Hypertensive retinopathy is a lesion of the retinal vessels against the background of a persistent increase in blood pressure in patients with hypertension. The main symptoms are visual impairment, increased visual fatigue, redness of the eyes, headache, the appearance of “floating opacities” and “flies” in front of the eyes. Pathology is diagnosed based on the results of ophthalmoscopy, visometry, tonometry, biomicroscopy. Patients are indicated for systemic hypotensive therapy and hypolipidemic agents. Additionally, retrobulbar administration of retinoprotectors and the appointment of vitamins of group C, A and B.
H35.0 Background retinopathy and retinal vascular changes
Hypertensive retinopathy is a widespread pathology that occurs everywhere. The disease was first described by the English ophthalmologist Marcus Gunn in 1898. Microscopic signs of retinal vascular lesions are detected in persons aged 40 years and older, even in the absence of a history of hypertension. Stages III and IV of the disease are diagnosed in 2-15% of patients suffering from hypertension. Specific changes in ophthalmoscopy in children with arterial hypertension are observed in 3-5% of cases. Men and women get sick with the same frequency.
The causes of the pathology are essential and symptomatic arterial hypertension. The main trigger factors include overweight, excessive salt intake, smoking, stress, low level of physical activity, alcohol abuse. There is a genetic predisposition to the occurrence of the disease. The risk group includes people with decompensated hypertension, heart disease, atherosclerosis, diabetes mellitus. Scientists have proved that the symptoms of hypertensive retinopathy are often found in patients suffering from senile dementia, but the trigger factors for the development of pathology in senile dementia could not be established.
The features of retinal hemocirculation largely depend on the indicators of systemic blood pressure. In the pathogenesis of the initial (vasoconstrictor) stage, an important role is assigned to vasospasm, which is combined with an increase in the tone of the arterioles of the retina of the eye. Arteriospasm is based on the launch of local autoregulatory reactions. Morphologically, the focal narrowing of arterioles is determined, which eventually transforms into generalized. Prolonged increase in pressure causes thickening of the inner layer (intima) and hyperplasia of the middle layer (media). Pathological changes in the intima-media complex progress very quickly.
In the pathogenesis of the sclerotic stage, the degeneration of hyaline fibers comes to the fore. Narrowing of arterioles and dilation of veins in certain areas leads to the formation of an arteriovenous intersection (Salus-Gun’s symptom). With the I degree of this symptom, the vein is depressed at the point of its intersection by the artery, the II degree – before the intersection, the vein forms an arc and sharply thinns under the artery, the III degree – in the center of the arcuate bend, the vein becomes invisible. Due to structural disorders in the arteriolar and venular junctions, the light reflex expands.
Involutional sclerosis potentiates a sharp narrowing of the arterioles. The vessels become pale and convoluted, resembling a “silver wire” (a positive symptom of Gwist). Necrosis of myocytes and endotheliocytes provokes retinal ischemia and increased permeability of the hematoretinal barrier, which is characteristic of exudative changes. With the atypical course of the disease, the stages of the process are disrupted, in the early stages it is possible to identify a number of changes (microaneurysms, hemorrhages), which normally occur only with pronounced arteriovenous intersections.
Currently, there are a large number of approaches to systematization of changes in the fundus in hypertensive retinopathy. The correlation between arterial hypertension and retinal damage is most accurately reflected in the Keith Wagener Barker Classification (KWB), developed back in 1939. Taking into account the clinical signs , the following stages of the disease are distinguished:
- Stage 1. The pathological process extends only to the vessels of the inner shell of the eye, the changes are reversible. There is a violation of the ratio of the diameter of veins and arteries due to the narrowing of the latter. Single arteriovenous intersections are determined, the Salus I symptom is positive.
- Stage 2. The initial signs of organic damage to the retina are revealed. The walls of retinal vessels are thickened, the light reflex is expanded. Due to the sealing of the vascular wall of the artery during ophthalmoscopy, they resemble copper or silver wire. In limited areas, zones of partial or complete obliteration of arterioles are visible.
- Stage 3. Symptoms of nerve fiber damage are added to the above-described manifestations. The ophthalmoscopic picture allows you to visualize plasmorrhagia and hemorrhages that spread to the posterior parts of the vitreous body. Accumulations of lipids have the appearance of yellowish “hard” exudates. Protein transudate is “soft”, grayish in color. In the area of ischemic retinal infarction, “cotton-like” foci are formed.
- Stage 4. The changes are irreversible. Marked progression of sclerotic vascular lesion is characteristic. Ophthalmoscopically visualized edema of the optic disc (OND). Degenerative changes can be traced from the inner shell of the eyeball. The risk of macular edema and retinal detachment is extremely high.
A long-term asymptomatic course is typical for the disease. The progression of pathology leads to deterioration of vision, redness of the eyes. Patients often complain of headache, increased fatigue with visual loads (reading, working at the computer, watching TV). At the III-IV stage of hypertensive retinopathy, the appearance of “flies” or “floating opacities” in front of the eyes is possible. With a sharp increase in blood pressure, photopsies and metamorphopsies are observed, which patients regard as signs of an “aura” before the onset of a hypertensive crisis.
The disease is very often complicated by subretinal hemorrhage, which can subsequently lead to retinal detachment. Choriopathy and optic neuropathy are progressing. In acute ischemic neuropathy, pronounced edema of OND occurs. In the severe course of the disease, signs of subatrophy of the optic nerve are traced. In the case of pronounced exudation, the pathological process affects the vitreous body, which provokes its turbidity. Patients with a history of hypertensive retinopathy are at risk of developing ocular migraine and ophthalmic hypertension.
In most cases, hypertensive retinopathy is an accidental diagnostic finding in individuals with a burdened history. Pronounced clinical symptoms are detected only in patients suffering from arterial hypertension or senile dementia for a long time. During physical examination, there are no changes on the part of the eyes. The main diagnostic methods are:
- Ophthalmoscopy. When examining the fundus in the central optical zone, local vasoconstriction in the OND region is visualized. The size of the lesion area is equal to half the diameter of the disc. Positive symptoms of Gwista and Salus I-III are determined.
- Measurement of intraocular pressure (IOP). Tonometry indicators slightly exceed the reference values. It is important to compare the data of systemic blood pressure with intraocular. Additionally, the study of the daily fluctuations of the IOP is shown.
- Visometry. There is no deterioration of visual functions in stage I-II of the disease. In patients with stage III-IV, visual acuity may decrease, but this phenomenon is caused by organic damage to the retina and the development of secondary complications.
- Examination of the anterior segment of the eye. With biomicroscopy of the eyeball, dilated vessels of the conjunctiva are determined. Persistent increase in blood pressure and frequent hypertensive crises lead to the formation of subconjunctival hemorrhages.
Etiotropic therapy is reduced to the appointment of systemic antihypertensive agents, the reception of which contributes to the normalization of blood pressure. With an increase in the level of low-density lipoproteins and blood cholesterol, the use of hypolipidemic agents with periodic monitoring of lipidogram indicators is indicated. Angioprotectors can be included in the treatment package, which improve retinal hemodynamics, prevent the development of ischemia. In order to accelerate the regeneration of retinal neurons, retrobulbar injections of retinoprotectors are prescribed. Additionally, vitamins A, C and B are recommended, which also have retinoprotective properties.
Prognosis and prevention
The outcome of the disease depends on the stage of the process. With the timely appointment of adequate treatment, the symptoms of the disease gradually regresses within 1 year. At the stage of sclerotic changes, it is almost impossible to influence retinal blood flow. Specific preventive measures have not been developed. Non-specific prevention includes monitoring and normalization of systemic arterial and intraocular pressure, blood lipids. In the presence of provoking factors, it is recommended to be examined by an ophthalmologist 4 times a year with mandatory ophthalmoscopy, visometry and IOP measurement.