https://www.aao.

org/munnerlyn-laser-surgery-center/angleclosure-glaucoma-19

Angle-Closure Glaucoma
DEC 18, 2013
Authors: Ani Khondkaryan, MD, and Brian A. Francis, MD, MS

Introduction
Acute angle closure is an urgent but uncommon dramatic symptomatic event with blurring of
vision, painful red eye, headache, nausea, and vomiting. Diagnosis is made by noting high
intraocular pressure (IOP), corneal edema, shallow anterior chamber, and a closed angle on
gonioscopy. Medical or surgical therapy is directed at widening the angle and preventing
further angle closure. If glaucoma has developed, it is treated with therapies to lower IOP.
Chronic angle-closure glaucoma is diagnosed by noting peripheral anterior synechiae on
gonioscopy, as well as progressive damage to the optic nerve and characteristic visual field
loss. Chronic angle-closure glaucoma is treated with therapies to lower intraocular pressure.
Definition
Angle-closure glaucoma (ACG) is a group of diseases in which there is reversible
(appositional) or adhesional (synechial) closure of the anterior-chamber angle. The angle
closure may occur in an acute or chronic form. In the acute form, the IOP rises rapidly as a
result of relatively sudden blockage of the trabecular meshwork by the iris via papillary
block mechanism. The chronic form may develop after acute angle closure where synechial
closure of the angle persists, or it may develop over time as the angle closes from prolonged
or repeated contact between the peripheral iris and the TM, which often leads to peripheral
anterior synechiae (PAS) and functional damage to the angle.

Classification
Clinical Classification
Classification of angle closure based on presence or absence of symptoms
Acute: abrupt onset of symptomatic elevation of IOP (> 21 mm Hg), resulting from
total closure of the angle, which is not self-limiting.
Subacute (or intermittent): abrupt onset of symptomatic elevation of IOP resulting
from total closure of the angle, which is self-limiting and recurrent.
Chronic: elevated IOP resulting from angle closure that is asymptomatic.
Common Vignette 1
A 50-year-old woman who has no eye symptoms is found during routine ophthalmic
examination to have elevated IOP of 42 mm Hg in both eyes. Funduscopy shows that the
optic nerve head appears normal with no evidence of glaucomatous neuropathy. Gonioscopy
shows that the anterior chamber angles are closed for almost the full circumference.
Common Vignette 2
A 64-year-old woman presents to the emergency room with severe pain around her right eye
of 4-hour duration, accompanied by blurred vision in the same eye. She is also nauseated.
Examination shows a red right eye with edematous cornea and a wide pupil that is
unresponsive to light. IOP is extremely elevated (60 mm Hg) only in the right eye. The
anterior chamber angle is closed in both eyes.
Other Presentations
Patients may present with spontaneously resolving symptoms of intermittent ache and/or
blurred vision with haloes around lights seen from one eye. Patients may also notice a change
in vision, which may represent longstanding chronic progressive visual field loss.
Epidemiology
The number of people in the world affected by glaucoma is approximately 45 million. One
third are from primary angle-closure glaucoma (PACG).
Half of cases leading to blindness are estimated to result from PACG.
The prevalence of PACG varies among different racial and ethnic groups. The highest
rates are reported in Inuit and Asian populations, and lowest rates are reported in
African and European populations. It is estimated that all forms of PACG account for
about 10% of glaucoma cases in the U.S., but up to 50% of glaucoma cases in Asian
populations. Among the white population in the U.S. and Europe the estimated
prevalence of PACG is 0.04% to 0.4%. The prevalence of PACG in the Inuit
population is estimated at 2.65% to 4.8%.
Women are 2 to 4 times more likely to have ACG than men.
Acute ACG is most common between the ages of 55 and 65 years.

Etiology
Angle closure can be primary, secondary to another eye disease, or drug induced. Eye
diseases that can cause ACG, include a thick cataractous lens (phacomorphic glaucoma);
ectopic lens (eg, in settings of trauma, as well as Marfans or Weill-Marchesani syndrome);
neovascularization of the angle secondary to diabetic retinopathy or ocular ischemia; and
tumors.
Sulfa-containing drugs can cause ACG by causing supraciliary body effusions. This form of
ACG has a distinctly different etiology and is not treated in the same fashion as PACG. It is
unresponsive to laser peripheral iridotomy and is treated with topical steroids and
discontinuation of the causative drug, as well as topical and systemic IOP lowering drugs.

Pathophysiology
Angle closure occurs when the peripheral iris is in contact with the trabecular meshwork
(TM), either intermittently (appositional closure) or permanently (synechial closure).
Specific mechanisms leading to angle closure can be divided into 2 categories:
Mechanisms that push the iris from behind. The most common reason is relative
pupillary block, but other reasons include plateau iris syndrome, enlarged or
anteriorly displaced lens, and malignant glaucoma.
Mechanisms that pull the iris into contact with the TM. Examples include contraction
of inflammatory membrane as in uveitis, fibrovascular tissue as in iris
neovascularization, or corneal endothelium as in iridocorneal endothelial syndrome.
Chronic intermittent friction between the iris and the TM can lead to progressive dysfunction
of the TM. With time, adhesions (synechiae) form between the iris and parts of the TM.
Eventually the TM is so dysfunctional or obstructed that aqueous outflow from the
eye is impaired and IOP rises.
Prolonged elevation of IOP leads anatomically to glaucomatous changes in the optic
nerve head and loss of optic nerve axons and functionally to progressive loss of the
visual field.
If untreated this process may progress to complete blindness.
Angle closure is usually chronic and progressive, but uncommonly it manifests as an acute
attack of complete closure with severe symptoms.

Diagnostic Approach
Acute ACG presents with a change in vision or with severe acute symptoms. Chronic ACG is
often discovered incidentally during routine examination or during examination for another
reason. ACG can also present with intermittent symptoms, change in vision, or severe acute
symptoms such as pain in the affected eye, headache, and associated nausea or vomiting.
Patients who are suspected of having ACG should be referred to ophthalmology care
immediately.
History
Acute ACG is suggested by pain in the affected eye, blurred vision, halos around
lights seen from one eye, headache, and associated nausea or vomiting.
Many patients with chronic ACG are asymptomatic.
A history of ACG increases the risk of angle closure in the unaffected eye.
There may be intermittent ache and/or blurred vision with haloes around lights seen
from one eye, which resolve spontaneously.
The patient may report a change in vision.
Some medications increase the risk of ACG, such as anticholinergic topical ocular
medication (eg, pupil dilators) or systemic medication (eg, sulfonamides, topiramate,
phenothiazines) because they induce angle narrowing.
Examination
 Visual acuity should be tested because it may be decreased.
Examination of the eye may show it to be red with vascular congestion, corneal
edema, and a dilated unresponsive pupil.
The IOP may be raised above 21 mm Hg.
Investigations
The optic nerve head should be investigated by slit-lamp examination or funduscopy,
and may show typical changes of glaucoma such as a large optic cup and nerve fiber
loss.
Gonioscopy of both eyes should be performed when angle closure is suspected.
Gonioscopy refers to the technique used for viewing the anterior chamber angle of the
eye for evaluation of angle structures. Special contact lenses (gonioscopy lenses)
overcome the problem of total internal reflection of light rays from the chamber angle,
and allow visualization of the angle using obliquely inclined mirrors. The angle can
be closed even in the absence of any other symptoms or signs. If the clinician is
uncertain about the gonioscopic findings, he/she can refer the patient for objective
imaging of the angle either via ultrasound biomicroscopy or OCT.
Automatic testing of the visual field should be routinely done to assess the presence
and extent of glaucomatous visual field loss.
Objective quantitative assessment of optic nerve damage can be obtained by imaging
machines, such as Heidelberg retinal tomography, OCT, and GDx nerve fiber analysis.
Risk Factors
Strong:
Female gender: Women are 2 to 4 times more likely to have ACG than men.
Hyperopia: The anterior chamber depth and volume are smaller in hyperopic eyes.
Shallow peripheral anterior chamber: Having smaller anterior segment dimensions is
the main ocular risk factor for closure of the angle, with anterior chamber depth
having the strongest correlation with angle closure and ACG.
Second eye having angle closure: Anatomic factors of both eyes are virtually always
similar. An untreated fellow eye has a 40% to 80% chance of developing an acute
episode of angle closure over the next 5 to 10 years.
Inuit and Asian ethnicity: Highest rates of ACG are reported in Inuit and Asian
populations.
Weak:
Advanced age: Acute ACG is most common between the ages of 55 and 65 years. The
size of the lens increases progressively with age, thus crowding the region of the
anterior chamber angle, making it shallower.
Family history: Family history has been suggested as a risk factor, but is not
universally recognized.
Use of medications that induce angle narrowing: Anticholinergic topical pupil dilators
(eg, cyclopentolate or atropine) or systemic medication (eg, sulfonamides, topiramate,
phenothiazines)
History and Exam
Key diagnostic factors with common frequency:
Presence of risk factors: Key risk factors include female gender, Inuit or Asian
ethnicity, hyperopia, use of medication that can induce angle narrowing, and shallow
anterior chamber.
Elevated IOP: In healthy eyes, IOP is generally 10 to 21 mm Hg. In acute attacks, IOP
rises rapidly to relatively high levels, typically above 40 mm Hg.
Present in the acute and subacute forms but not with the chronic form of angle
closure:
 o Halos around lights
o Aching eye or brow pain
o Deep,dull,periocular headache
o Nausea, vomiting
o Reduced acuity
o Eye redness
o Corneal edema
o Fixed dilated pupil. Iris ischemia may cause the pupil to remain permanently
fixed and dilated.
Other diagnostic factors:
Common:

Incidental eye findings: In chronic disease, most patients are asymptomatic and ACG
is incidentally detected as part of an ophthalmic examination.
Blurred vision: In chronic disease, most patients are asymptomatic and ACG is
incidentally detected as part of an ophthalmic examination.
Uncommon: Change in vision; in effect this is new recognition of longstanding
chronic progressive visual field loss
Diagnostic Tests
First tests to order:
Gonioscopy:
Definitive test for diagnosing angle closure; gonioscopy of both eyes should be
performed on all patients in whom angle closure is suspected. It should also be
performed prior to instilling dilating medications to rule out eyes susceptible to angle
closure.
If angle closure is present, compression (indentation) gonioscopy with a four-mirror
or similar lens is particularly helpful to differentiate between appositional (reversible)
closure versus synechial (irreversible) angle closure, as well as allow for assessing the
extent of peripheral anterior synechiae.
Gonioscopy is also important for the detection of plateau iris and other specific
anatomic configurations.
Gonioscopy may be therapeutic in breaking the attack of acute angle closure.
Result: TM is not visible in angle closure because the peripheral iris is in contact with
it.
Slit lamp examination:
The best method of examining the optic disc is with the slit lamp combined with a
high magnification posterior pole lens. The anterior chamber depth should be noted
and the size of the phakic lens.
Result: shallow anterior chamber; and signs of glaucoma: large optic cup, narrowing
of the neuroretinal rim, splinter hemorrhage, nerve fiber loss
Automatic static perimetry:
Identifies the presence, and quantifies the amount, of glaucomatous visual field loss
during initial diagnosis and subsequently during follow-up care.
Result: visual field defects
Other tests to consider:
Ultrasound biomicroscopy
Can be ordered for objective documentation of angle closure when findings during
physical examination (gonioscopy) are not clear
 Useful for demonstrating specific etiologies for angle closure such as plateau iris or
supraciliary body fluid and for demonstrating dynamic changes in the angle during
light and dark, and after other provocative tests and after treatment
Result: closed angle; occludability of the angle in the dark vs. light; plateau iris or
supraciliary body fluid
Anterior segment optical coherence tomography:
Can be ordered for objective documentation of angle closure when findings during
physical examination (gonioscopy) are not clear
Useful for demonstrating dynamic changes in the angle during light and dark
Less capable of defining specific etiologies for angle closure due to inability to image
behind the iris
Result: closed angle, occludability of the angle in the dark versus light
Retinal OCT:
Can be used to assess loss of nerve tissue in and around the optic nerve objectively
and quantitatively
Result: quantifies neural tissue in and around the optic nerve
Heidelberg retinal tomography:
Can be used to assess loss of nerve tissue in and around the optic nerve objectively
and quantitatively
Presents this in relation to a nomogram derived from healthy eyes
Result: quantifies neural tissue in and around the optic nerve
GDx nerve fiber analyzer:
Can be used to assess loss of nerve tissue in and around the optic nerve objectively
and quantitatively
Result: quantifies neural tissue in and around the optic nerve

Differential Diagnosis
Disease/Condition Differentiating Differentiating Tests
Signs/Symptoms

Open-angle glaucoma Clinically Gonioscopy shows an open angle.

(primary and indistinguishable from
secondary) chronic ACG.

Other optic Visual field defects are IOP is normal. Gonioscopy shows an
neuropathies (eg, different from those of open angle. Optic nerve atrophy
compressive) glaucoma. (whitening of tissue) in contrast to loss
of tissue and cupping.

Eye trauma Acute red eye. Usually IOP usually normal. Gonioscopy
no nausea or vomiting. shows an open angle. The anterior
Hx of recent trauma. chamber depth is usually normal.
There may be signs of trauma on eye
exam and ocular adnexa (eyelid
ecchymosis, hyphema, inflammation).

Keratitis Acute red eye. Usually IOP usually normal. Gonioscopy

no nausea or vomiting. shows an open angle. The anterior
Conjunctival discharge. chamber depth is usually normal.
 Signs of infectious
infiltrate in the cornea.

Conjunctivitis, Acute Acute red eye. Usually
no nausea or vomiting.
Conjunctival discharge.
Signs of infectious
infiltrate in the cornea.
IOP usually normal. Gonioscopy
shows an open angle. The anterior
chamber depth is usually normal.

Corneal ulcer Acute red eye. Usually IOP usually normal. Gonioscopy
no nausea or vomiting. shows an open angle. The anterior
Recent foreign body, chamber depth is usually normal.
contact lens use, or
known poor eye closure
(eg, facial palsy).

Episcleritis or scleritis Acute red eye. Usually
no nausea or vomiting.
Known systemic disease,
such as rheumatoid
arthritis.
IOP usually normal. Gonioscopy
shows an open angle. The anterior
chamber depth is usually normal.

Chemical injury Acute red eye. IOP may be elevated, but gonioscopy
History of exposure to shows an open angle.
chemicals.

Diagnostic Criteria
Acute Angle-Closure Attacks
Presence of at least 2 of the following symptoms:
Ocular or periocular pain
Nausea or vomiting
Antecedent history of intermittent blurring of vision with haloes
Presenting IOP > 21 mm Hg
Presence of at least 3 of the following signs:
Conjunctival injection
Corneal epithelial edema
Mid-dilated unreactive pupil
Shallow anterior chamber
Chronic Angle-Closure Attacks
Developed for the use in prevalence surveys, it identifies 3 stages in the natural history of
angle closure:
Primary angle-closure suspect: an "occludable angle" with normal IOP, optic disc,
and visual field, without evidence of peripheral anterior synechiae (PAS)
Primary angle closure: an "occludable angle" with either raised IOP and/or primary
PAS; optic disc and field normal
Primary angle-closure glaucoma: primary angle closure with evidence of
glaucomatous damage to optic disc and visual field
Diagnostic Guidelines
Europe
The effectiveness of the Heidelberg Retina Tomograph and laser diagnostic glaucoma
scanning system (GDx) in detecting and monitoring glaucoma, Health Technology
Assessment NHS R&D HTA Programme, 2011.
North America
Comprehensive adult medical eye evaluation, American Academy of Ophthalmology,
2009.
Comprehensive adult eye and vision examination, American Optometric Association,
2005.
Primary angle closure, American Academy of Ophthalmology, 2009.
Screening
Which Population to Screen
Glaucoma is the second leading cause of blindness around the world. Half of these cases are
due to angle closure. Because angle closure is potentially preventable, screening is
immensely important.
Everyone aged 40 years or older undergoing an eye examination, either routinely or for a
specific reason, should be screened for angle closure.
Which Test to Use
The definitive test for the identification of angle closure and eyes at risk is gonioscopy.
Other methods to identify eyes at risk include ultrasound measurement of anterior chamber
depth (ACD) and determining the ACD to axial length ratio. High frequency ultrasound
(UBM) or anterior segment OCT may also be used to image the angle.
Treatment Approach
Initial Medical Management of Acute Episode
The immediate goal of treatment is to relieve the acute symptoms and decrease IOP, which is
usually achieved with medical therapy.
Oral or topical carbonic anhydrase inhibitors, topical beta-blockers, and topical alpha-
2 adrenergic agonists lower IOP through suppression of aqueous humor production.
Beta-blockers reduce IOP by around 20% to 30% within 1 hour of instillation.
Alpha-agonists reduce IOP by around 26% within 2 hours post-dose.
Carbonic anhydrase inhibitors, topical beta-blockers, or alpha-2 adrenergic agents
may be used as first-line therapies either alone or more typically in combination.
In patients where angle closure is thought to be secondary to pupillary block or plateau iris
syndrome, cholinergic agents (such as pilocarpine). 1[C] Evidence should be started after IOP
decreases to < 40 mm Hg.
Cholinergic agents can paradoxically result in shallowing of the anterior chamber and
narrowing of the angle in eyes with angle closure secondary to lens-induced mechanism or
aqueous misdirection (malignant glaucoma). They are therefore contraindicated in these
cases.
If these medical treatments are unsuccessful, hyperosmotic agents should be used.
Hyperosmotic agents are also used initially when pressures are exceedingly high.
Following resolution of the acute attack, definitive surgical treatment should be performed
within 24 to 48 hours with the aim of achieving a persistently open angle.
Definitive Surgical Management for Chronic ACG after Resolution of Acute Attack
Definitive treatment is aimed at achieving a persistently open angle:
Laser peripheral iridotomy (LPI), where a laser is used to make an opening in the iris,
is usually successful for acute angle-closure glaucoma (2[B] Evidence). LPI alleviates
pupillary block by allowing aqueous to bypass the pupil. The pressure differential
between anterior and posterior chambers is eliminated, and the iris loses its convex
configuration and falls away from the TM, resulting in opening or widening of the
angle. LPI is indicated in all eyes with primary angle closure and usually in fellow
 eyes as well, since the majority of fellow eyes will also develop glaucomatous
changes (Bain 1957, Lowe 1962, Hyams 1975).
Laser iridoplasty or gonioplasty can be considered in the presence of a patent LPI
with a residual appositional angle. An argon laser is used to place contraction burns in
the peripheral iris over its entire circumference in order to pull the peripheral iris
away from the TM.
If residual angle closure is attributable to the lens then lens then extraction surgery,
with or without goniosynechialys, is considered (2[B] Evidence)
Cholinergic agents may be used if there is residual angle closure after laser treatment.
These agents cause pupil constriction with thinning of the iris and its pulling away
from the inner eye wall and TM, thus opening the angle.
Persistently Elevated IOP in Patients with ACG Despite Surgery
If IOP remains elevated following these measures in acute angle-closure glaucoma, as well as
in cases of chronic angle-closure glaucoma, it is lowered in a fashion similar to open-angle
glaucoma with IOP-lowering medications, and if these are ineffective, then IOP-lowering
surgery.
Topical ophthalmic prostaglandin analogs work by increasing aqueous outflow.
They reach peak effectiveness 10 to 14 hours after administration, so they are not
used during acute attacks.
As chronic therapy, however, they are the most potent IOP-lowering agents available
and should be used first line.
Topical beta-blockers and alpha-2 adrenergic agonists may also be used. They are
typically used alone or in combination at the discretion of the physician.
Systemic carbonic anhydrase inhibitor chronic therapy is uncommonly used because of the
many adverse effects of chronic systemic use, and should be reserved for patients with
glaucoma refractory to other medical treatment.
Uncommonly IOP remains elevated despite all these measures, and in this case IOP-lowering
surgery, such as trabeculectomy or aqueous tube shunt implantation, is indicated.
Treatment Options
Acute

Patient Group Tx Line Treatment

Initial First Dynamic gonioscopy to attempt to break angle closure

presentation
First Carbonic anhydrase inhibitors and/or topical beta-blocker
and/or topical alpha-2 agonist:
Carbonic anhydrase inhibitors decrease aqueous humor
formation and are used commonly as first-line therapy in
combination with beta-blockers and alpha-2 agonists.
Topical dorzolamide and brinzolamide are preferred over
systemic acetazolamide and methazolamide. Topical beta-
blockers lower IOP through suppression of aqueous
humor production. Beta-blockers reduce IOP by around
20% to 30% within 1 hour of instillation. Topical alpha-2
adrenergic agonists lower IOP through suppression of
aqueous humor production. Alpha-agonists reduce IOP by
around 26% within 2 hours postdose.
Primary options:
 Acetazolamide: 125-250 mg orally (immediate-
release) up to four times daily, maximum 1000
mg/day; 250-500 mg intravenously every 2-4
hours, maximum 1000 mg/day
Betaxolol ophthalmic: (0.5%) 1-2 drops into the
affected eye(s) twice daily
Brinzolamide ophthalmic: (1%) 1 drop into the
affected eye(s) 2 or 3 times daily
Dorzolamide ophthalmic: (2%) 1 drop into the
affected eye(s) twice or three times daily
Levobunolol ophthalmic: (0.25%) 1-2 drops into
the affected eye(s) twice daily; (0.5%) 1-2 drops
into the affected eye(s) once daily
Methazolamide: 50-100 mg orally twice or three
times daily
Brimonidine ophthalmic: (0.1 to 0.2%) 1 drop into
the affected eye(s) 3 times daily
Timolol ophthalmic: (0.25% or 0.5%) 1 drop into
the affected eye(s) twice daily; (0.5% gel) 1 drop
into the affected eye(s) once daily

Adjunct Hyperosmotic agents:

If there is failure of initial medical treatment or IOP is
greater than 50 mm Hg, hyperosmotic agents are used to
control acute episodes of elevated IOP. They are rarely
administered for longer than a few hours because their
effects are transient. They are indicated in patients when
medical treatments are unsuccessful or if pressures are
exceedingly high.
Primary option: glycerine, 1-2 g/kg/dose orally,
repeat every 5 hours when required
Secondary option: mannitol, 1.5 to 2 g/kg/dose
intravenously over 30 minutes

Plus Laser peripheral iridotomy after acute attack resolved:

Laser peripheral iridotomy (LPI)is usually successful. LPI
alleviates pupillary block by allowing aqueous to bypass
the pupil. The pressure differential between anterior and
posterior chambers is eliminated, the iris loses its convex
configuration and falls away from the TM, resulting in
opening or widening of the angle. LPI is indicated in all
eyes with angle closure and usually in fellow eyes since
the majority of fellow eyes in patients with acute angle-
closure glaucoma also develop glaucomatous changes.

Ongoing

Patient Group Tx Line Treatment

Residual angle First Topical prostaglandin analog and/or topical beta-blocker
closure after laser and/or topical alpha-2 agonist:
peripheral These agents are typically used individually but may be
iridotomy with used in combination as well. They may be used in
elevated IOP refractory cases. Latanoprost has been associated with
lower incidence of conjuctival hyperemia than other
prostaglandin analogs. Topical ophthalmic prostaglandin
analogs work by increasing aqueous outflow reaching
peak effectiveness 10 to 14 hours after administration.
They are the most potent IOP-lowering agents.
Latanoprost and travoprost are preferred over
bimatoprost. Topical beta-blockers lower IOP through
suppression of aqueous humor production. Topical alpha-
2 adrenergic agonists lower IOP through suppression of
aqueous humor production. Topical cholinergic agonists
may or may not need to be continued.
Primary options:
Apraclonidine ophthalmic: (0.5%) 1-2 drops into
the affected eye(s) three times daily
Betaxolol ophthalmic: (0.5%) 1-2 drops into the
affected eye(s) twice daily
Bimatoprost ophthalmic: (0.03%) 1 drop into the
affected eye(s) once daily at night
Latanoprost ophthalmic: (0.005%) 1 drop into the
affected eye(s) once daily at night
Levobunolol ophthalmic: (0.25%) 1-2 drops into
the affected eye(s) twice daily; (0.5%) 1-2 drops
into the affected eye(s) once daily
Travoprost ophthalmic: (0.004%) 1 drop into the
affected eye(s) once daily at night
Brimonidine ophthalmic: (0.1 to 0.2%) 1 drop into
the affected eye(s) three times daily
Timolol ophthalmic: (0.25% or 0.5%) 1 drop into
the affected eye(s) twice daily; (0.5% gel) 1 drop
into the affected eye(s) once daily

Carbonic anhydrase inhibitors:

Carbonic anhydrase inhibitors decrease aqueous humor
formation. Topical dorzolamide and brinzolamide are
preferred over systemic acetazolamide and
methazolamide. Systemic carbonic anhydrase inhibitor
chronic therapy is uncommonly used because of the many
adverse effects of systemic use, and should be reserved
for patients with glaucoma refractory to other medical
treatment.
Primary options:
Brinzolamide ophthalmic: (1%) 1 drop into the
affected eye(s) twice or three times daily
Dorzolamide ophthalmic: (2%) 1 drop into the
 affected eye(s) twice or three times daily
Secondary options:
Acetazolamide: 125-250 mg orally (immediate-
release) up to four times daily, maximum 1000
mg/day; 250-500 mg intravenously every 2-4
hours, maximum 1000 mg/day
Methazolamide: 50-100 mg orally twice or three
times daily

Adjunct Argon laser peripheral iridoplasty (when there is a

(in cases component of plateau iris):
of plateau ALPI is a procedure during which contraction burns are
iris) placed in the peripheral iris with the aim of thinning it and
pulling it away from the TM.

Adjunct Lens extraction surgery:

If residual angle closure is attributable to the lens pushing
forward the iris, then lens extraction surgery with or
without goniosynechialysis is considered.

Adjunct Topical cholinergic agonists:

Cholinergic agents may be used if there is residual angle
closure after laser treatment. These agents cause pupil
constriction with thinning of the iris and its pulling away
from the inner eye wall and TM, thus opening the angle.
Instillation frequency and concentration of pilocarpine is
determined by response. Patients with heavily pigmented
irides may require higher strengths. In acute attack 1% to
2% is the preferred solution. Stronger miotics may
increase the pupillary block. Patients may be maintained
on pilocarpine as long as IOP is controlled and no
deterioration in visual fields occurs.
Primary option: Pilocarpine ophthalmic (1-2%) 1 drop
into the affected eye(s) up to 4 times daily

Adjunct Trabeculectomy or tube shunt implantation:

Uncommonly IOP remains elevated despite medical and
surgical measures, and in this case IOP-lowering surgery,
such as trabeculectomy or tube shunt implantation, is
indicated.

Emerging Therapies
Emerging Surgical Treatment for Acute Angle Closure Attacks
It has been suggested that an acute attack of angle closure can be terminated by surgical
means such as an anterior chamber paracentesis to acutely lower IOP and break the cycle of
rising IOP. It may also allow clearing of the corneal edema to facilitate LPI. Other reports
recommend laser iridoplasty, corneal indentation, cataract or clear lens extraction.
Emerging Surgical Treatment for Chronic Angle-Closure Glaucoma
The treatment of chronic angle-closure glaucoma is similar to that of open-angle glaucoma.
Recently developed procedures to treat chronic angle-closure glaucoma include the Ex-
PRESS glaucoma implant, canaloplasty, trabectome, and trabecular micro-bypass stent.
[Francis, et al 2011] [1398 Chai CL. 2010]
Treatment Guidelines
Asia
Clinical practice guidelines: glaucoma, Singapore Ministry of Health, 2010. Evidence-based
guidelines on the treatment of glaucoma. The goal of treatment is to maintain useful visual
function and patient's quality of life by lowering IOP. Treatment options for lowering IOP are
discussed.
Europe
The effectiveness of the Heidelberg Retina Tomograph and laser diagnostic glaucoma
scanning system (GDx) in detecting and monitoring glaucoma, Health Technology
Assessment NHS R&D HTA Programme, 2011.
North America
Comprehensive adult medical eye evaluation, American Academy of Ophthalmology,
2009.
Comprehensive adult eye and vision examination, American Optometric Association,
2005.
Primary angle closure, American Academy of Ophthalmology, 2009.
Prognosis
Acute Angle Closure
After the resolution of the acute episode, eyes should be assessed for degree of angle closure,
the presence of PAS, degree of cataract, and optic disc and visual field damage. IOP should
be checked multiple times to detect asymptomatic rise in IOP. The second eye should be
assessed and treated to prevent attack.
The prognosis is favorable if the IOP can be controlled. IOP is reported to be controlled with
laser peripheral iridotomy alone in 42% to 72% in whites, more often than in Asians.
Chronic Angle-Closure Glaucoma
With control of the IOP, progressive visual deterioration can be controlled. The efficacy of
peripheral iridotomy for disease control depends on both the underlying mechanism and the
stage of the disease when diagnosed.
Greater extent of PAS, a higher presenting IOP, and a larger cup-to-disc ratio are all
predictors of poor pressure control following iridotomy.
Once glaucomatous optic neuropathy has developed (defined as structural damage to the disc
and/or visual field loss), virtually all cases (94% to 100%) will require further treatment to
control IOP.
Monitoring
Following iridotomy, patients may have an open anterior-chamber angle or an anterior-
chamber angle with a combination of open sectors and areas occluded by irreversible
iridotrabecular synechiae.
After the acute episode of angle closure has been addressed, patients who are found to have
glaucomatous optic neuropathy should be followed up periodically, probably every 3 to 6
months, similar to patients with primary open-angle glaucoma, to ensure IOP is controlled
and there is no further glaucomatous progression of optic nerve or visual field changes.
Patients who do not have glaucomatous optic neuropathy should be followed up periodically,
approximately every 6 to 12 months, to detect further closure of the angle or elevation of
IOP.
Complications
Complications Likelihood Timeframe

Fellow eye attack: High Variable

The fellow eye, which usually shares the anatomic
predisposition for increased pupillary block, is at high risk for
developing acute angle closure. An untreated fellow eye has a
40% to 80% risk of developing an acute attack. It is
recommended that the contralateral eye be treated
prophylactically with laser peripheral iridotomy if the chamber
angle is found to be anatomically narrow (Bain 1957, Lowe
1962, Hyams 1975).

Retinal vein occlusion: Medium Short-term

This complication may be prevented by prompt reduction of
IOP. Once it occurs there is no specific immediate treatment.

Loss of vision: Medium Short-term

This complication may be prevented by prompt reduction of
IOP.

Permanent decrease in visual acuity: Medium Variable

Patients with primary angle-closure glaucoma (PACG) often
present with higher IOP and more advanced visual field loss
than those with primary open-angle glaucoma (POAG). These
finding suggest that PACG is a more IOP-dependent disease.
Following successful treatment of acute primary angle-closure,
there is some evidence that retinal nerve fiber layer thickness
significantly decreases within 16 weeks after the attack.
Adequate and prompt treatment with lowering of IOP will
reduce the risk for permanent injury to the retinal ganglion cells
and axons.

Repeat episode of acute ACG: Low Variable

If the mechanism of angle closure was not eliminated, an acute
episode can recur. The clinician should look for the specific
mechanism of angle closure, and treat it accordingly. It is also
important to verify that the peripheral iridotomy is patent.

Clinical Evidence References

1[C]
Intraocular pressure: there is poor-quality evidence that in people with angle closure
glaucoma receiving acetazolamide, low dose pilocarpine, an intensive pilocarpine regimen, or
pilocarpine ocular inserts all reduced intraocular pressures after 2 hours with no significant
difference among groups. More info at BMJ Clinical Evidence.
2[B]
Symptom improvement and intraocular pressure: there is medium-quality evidence that for
people with uniocular acute angle closure glaucoma, there is no significant difference
between surgical iridectomy and laser iridotomy in improvements in intraocular pressure
after 3 years. Poor-quality evidence has not shown whether surgical iridectomy is more
effective than laser iridotomy in improving visual acuity at 3 years in people with uniocular
acute angle closure glaucoma. More info at BMJ Clinical Evidence.
Evidence Level A
Systematic reviews (SRs) or randomized controlled trials (RCTs) of > 200 participants
Evidence Level B
Randomized controlled trials (RCTs) of < 200 participants, methodologically flawed RCTs of
> 200 participants, methodologically flawed systematic reviews (SRs) or good quality
observational (cohort) studies
Suggested Reading
1. World Glaucoma Association. Third Consensus Meeting: Angle Closure Glaucoma.
Hollywood, FL. May 3, 2006.
2. Basic and Clinical Science Course (BCSC) Section 10: Glaucoma. San Francisco:
American Academy of Ophthalmology.
3. Preferred Practice Patterns: Primary Angle Closure PPP - 2010. San Francisco:
American Academy of Ophthalmology.
4. Quigley HA, Broman AT. The number of people with glaucoma worldwide in 2010
and 2020. Br J Ophthalmol. 2006;90:262-267.
5. Quigley HA. Number of people with glaucoma worldwide. Br J Ophthalmol.
1996;80:389-393.
6. Bankes JL, Perkins ES, Tsolakis S, et al. Bedford glaucoma survey. Br Med J.
1968;1:791-796.
7. Bengtsson B. The prevalence of glaucoma. Br J Ophthalmol. 1981;65:46-49.
8. Foster PJ, Johnson GJ. Glaucoma in China: how big is the problem? Br J Ophthalmol.
2001;85:1277-1282.
9. He M, Foster PJ, Johnson GJ, et al. Angle-closure glaucoma in East Asian and
European people. Different diseases? Eye. 2006;20:3-12.
10. Drance SM. Angle closer glaucoma among Canadian Eskimos. Can J Ophthalmol.
1973;8:252-254.
11. Johnson GJ and Foster PJ. Can we prevent angle-closure glaucoma? Eye.
2005;19:1119-1124.
12. Klein BE, Klein R, Sponsel WE, et al. The Beaver Dam Eye Study. Prevalence of
glaucoma. Ophthalmology. 1992;99:1499-1504.
13. Ritch R, Lowe RF. ACG: Mechanisms and Epidemiology. In: Ritch R, Shields MB,
Krupin T, eds. The glaucomas. 2nd ed. St. Louis, MO: CV Mosby; 1996:814.
14. Thomas R, George R, Parikh R, et al. Five year risk of progression of primary angle
closure suspects to primary angle closure: a population based study. Br J Ophthalmol.
2003;87:450-454.
15. Van Herick W, Shaffer RN, Schwartz A. Estimation of width of angle of anterior
chamber. Incidence and significance of the narrow angle. Am J Ophthalmol.
1969;68:626-629.
16. Devereux JG, Foster PJ, Baasanhu J, et al. Anterior chamber depth measurement as a
screening tool for primary angle-closure glaucoma in an East Asian population. Arch
Ophthalmol. 2000;118:257-263.
17. Aung T, Friedman DS, Chew PT, et.al. Long-term outcomes in Asians after acute
primary angle closure. Ophthalmology. 2004;111:1464-1469.
18. Chong YF, Irfan S, Menege MS. AACG: an evaluation of a protocol for acute
treatment. Eye. 1999;13:613-616.
19. Foster PJ, Buhrmann R, Quigley HA, et al. The definition and classification of
glaucoma in prevalence surveys. Br J Ophthalmol. 2002;86:238-242.
20. Hung L, Yang CH, Chen MS. Effect of pilocarpine on anterior chamber angles. J
Ocul Pharmacol Ther. 1995;11:221-226.
21. Ritch R. The treatment of chronic angle-closure glaucoma. Ann Ophthalmol.
1981;13:21-23.
22. Quigley HA. Long-term follow-up of laser iridotomy. Ophthalmology. 1981;88:218-
224.
23. American Academy of Ophthalmology. Laser peripheral iridotomy for pupillary-
block glaucoma. Ophthalmology. 1994;101:1749-1758.
24. Ng WS, Ang GS, Azuara-Blanco A. Laser peripheral iridoplasty for angle-closure.
Cochrane Database Syst Rev. 2008;(3):CD006746.
25. Harasymowycz PJ, Papamatheakis DG, Ahmed I, et al. Phacoemulsification and
goniosynechialysis in the management of unresponsive primary angle closure. J
Glaucoma. 2005;14:186-189.
26. Greve EL. Primary ACG: extracapsular cataract extraction or filtrating procedure? Int
Ophthalmol. 1988;12:157-162.
27. Gunning FP, Greve EL. Lens extraction for uncontrolled glaucoma. J Cataract
Refract Surg. 1998;24:1347-1356.
28. Chen MJ, Chen YC, Chou CK, et al. Comparison of the effects of latanoprost and
travoprost on intraocular pressure in chronic angle-closure glaucoma. J Ocul
Pharmacol Ther. 2006;22:449-454.
29. Aung T, Tow SL, Yap EY, et al. Trabeculectomy for acute primary angle closure.
Ophthalmology. 2000;107:1298-1302.
30. Honrubia F, Garca-Snchez J, Polo V, et al. Conjunctival hyperaemia with the use of
latanoprost versus other prostaglandin analogues in patients with ocular hypertension
or glaucoma: a meta-analysis of randomised clinical trials. Br J Ophthalmol.
2009;93:316-321.
31. Masselos K, Bank A, Francis IC, et al. Corneal indentation in the early management
of acute angle closure. Ophthalmology. 2009;116:25-29.