bubble_chart Overview

Chronic angle-closure glaucoma accounts for more than 50% of primary glaucoma cases, with 84% occurring in individuals over 30 years old, mostly affecting both eyes. This indicates that it is one of the common eye diseases among middle-aged and elderly people. Most cases of chronic angle-closure glaucoma have a history of repeated minor attacks, while some develop gradually without noticeable symptoms. It can only be distinguished from chronic simple glaucoma through gonioscopy.

bubble_chart Etiology

1. Internal factors: Anatomical and physiological factors.

(1) Variations within the normal range of anatomical structure and genetic defects: such as microphthalmos, small-angle membrane, hyperopia, shallow anterior chamber, and high-rolled red membrane edge, which result in a shallow anterior chamber and narrow angle, leading to impaired aqueous humor outflow.

(2) Physiological changes: Pupillary block, shallow anterior chamber, and narrow angle, with grade II pupil dilation being a key condition. Additionally, with advancing age, the lens grows progressively closer to the pupillary margin, creating pupillary block between the iris and lens, causing the posterior chamber pressure to exceed the anterior chamber pressure. Coupled with weakened elasticity of the corneal-scleral membrane and its inability to compensate for sudden pressure increases, the peripheral iris is pushed forward, resulting in iris bombe and angle closure, leading to increased intraocular pressure.

2. External factors

(1) Emotional hormones: Dysfunction of the central nervous system, imbalance of excitation and inhibition in the cerebral cortex, and impairment of the diencephalic intraocular pressure regulation center. Vascular motor nerve dysfunction causes congestion and edema of the pigment membrane, while sympathetic nerve excitation dilates the pupil, both of which can push the iris root toward the periphery, obstructing the angle.

(2) Pupil dilation due to mydriatic drops, dark room testing, or prolonged movie or TV watching can dilate the pupil, obstruct the angle, and lead to increased intraocular pressure.

Schematic diagram of angle-closure glaucoma onset:

bubble_chart Pathological Changes

Elevated intraocular pressure can lead to a series of pathological tissue changes in the eye.

1. Acute phase: Manifested as circulatory disturbances and tissue edema in the eye, corneal edema, congestion and edema of the iris and ciliary body, and even exudation, dilation of blood vessels in the bulbar conjunctiva, and dilation, congestion, or even hemorrhage of retinal blood vessels.

In the initial stage of acute angle-closure glaucoma, the iris stroma is highly congested and edematous, and the iris root shifts forward to closely contact the trabecular meshwork, making the anterior chamber angle narrower or completely occluded. During this period, the anterior chamber angle is merely in contact without fibrous adhesion, and the acute symptoms can be relieved after the acute phase. If improperly treated or recurrent, prolonged contact between the iris root and the trabecular meshwork can lead to fibrosis and degeneration of the iris stroma and the trabecular meshwork, resulting in permanent adhesions. The occluded anterior chamber will not reopen, and Schlemm's canal may become deformed due to compression, permanently losing its aqueous humor drainage function.

2. Chronic phase: Manifested as tissue degeneration or atrophy, such as bullous keratitis caused by corneal degeneration, atrophy and pigment loss of the iris and ciliary body, retinal and optic nerve atrophy, and the formation of a typical glaucomatous optic cup.

Primary glaucoma often affects both eyes, may occur sequentially, and has a familial genetic predisposition.

bubble_chart Clinical Manifestations

According to the morphology of the anterior chamber angle, it can be further divided into two types:

**Iris Bombe Type**: The anterior chamber is shallow, the angle is narrow, and the iris is bulging. During an attack, intraocular pressure rises, accompanied by rainbow vision, blurred vision, dizziness, and eye distension. After repeated attacks, the baseline pressure (the lowest intraocular pressure over 24 hours) gradually increases. Peripheral anterior synechiae (PAS) appear in the angle, adhering to the back of the cornea. During high intraocular pressure, the pupil dilates to grade I.

**Iris Plateau Type**: This is a type of angle-closure glaucoma without pupillary block, also known as short-angle glaucoma. In these patients, the depth of the anterior chamber is normal, and pupillary block is not significant. The main issue is that the peripheral iris is highly folded and tightly adheres to the trabecular meshwork, obstructing aqueous outflow.

The iris appears highly folded, with a deep central anterior chamber but a narrow angle. Under gonioscopy, the anterior surface of the iris appears "normal" or even slightly concave (grade I). However, the iris root is elongated and may protrude into the angle, forming a plateau iris. Hence, it is also called root-insertion glaucoma. When the pupil dilates, the peripheral iris folds into the narrow angle and contacts the trabecular meshwork, obstructing aqueous outflow at the apex of the angle. However, the changes in the four quadrants of the anterior chamber angle are not uniform, with significant differences in width between quadrants. This is one of the key diagnostic criteria for chronic angle-closure glaucoma.

1. Attacks are often triggered by emotional disturbances, fatigue, or prolonged reading, manifesting as rainbow vision, foggy vision, and eye distension, which may resolve spontaneously after rest or sleep.

2. There may be grade I or grade II ciliary congestion in the anterior segment (sometimes absent). The angle shows extensive, permanent synechiae, appearing closed or with peripheral iris folds adhering to the trabecular meshwork, resulting in a shallow anterior chamber, narrow angle, angle closure, and obstructed aqueous outflow.

3. Intraocular pressure rises suddenly in a cyclical pattern. Miotics alone cannot lower the pressure. Initially, the intervals between attacks are long, but they gradually worsen due to angle synechiae, leading to persistent high intraocular pressure.

4. The fundus shows no changes in the early stages, but in the advanced stage, optic nerve atrophy becomes the dominant feature, forming a glaucomatous cup.

5. Visual field damage resembles that of primary open-angle glaucoma. Vision gradually declines until complete loss occurs.

bubble_chart Diagnosis

1. Iris Bombe Type

(1) Recurrent intermittent elevation of intraocular pressure and eye pain, often accompanied by grade I congestion and rainbow vision. Generally, major attacks are only minor episodes or mild subjective symptoms.

(2) There is slight pigmentation behind the corneal membrane, but no glaucomatous flecks or iris atrophy.

(3) When intraocular pressure rises to 4.7 kPa (35 mmHg), the angle partially closes. However, when the pressure returns to normal, the angle also normalizes.

(4) Provocative tests—positive dark room and prone dark room tests.

(5) In advanced stages, glaucomatous changes appear successively in the fundus and visual field.

2. Plateau Iris Type

(1) No obvious symptoms in the early stage, with a slow rise in intraocular pressure.

(2) The iris root is elongated, the angle entrance is narrow, the iris surface is flat, the central anterior chamber is deep, and the angle is short.

(3) Pupil dilation.

(4) After peripheral iridectomy, pupil dilation can induce an attack.

(5) In advanced stages, typical glaucomatous visual field and fundus changes occur.

bubble_chart Treatment Measures

1. Early stage: Peripheral iridectomy or laser iridotomy can be performed.

2. Chronic stage: Frequent attacks, peripheral anterior synechiae, contact between the iris and trabecular meshwork, inability to reopen the angle, decreased aqueous outflow function, and even damage to the optic disc and visual field may occur. Trabeculectomy can be performed to relieve pupillary block and facilitate external drainage.

3. Plateau iris syndrome glaucoma: This type of glaucoma is primarily treated with strong miotics such as 4% pilocarpine or 0.06% echothiophate iodide. 1% pilocarpine cannot flatten the abundant, thick peripheral iris folds. Some advocate surgical treatment, performing a large sector iridectomy, followed by continued miotic therapy to manage residual glaucoma.

4. For the contralateral eye in cases of unilateral onset, prophylactic peripheral iridectomy or laser iridotomy may be performed.