Primary closed-angle glaucoma: causes, symptoms, diagnosis, treatment

Closed-angle glaucoma, developing with predisposing to this disease forms of the iris, is called primary closed-angle. Pathology can be with acute, subacute and secondary chronic closure of the angle with pupillary block or flat iris. In all forms of angle closure, the basis is a mechanical blockade of the outflow of aqueous humor through the trabecular meshwork by the peripheral part of the iris. In primary acute, subacute and chronic closure of the angle, relatively high pressure behind the iris pushes it forward. In the flat form, the iris is pushed forward by rotated ciliary processes.

The term "primary" is misleading because it implies an unknown mechanism, although in fact the mechanism of disease development is clear. However, this definition continues to be used, it distinguishes primary glaucoma from secondary closed-angle glaucoma, such as neovascular, neoplastic and other forms.

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Epidemiology of primary angle-closure glaucoma

Among patients of the white race, the prevalence of narrow angle reaches 2%, and the incidence of acute angle-closure glaucoma is 0.1%. In Eskimos, the incidence of this disease is 40 times higher. Acute angle-closure glaucoma is less common among the black population; they more often develop chronic angle-closure glaucoma. In people of the Asian race, the incidence of acute angle-closure glaucoma is higher than in the white race, but lower than in Eskimos. The ratio of acute angle-closure glaucoma in women to men is three to four. The highest prevalence of the disease by age is 55-65 years. Risk factors are hyperopia and a small anterior chamber.

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Pathophysiology of primary angle-closure glaucoma

The compression of the iris sphincter against the anterior capsule of the lens causes an increase in pressure behind the iris, causing it to bend forward in susceptible individuals and closing the trabecular meshwork. As a result, intraocular pressure increases. The contact of the pupil with the lens and the increase in pressure behind the iris is called a relative pupillary block. If the relative pupillary block is quite extensive and the angle is very narrow, the trabecular meshwork is completely blocked, intraocular pressure increases sharply, and acute angle-closure glaucoma develops. If the relative pupillary block is weak, the angle is narrow but not closed, and the trabecular meshwork is blocked only over a small area, then intraocular pressure increases very slowly, often over many years. This process is called chronic primary angle closure. Subacute angle-closure glaucoma is between acute and chronic in terms of development time, depending on the time it takes for intraocular pressure to increase.

Symptoms of Primary Angle-Closure Glaucoma

Acute angle closure

Symptoms range from mild one-sided blurred vision and pain to severe pain, nausea, vomiting, and sweating. These symptoms usually worsen in the evening. Attacks can be triggered by fatigue, poor lighting, stress, and prolonged close-up work.

Subacute angle closure

Symptoms of subacute angle closure include intermittent pain attacks and blurred vision. Symptoms develop in low light, stress, fatigue, and working close to the eyes. Sleep may interrupt the onset of an attack. This condition may be mistaken for a migraine headache.

Chronic angle closure

The absence of symptoms is typical. When the angle is completely closed, the pressure increases sharply, and the patient may complain of pain.

Diagnosis of primary angle-closure glaucoma

Biomicroscopy and gonioscopy

Acute angle closure

When examining the affected eye, a slightly dilated pupil, pronounced mesjunctival injection, corneal edema, and a shallow anterior chamber are determined. The iris is often in the position of a classic bombage. Intraocular pressure can reach 80 mm Hg. Light and precise suspension and opalescence are often visible. Gonioscopy is often difficult due to corneal edema. If possible, the iris is visible, covering the trabecular meshwork.

It is necessary to carefully examine the second eye, since it almost always also has a shallow anterior chamber with a narrow angle.

Subacute angle closure

The affected eye may be quiescent or have slight conjunctival injection, cellular suspension, and opalescence if the attack was recent. The anterior chamber may be slightly shallow, and a mild form of iris bombing is possible. Gonioscopy reveals a narrow but not closed angle.

Chronic angle closure

The eye is usually calm, the angle is slightly narrow. Gonioscopy shows a narrow angle with wide areas of peripheral anterior synechiae. In milder cases, the trabecular meshwork is visible in small areas of the angle.

Posterior pole

Acute angle closure

At the onset of increased intraocular pressure, the optic nerve disc is swollen and hyperemic. A prolonged attack leads to the appearance of disc pallor with visual field defects disproportionate to the excavation of the optic nerve disc (OND).

When the intraocular pressure is higher than the diastolic pressure, arterial pulsation is detected in the optic nerve head. If the intraocular pressure exceeds the perfusion pressure of the central retinal artery, retinal ischemia develops.

Subacute angle closure

With frequent attacks over a long period of time, the excavation of the optic disc expands.

Chronic angle closure

Typical changes associated with prolonged increase in intraocular pressure are observed on the optic nerve disc.

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Treatment of primary angle-closure glaucoma

Acute angle closure

To stop attacks of acute angle-closure glaucoma, it is necessary to eliminate the relative pupillary block. Mandatory treatment is peripheral iridectomy, which prevents further attacks of pressure increase.

When compression (gonioscopy with compression) is applied to the central area of the cornea with a Zeiss lens, the angle occasionally opens, leading to a transient increase in pressure in the anterior chamber and mechanical opening of the angle.

The attack can be interrupted pharmacologically by acting on the sphincter or dilator of the iris. In this case, the sphincter of the iris moves away from the surface of the lens to the critical zone of 4-5 mm, but this method is not always successful and can worsen the situation with further strengthening of the relative pupillary block. In addition, the attack is interrupted with the help of drugs that suppress the production of aqueous humor and osmotic agents, which reduces intraocular pressure and dehydrates the vitreous body, allowing the iris-lens diaphragm to shift backwards. As a result, the hydrodynamics that led to the development of the relative pupillary block change.

The most common method of treatment is the initial reduction of pressure with osmotic drugs and agents that reduce the production of intraocular fluid. After the disappearance of corneal edema, peripheral laser iridotomy is performed.

Subacute angle closure

The main method of treatment is laser peripheral iridotomy.

Chronic angle closure

Treatment involves laser peripheral iridotomy to prevent further angle closure. Damage may already have occurred in the trabecular meshwork, and despite a functioning iridotomy, intraocular pressure remains high, necessitating continued use of intraocular pressure-lowering medications.