Acute Angle-Closure Glaucoma in Emergency Medicine 

Updated: Nov 19, 2018
Author: Joseph Freedman, MD; Chief Editor: Steven C Dronen, MD, FAAEM 



Glaucoma is a nonspecific term used for several ocular diseases that ultimately result in increased intraocular pressure (IOP) and decreased visual acuity. Acute angle-closure glaucoma (AACG) is an ocular emergency and receives distinction due to its acute presentation, need for immediate treatment, and well-established anatomic pathology.[1] Rapid diagnosis, immediate intervention, and referral can have profound effects on patient outcome and morbidity.

The acute angle closure literature has been plagued by the lack of a uniform definition and specific diagnostic criteria. Only in recent years has there been a strong push to standardize the definitions of the various forms of angle closure disease. Primary angle closure, primary angle-closure glaucoma, acute angle closure, and acute angle-closure glaucoma were previously used interchangeable. Now, acute angle closure is defined as at least 2 of the following symptoms: ocular pain, nausea/vomiting, and a history of intermittent blurring of vision with halos; and at least 3 of the following signs: IOP greater than 21 mm Hg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, and shallower chamber in the presence of occlusion.

Primary angle closure is defined as an occludable drainage angle and features indicating that trabecular obstruction by the peripheral iris has occurred (ie, peripheral anterior synechiae, increased IOP, distortion of iris fibers [iris whorling], lens opacities, excessive trabecular pigmentation deposits). An eye in which contact between the peripheral iris and the posterior trabecular meshwork is considered possible based on ocular anatomy is termed primary angle closure suspect. The term glaucoma is added if glaucomatous optic neuropathy is present.


AACG represents the end stage of processes resulting in the compromised egress of aqueous humor circulation and the subsequent increase in IOP. Aqueous humor is produced by the ciliary body in the posterior chamber of the eye. It diffuses from the posterior chamber, through the pupil, and into the anterior chamber. From the anterior chamber, the fluid is drained into the vascular system via the trabecular meshwork and Schlemm canal contained within the angle.

Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals to AACG. These include shallower anterior chambers, thinner ciliary bodies, a thinner iris, anteriorly situated thicker lens,[2] and a shorter axial eye length. Recent studies have suggested that increased iris thickness and cross-sectional area are associated with increased risk.[3] Of the many predisposing anatomical variations, a narrow angle has the most devastating consequences.

In the traditional model of AACG, the eye's natural response of dilation to environmental or chemical stimuli results in a pathologic iris-lens apposition. The apposition and contact between the lens and the iris is called pupillary block. Furthermore, pupillary block describes a state in which the forward-most surface of the lens is anterior to the plane of the iris insertion into the ciliary body. As a result, aqueous flow from the posterior chamber to the anterior chamber is obstructed or altogether blocked. When pupillary block occurs in conjunction with the iris, the increasing pressure in the posterior chamber causes the pliable iris, particularly the peripheral region, to bow forward in a process termed iris bombé. Iris bombé further closes the already narrow angle and compromises aqueous drainage, thus increasing IOP.

Recent research has suggested an alternative pathophysiologic pathway for AACG. Cronemberger et al propose that acute events can be traced to an autonomic imbalance in individuals with AACG, specifically increased sympathetic tone. Furthermore, the iris dilator muscles in these individuals have been found to be more developed and stronger. In instances of increased ocular sympathetic tone, including emotional distress, low light conditions, or after sympathomimetic drug use, contraction of the iris dilator muscles leads to pupil dilatation and thickening of the middle-peripheral iris. This thickening can lead to angle closure, thereby obstructing the outflow of aqueous humor.[4]

Other proposed mechanisms of AACG include plateau iris, lens swelling, and ciliary block. Plateau iris is less common than pupillary block and is due to anterior insertion of the iris. The superfluous and crowded iris tissue blocks the trabecular meshwork and again leads to increased IOP.

Lens swelling and ciliary block are extremely rare. Lens swelling occurs in cases of cataracts in which hydration forces cause enlargement of the lens and subsequent crowding of the anterior chamber. Forces posterior to the lens can push the lens and iris forward causing ciliary block or vitreous pressure. This can be seen in panretinal photocoagulation, scleral buckles, and uveitis.



United States

AACG occurs between 1 and 40 times for every 1000 Americans depending on their ethnicity.


Outcome after AACG is dependent on duration from onset to treatment, underlying ocular disease, and ethnicity. The degree of IOP elevation has been shown to have less impact on future visual acuity. Studies report that as many as two thirds of individuals with AACG had no visual field loss. However, Asians appear to be more refractory to the initial medical management, and, even after definitive treatment, they experience a progressive increase in IOP and deterioration in visual acuity.[5]


AACG occurs in 1 of 1000 whites, about 1 in 100 Asians, and as many as 2-4 of 100 Eskimos.[6, 7]


AACG predominately affects females because of their shallower anterior chamber.


Elderly patients in their sixth and seventh decades of life are at greatest risk.




Classically, patients are elderly, suffer from hyperopia, and have no history of glaucoma. Most commonly, they present with periorbital pain and visual deficits.[8] The pain is boring in nature and associated with an ipsilateral headache. Patients note blurry vision and describe the phenomenon of "seeing halos around objects."

Careful investigation may elucidate a precipitating factor, such as dim light or medications (eg, anticholinergics, sympathomimetics).

In a large percentage of patients, extraocular symptoms and systemic manifestations are the chief complaint. Patients present with headache and may receive medications for migraines or an evaluation for a subarachnoid hemorrhage. Several case reports discuss patients presenting with vomiting and abdominal pain that were misdiagnosed with gastroenteritis.[9]


The emergency department evaluation of the eye includes visual acuity, the external eye, visual fields, a funduscopic examination, pupils, ocular motility, and IOP. All of these tend to be affected in AACG.

Slit-lamp evaluation may reveal corneal edema, synechiae, irregular pupil shape or function, or segmental iris atrophy.

Patients complain of blurred vision, and testing reveals decreased visual acuity in the affected eye, often the ability to detect hand movements only. Commonly, they are unable to identify numbers and letters on distance charts or near cards.

Cornea and scleral injection and ciliary flush are present. The obviously edematous and cloudy cornea obscures the funduscopic examination.

Increased IOP (normal limit, 10-20 mm Hg) and ischemia result in pain on eye movement, a mid-dilated nonreactive pupil, and a firm globe. Clinicians must take a comprehensive history and perform a thorough physical examination to ensure that this time-sensitive diagnosis is not missed.


Shallower anterior chambers; anteriorly situated lens; shorter axial eye length; thick iris; overdeveloped iris dilator muscles; and a narrow angle lead to a higher propensity for development of AACG.

Precipitating factors include drugs (ie, sympathomimetics, anticholinergics, antidepressants [SSRIs], anticonvulsants, sulfonamides, cocaine, botulinum toxin),[10, 11, 12, 13, 14] dim light, and rapid correction of hyperglycemia.

Case reports have identified AACG associated with carotid-cavernous sinus fistula, trauma, prone surgical positioning, and giant cell arteritis.[14, 15, 16]





Laboratory Studies

The diagnosis of acute angle-closure glaucoma (AACG) is predicated upon the clinical presentation of painful vision loss and a physical examination revealing a fixed mid-dilated pupil. No definitive laboratory or imaging studies are available. However, tonometry must be performed and must demonstrate increased intraocular pressure (IOP).



Prehospital Care

The patient should be brought to the hospital in an expeditious manner to have intraocular pressure (IOP) reduced. The patient should remain in the supine position as long as possible. The urge to wear eye patches, covers, or blindfolds should be resisted. By maintaining the conditions that cause pupillary dilation, these articles help perpetuate the attack. Their potential negative effects outweigh any presumed benefit.

Emergency Department Care

The treatment of acute angle-closure glaucoma (AACG) consists of IOP reduction, suppression of inflammation, and the reversal of angle closure. Once diagnosed, the initial intervention includes acetazolamide, a topical beta-blocker, and a topical steroid.

Acetazolamide should be given as a stat dose of 500 mg IV followed by 500 mg PO. A dose of a topical beta-blocker (ie, carteolol, timolol) will also aid in lowering IOP. Studies have not conclusively demonstrated the superior neuronal or visual field protectiveness of one beta-blocker over another. Both beta-blockers and acetazolamide are thought to decrease aqueous humor production and to enhance opening of the angle. An alpha-agonist can be added for a further decrease in IOP.

Inflammation is an important part of the pathophysiology and presenting symptomology. Topical steroids decrease the inflammatory reaction and reduce optic nerve damage. The current recommendation is for 1-2 doses of topical steroids.

Addressing the extraocular manifestations of the disease is critical. This includes analgesics for pain and antiemetics for nausea and vomiting, which can drastically increase IOP beyond its already elevated level. Placing the patient in the supine position may aid in comfort and reduce IOP. It is also believed that, while supine, the lens falls away from the iris decreasing pupillary block.

After the initial intervention, the patient should be reassessed. Reassessment includes evaluating IOP, evaluating adjunct drops, and considering the need for further intervention, such as osmotic agents and immediate iridotomy.

Approximately 1 hour after beginning treatment, pilocarpine, a miotic that leads to opening of the angle, should be administered every 15 minutes for 2 doses. In the initial attack, the elevated pressure in the anterior chamber causes a pressure-induced ischemic paralysis of the iris. At this time, pilocarpine would be ineffective. During the second evaluation, the initial agents have decreased the elevated IOP and hopefully have reduced the ischemic paralysis so pilocarpine becomes beneficial in relieving pupillary block.

Pilocarpine must be used with caution. Theoretical concerns exist about its mechanism of action. By constricting the ciliary muscle, it has been shown to increase the axial thickness of the lens and to induce anterior lens movement. This could result in reducing the depth of the anterior chamber and worsening the clinical situation in a paradoxical reaction. Despite this, pilocarpine is recommended to be used as an additional agent.[17]

No standard rate of reduction for IOP exists; however, Choong et el identified a satisfactory reduction as IOP less than 35 mm Hg or a reduction greater than 25% of presenting IOP.[16] If the IOP is not reduced 30 minutes after the second dose of pilocarpine, an osmotic agent must be considered. An oral agent like glycerol can be administered in nondiabetics. In diabetics, oral isosorbide is used to avoid the risk of hyperglycemia associated with glycerol. Patients who are unable to tolerate oral intake or do not experience a decrease in IOP despite oral therapy are candidates for IV mannitol.

Hyperosmotic agents are useful for several reasons. They reduce vitreous volume, which, in turn, decreases IOP. The decreased IOP reverses iris ischemia and improves its responsiveness to pilocarpine and other drugs. Osmotic agents cause an osmotic diuresis and total body fluid reduction. They should be administered with caution in cardiovascular and renal patients. Choong et el demonstrated that 44% of patients required the addition of an osmotic agent to decrease IOP.[18] Repeat doses may be necessary if no effect is seen and if tolerated by the patient.

When medical therapy proves to be ineffective, corneal indentation (CI) can be used as a temporizing measure to reduce IOP until definitive treatment is available. As the cornea is indented, aqueous humor is displaced to the periphery of the anterior chamber, which serves to temporarily open the angle. This leads to immediate reduction of IOP and occasionally may completely abort the attack. After applying topical anesthetic, any smooth instrument can be used to perform this procedure, including a gonioprism (ideal, if available), or a cotton-tipped applicator. Obviously, a concern with performing CI is the possibility for damage to the corneal epithelium, which may complicate the patient’s course.[19]

Laser peripheral iridotomy (LPI), performed 24-48 hours after IOP is controlled, is considered the definitive treatment for AACG. Furthermore, LPI may be offered prophylactically to individuals anatomically predisposed to AACG if identified before the first acute attack. While LPI is the current definitive treatment, evidence suggests that argon laser peripheral iridoplasty (ALPI) and anterior chamber paracentesis (ACP) may have increasing roles in the management of AACG.

In ALPI, burns are made in the peripheral iris resulting in iris contraction and opening of the angle. Some studies suggest ALPI causes a more immediate decrease in IOP, resulting in better outcomes with fewer side effects than systemic therapy.[20] However, a recent randomized-controlled trial comparing LPI plus ALPI compared with ALI alone failed to show improved outcomes with ALPI as an adjunctive therapy.[21] Systemic therapy must still be used with ACP, but ACP appears to instantaneously relieve symptoms.

An additional alternative is lens extraction. Although its role in AACG has not been completely established, it has been proven to effectively reduce IOP without the need for medication postoperatively. Furthermore, it offers a therapeutic advantage for individuals with coexisting cataracts.[22]

The choice of which therapy to use will be made by an ophthalmologist who will evaluate all patients via gonioscopy with complete inspection of the angle. At institutions where ophthalmologic consultation is immediately available, initial treatment should be performed in conjunction with the specialist.

If ophthalmologic consultation is not immediately available, the emergency department physician must begin pharmacologic therapy as described above. After appropriate therapy aimed at IOP reduction, ophthalmologic evaluation must be ensured by transferring the patient, if necessary. If the IOP is unchanged or increased, with appropriate pharmacologic therapy, the attack most likely will terminate only with LPI. Because outcome is adversely affected by the duration of symptoms, expeditious evaluation by a specialist is required. Ocular massage through a closed eyelid may be performed while waiting for ophthalmology if no other treatment reduces IOP.


Ophthalmologic consultation should be obtained as soon as possible because acute-angle closure glaucoma is an ophthalmic emergency.



Medication Summary

The goal in treatment of AACG is to reduce IOP. Medical management is the first step. A prompt reduction in IOP using topical and systemic medication decreases the duration of elevated IOP and the potential for a permanent reduction in visual acuity. IOP reduction is accomplished via suppressing aqueous humor production, eliminating pupillary block, and reversing inflammation. As with any medical intervention, intimate knowledge of the drugs, their indications, contraindications, and potential side effects can aid the physician in providing the best treatment and a favorable outcome.

Carbonic anhydrase inhibitors

Class Summary

These are first-line agents that should be used immediately during the initial intervention. They reduce bicarbonate production in the ciliary epithelium and therefore decrease aqueous formation.

Acetazolamide (Diamox)

Reduces rate of aqueous humor formation by direct inhibition of enzyme carbonic anhydrase (CA) on secretory ciliary epithelium, causing, in turn, a reduction in IOP. More than 90% of CA must be inhibited before IOP reduction can occur. May reduce IOP by 40-60%. Effects are seen in about an hour, they peak in 4 h, and trough in about 12 h. Derived chemically from sulfa drugs. If one form is not well tolerated, another form may be better or lower dose of the drug may better tolerated. IV administration of this medication may be used for rapid relief of increased IOP. A beneficial effect occurs when used with miotics or mydriatics.

Methazolamide (Neptazane)

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

Beta-adrenergic blockers

Class Summary

These agents may lower IOP via their suppression of aqueous humor production and probably not through any affects on the pupil.

Timolol ophthalmic (Timoptic, Timoptic XE)

Reduces elevated and normal IOP by reducing aqueous humor production or possibly the outflow.

Carteolol ophthalmic (Ocupress)

Nonselective beta-adrenergic receptor. Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic activity (ISA), with possibly fewer cardiac and lipid profile adverse effects. Precise mechanism by which carteolol decreases IOP is thought to be through reduction of aqueous formation.

Levobetaxolol (Betaxon)

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

Levobunolol (AKBeta, Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and may increase outflow of aqueous humor.

Dosages of more than 1 gtt of 0.5% levobunolol twice daily have not been shown to be more effective. If IOP not at satisfactory level on this regimen, concomitant therapy can be instituted. However, do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously.

Alpha-adrenergic agonists

Class Summary

These agents are used as adjunct agents to further decrease IOP secondary to their affect on aqueous humor production.

Apraclonidine (Iopidine)

Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Suppresses aqueous production. Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. Apraclonidine is relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

Brimonidine (Alphagan, Alphagan-P)

Selective alpha2 receptor that may reduce aqueous humor formation, may decrease inflow, or may increase uveoscleral outflow.


Class Summary

These agents reduce ocular inflammation thereby providing symptomatic relief and augmenting the affects of other medications.

Prednisolone ophthalmic (AK-Pred, Econopred)

Used in treatment of acute inflammations following eye surgery or other insults to the eye.

In cases of bacterial infections, concomitant use of anti-infective agents is mandatory. If signs and symptoms do not improve after 2 d, reevaluate the patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.

Ophthalmic agents, miotic

Class Summary

These agents pull the peripheral iris tissue away from the trabecular meshwork helping to eliminate obstructed aqueous humor flow. They are ineffective during the initial period due to the ischemic paralysis of the iris. Miotics should be used after the immediate management and initial reduction of IOP.

Pilocarpine ophthalmic (Pilagan, Pilocar, Pilostat)

Patients may be maintained on pilocarpine as long as IOP is controlled and no deterioration in visual fields is present. May be used alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.

Frequency of instillation and concentration are determined by patient's response. Individuals with heavily pigmented irides may require higher strengths.


Class Summary

Hyperosmotic agents increase serum osmolarity and cause a fluid shift from the eye into the vascular space. The subsequent osmotic diuresis reduces IOP.

Glycerin (Osmoglyn)

Used in glaucoma to interrupt acute attacks. Reduces IOP through its diuretic effects. Adds to tonicity of blood until metabolized and eliminated by kidneys. Maximal reduction of IOP occurs 1 h after glycerin administration. The effect lasts approximately 5 h.

Isosorbide (Ismotic)

In the eyes, creates an osmotic gradient between plasma and ocular fluids. Induces diuresis by elevating osmolarity of glomerular filtrate, thereby hindering tubular reabsorption of water. May be used to interrupt an acute attack of glaucoma. Use when less risk of nausea and vomiting, compared with other oral hyperosmotic agents, is needed.

Mannitol (Osmitrol)

Reduces elevated IOP when pressure cannot be lowered by other means.

Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h.

In children, assess for adequate renal function by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 1 mL/h over 1-3 h.



Further Outpatient Care

Patients remain on oral acetazolamide, pilocarpine, and beta-blockers or alpha-agonists until definitive treatment. After laser peripheral iridotomy (LPI), 33% of patients require topical medication to maintain lower intraocular pressure (IOP).

Further Inpatient Care

A low threshold for admission should be used with acute angle-closure glaucoma (AACG) patients. Immediate ophthalmologic consultation must be arranged and admission may be required based on their treatment protocol and the patient's response to therapy. Patients who received osmotic agents may require electrolyte and volume status monitoring, particularly those with co-morbid illnesses.


Fellow eye surgery


Complications may include the following:

  • Permanent decrease in visual acuity

  • Repeat episode

  • Malignant glaucoma

  • Fellow eye attack

  • Central retinal artery occlusion

  • Central retinal vein occlusion


Several studies evaluated patients after treatment for AACG and demonstrated favorable outcomes. With adequate treatment, most patients recover their lost vision. In whites, IOP was controlled with LPI alone in 65-76%. Asians more often have medically refractory initial attacks and require medications after LPI.[5] They also have higher rates of vision loss and subsequent increases in IOP.[5] It has been hypothesized that the initial attack is often more severe in Asians resulting in greater trabecular damage. Another possibility is the formation of peripheral synechiae (adhesions) causing a creeping angle reclosure.

Patient Education

For patient education resources, see the Glaucoma Center, as well as Acute Angle-Closure Glaucoma, Glaucoma FAQs, Glaucoma Overview, and Understanding Glaucoma Medications.


Questions & Answers


What is acute angle-closure glaucoma (AACG)?

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

How common is acute angle-closure glaucoma (AACG) in the US?

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

What is the race-related incidence of acute angle-closure glaucoma (AACG)?

Is acute angle-closure glaucoma (AACG) more common in males or females?

What are the age-related demographics of acute angle-closure glaucoma (AACG)?


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

What are the physical exam findings in acute angle-closure glaucoma (AACG)?

What causes acute angle-closure glaucoma (AACG)?


What are the differential diagnoses for Acute Angle-Closure Glaucoma in Emergency Medicine?


Which lab studies are indicated in the workup of acute angle-closure glaucoma (AACG)?


What prehospital care is indicated for acute angle-closure glaucoma (AACG)?

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

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

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

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

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

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

Which specialist consultations are indicated in the treatment of acute angle-closure glaucoma (AACG)?


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

Which medications in the drug class Hyperosmotics are used in the treatment of Acute Angle-Closure Glaucoma in Emergency Medicine?

Which medications in the drug class Ophthalmic agents, miotic are used in the treatment of Acute Angle-Closure Glaucoma in Emergency Medicine?

Which medications in the drug class Corticosteroids are used in the treatment of Acute Angle-Closure Glaucoma in Emergency Medicine?

Which medications in the drug class Alpha-adrenergic agonists are used in the treatment of Acute Angle-Closure Glaucoma in Emergency Medicine?

Which medications in the drug class Beta-adrenergic blockers are used in the treatment of Acute Angle-Closure Glaucoma in Emergency Medicine?

Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Acute Angle-Closure Glaucoma in Emergency Medicine?


What further outpatient care is indicated in the treatment of acute angle-closure glaucoma (AACG)?

When is inpatient care indicated in the treatment of acute angle-closure glaucoma (AACG)?

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

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

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

What educational resources are available for patients with acute angle-closure glaucoma (AACG)?