Journal of Current Glaucoma Practice

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VOLUME 13 , ISSUE 3 ( September-December, 2019 ) > List of Articles

REVIEW ARTICLE

Drug-induced Acute Angle-closure Glaucoma: A Review

Michael C Yang, Ken Y Lin

Keywords : Acute angle-closure glaucoma, Acute angle-closure crisis, Adrenergic drugs, Drug-induced, Drug-induced acute angle-closure glaucoma, Iatrogenic, Paradoxical pilocarpine reaction, Pupillary block

Citation Information : Yang MC, Lin KY. Drug-induced Acute Angle-closure Glaucoma: A Review. J Curr Glaucoma Pract 2019; 13 (3):104-109.

DOI: 10.5005/jp-journals-10078-1261

License: CC BY-NC 4.0

Published Online: 01-12-2019

Copyright Statement:  Copyright © 2019; Jaypee Brothers Medical Publishers (P) Ltd.


Abstract

Aim: Our goal is to review current literature regarding drug-induced acute angle-closure glaucoma (AACG) and provide ophthalmologists and general practitioners with a thorough understanding of inciting medications and treatment pitfalls to be avoided. Background: Drug-induced AACG is an ophthalmological emergency that ophthalmologists and general practitioners should be familiar with, given its potentially blinding consequences. Common anatomical risk factors for AACG include a shallow anterior chamber depth, short axial length, plateau iris configuration, thick lens, anteriorly positioned lens, and rarely, intraocular tumor. Demographic risk factors include female sex, Asian ethnicity, family history, and advanced age. In patients with predisposing factors, acute angle closure can be triggered by various classes of medications including adrenergic agonists, anticholinergics, cholinergics, sulfonamides, supplements, and serotonergic medications. Physicians prescribing such inciting medications should be aware of their potentially sight-threatening adverse effects and to inform patients of the warning symptoms. Patients typically present with elevated intraocular pressure (IOP), headache, nausea, blurry vision, and halos around lights. Review results: There are two main mechanisms of drug-induced AACG, both with different treatment strategies. The first mechanism of drug-induced AACG is pupillary block and iridocorneal angle closure secondary to thickening of iris base with mydriasis. The second mechanism of drug-induced AACG is anterior displacement of the lens–iris diaphragm due to mass effect (e.g., blood, misdirected aqueous humor, and tumors), uveal effusion, or weakened zonules. Conclusion: This paper reviews drug-induced AACG, high-risk anatomical features, underlying mechanisms, inciting medications, and options for treatment and prevention. Clinical significance: With proper understanding of the underlying mechanism of drug-induced AACG, physicians can respond promptly to save their patients’ vision by employing the correct treatment strategy.


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