How is acute angle-closure glaucoma (AACG) treated?

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

The treatment of acute angle-closure glaucoma (AACG) consists of IOP reduction, suppression of inflammation, and the reversal of angle closure. Once diagnosed, the initial intervention includes acetazolamide, a topical beta-blocker, and a topical steroid.

Acetazolamide should be given as a stat dose of 500 mg IV followed by 500 mg PO. A dose of a topical beta-blocker (ie, carteolol, timolol) will also aid in lowering IOP. Studies have not conclusively demonstrated the superior neuronal or visual field protectiveness of one beta-blocker over another. Both beta-blockers and acetazolamide are thought to decrease aqueous humor production and to enhance opening of the angle. An alpha-agonist can be added for a further decrease in IOP.

Inflammation is an important part of the pathophysiology and presenting symptomology. Topical steroids decrease the inflammatory reaction and reduce optic nerve damage. The current recommendation is for 1-2 doses of topical steroids.

Addressing the extraocular manifestations of the disease is critical. This includes analgesics for pain and antiemetics for nausea and vomiting, which can drastically increase IOP beyond its already elevated level. Placing the patient in the supine position may aid in comfort and reduce IOP. It is also believed that, while supine, the lens falls away from the iris decreasing pupillary block.

After the initial intervention, the patient should be reassessed. Reassessment includes evaluating IOP, evaluating adjunct drops, and considering the need for further intervention, such as osmotic agents and immediate iridotomy.

Approximately 1 hour after beginning treatment, pilocarpine, a miotic that leads to opening of the angle, should be administered every 15 minutes for 2 doses. In the initial attack, the elevated pressure in the anterior chamber causes a pressure-induced ischemic paralysis of the iris. At this time, pilocarpine would be ineffective. During the second evaluation, the initial agents have decreased the elevated IOP and hopefully have reduced the ischemic paralysis so pilocarpine becomes beneficial in relieving pupillary block.

Pilocarpine must be used with caution. Theoretical concerns exist about its mechanism of action. By constricting the ciliary muscle, it has been shown to increase the axial thickness of the lens and to induce anterior lens movement. This could result in reducing the depth of the anterior chamber and worsening the clinical situation in a paradoxical reaction. Despite this, pilocarpine is recommended to be used as an additional agent. [17]

No standard rate of reduction for IOP exists; however, Choong et el identified a satisfactory reduction as IOP less than 35 mm Hg or a reduction greater than 25% of presenting IOP. [16] If the IOP is not reduced 30 minutes after the second dose of pilocarpine, an osmotic agent must be considered. An oral agent like glycerol can be administered in nondiabetics. In diabetics, oral isosorbide is used to avoid the risk of hyperglycemia associated with glycerol. Patients who are unable to tolerate oral intake or do not experience a decrease in IOP despite oral therapy are candidates for IV mannitol.


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