PRIMARY ANGLE CLOSURE GLAUCOMA

PRESENTER: DR ANNAPURNA PUNTA

MODERATOR: PROF AMIT MAITREYA
PRIMARY ANGLE CLOSURE GLAUCOMA
Angle closure glaucoma (ACG) results from appositional or synechial closure of the anterior
chamber angle leading to reduction in aqueous outflow facility, IOP elevation, and
subsequent damage to the optic nerve with associated visual field loss. There are primary and
secondary forms of angle closure glaucoma . In primary angle closure, the mechanism
causing disease is primarily pupillary block, being either functional or absolute, while in
secondary forms there are other underlying causes.
Primary angle-closure suspect (PACS) or anatomic narrow angle – An eye in which the
anterior chamber angle recess has an abnormally narrow angular width. The peripheral iris is
located close to, but not touching, the posterior pigmented trabecular meshwork (TM). No
PAS are present. IOP, optic nerve, and visual field are normal.
Primary angle closure (PAC) – An eye that has a primary anatomic narrow angle and
evidence that trabecular obstruction by the peripheral iris has occurred, such as peripheral
anterior synechiae (PAS), elevated IOP, iris whorling or sectoral atrophy, and excessive
pigment deposition on the trabecular surface. The eye does not have glaucomatous damage of
the optic nerve.
Primary angle closure glaucoma (PACG)-iridotrabecular contact is present in three or more
quadrants of the drainage angle in the presence of documented optic nerve damage and visual
field loss.
Secondary angle closure is caused by an underlying identifiable pathologic etiology, such as
neovascularization or uveitis. If angle closure results in elevated IOP that causes
glaucomatous optic disc damage, it is referred to as secondary angle closure glaucoma.Both
primary and secondary angle closure can result in acute angle closure attacks and chronic
angle closure leading to glaucoma.

Etiology
See Pathophysiology section below.
Risk Factors
A large number of risk factors have been identified:
• Hyperopia
• Family history of angle closure
• Advancing age
• Female gender
• Asian or Inuit descent
• Shallow anterior chamber depth
• Shorter axial length
• Thicker lens
Pathophysiology
Primary angle closure glaucoma is caused by relative pupillary block in the majority of cases.
In pupillary block, aqueous humor encounters increased resistance as it flows from the
posterior to anterior chamber through the iris-lens channel. Some degree of relative pupillary
block is present in most phakic eyes. The risk of pupillary block is highest with a mid-dilated
pupil where there appears to be maximum contact between the iris and the lens. In eyes with
angle closure, other factors exacerbate the block, such as the front lens surface being anterior
to the plane of iris insertion into the ciliary body base. The increased pressure gradient across
the pupil causes the peripheral iris to bow forward and cover some or all of the filtering
portion of the trabecular meshwork, resulting in appositional angle closure. Peripheral
anterior synechiae form after prolonged or repeated contacts of the peripheral iris with TM.
Another mechanism thought to be important in primary angle closure is iris angle crowding,
which is caused by a thickened peripheral iris filling the space between the TM and angle
recess under dark conditions.
Eyes that experience angle closure are not only anatomically different than normals — they
have shorter axial lengths, shallower anterior chambers, thicker and relatively anteriorly
positioned lenses, and flatter corneas — but they are also physiologically different. Thicker
irides may increase the posterior to anterior pressure differential. Dynamic factors in angle
closure eyes that can contribute to increased pupillary block are the tendency to retain more
iris volume after dilation and choroidal expansion causing forward lens movement. As
imaging modalities, such as ultrasound biomicroscopy and anterior segment optical
coherence tomography improve, these dynamic factors will be better studied and understood.
A less common cause of primary angle closure is anterior non-pupillary block. This is
observed in eyes in which angle closure progresses despite a patent iridotomy, for example,
as seen in plateau iris. Plateau iris configuration is characterized by a normal central anterior
chamber depth, flat iris profile, and crowding of the angle by the iris base. There is a forward
displacement of the iris base by anteriorly located ciliary processes that can lead to
subsequent angle closure. Plateau iris syndrome occurs when an eye with plateau iris
configuration develops a closed angle. Prominent last iris roll is another mechanism of
anterior nonpupillary block in which a very thick iris with prominent peripheral
circumferential folds becomes more pronounced and contacts trabecular meshwork with
dilation.
Secondary angle closure glaucoma is caused by a myriad of other eye diseases . There are
several secondary causes of angle closure that involve relative and absolute pupillary block.
In phacomorphic glaucoma, the mass effect of a thickened or intumescent cataract pushes the
iris forward and causes pathological angle narrowing. Forward displacement of the lens in
ectopia lentis or microspherophakia can also push the iris forward and shallow the angle.
Absolute pupillary block occurs when there is no movement of aqueous through the pupil
because of 360o posterior synechiae between the iris and a crystalline lens, an intraocular
lens, capsular remnants, or the vitreous face. In secondary angle closure glaucoma without
pupillary block, angle closure is due to either a.) contraction of an inflammatory,
hemorrhagic, or vascular membrane in the angle leading to PAS, or b.) forward displacement
of the lens-iris diaphragm, often associated with ciliary body swelling and anterior rotation.

Mechanisms that push the iris forward from behind

• Relative pupillary block (primary angle closure)
• Plateau iris configuration (primary angle closure)
• Absolute pupillary block – 360 degree posterior synechiae secluding pupil
• Aqueous misdirection or malignant glaucoma
• Ciliary body swelling, inflammation or cysts
• Choroidal swelling, effusions, or detachments
• Posterior segment tumors or space-occupying substances (silicone oil or gas
bubble)
• Contracting retrolental tissue as seen in retinopathy of prematurity
• Anteriorly displaced lens
• Encircling retinal bands/buckles
Mechanisms that pull the iris forward into contact with the trabecular meshwork
• Contraction of inflammatory membrane or fibrovascular tissue
• Iridocorneal endothelial (ICE) syndrome with migration of corneal
endothelium
• Fibrous ingrowth
• Epithelial downgrowth
• Iris incarceration in traumatic or surgical wound
Primary prevention :Screening
Given the high prevalence and morbidity of angle closure glaucoma in many countries, there
is a need for quick, inexpensive screening methods that do not require highly skilled
operators.
Oblique flashlight test uses a penlight that is held next to the temporal side of an eye with the
beam of light parallel to the iris and shining across the anterior chamber. If there is a shadow
projected onto the nasal iris, the angle is narrow because the iris is bowed forward and
blocking the path of light. If there is no shadow, the anterior chamber angle is considered
open. Because of variability in flashlight illumination and subjectivity in assessment of the
test result, however, this test has a relatively low specificity.
The Van Herick method uses a narrow slit beam at 60o onto the cornea just anterior to the
limbus to evaluate the anterior chamber depth. If the distance from the anterior iris surface to
the posterior corneal surface is less than one-fourth the corneal thickness, the angle may be
narrow and should undergo gonioscopy. Modification of this method by creating additional
grades, called the limbal chamber depth test, outperformed central anterior chamber depth (as
measured by optical pachymetry and ultrasound) and autorefraction as a screening tool for
the detection of occludable drainage angles identified by gonioscopy.
Laser peripheral iridotomy for narrow angles
The goal of screening for narrow angles is to identify patients at risk of developing angle
closure and to treat prophylactically with a laser peripheral iridotomy (LPI). Patients with
narrow but open angles should be followed for IOP elevation, progressive angle narrowing,
and development of PAS. There is no evidence that iridotomy is indicated for narrow but
open angles with normal IOP; however, LPI is fairly safe and can prevent a potentially
vision-threatening outcome so the risks and benefits must be carefully considered in each
case and discussed with the patient in details.

Indications for laser peripheral ridotomy

• Elevation of previously normal IOP
• Presence of potentially occludable angle
• PAS attributable to episodes of angle closure
• Progressive narrowing of the angle
• Requirement for medication that may provoke pupillary block (i.e. —
antidepressants, anticholinergics, etc.)
• Symptoms that suggest prior or intermittent subacute angle closure
• Situation limiting a patient’s ability to immediately receive ophthalmic care
(e.g.,frequent travel to less developed countries where treatment may not be readily available,
lack of insurance, and poor access to transportation)
• Having another eye disorder that requires frequent dilated eye exams (e.g.
diabetic retinopathy)
• History of acute PAC in other eye
Diagnosis
Diagnosis of both primary and secondary angle closure glaucoma is based on history and eye
exam. Gonioscopy is the gold standard for evaluating the anterior chamber angle, but
imaging modalities assist in quantifying and objectifying angle characteristics. To distinguish
between primary and secondary causes, the clinician must actively look for signs and
symptoms of possible secondary causes and rule each out before the patient can be diagnosed
with primary angle closure glaucoma .
History
 • History of present illness – typical signs and symptoms of acute or subacute
angle closure attacks (see Signs and Symptoms sections) and if patient was upset or in the
dark when symptoms started
• Past ocular history
• Trauma – can cause zonular weakness or dehiscence allowing lens to displace
anteriorly
• Incisional or laser surgery – can cause anterior chamber inflammation or
predispose to epithelial/fibrous ingrowth; may also lead to aqueous misdirection (e.g. after
LPI) or ciliary body engorgement (e.g. after extensive panretinal photocoagulation).
• History of prior retinal vein occlusion – can cause angle neovascularization or
ciliary body engorgement rotating lens forward
• Past medical history – history of diabetes or carotid stenosis disease that can
cause angle neovascularization
• Medications – use of systemic medications, such as sulfonamide, topiramate,
and phenothizaines, that may cause ciliary body engorgement or suprachoroidal effusion; use
of medications to treat allergy, bladder dysfunction, or depression; use of anticholinergics or
sympathomimetics that can dilate pupil
• Family history of acute angle glaucoma
Physical examination
• Refractive status – hyperopic eyes tend to have shallower anterior chamber
angles which places them at risk for angle closure
• Pupil size and reactivity
• Slit lamp exam
• Conjunctiva – injection
• Cornea – clarity, presence of edema, evidence of surgical or traumatic wounds
• Anterior chamber – central and peripheral depth, inflammation
• Iris – areas of atrophy, mass, neovascularization, or posterior synechiae
• Lens – thickness, phacodonesis, subluxation, glaucomflecken (necrosis of
anterior lens capsule; may indicate previous attacks)
• Intraocular pressure measurement, preferably with applanation prior to
gonioscopy
• Gonioscopy of both eyes with indentation to evaluate for appositional versus
synechial angle closure
• Evaluation of fundus and optic nerve – dilation is often not advisable in
primary angle closure attack until an iridotomy has been performed and/or the acute attack
has resolved as dilation can exacerbate the condition. In contrast, dilation may be permissible
as the appropriate treatment in certain forms of secondary angle closure. The fundus should
be examined for underlying causes leading to the angle closure.
Signs
Signs of a primary anatomic narrow angle on slit lamp exam can be subtle and include a
shallow anterior chamber and an anteriorly bowed iris.
Both primary and secondary forms of angle closure can cause acute angle closure attacks.
The intraocular pressure usually exceeds 40 mmHg and may rise to as high as 80 mmHg. The
conjunctiva is significantly injected. The cornea develops stromal and microcystic edema in
response to the acute rise in eye pressure and decompensation of the endothelial pump
mechanism. Iris sphincter ischemia leads to a fixed, mid-dilated pupil. Sectoral iris atrophy
may occur, releasing pigment into the anterior chamber that dusts the corneal endothelium
and anterior lens capsule. The overall anterior chamber is shallow. The center is usually
formed, but the mid-peripheral iris bows forward and may touch the peripheral cornea. Often
there is anterior chamber inflammation. The fundus is typically difficult to examine because
of corneal edema. If visualized, the optic nerve head may be hyperemic and edematous. The
angle is often difficult to examine with gonioscopy because of corneal edema, but if
visualized, reveals contact of the peripheral iris with cornea.
In the aftermath of an acute attack, pupillary distortion may result if there is permanent
sphincter damage and/or iris atrophy. Anterior lens capsule opacities, known as
glaukomflecken, may result from damage to the anterior lens epithelium from high
intraocular pressure. The angle may have permanent synechiae formation. Intraocular
pressure may be low if the ciliary body is so ischemic that aqueous humor production is
compromised. As the ciliary body recovers, normal aqueous humor production resumes and
the intraocular pressure rises.
ACG exhibits signs of optic neuropathy in the typical glaucomatous pattern with increased
cupping of the optic nerve and retinal nerve fiber layer dropout.
Summary of Clinical Findings in Various Types of Secondary Angle Closure Glaucoma
• Neovascularization of the angle – blood vessels from iris that cross scleral spur to
arborize along trabecular meshwork, Peripheral Anterior Synechiae (PAS)
• Anterior chamber inflammation – keratic precipitates, posterior synechiae, iris
bombé, inferior PAS (as opposed to primary angle closure where PAS tend to develop
superiorly)
• Iridocorneal endothelial (ICE) syndrome – beaten-bronze corneal
endothelium, corneal edema, high PAS that can extend anterior to the Schwalbe line, iris
atrophy, corectopia
• Drug induced (e.g. systemic topiramate) – acute bilateral disease, acute
myopic shift, uniformly shallow chamber with anterior iris and lens displacement,
ciliochoroidal effusion or detachment
• Aqueous misdirection (malignant glaucoma) – flattening of central and
periperhal anterior chamber, anterior displacement of lens (cystralline or intraocular lens) or
vitreous face, clear “aqueous” zones in vitreous
 • Lens-induced angle closure – thick cataract, unstable or subluxed lens
• Nanophthalmos – small but normal eye with short axial length, microcornea,
large lens, and thickened sclera; choroidal effusion
• Retinopathy of prematurity or persistent hyperplastic primary vitreous –
contracting retrolental tissue
• Iris or ciliary body mass lesions or cysts – irregular contour of iris or
neovascularization, hyphema or vitreous hemorrhage, episcleral sentinel vessel, ciliary body
mass through dilated pupil or on ultrasound biomicroscopy
• Posterior segment mass or large serous retinal detachment – signs of each on
funduscopic exam
• Epithelial and/or fibrous downgrowth – wound dehiscence or gape, epithelial
cysts in anterior chamber adjacent to wound, gray sheetlike membrane covering anterior
segment structures that whitens with argon laser
• Pseudophakic or aphakic pupillary block – pupilary obstruction or synechiae
to anterior hyaloid surface, the intraocular lens, or posterior capsule
• Ciliary body engorgement associated with retinal vascular occlusion or
panretinal photocoagulation – anterior rotation of iris and lens; retinal signs of each
underlying etiology, e.g. retinal hemorrhages for vein occlusion and extensive retinal laser
scars from photocoagulation.
• Retinal surgery
• Encircling scleral buckle – relatively deep central anterior chamber with
peripheral iris flattening, choroidal effusion
• Pars plana vitrectomy - pupillary block from expansile gases pushing iris and
lens forward, silicone oil in the anterior chamber, non-patent iridotomy
Symptoms
Patients with anatomic narrow angles without acute angle closure are typically asymptomatic
in both the primary and secondary forms. Similarly, primary and secondary chronic angle
closure patients often experience no symptoms unless they develop end-stage glaucoma, in
which case they may complain of decreased vision or reduced peripheral vision.
Acute angle closure, on the other hand, usually presents with dramatic symptoms from the
quick rise in intraocular pressure. Patients complain of blurred vision, rainbows, halos around
lights, or even transient loss of vision. They often have intense pain that may be localized to
the eye, may follow the trigeminal distribution, or may be described as diffuse discomfort.
Nausea and vomiting are common.
Subacute or intermittent angle closure attacks are brief episodes of angle closure that resolve
spontaneously. Patients experience the above symptoms of acute angle closure, but on a
milder scale. They will typically experience some blurring of the vision or halos with mild to
moderate eye pain, brow ache, or headache. These attacks are often resolved by entering a
well lit room which may cause miosis or sleep as sleep-induced miosis ameliorates the lesser
degree of pupillary block in these patients.
Clinical diagnosis
Gonioscopy
The key to diagnosis of anatomic narrow angle or angle closure is gonioscopy, which is still
the gold standard method of angle evaluation. The ideal way to perform gonioscopy is in a
dark room using a small rectangle of light only as bright as necessary to view the angle
structures, as light can open an appositionally closed angle in about one-third of cases.
Dynamic or compression or indentation gonioscopy is essential to differentiate appositional
closure from synechial closure. Gentle pressure on the cornea with the goniolens pushes back
the iris and reveals whether the angle can be opened any further; if not, synechial closure is
present. This maneuver can also help break acute attacks by forcing fluid into the periphery
and opening areas of appositional closure.
Occludable angles are typically described as eyes in which the posterior, usually pigmented,
trabecular meshwork is seen for less than 90° of the angle circumference or if the angle width
is less than 20°.
Angle Grading and Classification Systems
A. Scheie system (R)
0 – entire angle visible with wide ciliary body band I – last roll of iris obscuring part of the
ciliary bodyII – nothing posterior to trabecular meshwork visibleIII – posterior portion of
trabecular meshwork not visible IV – no structures posterior to Schwalbe’s line visible
Pigmentation graded 0 (no pigmentation) to 4 (heavily pigmented)
B. Shaffer system (R)
0 – closed or slit 1 – extremely narrow, ≤10 degrees2 – narrow, 20 degrees3 – open, 20-35
degrees4 – wide open, 35-45 degrees
C. Spaeth system (R)
Level of iris insertion:A – anterior to trabecular meshwork B – anterior to posterior limit of
trabecular meshworkC – posterior to scleral spurD – into the mid-ciliary body face (anterior
ciliary body band visible)E – posterior ciliary body (wide band of ciliary body band visible)
Angle width – estimated in degrees from line tangential to the trabecular meshwork to line
tangential to the iris surface one third of the way from the periphery (ranges from 0 - 40
degrees)
Curvature of iris:
r – regular configuration, no significant forward or backward arching of iris – steep or
forward bowing (convex) curveq – queer or posterior bowing (concave) curve
Pigmentation: 0 (no pigment) to 4 (heavy pigmentation)
Change in angle configuration after indentation performed described by putting the original
insertion in parenthesis, followed by the insertion after indentation. For example, if
indentation shows that the insertion is actually a D when it originally appeared to be a C, it is
indicated as a (C)D.
Photos Courtesy of Sarwat Salim, MD, University of Tennessee

•Chronic Angle Closure Glaucoma

•Combined Mechanism Glaucoma with Scattered PAS

•PAS in a patient with ICE Syndrome

Provocative tests: Various provocative tests have been developed in an attempt to separate
out patients who may be at higher risk of angle closure. In these tests, different maneuvers are
used in an attempt to induce pupillary block, and then the pressure is rechecked and the angle
is examined for narrowing. A test is considered positive if the IOP increases by 8 or more
mmHg. In the dark room test, patients are placed in a dark room for 1-2 hours to dilate the
pupil and increase resistance at the lens-iris channel.
The prone test involves placing the patient in the prone position for 1-2 hours without
sleeping to anteriorly displace the lens and increase pupillary block. These tests have not
been found to be very predictive of angle closure. Combining anterior chamber imaging (e.g.
ultrasound biomicroscopy) with provocative testing assists in detecting apposition and allows
measurement of various parameters of the angle, but their ability to predict future angle
closure is not well established.
Pharmacologic provocative tests using mydriatic eye drops to increase pupillary block via
pupil dilation have fallen out of favor as they carry a significant risk of angle closure in and
of themselves.

Imaging modalities: To supplement information obtained through gonioscopy, there are

several anterior segment imaging devices available that provide detailed images of structures
and quantitative measurements. They are useful in primary angle closure but can also help
detect secondary cases of angle closure, such as ciliary body masses or anterior rotation. At
this time, there are no widely agreed upon quantitative measurement cutoffs obtained from
these devices that distinguish a narrow angle from an open one.
Ultrasound biomicroscopy (UBM):This high-frequency B scan ultrasound provides high-
resolution cross-sectional images of the anterior segment of the eye to the anterior vitreous.
Because it uses sound, it can pass through opaque structures to visualize structures hidden
from direct clinical examination, such as the ciliary body. It is particularly helpful for
evaluating plateau iris and other ciliary body pathology. The disadvantages of UBM
include: requirement of a water bath immersion, specialized equipment, and a skilled
technician to operate; it is also relatively costly and time consuming.
Anterior segment OCT (AS-OCT): This modality uses a diode light source instead of sound
to produce highly detailed images of the cornea, angle region, and anterior ciliary body
similar to those seen with UBM. Compared to UBM, AS-OCT is unable to image structures
posterior to the iris plane well because of posterior pigmented iris shadowing and scleral light
scattering. The advantages of AS-OCT are that it is a noncontact exam: the patient can be
imaged in an upright position avoiding positional lens changes, and all four quadrants can be
scanned at once.
Scheimpflug photography
Digital images of the anterior chamber angle can be obtained using a Scheimpflug camera.
Rotating versions of the camera provide three-dimensional photos that can be analyzed by
computer software to measure specific parameters of the angle. The camera has an easy-to-
use slit lamp type configuration but is expensive and requires special equipment. It cannot
image the ciliary processes or body behind the iris.
Optic nerve assessment and imaging, retinal nerve fiber layer analysis, and visual field testing
should be preformed to assess for signs of glaucomatous optic neuropathy in any patient with
angle narrowing or angle closure glaucoma.
Differential diagnosis
The main entities to distinguish are primary angle closure versus secondary causes of angle
closure because treatment may differ depending on the etiology. Primary disease tends to be
bilateral, while disease caused by a secondary etiology may be unilateral or bilateral. Please
refer to the previous tables for various causes of secondary angle closure glaucoma.
Management
The overall goals for management are to reverse or prevent the angle closure process, control
intraocular pressure elevation, and prevent damage to the optic nerve. Some primary and
secondary forms of angle closure may be treated similarly, while others require very different
treatment approaches based on their underlying pathophysiology. IOP is lowered with
glaucoma medications. Iridotomy is an essential part of treatment in PAC, but may not be
indicated in some forms of secondary angle closure glaucoma. Trabeculectomy and tube
shunts may also not be indicated for certain secondary forms of angle closure glaucoma.

Medical therapy
Acute angle closure glaucoma
The role of medical therapy in acute angle closure attacks is to lower IOP, reduce pain, and
clear corneal edema in preparation for iridotomy. The medications below can be used,
provided the patient has no condition contraindicating them:
Topical
• Beta blockers
 • Selective alpha agonists
• Carbonic anhydrase inhibitors
• Miotics (e.g., pilocarpine 2%) may help break an early angle-closure attack,
but may be ineffective if the iris is already ischemic. High-concentration miotics (e.g.,
pilocarpine 4%) should be avoided because of the potential for forward displacement iris-lens
diaphragm.
• Prostaglandin analogues – unreliable effect in acute attack because of slow
onset of action
• Hyperosmolar agent (e.g. 5% sodium chloride) – assists in clearing corneal
edema
• Prednisolone 1% - decreases inflammation
Systemic
• Carbonic anhydrase inhibitors – oral acetazolamide’s maximum IOP reduction
is reached in 2-4 hours and lasts for 6-8 hours. Intravenous acetazolamide drops the IOP
within 2 minutes with a peak effect noted by 10-15 minutes. In acute situations, a single dose
of 500 mg acetazolamide should be given orally if the patient is not vomiting. Regular
acetazolamide is preferred over the sustained-release sequel form because of quicker onset of
action. If the patient is vomiting, acetazolamide can be given intravenously.
• Osmotic agents
1. Mannitol can decrease the IOP 30 mm Hg or more within 30 minutes of
administration. The recommended intravenous dose is 0.5-1.5 g/kg body weight as a 15% or
20% solution, delivered at 3 to 5 mL/minute. Frail patients with cardiac or conditions may
develop circulatory overload, pulmonary edema, congestive heart failure, and electrolyte
imbalance. A rapid reduction in cerebral volume may result in subdural hematomas from vein
rupture between the sagittal sinus and cortical surface. Therefore, patients receiving IV
mannitol should be monitored in a hospital setting.
2. Oral osmotic agents:
• Glycerin: 1 to 1.5 g/kg body weight of a 50% solution. Onset of pressure
reduction is typically 10 to 30 minutes. Avoid in diabetics because the increased caloric load
can cause ketoacidosis.
• Isosorbide is commercially available as a 45% (45 g/100 mL) solution
(Ismotic; Alcon Surgical). The recommended dose is 1 to 1.5 g/kg body weight. Its effect is
similar to glycerin’s but is safe for use in diabetics because it is not metabolized.
• Although less common, oral agents can also cause subdural hematomas.
Headache and gastrointestinal upset are common adverse reactions.
Paracentesis Can be perfomed in an acute setting. Technically, it can be difficult to perform
on a phakic eye in pain with a shallow chamber, and there is a risk of permanent damage to
the cornea, lens, and iris. Devastating complications such as endophthalmitis and choroidal
hemorrhage from a rapid pressure drop may occur. Also the effects are typically short-term,
because, as the ciliary body begins to form aqueous again, the IOP will inevitably rise. This
procedure can be used in cases of extreme IOP elevation to “buy time” until medications take
effect or iridotomy can be performed.
Laser Iridotomy Should be performed as soon as possible in the affected eye and in the
contralteral eye to avoid an attack of acute angle closure glaucoma in the future.
Chronic angle closure glaucoma
Very few studies exist to address medical therapy in chronic angle closure glaucoma after
laser iridotomy. In cases where elevated IOP becomes an issue, aqueous suppressants are
helpful in reducing IOP.[32] Prostaglandin analogues have been shown to be effective in
lowering IOP, even in angles that are partially closed.[32] [33] Evidence is not conclusive,
however, regarding their effectiveness in cases of 360° degrees of synechial closure.[34] The
role of PI and other surgical interventions are described below.
Peripheral iridotomy
See Primary prevention section for information regarding prophylactic LPI for narrow angles.
Acute Angle Closure and Fellow Eyes
In angle closure secondary to pupillary block, an iridotomy is the definitive treatment. Laser
peripheral iridotomy (LPI) is considered an effective and safe treatment. It often breaks an
attack of acute angle closure and can prevent future attacks. An incisional iridectomy may be
necessary in cases of cloudy corneas, flat anterior chamber, poor patient cooperation at the
laser, or inability to substantially lower the IOP with medications after a failed LPI attempt.
The fellow eyes of patients that have undergone primary acute angle-closure are generally at
significant risk for an acute attack and should receive an iridotomy. An untreated fellow eye
has a 40% to 50% chance of developing an acute PAC attack over the next 5 to 10 years.
Chronic miotic therapy is not an acceptable alternative, as 50% of contralateral eyes of
individuals suffering acute PAC developed acute attaks when treated with pilocarpine alone.
This is in contrast to the 1.8% of patients treated with prophylactic incisional iridectomy who
developed an attack during this same time period.
Chronic Angle Closure and Angle Closure Glaucoma
LPI relieves the pupillary block component in chronic disease and may halt the progression
of synechial closure and progressive IOP elevation. Its ability to control IOP, however, may
not be long-lasting, especially in eyes where glaucomatous optic neuropathy has already
developed. Additional medications or surgical treatment is often necessary. In cases where
LPI does successfully lower IOP, eyes still need to be monitored routinely as IOP can
increase months or years after the procedure.

Persistent or progressive rise in IOP after LPI

•Damage to trabecular meshwork and/or formation of PAS has occurred when iridocorneal
apposition present
•Pupillary block may recur if iridotomy becomes occluded
• Factors other than pupillary block causing angle closure may have gone unrecognized until
after the LPI (e.g. plateau iris syndrome)
•Angle closure may have been superimposed on pre-exisitng open angle glaucoma or another
eye condition causing IOP elevation, such as pseudoexfolation
•There may be co-existing chronic open angle glaucoma
Complications of LPI
The most common complications of LPI are transient bleeding at site of treatment, hyphema,
postoperative pressure spike, and anterior chamber inflammation. Occasionally, patients may
complain of a seeing a double image if the lid does not cover the iridotomy site. More severe
but rare complications include aqueous misdirection and injury to the cornea, lens, or retina.
Iridoplasty
In laser iridoplasty, contraction burns of long duration, low power, and large spot size are
placed on the peripheral iris to contract the iris stroma and physically pull the iris from the
drainage angle in an attempt to open the angle. In acute angle closure, iridoplasty has been
found effective and safe in short-term lowering of IOP. It can be used in cases that are
medically unresponsive, in which systemic carbonic anhydrase inhibitors must be avoided,
when immediate iridotomy is not possible, or rarely when the attack continues despite a
successful LPI. It is the procedure of choice for plateau iris syndrome when the angle fails to
open and IOP remains elevated despite a patent peripheral iridotomy. In chronic cases of
angle closure, iridoplasty may slightly decrease the formation of PAS.
It is important to note that iridoplasty does not eliminate pupillary block, so iridotomy
remains necessary if pupillary block is the mechanism of angle closure. Potential
complications include IOP spike, iris atrophy from destruction of iris vessels, corneal burns,
marked anterior chamber inflammation, and corneal endothelial damage.
Cataract extraction
In PAC, since the lens is a key player in development of relative pupillary block, it makes
sense that cataract extraction can lower IOP in both acute and chronic angle closure. Removal
of the lens from an eye with a crowded anterior chamber opens the angle and may prevent or
reduce PAS formation. In one study, early phacoemulsification was found to be better than
LPI at preventing IOP rise after an acute angle closure event was controlled
medically.Cataract extraction in the setting of an acute angle-closure attack, however, is
technically difficult. The eye is inflamed with significant corneal edema, a shallow anterior
chamber, an atrophic and atonic iris that is difficult to dilate, and possible zonular weakness.
It may be more prudent to control the acute attack with medications and LPI first and then
wait to perform surgery when the eye has recovered and is less inflamed.
In the chronic phase when patent laser iridotomy and medical treatment have failed to
adequately control IOP, lens extraction many months after the initial attack has been found to
reduce IOP and reduce the need for IOP medications. Cataract extraction can be combined
with goniosynechialysis to further improve IOP control in the short term. Methods of
goniosynechialysis include breaking synechiae with a heavy viscoelastic (viscogonioplasty),
forceps, or a cyclodialysis spatula.
In lens-induced ACG, which includes phacomorphic glaucoma and angle closure due to
forward subluxation of the lens, the definitive treatment is lensectomy. Acute attacks can be
first controlled with medical therapy and/or LPI with lens extraction performed when the eye
is quiet.
Filtration surgery
Filtration surgery has been performed for both acute and chronic angle closure glaucoma. The
indications to perform filtration surgery in PACG are similar to those for surgery in POAG.
In chronic cases, surgery is considered if the optic neuropathy is progressing and IOP is at a
level believed to be contributing to the progression. Reasons for performing filtration surgery
in the setting of an acute closure attack include medical unresponsiveness, lack of laser
availability, or signs of glaucomatous optic neuropathy already present. The same techniques
of filtration surgery are used as in POAG, although some surgeons advocate tighter suturing
of the trabeculectomy flap to avoid low IOP in the immediate postoperative period. A low
IOP may contribute to further anterior chamber shallowing, which may lead to a higher rate
of malignant glaucoma postoperatively
Whether to perform filtration surgery versus a tube shunt procedure for secondary angle
closure glaucoma depends on the underlying etiology. In most cases, dealing with the
underlying pathology (e.g. stopping topiramate in drug-induced glaucoma, removing the lens
in lens-induced glaucoma) will slow or stop the progression of disease. If medical therapy is
not sufficient to control IOP, even when the primary pathology has been addressed, glaucoma
surgery may be necessary and filtration surgery may be appropriate. Conditions such as
neovascular glaucoma and ICE, however, tend to do better with glaucoma drainage
implants. (see below). It has been proposed that combined phacotrabeculectomy may be more
effective at controlling IOP than cataract extraction alone. Recent study results have been
mixed, with some showing phacoemulsification as being superior for deepening the chamber,
[58] the two procedures being equal in terms of IOP control, and combined procedures being
superior for IOP control. Of note, one randomized control trial found that patients who
undergo combined procedures have more postoperative complications and progression of
their optic neuropathy compared to the phacoemulsification alone group, so the risks and
benefits of each procedure need to be carefully considered in each case until more definitive
evidence is available.
Glaucoma drainage implants
A limited number of studies look at the use of tube shunt devices in PACG. PACG eyes are
often placed into the category of refractory glaucoma along with other types of glaucoma and
thus are not separately evaluated. Based on the limited data available in these studies,
tube implants appear effective in controlling IOP in PACG.[62] Drainage implants are
considered more effective than filtering procedures in neovascular glaucoma and ICE
syndrome because, in these diseases, a fibrovascular membrane often grows over the
sclerostomy site causing bleb failure.
Other surgical procedures
 • May be required depending on the etiology of the underlying disease.
• Aqueous misdirection: Nd:YAG laser can be used to disrupt the anterior
vitreous in aphakic and pseudophakic eyes. If that is not successful, definitive surgical
treatment in the form of vitrectromy with anterior hyaloid disruption combined with an
anterior chamber deepening procedure may be indicated.
• Epithelial and/or fibrous downgrowth: radical surgery to remove the
intraocular membrane and affected tissues may be necessary.
• Angle closure that develops after retina surgery may require removing or
loosening encircling bands, opening up iridectomy sites, or removing silicone oil.
Surgical follow up
Patients typically need to be watched closely in the immediate postoperative period,
sometimes weekly for several months. Once IOP control is achieved and the eye is stabilized,
follow up can follow the schedule of routine PACG patients.
Complications
Complications of acute angle attacks are the result of a rapid, extreme rise in IOP. Possible
sequelae include corneal decompensation, cataractous lens changes, iris ischemia resulting in
atrophy and distortion, ciliary body shutdown with resultant hypotony, central retinal vein
occlusion, optic nerve ischemia, and acute permanent vision loss.
Complications of chronic disease include all the same ones that can be seen in acute disease.
The difference in chronic disease is that these conditions develop in a more insidious fashion
over a longer period of time. These patients typically have asymptomatic progression of
glaucomatous optic neuropathy with corresponding visual field defects developing over time.
Prognosis
Primary angle closure suspects
The overall likelihood of an individual with a narrow angle developing acute angle closure in
the United States is less than 10%. A prospective multicenter study, however, found that
patients judged to be at risk for developing ACG by experienced ophthalmologists through
careful slit lamp exam and gonioscopy had a 30% risk of developing angle closure within 5
years when no prophylactic intervention was performed.See “Primary Prevention” for
recommendations regarding prophylactic LPI in PACS.
In contrast, fellow eyes in which the other eye has already suffered an acute angle closure
attack have a much worse prognosis without prophylactic treatment. An untreated fellow eye
has a 40% to 50% chance of developing an acute PAC attack over the next 5 to 10 years.An
iridectomy or iridotomy virtually eliminates the risk.The long-term fate (4–6 years) in terms
of IOP and glaucomatous optic neuropathy is good for most fellow eyes after LPI with the
majority not requiring any additional glaucoma treatment and retaining good vision.
Acute angle closure
In an eye suffering an acute angle-closure attack, the long-term outcomes vary depending on
ethnicity (which may be a reflection of mechanism of angle closure), duration of attack, and
severity of attack in terms of whether or not it can be aborted by medical treatment alone. If
promptly treated, most (60%–75%) symptomatic episodes of angle closure recover without
visual field or optic disc damage in the short term.Six months post-attack, one study reported
38% of eyes to have visual field loss secondary to nerve fiber bundle loss. In another study, 2
- 16 weeks after an attack, changes were noted in optic disk morphology, with preferential
loss in the superotemporal and inferotemporal areas.
The longer the duration of an attack and the more difficult to manage, the worse the outcome
for the eye, regardless of the initial IOP measurement. Patients with a 24 to 72 hour delay in
presentation had a relative risk of 2.78 for developing chronic glaucoma, whereas those
requiring laser iridotomy to control IOP or a trabeculectomy had relative risks of 3.63 and
4.83, respectively. In Singapore, risk of visual field loss was significant if the duration of
symptoms was longer than 7 days.
Even despite successful termination of an acute attack by surgical iridectomy, late IOP
increase is reported in 19% to 24% of cases.There may be ethnic differences in the rate of
IOP control by LPI alone. A greater extent of PAS, a high presenting IOP, and a larger cup to
disc ratio have been reported as predictors of poor pressure control following iridotomy.A
significant portion of patients go on to develop PACG and require further medical or surgical
intervention in an attempt to control their disease. Unfortunately, up to 20% these patients
deteriorate to lose significant vision and are classified as blind in that eye.
Chronic angle closure glaucoma
Asymptomatic angle-closure patients present with more severe visual field defects than
symptomatic patients.In one study which examined visual field loss on presentation, 52.8%
of asymptomatic PACG had end stage visual field loss by Advanced Glaucoma Intervention
Study criteria compared to only 17.5% of symptomatic PAC cases. Although presenting IOP
was considerably higher in the symptomatic group, the level of IOP was not found to be a
significant predictor for visual field outcome. It is likely that the duration of elevated IOP has
a major influence in causing optic nerve damage in PACG, possibly more so than the level of
IOP. Once glaucomatous optic neuropathy has developed, almost all cases will require further
treatment to control IOP (94%–100%). Closer monitoring of IOP is recommended in CACG
compared to POAG, despite the efficacy of medical therapy. Chronic angle-closure glaucoma
tends to progress more quickly and fail medical therapy sooner than POAG.With aggressive
management, however, chronic ACG patients can maintain stable fields and long-term IOP
control.
Secondary Angle Closure
The prognosis for secondary angle closure patients depends on the underlying etiology. Early
recognition of the underlying pathology and timely directed treatment helps to improve
outcomes.

REFRENCES
American academy of ophthalmology