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Acute Closed Angle Glaucoma

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Last Update: January 2, 2023.

Continuing Education Activity

Acute angle-closure glaucoma is an ocular emergency that results from a rapid increase in intraocular pressure due to outflow obstruction of aqueous humor. Several factors lead to the obstruction in acute angle-closure glaucoma, but the major predisposing factor is the structural anatomy of the anterior chamber, leading to a shallower angle between the iris and the cornea. Acute angle-closure glaucoma presents as a sudden onset of severe unilateral eye pain or a headache associated with blurred vision, rainbow-colored halos around bright lights, nausea, and vomiting. The physical exam will reveal a fixed midpoint pupil and a hazy or cloudy cornea with marked conjunctival injection. This activity reviews the evaluation and management of patients with acute angle-closure glaucoma and highlights the role of the interprofessional team in managing patients with this condition.


  • Describe the pathophysiology of acute angle-closure glaucoma.
  • Summarize how a patient with acute angle-closure glaucoma is likely to present.
  • Identify the critical immediate steps to take when managing a patient with acute angle-closure glaucoma.
  • Outline the role of a collaborative interprofessional team in providing well-coordinated care to patients presenting with acute angle-closure glaucoma.
Access free multiple choice questions on this topic.


Glaucoma is a set of ocular disorders often defined by increased intraocular pressures leading to optic neuropathy and vision loss if untreated.[1] Glaucoma has traditionally been classified as open-angle or closed-angle and as primary or secondary. The angle refers to the angle between the iris and the cornea in the anterior chamber, which can become structurally obstructed. By definition, primary glaucomas are not associated with known ocular or systemic disorders and usually affect both eyes. Secondary glaucomas are associated with ocular or systemic disorders and are often unilateral. Acute angle-closure glaucoma is a subset of primary angle-closure glaucoma.

The commonly accepted range for intraocular pressure is 10 to 22 mmHg. Three factors that affect the intraocular pressure are the rate of production of aqueous humor by the ciliary body, the resistance to aqueous outflow through the trabecular meshwork and Schlemm’s canal, and the episcleral venous pressure. The normal flow of aqueous humor starts in the ciliary body, goes through the pupil, and out through the trabecular meshwork and Schlemm's canal in the angle of the anterior chamber. In acute angle-closure glaucoma, intraocular pressure increases rapidly due to outflow obstruction of the aqueous humor. Several factors lead to the obstruction in acute angle-closure glaucoma, but the major predisposing factor is the structural anatomy of the anterior chamber leading to a shallower angle.[2][3]


Blockage to the flow of aqueous humor occurs due to a number of predisposing anatomic variations. These variations include a shallower anterior chamber, lens size, anterior location of the iris-lens diaphragm, and a narrow entrance to the anterior chamber angle. The shallower anterior chamber angle leads to a large area of the iris and lens being in contact with each other, slowing the flow of aqueous humor from the posterior chamber to the anterior chamber. This, in turn, leads to a pressure difference between the chambers called a pupillary block.[4] 

The pupillary block causes bowing of the iris, which narrows the angle of the anterior chamber further. This cycle will perpetuate increasing intraocular pressures leading to the clinical presentation of acute angle-closure glaucoma.


There are several risk factors for acute angle-closure glaucoma, including age, gender, race, and family history.[5]

  • Age: The average age at presentation is 60, and prevalence increases thereafter. This is felt to be due to the increasing size of the lens with age.
  • Gender: There is a 4 to 1 ratio of the incidence of angle-closure glaucoma in women versus men.
  • Race: Angle-closure glaucoma is more common in Southeast Asians, Chinese, and Eskimos. It is uncommon in black populations. In whites, acute angle-closure glaucoma accounts for 6% of all glaucoma diagnoses.[6]
  • Family history: Ocular anatomic features are inherited. 


An acute attack of angle-closure glaucoma is precipitated by pupillary dilatation, leading to increasing iris and lens contact increasing the pupillary block.[7] The increasing pupillary block leads to bulging of the iris, acutely closing the angle between the iris and cornea, thus obstructing the aqueous humor outflow tract. The intraocular pressure rises acutely, leading to symptomology.

History and Physical

Acute angle-closure glaucoma presents as a sudden onset of severe unilateral eye pain or a headache associated with blurred vision, rainbow-colored halos around bright lights, nausea, and vomiting. The physical exam will reveal a fixed midpoint pupil and a hazy or cloudy cornea with marked conjunctival injection (most prominent at the limbus). Intraocular pressure will be elevated and can be as high as 60 to 80 mm Hg in an acute attack. A mild amount of aqueous flare and cells may be seen. The optic nerve may also be swollen during an acute attack.[8][9]


Measuring elevated intraocular pressure is diagnostic. There is no need for any imaging studies. A basic metabolic panel should be checked if osmotic agents are used in the treatment regime. A gonioscopic examination by an ophthalmologist to verify angle-closure makes the definitive diagnosis. Gonioscopy of the unaffected eye will reveal a narrow occludable angle given the anatomic predisposing factors to acute angle-closure glaucoma (See other issues for further discussion). Glaucomflecken (grey-white opacities on the anterior lens capsule) may be visible if previous attacks of angle-closure glaucoma have occurred.[10]

Treatment / Management

The medical treatment for acute angle-closure glaucoma aims to decrease the intraocular pressure by blocking the production of aqueous humor, increasing the outflow of aqueous humor, and reducing the volume of the aqueous humor.[11][12]

Initial medical therapy includes a combination of the following medications:

  • Intravenous acetazolamide 500 mg to block the production of aqueous humor.
  • Intravenous mannitol 1 to 2 grams/kg can be given (if there is no contraindication) to rapidly reduce the volume of aqueous humor.
  • Topical beta-blocker (timolol 0.5%) one drop to block the production of aqueous humor.
  • Topical alpha 2-agonist (apraclonidine 1%) one drop to block the production of aqueous humor.
  • Topical pilocarpine 1% to 2% one drop every 15 minutes for two doses once intraocular pressure is below 40 mm Hg to increase the outflow of aqueous humor. This is not effective at higher pressures due to pressure-induced ischemic paralysis of the iris.

Intraocular pressure needs to be checked every hour.

Definitive treatment is peripheral iridectomy after the acute episode subsides. Laser iridectomy is the treatment of choice. Surgical iridectomy is indicated when laser iridectomy can not be accomplished. Iridectomy relieves the pupillary block as the pressure between the posterior and anterior chamber approaches zero by allowing the flow of aqueous humor through a different route. Iridectomy should be as peripheral as possible and covered by the eyelid to avoid monocular diplopia through this second hole in the pupil.[13]

Differential Diagnosis

  • Allergic conjunctivitis
  • Bacterial conjunctivitis (pink eye)
  • Viral conjunctivitis 
  • Drug-induced glaucoma
  • Malignant glaucoma
  • Neovascular glaucoma
  • Phacomorphic glaucoma
  • Senile cataract (age-related cataract)
  • Lens subluxation[14]
  • Migraine headache[15]
  • Cluster headache
  • Suprachoroidal hemorrhage


The prognosis depends on early detection and prompt treatment of acute closed-angle glaucoma. A study conducted on 116 cases of acute angle-closure glaucoma concluded that the delay in presentation and the time taken to end the acute episode was the most important factor in determining the final outcome of these patients. High intraocular pressure was less effective in determining the long-term prognosis of this condition.[16]


If acute closed-angle glaucoma is not detected and treated in its initial stages, it can lead to temporary loss of vision or blindness. There is a loss of peripheral vision, followed by a loss of central vision. There can be a significant increase in IOP in patients with peripheral patent iridotomy and a flat anterior chamber. This condition is called malignant glaucoma. This condition is difficult to treat and progressively leads to blindness.[17]

Deterrence and Patient Education

Patients with a history of acute angle-closure glaucoma should avoid dim light. Pupils dilate in response to dim light, further narrowing the iridocorneal angle. Patients with hypermetropia are at an increased risk of developing angle-closure glaucoma.

Pearls and Other Issues

An untreated opposite eye has a 40% to 80% chance of developing an acute attack of angle-closure glaucoma over 5 to 10 years as it shares the same anatomic predisposing factors as the first eye.[18] Hence peripheral iridectomy should be performed in the other eye as well as the affected eye.

The gender and ethnicity predisposing factors to acute angle-closure glaucoma hint at a genetic predisposition to the disease in certain populations. Recent large-scale studies have shown a clear association to several genes and genetic loci with primary open-angle glaucoma, but evidence for acute angle-closure glaucoma is sparse. So far, only one study has shown a genetic locus on Chromosome 11 that can cause acute angle-closure glaucoma. Studies have been conducted on possible therapeutic targets in patients with early-onset glaucoma based on molecular and cellular events caused by MYOC, OPTN, and TBK1 mutations.[19]

Enhancing Healthcare Team Outcomes

Acute angle-closure glaucoma is best managed by an interprofessional team, including an ophthalmologist, family clinician, an ophthalmology nurse, and the pharmacist. After managing the emergency with eye drops, the patient should be scheduled for an iridectomy. Clinicians need to be aware that the other eye is also at risk for acute angle-closure glaucoma, and prophylactic surgery is recommended.

The outcomes for patients with acute angle-closure glaucoma are good following treatment. However, delay in treatment can lead to damage to the optic nerve and vision loss.

Review Questions


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Pohl H, Tarnutzer AA. Acute Angle-Closure Glaucoma. N Engl J Med. 2018 Mar 08;378(10):e14. [PubMed: 29514027]
Sun X, Dai Y, Chen Y, Yu DY, Cringle SJ, Chen J, Kong X, Wang X, Jiang C. Primary angle closure glaucoma: What we know and what we don't know. Prog Retin Eye Res. 2017 Mar;57:26-45. [PubMed: 28039061]
Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2014 May 14;311(18):1901-11. [PMC free article: PMC4523637] [PubMed: 24825645]
Anderson DR, Jin JC, Wright MM. The physiologic characteristics of relative pupillary block. Am J Ophthalmol. 1991 Mar 15;111(3):344-50. [PubMed: 2000905]
Ahram DF, Alward WL, Kuehn MH. The genetic mechanisms of primary angle closure glaucoma. Eye (Lond). 2015 Oct;29(10):1251-9. [PMC free article: PMC4815686] [PubMed: 26206529]
Bourne RR, Taylor HR, Flaxman SR, Keeffe J, Leasher J, Naidoo K, Pesudovs K, White RA, Wong TY, Resnikoff S, Jonas JB., Vision Loss Expert Group of the Global Burden of Disease Study. Number of People Blind or Visually Impaired by Glaucoma Worldwide and in World Regions 1990 - 2010: A Meta-Analysis. PLoS One. 2016;11(10):e0162229. [PMC free article: PMC5072735] [PubMed: 27764086]
Collignon NJ. Emergencies in glaucoma: a review. Bull Soc Belge Ophtalmol. 2005;(296):71-81. [PubMed: 16050422]
Watkinson S. Assessment and management of patients with acute red eye. Nurs Older People. 2013 Jun;25(5):27-34; quiz 35. [PubMed: 23914708]
Garala P, Bansal A. Acute Secondary Optic Neuropathy as a Complication of a Single Episode of Acutely Raised Intraocular Pressure: A Case Series. J Glaucoma. 2019 Jan;28(1):e10-e13. [PubMed: 30234746]
Shaw AD, Burnett CA, Eke T. A simple technique for indirect gonioscopy for patients who cannot be examined at the slit lamp. Br J Ophthalmol. 2006 Sep;90(9):1209. [PMC free article: PMC1857408] [PubMed: 16929072]
Anwar F, Turalba A. An Overview of Treatment Methods for Primary Angle Closure. Semin Ophthalmol. 2017;32(1):82-85. [PubMed: 27686782]
He M, Jiang Y, Huang S, Chang DS, Munoz B, Aung T, Foster PJ, Friedman DS. Laser peripheral iridotomy for the prevention of angle closure: a single-centre, randomised controlled trial. Lancet. 2019 Apr 20;393(10181):1609-1618. [PubMed: 30878226]
Xing X, Huang L, Tian F, Zhang Y, Lv Y, Liu W, Liu A. Biometric indicators of eyes with occult lens subluxation inducing secondary acute angle closure. BMC Ophthalmol. 2020 Mar 05;20(1):87. [PMC free article: PMC7059282] [PubMed: 32138781]
Renton BJ, Bastawrous A. Acute Angle Closure Glaucoma (AACG): an important differential diagnosis for acute severe headache. Acute Med. 2011;10(2):77-8. [PubMed: 22041605]
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Shahid H, Salmon JF. Malignant glaucoma: a review of the modern literature. J Ophthalmol. 2012;2012:852659. [PMC free article: PMC3321564] [PubMed: 22545204]
Atalay E, Nongpiur ME, Baskaran M, Sharma S, Perera SA, Aung T. Biometric Factors Associated With Acute Primary Angle Closure: Comparison of the Affected and Fellow Eye. Invest Ophthalmol Vis Sci. 2016 Oct 01;57(13):5320-5325. [PubMed: 27727395]
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Nuessle S, Luebke J, Boehringer D, Reinhard T, Anton A. [Acute angle closure : An ophthalmological emergency in the emergency room]. Med Klin Intensivmed Notfmed. 2022 Mar;117(2):137-143. [PMC free article: PMC8897352] [PubMed: 33580819]

Disclosure: Babak Khazaeni declares no relevant financial relationships with ineligible companies.

Disclosure: Leila Khazaeni declares no relevant financial relationships with ineligible companies.

Copyright © 2023, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK430857PMID: 28613607


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