecretory glaucoma. Diakarb is administered orally at a dose of 0,1250,25 g from 1 to 3 times a day. After three days of taking diakarba, it is recommended to take a break for 12 days. The appointment of glycerol and chlorpromazine occurs once with acute increases in intraocular pressure. It is necessary to decide on the surgical treatment of open-angle glaucoma individually, taking into account the form of glaucoma, the level of intraocular pressure, the coefficient of ease of outflow, the state of the angle of the anterior chamber, the field of view and the general status of the patient. The main indications for surgery are a persistent and significant increase in intraocular pressure, despite the use of various antihypertensive drugs; progressive deterioration of the visual field; negative dynamics of clinical data (the state of the iris, the angle of the anterior chamber, the optic nerve), i.e., the unstabilized nature of the course of the glaucomatous process. In recent years, laser methods have been used to treat primary glaucoma. In the case of open-angle glaucoma, the use of laser goniopuncture and trabeculospasis with argon or ruby lasers is effective. The most effective in the drug treatment of angle-closure glaucoma are miotic drugs, mainly cholinomimetic drugs (pilocarpine, carbacholine, aceclidine). It is also possible to prescribe a 0,250,5% solution of timolol. Strong anticholinesterase miotics (armin, phosphacol, tosmilen), promoting a sharp constriction of the pupil, can cause pupillary block, so they are usually not prescribed for closed-angle glaucoma. In this form of glaucoma, adrenomimetic drugs (adrenaline, fethanol, clonidine) are also contraindicated due to their mydriatic properties and the possibility of blocking the iridocorneal angle of the anterior chamber. General agents for reducing intraocular pressure include diacarb and glycerol used orally. With insufficient drug therapy, surgical and laser treatment is also used. Laser treatment consists of laser iridectomy and iridoplasty. Treatment of an acute attack of glaucoma. An acute attack of glaucoma requires urgent specialized care, the main purpose of which is to reduce intraocular pressure and thus normalize impaired blood circulation in the eye, restore metabolism in the tissues of the eye and the optic nerve. On an outpatient basis, treatment begins with instillations of a 1% (preferably 2%) solution of pilocarpine hydrochloride every 15 minutes for 1 hour, then every 30 minutes for the next 2 hours and then every hour. Instead of pilocarpine, a 1,53% solution of carbocholine can be administered. A 0,5% solution of Optimol is also instilled. Simultaneously with miotics, 0,5 g of diacarb or glycerol (50% glycerol solution) is prescribed orally at the rate of 11,5 g of glycerol per 1 kg of body weight. The decrease in intraocular pressure after taking glycerin begins after about 30 minutes, and after 1 1,5 hours its maximum reduction is achieved. Upon completion of emergency measures, the patient is sent to inpatient treatment. In the hospital, if the effect of previous treatment is insufficient after 23 hours and in the absence of arterial hypotension, the administration of chlorpromazine, which produces a pronounced sedative effect, is indicated. The drug reduces blood and intraocular pressure. The decrease in intraocular pressure under the influence of chlorpromazine is due to a decrease in the production of aqueous humor. Aminazine is administered as part of a lytic mixture containing a 2,5% solution of aminazine (1 ml), a 1% solution of diphenhydramine (2 ml) and a 2% solution of promedol (1 ml). Solutions of these medications are collected into one syringe, after which they are administered intramuscularly. After administration of the lytic mixture, patients must remain in bed for 34 hours in a horizontal position to prevent orthostatic collapse. In cases of severe corneal edema, eye baths with a 2040-810% glucose solution are indicated. If the described drug treatment does not stop an acute attack of glaucoma within XNUMX hours, anti-glaucoma surgery is performed. General drug treatment for primary glaucoma includes the prescription of drugs that improve metabolic processes in the retina and optic nerve. Vasodilators and drugs that affect tissue metabolic processes are means that stabilize visual functions in patients with glaucoma with normal intraocular pressure. Of these drugs, the most widely used internally are nicotinic acid (0,05 g 23 times a day for two to three weeks), nikoshpan (1 tablet 23 times a day for two to three weeks), noshpa (0,04 g 23 times a day), nigexin (0,25 g 34 times a day for the first 23 weeks and 2 times a day for another two weeks), aminalon (0,5 g 3 times a day for a month or more), Cavinton (0,005 g 23 times a day), Complamin (0,15 g 23 times a day), Trental (0,1 g 23 times a day), Riboxin (0,2 g 23 times a day), glio6, or pyridoxylate (0,1 g 23 times a day), biogenic stimulants (PhiBS subcutaneously, 0,5 ml, 1520 injections per course), 1% solution of sodium salt of ATP (1 ml intramuscularly daily, 3 injections per course), 0,25% solution of cytochrome C (4 ml intramuscularly every other day, 1015 injections per course), B vitamins. A combination of drugs is advisable. To stabilize visual functions, patients with glaucoma are prescribed a medicinal complex, including Eleutherococcus (30 drops 3 times a day for a month), cytochrome C (0,25% solution, 4 ml intramuscularly every other day, 1015 injections per course) and ascorbic acid (orally 0 g 1 times a day for a month). The specified drug treatment for patients with glaucoma is carried out in courses lasting 3 month 1 times a year, taking into account the need to normalize intraocular pressure. LECTURE No. 26. Congenital and secondary glaucoma 1. Congenital glaucoma There is hereditary congenital glaucoma (about 15% of cases) and intrauterine (about 85% of cases), which occurs as a result of exposure to various pathological factors on the fetal eye, which is a consequence of malformations of the anterior part of the eye. An increase in intraocular pressure occurs due to a violation of the outflow of intraocular fluid due to the closure of the iridocorneal angle of the anterior chamber by unresolved embryonic mesodermal tissue. Less common causes of aqueous humor retention are the anterior attachment of the iris and intratrabecular and intrascleral changes. Congenital glaucoma manifests itself in three forms: simple (actual hydrophthalmos) with changes in the angle of the anterior chamber of the eye (the most common); congenital glaucoma with anomalies in the anterior part of the eye or the entire eye (aniridia, ectopia of the lens, microphthalmos, etc.); congenital glaucoma with phakomatoses (angiomatosis, neurofibromatosis). Often, congenital glaucoma appears in newborns or in the first six months of a child's life, as well as in the first year of life. Congenital glaucoma is characterized by a progressive course. There are the following stages of the disease: initial, advanced, advanced, almost absolute and absolute. According to the state of intraocular pressure, it is possible to distinguish compensated, uncompensated and decompensated congenital glaucoma. The onset of the disease is manifested by photophobia, lacrimation, dullness of the cornea; the length of the sagittal axis of the eye and the diameter of the cornea are normal or slightly enlarged. An increase in the length of the sagittal axis of the eye, the diameter of the cornea and an increase in corneal edema occur in the advanced stage due to further stretching of the membranes of the eyeball. There are ruptures of the Descemet's membrane and clouding of the cornea. The anterior chamber becomes deeper. Changes occur in the iris in the form of atrophy and stromal hypoplasia, depigmentation. The pupil is dilated. Excavation of the optic nerve head, decreased visual acuity, and narrowing of the field of view on the nasal side to 45-35° are observed (if the child’s age allows them to be examined). The progressive stage of the disease is determined by a sharp increase in the length of the sagittal axis of the eye and the diameter of the cornea. The limbus is stretched. The sclera becomes thinner, and the choroid appears through it in a bluish-bluish color. The anterior chamber is deep. There are degenerative changes in the cornea. The pupil is wide. The optic disc is grayish in color, its excavation increases. There is a sharp decrease in visual acuity, a concentric narrowing of the field of vision, mainly on the nasal side (up to 15°). In the stage of almost absolute and absolute glaucoma, all these phenomena increase, complications often develop (subluxation and dislocation of the lens, intraocular hemorrhages, complicated cataracts, retinal detachment, etc.), vision is reduced to light perception with an incorrect projection, and in the absolute stage complete blindness is observed. Treatment. Treatment of congenital glaucoma is surgical. In order to eliminate embryonic tissue and improve the outflow of intraocular fluid into Schlemm's canal, in most cases, operations are performed in the area of the anterior chamber angle, as they are the most effective. Despite the age of the child, the operation must be performed urgently. Drug treatment is additional to surgical treatment (before and after surgery). Among medications, a 12% solution of pilocarpine hydrochloride, a 0,055% solution of Armin, a 0,013% solution of phosphacol and a 23% solution of aceclidine, a 0,25% solution of Optimol are prescribed locally. Diacarb or glycerol is taken orally (in doses corresponding to the body weight and age of the child). General strengthening and desensitizing therapy is carried out. 2. Juvenile (juvenile) glaucoma It develops at a young age due to congenital defects in the structure of the iridocorneal angle of the iris, there is a hereditary transmission of these defects. Usually people older than thirty years are ill. For some patients, changes in the iris are characteristic (hypoplasia, large crypts or their almost complete absence, eversion of the pigment sheet, coloboma), for others, the first symptoms appear in the second decade of life, develop slowly, the cornea is of normal size, the anterior chamber is deep. In the diagnosis of erased forms, gonioscopic and tonographic studies are important. Many patients with juvenile glaucoma have a remnant of germinal mesodermal tissue in the anterior chamber angle. Topical application of various miotic drugs (pilocarpine, carbacholin, aceclidine, phosphakol, armin), as well as clonidine and optimol, is shown, diacarb is prescribed orally. In the absence of compensation for the glaucomatous process and the deterioration of visual functions, an operation is indicated. 3. Secondary glaucoma The increase in intraocular pressure that occurs with secondary glaucoma is the result of another disease of the eye (or the whole body) or damage to the eye. Glaucoma can develop at various times after cataract removal. An increase in intraocular pressure in the early stages after cataract extraction is associated with pupillary block as a result of obstruction of the pupil by the vitreous body, residual lens masses, or air introduced into the eye. The reason for the increase in ophthalmotonus in the later stages after cataract removal may be pupillary or angular blockade, which developed as a result of postoperative complications (iridocyclitis, goniosinechia). Occasionally, glaucoma in an aphakic eye may be a manifestation of primary open-angle glaucoma not identified prior to cataract extraction. The differential diagnosis is based on the data of tonometric, tonographic studies and gonioscopy of both eyes. Treatment consists of dilating the pupil, reducing ophthalmotonus, reducing the production of intraocular fluid, eliminating the inflammatory reaction, and also depends on the cause of the increase in intraocular pressure. They use in the form of instillations a 12% solution of pilocarpine hydrochloride, preparations of timolol maleate (0,250,5% timoptik, 0,250,5% ofthimolol, 0,250,5% proxodolol, etc.), combined preparations (fotil, timpilo ), Diacarb is prescribed orally at a dose of 0,1250,25 g 23 times a day. If ineffective, surgical intervention is indicated. Secondary glaucoma in iridocyclitis and uveitis The causes of this disease are anterior uveitis occurring in the acute period with exudation into the anterior chamber of the eye. The exudate contributes to the closure of the filtering zone of the angle of the anterior chamber and the deterioration of the outflow of intraocular fluid. Changes in the vessels of the uveal tract (expansion of capillaries, blood stasis) associated with the inflammatory process are of great importance. In chronic uveitis, the development of secondary glaucoma occurs as a result of the formation of posterior circular synechia of the pupil, goniosynechia, which are the result of a normal outflow of aqueous humor, which leads to a sharp increase in intraocular pressure. In secondary glaucoma, which is a complication of chronic uveitis, in the light of a slit llama, single precipitates are found on the posterior surface of the cornea, in the corner of the anterior chamber, exudate, goniosinechia. The diagnosis is made on the basis of tonometry, elastometry, tonography, biomicroscopy and gonioscopy data. Precipitates located on the posterior surface of the cornea distinguish secondary uveal glaucoma from primary. First of all, the underlying disease is treated. In the acute stage, especially with the formation of posterior synechiae, patients are prescribed applications with a 0,1% solution of adrenaline hydrochloride or a solution of adrenaline is injected subconjunctivally 0,25 ml once a day. Mydriatic agents are used: 1% solution of homatropine hydrobromide, 0,25% solution of scopolamine hydrobromide, 1% solution of mezatone. Corticosteroid drugs are used locally: 0,52,5% hydrocortisone suspension, 0,3% prednisolone solution, 0,1% dexamethasone solution, Sofradex drops. To reduce intraocular pressure, diacarb is administered orally at a dose of 0,1250,25 g 23 times a day. A persistent increase in intraocular pressure and the ineffectiveness of medical treatment lead to the need for surgical treatment. Secondary glaucoma with circulatory disorders in the vessels of the eye, orbit and intraocular hemorrhages The causes of this pathology are most often thrombosis of the central retinal vein, less often venous circulation disorders in the orbit (inflammatory processes, edematous exophthalmos, etc.), impaired venous outflow in the anterior ciliary veins, intraocular hemorrhages. Pathological changes in the outflow of aqueous humor (development of connective tissue moorings) lead to secondary glaucoma with thrombosis of the central retinal vein. In the case of hemophthalmia, the causes of an increase in intraocular pressure are deposits filling the filtering system in the zone of corneoscleral trabeculae of hemosiderin and other blood decay products due to intraocular hemorrhages. Further, in the corner of the anterior chamber, the formation of connective tissue with newly formed vessels occurs. These changes increase the resistance to the outflow of aqueous humor and are the consequences of a persistent increase in intraocular pressure. Retinopathy of various etiologies can contribute to the development of secondary glaucoma. The clinical picture is determined by the underlying disease. Secondary hemorrhagic glaucoma with thrombosis of the central retinal vein develops 38 months after the onset of the disease and is characterized by a severe course. Various processes in the orbit can lead to a significant increase in intraocular pressure (up to the development of an attack of glaucoma). The diagnosis is based on the clinical picture of the underlying disease and the data of tonometric, tonographic studies and gonioscopy. Treatment begins with treatment of the underlying disease. The prescription of miotic drugs is carried out in the absence of newly formed vessels in the iris. Their presence indicates the need to recommend instillation of solutions of adrenaline, clonidine, optimol, and corticosteroids. Medications that promote the resorption of hemorrhages are prescribed: local instillation of a 3% solution of potassium iodide, a 0,1% solution of lidase, lidase and vitreous are prescribed intramuscularly. LECTURE No. 27. Cataract Cataract - partial or complete clouding of the substance or capsule of the lens with a decrease in visual acuity up to its complete loss. There are primary and secondary cataracts, acquired and congenital. Congenital cataracts can be hereditary or result from intrauterine developmental disorders, such as infections in the mother, such as rubella, etc. Etiopathogenesis and pathological anatomy. Depending on the etiological factor, several groups of cataracts are distinguished: senile, traumatic, complicated, radiation, toxic and metabolic. The mechanism of development of age-related cataracts is multifactorial and is not yet fully understood. With age, the mass and thickness of the lens increase, and its refractive power decreases. The nucleus of the lens is compressed by new layers of fibers forming concentrically and becomes harder. As a result, the transparency of the lens is sharply reduced. Chemically altered core proteins gradually stain. With age, the lens takes on shades from yellow to brown. A blunt, non-penetrating wound can cause clouding of the lens, affecting part or all of it. The initial manifestation of a contusion cataract is often a stellate or rosette-like opacification, usually located in the center of the lens, where the back of the lens is involved. Rosette-shaped cataracts can progress to complete opacification. In some cases, the lens capsule ruptures with blunt trauma, followed by swelling of the lens fibers, resulting in clouding of the lens. Complicated cataracts often form against the background of chronic uveitis of various origins due to the toxic effects of inflammatory products on the lens. The lens is very sensitive to radiation: infrared radiation, which causes damage to the anterior capsule of the lens in the form of peeling of the surface layers, ultraviolet radiation (290-329 nm), ionizing radiation. As a result of exposure to a number of chemicals (naphthalene, dinitrophenol, thallium, mercury, ergot), toxic cataracts develop. The ingress of alkali into the conjunctival cavity causes damage to the conjunctiva, cornea and iris and often leads to the development of cataracts. Alkaline compounds easily penetrate the eye, reduce the acidity of chamber moisture and reduce the level of glucose in it. Cataract occurs in some metabolic diseases: diabetes mellitus, galactosemia, hypocalcemia, Westphal-Wilson-Konovalov's disease, myotonic dystrophy, protein starvation. In diabetes mellitus, with an increase in blood sugar levels, the glucose content in the chamber humor and lens increases. Water then enters the lens, causing the lens fibers to swell. Edema affects the refractive power of the lens. In 75% of patients with classic galactosemia, cataracts usually develop during the first weeks after birth. The accumulation of galactose inside the lens leads to an increase in intracellular pressure, fluid enters the nucleus of the lens, and the layers of the cortex take on the appearance of “oil drops” visible in transmitted light. Cataracts can form in any condition that leads to a decrease in calcium levels in the blood: tetany, spasmophilia, rickets, renal failure. In Westphal Wilson-Konovalov disease, copper metabolism is impaired. A golden-brown Kaiser-Fleischner ring appears, which is formed by pigment granules. The ring is separated from the corner of the eye by a strip of transparent corneal tissue. With miotic dystrophy, patients develop multicolored iridescent crystals in the posterior intracapsular layers of the lens. The disease is hereditary. Pathoanatomical changes in cataracts are manifested depending on the location, type and degree of clouding of the lens. The following types of cataracts are distinguished: polar, suture, nuclear, capsular, zonular, complete, membranous. With polar cataracts, changes in the lens form in the intracapsular layers of the anterior or posterior pole of the capsule. Suture cataracts are manifested by opacification of the Y-shaped suture of the nucleus. Congenital nuclear cataract is an opacification of any embryonic nucleus. Capsular cataract is a limited opacification of the epithelium and anterior capsule of the lens. Zonal cataract is a bilateral symmetrical lesion. A complete cataract is a clouding of all lens fibers. Membranous cataract occurs when the proteins of the lens are reabsorbed. In this case, the anterior and posterior capsules of the lens are fused into a hard membrane. clinical picture. The clinical picture of cataract in the primary form is manifested by complaints of decreased visual acuity. Sometimes the first symptoms of cataract are distortion of objects, monocular polyopia (multiple vision of objects). In the clinical course of senile cataracts, initial, immature, mature and overmature stages are distinguished. In the initial stage, patients may have no complaints, others note a decrease in visual acuity, the appearance of “flying spots”, and sometimes polyopia. During a biochemical study at this stage, the appearance of intracapsular bubbles and separation of the lens fibers are determined. After 23 years, the stage of immature cataract begins. At this stage, the phenomena of hydration of the lens increase, and patients complain of a sharp decrease in vision. The immature cataract stage lasts for years. Gradually, the lens begins to lose water, and the clouding acquires an intense gray tint and becomes uniform. The stage of mature cataract occurs. At this stage, the figure of a lens star and intense opacification in the area of the lens sutures are visible. Patients complain of a lack of objective vision. With overripe cataracts, the cortex transforms into a liquefied milky mass, which undergoes resorption, and the volume of the lens decreases. With nuclear cataracts, central vision is impaired early, and distant vision is more affected. Temporary myopia may occur. In side light, the lens in these cases has a light green tint. Complications of cataracts are phacolytic glaucoma, phacogenous iridocyclitis. Phacolytic glaucoma develops in immature cataracts due to the absorption of a decaying substance during swelling of the lens, an increase in its volume and as a result of a violation of the outflow of intraocular fluid. When cataract masses fall into the anterior chamber of the eye and their resorption is delayed, iridocyclitis may occur, associated with the development of hypersensitivity to the lens protein. Treatment. Conservative cataract therapy is used for initial lens opacification to prevent its progression. Medicines used to treat cataracts contain a means for correcting metabolic processes, normalizing electrolyte metabolism, redox processes and reducing lens edema (oftankatachrome, soncatalin, vitaiodurol, quinax). Surgical treatment (removal of the cataract) remains the main treatment for lens opacity. Indications for surgical treatment are set individually. It depends on the state of visual functions, the nature and intensity of the clouding of the lens. Removal can be intracapsular or extracapsular. With intracapsular removal, the lens is removed in a capsule. With extracapsular removal, after opening the anterior capsule of the lens, the nucleus is squeezed out, and the lens masses are sucked off. A method has been developed for removing cataracts through tunnel incisions, which are sutured. Currently, the main methods of cataract removal in children include suction, ultrasonic phacoemulsification and mechanical removal of the lens. 1. Cataracts in children In accordance with the classification proposed by E. I. Kovalevsky in 1970, the following forms of cataracts in children should be distinguished. By origin, they are divided into: congenital (hereditary, intrauterine); consistent due to local processes (uveitis, congenital glaucoma, injuries, etc.) and due to general diseases (infectious and neuroendocrine diseases, radiation sickness, metabolic diseases, etc.); secondary (postoperative). By localization, cataracts are: polar, nuclear, zonular, coronary, diffuse, membranous, polymorphic, anterior and posterior (cup-shaped, rosette). According to the absence or presence of complications and concomitant changes, cataracts are divided into: simple (except for opacities, there are no other changes), with complications (nystagmus, amblyopia, strabismus), with concomitant changes (congenital malformations of the eye, microphthalmos, aniridia, coloboma of the vascular tract, retina, optic nerve, etc., acquired by pathology of posterior and anterior synechiae, subluxation and dislocation of the lens, vitreous hernia). According to the degree of visual impairment: the first degree of cataract visual acuity is 0,3 and above), the second is 0,20,05, the third is below 0,05. 2. Congenital cataracts (cataractae congenitae) Anterior and posterior polar cataracts (cataractae polaris anterior et posterior) are diagnosed by their location at the poles of the lens. Opacities are clearly visible in transmitted light and biomicroscopy. Anterior polar cataracts can also be detected on examination with lateral illumination. Polar cataract has the appearance of a dense white disk with a diameter of not more than 2 mm, quite clearly delimited from the surrounding transparent areas of the lens. When the eyeball moves, the anterior polar cataract is viewed in transmitted light moving in the direction of eye movement, while the posterior polar cataract moves in the opposite direction. These types of cataracts usually do not affect visual acuity and are not subject to surgical treatment. Zonular (layered) cataract (cataracta zonularis) is the most common congenital pathology of the lens. In transmitted light, a zonular cataract is a gray, lighter in the center disk 56 mm in diameter with radiar processes ("riders") against the background of a pink reflex of the fundus. In the light of a slit lamp, clouding is visible in the form of a disk located in the central sections and surrounded by a transparent substance of the lens. Along the edge of the disk, which consists of separate opacification zones, additional opacities in the form of protrusions are visible. The degree of vision loss depends on the intensity of the clouding. Unlike other types of congenital opacities, zonular cataract can progress in the first years of a child's life. Diffuse (complete) cataracts (cataracta diffusa) are visible even with side lighting. The pupil area is diffusely gray, vision is sharply reduced. One of the varieties of congenital cataracts is membranous cataract (cataracta membranacea), which has a gray (white), often homogeneous color. This type of cataract is diagnosed according to the biomicroscopic picture (deeper anterior chamber, iridodonesis, direct optical section of the lens) and echography data (one echopic from the lens instead of two). Such cataracts also significantly reduce visual acuity and, like diffuse ones, are subject to removal. All rare lens opacities (coral-shaped, pyramidal, etc.) of congenital genesis of various localization and severity, on which the degree of vision loss depends, are taken for polymorphic cataract. 3. Diagnosis of cataracts in children When examining a child, it is important to find out how the mother’s pregnancy proceeded, whether there were any harmful effects on her body (rubella, influenza, chicken pox, oxygen starvation of the fetus as a result of heart disease in the mother, lack of vitamin A in the pregnant woman’s diet, etc. ), at what weight and whether the child was born full-term, and whether he was kept in an oxygen tent after birth. Find out the presence in the anamnesis of general (tuberculosis, diabetes, infectarthritis, etc.) and local (uveitis, trauma, etc.) processes that can cause the occurrence of sequential cataracts. An examination of the eye is always preceded by a brief acquaintance and establishment of contact with the child, then visual functions are determined. In young children, when it is not possible to determine vision by classical methods, one should pay attention to how they orient themselves in the environment, whether they have shaped vision (whether they reach for a toy that is shown at various distances from the eye, whether they move freely) . Visual acuity in older children and adults should be determined according to the tables (up to two units) with both narrow and wide pupils, with and without correction, since this is important in clarifying the indications and choosing the method of surgical intervention. If the patient has light projection, it should be established whether it is correct. If the projection of light on the eye with a cataract is incorrect and it is impossible to examine the deeper parts of the eye (vitreous body, retina, optic nerve, choroid) using visual methods, echo-ophthalography is performed, which allows to detect changes in the vitreous body, retinal detachment, etc. The study of the visual field in patients with cataracts can be carried out on the projection-registration perimeter with an object of the greatest brightness and magnitude, as well as on the desktop perimeter with a luminous object or a candle. Approximately the field of view is also determined in the process of studying the light projection. You should not immediately resort to forcible examination of the child (with the help of eyelid lifters). During an external examination, attention is paid to the position and excursion of the eyeballs (in case of strabismus, the magnitude of the Hirschberg deviation is determined), the presence of nystagmus and other complications, as well as concomitant congenital anomalies. Further, under conditions of mydriasis (caused by 0,10,25% scopolamine, 1% homatropine, etc.), an examination is carried out with a side lamp, a combined method and in transmitted light. During an eye examination, young children are occupied by showing bright toys and talking. When examining the eyes, you can see clouding of the lens in the form of a gray disk (zonular cataract) or a gray dot (anterior polar cataract), etc. You should pay attention to which direction the clouding shifts when the eye moves. This allows us to judge their topography in the lens. When the lens is subluxated (dislocated), its edge is visible; also, with dislocation, changes in the depth of the anterior chamber, trembling of the iris (iridodonesis), congestive injection of the eye are noticeable, and increased ophthalmotonus can be detected by palpation. In the absence of opacities in the lens, its pathology can be indirectly judged by visual acuity and accommodative ability. When examining the cornea, scars can be detected, indicating a perforated wound in the past and the traumatic origin of the cataract, as well as a former surgical intervention. Particular attention is paid to the depth and uniformity of the anterior chamber. A deep and sometimes uneven chamber occurs with aphakia, dislocations of the lens, and iridodonesis (trembling of the iris) is often observed during eye movement. Posterior synechia, subatrophy of the iris, expressed in some fuzziness of its pattern and depigmentation, indicate past uveitis and suggest (together with an assessment of the anamnesis and biomicroscopic picture) a consistent (complicated) nature of lens opacity. The presence of a coloboma of the iris upward indicates a former surgical intervention. In some cases, with partial clouding of the lens, ophthalmoscopy is possible, which sometimes makes it possible to detect severe congenital pathology in the fundus (coloboma of the retina, choroid, etc.). 4. Sequential (complicated) cataracts (cataractae complicatae) Sequential cataracts in children of different ages can occur with eye damage, uveitis, congenital glaucoma, diabetes, infectious nonspecific polyarthritis (Still's disease), etc. Cataracts against the background of tuberculous uveitis are observed in about 1/5 of sick children, in most cases after iridocyclitis. Usually one eye is affected. Opacification of the lens begins with its posterior sections in the form of a grayish veil or dots, as a result of which visual acuity is somewhat reduced. The turbidity may stabilize or regress. In some cases, the process progresses up to a complete clouding of the lens and a decrease in vision to light perception. Eye damage due to infectious nonspecific polyarthritis, along with corneal dystrophy and uveitis, can be accompanied in most cases by cataracts. The process is usually two-way. Initially, opacities appear at the anterior surface of the lens, in the pupillary zone, in the form of pinpoint whitish-gray inclusions. Gradually they capture the cortical part of the lens to the embryonic nucleus, in rare cases reaching the central and then the posterior parts of the lens. The peripheral parts of the lens often remain transparent. Some children experience gross changes in the anterior capsule of the lens, caused by the organization of a whitish exudate with newly formed vessels and pigment inclusions. In this case, vision is reduced to light perception with correct projection. Opacities of the lens in infectious nonspecific polyarthritis and tuberculous uveitis are observed in children older than one year. The most severe types of cataracts develop in predominantly older children with an acute course of the process in the eye. Cataract in congenital glaucoma occurs in its advanced stage, with a pronounced stretching of the corneoscleral capsule of the eye. Progressive cup-shaped gray opacities appear under the posterior lens capsule. The entire posterior capsule, posterior cortical and middle layers gradually become cloudy. The anterior lens capsule and anterior layers remain translucent for a long time. Cataracts in children with hydrophthalmos can be unilateral or bilateral, but they usually do not occur simultaneously. Diabetic cataract in children occurs in two clinical varieties: one is characterized by classical manifestations (the presence of subcapsular vacuoles and opacities, consisting of whitish dots, spots, flakes, extending to the cortical regions and beyond), the other combines atypical signs of cataract development, in which there is often no subcapsular opacities and vacuoles. The pathology of the lens is detected at any duration of the disease. Of primary importance is the severity of the process. 5. Senile cataract (cataracta senilis) Senile cataracts are characterized by a slow progressive loss of vision. With initial cataracts (cataracta incipiens), visual acuity is usually high. With side illumination, no changes from the side of the lens can be detected. In transmitted light with a dilated pupil against the background of a pink reflex, one can see opacities on the periphery along the equator of the lens in the form of spokes or strokes or in the center if the cataract is nuclear. If a patient has an immature (swelling) cataract (cataracta nondum matura s. intumescens), he complains of a significant decrease in vision. When illuminated from the side, a gray cloudy lens is visible in the pupil area. The lens may swell, causing the anterior chamber to become shallow. due to the existing transparent areas in the lens, the shadow of the iris is visible on it in lateral lighting, as well as a reflex from the fundus in transmitted light. Swelling of the lens can cause increased intraocular pressure. Patients with mature cataracts (cataracta matura) are practically blind. Visual acuity is equal to light perception or hand movement near the face; there is no shadow from the iris, there is no reflex from the fundus. If the cataract is overripe (cataracta hypermatura), then cholesterol deposits are observed in it in the form of white plaques on the anterior capsule of the lens, the nucleus may descend downwards, as the cortical substance liquefies. White plaques and a drooping nucleus are visible on combined examination and under the slit lamp. Treatment of congenital and senile cataracts. Congenital cataracts that hardly affect visual acuity (for example, polar cataract, suture cataract) cannot be treated. Zonular, diffuse, membranous, nuclear and other cataracts are removed when visual acuity decreases to 0,2, and also if vision does not increase with pupil dilation. As a rule, the operation is performed on children under two years of age. At a later age, surgical intervention is less advisable, since amblyopia develops, which requires long-term postoperative treatment. With diffuse (complete) opacities of the lens, cataract extraction is performed. In the case of zonular and other partial cataracts, the operation is performed in two stages: first, the anterior lens capsule is dissected, and then, after 1012-XNUMX days, a simple (without iridectomy) extracapsular cataract extraction is performed. Intracapsular congenital cataracts are almost never removed, since the zonium ligaments in children are strong, elastic, and, in addition, their lens is firmly connected with the vitreous body. With membranous cataracts, the operation of dissection of the excision of the lens capsule is indicated. Senile cataracts are treated depending on the stage of the process and the state of the visual function. In the initial stage, the appointment of vitamin drops (cysteine, withiodurol, etc.) is shown, with a mature cataract, intracapsular extraction. If visual acuity is very low, the patient is practically blind, and the cataract is not quite mature, intracapsular extraction is also performed. In elderly people, unlike children, due to the presence of a dense nucleus in the lens, it is often necessary to perform an iridectomy during surgery, i.e., the so-called combined cataract extraction is performed. If an iridectomy is not performed, the operation is called simple cataract extraction. Treatment of consecutive cataracts is carried out depending on the etiology of the process and the degree of vision loss. For example, in diabetes, lens opacities may disappear under the influence of insulin therapy. Before prescribing a patient for surgery, it is necessary to have the following additional data: the conclusion of the therapist to exclude somatic contraindications to surgical intervention, the results of chest x-ray, positive conclusions of the otolaryngologist and dentist, sowing from the conjunctiva, reaction to toxoplasmosis, Wasserman reaction, blood tests (general, coagulability and bleeding time), urinalysis. On the eve of the operation, it is necessary to cut the eyelashes and shave the eyebrows. On the morning of the operation, a cleansing enema is done, the patient does not eat. Children are operated under anesthesia, adults under local anesthesia. The operating field is treated with alcohol, smeared with iodine, covered with sterile napkins. In the postoperative period, the patient is on strict bed rest in the supine position for three days. For the prevention of postoperative iridocyclitis, mydriatics and anti-inflammatory drugs are prescribed. If the depth of the anterior chamber is not restored on the second or third day, this indicates poor adaptation of the edges of the postoperative wound or detachment of the choroid. In such cases, repeated intervention is required. Author: Shilnikov L.V.
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