Fundus of the eye in hypertension: location of blood vessels, possible changes and preventive measures. Vascular changes in the fundus of the eye in common diseases Variants of changes in the fundus of the eye

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

With hypertension of any origin, changes in the vessels of the fundus are noted. The severity of these changes depends on the height of blood pressure and the duration of hypertension. In hypertension, there are three stages of changes in the fundus of the eye, which successively replace each other:

1. stage of functional changes - hypertensive retinal angiopathy;
2. stage of organic changes - hypertensive angiosclerosis of the retina;
3. stage of organic changes in the retina and optic nerve - hypertensive retinopathy and neuroretinopathy.

Initially, the arteries narrow and the veins expand; the walls of the vessels, primarily the arterioles and precapillaries, gradually thicken.

With ophthalmoscopy, the severity of atherosclerosis is determined. Normally, the walls of the retinal blood vessels are not visible during examination, but only a column of blood is visible, along the center of which there is a bright strip of light. With atherosclerosis, the vascular walls become denser, the reflection of light on the vessel becomes less bright and wider. The artery is already brown, not red. The presence of such vessels is called the “copper wire” symptom. When fibrous changes completely cover the blood column, the vessel looks like a whitish tube. This is a symptom of the “silver wire”.

The severity of atherosclerosis is also determined by changes in the intersections of the arteries and veins of the retina. In healthy tissues, at the intersection sites, a blood column in the artery and vein is clearly visible, the artery passes in front of the vein, they intersect at an acute angle. With the development of atherosclerosis, the artery gradually lengthens and, when pulsating, begins to compress and expand the vein. With first-degree changes, there is a conical narrowing of the vein on both sides of the artery; with second-degree changes, the vein bends in an S-shape and reaches the artery, changes direction, and then behind the artery returns to its normal direction. With third degree changes, the vein in the center of the chiasm becomes invisible. Visual acuity with all of the above changes remains high. At the next stage of the disease, hemorrhages appear in the retina, which can be pinpoint (from the capillary wall) and streak-like (from the arteriole wall). With massive hemorrhage, blood breaks from the retina into the vitreous body. This complication is called hemophthalmos. Total hemophthalmos often leads to blindness, since blood cannot be absorbed in the vitreous body. Minor hemorrhages in the retina can gradually resolve. A sign of retinal ischemia is “soft exudate” - cotton-like whitish spots in the retinal rim. These are microinfarctions of the layer of nerve fibers, areas of ischemic edema associated with the closure of the lumen of the capillaries.

In malignant hypertension, as a result of high blood pressure, fibrinous necrosis develops from the vessels of the retina and optic nerve. In this case, pronounced swelling of the optic nerve head and retina is noted. Such people have decreased visual acuity and a defect in the visual field.

In hypertension, the choroidal vessels are also affected. Choroidal vascular insufficiency is the basis for secondary exudative retinal detachment in toxicosis of pregnancy. In cases of eclampsia - a rapid increase in blood pressure - a generalized spasm of the arteries occurs. The retina becomes “wet” and there is pronounced retinal edema.

When hemodynamics normalize, the fundus quickly returns to normal. In children and adolescents, changes in retinal vessels are usually limited to the stage of vasospasm.

Currently, the diagnosis of “arterial hypertension” is established if there is a history of a stable increase in systolic arterial (above 140 mm Hg) and/or diastolic (above 90 mm Hg) pressure (normal 130/ 85). Even with a slight increase in blood pressure, untreated arterial hypertension leads to damage to target organs, which are the heart, brain, kidneys, retina, and peripheral vessels. With arterial hypertension, microcirculation is disrupted, hypertrophy of the muscular layer of the vascular wall, local spasm of the arteries, congestion in the venules, and a decrease in the intensity of blood flow in the capillaries are noted.

Changes detected during ophthalmoscopic examination in some cases are the first symptoms of hypertension and can help in establishing a diagnosis. Changes in the retinal vessels during different periods of the underlying disease reflect its dynamics, help determine the stages of disease development and make a prognosis.

Stages of changes in retinal vessels in arterial hypertension

To assess fundus changes caused by arterial hypertension, use the classification proposed by M. L. Krasnov, according to which three stages of changes in retinal vessels are distinguished.

The first stage - hypertensive angiopathy - is characteristic of stage I of hypertension - the phase of functional vascular disorders. At this stage, narrowing of the arteries and dilatation of the retinal veins occur, the ratio of the caliber of these vessels becomes 1:4 instead of 2:3, uneven caliber and increased tortuosity of the vessels are noted, and a symptom of arteriovenous decussation of the first degree (Salus-Gunn symptom) may be observed. Sometimes (in about 15% of cases) in the central parts of the retina there is a corkscrew-shaped tortuosity of small venules (Gwist's symptom). All these changes are reversible; when blood pressure normalizes, they regress.

The second stage is hypertensive angiosclerosis of the retina - the stage of organic changes. There is unevenness in the caliber and lumen of the arteries, and their tortuosity increases. Due to hyalinosis of the artery walls, the central light strip (reflex along the vessel) becomes narrower and acquires a yellowish tint, which makes the vessel resemble light copper wire. Later, it narrows even more and the vessel takes on the appearance of a silver wire. Some vessels are completely obliterated and are visible as thin white lines. The veins are somewhat dilated and tortuous. This stage of arterial hypertension is characterized by the symptom of arteriovenous decussation - the Salus-Hun symptom). The sclerotic elastic artery crossing the vein pushes it down, causing the vein to bend slightly (Salus-Gunn I). With arteriovenous decussation of degree II, the bend of the vein becomes clearly visible and arched. It appears thinner in the middle (Salyus-Gunn II). Later, the venous arch at the intersection with the artery becomes invisible, the vein seems to disappear (Salyus-Gunn III). Bends in the vein can provoke thrombosis and hemorrhage. Newly formed vessels and microaneurysms may be observed in the area of ​​the optic nerve head. In some patients, the disc may be pale, monochromatic with a waxy tint.

The stage of hypertensive retinal angiosclerosis corresponds to the phase of a sustained increase in systolic and diastolic blood pressure in stage IIA and IIB hypertension.

The third stage is hypertensive angioretinopathy and neuroretinopathy. In the fundus, in addition to changes in blood vessels, hemorrhages in the retina, swelling and white foci that look like lumps of cotton wool appear, as well as small white foci of exudation, sometimes with a yellowish tint, and areas of ischemia appear. As a result of disturbances in neuroretinal hemodynamics, the condition of the optic nerve head changes, its swelling and unclear boundaries are noted. In rare cases, with severe and malignant hypertension, a picture of a congestive optic disc is observed, and therefore there is a need for differential diagnosis with a brain tumor.

A cluster of small lesions around the macula forms a star shape. This is a sign of a poor prognosis not only for vision, but also for life.

The condition of the retinal vessels depends on the level of blood pressure, the magnitude of peripheral resistance to blood flow and, to a certain extent, indicates the state of the contractility of the heart. With arterial hypertension, diastolic pressure in the central retinal artery increases to 98-135 mm Hg. Art. (at a norm of 31-48 mm Hg). In many patients, the field of vision changes, visual acuity and dark adaptation decrease, and light sensitivity is impaired.

In children and adolescents, changes in retinal vessels are usually limited to the stage of vasospasm.

The changes in the retinal vessels identified by the ophthalmologist indicate the need for active treatment of hypertension.

Pathology of the cardiovascular system, including arterial hypertension, can cause acute circulatory disorders in the retinal vessels.

Acute obstruction of the central retinal artery

Acute obstruction of the central retinal artery (CRA) and its branches can be caused by spasm, embolism or thrombosis of the vessel. As a result of obstruction of the central retinal artery and its branches, ischemia occurs, causing dystrophic changes in the retina and optic nerve.

Spasm of the central retinal artery and its branches in young people is a manifestation of vegetative-vascular disorders, and in older people, organic damage to the vascular wall often occurs due to arterial hypertension, atherosclerosis, etc. Several days and even weeks before the spasm, patients may complain of temporary fogging vision, sparks, dizziness, headache, numbness of fingers and toes. The same symptoms can occur with endarteritis, certain poisonings, eclampsia, infectious diseases, with the introduction of anesthetics into the mucous membrane of the nasal septum, or with the removal of a tooth or its pulp. Ophthalmoscopy reveals narrowing of all or individual branches of the central retinal artery with ischemia around. Obstruction of the trunk of the central retinal artery occurs suddenly, often in the morning, and is manifested by a significant decrease in vision, up to complete blindness. If one of the branches of the central retinal artery is damaged, visual acuity may be preserved. Defects are detected in the field of view.

Central retinal artery embolism

Embolism of the central retinal artery and its branches is more often observed in young people with endocrine and septic diseases, acute infections, rheumatism, and trauma. Fundus ophthalmoscopy reveals characteristic changes in the area of ​​the central fovea - a cherry spot - a symptom of a “cherry pit”. The presence of the spot is explained by the fact that in this area the retina is very thin and the bright red choroid is visible through it. The optic disc gradually becomes pale, and its atrophy occurs. In the presence of the cilioretinal artery, which is an anastomosis between the central retinal artery and the ciliary artery, there is additional blood flow in the macula area and the “cherry pit” symptom does not appear. Against the background of general retinal ischemia, the papillomacular area of ​​the fundus may have a normal color. In these cases, central vision is preserved.

With embolism of the central retinal artery, vision is never restored. With a short-term spasm in young people, vision can return completely, but with a long-term spasm, an unfavorable outcome is possible. The prognosis for elderly and middle-aged people is worse than for young people. When one of the branches of the central retinal artery is blocked, ischemic edema of the retina occurs along the affected vessel, vision is only partially reduced, and loss of the corresponding part of the visual field is observed.

Treatment of acute obstruction of the central retinal artery and its branches consists of the immediate administration of general and local vasodilators. Under the tongue - a nitroglycerin tablet, under the skin - 1.0 ml of a 10% caffeine solution, inhalation of amyl nitrite (2-3 drops on a cotton swab), retrobulbar - 0.5 ml of a 0.1% solution of atropine sulfate or a solution of prick (10 mg per administration, daily for several days), 0.3-0.5 ml of 15% complamin solution. Intravenously - 10 ml of a 2.4% solution of aminophylline, intramuscularly - 1 ml of a 1% solution of nicotinic acid as an activator of fibrinolysis, 1 ml of a 1% solution of dibazol, 2 ml of a 2% solution of papaverine hydrochloride, 2 ml of 15% complamine.

A 1% solution of nicotinic acid (1 ml), a 40% solution of glucose (10 ml) is also administered intravenously, alternating it with a 2.4% solution of aminophylline (10 ml). If the patient has general diseases (cerebrovascular accidents, myocardial infarction), anticoagulant therapy is indicated. For thrombosis of the central retinal artery resulting from endarteritis, retrobulbar injections of fibrinolysin with heparin are given against the background of intramuscular administration of heparin in a dose of 5000-10,000 units 4-6 times a day under the control of blood clotting and prothrombin index. Then indirect anticoagulants are prescribed internally - 0.03 ml finilin 3-4 times on the first day, and subsequently - 1 time per day.

Orally take aminophylline 0.1 g, papaverine 0.02 g, dibazol 0.02 g, no-shpu 0.04 g, nigexin 0.25 g 2-3 times a day, trental 0.1 g 3 times a day.

Intramuscular administration of a 25% solution of magnesium sulfate, 5-10 ml per injection, is indicated. Anti-sclerotic agents (iodine preparations, methionine 0.05 g, miscleron 0.25 g 3 times a day), vitamins A, B 6, B, 2 and C are prescribed in normal doses.

Thrombosis of the central retinal vein

Thrombosis of the central retinal vein (CRV) occurs mainly in hypertension, atherosclerosis, diabetes mellitus, and more often in the elderly. In young people, the cause of thrombosis of the central retinal vein can be a general (influenza, sepsis, pneumonia, etc.) or focal (usually diseases of the paranasal sinuses and teeth) infection. Unlike acute obstruction of the central retinal artery, thrombosis of the central retinal vein develops gradually.

In the prethrombosis stage, venous congestion appears in the fundus. The veins are dark, dilated, tortuous, arteriovenous crossovers are clearly visible. When performing angiographic studies, a slowdown in blood flow is recorded. When thrombosis begins, the retinal veins are dark, wide, tense, there is transudative tissue edema along the veins, and there are pinpoint hemorrhages on the periphery of the fundus along the terminal veins. In the active stage of thrombosis, vision suddenly deteriorates and then completely decreases. During ophthalmoscopy, the optic disc is swollen, the boundaries are washed away, the veins are dilated, tortuous and intermittent, often immersed in the edematous retina, the arteries are narrowed, and hemorrhages of various sizes and shapes are observed.

With complete thrombosis, hemorrhages are located throughout the retina, and with branch thrombosis, they are localized only in the area of ​​the affected vessel. Thrombosis of individual branches most often occurs in the area of ​​arteriovenous junctions. After some time, white foci form - accumulations of protein, degeneration. Under the influence of treatment, hemorrhages can partially resolve, resulting in improved central and peripheral vision.

In the central zone of the fundus after complete thrombosis, newly formed vessels often appear that have increased permeability, as evidenced by the free release of fluorescein during angiographic examination. Complications of the late period of central retinal vein thrombosis are recurrent preretinal and retinal hemorrhages, hemophthalmos associated with newly formed vessels.

After thrombosis of the central retinal vein, secondary hemorrhagic glaucoma, retinal degeneration, maculopathy, proliferative changes in the retina, and optic nerve atrophy often develop. Thrombosis of individual branches of the central retinal vein is rarely complicated by secondary hemorrhagic glaucoma; dystrophic changes in the central region of the retina appear much more often, especially when the temporal branch is affected, since it drains blood from the macular part of the retina.

If retinal veins are obstructed in patients with hypertension, it is necessary to reduce blood pressure and increase perfusion pressure in the vessels of the eye. To reduce blood pressure, it is necessary to give a clonidine tablet, and to increase perfusion pressure in the vessels of the eye, reduce swelling in the area of ​​venous stagnation and reduce extravasal pressure on the intraocular vessels, ethacrynic acid 0.05 g and diacarb 0.25 g 2 times a day are recommended for 5 days, as well as installation of a 2% pilocarpine solution. Plasma inogen has a beneficial effect. Heparin and corticosteroids are administered parabulbarly, rheopolyglucin and trental are administered intravenously, heparin is administered intramuscularly, the dose of which is set depending on the blood clotting time: it should be increased by 2 times compared to the norm. Then indirect anticoagulants (phenyline, neodecumarin) are used. Among the symptomatic drugs recommended are angioprotectors (Prodectin, Dicinone), drugs that improve microcirculation (Complamin, Teonicol, Trental, Cavinton), antispasmodics (papaverine, no-shpa), corticosteroids (Dexazone retrobulbar and subconjunctival), vitamins, anti-sclerotic drugs. In the later stages (after 2-3 months), laser coagulation of the affected vessels is performed using the results of fluorescein angiography.

It is important to know!

Retinoblastoma is the most common malignant neoplasm in pediatric ophthalmology. This is a congenital tumor of the embryonic structures of the retina, the first signs of which appear at an early age. Retinoblastoma can occur sporadically or be inherited.

The fundus of the eye is a natural “window” in the human body, allowing a detailed assessment of the condition of small vessels. As is known, when blood pressure increases, they are affected first, which cannot but affect the picture of the fundus. These changes are the result of damage and adaptive changes in blood vessels and blood circulation in response to hypertension.

According to various data, the incidence of such changes varies widely (from 3 to 95%) among patients with arterial hypertension and depends on many factors. Examination of the fundus can help identify initial changes in individuals with asymptomatic increases in pressure; it is extremely important for malignant hypertension and frequent crises.

Most patients with changes in the fundus do not present any complaints. However, in severe cases, decreased vision and headaches may occur.
Risk factors include:
- African race;
- age;
- seminal predisposition;
- obesity;
- smoking;
- stress;
- alcohol;
- passive lifestyle.

Classification

In the countries of the former USSR, when describing changes in the fundus during arterial hypertension, it is customary to use the Krasnov-Vilenkina classification:
1) hypertensive angiopathy. Functional (transient) changes are noted in the fundus: dilation of the veins, an increase in the angle of their divergence of the 2nd and 3rd orders (the “tulip” symptom), narrowing of the arteries. Mild hyperemia of the optic disc is possible. All these phenomena are reversible and disappear as the underlying disease is cured;
2) hypertensive angiosclerosis. In addition to the symptoms listed above, there is a thickening of the walls of the arteries, a decrease in their lumen, and therefore the vessels are visible not pink-red, but yellow-red (symptom of “copper wire”). Subsequently, the lumen of the artery is completely blocked as a result of intimal growth and it acquires a whitish tint (the “silver wire” symptom). Compaction of the artery at the site of intersection with the vein leads to compression of the vein, and symptoms of vascular intersection appear (symptoms of Salus Hun). Corkscrew-shaped tortuosity of blood vessels in the paramacular region may be detected (Gwist's sign);
3) hypertensive retinopathy. Along with the changes described above, damage to the retina is noted: swelling, hemorrhage, whitish and yellowish spots, plasmorrhagia along the nerve fibers, which form a ring or star shape around the macula. Patients may experience decreased visual acuity;
4) hypertensive neuroretinopathy. All of the above changes are detected in the fundus with the involvement of the optic nerve in the process. The optic disc becomes swollen and enlarged, and the swelling spreads to the surrounding retina.

Abroad they use the Keith-Wagner-Barker classification, which practically corresponds to the Krasnov-Vilenkina classification adopted in our country. Less commonly used is Scheie's classification, which distinguishes 5 stages for hypertensive and atherosclerotic changes.

It is widely believed that the stages transform into one another and accompany the stages of hypertension. However, this is not entirely true. Moreover, changes in the fundus often have much less diagnostic and prognostic value than general practitioners, cardiologists and neurologists give them.

Treatment of ocular complications of arterial hypertension consists of lifestyle changes and drug therapy. It is important to note that in the presence of signs of optic neuropathy, a sharp decrease in blood pressure can lead to ischemic damage to the optic nerve.

Manifestations of arterial hypertension in the fundus

The vessels of the retina, choroid and optic nerve have differences in structure. This explains the variety of manifestations of arterial hypertension in the fundus.

Changes in arteriolar lumen diameter are an essential component of the regulation of systemic blood pressure levels. Thus, a 50% decrease in lumen leads to a 16-fold increase in blood pressure. If a change in the caliber of blood vessels is associated only with an increase in blood pressure, then after its normalization, the fundus picture returns to normal. Atherosclerotic changes in the walls of blood vessels can also play a role - in this case, changes in the fundus are irreversible. For this reason, the first symptom to judge the presence of arterial hypertension is a change in the caliber of blood vessels. The normal artery/vein thickness ratio is 2/3. When blood pressure rises, as a rule, arterioles begin to narrow and veins begin to expand. These changes may be uneven throughout the same vessel.

When the vessels of the fundus of the eye are damaged by atherosclerosis, characteristic manifestations are determined, such as the symptom of “copper” and “silver wire”. Normally, along the lumen of the vessel during ophthalmoscopy, a light reflex is visible, which is formed due to the reflection of light from the column of blood in it. As the walls thicken and sclerose, light begins to be reflected from them, as a result of which the reflex becomes wider and less bright, acquires a brown tint (hence the “copper wire” symptom), and if the process progresses, it becomes whitish (the “silver wire” symptom).

The symptom of arteriovenous decussation, or the Salus-Gunn symptom, is considered the most pathognomonic for arterial hypertension. It is caused by sclerosis of the walls of the arteriole, as a result of which its thickened wall reflects light more strongly, shading the underlying vein.

There are three degrees:
Salus I– compression of the vein at the intersection with the artery. The vein is thinned on both sides, conically narrowed.
Salus II– the same picture is visible as with Salus I, but the vein bends before the decussation with the formation of an arch.
Salus III– the vein under the artery at the intersection and along the edges of the intersection is not visible; it is thinned, curved and, near the intersection, expanded due to a violation of the outflow of venous blood. The vein is deeply pressed into the retina.

The next sign of increased blood pressure is a violation of the normal branching of blood vessels. Normally, they diverge at an acute angle, and in the presence of hypertension, this angle can even reach 180 degrees (symptom of “tulip” or “bull horns”). Elongation and tortuosity of the vessels may also be observed. The Gwist sign or “corkscrew” sign is the increased tortuosity of the venules in the macular zone.

Retinal hemorrhages are more serious in terms of prognosis for life. They arise due to the penetration of red blood cells through the altered vascular wall, its rupture due to increased blood pressure or due to previous microthrombosis. Most often, hemorrhages occur near the optic disc in the layer of nerve fibers and have the appearance of radially diverging stripes or streaks. In the macular area, hemorrhages resemble a star figure.

Impaired retinal nutrition in hypertension can lead to infarctions of small areas of nerve fibers, which entails the appearance of cotton wool-like, “soft” exudates. “Hard” exudates are less pathognomonic for arterial hypertension, but, nevertheless, can be detected in this disease. They can be pointy or large, round or irregular in shape; in the macular zone they often form a star shape.

Swelling of the retina and optic disc is determined in severe arterial hypertension and often accompanies the above-described changes in the fundus.

Also, a consequence of increased blood pressure can be occlusions and thromboses of the retinal vessels.

In rare cases, changes can be observed in the choroid of the eye: Elshing spots - dark spots surrounded by a light yellow or red halo; Siegrist stripes – linear hyperpigmented spots along the choroidal vessels; exudative retinal detachment. Their cause is a violation of microcirculation in this membrane of the eye in severe arterial hypertension.

The degree and duration of arterial hypertension often, but not always, determine the severity of changes in the fundus. In some cases, against the background of increased blood pressure, signs of damage to the retinal vessels are not detected, while in others, on the contrary, the picture of the fundus indicates severe damage to the internal organs, despite compensated pressure. The identified changes in the retina are not specific only to arterial hypertension. Various conditions may be associated with hypertensive retinopathy: ethnicity, smoking, increased intima-media thickness and plaque in the carotid artery, decreased elasticity, increased blood cholesterol, diabetes, increased body mass index.

Some changes tend to spontaneously resolve after normalization or stabilization of blood pressure, and therefore the picture of the fundus after some time can be strikingly different in one patient. To a greater extent, this applies to the initial stages of hypertension. Studies have shown that, even without taking into account the individual characteristics of the structure of the vascular tree of each person, the width and tortuosity of the vessels can vary even within one day. The caliber can change throughout one vessel and is also not constant. From the above, it is easy to conclude that this variability, as well as the method of examination, and the qualifications of the ophthalmologist who examined the fundus, lead to a significant discrepancy in medical reports. This fact is supported by data from one study that assessed interrater agreement in assessing microvascular changes. Thus, it was lowest when assessing arteriolar narrowing, and higher when assessing the symptoms of chiasm (Salus-Gunn symptom). Opinions most often coincided when identifying hemorrhages and exudates.

Studies have shown a low prevalence of retinal changes in patients with hypertension (3-21%). Half of people without signs of hypertensive retinopathy suffered from high blood pressure. However, changes in the fundus were rarely found in healthy people (specificity - 88-98%). Narrowing of arterioles in 32-59% indicated hypertension, the presence of the Salus-Hun symptom - in 44-66%. Moreover, the latter can also be detected both in people with arterial hypertension and in healthy people or with age-related changes. The occurrence of Gwist's symptom in patients with increased blood pressure, according to various authors, ranges from 10 to 55% of cases.

The presence of hemorrhages and exudates in the fundus in 43-67% indicated arterial hypertension. At the same time, in the Beaver Dam eye study and the Blue Mountains eye study, there were no significant differences in the frequency of detection of hemorrhages and exudates in patients with normal and high blood pressure over the age of 65 years.

Diagnostic value

Many studies have been aimed at identifying the prognostic value of changes in the fundus in diseases of the cardiovascular system. Their connection with the development of stroke turned out to be most clear. It is important to note that the risk of its occurrence doubled in patients with retinopathy, regardless of blood pressure level. The presence of changes in the retina also doubles the risk of left ventricular hypertrophy. Patients with hemorrhages and exudates in the fundus significantly have a greater thickness of the intima-media layer of the carotid artery. Data on the relationship between hypertensive angiopathy and microalbuminuria are contradictory.

Some studies have found that a decrease in the diameter of the retinal arteries may be an independent risk factor for the development of arterial hypertension. Thus, the presence of this sign in middle-aged and elderly patients with normal blood pressure indicated a 60% risk of developing hypertension in the next three years, and the correlation between the degree of narrowing and the risk of developing hypertension did not depend on other factors.

Thus, studies often find an association between hypertensive retinopathy, blood pressure levels and cardiovascular mortality. However, the low predictive value of the identified changes in the retina does not allow us to give a clear answer to the question: does a given person’s blood pressure increase or not. Fundus examination has limited diagnostic value in patients with hypertension, except in acute emergencies caused by elevated blood pressure.

Fundus changes are one of the most common manifestations of hypertension. They often precede a persistent increase in blood pressure and are the only easily directly observable manifestation of the early stage of hypertension.

Severe changes in the fundus should be considered as a sign of a malignant course of hypertension.

The picture of fundus changes in hypertension is extremely diverse:

a) Hypertensive retinal angiopathy is inherent in the first phase of hypertension - functional vascular disorders and unstable pressure.

There are no organic changes in the vessels of the eye yet. However, due to passive expansion of both veins and arteries, hyperemia of the fundus may be observed. Subsequently, spasm of the arteries occurs, which manifests itself in a number of vascular symptoms, among which the most characteristic are Gwist’s symptom (corkscrew-shaped tortuosity of small veins surrounding the area of ​​the macula) and the Hun-Salus symptom (crossing of blood vessels).

If a tense artery lies over a vein, it can compress it to varying degrees. Salus I - the vein lying under the artery seems somewhat thinned, its lumen is narrowed; this corresponds to the initial phase of the disease. Salus II - the vein not only has a narrowed lumen, but does not go in a straight line, but makes a bend in the form of an arc. Salus III - in the arch formed by the vein, there is a break; on both sides of the artery, for some distance the vein seems to disappear.

b) Hypertensive angiosclerosis (angiosclerosis retinae hypertonica) is the second stage of changes in the fundus and confirms that the damage concerns mainly the vessels and is already organic in nature. In this case, the symptoms of Salus II and III and the symptom of “copper or silver wire” prevail.

c) Hypertensive angioretinopathy and neuroretinopathy are further manifestations of disease progression. These changes occur due to increased vascular permeability.

In the fundus, in addition to vascular changes, swelling, hemorrhages and white spots appear, which indicates involvement of the retina in the process. Hemorrhages occur in the form of petechiae and streaks, which is typical for varying degrees of vascular damage. The appearance of streak-shaped hemorrhages indicates damage to the large branches of the central retinal artery located in the layer of nerve cells and indicates a deterioration in the patient’s condition.

When the lesions are located in the area of ​​the macula, a “star” figure is formed. Usually, when the lesions are centrally located, vision decreases significantly. When these changes appear, the prognosis is poor not only in terms of vision, but also in life, especially if the retinopathy is renal.

Fundus changes in hypertension

The vast majority of patients with hypertension exhibit various changes in the fundus of the eye in the retinal vessels, retina and optic nerve.

The most common changes in the caliber of arteries, which narrow either throughout or in certain areas. If normally an artery is 1.5 times narrower than the vein corresponding to it in caliber (a:u = 2:3), then here this ratio can reach 1:4. Such changes are considered functional, i.e. reversible, and therefore real narrowing can only be observed in young patients. According to the most commonly used classification by M. L. Krasnov, such changes are classified as hypertensive retinal angiopathy.

Very important importance is attached to changes in the course of retinal vessels, especially the symptom of arteriovenous junction (Adamyuk-Hun-Salus). Weak compression of the vein underlying the artery (it bends, changing its normal course) also occurs in healthy people, and a pronounced decussation symptom is especially characteristic of the phase of sclerotic changes in the vascular wall. At the site of natural crossing, the sclerotic artery compresses the vein in such a way that the distal end of the vein expands due to stagnation, and the proximal one has a narrowing in the form of a candle flame on the other side of the cross. With the strongest pressure, it seems that the vein directly under the artery seems to disappear.

As organic changes in the vascular wall progress, it loses its transparency and symptoms of “copper” and “silver wire” are formed. Moreover, in some areas the column of blood is almost or not at all visible through such a wall.

These changes belong to the concept of hypertensive angiosclerosis of the retina (according to the same classification).

It is also characterized by the formation of the Adamyuk-Twist symptom - a corkscrew-shaped tortuosity of small venous trunks radially surrounding the foveal region.

Hypertensive retinopathy and neuroretinopathy occur due to increased vascular permeability. Then hemorrhages appear in the retinal tissue, varying in size and shape, swelling of the retina from mild to severe, which can lead to exudative detachment, as well as “hard” exudates (yellowish, clearly defined, shiny) and “soft” in the form of lumps of cotton wool (local infarctions in the area of ​​capillary blockage).

With these manifestations of hypertensive retinopathy, the formation of a “star” figure in the posterior pole of the eye is possible (exudates are arranged in accordance with the location of the retinal nerve fibers), which was previously called the “albuminuric star”.

The degree of papilledema can be expressed in hypertensive neuropathy to varying degrees.

These kinds of changes in the retina and optic nerve are usually observed in severe hypertension, and with adequate therapy they can undergo reverse development (more often in young people). In this regard, the observations of R. A. Batarchukov, I. I. Titov and I. P. Krichagin regarding “siege” hypertension in besieged Leningrad during the Great Patriotic War are indicative. Such manifestations of hypertension occurred in approximately a third of patients and responded well to treatment.

It should be noted that all of these changes in the fundus occur in hypertension of various origins. At the same time, it is not possible to find any characteristic symptoms indicating one or another nature of the increase in blood pressure, for example, diseases of the renal vessels or kidney parenchyma, severe toxicosis of pregnancy, and some endocrine diseases.

To sum it all up, you should remember:

— There is no strict parallelism between the severity of hypertension and the severity of its manifestations in the fundus.

— The most significant sign of persistent hypertension is focal narrowing of the arteries, a pronounced symptom of arteriovenous junction.

— It is impossible to reliably establish the cause of secondary arterial hypertension from the fundus picture.

Changes in the organ of vision with arterial hypertension

Arterial hypertension accompanies a group of diseases in which, as a result of at least three measurements at different times, systolic blood pressure (BP) is or exceeds 140 mmHg. Art. diastolic - 90 mm Hg. Art. It is more common between the ages of 40-69 years.

Classification

The European classification of hypertensive retinopathy distinguishes four stages of the disease:

Stage 1 - there are no changes in the fundus.

Stage 2 - narrowing of the arteries.

Stage 3 - the presence of symptoms characteristic of stage 2, in combination with retinal hemorrhages and/or exudate.

Stage 4 - the presence of symptoms characteristic of stage 3, combined with papilledema.

In the CIS countries they use the classification of M.L. Krasnova (1948), who distinguishes three stages of development of fundus changes in arterial hypertension, gradually transforming into one another:

I. Hypertensive angiopathy - functional changes in retinal vessels.

II. Hypertensive angiosclerosis is organic changes in the vessels of the retina.

III. Hypertensive retino- and neuroretinopathy damages not only blood vessels, but also retinal tissue and the optic nerve.

Clinical picture and diagnosis

An examination by an ophthalmologist for arterial hypertension is mandatory and includes viziometry, measurement of intraocular pressure, perimetry and ophthalmoscopy (with fundus lenses), fluorescein angiography (FA) and optical coherence tomography (OCT) of the retina, rheoophthalmography, Dopplerography of the vessels of the brain and spine.

At the stage of angiopathy (functional changes in retinal vessels), a decrease in central and peripheral vision is not observed; it is characterized by narrowing of the arteries, dilatation of the veins and tortuosity of the retinal vessels. In this regard, the normal ratio of arteries and veins of the retina (2.3) in the hundred-

ron increase - up to 1. 4. Characteristic is the Salus-Hun symptom of the 1st degree (symptom of arteriovenous intersection) - a slight narrowing of the vein under the pressure of the artery at the site of their intersection. In the central sections, around the macula, a corkscrew-shaped tortuosity of small venules appears (Gwist's symptom).

The stage of angiosclerosis (organic changes in the vessels of the retina) corresponds to the NA and BE stages of hypertension, a decrease in central

and peripheral vision is not typical. When examining the fundus, narrowing, uneven caliber and the appearance of “side stripes” along the retinal arteries are observed. The vessels appear as if they are double-circuited due to thickening and decreased transparency of the vascular wall. The central reflex along the arterioles becomes wider and acquires a golden hue - a symptom of copper wire. This picture is explained by lipoid infiltration of the vascular wall with protein deposits. With organic degeneration of the vessel wall (fibrosis, deposits of hyaline, amyloid, lime), the silver wire symptom occurs in the form of a bright white vascular reflex. The veins are dilated and tortuous. Characteristic symptoms are Salus-Hun II (a symptom of a venous arch; it consists of partial compression of the vein and an arc-shaped displacement to the side and into the thickness of the retina) and Salus-Hun III (a visible “break” of the vein under the artery).

The stage of retino- and neuroretinopathy (organic changes in the retina and optic nerve) is observed in stages IIIA and IIIB of hypertension. It is always a marker of severe complications of arterial hypertension, in particular kidney pathology. Visual acuity, as a rule, decreases with damage to the macular area (ischemia, hemorrhage, edema) and in the late stage of neuroretinopathy. Perimetry in modern conditions (computer static perimetry) allows us to identify early functional changes in the visual analyzer: decreased light sensitivity, expansion of the blind spot, as well as the presence of scotomas at the stage of retinopathy and narrowing of visual fields. At this stage, obstruction of precapillary arterioles and capillaries with the appearance of ischemic zones and disruption of the blood-retinal barrier lead to the occurrence of foci of exudation, hemorrhages, edema of the retina and optic nerve head, and less often - newly formed vessels and microaneurysms.

Hemorrhages, depending on their location relative to the areas and layers of the retina, can be in the form of streaks, stripes, flames or spots. Preretinal hemorrhages can also be detected. Along the vascular arcades, as a result of ischemia and plasmorrhagia, “loose” gray-white foci are formed, resembling lumps of cotton wool - the so-called cotton wool exudates. “Hard” exudates appear as small foci with clear boundaries of white (ischemia + protein infiltration) or yellow (lipids + cholesterol) color.

They appear more often in the central sections and form a “star figure” in the area of ​​the macula. In hypertensive crises or malignant hypertension, the choroid may be involved in the pathological process: focal infarctions (Elshing's lesions) and fibrinoid vascular necrosis (Sigrist's lines).

An increase in the size of the optic disc, blurring of its boundaries and protrusion into the vitreous body, as well as the appearance of a waxy tint are characteristic of papilledema (neuroretinopathy).

During fluorescein angiography, local areas of choriocapillary occlusion can be seen, especially in malignant hypertension. It should be noted that the manifestations described above may be preceded by changes in the retina.

Differential diagnosis

Differential diagnosis of the identified changes should be carried out with congestive optic disc, with retinopathy due to diabetes, collagenosis, blood diseases, and radiation damage.

Complications

Complications of the eyes in hypertension are: spontaneous recurrent subconjunctival hemorrhages, thrombosis of the central retinal vein or its branches, acute obstruction of the central retinal artery or its branches, microaneurysms of the retinal arteries, anterior ischemic optic neuropathy, hemophthalmos, secondary vascular glaucoma.

Most often, hypertensive retinopathy is a bilateral disease, and the severity of changes in the fundus is often asymmetrical, which depends on the different degrees of vascular damage and blood supply to the right and left hemispheres. The severity of vascular disorders can be determined by computer rheoophthalmography or Dopplerography of the vessels of the brain and spine. Characterized by the presence of venous stasis, impaired venous outflow, a decrease in the linear and volumetric velocity of blood flow, spasm of medium and small vessels, and a decrease in the rheo-ophthalmic coefficient.

Treatment

Treatment is carried out on an outpatient and inpatient basis, together with a therapist. A prerequisite for successful treatment and prevention of further complications is blood pressure compensation. In the treatment of the underlying disease, antihypertensive and diuretic drugs are used in doses appropriate to the patient’s age, nature and severity of the disease. To compensate for pathological changes in the retina, angioprotectors, antiplatelet agents, antioxidants, vasodilators, venotonics, and neuroprotectors are prescribed. According to indications, laser coagulation of pathologically altered areas of the retina is performed.

In fact, the fundus is what the back of the eyeball looks like when viewed upon examination. Here the retina, choroid and optic nerve nipple are visible.

The color is formed by retinal and choroidal pigments and can vary among people of different color types (darker for brunettes and black people, lighter for blonds). Also, the intensity of the fundus coloring is affected by the density of the pigment layer, which can vary. With a decrease in pigment density, even the vessels of the choroid - the choroid of the eye with dark areas between them - become visible (Parkert picture).

The optic disc appears as a pinkish circle or oval up to 1.5 mm in cross section. Almost in its center you can see a small funnel - the exit point of the central blood vessels (central artery and vein of the retina).

Closer to the lateral part of the disc, another cup-like depression can rarely be seen; it represents a physiological excavation. It looks slightly paler than the medial part of the optic disc.

Normal fundus, on which the optic nerve papilla (1), retinal vessels (2), fovea (3) are visualized

The norm in children is a more intense coloration of the optic disc, which becomes paler with age. The same is observed in people with myopia.
Some people have a black circle around the optic disc, which is formed by an accumulation of melanin pigment.

The arterial vessels of the fundus look thinner and lighter, they are more straight. Venous ones are larger in size, in a ratio of approximately 3:2, and more convoluted. After the optic nerve leaves the nipple, the vessels begin to divide according to a dichotomous principle, almost to the capillaries. At the thinnest part that can be determined by fundus examination, they reach a diameter of only 20 microns.

The smallest vessels gather around the macula area and form a plexus here. Its greatest density in the retina is achieved around the macula - the area of ​​​​best vision and light perception.

The area of ​​the macula (fovea) itself is completely devoid of blood vessels; its nutrition comes from the choriocapillaris layer.

Age characteristics

The fundus of the eye in newborns is normally light yellow in color, and the optic disc is pale pink with a grayish tint. This slight pigmentation usually disappears by the age of two. If a similar pattern of depigmentation is observed in adults, this indicates optic nerve atrophy.

The afferent blood vessels in a newborn are of normal caliber, while the efferent blood vessels are slightly wider. If childbirth was accompanied by asphyxia, then the fundus of the children will be dotted with small pinpoint hemorrhages along the arterioles. Over time (within a week) they resolve.

With hydrocephalus or another cause of increased intracranial pressure in the fundus, the veins are dilated, the arteries are narrowed, and the boundaries of the optic disc are blurred due to its swelling. If the pressure continues to increase, the optic nerve nipple swells more and more and begins to push through the vitreous body.

Narrowing of the arteries of the fundus accompanies congenital atrophy of the optic nerve. His nipple looks very pale (more so in the temporal areas), but the boundaries remain clear.

Changes in the fundus of the eye in children and adolescents can be:

• with the possibility of reverse development (no organic changes);
• transient (they can only be assessed at the moment of their appearance);
• nonspecific (no direct dependence on the general pathological process);
• predominantly arterial (without changes in the retina characteristic of hypertension).

With age, the walls of blood vessels thicken, causing small arteries to become less visible and, in general, the arterial network to appear paler.

The norm in adults should be assessed taking into account concomitant clinical conditions.

Research methods

There are several methods for checking the fundus. An ophthalmological examination aimed at studying the fundus of the eye is called ophthalmoscopy.

An examination by an ophthalmologist is performed by magnifying the illuminated areas of the fundus with a Goldmann lens. Ophthalmoscopy can be performed in forward and reverse view (the image will be inverted), which is due to the optical design of the ophthalmoscope device. Reverse ophthalmoscopy is suitable for general examination; the devices for its implementation are quite simple - a concave mirror with a hole in the center and a magnifying glass. Direct is used when a more accurate examination is needed, which is carried out with an electric ophthalmoscope. To identify structures invisible in normal lighting, illumination of the fundus with red, yellow, blue, yellow-green rays is used.

Fluorescein angiography is used to obtain an accurate picture of the retinal vascular pattern.

Why does the fundus of the eye hurt?

The reasons for changes in the fundus picture may relate to the position and shape of the optic disc, vascular pathology, and inflammatory diseases of the retina.

Vascular diseases

The fundus of the eye most often suffers from hypertension or eclampsia during pregnancy. Retinopathy in this case is a consequence of arterial hypertension and systemic changes in arterioles. The pathological process occurs in the form of myeloelastofibrosis, less commonly hyalinosis. The degree of their severity depends on the severity and duration of the disease.

The result of an intraocular examination can establish the stage of hypertensive retinopathy.

First: slight stenosis of arterioles, the beginning of sclerotic changes. There is no hypertension yet.

Second: the severity of stenosis increases, arteriovenous crossovers appear (the thickened artery puts pressure on the underlying vein). Hypertension is noted, but the condition of the body as a whole is normal, the heart and kidneys are not yet affected.

Third: constant vasospasm. In the retina there is effusion in the form of “lumps of cotton wool”, small hemorrhages, swelling; pale arterioles have a “silver wire” appearance. Hypertension levels are high, the functionality of the heart and kidneys is impaired.

The fourth stage is characterized by the fact that the optic nerve swells and the blood vessels undergo critical spasm.

If the pressure is not reduced in time, then over time, occlusion of the arterioles causes a retinal infarction. Its outcome is atrophy of the optic nerve and death of cells in the photoreceptor layer of the retina.

Arterial hypertension can be an indirect cause of thrombosis or spasm of the retinal veins and central retinal artery, ischemia and tissue hypoxia.

Examination of the fundus for vascular changes is also required in case of systemic disturbances in glucose metabolism, which leads to the development of diabetic retinopathy. Excess sugar in the blood is detected, osmotic pressure increases, intracellular edema develops, the walls of the capillaries thicken and their lumen decreases, which causes retinal ischemia. In addition, microthrombi form in the capillaries around the foveola, and this leads to the development of exudative maculopathy.

During ophthalmoscopy, the fundus picture has characteristic features:

• microaneurysms of retinal vessels in the area of ​​stenosis;
• an increase in the diameter of the veins and the development of phlebopathy;
• expansion of the avascular zone around the macula due to capillary closure;
• the appearance of a hard lipid effusion and soft cotton-like exudate;
• microangiopathy develops with the appearance of couplings on the vessels, telangiectasias;
• multiple small hemorrhages at the hemorrhagic stage;
• the appearance of an area of ​​neovascularization with further gliosis - the proliferation of fibrous tissue. The spread of this process can gradually lead to tractional retinal detachment.

DZN

Pathology of the optic nerve disc can be expressed in the following:

• megalopapilla - measurement shows an increase and pallor of the optic disc (with myopia);
• hypoplasia – a decrease in the relative size of the optic disc in comparison with the retinal vessels (with hypermetropia);
• oblique ascension – the optic disc has an unusual shape (myopic astigmatism), the accumulation of retinal vessels is shifted to the nasal region;
• coloboma – a defect of the optic disc in the form of a notch, causing visual impairment;
• symptom of “morning glow” – mushroom-shaped protrusion of the optic disc into the vitreous body. Ophthalmoscopy descriptions also indicate chorioretinal pigmented rings around an elevated optic disc;
• congestive nipple and edema - enlargement of the optic nerve nipple, its pallor and atrophy with increased intraocular pressure.

Pathologies of the fundus of the eye also include a complex of disorders that occur in multiple sclerosis. This disease has multiple etiologies, often hereditary. In this case, the myelin sheath of the nerve is destroyed against the background of immunopathological reactions, and a disease called optic neuritis develops. An acute decrease in vision occurs, central scotomas appear, and color perception changes.

In the fundus one can detect sharp hyperemia and swelling of the optic disc, its boundaries are erased. There is a sign of optic nerve atrophy - blanching of its temporal region, the edge of the optic disc is dotted with slit-like defects, indicating the onset of atrophy of the retinal nerve fibers. Narrowing of the arteries, formation of couplings around the vessels, and macular degeneration are also noticeable.

Treatment for multiple sclerosis is carried out with glucocorticoid drugs, since they inhibit the immune cause of the disease, and also have an anti-inflammatory and stabilizing effect on the vascular walls. Injections of methylprednisolone, prednisolone, and dexamethasone are used for this purpose. In mild cases, corticosteroid eye drops such as Lotoprednol can be used.

Retinal inflammation

Chorioretinitis can be caused by infectious-allergic diseases, allergic non-infectious, post-traumatic conditions. In the fundus, they appear as many rounded formations of light yellow color, which are located below the level of the retinal vessels. The retina has a cloudy appearance and a grayish color due to the accumulation of exudate. As the disease progresses, the color of inflammatory foci in the fundus may approach whitish, as fibrous deposits form there and the retina itself becomes thinner. The retinal vessels remain virtually unchanged. The outcome of retinal inflammation is cataract, endophthalmitis, exudative, and in extreme cases, atrophy of the eyeball.

Diseases affecting the retinal vessels are called angiitis. Their causes can be very diverse (tuberculosis, brucellosis, viral infections, mycoses, protozoa). The ophthalmoscopy picture shows vessels surrounded by white exudative couplings and stripes, areas of occlusion and cystic edema of the macula area are noted.

Despite the severity of the diseases causing fundus pathologies, many patients initially begin treatment with folk remedies. You can find recipes for decoctions, drops, lotions, compresses from beets, carrots, nettles, hawthorn, black currants, rowan berries, onion peels, cornflowers, celandine, immortelle, yarrow and pine needles.

I would like to draw your attention to the fact that by taking home treatment and delaying a visit to the doctor, you may miss the period of development of the disease at which it is easiest to stop it. Therefore, you should regularly undergo ophthalmoscopy with an ophthalmologist, and if pathology is detected, carefully follow his instructions, which you can supplement with folk recipes.