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Fundus changes in hypertension. Vision under pressure

The human body is an extremely complex structure, all parts of which work in close relationship with each other. It is therefore not surprising that in many cases of the disease general cause significant changes in the condition of the eyes, and sometimes lead to significant impairment of visual functions. Therefore, many patients with general somatic diseases require observation by an ophthalmologist, as well as timely and correct correction of eye disorders.
HYPERTENSION DISEASE, WHAT IS IT?
Hypertension is one of the most common diseases among the peoples of the world. How special shape Hypertension was identified 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 emotions negative character.
Currently, hypertension is understood as a disease accompanied by an increase in blood pressure and caused by a primary violation of cortical and subcortical regulation vascular system as a result of a disorder of higher nervous activity with subsequent involvement in pathogenetic mechanism humoral factors.
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 occurs, as a rule, with an increase in pressure, but its level often changes. Pronounced organic changes are usually not detected.
Stage II, phase B (stable) is 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 detected, in particular, the porosity of the vascular walls increases, and the development of dystrophic changes.
Stage III, especially phase B (decompensated), is characterized by sharp dystrophic and sclerotic changes in organs and tissues (arteriolohyalinosis, arteriolonecrosis).
VARIANTS FOR 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.
By clinical course distinguish benign and malignant forms of the disease. The latter form is relatively rare and is characterized by a rapidly progressive course, early organic damage to the heart, cerebral vessels and, most importantly, the kidneys and eyes.
EYE AND HYPERTENSION?
The main changes in the 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 RETINAL HEMORRHAGES?
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, it only breaks inner part the walls of the vessel and the blood, permeating the vascular wall, forms a kind of case.
Vascular ruptures are associated with the action of three factors: increased blood pressure, decreased elasticity vascular wall, changes in the condition of the blood (increased viscosity).
Hemorrhages are especially often found near the disc optic nerve 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 ON THE EYE FOUNDUS?
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 mainly near large vessels, not far from the optic nerve head. They quickly arise, reach maximum size(up to the size of the optic nerve head) for several 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 discovery of this symptom is a reason to take very active measures, as this indicates that similar events may occur in other target organs. pathological processes, which is already a threat to the patient’s life.
WHAT IS HARD EXUDATE ON THE EYE FOUNDUS?
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 dissolve, but this the process is underway very slowly, over several months or even years.
CAN THERE BE SWELLING OF THE RETINA AND OPTIC NERVE?
Edema of the retina and optic nerve head is one of the important symptoms 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. At great content The protein of the retina loses its transparency, becomes grayish-white, and the vessels are covered in places with edematous tissue.
Edema of the optic nerve head can be expressed in varying degrees - from slight blurring of its contour to a picture of 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.
VISUAL FUNCTIONS 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 of the boundaries of the visual field, as well as an 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 macular spot, 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 late stage neuroretinopathy.
CLASSIFICATION OF HYPERTENSIVE CHANGES IN THE OPICULUM
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.
PROGNOSIS FOR VISION IN 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 level 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 substances that increase blood pressure, and therefore to a further increase vascular tone. Thus, there arises vicious circle, causing the malignant course of the disease. It should be noted that modern methods Treatments can in many cases 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), pronounced 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 minor and consist of an expansion of the blind spot, the appearance of individual scotomas and a concentric narrowing of the visual field.
It should be noted that the picture 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. Individual symptoms neuroretinopathy, especially the star macular figure, may be absent. However, a pronounced picture of neuroretinopathy can be combined with satisfactory general condition and undergo reverse development. Despite these reservations, clinical picture 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 sick.
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.

The fundus of the eye is a natural “window” into 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 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 countries 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. Possible mild hyperemia optic nerve head. 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 point of intersection, expanded due to a violation of the outflow 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 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 in rare cases changes can be observed in choroid eyes: Elshing spots - dark spots surrounded by a light yellow or red halo; Siegrist stripes – linear hyperpigmented spots along the choroidal vessels; exudative detachment retina. 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 defeat internal organs, despite compensated pressure. The identified changes in the retina are not specific only to arterial hypertension. Various states may be associated with hypertensive retinopathy: ethnicity, smoking, increased intima media thickness, and the presence of plaques in carotid artery, decreased elasticity, increased cholesterol in the blood, 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 initial stages hypertension. Research has shown that, even without taking into account individual characteristics 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 rare 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 data different 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: blood pressure increases in this person or not. Fundus examination is limited diagnostic value in patients with arterial hypertension, with the exception of acute emergency conditions caused by increased blood pressure.

Hypertensive changes in the fundus

The human body functions as a single mechanism, so disruptions in the functioning of any of physiological systems may lead to serious consequences. High blood pressure can interfere with normal functioning visual system caused by hemorrhage from the retinal vessels. In patients with acute obstruction of the central artery in the retina, vision deteriorates sharply.

According to the study different doctors we can say that 50 - 95% of people with hypertension experience changes in the fundus of the eye. Indicators depend on the age of the patient, the course of the disease, and concomitant ailments. Very difficult to diagnose hypertensive changes fundus on early stages development of the disease. The most common diseases are: retinal angiopathy, retinal arteriosclerosis, retinopathy, malignant hypertension.

Hypertensive angiopathy of the retina is characterized by uneven narrowing of the lumen of the arteries and dilation of the veins. As a result of these processes, the venous tree is full-blooded with clearly visible branches, and the arterial tree is poor. Sometimes symptoms of Gwist and decussation are noticeable.

Hypertensive atherosclerosis of the retina is accompanied by signs of angiopathy with symptoms of copper and silver wire, dense retinal exudates and minor hemorrhages also appear. In patients childhood The angiosclerotic stage is always absent.

Hypertensive retinopathy is accompanied by irreversible destruction of blood vessels and retinal tissue, and neuroretinopathy (damage to the optic nerve) is also quite often observed. The disease develops very quickly - swelling in the fundus of the eye forms in the area of the peripapillary retina and optic nerve, hemorrhages are noticeable, cotton-like and thickened retinal exudates appear. Patients with angioretinopathy develop maculopathy in the fundus, which has the appearance of a star with multiple rays. This is explained by clearly visible deposits of cholesterol in the nerve fibers passing through the retina.

Malignant hypertension is characterized by pronounced changes in the fundus of the eye, such as neuroretinopathy. As a rule, these changes are the first signs of the transition of hypertension to a malignant disease. In patients, blood pressure increases, the lumens of blood vessels narrow, fibrinoid necrosis of arterioles, and arteriolar hyperplasia appear. The disease spreads throughout the body, the kidneys are most affected, so people with nephritis are more susceptible to the disease. The risk group is people aged 30 to 50 years.

The main symptoms of malignant hypertension when diagnosing the fundus are: swelling of the peripapillary retina and optic nerve; narrowing of the lumen of the arteries and expansion of the veins, the appearance of hemorrhages (point and striped), the formation of cotton-like exudates and a macular star. However, the described symptoms may accompany other diseases that are not malignant in nature. For example, autopsies showed that not all those who died from this disease had fundus changes. Therefore, when indicated symptoms patients should monitor their health very carefully and remember that all benign diseases can become malignant over time.

Hypertension is insidious in that at first it goes unnoticed by the patient. No one will pay due attention to symptoms such as occasional dizziness, irritability, and decreased performance. Starting with a deviation from normal blood pressure towards an increase in moments emotional overexcitation, hypertension then leads to very serious diseases of various human organs.

The effect of hypertension on the fundus of the eye

One of the organs that suffers from hypertension is the eyes. The main negative changes occur in the fundus of a person with hypertension.

Let us consider in more detail the fundus of the eye in hypertension. At the first examination of the fundus of the eye, an ophthalmologist can determine the dilation of the veins of the retina and the narrowing of the arteries. Due to the high tone, the dense ophthalmic artery compresses the vein at the intersection. The degree of severity of the above changes in the vessels of the fundus will depend on the duration of a person’s hypertension and on the height of his blood pressure.

In medicine, the following stages of fundus changes in hypertension are distinguished:

stage of hypertensive angiopathy of the retina (functional changes);

stage of hypertensive angiosclerosis of the retina (organic changes);

stage of hypertensive angioretinopathy and neuroretinopathy (organic changes in the optic nerve and retina).

With hypertensive angiopathy of the retina, which corresponds to the first stage of hypertension, dilation of the retinal veins and narrowing of the arteries occurs. These changes are reversible. When blood pressure normalizes, the vessels of the retina return to normal.

With hypertensive angiosclerosis of the retina, further expansion of the veins and hardening of the arteries occurs. Increased tortuosity of the vessels of the eye can lead to hemorrhage. Microaneurysms appear in the area of the optic nerve. This stage corresponds to persistently elevated blood pressure.

With hypertensive angioretinopathy and neuroretinopathy, the condition of the fundus is further aggravated. In the fundus, in addition to retinal hemorrhages and vascular changes, foci of exudation and ischemia appear. The condition of the optic nerve changes. In patients, visual acuity and field of vision are lost, photosensitivity is impaired, and visual functions are significantly impaired.

The effect of blood pressure on the organs of vision once again proves the complex interconnected structure of the human body.

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Most often, fundus diagnostics is prescribed to study retinal pathologies, which can be an independent disease, or can be a symptom of a number of other diseases. With the help of this mirror, light from a small source located nearby is collected into a narrow, directional beam. It illuminates the fundus of the eye, which the doctor can see through the hole in the mirror and through the person's pupil.

Fundus examination - ophthalmoscopy - is absolutely harmless to the patient and does not lead to vision deterioration. Ophthalmoscopy allows you to see the inner membranes of the eyeball - the retina and choroid, as well as the arteries and veins of the retina, the disc optic nerve-all together this is called the fundus of the eye. Any changes or deviations from the norm identified during fundus examination tell a specialist a lot.

In some cases, only ophthalmoscopy allows us to identify a disease in which, apart from changes in the fundus, there are no general symptoms. This is why those suffering from cardiovascular disease endocrine diseases, metabolic disorders, diseases of the central nervous system, and the organ of vision, fundus examinations are periodically performed. This is done using an ophthalmoscope - a round concave mirror with a hole in the center.

Ophthalmoscopy is a method of examining the fundus of the eye (retina and its vessels, optic nerve, choroid) which is based on the reflection of light rays from the fundus of the eye. In simple terms, this is an examination of the eye from the inside. The study is carried out using a special device - an ophthalmoscope. The doctor directs a beam of light (emanating directly from the device’s lamp or reflected from another source) into the patient’s eye (through the pupil onto the retina) and in certain positions examines various parts of the fundus of the eye: the optic disc, the macula.

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:

stage of functional changes - hypertensive retinal angiopathy;
stage of organic changes - hypertensive angiosclerosis of the retina;
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. Normal walls blood vessels the retina is 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. N healthy tissues at the intersection points, the 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, there is pronounced swelling of the optic nerve head and retina. 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 changes in the fundus of the eye caused by arterial hypertension, use the classification proposed by M. L. Krasnov, according to which three stages of changes in the 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 (about 15% of cases) in central departments retina there is a corkscrew-shaped tortuosity of small venules (Gwist's sign). 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 arterial walls, the central light strip (reflex along the course of the vessel) becomes narrower and acquires a yellowish tint, which gives the vessel a resemblance to 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 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. For arterial hypertension diastolic pressure in the central retinal artery it rises 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 disorders blood circulation 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 it more often occurs organic lesion vascular wall due to arterial hypertension, atherosclerosis, etc. Several days and even weeks before the spasm, patients may complain of temporary blurred vision, the appearance of 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, 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 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 acute obstruction the central retinal artery and its branches is to immediately prescribe 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(violations cerebral circulation, 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 oral anticoagulants are prescribed indirect action- finilin 0.03 ml 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.

Shown intramuscular injection 25% magnesium sulfate solution, 5-10 ml per injection. 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, more often in older people. 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 venous stagnation and reducing extravasal pressure on the intraocular vessels, ethacrynic acid 0.05 g and diacarb 0.25 g 2 times a day for 5 days are recommended, as well as the installation of a 2% solution of pilocarpine. 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. From symptomatic remedies recommend 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 late dates(after 2-3 months) laser coagulation of the affected vessels is performed using the results of fluorescein angiography.

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 have 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.

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.

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.

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.

Diagnostic value

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.

Retinal changes in arterial hypertension

Symptoms. Most often, high blood pressure does not cause any eye symptoms. Changes in the retina, in particular changes in the blood vessels associated with high blood pressure, are detected only when examining the fundus of the eye. It is possible that some deviations from normal vision may occur (decreased visual acuity, hemorrhage in the conjunctiva), which leads to an increase in pressure that was not previously noted.

Treatment. A decrease in blood pressure to normal is usually sufficient to eliminate most of the noted retinal disorders. In some cases it is necessary to carry out special course ophthalmic treatment, especially if this disorder is accompanied by other disorders (glaucoma, diabetes, etc.).

Deterioration of vision due to hypertension

In blood pressure without the use of antihypertensive drugs, magnetic resonance imaging (MRI) revealed periventricular changes. Subsequently, a J-shaped relationship was shown between the incidence of silent brain damage and the magnitude of the nocturnal decrease in blood pressure: multiple lacunae on MRI were found in 56% of over-dippers, 38% of non-dippers, and only in 6% of patients with a preserved circadian blood pressure rhythm. Signs of periventricular edema were found in 44% of over-dippers, 22% of non-dippers and 18% of patients with normal blood pressure reduction.

The effect of arterial hypertension on vision

IN last years Studies have been conducted showing the relationship between an excessive decrease in blood pressure at night and the progression of visual impairment in patients over 50 years of age due to ischemic neuropathy anterior branch of the optic nerve. The cause of this complication is considered to be a decrease in blood flow in the posterior ciliary artery, which can lead to infarction of the optic nerve nipple, manifested by its swelling. According to Hayreh et al. patients who developed this complication were characterized by a significantly more pronounced nocturnal decrease in blood pressure (25.3% for SBP and 31.2% for DBP) compared to normal values (10-20%). Moreover, patients whose vision loss progressed also had a significantly greater decrease in blood pressure at night than those whose visual impairment was stable (respectively 35.3% versus 26.8% for SBP and 30.5% versus 19. 6% for DBP). The data from this study supported the hypothesis that an excessive nocturnal decrease in blood pressure may be a factor provoking the development of ischemic optic neuropathy. Subsequently, the authors came to the conclusion that relative hypotension at night and in the morning may be important for the development of this complication.

Blood pressure studies

Studies conducted using ABPM have confirmed the importance of pulse pressure as an independent risk factor for the development of cardiovascular complications. At the same time, an abrupt increase in risk is observed when the average daily pulse blood pressure is >53 mm Hg. Art. while critical level in relation to clinical pulse pressure, 60 mmHg is considered. Art.

The results of the Syst-Eur study made it possible to establish that the main factors determining daily fluctuations in blood pressure in elderly patients with ISAH are gender, age, smoking, and alcohol intake. Thus, the average daily values of SBP and DBP tended to be higher in men (150 ± 15/82 ± 9 mm Hg) than in women (147 ± 17/79 ± 10 mm Hg), however, the differences between sexes were significant. differences were only for diastolic blood pressure.

It is known that blood pressure increases acutely with smoking, possibly due to sympathetic stimulation. Population studies have shown that in smokers blood pressure in traditional measurements increases by 1-2 mm Hg. Art. higher than non-smokers. The Syst-Eur study did not reveal significant differences in the level of clinical blood pressure between smokers and non-smokers, while the average daily systolic blood pressure increased by 3 mm Hg. Art. for every 10-year increase in age, it was significantly higher in smokers.

Changes in blood pressure depending on age

The same study demonstrated clear dynamics of average daily blood pressure values depending on age. The average daily DBP in men was 2 mm Hg. Art. higher than in women and decreased by 1.5 mm Hg. Art. for every 10 years of increase in age. The day-night difference increased by 2 mm Hg. Art. for every 10 mm Hg. Art. increase in blood pressure measured traditional method, and decreased by 5 mm Hg. Art. for every 10 years as age increased, it was 2 mmHg. Art. higher in women than in men by 6 mm Hg. Art. more in smokers.

In addition, the degree of nocturnal BP reduction was closely correlated with gamma-glutamyl transferase levels, used as an index of alcohol intake.

In elderly patients, the morning rise in blood pressure has its own characteristics, which plays a role in important role in a complex of unfavorable neurohumoral and hemodynamic changes, which determine a significantly higher frequency of cardiovascular and cerebrovascular accidents during this period of the day. Thus, according to Carmona J. et al., when comparing the magnitude and rate of rise in blood pressure during 6 morning hours (3 hours before the patient gets up and 3 hours after), in patients over 60 years of age, a sudden jump in blood pressure is recorded much more often, than in young and middle-aged patients. According to these data, more than 75% of cardiovascular events in elderly patients are recorded during these hours.

Blood pressure variability is an independent risk factor for the development of cardiovascular accidents and tends to increase with increasing age.

Visual impairment and arterial hypertension

At hypertensive crisis Sudden blindness may occur due to arteriolar spasm and retinal ischemia. In addition, a sharp increase in blood pressure can lead to blindness due to ischemic papilledema. To treat acute hypertensive retinopathy, it is necessary to lower blood pressure - but not too sharply, since sharp deterioration blood supply can lead to optic disc infarction.