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Button END Topics Basic Laser Physics Laser-Tissue Interactions
Retinal Applications Glaucoma Applications
Laser Trabeculoplasty: Questions in Clinical Practice
Perspective: Selective Laser Trabeculoplasty
Laser Trabeculoplasty: Ophthalmic Technology Assessment
Endoscopic Surgery of the Anterior Segment
Perspective: Endoscopic Cyclophotocoagulation
Angle-Closure Glaucoma
ELT: An Effective MIGS Procedure for OAG
Video: Laser Peripheral Iridotomy
Other Anterior Segment Applications Photoablative Refractive
Surgery Phototherapeutic Keratectomy Femtosecond Laser
Keratoplasty Femtosecond Laser Refractive Cataract Surgery
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Back Next Angle-Closure Glaucoma DEC 18, 2013
Glaucoma googleoff: index Add to My To-Do List Recommend Go to
User Comments Views2 googleon: index Authors: Ani Khondkaryan,
MD, and Brian A. Francis, MD, MS IntroductionAcute 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 ExamKey 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 TestsFirst 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 OptionsAcuteInitial 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
DefinitionAngle-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. ClassificationClinical
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.
EtiologyAngle 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. PathophysiologyAngle 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 ApproachAcute 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/Co Differenti Differentiat

ndition ating ing Tests
Signs/Symptoms
Open-angle Clinically Gonioscopy
glaucoma (primary indistinguishable shows an open
and secondary) from chronic angle.
ACG.
Other optic Visual field IOP is
neuropathies (eg, defects are normal.
compressive) different from Gonioscopy shows
those of an open angle.
glaucoma. Optic nerve atrophy
(whitening of
tissue) in contrast
to loss of tissue
and cupping.
Eye trauma Acute red IOP usually
eye. Usually no normal.
nausea or Gonioscopy shows
vomiting. Hx of an open angle. The
recent trauma. anterior chamber
depth is usually
normal. There may
be signs of trauma
on eye exam and
ocular adnexa
(eyelid ecchymosis,
hyphema,
inflammation).
Keratitis Acute red IOP usually
eye. Usually no normal.
nausea or Gonioscopy shows
vomiting. Conjun an open angle. The
ctival discharge. anterior chamber
Signs of infectious depth is usually
infiltrate in the normal.
cornea.
Acute red IOP usually
Conjunctiviti eye. Usually no normal.
s, Acute nausea or Gonioscopy shows
vomiting. Conjun an open angle. The
ctival discharge. anterior chamber
Signs of infectious depth is usually
 infiltrate in the normal.
cornea.
Corneal Acute red IOP usually
ulcer eye. Usually no normal.
nausea or Gonioscopy shows
vomiting. Recent an open angle. The
foreign body, anterior chamber
contact lens use, depth is usually
or known poor normal.
eye closure (eg,
facial palsy).
Episcleritis Acute red IOP usually
or scleritis eye. Usually no normal.
nausea or Gonioscopy shows
vomiting. Known an open angle. The
systemic disease, anterior chamber
such as depth is usually
rheumatoid normal.
arthritis.
Chemical Acute red IOP may be
injury eye. History of elevated, but
exposure to gonioscopy shows
chemicals. an open angle.
Diagnostic CriteriaAcute 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 GuidelinesEurope 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.
ScreeningWhich 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 ApproachInitial 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
Treatment
Patie T
nt Group x Line
Initial Dynamic gonioscopy to
presentation Fi attempt to break angle closure
rst
Carbonic anhydrase
Fi inhibitors and/or topical beta-blocker
rst 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
Hyperosmotic agents: If
A there is failure of initial medical
djunct 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
Laser peripheral iridotomy
P after acute attack resolved: Laser
lus 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
Treatment
Patie T
nt Group x Line
Topical prostaglandin analog
Resi Fi and/or topical beta-blocker and/or
dual angle rst topical alpha-2 agonist: These
closure after agents are typically used individually
laser but may be used in combination as
peripheral well. They may be used in refractory
iridotomy cases. Latanoprost has been
with associated with lower incidence of
elevated conjuctival hyperemia than other
IOP 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
Argon laser peripheral
A iridoplasty (when there is a
djunct (in component of plateau iris): ALPI is
cases of a procedure during which
plateau contraction burns are placed in the
iris) peripheral iris with the aim of
thinning it and pulling it away from
the TM.
Lens extraction surgery: If
 A residual angle closure is attributable
djunct to the lens pushing forward the iris,
then lens extraction surgery with or
without goniosynechialysis is
considered.
Topical cholinergic
A agonists: Cholinergic agents may
djunct 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
Trabeculectomy or tube
A shunt implantation: Uncommonly
djunct 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 TherapiesEmerging 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 GuidelinesAsiaClinical 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.
PrognosisAcute 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. MonitoringFollowing 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
Lik Tim
elihood eframe
Fellow eye attack: The
fellow eye, which usually shares Hig Vari
the anatomic predisposition for h able
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: This complication may Me Sho
be prevented by prompt reduction dium rt-term
of IOP. Once it occurs there is no
specific immediate treatment.
Loss of vision: This
complication may be prevented by Me Sho
 prompt reduction of IOP. dium rt-term
Permanent decrease in
visual acuity: Patients with Me Vari
primary angle-closure glaucoma dium able
(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 Low
ACG: If the mechanism of angle Vari
closure was not eliminated, an able
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 References1[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
World Glaucoma Association. Third Consensus Meeting: Angle Closure
Glaucoma. Hollywood, FL. May 3, 2006.
Basic and Clinical Science Course (BCSC) Section 10: Glaucoma. San
Francisco: American Academy of Ophthalmology.
Preferred Practice Patterns: Primary Angle Closure PPP - 2010. San
Francisco: American Academy of Ophthalmology.
Quigley HA, Broman AT. The number of people with glaucoma worldwide
 in 2010 and 2020. Br J Ophthalmol. 2006;90:262-267.
Quigley HA. Number of people with glaucoma worldwide. Br J Ophthalmol.
1996;80:389-393.
Bankes JL, Perkins ES, Tsolakis S, et al. Bedford glaucoma survey. Br
Med J. 1968;1:791-796.
Bengtsson B. The prevalence of glaucoma. Br J Ophthalmol. 1981;65:46-
49.
Foster PJ, Johnson GJ. Glaucoma in China: how big is the problem? Br J
Ophthalmol. 2001;85:1277-1282.
He M, Foster PJ, Johnson GJ, et al. Angle-closure glaucoma in East Asian
and European people. Different diseases? Eye. 2006;20:3-12.
Drance SM. Angle closer glaucoma among Canadian Eskimos. Can J
Ophthalmol. 1973;8:252-254.
Johnson GJ and Foster PJ. Can we prevent angle-closure glaucoma? Eye.
2005;19:1119-1124.
Klein BE, Klein R, Sponsel WE, et al. The Beaver Dam Eye
Study. Prevalence of glaucoma. Ophthalmology. 1992;99:1499-1504.
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.
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.
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.
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.
Aung T, Friedman DS, Chew PT, et.al. Long-term outcomes in Asians after
acute primary angle closure. Ophthalmology. 2004;111:1464-1469.
Chong YF, Irfan S, Menege MS. AACG: an evaluation of a protocol for
acute treatment. Eye. 1999;13:613-616.
Foster PJ, Buhrmann R, Quigley HA, et al. The definition and classification
of glaucoma in prevalence surveys. Br J Ophthalmol. 2002;86:238-
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Hung L, Yang CH, Chen MS. Effect of pilocarpine on anterior chamber
angles. J Ocul Pharmacol Ther. 1995;11:221-226.
Ritch R. The treatment of chronic angle-closure glaucoma. Ann
Ophthalmol. 1981;13:21-23.
Quigley HA. Long-term follow-up of laser iridotomy. Ophthalmology.
1981;88:218-224.
American Academy of Ophthalmology. Laser peripheral iridotomy for
pupillary-block glaucoma. Ophthalmology. 1994;101:1749-1758.
Ng WS, Ang GS, Azuara-Blanco A. Laser peripheral iridoplasty for angle-
closure. Cochrane Database Syst Rev. 2008;(3):CD006746.
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.
Greve EL. Primary ACG: extracapsular cataract extraction or filtrating
procedure? Int Ophthalmol. 1988;12:157-162.
Gunning FP, Greve EL. Lens extraction for uncontrolled glaucoma. J
Cataract Refract Surg. 1998;24:1347-1356.
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.
Aung T, Tow SL, Yap EY, et al. Trabeculectomy for acute primary angle
closure. Ophthalmology. 2000;107:1298-1302.
Honrubia F, Garca-Snchez J, Polo V, et al. Conjunctival hyperaemia with
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patients with ocular hypertension or glaucoma: a meta-analysis of
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29.

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