CLINICAL METHODS IN DIAGNOSIS OF
POAG
OPTIC DISC
1.2-1.4 million axons/ 5000 loss/year
10% Magnocellular
90% ParvoSIZE AND SHAPE
DD: 1.5mm
Surface: 2.1-2.8mm2 (π/4xHDxVD)
AGE: no change after 3-10 years
RACE: African>Asian>Mexican>Caucasian
REFRACTIVE ERROR:independent [–5-+5DS]
Positive correlation to rim and cup size
Vertically oval (VDmax>HDmin by 10%)
Abnoral shape or tilted: corneal astigmatism- amblyopia
RIM SIZE AND SHAPE
Related to disc size (+)
ISNT rule (vert. oval disc/ Horizontal oval cup)
Positive correlation to ret. arteriole diameter
IT-ST-HT- IN-SN (predilection, mainly DIFFUSE loss)
ST: sharp border cup-rim
IT: some sloping (but NFL normal)
Pallor: ? Non-glaucomatous (increased cup size)
OPTIC DISC CUP
Increases with disc size
Horizontally oval
Depth:  with disc size (deepest: JPOAG, Shallowest: high
myopic type of POAG)- negative correlation to PPA
CD RATIO
H>V hence H/V>1.0 but in early to medium G <1.0
Normal range:0.0-0.9
Independent of optic media magnification
HCD/VCD: independent of cup and disc size
RNFL
Ganglion cells axons+astrocytes+ Muller cell processes
Visibility: unevenly distributed/ with age
IT>ST>SN>IN>S>I>HT>HN
Correlates with rim thickness, retinal artery caliber and
foveolar location
Sandwich arrangment
Red –free/ wide beam
Achromatic white light
Clinical examination
Direct
Indirect
Slit lamp
ophthalmoscope ophthalmoscope
•Red-free
•No stereo-
•Young children
•Uncooperative
•High myopes
•Opacities
90D
78D
60D
FCL
DISC CHANGES IN POAG
GENERALIZED
• Large cup
• Cup asymmetry
• Progressive  in cup size
• Saucerisation
FOCAL
• Notching
•Vertical elongation
•Cupping of rim margin
•Regional pallor
•Splinter haemorrhage( specificity, early-med
advanced, IT-ST, Progression, NTG)
LESS SPECIFIC
•Exposed lamina cribrosa
•Nasal displacement
•Baring of circumlinear vessels/ constriction of arterioles
•PP crescent (spatial correlation with NRR loss)
•Shunt vessels of optic disc (advanced stage)
RNFL CHANGES
•Focal defects
wedge shaped (disc border-broad base to temporal raphe)
20%, always pathologic but not pathognomonic
v: from early to medium advanced G and  very advanced
Associated with notching, haem, PPA in that sector/NTG
50% loss of thickness: visible
• Diffuse (commoner, more difficult to see)
Sequence of sectors regarding RNFL visibility
Retinal vessels( clearer- sharper)
RECORDING OF FINDINGS
1. CD ratio: poor description
2. NRR: colour, contour, width
3. Diagram
4. PHOTO (stereo+ magnification)
AQUEOUS HUMOUR DYNAMICS
GOLDMAN EQUATION: IOP= (F/C)+P
PRODUCTION
Rate: 2-3 μl/min (1% turnover/min)
Pigmented+non-pigmented cells
•Active transport (70%)
•Ultrafiltration (20%)
•Osmosis (10%)
OUTFLOW
0.22-0.28 μl/min /mmHg
•Trabecular (90%)
•Uveoscleral (10%)
EPISCLERAL VENOUS
PRESSURE
10mmHg
IOP
Mean 16mmHg SD:3mmHg (10-22mmHg)
Non Gaussian distribution, skew to R (>40y)
•Diurnal variation/ Seasonal (W>S)
•Heart beat/ respiration
•Exercise/ Posture
•Fluid intake
•Medication (systemic, topical, alcohol, caffeine, cannabis))
•Age
•F>M after 40y
•Genetically influenced
IOP MEASUREMENT
1. Applanation tonometry (Imbert-fick: P= F/A)
Goldmann, Perkins
Airpuff (overestimate)
Tonopen (scar, oedema)
2. Indentation: Schiotz
3. Digital pressure
SOURCES OF ERROR
• Squeezing
•Valsalva
•Pressure on globe
•Tight collars
•Calibration
•EOM force to restricted globe
• FL: IOP and vice versa
• corneal astigmatism
• corneal oedema
•scar 
•CL 
•Central corneal thickness (LASIK, PRK)
• Post scleral buckling