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  Schlemm’s 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 pupil

Trabecular route 90 % anterior chamber

Schlemm’s canal uveoscleral route (10%)

suprachoroidal space ciliary body

leaves the eye
through episcleral vein 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  Schwalbe’s line
– Sclera  scleral spur
– Iris  iris processus
– Ciliary body  angle recess
 Aqueous outflow
a. Uveal
meshwork
b. Corneoscleral
meshwork
c. Schwalbe’s line
d. Schlemm’s
canal
e. Collector
channels
f. Ciliary body
g. Scleral spur
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).
 Goldmann’s 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

• Schwalbe’s 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 Schwalbe’s 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

• Schlemm’s 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 : 45 degrees angle

III : 20 - 25 degrees angle
II : 20 degrees angle  closed
I : 10 degrees angle  closed
• Slit angle : less than 10 degrees,
• Grade 0 : 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.
DR.KUKUH PRASETYO
081286668052