Glaucoma

dr. Rani Himayani, Sp.M

 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,
 Cause of third permanent blindness.

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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
Humor
outflow

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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,
• Macrophage, lens cell at the trabecular meshwork.
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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

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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 and trabeculum,
– Pathogenesis: anterior forces / posterior forces
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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
• Glaucomatous visual field defects, central
tunnel vision,
• Minimal clinical signs.

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 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,
– Narrow entrance to the chamber angle.

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 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,
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(+),
– 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
• 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,
• Mal development 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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 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).
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 Goldmann’s 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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 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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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

anatomy
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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

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 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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 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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