Ocular hypertension is an increase in intraocular pressure above 20 mmHg in the absence of glaucomatous changes in the fundus. Common symptoms for all forms are headache, blurred vision, a feeling of discomfort in the eye socket. The complex of diagnostic measures includes tonometry, biomicroscopy of the eye, gonioscopy, tonography. In ocular hypertension, hypotensive therapy is indicated, which is reduced to instillation 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.
Ocular hypertension 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 disc (OND). According to the statistics available in ophthalmology, nosology is diagnosed in 7.5% of the population over the age of 40. After 50 years, this figure reaches about 20%. Patients with increased intraocular pressure are at risk of developing glaucoma. It is proved 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 ocular hypertension
The reason for the essential form is age–related changes in the circulation of watery moisture. The disease occurs against the background of hormonal imbalance in women of menopausal age. The development of the symptomatic form leads 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 administration of the drug.
- Traumatic injuries. The reactive nature of the disease is associated with irritation of pain receptors on the surface of the iris and cornea. Acute ocular hypertension occurs in response to dislocation of the lens.
- Surgical interventions. An increase in ophthalmotonus provokes obturation of the drainage network by fragments of the lens, pigment or pseudoexfoliative material. Ocular hypertension develops with the use of viscoelastic drugs during surgery. In the postoperative period, the increase in IOP is associated with a local inflammatory reaction, pupillary and ciliary block.
- Posner-Schlossman syndrome. This pathology causes glaucocyclitic crises, which are accompanied by a sharp increase in pressure without changes in FCA.
- Intoxication. An increase in IOP is provoked by chronic tetraethyl lead intoxication, furfural poisoning or uncontrolled intake of drugs containing sanguinarine.
- Uveit. Inflammation of the uveal tract provokes an increase in fluid secretion, trabecular edema and accumulation of exudate in the FCA, which leads to a transient increase in IOP.
- Endocrine diseases. Ocular hypertension is caused by hormonal imbalance on the background of hypercorticism or hypothyroidism in the anamnesis.
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 IOF, even its moderate secretion potentiates an increase in pressure. Normally, in elderly patients, obstructed circulation of intraocular fluid is associated with its reduced production, therefore ophthalmopathology does not develop. The occurrence of symptomatic ocular hypertension is caused by an increase in IOF production or a reversible violation of the outflow of watery moisture, which causes edema of the trabecular network, accumulation of exudate or blood in the area of the angle of the anterior chamber of the eye (FCA).
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 capacity of the ciliary body. Inhibition of proteases and phagocytosis of trabecular endotheliocytes plays a leading role in the pathogenesis of the steroid form of the disease. Violation of ion exchange leads to sodium retention and swelling of the drainage network. Polymerization of molecules on the surface of the trabecular tissue potentiates an increase in the nucleus and cell size. Corticosteroids inhibit the production of prostaglandins, whose function is to reduce IOP and improve the outflow of IOF.
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 ocular hypertension. A temporary increase in IOP develops against the background of a pathological process unrelated to glaucoma.
- Essential ocular hypertension. It is characterized by a slight increase in ophthalmotonus at normal IOF outflow rates.
- 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 ocular hypertension
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 the intensity of IOF production gradually decreases with age. In most cases, ocular hypertension occurs symmetrically in both eyes. Patients report frequent headache. The exception is the symptomatic form against the background of a glaucomocyclitic crisis. With this pathology, one eye is affected. During the crisis, patients complain of discomfort, the appearance of “fog” and iridescent circles in front of their eyes. Pain syndrome is usually absent.
With a steroid type of disease, intraocular pressure increases gradually. In the reactive variant, signs of ocular hypertension increase for 2-6 hours after injury or surgery. Patients complain of a foreign body sensation, blurred vision, pronounced soreness. Dyspeptic manifestations (nausea, vomiting) are rarely noted. Specific symptoms of uveal form include hyperemia of the eye, photophobia and increased lacrimation. The disease can lead to an irreversible decrease in visual functions.
A common complication of symptomatic ocular hypertension is secondary glaucoma, which is a consequence 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 of the eyelids, the occurrence of ptosis. The reactive variant of nosology is complicated by hypertensive epithelopathy. Uveal ocular hypertension on the background of panuveitis leads to irreversible loss of visual functions.
Diagnosis of the disease is a great difficulty. The measurement of IOP causes psychological stress in the patient, which often provokes an increase in ophthalmotonus and the occurrence of false ocular hypertension. A special ophthalmological examination requires:
- Tonometry. The objective criterion of ocular hypertension is an increase in IOP of more than 20 mmHg with two consecutive measurements. In the symptomatic form, the indicators of ophthalmotonus can reach 40-60 mm Hg.
- Biomicroscopy of the eye. This is the only method that allows the diagnosis of symptomatic ocular hypertension in Posner-Schlossman 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 indicators. 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 FCA of the eye is visualized. The depth of the camera is within the normal range. In patients with a reactive form, viscoelastic residues are detected in the anterior chamber.
For differential diagnosis with glaucoma, gonioscopy, ophthalmoscopy, perimetry and visometry are performed. Unlike glaucoma in ophthalmic hypertension, intraocular pressure indicators do not affect visual functions, FCA is unchanged. Pathology is not accompanied by changes on the part of the OND and the inner shell of the eyeball. The boundaries of the field of view correspond to the reference values.
Treatment of ocular hypertension
Therapeutic tactics are reduced to the appointment of antihypertensive agents. The target level of intraocular pressure is 20-13 mm Hg. Treatment begins with the appointment of one drug from the group of beta-blockers. With low efficacy, combination therapy is indicated. The most common treatment regimen includes the use of two beta-blockers. In the absence of an effect, ophthalmologists prescribe a combination of a beta-adrenoblocker with an M-cholinomimetic or a carbonic anhydrase inhibitor. When choosing a combined tactic, it is necessary to change the treatment regimen 2-3 times a year in order to prevent the development of tolerance to drugs. The leading role in the treatment of symptomatic ocular hypertension is the elimination of the causal factor.
With the steroid nature of the disease, intraocular pressure normalizes within 2-3 weeks after the withdrawal of corticosteroids. If there is a need to continue therapy, replacement with nonsteroidal anti-inflammatory drugs is indicated. Antihypertensive agents are prescribed only when an IOP of 40-60 mm Hg is reached. The tactics of treatment of the reactive form is reduced to the local use of drugs of the group of beta-blockers, carbonic anhydrase inhibitors or α-adrenomimetics. With an increase in IOP after surgery due to the accumulation of viscoelastic or shaped elements in the anterior chamber, its decompression is carried out. Identification of a mechanical obstacle in the way of IOF outflow requires its removal surgically.
Prognosis and prevention
The prognosis for life and visual functions in ocular hypertension 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 hypotensive therapy on the eve of surgery. Patients working with tetraethyl lead and furfural are recommended to use personal protective equipment (glasses, masks). When taking medications with sanguinarine and corticosteroids, it is necessary to monitor the level of IOP.