Open–angle glaucoma is a chronic eye pathology with a tendency to progression, characterized by increased intraocular pressure and damage to the optic nerve. Clinical symptoms are represented by a decrease in visual acuity and accommodation, painful sensations. The main diagnostic measures are tonometry, gonioscopy, optical coherence tomography, perimetry and ophthalmoscopy. The components of the complex treatment of open-angle glaucoma are laser surgery methods, surgical interventions (sinusotrabeculectomy, sclerectomy) and conservative therapy.
Primary open-angle glaucoma (POAG) is considered as a disabling disease, including periodic or regular increase in intraocular pressure (IOP) above individually tolerated values, violation of the integrity of the optic nerve disk and retinal ganglion cells, as well as decreased vision. In open-angle glaucoma, unlike closed-angle glaucoma, IOP increases when the angle of the anterior chamber of the eye is open. According to the World Health Organization (WHO), more than 70 million patients with open-angle glaucoma have been registered in the world. To date, the disease is in second place among the causes of vision loss. Pathology is most common in people after 60 years (3-4%). After the age of 45, POAG is diagnosed in 2% of the population. There are rare cases of the development of this pathology in persons under 18 years of age.
Open-angle glaucoma refers to a number of diseases that have a genetic predisposition with polygenic transmission mechanisms. This pathology has many prerequisites, but the starting etiological factor of POAG has not been established. Functional blockade of the scleral sinus plays a key role in the development of open-angle glaucoma. Such features of the eyeball anatomy as a low degree of differentiation or pathology of attachment of the scleral spur and ciliary muscle, a decrease in the angle of inclination of the Schlemm canal lead to POAG. These changes progress with the age of the patient.
It was found that long-term intake of glucocorticoids, reducing the permeability of the trabecular network, inhibits the outflow of watery moisture. The consequence is damage to the optic nerve disc under the influence of high IOP. An important link in the pathogenesis of POAG is a violation of the mechanisms of regulation of blood circulation in the area of the optic nerve disc. The tendency to develop POAG increases in patients with atherosclerosis, hypertension, diabetes mellitus, myopia, as well as pathological conditions accompanied by metabolic disorders.
Symptoms of open-angle glaucoma
From a clinical point of view, there are such forms of open-angle glaucoma as simple primary open-angle glaucoma, pseudoexfoliative open-angle glaucoma, pigmented glaucoma and normal pressure glaucoma.
Simple primary open-angle glaucoma leads to damage to both eyes. In the early stages of development, pathology is characterized by an asymptomatic course. Then there are such subjective symptoms as rainbow circles when fixing the gaze on direct rays of light, reduced accommodation, fog and flickering in front of the eyes. When the IOP tolerance values are exceeded, patients complain of headache with irradiation into the eyes and brow arches.
The pseudoexfoliative form of open-angle glaucoma is characteristic of patients with a history of exfoliative syndrome. With this pathology, a thin layer of amyloid-like substance is deposited in the area of the structures of the anterior pole of the eyeball. Pseudoexfoliative glaucoma is the cause of eye damage to varying degrees. Pathognomonic symptoms of the disease are a change in the contour of the pupil, depigmentation of the central part of the iris, phacodon (trembling of the lens during eye movements). Higher values of IOP are characteristic than in other forms of the disease, and the progrediency of the course.
Pigmented glaucoma develops as a result of the introduction of the iris pigment into the corneal-scleral septum by the fluid flow. Violation of the circulation of watery moisture is a prerequisite for an increase in pressure.
Normal pressure glaucoma is observed after 35 years. Damage to both eyes occurs to varying degrees. The classic glaucoma clinic develops at normal IOP values and an open angle of the anterior chamber. The trigger is arterial hypertension against the background of spasm of large vessels.
The key importance in the diagnosis of the disease is the measurement of intraocular pressure using techniques such as tonometry, elastotonometry and daily tonometry, which allows you to record changes in IOP throughout the day. It is also necessary to examine the structures of the fundus, the field of vision and the angle of the anterior chamber of the eye.
The gonioscopy method allows you to visualize the open angle of the anterior chamber of the eye, medium width, increased pigmentation, increased density and the development of sclerotic changes in the corneal-scleral trabecula. The perimetry method determines the narrowing of the visual fields. The reason is the appearance of paracentral cattle, Bierum scotoma and an increase in the diameter of the blind spot. Narrowing develops from the nasal half and complete blindness occurs at the terminal stages of the disease.
During ophthalmoscopy, pallor and expansion of the boundaries of the vascular funnel of the optic nerve disc are observed. The progression of pathology leads to atrophy of the second pair of cranial nerves and vascular plexuses of the eyeball, followed by the development of a ring of prepapillary atrophy. It is possible to assess in more detail the degree of the pathological process in the area of these structures using optical coherence tomography and laser scanning ophthalmoscopy. Differential diagnosis of POAG should be carried out with senile cataract.
Treatment of open-angle glaucoma
The first stage in the etiotropic treatment of open-angle glaucoma is hypotensive therapy. To do this, prescribe drugs to improve the outflow of intraocular fluid of the prostaglandin group (latanoprost, travoprost) and M-cholinomimetics (pilocarpine hydrochloride). In order to reduce the production of intraocular fluid, the appointment of adrenoblockers (timolol, proxodolol), carbonic anhydrase inhibitors (diacarb), alpha-2 agonists (brimonidine) is effective. Osmotic diuretics (mannitol) help to reduce IOP. Vitamin preparations and flavonoids (alpha-tocopherol, gamma-aminobutyric acid), calcium channel blockers (nifedipine) and non-enzyme antioxidants (ethylmethylhydroxypyridine succinate) are used as neuroprotective therapy.
Laser treatment methods have limited indications for open-angle glaucoma. Laser iridectomy is indicated in the presence of a narrow corneal-scleral angle. Laser trabeculoplasty is used only with low efficiency of conservative therapy. Surgical intervention in open-angle glaucoma consists in performing a sinustrabeculectomy, which is one of the non-penetrating filtering operations.
During the first 10 days after surgery, you should refrain from eating salted and pickled food, as well as alcoholic beverages. Patients should avoid getting water into the area of surgical intervention, it is impossible to rub the eye. During this period, it is recommended to sleep on the side opposite to the surgical wound and limit physical activity. At the end of the rehabilitation period, it is necessary to be examined by an ophthalmologist 2 times a year.
Prognosis and prevention
Modern methods of ophthalmology cannot ensure a complete recovery of patients with glaucoma, but treatment is necessary, because this pathology is characterized by a progressive course and in the terminal stages of the disease leads to irreversible loss of vision. The prognosis for glaucoma in the early stages is favorable for life and performance. The reason for establishing a disability group is a sharp decrease in visual acuity.
Prevention of POAG is reduced to regular examination by an ophthalmologist of patients after 40 years, as well as all persons at risk. All patients with an established diagnosis of glaucoma should be registered at the dispensary and visit an ophthalmologist 1 time every 2-3 months.