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Primary and secondary open-angle glaucoma
Last reviewed: 05.07.2025

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Primary open-angle glaucoma without visible glaucomatous damage is called ocular hypertension (a condition in which the intraocular pressure is above 21 mm Hg). This condition should also be classified as glaucoma. The development of glaucomatous damage can occur both at intraocular pressure above 21 mm Hg and at lower values. However, the likelihood of this happening increases with increasing pressure.
Causes open-angle glaucoma
The pathogenesis of open-angle glaucoma is associated with a disruption of the normal function of the eye drainage system, through which fluid is drained from it; dystrophic and degenerative changes are always found in the drainage zone of the limbus. In the initial stage of the disease, these changes are minimal: the trabecular plates thicken, the intrabecular slits and especially the Schlemm's canal narrow. Later, the trabecula almost completely degenerates, the slits in it disappear, the Schlemm's canal and some of the collecting canals overgrow. In the late stages of glaucoma, degenerative changes in the eye are secondary and are associated with the effect of increased intraocular pressure on the tissue. In open-angle glaucoma, the trabeculae shift toward the outer wall of the Schlemm's canal, narrowing its lumen. This condition is called a functional block of the venous sinus of the sclera. Sinus block occurs more easily in eyes with an anatomical predisposition, i.e. with an anterior position of the venous sinus of the sclera, weak development of the scleral spur and a relatively posterior position of the ciliary muscle. All changes in the drainage system of the eye depend to a certain extent on nervous, endocrine and vascular disorders. Therefore, primary glaucoma is combined with such diseases as atherosclerosis, hypertension, diabetes mellitus, lesions of the subtubercular region. The degree and nature of degenerative changes in the drainage apparatus in glaucoma are determined by genetic factors. As a result, open-angle glaucoma is often familial.
Risk factors
Risk factors for primary open-angle glaucoma include old age, heredity, race (representatives of the Negroid race are 2-3 times more likely to get sick), diabetes mellitus, glucocorticoid metabolism disorders, arterial hypotension, myopic refraction, early hyperopia, and pigment dispersion syndrome.
Symptoms open-angle glaucoma
Most often, open-angle glaucoma begins and progresses unnoticed by the patient, who does not experience any unpleasant sensations and consults a doctor only when severe visual impairments appear (advanced or advanced stages); at these stages, achieving stabilization of the process becomes very difficult, if not impossible.
With open-angle glaucoma, it can be confused with cataracts, leaving the patient untreated and allowing the development of incurable blindness.
With cataracts, intraocular pressure is normal, and when examined in transmitted light, the pink glow of the pupil is weakened and black streaks and spots of more intense opacities can be distinguished against its background.
In glaucoma, intraocular pressure increases, the visual field begins to progressively narrow on the nasal side, the pupil glows bright pink in transmitted light (if there is no concomitant cataract), and the optic disc becomes grayish, the vessels along its edge bend (glaucomatous excavation). The same changes are characteristic of open-angle glaucoma with normal intraocular pressure. In addition, this type of glaucoma is characterized by hemorrhages on the optic disc, pericapillary atrophy, shallow excavation of the optic disc, sometimes with a pale neuroretinal ring, gliosis-like changes in the retina, and some changes in the conjunctival vessels. All these symptoms are determined by an ophthalmologist and indicate additional factors involved in the mechanism of glaucomatous damage in this type of glaucoma. In normal cerebrospinal fluid pressure glaucoma, acute hemodynamic disturbances (hemodynamic crises, decreased blood pressure at night, vascular spasms) and chronic disturbances of blood microcirculation in the optic nerve disc (venous dyscirculation, microthrombosis) are observed in the retrobulbar region of the optic nerve.
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Treatment open-angle glaucoma
The slightest suspicion of glaucoma requires a detailed examination in specialized offices or even in a hospital.
Patients with glaucoma should be under the regular observation of an ophthalmologist (visit the doctor 2-3 times a year, and more often if necessary), who monitors the field of vision, visual acuity, intraocular pressure level, and the state of the optic nerve. This allows us to judge the dynamics of the pathological process, promptly change the medication regimen, and in the absence of normalization of intraocular pressure under the influence of drops, recommend a transition to surgical treatment - traditional or laser. Only such a set of measures can help preserve visual functions for many years. Any antiglaucoma surgery aims only to reduce intraocular pressure, i.e., in essence, it is a symptomatic method of treatment. It does not imply improvement of visual functions or getting rid of glaucoma.
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Prevention
The basis for preventing blindness from glaucoma is early detection of the disease. For this purpose, all people over forty years of age should instrumentally measure intraocular pressure once every 2-3 years. In cases where there are patients with established glaucoma, their relatives should do this from the age of thirty-five, while it is desirable to evaluate the visual field using the perimeter and examine the optic nerve disc.
Forecast
The prognosis for normal-tension glaucoma is similar to that for high-tension glaucoma. Without adequate therapy to lower intraocular pressure, blindness may occur. However, a feature of normal-tension glaucoma is that, despite the pronounced visual impairment, cases of complete blindness are rare. This is explained by the fact that with age, the role of vascular risk factors causing this type of glaucoma (low blood pressure and vascular regulation disorders) weakens.