Investigation of the volumetric structure of ophthalmoscopic objects. Description of the fundus of the eye Disk hyperemia, small single hemorrhages in the layer of nerve fibers

OCULAR FUNDUS (fundus oculi) - the inner surface of the eyeball visible during ophthalmoscopy: the optic disc, the retina with the central artery and central vein, and the choroid.

An extremely important area of ​​​​the retina, which has the function of central vision (the highest vision in the retina), is yellow spot(s. macula lutea) with a central fossa (fovea centralis). The yellow spot is located outside approximately 2 diameters of the disk from its temporal border; its center is slightly below the horizontal line passing through the middle of the disc. The yellow spot stands out in a darker color; it has the form of a horizontally located oval, along the edge of which often, especially at a young age, a silvery-white arc or ring is noted - a macular reflex. This light reflex occurs due to the thickening of the retina in the form of a roller around the macula. In the center of the yellow spot, a darker round spot is visible - a dimple (foveola) with a shiny dot in the middle. In older people, the yellow spot stands out less clearly, while light reflexes are usually weakly expressed or completely absent; its position in this case is judged by a darker color and the absence of blood vessels.

With conventional ophthalmoscopy, the yellow color of the spot is indistinguishable against the red background of G.; it can be seen only with ophthalmoscopy in redless light, proposed by Vogt (A. Vogt, 1913). This method is used to study the retina and optic disc. When examining with a light source devoid of red rays using a blue-green light filter, G. appears to be colored green-blue, the retinal vessels appear almost black, the yellow spot is lemon-yellow, and thin vascular branches invisible at conventional ophthalmoscopy (tsvetn. fig. 5), since short-wave rays are reflected mainly from the surface of the retina. Dimmer (F. Dimmer) found that the yellow color depends on the pigment located in the retina in the macula. In addition to redless, for ophthalmoscopy, light colored differently with the help of light filters is used.

In 1960, a comprehensive method for the study of G. by light of various spectral compositions was developed, including comparative ophthalmoscopy in blue, yellow, red, redless, yellow-green and purple light (see Ophthalmoscopy).

In the study of G. in redless and yellow-green light, you can see the course and distribution of the nerve fibers of the retina. These fibers in the form of white stripes start from the disk, bend over its edge and diverge in a fan-like fashion. Near the disc, the fibers are coarser and more clearly defined than at the periphery. Some of them follow the direction of large vessels and reach the periphery, some go to the macula, forming a papillomacular bundle. At the macula, some fibers are steeply bent, take a vertical direction, and, bordering the macula from the temporal side, are lost in it. The fibers going up and down from the disc do not participate in the formation of the papillomacular bundle; they bend and cross at an obtuse angle, and partly, without crossing, go to the periphery. The blood circulating in the vessels of the retina and choroid can be determined by fluorescein angiography (see). With its help, it is possible to clarify the causes of circulatory insufficiency in the vessels of the retina (obturation, spasm), to identify patol, processes in the macula and optic nerve that are indistinguishable during ophthalmoscopy, to differentiate tumor and inflammatory processes, early vascular changes in diabetes.

The peripheral border of G. corresponds to the jagged line (ora serrata); it has a darker color and is visible with an enlarged pupil and a maximum deviation of the eye in the corresponding direction. G.'s periphery is better seen when using a special research method, which consists in local depression of the eyeball and observation with a slit lamp (see) through a gonioscope with an appropriate mirror (see Gonioscopy).

Pathological changes in G. are caused by damage to the optic nerve, the retina and vascular membranes of the eye, as well as the boundary membrane of the vitreous body.

Ophthalmoscopically, with damage to the optic nerve, there are changes accompanied by hyperemia and edema of the optic disc - congestive nipple, ischemic disc edema, pseudocongestive nipple (see Congestive nipple), neuritis; atrophic changes (primary and secondary atrophy of the optic nerve), tumors of the optic disc and developmental anomalies (see Optic nerve). In some cases, changes are detected ophthalmoscopically only when the process, having begun somewhere in the optic nerve behind the eye, reaches the disc (retrobulbar neuritis, descending atrophy).

Patol, changes in the retina are ophthalmoscopically characterized by the appearance of diffuse opacities in it or limited white foci, hemorrhages and dyspigmentations, vascular changes. These changes are based on inflammatory (see Retinitis), circulatory-metabolic (see Retinopathy), dystrophic processes, circulatory disorders and developmental anomalies (see Retina).

Changes in the choroid, visible during ophthalmoscopy, are the result of inflammatory, degenerative, sclerotic processes, neoplasms and developmental anomalies. In most cases, inflammatory processes of the choroid are focal in nature (see Choroiditis). At the same time the pigment epithelium of a retina is involved in process owing to what in the field patol, changes there is an accumulation of lumps of a pigment. Gradually, on the site of inflammatory foci, atrophic changes occur, which are the main ophthalmoscopic sign of damage to the choroid. Some changes in G.'s, for example, the protrusion of the disc with a congestive nipple, a mottled reflex on the arteries with diabetic retinal angiopathy, are better detected with ophthalmochromoscopy. Microaneurysms in diabetic retinal angiopathy are well detected by fluorescein angiography.

Clinical and diagnostic characteristics of fundus changes

Illustrations for the table

Rice. 6 - 10. Pathological changes in the fundus. Rice. 6. Neurofibromatosis. Rice. 7. With tuberous sclerosis of the brain. Rice. 8. Multiple retinal angiomas. Rice. 9. With amaurotic idiocy. Rice. 10. Pseudoneuritis of the optic nerve.

Rice. 11 - 26. Rice. 11. The initial congestive nipple (the arrow indicates the arc around the nipple light reflex). Rice. 12. A pronounced congestive nipple, at the upper edge of its hemorrhage (indicated by an arrow). Rice. 13. Pseudocongestive nipple on the basis of drusen (indicated by arrows). Rice. 14. Pseudo-congestive nipple on the basis of drusen hidden in its depth (indistinguishable from a true congestive nipple). Rice. 15. Hidden druse (indicated by an arrow) (distinguishable with ophthalmochromoscopy). Rice. 16. Optic neuritis. Rice. 17. Primary (simple) atrophy of the optic nerve. Rice. 18. Secondary atrophy of the optic nerve (arrow indicates an atrophic corolla around the disc). Rice. Fig. 19. Atrophic optic disc when examined in normal light (Fig. 19 and 20 the image is enlarged). Rice. 20. An atrophic optic disc appears blue when examined in purple light. Rice. 21. Axial (axial) atrophy of the optic nerve (arrow indicates blanching of the temporal half of the disc). Rice. 22. Axial atrophy of the optic nerve when examined in purple light (pale temporal half appears blue). Rice. 23. Axial atrophy of the optic nerve when examined in yellow-green light - a symptom of a break in the pattern of nerve fibers (indicated by an arrow). Rice. 24. Obstruction of the central retinal vein (arrows indicate hemorrhage). Rice. 25. Obstruction of the branch of the central retinal vein (arrow indicates hemorrhage). Rice. 26. Obstruction of the branch of the central retinal vein when examined in redless light (arrow indicates hemorrhage).

Rice. 27-42. Rice. 27. Obstruction of the central retinal artery (arrows indicate narrowed arteries). Rice. 28. Hypertensive angiopathy of the retina (Gwist symptom). Rice. 29. Symptom of decussation of the first degree (Salus I; indicated by arrows). Rice. 30. Symptom of decussation of the second degree (Salus II; indicated by arrows). Rice. 31. Symptom of decussation of the third degree (Salus III; indicated by the arrow). Rice. 32. Hypertensive retinopathy. Rice. 33. Hypertensive retinopathy (the arrow indicates the figure of a star). Rice. 34. Ischemic edema of the optic disc. Rice. 35. Dry form of senile macular degeneration. Rice. 36. Wet form of senile macular degeneration (indicated by an arrow). Rice. 37. Ring dystrophy of the retina (the arrow indicates the shape of the ring). Rice. 38. Hypertensive neuroretinopathy (the arrow indicates the figure of a star). Rice. 39. Diabetic angiopathy of the retina. Rice. 40. Microaneurysms on examination in normal light. Rice. 41. Microaneurysms on examination in redless light (the same area as in Fig. 40). Rice. Fig. 42. Microaneurysms in fluorescein angiography. Fig. 42. 6. Neurofibromatosis. Rice. 7. With tuberous sclerosis of the brain. Rice. 8. Multiple retinal angiomas. Rice. 9. With amaurotic idiocy. Rice. 10. Pseudoneuritis of the optic nerve.

Rice. 43 - 58. Rice. 43. Simple diabetic retinopathy. Rice. 44. Proliferating diabetic retinopathy (the arrow indicates the "wonderful network" of newly formed vessels). Rice. 45. Proliferating diabetic retinopathy (the arrow indicates a strand of connective tissue). Rice. 46. ​​Retinopathy in anemia. Rice. 47. Retinopathy in polycythemia. Rice. 48. Retinopathy in chronic lymphocytic leukemia (arrow indicates light foci bordered by hemorrhage). Rice. 49. Rheumatic retinovasculitis. Rice. 50. Disseminated tuberculous chorioretinitis (arrow indicates a light focus). Rice. 51. Disseminated tuberculous chorioretinitis on examination in blue light. Rice. 52. Central tuberculous chorioretinitis. Rice. 53. Central tuberculous chorioretinitis on examination in redless light. Rice. 54. Tuberculous retinal periphlebitis (arrows indicate muffs on veins). Rice. 55. Congenital toxoplasmic chorioretinitis (arrows indicate atrophic foci). Rice. 56 and 57. Congenital syphilitic chorioretinitis. Rice. 58. Diffuse syphilitic neuroretinitis - atrophy of the choroid.

Name of fundus changes	Diseases or conditions that can lead to fundus changes	Ophthalmoscopy data	With what pathology of the fundus it is necessary to differentiate
CHANGES DUE TO VASCULAR PATHOLOGY
Retinal angiopathy, hypertensive	I stage of hypertension	Narrowing of the arteries and dilatation of the retinal veins, moderately pronounced unevenness of the caliber of the arteries (functional). Mild symptom of arteriovenous decussation of the first degree (symptom of Salus I). Some patients have a corkscrew-like tortuosity of the veins of the macula (Guist's symptom - Fig. 28). Inconsistently: veiled contours of the optic disc	Renal angiopathy of the retina. Diabetic retinal angiopathy
Retinal angiopathy, hypertensive, traumatic	craniocerebral	Expansion of the retinal veins, uneven caliber, tortuosity of the branches in the area of ​​the macula. The arteries are narrowed, the reflex strip on them is expanded. In some places, symptoms of arteriovenous chiasm. Hemorrhages may occur. With a deterioration in the general condition, a picture of a congestive optic disc often develops.	Hypertensive angiopathy, hypertensive neuroretinopathy
Retinal angiopathy, hypertensive renal		Narrowing of the arteries, as a rule, without signs of sclerosis of the vascular wall. Occasionally symptoms of first-degree decussation (Salus I). No Gwist sign. Some patients have constrictions on the arteries, giving them the appearance of a rosary. Moderate swelling of the peripapillary retina	Hypertensive angiopathy
Angiosclerosis of the retina, hypertensive	II-III stages of hypertension	Narrowing of the arteries and expansion of the retinal veins, uneven caliber of the arteries. Symptom of crossover of the first and second degree (Salus I and II - Fig. 29 and 30). More rarely Salus III (Fig. 31). Expansion of the reflex strip on the arteries. In some places, a reflex strip of yellow color (a symptom of copper wire), in some places white color(silver wire symptom). Along the arteries in limited areas, lateral accompanying stripes. Expansion and tortuosity of veins. Inconstantly: retinal edema, hemorrhages in the form of single dots and strokes. Ophthalmochromoscopy: mottled reflex on the arteries when examined in redless light. In yellow-green light, uneven caliber and side accompanying stripes are better detected. In yellow light, hemorrhages are detected that are indistinguishable in ordinary light.	Age-related angiosclerosis of the retina
retinopathy hypertonic	IV stage of hypertension	Narrowing of the arteries, their straightness. Impoverishment of the vascular tree. Uneven caliber of arteries and reflex bands. Salus I. Guist's symptom, a symptom of copper, less often silver wire. In some places accompanying stripes along the arteries. Hemorrhages. Large cotton-wool foci, as well as small dystrophic white and yellowish foci in the area of ​​the macula. Retinal edema around the disc (Fig. 32)	Diabetic retinopathy, retinovasculitis, hypertensive renal retinopathy
Neuroretinopathy hypertensive	IV stage of hypertension (the threat of transition to a malignant form)	Narrowing of the arteries, their straightness. Impoverishment of the vascular tree. Uneven caliber of arteries and reflex bands. Salus I. Guist symptom. A symptom of copper, less often silver wire. In some places accompanying stripes along the arteries. Severe edema of the optic disc and retina in the central region. A large number of hemorrhages and cotton wool foci. Small foci in the region of the macula may form the shape of a star (Fig. 33). Ophthalmochromoscopy: in redless light, a speckled reflex on the arteries. In red light, early signs of macular area dyspigmentation	Hypertensive renal neuroretinopathy
retinopathy hypertonic renal	Acute nephritis, chronic nephritis, toxicosis of pregnant women	Narrowing of the arteries without signs of sclerosis of the vascular wall. Occasionally symptoms of first-degree chiasm. No Gwist sign. Some patients have constrictions on the arteries, giving them the appearance of a rosary. Moderately pronounced edema of the peripapillary retina. Cotton-wool lesions and degenerative small lesions. Hemorrhages. Severe retinal edema	Hypertensive retinopathy
Neuroretinopathy, hypertensive renal	Hypertensive	Narrowing of the arteries without signs of sclerosis of the vascular wall. Rarely Salus I. Absence of Guist symptom. Some patients have constrictions on the arteries, giving them the appearance of a rosary. Moderately pronounced edema of the peripapillary retina. Cotton-wool foci and dystrophic small foci. Hemorrhages. Severe swelling of the retina and optic nerve (congestive nipple). Sharply narrowed arteries in some places disappear in the edematous tissue. Dry foci form the figure of a star (Fig. 38). Possible retinal detachment	Hypertensive neuroretinopathy, congestive optic disc
Diabetic retinal angiopathy	Diabetes	Preferential changes in the veins of the retina: the veins are dilated, tortuous, their caliber is uneven. Microaneurysms are usually in the area of ​​the macula. The arteries are little changed (arterial damage is noted in sclerotic and hypertensive forms of the disease). Single hemorrhages (Fig. 39). Ophthalmochromoscopy: in redless light, microaneurysms are revealed that are indistinguishable in ordinary light (Fig. 40 and 41). In yellow light, small and deep-seated hemorrhages become visible. Fluorescein angiography reveals a large number of microaneurysms that are indistinguishable during ophthalmoscopy (Fig. 42)	Hypertensive angiopathy
retinopathy diabetic	Diabetes	Preferential changes in the veins of the retina: the veins are dilated, tortuous, their caliber is uneven. Microaneurysms are usually in the area of ​​the corpus luteum. The arteries are little changed (arterial damage is observed in sclerotic and hypertensive forms of the disease). Waxy lesions of irregular shape (Fig. 43). Yellowish tinge of the fundus. In some cases, the foci form a figure encircling	Hypertensive retinopathy, senile retinopathy
		schey dystrophy of the retina. Some patients have white, cotton-like lesions. Large hemorrhages. Thrombosis of the central retinal vein is possible. Ophthalmochromoscopy: in blue light, a change in the color of the fundus is better detected, in redless light - microaneurysms that are indistinguishable in ordinary light. In yellow light, small and deeply located hemorrhages are visible. Fluorescein angiography reveals a large number of microaneurysms that are indistinguishable during ophthalmoscopy
retinopathy diabetic proliferating	Diabetes	Preferential changes in the retinal veins: the veins are dilated, tortuous, their caliber is uneven. Microaneurysms are usually in the area of ​​the macula. The arteries are little changed (arterial damage is noted in sclerotic and hypertensive forms of the disease). Wax-like foci of irregular shape. Yellowish tinge of the fundus. In some cases, the foci form a figure of girdle retinal dystrophy. Some patients have white cotton-like lesions. Large hemorrhages. Thrombosis of the central retinal vein is possible. Newly formed vessels from single branches, loops to the formation of a "wonderful network" (Fig. 44). Light moorings due to proliferation of connective tissue (Fig. 45). Possible: traction retinal detachment, vitreous hemorrhage. Ophthalmochromoscopy: redless light reveals microaneurysms that are indistinguishable in ordinary light. In yellow light, small and deep-seated hemorrhages become visible. In blue light, the change in the color of the fundus is better seen. Fluorescein angiography reveals a large number of microaneurysms, small newly formed vessels that are not distinguishable during conventional examination.	Hypertensive retinopathy, fibroplasia of other etiologies
Angiosclerosis retina	Universal angiosclerosis	Narrowing of the arteries, their straightness. Impoverishment of the vascular tree. Uneven caliber of arteries and reflex bands. Salus I. Guist symptom. A symptom of copper, less often silver wire. In some places accompanying stripes along the arteries. Ophthalmochromoscopy: in redless light - mottled reflex on the arteries. In red light, early signs of macular area dyspigmentation	Hypertensive angiosclerosis of the retina
retinopathy senile	Aging	Narrowing of the arteries, their straightness. Impoverishment of the vascular tree. Uneven caliber of arteries and reflex bands. Salus I. Symptom of copper, rarely silver wire. In some places accompanying stripes along the arteries. In addition, as a result of dyspigmentation, the macula acquires a mottled appearance - a dry form of macular dystrophy (Fig. 35) or an effusion appears under the retina in the area of ​​the macula - a wet form of macular dystrophy (Kunt-Junius discoid dystrophy; Fig. 36). Small foci can form a figure of annular retinal dystrophy around the altered macula (Fig. 37). Druses of the vitreous plate are often found. Ophthalmochromoscopy: in redless light, signs of the senile form of edematous-fibroplastic syndrome of the macula (stationary reflexes, edema, cystic dystrophy, hole in the macula, fibroplasia) are better visible, in indirect red light, retinal drusen become visible, indistinguishable in ordinary light	Hypertensive retinopathy, diabetic retinopathy, macular melanoblastoma, transudative macular degeneration in myopia
retinopathy traumatic	Combination of blunt trauma of the skull and general contusion, intense compression of the trunk	Whitish swelling of the retina. White cotton-wool-like foci of various sizes and shapes, sometimes overlapping altered vessels. A large number of hemorrhages located both in the retina and preretinally. Process regresses slowly	Central vein thrombosis, hypertensive neuroretinopathy
Obstruction of the central retinal artery	Vasomotor dystonia, hypertension, endocarditis	A sharp narrowing of the central artery with a normal caliber of the veins. In places, collapsed arteries look like white stripes. In some areas, with incomplete closure of the lumen of the vessel, an intermittent blood flow is visible. Opacification of the retina of the central region is characteristic in the form of a light field with a cherry-red spot, located in accordance with the central fossa (Fig. 27). Possible obstruction of only one of the branches	Central exudative chorioretinitis, retinovasculitis
Obstruction of the central retinal vein	Hypertension, diabetes mellitus, arteriosclerosis, thrombophlebitis, endangiitis obliterans	The disk is swollen, hyperemic, its borders are veiled or almost indistinguishable. The veins are dilated and tortuous. The arteries are constricted. The retina is edematous, especially around the disc and in the central region. Possible cystic macular edema. A large number of hemorrhages are characteristic: around the disk they can be located like tongues of Flame (Fig. 24), and on the rest of the fundus in the form of smears, spots, strokes, splashes and dots. White cotton-like lesions are also observed. With obstruction of one of the branches of the central vein, hemorrhages, edema and white lesions are located, respectively, in the affected area (Fig. 25). Ophthalmochromoscopy: in redless light, retinal edema, cystic macular degeneration and white foci are better detected (Fig. 26)	Congestive optic disc, hemorrhagic retinovasculitis
Ischemic papilledema	Hypertension, atherosclerosis, obliterating endarteritis, rheumatic vasculitis, cervical osteochondrosis	Pale edema of the optic disc, giving it the appearance of a moderately protruding congestive nipple with a milky white or yellowish color (Fig. 34). Arteries are sharply narrowed. The veins are dilated. There may be hemorrhages that are located both on the disc and around it. Characteristic is the absence of an arc reflex near the disk. In acute edema, optic nerve atrophy usually develops after 2-3 weeks.	congestive optic disc, optic neuritis, pseudocongestive optic disc
congested nipple	Brain tumor, other diseases c. n. s., causing an increase in intracranial pressure (inflammatory diseases of the brain and its membranes, skull deformity, etc.), general diseases (hypertension, diseases of the kidneys, blood, etc.), diseases of the orbit and eyes	There are initial, pronounced, pronounced congestive nipple and congestive nipple in the stage of atrophy. In the initial stage, partial veiling of the boundaries of the optic nerve head, moderate varicose veins, and retinal edema are visible in places. Around the disc is an arc peripapillary light reflex (Fig. 11). A small protrusion of the disc is better detected with ophthalmochromoscopy and biomicroscopy. With a pronounced congestive nipple, the disc is enlarged in size and stands in the vitreous body by 2-7 D (0.6-2 mm), its borders are veiled, the veins are dilated and tortuous, the arteries are narrowed. Vessels are bent over the edge of the disk and in some places seem to be interrupted in the edematous tissue of the retina. Hemorrhages on the disc and adjacent retina are possible (Fig. 12). With a pronounced congestive nipple, the protrusion of the disc reaches 5--7 D (1.5-2 mm) or more, the diameter of the disc is significantly increased, there are more hemorrhages, the borders of the disc are blurred. The retina is edematous, small light foci are visible in it, sometimes forming a star figure in the area of ​​the macula. In the stage of atrophy, the disc becomes pale, its edema decreases, the arteries narrow, there are fewer small branches, and hemorrhages resolve. The light reflex near the disk disappears. Later on, optic atrophy develops.	Pseudocongestive nipple, optic neuritis, ischemic optic edema, obstruction of the central retinal vein, neuroretinopathy
optic nerve atrophy	Diseases of the brain and its membranes, multiple sclerosis, intoxication, hypertension, atherosclerosis, injuries, hereditary diseases	A constant symptom is blanching of the optic disc. The vessels are constricted. The boundaries of the disk can be clear - primary (simple) atrophy (Fig. 17) or veiled - secondary atrophy. With secondary atrophy, changes in the fundus around the disc can be observed (Fig. 18). Ophthalmochromoscopy: in purple light, the white disc becomes Blue colour(fig. 19 and 20)	Paleness of the optic disc in blood diseases, constitutional discoloration of the disc
CHANGES DURING INFLAMMATORY PROCESSES
Tuberculous retinal periphlebitis	Incomplete, intrathoracic tuberculosis	Recurrent, often massive vitreous hemorrhages. After resorption of hemorrhages, light, slightly protruding foci, located, as a rule, on the periphery of the fundus, fibrous bands become visible. White accompanying stripes are noted along the veins. Muffs on the veins. Violation of the normal course and caliber of the veins. These changes are better seen in redless light (Fig. 54)	Periflebitis of various etiologies
Optic neuritis	Inflammatory diseases of the brain and its membranes, general infections (flu, malaria, tuberculosis, brucellosis), toxic-allergic diseases, local foci of inflammation (paranasal sinuses, nasopharynx, mouth), inflammation of the membranes of the eye and orbit	The optic disc is hyperemic, its borders are veiled. Arteries are not changed, veins and capillaries are dilated (Fig. 16). There may be hemorrhages on the disc, less often white exudative foci. Hemorrhages and accumulations of exudate are also noted near the disk on the retina. In more rare cases, there may be severe disc edema	Congestive nipple, pseudoneuritis, ischemic optic edema
Optic neuritis retrobulbar	Multiple sclerosis, diseases of the paranasal sinuses and orbit, common infectious diseases (flu, etc.) and intoxication (tobacco-alcohol, etc.)	Characteristic is the absence of changes in the fundus with reduced central vision and the presence of a central scotoma. When examining in redless light, the veiled contours of the disk, its edema and arc reflex. If the focus of inflammation is located near the eyeball, then the process proceeds according to the type of optic neuritis	Congestive nipple, optic neuritis, ischemic edema, onset of descending optic nerve atrophy in tumors of the frontal lobe of the brain
Neuroretinitis syphilitic diffuse	Acquired syphilis (II-III stage)	Stormy start. Severe diffuse edema of the retina and optic nerve. Opacification of the posterior vitreous. Later, extensive atrophy of the choroid, retina and optic nerve develops. The pigment layer is preserved only in the area of ​​the macula (Fig. 58)	Diffuse chorioretinitis of tuberculosis, toxoplasmosis and other etiologies
Chorioretinitis syphilitic congenital	congenital syphilis	There are three main types of fundus changes. The first, the most frequent, is characterized by small pigmented clumps, alternating with small light foci. Because of the characteristic appearance, it was called "salt and pepper" retinitis (Fig. 56). Ch. is amazed. arr. the periphery of the bottom of the eye, but the foci can also be located in the central region. The second type is large pigmented atrophic foci or light pink atrophic foci, sometimes merging with each other (Fig. 57). The foci are located on the extreme periphery of the fundus. The third type proceeds as retinitis pigmentosa	Congenital dystrophies of the fundus of the eye, retinitis pigmentosa of another etiology
Chorioretinitis toxoplasmosis congenital	congenital toxoplasmosis	Mostly in the central region of the bottom of the eye, light foci of various sizes, round or oval, with clear boundaries. Characteristic is the accumulation in the foci, especially along the edges, of a significant amount of dark pigment. Often there is a large central focus, resembling a congenital coloboma of the choroid (Fig. 55). There may also be optic nerve atrophy, retinal fibroplasia and accumulation of connective tissue in the vitreous body - pseudoglioma	Disseminated chorioretinitis of tuberculous and other etiologies, retinoblastoma
Chorioretinitis toxoplasmosis acquired	Acquired Toxoplasmosis	The disease can proceed according to the type of central retinitis or chorioretinitis with the formation of prominent grayish foci surrounded by hemorrhages. Perhaps the course of the type of exudative neuroretinitis or diffuse chorioretinitis. Primary and secondary lesions of the retinal vessels are often noted.	Chorioretinitis of tuberculous and other etiologies
Disseminated tuberculous chorioretinitis - metastatic focal lesions of the choroid proper with involvement of the retina	Tuberculosis of all localizations	Foci, as a rule, of different age, located in the posterior part of the fundus outside the macula. Fresh ones are yellowish or whitish in color with veiled outlines and sometimes bordered with hemorrhage. The old ones are lighter with clear boundaries and accumulations of pigment, often forming a corolla. Small clumps of pigment are visible between the foci (Fig. 50). Ophthalmochromoscopy: in blue light, old foci are less clearly visible, fresh ones are better detected (Fig. 51)	Disseminated chorioretinitis of other etiology (Toxoplasmosis, viral and other infections)
Chorioretinitis tuberculous central	Tuberculosis of all localizations	In the region of the macula, there is a relatively large, protruding exudative focus of yellowish or gray-slate color with perifocal retinal edema (exudative form). Around the focus, hemorrhages are possible in the form of spots or a corolla - an exudative-hemorrhagic form (Fig. 52). Perifocal edema and the by-pass beam reflexes caused by it are better seen in redless light (Fig. 53)	Transudative macular degeneration, central granulomatous process in syphilis, brucellosis, malaria, etc.
Retinochoriovasculitis with perivascular infiltration and hyalinosis of the vessel wall	lupus erythematosus	Uneven caliber of the retinal arteries, in places their obliteration, microaneurysms, hemorrhages, cotton-wool foci, disc edema. The outcome may be retinal fibrosis. Fibrosis of the choroid. Atrophy of the optic nerves	Hypertensive retinopathy, diabetic retinopathy
Atrophy of the optic nerve, axial	Multiple sclerosis and other diseases of c. n. s., diseases of the paranasal sinuses, common infections and intoxications	Paleness of the temporal half of the optic disc with increased clarity of its temporal border (Fig. 21). Narrowing of the arteries. Ophthalmochromoscopic picture: in purple light, the temporal half of the disc is blue (Fig. 22), in yellow-green - a symptom of a break in the pattern of nerve fibers (Fig. 23). With fluorescein angiography - a symptom of a striped frame	Severe physiological excavation of the optic disc
Optic nerve atrophy, syphilitic	Dorsal tabes	The optic disc is pale with a characteristic grayish tint. Disc borders are clear. Arteries are narrowed only in advanced cases. The process is usually two-way.	Simple atrophy of the optic nerve of another etiology
Retinal nodular periarteritis	Nodular periarteritis	Yellowish-brown nodules on arteries. Hemorrhages. Edema of the retina and optic disc. Some patients have thrombosis of the retinal arteries. In the presence of hypertensive or renal syndrome, the development of malignant neuroretinopathy and serous retinal detachment is possible.	Rheumatic retinovasculitis, hypertensive neuroretinopathy
Retinovasculitis rheumatic	Rheumatism	Along the retinal vessels there are lateral accompanying stripes, in some places a grayish color of the sleeve. In the retina along the vessels there are small grayish foci. With the involvement of several vessels, large white effusion foci are visible near the optic disc, overlapping the vascular bundle (Fig. 49). Possible "hemorrhages and swelling of the retina	Retinovasculitis with nodular periarteritis
CHANGES IN BLOOD DISEASES
Retinopathy with anemia	Anemias: aplastic, hypochromic, pernicious, secondary	The color of the fundus is pale pink. The optic disc is discolored. The veins are dilated and tortuous. The difference in color of veins and arteries is reduced. Intermittent changes: in purple light, blue optic disc and fundus. With a decrease in the number of red blood cells below 50% of the norm, in addition, hemorrhages in the form of strokes, round spots and flames. Characteristic are hemorrhages with a white center (Fig. 46). White cottony patches. There may be peripapillary retinal edema around the disc. With a more severe course of the process, preretinal hemorrhages and hemorrhages in the vitreous body. Congested nipples, rarely neuritis. Atrophy of the optic nerve. Possible retinal detachment	Optic atrophy of other etiology, congestive nipple, optic neuritis
Retinopathy in chronic myelogenous leukemia	Chronic myeloid leukemia	The color of the fundus is orange or yellow. The veins are dilated. With a severe course of the hemorrhage process, some of them with a white center. Possible hyperemia of the disk, swelling of it and the peripapillary retina. Sometimes cottony patches	Optic neuritis
Retinopathy in acute leukemia	Acute leukemia	Pale background of the fundus. Arteries are discolored. The veins are dilated. Polymorphic hemorrhages. The optic disc is pale, the contours of the disc are veiled. Ophthalmochromoscopy: when examined in purple light, the optic disc is blue-purple. When examined in yellow-green light, the preserved pattern of nerve fibers is visible.	Congested nipple in the stage of atrophy
Retinopathy in chronic lymphocytic leukemia	Chronic lymphocytic leukemia	The disc acquires a yellowish tint, its borders are veiled. The arteries are constricted. The veins are dilated and tortuous. Numerous hemorrhages. Some patients have pale yellow foci located along the periphery of the fundus. The foci may be bordered by hemorrhage (Fig. 48)	Ascending optic nerve atrophy, chorioretinitis
Retinopathy in polycythemia	Polycythemia	The background of the fundus is dark red with a bluish tint. The veins are cyanotic, sharply dilated and tortuous (Fig. 47), the arteries almost do not differ in color from the veins. With the progression of the disease, in addition, small hemorrhages	pseudoneuritis
CHANGES IN OTHER DISEASES
Choroid angioma	Encephalotrigeminal neuroangiomatosis (Sturge-Weber disease)	Glaucomatous excavation of the optic disc. Often, myelin fibers are visible near the disc. The veins are dilated and tortuous. Possible angioma of the choroid. In some cases, peripapillary squamous retinal detachment	Primary glaucoma, choroid melanoblastoma
Retinal angiomatosis	Retino-cerebellovisceral angiomatosis (Hippel-Lindau disease)	Angiomas in the form of round glomeruli various sizes- from small to large nodes exceeding the diameter of the optic nerve head. A pair (vein, artery) of dilated, tortuous vessels approaches each tangle (Fig. 8). Newly formed vessels and focal changes in the retina are observed	Racemose aneurysms of retinal vessels. Proliferating diabetic retinopathy
retinal dystrophy	Amaurotic	In the early childhood form, characteristic changes in the central part are found at the bottom of the eye in the form of a grayish-white area with a bright red spot in the center, located corresponding to the central fossa (Fig. 9). With a late childhood form, atrophy of the optic nerve develops	Pigmentary degeneration of the retina, changes in the fundus of the eye with reticuloendothelial sphingomyelosis
Atypical retinal dystrophy	Laurence-Moon-Biedl syndrome	Accumulations of pigment in the form of small rounded or striped foci. In 15% - accumulations of the type of bone bodies typical of pigmentary dystrophy. In most patients, along with pigment clusters, whitish small foci are found.	Pigmentary retinal dystrophy
Tumor-like formations of the optic disc and retina of the hamartoma type	Neurofibromatosis (Recklinghausen's disease)	On the optic disc there are tumor-like formations of a whitish or yellowish color with a shiny surface (Fig. 6). Small nodules and plaques of yellow or white color are visible on the retina	Changes in the fundus of the eye in tuberous sclerosis
	Tuberous sclerosis of the brain (Bourneville disease)	Hemorrhages are possible on the retina, resembling mulberries (Fig. 7). Similar growths are possible on the optic nerve head. There may be obvious and hidden drusen of the optic disc	Fundus changes in neurofibromatosis
pseudoneuritis	High farsightedness, delayed embryonic stage of optic nerve development	The optic disc is hyperemic, its borders are veiled. Pronounced tortuosity of vessels (Fig. 10). The caliber of the arteries is not changed, atypical course of the vessels and other anomalies of their development are often observed	Optic neuritis
Pseudocongestive nipple	Drusen of the optic nerve head, constitutional features of the structure of the optic nerve head	The pseudocongestive nipple, caused by obvious drusen, has a bumpy appearance, its edges are scalloped, the caliber of the vessels is not changed (Fig. 13). With a pseudocongestive nipple due to hidden drusen (Fig. 14), the correct diagnosis can be made with biomicroscopy or ophthalmochromoscopy: in indirect red light, latent drusen become visible as rounded luminous formations (Fig. 15)	Congestive nipple, subtraction cones in myopia, ischemic optic nerve edema

Bibliography Arkhangelsky VN Morphological bases of ophthalmic diagnostics, M., 1960; Berezinskaya D. I. Fundamentals of ophthalmoscopic diagnosis, M., 1960; Vodovozov A. M. Ophthalmochromoscopy, Atlas, M., 1969, bibliogr.; Volkov V. V., Gorban A. I. and Dzhaliashvili O. A. Clinical examination of the eye with the help of instruments, L., 1971; Multi-volume guide to eye diseases, ed. V. N. Arkhangelsky, vol. 1, book. 2, p. 16, M., 1962, bibliography; Plitas P. S. Ophthalmoscopic atlas, M., 1960; Radzikhovsky B.A. Ophthalmoscopic diagnostics (with an ophthalmoscopic atlas), Chernivtsi, 1957; Radnot M. Atlas of eye diseases, trans. from Hungarian., vol. 2, Budapest, 1963; Shulpina N. B. Biomicroscopy of the eye, M., 1974, bibliogr.; Der Augenarzt, hrsg. y. K. Velhagen, Bd 1, S. 559, Lpz., 1969, Bibliogr.; System of ophthalmology, ed. by S. Duke Elder, v. 5, L., 1970; Trevor-Roper P.D. The eye and its disorders, Oxford, 1974.

H. K. Ivanov; tabular compiler. A. M. Vodovozov.

Information for specialists

Differential diagnosis of congestive optic disc

• retrobulbar neuritis (more often a unilateral process, deterioration of visual functions, discomfort, pain in the eye, aggravated by movement, swollen optic disc, negative dynamics);
• prethrombosis / thrombosis of the CVS (more often unilateral, vision improvement in the evening, ophthalmohypertension is possible on the diseased eye, the optic disc is edematous, relative scotomas or concentric narrowing are possible with perimetry, negative dynamics);
• anterior ischemic optic neuropathy;
• compression optic neuropathy;
• toxic optic neuropathy;
• Foster-Kennedy syndrome;
• pseudocongestive optic disc (myopia, latent hypermetropia, no changes in perimetry and tonometry, no dynamics);
• Druses of the optic nerve disc;
• atrophy of the optic disc;

Complaints

These complaints are inherently symptoms of intracranial hypertension (ICH) and not symptoms of congestive optic disc (PAD).

Headache

The most common symptom (rarely absent in ICH), may appear at any time of the day, but is more disturbing when waking up, or interrupts sleep in the morning; aggravated by movement, stooping, coughing, or other type of Valsalva maneuver; may be generalized or local; the doctor, as a rule, leads to pain intensifying within 6 weeks; patients who have suffered from headaches before may report a change in their nature.

Nausea and vomiting

Occurs in severe forms. May relieve headache, may appear without pain or before pain. The next step after nausea and vomiting is impaired consciousness.

Disturbance of consciousness

From mild to severe forms; sudden significant disturbances are a symptom of damage to the brain stem with tenitorial or cerebellar herniation and require urgent action.

Pulsating ringing and tinnitus

visual symptoms

More often absent, but possible: transient blurred vision for a few seconds (paleness of colors, usually in both eyes, especially when moving from a horizontal to a vertical position, or flickering, as if the lights are quickly turned on and off). Blurred vision, narrowing of the visual field, and impaired color perception may occur. Sometimes, with paralysis of the sixth cranial nerve or its tension over the pyramid, diplopia occurs. Visual acuity remains good except in later stages of the disease.

Epidemiology

Congestive optic disc does not occur in all patients with intracranial hypertension. It is very rare in children, especially in infancy (this is due to open fontanelles that compensate for the increase in pressure). But in all patients with MD, an intracranial neoplasm should be suspected first and foremost until another cause is proven.

A recurrent increase in intracranial pressure (ICP) may occur without a congested disc due to glial scarring of the disc during the first episode.

Congestive ONH is sometimes found during routine examination of an asymptomatic patient. In these cases, it is necessary to ask about the drugs taken, the presence of a history of traumatic brain injury.

Etiology

The term congestive optic disc is often misused to describe swollen optic nerve due to infection, inflammation, or infiltration of the disc itself. In these cases, the deterioration of visual functions occurs at the very beginning of the disease, and in case of MDD - at final stages. The term is appropriate if intracranial hypertension itself is the result of infection, inflammation, or infiltration. The cause of congestive optic disc is intracranial hypertension. In other words, HPD is one of the symptoms of intracranial hypertension, along with headache, nausea, vomiting, and impaired consciousness, which in most cases is bilateral (with the exception of cases of severe hypotension in one eye or Foster-Kennedy syndrome).

Intracranial hypertension is divided into four types:

1. parenchymal - develops as a result of volumetric intracranial processes: tumors, hematomas, brain abscesses, etc., traumatic brain edema, general intoxication with neurotoxins of exogenous or endogenous origin;
2. vascular - develops as a result of vascular diseases of the brain: cerebral thrombosis, thrombosis of the superior sagittal sinus, mastoiditis with thrombosis of the transverse or sigmoid sinus; extracerebral vascular diseases: hypertensive encephalopathy in cases of malignant hypertension of any etiology, glomerulonephritis, eclampsia, etc., obstruction of cerebral venous outflow in congestive heart failure, superior vena cava syndrome, volumetric intrathoracic processes or injuries;
3. caused by a violation of the dynamics of the cerebrospinal fluid - develops as a result of obstruction of the CSF circulation pathways in tumors, hematomas, narrowing of the Sylvian aqueduct, infection; CSF malabsorption in acute meningitis, subarachnoid hemorrhage, carcinomatous meningitis, sarcoidosis;
4. idiopathic - diagnostic criteria are: symptoms of increased intracranial pressure (headache, swelling of the optic nerve head, cerebrospinal fluid pressure more than 25 cm of water column), but the composition of the cerebrospinal fluid is normal, there are no topical neurological symptoms, there are no suspicions of intracranial venous thrombosis, and computed or magnetic resonance imaging shows the normal structure of the skull and brain).

Examination of a patient with congestive optic disc

In addition to clarifying neurological problems (the nature of the headache and the history of the development of the disease, the presence of a history of episodes of fever), the following is necessary:

• assessment of eyeball motility and carrying out a cover-test when looking directly and at the extreme positions of the eyes at eight points (abducens nerve palsy can be combined with ICH), check for pain on movement;
• assessment of pupillary reactions (relative afferent pupillary defect, as a rule, is absent, since visual functions do not suffer before the onset of atrophy of the optic disc, but it is necessary to remember the complaints described above);
• assessment of visual acuity, color sensitivity, refractometry (detection of latent hypermetropia and the difference in refraction above the disk);
• perimetry (look for concentric narrowing, scotomas);
• tonometry (pay attention to the asymmetry of IOP);
• binocular ophthalmoscopy in dynamics with photography of the fundus to objectify dynamic observation;
• Ultrasound of the orbits (detection of orbital causes of edema, optic disc drusen, measurement of the thickness of the optic nerve and prominence of the optic nerve head);

Classification of congestive optic disc by stages

Congestive optic disc can be graded in several stages according to the Friesen scale (the scale is based on a study using fundus photography and showed good reproducibility between different observers; specificity ranged from 88% to 96%, sensitivity between 93% and 100%; results were more accurate when examined in red-free light).

0 stage

Normal ONH with nasal and temporal borders, blurred overlying bundles of nerve fibers in inverse proportion to the diameter of the disc (slight blurring with a large disc, and vice versa). The location of the near-discal bundles of nerve fibers is strictly radial, without tortuosity of diverging axons. Blurring of the upper and lower boundaries is not taken into account due to the large number of normal options. Rarely, the major vessels may be covered by overlying nerve fibers at the border of the disc, usually at the superior pole.

1 stage

Excessive (in relation to the diameter of the disc) blurring of the nasal border of the optic disc, with a violation of the normal radial arrangement of the bundles of nerve fibers. The temporal part remains normal, at least within the papillomacular sector. These changes lead to the formation of a thin grayish halo around the circumference of the optic disc, the temporal side of the ONH is not affected by edema (C-shaped edema), and the excavation is clearly defined (generally best assessed with low magnification and indirect ophthalmoscopy).

2 stage

There is a prominence of the nasal part of the ONH and blurring of the temporal margin. The halo surrounds the disk completely. Concentric or radial retinochoroidal folds may appear already at this stage. Excavation is still clearly defined.

3 stage

There is a prominence of the temporal border and a clear increase in the diameter of the ONH. Prominent borders overlap one or more segments of large retinal vessels (vessels are buried in edematous tissue), or become invisible in the place where they, bending, leave the disc. The halo has a flared outer fringed edge. Excavation can be smoothed out.

4 stage

Prominence of the entire OD in combination with smoothing of the excavation or its compression to the size of a gap, or with partial immersion of large vessels in the edematous tissue not only on the edge, but also on the surface of the disc.

5 stage

The increase in disc prominence exceeds the expansion of its diameter. The optic disc is a relatively smooth, domed protrusion with a narrow and indistinctly demarcated halo. The vessels bend sharply, climbing a steep slope, partially or completely immersed in the edematous tissue over the entire surface of the disc.

Stages 1 and 2 can be assessed as mild papilledema, stage 3 as moderate, and stages 4 and 5 as severe.

Early symptoms of congestive optic disc that may help in diagnosis

Disc hyperemia, small single hemorrhages in the layer of nerve fibers

The absence in the classification of indications of hyperemia (or pallor), hemorrhages and cotton-like foci is intentional, due to the significant variability of these signs under various pathogenetic conditions, as well as in different patients under the same conditions. However, in each case, it is very appropriate to make a note about the presence or absence of each of these signs. Obviously, the more complete the information, the easier it is to find the root cause, and the more noticeable any changes in appearance over time.

As the stagnation progresses, the number and size of hemorrhages increase, foci of soft exudates, retinal folds and choroids appear.

After a few months, hyperemia is replaced by pallor, excavation is smoothed out - secondary atrophy is formed. Small, shiny, crystalline deposits may appear on the disc surface (disk pseudodruse).

Spontaneous venous pulsation

The symptom is useful and confirming the optic disc in those cases where the pulsation was recorded earlier and when observed in dynamics, it disappears. Here we can talk about negative dynamics. Also, when evaluating the effectiveness of treatment, the restoration of pulsation indicates a positive trend. But it must be remembered that pulsation is absent in 10% of healthy people, and with intracranial hypertension it disappears when ICP increases more than 190 mm of water column.

retinal reflexes

Peripapillary reflex

In the initial stages, the reflex is located closer to the disc, weakly expressed as a fragment of an arc (more often determined from the nasal side), the closer it is to the disc, the thinner and brighter, as the edema increases, the reflex becomes wider, fades and moves away to the periphery, usually upper and lower the edges of the reflex are farther from the disk than the middle, the edges do not close (in severe cases, the edema extends to the temporal part and the reflex is located on both sides - "ON in brackets").

supra-papillary reflex

It is formed if the vascular funnel contours (ring-shaped reflex at the top of the optic disk around the excavation)

Pathological reflexes of the fundus

The foveolar reflex takes the form of a blurred spot, the normal macular reflex becomes pathological, and then they disappear; if the edema increases, glare and linear reflexes appear.

Features of retinal reflexes in other conditions

• pseudocongestive optic disc- peripapillary reflex is located concentrically relative to the disk; the edges can close, forming a ring;
• Druzy ONH- the peripapillary reflex is located on the side of the drusen;
• retrobulbar neuritis- the macular reflex becomes pathological - it expands, loses its clear outline, breaks into separate highlights, then becomes indistinguishable as an annular formation; glare reflexes appear in its place; the foveolar reflex takes the form of a blurred spot, its mobility increases, disappears together with or a little later than the macular reflex, in some patients, especially with a long course, linear reflexes between the disc and the macula become visible;
• primary atrophy of the optic disc- weakening and disappearance of all reflexes (atrophy of the layer of nerve fibers), the reflex on the vessels becomes brighter, and then uneven and mottled as in atherosclerosis;
• secondary atrophy of the optic disc- a distinctive feature is the presence of a peripapillary reflex (the borders of the disk are not always convincing).

Ophthalmochromoscopy for congestive optic disc

• in redless light: The optic disc becomes light green in color, small dilated vessels become visible in large numbers, the disk seems to be covered with a vascular network, lateral accompanying stripes along large vessels are visible better than in ordinary light, the pattern of nerve fibers is clearly visible, they are thickened, the spaces between the fibers are expanded, hemorrhages visible better and in greater numbers, disc prominence looks more prominent, reflexes and perripapillary retinal edema are more distinct;
• in red light: in some patients, the phenomena of stagnation are indistinguishable, the outlines of the disk contour appear, especially well in indirect illumination (the sign is not pathognomonic, since it does not occur in everyone and no dependence on the cause of edema has been identified); deeply located disk drusen are found, indistinguishable in ordinary light (round-shaped light / "luminous" formations with a paradoxical shadow, resembling bubbles, merging into lumps or resembling a mulberry);
• in purple light: disk in the form of a red-purple blurred spot surrounded by a wide blue jagged border.

Tactics

1. Compare current data with previous inspections.
2. Carefully record the current state of the ONH (better if it is a photograph).
3. Re-examination after 1–2 weeks with the same set of examinations.
4. When making a diagnosis of MDD - a consultation with a neurologist to decide on the tactics of management, referral to CT or MRI of the brain, orbits and optic nerve.
5. If, as a result, idiopathic intracranial hypertension is exhibited - the supervision of a therapist (control of blood pressure, body mass index in dynamics).

Forecast

In the natural course, the stagnant disc turns into secondary atrophy with loss of visual functions.

The most prominent part of the fundus is the nipple (disc) of the optic nerve, and the study usually begins with it. The nipple is located medially from the posterior pole of the eye and enters the ophthalmoscopic field of view if the examined person turns the eye to the nose by 12-15°.

Against the red background of the fundus, the optic nerve papilla stands out with its clear boundaries and pink or yellowish-red color. The color of the nipple is determined by the structure and ratio of the anatomical elements that form it: arterial capillaries, grayish nerve fibers and the whitish cribriform plate underlying them. The nasal half of the nipple contains a more massive papillomacular bundle of nerve fibers and is better supplied with blood, while in the temporal half of the nipple the layer of nerve fibers is thinner and the whitish tissue of the cribriform plate is more visible through it. Therefore, the outer half of the optic papilla almost always looks lighter than the inner half. For the same reason, due to the greater contrast with the background of the fundus, the temporal edge of the nipple is outlined more sharply than the nasal one.

However, the color of the nipple and the clarity of its borders vary markedly. In some cases, only extensive clinical experience and dynamic monitoring of the state of the fundus make it possible to distinguish the normal variant from the pathology of the optic nerve papilla. Such difficulties arise, for example, with the so-called false neuritis, when the normal nipple has fuzzy contours and appears to be hyperemic. Pseudoneuritis mostly occurs with medium and high hypermetropia, but can also be observed with myopic refraction (MI Averbakh, 1949).

In doubtful cases Shik (Schieck, 1930) recommends paying attention to the vascular funnel of the optic nerve papilla: it is clearly expressed in pseudoneuritis and is not visible in inflammation or stagnation.

Often, the optic nerve papilla is surrounded by a white (scleral) or dark (choroidal, pigmented) ring. The first ring, also called the cone, is usually the rim of the sclera, visible as a result of the hole in the choroid through which the optic nerve passes is wider than the hole in the sclera. Sometimes this ring is formed by glial tissue surrounding the optic nerve. The scleral ring is not always complete and may be sickle or crescent shaped. As for the choroidal ring, it is based on the accumulation of pigment along the edge of the hole in the choroid. In the presence of both rings, the choroidal ring is located more peripherally than the scleral one; often it occupies only part of the circumference.

The optic papilla most often has the shape of a circle or a vertical oval and very rarely a transverse oval shape. Astigmatism of the examined eye can distort the true shape of the nipple and give the doctor a false impression of its shape. A similar distortion of the shape of the nipple can also be observed as a result of errors in the examination technique, when, for example, during reverse ophthalmoscopy, the magnifying glass is placed too obliquely to the line of observation.

The horizontal size of the nipple is on average 1.5-1.7 mm. Its visible dimensions, like other elements of the fundus, are much larger during ophthalmoscopy and depend on the refraction of the eye under study and the method of examination.

The optic nerve papilla can be located with its entire plane at the level of the fundus of the eye (flat nipple) or have a funnel-shaped depression in the center (excavated nipple). The recess is formed due to the fact that the nerve fibers leaving the eye begin to bend at the very edge of the scleral-choroidal canal. A thin layer of nerve fibers in the central region of the optic papilla makes the underlying whitish lamina cribrosa more visible, and therefore the excavation site appears particularly light. Often here you can find traces of holes in the lattice plate in the form of dark gray dots. Sometimes physiological excavation is located paracentrally, somewhat closer to the temporal edge of the nipple. From pathological types of excavations, it is distinguished by a small depth (less than 1 mm) and the main obligatory presence of a rim of normally colored nipple tissue between its edge and the excavation edge.

A pronounced depression at the site of the optic nerve papilla can be observed in congenital colobomas. In such cases, the nipple is often surrounded by a white rim with pigment inclusions and seems somewhat enlarged. A significant difference in the level of the nipple and the retina leads to a sharp bending of the vessels and creates the impression that they do not appear in the middle of the nipple, but from under its edge. Rarely encountered defects (pits) in the tissue of the nipple and pulpy, myelinated fibers, which look like bright white shiny elongated spots, are also associated with an anomaly of development. They can sometimes be located on the surface of the nipple, cover it; with inattentive examination, they can be mistaken for a bizarre nipple.

In diseases of the optic nerve, mainly occurring in the form of inflammation or stagnation, the nipple may acquire a red, grayish-red or dull red color and the shape of an elongated oval, irregular circle, kidney-shaped or hourglass. Its dimensions, especially with stagnation, often exceed the usual 2 times or more. The borders of the nipple become fuzzy, blurry. Sometimes the outlines of the nipple cannot be caught at all, and only the vessels emerging from it make it possible to judge its location in the fundus.

Atrophic changes in the optic nerve are accompanied by whitening of the nipple. A gray, grayish-white or grayish-blue nipple with sharp borders is observed with primary atrophy of the optic nerve; a dull white nipple with fuzzy contours is characteristic of secondary optic nerve atrophy.

Distinguish between atrophic and glaucomatous pathological excavation of the optic nerve papilla. The first is characterized by a whitish color, regular shape, slight depth, gentle edges and a slight bend in the vessels at the edge of the nipple. Glaucomatous excavation grayish or grayish-green in color, much deeper, with undermined edges. Bending over them, the vessels seem to break off and at the bottom of the excavation, due to the deep occurrence, they are less distinguishable. They are usually displaced to the nasal edge of the nipple. Around the latter, a yellowish rim (halo glaucomatosus) is often formed.

In addition to excavations of the nipple, there is also a bulging, protrusion of it into the vitreous body. Especially pronounced bulging of the nipple occurs with congestion in the optic nerve (the so-called mushroom nipple).

From the middle of the nipple of the optic nerve or somewhat medially from the middle, the central retinal artery (a. centralis retinae) emerges. Next to her, laterally, enters the nipple central vein retina (v. centralis retinae).

On the surface of the nipple, the artery and vein are divided into two vertical branches - the upper and lower (a. et v. centralis superior et inferior). Each of these branches, leaving the nipple, is again divided into two branches - temporal and nasal (a. et v. temporalis et nasalis). In the future, the vessels tree-like break up into smaller and smaller branches and spread along the fundus of the eye, leaving a yellow spot free. The latter is also surrounded by arterial and venous branches (a. et v. macularis), directly extending from the main vessels of the retina.

Sometimes the main vessels divide already in the optic nerve itself, and then several arterial and venous trunks immediately appear on the surface of the nipple. Occasionally, the central retinal artery, before leaving the nipple and making its usual path, twists in a loop and protrudes somewhat into the vitreous body (prepapillary arterial loop).

With an ophthalmoscopic examination, arteries can be easily distinguished from veins. They are thinner than the latter, lighter than them and less crimped. Light stripes stretch along the lumen of the larger arteries - reflexes formed due to the reflection of light from a column of blood in the vessel. The trunk of such an artery, as if divided by the indicated stripes, seems to be double-circuit. The veins are wider than the arteries (their calibers are respectively 4:3 or 3:2), painted in cherry red, more tortuous. The light strip along the course of the veins is much narrower than along the course of the arteries. On large venous trunks, the vascular reflex is often absent. Often there is a pulsation of the veins in the region of the nipple of the optic nerve.

In the eyes with high hypermetropia, the tortuosity of the vessels is more pronounced than in the eyes with myopic refraction. Astigmatism of the examined eye, not corrected with glasses, can create a false impression of the uneven caliber of the vessels.

In many parts of the fundus of the eye, a decussation of arteries with veins is visible, and both an artery and a vein can lie in front.

A change in the caliber of blood vessels occurs as a result of violations of vascular innervation, pathological processes in the walls of blood vessels and varying degrees of their blood supply. Expansion of blood vessels, especially veins, is observed with inflammation of the retina. In circulatory disorders associated with blockage of the vessel, the veins are also dilated, while the arteries are narrowed. If the transparency of their walls is not disturbed during spasm of the arteries, then with sclerotic changes, along with a narrowing of the lumen of the vessels, a decrease in their transparency is noted. In severe cases of such conditions, the vascular reflex acquires a yellowish tint (a symptom of copper wire). Along the edge of vessels that reflect light more strongly, white stripes appear. With a significant narrowing of the arteries and compaction of their walls, the vessel takes the form of a white thread (a symptom of a silver wire). Often, small vessels become more tortuous and uneven in thickness. Corkscrew-like tortuosity of small veins occurs in the region of the macula (Relman-Guist symptom). In places where the vessels cross, compression of the underlying vein by the artery can be observed (Hunn-Salus symptom). Pathological phenomena also include the occurrence of arterial pulsation, especially noticeable at the site of the bending of the vessels on the papilla of the optic nerve.

In the posterior pole of the eye lies the most functionally important region of the retina - the yellow spot (macula lutea). It can be seen if the subject directs his gaze to the light "glare" of the ophthalmoscope. But at the same time, the pupil narrows sharply, which makes it difficult to study. It is also interfered with by light reflexes that occur on the surface of the central part of the cornea. Therefore, when examining this area of ​​the retina, it is advisable to use non-reflex ophthalmoscopes, resort to pupil dilation (where possible) or direct a less bright beam of light into the eye.

With conventional ophthalmoscopy (in achromatic light), the yellow spot looks like a dark red oval, bordered by a shiny stripe - the macular reflex. The latter is formed due to the reflection of light from a roller-like thickening of the retina along the edge of the macula. The macular reflex is better expressed in young people, especially in children, and in eyes with hyperopic refraction. The macula lutea is surrounded by separate arterial branches, somewhat reaching its periphery. The size of the yellow spot varies markedly. So, its larger horizontal diameter can have a value from 0.6 to 2.9 mm.

In the center of the macula is a darker round spot - the central fossa (fovea centralis) with a shiny bright dot in the middle (foveola). The diameter of the central fossa averages 0.4 mm.

The ophthalmologist, by changing the position of the eye relative to the eye of the subject and forcing him to move his gaze in different directions, can also examine the rest of the fundus. With the maximum dilated pupil, only a small area of ​​the fundus at the limbus 8 mm wide remains inaccessible to research.

The general color of the fundus is made up of the color shades of the rays emerging from the examined eye and mainly reflected by the retinal pigment epithelium, the choroid, and partly by the sclera. The normal retina, when examined in achromatic light, reflects almost no rays and therefore remains transparent and invisible.

Depending on the pigment content in the pigment epithelium and in the choroid, the color and general pattern of the fundus noticeably changes. Most often, the fundus appears uniformly colored red with a lighter periphery (Fig. 13, a). In such eyes, the pigment layer of the retina hides the pattern of the underlying choroid. The more pronounced the pigmentation of this layer, the darker the fundus looks.

Rice. 13. Fundus

a — differently colored fundus; b - spotty or parquet fundus; c — weakly stained (albinotic) fundus of the eye; g — an eyeground of newborns; e - fundus of the eye during ophthalmoscopy in redless light; f — fundus of the eye during ophthalmoscopy in yellow-green light.

The pigment layer of the retina may contain little pigment and then the choroid appears through it. The fundus appears bright red. It shows choroidal vessels in the form of densely intertwined orange-red stripes converging to the equator of the eye. If the choroid is rich in pigment, then its intervascular spaces take the form of elongated spots or triangles. This is the so-called spotted, or parquet, fundus (fundus tabulatus) (Fig. 13, b).

In cases where there is little pigment in both the retina and the choroid, the fundus of the eye, due to the stronger translucence of the sclera, looks especially bright. Against this background, the optic nerve papilla and retinal vessels are more sharply contoured and appear darker. The choroidal vessels are clearly visible. The macular reflex is poorly expressed or absent. Weakly pigmented fundus (Fig. 13, c) is most often found in albinos, which is why it is also called albino.

Similar in color to the albino eye fundus of newborns (Fig. 13, d). But their optic papilla is pale gray with indistinct contours. The veins are wider than usual. Macular reflex is absent. From the second year of life, the fundus of the eye of children almost does not differ from the fundus of adults.

Pathological changes in the vascular and retinal membranes are very diverse and can manifest themselves in the form of diffuse opacities, limited foci, hemorrhages and pigmentation.

Diffuse opacities of larger or smaller sizes give the retina a dull grey colour and especially sharply protrude in the area of ​​the nipple of the optic nerve. Localized retinal lesions may vary in shape and size and may be light white, light yellow, or bluish yellow in color. Located in the layer of nerve fibers, they take a dashed shape; in the region of the yellow spot form a figure resembling a star. The round shape and pigmentation of the foci are observed when the process is localized in the outer layers of the retina. Fresh focal changes in the choroid are darker than retinal and less clearly defined. As a result of the subsequent atrophy of the choroid, the sclera is exposed in these areas and they take the form of white, sharply limited foci of various shapes, often surrounded by a pigmented rim. Retinal vessels usually pass over them. Hemorrhages of the choroid are relatively rare and, being covered by the pigment epithelium, are poorly distinguishable. Fresh retinal hemorrhages have a cherry-red color and vary in size: from small, punctate extravasates to large, occupying a vast area of ​​the fundus. When localized in the layer of nerve fibers, hemorrhages appear as radial strokes or triangles with their apex facing the optic nerve papilla. Preretinal hemorrhages are round or transversely oval. In rare cases, hemorrhages resolve without a trace, but more often they leave behind whitish, gray or pigmented atrophic foci.

Age-related macular degeneration (AMD: Age-related macula degeneration) is a disease of the central retina that occurs in old age and leads to a decrease in central vision.
The job of the retina is to absorb and convert light into nerve impulses. The structure and functions of the retina in its various zones are not the same.

When looking at a distant object, such as the moon, the eyes are in such a position that the image of the moon is projected directly onto the center of the retina. This center, which appears slightly yellow due to xanthophyll pigment, is called the lutea macula or "yellow spot" (Lat. Macula: spot / Lat. Lutea: yellow). While the periphery of the retina is specialized in the perception of movements (mainly large objects), the center is responsible for spatial vision. This means that the center of the retina perceives even tiny objects, and two points extremely close to each other are identified by it as separate. The resolving power of the retina is expressed by visual acuity. A healthy person (with corrective lenses if necessary) has a visual acuity of 100%, or, as defined by ophthalmologists, 1.0 or 20/20.

The high resolution is the result of a denser arrangement of visual receptors in the macula than in any other area of ​​the retina. In addition, in this area, the ratio of cone cells to ganglion cells is almost 161. Therefore, macula receptors are connected directly to the brain through retinal nerve cells.

If the quality of the image on the retina is not perfect, such as in nearsighted people without glasses, visual acuity will be less than 100%. What is 100% visual acuity, or equal to 1.0? This means that two different points that are very close to each other must be perceived separately by the eye. If visual acuity is 0.5, or, in other words, 50% visual acuity, then in order for two points to be distinguished as separate objects, they must be twice as far apart as compared to the visible points at visual acuity 1.0. This distance should be four times greater at 25% visual acuity, etc. On a vision chart examination, a patient with 0.5 vision only identifies letters or numbers twice as large as a person with 1.0 vision can see. If a myopic patient is examined with correct spectacles (or contact lenses), the results become normal again. However, if the retina itself is changed, which may be associated with the death of receptor cells or their partial damage, a decrease in visual acuity occurs, which cannot be corrected with glasses. This problem is especially important for the macular area.

Like all organs, the retina also undergoes the aging process during life. Even in a healthy person, there is a slow decrease in the number of receptor and nerve cells. The pigment epithelium, located directly behind the retina and continuously absorbing the remnants of parts of the receptor cells, gradually forms deposits of waste substances that are difficult to process. The blood supply to the next layer, the choroid, also decreases with age.

The ability of the choroid to transport heat and regulate the required volume of blood usually decreases with age, which is reflected in the nutrition of the retina. In addition, deposits of unprocessed products, mainly fat deposits, increasingly impede the transport of substances from the retina to the choroid, and vice versa.

Normally, the macula receives a relatively small amount of oxygen from the vessels of the retina, mainly it enters the macular region from the choroid. This is the reason why the macula especially suffers from age-related disorders caused by the deposition of fatty deposits from the choroid adjacent to it. Another important factor is that the macula is more exposed to light and its damaging effects than other areas of the retina.

The difference between the normal aging of the macular area and some of the pathological processes occurring in it is sometimes subtle. Many older people develop overt changes in the macula, which can lead to severe vision loss. The precursor to such defects is the visual entrainment of a number of deposits in the retina, called drusen. Drusen are small, lump-like formations primarily composed of fat; they are located between the pigment epithelium and the choroid. When examining the eyes, they can be identified as small yellowish spots located behind the retina.

If the aforementioned drusen are relatively large, without clear boundaries and tend to shine (become confluent), then the risk of developing macular degeneration (Lat. Degeneratio: degeneration) increases. Degeneration is defined as the reorganization of tissue from a more complex form to a simpler one, as well as the transition from a properly functioning state to an incapacitated level. The first stage of AMD is changes in the structure of the pigment epithelium, determined by ophthalmoscopy.

It can be seen that instead of the usual homogeneous pink fundus reflex, dark and light foci are detected in the macular region. A patient with such changes no longer has 100% vision, and, depending on the severity of these changes, it ranges between 20 and 80%.
The lowest visual acuity that can be "adequate" for reading a newspaper (perhaps with reading glasses) is approximately 30%. AMD may stop at this first stage (changes in the pigment epithelium) and not develop further. Otherwise, there may be further deterioration, and the subsequent development of an atrophic form or progression of the process contributes to the emergence of a "wet" form of the disease (Gr. atrophein: without food). The development of atrophic degeneration may be associated with the risk of severe tissue loss and a significant deterioration in visual functions. The macular changes just described are otherwise known as dry AMD.

The dry form of AMD can go into the wet form. Nature, whenever possible, always strives to restore the body's own failures. Therefore, blood vessels can grow from the choroid into the degeneratively altered macula under the pigment epithelium. They can even break through the pigment epithelium and continue to grow between this layer and the retina. Such compensatory processes actually do more harm than good. Unlike healthy capillaries, newly formed blood vessels are not watertight. Fluid, sometimes even blood, can leak out and enter both under and into the retina, thus causing the wet form of AMD.

These blood vessels and exudate lead to local detachments and displacements of retinal receptor cells. As a result, the rods and cones are no longer where they should be, while the blood supply to the retina becomes even more inefficient. If an image is projected onto a detached part of the retina, the brain receives information that is topographically (spatially) incorrect. This is the reason why the wet AMD patient does not see the doorway as a rectangle, but rather as a twisted or undulating structure. This phenomenon, called metamorphopsia (Gr.metamorphopsein: to see something tilted), is pathognomonic (obligatory manifestation) for lesions of the macular zone.

We list the most important symptoms of AMD: in the dry form of AMD there is a decrease in visual acuity of one degree or another, in the wet form of AMD there is a significant decrease in vision associated with metamorphopsia.

Loss of vision is a heavy burden for the elderly. It is reassuring to know that AMD will not completely blind the patient. He may have trouble reading or seeing details, but complete blindness will not occur unless there are other eye conditions (such as glaucoma) because other areas of the retina remain intact.
A patient with AMD has a fairly good orientation in space and can move freely, as the disease does not affect the peripheral areas of the retina.

How common is AMD?
There are some very rare hereditary forms of macular degeneration that appear in childhood or at a young age. These forms of macular degeneration should not be confused with AMD, which is a problem in the elderly. AMD is rare in middle age, but the likelihood of developing AMD is greatly increased in the elderly. Approximately 1.5% of people aged 52-64 have AMD, while this figure rises to 10-20% among those aged 65-75 and approximately 35% of people aged 75-84 have this pathology. It's safe to say that anyone who lives long enough will almost certainly develop AMD. As life expectancy increases, a corresponding increase in the number of patients with AMD can be expected in the future.

Pathogenesis and prevention of AMD.
The pathogenesis of AMD is not fully known, so attempts to treat this pathology are still at a very early stage.

Without a doubt, there is some genetic predisposition to the disease: children of parents suffering from AMD are at greater risk of developing the disease in the future. People with pale skin and those who complain of increased sensitivity to bright light are more likely to suffer from this disease. Other risk factors are similar to those that cause arteriosclerosis: AMD is more commonly seen in association with smoking and elevated blood lipids. There is also evidence that vitamin deficiencies, especially vitamins E and C, as well as vitamin A, may hasten the development of AMD. The general rules that have been established to prevent arteriosclerosis can also be regarded as preventive measures for AMD: smoking abstinence, a vitamin-rich and low-calorie diet, exercise, etc. Since light appears to play a significant role in the pathogenesis of AMD, high-quality UV-absorbing sunglasses are recommended, especially at sea, in the snow, and in the mountains.

There is no specific therapy for the dry form of AMD. A diet rich in vitamins is usually recommended, sometimes nutritional supplements of gingko preparations.

With the wet form of AMD, the destruction of newly formed pathological blood vessels (neovascularization) is carried out with a laser. These vessels are indeed destroyed after laser treatment. However, we must not forget that a) during laser treatment, healthy tissue also suffers; b) the main cause of AMD is not affected.

Recently, laser therapy has been complemented by photodynamic therapy. To perform this therapeutic measure, intravenous administration of a photosensitive chemical preparation is performed. This substance is mainly deposited on the walls of newly formed and pathologically altered blood vessels. The interaction of this substance with a non-thermal laser leads to a biochemical reaction, which ends with the closure and, in the future, the destruction of the “marked” newly formed blood vessels. In most cases, after this therapy, it is necessary to conduct frequent and rather extensive examinations and re-treatment, since the main cause of the disease is not eliminated. There are great hopes for photodynamic therapy, but it remains to be determined how significant the benefits of long-term results of this type of treatment are.

In other therapeutic approaches, the newly formed blood vessels are removed surgically, or the retina is completely separated, rotated, and fixed in position so that the macula is in contact with an area of ​​still healthy pigment epithelium. However, such treatment is possible only in very few cases, and some of its results are still unclear.

Until now best recommendation for patients with AMD, there is a thorough and complete consultation with an ophthalmologist, as well as an optician working with patients with low vision. The use of magnifying devices is recommended, which may allow patients with severe forms of AMD to regain some ability to read at least selected documents and texts.

AMD and glaucoma.
Glaucoma does not increase the risk of AMD, however, if the degeneration develops in patients with glaucoma, it is especially dangerous. Glaucomatous lesions are characterized by the development of visual defects in the periphery, while central vision remains normal for a long time. If a patient has both glaucomatous visual field defects and AMD-related visual acuity loss, his vision is doubly affected. This once again emphasizes the need to treat glaucoma, even if no subjective changes are detected. The glaucoma patient should be aware of the possibility of developing AMD in the future and understand that the preservation of visual fields is especially important in this case.

Depends on the presence of capillaries. The thickness of their layer is equivalent to the thickness of the layer of nerve fibers, and therefore fine the color gradation is different: from almost red in the nasal part to pale pink in the temporal part. In young people, the color is often yellow-pink; in children under 1 year old, the color of the disc is pale gray.

In case of pathology, the optic disc can be decolorized, hyperemic, bluish-gray. Monotony of color - abnormal development of the optic disc (often with amblyopia) is observed with tapetoretinal dystrophy, in old age.

Borders.

Clear ok or obscured by pathology. The ophthalmoscopic border of the disc is the edge of the choroid. When there is an underdevelopment of the choroid, an oblique position of the disc or stretching of the posterior pole of the eye with myopia (myopic cone) - the choroid moves away from the edge of the disc.

The senile halo is a peripapillary zone of atrophy without noticeable disorders of visual functions.

Dimensions.

Note normal size (true size 1200-2000 microns), enlarged or reduced. In hypermetropic eyes, the discs are usually visually smaller, in emmetropic eyes they are larger. With age, the dimensions of the disk do not change, but part of the supporting tissue atrophies, this atrophy is manifested by flattening of the optic disc.

Form. Normally round or slightly oval.

The central recess (vascular funnel, physiological excavation) is the place of entry and exit of retinal vessels. Formed by 5-7 years. The maximum diameter is normally 60% of the disk diameter (DD), the area is 30% of the total disk area. In some cases, excavation is absent and the central part of the disk is occupied by glial and connective tissue (Kunt's meniscus) and retinal vessels. Sometimes (in 6% of emmetropes) physiological excavation reaches the depth of the cribriform plate of the sclera and the latter is visible as a white oval with dark dots.

Pathological excavation (glaucoma) differs in size, depth, progressive course up to a breakthrough to the edge of the ONH (the ratio of diameters E / D from 0.3 to 1.0), the presence of parallax of the vessels along the edge of the disc.

Level in relation to the plane of the fundus.

Fine the nasal, upper, and lower portions of the optic disc are somewhat elevated compared to the surrounding retinal tissue (vitreous prominence), and the temporal portion is at the same level as the retina.

Atypical optic disc ("oblique disc") - occurs in 1% of cases in healthy eyes. Due to the oblique course of the ONH in the scleral canal, such a disk has a narrowed shape in the horizontal meridian, a flat position of the entire temporal side, and an undermined nasal edge of the excavation.

Edema of the optic disc:

Inflammatory (neuritis-papillitis),

Circulatory (anterior ischemic neuropathy, disc vasculitis - incomplete CVD thrombosis),

Hydrodynamic (stagnant disk).

Pseudostagnant disk- in ¼ of patients with hypermetropia, it can also be caused by drusen. The reason is the hypertrophy of glial tissue in the central depression of the disc during fetal development. The degree of expression is different. Often this is an increase in the saturation of the pink color, some blurring of the nasal, upper and lower borders in the normal state of the retinal vessels. To exclude pathology, dynamic observation is necessary with the control of visual functions, control of the size of the blind spot (not enlarged here).

Underdevelopment of the papillomacular sector of the disc: The optic disc is bean-shaped. The temporal sector is absent, pigment deposition is noted in this area.

disc entry coloboma- in the region of the disc, a wide hole 2-2.5 DD in size, surrounded by pigment, is visible. At the bottom of the hole, which is 3-4 diptries below the level of the retina, a pink disk is visible. The central vessels climb along the lateral surface of this cavity to the surface of the retina. Visual functions, as a rule, are not disturbed.

Myelin sheaths of fibers in the disc region and retina (in 0.3% of people). Normally, in humans, the border of their distribution is the cribriform plate. Ophthalmoscopically, myelin fibers with clear boundaries, coming from the depths of the disk, resemble white flames. Retinal vessels are lost in these tongues. Vision is not affected.

Disc inversion- the reverse arrangement, while the vessels of the retina are located in the temporal half of the disk, and not the nasal one.

Symptom of Kestenbaum- a decrease in the number of vessels on the disk less than 7 (symptom of optic nerve atrophy).

Disc drusen- abnormal hyaline bodies in the form of yellowish-white nodules located on the surface of the disc or in its tissue. Discs with drusen are not hyperemic, the borders can be scalloped, there is no exudate and venous stasis. Physiological excavation is smoothed, the edges are blurred, uneven. In doubtful cases, fluorescein angiography.

Evulsion- tearing out of the optic nerve from the scleral ring. Ophthalmoscopically, a hole is seen instead of a disc.

avulsion- rupture, detachment of the disc from the scleral ring. The disk remains in place. Visual acuity = 0.

Omnubelation- periodic fogging, transient loss of vision, manifested by an increase in intracranial pressure.

In newborns, it is light yellow, corresponding in size to the area of ​​the optic disc. By the age of 3-5 years, the yellowish background decreases and the macular area almost merges with the pink or red background of the central zone of the retina. Localization is determined mainly by the avascular central zone of the retina and light reflexes, located approximately 25 0 temporal to the ONH. The macular reflex is determined mainly up to 30 years, then gradually fades away.

Retina

Transparency.

Fine transparent (even a layer of pigment epithelium). The thickness at the optic disc is 0.4 mm, in the area of ​​the macula 0.1-0.03 mm, at the dentate line 0.1 mm. The background of the fundus is pink. It is necessary to examine the near, middle and extreme periphery.

The first zone, otherwise - the posterior pole - a circle, the radius of which is equal to twice the distance from the optic disc to the foveola. The second - the middle zone - a ring located outward from the first zone to the nasal part of the dentate line and passing through the temporal part in the equatorial region. The third zone is the rest of the retina anterior to the second. She is the most prone to retinopathy.

Parquet fundus- an uneven red color, on which the stripes formed by the vessels and darker areas between them are visible. This is due to a small amount of retinal pigment and a large amount of choroid pigment (normal variant).

Aspid fundus- the background is slate gray. The norm for people of the dark race.

Albinotic fundus: pale pink color (little pigment in the retinal pigment epithelium and choroid, and the sclera is visible). The vascular pattern of the choroid is clearly visible.

"Thinning of the retina"- this ophthalmological term is incorrect in principle, since even the absence of the retina does not lead to a change in the color of the fundus. If large and medium vessels of the choroid are visible through the retina, this means that the retinal pigment epithelium layer and the vascular choriocapillary layer have died.

A) caliber.

Note the state of the caliber of the vessels (arteries and veins): normal caliber, narrowed, dilated, obliterated. With narrowing of the arteries, note the arteriovenous ratio.

normal difference in the ratio of caliber A and B is most pronounced in newborns 1:2, decreases with age - in adults 2:3 and increases again in the elderly.

B) The course of blood vessels.

Note: normal, pathological tortuosity, arteriovenous chiasm.

The CAS and the CVS have 4 branches each, supplying blood to 4 quadrants of the retina - the upper and lower temporal, upper and lower nasal. Vessels pass in the layer of nerve fibers, small branches branch to the outer mesh layer. Before the first branching, the vessels are called the vessels of the first order, from the first to the second - the vessels of the second order, etc.