Angle Closure Glaucoma

Angle Closure Glaucoma  

7 Interesting Facts of Angle Closure Glaucoma  

  1. Angle-closure glaucoma is a form of glaucoma caused by narrowing or closure of the ocular anterior chamber angle resulting in increased intraocular pressures
    • Can be an acute process with more immediate signs and symptoms, or may be insidious, chronic, and asymptomatic
    • Usually results in optic disk damage and associated visual field loss
  2. Diagnosis of angle closure is based on gonioscopy
  3. Majority of patients with chronic angle-closure glaucoma are asymptomatic; vision loss can occur in advanced disease
    • May be noted on routine eye examinations or incidentally during other ocular evaluations
    • Consult ophthalmologist for patients with intraocular pressure exceeding 20 mm Hg 
  4. Acute angle-closure crisis is an ocular emergency
    • Symptoms include acute onset of eye pain, blurred vision, headache, nausea, and vomiting
    • Signs include red eye, fixed and mid-dilated pupil, hazy cornea, and highly elevated intraocular pressures
  5. Initial treatment of acute angle closure is aimed at decreasing intraocular pressure
  6. Definitive treatment of angle closure is laser peripheral iridotomy, with prophylactic iridotomy in fellow eye if chamber angle is anatomically narrow
  7. Prompt and effective treatment of angle closure can often prevent glaucomatous optic neuropathy or significant visual deficits from occurring


  • Failure to consider glaucoma as the cause of headache, particularly in older adult patients
  • Omission of gonioscopy in evaluation of suspected glaucoma (will lead to incorrect diagnosis)
  • Failure to evaluate fellow eye for similar anatomic predisposition and treat prophylactically, if indicated (approximately 50% of fellow eyes develop acute angle-closure crisis within 5 years)
  • Glaucoma is a group of optic neuropathies characterized by optic disk damage and associated visual field loss; increased intraocular pressure is a major modifiable risk factor
    • Leading cause of global irreversible blindness 
    • 2 major subtypes: open angle and angle closure, based on status of eye’s drainage system 
  • Angle-closure glaucoma is increased intraocular pressure caused by narrowing or closure of the anterior chamber angle (junction of iris and cornea)
    • Can be an acute process with more immediate signs and symptoms, or may be an insidious, chronic or intermittent, asymptomatic process
    • Generally bilateral; acute attacks are usually unilateral


  • Broadly classified as: 
    • Primary: no cause identified, other than anatomic predisposition
    • Secondary: result of other ocular conditions (eg, neovascularization, inflammation, trauma, obstruction from enlarging cataract in a small eye)
  • Traditionally based on presence of symptoms (subjective, highly variable) 
    • Acute: sudden onset of symptomatic intraocular pressure elevation from total angle closure
    • Subacute or intermittent: self-limited and recurrent episodes of sudden intraocular pressure elevation; symptoms may be mild or even absent
    • Chronic: chronic, asymptomatic elevated intraocular pressure from angle closure
  • Based on natural history (objective, preferred) 
    • Primary angle-closure suspect
      • Contact between iris and trabecular meshwork is possible
      • Intraocular pressure within reference range
      • No optic neuropathy
    • Primary angle closure
      • Evidence that trabecular meshwork obstruction by peripheral iris has occurred, such as:
        • Elevated intraocular pressure
        • Peripheral anterior synechiae (adhesions between iris and trabecular meshwork)
      • No optic neuropathy
    • Primary angle-closure glaucoma
      • Same criteria as primary angle closure, but with presence of glaucomatous optic neuropathy
        • Glaucomatous optic neuropathy consists of optic disk cupping from loss of axons, blood vessels, and glial cells; may result in functional vision loss
    • Acute angle-closure crisis 
      • Occluded angle with symptomatic high intraocular pressure
      • Uncommon ophthalmologic emergency requiring immediate treatment

Clinical Presentation


  • Majority of patients at risk for primary angle-closure glaucoma are asymptomatic; visual loss can occur in advanced disease 
    • Often discovered incidentally during routine eye examination
  • Ocular history may include family history of angle-closure glaucoma or personal history of intermittent, symptomatic angle closure episodes (eg, after stress or dilated eye examinations) 
  • Inquire about recent environmental or medication exposures that can induce acute, as well as asymptomatic, angle closure 
    • In anatomically predisposed eyes, pupil dilation can cause iris apposition to the angle structures, leading to increased intraocular pressures; if the rise in intraocular pressure is acute, this can result in acute angle closure. Common causes of pupillary dilation include:
      • Spontaneous
        • Dim lighting
        • Emotional stress
        • Severe pain
      • Pharmacologic-induced 
        • Sympathomimetics: β₂-agonists (eg, albuterol), α-agonists (eg, phenylephrine), nasal decongestants (eg, phenylpropanolamine), amphetamines, and cocaine
        • Anticholinergics: tricyclic antidepressants (eg, imipramine), selective serotonin reuptake inhibitors (eg, paroxetine, citalopram, fluvoxamine), and muscarinic antagonists (eg, atropine, oxybutynin, tropicamide); botulinum toxin
        • Idiosyncratic: sulfa-containing drugs, hydrochlorothiazide, topiramate, promethazine, escitalopram; serotonin and noradrenaline reuptake inhibitors (eg, venlafaxine)
  • Acute angle-closure crisis may present with sudden onset of symptoms, including: 
    • Ocular pain or headache
    • Blurred vision; occasionally multicolored halos around lights
    • Nausea and/or vomiting
    • Abdominal pain (can simulate appendicitis or gastroenteritis in some patients) 

Physical examination

  • Physical signs of acute angle-closure crisis include:
    • Conjunctival erythema
    • Increased tears
    • Fixed, mid-dilated pupil
      • May also be asymmetrical, poorly reactive to light, and have an afferent defect
    • Corneal edema (stromal and epithelial) with resultant decreased visual acuity
    • Gentle palpation of globe with lids closed may reveal it to be firm or rock-hard
    • Shallow anterior chamber (determined by slit lamp examination); often narrow angle in other eye (determined on gonioscopic evaluation by ocular specialist)


  • Anatomic block of aqueous humor outflow at the angle of the eye, which can result in increased intraocular pressure and optic nerve damage with accompanying retinal ganglion loss
    • Typically, aqueous humor is produced by the ciliary body, flows through the pupil into the anterior chamber, and exits at the anterior chamber angle via the trabecular meshwork into Schlemm canal (ie, sinus venosus sclerae)
    • Blockage may be appositional or synechial
      • Appositional angle closure: iris rests against and covers the trabecular meshwork; may be intermittent
        • In eyes with a narrow anterior chamber angle, dilation increases the iris volume, predisposing to angle closure 
      • Synechial angle closure: iris permanently adheres to trabecular meshwork, owing to fibrosis between the surfaces
    • Multiple mechanisms have been recognized
      • Pupillary block is the primary anatomical mechanism of angle narrowing (75% of cases) 
        • Blockage of aqueous humor flow from posterior to anterior chamber at the pupil; results in increased posterior segment pressure, causing iris to bow anteriorly and narrow or close the angle of the eye
      • Other mechanisms include plateau iris configuration (narrow angle due to an anteriorly positioned ciliary body with deep central anterior chamber)

Risk factors and/or associations

  • Older age
    • Risk increases as lens thickens (cataract formation) and anterior chamber depth becomes more shallow with age 
  • Females are at higher risk 
  • Family history of angle closure, especially first-degree relatives
    • Anatomic features are inherited
  • Asian descent 
Other risk factors/associations
  • Other ocular biometric risk factors include: 
    • Thick, anteriorly positioned, crystalline lens
    • Shallow anterior chamber depth
    • Small eyes; short axial length (hyperopia)

Diagnostic Procedures

Primary diagnostic tools

  • Initial emergency department or nonophthalmologic clinician evaluation for acute angle crisis
    • Diagnosis is based on suggestive history and physical examination: 
      • Obtain best-corrected visual acuity (Snellen chart) and visual fields (by confrontation)
        • Vision may be decreased in acute attack, owing to edematous, hazy cornea
      • Evaluate external eye for trauma and assess pupils for abnormal size, shape, or reactivity, and presence of relative afferent pupillary defect
        • Pupil may be fixed and mid-dilated (usually 3-6 mm); may have asymmetric or oval shape 
        • Relative afferent pupillary defect (ie, Marcus Gunn pupil) may be present with asymmetric optic nerve damage or elevated intraocular pressure
      • Examine with slit lamp (if available) for signs, including: 
        • Conjunctival hyperemia
        • Corneal edema (hazy, cloudy)
        • Shallow anterior chamber
      • Observe fundus by nondilated direct funduscopy
        • Optic disk may have cupping, indicating glaucomatous changes; not typically seen in acute stages
      • Determine intraocular pressure (tonometry)
        • Common methods include electronic, manual (eg, Schiøtz), or applanation tonometers
          • Intraocular pressure reference range:10 to 20 mm Hg
          • Consult ophthalmologist for patients with intraocular pressure exceeding 20 mm Hg
          • Emergent consultation with ophthalmologist is required for patients with intraocular pressures above 30 mm Hg, as they require rapid treatment
            • Intraocular pressure measurements are typically above 40 mm Hg in patients with acute angle closure 
  • Ophthalmologic examination by ocular specialist
    • Complete history and diagnostic bilateral eye evaluation, including the following specific key elements:
      • Refractive status and visual field evaluation
        • Hyperopic (ie, shortened) eyes have increased risk of primary angle closure
        • Automated static perimetry often used to evaluate for visual field loss
      • Slit lamp biomicroscopy evaluation of anterior segment
        • Conjunctival hyperemia (in acute cases)
        • Corneal edema (in acute cases) and endothelial cell loss
        • Inflammation (suggests current or recent attack)
        • Anterior chamber depth narrowing, central and peripheral
        • Iris abnormalities (eg, atrophy, whorling, posterior synechiae, pupil irregularities)
        • Lens changes, such as cataract and glaukomflecken (gray-white, patchy anterior cortical lens opacities)
      • Intraocular pressure (typically using contact applanation tonometry)
      • Gonioscopy on both eyes to visualize the anterior segment and anterior chamber angle anatomy
        • Essential to diagnose angle closure
          • Currently defined as an angle in which 180° or more of the posterior trabecular meshwork cannot be seen 
        • Narrow anterior chamber angle is typically bilateral
          • Wide open angle in fellow eye suggests alternative diagnosis, such as secondary angle-closure glaucoma (eg, iris neovascularization, synechiae due to inflammatory process, intraocular tumors, congenital anterior chamber angle abnormalities)
      • Anterior segment imaging is considered when anterior chamber angle anatomy is difficult to assess on gonioscopy
        • Ultrasonographic biomicroscopy
        • Anterior segment optical coherence tomography
      • Evaluate fundus and optic nerve using direct ophthalmoscopy or slit lamp biomicroscope with an indirect lens
        • Avoid pupil dilation initially, as dilation can precipitate acute angle-closure crisis
        • May show evidence of glaucomatous optic nerve damage (eg, large optic cup, nerve fiber loss)
    • Diagnose primary angle-closure suspect based on:
      • Anatomical presence of iridotrabecular contact of 180° or more on gonioscopy
      • No elevated intraocular pressure or optic nerve damage
    • Diagnose primary angle closure based on:
      • Iridotrabecular contact of 180° or more on gonioscopy
      • Presence of either elevated intraocular pressure or peripheral anterior synechiae; no optic nerve damage
    • Diagnose primary angle-closure glaucoma based on:
      • Iridotrabecular contact of 180° or more on gonioscopy
      • Presence of peripheral anterior synechiae, elevated intraocular pressure, and optic neuropathy
    • Diagnose acute angle-closure crisis based on:
      • Occluded angle on gonioscopy with symptomatic high intraocular pressure


  • Ultrasonographic biomicroscopy
    • Allows real-time, high-resolution images of anterior chamber angle and other anterior segment structures to aid in determining presence and mechanism of angle closure
    • Requires skilled operator and patient cooperation (direct contact with eye)
  • Anterior segment optical coherence tomography
    • Allows noncontact imaging of entire anterior chamber in a single image to assess angle, iris, and lens parameters 
    • May be superior to gonioscopy in diagnosis of closed angles 

Functional testing

  • Automated static perimetry
    • Test to determine visual field loss
    • Light stimuli of same size, but different intensity, are presented randomly in predetermined locations of visual fields and patient responses are recorded


  • Tool to determine intraocular pressure; various methods available 
  • Typical emergency department methods use impression tonometry, which measures the resistance of the cornea to indentation by an applied force 
    • Schiøtz tonometry
      • Uses a plunger (3-mm diameter) to deform the cornea; tonometer foot is placed vertically onto the anesthetized cornea and clinician reads pressure off scale
      • Patient must be in supine position
    • Handheld, digital instrument (eg, Tono-Pen XL)
      • Device is held perpendicular to corneal surface and anesthetized cornea is gently and briefly touched; repeated several times and average is read out on display screen
      • Patient can be in any position; device has smaller footprint than Schiøtz tonometer and uses sterile tip covers
        • Slightly less accurate than Schiøtz tonometry
  • Applanation tonometry (eg, Goldmann tonometry) is typically used by eye specialists; most accurate 
    • Planar surface of device is pressed against the cornea; used with slit lamp
  • Determination of intraocular pressure 
  • Suspected penetrating globe injuries
  • Relative contraindications include:
    • Corneal defects
    • Infection (unless using sterile cover)
    • Uncooperative patient (may induce injury)
  • Corneal abrasions (rare)
  • Intraocular pressure
    • Reference range: 12 to 20 mm Hg
    • Between 20 and 30 mm Hg requires urgent ophthalmologist referral
    • Above 30 mm Hg requires immediate ophthalmologist consultation and treatment
  • Ophthalmologic technique for visualizing the structures in the anterior chamber angle and determining whether angle is open or closed 
  • Handheld, mirrored instrument (goniolens) is placed on patient’s eye to examine angle of eye in conjunction with slit lamp
    • Evaluates angle anatomy, presence of iridotrabecular contact and/or peripheral anterior synechiae, and plateau iris configuration 
      • Iridotrabecular contact is defined as the iris appearing to contact the anterior chamber angle at the posterior pigmented trabecular meshwork or further anterior structures 
    • With indentation, presence of peripheral anterior synechiae can be determined 
      • If cornea is edematous because of an acute attack of angle closure, topical glycerin can help clear edema to allow visualization of angle 
  • Binocular evaluation of all patients in whom angle closure is suspected 
  • Verification of improvement in angle configuration after treatment 
  • Suspicion for open globe injury 
  • Immediate postoperative period 
  • Hyphemia 
  • Corneal abrasions 
  • External ocular infection, active keratitis or conjunctivitis 
  •  Corneal vascular disorders with corneal melts or peripheral ectasias 
  • Corneal scars 
  • Occludable angle risk currently defined as angle in which 180° or more of the posterior trabecular meshwork cannot be seen 
  • Various grading systems (eg, Shaffer, Scheie, Spaeth) are used to evaluate functional status of angle, degree of closure, and risk of further closure, based on gonioscopic findings 
  • Both eyes must demonstrate narrow anterior angle to support the diagnosis of angle-closure glaucoma; if only 1 angle is narrow, search for a secondary cause is indicated 

Differential Diagnosis

Most common

  • Anterior uveitis
    • Inflammatory process of the anterior uvea (iris and ciliary body)
    • Symptoms of acute disease include rapid onset (over few hours to days) of eye pain, redness, and decreased visual acuity; other symptoms include photophobia
    • Differentiate by clinical examination; notably uveitis is recognized by presence of flare and cells in anterior chamber and by intraocular pressure within reference range
  • Endophthalmitis
    • Inflammatory process of the intraocular fluids (aqueous and/or vitreous humors); typically infectious
      • Usually there is recent history of trauma or surgery, but it can be endogenous
    • Presentation can include eye pain, redness, decreased vision, and corneal edema; may also include low intraocular pressure
    • Presence of anterior (hypopyon) and/or vitreous inflammatory cells on clinical examination aids in differentiation
      • Ultrasonography is useful in evaluating endophthalmitis, especially for posterior involvement
    • Culture and sensitivity can be confirmatory
  • Corneal abrasion
    • Typically presents with acutely painful, red eye; can have decreased vision
      • Blepharospasm, photophobia, and tearing can also be present
    • Often includes recent history of trauma to eye from foreign body; usually no nausea or vomiting
    • Diagnosed by corneal staining with fluorescein on slit lamp examination; intraocular pressure is typically within reference range
  • Corneal ulcer
    • Presenting symptoms can include acutely painful, red eye; can have decreased vision
    • Can have history of trauma or contact lens wear; usually no nausea or vomiting
    • Clinical examination reveals localized corneal opacity with surrounding corneal edema; intraocular pressure is typically within reference range
  • Cluster headache
    • Primary headache characterized by clustered attacks of brief, unilateral, severe pain typically orbital or supraorbital in location
    • Similarly, associated with unilateral pain and conjunctival injection; other symptoms of cluster headache include cranial nerve parasympathetic symptoms of unilateral eyelid swelling, lacrimation, rhinorrhea, miosis, and ptosis
    • Differentiate based on history and ocular examination; intraocular pressure is typically within reference range
  • Secondary causes of anterior angle closure
    • Require differentiation by ophthalmologist
      • Pulling mechanism caused by iris membrane contracture (eg, neovascularization, contracture of inflammatory precipitates, synechiae after anterior segment surgery, congenital abnormalities) 
      • Pushing mechanisms that push the iris or ciliary body forward, caused by: 
        • Secondary pupil block (eg, uveitis with secondary posterior synechiae, malpositioned intraocular lens)
        • Retinal conditions (eg, intraocular tumors, choroidal hemorrhage)
        • Aqueous misdirection (malignant glaucoma); typically occurs after intraocular surgery in patients with a history of glaucoma

Treatment Goals

  • Reverse or prevent angle closure process
  • Control intraocular pressure
  • Prevent damage to optic nerve and preserve vision in presenting eye and fellow eye

Admission criteria

  • May be indicated for patients requiring intensive treatment of acute angle-closure crisis 
    • Allows close monitoring after surgical procedures in patients at high risk for postoperative complications or for patients with special medical or social needs

Recommendations for specialist referral

  • Emergent referral to an ophthalmologist is required for acute angle-closure crisis
  • Refer any patient with elevated intraocular pressures (20 mm Hg or higher) to ophthalmologist for further evaluation and treatment 

Treatment Options

Treatment of angle closure depends on disease process and underlying mechanism

  • Acute angle-closure crisis is an ophthalmologic emergency
    • Emergency department treatment of acute angle closure
      • Consult ophthalmologist immediately for evaluation and recommendation of appropriate initial treatment
      • If intraocular pressure exceeds 30 mm Hg, administer medications to reduce intraocular pressure and relieve acute symptoms 
        • Decrease production of aqueous humor
          • The following medications are typically used in combination and given concurrently, but each may be used alone:
            • β-blocker (eg, timolol)
            • α-agonist (eg, apraclonidine)
            • Carbonic anhydrase inhibitor (eg, dorzolamide)
              • In sickle cell disease, use single oral dose of methazolamide 50 mg 
        • Decrease inflammation with prednisolone 
        • Constrict pupil with cholinergic agent (eg, pilocarpine) 
        • Consider establishing osmotic gradient with hyperosmotic agent (eg, mannitol) 
        • Treat symptoms of nausea (eg, ondansetron) and pain (eg, morphine or hydromorphone) as indicated
  • Ophthalmology specialist management
    • Acute angle-closure crisis
      • Use medical therapy first to reduce pain, lower intraocular pressure, and clear corneal edema; includes some or all of the following (based on patient’s physical and medical status), if not already provided by emergency clinician: 
        • Topical β₂-adrenergic antagonists
        • Topical α₂-adrenergic agonists
        • Carbonic anhydrase inhibitors (topical [preferred], oral, or IV)
        • Topical miotics
        • Oral or IV hyperosmotic agents
      • Consider corneal indentation to help break pupillary block; may use cotton-tipped applicator and 4-mirror gonioscope 
        • May be attempted at 30-second intervals to open appositionally closed trabecular meshwork and allow some outflow of aqueous humor 
          • Can cause increased pain and momentarily increased pressures
      • Perform iridotomy as soon as possible 
        • Laser iridotomy is the preferred surgical treatment of acute angle-closure crisis, after initial medical therapy
          • Rarely, surgical iridectomy may be necessary if laser iridotomy is unsuccessful
        • Perform prophylactic iridotomy in fellow eye if chamber angle is anatomically narrow
          • Nearly 50% of fellow eyes develop acute angle-closure crisis within 5 years
    • Primary angle-closure suspect 
      • Follow for development of elevated intraocular pressure, progressive narrowing, or synechial angle closure
      • Consider iridotomy to reduce risk of developing angle closure
      • Educate patient on risk for acute angle-closure crisis
        • Avoid medications that could cause pupil dilation and precipitate crisis (eg, decongestants, motion sickness medication, anticholinergics)
        • Provide symptom education and instructions on when to seek immediate care
    • Primary angle closure and primary angle-closure glaucoma
      • Perform iridotomy 
      • Additional treatment after iridotomy is aimed at lowering intraocular pressure to prevent or limit damage to an already compromised optic nerve; this can include medications and/or surgery 

Drug therapy

  • Acute angle-closure crisis
    • Initiate drug therapy immediately to decrease intraocular pressure; immediately refer patient to specialist
    • Usually used together as part of multidrug regimen at presentation
    • Instill drops at least 1 minute apart to allow for proper absorption of each medication 
  • β₂-adrenergic antagonists
    • Suppress aqueous humor production
    • Caution in patients with asthma or cardiac conditions
      • Timolol
        • Timolol Maleate Ophthalmic drops, solution; Adults: Instill 1 drop of a 0.5% solution in affected eye(s). 
  • α₂-adrenergic agonists
    • Decrease aqueous humor production
      • Apraclonidine
        • Apraclonidine Hydrochloride Ophthalmic drops, solution; Adults: 1 drop into the affected eye(s) every 8 hours. 
  • Miotics
    • Increase aqueous outflow by constricting pupil
    • Give after intraocular pressure has been reduced to less than 50 mm Hg
      • Pilocarpine
        • Pilocarpine Hydrochloride Ophthalmic drops, solution; Adults: 1 drop of a 1% or 2% solution into affected eye(s); may be repeated every 15 minutes. 
  • Carbonic anhydrase inhibitors
    • Decrease aqueous fluid production
      • Dorzolamide
        • Dorzolamide Hydrochloride Ophthalmic drops, solution; Adults: Instill 1 drop of a 2% solution into the affected eye(s) every 8 hours. 
      • Acetazolamide
        • Oral
          • Acetazolamide Oral tablet; Adults: 250 mg PO every 4 hours.
            • Alternately, treatment of some acute types of glaucoma has been initiated with a dose of 500 mg, followed by 125 to 250 mg PO every 4 hours 
        • IV
          • Acetazolamide Sodium Solution for injection; Adults: 500 mg IV. If needed, may repeat the dose in 2 to 4 hours.
  • Corticosteroids
    • Reduce ocular congestion and inflammation
    • Prednisolone
      • Prednisolone Acetate Ophthalmic drops, suspension; Adults: 1 drop in the affected eye(s) every 15 minutes for 4 doses. 
  • Hyperosmotic agents
    • Decrease vitreous humor volume
    • Consider when intraocular pressure is exceedingly high or initial treatment is unsuccessful
      • Mannitol
        • Mannitol Solution for injection; Adults: 1.5 to 2 g/kg IV as 15% to 20% mannitol over at least 30 minutes. 

Nondrug and supportive care

Laser peripheral iridotomy 

General explanation

  • A small, full-thickness hole is created in peripheral iris with laser allowing aqueous humor to bypass pupillary block 
    • Eliminates pressure gradient between posterior and anterior chambers
    • Widens anterior chamber angle


  • Angle closure 
  • Angle-closure glaucoma 
  • Angle closure suspect, especially if there is:
    • Angle closure present in fellow eye
    • Family history of angle-closure glaucoma
    • Need for repeated dilated eye examinations
    • Limited access to ophthalmic care, especially in high-risk patient


  • Increased intraocular pressure 
  • Laser burns to cornea, lens, or retina 
  • Late-onset corneal edema 
  • Posterior synechiae development 
  • Hemorrhage or hyphemia 
  • Iritis 
  • Development of glare or halos 


  • Monitor intraocular pressure closely for the first year after acute angle-closure crisis (eg, every 3-6 months) 
  • Postiridotomy, follow patients with residual narrow angles or those with open angle and some peripheral anterior synechiae at appropriate intervals 
    • Repeat gonioscopy to determine any interval changes
  • Patients treated with topical medications are monitored for local and systemic adverse effects and toxicity


  • Attack in fellow eye
    • Fellow eye at high risk for developing acute angle closure owing to underlying anatomic similarities
  • Loss of vision
  • Permanent visual acuity decrease
  • Recurrent episode of acute angle closure (if cause of angle closure is not treated)


  • Prompt and effective treatment of angle-closure crisis can often prevent glaucomatous optic neuropathy or significant visual deficits from occurring 
    • With elevated intraocular pressure, optic neuropathy can occur rapidly
      • Left untreated, may result in progressive permanent vision loss; fellow eye also at risk (in one small study, approximately 50% of fellow eyes developed acute angle-closure crisis within 5 years) 
    • Acute angle-closure crisis can also be self-limited and resolve spontaneously; may recur 
  • Chronic angle closure is usually asymptomatic and progressive with loss of visual field
  • Patients with untreated primary angle-closure glaucoma typically develop progressive vision loss; can result in bilateral blindness 
    • Visual field loss is most often undetected until almost 20% to 40% of retinal ganglion cells have irreversible damage

Screening and Prevention

At-risk populations

  • World Glaucoma Association states angle closure case detection or opportunistic screening should be performed in all persons aged 40 years or older who are undergoing an eye examination 
    • While a shallow anterior chamber is strongly associated with angle closure, use of anterior chamber depth for population-based screening remains unproven 
  • American Academy of Ophthalmology recommends eye examination, which includes glaucoma screening, by an eye professional for general eye health, for patients with no signs, symptoms, or risk factors for ocular disease: 
    • General population
      • Aged 40 years: 1 examination
      • Aged 41 to 54 years: every 2 to 4 years
      • Aged 55 to 64 years: every 1 to 3 years
      • Aged 65 years or older: every 1 to 2 years


Babineau MR et al: Ophthalmologic procedures in the emergency department. Emerg Med Clin North Am. 26(1):17-34, v-vi, 2008


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