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Glaucoma, Angle Closure, Acute Clinical Presentation

  • Author: Robert J Noecker, MD, MBA; Chief Editor: Hampton Roy, Sr, MD  more...
Updated: Nov 25, 2015


In acute primary ACG, the anterior chamber angle is blocked suddenly and IOP rises rapidly, and the patient may present with dramatic symptoms, as follows:

  • Onset of severe ocular pain, nausea and vomiting, headache, and blurred vision is sudden.
  • Patients may complain of seeing haloes around lights. Haloes and blurry vision are the result of corneal edema.
  • The attack may have been precipitated by pupillary dilation, possibly during an ophthalmic examination. Patients with acute ACG are extremely uncomfortable and distressed.

Some patients may experience intermittent episodes of partial angle closure and relatively elevated IOP without ever experiencing a frank attack of ACG.

Patients may be totally asymptomatic, or they may report incidents of mild pain with slightly blurred vision or seeing haloes around lights. These symptoms resolve spontaneously as the angle reopens.



Examination of a patient who presents with suspected ACG should include gonioscopy, tonometry, biomicroscopy, and ophthalmoscopy, as follows:

  • Diagnosis of ACG is made by gonioscopic visualization of an occluded anterior chamber angle.
  • Tonometry demonstrates an elevated IOP, which may be as high as 40-80 mm Hg.
  • Biomicroscopy may reveal a fixed or sluggish and middilated pupil, a shallow anterior chamber, corneal epithelial edema and bullae, ciliary injection, and cells and flare. Diffuse lacrimation may be present.
  • Ophthalmoscopy may reveal a swollen optic disc in an acute attack or excavation if episodes have been chronic. Unilateral involvement and worsening symptoms are common in acute attacks. [6]

If an attack persists or if several milder incidents of angle closure have occurred in the past, peripheral anterior synechiae and adhesions may be visible between the cornea and iris. Peripheral anterior synechiae may destroy the trabecular meshwork, while adhesions may cause necrosis and permanent dilation of the iris.

Glaucoma flecks (also known as flecken glaucoma), or vesicles on the anterior subcapsular lens, also may be seen if acute angle closure has occurred in the past.

Gray atrophy of the stroma of the iris provides further evidence of a prior attack, if the attack occurred 3 weeks or more prior to examination.



Pupillary block is the most common cause of ACG. Normally, aqueous humor is made by the ciliary epithelial cells in the posterior chamber and flows through the pupil to the anterior segment, where it can drain out of the eye through the trabecular meshwork and Schlemm canal. If contact occurs between the lens and the iris, aqueous accumulates behind the pupil, increasing posterior chamber pressure and forcing the peripheral iris to shift forward and block the anterior chamber angle. The anterior surface of the iris may be apposed to the posterior surface of the cornea or to the trabecular meshwork. This blockage causes accumulation of aqueous in the anterior chamber and an acute rise in IOP.

Plateau iris is a condition in which anterior insertion of the iris to the ciliary body causes the anterior chamber angle to become occluded on dilation of the pupil. The iris may insert on the anterior edge of the ciliary body, close to the trabecular meshwork. It may cause the patient to have genetically narrow angles despite a normal anterior chamber depth. The iris also may appear unusually flat, not bowed as might be expected in ACG. Often, an element of pupillary block exists in cases of plateau iris glaucoma, in which case peripheral iridectomy will lower IOP. If the patient continues to develop angle closure on pupillary dilation after iridectomy has been performed, continue performing miotic therapy to prevent recurrence. A diagnosis of plateau iris can be confirmed with ultrasound biomicroscopy.

Hyperopia: Patients with hyperopic eyes are more likely to have shallow anterior chambers and narrow angles. These patients are predisposed to develop ACG.[7] Dilation of the eye may precipitate an attack of acute ACG because the peripheral iris relaxes when dilated to midposition. When the iris is relaxed, it may bow anteriorly and maximize iris-lens apposition, possibly causing pupillary block.

Several medications have been implicated in causing acute ACG.[8] Sulfa-derivative medications, including acetazolamide, sulfamethoxazole, and hydrochlorothiazide, have all been reported to cause acute attacks. Topiramate, a newer antiepileptic medication, has recently been implicated in causing acute narrow-angle glaucoma. Also a sulfa-derivative medication, topiramate blocks glutamate receptors and is labeled for use in treating seizures.[9] The presumed mechanism of angle closure involves swelling of the ciliary body with anterior displacement of the lens-iris diaphragm. Stopping the medication is effective in treating this condition and requires a high index of suspicion by the treating physician.

Other causes: Several mechanisms can cause the iris-lens diaphragm to be pushed forward. A space-occupying lesion (eg, tumor, swelling associated with ciliary body inflammation) may cause the iris to block the trabecular meshwork. Other conditions associated with this mechanism include central retinal vein occlusion, placement of a scleral buckle, history of panretinal photocoagulation, and nanophthalmos.

Contributor Information and Disclosures

Robert J Noecker, MD, MBA Associate Professor, Department of Ophthalmology, University of Pittsburgh School of Medicine; Director, Glaucoma Service, Vice Chair, Department of Ophthalmology, University of Pittsburgh Medical Center Eye Center

Robert J Noecker, MD, MBA is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society, American Medical Association, American Society of Cataract and Refractive Surgery

Disclosure: Received consulting fee from Allergan for consulting; Received grant/research funds from Allergan, Zeiss, Lumenis for other; Received honoraria from Allergan, Alcon, Lumenis, Endo-optics for speaking and teaching.


Malik Y Kahook, MD Clinical Instructor of Ophthalmology, Fellow in Glaucoma, Department of Ophthalmology, University of Pittsburgh Medical Center

Malik Y Kahook, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Association for Research in Vision and Ophthalmology, Colorado Medical Society

Disclosure: Received consulting fee from Alcon for consulting.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Martin B Wax, MD Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon Laboratories, Inc

Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Society for Neuroscience

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Kilbourn Gordon, III, MD, FACEP Urgent Care Physician

Kilbourn Gordon, III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology, Wilderness Medical Society

Disclosure: Nothing to disclose.

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