Ophthalmohypertension - causes and treatment. Elevated IOP or ocular hypertension: symptoms of the disease and how it differs from glaucoma Ocular hypertension

Various eye diseases are becoming more common today. Vision problems affect people of different ages and social statuses. One of the most common ophthalmic ailments can be called ocular hypertension. This problem is characterized by an increase in eye pressure to levels greater than 27 millimeters of mercury. Most often, this problem is faced by older people or representatives of the middle age category.

It is important to note that there are two types of ocular hypertension:

• Symptomatic.
• Idiopathic (essential).

The first type of ocular hypertension does not apply to independent diseases. The disorder is only a symptom of some ophthalmic disease or disease of another organ system. Also, the cause of this problem can be exposure to toxic substances and a number of drugs.

Self-induced hypertension has an unclear etiology. It occurs most often in middle-aged and elderly people. It has not yet been possible to find out the exact causes of the development of the disease in any of the cases. It should be emphasized that this type of disorder, as it appears out of nowhere, is often able to disappear without a trace.

Features of symptomatic hypertension

Symptomatic variety of ophthalmohypertension is divided into several main types:

• Toxic - occurs against the background of acute or chronic poisoning with toxic substances.
• Corticosteroid - develops as a result of prolonged use of drugs of this group.
• Endocrine - occurs as a concomitant symptom of some diseases of the endocrine system. It is often diagnosed during menopause in women and in patients with severe forms of thyroiditis. Also, the disease is diagnosed with other serious disorders associated with the work of the endocrine glands.
• Ophthalmic uveal - develops against the background of some inflammatory processes of the eye. Often diagnosed with glaucoma, iridocyclitis, etc.
• Diencephalic - occurs as a concomitant symptom with serious disorders of certain parts of the brain.

Description of self-hypertension

Idiopathic, or, as it is commonly called, essential hypertension occurs for unclear reasons. However, doctors single out one of the hypothetical causes of such a pathology - this is the abundant content of the intraocular fluid during the period of normal intensity of the lacrimal outflow.

As a rule, the type of disorder under consideration is not accompanied by violations of the structure of the shell of the eye and a decrease in the quality of vision. It should be noted that with this type of disorder, there is a moderate increase in intraocular pressure up to 35 mm Hg. Patients with such a problem should be constantly monitored by an ophthalmologist, since in some cases (15-20%) such a disease creates a fertile ground for the development of glaucoma. With an uncomplicated course, this type of problem does not require the use of therapeutic measures.

Characteristic signs of pathology

Detecting any kind of ocular hypertension on your own is quite problematic. The fact is that the disorder does not have pronounced symptoms. The patient may not notice the presence of the problem for years. This is completely unsafe, because in some cases, ocular hypertension gives rise to the development of quite serious ophthalmic pathologies.

However, especially attentive people may still notice some minor changes in vision and sensation in the ocular surface area.

The described problem is characterized by the following manifestations:

• Decreased color clarity.
• Rapid eye fatigue.
• The occurrence of migraine-like pain.
• Increased lacrimation due to eye strain.

Many people attribute all of the above signs to banal fatigue and do not pay due attention to the problem. It is worth noting that in 25% of cases, these symptoms indicate the presence of eye pressure. Therefore, paying attention to such manifestations, especially if they are regular, you should definitely visit an ophthalmologist.

It is important to remember that eye pressure is often the cause of glaucoma. This disease, in turn, often ends in partial loss of vision or complete blindness.

Diagnostic methods and therapy

If you suspect any problems in terms of vision, you must definitely contact an ophthalmologist.

For the diagnosis of eye pressure, several main directions in ophthalmological research are used.

At the initial stage, examinations are carried out for the presence of glaucoma. If this ailment can be completely excluded, then the diagnosis under consideration is most often established.

To determine the presence of this problem, the doctor may resort to the following examination options:

• External examination and questioning for complaints.
• Checking the quality of visual acuity.
• Performing an ophthalmoscopy.
• The use of tonographic research.
• Implementation of various tests.
• Tomography.

The main emphasis in such an examination is on ophthalmoscopy. A modern ophthalmoscope allows you to examine the fundus in detail and detect characteristic changes. This gives great chances for timely detection of the problem and an accurate diagnosis. After the presence of intraocular pressure is confirmed, the doctor evaluates the nature of the course of the disease and tries to determine the exact causes. The latter is extremely important for the selection of an adequate method of therapy. For the treatment of symptomatic eye pressure, an important point is to eliminate the cause of the pathology. It is on this that the selection of effective means is based.

In cases where the problem is caused by increased tear secretion, the patient may be prescribed eye drops that increase the outflow of fluid or reduce the production of tear secretion. The choice of eye preparations is made taking into account all the features of the disease. Particular attention is paid to the hemodynamics of the patient's eyes.

A few words about prevention

Despite the fact that in many cases it is a benign type of intraocular pressure that is diagnosed, we should not forget that this problem is one of the leading factors leading to the development of a serious pathology (secondary glaucoma). Every person who pays attention to vision problems or discomfort in the cornea should visit a doctor. It is possible that the cause of the trouble has nothing to do with the disease described. But, you can be sure of this only by visiting a specialist.

Examination of the fundus with an ophthalmoscope takes only a few minutes. But this diagnostic method allows you to exclude or confirm the presence of this problem with a high degree of probability. Having spent quite a bit of your time, you can get an excellent chance for a quick and favorable relief of the development of serious ophthalmic diseases.

• Patients with a history of comorbidities.
• People who have seen but not confirmed signs of eye pressure.
• Representatives of the middle and elderly age group (after 40 years).
• People with a burdened heredity in terms of ophthalmic diseases.

It is important to remember that timely diagnosis eliminates or significantly reduces the risk of developing serious and sometimes irreversible problems.

14-12-2012, 19:50

Description

Dominant concept of ophthalmohypertension

Ophthalmohypertension is called anything non-glaucomatous increase in IOP. To date, the concept of ocular hypertension has not been finalized. The dominant concept that has developed over the past 20 years is discussed below. According to this concept, ophthalmohypertension syndrome can be diagnosed under the following conditions:

• the level of ophthalmotonus is outside the statistical norms (true IOP > 20 mm Hg);
• CPC is open;
• The optic disc and visual field do not have changes characteristic of glaucoma;
• such changes do not occur during long-term (long-term) observation.

Since the last point cannot always be fulfilled, it is usually ignored when diagnosing ophthalmohypertension. It follows that the diagnosis of glaucoma can only be established after the appearance of glaucomatous changes in the visual field or ONH.

The above concept has both strengths and weaknesses. Before considering them, let us dwell on the results of some specific studies.

J. Wilensky and J. Podos (975) reported the results of follow-up for 5-14 years in 50 persons with ocular hypertension. During this time, glaucomatous visual field changes appeared in 5 (5%) eyes out of 100.

Of 152 persons with ocular hypertension identified during a preventive examination in the city of Skovde, 14 (9.2%) had glaucoma within 10 years.

The benign hypertension of the eye is also evidenced by the fact that intraocular pressure tends to gradually decrease. For example, E. Linner (1973) noted a decrease in intraocular pressure by an average of 2.2 mm Hg. Art. for 10 years in 92 patients with ocular hypertension.

Criticism of the dominant concept

The above data indicate the advisability of separating ophthalmohypertension and glaucoma. At the same time, it should be noted that modern ideas about ocular hypertension are very vague and the criteria for diagnosing this condition, as well as the differential diagnosis of ophthalmohypertension and the initial stage of glaucoma, are unclear. Let us dwell on some controversial issues related to the concept of ocular hypertension.

1. As already noted, hypertension includes such cases when intraocular pressure, with a single or repeated measurement, exceeds the upper limit of the statistical norm. However, single, and often repeated pressure measurements can give a significant error even if the procedure is carried out flawlessly. This is due to the excitement of the subject in connection with the possibility of detecting a disease or an upcoming unpleasant procedure. An involuntary increase in the tone of the extraocular muscles of the eye and eyelids when the tonometer approaches the eye and the total arterial pressure due to the excitement of the subject in some cases can lead to an increase in intraocular pressure.
2. The maximum value of normal intraocular pressure is considered to be 20-21 mm Hg. Art. when measured with a Goldman tonometer (24 mm Hg according to Maklakov). This figure is obtained by adding the average value of ophthalmotonus (15-16 mm Hg) with twice the standard deviation (?) for young people (2.5 mm Hg). With this method of calculating the upper limit, about 2.5% of healthy young people are unjustifiably included in the group of patients with ophthalmohypertension.

   We consider it expedient to calculate the upper limit of the norm according to the formula: Pmax \u003d M ± 2.6?. In this case, only in 0.5% of healthy eyes the pressure will be higher than normal. In our opinion, one should take the values ​​of M and?, which are typical for the age group of 30-38 years. This age is closer to the one in which they suffer from glaucoma, but there are practically no glaucoma patients among people of this age. With this calculation method, the upper limit of normal intraocular pressure will not be 20, but 23.3 mm Hg. Art. (26 mm Hg according to the old tables for the Maklakov tonometer). Therefore, only a pressure of 24 mm Hg. Art. and above, can be considered as definitely increased, which, by the way, corresponds to the standards that are accepted in our country.

   Change in the upper limit of normal by 3 mm Hg. Art., as in the studies of foreign authors presented above, will lead to a decrease in the frequency of hypertension significantly more than times. This will significantly increase the incidence of glaucomatous changes in the optic nerve head and visual field in hypertension.

3. It is difficult to agree with ideas about glaucoma as a disease that always progresses rapidly and leads to changes in the optic nerve head and visual field. Our experience shows that the course of the glaucomatous process is very diverse. As for the duration of the period between the increase in pressure and the appearance of changes in the visual field, it varies over a wide range, the boundaries of which cannot be specified. In this regard, in some cases, hypertension of the eye, apparently, is the initial stage of glaucoma with a mild, benign course.
4. Most authors who have studied eye hypertension, for some reason, use this concept only in connection with primary open-angle glaucoma. It remains unclear what to do with other forms of glaucoma. In particular, is it possible to make a diagnosis of angle-closure glaucoma in those cases of blockade of the anterior chamber angle, when there are no changes in the optic disc and visual field? It is known that angle-closure glaucoma does not always have a progressive course and the disease is limited to prodromal attacks with a moderate increase in intraocular pressure, not accompanied by changes in either the visual field or the optic nerve head indefinitely, sometimes throughout the patient's life.

The same can be attributed to secondary glaucoma. Should the diagnosis of glaucoma be made in the case of traumatic recession of the anterior chamber angle, if intraocular pressure is constantly elevated in the normal state of the visual field?

These questions remain unanswered. Meanwhile, to be consistent, in the above cases, one should also make a diagnosis of ophthalmohypertension, and not glaucoma [Volkov VV et al., 1985].

Classification of ophthalmic hypertension

All cases of non-glaucomatous increase in IOP can be divided into three main groups:

• pseudohypertension of the eye;
• essential ophthalmic hypertension;
• symptomatic ocular hypertension.

As already noted, in some healthy people, IOP goes beyond the statistical standards. The frequency of such cases depends on the methodology for calculating the standards. In such people, a relatively high level of IOP is their individual norm. Pseudohypertension should also include a short-term increase in IOP during tonometry.

Essential ophthalmohypertension occurs for no apparent reason. Its frequency, like primary OAG, increases with age. Differential diagnosis of essential ophthalmohypertension and initial OOH is associated with great difficulties.

To symptomatic ophthalmic hypertension include a short-term or long-term increase in IOP, which occurs as one of the symptoms of non-glaucomatous diseases. Symptomatic hypertension should not be confused with either primary or secondary glaucoma. In primary glaucoma, an increase in IOP is not only a symptom of the disease, but also the most important link in its pathogenesis. In secondary glaucoma, an increase in IOP is not a symptom of the disease, but its consequence: after the treatment of the underlying disease, glaucoma persists. Secondary glaucoma occurs as a result of an organic lesion of the eye, causing a violation of the outflow of aqueous humor. Symptomatic hypertension is more often associated with hypersecretion of aqueous humor or a temporary violation of its outflow (edema of the trabeculae, exudate and blood in the APC).

Essential ophthalmohypertension

Essential ophthalmohypertension is characterized by moderate increase in IOP, open AUC, outflow indicators within the normal range, no changes in the optic disc and visual field during long-term follow-up (for several years).

Unlike glaucoma, the direct cause of an increase in IOP in essential hypertension is not a pathological blockade in the aqueous humor outflow system, but imbalance in age-related changes in its circulation in the eye[Nesterov A.P., 1982]. As you know, in old age, both the production of aqueous humor and the ease of its outflow decrease to approximately the same extent. Both processes balance each other, and IOP does not change significantly. Ophthalmohypertension occurs when changes in fluid outflow are not accompanied by corresponding changes in its production. In some cases, fluid hypersecretion may also be noted, apparently associated with hormonal disorders in the body [Suprun A. V., Rudinskaya G. M., 1974].

Thus, ophthalmohypertension occurs as a consequence relative or true hypersecretion of aqueous humor. It can be assumed that the high level of moisture production is due to a fairly intense blood circulation in the eye, the preservation of the ciliary epithelium, and the absence of noticeable metabolic disorders. This explains the high level of tolerant IOP and the absence of pronounced dystrophic changes in the anterior choroid in individuals with hypertension. According to S. N. Basinsky and I. N. Cherkasova (1984), the hemodynamic parameters of the eyes in patients with ophthalmohypertension are higher than in healthy people of the same age and in patients with initial OAG.

Age changes unlike pathological ones, they usually appear in both eyes, so changes in IOP with hypertension are also symmetrical in most cases. It should also be noted that the differences in age-related changes in the systems of production and outflow of moisture gradually decrease, as a result of which ophthalmohypertension has a stable or regressive course. E. Linner (1976) observed the condition of the eyes in 92 people with ophthalmohypertension without changes in the visual field and optic disc, who did not receive any treatment. During the observation period, IOP decreased by an average of 2.2 mm Hg. Art. by reducing moisture production by 25%. According to our data (40 people, observation for more than 8 years), hypertension had a stable course in 28 (35%) eyes out of 80 and regressed in 24 (30%), 14 people (28 eyes, 35%) developed glaucomatous changes in field of view and optic nerve.

Unlike hypertension in glaucoma, a decrease in the outflow of aqueous humor is more often observed. The pathological process is rarely perfectly symmetrical, therefore asymmetry in the condition of two eyes is a characteristic sign of glaucoma. A low level of aqueous humor production is associated with circulatory and metabolic disorders. Regardless of whether these disorders occur primarily or as a result of increased IOP, they cause a decrease in the level of tolerant IOP and often the occurrence of degenerative changes in the iris and ciliary body.

Differential diagnosis of ophthalmic hypertension and glaucoma

According to the above concept, ophthalmohypertension is characterized by a moderate increase in IOP, a mildly pronounced decrease in the ease of outflow (not lower than 0.10 mm / min per 1 mm Hg), a normal or increased level of moisture production, and the absence of noticeable dystrophic changes in the iris and ciliary body , a symmetrical condition of both eyes and a stable or regressive course.

OAGs are characterized violations of the outflow and production of aqueous humor, dystrophic changes in the anterior choroid, asymmetry in the condition of paired eyes, the progressive course of the disease. Pronounced pigmentation of the trabeculae, large size of the physiological excavation of the ONH (E/D? 0.6), especially in combination with the vertical oval shape of the excavation and the phenomenon of retraction of the temporal half of the ONH, are not typical for ophthalmohypertension. Well-defined water and laminar veins and their adequate response to eye compression indicate a good state of both production and outflow of aqueous humor, which is extremely rare in glaucoma.

To assess the totality of risk factors and the initial symptoms of the disease, methods based on mathematical analysis are proposed. Particularly promising is the use linear discriminant function. With its help, several diagnostic tables have been developed, oriented to the different equipment of medical institutions with diagnostic equipment [Abakumova L. Ya. et al., 1980]. For the most convenient tables in clinical practice, programs have been compiled that can easily be entered into microcalculators with a memory device [Cherkasova IN, Listopadova NA, 1987]. The use of microcalculators saves the doctor from calculations and reduces the time spent on processing the received data to 2-3 minutes. However, it must be emphasized that diagnostic tables allow only the degree of risk of developing glaucoma to be assessed and do not completely guarantee against errors in borderline cases. The final diagnosis is established by the doctor, not the microcalculator.

In practical work, the phased differential diagnosis of hypertension and glaucoma seems to be optimal. At the first stage after the discovery of elevated IOP rule out false hypertension, which is a consequence of the patient's excitement at the time of performing tonometry or the tonometrist's collision. If during the time spent on carrying out several repeated tonometry with an interval of several minutes, IOP normalizes, then hypertension can be attributed to false. At the same time, an entry is made in the outpatient card about the increased reaction of the patient to tonometry. Persons with false hypertension are not subject to treatment or special observation.

Second phase allows you to set an explicit OGG. At the same time, marginal excavation of the optic disc, or visual field defects characteristic of glaucoma, or both symptoms are detected.

Purpose of the third stage- Diagnosis of overt ophthalmohypertension. Criteria for such a diagnosis include symmetry in the state of both eyes, well-defined aquatic and laminar veins, values ​​of the coefficient of ease of outflow above 0.14 mm / min per 1 mm Hg. Art., the absence of noticeable dystrophic changes in the iris, severe pigmentation of the trabeculae and pseudoexfoliation, the normal state of the visual field and optic disc. IOP should not exceed 30 mm Hg. Art. Such patients should be observed for several years without any treatment.

Fourth stage especially difficult. Its goal is to identify initial OAG without visual field defects or with minor and indeterminate defects. Such a diagnosis can be established if an increase in IOP is associated with additional symptoms: the ease of outflow is below 0.10 mm / min per 1 mm Hg. Art., inadequate response of water veins to eye compression, pronounced dystrophic changes in the iris, the appearance of pseudoexfoliations, intense pigmentation of trabeculae, microsymptoms from the optic disc (flattening of the temporal half of the optic disc, vertical oval excavation, E/D? 0.6). The diagnosis of glaucoma becomes more reliable if a marked asymmetry is found in the state of fellow eyes or glaucoma is detected in blood relatives of the examined patient. Risk factors also include diabetes mellitus, severe atherosclerosis, and vascular hypotension. In cases that are not sufficiently clear in terms of diagnostics, it is advisable to establish a diagnosis of high-risk ophthalmohypertension. Such patients are prescribed medication, and sometimes laser treatment.

Fifth stage consists in the dynamic monitoring of individuals with ocular hypertension and ophthalmohypertension at increased risk. A progressive increase in IOP, the appearance or increase in the severity of other risk factors and microsymptoms make it possible to establish a diagnosis of glaucoma, and, conversely, a stable condition of the eyes for several years and especially a spontaneous decrease in IOP to a normal level give grounds to exclude glaucoma.

Symptomatic hypertension of the eye

As the name implies, an increase in IOP is one of the symptoms of a general or local disease. Symptomatic hypertension is usually temporary. The increase in pressure is caused either by an increase in the rate of production of aqueous humor, or by transient changes in the outflow of fluid (edema of the trabeculae, exudate in the angle of the anterior chamber, etc.). In some cases, hypertension disappears, despite the fact that the underlying disease persists, in others - only after it has been cured. However, the transition of symptomatic hypertension to secondary glaucoma is possible if irreversible changes occur in the drainage apparatus of the eye.

All varieties of symptomatic hypertension can be combined into the following main groups.

1. Uveal hypertension:
   • iridocyclitis with hypertension,
   • glaucoma crises,
   • reactive hypertension of the eye.
2. Toxic hypertension.
3. Corticosteroid hypertension.
4. Diencephalic and endocrine hypertension.

Increased blood pressure in uveitis associated either with hypersecretion of aqueous humor, or with an increase in outflow resistance as a result of trabecular edema and exudate deposition in the anterior chamber angle. If the deterioration of the outflow becomes permanent due to the formation of goniosynechia and damage to the trabeculae, then uveal hypertension turns into secondary post-inflammatory glaucoma.

Uveitis with hypertension is sometimes mistaken for an acute attack of primary glaucoma. In differential diagnosis the whole clinical picture of the disease must be taken into account: medical history, complaints, the nature of the injection of the eye, the presence or absence of precipitates on the cornea, the depth of the anterior chamber, the width of the pupil.

glaucoma cycling crises, or Posner-Schlossman syndrome, develops in people of both sexes aged 20-60 years. It is characterized by repeated crises, consisting in a sharp increase in IOP without any specific cause. As a rule, one eye suffers, bilateral lesions are rare. During a crisis, the patient has a feeling of slight discomfort in the eye, blurred vision and rainbow circles appear. IOP rises to 40-60 mm Hg. Art., however, unlike an attack of ZUG, pain does not occur. Biomicroscopy reveals slight corneal edema and a small amount of small corneal precipitates, which in some cases disappear within a few days, which can make a correct diagnosis difficult. The anterior chamber is of medium depth, the pupil is dilated, the angle of the anterior chamber is open, there are neither posterior synechia nor goniosynechia. In many patients, signs of APC and iris root dysgenesis are revealed: anterior attachment of the iris, a layer of uveal tissue in the APC bay and on the trabecula, areas of hypoplasia in the iris root. T. Jerndal et al. (1978) examined the trabeculae of a patient with Posner-Schlossmann syndrome using scanning electron microscopy and found a weakly fenestrated endothelial membrane on the trabecular surface between the Schwalbe ring and the scleral spur.

During a crisis, the resistance to the outflow of aqueous humor from the eye increases sharply, while fluid production increases. In a calm period, these indicators return to normal.

Etiology and pathogenesis of the disease unclear. There are indications of a possible role for autoimmune factors. During a crisis in the moisture of the anterior chamber, the content of prostaglandin E is increased. This may affect the production of intraocular fluid. T. Jerndal et al. (1978) consider this syndrome as a kind of congenital glaucoma caused by dysgenesis of the APC.

The duration of each crisis varies from a few hours to 2-4 weeks. The prognosis is satisfactory. In most cases, after the crisis, no traces remain, however, in some cases, defects in the field of view and excavation of the optic disc occur. Posner-Schlossman syndrome can be combined with primary OAG.

Treatment includes the use of antihypertensive (pilocarpine, timolol, diacarb) and anti-inflammatory (corticosteroids, indomethacin) agents.

Reactive hypertension of the eye occurs with severe pain irritation of the iris and cornea receptors (eye injuries, iritis, iridocyclitis, keratitis). Due to the short duration of the increase in intraocular pressure, the question of the differential diagnosis of reactive hypertension and glaucoma usually does not arise.

It has been established that chronic intoxication with sanguinarine, tetraethyl lead, furfural can lead to impaired regulation of intraocular pressure [Skripnichenko 3. M., 1957; Kasimova M. D., 1966]: instability of ophthalmotonus, its periodic or constant increase are noted. The immediate cause of the increase in intraocular pressure during poisoning with tetraethyl lead and furfural is an increase in the rate of formation of intraocular fluid. Soon after the cessation of the action of the toxic factor, the ophthalmotonus and hydrodynamics of the eye return to normal.

Diagnosis of toxic hypertension is based primarily on establishing the fact that the patient has been exposed to one of the poisons listed above for some time. In the study of the hydrodynamics of the eye, the hypersecretory nature of glaucoma is established. To establish the correct diagnosis, it is very important to detect common symptoms of intoxication of the body.

Cortisone hypertension occurs with prolonged local or general use of corticosteroids or ACTH. Corticosteroid-induced ocular hypertension is easily differentiated from primary glaucoma. After discontinuation of the drug, ophthalmotonus and hydrodynamics of the eye quickly normalize.

Diencephalic hypertension is a borderline condition between symptomatic and essential ocular hypertension. It is due to increased secretion of aqueous humor with a normal value of the outflow easiness coefficient. The disease often occurs in women aged 35-65 years, who have mild hormonal and diencephalic disorders. It is similar to open-angle glaucoma. The course of the disease is favorable. Visual functions are preserved for a long time [Vilenkina A. Ya., 1958]. However, with a prolonged course of the disease, the drainage system of the eye is secondarily affected. In such cases, hypersecretory hypertension of the eye turns into retention open-angle glaucoma [Khizhnyakova IN, 1968].

Symptomatic hypertension can also occur with endocrine lesions: Itsenko-Cushing syndrome [Pantieleva V. M., Bunin A. Ya., 1974], hypothyroidism [Chentsova O. B. et al., 1978] and pathological menopause in women [Suprun A. V ., Rudinskaya G. M., 1974]. Endocrine hypertension appears to be associated with dysfunction of the hypothalamus.

Differential diagnosis of diencephalic and essential hypertension and primary glaucoma is based on the same principles. It should also be noted the transient nature of the increase in IOP, the combination of an increase in ophthalmotonus with a deterioration in the general condition (headache, nausea, general weakness, palpitations). Miotics do not reduce IOP [Khizhnyakova IN, 1973]. The detection of other hypothalamic and endocrine disorders is essential for establishing the correct diagnosis.

Consider the essence of the concept of essential hypertension: what is it from the point of view of the mechanism of the onset of the disease, its classification, causes, symptoms, principles of diagnosis, therapy, and prevention.

Origin theories

Essential hypertension is a repeated increase in blood pressure above the level of 140/90 of unclear etiology. There are primary and secondary forms of the disease. The first is hypertension of unclear etiology, the second is a sign of a disease of a particular organ.

There are several assumptions about the mechanism of the occurrence of pathology:

• stress or neurogenic theory, the essence of which is the extreme activity of the sympathetic nervous system: a massive release of neurotransmitters into the blood leads to vascular spasm, increased blood pressure;
• humoral - based on an imbalance of vasodilator, vasoconstrictor biocomponents with a predominance of vasoconstrictor;
• membrane - the result of a genetic breakdown of smooth muscle membrane pumps, they stop pumping sodium out of the cell, which causes vascular spasm;
• renal - a consequence of kidney disease, characterized by sodium accumulation, fluid retention, an increase in its volume in the bloodstream, activation of pressor substances, arterial spasm;
• receptor - a change in the work of baro-, chemoreceptors, an increase in the content of carbon dioxide occurs, which gives a signal to the medulla oblongata to increase pressure.

ICD code 10

The International Classification of Diseases (ICD 10) has several gradations of pathological conditions associated with high blood pressure.

Essential primary hypertension according to ICD-10 has the code I10, implies the primary variant of the disease (Hypertensio arterialis essentialis (primaria)). Code I10-I15 - hypertensive diseases, including a secondary form of pathology in accordance with the affected target organ. On the form under the code I10, ICD 10 takes up to 90% of all high blood pressure.

Primary hypertension usually debuts at the age of about 40 years, is characterized by a progressive increase in pressure, both systolic and diastolic at the same time. An isolated increase in one of them is possible.

The main danger of the disease is untimely diagnosis, late visit to the doctor. The result - a hypertensive crisis, sometimes - unpredictable consequences.

Classification

In addition to ICD10, the disease is classified clinically.

By the nature of the flow

Hypertension is usually divided into a disease with a benign or malignant course. Benign is stopped by taking medications. At the same time, the general well-being of the patient is practically not disturbed, the quality of life does not suffer, the internal target organs function normally.

The malignant form of hypertension brings unpleasant surprises: a spontaneous increase in blood pressure to crisis levels, insufficient effectiveness of drugs, damage to internal organs with a change in their functional potential. Moreover, the disease sometimes develops at lightning speed, it is diagnosed already at the stage of serious complications.

By severity

Hypertension is divided into three degrees of severity:

1. mild or the first is characterized by an increase in pressure without involvement of organs in the pathological process (tonometry from 140/90 to 160/100);
2. the middle or second one indicates damage to internal organs with the preservation of their functions (180/110);
3. severe or third - indicates changes in the internal organs with a violation of their functional potential, failure to work (BP over 180/110).

There is also: upper pressure - more than 140, lower - less than 90 units.

By stages

In addition to the severity, there are stages of hypertension. There are also three of them:

1. the first - there are no symptoms, the organs are intact;
2. the second is the debut of pathology in the endothelium of the arteries, thickening of the heart muscle while maintaining the functionality of the organs, that is, objective indicators of organ damage are determined in the absence of symptoms on their part;
3. the third - structural changes in the vascular wall, damage to the heart, kidneys, brain, in other words, there are both objective data and clinical manifestations.

Classification according to clinical symptoms makes it possible to prescribe the correct clinical and laboratory examination, choose adequate therapy, and calculate the negative consequences.

Causes of pathology

The exact triggers of the pathology are not clear. About half of all cases of essential hypertension are hereditary. In addition, primary hypertension, the causes of which are established, occurs when:

• a set of extra pounds, which significantly increase the risk of developing the disease, especially when combined with little physical activity;
• nicotine addiction is another provocateur of high blood pressure: tobacco poison causes myocardial ischemia;
• excessive salt intake, leading to water retention in the body, an increase in the volume of circulating fluid in the bloodstream, an increase in blood pressure;
• irrational nutrition: fast food, lack of vitamins, minerals, alcohol abuse, coffee, strong tea, sweet soda;
• stress;
• diabetes mellitus, other malfunctions of the endocrine glands.

The causes of the disease are very important for understanding the mechanism of its development, and therefore, choosing the right tactics for managing the patient.

Clinical manifestations

The symptom complex of primary hypertension is caused by damage to target organs: the heart, blood vessels, kidneys, and brain. For a long time, hypertension is asymptomatic, and special diagnostic methods are needed to detect it. The risk of death, the choice of therapeutic tactics depends on the root cause.

First (initial) stage

This is the clinical latency period. The only signs can be considered weakness, migraine, increased blood pressure. Symptoms of essential hypertension are manifested by severe overexertion, physical exertion, overeating, excessive consumption of coffee, alcohol. Over time, the load on the vessels leads to cardiac pathology.

Second (crisis) stage

Pain behind the chest

The possibility of developing a crisis is the danger of the second stage. It is important not to miss the first symptoms: high blood pressure, migraine pain, pre-syncope. This is a reason for the patient to contact a doctor who prescribes an examination, complex antihypertensive therapy.

Third (severe) stage

It is characterized by high blood pressure, encephalopathy, memory impairment, dementia, cardiovascular insufficiency, kidney pathology. This leads to a metabolic disorder, protein in the urine, and creatinine in the blood. Changes in organs, as a rule, are irreversible, require constant monitoring by a doctor, periodic hospitalization, and treatment adjustments. At this stage, heart attacks, strokes, and a coma often occur.

Metabolic syndrome is diagnosed if a combination of three of the following five factors is diagnosed:

• visceral-abdominal obesity;
• high blood sugar on an empty stomach;
• BP more than 130/85;
• lowering the level of HDL cholesterol - cholesterol, high density lipoproteins;
• a high level of TG (triglycerides) is an indicator of lipid metabolism disorders.

Metabolic syndrome determines the degree of risk of complications, the likelihood of death.

Diagnostics

Symptomatically, hypertension is difficult to distinguish from other diseases. Take into account the age of the patient, consistently high blood pressure numbers, their correction with drugs. However, for an accurate diagnosis, a complete clinical and laboratory examination is necessary, the basis of which is pressure monitoring. In addition, use:

• history taking, physical examination of the patient;
• UAC, OAM;
• biochemistry of blood with tests for hormones;
• creatinine clearance, degree of microalbuminuria to detect hypertensive nephropathy;
• pulsometry of large vessels;
• orthostatic tests with blood pressure measurement;
• ECG, EchoCG (to determine the degree of left ventricular hypertrophy);
• Ultrasound of the carotid arteries for the diagnosis of atherosclerotic vascular lesions;
• dopplerography;
• fundus examination;
• consultation with a gynecologist, endocrinologist.

The choice of the optimal tactics of patient management, the development of complications, and the prognosis of life expectancy depend on the timely diagnosis.

The choice of treatment tactics

The main goal of therapy for essential hypertension is to balance blood pressure, optimal comfort of the internal organs. To do this, you need to radically change your habits, first of all. With excess weight, hypodynamia, love for alcohol, cigarettes, getting rid of hypertension or at least curbing it will not work. The second step on the way to maintaining the quality of life is the regular intake of drugs prescribed by the attending physician. The third is control over your emotions.

Medications

Essential hypertension of the first or second degree has a favorable course, the prognosis, since it is well treated if the drugs are taken regularly.

Medicines are prescribed only by a doctor. Self-medication can be tantamount to a sentence, since it is impossible to choose the right group of antihypertensive drugs without examination. Complex therapy of the disease involves a decrease in pressure when prescribed:

• (especially if a crisis has developed) - Lasix, Triampur, Diakarb;
• : Prestarium, Enam, Ramipril, Perindopril, Trandolapril - help to avoid complications, relieve stress on target organs;
• : Lacidipine, Lecarnidipine, Isradipine - relax the wall of the arteries, relieve angiospasm, recommended for coronary artery disease (coronary heart disease);
• reduce cardiac load - Carvedilol, Labetalol, Betaloc ZOK;
• improve blood flow, thereby normalizing blood pressure - Tamsulosin, Pyrroxan, Tropafen;
• imidazoline receptor controllers are recommended for patients with endocrine pathologies: obesity, diabetes mellitus, they improve metabolism while lowering blood pressure, have a pronounced peripheral sympatholytic activity - Moxonidine, Rilmenidine;
• have a selective effect, belong to modern medicines - Losartan, Valsartan.

If atherosclerosis is detected, they are additionally connected, the development of complications dictates the appointment of anticoagulants: Heparin, Hirudin, Lepirudin; : Indobufen, Thrombo-AS, Tirofiban; digitalis preparations such as Digoxin (with great care, exclusively under the supervision of a physician): Nitrong, Sustonit, Sustak forte; neurological symptoms require correction with drugs that improve cerebral circulation: Cavinton, Cerebrolysin, Piracetam. Medications are taken in parallel with non-drug therapies.

Non-drug therapy

A large role in the treatment of essential hypertension belongs to therapy without drugs:

• diet;
• healthy lifestyle;
• physical activity with a reasonable dosage;
• psychotherapeutic measures;
• auto-training;
• yoga;
• acupuncture;
• herbs;
• physio-, hirudotherapy.

The diet, first of all, involves the restriction of salt to 5 g / day, the exclusion of alcoholic beverages, coffee, strong tea, and the restriction of fats. All this in order to prevent an increase in blood pressure, stress on the vascular system, and the risk of damage to internal organs.

The diet includes fruits and vegetables. Products containing potassium, magnesium: beans, buckwheat, oatmeal, nuts, dried fruits, spinach, mushrooms, pumpkin; watermelon, apricots, tomatoes, citrus fruits, sea kale, potatoes, cocoa, bran.

The role of physical activity is great. Weightlifting, any overexertion is prohibited, swimming, walking are optimal.

The debut of primary hypertension can be stopped or mitigated by herbs, physiotherapy. Consultation with a doctor is required. For example, with hypertension, St. John's wort, Eleutherococcus, lemongrass, goat's rue are contraindicated. Useful - decoctions of valerian root, sage, eucalyptus - they reduce pressure.

The priority physiotherapeutic procedure is electrosonotherapy. In general, it is better to engage in physiotherapy in sanatorium conditions. Apply general galvanization, electrophoresis with Aminazine, Obzidan, low-frequency magnetotherapy, aerophytotherapy with esters of orange, lemon, juniper, lavender, vanilla, UHF, darsonval, laser.

Very effective massage and baths:

• sodium chloride - dilates blood vessels (12 procedures for 15 minutes);
• radon - prevent the pathology of the vascular system (10 procedures for 10 minutes);
• carbonic - have a sedative effect, but are prohibited during jumps in blood pressure (multiplicity of 10 to 10);
• coniferous - anti-neurotic, normalize sleep (multiplicity of 15 to 15).

All physiotherapy and non-drug treatments are indicated only in the first stage of the disease. Blood pressure above 160/100 suggests caution. However, the development of complications or their risk requires radical therapy.

Effects

The existence of hypertension for a long time leads to organ damage. All complications are conditionally divided into two groups:

• hypertensive, caused by the destruction of blood vessels due to the long-term effect of hypertension, direct mechanical effects on the heart, blood vessels. These include: stroke (acute cerebrovascular accident), the development of heart failure, subarachnoid hemorrhage, myocardial hypertrophy, retinal hemorrhage, optic nerve edema, aortic aneurysm, malignant hypertension;
• atherosclerotic, associated with vascular atherosclerosis, they can also form against the background of normal pressure, but they usually have a more severe course, an early debut. These include: ischemic heart disease, myocardial infarction, sudden cardiac arrest, stroke (hemorrhage due to atherothrombosis), peripheral arterial disease, renal artery stenosis, chronic renal failure.

Essential hypertension is characterized by many complications. All of them are extremely serious, deserve special attention, are treated only inpatients. The patient is observed around the clock, emergency therapy is designed to alleviate the patient's condition, to prevent the progression of complications. In the future, it is to reduce the frequency of crises and prolong the life of the patient.

Prevention, prognosis

Prevention rules are simple:

• dosed physical activity;
• lack of stress;
• a balanced diet of an atherogenic (fat restriction) profile;
• refusal of alcohol, nicotine, drugs;
• taking medications only as prescribed by a doctor;
• control over extra pounds;
• continuous monitoring of blood pressure;
• daily half-hour walks in the fresh air.

The prognosis depends on the stage of the disease, its course (benign or malignant), on age, the potential of internal organs, and compliance with medical prescriptions.

According to WHO, life expectancy with pressure correlation:

• 120/80 - 74 years old;
• 130/90 - 68 years;
• 140/100 - 63 years old;
• 150/110 - 55 years old.

Early diagnosis, correct treatment is the basis of a favorable prognosis. Pressure should be measured in the morning and evening, drugs should be taken regularly, they should be changed only according to the scheme drawn up by the doctor. Hypertension of the third degree with damage to target organs, frequent crises is considered an unfavorable sign.

Last update: September 28, 2019

is an increase in intraocular pressure above 20 mm Hg. Art. in the absence of glaucomatous changes in the fundus. Common symptoms for all forms are headache, blurred vision, discomfort in the orbit. The complex of diagnostic measures includes tonometry, eye biomicroscopy, gonioscopy, tonography. With ocular hypertension, antihypertensive therapy is indicated, which is reduced to instillations of beta-blockers or their combination with M-cholinomimetics, carbonic anhydrase inhibitors. The treatment of the symptomatic form is based on the elimination of the etiological factor.

General information

Ophthalmohypertension is a widespread pathology. In 35% of cases it has a stable course, in 30% it regresses with age, in 35% it leads to the development of glaucomatous changes in the retina and optic nerve head (OND). According to the statistics available in ophthalmology, nosology is diagnosed in 7.5% of the population over the age of 40 years. After 50 years, this figure reaches about 20%. Patients with elevated intraocular pressure are at risk for developing glaucoma. It has been proven that in the absence of correction of ophthalmotonus for 10 years, complications occur in 5-9.2% of patients. The disease occurs on average 10 times more often than glaucoma.

Causes of ophthalmohypertension

The reason for the essential form is age-related changes in the circulation of aqueous humor. The disease occurs against the background of hormonal imbalance in menopausal women. The development of a symptomatic form lead to:

• The use of corticosteroids. The hydrodynamics of the eye is disturbed both with prolonged instillations of hormonal agents and with their oral administration. Local use of glucocorticosteroids causes an increase in IOP after a few weeks, systemic - after 2-4 years. Intensive steroid therapy potentiates an increase in ophthalmotonus 1-2 hours after drug administration.
• Traumatic injuries. The reactive nature of the disease is associated with irritation of pain receptors on the surface of the iris and cornea. Acute ophthalmohypertension occurs in response to the dislocation of the lens.
• Surgical interventions. An increase in ophthalmotonus provokes obturation of the drainage network with lens fragments, pigment, or pseudoexfoliative material. Ocular hypertension develops with the use of viscoelastic drugs during surgery. In the postoperative period, an increase in IOP is associated with a local inflammatory reaction, pupillary and ciliary block.
• Syndrome Posner-Schlossmann. This pathology becomes the cause of glaucoma cyclistic crises, which are accompanied by a sharp increase in pressure without changes in the CPC.
• Intoxication. An increase in IOP provokes chronic tetraethyl lead intoxication, furfural poisoning, or uncontrolled intake of drugs containing sanguinarine.
• Uveitis. Inflammation of the uveal tract provokes an increase in fluid secretion, trabecular edema, and accumulation of exudate in the APC, which leads to a transient increase in IOP.
• Endocrine diseases. Ophthalmohypertension is caused by hormonal imbalance against the background of hypercortisolism or hypothyroidism in history.

Pathogenesis

The mechanism of development of ocular hypertension directly depends on the form of pathology. With the essential nature of the disease, due to a violation of the outflow of intraocular fluid, even its moderate secretion potentiates an increase in pressure. Normally, in elderly patients, the difficult circulation of intraocular fluid is associated with its reduced production, so ophthalmopathology does not develop. The occurrence of symptomatic ophthalmohypertension is due to an increase in the production of intraocular fluid or a reversible violation of the outflow of aqueous humor, which causes edema of the trabecular meshwork, accumulation of exudate or blood in the area of ​​the angle of the anterior chamber of the eye (AEC).

Individuals with this nosology have a history of imaginary or true hyperproduction of intraocular fluid. This is due to the intensive blood supply to the membranes of the eye, the high functional ability of the ciliary body. In the pathogenesis of the steroid form of the disease, the inhibition of proteases and phagocytosis of trabecular endotheliocytes plays a leading role. Violation of ion exchange leads to sodium retention and swelling of the drainage network. Polymerization of molecules on the surface of trabecular tissue potentiates an increase in the nucleus and cell size. Corticosteroids inhibit the production of prostaglandins, the function of which is to reduce IOP and improve the outflow of intraocular fluid.

Classification

Ocular hypertension has many variants of development. According to the etiology, the disease is classified into uveal, reactive and steroid forms. From a clinical point of view, there are:

• Symptomatic ophthalmohypertension. A temporary increase in IOP develops against the background of a pathological process that is not related to glaucoma.
• Essential ocular hypertension. It is characterized by a slight increase in ophthalmotonus with normal outflow of intraocular fluid.
• Pseudohypertension of the eye. This is an excess of intraocular pressure, which occurs as a result of stress before visometry in healthy people.

Symptoms of ophthalmohypertension

Clinical manifestations of pathology are determined by the variant of development. Essential ocular hypertension is characterized by a stable or regressive course. This is due to the fact that with age, the intensity of HBF production gradually decreases. In most cases, ophthalmohypertension occurs symmetrically in both eyes. Patients report frequent headaches. An exception is the symptomatic form against the background of a glaucoma-cyclitic crisis. With this pathology, one eye is affected. During a crisis, patients complain of discomfort, the appearance of "fog" and iridescent circles before their eyes. Pain syndrome is usually absent.

In the steroid type of the disease, intraocular pressure rises gradually. In the reactive variant, signs of ocular hypertension increase within 2-6 hours after injury or surgery. Patients complain of foreign body sensation, blurred vision, severe pain. Rarely observed dyspeptic manifestations (nausea, vomiting). Specific symptoms of the uveal form include ocular hyperemia, photophobia, and increased lacrimation. The disease can lead to irreversible visual impairment.

Complications

A common complication of symptomatic ophthalmohypertension is secondary glaucoma, which is the result of irreversible changes in the trabecular apparatus. Undesirable consequences of the steroid form are represented by thickening of the cornea, the formation of posterior capsular cataracts, the formation of ulcerative defects on the surface of the cornea. Possible atrophic changes in the eyelids, the occurrence of ptosis. The reactive variant of the nosology is complicated by hypertensive epitheliopathy. Uveal ophthalmohypertension against the background of panuveitis leads to an irreversible loss of visual functions.

Diagnostics

Diagnosis of the disease is very difficult. Measurement of IOP causes psychological stress in the patient, which often provokes an increase in ophthalmotonus and the occurrence of false ophthalmohypertension. A special ophthalmological examination requires:

• Tonometry. An objective criterion for ocular hypertension is an increase in IOP of more than 20 mm Hg. Art. with two consecutive measurements. With a symptomatic form, ophthalmotonus indicators can reach 40-60 mm Hg. Art.
• Biomicroscopy of the eye. This is the only method that allows you to establish the diagnosis of symptomatic ophthalmohypertension in Posner-Schlossmann pathology. The biomicroscopic picture includes a slight swelling of the cornea, small precipitates that disappear 2-3 days after the crisis. In the reactive form, corneal edema is determined.
• Tonography. The study of the hydrodynamics of the eye makes it possible to graphically record changes in IOP. The verification of the form of the disease is based on the measurement of the minute volume of intraocular fluid and the coefficient of ease of its outflow.
• Gonioscopy. With this nosology, an open ACL of the eye is visualized. The depth of the chamber is within the normal range. In patients with a reactive form, viscoelastic residues are determined in the anterior chamber.

For differential diagnosis with glaucoma, gonioscopy, ophthalmoscopy, perimetry and visometry are performed. In contrast to glaucoma, in ophthalmohypertension, intraocular pressure indicators do not affect visual functions, APC is unchanged. Pathology is not accompanied by changes in the optic disc and the inner shell of the eyeball. The boundaries of the field of view correspond to the reference values.

Treatment of ophthalmohypertension

Therapeutic tactics is reduced to the appointment of antihypertensive drugs. The target level of intraocular pressure is 20-13 mm Hg. Art. Treatment begins with the appointment of one drug from the group of beta-blockers. With low efficiency, combination therapy is indicated. The most common treatment regimen includes the use of two β-blockers. If there is no effect, ophthalmologists prescribe a combination of a β-blocker with an M-cholinomimetic or a carbonic anhydrase inhibitor. When choosing a combined tactic 2-3 times a year, it is necessary to change the treatment regimen in order to prevent the development of tolerance to drugs. The leading role in the treatment of symptomatic ophthalmohypertension is the elimination of the causative factor.

With the steroid nature of the disease, intraocular pressure normalizes within 2-3 weeks after the abolition of corticosteroids. If there is a need to continue therapy, a replacement with non-steroidal anti-inflammatory drugs is indicated. Antihypertensive drugs are prescribed only when IOP reaches 40-60 mm Hg. Art. The tactics of treating the reactive form is reduced to the local use of drugs from the group of β-blockers, carbonic anhydrase inhibitors or α-adrenergic agonists. With an increase in IOP after surgery due to the accumulation of viscoelastic or formed elements in the anterior chamber, it is decompressed. Identification of a mechanical obstruction to the outflow of intraocular fluid requires its removal by surgery.

Forecast and prevention

The prognosis for life and in relation to visual functions in ophthalmohypertension is favorable. The cause of complete loss of vision may be the uveal form, which is often associated with a long course of panuveitis. Specific preventive measures have not been developed. Nonspecific prevention is reduced to the elimination of hormonal imbalance, the appointment of antihypertensive therapy on the eve of surgery. Patients working with tetraethyl lead and furfural are recommended to use personal protective equipment (glasses, masks). When taking drugs with sanguinarine and corticosteroids, it is necessary to control the level of IOP.

Glaucoma is a disease that, in the overwhelming majority of cases, is manifested by an increase in intraocular pressure, a progressive narrowing of the visual field, and specific changes in the optic nerve, ultimately leading to its atrophy.

Ophthalmohypertension is an increase in intraocular pressure, in which there are no changes characteristic of primary glaucoma.

Types of ocular hypertension

Ophthalmohypertension is divided into essential and symptomatic.

Essential ophthalmohypertension develops in middle-aged and elderly people. The reasons for its development have not been fully elucidated. With age, both a decrease in the secretion of intraocular fluid and a decrease in the ease of its outflow are noted. Both processes are balanced, and intraocular pressure remains within the normal range. Essential hypertension of the eye occurs when there is an imbalance between the secretion and outflow of aqueous humor with a predominance of the former, which leads to an increase in intraocular pressure.
Essential ophthalmohypertension is characterized by a moderate and usually symmetrical increase in intraocular pressure (IOP) in both eyes, the absence of glaucoma-specific changes in the optic nerve head and visual field. Indicators of hydrodynamics and hemodynamics are symmetrical in both eyes. Indicators of the outflow from the eye of aqueous humor remain within the normal range. According to a number of authors, ophthalmohypertension has a stable or regressive course, since with age, differences in the systems of production and outflow of intraocular fluid gradually decrease.

Symptomatic ophthalmohypertension occurs due to any diseases of the eye or body, as well as under the influence of certain medications and toxic effects. This is not an independent disease, but only a manifestation of some other pathology. Ophthalmohypertension is also not accompanied by the development of glaucoma-specific changes in the optic disc and visual field, but with a long course it can smoothly turn into secondary glaucoma with all its inherent signs.

Symptomatic ophthalmohypertension is characterized by periodic short-term or prolonged rises in intraocular pressure.

There are several types of symptomatic hypertension:

• Uveal hypertension is observed against the background of inflammatory diseases of the eye, such as iritis, iridocyclitis, keratoiridocyclitis, with glaucoma cyclitis crises.
• Toxic hypertension develops under the influence of chronic intoxication with tetraethyl lead, furfural and other substances.
• Corticosteroid ophthalmohypertension occurs with prolonged local or general use of corticosteroid drugs.
• Symptomatic endocrine and ophthalmohypertension can be observed in some diseases: Itsenko-Cushing syndrome, hypothyroidism, thyrotoxicosis, pathological menopause in women.
• Diencephalic hypertension is often part of the symptom complex of diencephalic, in particular hypothalamic disorders that occur with inflammatory pathology of the corresponding area of ​​the brain.

What worries?

Clinically, ophthalmohypertension is manifested by a feeling of fullness of the eyeball, aching in one or two eyes, and a headache. It is often discovered incidentally as a result of prophylactic measurement of intraocular pressure and in the absence of any subjective sensations in the patient.

Diagnostics

In the absence of apparent causes, the diagnosis of ophthalmohypertension is established after exclusion of primary glaucoma. It is necessary to conduct all studies used in the diagnosis of glaucoma:

• Checking visual acuity and fields (visometry, perimetry);
• Measurement of intraocular pressure in the evening and morning hours (daily tonometry);
• Examination of the fundus (ophthalmoscopy);
• Inspection of the angle of the anterior chamber (gonioscopy);
• Study of eye hydrodynamics (tonography);
• Various loading or unloading tests that provoke a change in intraocular pressure;
• Retinal tomography (HRT), which allows you to assess the condition of the optic nerve head.

If an extraocular pathology is suspected, other diagnostic tests may be needed: a study of hormonal status, ultrasound dopplerography of cerebral vessels, etc. Of decisive importance in the differential diagnosis of hypertension of the eye and initial open-angle glaucoma is the dynamic monitoring of the state of the organ of vision.

Treatment

To normalize intraocular pressure, it is necessary to eliminate the cause that caused hypertension: treatment of the underlying disease, identification and elimination of a toxic factor, correction of the level of certain hormones, and so on. Treatment is carried out in conjunction with the appropriate specialist.

To reduce intraocular pressure, antihypertensive therapy is prescribed - eye drops or tablets for oral administration with a different mechanism of action: reducing the secretion of aqueous humor, improving outflow, or acting on both processes. The choice of this or that drug is made by an ophthalmologist, based on data on the hemodynamics of the eye, obtained as a result of a comprehensive diagnostic examination.

The patient's task is to consult a doctor in a timely manner, even if the symptoms that disturb him are intermittent and pass quickly, because. despite the considered favorable prognosis, in certain cases, ophthalmohypertension leads to the development of secondary glaucoma, a serious and difficult-to-treat disease.