Download MBBS Ophthalmology PPT 42 Primary Open Angle Glaucoma Lecture Notes

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Acknowledgement

? Figures and photographs - Courtesy

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Kanski's Clinical Ophthalmology

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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 managing
primary open angle glaucoma

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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 blindness

in India

? Not reversible

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? More than 50% of patients unaware of

disease.

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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 ocular

diseases 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 7th

decades 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,Graves

disease

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Pathogenesis of POAG

? Decrease in aqueous outflow facility due to

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increased resistance to outflow leads to rise

in IOP

? Two theories of axonal loss in optic disc

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? 1. Mechanical: Distortion of lamina cribrosa

leading to impaired axoplasmic flow

2. Vascular: Optic disc ischaemia with

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defective autoregulation of blood vessels

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FORMATION OF AQUEOUS HUMOR

CILIARY 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 plana

DIFFUSION

SECRETION

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(80-90%)

ULTRA-
FILTRATION

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FORMATION PROCESSES 10
Formation of aqueous humor

? Diffusion and ultrafiltration are both

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passive mechanisms so no active cellular

partcipation 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/minute

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Table 1. Constituents of Human Aqueous Humor*

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Constituent (?mol/mL) Anterior Chamber

Aqueous

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Plasma

Ascorbate

1.06

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0.04

Bicarbonate

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22.0

26.0

Calcium

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2.5

4.9

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Chloride

131.0

107.0

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Glucose

2.8

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5.9

Lactate

4.5

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1.9

Magnesium

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1.2

1.2

Phosphate

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0.6

1.1

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Potassium

22.0

26.0

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Sodium

152.0

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148.0

Urea

6.1

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7.3

Protein (gm/dL)

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0.024

7.0

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pH

7.21

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7.4
Differences 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 of

1.06 0.04

Ascorbate

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micromol/ml micromol/ml

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-Excess of Lactate

4.5 1.9

micromol/ml micromol/ml

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-Excess of Chloride &

certain amino acids

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Functions 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.

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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's

optical 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 dependent

process

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Ciliary processes

Aqueous Humor in PC

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through pupil

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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

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TRABECULAR MESHWORK

-A sponge work of
connective tissue

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beams arranged as
super-imposed
perforated sheets.
-It's extracellular spaces
contain hydrophilic

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glycosaminoglycans &

collagen.

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-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 meshwork

Corneo-scleral meshwork

Juxta-canalicular tissue

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Endothelial lining of SC

Schlemm's Canal

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UVEAL MESHWORK

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-Extends from the iris

root & 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 the

lateral wall of scleral

sulcus

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-Flattened perforated

sheets, 8-15 layers

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-Openings of 5-50

microns 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 normal

resistance to

aqueous outflow .

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-Connects the

corneoscleral

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meshwork with

schlemm'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 outflow


UVEO-SCLERAL OUTFLOW

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Trans-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 be

identified 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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---------

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Grade
IV

III

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II

I
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 defects

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Optic disc changes in glaucoma

? Early changes

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o Retinal nerve fibre layer atrophy

o 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 haemorrhages

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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 alterations
o 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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Recording 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 defect

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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 the
horizontal line.
? Double arcuate/ring scotoma

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Progression of field defects

? Roenne's central nasal step:
Sharp right angled defect at the horizontal

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meridian when arcuate scotomas run in
different arcs
? Peripheral field defects
? Advanced defects
Residual Tubular vision

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Temporal island of vision

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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 before
final interpretation

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Enlarged blind spot

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Superior arcuate scotoma

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Bjerrum's scotoma

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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 glaucoma

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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 surgery

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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 needed

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Topical drugs used for POAG therapy

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? Prostaglandin/Prostamides
Latanoprost, Bimatoprost, Travoprost
? Beta blockers
Timolol maleate, Betaxolol
? Carbonic anhydrase inhibitors

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Dorzolamide, Brinzolamide
? Sympathomimetics
Brimonidine, Apraclonidine
? Parasmpathomimetics

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Pilocarpine

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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Laser treatment

? Indications
Target IOP not achieved with medical

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therapy
Non compliance of medical therapy

Argon/ Diode Laser Trabeculoplasty (ALT)
Selective Laser Trabeculoplasty (SLT)

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Surgical therapy

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? Indications
v 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 therapy
v Advanced glaucoma

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Surgical therapy

? Filtration surgery : Trabeculectomy
? Modified trabeculectomy :

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Use of antifibrotic agents
Mitomycin/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