Hypertensive and eye changes

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

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

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

When ophthalmoscopy determine the severity of atherosclerosis. Normally, the walls of the blood vessels of the retina are not visible when viewed, and only the blood column is visible, in 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 a symptom of "copper wire". When the fibrous changes completely cover the blood column, the vessel looks like a whitish tubule. This is a symptom of "silver wire".

The degree of severity of atherosclerosis is also determined by changes in the intersections of the arteries and veins of the retina. In healthy tissues, a blood column in the artery and vein is clearly seen in the intersection, 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 squeeze and unfold the vein. With changes in the first degree, there is a conical narrowing of the vein on either side of the artery; with changes in the second degree, the vein flexes in an S-shape and reaches the artery, changes direction, and then returns to its normal direction behind the artery. With changes of the third degree, the vein at the center of the cross becomes invisible. The visual acuity for all the above changes remains high. At the next stage of the disease, hemorrhages appear in the retina, which can be small-dotted (from the capillary wall) and dashed (from the arteriolar wall). With massive hemorrhage, blood breaks out of the retina into the vitreous. Such a complication is called hemophthalmia. Total hemophthalm often leads to blindness, since in the vitreous body the blood can not dissolve. Minor hemorrhages in the retina can gradually resolve. A sign of retinal ischemia is a "soft exudate" - cottonish whitish spots in a reticular rim. These are microinfarctions of the layer of nerve fibers, zones of ischemic edema, associated with the closure of the lumen of the capillaries.

With malignant hypertension, as a result of high blood pressure, fibrinous necrosis from the retina and optic nerve vessels develops. At the same time there is marked swelling of the optic nerve and mesh shell. Such people have reduced visual acuity, there is a defect in the field of vision.

In hypertensive disease, the vessels of the choroid are also affected. Choroidal vascular insufficiency is the basis for secondary exudative retinal detachment in toxicosis of pregnant women. In cases of eclampsia - a rapid increase in blood pressure - there is a generalized spasm of the arteries. The retina becomes "wet", there is a pronounced retinal swelling.

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

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

Identified in ophthalmoscopic examination, changes in some cases are the first symptoms of hypertensive disease and can help in establishing a diagnosis. Changes in the vessels of the retina in different periods of the underlying disease reflect its dynamics, help determine the stages of the development of the disease and make a prediction.

[1], [2], [3], [4], [5], [6], [7], [8],

Stages of changes in the vessels of the retina in hypertension

To assess changes in the fundus due to hypertension, the classification proposed by ML Krasnov is used, according to which three stages of changes in the retinal vessels are distinguished.

The first stage - hypertonic angiopathy - is typical for the first stage of hypertensive disease - the phase of functional vascular disorders. At this stage arteries narrowing and retinal veins widen, the ratio of the caliber of these vessels becomes 1: 4 instead of 2: 3, irregularity of the caliber and an increase in the tortuosity of the vessels are noted, a symptom of the arteriovenous intersection of the 1st degree (the Salus-Gunn symptom) can be observed. Sometimes (approximately 15% of cases) in the central parts of the retina there is a corkscrew sinuosity of small venules (Gvist's symptom). All these changes are reversible; when they normalize their blood pressure, they regress.

The second stage - hypertonic angiosclerosis of the retina - stage of organic changes. Unevenness of the caliber and lumen of arteries is noted, their crimp increases. In connection with the hyalinosis of the walls of the arteries, the central light strip (reflex along the vessel) becomes narrower, acquiring a yellowish shade, which gives the vessel a resemblance to a light copper wire. Later, it narrows even more and the vessel takes the form of a silver wire. Some vessels are completely obliterated and visible in the form of thin white lines. The veins are somewhat enlarged and tortuous. For this stage of arterial hypertension, a symptom of arteriovenous crosshair is a symptom of the Salus-Gunn). A sclerosed elastic artery crossing the vein pushes it down, causing the vein to slightly flex (Salus-Gunn I). In arteriovenous crosshairs of the second degree, the vein bend becomes distinctly visible, arcuate. It seems thinned in the middle (Salus-Gunn II). Later, the venous arch becomes invisible at the intersection of the artery and the vein disappears (Salus-Hun III). Vein bends can provoke thrombosis and hemorrhage. In the region of the optic nerve disk, newly formed vessels and microaneurysms can be observed. At the part of patients the disk can be pale, monophonic with a wax tint.

The stage of hypertonic angiosclerosis of the retina corresponds to the phase of steady increase in systolic and diastolic arterial pressure in hypertensive disease IIA and IIB stage.

The third stage is hypertensive angioretinopathy and neuroretinopathy. On the fundus, in addition to vessel changes, hemorrhages to the retina, edema and white foci resembling clots of cotton wool, as well as small white foci of exudation, sometimes with a yellowish tinge, appear ischemia. As a result of the disturbance of neuroretinal hemodynamics, the condition of the optic nerve disc changes, its swelling and border blurriness are noted. In rare cases, with severe and malignant hypertension, a picture of the stagnant optic nerve disk is observed, which necessitates differential diagnosis with a brain tumor.

The accumulation of small foci around the yellow spot form the figure of a star. This is a sign of a poor prognosis not only for sight, but for life.

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

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

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

The pathology of the cardiovascular system, including arterial hypertension, can cause acute circulatory disturbances in the retinal vessels.

Acute obstruction of the central artery of the retina

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

Spasm of the central artery of the retina and its branches in young people is a manifestation of vegetative disorders, and in elderly people there is an organic lesion of the vascular wall in connection with arterial hypertension, atherosclerosis, etc. For a few days and even weeks before the spasm, patients can complain about temporary fogging vision, the appearance of sparks, dizziness, headache, numbness of the fingers and toes. The same symptoms can occur with endarteritis, some poisoning, eclampsia, infectious diseases, with the introduction of anesthetics in the mucosa of the nasal septum, the removal of the tooth or its pulp. When ophthalmoscopy, the narrowing of all or individual branches of the central artery of the retina with ischemia is revealed. The obstruction of the trunk of the central artery of the retina arises suddenly, more often in the morning hours, and is manifested by a significant decrease in vision, up to complete blindness. The visual acuity can be preserved if one of the branches of the central artery of the retina is damaged. Defects are detected in the field of view.

[9], [10], [11], [12], [13], [14]

Embolism of the central artery of the retina

The embolism of the central artery of the retina and its branches is more often observed in young people with endocrine and septic diseases, acute infections, rheumatism, and trauma. When ophthalmoscopy of the fundus reveals characteristic changes in the central fossa of the cherry blot - a symptom of the "cherry bones". The presence of the spot is explained by the fact that in this area the retina is very thin and a bright red vascular membrane shines through it. The disc of the optic nerve gradually turns pale, and its atrophy sets in. In the presence of a ciliary regulating artery, which is an anastomosis between the central artery of the retina and the ciliary artery, there is additional blood flow in the area of the macula and the symptom of the cherry bones does not appear. Against the background of general retinal ischemia, the papillomacicular area of the fundus can be of normal color. In these cases, central vision is preserved.

With embolism of the central artery of the retina, vision is never restored. With a short-term spasm in young people, vision can return completely, with a prolonged same unfavorable outcome is possible. The prognosis of elderly and middle-aged people is worse than that of the young. When one of the branches of the central artery of the retina is blocked, the retinal ischemic edema develops along the affected vessel, the vision is only partially reduced, the corresponding field of vision falls out.

Treatment of acute obstruction of the central artery of the retina and its branches consists in the immediate administration of general and local vasodilators. Under the tongue is a tablet of nitroglycerin, under the skin - 1.0 ml of 10% caffeine solution, inhalation of amyl nitrite (2-3 drops on the cotton wool), retrobulbarno - 0.5 ml of 0.1% solution of atropine sulphate or prikol solution (10 mg per one administration, every day for several days), 0.3-0.5 ml of 15% solution of Complamine. Intravenous - 10 ml of a 2.4% solution of euphyllin, intramuscularly - 1 ml of a 1% solution of nicotinic acid as an activator of fibrinolysis, 1 ml of a 1% solution of dibazolum, 2 ml of a 2% solution of papaverine hydrochloride, 2 ml of 15% of complamine.

Intravenous 1% solution of nicotinic acid (1 ml), 40% glucose solution (10 ml), alternating with a 2.4% solution of euphyllin (10 ml) is also administered intravenously. If the patient has common diseases (cerebral blood flow disorders, myocardial infarction), anticoagulant therapy is indicated. When thrombosis of the central artery of the retina, resulting from endarteritis, retrobulbarno injections of fibrinolysin with heparin against intramuscular injection of heparin at a dose of 5000-10 000 ED 4-6 times a day under the control of blood clotting and prothrombin index. Then, anticoagulants of indirect action are administered inside - 0.03 ml of finylin 3-4 times in the first day, and then - once a day.

Inside take eufillin 0.1 g, papaverine 0,02 g, dibazol 0,02 g, but-spine to 0,04 g, nyheksin to 0.25 g 2-3 times a day, trental to 0.1 g 3 times a day.

Intramuscular injection of a 25% solution of magnesium sulfate 5-10 ml per injection was shown. Antisclerotic drugs (iodine preparations, methionine at 0.05 g, Misciliron 0.25 g 3 times a day), vitamins A, B ₆, B, ₂ and C are prescribed in usual doses.

[15], [16], [17], [18]

Central retinal vein thrombosis

Thrombosis of the central vein of the retina (CVC) occurs mainly in hypertensive disease, atherosclerosis, diabetes, more often in the elderly. In young people, the cause of venous thrombosis of the central vein of the retina may be general (influenza, sepsis, pneumonia, etc.) or focal (more often the disease of the paranasal sinuses and teeth) infection. Unlike acute obstruction of the central retinal artery, the central vein of the retina develops gradually.

In the stage of prethrombosis, the venous stasis appears on the fundus. The veins are dark, enlarged, convoluted, arterio-venous crossings are clearly pronounced. When performing angiographic studies, a slowing of the blood flow is recorded. When the thrombosis begins, the veins of the retina are dark, wide, tense, along the veins - transudative swelling of the tissue, on the periphery of the fundus in the course of the terminal veins there are pinpoint hemorrhages. In the active stage of thrombosis, there is a sudden deterioration, and then a complete decrease in vision. With ophthalmoscopy, the optic nerve disc is swollen, the borders are washed away, the veins are enlarged, convoluted and intermittent, often immersed in a swollen retina, arteries are narrowed, hemorrhages of different size and shape are observed.

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

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

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

If the veins of the retina are blocked in patients with essential hypertension, it is necessary to lower arterial 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 edema in the area of venous stasis and reduce extravasal pressure on intraocular vessels, ethacrylic acid is recommended at 0.05 g and diacarb 0.25 g twice daily for 5 days, as well as installation of a 2% solution of pilocarpine. Favorable action has plasma inogen. Parabulbarno enter heparin and corticosteroids, intravenously - reopolyglucin and trental, intramuscularly - heparin, the dose of which is set depending on the time of blood coagulation: it should be increased 2 times in comparison with the norm. Then apply anticoagulants of indirect action (Phenylinum, neodekumarin). Symptomatic agents recommend angioprotectors (prodektin, dicinone), drugs that improve microcirculation (komplamin, theonikol, trental, cavinton), spasmolytic drugs (papaverine, no-shpa), corticosteroids (retrobulbarno and conjunctivitis dexazone), vitamins, antisclerotic drugs. In late terms (2-3 months), laser coagulation of the affected vessels is performed using the results of fluorescent angiography.

[19], [20], [21], [22]