Glaucoma

Dr. Sugiarti Kadarhartono, SpMK

Dr. Sutarya Enus, SpMK
Dr. Andika Prahasta, SpM

Definition of Glaucoma
Glaucoma is an optic disc neuropathy
which is characterized by:

High intra ocular pressure (IOP) > 21 mHg,

Optic nerve fibers death optic disc damage,
Progressive visual field defect,
Cause of third permanent blindness.

Incidence
Primary glaucoma is:
hereditary
female > male
especially at age > 40 years

Incidence

Congenital glaucoma
age 0 - 2 years
Infantile glaucoma
age > 2 years
Juvenile glaucoma
age > 15 year
Secondary glaucoma: glaucoma as a
complication from other eye disease

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.

Aqueous outflow
AH fills posterior chamber pupil
anterior chamber leaves the eye by two
different routes:
90% trabecular route Schlemms canal
leaves the eye episcleral vein.
10% uveoscleral route: passes ciliary body
suprachoroidal space venous system in the
ciliary body.

Aqueous outflow
AH fills posterior chamber
Trabecular route

pupil
90 %

Schlemms canal

uveoscleral route (10%)

suprachoroidal space
leaves the eye
through episcleral vein

anterior chamber

ciliary body

venous system in the ciliary body

Aqueous outflow
Normal outflow of
aqueous humour:
a. Conventional
trabecular route
b. Uveoscleral route
c. Through the iris

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

Descemet membrane
Sclera
Iris
Ciliary body

Schwalbes line
scleral spur
iris processus
angle recess

Aqueous outflow
Uveal
meshwork
b. Corneoscleral
meshwork
c. Schwalbes line
d. Schlemms canal
e. Collector
channels
f. Ciliary body
g. Scleral spur
a.

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,
Macrophage, lens cell at the trabecular meshwork.

Trabecular Meshwork
The TM is devided into three portions:
Uveal meshwork, large spaces, resistance ,
Corneoscleral meshwork, smaller space,
Endothelial meshwork, major proportion of
normal resistance to aqueous outflow.

Obstruction of aqueous flow usually at

trabecular meshwork high IOP.

Anatomy of
Trabecular
Meshwork

Intra Ocular Pressure (IOP)

Normal IOP < 21 mm Hg,
IOP > 21 mm Hg glaucoma suspect,
Diurnal fluctuation of IOP in 24 hour:
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.

Pathogenesis of
Glaucomatous Damage
There are two current theories:
The indirect ischaemic theory: IOP -- nerve
fiber death + interfering of micro circulation of
the optic disc,
Direct mechanical theory: IOP -- damage
retinal nerve fiber at the optic disc.

Classification of the glaucomas

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

Primary glaucomas
High IOP is not associated with any ocular
disorder
Open angle
Angle closure
Congenital (developmental)

Secondary glaucomas
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 and
trabeculum,
Pathogenesis: anterior forces / posterior forces

Secondary Glaucoma
Mechanism of obstruction in
secondary glaucoma:
a.

Pre-trabecular
obstruction (membrane)

b.

Trabecular obstruction
(pigment granules)

c.

Secondary angle closure

by pupil block

d.

Secondary angle closure

without pupil block

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.

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

Schiotz Tonometer

Portable, simple, low cost,

Measure the depth of indentation of
cornea by a plunger with
specific weight,
5 mm indentation represent as each
scale of Schiotz which converted into
mmHg by Freidenwald table,
Low accuracy because it is
influenced by ocular rigidity (high
myop, DM, corneal leucoma).

Goldmanns Applanation
Tonometer
More accurate, not influenced by ocular rigidity,
The foot plate of the plunger is smaller (3.06 mm),
Disadvantages: cannot be applied to

Corneal edema
Keratitis, corneal ulcer
Keratokonus
High astigmatic

Tonography
To estimate outflow facility of HA,
Principal: to express fluid from the eye by
continuous pressing to the eye, maximal
flows,
Placing Schiotz type tonometer 2-4 minutes,
Compare IOP at 0 and after 4 minutes
outflow facility (C),
Normal C > 0.18.

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

Gonioscopy
Three main purposes of gonioscopy:
Identification of abnormal angle structure,
Estimating the width of the chamber angle,
Visualization of the angle during this following
procedures: goniotomy, laser trabeculoplasty.

Indentation Gonioscopy

Identification of angle structures

Schwalbes line as an opaque line is a
peripheral termination of Descemet
membrane,

Identification of angle structures

Trabecular meshwork has a ground glass
appearance, stretches from Schwalbes line
to scleral spur.
Consists of two part:
The anterior, nonfunctional, non pigmented
part, whitish color,
The posterior, functional, pigmented part,
greyish-blue translucent.

Identification of angle structures

Schlemms canal, slightly darker line, deep
to the posterior trabeculum,
Scleral spurs, most anterior of sclera,
narrow, dense, often shiny, whitish band. As
a landmark for laser trabeculoplasty.

Identification of angle structures

Ciliary body stands behind the scleral spur as dull
brown band. The width depends on iris insertion.
Curve of the corner at the margin of the ciliary body
Iris processes

The angle recess dipping of the iris, it inserts into

the ciliary body.
Iris processes, small extension of the anterior
surface of the iris, inserted at the level of scleral
spur.

Identification of angle structures

Angle classification by Shaffer

Grade IV
III
II
I
Slit angle
Grade 0

: 45 degrees angle
: 20 - 25 degrees angle
: 20 degrees angle closed
: 10 degrees angle closed
: less than 10 degrees,
: closed angle, iridocorneal
contact.

Shaffer Grading

Ophthalmoscopy of the optic disc

1.2 million axons pass 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.

Ophthalmoscopy of the optic disc

Nerve fiber layer anatomy

Ophthalmoscopy of the optic disc

Normal nerve fiber layer

Ophthalmoscopy of the optic disc

Normal nerve fiber layer

Diffuse nerve fiber atrophy

Ophthalmoscopy of the optic disc

Scleral canal, the opening of 1.2 million nerve
fiber leaves the eye, oval, vertical, 1.75 mm in
diameter,
The lamina cribrosa, plate of collagenous
connective tissue, 200-400 pore, containing retinal
nerve fiber bundles,
The large pores have thin connective tissue
supports, and large nerve fibers, vulnerable to
glaucomatous damage.

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 outer edge of
the cup and the outer margin of the disc, the color
is pink 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.

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.

Optic disc changes in glaucoma

Normal disc with small cup

Optic disc changes in glaucoma

Large physiological
cups

Optic disc changes in glaucoma

Progressive loss of the retinal nerve fibers
notching / thinning of neuroretinal rim (NRR)
The cup is enlarged :
concentrically diffuse thinning of NRR
localized expansion notching of NRR

Double angulation of the blood vessel

bayoneting sign,
Arterial and vein nasalisation,

Optic disc changes in glaucoma

Cup and disc ratio > 0.6,
Peripapillary atrophy at temporal region,
Splinter-shaped hemorrhage on the disc
margin.

Optic disc changes in glaucoma

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
sea of darkness, the sharpest is at the top of island.

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,

Visual Fields in Glaucoma

Peripheral scotoma that spreads and
coalesce to the paracentral scotoma
Leaving central island and accompanying
temporal island, even if the central vision is
still normal
Temporal island total blindness

Visual Fields
in Glaucoma

Classification

Primary open-angle glaucoma

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

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,
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.

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

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,
Narrow entrance to the chamber angle.

PACG stage
Five overlapping stage:

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

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.

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.

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.

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 (+),

Acute congestive
angle-closure glaucoma
Wide pupil, slow / negative light
reflex,
Papilla edema, retinal edema,

Acute congestive
angle-closure glaucoma

Acute congestive
angle-closure glaucoma
Differential diagnosis:
Red eyes:
acute glaucoma, 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

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.

Postcongestive
angle-closure glaucoma

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

Chronic closed-angle glaucoma

Signs and therapy are similar as simple
glaucoma:
Trabeculectomy,
Laser gonioplasty to make an angle,
Argon Laser Trabeculopasty (ALT)

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,
Poorly prognosis.

Primary Congenital Glaucoma

Clinical signs:
Depends on the age of onset and the level of
IOP,
According to age of onset there are 3 types:
True congenital glaucoma (40%). IOP elevated
intrauterine buphthalmos,
Infantile glaucoma (55%) manifest after birth,
Juvenile glaucoma: IOP at 2-16 years of age, with
clinical manifestation the same as POAG.

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.

Primary Congenital Glaucoma

Treatment:

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.

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

Secondary Glaucoma

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

Therapy
Nerve fiber damage caused by glaucoma is
irreversible,
Principal of therapy is to decrease IOP medically
or surgically to maintain the current condition,
The purposes of decreasing the IOP is to reduce
progressivity of the nerve fiber damage and visual
field defect,
Early finding.

Indications of Medical Treatment

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

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.

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.

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.

Surgical treatment
Treatment for absolute glaucoma:
cyclocryo coagulation destroys the ciliary body
to decrease HA production,
enucleation if all treatment is not successfull.

Laser treatment:
iridotomy
gonioplasty
trabeculoplasty

Good Prognosis
Early and right diagnosis,
Adequate control of IOP by medical /
surgical treatment,
Compliance of the patients for checking
their IOP and use medical treatment,
Case finding among glaucoma family.