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CLINICAL METHODS IN DIAGNOSIS OF POAG

CLINICAL METHODS IN DIAGNOSIS OF POAG. OPTIC DISC 1.2-1.4 million axons/ 5000 loss/year 10% Magnocellular 90% Parvo- SIZE 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]

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CLINICAL METHODS IN DIAGNOSIS OF POAG

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  1. CLINICAL METHODS IN DIAGNOSIS OF POAG OPTIC DISC 1.2-1.4 million axons/ 5000 loss/year 10% Magnocellular 90% Parvo- SIZE 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

  2. 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)

  3. 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

  4. 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

  5. Clinical examination

  6. 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)

  7. 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)

  8. RECORDING OF FINDINGS • CDratio: poor description • NRR: colour, contour, width • Diagram • PHOTO (stereo+ magnification)

  9. 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%)

  10. 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

  11. IOP MEASUREMENT • Applanation tonometry (Imbert-fick: P= F/A) • Goldmann, Perkins • Airpuff (overestimate) • Tonopen (scar, oedema) • Indentation: Schiotz • Digital pressure

  12. 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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