Glaucoma
By – Dr. Rabawit Habtewold
Assistant professor of
Ophthalmology
Yekatit 12 HMC
Contents
• Introduction
– Definition
– Anatomy & physiology
• Patient evaluation
• Classification
• Treatment
Introduction
Glaucoma is a group of disease that have in
common a characteristic optic neuropathy
with associated visual field loss for which
elevated IOP is one of primary risk factors.
• Normal IOP: 10-21 mmHg
• Is a significant cause of blindness in the united
stated and the most frequent cause of blindness
among African Americans.
• Second leading cause of blindness worldwide
• Usually insidious because symptoms and
noticeable visual field defects occur in late
stages of the disease. = silent blinder
• Factors that determine IOP
1. Rate of aqueous humor production by
ciliary body
2. Resistance to aqueous outflow across the
Trabecular meshwork-Schlemm’s canal
system
3. The level of episcleral venous pressure
Anatomy
Physiology
Aqueous Production
– Active secretion
• 80%, NPE ciliary body
– Passive secretion
• 20% , ultrafiltration, diffusion
• Dependent on capillary pressure, plasma oncotic pressure, IOP
• Aqueous drainage
– Trabecular meshwork (convetional), 90%
– Uveoscleral(unconventional), 10%
• Conventional
– PC => Pupil => AC =>
Trabecular meshwork =>
sclemm canal =>
collector channels =>
episcleral venous system
• Unconventional
– PC => Pupil => AC =>
root of iris & CB face =>
suprachoroidal space
Patient evaluation
• History
– Pain
– Redness
– Haloes around light
– Reduction of vision
– Reduction in visual field
– Family history of glaucooma
– Trauma
– Systemic illness and surgery
• P/E
– Visual acuity:
• The VA of glaucoma patient ranges from normal to
NLP in advanced or terminal disease.
• A normal VA does not rule out glaucoma
– Tonometry:
• The normal IOP ranges from 10-21 mmHg, but normal
tension range does not always rule out glaucoma.
• Conversely, high measurement of IOP (greater than
22) does not always tell a glaucoma (especially when
IOP is less than 30)
• Slit lamp microscopy;
Ciliary injection in AACG
Cornea could be steamy (cloudy) in AACG
Anterior chamber reaction
Anterior chamber could be shallow in AACG
Pupil could be dilated and fixed
Pseudo exfoliation materials at pupillary border in PXG
Neovascularization of the pupil in NVG
• Gonioscopy
– Gonioscopy is an essential diagnostic tool and
examination technique used to visualize the
structures of the anterior chamber angle.
Angle status (open, closed narrow)
Inspect vessels, pigmentation, etc
• Optic nerve head assessment
– Glaucomatous optic neuropathy is a progressive
degeneration of RGCs and their axons, with damage
extending from the optic nerve to the major visual
centers in the brain
– The optic nerve head is usually
• round or slightly oval in shape and contains a central cup.
VCDR 0.1 – 0.4
• Neuroretinal rim has uniform width and a color that
ranges from orange to pink.
• Respect ISNT rule
ISNT Rule
• In normal eyes the thickness of the NRR along
the cardinal meridians of the optic disc
decreases in order
– Inferior
– Superior
– Nasal
– Temporal
• Cupping - consists of
loss of axons, blood
vessels, and glial cells.
• The tissue between the
cup and the disc margin
is called the neural rim
or neuroretinal rim
• Sign of glaucoma
– large optic cup
– Asymetrical of the cup
>0.2
– Progressive enlargement
of cup
– Splinter hemorrhage
• Early
– VCDR <0.65
• Moderate
– VCDR 7 – 8.5
• Advanced
– VCDR >8.5
• Theories:
• Mechanical theory:
– direct compression of axonal fibers with distribution of lamina
cribosa plates => interuption of axoplasmic flow => death of
RGCs.
• Ischemic theory:
– decrease optic nerve perfusion=> intraneural ischemia
• Examination:
– slit lamp combined with 60,78 or 90 D lens
GONH
• Visual field is the area of vision perceived
simultaneously by a fixating eye.
• Boundaries of FV
– 100-1100 temporal
– 70-750 inferior
– 600 nasal
– 600 superior
Methods of measuring visual field
• Confrontation
• Kinetic Perimetry
– Stimulus is moved from a non-seeing area of the visual
field to a seeing area along a set meridian
– Tangent screen
• Static automated perimetry:
– Retinal sensitivity at a specific location is determined
by varying the brightness of the test targets
– The size and location of the test targets remain constant
• Kinetic Goldman • Static Humphrey
• Glaucomatous visual field defects include the
following:
– arcuate or Bjerrum scotoma
– nasal step
– paracentral scotoma
– altitudinal defect
– generalized depression
– temporal wedge (rare)
Paracentral scotoma
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Arcuate scotoma
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Nasal step
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Tubular field
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Progression of glaucomatous damage
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0
Loss of visual field
Clear image of a road.
Note runner with white shirt on the left.
Glaucoma Visual Field Loss
LEFT EYE
Arc shaped loss of sensitivity starting
from the normal blind spot
(near where the runner is)
into the inside (nasal) field of vision
Glaucoma - severe visual
field loss. Only a small central island
of vision remains. The centre of
the vision is cut through horizontally
as well
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Characteristic pattern to loss of visual field
Rim of optic nerve
becomes thinner as
disc caves in and
becomes more cupped
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Classification of glaucoma
1. Primary open angle glaucoma
2. Primary angle closure glaucoma
3. Secondary glaucoma
4. Infantile or Congenital glaucoma
Open angle glaucoma
Primary open angle glaucoma
(POAG):
Risk factors:
Clinical feature:-
– insidous onset – Age
– slow progression – race : black > white
– Painless – family history
– bilateral, can be asymmetric – controversy: myopia,
– IOP >22 mmHg DM, cardiovascular
– glaucomatous ONH disease
– visual field loss – CRVO
– gonioscopy: opened angle
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Secondary open-angle glaucoma:
1.Pseudoexfoliation syndrome:
- deposition of a distinctive fibrillar material in anterior segment
- unilateral or bilateral
- Common in East Africans
- age > 70 years
- angle; heavy pigment
- pupillary margin
- poorly dilated pupils
- poor prognosis
- laser treatment: very effective
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2. Lens-induced glaucoma:
2.1 Phacolytic glaucona:
- leakage of lens protein through the capsule
- debris obstructs TM.
- mature or hypermature cataract
- elderly patients of history poor vision
- Management: cataract extraction
2.2 Lens particle glaucoma:
- lens cortex obstructs TM.
- occur within weeks of the initial surgery or trauma
- Management: - medication
- surgery if failed medication
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3. Ocular inflammation:
Mechanism:
- edema of the TM
- TM endothelial cell dysfunction
- blockage of the TM. by fibrin and inflammatory cells
- PGs-mediated breakdown of the blood-aqueous barrier
- steroid-induced reduction in aqueous outflow through
the TM.
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4.Accidental and surgical trauma:
4.1 Hyphema: more common following recurrent hemorrhage
• increase IOP:
– obstruction of TM. with RBC,inflammatory cell
– direct injury of the TM.
• Sickle cell hemoglobinopathies: increase incident of glaucoma
4.2 Surgical trauma:
- usually transient
- retained viscoelastic substance after cataract surgery
5. Steroid induced glaucoma:
- prolonged used of topical, periocular, inhaled or systemic steroid
- increase resistance to aqueous outflow in the TM.
Acute angle closure glaucoma
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Angle-closure glaucoma
Risk factor:
1. race : East Asians
2. ocular biometrics : shallow anterior chamber
thick lens
short axial length
3. age
4. gender: women 2-4 times common than men
5. family history
6. hyperopic
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Acute primary angle closure glaucoma
-symptoms:-Redness, ocular pain, - Diagnosis: gonioscopy
headache, decrease vision, nausea and
vomiting
- Management: -
- sign: - high IOP iridectomy
- mid dilated, sluggish and
often irregular pupil -
- corneal epithelial edema cholinergic agent,
- congested episcleral and adrenergic drops, diamox,
conjunctival blood vessels glycerol or manitol
- shallow anterior chamber
- fellow eye: prophylaxis
- a mild amount of aqueous
flare and cell PI
Chronic angle closure glaucoma
• major cause of blindness in Asia
• mechanism: creeping angle closure ( slow formation of PAS )
• PAS: peripheral anterior synechiae is an adhesion between peripheral part of the
cornea with the iris causing closure of the angle structure
• sign:
– permanent PAS
– rise IOP
– progressive cupping
– loss of visual field
• Management:
1. Peripheral iridectomy (Excision of the peripheral iris to create an opening hole for the
passage of aqueous from PC to AC)
2. Antiglaucoma drug
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Secondary angle closure with pupillary block
Lens induced angle closure:
1. Phacomorphic glaucoma:
- rapid onset
- intrumescent lens
- different of anterior chamber depth between 2 eyes
2. Ectopia lentis:
- displacement of lens
- Management: iridectomy, lens extraction
3. Aphakia or pseudophakic angle-closure glaucoma
- pupillary block by intact viterous face
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Phacomorphic glaucoma
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Secondary angle closure without pupillary
block
1.Neovascular glaucoma:
- most common causes: DM, CRVO
- neo-vascularization of iris and TM. => PAS
- poor prognosis
- Management: - Laser
- treat underlying disease like treat diabetes
Mechanism
• When there is hypoxia of retinal cells new vessels will develop on the retina
and iris due to the release of angiogenic factor. The wall of these new vessels
is weak which can easily bleed resulting in a retinal hemorrhage or hyphema.
• The new vessels can also block the anterior chamber angle
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Secondary angle closure without pupillary block:
2. Inflammation:
- formation of posterior synechiae, peripheral
anterior synechiae
- Management: aqueous suppressant, corticosteriod
3. Trauma:
- peripheral anterior synechiae
4. Drug induced secondary angle closure glaucoma:
- antiepileptic, antidepressant
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Childhood glaucoma
Primary congenital glaucoma:
- 50-70 % of congenital glaucoma
- 65 % male
- 70 % bilateral
- most case : sporadic
- genetic:
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Primary congenital glaucoma:
Clinical features:
- Clinical triad: epiphora, photophobia, blepharospasm
- Buphthalmos : corneal diameter > 12 mm. during the first year of
life
- corneal edema
- gonioscopy: open
- cupping may be reversible if IOP is lower (Unlike adult
glaucoma)
- Management: goniotomy or trabeculotomy
medication ( timolol and diamox )
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Childhood glaucoma
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Treatment of glaucoma
I. Medical management of
glaucoma
Medical agents:
Goal of treatment:
1. Beta-adrenergic antagonists
- lowest risk
2. Parasympathomimetic ( miotic )
- fewest side effect agent
- least disruption of patient’s life 3. Carbonic anhydrase inhibitors
Target IOP: 4. Adrenergic agonist
- severity of the damage 5. Hypotensive lipids
- life expectancy 6. Combination medications
- associated risk factor 7. Hyperosmotic agents
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Surgical therapy for glaucoma
Angle closure glaucoma:
1. Laser iridectomy:
indication: pupillary block
complication: focal lens or corneal damage
retinal detachment
bleeding
IOP spike
2.Incisional Peripheral iridectomy
3. Cataract extraction
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Congenital glaucoma:
Goniotomy: clear cornea
Trabeculotomy: cloudy cornea
Tube shunt implantation
Indication-failed trabeculectomy
-neovascular glaucoma
-uveitic glacoma
Ahmed valve, Baerveldt, Krupin, Molteno
Trabeculectomy
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Intra-operative Complications of
trabeculectomy
• Button-hole conjunctiva
• Haemorrhage
• Vitreous loss
• Cataract
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Postoperative complications
• Flat anterior chamber
• Leak
• Excessive filtration
• Choroidal detachments
• Hypotony
• Suprachoroidal haemorrhage
• Encapsulated blebs
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MANAGEMENT OF END STAGE
GLAUCOMA
• Atropine and dexamethasone
• Retrobulbar alcohol/ CPZ injection
• Enucleation
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Thank you
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