Closed-angle glaucoma

Primary angle-closure glaucoma is 2-3 times less common than primary open-angle glaucoma. Women are more likely to get sick than men.

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Pathogenesis

Genetic, nervous, endocrine and vascular factors play a certain role in the pathogenesis of primary closed-angle glaucoma. Primary closed-angle glaucoma has the same cardinal symptoms as open-angle glaucoma: increased intraocular pressure, narrowing of the visual field on the nasal side, development of glaucomatous atrophy of the optic nerve with the formation of a characteristic excavation of its disk on the fundus.

Heredity determines the structural features of the eye that predispose 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, more often hypermetropic clinical refraction of the eye, increased volume of the vitreous body). Functional factors include pupil dilation in the eye with a narrow angle of the anterior chamber, increased intraocular moisture, increased blood filling of the intraocular vessels.

There are two mechanisms for the development of primary angle-closure glaucoma: pupillary block and the formation of a fold with an anatomically flat iris.

Pupillary block occurs when the pupil is too tightly attached to the lens, causing internal fluid to accumulate in the posterior chamber of the eye, causing the root of the iris to bulge toward the anterior chamber and block its angle.

When the pupil dilates, the root fold of the iris closes the filtration zone of the narrow angle of the anterior chamber in the absence of pupillary block.

As a result of fluid accumulation in the posterior chamber, the vitreous body shifts forward, which can lead to a vitreocrystalline lens block. In this case, the root of the iris is pressed by the lens to the anterior wall of the anterior chamber angle. In addition, goniosynechiae (adhesions) are formed, and the root of the iris fights with the anterior wall of the anterior chamber angle and obliterates it. Most often, patients with a pupillary block (80%) with primary angle-closure glaucoma are encountered.

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Symptoms closed-angle glaucoma

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Acute attack of glaucoma

The pupil is narrowed by the sphincter muscle of the iris, which is innervated by the parasympathetic part of the autonomic nervous system. The pupil is dilated by the dilator muscle of the iris, which is innervated by the sympathetic part of the autonomic nervous system. There are situations when both muscles of the iris are active simultaneously, i.e. they work in opposite directions, which increases the pressure of the iris on the lens. This is observed during emotional stress or shock. A similar situation is possible during sleep. The course of the disease is wave-like with attacks of restless interictal periods. Acute and subacute attacks of primary closed-angle glaucoma are distinguished, during which intraocular pressure increases.

During an attack, optic nerve atrophy develops so rapidly that assistance must be provided immediately.

An acute attack of glaucoma can be provoked by stressful situations, staying in the dark, prolonged work in a bent position, instillation of mydriatics into the eye, and side effects of some commonly used medications.

Severe pain appears in the eye, radiating to the corresponding brow or half of the head. The eye is red, the vascular pattern on the conjunctiva and sclera is sharply intensified. The cornea looks rough, dull, cloudy compared to the transparent, shiny healthy cornea; a wide oval pupil is visible through the cloudy cornea, which does not react to light. The iris changes layer color (usually becomes greenish-rusty), its pattern is smoothed out, unclear. The anterior chamber is either very small or completely absent, which can be seen with focal (lateral) lighting. Palpation of such an eye is painful. In addition, a stony density of the eyeball is felt. Vision is sharply reduced, it seems to the patient that there is a thick fog in front of the eye, rainbow circles are visible around light sources. Intraocular pressure increases to 40-60 mm Hg. As a result of narrowing of some of the vessels, focal or sectoral necrosis of the iris stroma develops with subsequent aseptic inflammation. Formation of posterior synechiae at the edge of the pupil, goniosynechia, deformation and displacement of the pupil. Often, due to severe pain in the eye due to compression of sensitive nerve fibers, arterial pressure increases significantly, nausea and vomiting occur. For this reason, this clinical condition is mistakenly assessed as a hypertensive crisis, dynamic cerebrovascular accident or food poisoning. Such errors lead to the fact that the patient's intraocular pressure is reduced too late, when the disorders in the optic nerve become irreversible and lead to the development of chronic closed-angle glaucoma with constantly elevated intraocular pressure.

A subacute attack of primary angle-closure glaucoma occurs in a milder form if the anterior chamber angle does not close completely or not tightly enough. Subacute attacks are characterized by no strangulation of the vessels and no necrotic or inflammatory processes in the iris. Patients usually complain of blurred vision and the appearance of rainbow circles when looking at light. Pain in the eyeball is mild. On examination, slight corneal edema, moderate pupil dilation, and hyperemia of the episcleral vessels are noted. After a subacute attack, there is no deformation of the pupil, segmental atrophy of the iris, or formation of posterior synechiae and goniosynechia.

Course of primary angle-closure glaucoma with pupillary block

Glaucoma is usually detected during an acute or subacute attack. In the early stages of the disease, intraocular pressure increases only during attacks, and is normal between attacks. After repeated attacks, chronic glaucoma develops, the course of which has much in common with the course of primary open-angle glaucoma: intraocular pressure increases constantly, and changes in the visual field and optic disc characteristic of glaucoma develop.

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Subacute attack of glaucoma

This form is very rare and occurs if there are anatomical predispositions in the eyes (reduced size of the eyeball, large lens, massive ciliary body). Fluid accumulates in the posterior part of the eye. The iris-lens diaphragm moves forward and blocks the angle of the anterior chamber. In this case, the lens can be pinched in the ring of the ciliary body.

Clinical picture of an acute attack of glaucoma. During examination, a tight fit of the iris with its entire surface to the lens is noted, as well as a very small, slit-like anterior chamber. Conventional treatment of this form of primary closed-angle glaucoma is ineffective, so 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 pupillary block, with a flat iris, the closure of the angle of the anterior chamber occurs due to the anatomical structure, in which the iris, which is in the extreme anterior position, blocks the angle of the anterior chamber. When the pupil dilates, the periphery of the iris thickens and folds form. Complete closure of the iridocorneal angle may occur. The outflow of aqueous humor is disrupted, and intraocular pressure increases. With age, the likelihood of such a condition increases. In order for an attack to occur with closure of the angle of the anterior chamber, the pupil must be greatly dilated. Compared to pupillary block, closure of the angle with a flat iris is much less common, but a combination of both options is observed, sometimes it is difficult to distinguish between them. An 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 during pupil dilation under the influence of mydriatics, emotional arousal, or being in the dark.

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Treatment closed-angle glaucoma

Due to the high intraocular pressure and the severe syndrome, urgent treatment is necessary. The main goal is to remove the iris from the trabecular meshwork and thus facilitate the outflow of aqueous humor. First, it is necessary to equalize the pressure in the anterior and posterior chambers of the eye. To do this, an artificial opening is made on the periphery of the iris using a laser beam or a surgical method. In this way, the aqueous humor receives a new outflow path and penetrates into the anterior chamber independently of the pupil. The first procedure is called laser iridotomy, and the other is surgical iridectomy. However, both procedures are difficult to perform when the intraocular pressure is too high. Laser iridotomy is difficult due to corneal edema and problematic examination of the internal structures of the eye, so there is a risk of laser damage to other eye tissues. Surgery in an eye with high pressure is also risky: eye tissue displaced forward by high intraocular pressure may be pinched in the incision.

For these reasons, it is first necessary to reduce the intraocular pressure with medication, at least during the first hours of an acute attack of glaucoma. Eye drops, which are usually used to treat chronic glaucoma, are useless in closed-angle glaucoma. The drugs are practically not absorbed by the tissues of the eye, since the diffusion of the drug is very difficult. In this regard, it is necessary to prescribe powerful systemic drugs. Such drugs are not applied locally (in the form of drops or ointments), but are administered as tablets or intravenous injections and reach the area they act on due to circulation in the general bloodstream. These substances, such as 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 the 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, it is necessary to achieve constant moderate miosis (narrowing of the pupil). It is sometimes sufficient to prescribe a medium dose of a miotic drug at night.

Prevention

The most important thing is to prevent severe pupil dilation. In severe cases, especially if attacks have already occurred, it is necessary to conduct light medicinal miosis, especially at night. In the case of a combination of two possible mechanisms of attack development (closure of the angle by a flat iris and pupillary block), peripheral iridotomy is indicated for prevention.

It is desirable to prevent the development of an acute attack of glaucoma. For this purpose, both iridotomy and iridectomy are indicated. Such measures are necessary in the event that during the examination the ophthalmologist determines the occurrence of an acute attack, or when an acute attack of angle-closure glaucoma has already occurred in the fellow eye.

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