COLSED ANGLE GLAUCOMA

9/4/2015

ANIL REGMI
Medical student
NGMC

Glaucoma:

It is the chronic, progressive optic

neuropathy caused by a group of ocular
condition, which lead to damage of optic
nerve with loss of visual function. Most
common risk factor is raised IOP.

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pathogenesis:
1. mechanical change due to raised IOP:
Raised IOP

Mechanical pressure to lamina cribrosa

Backward displacement and compaction of laminar

plates

Narrows the opening through which axon passes

Damage the nerve fibre bundle

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2. Vascular perfusion:
Raised IOP

Mechanical pressure on lamina cribrosa

Decrease capillary blood flow

Decrease perfusion to the optic nerve head

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CLOSE ANGLE GLAUCOMA

It includes the spectrum of condition in

which peripheral iris moves forward to block
the openings of the trabecular meshwork in
an occludable angle causing rise in intra
ocular pressure.

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Epidemiology:
Common in Asians and Eskimos
Uncommon in African and Caucasians
Age: 4th to 5th decade
Sex: female: male = 4: 1
First degree relative are at increased risk

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Predisposing factors:
1.

Anatomical:

Short eye
Smaller corneal diameter
Shallow anterior chamber
Relative anterior positioning of lens-iris and
diaphragm.

.
.
.

2. Physiological:
.
.

Dim illumination
Emotional stress

3. Pharmacological :
.

Use of mydriatic drug like atropine, tropicamide

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Clinical features:
Generally bilateral though the involvement
of two eye is often asymmetrical.
Number of clinical subtypes have been
described.

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1. Primary angle closure

glaucoma suspect
Shallow anterior chamber with occludable
angle (angle recess < 20 )
No other gonioscopic abnormalities are
present.
Provocative test:
dark room test : IOP rise by 8mm Hg.

mydriatic provocative test : 2%

pilocarpine
No any clinical symptoms.

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2. Subacute or intermittent
primary angle closure glaucoma
Shallow anterior chamber with occludable
angle (angle recess < 20 )
IOP rise suddenly while reading in dim light,
watching the film in darkened room for
short period followed by spontaneous
resolution of pupillary block, which is
possible due to physiological myosis, which
occur during sleep.

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Patient complains:
Unilateral headache or brow ache.
Blurring of vision
Unbroken colored halos around light during
episodes.
Between the recurrent attacks, eyes are
free of symptoms and only sign of narrow
angle recess, clumping of pigment in angle,
or occasional peripheral anterior synechiae.

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3. Acute Primary angle closure

glaucoma
It is caused by sudden occlusion of entire
angle with resultant acute rise in IOP to
extremely high level.
Patient complains:
Severe unilateral headache.
Diminution of vision in red eye.
Nausea may be frequently associated.

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On examination:
Corneal edema
Shallow anterior chamber
Iris bombe with vertically oval.
Mid dilated pupil.
After resolution of corneal edema,
gonioscopically closed angle can be seen
i.e. extensive irido-corneal synechiae and
optic disc may be found to be either
hyperemic or normal.

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4. Chronic primary angle

closure glaucoma:
It is said if IOP is chronically raised in eyes if
synechial closure over at least 180 degree.
Change in optic nerve head or visual field may or
may not be present.
Causes:
a. repeated subacute attacks of primary angleclosure glaucoma

Extensive synechial closure

Chronoically elevated IOP

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b. acute primary angle closure glaucoma, which

persists more than few hours

Irreversible synechial closure of angle and

permanent damage to trabecular meshwork.
c.

asymptomatic or creeping angle closure

Synechial closure occurs within depth of angle.

Progressively involves the entire angle.

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Treatment:
Acute congestive glaucoma is the
emergency condition and need to be
controlled immediately.
Management is essentially surgical.
Medical therapy is given as an emergency
and temporary measure in order to
decrease IOP before ready for operation.

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Medical therapy:
1. systemic hyperosmotics to decrease IOP given
as soon as diagnosed.
i.v. Mannitol (1gm/kg body wt)
Oral glycerol (1.5gm/kg)
2. tab. Acetazolmide
3. Analgesics and antiemetics
4. Pilocarpine eyedrops started after IOP is bit
lowered by hyperosmolar agents.
5. Beta-blocker 0.5% Timolol BD
6. Corticosteroid eyedrop. E.g. dexamethasone 34times/day to reduce inflammation.
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Surgical treatment:
Peripheral laser iridotomy:
Indications:
. Peripheral anterior synechiae: <50% of
angle
. Prophylactic
. Bypass pupillary block
. A hole is made in peripheral iris allowing
the aqueous to drain directly from posterior
chamber to region of trabecular meshwork.
. Laser iridotomy : non invasive method
1.

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2. Trabeculectomy (filtration surgery)

Indication:
IOP not controlled within 12 hours of
vigorous medical therapy
Peripheral anterior synechiae: >50% of
angle
It provides an alternative to angle of
drainage of aqueous from anterior chamber
into subconjunctival space.

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MCQs
1. All of following anatomical change
predispose to primary angle closure
glaucoma expect?
a. Small cornea
b. Flat cornea
c. Shallow anterior chamber
d. Short axial length of eyeball

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2. All are the feature of acute attack of

primary narrow angle glaucoma expect?
a. IOP raised up to 40-70mm Hg
b. Eye red, painful, and tender
c. Disc shows glaucomatous cupping
d. Fellow eye also shows shallow anterior
chamber

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3. The most common provocative test for

angle closure glaucoma is:
a. Water drink test
b. Dark room test
c. Mydriatic-miotic test
d. Homatropine mydriatic test

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PBQs
1.

a)
b)
c)

A 55 years old patient with moderate

hypermetropia in both eyes presented in
emergency department with sudden painful
diminution of vision. O/E, her right eye was
red with high IOP and shallow anterior
chamber and her left eye also had shallow
anterior chamber.
What is your most likely diagnosis?
Write about the treatment?
Write briefly about the aqueous secretion and
drainage?
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THANK YOU
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