Angle closure glaucoma

Angle Closure Glaucoma
Moderator: Dr. Shivanand Bubanale
Presentor: Dr. Arushi Prakash

Contents
 Glaucoma- definition
 - history
 Angleclosureglaucoma–definition
 classification
 Grading of anglewidth
 Mechanismsof angleclosureglaucoma
 Epidemiology
 Provocativetests
 Acuteprimary angleclosureglaucoma
 clinical presentation
 treatment
sequalae
 Plateau irisconfiguration
 Pseudoplateau irissyndrome

Contents
 Phacomorphic Glaucoma
 Secondary angle closure glaucomas
 Neovascular glaucoma
 Iridocorneal endothelial syndrome
 Posterior polymorphousdystrophy
 Epithelial downgrowth
 Fibrovascular ingrowth
 Flat anterior chamber
 Iridoschisis
 Inflammatory glaucomas
 Ciliary body glaucoma
 Intraocular tumors
 Nanophthalmos

Contents
 Posterior Scleritis
 Central retinal vein occlusion
 Post ocular surgery glaucomas
 Retinopathy of prematurity
 Microspherophakia

Glaucoma
Glaucoma is a group of disorders characterized
by a progressive optic
neuropathy resulting in a
characteristic appearance of
the optic disc and specific pattern of irreversible
visual field defects that are associated
frequently but not invariably with raised
intraocular pressure.

History of GlaucomasHistory of Glaucomas
08/22/15

History of Glaucomas
Term acute glaucoma first used by Lawrence to describe
severe ocular inflammation
MacKenzie emphasized firmness to touch
Von Graefe observed progressive optic disc cupping and
stressed the importance of elevated intraocular pressure and
the beneficial effect of iridectomy
Curran and Banzinger introduced the concept of physiologic
obstruction of aqueous humor flow through the pupil from
the posterior chamber to the anterior chamber (pupillary
block)

Curran reported success with surgical peripheral iridectomy in
eyes with shallow anterior chambers but not in eyes with
chambers of normal dephth
The introduction of gonioscopy and the recognition of synechial
angle closure provided the basis for the differentiation of open
angle and angle closure glaucomas

Rosengren demonstrated that anterior chamber in eyes with
“acute congestive glaucoma” was significantly shallower than in
normal eyes
Lowe investigated biometry of eyes with angle closure glaucoma
And introduced the concept of polygenic inheritance
Becker introduced acetazolamide

Before that, eyes with acute angkle closure glaucoma were
prepared for surgery by intensive miotic therapy, purges and the
application of leeches
Use of hyperosmotic agents to withdraw fluid from the eye
began with
intravenous urea
then, intravenous mannitol
and finally, oral agents

Surgical treatment of angle closure glaucoma has been
revolutionized with the development of laser iridotomy and
iridoplasty.

Angle closure Glaucoma
the term “angle closure” refers to occlusion of the trabecular
meshwork by the peripheral iris, obstructing aqueous outflow.
It may be-
Primary- in an anatomically predisposed eye
Secondary- to another ocular condition

Nomenclature and Classification
Historically the angle-closure glaucoma nomenclature has been
confusing:
conditions were sometimes classified by the time course of the
disease,
sometimes by the effects of the angle closure, and
sometimes by the presumptive pathophysiology of the angle
closure

Nomenclature and Classification
Angle-closure glaucoma has been described by the
adjective pairs congestive/non-congestive and
compensated/uncompensated.
These terms have been abandoned because they lack
specificity.
The congestion and corneal decompensation are
usually a function of the rapidity with which the
pressure rises,
or reflect underlying causal phenomena such as
uveitis.
Similarly the terms acute, subacute, and chronic have often
been used to reflect the time course and/or presence of
symptoms.
Abrupt and total angle closure is acute; recurrent and self-
limiting episodes of closure with elevated intraocular
pressure (IOP) are subacute; and asymptomatic elevated

Twenty-first century consensus
classification
The new classification of primary angle-closure disease relies on three
simple categories:
IOP measurement,
Gonioscopy,
and disc and visual field evaluation.
In other words, the presenting
patient’s clinical examination alone determines the staging of the disease,
regardless of the presence, absence, or reliability of symptom history,
alleged duration, intermittency of problems, etc.

classification
1. Primary angle closure SUSPECT (PAC suspect):
greater than 270° of irido-trabecular contact
 absence of peripheral anterior synechiae (PAS)
normal IOP,disc,and visual field.
In other words,the suspect eye has normal
IOPs, optic nerves and visual fields, i.e., no signs of clinical
glaucoma, but whose angle before indentation gonioscopy is
graded as a Shaffer grade 2 or less, without PAS on
compression.
The angle is at risk.

classification
2. Primary angle CLOSURE (PAC):
greater than 270° of irido-trabecular contact with
either elevated IOP
and/or PAS
 normal disc and visual field examinations.
 In other words, angle closure demonstrates irido-trabecular
contact in 75% of the angle, with either PAS or elevated
IOPs, but without disc and visual field changes.
The angle is abnormal in structure (PAS) or function (elevated IOP).

classification
3. Primary angle-closure GLAUCOMA (PACG):
Greater than 270° of irido-trabecular contact
 elevated IOP
optic nerve and visual field damage.
In other words, angle closure glaucoma manifests the criteria of
closure above,plus demonstrable disc and/or visual field
changes.
The angle is abnormal in structure and function,with optic
neuropathy.

08/22/15
To apply this classification mastery of gonioscopy is required
Irido-trabecular contact needs to be identified as present or
absent,
and then discriminated as either appositional (by indenting
and revealing angle structures) or synechial,
while documenting the latter’s extent (in terms of degrees or
total clock hours)
A goniolens larger than the corneal diameter may allow
better resolution of angle structures, but successful
indentation to view deeper into the angle is usually not
possible.

Newer Imaging Technologies
08/22/15
1. Ultrasonic biomicroscopy (UBM)
With tissue penetration of 4 mm, a UBM’s resolution
typically includes angle structures as well as imaging of the
anterior lens and anterior ciliary processes; images appear as
radial slices of one portion of the angle
Ultrasonic biomicroscopy of angle closed
(star) in darkness-induced dilation
Ultrasonic biomicroscopy of angle opened
(star) in light-induced
miosis.

Newer Imaging Technologies
08/22/15
2.Anterior segment ocular coherent tomography (AS-OCT)
uses infrared light while examining a sitting patient without
direct ocular contact, Images comprise a 180°-diameter slice
of the anterior segment, currently limited to but a few clock
hours (e.g., 3–9 o’clock scan), but dramatically capture the
pupil and irido trabecular
configuration in high definition.Anterior segment ocular coherent
tomography 180°image of
narrow angles pre iridotomy

Classification by mechanisms
Angle closure can be caused by one or a combination of the
following:
(1) Abnormalities in the relative sizes or positions of the anterior
segment structures
(2) Abnormalities in the absolute sizes or positions of the
anterior segment structures
(3) Abnormal forces in the posterior segment that alter the
anatomy of the anterior segment

Mechanisms of Angle Closure Glaucoma
I. Pupillary Block
A. Relative pupillary block (primary angle closure)
B. Miotic- induced angle closure
C. Posterior synechiae
1. Crystalline lens
2. Intraocular lens
3.Anterior hyaloid face

II.Plateau Iris
A.True plateau iris
B. Pseudoplateau iris- iris and ciliary body cysts

08/22/15
III. Lens Induced angle closure
A. Intumescent lens (phakomorphic)
B.Anterior lens subluxation
1.Trauma
2. Exfoliation syndrome
3. Hereditary disorders
C. Drug sensitivity e.g. Sulfonamides

IV. Malignant (ciliary block) glaucoma
A. Phakic
B. Pseudophakic
C.Aphakic

D.Assosiated with other conditions
1.After panretinal photocoagulation
2.After scleral buckling procedures
3.After central retinal vein occlusion
4. Intraocular tumors
5. Posterior scleritis
6. Retrolenticular tissue contracture
a. Retinopathy of prematurity
b. Persistent hyperplastic primary vitreous
7. Uveal effusion from adjacent inflammation
a. Posterior scleritis
b.Aquired immunodeficiency syndrome

Pupillary block Glaucoma
08/22/15
Pupillary block is the fundamental mechanism underlying the
spectrum of PrimaryAngle Closure disease
It may be absolute, as when then iris is completely bound
down to the lens by posterior synechiae
But, most often is a functional block, termed relative
pupillary block.

Pupillary block Glaucoma
08/22/15
Its pathophysiology involves:
(1) lens– iris apposition at the pupil, with resultant bowing
forward of the peripheral iris as aqueous pressure builds up
in the posterior chamber;
and (2) an anatomically predisposed eye that allows the
anterior displaced peripheral iris to occlude the trabecular
meshwork.

Other Demographic risk Factors
08/22/15
• AGE
• Commonly seen with the most frequency in the 6th
and 7th
decades of life
• Several age-associated changes can include progressive
relative pupillary block from a combination of
1. increasing lens thickness,
2. more anterior positioning of the lens,
3. and pupillary miosis

08/22/15
These age-related changes increase the contact between the
iris and lens, potentiate pupillary block and reduce anterior
chamber depth and volume.
Estimated central anterior chamber depth decreases
0.01mm/year

08/22/15
however, PACG with pupillary block
can occur in patients of any age, and rarely even in children –
though the etiologies among the young are almost always
developmental or secondary

08/22/15
GENDER
2 to 3 times more commonly seen in women than men
Because of shallow anterior chambers

HEREDITY
Most cases of PACG with pupillary block are sporadic in
nature
Shallow anterior chambers and narrow angles have been
reported as more common in relatives of patients with PACG
than in individuals whose relatives do not have the disorder

Refractive error
08/22/15
prevalence much higher in individuals with hyperopic eyes,
which typically have shallow anterior chambers
and short axial lengths
 Although rare, angleclosure glaucoma can occur in myopic
eyes

Other Risk factors
08/22/15
Occurs more commonly in the winter months.

attributed to low levels of illumination,

increased cloudiness,

changeable weather,
Central corneal thickness – a recently recognized risk factor
for POAG – does not
seem to have an association with PACG

Ocular risk factors and
mechanisms
08/22/15
Ocular risk factors cluster around a variety of findings, each of
which reflects smaller ocular dimensions:
1. Shallow anterior chamber both centrally and peripherally.
 2. Decreased anterior chamber volume.
3. Short axial length of the globe.
4. Small corneal diameter.
5. Increased posterior corneal curvature (i.e., decreased radius of
posterior corneal curvature).
6. Decreased corneal height.

08/22/15
7.Anterior position of the lens with respect to the ciliary body.
8. Increased curvature of the anterior lens surface.
9. Increased thickness of the lens.
10. More anterior insertion of the iris into the ciliary body, giving
a narrower approach to the angle recess, and possible anomalies of
iris histology.
11.Thinning of the ciliary body is reportedly associated with
anterior movement of the lens, increased lens thickness and
decreased anterior chamber depth.

08/22/15
• Three measures in particular show particularly high
correlations
with angle-closure disease:
• (1) reduced axial anterior chamber depth and volume
• (2) thicker lens; and
• (3) steeper radii of corneal curvature

• The biometric peculiarities of eyes predisposed to angle-
closure glaucoma are accentuated by three trends associated
with aging.
• First, the lens grows in thickness throughout life.
• Second, the lens assumes a more anterior position with age.
• Third, the pupil becomes increasingly miotic with age.
• All of these
• age-associated changes increase the contact between the iris
and lens, potentiate pupillary block, and reduce anterior
chamber depth and volume. It is estimated that central
anterior chamber depth decreases 0.01 mm/year.
08/22/15

08/22/15
Somehow the junction of the lens and iris at the pupillary plane
modulates the flow of aqueous from the posterior to the anterior
chamber, but it apparently is not a simple matter of direct contact
between lens and iris
it includes-
iris–lens channel:
It is an extremely thin (<5 microns),
fluid-filled, flat, doughnut shaped
passage between the posterior iris surface
and the anterior lens,
circumferentially extending beyond the edges of the pupil.

08/22/15
This dynamic and pulsatile fluid‘structure’ provides
normal
resistance to aqueous flow from the posterior to anterior
chambers.
This thus functions as a relative one-way valve to sustain
a minimally
higher pressure in the posterior chamber than in the
anterior
chamber, hence directing anterior flow forward
The resistance to flow has classically been referred to as
relative pupillary block

if the peripheral iris bows forward enough to cover the
trabecular meshwork, the normal outflow of aqueous humor
from the anterior chamber would be blocked and the IOP
could increase.
Angle closure disease typically occurs in eyes with small
anterior segments in which even a relatively small forward
bow of the peripheral iris may contact the trabecular
meshwork.
08/22/15

08/22/15
Moderate pupillary dilation is historically the most
recognizable cause of increased pupillary block, frequently
due to pharmacologic dilation.
 the posterior vector of force of the iris sphincter muscle
reaches its maximum when the pupil is moderately dilated to
a diameter of 3.0–4.5 mm.
Also, in a midilated pupil, the peripheral iris is under less
tension and is more easily pushed forward into contact with
the trabecular meshwork.
 Lastly, dilation may also thicken and bunch the peripheral
iris in the angle.

 In contrast, when the pupil is widely dilated,there is little or no
contact between the lens and the iris and minimum pupillary
block.
Therefore, acute angle-closure glaucoma rarely occurs while
the pupil is in the actual process of dilating due to mydriatic
eye drops: the dilation occurs rapidly enough that pupillary
block does not have time to develop.
Rather, pupillary block‘classically’ occurs as the pupil
constricts over hours following dilation, presumably because
the mid-dilation is prolonged as the mydriatic effect slowly
reverses.
08/22/15

08/22/15
Pupillary block can also be increased by marked pupillary miosis
There are several everyday life‘triggers’ for precipitating attacks of acute
PACG
emotional upset (e.g., bad news, pain, fear, illness, an accident)
or dim illumination (e.g., in a restaurant or theater).
Emotional upset is thought to dilate the pupil through increased
sympathetic tone to the iris dilator muscle, whereas dim illumination
dilates the pupil through decreased cholinergic tone to the iris sphincter
muscle.
Similarly, the forward movement of the lens, which occurs in a variety of
situations such as reading, changes in body position, and miotic therapy,
has been implicated as a trigger.
Diurnal variations in the anterior chamber depth with parasympathetic
fluctuations and pupillary diameter, and diurnal variations in aqueous
secretion have also been suggested as contributory factors

Provocative tests
08/22/15
These were designed to elevate IOP in conjunction with
occlusion of the angle, so as to indicate which eyes‘at risk’
merit surgical intervention.
Most provocative tests were designed to resemble
‘physiologic’ situations, in the hope that the test would
mimic the natural history of the condition.

Provocative tests
1) Mydriatic stimulation-
A weak, short-acting parasympatholytic agent
such as tropicamide 0.5% or a weak
sympathomimetic such as hydroxyamfetamine,
to mildly dilate the pupil (raise the IOP >8mmhg
is consider positive)

(2) Dark room testing to induce physiologic miosis
(3) A prone test
with the head resting on one’s arms on a table
shifting the lens
anteriorly without dilation;
(4) Complex pharmacologic provocations,
mixture of cycloplegics or mydriatics with
pilocarpine.

Subacute or intermittent PACG presents with
-unilateral headache
-blurring of vision
-unbroken coloured haloes
With spontaneous resolution of symptoms

Acute PACG
1)Unilateral sudden onset of pain or aching on the side of the
affected eye.
2)This pain is accompanied by blurred vision or
colored haloes around lights
3)Ocular congestion and corneal edema
4) and sometimes nausea, vomiting, and sweating.
The pain usually occurs in the trigeminal distribution, and is
locally experienced by the patient as in the eye; or it can
manifest as referred pain in the orbit, head, ear, sinuses, or
teeth.

Physical findings in acute angle-closure glaucoma with
pupillary block
08/22/15
• Findings during an acute attack of angle-closure glaucoma
• Two of the following symptom sets:
 Periorbital or ocular pain
 Diminished vision
 Specific history of rainbow haloes with blurred vision
 IOP higher than21 mmHg
• plus three of the following findings:
 Ciliary flush
 Corneal edema
 Shallow anterior chamber
 Anterior chamber cell and flare
 Mid-dilated and sluggishly reactive pupil
 Closed angle on gonioscopy
 Diminished outflow facility
 Hyperemic and swollen optic disc
 Constricted visual field

Acute congestive angle-closure glaucoma
• Severe corneal oedema
• Complete angle closure
(Shaffer grade 0)
• Dilated, unreactive,
vertically oval pupil
• Shallow anterior
chamber
• Ciliary injection
Signs

08/22/15
• Findings suggesting previous episodes of acute angle-
closure glaucoma
 Peripheral anterior synechiae
 Posterior synechiae to lens
 Glaukomflecken
 Sector or generalized iris
atrophy
 Optic nerve cupping and/
or pallor
 Visual field loss
 Diminished outflow facility

Differential diagnosis of acute angle-
closure glaucoma
08/22/15
• Evidence of compromised angle on gonioscopy
or shallow anterior chamber
Ciliary block glaucoma (aqueous misdirection or
malignant glaucoma)
Neovascular glaucoma
Iridocorneal endothelial syndrome
Plateau iris syndrome with angle closure
Secondary angle closure with pupillary block (e.g.,
posterior scleritis)
Cilio-choroidal detachments (bilateral)

08/22/15
• High-pressure open-angle glaucomas masquerading
as acute angle closure
Glaucomatocyclitic crisis
Herpes simplex keratouveitis
Herpes zoster uveitis
Sarcoid uveitis
Pigmentary glaucoma
Exfoliative glaucoma (may have associated angle closure)
Post-traumatic glaucoma
Phacolytic glaucoma
Steroid-induced glaucoma

Primary angle-closure suspect
1)Prophylactic laser iridotomy is recommended iridotomy
widens the angle by about two grades
2)If significant ITC persists after iridotomy
-laser iridoplasty
-lens extraction

Treatment of acute
PACG
IMMEDIATE MEDICALTHERAPY
PROTECTION OF FELLOW EYE
LASER IRIDOTOMY IN BOTH INVOVED
AND FELLOW EYE
LONGTERM GLAUCOMA SURVEILLANCE AND IOP
MANAGEMENT OF BOTH EYES

Hyperosmotic agents
Raise serum osmotic pressure removing fluid from eye especially
from vitreous
In addition, vitreous dehydration allows lens to move posteriorly
deepeningAC and facilitating opening of the angle
Pressure decreases within 30-60 minutes after administration and
effect lasts 5-6 hrs
Oral glycerol 50% 1-1.5g/kg
Isosorbide 1.5-2g/kg in diabetics (not metabolized)
Mannitol 20% 1-2g/kg given intravenously over 45 minutes has a
greater hypotensive effect.
Adverse effects- thirst, headache. Hyperosmolar coma can be a
serious complication due to severe CNS dehydration.
Patients with renal or cardiovascular disease or those already
dehydrated by vomiting are at risk. 08/22/15

Inhibitors of Aqueous Humor
Secretion
Carbonic anhydrase inhibitors
Acetazolamide
Highly effective in angle closure glaucomas
May open some closed angles even in prescence of ischemic iris
atrophy and paralysis of pupil
Aim is to give large dose quickly- 500mg intravenously,
advantageous when vomiting is present,
onset is rapid
May be given orally but onset of action
is not rapid After oral therapy plasma
levels last for 4 to 6 hours
Adverse reactions are uncommon but there is a remote chance of
sensitivity since it is a sulphonamide 08/22/15

β blockers - Beta adrenergic antagonists are
additive with acetazolamide but have a more
prolonged onset of action than intravenous
acetazolamide in acute angle closure glaucoma.
They are more useful in later stages of treatment and in
maintaining reduced intraocular pressure before laser
iridotomy
α adrenergic agonists – by means of vasoconstriction
they reduce aqueous production and increase
uveoscleral flow.
08/22/15

DRUGS THAT INCREASE AQUEOUS
OUTFLOW
Prostaglandin Analogs- Low concentrations PGF2α lower
intraocular pressure without inducing ocular inflammation by
increasing uveoscleral outflow, by increasing permeability of
tissues in cilliary muscle or by an action on episcleral vessels.
Side effects include increased iris
pigmentation, thickening and darkening
of eyelashes.
No systemic side effects
08/22/15

Topical steroids
-To reduce anterior chamber inflammation and
the chance of both anterior and posterior
synechiae formation, may be administered
after the acute attack is broken

ROLE OF PILOCARPINE in
pacg ??
WHAT MAKESTHE USE OF PILOCARPINE
APPEALING?
- It constricts pupil, which‘retracts’ the peripheral
iris from its contact with the angle
- So Miotic agents’ were used in managing
acute disease, and as preventive
therapy for the fellow
eye or until an iridotomy can be arranged

But prophylactic’ pilocarpine in these fellow
eyes may have been the precipitating cause of
PACG
Two major intraocular mechanic situations that miotics
exacerbate:
(1) Pilocarpine’s effects on ciliary body and zonular responses
allow the lens shape to become more convex, while
facilitating its anterior movement, thus shallowing the
anterior chamber, with peripheral compromise of the irido-
trabecular angle

(2) Miotics induce increased convexity of the iris as the lens
advances which, with the simultaneous miotic-induced
miosis, predisposes the lens–iris channel to greater
resistance to aqueous flow.
The result is frequently an inadvertent worsening of
pupillary block.

 SOWHERE PILOCARPINE CAN BE
USED?
Before immediate laser iridotomy or
iridoplasty
-To induce miosis to maximally stretch the
peripheral iris
In plateau iris

IT IS NOT EFFECTIVE IN ACUTE ATTACKS
- The IOP is so high that the pupillary sphincter
muscle is ischemic and unresponsive to topical
miotic agents.

WHENTO CONSIDERTHE ACUTE ATTACK BEEN
TERMINATED?
- Until the IOP is reduced and sustained at the
lowest possible levels. Because IOP may fall
temporarily with medical treatment as profound
hyposecretion and hypotony can follow an acute
attack of PACG
- The angle is as open as physically possible
on gonioscopy.

Slit-lamp maneuvers in management of acute PACG
To often accelerate corneal clarity
Such Maneuvers include:
1) Axially depressing the central cornea with a
small gonioprism (e.g.,the Zeiss four-mirror
lens) or with a blunt instrument(e.g., a muscle
hook or moist cotton swab),

2.Applying digital massage to the globe after retrobulbar anesthesia.
This technique is used to dehydrate the vitreous cavity and
lower IOP
3. Performing an anterior chamber paracentesis,under topical
anesthesia,with a small-gauge disposable sterile needle

Laser interventions for acute PACG
1.Peripheral laser iridotomy,
2.A peripheral iridoplasty (gonioplasty)
3.A pupilloplasty with Nd:YAG or argon
instruments, is the definitive treatment for acute angle-
closure

WHENTO DO IRIDOTOMY?
DIRECTLY- if an acute attack terminated by medical means
OR
WAIT 1-2 DAYS-
For the cornea to clear and intraocular
inflammation to subside

ROLE OF IRIDECTOMY
Surgical iridectomy
- Is a relatively safe and simple procedure
BUT invasive
- complications such as cataract, bleeding, and
endophthalmitis can accur

Surgical iridectomy reserved for situations such as:
1)The laser fails to produce a patent iridotomy;
2) Laser iridotomies repeatedly close;
3) A laser is neither available nor functioning
properly;
4) Opacities of the cornea interfere with laser treatment;
5)The patient is uncooperative or unable to sit at the slit lamp

2) Peripheral laser iridoplasty (gonioplasty)
can be use in
a)Acute PACG from pupillary block
-unresponsive to medical treatment where a perforating
laser iridotomy is precluded by excessive shallowing of the
anterior chamber, inflammation, or corneal edema
b) plateau iris syndrome; and
c) acute phacomorphic angle closure.

3) Laser pupilloplasty
PRINCIPAL
It interrupt pupillary block by distorting the pupil
into a tear-shaped configuration, focally
interrupting decreased flow through the iris–
lenticular junction, thus facilitating aqueous
to flow into the anterior chamber

SURGICAL MANAGEMENT
When to go for surgical option?
If IOP elevation persists despite a patent laser iridotomy and
subsequent medical therapy
1)filtering surgery alone;
2)lens extraction alone, with or without
goniosynechialysis;
3) combined lens extraction with trabeculectomy;
4)or goniosynechialysis alone

MANAGEMENT OF FELLOW EYE
-Is initiated with medical treatment to reduce the
IOP, until the acute attack is resolved and
-A prophylactic iridotomy can be performed
--vigorous surveillance with periodic gonioscopic, disc, and
field assessments

Instructions to patient
Need for lifelong care even when iridotomy has
apparently‘cured’ their acute glaucoma.
 Once optic nerve damage is demonstrated after an
acute attack – i.e.PACG is manifest – iridotomy
won’t sufficiently control pressure, and
supplemental medical therapy or surgery is required.
 More frequent gonioscopy examination is required

Sequelae of acute PACG
Elevated IOP-
-may occur as a result of release of pigment and other debris,
-incomplete or sealed iridotomy,
-unrecognized plateau iris syndrome,
- inflammation,
-extensive PAS,
- corticosteroid administration

Visual field loss
-Typical glaucomatous visual field loss following an acute attack
of PACG occurs in the minority of eyes (about 40%)
-Nerve fiber layer loss can be demonstrated in most patients
whose attack’s duration was longer than 48 hours.

--Visually significant cataract
--Corneal damage
--Loss of endothelial cells
-- superficial corneal surface burns
- Corneal decompensation

Plateau iris
--Plateau iris refers On gonioscopy, that the iris assumes
a steep approach at its insertion before flattening
centrally
plateau iris is divided into two entities
1)‘plateau iris configuration’
2)‘plateau iris syndrome

On Gonioscopy,
The iris appears flat from the pupillary margin to the
periphery and creates a narrow angle recess and the potential
for angle closure
 Koeppe gonioscopy- double hump or S-sign of a peripherally
elevated roll of iris is seen ,where the forwardly positioned ciliary
processes prevent the peripheral iris from falling backward in
the supine position

many cases, plateau iris configuration is accompanied by
some degree of pupillary block, which exacerbates the
problem.
Therefore, it is often not possible on clinical grounds to
differentiate between a pupillary block PAC and a plateau iris
configuration embarrassing the angle until after an iridotomy
has been performed.
In conditions precipitated by pupillary block, iridotomy will
cause the iris to fall back and the peripheral chamber to
deepen; whereas in plateau iris, the peripheral angle remains
unchanged.
08/22/15

Patients with plateau iris configuration (and plateau iris
syndrome)
should be warned to avoid agents which have a potential
for dilating the pupil
These include any medication
with anticholinergic activity such as antihistamines,
phenothiazine
antianxiety agents, antidepressants, and drugs used for
incontinence and for diarrhea
08/22/15

-Plateau iris syndrome refers to the
development of angle closure either
spontaneously or after pharmacologic dilation
,in an eye with a patent iridotomy
angle closure occurs because the ciliary processes are rotated
forward.

presentation
- -Seen in young patients
- - Aged 30–40 years old
- Occurs equally among men and women
presents with or without symptoms occurring days, weeks,
months, or years after iridotomy or other intraocular surgery
If not diagnosed and treated properly, repeated episodes of
angle closure can progress to PAC or PACG: increasing
numbers of PAS, persistent elevation of IOP, and ultimate
glaucomatous damage

Differential diagnosis of plateau iris
syndrome
1)Extensive PAS due to any cause;
2)Imperforate or occluded iridotomy with persistent pupillary
block
3) Multiple cysts of the iris or ciliary body
4) Ciliary block glaucoma
5) Open-angle glaucoma with anatomically narrow angles(as
with increasing cataract formation); and the effect of chronic
topical corticosteroids or cycloplegic agents

treatment
Iridotomy.
Usually the first treatment for plateau iris syndrome
Peripheral iridoplasty –
If UBM imaging is available, it may be the initial
Treatment since iridotomy often does not change the
anterior Segment anatomy
 Miotic agents
can be tried to minimize pupillary dilation (e.g., pilcocarpine
1–2% 2–4 times a day)

Argon laser peripheral iridoplasty (gonioplasty)
- if the response to miotics is inadequate,
-or if the patient is unable or unwilling to use them longterm
 Filtration surgery,or glaucoma drainage devices
- If iridoplasty plus medical therapy cannot control
the IOP adequately

 Cataract extraction with IOL implant
-Effective in allowing the ciliary
processes to move posteriorly and improve
pressure control; but apposition has been
documented to persist even after lens
removal

Care to be taken after an iridotomy
done in plateau iris
 Eyes should be examined periodically for signs
of elevated IOP, peripheral synechia and
glaucomatous damage.
 Pupillary dilation should be undertaken with
care, even after iridotomy

•Primary cysts of the iris and ciliary body
usually arise from the
epithelial layers.
•The cysts can be single or multiple and
involve oneor both eyes
•In most cases the cysts remain stationary
and cause no harm.
•In rare cases the cysts are
sufficient in size and number
to lift the iris forward and cause
angle-closure glaucoma without
pupillary block.

MANAGEMENT
If the cysts causing angle closure are visible
-Punctured with an argon or Nd:YAG laser
If the cysts are not visible
-If UBM has identified their location it is possible
to puncture them by first doing a laser
iridotomy over the involved area

Medical therapy
- May be required after cyst puncture if extensive PAS are
present.
 Filtering surgery
-In a few cases where the cysts cannot be treated with a laser

PHACOMORPHIC GLAUCOMA
An abnormal lens either compromises
1)The lens–iris channel (pupillary block)
- can develop slowly with an age-related cataract or
-rapidly with a traumatic, swollen cataract.
2)Mechanically pushes the peripheral iris
forward into the angle structures

Usually unilateral and resembles PACG,
except
for the presence of
Intumescent lens and
A normal anterior chamber depth in
the fellow eye.

TREATMENT
Medical treatment is identical to that of PACG
The definitive treatment
-cataract extraction.
 Role of iridotomy
If cataract extraction is not possible
-because of extenuating circumstances
(e.g.,gravely ill patient )or must be delayed

Secondary
Angle Closure
Glaucomas 08/22/15

Secondary angle-closure
glaucoma
When a related or identifiable ophthalmic
condition is known to be present with the onset of angle
closure, it is referred to as secondary.
(replaces the category of‘combined (mixed)
mechanism glaucoma’)
Two different fundamental mechanisms:
1)Anterior pulling mechanism
2)Posterior pushing mechanism

1)Anterior pulling mechanism
With the anterior pulling
mechanism, the
peripheral iris is pulled forward
onto the trabecular
meshwork by the contraction
of a membrane,
inflammatory exudate, or
fibrous band

As the membrane, band, or inflammatory material contracts,
it acts like a zipper to
form permanent PAS, which can be spotty and irregular or
diffuse and quite regular.
 Pupillary block plays little or no role in this mechanism.
08/22/15

Neovascular Glaucoma
caused by a fibrovascular membrane that develops on the
surface of the iris and the angle.
 At first the membrane merely covers the angle structures,
but then it contracts to form PAS
Almost always associated with some form of ocular ischemia
Has also been refered to as –
thrombotic glaucoma,
hemorrhagic glaucoma,
diabetic hemorrhagic glaucoma,
congestive glaucoma,
and rubeotic glaucoma 08/22/15

important to distinguish the terms neovascular glaucoma and
rubeosis iridis
pathogenesis of neovascular glaucoma is that retinal ischemia
liberates angiogenic factors that diffuse forward and induce
new vessel formation on the iris and in the angle.
Capillary occlusion or ischemia appears to be the initiating
event in this process, similar to the production of an
angiogenic factors by solid tumors
08/22/15

Ocular vascular disease
Central retinal vein occlusion
Central retinal artery occlusion
Branch retinal vein occlusion
Branch retinal artery occlusion
Sturge-Weber syndrome with choroidal hemangioma
Leber’s miliary aneurysms
Sickle cell retinopathy
Diabetes mellitus
Extraocular disease
Carotid artery disease/ligation
Ocular ischemia
Aortic arch syndrome
Carotid-cavernous fistula
Giant cell arteritis
Pulseless disease
08/22/15

Assorted ocular diseases
Retinal detachment
Eales’ disease
Coats’ disease
Retinopathy of prematurity
Persistence and hyperplasia of the primary vitreous
Retinoschisis
Glaucoma
Open-angle
Angle-closure
Secondary
Norrie’s disease
Stickler’s syndrome 08/22/15

Trauma
Essential iris atrophy
Neurofibromatosis
Lupus erythematosus
Marfan’s syndrome
Recurrent hemorrhages
Vitreous wick syndrome
Ocular neoplasms
Malignant melanoma
Retinoblastoma
Optic nerve glioma associated with venous stasis
Metastatic carcinoma
Reticulum cell sarcoma
Medulloepithelioma
Squamous cell carcinoma conjunctiva
Angiomatosis retinae 08/22/15

Ocular inflammatory disease
Chronic uveitis
Endophthalmitis
Sympathetic ophthalmia
Syphilitic retinitis
Vogt-Koyanagi-Harada syndrome
Ocular therapy
Cataract excision (especially in diabetics)
Vitrectomy (especially in diabetics)
Retinal detachment surgery
Radiation
Laser coreoplasty
08/22/15

Diabetes mellitus is associated with about one-third of the
cases of neovascular glaucoma;
Central retinal vein occlusion with another third;
and a variety of conditions with the last third – with carotid
occlusive disease being the most common in the last group
08/22/15

Clinical Presentation
acute onset of pain, tearing, redness, and blurred vision some
cases (weeks to months) before the onset of the pain and
redness
ciliary injection, a hazy cornea from epithelial edema, a deep
anterior chamber with moderate flare, a hyphema, a small
pupil, and new vessels on the iris and in the angle.
Clinically the new vessels are first detected as small tufts at
the pupillary margin. Occasionally new vessels are seen first
in the angle if the tufts near the pupil are obscured by dark
iris pigment

The neovascularization progresses over the iris surface and
into the angle.The new vessels extend from the iris root
across the ciliary body and scleral spur, where they arborize
over the trabecular meshwork.
may be difficult to distinguish new vessels from normal iris
vessels
08/22/15

Normal iris vessels Neovascularization
Uniform size irregular size
Radial course Irregular course
Do not branch within the
iris
Branch frequently
Lie in the stroma Lie on the iris surface
08/22/15

08/22/15
Stages of neovascular glaucoma.
(A) Pre-glaucoma stage with new vessels appearing at pupillary
margin and in angle.
(B) Open-angle glaucoma stage with new vessels spreading and
fibrovascular tissue covering angle.
(C) Heavy neovascularization and extensive peripheral anterior
synechiae.
(D) Regression stage with angle sealed and vessels less visible.

AN ACUTE EPISODE IN NVG
Treated by
-Maximal IOP-reduction medical therapy,
-Atropine for relief and to maximally dilate the
pupil before iris mobility is lost,
-Corticosteroid.
-Panretinal photocoagulation or retinal
cryoablation to prevent total angle closure.

If the eye has good visual potential, and if the
neovascular membrane has regressed
-Filtering surgery can be successful, especially
when augmented with antimetabolites.
-Glaucoma drainage implants appear to be
Successful

Eyes with limited or no vision can often be made
comfortable using
-Cycloplegic agents
-Topical corticosteroids regardless of the
IOP.

Cyclodestructive procedures
May be appropriate if
the patient infirm for surgery, has too little
visual potential to procede with filtration
or tube surgery, or requires immediate pain relief.

Cyclocryotherapy is usually applied at
-60°C to -80°C, using a large-tip
probe with its anterior edge 2.5 mm
posterior to the limbus. Six to eight
60-second freezes are placed over
half of the Circumference of the
ciliary body.
Complications
 iridocyclitis, hypotony, pain, cataract, and
 phthisis bulbi.

Diode laser cyclodestruction
for patients with poor vision or poor visual prognosis and for
those for whom a glaucoma drainage device operation may
be inadvisable
Retrobulbar alcohol injections and enucleation are
appropriate treatments for eyes either with no useful vision
or with intractable
pain that does not respond to medical
therapy and ciliodestructive procedures

Goniophotocoagulation direct laser treatment to
new vessels in the angle it may be a useful
adjunct to panretinal photocoagulation in
certain situations.ountered when full
panretinal photocoagulation is not totally
successful in reducing the angiogenic stimulus.
Intravitreal bevacizumab-through pars plana

Iridocorneal endothelial
syndrome
Fundamental defect is in the corneal endothelium, that forms
a membrane over the anterior surface of the iris and the
angle structures.
this membrane on contracting , distorts the iris and closes
the angle
Clinical presentation
Clinical entities – 1) Progressive iris atrophy,
2)Chandler’s syndrome,
3)Cogan-Reese syndrome

Iridocorneal endothelial syndrome

early to mid adult life,
White> Blacks
Women> Men
The patients usually notice change in iris or pupil,
disturbance in their vision, or mild ocular discomfort.
Few familial cases, mostly medical and family hostories
unrevealing
08/22/15

Progressive (essential) iris atrophy - corectopia and
ectopion uvea(The synechiae lift the iris off the surface of the
lens
 The iris dissolution begins as a patchy disappearance of the
stroma and progresses to full-thickness holes
‘stretch holes’- in quadrants away from pupillary
displacement due to traction
‘melt holes’- without correctopia and ischaemic in nature

Advanced essential iris atrophy with
polycoria.

Chandler’s syndrome
Chandler’s syndrome is the most common variant of
the ICE
- Marked corneal changes
- Corectopia is minimal or absent.
The endothelium has a hammered silver appearance.
In contrast to the marked corneal changes, the iris involvement is
generally
mild and limited to superficial stromal dissolution
- Peripheral anterior synechiae form, but they
are not as diffuse and do not extend as far
anteriorly as in progressive iris atrophy. For this
reason glaucoma is often mild

The Cogan-Reese, or iris nevus,
syndrome

Occurrence of pigmented lesions of the iris
Pedunculated iris nodules
diffuse pigmented lesions
Some eyes have both
08/22/15

treatment
Hypertonic solutions or soft contact lenses
- If corneal edema produces pain or reduced vision if IOP is
reduced eventually require
- penetrating keratoplasty
 Goniotomy
 Filtering surgery or glaucoma drainage devices
are often required to control glaucoma

Posterior polymorphous
dystrophy
Glaucoma occurs in 10–15% of patients
-presents with corneal edema, iris atrophy, mild corectopia,
and iridocorneal adhesions
-maintain good vision throughout lives
-cluster or linear arrangement of vesicles in
the posterior cornea surrounded by a gray haze

treatment
Most cases of posterior polymorphous dystrophy require no
treatment.
Eyes with glaucoma are treated with medication and then
filtering surgery as necessary

Epithelial downgrowth
Epithelial downgrowth (also called epithelial ingrowth)
occurs when an epithelial membrane enters an eye through a
wound and then proliferates over the corneal endothelium,
trabecular meshwork,anterior iris surface, and vitreous face

Cataract surgery is the most common cause of epithelial
downgrowth.
 also been reported after penetrating
keratoplasty, glaucoma surgery, penetrating
trauma, and unsuccessful removal of epithelial
cysts of the anterior segment

presentation
. evidence of current or past wound leak and are hypotonic if
the fistula is still functional.
- a grayish white membrane with a scalloped, thickened
leading edge on the posterosuperior corneal surface.The
cornea overlying the membrane may be edematous, and the
iris may be drawn up to the old wound or incision.

diagnosis
Clinically on examination
Involvement of the iris is dramatically demonstrated when it
is treated with large, low-energy argon laser burns (200–500
m, 100–400 mW, 0.1 second), which turn
the epithelial membrane white. (Normal iris
does not respond this way.)
Aqueous humor can be aspirated, passed through
a Millipore filter, and then examined to identify
epithelial cells

treatment
The treatment of epithelial downgrowth is often difficult and
unrewarding.
The corneal portion of the membrane can then be destroyed
with cryotherapy or chemical cauterization.
The affected iris can be excised, and cryotherapy can be
applied to any remaining membrane on the ciliary body and
retina

alternative approach is to do an en-bloc excision of all involved
tissues.

Fibrovascular ingrowth
Fibrovascular tissue can grow into an eye if there is an open
wound after penetrating trauma or surgery
occurs more frequently if the trauma or surgery is associated
with hemorrhage, inflammation, or incarcerated
tissue
Fibrovascular ingrowth usually causes glaucoma when the
membrane covers the angle and then contracts to form
peripheral anterior synechiae
Other factors contributing to the glaucoma include uveitis or
pupillary block.

treatment
 Medical therapy.
 In some cases posterior glaucoma drainage
device implantation or cyclophotocoagulation

Flat anterior chamber
A flat anterior chamber after penetrating trauma or surgery
can lead to the formation of PAS and secondary angle-closure
glaucoma without pupillary block
In most of the studies secondary angle-closure glaucoma was
common if the anterior chamber was flat for 5 days or longer

TREATMENT
Following re-formation of a flat anterior chamber, the
residual secondary angle-closure glaucoma is treated with
standard medical therapy.

08/22/15
Malignan
t
Glaucoma
Choroidal
Detachme
nt
Pupillary
Block
Suprachor
oidal
Hemorrha
ge
Wound
Leak
Central
anterior
chamber
Flat or
shallow
Shallow May be
normal
Flat or
shallow
Flat or
shallow
Intraocular
pressure
Normal or
elevated
Low Normal or
elevated
Normal or
elevated
Low
Fundus
appearance
Usually
normal
Large,
smooth,
brown
mass
Usually
normal
Dark
brown or
dark
red
elevation
Choroidals
may be
present
Suprachoro
idal fluid
Absent Present Absent Present Absent
Relief by
drainageof
suprachoroi
No Yes No Yes No

08/22/15
Malignan
t
Glaucoma
Choroidal
Detachme
nt
Pupillary
Block
Suprachor
oidal
Hemorrha
ge
Wound
Leak
Relief by
iridectomy
No Yes No Yes No
Patent
iridectomy
Yes Yes No Yes Yes
Onset Usually
within
days,
but may be
months
Usually
within
first week
Anytime Immediatel
y or within
first few
days
Usually
within
first few
days but
may be
late with
adjunctive
antimetabo
lites

Iridoschisis
usually bilateral and tends to involve the lower iris quadrants
Glaucoma occurs in about 50% of the patients and is usually
related to the development of PAS in the region of the iris
strands.
Elevated IOP and iridoschisis are usually
managed by medical therapy.
 A laser iridotomy should be
performed( If pupillary block)

INFLAMMATION
Inflammation can produce glaucoma through a variety of
mechanisms,
 Including increased viscosity of the aqueous humor,
Obstruction of the trabecular meshwork by inflammatory
cells and debris,
Scarring of the outflow channels ,
Elevated episcleral venous pressure,
Forward displacement of the lens–iris diaphragm,
Pupillary block from posterior synechiae

PATHOGENESIS
1)Peripheral anterior synechiae
2)Posterior synechiae
3)Forward rotation of ciliary body

Management
Pupillary dilatation-
(i) gives comfort and rest to the eye by relieving spasm of iris
sphincter and ciliary muscle,
(ii) prevents the formation of synechia and may break the
already formed synechia,
(iii) reduces exudation by decreasing hyperaemia and vascular
permeability and
(iv) increases the blood supply to anterior uvea by relieving
pressure on the anterior ciliary arteries

Corticosteroids
Immunosuppresive theraphy-
Antiglaucoma medical theraphy
Surgical theraphy
1)Iridotomy
2)Argon laser trabeculoplasty
3)Filtration surgery
4)Antifibrotic filtration surgery
5)Cyclodestructive surgery

Posterior pushing (or
rotational)
mechanism
The peripheral iris is displaced forward by the lens, vitreous, or ciliary body
The posterior pushing mechanism is often accompanied by swelling and
anterior rotation of
the ciliary body, which further acts to close the angle.

the role of the ciliary body in ‘pushing’
forms of secondary angle-closure
glaucoma
1) When the anterior uveal tract swells from
inflammation or vascular congestion, the
ciliary ring is narrowed, which reduces
tension on the zonules, permits the lens to
come forward, and displaces the peripheral
iris.

2)When the ciliary body swells, it also rotates forward about
its attachment to the scleral spur, which again loosens the
Zonules and displaces the root of the iris
3) Ciliary body swelling is often accompanied by the
acumulation of suprachoroidal and supraciliary
fluid, which further rotates the ciliary body and
iris root into the angle

Ciliary block glaucoma
(aqueous misdirection,hyaloid block glaucoma
and posterior aqueous entrapment)
-commonly complication of a filtering procedure in
eyes with pre-existing angle-closure glaucoma or
shallow anterior chambers(2–4% of patients )
- ‘Triggers’
 laser iridotomy,
 miotic usage,
 infectious endophthalmitis,
 retinal conditions,
 hyperplastic ciliary processes

OCULAR MANIFESTATIONS
- Red, painful eye is most commonly seen after surgery for
acute angle-closure glaucoma.
-The condition usually occurs immediately after surgery but
may occur during surgery or months to years later;
-Its development often corresponds to the cessation of
cycloplegic therapy or the institution of miotic drops

-The key is that the IOP is elevated and the
anterior chamber is axially shallow without iris
Bombe.
-A high index of suspicion is necessary to make
the appropriate diagnosis, since initially the IOP
may not be elevated much.

DIAGNOSIS
 Patent iridectomy must be established (to rule out pupillary block)
High-resolution ultrasound biomicroscopy
It reveals anterior rotation of the ciliary body against the
peripheral iris and forward displacement of the posterior
chamber intraocular lens, as well as a shallow central anterior
chamber, all of which are reversible

DIFFERENTIAL DIAGNOSIS
1) Pupillary block-patent iridectomy will rule out
2) Suprachoroidal hemorrage - USG or
Ophthalmoscopy reveal the presence of single or
multiple elevations of choroid
3)Serous choroidal effusion

treatment
 To move the lens-iris diaphragm back and relax the
ciliary muscle
-Mydriatics and Cycloplegics
 To decrease aqueous production
-Topical -blockers, oral or topical carbonic anhydraseβ
inhibitors, and -agonistsα

FELLOW EYE
If a narrow angle is present in the fellow eye, a
laser peripheral iridectomy is performed before
any other surgical procedures

Nd:YAG) laser may be used in aphakic and
pseudophakic patients
Pars plana vitrectomy
When medical or laser therapy fails, or in phakic eyes for
which laser treatment is not a good option,

Intraocular tumors
Ocular malignant melanoma is frequently associated with
glaucoma
Mechanisms,
1) Direct extension into the trabecular meshwork
2) Seeding of tumor cells into the outflow
channels
3)Obstruction of the meshwork by pigment
or pigment-laden macrophages,
4)Neovascularization,
5)PAS,iridocyclitis, and hyphema

Nanophthalmos
 Refers to an eye that is normal in shape
but small in size.
 Ratio of the volume of the lens
to the volume of the eye is 10–25% instead of
the normal 3–4%.

FACTORS IN DEVLOPMENT OF
GLAUCOMA IN NANOPHTHALMOS
1) Little anatomic reserve
2) Development of a choroidal effusion.(as thick
sclera obstructing flow through the vortex veins)
 Frequently develop angle-closure glaucoma in
the fourth to sixth decades of life.

management
Laser iridotomy-if narrowing of angle present
Laser gonioplasty-if angle not does not deepen on laser
iridotomy
Antiglaucoma theraphy
Unroofing of at least two vortex veins to relieve venous
obstruction

POSTERIOR SCLERITIS
Posterior scleritis causes
 Choroidal effusion,
 Swelling, and anterior rotation
of the ciliary body, as well as secondary angle-
closure glaucoma without pupillary block.

Management-
Antiglaucoma theraphy to control IOP
Systemic NSAIDS
Topical and systemic corticosteroids

Central retinal vein occlusion
 It interferes with the venous drainage of the uveal tract,
causing swelling and anterior rotation of the ciliary body.
 It also causes transudation of fluid into the
choroid, retina, and vitreous.The fluid acts like
an acutely developing posterior mass that
Displaces the lens–iris diaphragm causing
glaucoma

Management
Antiglaucoma theraphy
Laser iridotomy if pupillary block present
Laser gonioplasty
If ischemia is present –retinal ablation should be performed

Scleral buckling procedure
After a scleral buckling procedure, it is common for the
anterior chamber to be shallow for a few days.
In 1–2% of eyes, this condition progresses to angle-closure
glaucoma without pupillary
block.
Most cases of postscleral buckling angle closure
glaucoma can be treated medically until the
anterior chamber deepens
spontaneously

Panretinal photocoagulation
Photocoagulation may break the blood–ocular barriers and
cause a transudation of fluid into the retina, choroid, and
vitreous
Most individuals with angle closure after PRP
are asymptomatic,although an occasional
patient complains of ocular discomfort or headache
Most cases managed medically

Retinopathy of prematurity
Mechanisms include
 Neovascularization,
 Pupillary block, and
 Pushing forward of the lens–iris diaphragm

POSTERIOR PUSHING MECHANISM
WITH PUPILLARY BLOCK-dislocated
lens

Microspherophakia
-Pupillary block and glaucoma occur through one of two
mechanisms: either the lens dislocates into the pupil and
anterior chamber or long zonules allow the lens to come into
pupil.

y
08/22/15
# Becker-Shaffer's Diagnosis and
Therapy of the Glaucomas; 8th Ed.
# Shields Textbook of Glaucoma; 2nd Ed.
# American Academy of Ophthalmology
BCSC. Section 10; 2011-2012
# Parson's Diseases of the Eye; 21st Ed.
# Comprehensive Ophthalmology by A K
Khurana; 4th Ed.

Angle closure glaucoma

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