Primary Angle-Closure Glaucoma Clinical Presentation

Updated: May 09, 2016
  • Author: Clement Chee-yung Tham, BM, BCh, MA, FRCS(Glasg); Chief Editor: Hampton Roy, Sr, MD  more...
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Presentation

History

Primary angle-closure glaucoma (PACG) is usually asymptomatic because of its slow onset, as opposed to acute angle-closure glaucoma (AACG), which presents with pain and nausea due to the rapid intraocular pressure (IOP) increase. However, patients with PACG may report transient eye pain, headache, and/or halo visualization.

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Physical

Insertion of the iris at or anterior to the scleral spur is rare in young individuals, and, in many eyes with angle-closure glaucoma that have such an insertion, creeping angle closure is the underlying reason. It occurs in eyes with slightly deeper anterior chambers than are found in AACG. Gradual shortening of the angle in the presence of iris bombé brings the peripheral iris close to the external angle wall more anteriorly, narrowing the gap between the iris and the trabecular meshwork. Eventually, AACG may supervene, or PAS may permanently occlude the trabecular meshwork and lead to elevated IOP and glaucomatous damage.

The IOP in eyes with primary angle closure (PAC) may be normal or elevated. As peripheral anterior synechiae (PAS) formation progresses in the absence of intermittent attacks, IOP rises gradually as less and less functional meshwork becomes available. In eyes with intermittent attacks, IOP rises more rapidly relative to the extent of PAS formation caused by recurrent damage to the trabecular meshwork by the transient angle closure.

Other signs 

Blotches of pigment on the meshwork, particularly in the superior angle, or deposits of black pigment in the angle of a lightly pigmented iris are highly suggestive of previous appositional closure. If the angle opens, this deposited line of pigment shows the extent of previous angle closure and sometimes can be a helpful diagnostic feature.

The anterior chamber is quiet and usually deeper than in eyes with AACG.

The pupil is normal.

The gradual elevation of IOP does not result in corneal endothelial decompensation, and corneal edema is rare. The IOP is usually less than 40 mm Hg and does not reach the levels found in AACG. Symptoms are absent until the pressure rises high enough to affect the cornea or until extensive visual field damage has occurred. Although iridotomy will eliminate the pupillary block, IOP often remains elevated, and further medical treatment or surgery is required.

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Causes

Causes of PACG include PAS formation, plateau iris, combined mechanism glaucoma, mixed mechanism glaucoma, and miotic-induced glaucoma.

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