eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Angle Closure, Acute

Author: 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
Coauthor(s): Malik Y Kahook, MD, Clinical Instructor of Ophthalmology, Fellow in Glaucoma, Department of Ophthalmology, University of Pittsburgh Medical Center
Contributor Information and Disclosures

Updated: Jun 18, 2009

Introduction

Background

Angle-closure glaucoma (ACG) is a condition in which the iris is apposed to the trabecular meshwork at the angle of the anterior chamber of the eye. When the iris is pushed or pulled anteriorly to block the trabecular meshwork, the outflow of aqueous from the eye is blocked, which causes a rise in intraocular pressure (IOP). If closure of the angle occurs suddenly, symptoms are severe and dramatic. Immediate treatment is essential to prevent damage to the optic nerve and loss of vision. If closure occurs intermittently or gradually, ACG may be confused with chronic open-angle glaucoma.

Pathophysiology

Angle closure may occur via 2 mechanisms. The iris may be pushed forward into contact with the trabecular meshwork, as in pupillary block or plateau iris, or it may be pulled anteriorly, as occurs with other inflammatory conditions. In either case, the position of the iris causes the normally open chamber angle to close. Aqueous humor that should drain out of the anterior chamber is trapped inside the eye. Pain, blurred vision, and nausea may occur if the ensuing rise in pressure is sudden. Glaucomatous damage to the optic nerve also may occur due to the increased IOP, either in a sudden attack or in intermittent episodes over a long period of time.

Frequency

United States

Fewer than 10% of US glaucoma cases are due to ACG. Hyperopes are at increased risk for acute ACG because their anterior chamber angles are relatively shallow.

International

ACG is more common than open-angle glaucoma in Asia.

Mortality/Morbidity

Accurate early diagnosis and treatment help prevent visual damage.

Race

Races with an anatomically narrower angle, such as Asians and Eskimos, have a higher incidence of ACG than whites. Incidence among American Indians is lower than among whites.

Sex

Among white patients, the incidence of ACG is 3 times higher in women than in men. In black patients, men and women are affected equally.

Age

In older people, incidence of primary ACG increases as the lens enlarges, and the depth and volume of the anterior chamber decrease.

Clinical

History

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

Physical

• Examination of a patient who presents with suspected ACG should include gonioscopy, tonometry, biomicroscopy, and ophthalmoscopy.
  • 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.
• 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.

Causes

• 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. 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. 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. 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.

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