Acute Closed Angle Glaucoma

Article Author:
Babak Khazaeni
Article Editor:
Leila Khazaeni
6/3/2019 5:24:19 PM
PubMed Link:
Acute Closed Angle Glaucoma


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 10-22 mm Hg. Three factors affect intraocular pressure:  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.  There are several factors leading 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]


Blockage of the 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 differential between the chambers called a pupillary block.[3]  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 a number of risk factors for acute angle closure glaucoma which include age, gender, race and family history.[4]

  • Age: 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 4:1 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.[5]
  • 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.[6]  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 track.  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.[7]  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 cell may be seen.  The optic nerve may also be swollen during an acute attack.


Measuring an elevated intraocular pressure is diagnostic.  There is no need for any imaging studies.  A basic metabolic panel should be checked if osmotic agents will be initiated for treatment.  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.

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.[8][9]

Initial medical therapy includes a combination of the following medications:

  • Intravenous acetazolamide 500 mg to block the production of aqueous humor.
  • Intravenous mannitol 1-2 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%-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.

Emergently consult ophthalmology as you begin treatment.

Definitive treatment is peripheral iridectomy after the acute episode subsides.  Laser iridectomy is the treatment of choice.  Surgical iridectomy is indicated when laser 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. 

Pearls and Other Issues

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

Enhancing Healthcare Team Outcomes

Acute angle closure glaucoma is best managed by a multidisciplinary team that also includes an ophthalmology nurse and the pharmacist. After managing the emergency with eyedrops, the patient should be scheduled for iridectomy. Clinicians need to be aware that the other eye is also at risk for acute angle close glaucoma and prophylactic surgery is recommended.

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


[1] Pohl H,Tarnutzer AA, Acute Angle-Closure Glaucoma. The New England journal of medicine. 2018 Mar 8;     [PubMed PMID: 29514027]
[2] Primary angle closure glaucoma: What we know and what we don't know., Sun X,Dai Y,Chen Y,Yu DY,Cringle SJ,Chen J,Kong X,Wang X,Jiang C,, Progress in retinal and eye research, 2016 Dec 28     [PubMed PMID: 28039061]
[3] The physiologic characteristics of relative pupillary block., Anderson DR,Jin JC,Wright MM,, American journal of ophthalmology, 1991 Mar 15     [PubMed PMID: 2000905]
[4] Ahram DF,Alward WL,Kuehn MH, The genetic mechanisms of primary angle closure glaucoma. Eye (London, England). 2015 Oct;     [PubMed PMID: 26206529]
[5] Number of People Blind or Visually Impaired by Glaucoma Worldwide and in World Regions 1990 - 2010: A Meta-Analysis., Bourne RR,Taylor HR,Flaxman SR,Keeffe J,Leasher J,Naidoo K,Pesudovs K,White RA,Wong TY,Resnikoff S,Jonas JB,, PloS one, 2016 Oct 20     [PubMed PMID: 27764086]
[6] Emergencies in glaucoma: a review., Collignon NJ,, Bulletin de la Societe belge d'ophtalmologie, 2005     [PubMed PMID: 16050422]
[7] Assessment and management of patients with acute red eye., Watkinson S,, Nursing older people, 2013 Jun     [PubMed PMID: 23914708]
[8] An Overview of Treatment Methods for Primary Angle Closure., Anwar F,Turalba A,, Seminars in ophthalmology, 2017     [PubMed PMID: 27686782]
[9] Primary Angle Closure Preferred Practice Pattern(®) Guidelines., Prum BE Jr,Herndon LW Jr,Moroi SE,Mansberger SL,Stein JD,Lim MC,Rosenberg LF,Gedde SJ,Williams RD,, Ophthalmology, 2016 Jan     [PubMed PMID: 26581557]
[10] Biometric Factors Associated With Acute Primary Angle Closure: Comparison of the Affected and Fellow Eye., Atalay E,Nongpiur ME,Baskaran M,Sharma S,Perera SA,Aung T,, Investigative ophthalmology & visual science, 2016 Oct 1     [PubMed PMID: 27727395]