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

Updated: Nov 19, 2018
  • Author: Joseph Freedman, MD; Chief Editor: Steven C Dronen, MD, FAAEM  more...
  • Print
Answer

AACG represents the end stage of processes resulting in the compromised egress of aqueous humor circulation and the subsequent increase in IOP. Aqueous humor is produced by the ciliary body in the posterior chamber of the eye. It diffuses from the posterior chamber, through the pupil, and into the anterior chamber. From the anterior chamber, the fluid is drained into the vascular system via the trabecular meshwork and Schlemm canal contained within the angle.

Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals to AACG. These include shallower anterior chambers, thinner ciliary bodies, a thinner iris, anteriorly situated thicker lens, [2] and a shorter axial eye length. Recent studies have suggested that increased iris thickness and cross-sectional area are associated with increased risk. [3] Of the many predisposing anatomical variations, a narrow angle has the most devastating consequences.

In the traditional model of AACG, the eye's natural response of dilation to environmental or chemical stimuli results in a pathologic iris-lens apposition. The apposition and contact between the lens and the iris is called pupillary block. Furthermore, pupillary block describes a state in which the forward-most surface of the lens is anterior to the plane of the iris insertion into the ciliary body. As a result, aqueous flow from the posterior chamber to the anterior chamber is obstructed or altogether blocked. When pupillary block occurs in conjunction with the iris, the increasing pressure in the posterior chamber causes the pliable iris, particularly the peripheral region, to bow forward in a process termed iris bombé. Iris bombé further closes the already narrow angle and compromises aqueous drainage, thus increasing IOP.

Recent research has suggested an alternative pathophysiologic pathway for AACG. Cronemberger et al propose that acute events can be traced to an autonomic imbalance in individuals with AACG, specifically increased sympathetic tone. Furthermore, the iris dilator muscles in these individuals have been found to be more developed and stronger. In instances of increased ocular sympathetic tone, including emotional distress, low light conditions, or after sympathomimetic drug use, contraction of the iris dilator muscles leads to pupil dilatation and thickening of the middle-peripheral iris. This thickening can lead to angle closure, thereby obstructing the outflow of aqueous humor. [4]

Other proposed mechanisms of AACG include plateau iris, lens swelling, and ciliary block. Plateau iris is less common than pupillary block and is due to anterior insertion of the iris. The superfluous and crowded iris tissue blocks the trabecular meshwork and again leads to increased IOP.

Lens swelling and ciliary block are extremely rare. Lens swelling occurs in cases of cataracts in which hydration forces cause enlargement of the lens and subsequent crowding of the anterior chamber. Forces posterior to the lens can push the lens and iris forward causing ciliary block or vitreous pressure. This can be seen in panretinal photocoagulation, scleral buckles, and uveitis.


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!