CLINICAL METHODS IN DIAGNOSIS OF POAG OPTIC DISC

CLINICAL METHODS IN DIAGNOSIS OF POAG OPTIC DISC

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

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 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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