Changes in the organ of vision in arterial hypertension. Ocular hypertension
Changes in the fundus of the eye in hypertension are very common and have great diagnostic and prognostic value.
Examination of the fundus in hypertensive disease can give the first indication of the presence of hypertension in a patient, allows you to clarify the degree and nature of changes in the vascular system. Therefore, the study of the organ of vision in patients with hypertension should be carried out systematically.
Ophthalmoscopy most often shows tonic narrowing of the retinal arterioles, usually of a uniform nature. Normally, retinal arterioles are almost equal in size to veins. Since the lumen of the veins does not change in the initial stages of hypertension, the degree of narrowing of the arterioles is assessed in comparison with their venules. Of course, these measurements are by eye inaccurate. Special methods for determining the caliber of small vessels have shown a very high frequency of narrowing of the retinal arterioles in hypertension.
Against the background of evenly narrowed arterioles in the fundus of the eye with hypertension, there are also focal changes that sometimes give the vessels a clearly-shaped appearance. It is believed that they are caused not only by tonic contraction of the vascular walls, but also by structural changes in them such as arteriolosclerosis. These pictures are usually observed in the later stages. They seem to be a very common, if not obligatory, symptom of these stages.
Retinal arterioles in ophthalmoscopy often take the form of reflective strips - or narrow shiny white (silver wire symptom), wider yellowish (copper wire symptom).
It is assumed that the former are associated with an increased tonic contraction of the arterioles, while the latter are associated with a thinning of their walls (the blood in the vessel shines through). Vessels like silver wire are in the early stages of the disease, vessels like copper wire - in the later stages.
In the fundus of the eye with hypertension, a corkscrew-shaped tortuosity of the veins around the macula is noted; attach great importance to the depression of the artery into the lumen of the dilated vein above or below its decussation. The symptom of crossover occurs in most patients with hypertension, even in the early stages of the disease. It depends on the expansion of the veins of the retina, on the contraction and rigidity of the arteries. It was believed that a different degree of its severity corresponds to the successive stages of the development of the disease, but later it was proved that all three degrees can occur already in the first stage of the disease.
The expansion of the retinal veins in hypertension is apparently associated with the state of hypoxia of their walls, caused by narrowing of the arterioles, and in some cases - with stagnation as a result of increased intracranial pressure.
Then, due to vascular changes, more severe symptoms appear from the fundus of the eye with hypertension - swelling of the retina (especially in the region of the optic nerve papilla), retinal hemorrhage, and the formation of special short yellowish spots. These changes are united by the term hypertensive retinopathy.
Previously, it was believed that retinopathy is inherent only in rapidly progressive forms of hypertension with symptoms of nephroangiosclerosis. It is now generally accepted that it can also occur with hypertension of the usual, slow course in the later stages. The more rapidly the disease proceeds, the more often retinopathy occurs.
There is no doubt that changes in the fundus of the eye in hypertension are caused by vascular disorders: spasms, increased permeability of their walls, as well as arteriolonecrotic and arteriolosclerotic changes in the retina - a direct result of a violation of vascular permeability. It is judged by the vagueness of the boundaries of the papilla of the optic nerve, especially from the temporal side, as well as by clouding of the retina (arterioles are visible only in certain areas). Usually there is a congestive optic papilla.
Outpourings of blood into the retina are located along the radii around the nipple, along the course of the vessels; they arise per diapedesin and are multiple. In addition, there are extensive hemorrhages resulting from retinal vein thrombosis due to increased intracranial pressure.
Spots in the retina were previously considered as a consequence of the deposition of lipids from the blood; it is now believed that they arise as a result of the deposition of proteinaceous masses. It is possible that white spots are the outcome of small hemorrhages. The assumption about the necrotic nature of such spots is refuted by observations.
Undoubtedly, spots in the retina are one of the manifestations of severe changes in the fundus of the eye in hypertension; they, like hemorrhages, lead to a significant visual impairment, and sometimes to loss of it; but in a number of patients, as the condition improves, the spots may decrease.
With a strong retina, detachment sometimes occurs. An equally serious complication of the disease is the so-called retinal artery embolism. This name is incorrect, since there is no embolus in the artery. We are talking about the most acute spastic contraction of the lumen of the artery, followed by retinal ischemia and loss of vision. In more favorable cases, it is soon restored, sometimes even completely. If the spasm of the central artery leads not only to ischemia, but also to atrophy and necrosis of the retina, blindness occurs. Thrombosis of the central artery is also possible, it is often combined with strokes.
After examining the fundus in hypertension, sometimes there is a need for more subtle methods for studying changes in retinal vessels. Such methods could contribute both to correct understanding of the pathogenesis and early diagnosis of the disease.
The article was prepared and edited by: surgeon
For citation: Nesterov A.P. Changes in the fundus of the eye in hypertension // BC. Clinical ophthalmology. 2001. No. 4. S. 131
Changes of the eye fundus in arterial hypertension
Nesterov A.P.
The article consists of the lecture for physicians and ophthalmologists. Symptoms of functional changes in the central retinal vessels, features of hypertonic angiosclerosis of retinal vessels, peculiarities of hypertonic retinopathy and neuroretinopathy are discussed in the article and recommendations for treatment of the hypertonic retinopathy are given.
The frequency of damage to the fundus in patients with hypertension (AH), according to various authors, varies from 50 to 95%. This difference is partly due to age and clinical differences in the studied group of patients, but mainly due to the difficulty of interpreting the initial changes in the retinal vessels in hypertension. Internists attach great importance to such changes in the early diagnosis of GB, determining its stage and phase, as well as the effectiveness of the therapy. The most interesting in this regard are the studies of R. Salus. Under the conditions of a well-organized experiment, he showed that the diagnosis of HD, made by him according to the results of ophthalmoscopy, turned out to be correct only in 70% of cases. Errors in diagnosis are associated with significant individual variations in retinal vessels in healthy individuals, and some of the variants (relatively narrow arteries, increased tortuosity of vessels, the “crossover” symptom) can be misinterpreted as hypertensive changes. According to the observations of OI Shershevskaya, with a single check of an unselected contingent of patients with GB, specific changes in the retinal vessels are not detected in 25-30% of them in the functional period of the disease and in 5-10% in the late phase of the disease.
Retinal and optic nerve vessels
The central retinal artery (CAS) 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 the thinning (from 20 to 10 microns) of all its layers. Within the eye, the CAC divides repeatedly dichotomously. Starting from the second bifurcation, the branches of the CAS lose their characteristic features of the arteries and turn into arterioles.
The supply of the intraocular part of the optic nerve is carried out mainly (with the exception of the neuroretinal layer of the optic disc) from the posterior ciliary arteries. Posterior to the cribriform plate of the sclera, the optic nerve is supplied with centrifugal arterial branches coming from the CAC and centropetal vessels coming from the ophthalmic artery.
The capillaries of the retina and optic disc have a lumen with a diameter of about 5 microns. They start from precapillary arterioles and join into venules. The endothelium of the capillaries of the retina and the 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 ONH is the central retinal vein (CRV).
The adverse effect of various factors on the retinal circulation is smoothed out due to vascular autoregulation, which ensures optimal blood flow using local vascular mechanisms. Such blood flow ensures the normal course of metabolic processes in the retina and optic nerve.
Pathomorphology of retinal vessels in GB
Pathological changes in the initial transient stage of the disease are hypertrophy of the muscle layer and elastic structures in small arteries and arterioles. Stable arterial hypertension leads to hypoxia, endothelial dysfunction, plasma impregnation of the vascular wall, followed by hyalinosis and arteriolosclerosis. In severe cases, fibrinoid necrosis of arterioles is accompanied by thrombosis, hemorrhages and microinfarctions of the retinal tissue.
Retinal vessels in GB
Two vascular trees are clearly visible in the fundus: arterial and venous. It is necessary to distinguish: (1) the severity of each of them, (2) branching features, (3) the ratio of the caliber of arteries and veins, (4) the degree of tortuosity of individual branches, (5) 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 CAS, refraction, and the state 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. In hypermetropia, retinal vessels appear wider and brighter on ophthalmoscopy than in emmetropia, while in myopia they become paler. Age-related thickening of the vascular wall makes small branches less noticeable, and the arterial tree of the fundus in the elderly looks depleted.
With GB, 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 (Fig. 4, 1, 5). It should be noted that in some cases, provided that the elasticity of the vessels is preserved, in patients with HD, not only venous, but also arterial plethora is observed. Changes in the arterial and venous vascular bed are also manifested in a change in the arterio-venous ratio of retinal vessels. Normally, this ratio is approximately 2:3; in patients with HD, it often decreases due to narrowing of the arteries and dilation of the veins (Fig. 1, 2, 5).
Narrowing of the retinal arterioles in GB is not an obligatory symptom. According to our observations, a pronounced narrowing, which can be determined clinically, occurs only in half of the cases. Quite often only separate arterioles are narrowed (fig. 2, 5). Characterized by the unevenness of this symptom. It is manifested by the asymmetry of the state of the arteries in paired eyes, the narrowing of only individual vascular branches, and the uneven caliber of the same vessel. In the functional phase of the disease, these symptoms are caused by unequal tonic contraction of blood vessels, in the sclerotic phase - by uneven thickening of their walls.
Much less often than the narrowing of the arteries, with GB their expansion 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 the form of an uneven chain with swellings and interceptions (Fig. 5, 7, 9).
One of the frequent symptoms of hypertensive angiopathy is a violation of the normal branching of the retinal arteries. Arteries usually 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 a right and even obtuse angle (“bull horns symptom”, Fig. 3). The greater the branching angle, the greater the resistance to blood flow in this zone, the stronger the tendency to sclerotic changes, thrombosis and disruption of the integrity of the vascular wall. High arterial pressure and large pulse amplitude are accompanied by an increase not only in lateral, but also in longitudinal stretching of the vascular wall, which leads to elongation and tortuosity of the vessel (Fig. 5, 7, 9). In 10-20% of patients with GB, there is also a tortuosity of the perimacular venules (Gvist's symptom).
Essential for the diagnosis of hypertonic fundus is the symptom of the Gunn-Salus chiasm. The essence of the symptom lies in the fact that at the site of intersection with the compacted artery of the venous vessel, a partial squeezing of the latter occurs. There are three clinical degrees of this symptom (Fig. 4). The first degree is characterized by a narrowing of the lumen of the vein under the artery and near the junction of the vessels. A feature of the second degree is not only partial squeezing of the vein, but also its displacement to the side and into the thickness of the retina (“arc symptom”). The third degree of decussation of the vessels is also characterized by a symptom of the arch, but the vein under the artery is not visible and seems to be completely compressed. The symptom of decussation and venous compression is one of the most frequent in GB. However, this symptom can also be found in retinal arteriosclerosis without vascular hypertension.
Symptoms pathognomonic for retinal arteriosclerosis in HD include the appearance of side bands (“cases”) along the vessel, symptoms of “copper” and “silver” wire (Fig. 5). The appearance of white side stripes is explained by the thickening and decrease in the transparency of the vascular wall. The streaks are visible along the edge of the vessel, as there is a thicker wall layer and a thinner layer of blood compared to the central part of the vessel. At the same time, the light reflection from the anterior surface of the vessel becomes wider and less bright.
Symptoms of copper and silver wire (terms proposed by M. Gunn in 1898) are interpreted ambiguously by various authors. We adhere to the following description of these symptoms. The symptom of copper wire 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 plasma impregnation of the vascular wall with lipoid deposits. The 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 to be completely empty.
Retinal hemorrhages
Hemorrhages in the retina in GB occur by diapedesis of erythrocytes through the altered wall of microvessels, rupture of microaneurysms and small vessels under the influence of high pressure or as a consequence of microthrombosis. Especially often hemorrhages occur in the layer of nerve fibers near the optic disc. In such cases, they look like radial strokes, stripes or flames (Fig. 9). In the macular zone, hemorrhages are located in the layer of Henley and have a radial arrangement. Much less often, hemorrhages are found in the outer and inner plexiform layers in the form of irregularly shaped spots.
Retinal "exudates"
For GB, the appearance of soft exudates resembling cotton wool is especially characteristic. These greyish-white, loose-looking anteriorly protruding lesions appear predominantly in the parapapillary and paramacular zones (Fig. 8, 9). They arise quickly, reach their 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 section 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 congestive discs, diabetic retinopathy, CVD occlusion, and some other retinal lesions in which necrotic processes develop in arterioles.
Unlike cotton-wool lesions, hard exudates in GB have no prognostic value. They can be punctate and larger, rounded or irregular in shape (Fig. 7, 8), located in the outer plexiform layer and consist of lipids, fibrin, cellular debris and macrophages. It is believed that these deposits result from the release of plasma from small vessels and the subsequent degeneration of tissue elements. In the macular region, solid lesions are banded and radially arranged, forming a complete or incomplete star figure (Fig. 8, 9). They have the same structure as other solid foci. With the improvement of the patient's condition, the figure of the star may resolve, but this process takes a long time - for several months or even several years.
Edema of the retina and optic disc
Edema of the retina and optic disc, combined with the appearance of soft foci, indicates a severe course of GB (Fig. 7, 9). Edema is localized mainly in the peripapillary zone and along the large vessels. With a high content of proteins in the transudate, the retina loses its transparency, becomes grayish-white, and the vessels are sometimes covered with edematous tissue. Edema of the optic disc can be expressed in varying degrees - from a slight blurring of its contour to a picture of a developed congestive disc. A congestive disc in GB is often associated with peripapillary retinal edema, retinal hemorrhages, and cotton wool lesions (Fig. 9).
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 isopters and the boundaries of the field of view, as well as an expansion of the "blind spot". With severe retinopathy, scotomas can be detected, localized in the paracentral region of the visual field.
Visual acuity decreases much less frequently: with ischemic maculopathy, macular hemorrhages, with the occurrence of edematous maculopathy and with the formation of an epiretinal membrane in the late stage of neuroretinopathy.
Classification
hypertonic fundus changes
Currently, there is no generally accepted classification of hypertensive angioretinopathy. In Russia and neighboring countries (the former republics of the USSR), the most popular classification is M.L. Krasnov and its modifications. M.L. Krasnov singled out three stages of fundus changes in HD:
1. hypertensive angiopathy, characterized only by functional changes in the retinal vessels;
2. hypertensive angiosclerosis;
3. hypertensive retinopathy and neuroretinopathy, in which not only the vessels are affected, but also the retinal tissue, and often the optic disc.
The author divided retinopathy into 3 subgroups: sclerotic, renal and malignant. The most severe changes in the retina are observed in renal and especially malignant forms of HD (Fig. 9).
The stages of GB and the prognosis for the life of the patient 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 retinal hemorrhages, the appearance of areas of ischemia, non-perfused areas, cotton-like exudates, as well as a pronounced edema of the optic disc, peripapillary retina indicate a 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 in treating the underlying disease. To reduce retinal ischemia, vasodilators are used, which mainly dilate the vessels of the brain and eyes (trental, cavinton, ksavin, stugeron). Oxygen inhalation is often used to reduce hypoxia. However, oxygen can cause retinal vasoconstriction. Therefore, we prefer to prescribe inhalations of carbogen, which, in addition to oxygen, contains carbon dioxide (5-8%). Carbonic acid has a strong vasodilatory effect on the vessels of the brain and eyes. To improve the state of blood rheology and prevent the occurrence of thrombosis, antiplatelet agents are used. It should be borne in mind that the elimination of retinal ischemia can lead to the development of postischemic reperfusion syndrome, which consists in excessive activation of free radical processes and lipid peroxidation. Therefore, constant intake of antioxidants (alpha-tocopherol, ascorbic acid, veteron, diquertin) is essential. It is useful to prescribe angioprotectors, especially doxium. 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 is prescribed using a low-energy infrared diode laser.
Literature
1. Vilenkina A.Ya. // Collection of materials NIIGB im. Helmholtz. - M., 1954. - S. 114-117.
2. Katsnelson L.A., Forofonova T.I., Bunin A.Ya. // Vascular diseases of the eye. - M. 1990.
3. Komarov F.I., Nesterov A.P., Margolis M.G., Brovkina A.F. // Pathology of the organ of vision in general diseases. - M. 1982.
4. Krasnov M.L. // Vestn. ophthalmol. - 1948. - No. 4., S. 3-8.
5. Rokitskaya L.V. // Vestn. ophthalmol. - 1957. - No. 2. - S. 30-36.
6. Sidorenko E.I., Pryakhina N.P., Todrina Zh.M. // Physiology and pathology of intraocular pressure. - M. 1980. - S. 136-138.
7. Shershevskaya O.I. // Eye damage in some cardiovascular diseases. - M. 1964.
8. Harry J., Ashton N. // Trans. Ophthalmol. soc. UK. - 1963. - V. 83. - P. 71-80.
9. McLeod D. // Brit. J. Ophthalmol. - 1976. - V. - 60. - 551-556.
10 Walsh J.B. // Ophthalmology. - 1982. - V. - 89. - P. 1127-1131.
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 need the supervision of an ophthalmologist, as well as timely and correct correction of eye disorders.
HYPERTENSION, WHAT IS IT?
Hypertension is one of the most common diseases among the peoples of the world. As a special form of hypertension isolated 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 violation of the cortical and subcortical regulation of the vascular system as a result of a disorder of higher nervous activity, followed by the involvement of humoral factors in the pathogenetic mechanism.
STAGES OF HYPERTENSION?
In the course of hypertension, three stages are distinguished, 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, an increase in blood pressure and other symptoms of the disease (headache, dizziness, periodic visual disturbances, etc.) appear under certain conditions (especially after psycho-emotional overstrain) for a while, and then, under the influence of rest and treatment, the pressure returns to normal. However, already at this stage, angiospasms can be observed, both generalized and local (cerebral, coronary vessels).
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. In this period of the disease, organic changes in the vessels are already detected, in particular, the porosity of the vascular walls increases, dystrophic changes develop in organs and tissues.
Stage III especially phase B (decompensated), characterized by sharp dystrophic and sclerotic changes in organs and tissues (arteriologialinosis, arteriolonecrosis).
VARIANTS OF THE COURSE OF THE DISEASE?
Both functional and sclerotic changes in the vessels can develop in different organs not to the same extent, which causes various 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, cerebral vessels and, which is especially characteristic, of 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 lesions of the fundus in patients with hypertension, according to various authors, varies from 50% to 95%.
The first manifestations of changes are the narrowing of the arteries and the expansion of the veins of the retina. In places of arteriovenous intersection, 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 walls of the retinal arteries occurs, which eventually leads to their desolation due to stenosis of the lumen. Such changes are called copper and silver wire symptoms.
CAN THERE BE HEMORRHAGES INTO THE RETINA?
As a result of the release of erythrocytes through the stretched and defective capillary wall in hypertensive patients, small hemorrhages (hemorrhages) may occur in the retina. In addition, hemorrhages are characteristic of ruptures of small vessels, capillaries or microaneurysms.
In some cases, only the inner part of the vessel wall is torn and the blood, impregnating the vascular wall, forms a kind of case.
Vessel ruptures are associated with the action of three factors: an increase in blood pressure, a decrease in the elasticity of the vascular wall, a change in the state of the blood (an increase in its viscosity).
Especially often hemorrhages are found near the optic disc in the layer of nerve fibers.
Banded hemorrhages in the area around the optic nerve are especially characteristic of hypertension. Hemorrhages in the peripheral parts are also not uncommon, but they are considered as a sign of arteriosclerosis, developing either independently, or as a consequence of hypertension.
WHAT IS SOFT EXUDATE ON THE EYE?
In addition to hemorrhages, hypertensive retinopathy is characterized by the appearance of formations called exudates on the fundus.
These are grayish-white in color, loose in appearance, with somewhat fuzzy contours, protruding foci appear mainly 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. When the cotton-wool focus is resorbed, it decreases in size and flattens. At the same time, hemorrhages and red dots - microaneurysms are often found at the site of the focus. 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 heart attacks in the fundus.
The detection of this symptom is a reason for taking very active measures, since this indicates that similar pathological processes can occur in other target organs, which is already a threat to the patient's life.
WHAT IS A SOLID EXUDATE ON THE EYE?
Another type of formations in the fundus of the eye in hypertensive patients - "hard" foci do not have such an important prognostic value, although they indicate a far-reaching process.
It is believed that these deposits result from the release of plasma from small vessels and the subsequent degeneration of tissue elements. In the macular region, solid foci are banded and radially arranged, forming a complete or incomplete star figure. With the improvement of the patient's condition, the figure of the star may resolve, but this process is very slow, over several months or even years.
CAN THERE BE A RETINA AND OPTIC NERVE Swelling?
Edema of the retina and optic nerve head is one of the important symptoms of hypertensive retinopathy. Edema is localized mainly in the peripapillary zone and along the 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 its transparency, becomes grayish-white, and the vessels are covered with edematous tissue in places.
Edema of the optic disc can be expressed in varying degrees - from a slight blurring of its contour to a picture of a developed congestive disc. In the latter case, the prognosis is serious, especially if such a picture is combined with cotton-like exudates in the retina, hemorrhages, and clouding of the peripapillary retina. However, if the treatment of arterial hypertension is effective, disc edema and other symptoms of neuroretinopathy gradually disappear.
VISUAL FUNCTIONS IN HYPERTENSION?
A decrease in 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 field of view, as well as an expansion of the blind spot. With severe retinopathy, scotomas can be detected, often localized in the paracentral region.
Visual acuity decreases much less frequently: with ischemic lesions of the macula, with macular hemorrhages, with extravasation of fluid into the macular area 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 EYE
Currently, 4 degrees of vascular changes in the retina are usually distinguished in arterial hypertension.
1.HYPERTONIC ANGIOPATHY OF THE RETINA
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 tortuosity of the vessels in the paramacular region, decussation (I degree), uneven caliber of the arteries
2. HYPERTENSION ARTERIOSCLEROSIS OF THE RETINA
The symptoms described above, as well as the accompanying stripes and a wide reflex on the arteries, symptoms of decussation, copper and silver wire. Hard lesions and single hemorrhages are also possible.
3. EARLY HYPERTENSION NEURORETINOPATHY
Symptoms of angiopathy (see point 1), edema of the optic disc and peripapillary retina, hemorrhages, cotton-wool and hard lesions
4. LATE HYPERTENSION NEURORETINOPATHY
Symptoms of hypertensive arteriosclerosis (see paragraph 2) in combination with edema of the optic disc and peripapillary retina, cotton-wool lesions, hard exudates and hemorrhages. Sometimes symptoms of epithelial fibrosis in the posterior pole of the eye, collapse and destruction of the vitreous.
PROGNOSIS FOR VISION IN HYPERTENSION
The stage of hypertension and the prognosis for the life of the patient 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 correlation between them. In any case, multiple retinal hemorrhages, the appearance of areas of ischemia and cotton-like exudates, as well as pronounced edema of the optic disc and peripapillary retina indicate a severe progressive nature of the disease and the need to change and intensify therapeutic measures.
Modern therapeutic agents allow in many cases to achieve a 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 captures various organs, especially the kidneys. Changes in the arterial vessels of the kidneys lead not only to a violation of their functions, but also to the release of pressure-increasing substances, and, consequently, to a further increase in vascular tone. Thus, a vicious circle arises, causing a malignant course of the disease. It should be noted that modern methods of treatment allow in many cases to stop or slow down the progression of the disease, but the prognosis for malignant hypertension always remains serious.
The disease often begins at the age of 30-50 years, but it 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 vessels is possible.
In typical cases, changes in the fundus are very pronounced, like 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 edema of the retina), pronounced narrowing of the arteries and dilation of the veins, pinpoint and streaked hemorrhages, exudative foci, especially cotton-wool foci and macular star figure. The lesion to some extent captures the entire fundus of the eye, but is especially pronounced in its posterior section. Often in the back of the vitreous body you can see hemorrhages, flaky opacities and destructive changes.
Functional changes are relatively small and consist in the expansion of the blind spot, the appearance of separate scotomas and the concentric narrowing of the visual field.
It should be noted that the picture of neuroretinopathy described above is a frequent but not obligatory finding in malignant arterial hypertension. In some patients who died from this disease, there were no noticeable changes in the fundus. Individual symptoms of neuroretinopathy, especially the figure of a macular star, may be absent. At the same time, a pronounced picture of neuroretinopathy can be combined with a satisfactory general condition and undergo regression. 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 HYPERTENSION NEURORETINOPATHY?
Therapy of hypertensive neuroretinopathy consists primarily in the treatment of the underlying disease. To reduce retinal ischemia, vasodilators are used, which mainly dilate the vessels of the brain and eye (trental, cavinton).
Many authors recommend oxygen therapy. However, oxygen can cause narrowing of the retinal arteries. Therefore, we prefer to use carbogen inhalations, which, in addition to oxygen, contain carbon dioxide (5-8%). Carbonic acid has a strong vasodilating effect on the 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 retinal hemorrhages, ascorbic acid with rutin is prescribed. More effective in such cases is etamsylate, which also has an angioprotective effect. It is useful to prescribe an angioprotector, especially calcium dobesilate.
For resorption of hemorrhages and transudate, electrophoresis with lidase, papain or other proteolytic enzymes is used. It is useful to prescribe vitamins (A, group B, E), especially in cases where the patient has a reduced 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 reduced appetite) or endogenous hypovitaminosis develop.
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 need the supervision of 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. As a special form of hypertension isolated a little more than half a century ago.
According to scientists, hypertension is a kind of neurosis of 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 violation of the cortical and subcortical regulation of the vascular system as a result of a disorder of higher nervous activity, followed by the involvement of humoral factors in the pathogenetic mechanism.
Stages of hypertension
In the course of hypertension, three stages are distinguished, 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, an increase in blood pressure and other symptoms of the disease (headache, dizziness, periodic visual disturbances, etc.) appear under certain conditions (especially after psycho-emotional overstrain) for a while, and then, under the influence of rest and treatment, the pressure returns to normal. However, already at this stage, angiospasms can be observed, both generalized and local (cerebral, coronary vessels).
Stage II, phase A (labile)- the disease proceeds, 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) characterized by a relatively stable and often significant increase in blood pressure. In this period of the disease, organic changes in the vessels are already detected, in particular, the porosity of the vascular walls increases, dystrophic changes develop in organs and tissues.
Stage III, especially phase B (decompensated), is characterized by sharp dystrophic and sclerotic changes in organs and tissues (arteriologialinosis, arteriolonecrosis).
Variants of the course of the disease?
Both functional and sclerotic changes in the vessels can develop in different organs not to the same extent, which causes various 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, cerebral vessels and, which is especially characteristic, of the kidneys and eyes.
The eye and hypertension?
Major changes from organ of vision in hypertension occur in the fundus and can be assessed by ophthalmoscopy.
The frequency of lesions of the fundus in patients with hypertension, according to various authors, varies from 50% to 95%.
The first manifestations of changes are the narrowing of the arteries and the expansion of the veins of the retina. In places of arteriovenous intersection, 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 walls of the retinal arteries occurs, which eventually leads to their desolation due to stenosis of the lumen. Such changes are called copper and silver wire symptoms.
Can there be hemorrhages in the retina?
As a result of the release of erythrocytes through the stretched and defective capillary wall in hypertensive patients, small hemorrhages (hemorrhages) may occur in the retina. In addition, hemorrhages are characteristic of ruptures of small vessels, capillaries or microaneurysms.
In some cases, only the inner part of the vessel wall is torn and the blood, impregnating the vascular wall, forms a kind of case.
Vessel ruptures are associated with the action of three factors: an increase in blood pressure, a decrease in the elasticity of the vascular wall, a change in the state of the blood (an increase in its viscosity).
Especially often hemorrhages are found near the optic disc in the layer of nerve fibers.
Banded hemorrhages in the area around the optic nerve are especially characteristic of hypertension. Hemorrhages in the peripheral parts are also not uncommon, but they are considered as 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 on the fundus.
These are grayish-white in color, loose in appearance, with somewhat fuzzy contours, protruding foci appear mainly 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. When the cotton-wool focus is resorbed, it decreases in size and flattens. At the same time, hemorrhages and red dots - microaneurysms are often found at the site of the focus. 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 heart attacks in the fundus.
The detection of this symptom is a reason for taking very active measures, since this indicates that similar pathological processes can 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 formations on the fundus of the eye in hypertensive patients - "hard" foci do not have such an important prognostic value, although they indicate a far advanced process.
It is believed that these deposits result from the release of plasma from small vessels and the subsequent degeneration of tissue elements. In the macular region, solid foci are banded and radially arranged, forming a complete or incomplete star figure. With the improvement of the patient's condition, the figure of the star may resolve, but this process is very slow, over several months or even years.
Can there be swelling of the retina and optic nerve?
Edema of the retina and optic disc- one of the important symptoms of hypertensive retinopathy. Edema is localized mainly in the peripapillary zone and along the 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 its transparency, becomes grayish-white, and the vessels are covered with edematous tissue in places.
Optic disc edema can be expressed to varying degrees - from a slight blurring of its contour to a picture of a developed-stagnant disk. In the latter case, the prognosis is serious, especially if such a picture is combined with cotton-like exudates in the retina, hemorrhages, and clouding of the peripapillary retina. However, if the treatment of arterial hypertension is effective, disc edema and other symptoms of neuroretinopathy gradually disappear.
How do visual functions behave in hypertension?
A decrease in dark adaptation is one of the earliest functional signs in hypertensive angiopathy and retinopathy.
At the same time, there is a moderate narrowing the boundaries of the field of view, as well as widening the blind spot. With severe retinopathy, scotomas can be detected, often localized in the paracentral region.
Visual acuity decreases much less frequently: with ischemic lesions of the macula, with macular hemorrhages, with extravasation of fluid into the macular area 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, 4 degrees of vascular changes in the retina are usually distinguished in arterial hypertension.
1. HYPERTONIC ANGIOPATHY OF THE RETINA
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 tortuosity of the vessels in the paramacular region, decussation (I degree), uneven caliber of the arteries
2. HYPERTENSION ARTERIOSCLEROSIS OF THE RETINA
The symptoms described above, as well as the accompanying stripes and a wide reflex on the arteries, symptoms of decussation, copper and silver wire. Hard lesions and single hemorrhages are also possible.
3. EARLY HYPERTENSION NEURORETINOPATHY
Symptoms of angiopathy (see point 1), edema of the optic disc and peripapillary retina, hemorrhages, cotton-wool and hard lesions
4. LATE HYPERTENSION NEURORETINOPATHY
Symptoms of hypertensive arteriosclerosis (see paragraph 2) in combination with edema of the optic disc and peripapillary retina, cotton-wool lesions, hard exudates and hemorrhages. Sometimes symptoms of epithelial fibrosis in the posterior pole of the eye, collapse and destruction of the vitreous.
What is the prognosis for vision in hypertension?
The stage of hypertension and the prognosis for the life of the patient 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 correlation between them. In any case, multiple retinal hemorrhages, the appearance of areas of ischemia and cotton-like exudates, as well as pronounced edema of the optic disc and peripapillary retina indicate a severe progressive nature of the disease and the need to change and intensify therapeutic measures.
Modern therapeutic agents allow in many cases to achieve a 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 captures various organs, especially the kidneys. Changes in the arterial vessels of the kidneys lead not only to a violation of their functions, but also to the release of pressure-increasing substances, and, consequently, to a further increase in vascular tone. Thus, a vicious circle arises, causing a malignant course of the disease.
It should be noted that modern methods of treatment allow in many cases to stop or slow down the progression of the disease, but the prognosis for malignant hypertension always remains serious.
The disease often begins at the age of 30-50 years, but it 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 vessels is possible.
In typical cases, changes in the fundus are very pronounced, like 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 edema of the retina), pronounced narrowing of the arteries and dilation of the veins, pinpoint and streaked hemorrhages, exudative foci, especially cotton-wool foci and macular star figure.
The lesion to some extent captures the entire fundus of the eye, but is especially pronounced in its posterior section. Often in the back of the vitreous body you can see hemorrhages, flaky opacities and destructive changes.
Functional changes are relatively small and consist in the expansion of the blind spot, the appearance of separate cattle and concentric narrowing of the field of view.
It should be noted that the picture of neuroretinopathy described above is a frequent but not obligatory finding in malignant arterial hypertension. In some patients who died from this disease, there were no noticeable changes in the fundus. Individual symptoms of neuroretinopathy, especially the figure of a macular star, may be absent.
At the same time, a pronounced picture of neuroretinopathy can be combined with a satisfactory general condition and undergo regression. 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 of hypertensive neuroretinopathy consists primarily in the treatment of the underlying disease. To reduce retinal ischemia, vasodilators are used, which mainly dilate the vessels of the brain and eye (trental, cavinton).
Many authors recommend oxygen therapy. However, oxygen can cause narrowing of the retinal arteries. Therefore, we prefer to use carbogen inhalations, which, in addition to oxygen, contain carbon dioxide (5-8%). Carbonic acid has a strong vasodilating effect on the 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 retinal hemorrhages, ascorbic acid with rutin is prescribed. More effective in such cases is etamsylate, which also has an angioprotective effect. It is useful to prescribe an angioprotector, especially calcium dobesilate.
For resorption of hemorrhages and transudate, electrophoresis with lidase, papain or other proteolytic enzymes is used. It is useful to prescribe vitamins (A, group B, E), especially in cases where the patient has a reduced 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 reduced appetite) or endogenous hypovitaminosis develop.
Article from the appendix to the book: .
Unfortunately, hypertension (hypertensive disease or arterial hypertension) is a very common disease of the cardiovascular system, characterized by a gradual increase in blood pressure (from 140/90 mm Hg and above). Hypertension is fraught with the fact that due to high blood pressure, the risk of premature death of the patient increases significantly. The most common complications of hypertension are damage to the heart (myocardial infarction), brain (stroke) and kidneys (renal failure).
However, few people know that high blood pressure has a very detrimental effect on vision: in 80% of hypertensive patients, the blood vessels of the retina are affected and hypertensive retinopathy develops. Here is what the retinas of a healthy person and a person with hypertensive retinopathy look like:
In the initial stages of hypertension, a person usually does not observe any deterioration in vision. Pathological changes in the blood vessels of the retina are detected only with a thorough examination of the fundus by an ophthalmologist using a special device.
However, as hypertension progresses, further deterioration of the retinal vascular network is manifested by the appearance of "flies" before the eyes, objects begin to blur, vision deteriorates (especially at night). Sometimes a red veil is observed, which indicates that under the influence of constant high pressure, the delicate capillaries of the retina do not withstand and burst, causing hemorrhages:
A very thin and delicate retina (it is like newsprint in thickness), weakened by hypertensive retinopathy, sometimes does not withstand and exfoliates and / or breaks, which manifests itself in visual impairment, narrowing of the visual field and the appearance of opaque dark spots on it.
Another manifestation of hypertension that is dangerous for vision is swelling of the optic disc due to the ingress of blood cells and plasma into the retina through weakened capillary walls:
Due to this edema, the transmission capacity of the optic nerve decreases, which contributes to an even greater deterioration in vision.
Hypertension over time leads to a qualitative change in the composition of the blood, which increases the risk of blood clots that clog blood vessels, disrupting blood circulation. If thrombosis (blockage by blood clots) of the veins or arteries of the retina occurs, then this is fraught with partial or complete loss of vision in this eye.
Well, perhaps the most serious threat to vision in hypertension is a stroke, which can lead to complete blindness if the optic nerve or visual center in the occipital region of the brain is disrupted.
It should be especially noted that the simultaneous exposure of the eyes to high blood pressure and sharply increases the risk of senile blindness.
In more detail about the stages (or stages) of the impact of high blood pressure on the human visual system, an experienced ophthalmologist tells in this video:
From the foregoing, a single correct conclusion follows: since high blood pressure is the cause of pathological changes in the retina, everything possible should be done to lower this pressure, and ideally, bring it back to normal.
How can I do that? And is it really possible to do it at all? Have you ever met people who followed the advice of doctors and got rid of hypertension forever? Most likely no.
Fortunately, there is a technique that helps to normalize blood pressure and get rid of hypertension naturally without the help of medications. The author of this technique is Nikolai Grigorievich Mesnik, a practicing doctor and a hypertensive patient in the past.
Nikolai Grigorievich called his method "psychophysical method". The secret of its effectiveness lies in the restoration of broken connections in the mechanisms of natural regulation of blood pressure (starting from the cerebral cortex and other structures of our body).
Evaluate the effectiveness of the methodology of Mesnik N.G. you can, following the recommendations from the video, where the author of the technique demonstrates simple tricks to lower blood pressure:
All the nuances of the psychophysical method Mesnik N.G. disclosed in his author's video course "HYPERTENSION - NO!":
I hope this article will help you keep your eyes healthy in the future by minimizing the negative impact of such a powerful factor as high blood pressure.
Be healthy and happy!
