Definition of Glaucoma

Glaucoma is an optic disc neuropathy

which is characterized by:

– Optic nerve fibers death  optic disc damage

– Progressive visual field defect
– High intra ocular pressure (IOP) > 21 mHg
 Incidence
• Primary glaucoma is:
– hereditary
– female > male
– especially at age > 40 years
• Secondary glaucoma: glaucoma as a
complication from other eye disease
• Congenital glaucoma  age 0 - 2 years
• Infantile glaucoma  age 2 - 5 years
• Juvenile glaucoma  age 5- 15 year
 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
 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
 Pathogenesis of
Glaucomatous Damage

There are two current theories:

– 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 glaucoma
• angle closure glaucoma
Factor contributing IOP :
• primary glaucoma
• 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
 Intra Ocular Pressure (IOP)
• Normal IOP 10-21 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
 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, (5gr, 7.5gr, 10gr)
 The 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
 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.
• 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.
Normal disc with small cup
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
• Bayoneting sign (Double angulation of the blood vessel)
• Arterial and vein nasalisation
• Cup and disc ratio > 0.6
• Peripapillary atrophy at temporal region
• Splinter-shaped hemorrhage on the disc margin.
Optic disc changes in glaucoma
OCT
 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 Rhone
• 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
Perimetry
 Classification
• Primary open-angle glaucoma
• Secondary open-angle glaucoma
• Primary closed-angle glaucoma
• Secondary closed-angle glaucoma
• Primary congenital glaucoma
• Secondary congenital glaucoma
 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,
• Trabecular meshwork has a ground glass
appearance, stretches from Schwalbe’s line to
scleral spur.
• Schlemm’s canal, slightly darker line, deep to the
posterior trabeculum,
• Scleral spurs, most anterior of sclera, narrow,
dense, often shiny, whitish band.
 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 Shaeffer
• 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.
Shaeffer Grading
 Primary Open-Angle 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
Symptom :
•Rapidly progressive impairment of vision, sometimes the vision
1/300 – 0
•Eye ache and frontal headache
•Congestion, nausea, vomiting
Sign :
•Ciliary and conjunctival injection
•IOP > 50 mmHg, dilated pupil, unreactive.
•Cornea: epithelial edema, KP(+), vesicle
•Ant chamber: shallow  PAS, flare / cell (+)
•Wide pupil, slow / negative light reflex
 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:
o Creeping PAS  laser iridotomy / trabeculectomy
o After intermittent and laser iridotomy  drug >
o Combination of POAG with narrow angle  laser iridotomy + medical
 trabeculectomy
• 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 glaucoma
• Neovascular glaucoma
• Inflammatory glaucoma
• Phacolytic glaucoma
• Red cell glaucoma
• 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
• Latanoprost : increase the 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.
Trabeculectomy
• VIDEO
 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.