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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.
Headache
Nausea, vomiting
Reduced acuity
Eye redness
Corneal edema
Engorged conjunctival vessels
Elevated IOP
Diagnostic Tests
Slit-lamp examination
Ultrasound biomicroscopy
Retinal OCT
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
Topical prostaglandin analog and/or topical beta-blocker and/or topical alpha-2 agonist
Definition
Classification
Clinical Classification
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.
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).
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%.
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).
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.
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.
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.
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
Examination of the eye may show it to be red with vascular congestion, corneal edema,
and a dilated unresponsive pupil.
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.
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)
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:
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.
Diagnostic Tests
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.
Gonioscopy is also important for the detection of plateau iris and other specific anatomic
configurations.
Result: TM is not visible in angle closure because the peripheral iris is in contact with it.
Result: shallow anterior chamber; and signs of glaucoma: large optic cup, narrowing of
the neuroretinal rim, splinter hemorrhage, nerve fiber loss
Identifies the presence, and quantifies the amount, of glaucomatous visual field loss
during initial diagnosis and subsequently during follow-up care.
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
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
Can be used to assess loss of nerve tissue in and around the optic nerve objectively and
quantitatively
Can be used to assess loss of nerve tissue in and around the optic nerve objectively and
quantitatively
Differential Diagnosis
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
Nausea or vomiting
Conjunctival injection
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
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.
Screening
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.
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
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.
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
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.
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
Primary options:
Ongoing
Primary options:
Primary options:
Secondary options:
Emerging Therapies
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.
Asia
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
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.
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
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
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
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