Changes in the organ of vision in arterial hypertension. Fundus of the eye in arterial hypertension

3-01-2011, 13:23

Description

The human body is an extremely complex structure, all parts of which work in close relationship with each other.

Therefore, it is not surprising that in many cases, diseases of a general nature cause significant changes in the condition of the eyes, and sometimes lead to significant visual impairment. Therefore, many patients with general somatic diseases require observation by an ophthalmologist, as well as timely and correct correction of eye disorders.

Hypertension, what is it?

Hypertonic disease- one of the most common diseases among the peoples of the world. Hypertension was identified as a special form a little more than half a century ago.

According to scientists, hypertension is a kind of neurosis of the higher nerve centers that regulate blood pressure, which is caused by their overstrain as a result of prolonged and inhibited effects and negative emotions.

Currently, hypertension is understood as a disease accompanied by an increase in blood pressure and caused by a primary disruption of the cortical and subcortical regulation of the vascular system as a result of a disorder of higher nervous activity with subsequent involvement of humoral factors in the pathogenetic mechanism.

Stages of hypertension?

During hypertension there are three stages, each of which in turn is divided into two phases.

Stage I, phase A refers to the very initial period of the disease and is manifested by an increase in blood pressure in response to emotional and physical stimuli.

Stage I, phase B- transient hypertension. At this stage, increased blood pressure and other symptoms of the disease (headache, dizziness, periodic visual disturbances, etc.) appear under certain conditions (especially after psycho-emotional stress) for some time, and then under the influence of rest and treatment, the pressure normalizes. However, already at this stage, vasospasms, both generalized and local (cerebral, coronary vessels), can be observed.

Stage II, phase A (labile)- the disease usually occurs with increased blood pressure, but its level often changes. Pronounced organic changes are usually not detected.

Stage II, phase B (stable) characterized by a relatively stable and often significant increase in blood pressure. During this period of the disease, organic changes in the vessels are already revealed, in particular, the porosity of the vascular walls increases, and degenerative changes develop in organs and tissues.

Stage III, especially phase B (decompensated), is characterized by sharp dystrophic and sclerotic changes in organs and tissues (arteriolohyalinosis, arteriolonecrosis).

Variants of the course of the disease?

Both functional and sclerotic changes in blood vessels can develop in different organs far from the same extent, which also causes different clinical variants of hypertension.

According to the clinical course, benign and malignant forms of the disease are distinguished. The latter form is relatively rare and is characterized by a rapidly progressive course, early organic damage to the heart, brain vessels and, most importantly, the kidneys and eyes.

Eye and hypertension?

Major changes from organ of vision in hypertension occur in the fundus and can be assessed using ophthalmoscopy.

The frequency of fundus lesions in patients with hypertension, according to various authors, varies from 50% to 95%.

The first manifestations of changes are narrowing of the arteries and dilation of the retinal veins. In places of arteriovenous crossover, compression of the vein by a denser artery occurs due to its higher tone.

What happens to the arteries of the eye?

In addition, in patients with hypertension, sclerosis of the wall of the retinal arteries occurs, which ultimately leads to their emptying due to stenosis of the lumen. These changes are called copper and silver wire symptoms.

Can there be hemorrhages in the retina?

As a result of the release of red blood cells through a stretched and defective capillary wall, small hemorrhages (bleeds) in the retina may occur in patients with hypertension. In addition, hemorrhages are characteristic of ruptures of small vessels, capillaries or microaneurysms.

In some cases, only the inner part of the vessel wall ruptures and the blood, permeating the vascular wall, forms a kind of sheath.

Vascular ruptures are associated with the action of three factors: an increase in blood pressure, a decrease in the elasticity of the vascular wall, and a change in the condition of the blood (increase in its viscosity).

Especially often, hemorrhages are found near the optic nerve head in the layer of nerve fibers.

Hypertensive disease is especially characterized by banded hemorrhages in the area around the optic nerve. Hemorrhages in the peripheral parts are also not uncommon, but they are considered a sign of arteriosclerosis, developing either independently or as a consequence of hypertension.

What is soft exudate in the fundus?

In addition to hemorrhages, hypertensive retinopathy is characterized by the appearance of formations called exudates in the fundus.

These are grayish-white in color, loose in appearance, with somewhat unclear contours, protruding foci that appear primarily near large vessels, not far from the optic nerve head. They arise quickly, reach their maximum size (up to the size of the optic nerve head) within a few days, but never merge with each other. There may be small hemorrhages around some foci. As the cotton wool-like focus dissolves, it decreases in size and becomes flattened. At the same time, hemorrhages and red dots - microaneurysms - are often found at the site of the lesion. In fact, the cause of the appearance of these formations is a local circulatory disorder in the layer of nerve fibers, which leads to the development of local infarctions in the fundus.

The detection of this symptom is a reason to take very active measures, since this indicates that similar pathological processes may occur in other target organs, which is already a threat to the patient’s life.

What is hard exudate in the fundus?

Another type of formation in the fundus of hypertensive patients, “hard” lesions, do not have such an important prognostic value, although they indicate an advanced process.

It is believed that these deposits arise as a result of the release of plasma from small vessels and subsequent degeneration of tissue elements. In the macular region, solid lesions have a banded shape and a radial arrangement, forming a complete or incomplete star figure. As the patient's condition improves, the star figure may resolve, but this process occurs very slowly, over several months or even years.

Could there be swelling of the retina and optic nerve?

Swelling of the retina and optic nerve head- one of the important symptoms of hypertensive retinopathy. Edema is localized mainly in the peripapillary zone and along large vessels. If the effusion (transudate) contains little protein, then the retinal tissue remains transparent, and its inner surface reflects more than usual. With a high protein content, the retina loses transparency, becomes grayish-white and the vessels are covered in places with edematous tissue.

Papilledema can be expressed to varying degrees - from slight blurring of its contour to a picture of a developed-stagnant disk. In the latter case, the prognosis is serious, especially if this picture is combined with cotton wool-like exudates in the retina, hemorrhages and opacification of the peripapillary retina. However, if treatment of arterial hypertension is effective, disc swelling and other symptoms of neuroretinopathy gradually disappear.

How do visual functions behave in hypertension?

Decreased dark adaptation is one of the earliest functional signs in hypertensive angiopathy and retinopathy.

At the same time, there is a moderate narrowing boundaries of the field of view, as well as expansion of the blind spot. With severe retinopathy, scotomas can be found, most often localized in the paracentral region.

Visual acuity decreases much less frequently: with ischemic damage to the macula, with macular hemorrhages, with transudation of fluid into the macular zone of the retina from altered capillaries and with the formation of an epiretinal membrane in the late stage of neuroretinopathy.

Classification of hypertensive changes in the fundus

Currently, there are usually 4 degrees of vascular changes in the retina in arterial hypertension.

1. HYPERTONIC RETINAL ANGIOPATHY

The arteries are narrowed, the arterial tree is poor, the veins are dilated, the venous tree is full-blooded, branched, there may be symptoms of vascular tortuosity in the paramacular region, decussation (I degree), uneven caliber of the arteries

2. HYPERTENSIVE RETINAL ARTERIOSCLEROSIS

The symptoms described above, as well as the accompanying stripes and wide reflex on the arteries, symptoms of chiasm, copper and silver wire. Hard lesions and isolated hemorrhages are also possible

3. EARLY HYPERTENSIVE NEURORETINOPATHY

Symptoms of angiopathy (see point 1), swelling of the optic nerve head and peripapillary retina, hemorrhages, cotton wool-like and hard lesions

4. LATE HYPERTENSIVE NEURORETINOPATHY

Symptoms of hypertensive arteriosclerosis (see point 2) in combination with edema of the optic disc and peripapillary retina, cotton wool-like lesions, hard exudates and hemorrhages. Sometimes symptoms of epithelial fibrosis in the posterior pole of the eye, collapse and destruction of the vitreous body.

What is the prognosis for vision with hypertension?

The stage of hypertension and the prognosis for the patient’s life are determined by the height of blood pressure and the severity of vascular changes in the kidneys, heart and brain. These changes are not always parallel with changes in the retina, but there is still a certain correlative relationship between them. In any case, multiple hemorrhages in the retina, the appearance of areas of ischemia and cotton wool-like exudates, as well as severe swelling of the optic nerve head and peripapillary retina indicate the severe progressive nature of the disease and the need to change and intensify therapeutic measures.

Modern therapeutic agents make it possible in many cases to achieve significant improvement in the course of the disease and reverse the development of symptoms of hypertensive neuroretinopathy.

Malignant arterial hypertension

Malignant hypertension is characterized by very high blood pressure, widespread vasoconstriction, arteriolar hyperplasia and fibrinoid necrosis of arterioles. The lesion affects various organs, especially the kidneys. Changes in the arterial vessels of the kidneys lead not only to disruption of their functions, but also to the release of pressure-increasing substances, and therefore to a further increase in vascular tone. Thus, a vicious circle arises, causing the malignant course of the disease.

It should be noted that modern treatment methods make it possible in many cases to stop or slow down the progression of the disease, but the prognosis for malignant hypertension always remains serious.

The disease most often begins at the age of 30-50 years, but can occur much earlier, especially in people suffering from nephritis. A transition to the malignant phase of previously benign hypertension in elderly patients with altered blood vessels is possible.

In typical cases, changes in the fundus are very pronounced, similar to neuroretinopathy. Often these changes are the first clinical symptoms indicating the transition of hypertension to a malignant form.

The most characteristic are edema of the disc and peripapillary retina (or widespread retinal edema), severe narrowing of the arteries and dilatation of the veins, punctate and streak hemorrhages, exudative foci, especially cotton wool lesions and macular star figure.

The lesion to one degree or another covers the entire fundus of the eye, but is especially pronounced in its posterior part. Often, hemorrhages, flocculent opacities, and destructive changes can be seen in the posterior part of the vitreous.

Functional changes are relatively small and consist of expansion of the blind spot, the appearance of individual scotomas and concentric narrowing of the field of view.

It should be noted that the pattern of neuroretinopathy described above is a common, but not obligatory, finding in malignant arterial hypertension. Some patients who died from this disease had no noticeable changes in the fundus. Some symptoms of neuroretinopathy, especially the star macular figure, may be absent.

At the same time, a pronounced picture of neuroretinopathy can be combined with a satisfactory general condition and undergo reverse development. Despite these reservations, the clinical picture of neuroretinopathy should be considered as a sign indicating a possible transition of the disease to a malignant form and the need for more intensive treatment of the patient.

How to treat hypertensive neuroretinopathy?

Therapy for hypertensive neuroretinopathy consists primarily of treating the underlying disease. To reduce retinal ischemia, vasodilators are used, which dilate mainly the vessels of the brain and eye (Trental, Cavinton).

Many authors recommend oxygen therapy. However, oxygen can cause the retinal arteries to narrow. Therefore, we prefer to use inhalation of carbogen, which, in addition to oxygen, contains carbon dioxide (5-8%). Carbon dioxide has a strong vasodilating effect on the blood vessels of the brain and eyes. Inhalations are prescribed for 3–4 weeks, 1–2 sessions per day. The duration of each session is 15 minutes.

In cases where there is swelling of the optic nerve head and retina, diuretics are useful. To prevent new hemorrhages in the retina, ascorbic acid with rutin is prescribed. Etamsylate, which also has an angioprotective effect, is more effective in such cases. It is useful to prescribe angioprotectors, especially calcium dobesilate.

To resolve hemorrhages and transudate, electrophoresis with lidase, papain or other proteolytic enzymes is used. The administration of vitamins (A, group B, E) is useful, especially in cases where the patient has a decreased appetite or suffers from diseases of the gastrointestinal tract, biliary tract and liver. It should be borne in mind that in such cases exogenous (with decreased appetite) or endogenous hypovitaminosis develops.

Article from the appendix to the book: .

Hypertension is an independent, chronically progressive disease.

There are four degrees of severity of hypertension based on diastolic pressure:

borderline hypertension (90-94 mm Hg);
benign hypertension (95-104 mm Hg);
moderate-to-severe hypertension (105-114 mm Hg);
severe hypertension (115 mmHg and above).

The duration of these periods of disease development varies and depends on many factors.

Stages of development of hypertension

The World Health Organization identifies the following stages of development hypertension:

stage I: hypertension without changes in organs;
stage II: hypertension with minor organic changes, such as proteinuria, left ventricular hypertrophy, hypertensive retinopathy (changes in the retina) grade I-II;
stage III: hypertension with severe organic damage, such as heart failure, periodically recurring “failure of a man,” grade III-IV hypertensive retinopathy, complications in the brain, renal failure.

Symptoms of hypertension

Hypertension can occur for a long time without any noticeable clinical symptoms. High blood pressure discovered by chance.

However, patients often experience early morning pain in the back of the head, dizziness, are less able to tolerate physical activity, and during special physical efforts a feeling of suffocation and palpitations appear.

Diagnosis of hypertension

Arterial hypertension is diagnosed after receiving the results of multiple measurements. For research, the method of intermediate measurement with a tonometer with a rubber cuff is most often chosen.

A diagnostic method is also 24/7 automatic blood pressure measurement, which avoids errors in human measurements.

In diagnosing hypertension, in addition to measuring blood pressure, it is also important to determine whether hypertension is primary or secondary. Assessing the degree of organ damage is important.

Consequences of hypertension for vision

Hypertension leads to changes in most organs and tissues. But some organs are especially susceptible, such as the heart, brain, kidneys, eyes (retina), large vessels. Untreated hypertension leads to left ventricular hypertrophy and failure.

With hypertension, characteristic changes are found in the vessels of the retina, visible during fundus examination. Based on these changes, the severity of the disease can be determined. For this purpose, the Keith and Wegener classifications are used, which determine the stages of vascular changes at the bottom of the eye.

Less severe changes corresponding to stages I and II consist of narrowing of the arterioles, disruption of the shape of the lumen, coarsening of the walls, and during stage II - compression of the veins by the arterioles crossing them. Changes in stages I and II accompany mild hypertension; atherosclerosis plays an important role in their occurrence.

More severe changes retina, which appear in stages III and IV, are characterized by the presence of signs of possible penetration of plasma and blood cells into the retina - which leads to the formation of degenerative foci of the retina, as well as, in stage IV, pronounced swelling of the optic disc. The form of stage III and IV changes is characterized by blockage of small-caliber arterioles. The appearance of petechiae and foci of degeneration is a symptom of necrosis of the arteriolar wall and developing malignant hypertension, which leads to papilledema.

The most important structural change in blood vessels in arterial hypertension is hypertrophy of the central mucosa. In subsequent periods, glazing, segmentation, atrophy and fibrosis of the inner membrane occur. The lumens of blood vessels undergo gradual narrowing.

The frequency of fundus damage in patients with hypertension, according to various authors, varies from 50 to 95%. This difference is caused partly by age and clinical differences in the patient population studied, but mainly by the difficulty of interpreting the initial changes in the retinal vessels in hypertension.

Doctors attach great importance to such changes in the early diagnosis of hypertension, determining its stage and phase, as well as the effectiveness of the therapy.

Errors in diagnosis may be associated with significant individual variations in the retinal vessels in healthy people, and some of the variations (relatively narrow arteries, increased vascular tortuosity, crossover sign) may be incorrectly interpreted as hypertensive changes.

Vessels of the retina and optic nerve

1 - DZN
2 - optic nerve funnel with central retinal vessels;
3 - n. nasal arteriole;
4 - n. nasal venule;
5 - n. temporal venule;
6 - n. temporal arteriole;
7 - yellow spot with c. pit;
8 - c. temporal arteriole;
9 - c. temporal venule;
10 - in. nasal arteriole;
11th century nasal venule.

The central retinal artery in its orbital section has a structure typical of medium-sized arteries. After passing through the cribriform plate of the sclera, the thickness of the vascular wall is halved due to thinning (from 20 to 10 µm) of all its layers. Inside the eye, the artery divides dichotomously many times. Starting from the second bifurcation, its branches lose their inherent characteristics of arteries and turn into arterioles.

The intraocular part of the optic nerve is supplied mainly (with the exception of the neuroretinal layer of the optic nerve head) from the posterior ciliary arteries. Posterior to the lamina cribrosa of the sclera, the optic nerve is supplied by centrifugal arterial branches originating from the central retinal artery and centropetal vessels originating from the ophthalmic artery.

The capillaries of the retina and optic disc have a lumen with a diameter of about 5 µm. They start from precapillary arterioles and connect to venules. The endothelium of the retinal capillaries and optic nerve forms a continuous layer with tight junctions between cells.

Retinal capillaries also have intramural pericytes, which are involved in the regulation of blood flow. The only blood collector for both the retina and the optic nerve head is the central retinal vein.

The adverse effects of various factors on retinal blood circulation are smoothed out due to vascular autoregulation, which ensures optimal blood flow using local vascular mechanisms. This blood flow ensures the normal course of metabolic processes in the retina and optic nerve.

Pathomorphology of retinal vessels in hypertension

Pathomorphological changes in the initial transient stage of the disease consist of hypertrophy of the muscle layer and elastic structures in small arteries and arterioles.

Stable arterial hypertension leads to

hypoxia,
endothelial dysfunction,
plasmatic impregnation of the vascular wall with subsequent hyalinosis and arteriolosclerosis.

In severe cases, fibrinoid necrosis of arterioles is accompanied by thrombosis, hemorrhages and microinfarctions of retinal tissue.

Retinal vessels

Two vascular trees are clearly visible in the fundus: arterial and venous. It is necessary to distinguish:

the severity of each of them,
branching features,
ratio of the caliber of arteries and veins,
degree of tortuosity of individual branches,
the nature of the light reflex on the arteries.

The severity and richness of the arterial tree depend on the intensity of blood flow in the central artery, refraction and the condition of the vascular wall. The more intense the blood flow, the better the small arterial branches are visible and the more branched the vascular tree. With hypermetropia, the retinal vessels appear wider and brighter during ophthalmoscopy than with emmetropia, and with myopia they become paler. Age-related thickening of the vascular wall makes small branches less noticeable, and the arterial tree of the fundus in elderly people looks depleted.

In hypertension, the arterial tree often looks poor due to tonic contraction of the arteries and sclerotic changes in their walls. Venous vessels, on the contrary, often become more pronounced and acquire a darker, more saturated color. It should be noted that in some cases, provided that the elasticity of the vessels is preserved, in patients with hypertension, not only venous, but also arterial congestion is observed. Changes in the arterial and venous vascular beds also manifest themselves in changes in the arteriovenous ratio of retinal vessels. Normally, this ratio is approximately 2:3; in patients with hypertension, it often decreases due to narrowing of the arteries and dilation of the veins.

Narrowing of the retinal arterioles is not a necessary symptom. Severe narrowing, which can be determined clinically, occurs only in half of the cases. Often only individual arterioles narrow. The unevenness of this symptom is characteristic. It is manifested by asymmetry of the state of the arteries in paired eyes, narrowing of only individual vascular branches, and uneven caliber of the same vessel. In the functional phase of the disease, these symptoms are caused by unequal tonic contraction of the vessels, in the sclerotic phase - by uneven thickening of their walls.

Much less often than narrowing of the arteries, with hypertension, their dilation is observed. Sometimes both narrowing and dilation of arteries and veins can be seen in the same eye and even on the same vessel. In the latter case, the artery takes on the appearance of an uneven chain with swellings and interceptions.

One of the common symptoms of hypertensive angiopathy is disruption of the normal branching of the retinal arteries. Typically, the arteries branch dichotomously at an acute angle. Under the influence of increased pulse beats in hypertensive patients, this angle tends to increase, and it is often possible to see branching of the arteries at right and even obtuse angles (“bull horns symptom”). The greater the branching angle, the greater the resistance to blood movement in this zone, the stronger the tendency to sclerotic changes, thrombosis and disruption of the integrity of the vascular wall. High blood pressure and large pulse amplitude are accompanied by an increase in not only lateral, but also longitudinal stretching of the vascular wall, which leads to lengthening and tortuosity of the vessel. In 10–20% of patients, tortuosity of the perimacular venules is also observed (Gwist's sign).

The Hun–Salus intersection symptom is essential for the diagnosis of fundus hypertonicity. The essence of the symptom is that at the point of intersection of the venous vessel with a condensed artery, partial compression of the latter occurs.

There are three clinical degrees of this symptom.

The first degree is characterized by a narrowing of the lumen of the vein under the artery and near the intersection of the vessels.
A feature of the second degree is not only partial compression of the vein, but also its displacement to the side and into the thickness of the retina (“arch symptom”).
The third degree of vascular decussation is also characterized by an arch symptom, but the vein under the artery is not visible and seems completely compressed. The symptom of decussation and venous compression is one of the most common in hypertension. However, this symptom can also be found in retinal arteriosclerosis without vascular hypertension.

Symptoms pathognomonic for retinal arteriosclerosis in hypertension include the appearance of side stripes (cases) along the vessel, symptoms of copper and silver wire. The appearance of white lateral stripes is explained by thickening and decreased transparency of the vascular wall. The stripes are visible along the edge of the vessel, since there is a thicker layer of the wall and a thinner layer of blood compared to the central part of the vessel. At the same time, the light reflex from the front surface of the vessel becomes wider and less bright.

Copper wire symptom It is found mainly on large branches and is distinguished by an expanded light reflex with a yellowish tint. The symptom indicates sclerotic changes in the vessel with a predominance of elastic hypertrophy or plasmatic impregnation of the vascular wall with lipoid deposits.

Silver wire symptom appears on arterioles of the second or third order: the vessel is narrow, pale, with a bright white axial reflex, often it seems completely empty.

Retinal hemorrhages

Retinal hemorrhages in hypertension occur through diapedesis of red blood cells through the altered wall of microvessels, rupture of microaneurysms and small vessels under the influence of increased pressure or as a consequence of microthrombosis.

Especially often, hemorrhages occur in the layer of nerve fibers near the optic nerve head. In such cases, they take the form of radially arranged strokes, stripes or flames. In the macular zone, hemorrhages are located in the Genly layer and have a radial location.

Much less often, hemorrhages are found in the outer and inner plexiform layers in the form of irregularly shaped spots.

Retinal exudates

Hypertensive disease is especially characterized by the appearance of soft exudates resembling cotton wool. These grayish-white, loose-looking, anteriorly protruding lesions appear predominantly in the parapapillary and paramacular zones.

They arise quickly, reach maximum development within a few days, but never merge with each other. During resorption, the focus gradually decreases in size, flattens and fragments.

A cotton wool lesion is an infarction of a small area of nerve fibers caused by microvascular occlusion. As a result of the blockade, axoplasmic transport is disrupted, nerve fibers swell, and then fragment and disintegrate.

It should be noted that such foci are not pathognomonic for hypertensive retinopathy and can be observed with

stagnant disks,
diabetic retinopathy,
occlusion of the central retinal vein,
some other retinal lesions in which necrotic processes develop in the arterioles.

Unlike cotton wool lesions, hard exudates in hypertension do not have prognostic significance. They can be dotted or larger, round or irregular in shape, located in the outer plexiform layer and consist of lipids, fibrin, cellular debris and macrophages.

It is believed that these deposits arise as a result of the release of plasma from small vessels and subsequent degeneration of tissue elements. In the macular region, solid lesions have a banded shape and a radial arrangement, forming a complete or incomplete star figure. They have the same structure as other solid lesions. As the patient's condition improves, the star figure may resolve, but this process takes a long time over several months or even several years.

Swelling of the retina and optic nerve head

Swelling of the retina and optic nerve head, combined with the appearance of soft lesions, indicates a severe course of the disease.

Edema is localized mainly in the peripapillary zone and along large vessels. With a high content of proteins in the transudate, the retina loses transparency, becomes grayish-white, and the vessels are covered in places with edematous tissue.

Papilledema can be expressed to varying degrees, from slight blurring of its contour to a picture of a developed congestive disc. A congestive disc is often associated with peripapillary retinal edema, retinal hemorrhages, and cotton wool lesions.

Visual functions

Decreased dark adaptation is one of the earliest functional signs in hypertensive retinopathy.

At the same time, there is a moderate narrowing of the isopter and the boundaries of the visual field, as well as an expansion of the “blind spot”. With severe retinopathy, scotomas localized in the paracentral region of the visual field can be detected.

Visual acuity decreases much less frequently: with ischemic maculopathy, macular hemorrhages, with the occurrence of edematous maculopathy and with the formation of the epiretinal membrane in the late stage of neuroretinopathy.

Classification of hypertensive changes in the fundus

Currently, there is no generally accepted classification of hypertensive angioretinopathy. In Russia and neighboring countries (former republics of the USSR), the most popular classification is M.L. Krasnov and its modifications.

M.L. Krasnov identified three stages of fundus changes in hypertension:

hypertensive angiopathy, characterized only by functional changes in the retinal vessels;
hypertensive angiosclerosis;
hypertensive retino- and neuroretinopathy, which affects not only the vessels, but also the retinal tissue, and often the optic disc.

sclerotic,
renal and
malignant.

The most severe changes in the retina are observed in renal and especially malignant forms.

The stages of hypertension and the prognosis for the patient’s life are determined by the height of blood pressure and the severity of vascular changes in the kidneys, heart and brain. These changes are not always parallel with retinal lesions, but there is still a certain relationship between them. Therefore, multiple hemorrhages in the retina, the appearance of areas of ischemia, non-perfusion zones, cotton wool-like exudates, as well as severe swelling of the optic nerve disc and peripapillary retina indicate the severe progressive nature of the disease and the need to change and intensify therapeutic measures.

Treatment of hypertensive neuroretinopathy

Therapy for hypertensive (neuro)retinopathy consists of: treatment of the underlying disease.

To reduce ischemia the retina uses vasodilators that dilate mainly the vessels of the brain and eye (Trental, Cavinton, Xavin, Stugeron).

To reduce hypoxia Oxygen inhalation is often used. However, oxygen can cause constriction of the retinal vessels. Therefore, they prefer to prescribe carbogen inhalations, which in addition to oxygen contains carbon dioxide (58%). Carbon dioxide has a strong vasodilatory effect on the vessels of the brain and eyes.

To improve blood rheology and prevent the occurrence of thrombosis, antiplatelet agents are used.

It should be taken into account that elimination of retinal ischemia can lead to the development of post-ischemic reperfusion syndrome, which consists of excessive activation of free radical processes and lipid peroxidation. Therefore, constant intake of antioxidants (alfatocopherol, ascorbic acid, veton, diquertin) is essential.

The use of angioprotectors, especially doxium, is useful.

Preparations containing proteolytic enzymes (Wobenzym, papain, recombinant prourokinase) are used to resolve intraocular hemorrhages.

For the treatment of retinopathy of various origins, transpupillary irradiation of the retina using a low-energy infrared diode laser is prescribed.

With regular high blood pressure, target organs are affected: heart, brain, kidneys, fundus of the eye. The fundus of the eye in hypertension may be in a different state or remain unchanged. This is not an indicator of the stage of development of the disease, but simply a concomitant pathology that requires treatment. All changes that occur in the microvasculature of the body can be noticed during ophthalmoscopy in the fundus.

Patients who gradually develop hypertension may not understand the cause of their symptoms and may not seek treatment from their doctors. But changes in vision become a frequent reason for going to the hospital and the initial detection of pathologies such as hypertension and diabetes mellitus.

Dangerous symptoms

Changes in the retinal vessels are manifested by such symptoms and complaints as:

decreased visual acuity;
disturbance of color perception;
Pain in the eyes;
“floaters” before the eyes, regardless of the time of day;
narrowing of the field of view.

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

Symptoms eventually lead to optic atrophy or a series of complications associated with thrombosis or vascular obstruction, which is an ophthalmological emergency. The disease ends in blindness, affecting both eyes equally. An increased risk of progression of vascular pathology is observed in smokers, people leading a sedentary lifestyle, drinking alcohol and having excessive body weight.

Classification of pathologies

Changes in the fundus of the eye with hypertension were recorded in 75 percent or more of patients. Ophthalmologists use terminology such as:

Hypertensive angiopathy. Changes in vascular structures are temporary. They appear and disappear depending on the tonometer readings. The arteries are narrowed, and the veins are slightly dilated and form a “tulip” symptom. Redness of the nerve disc is observed.
Angiosclerosis. Added to the previous clinical picture is thickening of the arterial walls, a change in their color to yellow-red, which is also called the copper wire symptom. After blocking the blood flow in the artery, it becomes silvery in color, and the veins become more tortuous. Most often, the patient is bothered by floaters in the eyes; the stage is irreversible, but it is possible to stop the progression.

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

Retinopathy. The symptoms include damage to the retina, the appearance of hemorrhages on it and swelling. Plasmorrhages are observed along the nerve fibers, which resemble star figures. The disease is characterized by significant visual impairment.
Neuroretinopathy is a disease with a poor prognosis. The optic disc swells, a large number of hemorrhages into the retina, which leads to gradual atrophy of the nerve fibers.

There is an opinion that the stages of fundus pathology correspond to the stages of headache development. But this assumption is not true. The stages of diseases are in no way related to each other or to each other. And neuroretinopathy can appear at stage IIA headache.

Manifestations of headache at the bottom of the eye

The manifestations of arterial hypertension are varied, since various changes occur in the vascular structures. With a systemic increase in pressure, the arterioles thicken and narrow, and the veins dilate and become tortuous. The thickness of the arterioles increases, and the lumen of the veins increases and the wall weakens. Such metamorphoses are located unevenly and can be located within the same vessel.

Hypertensive angioretinopathy and neuroretinopathy are further manifestations of disease progression

With hypertension, a concomitant disease may be atherosclerosis, which affects the condition of the walls of blood vessels and clogs the lumen with small plaques or lipid deposits. Symptoms of the addition of atherosclerosis are a sign of “wire”, which can acquire a copper or silver tint during ophthalmoscopy.

Diagnostic methods

The fundus of the eye with hypertension is examined by an ophthalmologist. The examination device is a direct or indirect ophthalmoscope. The procedure is quick and painless, and is accessible to patients. More accurate information about the condition of the retina and fundus can be obtained using optical coherence tomography, which will cost more.

The supply of useful substances to the retina is carried out using blood vessels located in the fundus of the eye. The development of arterial hypertension leads to increased intraocular pressure. This is fraught with a decrease in visual acuity, pressing pain in the area of the superciliary arches, and a significant decrease in performance. Many people attribute migraines and “floaters before their eyes” to fatigue, lack of sleep or prolonged work at the computer. The fundus of the eye in hypertension may be damaged due to vascular spasm. There are cases when vision deteriorates directly during a hypertensive crisis, and then is restored back.

Causes of fundus changes

Arterial hypertension is an insidious disease that can be asymptomatic and is accidentally discovered only during a routine medical examination. Signs of changes in the fundus of the eye during hypertension resemble vascular inflammation caused by glaucoma, which is a local pathology.

Normal intraocular pressure is 12–22 mmHg. Art. If, in addition to changes in blood pressure, there are no other symptoms of glaucoma, we are talking about hypertension.

The development of hypertension can be provoked by:

bad habits (alcohol, smoking, drugs);
abuse of coffee and other tonics;
overweight, unhealthy diet, physical inactivity;
old age, genetic predisposition, chronic stress;
improperly functioning cardiovascular, endocrine and nervous systems.

Diagram of the eye structure

Fundus examination for hypertension is included in the list of mandatory preventive procedures, since its malignant course leads to damage to internal organs. Together with the vessels in the retina, the cerebral arteries suffer, which is fraught with an attack of hemorrhagic stroke.

With the help of a visual analyzer, more than 80% of information about the world around us is learned. Visual impairment due to hypertension is one of the serious complications of the disease. Increased blood pressure is accompanied by spasm of blood vessels, tension in their walls, and thickening of the blood, which can lead to retinal infarction, the formation of microthrombi, and hemorrhage.

Classification of vascular pathologies of the retina

With the help of ophthalmoscopy, even minor changes in the fundus of the eye are diagnosed in hypertension. Based on the nature of inflammation of the retinal vessels, the ophthalmologist determines the etiology of the disease in order to predict its further course and select the appropriate treatment. Sometimes contrast methods, such as angiography, are allowed. Eye pain accompanied by lacrimation may be of allergic origin, so it is important to differentiate these two conditions using therapeutic and ophthalmological examinations.

Among the fundus lesions associated with a persistent increase in blood pressure are:

Hypertensive angiopathy.
Hypertensive angiosclerosis.
Hypertensive retinopathy.
Hypertensive neuroretinopathy.

Hypertensive neuroretinopathy

These pathologies differ in the localization of inflammation, the size of the affected area and the level of vision loss. Damage to the optic nerve is very dangerous, since it is used to conduct nerve impulses from the receptors of the retina to the occipital lobe of the brain, where visually received information is processed. Changes in the eyes with hypertension gradually progress, which is fraught with negative consequences.

The above stages of development of retinal vascular lesions can transform into one another. First, inflammation of the eye arteries and veins occurs; they cannot withstand the excessive load caused by increased pressure in the body. Compensatory mechanisms are depleted, resulting in tissue sclerosis. The malignant course of the disease leads to generalized damage to the retina along with the optic nerve.

Signs of increased intraocular pressure

With cardiovascular diseases, performance and concentration levels are significantly reduced. The visual analyzer plays an important role in various activities. Hypertension and glaucoma negatively affect the condition of the retina.

Redness of the eye

The first symptoms of damage to the ocular vessels are:

redness of the protein membrane;
rapid development of fatigue during reading, prolonged work at the computer;
a person sees poorly in the twilight;
the field of view becomes smaller, the picture seems to blur;
pressing pain in the temporal region;
sunlight causes unpleasant sensations, “floaters appear before the eyes.”

People who naturally have very good vision begin to be frightened by the rapid development of symptoms of arterial hypertension. Today, there are various treatment methods, which include surgical correction, therapy with vitamins and minerals. Before starting to fight eye angiopathy, it is worth achieving normalization of blood pressure in the whole body.

Clinical picture of changes in the fundus in hypertension

The degree of vascular damage depends on the stage of the disease. At first, it may resemble fatigue caused by excessive load on the visual analyzer. As the symptoms progress, they intensify and do not disappear even after proper rest. People run to buy drops for conjunctivitis, put on safety glasses, try to avoid prolonged work at the computer, without realizing the true nature of the visual impairment. Unfortunately, many patients turn to the doctor when the disease has already significantly affected the level of vision.

The following periods are distinguished in the development of ocular hypertension:

Retinal angiopathy occurs from hypertension in a mild stage, which is accompanied by a short-term increase in blood pressure. Symptoms of the disease, such as headaches, “jumping midges” before the eyes, redness of the sclera, may disappear over time and then reappear. A slight dilation of the veins, together with spasm of the arteries, causes hyperemia of the fundus.
Hypertensive angiosclerosis. Pathological changes in the ocular vessels acquire an organic character. Discomfort and redness are accompanied by hardening of the arterial walls, which leads to the “copper wire symptom” (the vessels of the fundus become yellow-red). Over time, it develops into the “silver wire symptom,” characterized by a white tint. At the site of crossing of the vessels, compression of the ophthalmic vein is observed, which causes the Salus-Hun symptom.
Generalized retinopathy. Pathological changes from the vessels spread directly to the retina, causing its swelling, the appearance of white and yellowish spots, and figures in the form of a ring or a star form around the visual spot. At this stage of the disease, visual impairment is pronounced due to a decrease in its acuity.
Involvement of the optic nerve in the inflammatory process is neuroretinopathy. Its disc swells, and over time the entire retina becomes swollen. The permeability of blood vessels increases significantly, and their plasmatic cutting occurs.

At the last stage of development of ocular hypertension, an irreversible decrease in visual acuity occurs. Only timely treatment will help a patient with high blood pressure maintain the function of the visual analyzer and avoid dangerous complications.