Acute angle closure happens when fluid stops flowing through the canals in the eye, creating pressure that can damage the optic nerve.
Patients with primary angle closure can develop irreversible vision loss within a few hours, so it is important for all ophthalmologists to be able to correctly diagnose and appropriately manage it. Sometimes the diagnosis may not be obvious, but prompt diagnosis and treatment are critical to prevent permanent optic nerve damage.
Risks and Symptoms
Primary angle closure is usually caused by an anatomic problem: e.g., an occludable angle due to high iris insertion, a shallow anterior chamber in a hyperopic eye, a plateau iris that is being pushed forward by an anteriorly rotated ciliary body or lens rise from a growing cataract.
The history may give you clues that the patient is at risk for angle closure. Common risk factors include hyperopia, female gender, use of antihistamines and cold medications and advanced age.
Many patients describe the onset of their symptoms occurring while in the dark, during stressful situations or after having their eyes pharmacologically dilated. Symptoms include blurry vision, headache and halos around lights.
Intraocular pressure may be normal in the case of intermittent angle closure or if presenting early, so gonioscopy is key in the diagnosis. Ultrasound biomicroscopy and anterior segment optical coherence tomography can assist when the diagnosis is unclear. It is important to also perform gonioscopy of the contralateral eye. Indentation gonioscopy may be therapeutic in breaking the attack and can be attempted in all patients. Key exam findings of acute angle closure include a fixed mid-dilated pupil, ciliary flush, microcystic corneal edema, mid-peripheral iris bowing even with the center of the anterior chamber well formed, aqueous flare and cells, and glaucomflecken. The optic nerve should be evaluated to stratify prognosis, but without dilation.
Management
In most cases, acute angle closure is precipitated by pupillary block. Treatment can be medical, procedural or surgical.
Medical Treatment
Definitive treatment of pupillary block is laser peripheral iridotomy (LPI). If procedural intervention isn’t possible (due to location of patient or poor view of the iris due to corneal edema), medical treatment is a good temporizing measure. Timolol, brimonidine, dorzolamide and their pharmacological similar cousins are common drop treatments. Timolol is fastest with onset of action in about 20 minutes. Prostaglandin analogs act too slowly to be acutely useful.
If tolerated, strongly consider acetazolamide 500 mg IV or PO as soon as possible. Acetazolamide’s onset of action occurs in approximately 90 minutes and reaches peak effect in two to three hours. Be aware that acetazolamide depends on good renal function and can cause acidosis, renal stones, metabolic derangements and rarely Stevens-Johnson syndrome; avoid using it in patients with sickle cell disease.
In refractory cases, osmotic agents can be considered. Oral agents include glycerin and isosorbide but can cause nausea or GI upset. While highly effective, intravenous mannitol also results in significant fluid shifts that can cause or exacerbate major systemic issues including pulmonary edema, congestive heart failure, osmotic/metabolic derangements and severe central nervous system (CNS) complications. For this reason, patients receiving mannitol must be admitted to a medicine service for inpatient monitoring.
Procedural Treatment
If acute angle closure is due to pupillary block, we recommend a laser peripheral iridotomy (LPI), usually preceded by medical therapy or an anterior chamber paracentesis (AC tap).
Laser Peripheral Iridotomy
- Laser settings vary greatly amongst physicians. We usually use a YAG laser with 4.0-5.0 mJ energy. Patients are often pre-treated with pilocarpine to constrict the pupil; note pilocarpine can move the lens forward and therefore exacerbate some types of angle closure, but will make the LPI easier. A Blumenthal or Abraham Iridotomy lens is recommended for stabilization and visualization. Target the iris crypts and look for refluxed pigment. Transillumination helps confirm patency. Avoid placing the LPI in clock hours with intermittent lid exposure or those near the tear lake.
- Pre-treatment with argon laser can facilitate LPI in a dark iris and can reduce bleeding. We use a 50 um spot size, 10 ms duration, and 500 mW power.
- After LPI, give prednisolone and/or ketorolac four times daily for 5-7 days. Consider placing the patient on an aqueous suppressive agent until seen again.
Anterior Chamber Paracentesis
- An AC tap can be considered in certain situations when the patient cannot immediately undergo LPI, IOP is high enough to cause extreme pain or vomiting, or the cornea is too cloudy to allow for an LPI.
- An AC tap carries significant risks, especially if performed in phakic eyes, or eyes with neovascular glaucoma, and caution should be given before undertaking an AC tap in these patients.
- Apply proparacaine and a drop of betadine to the eye. Consider using a lid speculum. Using a 30-gauge needle on a plungerless syringe, enter the anterior chamber parallel to the iris plane. It usually only takes a few seconds to tap sufficiently. Use a drop of antibiotic before and after the procedure.
Surgical Treatment
Although LPI will decrease the risk of pupillary block, it doesn’t change the underlying anatomy that predisposes toward angle closure. That is why cataract surgery is indicated for post-LPI eyes with elevated intraocular pressure (IOP), occludable angles, or persistent angle closure attacks.
You can also consider concurrent goniosynechialysis for peripheral anterior synechiae or endoscopic cyclophotocoagulation to shrink the ciliary body. In chronic cases, it may not be possible to restore trabecular meshwork function. In these cases, angle-bypassing surgery may be necessary.
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About the authors: Lilian Nguyen, MD, is a clinical assistant professor, associate program director and director of medical student education at the University of Texas Health San Antonio Department of Ophthalmology. She completed her ophthalmology residency at the University of Texas Southwestern Medical Center and her glaucoma fellowship at Washington University in St. Louis.
Lynn W. Sun, MD, PhD, is completing her glaucoma fellowship at the University of Michigan Kellogg Eye Center. She completed her ophthalmology residency at the Medical College of Wisconsin and will be starting as a clinical assistant professor at Oregon Health & Science University Casey Eye Institute in autumn 2021.
The Academy’s YO Info Editorial Board is collaborating with YO leaders from our subspecialty society partners and thanks the American Glaucoma Society Jr. Members at Large, Davinder S. Grover, MD, PhD, and Paula Newman-Casey, MD, for recommending authors for this article.
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