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 (/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


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 l/min (1% turnover/min) Pigmented+non-pigmented cells Active transport (70%) Ultrafiltration (20%) Osmosis (10%)

OUTFLOW 0.22-0.28 l/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

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