AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Acute abdomen
Cluster headache
Gastritis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Imaging Studies

• Ultrasound biomicroscopy (UBM) - To visualize the angles and surrounding structures
• Anterior segment optical coherence tomography (OCT) - To view the angles and anterior ocular structures

Other Tests

• Gonioscopy

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Definitive treatment of ACG is laser iridotomy, or, if the iris cannot be accessed by laser, surgical iridectomy. Medical treatment is intended to prepare the patient for laser iridotomy. The cornea should be cleared with osmotic agents, the pupil should be constricted, and IOP should be lowered to prevent acute damage to the optic nerve.

Surgical Care

• Laser iridotomy: Treatment of choice for pupillary-block ACG is laser iridotomy. Iridotomy with an argon or Nd:YAG laser creates an opening in the iris through which aqueous humor trapped in the posterior chamber can reach the anterior chamber and trabecular meshwork. As aqueous flows into the anterior chamber through the iris defect, pressure behind the iris falls, allowing the iris to recede toward its normal position. This procedure opens the anterior chamber angle and relieves the blockade of trabecular meshwork. If the cornea is extremely cloudy or the patient cannot cooperate, incisional peripheral iridectomy may be performed instead of a laser procedure.
• Laser gonioplasty: Laser may be used to create stromal burns in the peripheral iris. As the iris contracts, the anterior chamber angle deepens. Use laser gonioplasty as treatment of ACG due to plateau iris and nanophthalmos, or use it as a temporary measure to open the angle until laser iridotomy can be performed.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The medical therapy for acute ACG is directed toward preparing the patient for laser or incisional iridotomy, which will create passage through the iris from the posterior to anterior chamber and will break an acute attack. IOP must be returned to normal, and the cornea must be cleared before a definitive procedure can be undertaken. In acute ACG, several drugs from different classes are used simultaneously to accelerate and maximize their pressure-lowering effects.

Drug Category: Alpha-adrenergic agonists

Topical adrenergic agonists, or sympathomimetics, decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and allergenicity.

Drug Category: Beta-blockers

Topical beta-adrenergic receptor antagonists decrease aqueous humor production by the ciliary body. Adverse effects of the beta-blockers are due to systemic absorption of the drug and include decreased cardiac output and bronchial constriction. In susceptible patients, this may cause bronchospasm, bradycardia, heart block, or hypotension. Pulse rate and blood pressure should be monitored in patients receiving topical beta-blocker therapy, and punctal occlusion may be performed after administration of the drops.

Drug Category: Miotic agents (parasympathomimetics)

Contract ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous. Miosis results from action of these drugs on pupillary sphincter. Adverse effects include brow ache, induced myopia, and decreased vision in low light.

Drug Category: Prostaglandin analogs

Increase uveoscleral outflow of the aqueous. One mechanism of action may be through induction of metalloproteinases in ciliary body, which breaks down extracellular matrix, thereby reducing resistance to outflow through ciliary body.

Drug Category: Carbonic anhydrase inhibitors

Reduce secretion of aqueous humor by inhibiting carbonic anhydrase in ciliary body. In acute ACG, may be given systemically but are used topically in patients with refractory open-angle glaucoma. Topical formulations are less effective, and their duration of action is shorter than many other classes of drugs. Adverse effects of topical carbonic anhydrase inhibitors are relatively rare, but they include superficial punctate keratitis, acidosis, paresthesias, nausea, depression, and lassitude.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Because some patients may experience transient increases in IOP after peripheral iridotomy, check every patient's IOP 1 hour after laser treatment. If medical treatment has not been successful by that time, repeat gonioscopic examination to rule out the presence of peripheral anterior synechiae. If peripheral anterior synechiae are found, the patient may need gonioplasty or incisional surgery.

Further Outpatient Care

• Once a peripheral iridotomy has been performed, the patient should continue using the medications that were chosen to treat the acute glaucoma for 1 day after leaving the hospital or clinic. Arrange a 1-day posttreatment visit. At this visit, check the IOP again, and examine the eye. After 1 day, the patient may discontinue the antiglaucoma medications that were used in the acute attack, but the patient should be maintained on corticosteroids for 1 week.
• Examine the patient's other eye gonioscopically and biomicroscopically to assess for narrow or occluded angles, as well as for evidence of prior attacks of ACG. If evidence of prior attacks or predisposition for future angle closure is seen, prophylactic peripheral iridotomy may be considered.

In/Out Patient Meds

• See Further Outpatient Care.

Complications

• Loss of vision can occur without prompt treatment.

Prognosis

• The prognosis is favorable with early detection and treatment.

Patient Education

• Inform the patient to promptly seek professional treatment if pain and/or decreased vision occur.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to diagnose ACG is the most important medicolegal area. Because patients present with remarkable systemic symptoms (eg, nausea, vomiting), the eyes may be overlooked as the source of the violent reactions. Ophthalmologists must have a high index of suspicion for acute ACG.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Cantor L, et al. Glaucoma. In: Basic and Clinical Science Course. Section 10. 1996-7.
• Epstein DL, Allingham RR, Schuman JS. Chandler and Grant's Glaucoma. 4^th ed. 1997.
• Hitchings RA. Glaucoma: current thinking. Br J Hosp Med. Mar 20-Apr 2 1996;55(6):312-4. [Medline].
• Lai JS, Tham CC, Chan JC. The clinical outcomes of cataract extraction by phacoemulsification in eyes with primary angle-closure glaucoma (PACG) and co-existing cataract: a prospective case series. J Glaucoma. Feb 2006;15(1):47-52. [Medline].
• Liesegang TJ. Glaucoma: changing concepts and future directions. Mayo Clinic Proceedings. 1996;71:689-694.
• Nolan W. Anterior segment imaging: ultrasound biomicroscopy and anterior segment optical coherence tomography. Curr Opin Ophthalmol. Mar 2008;19(2):115-21. [Medline].
• Shields MB. Textbook of Glaucoma. 4^th ed. 1998.
• Sihota R, Dada T, Gupta R, et al. Ultrasound biomicroscopy in the subtypes of primary angle closure glaucoma. J Glaucoma. Oct 2005;14(5):387-91. [Medline].
• Xu L, Cao WF, Wang YX, Chen CX, Jonas JB. Anterior chamber depth and chamber angle and their associations with ocular and general parameters: the Beijing Eye Study. Am J Ophthalmol. May 2008;145(5):929-36. [Medline].

Article Last Updated: May 20, 2008