Acute Angle-Closure Glaucoma (AACG)

Updated: Apr 07, 2023
Author: Albert P Lin, MD; Chief Editor: Inci Irak Dersu, MD, MPH 



Angle closure is defined as the apposition of iris to the trabecular meshwork, which results in increased intraocular pressure (IOP). In acute angle closure (AAC), the process occurs suddenly with a dramatic onset of symptoms, including blurred vision, red eye, pain, headache, and nausea and vomiting. The sudden and severe IOP elevation can quickly damage the optic nerve, resulting in acute angle-closure glaucoma (AACG).

AAC is a true ophthalmic emergency, and a delay in treatment can result in blindness. While immediate treatment can sometimes minimize the amount of visual loss, the best treatment is to stop its occurrence in susceptible individuals.[1, 2, 3, 4]


AAC occurs through a process termed pupillary block. Normally, aqueous humor is produced in the ciliary body, flows through the pupil into the anterior chamber, and drains into the trabecular meshwork to exit the eye. When the pupil is mid-dilated, the distance between the iris and the lens is the shortest, and the two structures can come into contact with each other in individuals at risk for angle closure. When this occurs, aqueous humor cannot flow through the pupil into the anterior chamber (pupillary block), and the aqueous pushes the iris forward. When the iris is pushed against the trabecular meshwork, aqueous humor cannot flow out of the eye (angle closure), resulting in a sudden rise in IOP.

The normal IOP is 10-21 mm Hg in AAC, and IOP typically exceeds 40 mm Hg. The sudden and severe elevation in IOP can cause irreversible optic nerve damage very quickly.  When optic nerve damage occurs, it is called acute angle-closure glaucoma.

Mechanisms other than pupillary block can contribute to primary angle closure, including plateau iris, use of certain medications, increased iris thickness, increased iris volume with dilation, hyperopia, and increased lens thickness in phacomorphic angle closure.


AACG is more common in older individuals. Among persons older than 40 years, AAC is more common in Inuit and Asian persons, less common in Whites, and least common in Blacks. While AACG usually accounts for a small proportion of glaucoma cases in the general population (0.6%, approximately 17 million world wide), it accounts for a significant number of glaucoma cases among persons of Eastern Asian and Southeast Asian descent (approximately 12 million). It is more common among women and individuals with hyperopia. Individuals with family history of AAC or who have had AAC in 1 eye are also at a higher risk.[2, 5, 6]


The prognosis is favorable with early detection and treatment. The best way to prevent loss of vision is to treat susceptible individuals prior to AAC.

Patient Education

AAC is a medical emergency that must be treated immediately. Even with immediate treatment, AAC may result in vision loss. The best method for preventing vision loss due to AAC is prophylactic treatment in patients with susceptible anatomy.

Patients need to promptly seek an eye care professional if symptoms (pain, decreased vision, headache, and vomiting) suggest AAC.




In acute angle closure (AAC), the intraocular pressure (IOP) rises rapidly, and the patient may present with dramatic symptoms, including the following:

  • Sudden onset of severe ocular pain, redness, blurry vision, headache, and nausea and vomiting
  • Patients may complain of seeing haloes around lights. Haloes and blurry vision result from corneal edema.
  • The attack may have been precipitated by pupillary dilation, which may result from activities such as going to a movie theater, taking over-the-counter medications that contain antihistamine for cold or allergy, or using dilation eye drops as part of an ophthalmic examination.
  • Patients with AAC may be extremely uncomfortable and distressed.

Some patients experience intermittent episodes of partial angle closure and relatively elevated IOP without experiencing a frank attack of AAC. These patients may report incidents of mild pain with slightly blurred vision or may report seeing haloes around lights. Some may be completely asymptomatic. Symptoms can resolve spontaneously if the angle reopens on its own.


A complete ophthalmic examination should be conducted in patients who present with suspected AAC. This examination should emphasize vision, pupil, gonioscopy, tonometry, slit-lamp examination, and optic nerve evaluation:

  • Diagnosis of AAC is based on gonioscopic visualization of an occluded anterior chamber angle in the affected eye and predisposing angle configuration (narrow occludable angle) in the contralateral unaffected eye.
  • Tonometry demonstrates an elevated IOP, which may be as high as 40-80 mm Hg.
  • Slit-lamp examination may reveal conjunctival injection, a fixed or sluggish and mid-dilated pupil, a shallow anterior chamber, corneal epithelial edema and bullae, and cells and flare. The patient may be sensitive to light, and the eye may be tearing and closed.
  • Ophthalmoscopy may reveal a swollen optic disc in an acute attack or excavation if episodes have been chronic or repetitive. Unilateral involvement and worsening symptoms are common in AAC.

If previous episodes of angle closure have occurred, the following may be visible:

  • Posterior and peripheral anterior synechiae- adhesions between the lens and iris and between the iris and trabecular meshwork.
  • Glaucoma flecks- subcapsular vesicles on front of the crystalline lens.
  • Atrophy of the iris- thinning and whitening of the iris.


Pupillary block is considered to be the most common cause of AAC. Normally, aqueous humor is made by the ciliary body and flows through the pupil to the anterior chamber, where it drains out of the eye through the trabecular meshwork and Schlemm's canal. If contact occurs between the lens and the iris, aqueous humor accumulates behind the pupil, increasing posterior chamber pressure and forcing the peripheral iris to shift forward. 

The trabecular meshwork is located between the iris and cornea, and the two structures form an angle that is normally 40°. Persons with susceptible anatomy have a narrow occludable angle, usually of less than 20°. When the iris is pushed forward by the aqueous humor in a narrow occludable angle, it becomes apposed to the trabecular meshwork. This blockage causes accumulation of aqueous humor in the anterior chamber and an acute rise in IOP.

Not all individuals with narrow occludable angle develop AAC, and mechanisms other than pupillary block play a role in development of AAC.

Plateau iris is a condition in which the iris is inserted more anteriorly into the ciliary body and the periphery of the iris is flat. The angle is narrow owing to the anterior iris insertion, and the flat iris bunches up to obstruct the angle when the eye is dilated.[7, 8]

Several medications have been implicated in causing acute ACC by producing swelling in the ciliary body and forward movement of the iris. Sulfa-derivative medications, including acetazolamide, sulfamethoxazole, and hydrochlorothiazide, and antiepileptic medication topiramate have been reported to cause acute attacks.[9, 10]

Persons of Asian descent have thicker irides, and increased iris thickness is associated with angle closure.[11, 12]

Pupillary dilation normally results in loss of iris volume, but this volume decrease is less in eyes that have had AAC; some of these eyes actually showed an increase in iris volume.[13, 14]

Individuals with hyperopia have smaller eyes, and the diameter of the eye (axial length) is shorter. The intraocular structures are spaced closer together. These patients are more likely to have shallow anterior chambers and narrow occludable angles.[1, 2, 3]

Lens volume increases with age and can decrease the amount of space in the anterior chamber via mass effect.[1, 2, 3]


Loss of vision or blindness can occur without prompt treatment.





Imaging Studies

Ultrasound biomicroscopy (UBM) and anterior segment optical coherence tomography (AS-OCT)

These imaging techniques can be used to visualize the angle and surrounding structures. They can provide objective and quantitative measurements to document changes to the angle before and after treatment. However, clinical assessment and the use of gonioscopy may be more practical and applicable if a patient has acute angle closure (AAC).[15]

Other Tests

The anterior chamber angle cannot be visualized through a slit lamp because the light reflected from the angle is reflected back into the eye. Gonioscopy is performed by applying a gonioscope onto the cornea after administration of a topical anesthetic. Four mirror lenses are useful to diagnose and, possibly, to break the block by applying pressure. It allows the clinician to quickly and accurately assess the angle without expensive machinery. It is an essential component of an ophthalmic examination in patients with suspected narrow angle and in patients with AAC.



Approach Considerations

The definitive treatment of acute angle closure (AAC) is surgical. The goal of medical treatment is to break the AAC in preparation for surgical intervention to prevent its recurrence.

Medical Care

Topical and oral medications are used to lower the IOP. Lowering the IOP minimizes damage to the optic nerve and allows the ocular tissue to be compressed.

If the IOP cannot be lowered sufficiently, an anterior chamber paracentesis (needle insertion) can be performed. This technique can be useful because it provides immediate relief to the distressed patient and facilitates tolerance of subsequent treatment. A consent form should be obtained for the risks (eg, inadvertent lens puncture, decompression retinopathy) and benefits prior to the procedure.

Compression gonioscopy then is performed by using a gonioscope to push down on the cornea and then easing up on it. The process is done repeatedly, and the force generated is translated intraocularly to break the contact between the iris and the lens (pupillary block) and apposition of the iris to the trabecular meshwork (angle closure). This temporarily restores the outflow of aqueous humor and normalizes the IOP.

Patients also may be placed in a supine position to allow the lens to move away from the anterior chamber to help restore the flow of aqueous humor.

When the eye is in AAC, the visualization into the anterior chamber is poor. Medications for eye pressure and inflammation are used to help clear up the cornea, to reduce intraocular inflammation, and to decrease iris edema. It is preferable to perform laser iridotomy when the condition can be optimized. If laser iridotomy cannot be performed and AAC continues, surgical iridectomy is indicated.

Surgical Care

Laser iridotomy

The treatment of choice for pupillary-block ACG is laser iridotomy. Iridotomy with an argon and/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 humor flows into the anterior chamber through the iris defect, pressure behind the iris falls, allowing the iris to fall back toward its normal position. This procedure opens the anterior chamber angle and relieves the blockade of trabecular meshwork. It also prevents future pupillary block and AAC.

Surgical iridectomy

If the cornea is extremely cloudy or the iris is too thick and an opening cannot be created using laser, incisional peripheral iridectomy can be performed in the operating room.

Laser iridoplasty

Argon laser may be used to create burns in the peripheral iris and to cause tissue contraction. This reduces iris thickness and creates additional space between the iris and the trabecular meshwork. Traditionally, this technique is indicated to prevent AAC in plateau iris and nanophthalmos but also can be used to augment the effect of iridotomy or iridectomy, if needed.[16, 17]

Cataract surgery

If the angle continues to be narrow and occludable after laser iridotomy and iridoplasty, especially in an older patient, cataract surgery is indicated to remove the cataract and its mass effect on the angle. If the patient has both a narrow occludable angle and a visually significant cataract (blurry vision due to cataract), cataract surgery is the treatment of choice. It opens the angle and improves vision.[18] Even without significant cataract, the Effectiveness of Early Lens Extraction for the Treatment of Primary Angle-closure Glaucoma (EAGLE) study, conducted in Asia, showed that clear lens extraction may be more efficacious and cost effective than laser iridotomy. The authors suggested that the crystalline lens may play a larger role in the mechanism of angle closure than previously thought and that early lens extraction can be considered as an option for first-line treatment.[19]


If the patient undergoes cataract surgery and there are bands of adhesion between the iris and the trabecular meshwork, the bands may be pulled apart during surgery to restore the flow of aqueous humor through the trabecular meshwork.

Glaucoma surgery

If permanent adhesions between the iris and trabecular meshwork have formed after AAC and IOP cannot be normalized with the other methods, traditional glaucoma surgery, such as a trabeculectomy or tube shunt, may be indicated.


Some of the potential complications of AAC include the following:

  • Cataract formation
  • Iris sphincter atrophy and permanently dilated pupil
  • Peripheral anterior synechia
  • Chronic angle closure glaucoma
  • Absolute glaucoma
  • Corneal decompensation
  • Optic atrophy


In most cases, the fellow eye has an occludable angle, and laser iridotomy should be performed as soon as possible.

Long-Term Monitoring

The patient must be monitored closely after the initial acute angle closure (AAC) to ensure the following:

  • The IOP is normalized and AAC does not recur.
  • Perform laser iridotomy once there is sufficient view into the anterior chamber.
  • Ensure the laser treatment is effective or if additional treatment, such as iridoplasty, is indicated.
  • Treat the patient until the inflammation has subsided and the pupil and vision return to normal. Gradually taper the medications.
  • Assess the contralateral eye and perform laser treatment, if needed.

Further Inpatient Care

Patients in AAC need to be treated until the IOP normalizes. IOP can increase after laser iridotomy, and the IOP should be checked 30-60 minutes after the treatment prior to releasing the patient.



Medication Summary

The medical therapy for acute angle closure glaucoma (AACG) is directed toward preparing the patient for surgical treatment. IOP must be returned to normal, and the cornea must be cleared before a definitive procedure can be undertaken. In AAC, several drugs from different classes are used simultaneously to accelerate and maximize their pressure-lowering effects.

Alpha-adrenergic agonists

Class Summary

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

Brimonidine (Alphagan P)

Selective alpha2-receptor that reduces aqueous humor formation and possibly increases uveoscleral outflow.

Apraclonidine (Iopidine)

Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Reduces IOP whether or not accompanied by glaucoma. Selective alpha-adrenergic agonist without significant local anesthetic activity. Has minimal cardiovascular effect.


Class Summary

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.

Levobunolol (Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production

Betaxolol ophthalmic (Betoptic-S)

Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.

Timolol maleate (Timoptic, Timoptic XE, Istalol, Betimol)

May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor.

Miotic agents

Class Summary

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.

Pilocarpine ophthalmic (Isopto Carpine)

A naturally occurring alkaloid, pilocarpine mimics muscarinic effects of acetylcholine at postganglionic parasympathetic nerves. Directly stimulates cholinergic receptors in the eye, decreasing resistance to aqueous humor outflow.

Instillation frequency and concentration are determined by patient's response. Individuals with heavily pigmented irides may require higher strengths. If other glaucoma medication is also being used, at bedtime, use gtt at least 5 min before gel. May use alone, or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.

Carbonic anhydrase inhibitors

Class Summary

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.

Acetazolamide (Diamox Sequels)

Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute ACG when delay of surgery desired to lower IOP.

Methazolamide (Neptazane)

Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.

Dorzolamide (Trusopt)

Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

Brinzolamide (Azopt)

Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than one topical ophthalmic drug is being used, administer drugs at least 10 min apart.

Dorzolamide HCl/ timolol maleate (Cosopt, Cosopt PF)

Carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.

Timolol is a nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion and may slightly increase outflow facility. Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly.

Prostaglandin, Ophthalmic

Class Summary

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.

Latanoprost (Xalatan, Xelpros)

Latanoprost may decrease IOP by increasing the outflow of aqueous humor. Patients should be informed about possible cosmetic effects to the eye/eyelashes, especially if uniocular therapy is to be initiated.

Travoprost (Travatan Z)

This agent is a prostaglandin F2-alpha analog. It is a selective FP prostanoid receptor agonist that is believed to reduce IOP by increasing uveoscleral outflow. Travoprost ophthalmic solution is used to treat open-angle glaucoma and ocular hypertension.

Bimatoprost (Lumigan, Latisse)

This agent is a prostamide analog with ocular hypotensive activity. It mimics the IOP-lowering activity of prostamides via the prostamide pathway. Bimatoprost ophthalmic solution is used to reduce IOP in open-angle glaucoma and ocular hypertension.

Latanoprostene bunod ophthalmic (Vyzulta)

Metabolizes rapidly in the eye to latanoprost acid, an F2 alpha prostaglandin analog. May increase the outflow of aqueous humor through the trabecular meshwork and uveoscleral route, which may in turn reduce intraocular pressure.

Rho Kinase Inhibitors

Class Summary

These agents may increase aqueous outflow by reversing structural and functional damage at the trabecular meshwork. The vasodilatory effect of rho kinase inhibitors may also reduce episcleral venous pressure.

Netarsudil ophthalmic (Rhopressa)

May reduce intraocular pressure by increasing the outflow of aqueous humor through the trabecular meshwork route.


Questions & Answers


What is acute angle-closure glaucoma (AACG)?

What is the pathophysiology of acute angle-closure glaucoma (AACG)?

What is the prevalence of acute angle-closure glaucoma (AACG)?

What is the prognosis of acute angle-closure glaucoma (AACG)?

What is included in patient education about acute angle-closure glaucoma (AACG)?


What are the signs and symptoms of acute angle-closure glaucoma (AACG)?

What is included in the ophthalmic exam for acute angle-closure glaucoma (AACG)?

Which physical findings are characteristic of acute angle-closure glaucoma (AACG)?

What causes acute angle-closure glaucoma (AACG)?

What are the possible complications of acute angle-closure glaucoma (AACG)?


What are the differential diagnoses for Acute Angle-Closure Glaucoma (AACG)?


What is the role of imaging in the diagnosis of acute angle-closure glaucoma (AACG)?

What is the role of gonioscopy in the diagnosis of acute angle-closure glaucoma (AACG)?


How is acute angle-closure glaucoma (AACG) treated?

What is the medical treatment for acute angle-closure glaucoma (AACG)?

What is the role of laser iridotomy in the treatment of acute angle-closure glaucoma (AACG)?

What is the role of iridectomy in the treatment of acute angle-closure glaucoma (AACG)?

What is the role of laser iridoplasty in the treatment of acute angle-closure glaucoma (AACG)?

What is the role of cataract surgery in the treatment of acute angle-closure glaucoma (AACG)?

What is the role of goniosynechialysis in the treatment of acute angle-closure glaucoma (AACG)?

What is the role of glaucoma surgery in the treatment of acute angle-closure glaucoma (AACG)?

What are the possible complications of acute angle-closure glaucoma (AACG)?

How is acute angle-closure glaucoma (AACG) prevented?

What is included in the long-term monitoring of patients with acute angle-closure glaucoma (AACG)?

What is included in inpatient monitoring of acute angle-closure glaucoma (AACG)?


What is the role of medications in the treatment of acute angle-closure glaucoma (AACG)?

Which medications in the drug class Prostaglandin, Ophthalmic are used in the treatment of Acute Angle-Closure Glaucoma (AACG)?

Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Acute Angle-Closure Glaucoma (AACG)?

Which medications in the drug class Miotic agents are used in the treatment of Acute Angle-Closure Glaucoma (AACG)?

Which medications in the drug class Beta-blockers are used in the treatment of Acute Angle-Closure Glaucoma (AACG)?

Which medications in the drug class Alpha-adrenergic agonists are used in the treatment of Acute Angle-Closure Glaucoma (AACG)?

Which medications in the drug class Rho Kinase Inhibitors are used in the treatment of Acute Angle-Closure Glaucoma (AACG)?