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Angle-Closure Glaucoma

DEC 18, 2013


Glaucoma
Views25

Authors: Ani Khondkaryan, MD, and Brian A. Francis, MD, MS

https://www.aao.org/munnerlyn-laser-surgery-center/angleclosure-glaucoma-19

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.

History and Exam

Key Factors for Acute Angle-Closure Glaucoma

 Presence of risk factors (eg, hyperopia, thick cataractous lens)

 Halos around lights

 Aching eye or brow pain

 Headache

 Nausea, vomiting

 Reduced acuity

 Eye redness

 Closed angle on gonioscopy

 Extremely elevated IOP

 Corneal edema
 Engorged conjunctival vessels

 Fixed dilated pupil

Key Factors for Chronic Angle-Closure Glaucoma

 Presence of risk factors

 Peripheral anterior synechiae on gonioscopy

 Elevated IOP

Diagnostic Tests

First Tests to Order

 Gonioscopy examination of anterior chamber angle

 Slit-lamp examination

 Automatic static perimetry

Other Tests to Consider

 Ultrasound biomicroscopy

 Anterior segment optical coherence tomography (OCT) of angle

 Evaluation of the optic nerve head by fundoscopy

 Retinal OCT

 Heidelberg retinal tomography

 GDx Nerve Fiber Analyzer

Treatment Options

Acute—Initial Presentation

 Dynamic gonioscopy

 Oral carbonic anhydrase inhibitors and/or topical beta-blocker and/or topical alpha-2
agonist
 Topical cholinergic agonists

 Hyperosmotic agents

 Laser peripheral iridotomy after acute attack resolved (once corneal edema resolves);
may consider lens extraction after acute attack resolved

Ongoing or Chronic Angle-Closure Glaucoma

 Topical prostaglandin analog and/or topical beta-blocker and/or topical alpha-2 agonist

 Carbonic anhydrase inhibitors

 Lens extraction surgery

 Trabeculectomy and/or tube shunt

 Consider surgical lysis of goniosynechiae

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 Marfan’s 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:

Halos around lights


Aching eye or brow pain
Deep, dull, periocular headache
Nausea, vomiting
Reduced acuity
Eye redness
Corneal edema
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 no IOP usually normal. Gonioscopy shows
nausea or vomiting. Hx of an open angle. The anterior chamber
recent trauma. 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 no IOP usually normal. Gonioscopy shows
nausea or vomiting. an open angle. The anterior chamber
depth is usually normal.
Conjunctival discharge.
Signs of infectious
infiltrate in the cornea.

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

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

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

Chemical injury Acute red eye. IOP may be elevated, but gonioscopy
shows an open angle.
History of exposure to
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 presentation First Dynamic gonioscopy to attempt to break angle closure

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
iridotomy with These agents are typically used individually but may be used
elevated IOP in combination as well. They may be used in 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
iris) ALPI is a procedure during which contraction burns are
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.

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
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5. Quigley HA. Number of people with glaucoma worldwide. Br J Ophthalmol.


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6. Bankes JL, Perkins ES, Tsolakis S, et al. Bedford glaucoma survey. Br Med J.
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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.
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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.
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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.
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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
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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.
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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-
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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.
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26. Greve EL. Primary ACG: extracapsular cataract extraction or filtrating procedure? Int
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27. Gunning FP, Greve EL. Lens extraction for uncontrolled glaucoma. J Cataract Refract
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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
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29. Aung T, Tow SL, Yap EY, et al. Trabeculectomy for acute primary angle closure.
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30. Honrubia F, García-Sánchez J, Polo V, et al. Conjunctival hyperaemia with the use of
latanoprost versus other prostaglandin analogues in patients with ocular hypertension or
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31. Masselos K, Bank A, Francis IC, et al. Corneal indentation in the early management of
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