What is the pathophysiology of acute angle-closure glaucoma (AACG)?

Updated: Jun 20, 2019
  • Author: Albert P Lin, MD; Chief Editor: Inci Irak Dersu, MD, MPH  more...
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AAC occurs through a process termed pupillary block. Normally, aqueous humor is produced in the ciliary body, flows through the pupil into the anterior chamber, and drains into the trabecular meshwork to exit the eye. When the pupil is mid-dilated, the distance between the iris and the lens is the shortest, and the two structures can come into contact with each other in individuals at risk for angle closure. When this occurs, aqueous humor cannot flow through the pupil into the anterior chamber (pupillary block), pushing the iris forward. When the iris is pushed against the trabecular meshwork, aqueous humor cannot flow out of the eye (angle closure), increasing IOP.

The normal IOP is 10-21 mm Hg. In AAC, and IOP typically exceeds 40 mm Hg. The sudden and severe elevation in IOP can cause irreversible optic nerve damage very quickly (acute angle-closure glaucoma).

Mechanisms other than pupillary block can also contribute to primary angle closure, including plateau iris, use of certain medications, increased iris thickness, increased iris volume with dilation, hyperopia, and increased lens thickness in phacomorphic angle closure.

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