Changes in the organ of vision in general diseases. What is the fundus of the eye and what can be learned from it? Vascular changes in the fundus

Metabolic problems, viral diseases and even the common cold can adversely affect the functioning of the fundus, especially these changes in the functioning of the organ of vision cause discomfort to people of age. In this article, we will look at the main root causes of retinal problems, learn how to diagnose various diseases and learn how to properly care for your eyes.

Causes of changes in the fundus of the eye in old age

In old age, most often the fundus of the eye changes due to chronic diseases, excessive fatigue and other factors. An experienced doctor, examining the retina, even without additional tests, can detect a large number of diseases, such as diabetes or hypertension.

diabetic retinopathy

The main reason for the development of this disease is glucose, or rather, its excess amount in the blood. The blood vessels of the fundus become fragile, they can even burst. The disease progresses slowly (with the exception of patients with high blood pressure), but without timely treatment, vision can deteriorate significantly and in some cases blindness occurs. In addition, due to vascular ruptures, hemorrhage occurs in the fundus, scars are formed and the retina is separated from the choroid.

Also, diabetic retinopathy negatively affects the work of the macula (a component of the eye, thanks to which we can distinguish small details), edema may form. In this case, the patient's vision always becomes worse, over time, macular edema can lead to blindness.

In the early stages, the disease is difficult to identify without examination, the symptoms appear already in advanced forms. That is why ophthalmologists recommend having a complete examination at least once every two years.

Retinopathy symptoms:
• discomfort or pain in the eyes while reading;
• flickering of bright dots or "flies" before the eyes;
• distortion of objects, lack of clarity or "fog" in the eyes;
• veil before the eyes and loss of vision;
• any other changes.

If you have at least one of these symptoms, you should immediately be examined by an experienced ophthalmologist. Since vision can still be preserved at an early stage, the neglected form leads to blindness.

Kidney disease and major fundus changes

Many people over 45 suffer from kidney disease. There is nothing surprising in this, because poor ecology and an unhealthy lifestyle have a bad effect on the work of the human body and the kidneys, as well, and since all systems are interconnected, vision also suffers.

Bright's kidney disease, together with high blood pressure, can lead to changes in the fundus of the eye, this pathology is called renal retinopathy. Renal retinopathy is observed in patients with narrow arterioles and arteries, with a wrinkled kidney and glomerulonephritis. During the course of the disease, edema of the retina is formed, its detachment may occur, and hemorrhages are visible near large vessels.

Elderly people suffering from diseases of the adrenal glands, renal hypertension and hypertension quite often develop hypertensive retinopathy - damage to the fundus caused by high blood pressure.

Stages of development of hypertensive retinopathy:
• angiopathy - functional changes in the vessels of the fundus;
• angiosclerosis - in this case, organic changes occur in the retinal vessels;
• retinopathy - pronounced foci of opacification around the vessels, the presence of hemorrhages;
• neuroretinopathy - clouding of the retina is observed on top of the optic disc, edema is formed.

How the fundus of the eye changes with blood diseases

With some types of blood diseases, changes in the fundus of the eye occur, hemorrhage of various shapes and sizes appears under the shell of the eye. Patients with myeloid leukemia (chronic form) may develop rounded lesions that are yellow-white in color. The background of the fundus becomes pale, and the boundaries of the optic nerve lose their clarity. Such changes occur in more than 80% of patients, while their vision deteriorates significantly.

In patients with lymphoid leukemia, there are no dramatic changes, there are small round hemorrhages and the color of the fundus changes slightly. Symptoms may disappear as the patient's condition improves.

In old age, some people suffer from anemia, in addition to general malaise, there may be problems with vision: paralysis of the muscles of the eyeball, hemorrhages of various shapes are formed (in the form of stripes, rounded shapes, and so on). Most of the hemorrhages accumulate around the macula, as well as the optic nerve. If the anemia is severe, star-shaped exudation and retinal detachment may occur in the macular region.

The main symptoms of retinal changes in blood diseases:
• the formation of edema;
• a large number of hemorrhages;
• loss of color of blood vessels;
• change in the color of the fundus;
• expansion of arteries and others.

Diagnosis of fundus changes

It is difficult to find out on your own what led to changes in the structure of the fundus, since there can be a large number of root causes. An accurate diagnosis and treatment method will be selected only by an ophthalmologist after certain examinations and checks.

During the examination, the doctor uses an ophthalmoscope (consists of a slit lamp and focusing lenses), it allows you to examine the eye and its components in more detail. In patients with diabetes, visual acuity is checked, gonioscopy is performed to monitor the condition of the optic nerve, its damage (glaucoma) leads to blindness. Tonometry will allow you to measure intraocular pressure, this event is extremely necessary, because diabetes mellitus increases the risk of developing glaucoma.

In hypertensive retinopathy, in addition to ophthalmoscopy, an ultrasound examination of the eyes, as well as an electrophysiological examination, are usually performed. Optical tomography of the retina can also detect kidney disease.

Remember that only experienced specialists should perform these and other types of examinations, the correct diagnosis and the preservation of your vision depend on their qualifications. Many diseases in the early stages are treatable, so it is very important to quickly identify the disease and choose the right therapy.

Features of treatment

Depending on the type of changes in the fundus and the type of disease, a treatment method is selected, so diabetic retinopathy can be fought through laser therapy, surgery, and medications help in the early stages. It is impossible to completely cure the disease, but it is quite possible to reduce the negative impact on the body and preserve vision. Sometimes you have to resort to repeated operations to stop retinal hemorrhage.

Laser photocoagulation for people over 45 years of age can be carried out in 1-2 sessions to stop the rapid development of proliferative retinopathy in patients with diabetes mellitus.

In the treatment of renal retinopathy, first of all, they try to eliminate the underlying disease, so it will not be possible to prescribe therapy without an examination by a nephrologist. Retinoprotectors, antioxidants, angioprotectors and other agents are usually used. Various preparations and vitamin complexes are also used, which help strengthen the walls of blood vessels. In addition, installations are carried out with keratoprojectors and tear substitutes.

Carefully select the type of operation if retinal detachment has occurred. Be sure to analyze in detail the changes in the fundus, the type of detachment, its prescription, vastness and other parameters. Pneumatic retinopexy can be used, during the operation, the doctor injects a gas bubble into the vitreous cavity with a syringe, it presses the retina into place.

There is also the so-called cryopexy - attachment of the retina to the choroid occurs through low temperature. In more complex cases, a vitrectomy is performed, during the operation the vitreous body is removed, and silicone oil is injected in its place, which is subsequently replaced with a saline solution.

As you can see, there are a large number of treatment methods, self-treatment in case of deterioration of vision can only harm, therefore, with any change in the work of the eyes, it is better to consult a doctor. If you treat the underlying diseases in a timely manner and take care of your eyes, then there should not be any special vision problems even in adulthood.

How to take care of your eyes after 45

Thanks to vision, we receive information from the world around us, having lost the ability to see, a person becomes vulnerable. To avoid unpleasant changes in your life, you need to take care of your eyes, special attention to this organ should be paid to people of middle and more honorable age.

Firstly, make sure that your workplace always has enough lighting, in the twilight your eyes get tired faster. Lamps and other lighting devices should give a bright and soft light, it is best to use table lamps with shades. If you work at a computer, then you should not sit too close to the monitor, the distance between the screen and your eyes should be at least 30-40 cm. It is not recommended to be too close to the TV, as well as watch it in the dark. Readers are not recommended to read books on the go or in transport, as the eyes in this position are very strained.

Secondly, in the process of work, do not forget about rest, it is ideal to take a short break every hour or at least do exercises for the eyes: look several times, close your eyes and take a break, blink more often and make rotational movements with eyeballs.

Thirdly, remember that a healthy lifestyle has a positive effect on the condition of the eyes. Your daily diet must be rich in foods containing vitamins A and D: cod liver, eggs, herring, cream and many others.

You can not neglect the hygiene of the eyes, you need to wash them more often with cooled boiled water, so you reduce the risk of infection and the development of conjunctivitis. Baths of green tea, infusion of linden flowers or chamomile have a positive effect on the eyes (1 tsp of dried plants is poured with a glass of boiling water and infused for 15-16 minutes).

Inspection or examination of the fundus is, in essence, endoscopy of the organ of vision - the eye. The fundus was first described in the middle of the 19th century. With the invention of the Helmholtz ophthalmoscope, the progress in the verification of pathological conditions has gone by leaps and bounds.

At the present stage of development of medical science, therapists and ophthalmologists should be given common tasks for the prevention of eye diseases. Moreover, a number of measures in the prevention of major eye diseases can be implemented only by the joint efforts of an ophthalmologist and a therapist.

In order to increase the effectiveness of preventive measures among the population, it is necessary to:

1. Establish close contact in the work of the local ophthalmologist and the local therapist.

2. To work out the therapist's tactics in providing first aid to patients with injuries of the organ of vision.

3. To work out the therapist's tactics in providing first aid to patients with "red eye syndrome".

4. Purposefully ensure timely consultation of an ophthalmologist for dispensary patients with chronic diseases (hypertension, diabetes mellitus, atherosclerosis, collagenoses, endocrine diseases, etc.).

5. Purposefully ensure timely consultation of an ophthalmologist for patients with diseases (tuberculosis, syphilis, AIDS, chlamydia).

6. Provide control of visual functions to all patients over 40 years of age at risk of glaucoma (vascular disease, diabetes, collagenoses).

7. Take into account the state of the organ of vision in occupational pathology.

8. Increase oncological vigilance during prophylactic examinations.

9. Take into account the state of refraction when examining patients.

In the process of teaching students, it is necessary to draw their attention to the fact that even a slight change in the organ of vision should be compared with other general and particular symptoms of the disease, the body as a whole, since there can be no pathology of the organ of vision in an absolutely healthy human body.

Identified pathological foci and changes in the eye often help a doctor of any specialty to correctly establish a general diagnosis and carry out pathogenetic treatment of the patient. For example, in neurosurgery, accurate diagnosis of neurological diseases is greatly facilitated by ophthalmic studies, which help to detect pathology at the earliest stages of its development. Late recognition of the disease leads to a belated surgical intervention, which becomes more dangerous for the patient's life, and hopes for the restoration of many functions, including visual ones, turn out to be very small.

In our time, there is no such specialist who would not sought
know more about eye pathology, and there is no doctor who
would did not use the conclusion of the ophthalmologist to clarify
diagnosis. Therefore, at an appointment with an ophthalmologist, you can always see
patients referred for consultation by a neuropathologist, therapist, obstetrician, gynecologist, endocrinologist, venereologist, etc., in addition, in hospitals of any profile, ophthalmologists carry out the same work.

The method of external examination of the organ of vision can relatively easily fix external pathology, such as drooping of the upper eyelid (ptosis), deviation of the eye outward, pupil dilation. These symptoms may indicate damage to the brain in the region of the nuclei of the oculomotor nerve.

Pupillary reflexes can be used to judge the state of the nervous system, which is important not only for clinicians, but also for physiologists, pathophysiologists, pharmacologists, and other specialists. But such purely external changes, which make it possible to draw conclusions about changes in the body, are not so frequent.

In the vast majority of diseases cause hardly visible changes in the eyes, and only with a thorough examination, the ophthalmologist finds the most diverse and often serious changes, especially in the fundus.

After the creation of the ophthalmoscope by G. Helmholtz in 1850, it became possible to see manifestations of hypertension, diabetes, diseases of the blood, kidneys, central nervous system and other pathologies of the body on the fundus.

Clinical and morphological changes are so characteristic that the state of the fundus can not only diagnose pathological processes in the body, but also predict their course. For example, changes in the fundus of the eye in hypertensive patients, accompanied by narrowing, desolation of blood vessels and large swelling of the retina with the formation of blurred white foci, indicate a very serious condition of the patient and a serious prognosis for his life.

Thus, the identified symptoms in the organ of vision are strongly recommended to be known to every practical doctor. When supervising a general practitioner, it is necessary to know the pathological changes in the fundus of patients, especially with the most common of the above diseases.

^ FUND CHANGES

INFLAMMATION OF THE OPTIC NERVE (NEURITIS) characterized by blurring of the borders as a result of the release of inflammatory products into the surrounding retinal tissue and hyperemia of the disc. The vascular funnel of the optic nerve is filled with exudate and appears to be continuous. Edema of the optic disc extends to the surrounding retina. The veins of the retina expand, the arteries narrow. Small dotted and striped hemorrhages, delicate whitish stripes appear along the vessels on the disk. With inflammation of the optic nerve, visual acuity drops sharply. When examining the visual field, central, paracentral scotomas are found.

The cause of optic neuritis can be diseases of the orbit, paranasal sinuses, teeth, tonsils, encephalitis, meningitis, multiple sclerosis. Inflammation of the optic nerve can be the result of common infections - influenza, all forms of typhus, malaria, syphilis, tuberculosis, childhood infections, blood diseases, endocrine disorders, intoxication with alcohol, lead, quinine, etc.

However, it should be remembered that with farsightedness (hypermetropic refraction), a picture of false neuritis may occur. The function of the eye does not change. A comprehensive examination of the patient excludes damage to the optic nerve.

Inflammation of the extraocular part of the optic nerve is called retrobulbar neuritis, while the focus of inflammation can be localized in the intracranial or orbital parts of the optic nerve. The cause of retrobulbar neuritis is not always possible to establish. Most often, it develops as a result of infectious diseases of the central nervous system (neuroinfection) and multiple sclerosis. A possible cause may be acute and chronic general infectious processes - influenza, tonsillitis, acute respiratory, herpetic diseases, rheumatism.

Retrobulbar neuritis usually develops and proceeds acutely. The main symptomatology is reduced to visual disorders - a decrease in visual acuity and changes in the visual field. Ophthalmoscopic changes are usually absent. Often, with retrobulbar neuritis, pain in the orbit is noted, which is associated with the involvement of the optic nerve sheaths in the process, the presence of a positive relative scotoma.

In acute neuritis, timely and correct treatment helps to maintain a sufficiently high visual acuity. In the case of chronic retrobulbar neuritis, there remains a significant decrease in visual acuity and a change in the visual field.

^ OPTICAL-CHIASMAL ARACCHNOIDITIS. Damage to the sheaths of the optic nerve can develop in the chiasmal part of it with optic-chiasmal arachnoiditis. The cause of optic-chiasmal arachnoiditis is most often a neuroinfection of viral etiology, as well as tonsillitis, inflammation of the paranasal sinuses, and sometimes craniocerebral trauma. Optic-chiasmal arachnoiditis develops acutely, and then becomes chronic.

Inflammation of the arachnoid, and then the pia mater in the chiasm and adjacent sections of the optic nerves leads to the expansion and increase in vascular permeability, the appearance of exudate, circulatory disorders and tissue hypoxia. Subsequently, productive inflammation leads to fibroplastic changes, fusion of the arachnoid and dura mater, the formation of strands and cysts, which leads to impaired blood circulation and compression of the nerve fibers in the chiasm region.

In the development of opto-chiasmal arachnoiditis, ophthalmic symptoms predominate - decreased visual acuity, the occurrence of central scotomas, segmental or concentric narrowing of the visual field. Three forms of opto-chiasmal arachnoiditis are clinically distinguished: in the form of symptoms of retrobulbar neuritis, or symptoms of chiasm tumors, or a complicated congestive disc.

Treatment of arachnoiditis is complex, taking into account the etiology of the process.

Fig.21. Atrophy of the optic disc.

^ TOXIC DAMAGE OF THE OPTIC NERVE BY METHYL ALCOHOL INTOXICATION. The pathological process develops in case of poisoning with pure methyl alcohol or its containing liquids. In addition to the general phenomena of intoxication, after 1-2 days (less often several hours), vision in both eyes decreases sharply, the pupils become wide, do not react to light, and after 2-3 weeks, atrophy of the optic nerve appears. Methyl alcohol causes degenerative changes in the retinal ganglion cell layer and the optic nerve trunk.

^ OPTIC NERVE DAMAGE IN ALCOHOL-
TOBACCO INTOXICATION. The lesion develops as a result of alcohol abuse and smoking, due to endogenous hypo and vitamin B deficiency, this causes degeneration of the nerve fibers of the optic nerve. The disease proceeds according to the type of bilateral chronic retrobulbar neuritis. Characteristically, these patients see better at dusk and in low light than during the day.

In addition, toxic damage to the optic nerve can occur when taking large doses of quinine, poisoning with lead, carbon disulfide, sulfonamides, after taking plasmacide, snake bite, etc.

^ STAGGING DISC OF THE OPTIC NERVE. The disease has a characteristic ophthalmoscopic picture, occurs as a result of an increase in intracranial pressure, which can be caused by a brain tumor, hemorrhage, abscess, cysts, etc. The most common congestive discs are observed in tumors of the posterior cranial fossa, especially in tumors of the cerebellum, tumors of the ventricles of the cerebral hemispheres , and are almost not observed in pituitary tumors. The faster the tumor grows, the earlier the congestive disc develops. Congestive discs are more common in malignant tumors than in benign ones.

^ Rice. 22. Congestive optic disc.

There are five stages in the development of a stagnant disc: 1) initial stagnant disc; 2) pronounced stagnant disc; 3) a pronounced stagnant disc; 4) stagnant disc with transition to atrophy; 5) atrophy of the optic nerve. In the initial stages of stagnation, slight veiling of the borders and moderate hyperemia of the optic nerve head are determined. During this period, the ophthalmoscopic picture can simulate optic neuritis. The function of the eye does not change. Gradually, the edema spreads to the center and to the entire disc, the protrusion of the disc into the vitreous body increases. In the region of the disk, the vessels, as it were, climb onto the prominant nerve, in places plunging into the edematous tissue. The veins are dilated, tortuous, the arteries are narrowed. In the stage of pronounced edema, hemorrhages are observed, most often linear, into the tissue of the disc and the retina adjacent to it, surrounding the edematous disc with a corolla. With prolonged existence of edema, if the cause that caused the stagnation of the optic disc is not eliminated, the disc acquires a grayish tint. At the same time, the protrusion and diameter of the disc decrease, the veins become less wide, the hemorrhages gradually resolve, atrophy of the optic nerve fibers occurs with a rapidly progressive decrease in visual acuity.

A congestive optic disc is characterized by a long-term preservation of visual functions. In the initial stages, periodic, short-term fogging appears, especially after physical exertion, which is associated with fluctuations in intracranial pressure. Visual acuity and visual fields remain normal for a long time even with pronounced edema of the optic nerve. Then the central vision slowly decreases, peripheral vision narrows. With the transition of the congestive disc to atrophy, the central vision rapidly falls and the field of view rapidly narrows.

The general condition of the patient and the outcome of the disease depend on the course of the disease.

A 41-year-old patient was taken to the hospital with complaints of headache.

History: underwent surgery - removal of a malignant tumor of the palate. Visual acuity - 1.0 in both eyes, in the fundus there is a slight blurring of the boundaries of the optic nerve and vein dilatation. This made it possible to suspect the onset of stagnation of the optic nerve head and, consequently, the possibility of tumor metastasis to the brain. A week later, the edema increased, the vessels in some places began to hide in the edematous tissue. After 2 weeks, the optic disc will protrude into the vitreous body. After another 2 weeks, the patient falls into a coma. On the section massive metastases: in the brain.

^ FOSTER-KENNEDY SYNDROME develops with tumors and other pathologies in the region of the basal part of the frontal lobe of the brain, less often the syndrome may manifest itself in opto-chiasmal arachnoiditis, diseases of the cerebral vessels. Foster-Kennedy syndrome is characterized by optic nerve atrophy in one eye and congestive optic disc in the other due to compression of the intracranial optic nerve, most often by a tumor, resulting in simple optic atrophy. Later, with an increase in intracranial pressure, a congestive disc develops in the other eye, and edema of the optic disc does not develop after its onset atrophy, since the communication between the subarachnoid space of the brain and the intersheath space of the optic nerve is blocked as a result of compression of the optic nerve.

^ VASCULAR PATHOLOGY OF THE ORGAN OF VISION. Changes in the vessels of the retina are most often associated with a pathological condition, the vessels of the body as a whole. Cardiovascular diseases are currently one of the main causes of disability and mortality, respectively, the pathology of the fundus vessels is increasing, leading to low vision, blindness and visual impairment not only among the elderly, but also in younger age groups. Basically, the disease manifests itself in the form of a change in the caliber of the vessels, the state of their walls, its permeability, tortuosity, decussations, and subsequent secondary changes in the retina and optic nerve head as a result of circulatory disorders.

ATHEROSCLEROSIS is a disease of the vascular system. Vascular damage is accompanied by a violation of protein-lipid metabolism, accompanied by a progressive accumulation of lipids in the inner lining of the arteries.

Leading mouth in the development of atherosclerosis is assigned to a violation of cholesterol metabolism, damage and degenerative changes in the vascular endothelium, increased blood pressure. Assessment of the state of the fundus vessels is an important additional factor in the analysis of general changes in the cardiovascular system of the body in atherosclerosis.

Clinically, with severe atherosclerosis, the vessels of the retina have their own specific status. In the arteries of large and small caliber, their unevenness and tortuosity are determined. Due to the thickening of the wall along the trunks, a light reflex with a yellowish-golden or whitish tint is determined - the phenomenon of copper and silver wire.

In some cases, the Gwist symptom is noted. Increased tortuosity and increased reflectivity of the vessels give the impression of increased vascularization of the retina. The development of aneurysms, dashed and spotty hemorrhages in the retina, and in some cases in the vitreous body with symptoms of partial or complete hemophthalmia, may develop macular degeneration of various types. Evaluation of changes in the fundus vessels helps to correctly determine the tactics of therapeutic measures.

^ CHANGES IN THE FUND OF THE EYE IN HYPERTENSION are very typical and varied depending on the stage of the disease. Analysis of ophthalmological changes in the fundus is currently a mandatory moment in the examination of patients with hypertension, since changes in the retinal vessels can be detected already in the early stages of the disease. It should be noted that in a quarter of patients with overt hypertension, ophthalmoscopy does not reveal changes in the vessels of the fundus.

There are three stages of fundus changes in hypertension, successively replacing one another: 1) hypertensive angiopathy - the stage of functional changes in retinal vessels; 2) hypertensive angiosclerosis - the stage of organic changes in the vessels of the retina; 3) hypertensive and neuroretinopathy - a stage of organic changes in the retina and optic nerve.

The first stage - initial (hypertensive angiopathy) - is characterized primarily by narrowing of the retinal arteries and expansion of the retinal veins. In this regard, the correct ratio of the caliber of arteries and veins (2:3) is violated in the direction of increasing this difference (1:4; 1:5). Uneven caliber and increased tortuosity of the retinal vessels are noted. In the central sections, a corkscrew-shaped tortuosity of small venules (Guist's symptom) is possible;
a slight narrowing of the vein under the pressure of the artery located above it. Symptoms of hypertensive angiopathy, characteristic of the period of functional changes in blood vessels, are unstable and can disappear with appropriate treatment of hypertension.

The second stage - transitional (hypertensive angiosclerosis) - is distinguished by a number of symptoms that characterize the stage of organic changes in retinal vessels, where hyperplasia of elastic membranes, fibrosis, lipoid infiltration, protein deposits, and areas of necrosis are found.

One of the early manifestations of angiosclerosis is a symptom of accompanying bands along the compacted wall, while the vessel seems to be double-circuit. The retinal arteries are narrow, tortuous, of uneven caliber, symptoms of copper and silver wire are pronounced.

In hypertensive angiosclerosis, a symptom of a pathological vascular decussation is often manifested - a symptom of Salus. There are three degrees of changes in the symptom of Salus: I - depression of the vein, II - arcuate bending of the vein at the point of intersection with the artery, III - visible break of the vein at the point of intersection. The most characteristic for angiosclerosis is the second stage. In one third of patients, the optic nerve disc appears pale with a waxy tint, and newly formed vessels and microneurysms may be noted in the area of ​​the disc.

The third stage - hypertensive retinopathy and neuroretinopathy - is characterized by gross violations in the entire vascular system of the patient. Focal opacities and hemorrhages in the retina join the above changes in the vessels of the retina. The optic nerve may be involved in the process. The ophthalmological picture at this stage depends on the pathogenesis of hypertension.

Arteriosclerotic retinopathy is manifested by sclerosis of the vessels and the unevenness of their caliber. From a decrease in blood flow in vessels with a narrow lumen, a symptom of a copper wire arises, and when the vessel is completely empty, it becomes like a silver wire. The most common symptom of hypertensive retinopathy is retinal hemorrhage.

^ Rice. 23. Hypetronic neuroretinopathy.

In most cases, these are small hemorrhages in the macular and paramacular regions. There is swelling of the retina, which often manifests itself along the vessels. In the central zone of the retina, there may be whitish foci that look like cotton balls, so-called hard exudates often appear - small, bright white, rounded foci with clear boundaries located in the outer layers of the retina. The optic nerve receives little blood and gradually atrophies.

Changes in visual functions in hypertension are very diverse and depend on damage to the retina and optic nerve.

Renal retinopathy, in addition to the narrowness of the vessels, retinal edema, changes in the optic nerve, is characterized by many small foci in the macula, which, when grouped, look like a star shape and a pronounced transudative syndrome. It manifests itself in a greater degree of retinal edema compared to hypertension. The edematous component is usually localized in the peripapillary zone, in the area of ​​the macula and along the large vascular branches. Typical are cotton-like foci located in the central parts of the fundus. Hemorrhagic syndrome is a little characteristic of renal retinopathy. The optic nerve with pronounced edema, pale in color, hemorrhages in the disc tissue are not typical.

Malignant hypertensive retinopathy develops in the terminal phase of both forms. This stage is characterized by gross retinal edema and more pronounced changes in the retina and optic nerve mentioned above. Optic nerve stasis is possible. The prognosis for such patients is poor.

^ ACUTE OBSTRUCTION OF THE CENTRAL RETINA ARTERY characterized by pathological changes in the form of a spasm of an arterial vessel (more often in hypertensive patients), or blockage of the lumen of the artery by an embolus (from the endocardium), or a thrombus, which lead to acute blood obstruction. Clinically, it is not always possible to determine exactly what caused the closure of the vessel lumen. Despite the difference in the causes of circulatory disorders, the clinical manifestations of all conditions are quite similar and characteristic. In all cases, retinal ischemia develops. If the vessel branch is affected, then retinal ischemia is limited; if the pathology concerns the entire trunk of the central retinal artery, then ischemia becomes common.

With ophthalmoscopy on a white background of the retina in the central macular region, a bright red spot is visible, the so-called "cherry stone" symptom. The appearance of such a spot is explained by the fact that in the central fossa the retina is very thin, it swells less and the choroid is visible through it. The optic disc is pale, its borders are blurred. With the defeat of the entire trunk of the artery, visual acuity decreases sharply, sometimes to the point of complete loss.

In acute arterial disorders in the retina, which is highly sensitive to the slightest changes in oxygenation, after 15 minutes of ischemia, retinal edema is morphologically detected, changes occur primarily in ganglion cells in the form of their initial tigrolysis. After 40 minutes, a pronounced edema of the retinal tissue is observed, with the restoration of blood circulation, within 40 minutes it is possible to expect a return of visual functions to one degree or another very rarely).

In the late period of the disease, atrophic and degenerative changes in the retina occur in all patients, and primary atrophy of the optic nerve develops. Arteries of uneven caliber are sharply narrowed, veins become narrow, acquire a rectilinear course.

^ THROMBOSIS OF THE CENTRAL RETINA VEIN unlike arterial obstruction, it develops more slowly, passing through several stages. With prethrombosis, patients usually do not complain. In the fundus, venous congestion is detected. The veins are dark, dilated, increased tortuosity. In the stage of incipient thrombosis, patients complain of blurring before the eye, especially in the morning (scotoma appears).

Ophthalmoscopically, the veins are dark, wide, tense, along their course a transparent transudative edema of the tissue is determined, on the periphery of the retina, along the terminal venous branches, dotted or spotted hemorrhages appear. With incomplete thrombosis, transudative edema of the tissues of the optic nerve and retina increases, and the number of hemorrhages increases. Vision is reduced.

In the stage of complete thrombosis in the fundus, massive hemorrhages are determined, the so-called “crushed tomato” symptom, the boundaries of the optic nerve are blurred. Visual acuity at this stage is sharply reduced. The prognosis is unfavorable. Against this background, an increase in intraocular pressure is possible, tonometric control is indicated.

^ Rice. 24. Thrombosis of the central retinal vein.

As the consequences of thrombosis of the central retinal vein reverse, a number of changes may develop: retinal neovascularization, central secondary retinal degeneration, retinal cystic maculopathy, retinal proliferative changes, vitreous fibrosis, secondary hemorrhagic glaucoma.

^ FUND CHANGES DURING PREGNANCY. The occurrence of toxicosis of pregnancy is evidenced by changes in the fundus, which appear earlier than other general symptoms of toxicosis, and often may be the only manifestation of it.

The dynamics of the pathology of the fundus can serve as an indicator of the course of the disease and the effectiveness of treatment. Therefore, along with a general examination of the patient, systematic monitoring of the fundus is necessary. Changes in the fundus appear at different stages of pregnancy, from the onset of toxicosis and in all its forms: vomiting, hydrops, nephropathy and hypertension. It must be borne in mind that pathological changes appear on the fundus no earlier than after 10-12 weeks of pregnancy.

Allocate early and late toxicosis (in the last months of pregnancy). Changes in the fundus of the eye during toxicosis of pregnant women are varied and numerous. Therefore, many classifications have been proposed, but there is no unified systematization of them.

All pathology fits mainly in changes in the state of blood vessels, optic nerve and retina. By their changes, the severity of the disease can be determined. First, changes in the vessels of the retina appear. If vascular changes are associated with an increase in blood pressure, then there is a violation of the ratio between the caliber of arteries and veins according to the type of angiopathy in hypertension. Further, the optic nerve is affected (neuritis, congestion and retina (edema, hemorrhage, retinal detachment).

The prognosis for toxicosis with damage to the fundus is always favorable more often for the child and difficult for the mother. When the fundus is damaged, the question of termination of pregnancy is raised, depending on the general condition of the patient, the duration of pregnancy, the nature and dynamics of changes in the fundus.

Experts recommend dividing the indications for interruption
pregnancies into absolute and relative. Absolute indications include: retinal detachment caused by toxicosis of pregnant women, hypertensive neuroretinopathy, optic neuritis, persistent angiospasm with high blood pressure, thrombosis of the central retinal vein. Relative indications are the initial form of angiospasm of the retinal vessels, previous retinopathy and retinal detachment due to toxicosis of pregnant women.

Often one has to deal with the issue of childbirth in women with a high degree of myopia (especially with large changes in the fundus of the myopic nature). As numerous observations show, natural childbirth rarely gives complications.

However, if the patient already had a retinal detachment in one eye or there are gross changes in the macular area, a tendency to hemorrhages, it is recommended to resort to turning off attempts (caesarean section before the onset of labor, forceps during childbirth). With severe retinopathy of pregnancy, regression of the entire pathology of the fundus is sometimes possible with the return of vision.

Patient A., aged 28, was with a second pregnancy in the maternity ward due to increased blood pressure. In history: the first pregnancy ended in termination due to severe toxicosis. The patient complains of blurred vision, headaches, general weakness. In the fundus, narrowing of the arteries, blurring of the borders, optic nerve head, and retinal edema are determined. The question of termination of pregnancy is raised to save the life of the patient, but the relatives and the patient herself categorically object to termination of pregnancy. The patient's condition deteriorates sharply, retinal edema increases, visual acuity drops to light perception, serous retinal detachment appears in both eyes. At the 8th month of pregnancy, a caesarean section is performed. The two twin boys are healthy, but the mother is left almost completely blind.

It should also be borne in mind that the absence of complaints of a drop in vision does not mean the absence of fundus lesions, therefore, it is necessary to periodically ophthalmoscope all pregnant women, regardless of the general well-being of the patient, and in case of toxicosis, this must be done more often.

Timely diagnosis of toxicosis of pregnant women and early treatment contribute to the preservation of not only vision, but also the life of the mother and child.

^ CHANGES IN THE ORGAN OF VISION IN DIABETES. Diabetes mellitus is one of the most common endocrine diseases. The number of patients with diabetes is increasing especially in highly developed countries; The prevalence of diabetes mellitus, the frequency and severity of the resulting complications gave it the character of a social disease, in connection with which, in 1965, the WHO Committee of Experts on Diabetes Mellitus was established.

The reasons for the development of diabetes are numerous. Great importance is attached to the genetic factor, overeating carbohydrates, obesity, stressful situations and, of course, local changes in the pancreas itself. Insulin deficiency plays a major role in the development of diabetes. Carbohydrate, protein, as well as water and salt metabolism is disturbed.

The basis of pathological changes is a generalized lesion of the vascular system of the body. Universal vascular damage is the cause of more frequent occurrence in diabetes, the vessels of the kidneys and eyes are especially often affected - this is in comparison with people who have had a stroke, myocardial infarction, gangrene of the lower extremities, gastric and intestinal bleeding.

Patients with diabetes are prone to inflammatory diseases in the form of eyelid skin eczema, blepharitis, blepharoconjunctivitis, chalazion, which is explained by the body's reduced resistance to various endo- and exogenous infections, and in some cases recurrent barley and blepharitis are the only symptoms of clinically pronounced or latent sugar, diabetes.

Characteristic of diabetes mellitus are changes in the vessels of the conjunctiva, especially in the area of ​​the limbus in the form of expansion of venules, microaneurysms and petechial hemorrhages. To a certain extent, with diabetes mellitus, changes in the cornea are possible (keratopathy, epithelial keratodystrophy, dry keratoconjunctivitis, central or peripheral stromal dystrophy with the deposition of pigment grains on the endothelium), a manifestation of polyneuropathy resulting from impaired microcirculation and metabolic changes.

A network of small newly formed vessels, the so-called rubeosis of the iris, appears and develops rather quickly on the iris, this is a manifestation of hypoxia in the tissues of the eyeball. In the future, newly formed vessels can spread into the angle of the anterior chamber, which contributes to the development of secondary glaucoma.

Damage to the vessels of the retina and optic nerve are the most severe manifestation of diabetes mellitus. During diabetic retinopathy, there are four stages in the development of damage to the vessels and the retina.

The first stage (diabetic preproliferative retinopathy) is characterized by changes only in the retinal veins in the form of their expansion and tortuosity, aneurysms from larger venous trunks, single microaneurysms. Visual functions are not impaired.

There are changes in the retinal tissue in the form of petechial hemorrhages at the posterior pole, initial exudation, single whitish foci and, accordingly, visual acuity decreases when the macular region is damaged.

^ Fig.25. Diabetic proliferative retinopathy.

Characterized by multiple hemorrhages, thrombosis of small venous vessels, yellowish or white exudates, which are often localized in the central part of the fundus. Retinal edema appears in the form of zones painted in a grayish-yellow color.

The second stage of diabetes (diabetic proliferative retinopathy) includes such a stage in the course of the process, when, in addition to the changes characteristic of the previous stages, newly formed vessels and proliferative changes appear in the tissue of the retina and vitreous body. Newly formed vessels in the proliferating connective tissue become thin and fragile, which constantly leads to new hemorrhages. Subsequently, traction retinal detachment, hypotension, or secondary hypertension may develop.

For a more favorable course of the disease and prevention of complications in all systems, including those of the organ of vision, proper treatment of the patient is necessary. - selection of medicines, their dosage, diet, mode of work and rest.

Diabetes can occur at any age and be combined with other diseases - sclerosis, hypertension, etc. Therefore, patients should be comprehensively examined by a therapist, constantly under the supervision of an endocrinologist and an ophthalmologist. If a diabetic patient is not treated carefully enough or does not follow prescriptions correctly, he may experience gross disturbances in blood sugar levels and develop hyperglycemia or hypoglycemia.

Diabetic hyperglycemic coma is caused by insulin deficiency, which causes ketoacidosis and the appearance of acetone in the urine, with dehydration occurring, effects on the brain of ketone bodies, decompensated acidosis, and electrolyte disturbance.

Symptoms increase gradually, over several hours or even days, a prodromal period preceding coma is possible: fatigue, weakness, dry mouth, increased thirst, polyuria, headaches, appetite suppression, nausea, often vomiting, abdominal pain. Then comes a coma - complete loss of consciousness, lack of response to stimuli. This condition is accompanied by noisy breathing - "Kussmaul's sick breath", - the smell of acetone from the mouth. The content of glucose in the blood exceeds 16 mmol / g.

Due to the sharp dehydration of the body, the tone of the eye decreases, hypotension develops. This is easy to verify by comparing the tone of the eye of a doctor and a patient, slightly palpating the eyeball with two index fingers through closed eyelids. The pupil in a diabetic coma narrows, sometimes a diabetic cataract can be observed.

Hypoglycemic coma develops with a rapid decrease in blood sugar and, as a result, low utilization of glucose by the brain tissue. It is usually observed in patients with diabetes mellitus with an excess of injected insulin and insufficient food intake.

A coma occurs quickly, starting with the precursors: hunger, weakness, trembling, headache, sweating, arousal turns into stupor and coma. The tone of the eyeballs is normal. At the beginning of the coma, there is an expansion of the pupils, and then their narrowing. The patient has a blurry image, doubling of objects.

^ VISUAL CHANGES IN NEXAPHOM DIABETES characterized by unquenchable thirst, increased diuresis with a decrease in urine density, lack of appetite, weight loss, dry mouth, nausea and vomiting, which is the cause of insufficient production of antidiuretic hormone. In contrast to diabetes mellitus, eye changes in this pathology are insignificant and are expressed in dryness of the conjunctiva and cornea, and a decrease in its sensitivity. Rarely, mild neuroretinopathy can be observed.

^ CHANGES IN THE FUND OF THE EYE IN BLOOD DISEASES. Changes in the fundus are usually associated with morphological and other changes in the composition of the blood, are not local in nature, being generalized, have a significant impact on all organs and systems, including the organ of vision.

So, with anemia, when the number of red blood cells and hemoglobin in the blood decreases sharply, the fundus of the eye appears discolored, and the vessels of the retina are paler. In severe and advanced forms of anemia, retinal vessels dilate, microaneurysms, microhemorrhages in the form of smears and stripes form, due to hypoxia, whitish-gray exudates form, retinal detachment is possible.

^ Fig. 26. Anemia.

With leukemia, the ophthalmoscopic picture is characterized by dilated veins, a pale yellowish color of the fundus due to infiltration of the choroid by lymphocytes and myelocytes. The optic disc is pale, edematous, the boundaries are often not defined. Retinal hemorrhages are observed and subconjunctival hemorrhages are common. In acute leukemia, the following are possible: stagnation of the optic nerve head, nystagmus, violation of the oculomotor muscles.

With erythremia, characterized by a sharp increase in the number of red blood cells and the appearance of their young forms, the fundus has a dark, cyanotic color, the arteries do not differ in color from the veins. The optic disc is edematous, red. Arteries are not changed. The veins are dilated and tortuous, along their course there is a large number of hemorrhages, which may resemble a picture of retinal vein thrombosis.

In some cases, with a blood disease, changes in the organ of vision are detected first, which serves as the basis for a detailed and targeted examination of the hematopoietic apparatus of patients.

Of no small importance for a general practitioner is knowledge of the pathology of the adnexal apparatus and the anterior segment of the organ of vision.

^ CHANGES IN THE POSITION OF THE EYELIDS, EYEBALL, PATHOLOGY IN THE ANTERIOR SECTION OF THE EYE

In the embryo, the eyelids are fused skin folds, which, at the end of fetal development, are separated and form the palpebral fissure. Normally, the open palpebral fissure on both sides of the same width, almond-shaped. Its length in an adult is on average 30 mm, height - from 10 to 14 mm. The eyelids should adhere to the eyeball and close when the palpebral fissure is closed. Closed eyelids can be called the fifth - anterior wall of the orbit, since it closes the entrance to the orbit and is a protection for the eyeball from the anterior most open side.

The eyeball is located strictly frontally in the orbit and does not protrude from the orbit. At rest, with the palpebral fissure open, the upper eyelid slightly covers the cornea from above up to 2 mm, the lower eyelid does not reach the limbus by 1-2 mm. The configuration, shape and size of the palpebral fissure can change with anomalies and various diseases. The eyeball is in the midline without retraction or displacement. The distance between the eyes is approximately 6 cm. The eye has an almost spherical shape. The average size of an adult human eye is approximately 24 mm.

The eye of a newborn is 16 mm long. The movements of the eyeball are carried out in full. Conjunctiva pale pink, shiny. The cornea is transparent. Its surface is mirror-like, spherical, smooth. Sensitivity should be normal - from the touch of a hair or a piece of cotton wool to the surface of the cornea, the patient under study blinks. The anterior chamber has an average depth, filled with a clear liquid - moisture. The iris is the same color in both eyes. The pupil is located in the center of the iris, has a correctly round shape, a diameter of 3 mm on average, in both eyes.

Pupiloscopy is the most common clinical method for examining pupils. First, it is advisable to study the pupils and pupillary reactions; in diffuse daylight, and then in a dark room to examine pupillary reactions to light. The method of accurately measuring pupils is called pupillometry.

With the help of special pupillometers, it is possible to measure the initial size of the pupil before the light reaction and the size of the constricted pupil after it is completed. Direct (direct illumination of the eye with light) and sympathetic - (response of the pupil of the unlit eye) pupillary reactions must be alive. When studying pupillary reactions to light, it is necessary to fix attention on the speed, constriction of the pupil, the scope of this constriction, the synchronism of pupil contraction in all radii. The reaction of the pupil - its narrowing during accommodation and convergence (due to the approach of an object from a distance of 20 cm) - is normal saved.

When examining pupillary reactions when the eyes are set at a close distance, it is necessary to pay attention, as well as in the study of pupillary light reaction, to the reaction rate, the scope of the constriction, and the concentricity of the constriction. Of particular note is whether there is a dissociation between the rate of pupillary reaction to light and to convergence. Normally, the reaction to convergence is slower than the reaction to light.

In the early stages of pathology, on the contrary, the reaction to light lags behind the reaction to convergence in time, or the rate of both reactions becomes the same. The reaction to the closing of the palpebral fissure is observed with an active attempt by the subject to close the eyelids, close the eyes, while the doctor prevents this with the thumbs of both hands placed on the eyelids. The expansion of the pupil, its return to the physiological form after the reaction to the closing of the palpebral fissure is observed in the palpebral fissure at the moment of opening the eyes.

The trigeminopupillary pupillary constriction reaction is caused by thermal, tactile, or some other irritation of the cornea, conjunctiva, and skin in the region of innervation of the first branch of the trigeminal nerve. Sensitive reactions of pupil dilation are observed with painful irritation, prick, pinch in any part of the body, especially in the neck. Pupillography is a method that allows you to record the course of pupillary reactions to light and to accommodation with convergence.

Various pharmacological tests can be used with great success, based on the fact that one group of substances (atropine, homatropine, scopolamine, etc.) depresses the parasympathetic nervous system, while another group (pilocarpine, ezerin, etc.), on the contrary, irritates, excites it and Finally, the third group (cocaine, adrenaline) excites the endings of the sympathetic nervous system.

With pathology in the activity of the parasympathetic and sympathetic systems, the reaction of the pupils to the introduction of the above substances will be different from the norm and unequal when the lesion is localized in one system or another. The pupil area with a transparent lens is usually black.

What kind of pathology can occur in the anterior part of the organ of vision in some common diseases? Let us dwell only on the most common and typical eye symptoms, which can be identified by a simple external examination.

^ PTOSIS (LOPPING OF THE UPPER EYELID) may be congenital or acquired. Congenital ptosis is most often bilateral. Ptosis can be complete or partial. The reason for it is the inferiority of the muscle that lifts the upper eyelid.

The etiology of acquired ptosis is paresis or paralysis of the levator. This pathology is often combined with paresis or paralysis of other muscles innervated by the oculomotor nerve. With the defeat of all the nuclei of the oculomotor nerve, ptosis is accompanied by paralysis of the motor muscles of the eye, the ciliary muscle, the muscle that narrows the pupil, as a result, the pupil will be dilated.

It is necessary to distinguish ptosis of the upper eyelid from the narrowing of the palpebral fissure in case of retraction of the eyeball - enophthalmos and blepharospasm, which accompanies the inflammatory process in the eye. With ptosis, folds appear on the skin of the forehead, the frontal muscle is included in the work to compensate for the activity of the muscle that lifts the upper eyelid. Some patients with severe ptosis and covering a significant part of the cornea with the eyelid for the convenience of vision are forced to raise their heads up - the “stargazer's position”. Ptosis can occur as a result of paralysis of the oculomotor nerve in various infections (botulism, typhoid, syphilis, influenza, meningitis, skull trauma, etc.).

Sympathetic ptosis develops with paralysis of the cervical sympathetic nerve, since the smooth muscle of Müller, innervated by the sympathetic nerve, is involved in lifting the eyelid. With paralysis of the Müllerian muscle, the upper eyelid droops slightly in one or both eyes, i.e. revealed incomplete ptosis. Sympathetic ptosis is usually associated with pupillary constriction and slight retraction of the eyeball.

The combination of these three symptoms (ptosis, miosis, enophthalmos) is known as Horner's syndrome. It should be noted that the narrowing of the palpebral fissure in sympathetic ptosis occurs not only due to the lowering of the upper eyelid, but also due to the upward movement of the lower eyelid, due to the contracture of the circular muscle due to the exclusion of the Müller muscle.

Sympathetic ptosis is also characterized by redness, an increase in the temperature of the skin of the corresponding half of the head. According to the clinical picture, sympathetic ptosis is difficult to distinguish from ptosis with paralysis of the oculomotor nerve. Helps in the diagnosis of the symptom of retraction of the eyeball and miosis. Paralysis of sympathetic innervation (ptosis) develops when the apex of the lungs is affected, neck and thyroid injuries.

Changes in the position of the eyeball can manifest as protrusion - exophthalmos, retraction - anophthalmos, displacement or deviation to the side, as well as twitching of the eye - nystagmus.

Unilateral rapidly developing exophthalmos is caused by pathological changes in the orbit due to inflammation, trauma or hemorrhage. With a slowly growing protrusion of the eye, one should always think about a neoplasm that can cause: also a displacement of the eye to the side, or an arteriovenous aneurysm. Since the eye socket is closely connected with the paranasal sinuses, it is necessary to consult an otolaryngologist for all processes in it. Bilateral exophthalmos, as a rule, is a consequence of endocrine disorders in Graves' disease and diencephalic syndrome.

Having found exophthalmos, it is necessary to apply all methods of examining the patient to establish the cause, type of exophthalmos and the degree of protrusion of the eyeball. To do this, use an external examination, palpation, auscultation of the orbit, exotalmometry, radiography and angiography. Normally, the protrusion of the eyeball is 17-19 mm with an allowable difference of 1.5 mm.

The degree of exophthalmos in millimeters is determined by the difference in the protrusion of the corneas of both eyes using a Hertel mirror exophthalmometer. In its absence, the degree of exophthalmos can be used to judge the width of the palpebral fissure (protrusion of the eyeball).

In the presence of exophthalmos, to clarify the diagnosis, it is necessary to clarify the following questions:

1. Unilateral exophthalmos or bilateral?

2. Speed ​​of development (rapid or slow appearance) and progression of exophthalmos.

3. Is exophthalmos reductible (displacement of the eyeball when pressed with fingers through the closed eyelids in the orbit).

4. Does exophthalmos pulsate or not?

5. The presence or absence of noise when listening in the orbit.

6. The presence or absence of x-ray data on painful changes in the walls of the orbit.

^ EXOPHTHALMOUS PULSING - a symptom complex, including: protrusion of the eye, synchronous pulsation of the eyeball from arterial blood entering the venous system through an arteriovenous aneurysm in the cavernous sinus or ophthalmic artery, and blowing noise. This noise is heard through the eyelids over the region of the orbit and temple during systole of the heart.

Compression of the carotid artery in the neck stops the pulsation and noise. Noise during pulsation deprives the patient of rest and is accompanied by headaches, diplopia is possible. Due to the difficulty of outflow of blood in arteriovenous aneurysms in the vessels of the conjunctiva, eyelids, retina, blood stasis is often noted, the veins are tortuous, dilated.

Paresis and paralysis of the oculomotor nerve are possible, since the disease occurs mainly with skull injuries - up to 75% of cases, therefore, consultation with a neuropathologist and neurosurgeon is required. Surgical treatment - ligation of the carotid artery in the neck or internal carotid artery inside the skull. A good effect is given by surgical intervention on the superior orbital vein.

^ INTERMITTING (INTERMITTED) EXOPHTHALMOUS - periodic protrusion of the eye and its disappearance. It is quite rare; predominantly in men, usually on one side. It is possible to provoke an attack of intermittent exophthalmos with a sharp tilt of the head, holding the breath, straining, squeezing the jugular vein. Exophthalmos develops with an increase in venous stasis in the orbit.

The reason is the congenital weakness of the avalvular veins of the orbit, their varicose expansion, relaxation of the fascia of the orbit. During an attack, in addition to exophthalmos, patients may have limited eye mobility, pupil dilation, a feeling of heaviness and pressure behind the eye. Surgical treatment - vein ligation.

^ ENDOCRINE EXOPHTHALMOUS. There are two separate forms of endocrine exophthalmos: 1, Benign or exophthalmos in patients with Graves' disease, 2. Malignant or Progressive exophthalmos. The cause of its development are disorders in the hypothalamic-pituitary-thyroid system.

^ EXOPHTHALMOUS IN PATIENTS WITH Graves' DISEASE is bilateral, slightly decreases with pressure on the eyeball and increases with head tilt and compression of the jugular veins. The eyeballs protrude moderately straight ahead, their mobility is preserved.

The palpebral fissures are dilated, there is a slight retraction of the upper eyelid, as a result of which most of the sclera remains exposed (Dalrymple's symptom); there is a lag of the upper eyelid when the eye is retracted downwards (Grefe's symptom); rare blinking (Stelwag symptom), convergence disorder - with a longer convergence, one eye deviates outward after a while (Mobius symptom), pigmentation of the skin of the upper eyelid (Yemenek symptom).

As a rule, patients do not complain, sometimes they are bothered by fatigue when reading or a feeling of a foreign body in the eye. Rarely disturbed by lacrimation, which appears periodically, endocrine exophthalmos usually does not affect vision and the condition of the fundus.

In case of malignant exophthalmos, as a rule, there is a bilateral protrusion of the eyeballs, rapidly emerging, progressive, reaching subluxation, sometimes dislocation, of the eyeballs.

In rare cases, exophthalmos can be unilateral. The exophthalmos is not reductible, there is a firm swelling of the eyelids, a pronounced chemosis, while the conjunctiva protrudes from the palpebral fissure.

The mobility of the eyeballs is limited due to paralysis of the external muscles of the eye. Patients are concerned about severe pain and irritation of the eyes; there is marked photophobia. Vision is reduced due to damage to the corneas - drying out from not closing the palpebral fissure, infiltrates and even ulceration.

^ Rice. 27. Appearance of a patient with Basedow's disease.

On the fundus, the phenomena of venous stagnation are noted. The field of view narrows in an irregularly concentric pattern. With endocrine exophthalmos, hormone therapy (cortisone, ACTH), X-ray therapy (irradiation of the pituitary region and the region of the orbits with significant doses) is used. According to indications, bands of edematous mucous membrane are excised.

ENOPHTHALM- retraction of the eye - appears with an increase in the volume of the orbit, with fractures of the walls of the orbit, mainly the lower wall, with atrophy of the orbital tissue, paralysis and paresis of the sympathetic nerve. Enophthalmos is also one of the signs of Bernard-Horner syndrome.

NYSTAGM- involuntary synchronous twitching or oscillation of the eyeballs, caused by central or local causes. Nystagmus in direction can be horizontal, vertical and rotational, in appearance - pendulum, jerky and mixed. The direction of nystagmus is assessed by its rapid phase of oscillation. For all types of nystagmus, speed, scope, degree, frequency and duration are also determined. The essence and etiology of nystagmus is established by neuropathologists, and in certain diseases - by otolaryngologists (diseases of the vestibular apparatus).

The development of nystagmus from local causes is based on congenital cataracts, corneal opacities, various underdevelopment of the eye, leading to low vision and elimination of macular fixation. Of the common causes, the occurrence of nystagmus is promoted by multiple sclerosis, meningitis, dropsy of the brain, lesions of the pons, cerebellum, pituitary gland, medulla oblongata, etc.

Nystagmus usually does not cause concern to patients, but they suffer greatly from low vision, which is difficult to correct.

Treatment of nystagmus is reduced to the elimination of the underlying cause. With horizontal nystagmus after surgical myoplastic operations, not only the amplitude of nystagmus decreases, but in some cases visual acuity in both eyes increases.

^ CHANGES IN THE ANTERIOR SECTION OF THE EYE. Identification of pathology in the anterior part of the eyeball is important in the diagnosis of common diseases. For example, the yellow color of the visible part of the conjunctiva and sclera indicates a liver disease that occurs with jaundice. It must be borne in mind that the icterus of the conjunctiva and sclera can only be detected in good daylight.

^ BLUE SCLERA SYNDROME - congenital disease. The bluish-blue color of the sclera is due to their thinness and translucence of the pigment of the vascular tract. This symptom (bilateral) is often accompanied by a triad: deafness, weakness of the articular and ligamentous apparatus, fragility of tubular bones with frequent fractures and dislocations (Van der Hove's syndrome). Blue sclera can be accompanied by heart disease, cleft palate, etc.

The appearance of a yellowish-brown-greenish ring along the corneal limbus (Kaiser-Fleischer rings) is observed with hepato-lenticular degeneration (Wilson's disease). It is difficult to detect the ring with the naked eye, it is necessary to conduct a biomicroscopic examination.

Pathological changes in the pupils play a huge role in the diagnosis of diseases. When assessing the state of the pupils, the doctor should focus on the size, shape, reaction of the pupils to light and when looking at a close object - with accommodation and convergence.

It is recommended to compare the examination data in one eye with the state of the pupil in the other eye, namely: with the equivalence of size, shape, pupil reaction not only to accommodation, but also to a direct and sympathetic reaction to light. It is important to establish whether there is a difference between the pupils.

Begin the study of the size of the pupils with uniform illumination of both eyes. If an unequal pupil size is recorded, then there is anisocoria. At rest, the physiological difference between both pupils can be no more than 0.25 mm.

The reaction to light is expressed by constriction of the pupils, the brighter the light entering the eye, the stronger it is. The reaction is more pronounced when the person was in the dark before or had his eye tightly closed. It must be borne in mind that in older people the reaction of the pupil (due to senile miosis) will be less indicative and not pronounced.

Of essential importance is the expansion of the pupil when applying pain or tactile irritation. In specialized institutions, pupillography is used to study pupils; cinematography and electrography. However, to assess their condition, all other specialists check the pupils with a simple examination.

Before examining the reaction of the pupils to light, one should always know whether belladonna preparations were used orally, atropine injections and atropine or any other mydriatic instillations. It should be borne in mind that the size and shape of the pupil can change with some eye diseases. For example, with glaucoma there is a tendency to dilate the pupil, with inflammation of the iris - to narrowing, and as a result of the formation of synechia (adhesions), it can change its shape.

Anisocoria can occur with spinal syphilis, tabes dorsalis, and progressive paralysis. In these cases, anisocoria is usually combined with a disorder of reflex reactions, which will be discussed below. In addition to these classical diseases, anisocoria also occurs in cases of skull trauma, brain tumors, hemorrhages and softening of the brain, with damage to the sympathetic and parasympathetic pathways due to basal serous meningitis.

^ MIOSIS (Pupil Constriction) often occurs with tabes, accompanied by anisocoria, immobility of the pupils (Arjail-Robertson symptom), with intracranial diseases (encephalitis), lesions of the meninges by a tumor. The pupil also narrows in otogenic meningitis on the side of the diseased ear.

An unfavorable sign for the prognosis is the transition of miosis to mydriasis, which occurs in the final stage of the disease. Miosis occurs with some exogenous and endogenous intoxications, for example, with poisoning with opium, morphine, bromine, aniline, mushrooms, alcohol, with uremia and Claude Bernard's syndrome.

Miosis can be observed with lesions in the medulla oblongata and with many other pathological changes in the central nervous system.

^ MYDRIASIS (Pupil Dilation) may be the result of paralysis of the oculomotor nerve (n. oculomotorius) and a number of intoxications (botulism, eclampsia of pregnant women, poisoning with atropine, cocaine, quinine, santonin and carbon dioxide). Mydriasis occurs with hysteria, accompanied by a temporary loss of vision, without organic changes in the eye.

Pathological reactions of pupils also play an important role in the diagnosis of diseases.

^ AMAUROTIC PUPIL IMMOBILITY may be associated with blindness (optic nerve atrophy or retinal damage), in which there is no direct and sympathetic reaction, the pupils are dilated. Other types of pupillary constriction reactions (the reaction of setting the eye at a close distance, the reaction to closing the palpebral fissure) are preserved.

Due to the lack of reaction to light, the reaction of the pupil to the closing of the palpebral fissure even becomes clearer. If one eye is blind, that is, there is damage to the retina or optic nerve of only one eye, then when this eye is illuminated, both direct and sympathetic reactions are absent. When the healthy eye is illuminated, there is a direct reaction in it and a sympathetic reaction in the pupil of the blind eye. In the case of a unilateral lesion, the pupillary reaction when placed at a close distance is preserved.

^ ABSOLUTE PUPIL STABILITY characterized by a lack of pupillary response to light (direct and sympathetic) and when the eyes are set at close range. This phenomenon is caused by damage to the motor oculomotor part of the pupillary arch, starting from the nuclei of the oculomotor nerve and reaching the sphincter of the pupil itself. Immobility is more often unilateral. It occurs in tuberculous meningitis (in the region of the base of the brain), syphilitic basal meningitis, with damage to the brain stem due to inflammatory, vascular or tumor processes. Pupil immobility can occur with botulism, vascular disorders of the brain, syphilis, lead poisoning, skull injuries, etc.

^ REFLECTOR IMMOBILITY OF PUPILS characterized by the absence of a direct and sympathetic reaction of the pupils to
light while maintaining pupillary response when the eye is set at a close distance. These reactions from the pupil are associated with damage to the central nervous system by neurolues (Arjail-Robertson symptom). Reflex immobility of the pupils can be characterized by great variety and severity.

^ Pupillotonia (EDY SYNDROME) - delayed or absent pupillary response to light and delayed pupillary response when eyes are placed at a close distance. Unilateral lesions and anisocoria are observed. It comes to light at frustration of a sympathetic innervation.

^ PATHOLOGICAL CHANGES IN THE LENS. Normally, the lens is a transparent body resembling a biconvex lens in shape. It is located just behind the iris, its central part is visible in the pupil area. With absolute transparency of the lens, the pupil appears black. With intense clouding of the lens substance, the pupil area acquires a gray or gray-white tint.

Clouding of the lens occurs most often with age (senile cataract). The reasons for such turbidity have not yet been fully identified.

^ Rice. 28. Polar cataract.

In addition to local disturbances in the eye, there are also general causes; accumulation of urotoxins in the blood, disturbances in the endocrine system, beriberi C, etc. There are diabetic cataracts, congenital cataracts in children with metabolic disorders in the prenatal period, as well as with various eye diseases.

In each case of developing cataracts, especially in young people, diabetes and other endocrine diseases, myotonia and tetany (after thyroid surgery) or harmful effects should be excluded: ergot poisoning, exposure to radiant energy (lightning cataracts, cataracts from x-rays, radium , cataract glassblowers, etc.). In all cases of clouding of the lens of the patient, an ophthalmologist should be consulted to clarify the etiology and treatment.

^ Rice. 29. Subluxation of the lens.

There may be changes in the position of the lens and its clouding in Marfan's syndrome (observed more often in men). The disease is accompanied by high growth, thin and elongated limbs, weak muscles.

^ HYPO AND AVITAMINOSIS A Vitamin A (retinol, axerophthol or antixerophthalmic) is one of the essential nutritional factors that ensures the normal course of biochemical and physiological processes and is involved in some body functions, including growth and the immune system.

Vitamin A and its aldehyde retinene are essential components of visual pigments, without which normal daytime, and especially twilight and night vision is impossible. It is also necessary for the normal functioning of epithelial structures that produce mucus.

The following animal products are richest in vitamin A: liver of cattle, pigs, fish (sharks, sea bass, cod, halibut), poultry, egg yolk, sour cream, cream, milk.

Carotenes - vitamin A precursors are found in leafy vegetables (sorrel, parsley, spinach, green onions), carrots, apricots, yellow-colored fruits, palm oil. Carotenes are converted to retinol in the intestines. They are less active compared to retinol. To obtain a similar effect in the course of treatment, it is necessary to take carotene at a dose 6 times greater than the dose of retinol.

More than half of the retinol that enters the body is absorbed in the small intestine, and then transported to the liver, where it accumulates in the form of retinol palmitate. The retina of the human eye in terms of the richness of the content of vitamin A is in second place, after its main depot - the liver. As needed, retinol is released into the blood, and then used by the epithelial cells of the body.

Vitamin A deficiency is a fairly common severe alimentary disease. Typical symptoms in this case are: stunting, damage to the skin and mucous membranes. Xerophthalmia is specific for vitamin A deficiency. Hypo- and avitaminosis A can be of exogenous and endogenous nature. Exogenous beriberi is due to insufficient intake of vitamin A and carotene from food during religious fasts, malnutrition, hunger in wartime, expeditions to the North, etc.

Endogenous avitaminosis develops in violation of the absorption of these substances in the gastrointestinal tract, increased need for them in physical overwork, liver diseases, including cirrhosis (alcoholic and others) and cachexia in cancer patients. Avitaminosis A can develop with dyspepsia in children, which occurs with prolonged diarrhea. Ocular manifestations of hypo- and avitaminosis A from dysfunction of rods and cones to structural changes in the conjunctiva, cornea and retina are referred to as xerophthalmia.

XEROPHTHALMIA- "dry eye" - manifests itself in both mild and severe forms. First of all, with it, the structure and functions of the pigment epithelium and photosensitive elements of the retina (rods) are disturbed, hemeralopia develops - “night blindness”. In children, there is a weakening of vision and a loss of the ability to spatial orientation in conditions of low light or twilight (some peoples have a specific definition of this condition - “chicken eyes”). In the youngest children, hemeralopia usually goes unnoticed.

With hemeralopia, there is a decrease in light sensitivity, a violation of the process of light adaptation, a change in the electroretinogram, a narrowing of the field of view, and, above all, colors. The fundus of the eye is usually not changed.

In the future, prexerosis, the earliest manifestation of xerosis, joins hemeralopia. Symptoms of xerosis are detected by biomicroscopy in the form of folding of the conjunctiva of the eyeball, in reducing its sensitivity and violation of luster. Outward, from the cornea on the bulbar conjunctiva, a triangular area appears, the base facing the cornea. This area is rough, not shiny, dull, dry, not wetted by tears. Often one or more of these spots appear in the nasal sections of the bulbar conjunctiva in the area of ​​​​the open palpebral fissure.

Both eyes are always involved in the process. In severe cases, the entire bulbar conjunctiva is affected. In typical cases of pronounced xerosis, Iskerek-Bito plaques appear on the conjunctiva. These are dull white spots located on both sides of the cornea in the area of ​​​​the eyelid gap. They are covered with a foamy or cheesy substance consisting of desquamated epithelium, or bacteria. The foamy substance is easily removed with a swab. Curd or cheese-like substance has a denser consistency. Plaques are not wetted by tears. These changes in conjunctival xerosis are reversible in most cases.

Corneal xerosis begins with punctate keratopathy, edema. The cornea loses its specular luster, transparency, sensitivity, becomes cloudy in patches, poorly or not wetted by tears. These changes in the cornea are also completely reversible.

With the destruction of the stroma in the cornea, ulcers occur, more often on the periphery. Large areas of destruction of the cornea and necrosis can occupy its center, and in severe cases, the entire surface. Such changes in the stroma lead to blindness.

The most severe lesion in xerophthalmia is keratomalacia - softening, melting and disintegration of the cornea. Eye damage in the vast majority of cases is paired. The process, as a rule, begins in the lower half of the corneas in the form of grayish or whitish superficial opacities; the keratinized epithelium is not wetted or sloughed off by tears. Destructive changes spread both over the surface and deep into the cornea. Quite quickly, sometimes within a day, the bottom of the infiltrated defect is perforated and the inner membranes, and sometimes the lens, fall out.

Keratomalacia develops in most cases in both eyes. Inflammatory phenomena are poorly expressed. Pain, photophobia and lacrimation are absent. There is little discharge from the conjunctival cavity, it is mucous or mucopurulent. The sensitivity of the corneas is sharply reduced, almost absent.

When a secondary infection is attached, purulent panophthalmitis may develop, followed by wrinkling of the eyeball. More often, as a result of intense scarring, a simple or fused thorn, or staphyloma, is formed. All these changes lead to a sharp decrease in vision or complete blindness. Keratomalacia usually develops with severe hypovitaminosis or avitaminosis A in children, mostly at an early age, up to 3 years.

The diagnosis is based on the characteristic clinical presentation of prexerosis, conjunctiva and cornea, and keratomalacia.

Determination of the level of vitamin A in the blood serum by the spectrophotometric method confirms its decrease. It is necessary to take into account the peculiarities of nutrition.

Treatment of xerophthalmia, which develops against the background of avitaminosis A, consists in prescribing vitamin A preparations orally or intramuscularly (in case of impaired absorption from the gastrointestinal tract).

Vitamin A is most effective when combined with other vitamins, especially the B group.

The prognosis for hemeralopia, prexerosis and xerosis is favorable, for keratomalacia - bad.

Prevention. The most important is the consumption, especially by children, of a sufficient amount of foods that contain vitamin A or carotene. Breastfeeding is essential as it is the main source of vitamin A for newborns. Topical instillations of a 30% solution of albucid and a broad-spectrum antibiotic ointment are applied against a possible secondary microbial infection.

^ CHANGES IN VISION IN AIDS. Acquired immunodeficiency syndrome was first identified in 1981 and created a rather alarming epidemiological situation in the world due to its relatively rapid spread, high mortality and lack of effective treatment.

The virus is transmitted through the blood. It is believed that infection passes through close contact with the patient: through sexual contact, intravenous injections, organ transplants and blood transfusions. The transmission of infection is not excluded when using brushes, razors and other objects shared with the patient. Children become infected from sick mothers in the antenatal and perinatal periods.

After infection, a flu-like illness is observed, then lymphadenopathy occurs, after which there may be an asymptomatic period for 1-14 years, then there is a progressive loss of body weight and, due to cellular immunodeficiency, patients become incredibly susceptible to infections: recurrent pneumonia, fungal lesions of the mucous membranes, miliary tuberculosis , chronic diarrhea, generalized lymphadenopathy, malaria, toxoplasmosis, Kaposi's sarcoma and other oncological diseases of the skin and internal organs. Death, as a rule, occurs from accidental diseases.

Eye manifestations in AIDS are diverse and are found on average in 75% of patients. In some cases, they are the first clinical signs of the disease. Moreover, the virus can be determined in the tear and in the epithelium of the conjunctiva. On the fundus of the eye with AIDS, cotton wool foci in the retina, isolated hemorrhages can be detected. Hemorrhages and cotton-wool lesions appear spontaneously and may disappear. The manifestation of cytomegalovirus retinitis is characteristic - retinal hemorrhages,
exudates, retinal vasculitis with massive leakage from the vessels, progression of the destructive process.

Cases of acute retinal necrosis, retinal periphlebitis, choroidal granulomas, papillitis, iridocyclitis, changes in accommodation, conjunctivitis, dry conjunctivitis, keratoconjunctivitis, cranial nerve palsies, skin sarcoma and Kaposi's conjunctiva in the form of single red, purple to blue-black spots, erythematous -popular formations.

Treatment of ocular manifestations of AIDS has so far been ineffective. The main efforts of doctors should be directed primarily to the prevention of AIDS infection, since scientists studying the problems of AIDS and its treatment cannot yet provide encouraging results.

So, from the given and far from complete information, the close connection of the organ of vision with the diseased organism is determined. Identification of the pathology of the eye and its functions, even by imperfect methods, makes it possible to clarify the diagnosis of a general disease. However, modern medicine as a science has been enriched by many technical achievements, it has become possible to conduct very subtle research in various fields of medicine, including ophthalmology. Therefore, it is recommended to consult patients with an ophthalmologist who uses modern optical equipment and special examination methods for this.

^ Chapter 4

The main task in the preparation of a dentist is to study the most common pathology of the organ of vision associated with diseases of the oral cavity and dentoalveolar system, mastering by students the skills necessary to provide emergency care for eye lesions isolated, combined and combined with lesions of the dentoalveolar system.

An important point for a dentist is knowledge of other diseases of the eye, both in adults and in children, the recognition of which and the timely referral to an ophthalmologist will make it possible to preserve vision, since the close anatomical relationship of the dentoalveolar system and the organ of vision, general innervation with a number of borderline areas is manifested by symptoms characteristic of a particular pathology.

At the present stage of development of medical science, dentists and ophthalmologists should be given general tasks for the prevention of eye diseases in preschool, school-age children and adults. Moreover, a number of measures in the prevention of major eye diseases can only be implemented through the joint efforts of ophthalmologists and dentists.

In order to increase the effectiveness of preventive measures among children and adults, it is necessary to:

1. 
   To acquaint a wide range of obstetrician-gynecologists, pediatricians, dentists with the causes and mechanism of development of anomalies of the maxillofacial region and the organ of vision.
2. 
   To revive health education work among young people to promote a healthy lifestyle, to fight against smoking, drunkenness, and drug addiction.
3. 
   Strengthen preventive measures to combat infectious diseases, stressful situations and injuries in pregnant women; in case of diseases of the expectant mother in the first trimester of pregnancy, provide rational drug therapy, exclude the use of teratogenic drugs.
4. 
   It is mandatory to consult an ophthalmologist for patients with congenital pathology of the maxillofacial region: hemangioma, lymphangioma, facial clefts, birth trauma of the maxillofacial region).
5. 
   Implementation of close contact in the work of the local pediatrician and the local pediatric dentist; in children under one year old, a mandatory examination by a dentist and an ophthalmologist with the entry of examination data into an outpatient card.
6. 
   It is necessary to instill in children the ability not only to brush their teeth and rinse their mouths with water after eating, but also to properly wash their faces and take care of the organ of vision.
7. 
   Mandatory consultation of an ophthalmologist in case of inflammatory diseases of the oral cavity in children with infectious diseases (measles, scarlet fever, mumps, diphtheria, etc.).
8. 
   Obligatory consultation by an ophthalmologist of persons with inflammatory processes of soft and bone tissues of the maxillofacial region (lymphaadenitis, odontogenic periostitis, acute odontogenic osteomyelitis, odontogenic phlegmon).
9. 
   Obligatory consultation by an ophthalmologist of elderly people with a neoplasm of the maxillofacial region.

The lack of a practical guide to eye diseases for students of the Faculty of Dentistry greatly reduces their ability to acquire basic skills in mastering the methods of studying the organ of vision, which are necessary for them in further medical work.

It is known that the combined pathology of the eyes and maxillofacial area is common, so dentists need knowledge of syndromes and symptoms with simultaneous damage to the eyes, oral cavity and dento-jaw system.

^ SHOT SYNDROME

In 1882, Leber first described keratoconjunctivitis with the formation of threads on the cornea. He considered the cause of it to be a disease of the cornea.

^ Rice. 30. Sjögren's syndrome.

Clinical symptoms are damage to the lacrimal and salivary glands, upper respiratory tract and gastrointestinal tract against the background of deforming polyarthritis. The disease develops slowly and flows chronically with remissions and exacerbations.

On the part of the eyes, complaints of patients are reduced to a feeling of pain, dryness, itching, burning, a feeling of sand in the eyes, difficulty opening the eyes in the morning, photophobia, fogging, lack of tears when laughing, crying, decreased visual acuity, pain in the eye. An objective examination shows photophobia, slight hyperemia of the eyelids, sometimes with thickening of their edges, "looseness" of the conjunctiva, viscous discharge in the conjunctival sac in the form of thin grayish elastic threads, which can be up to several centimeters long. Microscopy shows that these threads are nothing but epithelial cells and mucus.

Sometimes there is papillary hypertrophy.

The cornea becomes less transparent, loses its luster, has a matte appearance, is torn, especially in the lower section. On its surface, there are first mobile threads, then their number increases, and they become less mobile.

After removal of the threads, erosions may remain in the cornea, and later opacities with ingrowth of vessels, xerosis develop. The sensitivity of the cornea does not change.

Already in the early stages, the amount of lysozyme in the tear decreases (Kurbanaeva F.Sh., Gubastrullina S.N., 1970). Schirmer's test, as a rule, reveals a sharp decrease in the function of the lacrimal glands (can be from 0 to 3-5 mm).

Some time after the appearance of eye pathology, pathology occurs on the part of the oral mucosa, tongue. On the part of the oral cavity, dryness (xerostomia) is noted, which is associated with a decrease in the amount of saliva.

Saliva becomes dry and viscous, in connection with this, speech, the act of chewing and swallowing are difficult. Food is washed down with water.

After some time, there is absolutely no secretion of saliva from all the salivary glands (sialopenia). In the later period of the disease, a drop of thick, yellowish saliva can be squeezed out of the holes of the Stenon's duct with great difficulty. There may be recurrent enlargement of the salivary parotid glands, which is sometimes mistakenly regarded as mumps.

The mucous membrane of the mouth becomes dry, hyperemic, in places with the formation of fibrin. The red border of the lips also becomes dry. The tongue pattern is smoothed out, erosion and cracks may occur.

Sialography shows the absence of morphological changes in the parotid and submandibular glands.

Histological examination shows that in Sjögren's syndrome there is lymphocytic infiltration of the salivary and lacrimal glands, similar to the lymphocytic infiltration of glands in pernicious anemia (Williamson S., 1970 et al.), then atrophy of the salivary glands with very little inflammation.

In bacteriological examination of the oral mucosa in 13 out of 50 patients, an abundance of candida was found, which can greatly complicate the course of the process (N. S. Yartseva, S. D. Svetova, N. N. Storozheva, 1977). Dry mouth extends to the pharynx, esophagus, stomach, larynx, trachea, and nasopharyngeal, gastric, tracheobronchial, and other glands are also involved in the process. It has been established that in Sjögren's syndrome there is a sharp decrease in the amount of gastric contents while maintaining the acid-forming function of the secretory apparatus of the gastric mucosa. (N. S. Yartseva, S. D. Svetova, N. N. Storozheva, 1977).

Gastritis, colitis develops, hoarseness of voice and sometimes persistent dry cough appear. The mucous membrane of the urethra, vulva, vagina, rectum, anus is less commonly affected.

There may be erosive inflammation in the rectum.

Reduced secretion of sweat and sebaceous glands leads to dry skin.

Atrophy and induration may appear on the skin (often the forehead, hands, feet), there may be hyperkeratosis, hair loss. In areas of atrophy, the sensitivity of the “brush, as it were, in kid gloves” decreases.

Skin hyperpigmentation may occur. Almost all patients have arthropathy, often occurring in the form of chronic deforming polyarthritis. In addition, in many patients, all phenomena are combined with dental caries.

There may be subfebrile temperature, accelerated ESR, eosinophilia, normo and hypochromic anemia, first leukocytosis, then leukopenia. albumin-globulin shift, marked hyperproteinemia with significant hyperglobulinemia, liver dysfunction, abnormalities in the activity of the cardiovascular system, genitourinary system, paresis of the facial nerve, nervous manifestations, etc. The disease does not always occur with all symptoms simultaneously, however, dryness conjunctiva and cornea, oral and nasal mucosa are an indispensable feature of this syndrome (BM Pashkov, 1963, etc.). Sjögren himself in 1950, among all the symptoms, called dry keratoconjunctivitis as a fundamental symptom. The disease runs chronically for months and years. It is usually observed in women after 40 years, more often during menopause. Sometimes the disease begins at a younger age. Both eyes are always affected. The etiology and pathogenesis of this syndrome remain unclear. Previously, great importance was attached to endocrine disorders, then infections (Sjogren, 1933, Krakhmalyshkov LL, 1938). Currently, the disease is classified as collagenosis, a group of autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, periarteritis nodosa, etc., which are characterized by the presence of autoantibodies to cells or cellular contents in the blood (Williamson J. et al. 1970; Ruprecht K - W. et al., 1977, N. M. Tretyakov, P. N. Savina, 1966; Nakutina E. M. et al., 1973; Bronstein X. I., 1963; Kjfkham T. N., 1969 and etc.). A number of authors note an increase in thyroglobulin autoantibodies in Sjögren's syndrome and note the similarity of the histological picture in autoimmune thyroiditis and spontaneous myxidema with the histological picture of the salivary and lacrimal glands in Sjögren's syndrome.

For the early diagnosis of Sjögren's syndrome, L.A. Yudin, I.F. Romacheva et al. (1973) suggested the following research order:

1. 
   Study of the secretory function of the salivary glands.
2. 
   Cytological examination of secretion smears.
3. 
   radiosialography.
4. 
   Radiometric study of saliva.
5. 
   Scanning glands.
6. 
   Contrast x-ray examination of the glands (sialography, pantomosialography).
7. 
   Complete ophthalmic examination with simultaneous study of the functional state of the lacrimal glands.

For treatment, a solution of hyaluronidase 5 IU in 1 mm x 5-6 times was also used. per day in the form of drops, 1% gelatin solution or 10% blood serum solution in physiological saline, lysozyme solution, egg white, vaseline oil, fish oil, fibrinolysin, quinine solutions, peach, sea buckthorn, vaseline oil, Shinkarenko's drug. Ingestion of a 5% solution of pilocarpine. Some authors report a good effect of Dakrio-Biciron drops (0.1-0.2% bromhexine-BCL solution) with simultaneous ingestion of 12.5 mg bromhexine-BCL capsules. Galantamine 0.5% is also used in the form of drops and subcutaneous injections.

The retina is one of the thinnest components of the human eye; it belongs to the front edge of the brain, the most distant from it, part of the visual analyzer. The most complex structure allows the retina to be the first to perceive light, process and modify light energy into irritation. Changes in the fundus observed in more than half of the population.

I must say that changes in the fundus are observed up to 80% of people suffering from myopia. Often there are ruptures, thinning of the retina, which, if not properly treated in time, can develop into one of the severe complications of myopia - retinal detachment. This pathology becomes the main cause of poor vision, and often blindness. Changes in the fundus, which have not yet led to visual impairment (tears, tears, thinning) and which, if detected early, ophthalmologists can cure, are usually asymptomatic. Very rarely, the appearance of “flashes”, “lightning” before the eye can be signals.

However, not only nearsighted people may develop fundus changes and with the retina, since stress, colds, viral diseases, prolonged visual and physical exertion, poor ecology can cause such a problem.

Changes in the fundus can also be in middle-aged and elderly people due to slowly developing atherosclerosis, as a result of which the blood circulation of the eye worsens. This increases the risk of thinning and tearing of the retina, and consequently, detachment. Middle-aged and elderly people, even without problems with refraction (not wearing glasses) or suffering from age-related disorders (reading glasses), need a systematic examination of the retina.

Due to the high prevalence of hypertension (about 23%), the frequency of fundus pathology associated with this disease also increases. A woman during pregnancy and before childbirth must necessarily undergo an examination of the fundus to determine the method of delivery. Inspection of the retina does not take much time.

When diagnosing problems, appropriate treatment is prescribed: prophylactic laser coagulation of the retina. Modern lasers make it possible to treat not only thinning and ruptures, but also flat retinal detachments, which was previously impossible. With high and widespread retinal detachments, surgical treatment is prescribed, however, it is not always possible to “put” the detached retina in place, and “lost” vision may not return. However, even after successful operations, visual acuity is rarely restored to the initial level. Often, after surgical treatment of retinal detachment, astigmatism and the degree of myopia increase.

For the study, the pupils should be dilated, so you should not come to the clinic by car, the drops act for 3-4 hours, after which clear vision will be restored. If necessary, the doctor can immediately carry out the necessary medical procedures.

29-09-2014, 13:31

Description

OPTIC PAPILLA

Even in eyes with normal function, in some cases the papilla is unusually pale, in others, on the contrary, it seems too red, and sometimes it may have a bluish tint. In albino eyes, the papilla often appears somewhat veiled and has a grayish tint. With pathological hyperemia of the optic nerve, the papilla becomes so red that it can sometimes be difficult to distinguish from the surrounding parts of the fundus, while the boundaries of the papilla are slightly blurred.

Hyperemia of the papilla is observed with incipient inflammation of the optic nerve and retina, in persons with hypermetropic refraction, overstraining the eyes with increased work, and also when the eyes are exposed to radiant energy (ultraviolet rays). With meningitis, as well as tumors of the orbit of the optic nerve, hyperemia of the papilla is often the only manifestation of these diseases. However, with the diagnosis of simple hyperemia of the papilla, one must be very careful, given the possibility of deviation from the norm of the color of the papilla and the clarity of its wound, as well as the state of the retinal vessels, even in healthy holes. With greater confidence, we can talk about papilla hyperemia if there is a difference in the color of the papillae of both eyes, and also if repeated studies can note a change in the degree of hyperemia. But the best guarantee against errors, of course, is the experience gained by examining the fundus of a large number of normal eyes.

A sharp blanching of the papilla can be observed with ischemia of the optic sockeye salmon. Large trunks of retinal vessels are both narrowed and normal during ischemia of the papilla; the contours of the papilla remain clear. The classic examples of severe papillary ischemia are cases with complete rupture of the optic nerve, as well as cases with central artery embolism. Ischemia of the papilla can also sometimes be observed with retrobulbar neuritis of the optic nerve, a pronounced general anemia. If ischemia of the papilla is accompanied by vasoconstriction of the retina, then the latter may acquire a dull auricle and radial striation is noticeable on it. Paleness of the papilla associated with ischemia of the optic nerve can be both transient and acquire a persistent character, due to the atrophy of the optic nerve that occurs after ischemia.

A change in the color of the papilla to such an extent that it becomes white is usually observed with simple atrophy of the optic nerve. The white color of the papilla in this form of optic nerve atrophy (atrophia simplex) is explained by the fact that the process of descending atrophy of the nerve fibers also extends to the papilla, as a result of which the light-white cribriform plate, as well as the nerve fibers located under it, which also have white light, is more clearly visible. they are here covered with a myelip membrane.

The papilla with simple atrophy of the optic nerve differs not only in a pure white color (sometimes with a bluish tint), but also in sharp edges, as well as a clearly protruding pattern of the cribriform plate (mottled appearance). Large trunks of blood vessels may remain normal at first, but in older cases they are narrowed.

After neuritis optici (neuritic atrophy), the papilla of the optic nerve has a grayish-white color, its borders are blurred, the pattern of the cribriform plate is not visible, since in peuritic atrophy the atrophying nerve fibers are replaced by connective and ocular tissue, which give the white papilla a “dirty” shade.

Significant blanching of only the temporal part of the papilla is observed as a result of atrophy of the papillomacular bundle of optic fibers.

2. The edges of the papilla. The outline of the papilla, like its color, does not always appear the same even in normal eyes. The boundaries of the papilla stand out the sharper, the greater the contrast between the color of the papilla and the surrounding part of the fundus, in connection with this, in albuminotic eyes, the contours of the papilla appear fuzzy.

Usually, the vagueness of the boundaries of the papilla is observed with hyperemia, edema, and also with inflammation or an inflammatory process that has ended in the intraocular end of the optic nerve and the retina adjacent to it.

It must be borne in mind that the state of the edge of the papilla acquires diagnostic value, as a rule, only in combination with other changes in both the papilla itself and the surrounding retina, for example, blurring of the borders and white color of the papilla indicate neuritic atrophy of the optic nerve, and blurring of the borders hyperemic papilla is observed with inflammation of the optic nerve and retina.

The border of the papilla can be drastically changed and take on a completely unusual form in case of anomalies in the development of certain diseases localized at the entrance of the optic nerve. Here we will only talk about those changes that occur most often.

In myopic eyes, changes are often observed, cone (conus) or posterior staphyloma (staphyoma posticum), which are expressed in the fact that a whitish or yellowish, somewhat pigmented strip that looks like chamois. The width of the cone is different, from a barely noticeable lower to 2-3 PD. Sometimes the cone surrounds the entire papilla and is so wide that its outer edge reaches the macula. The reasons for the appearance of the cone are not the same. In some cases, the cone appears because when the posterior body of the bottom is stretched, the scleral canal with the optic nerve passing through it takes the form of an obliquely set cylinder, as a result of which part of the outer wall of the canal becomes visible.

In other cases, the cone appears because in the stretched myopic eye, the pigment epithelium is not up to the very edge of the papilla, and through the space devoid of pyment, the choroid becomes visible, and later, with the onset of atrophy of the latter, the discovered sclera is also visible. The nature of the border of the cone gives some indication of the further progression of the cone: if its lower border is sharply outlined, one can think that the stretching of the posterior part of the eye, and consequently the progression of the bone, has ended, but if the border is unclear, blurred, then this indicates that the process of stretching is still has not ended and the cone can increase.

The picture of the fundus is similar to that just described for ischemia of the lower cone (conus inferior), which is due to a congenital local defect in the choroid at the lower edge of the papilla. The border of the defect facing the papilla is often not clear enough, and therefore an inexperienced researcher can take the sharply defined outer border of the cone as the lower border of the papilla and, thus, interpret the picture under consideration simply as the presence in this case of such a papilla, which is enlarged in size. In such eyes, astigmatism is usually determined and they are amblyopic.

Another congenital malformation that can change the appearance of the papilla border is myelin (pulp) nerve fibers. They appear as white shiny spots or stripes starting on the papilla itself or at its edge, and, like tongues of flame, spreading to a greater or lesser distance from the papilla in different directions (Table 6, Fig. 3).

3. The size and shape of the papilla. First of all, it must be remembered that when examined directly in the mystical eye, the papilla seems larger than in the hypermetropic one, due to varying degrees of enlargement of the fundus, which has already been discussed in more detail above in the section “General remarks on ophthalmoscopic examination”. We can talk about a real increase in the size of the papilla only with its sharp edema (congestive nipple).

As for the shape of the papilla, it may not seem round, but oval with astigmatism, due to distortion of its image, as well as in the myopic eye with strongly pronounced posterior staphylomas, for the reason that the papilla in such eyes is located at some angle to the anterior-posterior axis of the eye and we see its perspective image in the form of a vertically set oval. The cone, in most cases, complements the elliptical diameter of the papilla, forming a disc.

4. The level of the papilla in normal eyes is in the same plane with the rest of the fundus. With pathological changes, both protrusion of the papilla into the vitreous body and deepening of the region of the papilla can be observed. The protrusion (prominence) of the papilla and the vitreous body occurs due to its swelling and occurs with inflammation of the optic nerve, and with a congestive nipple, prominence is the main and leading symptom of this disease.

The difference in level between the papilla and the rest of the fundus usually begins already on the retina, at some distance from the edge of the papilla, and is determined primarily by a change in the course of the vessels, which, at the border of the beginning elevation, bend and, as it were, crawl onto the edematous papilla. The curvature is particularly well seen in the veins, which here lose their peylex and appear darker than elsewhere. This symptom is of particular importance, since it is noticeable with the slightest forward prominence of the papilla. In addition, on the vessels, and again better on the veins, in the place where they make the greatest bend, there is a white transverse strip of light, as a result of which the vessel in this place becomes invisible and, as it were, is interrupted. The appearance of a transverse reflex is explained by the reflection of light by that part of the curved vessel, the direction of which at the bend approaches the direction of the rays coming from the ophthalmoscope, since the rays pass through the wall of this part of the vessel not in the transverse, but to some extent in the longitudinal direction (Fig. 37) .

Deepening or excavation of the papilla can be: physiological, atrophic and glaucomatous.

a) Physiological experiment differs from the pathological one in that the depression on the papilla occupies only its central or temporal part (Fig. 38).

The white color of the area is due to the fact that in this part of the papilla there is a depression that reaches the cribriform plate, which. as you know, it has a white color and shines through the thinned layer of nerve fibers. The amount of excavation varies greatly; it can occupy only a small part of the papilla, and sometimes it is so large that the normally stained, non-excavated part of the papilla looks like 1/6-1/8 of the papilla diameter. But without this narrow, normally colored band, excavation cannot be physiological and must be interpreted as pathological.

The kink of the vessels at the edge of the excavated area is often almost imperceptible, but in some cases it is quite clearly expressed and is determined by the disappearance of a light neutral strip on the vessels, and also because the vessel at the site of the bend seems darker. In cases where the excavation has steep edges, the vessels make such a sharp bend that a transverse reflex appears on them, the cause of which is described above, and it seems that the vessels at the edge of the excavation are interrupted and therefore, as if they are not a direct continuation of the vessels going along the bottom of the excavation. If the excavation is located eccentrically, the place of the inflection of the vessels is located at the very edge of the papilla, but no matter how pronounced the inflection of the vessels at the edge of the excavation, when crossing the edge of the papilla in all cases of physiological excavation, it does not bend, and this is another difference between physiological excavation and pathological.

b) Atrophic excavation observed with significant degrees of atrophy of the optic nerve and has a saucer shape. The indentation occupies the entire papilla, its edges sloping, and it never enters the cribriform plate, which always retains its normal position. The bottom of the excavation often has a mottled appearance due to the presence of a large number of grayish-blue spots on it. The appearance of spots, which are sometimes less visible even during physiological excavation, has the following explanation.

c) Glaucoma excavation it is usually complete, that is, it occupies the entire papilla. The cribriform plate, unlike atrophic excavation, does not retain its position; it, due to increased intraocular pressure, as the most pliable part of the outer shell of the eyeball, protrudes outward and therefore, in place of the papilla of the optic nerve, a deep cup-shaped depression is formed, often with undermined edges (Fig. 40). Sometimes glaucomatous excavation is also partial, that is, it captures only a certain part of the papilla.

The arteries of the retina, as a rule, are somewhat narrower than normal, the veins, on the contrary, are slightly dilated. The course of the vessels is very characteristic: the artery or sang, going along the fundus, having reached the edge of the excavation, makes a sharp bend, goes deep into the steep edge, and then reappears at the bottom of the excavation. The vessels running along the fundus, at the edge of the excavation (due to the bend), seem to be interrupted and have no visible connection with the vessels of the papilla (Table 7, Fig. 2).

5. Hemorrhages in the papilla can be observed in inflammatory processes and congestion (neuritis. optici, neurorctinitis, papillitis oedematosa) in the form of radially arranged stripes or limited red spots. Often, hemorrhages occur simultaneously both in the region of the papilla and in the retina adjacent to it. The radial location of hemorrhages is explained by the fact that the blood that has poured into the inner layers of the retina or papilla spreads along the course of the nerve fibers. Old hemorrhages acquire a darker (brown-red) color. It must be remembered that when ophthalmoscopy in direct v and ac, sometimes not only delicate radial stripes of hemorrhages are observed, but also the smallest branches of vessels, which also have different directions and, since with papillary edema phenomena they are visible only for some distance, an inexperienced researcher can take them for strips of blood.

6. Limited white lesions(plaques) found in neuritis. optici and papillitis oedematosa in the region of the papilla, are of different sizes and can partially cover the vessels. To spruce, they have the appearance of clear, shiny white stripes, which (are located rally and somewhat resemble myelin fibers, then the foci are the result of hypertrophy and degeneration of nerve fibers. If the foci have an irregularly round shape, a grayish tint, less clear contours and are arranged randomly, then they are exudates.In the later stages of neuritis and congested nipple, shiny white or yellowish-white lesions are sometimes observed, which are irregular in shape, fairly clear-cut and often located mainly in the temporal part of the papilla and adjacent retina.Such lesions are associated with processes hyaline degeneration.

RETINA

1. Hemorrhages. The delicate end vessels of the retina are more prone to hemorrhages, which can be caused by both general changes in the body and purely local causes. Retinal hemorrhages are a fairly common occurrence with important diagnostic value. Any hemorrhages at the bottom of the eye, found during ophthalmoscopic examination, can almost unmistakably be considered as retinal hemorrhages. This is explained by the fact that hemorrhages of the choroid are relatively rare and, moreover, they are difficult to notice, since they are located behind the pigment epithelium layer. The exception is Atonic eyes, in which, along with retinal hemorrhages, there may also be hemorrhages of the choroid, which is reborn here due to constant stretching, and therefore has a tendency to hemorrhages.

The form of retinal hemorrhages depends on which layers of the retina the blood has poured out. Oblong or striped hemorrhages are localized mainly in the layer of nerve fibers. Near the papilla, they, according to the location of the nerve fibers, usually have a radial arrangement. Hemorrhages located in the middle or outer layers of the retina have the shape of a roundish spot, which is outlined by a fairly clear, but wavy line. Hemorrhages occur most often around the circumference of the papilla.

Especially important are those that are localized in the macula, as they have a significant impact on the visual function of the eye. The amount of hemorrhage is different: with capillary hemorrhages, extravasations are usually observed as pinpoint, barely noticeable, in cases of violation of the integrity of larger vessels, hemorrhages can occupy a vast surface of the fundus.

In some cases, the blood that has poured out of the damaged vessel breaks through the outer layer of the retina and, spreading between the layer of rods and the pigment epithelium, causes a hemorrhagic retinal detachment of its own gender, which is usually so insignificant that it is not detected during ophthalmoscopic examination. It is also often observed that blood extravasation breaks through the inner boundary plate and spreads between the inner surface of the retina. Such hemorrhages are called preretinal. They are localized mainly in the region of the macula, but in rare cases they are also located in other places, for example, in the region of the papilla. Preretinal hemorrhages are easy to recognize already because they have a very characteristic round or transverse oval shape. Large vessels at their edge abruptly break off, since the hemorrhage completely closes not only the vessels, but also the rest of the parts of the fundus located behind the hemorrhage. After some time, you can notice that the lower dark red part of such a hemorrhage is separated by a horizontal line from the upper part, which has a pale red color (Table 14, Fig. 2). This phenomenon is associated with erythrocyte sedimentation. Sometimes the blood breaks through and penetrates the vitreous.

Retinal hemorrhages, as already mentioned, are of great diagnostic value, and as a particular symptom can be observed at any age with retinitis and retinopathy, as well as as a result of traumatic injuries. It must always be remembered that hemorrhages may be the first and only ophthalmoscopically detectable symptom of retinitis and retinopathy, and therefore not the first symptom indicating a general suffering of the whole organism.

As a private phenomenon, retinal hemorrhages are observed with changes in the composition of the blood, for example, in severe anemic conditions after large blood loss, and especially in malignant anemia. Often hemorrhages are also found in leukemia; they are localized in this disease mainly in the layer of nerve fibers. Retinal hemorrhages are also observed in infectious diseases: septicemia, typhoid fever, influenza, during attacks of malaria, etc., as well as in hemorrhagic diathesis: scorbute, Werlhof's disease, etc.

The cause of hemorrhages in women can also be endocrine disorders, leading to menstrual disorders. In old age, usually after 50 years, retinal hemorrhages occur on the basis of arteriosclerotic changes and are often localized in the area of ​​the macula. In the same area, hemorrhages are also found with high myopia. Hemorrhages are also associated with a sharp drop in intraocular pressure, which often occurs during antiglaucoma operations. Retinal hemorrhages can be of the most diverse nature with damage to the eyeball and bruises of neighboring areas, as well as with severe chest compressions and general contusions. Retinal hemorrhages are common in newborns. In the origin of these hemorrhages, birth trauma factors leading to severe circulatory disorders in the fetal head are of paramount importance.

Vascular changes

a) The caliber of vessels can be changed due to equal reasons:

1) weakening of the elasticity of the walls of blood vessels, as a result of various pathological processes in them;
2) violations of the innervation of blood vessels and
3) changes in the degree of blood filling of the vessels, under the influence of changes in blood pressure, violations of the conditions of outflow and inflow of blood, changes in intraocular pressure.

Expansion of arteries and veins occurs with leukemia and many other common diseases accompanied by high fever, as well as with various local pathological changes: injuries of both the eyeball itself and surrounding tissues, inflammatory processes in the eye and neighboring areas, as a reaction to sharp light stimuli and overstrain of accommodation, etc.

The reason for the narrowing of the arteries and veins, in some cases, are: spasm of the central artery, embolism of the central artery, rupture of the optic nerve, a sharp drop in total blood pressure; in others, vasoconstriction is a network of retinitis, chorieretinitis, and some optic nerve atrophy. In addition, vasoconstriction of the retina occurs in case of poisoning with quinine, lead, and in hypertension in nephritic processes.

Under certain conditions, not all retinal vessels appear dilated, but only the veins, while the arteries remain normal or further narrowed.

The reason for this condition of the vessels is often:
1) compression of the central vessels of the retina by tumors or inflammatory processes of the optic nerve and its surrounding tissues;
2) incomplete blockage of the central artery, due to embolism, thrombosis or spasm;
3) thrombosis of the central vein;
4) increased intraocular pressure (glaucoma).

b) Tortuosity of vessels. The expansion of the vessels in the transverse direction is accompanied by a simultaneous stretching of their walls in the longitudinal direction, therefore, with any ophthalmoscopically noticeable increase in the diameter of the vessels, their greater tortuosity is also noted and, conversely, each narrowing of the vessels leads to their straightening. Thus, the retinal vessels will be more tortuous in all those conditions in which there is an increase in the diameter of the vessels. However, with arteriosclerotic changes, which, as is known, lead to a decrease in the elasticity of the vessel walls, the diameter of the retinal vessels may remain normal or only slightly increased, while the tortuosity of the vessels is strongly pronounced. This can be explained by the fact that the walls of the vessel in this disease are more easily stretched in the longitudinal than in the transverse direction.

c) Central light strip, is a reflex that occurs due to the reflection of light by the cylindrical surface of a blood column moving in the vessels. The light strip has a uniform brightness only when the vessels lie on the spherical surface of the fundus. When the vessel deviates from the surface of the fundus, i.e., if the vessel makes such a bend that it is no longer in a plane perpendicular to the observer's visual line, the light strip at the place of the bend seems dim or even disappears altogether.

If the light strip disappears or seems unclear, dim over a significant extent of one or more vessels, then the following pathological conditions may be the cause of this:

1) complete or partial opacity of those layers of the retina that cover the vessels;
2) change in the transparency of the wall of the vessel itself.

Now it becomes clear why there is a complete or partial disappearance of the central light strip with diffuse (diffuse) opacification of the retina, which occurs with retinitis, necroretinitis, retinopathy, commotio retinae, embolism of the central artery, retinal detachment.

With a decrease in the transparency of the walls of the vessel itself, the reflex reflected by the blood column, although it is weaker, but the central light strip in some diseases, for example, arteriosclerosis, fatty degeneration and nervasculitis of the retinal vessels, is visible not only no worse, but sometimes even better than in normal eyes. This is probably due to the fact that the central light strip in these cases arises due to the reflection of light both by the blood column and by the clouded vessel wall. It should be noted, however, that in case of retinal vascular nervasculitis, the central light strip, although visible quite clearly, does not yet have its usual bright luster, and with fatty degeneration, in addition, it acquires a yellowish tint.

d) White helmets (accompanying stripes). Normally, one central light strip is visible on the retinal vessels, only sometimes two additional, barely noticeable white borders can be seen near the papilla on large trunks, running parallel to the central light strip. These borders, or as they are otherwise called "accompanying strips", can be seen in direct examination and they are nothing more than the visible wall of blood vessels. With thickening or clouding of the walls of blood vessels, white borders are clearly visible not only on large, but also on smaller trunks. Schematic figure 41, which shows a cross section of the vessel, makes it possible to clearly understand why the wall of the vessel, especially when its transparency is lowered, is visible in the form of two white borders extending into the distance of a red blood column.

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