Management of Acute Angle-Closure Glaucoma in an Emergent Setting

Acute angle-closure glaucoma (AACG) is an ocular emergency that causes sudden-onset eye pain, decreased vision, headache, and nausea or vomiting.¹ Primary AACG typically occurs in patients with narrow angles, which increases the risk of appositional closure and pupillary block and can lead to a sudden elevation of IOP.²

The management of AACG in an emergent setting focuses on reducing IOP to prevent optic nerve damage. Laser peripheral iridotomy (LPI) is often the definitive treatment for AACG secondary to pupillary block; however, patients with AACG may have significant corneal edema or inflammation that precludes an adequate view for LPI, or they may present in emergent settings where a laser is not immediately available. In this article, glaucoma specialists from hospitals across the country discuss their approaches to patients who present with AACG in an emergent setting.

DILRU AMARASEKERA, MD

Patients with AACG often present to our dedicated eye emergency room (ER). A thorough history and examination are performed to confirm the diagnosis. Because these patients’ pupils should not be dilated, B-scan ultrasound is performed to rule out posterior pathology as a mechanism for IOP elevation.

Therapy with three rounds of brimonidine and a fixed combination of dorzolamide and timolol is initiated immediately. If the IOP is not responsive, intravenous (IV) acetazolamide 500 mg is administered. If pressure reduction is still insufficient, then IV mannitol (1–2 g/kg) is administered after the patient is confirmed not to have any medical contraindications. IV mannitol dehydrates the vitreous and draws fluid from the eye, and treatment is often exceptionally effective at lowering the IOP and breaking the angle-closure episode.

The patient is seen in the clinic 1 or 2 days thereafter. If the cornea is clear enough for a view, an LPI is performed in the office. Often, the cornea is still highly edematous, and the anterior chamber is inflamed, increasing the risk of iridotomy closure or corneal damage from laser treatment. In this situation, an LPI is performed in the contralateral eye (if the angle is narrow), therapy with steroids and aqueous suppressants is continued in the affected eye, and an LPI is reattempted within 1 week if the view improves. If the view remains insufficient for an LPI or if the procedure does not decrease the IOP, phacoemulsification with or without glaucoma surgery is performed.

DANIEL PETKOVSEK, MD, AND MARY QIU, MD

In patients with elevated IOP for whom AACG is a concern, initial management is guided by their presentation. If they present through the ER, we recommend that they be admitted and initiate IOP-lowering topical therapy and IV acetazolamide. If these measures fail to improve the IOP within 1 or 2 hours and the patient is an appropriate candidate, IV mannitol (25–50 g in a 20% solution) is considered. It is important to advise the ER staff to avoid instilling pilocarpine, which can confound the exam if pupillary block is not the etiology of angle closure. If the patient is a clinic walk-in, therapy with topical drops and immediate-release oral acetazolamide is initiated.

In either of the aforementioned scenarios, a careful history is obtained, and a thorough examination is performed. If pupillary block appears to be the cause of angle closure, an LPI is performed. A discussion with the patient and a review of their medical history, however, may reveal a precipitating factor. For example, a history of trauma or topiramate use or a comparison of autorefraction and lensometer measurements may reveal a myopic shift and raise suspicion of a ciliary body effusion, which would change management.

If an LPI is successfully performed, the patient is monitored for a few hours to determine whether IOP control has improved, ideally to lower than 35 mm Hg. IOP-lowering medications are continued, and the patient is asked to return the next day for follow-up. If the fellow eye is at risk of angle closure, we perform an LPI on that eye as well.

If there is too much corneal edema for an LPI to be performed, treatment with topical glycerin may resolve the edema relatively quickly. This medication can be difficult to obtain, however, and can cause the patient significant discomfort. Usually, we try to avoid worsening the inflammation with too much laser energy (>100 to 150 mJ) and instead consider performing a surgical iridectomy or lensectomy. If an urgent lensectomy is needed, keratometry values can be obtained from the fellow eye to estimate the IOL power.

EILEEN BOWDEN, MD

When a patient presents to our institution with acutely elevated IOP from angle closure, medical therapy is initiated to break the attack. Treatment begins with topical IOP-lowering drops and oral acetazolamide. If the patient is nauseous (as is often the case), then IV acetazolamide is administered, and IV ondansetron is initiated to reduce their nausea. IOP measurements are taken frequently to assess the patient’s response to therapy. If the IOP is not adequately lowered with acetazolamide, IV mannitol is sometimes given to further decrease the aqueous volume.

Once the acute attack has resolved, the patient is scheduled for definitive treatment in the next 1 to 2 days. An LPI is performed in the eye that experienced the acute attack. If the cornea is edematous and impedes the view for laser treatment, then topical glycerin is administered. Underlying anatomic risk factors put the fellow eye at increased risk of AACG, so that eye is closely examined and treated with an LPI if needed.

If the IOP remains elevated after the LPI and residual angle closure is attributed to a forward-pushing mechanism from the lens, then a lensectomy with or without glaucoma surgery is considered. Once the acute symptoms have resolved, patients are evaluated for glaucomatous optic neuropathy with perimetry and OCT and asked to return periodically to ensure that their IOP is controlled and their glaucoma is not progressing.