POAG

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Primary open angle glaucoma

Dharanitharan M
Roll no:19
What is glaucoma ?
• The term glaucoma is derived from the
Greek word “glaukos” meaning “gray blue”
• Is the second leading cause of blindness
worldwide
• The third most common cause of blindness
in India
• Not reversible

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Definition of POAG
• Chronic, progressive optic neuropathy
characterised by morphological changes at
the optic nerve head and retinal nerve fibre
layer leading to characteristic visual field
changes, in the absence of other ocular
diseases or congenital anomalies (with or
without a raised IOP)

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Pathogenesis of POAG
• Decrease in aqueous outflow facility due to
increased resistance to outflow leads to rise
in IOP
• Two theories of axonal loss in optic disc
• 1. Mechanical: Increased IOP — blockage
of axoplasmic flow— optic atrophy
2. Vascular: Optic disc ischaemia with
defective autoregulation of blood vessels—
optic atrophy
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Aqueous humor outflow

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Major amount of aqueous humor leaves the
eye by

BULK FLUID FLOW

i.e. fluid flows along normal pressure


gradient through non-energy dependent
process

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Ciliary processes

Aqueous Humor in PC

through pupil

Anterior Chamber

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Trabeculo-canalicular outflow

*It is the main outlet for aqueous from the AC


*70-90% of total aqueous is drained by this route
UNCONVENTIONAL
OUTFLOW

*responsible for 10-25% of total aqueous outflow


UVEO-SCLERAL OUTFLOW

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Trans-corneal outflow
- Aqueous humor from anterior chamber
goes into tear film through cornea.
- Very little aqueous passes through this
pathway.
- Total volume of fluid transferred is limited
by high hydraulic resistance of the cornea.

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Clinical features of POAG
Symptoms
•Usually asymptomatic in early cases
•Mild headache and eye ache
•Frequent changes in presbyopic glasses
•Delayed dark adaptation
•Loss of peripheral vision
•Loss of central vision(late cases)

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Signs of POAG
• Normal anterior segment
• Pupil reaction to light may be sluggish(in
advanced cases only)
• Elevated IOP(More than 21 mm Hg) with
diurnal variation more than 5-8 mmHg
• Optic disc changes (Progressive,
asymmetric)
• Visual field defects
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Optic disc changes in glaucoma
• Early changes
o Retinal nerve fibre layer atrophy
o Vertically oval cup
o Asymmetry of the cups(More than 0.2
difference)
o Large cup(CD more than 0.6)
o Splinter haemorrhages

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Visual field defects in glaucoma
• Arcuate nerve fibres in the superior and
inferior temporal portions of the optic disc:
Most sensitive to damage
• Macular fibres : Most resistant to damage

CENTRAL VISION IS PRESERVED TILL


THE LAST IN GLAUCOMA

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Diagnostic work up/Investigations

• Tonometry
• Goniscopy: Open angles
• Perimetry: To detect visual field defects
• Slit lamp examination: To rule out causes
of secondary open angle glaucoma
• Fundus examination to document optic
disc changes
• Diurnal variation testing
• Provocative testing: Water drinking test
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Management of POAG
• Therapeutic choices

❑ Medical therapy

❑ Argon/Diode Laser Trabeculoplasty

❑ Filtration surgery

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Topical drugs used for POAG therapy
• Prostaglandin/Prostamides
Latanoprost, Bimatoprost, Travoprost
• Beta blockers
Timolol maleate, Betaxolol
• Carbonic anhydrase inhibitors
Dorzolamide, Brinzolamide
• Sympathomimetics
Brimonidine, Apraclonidine
• Parasmpathomimetics
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Pilocarpine
Systemic drugs used for POAG therapy

• Used rarely, for short term control of IOP


• Oral carbonic anhydrase inhibitors
Acetazolamide, Methazolamide

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Laser treatment
• Indications
Target IOP not achieved with medical
therapy
Non compliance of medical therapy

Argon/ Diode Laser Trabeculoplasty (ALT)


Selective Laser Trabeculoplasty (SLT)

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Surgical therapy
• Filtration surgery : Trabeculectomy
• Modified trabeculectomy :
Use of antifibrotic agents
Mitomycin/5FU
• Aqueous drainage devices:
Ahmed glaucoma valve

In cases with no/poor visual potential:


Cycloablative therapy with laser/cryo- Last
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resort
THANK YOU

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