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Presented by: Rami AbusalehPresented by: Rami Abusaleh
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
 Glaucoma comprise a group of diseases in which
damage to the optic nerve (optic neuropathy) is
usually caused by the effects of raised ocular
pressure acting at the optic nerve head And causing
ischemia.
Introduction
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Anatomy
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Anatomy
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 The intra-ocular pressure depends on the balance
between production and removal of aqueous
humour.
 Aqueous humour is produced from the ciliary
processes by active secretion and ultra filtration 
Post chamber  Through pupil  Ant chamber 
Drained
Basic Physiology
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 Drainage:
1) Conventional pathway  Through the trabecular
meshwork, Schlemm’s canal and episcleral veins.
2) Uveoscleral pathway  Across the ciliary body into
the supra-choroidal space and into the venous
circulation across the sclera.
Basic Physiology
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Grading
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Types of Glaucomas
Aquired Congenital
Primary 
1) open angle  Chronic
2) closed angel Acute or
.
Chronic.
Primary 
Risk factors :
1st
degree relatives (16% )
Hx of a Disease that presents in younger patients,
Juvenile Open Angle Glaucoma, 3 – 35 years of age.
GLCIA gene (localized to chromosome 1p)
Secondary 
Blood / Trauma
Inflammation
Pigment
Deposition
Drugs
Rubeosis Iridis
melanoma
Adhesion
Cataract
Secondary 
Ex.(causes aniridia or Rubella)
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Primary :
1) open angle Open Path to trabecular meshwork
but increased resistance to flow due to:
I. Drain Too slowly
II. Produced Too Quickly
III. extra-cellular material in the spaces.
2) closed angel Closed Path to trabecular meshwork
No Drain through it.
Classification
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1st
Video
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Open Angle Glaucoma
Onset: 50+ years of age
Symptoms (Usually none)
loss of central and peripheral vision.
Signs
 Elevated IOP
Visual field loss
Glaucomatous disk changes
N.B: Aka: chronic simple glaucoma (CSG) and primary open angle glaucoma (POAG)
N.B : in Acute Closed Angle glaucoma IOP might reach 60 mmHg.37 11
 Risk factors
 family history
 African American
 Trauma/steroid
 Examination :
 Visual acuity
 slit lamp ( normal IOP : 8 – 21 mmHg, usually in chronic open angle glaucoma 22 – 40
mmHg)
 Gonioscopy lens exam of the iridocorneal angle
 Examine the optic disc
Open Angle Glaucoma
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Closed Angle Glaucoma
Symptoms:
1. Severe eye pain (speical Pain) /Red eye
2. Blurred vision
3. Headache / Nausea / vomiting
Signs:
1. Teary eye
2. Corneal edema
3. Closed angle
4. Mid-dilated, fixed pupil
5. “Glaucomflecken”(Glaucoma spots)
6. Iris atrophy
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Narrow Angle
Glaucoma
Mid-dilated, fixed pupilMid-dilated, fixed pupil
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1) Open angle Meshwork Blockage by:
 Blood (hyphema) and blunt trauma
 Inflammatory cells in uveitis
 Pigment from the iris (Pigment dispersion syndrome)
 Deposition of material produced by the epithelium of the
lens, iris and ciliary body in the trabecular meshwork
(Pseudoexfoliative glaucoma)
 Drugs increasing trabecular meshwork resistance
(Steroids)
 Rubeosis Iridis : iris for new abnormal blood vessels
(neovascularization)
Secondary Glaucoma
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
 Hyphema
 Pseudoexfoliative glaucoma
 Neovascularization (Rubeosis Iridis )
 Pigment dispersion syndrome
 Large choroidal melanoma
Secondary Glaucoma
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2)Closed angle:
1)Rubeosis Iridis due to diabetic retinopathy or
central retinal vein occlusion.
2) Large choroidal melanoma pushing the iris
forward.
3) Cataract may swell, also pushing the iris
forward.
4) Uveitis may cause the iris to Adhere to the
trabecular meshwork.
Secondary Glaucoma
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 Onset: usually within 2 years old
 Symptoms
• Irritability
• Photophobia
• Epiphora (overflow of tears onto the face)
• Poor vision
 Signs
• Elevated IOP
• Buphthalmos (enlargement of the eyeball)
• Haab’s striae
• Corneal clouding
• Glaucomatous cupping
• Field loss
Congenital Glaucoma
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Congenital Glaucoma
Cloudy corneasCloudy corneas
BuphthalmosBuphthalmos
Haab’s striaeHaab’s striae
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Visual fields in glaucoma
EarlyEarly LateLate
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GLAUCOMA
Cup-to-disk ratioCup-to-disk ratio
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GLAUCOMA
NormalNormal
DISK CUPPINGDISK CUPPING
GlaucomaGlaucoma
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GLAUCOMA
Glaucomatous cuppingGlaucomatous cupping
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GLAUCOMA
The histology of glaucomatous optic nerve
cupping:
Normal:: Glaucomatous::
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 The main aim of treatment To prevent Further
Complications, Not to Restore vision loss,
by(Reduce and control of IOP)
 Modalities of treatment include:
1) Medical
2) Surgical
3) Laser
N.B: This value of target pressure varies from one person to the
other.
Treatment
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Medical Treatment
Topical Agents Example Action
Alpha-2 Agonists Apraclonidine Increase USO & DS
Beta Blockers Timolol Decrease secretion
Carbonic Anhydrase
Inhibitors Acetazolamide Decrease secretion
Dorzolamide  Decrease secretion
Prostaglandin Analogues Latanoprost Increase USO
Para-sympatho-mimetics Pilocarpine Increase outflow
Sympatho-mimetics Adrenaline Both DS & IO
*DS : Decrease secretion *IO : Increase Uveoscleral outflow
*USO : Increase Uveoscleral outflow
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
 BB Side effects :
I. exacerbation of Asthma .
II. exacerbation of heart block.
 If Not improved (IOP is still high), the options are
I. adding a drug
II. Laser
III. Surgical
Medical Treatment
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Video 2
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 Involves placing a series of laser burns (50 microns)
wide in the trabecular meshwork to improve
outflow.
 Increasing tendency towards surgical procedures
nowadays.
Laser Trabeculoplasty
Argon laserArgon laser
trabeculoplastytrabeculoplasty
FiltrationFiltration
proceduresprocedures37 30
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Video 3
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Filtration blebsFiltration blebs
Surgical Treatment
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Narrow Angle Glaucoma
PeripheralPeripheral
IridotomyIridotomy
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Video 4
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 Canaloplasty :Canaloplasty : For open angel (only )For open angel (only )
Surgical Treatment
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Video 5
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Thank You !!
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