Acute Angle-Closure Glaucoma in Emergency Medicine Treatment & Management

The patient should be brought to the hospital in an expeditious manner to have intraocular pressure (IOP) reduced. The patient should remain in the supine position as long as possible. The urge to wear eye patches, covers, or blindfolds should be resisted. By maintaining the conditions that cause pupillary dilation, these articles help perpetuate the attack. Their potential negative effects outweigh any presumed benefit.

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. ^[20]

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. ^[19] 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.

Hyperosmotic agents are useful for several reasons. They reduce vitreous volume, which, in turn, decreases IOP. The decreased IOP reverses iris ischemia and improves its responsiveness to pilocarpine and other drugs. Osmotic agents cause an osmotic diuresis and total body fluid reduction. They should be administered with caution in cardiovascular and renal patients. Choong et el demonstrated that 44% of patients required the addition of an osmotic agent to decrease IOP. ^[21] Repeat doses may be necessary if no effect is seen and if tolerated by the patient.

If patients fail medical management, there are surgical options (briefly touched on below).The ophthalmologist will evaluate all patients via gonioscopy (with complete inspection of the angle) to further decide the treatment course. At institutions where ophthalmologic consultation is immediately available, initial treatment should be performed in conjunction with the specialist.

If ophthalmologic consultation is not immediately available, the emergency department physician must begin pharmacologic therapy as described above. After appropriate IOP-reducing therapy is administered, ophthalmologic evaluation must be ensured by transferring the patient, if necessary. If the IOP is unchanged or continues to increase in spite of appropriate pharmacologic therapy, the attack will most likely persist without surgical management. Because outcome is adversely affected by the duration of symptoms, expeditious evaluation by a specialist is required. Ocular massage through a closed eyelid may be performed while waiting for ophthalmology if no other treatment reduces IOP.

Ophthalmologic consultation should be obtained as soon as possible because acute-angle closure glaucoma is an ophthalmic emergency.

When medical therapy proves to be ineffective, corneal indentation (CI) can be used as a temporizing measure to reduce IOP until definitive treatment is available. As the cornea is indented, aqueous humor is displaced to the periphery of the anterior chamber, which serves to temporarily open the angle. This leads to immediate reduction of IOP and occasionally may completely abort the attack. After applying topical anesthetic, any smooth instrument can be used to perform this procedure, including a gonioprism (ideal, if available), or a cotton-tipped applicator. Obviously, a concern with performing CI is the possibility for damage to the corneal epithelium, which may complicate the patient’s course. ^[22]

Laser peripheral iridotomy (LPI), performed 24-48 hours after IOP is controlled, is considered the definitive treatment for AACG. Furthermore, LPI may be offered prophylactically to individuals anatomically predisposed to AACG if identified before the first acute attack. While LPI is the current definitive treatment, evidence suggests that argon laser peripheral iridoplasty (ALPI) and anterior chamber paracentesis (ACP) may have increasing roles in the management of AACG.

In ALPI, burns are made in the peripheral iris resulting in iris contraction and opening of the angle. Some studies suggest ALPI causes a more immediate decrease in IOP, resulting in better outcomes with fewer side effects than systemic therapy ^[23] ; however, a recent randomized-controlled trial comparing LPI plus ALPI compared with ALI alone failed to show improved outcomes with ALPI as an adjunctive therapy. ^[24]  Systemic therapy must still be used with ACP, but ACP appears to instantaneously relieve symptoms.

An additional alternative is lens extraction. Although its role in AACG has not been completely established, it has been proven to effectively reduce IOP without the need for medication postoperatively. Furthermore, it offers a therapeutic advantage for individuals with coexisting cataracts. ^[25]