Primary open angle glaucoma
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Acknowledgement
? Figures and photographs - Courtesy
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Kanski's Clinical Ophthalmology2
Learning Objectives
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? At the end of this class the students shall be able to :? Define primary open angle glaucoma(POAG).
? Understand the pathophysiology and the
risk factors of POAG.
? Understand the clinical features of POAG.
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? Understand the fundamentals of managingprimary open angle glaucoma
3
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What is glaucoma ?? The term glaucoma is derived from the
Greek word "glaukos" meaning "gray blue"
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? Is the second leading cause of blindness
worldwide
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? The third most common cause of blindnessin India
? Not reversible
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? More than 50% of patients unaware ofdisease.
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Definition of POAG? Chronic, progressive optic neuropathy
characterised by morphological changes at
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the optic nerve head and retinal nerve fibre
layer leading to characteristic visual field
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changes, in the absence of other oculardiseases or congenital anomalies (with or
without a raised IOP)
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Etiopathogenesis
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? Multifactorial aetiology? Risk factors include:
?Elevated Intra Ocular Pressure(IOP)
(More than 21 mm Hg)
?Optic disc cupping
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?Increasing Age : More common in 5th to 7thdecades of life
?Race: More common and severe in Black
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population
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Etiopathogenesis
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?Heredity/ Family History: Risk of about
10% in siblings; 4% in off springs
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?Diabetes?Systemic Hypertension
? Myopia
?Thin central corneas
?Steroid usage
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? ?Migraine, Cigarette smoking,Gravesdisease
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Pathogenesis of POAG
? Decrease in aqueous outflow facility due to
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increased resistance to outflow leads to risein IOP
? Two theories of axonal loss in optic disc
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? 1. Mechanical: Distortion of lamina cribrosaleading to impaired axoplasmic flow
2. Vascular: Optic disc ischaemia with
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defective autoregulation of blood vessels8
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FORMATION OF AQUEOUS HUMORCILIARY PROCESSES
-approx. 70-80 radial folds in the pars plicata which form
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the site of aqueous production.
-Zonular fibers attach primarily in the valleys of the ciliary
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processes and also along the pars planaDIFFUSION
SECRETION
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(80-90%)ULTRA-
FILTRATION
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FORMATION PROCESSES 10Formation of aqueous humor
? Diffusion and ultrafiltration are both
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passive mechanisms so no active cellularpartcipation occurs.
? Active secretion is an active process.
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? Rate of formation of aqueous humor in a
healthy human eye is-
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2 - 3 microlitres/minute11
Table 1. Constituents of Human Aqueous Humor*
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Constituent (?mol/mL) Anterior Chamber
Aqueous
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PlasmaAscorbate
1.06
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0.04
Bicarbonate
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22.026.0
Calcium
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2.5
4.9
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Chloride131.0
107.0
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Glucose
2.8
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5.9Lactate
4.5
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1.9
Magnesium
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1.21.2
Phosphate
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0.6
1.1
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Potassium22.0
26.0
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Sodium
152.0
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148.0Urea
6.1
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7.3
Protein (gm/dL)
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0.0247.0
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pH
7.21
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7.4Differences between
aqueous humor & plasma
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AQUEOUS PLASMA-Marked deficit of
0.024 7.0
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proteins
gm/dl gm/dl
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-Marked excess of1.06 0.04
Ascorbate
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micromol/ml micromol/ml
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-Excess of Lactate4.5 1.9
micromol/ml micromol/ml
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-Excess of Chloride &
certain amino acids
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13Functions of aqueous humor
*Maintaining IOP :
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-important for early ocular development &maintaining global integrity throughout life.
*Serves as a vascular system for the avascular
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structures of the eye: cornea, lens & TM.
- by providing substrates & nutrients & removing
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metabolites.14
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Functions of aqueous humor*Delivering high concentration of Ascorbate:
- scavenges free radicals & protects against UV
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rays & other radiations.
*Local paracrine signaling & immune responses.
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*Colourless & transparent medium as part of eye'soptical system.
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Aqueous humor outflow
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Major amount of aqueous humor leaves the
eye by
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BULK FLUID FLOW
i.e. fluid flows along normal pressure
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gradient through non-energy dependentprocess
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Ciliary processes
Aqueous Humor in PC
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through pupil
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Anterior Chamber18
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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
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TRABECULAR MESHWORK
-A sponge work of
connective tissue
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beams arranged assuper-imposed
perforated sheets.
-It's extracellular spaces
contain hydrophilic
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glycosaminoglycans &
collagen.
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20-Inner portion
Uveal meshwork
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-Outer portion
Corneoscleral meshwork
-In between
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Juxta-canalicular(endothelial)meshwork
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Uveal meshworkCorneo-scleral meshwork
Juxta-canalicular tissue
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Endothelial lining of SC
Schlemm's Canal
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22UVEAL MESHWORK
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-Extends from the irisroot & ciliary body to
schwalbe's line.
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-Trabeculae are cord
like, 2-3 layer thick.
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-Openings of 25-75
microns size.
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CORNEOSCLERAL MESHWORK
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-Extends from SS to thelateral wall of scleral
sulcus
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-Flattened perforated
sheets, 8-15 layers
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-Openings of 5-50microns size
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JUXTACANALICULAR
(ENDOTHELIAL) MESHWORK
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-The outermost portion
of TM which mainly
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offers the normalresistance to
aqueous outflow .
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-Connects the
corneoscleral
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meshwork withschlemm's canal
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? Veins from the anterior part of ciliary body form the
Ciliary venous plexus
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Anterior ciliary veins & Episcleral veins
communicate with Schlemm's canal
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Schlemm's Canal
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20-30 Collector channels Aqueous Vein
Intra-scleral venous plexus
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Episcleral venous plexus
& Anterior Ciliary vein
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UNCONVENTIONAL
OUTFLOW
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*responsible for 10-25% of total aqueous outflowUVEO-SCLERAL OUTFLOW
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29Trans-corneal outflow
- Aqueous humor from anterior chamber
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goes into tear film through cornea.
- Very little aqueous passes through this
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pathway.- Total volume of fluid transferred is limited
by high hydraulic resistance of the cornea.
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ANGLE OF ANTERIOR
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CHAMBER
- The peripheral recess of anterior chamber is known as
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the angle of anterior chamber.- It is clinically visualized by gonioscopy.
- Starting at the root of iris & progressing anteriorly
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towards the cornea, the following structures can beidentified in a normal angle in an adult :
1) Ciliary body band (CBB) & root of iris
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2) Scleral spur (SS)3) Trabecular meshwork (TM)
4) Schwalbe's line (SL)
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GradeIV
III
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III
0
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Clinical features of POAG
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Symptoms? Usually asymptomatic in early cases
? Mild headache and eye ache
? Frequent changes in presbyopic glasses
? Delayed dark adaptation
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? 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
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advanced cases only)? Elevated IOP(More than 21 mm Hg) with
diurnal variation more than 5-8 mmHg
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? Optic disc changes (Progressive,
asymmetric)
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? Visual field defects36
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37Optic disc changes in glaucoma
? Early changes
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o Retinal nerve fibre layer atrophyo Vertically oval cup
o Asymmetry of the cups(More than 0.2
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difference)
o Large cup(CD more than 0.6)
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o Splinter haemorrhages38
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Advanced glaucomatous disc changes? Marked cupping (More than 0.7)
? Thinning of NRR (Neuroretinal rim)
? Lamellar dot sign
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? Vascular alterationso Nasal shifting of retinal vessels
o Bayonetting sign(convoluted path due to NRR
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loss)o Baring of circumlinear vessels and overpass
vessels
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o Multiple haemmorrhages at disc
? Glaucomatous optic atrophy
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41Recording and documenting disc changes
? Serial drawings (10 square grid) after
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seeing fundus by ophthalmoscopy/slit
lamp with +90D/+78D lens
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? Disc photography? HRT(Heidelberg retinal tomography)
? OCT (Optical coherence tomography)
? NFA(Nerve fibre analyser)
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Visual field defects in glaucoma? Arcuate nerve fibres in the superior and
inferior temporal portions of the optic disc:
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Most sensitive to damage
? Macular fibres : Most resistant to damage
CENTRAL VISION IS PRESERVED TILL
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THE LAST IN GLAUCOMA
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Progression of field defects
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? Isopter contraction: Generalised field
constriction
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? Baring of blind spot : Non specific(Exclusion of blind spot from central field)
? Paracentral scotoma: Wing shaped and
occurs above or below the blind spot in the
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Bjerrum's area(10-25 degrees from
fixation)
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Is the earliest clinically significant defect45
Progression of field defects
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? Seidel's scotoma: sickle shaped
Due to joining of blind spot and
paracentral scotoma
? Bjerrum's/Arcuate scotoma:
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Extension of Seidel's scotoma to reach thehorizontal line.
? Double arcuate/ring scotoma
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46Progression of field defects
? Roenne's central nasal step:
Sharp right angled defect at the horizontal
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meridian when arcuate scotomas run indifferent arcs
? Peripheral field defects
? Advanced defects
Residual Tubular vision
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Temporal island of vision47
Quantification of visual field defects
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? Visual field analyzer
Kinetic perimeter
Static perimeter (automated)
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Testing more than once is required beforefinal interpretation
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Enlarged blind spot
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Superior arcuate scotoma50
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Bjerrum's scotoma51
Roenne's nasal step
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Double arcuate
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10-2- Advanced VFD , macular split
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Advanced glaucoma54
Diagnostic work up/Investigations
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? Tonometry? Goniscopy: Open angles
? Perimetry: To detect visual field defects
? Slit lamp examination: To rule out causes
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of secondary open angle glaucoma? Fundus examination to document optic
disc changes
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? Diurnal variation testing
? Provocative testing: Water drinking test 55
Diagnosis
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? POAG: Raised IOP(More than 21 mm Hg),
glaucomatous optic disc cupping, visual
field changes.
? Ocular hypertension/glaucoma suspect:
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Raised IOP? NTG(Normal tension glaucoma):
glaucomatous optic disc cupping with or
without visual field changes with normal
IOP
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Management of POAG
? Therapeutic choices
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q Medical therapy
q Argon/Diode Laser Trabeculoplasty
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q Filtration surgery57
Basic principles of therapy
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? Make a correct diagnosis
? Set a target IOP
? Start with a single drug to lower IOP
? Switch to another group of drugs if needed
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? Add drugs from different groups(Combination therapy)
? Control IOP on minimal medication
? Monitor therapy and reset target IOP
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whenever needed58
Topical drugs used for POAG therapy
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? Prostaglandin/ProstamidesLatanoprost, Bimatoprost, Travoprost
? Beta blockers
Timolol maleate, Betaxolol
? Carbonic anhydrase inhibitors
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Dorzolamide, Brinzolamide? Sympathomimetics
Brimonidine, Apraclonidine
? Parasmpathomimetics
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59Pilocarpine
Systemic drugs used for POAG therapy
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? Used rarely, for short term control of IOP
? Oral carbonic anhydrase inhibitors
Acetazolamide, Methazolamide
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60Laser treatment
? Indications
Target IOP not achieved with medical
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therapyNon compliance of medical therapy
Argon/ Diode Laser Trabeculoplasty (ALT)
Selective Laser Trabeculoplasty (SLT)
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Surgical therapy
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? Indicationsv Target IOP not achieved with maximal
tolerated medical therapy and laser
trabeculoplasty
v Non compliance of medical therapy
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v Non availability of laser therapyv Advanced glaucoma
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Surgical therapy
? Filtration surgery : Trabeculectomy
? Modified trabeculectomy :
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Use of antifibrotic agentsMitomycin/5FU
? Aqueous drainage devices:
Ahmed glaucoma valve
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In cases with no/poor visual potential:Cycloablative therapy with laser/cryo- Last 63
resort
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