Hypertension and eye changes

With hypertension of any genesis, changes in the vessels of the fundus are observed. The degree of expression of these changes depends on the height of arterial pressure and the duration of hypertension. With hypertension, three stages of changes in the fundus area are distinguished, which successively replace each other:

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

At first, there is a narrowing of the arteries and expansion of the veins, and the walls of the vessels, primarily arterioles and precapillaries, gradually thicken.

Ophthalmoscopy determines the severity of atherosclerosis. Normally, the walls of the retinal blood vessels are not visible during examination, and only a column of blood is visible, along the center of which there is a bright light strip. 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 the "silver wire" symptom.

The severity of atherosclerosis is also determined by changes in the places of intersection of arteries and veins of the retina. In healthy tissues, a blood column in the artery and vein is clearly visible at the intersection, the artery passes in front of the vein, they intersect at an acute angle. As atherosclerosis develops, the artery gradually lengthens and, when pulsating, begins to squeeze and unfold 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 returns to its normal direction behind the artery. With third-degree changes, the vein in the center of the intersection becomes invisible. Visual acuity remains high with all of the above changes. At the next stage of the disease, hemorrhages appear in the retina, which can be fine-point (from the capillary wall) and streaky (from the arteriole wall). In case of massive hemorrhage, blood breaks through from the retina into the vitreous body. This complication is called hemophthalmos. Total hemophthalmos often leads to blindness, since the blood cannot be absorbed in the vitreous body. Small hemorrhages in the retina can gradually be absorbed. A sign of retinal ischemia is "soft exudate" - cotton-like whitish spots in the retinal rim. These are microinfarctions of the nerve fiber layer, zones 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 of the retinal vessels and optic nerve develops. In this case, pronounced edema of the optic nerve disc and retina is noted. Such people have decreased visual acuity, there is 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", there is pronounced retinal edema.

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

Currently, the diagnosis of "arterial hypertension" is established if the anamnesis indicates a stable increase in systolic arterial pressure (above 140 mm Hg) and/or diastolic pressure (above 90 mm Hg) (normal 130/85). Even with a slight increase in arterial 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 impaired, hypertrophy of the muscular layer of the vascular wall, local spasm of the arteries, congestion in the veins, and a decrease in the intensity of blood flow in the capillaries are noted.

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

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Stages of changes in the retinal vessels in arterial hypertension

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

The first stage - hypertensive angiopathy - is characteristic of stage I hypertension - the phase of functional vascular disorders. At this stage, the arteries narrow and the veins of the retina dilate, the ratio of the caliber of these vessels becomes 1:4 instead of 2:3, unevenness of the caliber and increased tortuosity of the vessels are noted, a symptom of arteriovenous crossing of the first degree (Salus-Gunn symptom) may be observed. Sometimes (in about 15% of cases) in the central parts of the retina there is a corkscrew tortuosity of small venules (Guist symptom). All these changes are reversible; when the arterial pressure is normalized, they regress.

The second stage is hypertensive angiosclerosis of the retina - the stage of organic changes. Unevenness of the caliber and lumen of the arteries is noted, their tortuosity increases. Due to hyalinosis of the arterial walls, the central light strip (reflex along the vessel) becomes narrower, acquires a yellowish tint, which makes the vessel look like a 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 slightly dilated and tortuous. This stage of arterial hypertension is characterized by the symptom of arteriovenous crossing - the Salus-Gunn symptom). The sclerotic elastic artery crossing the vein presses it down, as a result of which the vein slightly bends (Salus-Gunn I). With arteriovenous crossing of the II degree, the bend of the vein becomes clearly visible, arcuate. It appears thinned in the middle (Salus Gunn II). Later, the venous arch at the intersection with the artery becomes invisible, the vein seems to disappear (Salus Gunn III). The bends of the vein can provoke thrombosis and hemorrhages. Newly formed vessels and microaneurysms can be observed in the area of the optic nerve disc. In some patients, the disc can be pale, uniform in color with a waxy tint.

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

The third stage is hypertensive angioretinopathy and neuroretinopathy. In addition to changes in the vessels, hemorrhages in the retina, its edema and white foci similar to lumps of cotton wool, as well as small white foci of exudation, sometimes with a yellowish tint, and areas of ischemia appear on the fundus. As a result of the violation of neuroretinal hemodynamics, the state of the optic nerve disk changes, its edema and blurred boundaries are noted. In rare cases, with severe and malignant hypertension, a picture of congestion of the optic nerve disk is observed, in connection with which there is a need for differential diagnostics with a brain tumor.

The cluster of small foci around the macula forms a star shape. This is a sign of a bad prognosis not only for vision, but also for life.

The condition of the retinal vessels depends on the level of arterial pressure, the value of peripheral resistance to blood flow and to a certain extent indicates the state of the contractile ability of the heart. In arterial hypertension, the diastolic pressure in the central retinal artery increases to 98-135 mm Hg (with 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 the retinal vessels are usually limited to the angiospasm stage.

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

Cardiovascular pathologies, including arterial hypertension, can cause acute circulatory disorders in the retinal vessels.

Acute obstruction of the central retinal artery

Acute obstruction of the central retinal artery (CRA) and its branches may 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 degenerative changes in the retina and optic nerve.

Spasm of the central retinal artery and its branches in young people may be a manifestation of vegetative-vascular disorders, while in elderly people, organic damage to the vascular wall often occurs due to arterial hypertension, atherosclerosis, etc. Several days or even weeks before the spasm, patients may complain of temporary blurred vision, the appearance of sparks, dizziness, headache, numbness of the fingers and toes. The same symptoms may occur with endarteritis, some poisonings, eclampsia, infectious diseases, with the introduction of anesthetics into the mucous membrane of the nasal septum, tooth extraction 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, more 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 affected, visual acuity may be preserved. Defects are detected in the field of vision.

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Central retinal artery embolism

Embolism of the central retinal artery and its branches is more often observed in young people with endocrine and septic diseases, acute infections, rheumatism, and trauma. Ophthalmoscopy of the fundus reveals characteristic changes in the area of the central fossa - a cherry spot - the "cherry pit" symptom. The presence of the spot is explained by the fact that the retina in this area is very thin and the bright red vascular membrane shines 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 area of the macula lutea and the "cherry pit" symptom does not appear. Against the background of general retinal ischemia, the papillomacular area of the fundus may have a normal color. In these cases, central vision is preserved.

With embolism of the central retinal artery, vision is never restored. With a short-term spasm in young people, vision may return completely, but with a long-term spasm, an unfavorable outcome is possible. The prognosis in elderly and middle-aged people is worse than in 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 reduced only partially, and loss of the corresponding part of the visual field is observed.

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

1% nicotinic acid solution (1 ml), 40% glucose solution (10 ml) are also administered intravenously, alternating it with 2.4% euphyllin solution (10 ml). If the patient has general diseases (cerebrovascular accidents, myocardial infarction), anticoagulant therapy is indicated. In case of thrombosis of the central retinal artery caused by endarteritis, fibrinolysin with heparin is injected retrobulbarly against the background of intramuscular administration of heparin at a dose of 5000-10,000 U 4-6 times a day under the control of blood clotting and prothrombin index. Then indirect anticoagulants are prescribed orally - finilinum at 0.03 ml 3-4 times on the first day, and then - 1 time per day.

Take orally 0.1 g of euphyllin, 0.02 g of papaverine, 0.02 g of dibazol, 0.04 g of no-shpa, 0.25 g of nigexin 2-3 times a day, and 0.1 g of trental 3 times a day.

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

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Central retinal vein thrombosis

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

In the prethrombosis stage, venous congestion appears in the fundus. The veins are dark, dilated, tortuous, arteriovenous crossings are clearly visible. When performing angiographic studies, a slowdown in blood flow is recorded. With the onset of thrombosis, the retinal veins are dark, wide, tense, along the veins there is transudative edema of the tissue, on the periphery of the fundus along the terminal veins there are pinpoint hemorrhages. In the active stage of thrombosis, deterioration and then complete loss of vision occurs suddenly. During ophthalmoscopy, the optic nerve disc is edematous, the borders are washed out, the veins are dilated, tortuous and intermittent, often immersed in the edematous retina, the arteries are narrowed, hemorrhages of various sizes and shapes are observed.

In case of complete thrombosis, hemorrhages are located throughout the retina, and in case of branch thrombosis, they are localized only in the basin of the affected vessel. Thrombosis of individual branches most often occurs in the area of arteriovenous crossings. After some time, white foci are formed - accumulations of protein, degeneration. Under the influence of treatment, hemorrhages can partially resolve, as a result of which central and peripheral vision improves.

In the central zone of the fundus after complete thrombosis, newly formed vessels often appear, which have increased permeability, as evidenced by the free release of fluorescein during angiographic examination. Complications of the late period of thrombosis of the central retinal vein 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.

In case of retinal vein obstruction 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 tablet of clonidine, and to increase perfusion pressure in the vessels of the eye, reduce edema in the area of venous congestion and reduce extravasal pressure on the intraocular vessels, it is recommended to take ethacrynic acid at 0.05 g and diacarb at 0.25 g 2 times a day for 5 days, as well as instillations of a 2% solution of pilocarpine. Plasma inogen has a beneficial effect. Heparin and corticosteroids are administered parabulbarly, rheopolyglucin and trental intravenously, heparin 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 are used (phenylin, neodecoumarin). Symptomatic agents recommended include angioprotectors (prodectin, dicynone), drugs that improve microcirculation (complamin, theonikol, trental, cavinton), antispasmodic drugs (papaverine, no-shpa), corticosteroids (dexazone retrobulbar and under the conjunctiva), vitamins, and antisclerotic drugs. At later stages (after 2-3 months), laser coagulation of the affected vessels is performed using the results of fluorescent angiography.

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