GLAUCOM

A
 DEFINITION OF GLAUCOMA

Glaucoma is an optic disc neuropathy which is characterized

by:
High intra ocular pressure (IOP) > 21 mmHg,
Optic nerve fibers death optic disc damage,
Progressive visual field defect,
Glaucoma is the most common cause of blindness
worldwide and is the second major cause of blindness
in Indonesia

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 INCIDENCE

Primary glaucoma is:

hereditary
female > male
especially at age > 40 years

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 INCIDENCE

Congenital glaucoma since in the intrauterine

Infantile glaucoma after birth until 2 years
Juvenile glaucoma age 10 - 15 years
Secondary glaucoma: glaucoma as a complication
from other eye disease

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 AQUEOUS HUMOR SECRETION

80% is secreted by non pigmented ciliary

epithelium via active metabolic process that
depends on a number of enzymatic systems
(carbonic anhydrase enzyme),

20% is produced by passive processes as

ultrafiltration and diffusion.

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AQUEOUS OUTFLOW

AH fills posterior chamber pupil

Trabecular route 90 % anterior chamber

Schlemms canal uveoscleral route (10%)

suprachoroidal space ciliary body

leaves the eye
through episcleral vein venous system in the ciliary 6body
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 AQUEOUS
OUTFLOW

a. Uveal
meshwork
b. Corneoscleral
meshwork
c. Schwalbes line
d. Schlemms canal
e. Collector
channels
f. Ciliary body
g. Scleral spur
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AQUEOUS OUTFLOWS,
INFLUENCED BY:

High intra ocular pressure (IOP),

High episcleral pressure,
Aqueous viscosity: exudate, blood cell,
Ciliary block, pupillary block, posterior synechia,
Narrow / closed anterior chamber angle,
Narrowing of trabecular meshwork pore,
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Macrophage, lens cell at the trabecular
meshwork.
 TRABECULAR
MESHWORK

The TM is located at the anterior chamber angle, which consists:

Descemet membrane Schwalbes line
Sclera scleral spur
Iris iris processus
Ciliary body angle recess

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 INTRA OCULAR PRESSURE (IOP)

Normal IOP < 21 mm Hg,

IOP > 21 mm Hg glaucoma suspect,
Diurnal fluctuation of IOP in 24 hours:
IOP higher in the morning
IOP lower in the afternoon and evening
Ocular hypertension: IOP > 21 mmHg without any
nerve fiber damage,
Normal tension glaucoma: normal IOP, but
presenting glaucomatous signs.
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 PATHOGENESIS OF
GLAUCOMATOUS DAMAGE

There are two current theories:

The indirect ischaemic theory: IOP -- nerve fiber death + interfering micro
circulation of the optic disc,
Direct mechanical theory: IOP -- damage on retinal nerve fiber at the optic disc.

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CLASSIFICATION OF THE GLAUCOMAS

According to:
Outflow impairment: open angle and angle closure glaucoma,
contributing factors to IOP : primary and secondary glaucoma,
Age: congenital, infantile, juvenile, adult.

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 PRIMARY GLAUCOMAS

High IOP is not associated with any ocular disorder

Open angle
Angle closure
Congenital (developmental)

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 SECONDARY
GLAUCOMA

Aqueous outflow alters by ocular / non ocular disorders

IOP :
Secondary open angle glaucoma: pretrabecular,
trabecular and post-trabecular,
Secondary angle closure glaucoma caused by
apposition between the peripheral iris and11/16/17
trabeculum,
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Pathogenesis: anterior forces / posterior forces

 TONOMETRY

Two main methods of measuring IOP:

applanation force to flatten the cornea
indentation force to indent the cornea
The main types of tonometer:
The Schiotz tonometer uses a plunger with a preset weight to indent the cornea.
The amount of indentation is converted into mmHg by use of Friedenwald tables.

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 TONOMETRY

The main types of tonometer:

Goldmann tonometer consists of double prism with 3.06 mm
in diameter, applanation, more accurate,
Perkins tonometer, hand held, applanation,
The air puff tonometer, non contact, applanation, jet of air to
flatten the cornea.
Tono-pen
Gas Tonometer
Electrical Tonometer
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SCHIOTZ TONOMETER

Portable, simple, low cost,

Measure the depth of indentation of
cornea by a plunger with
specific weight (5 gr; 7,5 gr ; 10 gr)
The indentation represented in
Schiotz scale is converted into
mmHg by Freidenwald table,
Low accuracy because it is
influenced by ocular rigidity (high
myop, DM, corneal leucoma). 11/16/17 17
 GOLDMANNS
APPLANATION TONOMETER

More accurate, not influenced by ocular rigidity

The foot plate is smaller (3.06 mm)
Disadvantages: cannot be applied to
Corneal edema
Keratitis, corneal ulcer
Keratokonus
High astigmatism

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 TONOGRAPHY

To estimate outflow facility of HA,

Principle: to express the fluid flow from the eye by continuous pressing to the
eye
Place Schiotz tonometer for 2-4 minutes,
Compare IOP at 0 to 4 minutes outflow facility (C),
Normal C > 0.18.

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 PROVOCATION TEST

Water drinking test, dark room test, midriatic test, steroid test,
Positive if IOP at the end of the tests are more than 8 mmHg,
Indications:
Narrow / closed angle glaucoma
Normal tension glaucoma
Bias IOP

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 GONIOSCOPY

Three main purposes of gonioscopy:

To Identify the abnormal angle structure,
To Estimate the width of the chamber angle,
To Visualize the angle during these following procedures: goniotomy, laser
trabeculoplasty.

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IDENTIFICATION OF ANGLE
STRUCTURES

Trabecular meshwork has a ground glass

Schwalbes
appearance line (an from
stretching opaque line) is a peripheral
Schwalbes line to scleral
termination of Descemet membrane,
spur.
Consists of two parts:
The anterior: nonfunctional, non pigmented
part, whitish color,
The posterior: functional, pigmented part, 11/16/17 22
greyish-blue translucent.
IDENTIFICATION OF ANGLE
STRUCTURES

Schlemms canal: slightly darker line,

behind the posterior trabeculum,
Scleral spurs: anterior of sclera, narrow, dense, often
shiny,
Ciliarywhitish
body stands
band. behind the scleral
As a landmark for spur
laseras dull
trabeculoplasty.
brown band. The width depends on iris insertion.
Curve of the corner at the margin of the ciliary body
Iris processes
Iris processes, small extension of the anterior surface 11/16/17 23
\ of the iris, inserted at the level of scleral spur.
ANGLE CLASSIFICATION BY
SHAFFER

Grade IV: 45 degrees angle

III : 20 - 25 degrees angle
II : 20 degrees angle closed
I : 10 degrees angle closed
Grade 0 : closed angle, iridocorneal contact.

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 OPHTHALMOSCOPY OF THE OPTIC DISC

1.2 million axons passes across the retina and enter the
optic disc,
Fibers from the macula papillomacular bundle, straight
to the optic disc, most resistant,
Fibers from temporal of macula an arcuate path around
the papillomacular bundle supero and inferotemporal
of the optic disc, vulnerable to glaucomatous damage.

Nerve fiber layer

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anatomy
OPHTHALMOSCOPY OF THE OPTIC
DISC

Normal nerve fiber layer Diffuse nerve fiber atrophy

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 OPHTHALMOSCOPY OF THE
OPTIC DISC

The optic cup, pale depression in the center of the optic

cup, absent of nerve fiber,
The neuroretinal rim, tissue between the outer edge of the
cup and the outer margin of the disc, the color is pinkish
orange, uniform width, contains nerve fibers,
Nerve fibers death thinning of retinal rim,
High IOP posterior bowing of lamina cribrosa,
nasalisation of central retinal vessels.

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OPHTHALMOSCOPY OF THE OPTIC DISC

The cup-disc ratio: fraction of vertical and horizontal diameter cup and
diameter of the disc, normal c/d ratio is 0.3 or less.

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OPTIC DISC CHANGES IN GLAUCOMA

Normal disc with small cup 11/16/17 29

 OPTIC DISC CHANGES IN GLAUCOMA

Cup and disc ratio > 0.6,

Peripapillary atrophy at temporal region,
Splinter-shaped hemorrhage on the disc margin.

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OPTIC DISC CHANGES IN GLAUCOMA

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 NORMAL VISUAL FIELD
EXAMINATION

Nasally : 60 degrees
Temporally : 95 degrees
Superiorly : 50 degrees
Inferiorly : 70 degrees
The blind spot is located temporally 10-20 degrees
Visual field is an island of vision surrounded by the sea of
darkness, the sharpest is at the top of the island.

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 VISUAL FIELDS IN
GLAUCOMA

Baring of the blind spot

Localized paracentral scotoma at 10 - 20 degrees of
fixation at superior and inferior quadrant extension to
the blind spot Byerrum scotoma ring scotoma with
nasal step of Roenne,

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 VISUAL FIELDS IN GLAUCOMA

Peripheral scotoma that spreads and coalesces to the

paracentral scotoma
Leaving central island and accompanying temporal island,
even if the central vision is still normal
Temporal island total blindness

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 CLASSIFICATION

Primary open-angle glaucoma

Secondary open-angle glaucoma
Primary closed-angle glaucoma
Secondary closed-angle glaucoma
Primary congenital glaucoma
Secondary congenital glaucoma

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 PRIMARY OPEN-ANGLE
GLAUCOMA (SIMPLE
GLAUCOMA)

Bilaterally, not necessarily symmetrical,

absence of secondary causes of high IOP,
Glaucomatous optic nerve damage,
Open and normal angle, IOP > 21 mmHg,
Adult onset, hereditary, steroid
responsiveness,
Glaucomatous visual field defects, central
tunnel vision, 11/16/17 36

Minimal clinical signs.

 MANAGEMENT OF PRIMARY OPEN ANGLE
GLAUCOMA

Initial therapy is usually medical, except in

advanced cases,
Argon laser trabeculoplasty (ALT) if IOP is
uncontrolled despite maximal tolerated medical
therapy,
Trabeculectomy with / without antimetabolic drug
in refractory glaucoma,
Artificial filtering shunt: Achmed valve, Molteno
tube, Krupin- Denver valve.
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 SURGICAL INDICATIONS FOR
SIMPLE GLAUCOMA

Uncontrolled IOP by maximal medical treatment

Progressive disc damage and visual field defect
Drugs intolerance
Unable to buy the drugs
Poor compliance
Unable to do the regular control

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PRIMARY CLOSED-
ANGLE GLAUCOMA

Obstruction of aqueous outflow as a result of closure of

the angle by the peripheral iris
Anatomically predisposed, bilateral,
Predisposition:
Crowded anterior segment
Relatively anterior location iris lens diaphragm,
Shallow anterior chamber,
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Narrow entrance to the chamber angle.
 PACG STAGE

Five overlapping stages:

Latent
Intermittent (sub acute)
Acute (congestive and post congestive)
Chronic
Absolute

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LATENT ANGLE-CLOSURE GLAUCOMA

Shallow anterior chamber, convex-shape iris lens diaphragm, close iris to

cornea, normal IOP, occludable angle,
Treatment:
Good fellow eye without treatment, follow up,
PACG fellow eye laser iridotomy.

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 INTERMITTENT
ANGLE-CLOSURE GLAUCOMA

Rapid partial closure anterior chamber angle and reopening of the angle after
some rest,
Precipitating factors: physiological mydriasis, watching TV in dark room, prone
position, reading, sewing, emotion, stress,
Transient blurring of vision, halo, headache,
Recovery after some rest.

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 ACUTE CONGESTIVE
ANGLE-CLOSURE GLAUCOMA

Presentation:
Rapidly progressive impairment of vision,
sometimes the vision 1/300 0,
Eye ache and frontal headache,
Congestion, nausea, vomiting.

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 ACUTE CONGESTIVE
ANGLE-CLOSURE GLAUCOMA

Examination
Ciliary and conjunctival injection
IOP > 50 mmHg, dilated pupil,
unreactive.
Cornea: epithelial edema, KP(+), vesicle
Ant chamber: shallow PAS, flare / cell
(+),
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 ACUTE CONGESTIVE
ANGLE-CLOSURE GLAUCOMA

Wide pupil, slow / negative light reflex,

Papilla edema, retinal edema,

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 ACUTE CONGESTIVE
ANGLE-CLOSURE GLAUCOMA

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 ACUTE CONGESTIVE
ANGLE-CLOSURE GLAUCOMA

Differential diagnosis:
Red eyes:
conjunctivitis, iridocyclitis
Silent eyes:
simple glaucoma, ocular hypertension
Glaucomatous visual field defect:
anomaly of the optic nerve and retina
Papillary atrophy:
anomaly at optic nerve
Congenital megalocornea without high IOP
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 ACUTE CONGESTIVE
ANGLE-CLOSURE GLAUCOMA

Treatment:
Immediately decrease IOP with maximal drugs,
Wait for 24 hours evaluation,
Normal IOP, deep AC, open angle iridectomy,
High IOP, permanent AC closure > 50% trabeculectomy,
The fellow eye: preventive iridectomy.

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 POSTCONGESTIVE
ANGLE-CLOSURE GLAUCOMA

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 CHRONIC CLOSED-ANGLE GLAUCOMA

Clinical features of chronic CAG are similar as

POAG except gonioscopy of the angle is closed,
There are three mechanism of CCAG:
Creeping PAS laser iridotomy / trabeculectomy
After intermittent and laser iridotomy drug >
Combination of POAG with narrow angle laser
iridotomy + medical trabeculectomy
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 CHRONIC CLOSED-ANGLE GLAUCOMA

Signs and therapy are similar as simple glaucoma:

Trabeculectomy,
Laser iridoplasty to make an angle,
Argon Laser Trabeculopasty (ALT)

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 PRIMARY CONGENITAL GLAUCOMA

65% of patients are male, 1: 10.000,

Inheritance is autosomal recessive, bilateral,
Maldevelopment of the trabeculum and iridotrabecular
junction, abscent of angle recess, trabeculodysgenesis,
The iris insertion can be flat or concave,
Poor prognosis.

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 PRIMARY CONGENITAL GLAUCOMA

Clinical signs:
Depends on the age of the onset and the level of IOP,
According to the age of the onset there are 3 types:
True congenital glaucoma (40%). IOP elevated since in the intrauterine buphthalmos,
Infantile glaucoma (55%) manifesting after birth,
Juvenile glaucoma: IOP at 10-35 years of age, with clinical manifestation same as
POAG.

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 PRIMARY
CONGENITAL
GLAUCOMA

Examinations:
Corneal haze, lacrimation, photophobia and
blepharospasm,
Buphthalmos if IOP before the age of 3 usually
associated with axial myop, subluxated lens,
Break of Descemet membrane, endothelial
decompensation permanent stromal edema,
Reversible glaucomatous cupping.
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 PRIMARY CONGENITAL GLAUCOMA

Treatments:
Initial drug treatment,
Goniotomy if cornea is still clear,
Trabeculotomy at corneal clouding,
Trabeculectomy and trabeculotomy,
Trabeculectomy with antimetabolic agent,
--Outcome of the operation is poor.
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 SECONDARY GLAUCOMA

Inflammation and residual inflammation of the uveal tissue: iridocyclitis,

posterior synechia,
Immature cataract, hipermature cataract,
Lens luxation, lens subluxation,
Ischemic retina,
Sub choroidal bleeding,
Congenital anomaly of the eye

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 SECONDARY GLAUCOMA

Pigmentary gl. - Neovascular gl.

Inflammatory gl. - Phacolytic glaucoma
Red cell gl. - Ghost cell glaucoma
Angle recession glaucoma
Iridocorneal endothelial syndrome
Pseudoexfoliative glaucoma

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 THERAPY

Nerve fiber damage caused by glaucoma is

irreversible,
Principle of the therapy is to decrease IOP
medically or surgically to maintain the current
condition,
The purpose of decreasing the IOP is to reduce
progressivity of the nerve fiber damage and visual
field defect,
Early findings.
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 INDICATIONS OF MEDICAL TREATMENT

Simple glaucoma
Acute / chronic closed angle glaucoma
Maintain the diurnal IOP
Lower IOP before operation

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 REDUCING AQUEOUS PRODUCTION

Carbonic anhydrase inhibitor

acetazolamide 250 mg qid orally,
dorzolamide eye drop tid,
Beta-adrenergic antagonist:
beta-blocker (timolol maleat 0.25-0.5%) bid,
betaxolol 0.25% - 0.5% bid.
Adrenergic agonist:
depefeprine 0.5% - 2% bid.

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 OTHER ANTIGLAUCOMA DRUGS

Parasympathomimetic agents:
pilocarpin eye drop 2-4%, 2-6 x / day
carbachol 0.75% used after cataract operation
Increase the latanoprost uveoscleral flow
Hyperosmotic fluid
glycerol 50% 1-2 ml/kg body weight, drink all at once,
manitol 20% swift infusion preoperative, 1.5-3 ml/kg body
weight.
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 SURGICAL TREATMENT

Peripheral iridectomy:
Acute attack glaucoma, with good trabecular meshwork,
Preventive treatment from acute attack for the fellow eye.
Trabeculectomy for all types of glaucoma,
Goniotomy for congenital glaucoma if the cornea is
still clear,
Trabeculotomy for congenital glaucoma if the cornea
is edema.
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 SURGICAL TREATMENT

Treatment for absolute glaucoma:

cyclocryo coagulation destroys the ciliary body to decrease HA production,
enucleation if all treatment is not successful.
Laser treatment:
iridotomy
gonioplasty
trabeculoplasty

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 GOOD PROGNOSIS

Early and right diagnosis,

Adequate control of IOP by medical / surgical treatment,
Compliance of the patients to check their IOP and use medical treatment,
Case finding among glaucoma family.

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Thank
you
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