Closed-angle glaucoma
Last reviewed: 23.04.2024
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Pathogenesis
A certain role in the pathogenesis of primary closed-angle glaucoma is played by genetic, nervous, endocrine and vascular factors. Primary angle-closure glaucoma is characterized by the same cardinal symptoms as open-angle: increased intraocular pressure, narrowing the field of view from the nose, the development of glaucomatous atrophy of the optic nerve with the formation of a characteristic excavation of the disk on the fundus.
Heredity determines the structure of the eye, predisposing to the development of the disease. These features are in the anatomical structure of the eye (narrow angle of the anterior chamber, small size of the eyeball, small anterior chamber, large lens, short anteroposterior axis, often hypermetropic clinical refraction of the eye, increased vitreous volume). Functional factors include dilatation of the pupil in the eye with a narrow angle of the anterior chamber, an increase in moisture in the interior, an increase in the blood filling of the intraocular vessels.
There are two mechanisms for the development of primary closed-angle glaucoma: the pupillary block and the formation of a fold in an anatomically flat iris.
The pupil block arises as a result of tight fitting of the pupil to the lens, because of which the internal moisture accumulates in the posterior chamber of the eye, the root of the iris protrudes toward the anterior chamber and blocks the entire angle.
With the dilatation of the pupil, the basal fold of the iris closes the filtration zone of the narrow angle of the anterior chamber in the absence of the pupillary block.
As a result of the accumulation of fluid in the posterior chamber, the vitreous body moves anteriorly, which can lead to a vitreochrustic block. In this case, the root of the iris is pressed down by the lens to the front wall of the anterior chamber angle. In addition, goniosynchia (spikes) are formed, the battle of the iris root with the anterior wall of the anterior chamber angle and its obliteration are noted. Most often there are patients with a pupillary block (80%) with primary closed angle glaucoma.
Symptoms of the angle-closure glaucoma
Acute attack of glaucoma
The pupil contraction is carried out by the muscle - the sphincter of the iris, which is innervated by the parasympathetic part of the autonomic nervous system. The pupil is dilated by a muscle - the iris dilator, innervated by the sympathetic part of the autonomic nervous system. There are situations when both muscles of the iris are active simultaneously, that is, they work in opposite directions, because of this, the pressure of the iris on the lens increases. This is observed with emotional stress or shock. A similar situation is possible during sleep. The course of the disease is undulating with attacks of restless interstitial periods. There are sharp and subacute attacks of primary closed-angle glaucoma, during which the intraocular pressure rises.
During an attack, atrophy of the optic nerve develops so quickly that care should be provided urgently.
To provoke an acute attack of glaucoma can be stressful situations, stay in the dark, long work in an inclined posture, instillation into the eye of the mydriatic, side effects of some common medicine.
In the eye there are severe pains, irradiating to the corresponding overhead or half of the head. The eye is red, the vascular pattern on the conjunctiva and sclera sharply increases. The cornea looks rough, dull, unclear compared to a transparent, shiny, healthy cornea; Through a pinched cornea is seen a wide oval pupil that does not respond to light. Iris changes color layer (as a rule, it becomes greenish-rusty), its pattern is smoothed, unclean. The front camera is either very small, or none at all, which can be seen with focal (side) illumination. Palpation of such an eye is painful. In addition, there is a stony density of the eyeball. Vision is sharply reduced, the patient seems to have a thick fog before his eye, around the light sources rainbow circles are visible. Intraocular pressure rises to 40-60 mm Hg. Art. As a result of constriction of a part of the vessels, the phenomena of focal or sectoral necrosis of the iris stroma develop with subsequent aseptic inflammation. The formation of the posterior synechiae but the edge of the pupil, goniosinechia, deformity and pupil displacement. Often due to severe pain in the eye due to the compression of sensitive nerve fibers, blood pressure rises significantly, nausea and vomiting appear. For this reason, this clinical condition is mistakenly regarded as a hypertensive crisis, a dynamic disorder of cerebral circulation or food poisoning. Such errors cause the patient to start lowering intraocular pressure too late, when disturbances in the optic nerve become irreversible and lead to the development of chronic, closed-angle glaucoma with constantly increased intraocular pressure.
Subacute attack of primary closed-angle glaucoma occurs in a lighter form if the angle of the anterior chamber is not closed all over or is not tight enough. With subacute attacks, vagulation does not develop and necrotic and inflammatory processes in the iris do not occur. Patients usually complain about blurring the vision and the appearance of rainbow circles when looking at the light. Pain in the eyeball is mild. When examined, there is a slight corneal edema, a mild dilatation of the pupil, hyperemia of the episcleral vessels. After a subacute attack there is no deformation of the pupil, segmental atrophy of the iris, the formation of the posterior synechia and goniosinechia.
The course of primary closed angle glaucoma with a pupillary block
Glaucoma, as a rule, is found in an acute or subacute attack. In the early stage of the disease, intraocular pressure rises only during attacks, during interictal periods it is normal. After repeated attacks, chronic glaucoma develops, the course of which has much in common with the course of primary open-angle glaucoma: increased intraocular pressure is noted constantly, changes in the field of vision and the optic nerve disk are characteristic for glaucoma.
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Subacute attack of glaucoma
This form is very rare and arises if there are anatomical predispositions in the eyes (reduced size of the eyeball, large lens, massive ciliated body). In the back of the eye, fluid accumulates. The iridocharrow diaphragm mixes anteriorly and blocks the angle of the anterior chamber. In this case, the lens can be restrained in the ring of the ciliary body.
Clinical picture of acute attack of glaucoma. On examination, the iris is closely adhered to the lens by its entire surface, as well as a very small, slit-shaped anterior chamber. The usual treatment for this form of primary closed-glaucoma is ineffective, therefore it is called "malignant glaucoma".
Anatomically flat iris
Anatomically flat iris is one of the factors that can cause an increase in intraocular pressure. Unlike the pupillary block with a flat iris, the closing of the angle of the anterior chamber occurs due to an anatomical structure, in which the iris located in the forwardmost position blocks the angle of the anterior chamber. With the dilatation of the pupil, there is a thickening of the periphery of the iris and the formation of folds. There may be a complete closure of the iridocorneal angle. Outflow of aqueous humor is disturbed, and intraocular pressure rises. Over the years, the likelihood of such a state increases. In order to have an attack when the angle of the anterior chamber is closed, the pupil must be greatly expanded. Compared with the pupillary block, closing the angle with a flat iris occurs much less frequently, but a combination of both variants is observed, sometimes it is difficult to establish a difference between them. Acute or subacute attack occurs as a result of blockade of the narrow angle of the anterior chamber by the peripheral fold of the iris with the dilatation of the pupil under the influence of the mydriatic, emotional excitement, stay in the dark.
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Treatment of the angle-closure glaucoma
Due to the high level of intraocular pressure and pronounced syndrome, urgent treatment is necessary. The main goal is to remove the iris from the trabecular network and thus facilitate the outflow of watery moisture. First, you need to equalize the pressure in the anterior and posterior chambers of the eye. To do this, an artificial hole is made on the periphery of the iris by a laser beam or by a surgical method. Thus, watery moisture gets a new path of outflow and penetrates the anterior chamber irrespective of the pupil. The first procedure is called laser iridotomy, and the other is surgical iridectomy. However, both procedures are difficult to perform when intraocular pressure is too high. Laser iridotomy is difficult due to corneal edema and a problematic examination of the internal structures of the eye, so there is a risk of laser damage to other eye tissues. Surgical intervention in the eye with high blood pressure is also risky: the eye tissue displaced forward by the high intraocular pressure may be injured in the incision.
For these reasons, it is first necessary to reduce intraocular pressure with medication, but at least during the first hours after the onset of an acute attack of glaucoma. Eye drops, which are usually used in the treatment of chronic glaucoma, with closed angle glaucoma are useless. Medicines are not practically absorbed by the tissues of the eye, since the diffusion of the drug is very difficult. In this regard, the appointment of powerful systemic drugs. Such drugs are not applied topically (in the form of drops or ointments), and are given in the form of tablets or intravenous injections and reach the area that is affected by circulation in the general blood stream. These substances, for example acetazolamide, reduce the production of aqueous humor, and mannitol, like proteins, directs fluid from the eye into the bloodstream and thereby reduces intraocular pressure. When intraocular pressure is sufficiently reduced, eye drops are prescribed to reduce intraocular pressure, and laser treatment or surgery is performed.
To prevent a sharp increase in intraocular pressure should achieve a constant moderate myosis (narrowing of the pupil). There is enough appointment for the night of an average dose of a myotic drug.
Prevention
The most important is to prevent a strong pupil dilating. In severe cases, especially if the seizures have already occurred, it is necessary to perform an easy drug miosis, especially at night. When combined with two possible mechanisms for developing an attack, (closing the angle with a flat iris and a pupillary block), peripheral iridotomy is indicated for prevention.
It is advisable not to allow the development of an acute attack of glaucoma. For this purpose, both iridotomy and iridectomy are shown. Carrying out such activities is necessary in that case. If on examination the ophthalmologist determines the occurrence of an acute attack, or when an acute attack of closed-angle glaucoma has already occurred in the pair eye.