Author: Jennifer S Weizer, MD

Section Editor: Jonathan Trobe, MD

Deputy Editor: Howard Libman, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2017. | This topic last updated: Dec 22, 2015.

INTRODUCTION — Glaucoma is a group of eye diseases traditionally characterized by elevated intraocular

pressure (IOP). However, glaucoma is more accurately defined as an optic neuropathy and may not always be
associated with elevated IOP. Angle-closure glaucoma is characterized by narrowing or closure of the anterior
chamber angle.

This topic will discuss types of angle-closure glaucoma, diagnosis and treatment. A discussion of open angle
glaucoma is presented separately. (See "Open-angle glaucoma: Epidemiology , clinical presentation, and
diagnosis".)

DEFINITION

Glaucoma is defined as an optic neuropathy involving a characteristic atrophy of the optic nerve head, often
accompanied with typical visual field def ects [1]. Examination of a glaucomatous optic nerve reveals "cupping",
which looks like a "hollowing out" of the optic nerve head (picture 1). Glaucoma is typically, though not always,
associated with elevated intraocular pressure.

Angle-closure glaucoma is a form of glaucoma characterized by narrowing or closure of the anterior chamber
angle [2]. The normal anterior chamber angle provides drainage for the aqueous humor,the fluid that fills the
eyeball. When this drainage pathway is narrowed or closed, inadequate drainage of the aqueous humor leads ot
elevated intraocular pressure and damage to the optic nerve (figure 1A-B). Normal intraocular pressure is 8 to
21 mm Hg. In acute episodes of closed-angle glaucoma, pr essures are often 30 mm Hg or higher 3[ ].

Types of angle-closure glaucoma

Angle-closure glaucoma is divided into two main groups:

● Primary angle-closure — Patients are anatomically predisposed to this type of glaucoma; there is no
identifiable secondary cause.

● Secondary angle-closure — A secondary process is responsible for narrowing or closure of the anterior
chamber angle. Examples of secondary causes are a fibrovascular membrane that grows over the angle to
pull it closed, as in neovascular glaucoma, or a mass or hemorrhage in the posterior segment of the
eyeball that pushes the angle closed 4].
[

EPIDEMIOLOGY — After cataracts, glaucoma is the second leading cause of blindness in the world5].[ Angle-
closure glaucoma is more prevalent in populations of Asian descent, whereas open-angle glaucoma is more
common in populations of European or African descent 6 [ ]. In 2013, among people age 40 ot 80, there were an
estimated 20 million people with angle-closur e glaucoma worldwide with 75 percent in Asia [6]. This is
projected to increase to 32 million worldwide in 2020.

Risk factors — Risk factors that predispose to primary angle-closure glaucoma include [4,7-9]:

● Family history of angle-closure

● Age >60 years
 ● Female
● Hyperopia (farsightedness)
● Certain medications (table 1)
● Pseudoexfoliation (a condition in which abnormal flaky deposits onye
e surfaces can weaken the zonules
that support the lens and cause it to shift forward)
● Race

The highest rates of angle-closure are reported in Inuit and Asian populations 10-14],
[ and lower rates are
reported in populations of African and European origin [2,12,15,16].

PATHOGENESIS

Primary angle-closure — Aqueous humor is produced by the ciliary body, flows through the pupil, reaches the
anterior chamber angle and exits the eye. The balance between fluid production and drainage determines the
intraocular pressure.

In primary angle-closure, the lens is located too far forward anatomically and rests against the iris. This results
in pupillary block, a condition in which aqueous humor can no longer flow normally through the pupil. Pressure
builds up behind the iris, relative to the anterior chamber, causing the peripheral iris to bow forward and cover
all or part of the anterior chamber angle.

Prolonged or repeated contact between the iris and the angle can lead ot scarring and functional damage ot
the trabecular meshwork, the tissue in the angle that acts as a sie
ve through which the aqueous humor drains
(figure 1A-B). Once the optic nerve shows damage from the high intraocular pressure, the disease is called
primary angle-closure glaucoma.

If the entire angle is blocked suddenly, as occurs in complete pupillary block, the intraocular pressure rises
rapidly, and acute symptoms can occur. These attacks of acute angle-closure may resolve spontaneously and
recur repeatedly if not treated. Without treatment, vision loss and even blindness can occur quickly during the
attack (over hours to days), so acute angle-closure is a true ophthalmic emergency.

Patients with anatomically narrow angles are at risk for future angle-closure [2]. The width of their anterior
chamber angle is smaller than in the normal yee, and the peripheral iris is closer to the anterior chamber angle.

Chronic angle-closure — Chronic angle-closure results if only a portion of the angle is blocked at a time and
develops scarring. Over time, the angle may become progressively more closed. In this variation of the disease,
the intraocular pressure may be normal or only slightly elevated, in which case symptoms will likely not occur.
Patients with chronic angle-closure glaucoma may have more damage to the optic nerve and peripheral vision
when the diagnosis is established, compar ed to patients with symptomatic acute glaucoma, due o t absence of
symptoms, and thus delayed presentation.

Secondary angle-closure — Secondary angle-closure glaucoma results when the anterior chamber angle
becomes occluded as the e r sult of conditions that push the iris or ciliary body forward ("pushing" conditions) or
deform the iris so that it is e
r tracted into the angle ("pulling" conditions).

Pushing conditions include:

● Fibrosis of the pupil to the anterior surface of the lens

● Choroidal swelling or hemorrhage (due ot types of ophthalmic surgery, retinal laser treatment, posterior
scleritis, or drug reactions). Topiramate is the most common of the sulfa-based medicationsot cause this
rare, idiosyncratic reaction.

● Plateau iris syndrome (a developmental anomaly)

● A large or anteriorly displaced lens

 ● Aqueous misdirection (in which aqueous humor fills the vitreous cavity instead of flowing through the
pupil, most commonly as a er sult of ophthalmic surgery)

● Choroidal hemorrhage or effusion

● A space-occupying lesion in the posteriorsegment of the eyeball (such as a tumor or a gas bubble placed
during retinal surgery)

● Developmental syndromes causing fibrosis in the posterior segment of the eyeball

Pulling conditions include:

● Inflammation or blood in the angle itself that fibr

oses and contracts

● Neovascularization of the iris with a er sulting fibrovascular membrane (most commonly seen in poorly
controlled diabetes mellitus or ophthalmic artery insufficiency)

● Abnormal corneal endothelial cell proliferation

● Prolonged shallowing of the anterior chamberesulting

r in iris-angle contact due ot trauma or surgery

● Epithelial cell or fibroblast invasion of the angle [4]

CLINICAL PRESENTATION — The rapidity and degree of the intraocular pressure elevation from angle-closure
determines whether symptoms occur. If the intraocular pressure rises quickly, as is typical of acute primary
angle-closure, patients may experience some or all of the following symptoms:

● Decreased vision
● Halos around lights
● Headache
● Severe eye pain
● Nausea and vomiting

If the rise in intraocular pressure is slower and does not reach very high levels, the patient may be symptom-
free. This occurs in chronic angle-closure glaucoma. The patient may not notice damage to the peripheral
vision, which generally precedes decrease in central vision.

Signs that suggest a rapid rise in intraocular pressure include (picture 2):

● Conjunctival redness
● Corneal edema or cloudiness
● A shallow anterior chamber
● A mid-dilated pupil (4 to 6 mm) that reacts poorly to light

Signs and symptoms of acute glaucoma often occur in the veening, when lower light levels cause mydriasis,
and folds of the peripheral iris block the narrow angle [17].

DIAGNOSIS

Patients with the above signs or symptoms should undergo emergent ophthalmic examination of both eyes by
an ophthalmologist, including:

● Visual acuity
● Evaluation of the pupils
● Intraocular pressure
● Slit lamp examination of the anterior segments
 ● Visual field testing (either by confrontation [finger testing] or by formal methods, depending on the
acuteness of the clinical situation)
● Gonioscopy (see 'Gonioscopy' below)
● Undilated fundus examination

Pupillary dilation should be deferred in untreated cases of suspected angle-closure, as this may exacerbate the
condition.

On eye examination, patients who have experienced prior acute attacks of high intr aocular pressure may
demonstrate iris irregularity due to ischemia during the attack, glaucomflecken (scattered opacities) in the
anterior lens, normal or increased intraocular pressure, and cupping of the optic disc if narrow-angle glaucoma
is present.

Although angle-closure often presents in just one eye, it is important to examine the fellow eye as well. The
angle of the fellow eye may be similarly narrow, putting this eye at risk for future angle-closure attacks unless
prophylactic treatment is instituted.

Diagnostic tests

Gonioscopy — Gonioscopy is the gold-standard method of diagnosing angle-closure. This technique

involves using a special lens for the slit lamp, which allows the ophthalmologisto tvisualize the angle and
diagnose angle-closure (picture 3). Indentation gonioscopy refers to putting posterior pressure on the eyeball
with the lens used for gonioscopy. The pressure will widen the angle if it is not scarred completely closed; the
extent to which scarring has produced angle-closure helps to determine the severity and chronicity of the
angle-closure. Gonioscopy requires expertise and experience to perform reliably.

Slit lamp grading of anterior chamber depth — In this technique, the width of the angle is estimated yb
shining a light beam from the slit lamp on the peripheral anterior chamber. It is not as reliable as gonioscopy
for diagnosing angle-closure.

Ultrasound biomicroscopy — Specialized ultrasound of the anterior chamber can show angle-closure and
help to define the mechanism. The ultrasound biomicroscope instrument is costly and thus not widely
available. This technique also e
r quires specialized interpretation of the results.

Anterior segment optical coherence tomography — High definition anterior segment optical coher ence
tomography is being used as a modality ot image the drainage angle and detect eyes at risk for angle-closure
[18]. Findings suggest that eyes prone to developing angle-closure do not merely differ anatomically from
normal eyes, but may also respond differently to light stimuli [19]. As an example, when dilated ot the same
degree, the iris of an angle-closure eye tends to be thicker than the iris of a normal eye [20].

Provocative tests — Provocative tests most often do not provide additional information beyond the clinical
examination, and are not widely used because of their risks. In the dark o
r om provocation test, a patient rests
(awake) in a dark room for 30 minutes with his or her head in the prone position to encourage pupillary dilation
and forward displacement of the lens. Angle-closure is suggested if the intraocular pressure rises significantly
or if the angle appears more closed on gonioscopy. Clinical applicability is unknown.

In pharmacological tests, the pupil is dilated withphenylephrine or parasympatholytic mydriatic eye drops and
pilocarpine is instilled in an attempt o
t provoke an attack of angle-closure. This procedure involves risk and a
negative result does not absolutely rule out angle-closure [4]. Both eyes should not be tested simultaneously .
We do not recommend this test.

DIFFERENTIAL DIAGNOSIS

Other causes of a red eye may mimic acute primary angle-closure glaucoma. These include iritis, traumatic
hyphema, conjunctivitis, episcleritis, subconjunctiv
al hemorrhage, corneal abrasion, and infectious keratitis.
(See "Evaluation of the red eye".)
The primary care clinician may be able to distinguish acute primary closure from these conditions by the
presence of severe eye pain, headache, nausea and vomiting, a mid-dilated pupil, and possibly decreased
vision. Not every patient with acute angle-closure will demonstrate all of these signs and symptoms, however.

Secondary causes of angle-closure are best differentiated from primary angle-closure by an ophthalmologist
(see 'Secondary angle-closure' above). The treatment of these disorders differs from treatment of primary
angle-closure.

TREATMENT — Treatment of angle-closure involves prevention or reversal of angle-closure, as well as control

of intraocular pressure. A table to assist with the emergent management of severe acute angle-closure
glaucoma is provided (table 2).

Acute primary angle-closure glaucoma — There are no available trials comparing medical options for
treatment of acute angle-closure, and treatment recommendations are based on clinical experience 21].
[ When
an ophthalmologist is available for consultation within one hour of patient pr
esentation, patients with signs or
symptoms suggesting possible acute angle-closur e should be referred for emergent assessment and
treatment.

When there is likely to be an hour or more delay before a patient can be seen by an ophthalmologist, and the
suspicion of an acute attack is high, empiric tr
eatment should be initiated. For an acute primary angle-closure
attack, initial management involves prompt administration of pressure-lowering eye drops. A possible regimen
would be one drop each, one minute apart, of [21]:

● 0.5% timolol maleate (Timoptic)

● 1% apraclonidine (Iopidine), and
● 2% pilocarpine (Isopto Carpine)

Systemic medications (oral or IV acetazolamide, IV mannitol, or oral glycerol or isosorbide) to control the
intraocular pressure are often given. We suggest giving the patient two 250 mg tablets of acetaz olamide in the
office. The eye pressure should be checked 30 to 60 minutes after giving pressure-lowering drops and oral
acetazolamide. Systemic medications other than oral acetazolamide should be administered under the
guidance of an ophthalmologist, since angle-closur e should be confirmed before they are given.

If medical treatment is successful in reducing intraocular pressure, as is most often the case, corneal edema
and eye pain will typically lessen or er solve. Once the attack is broken, the treatment of choice is a peripheral
iridotomy. If laser peripheral iridotomy fails to remain patent, or the cornea is ot o cloudy to visualize the iris,
surgical peripheral iridectomy may be necessary.

Laser peripheral iridotomy — This procedure creates a tiny hole in the peripheral iris through which aqueous
humor can flow and reach the angle [22]. Once the iridotomy is patent, pupillary block is bypassed. Peripheral
iridotomy is usually created with a laser.

The intraocular pressure is rechecked 30 to 120 minutes after the iridotomy is performed, and mild steroid
drops are given for several days. Repeat gonioscopy is then performed to determine if the angle is wider. The
pupil is dilated to ensure that the intraocular pressure does not rise significantly, and to better assess any
glaucoma damage to the optic nerve.

Possible complications of laser peripheral iridotomy include:

● Increased intraocular pressure

● Inflammation
● Laser burns to the cornea, lens, or retina
● A ghost image in the vision
● Increased rate of cataract formation [23,24]
● Need for repeat treatment if the hole were to shrink or close spontaneously
The fellow eye should be examined. If a narrow angle is found, prophylactic laser peripheral iridotomy should
be performed to prevent future attacks of angle-closure [23]. Untreated, approximately 50 percent of fellow
eyes in acute angle-closure patients will have an angle-closure attack within five years [23,25].

Other surgery — In a few cases of angle-closure, goniosynechialysis may be performed in the operating
room at some point after a peripheral iridotomy is in place. In goniosynechialysis, adhesions thatesult
r in
scarring of the angle are mechanically lysed in an attempt to restore some drainage function. Results tend o
t
be better if the scarring has been present for less than one year [26].

Cataract surgery (phacoemulsification) with an intraocular lens implant also may resolve the issue of acute or
chronic primary angle-closure, once diagnosed, by removing the lens that may be crowding the angle [23,27-
29]. A randomized trial of 62 Chinese patients with cataracts who had been medically treated for acute primary
angle-closure found that early phacoemulsification was more effective than laser peripheral iridotomy in
preventing recurrence of intraocular pressure rise [30]. The role of phacoemulsification as definitive treatment
following an episode of angle-closure, especially in patients without significant catar
acts, remains to be
established.

Chronic angle-closure glaucoma — Laser peripheral iridotomy is the first step in treatment of patients with
chronic angle-closure glaucoma, to relieve any pupillary block component. The intraocular pressure may remain
elevated, however, if scarring has already damaged the drainage angle. In this case, the er maining glaucoma is
treated medically and surgically much as in open-angle glaucoma. (See"Open-angle glaucoma: Epidemiology ,
clinical presentation, and diagnosis".)

Secondary angle-closure glaucoma — Secondary angle-closure is managed by treating the cause of the angle-
closure if possible. Controlling the intraocular pressure medically and surgically afterwards is the next step,
much as in open-angle glaucoma. (See"Open-angle glaucoma: Epidemiology , clinical presentation, and
diagnosis".)

PATIENT INSTRUCTIONS — Patients who are known to have narrow angles but who have not yet undergone
laser peripheral iridotomy should avoid medicines that induce pupillary dilation and might provoke an angle-
closure attack. Such medicines include over-the-counter decongestants, motion sickness medications,
adrenergic agents, antipsychotics, antidepressants, and anticholinergic agents [2]. Once laser peripheral
iridotomy has been performed, these medications are no longer contraindicated.

People with a family history of primary angle-closure should undergo regular screening eye examinations for
this condition, particularly as they reach middle age. The examining ophthalmologist should per form
gonioscopy to assess for narrow angles, and evidence of prior angle-closure; laser peripheral iridotomy should
be performed if these are found.

PROGNOSIS — The outcomes of patients with angle-closur e depend on how early the disease is detected.
Because glaucoma damage o t the optic nerve is generally not reversible and can occur within a matter of hours
in the case of an acute angle-closure attack, it is important that an ophthalmologist see these patients
emergently to provide prompt diagnosis and treatment.

The fellow eye also must be evaluated as prophylactic treatment with laser peripheral iridotomy can prevent
future angle-closure. The outcome for patients with secondary angle-closure depends on the cause of the
angle-closure.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces ar e written in plain language, at the 5th to 6th grade
reading level, and they answer the four orfive key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-read materials.
Beyond the Basics patient education pieces ar e longer, more sophisticated, and more detailed. These articles
th th
are written at the 10 to 12 grade reading level and are best for patients who want in-depth information and
are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)

● Basics topic (see "Patient education: Angle-closure glaucoma (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Glaucoma involves a characteristic atrophy of the optic nerve head ("cupping"), often with peripheral vision
defects. Angle-closure glaucoma is characterized by narrowing or closure of the anterior chamber angle,
leading to elevated intraocular pressure and damage to the optic nerve. (See 'Definition' above.)

● Drainage of aqueous humor through the anterior angle is blocked by anatomic narrowing of the angle in
primary angle-closure glaucoma. Acute blockage is an ophthalmic emergency, since vision loss and
blindness may occur quickly. (See 'Primary angle-closure' above.)

● Patients with chronic angle-closure may not develop elevated intraocular pressure and symptoms, and
diagnosis may be delayed resulting in more vision loss than patients with acute angle-closur
e. (See
'Chronic angle-closure' above.)

● Secondary angle-closure is caused by a variety of processes that either push or pull the anterior chamber
angle closed. These may include fibrosis and scarring, drug reactions, neovascularization, or mass. (See
'Secondary angle-closure' above.)

● Patients with acute angle-closure glaucoma present with vision loss, headache, severe eye pain, light
halos, nausea, and vomiting. Exam reveals a red eye, corneal cloudiness or edema, a shallow anterior
chamber, and poorly reactive mid dilated pupil. Ophthalmologic examination is needed emer gently. (See
'Clinical presentation' above.)

● Diagnosis of angle-closure glaucoma is established by gonioscopy. Provocative tests are not

recommended. The fellow eye should be examined as well as the affected eye. (See 'Diagnostic tests'
above.)

● Patients with signs and symptoms suggesting an acute attack of angle-closure glaucoma require
emergency treatment by an ophthalmologist. A table to assist with the emergent management of severe
acute angle-closure glaucoma is provided (table 2). We recommend emergency use of topical ophthalmic
medications to reduce intraocular pressure (Grade 1C). These drugs may include a beta-blocker, an alpha
agonist, and an agent to produce miosis. We also suggest systemic medication ot decrease intraocular
pressure, which may include oral or IV acetazolamide, IV mannitol, oral glycerol, or isosorbide (Grade 2C).
Once the acute attack is controlled, definitive treatment for angle-closure glaucoma is a laser peripheral
iridotomy to provide a small drainage hole through the iris. (See'Treatment' above.)

● Patients with narrow anterior chamber angles, who are awaiting surgery, should be advised to avoid
decongestants and anticholinergic medications, which may precipitate an attack. (See'Patient
instructions' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

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