CLINICAL METHODS IN DIAGNOSIS OF POAG

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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
(p/4xHDxVD) AGE no change after 3-10 years RACE
AfricangtAsiangtMexicangtCaucasian REFRACTIVE
ERRORindependent 5-5DS Positive correlation
to rim and cup size
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Vertically oval (VDmaxgtHDmin 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)
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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 HgtV
hence H/Vgt1.0 but in early to medium G
lt1.0 Normal range0.0-0.9 Independent of optic
media magnification HCD/VCD independent of cup
and disc size
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RNFL Ganglion cells axonsastrocytes Muller cell
processes Visibility unevenly distributed/ ?with
age ITgtSTgtSNgtINgtSgtIgtHTgtHN Correlates with rim
thickness, retinal artery caliber and foveolar
location Sandwich arrangment Red free/ wide
beam Achromatic white light
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Clinical examination
Direct ophthalmoscope Indirect ophthalmoscope Slit lamp
Red-free No stereo- Young children Uncooperative High myopes Opacities 90D 78D 60D FCL
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• 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)

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• 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)

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• RECORDING OF FINDINGS
• CD ratio poor description
• NRR colour, contour, width
• Diagram
• PHOTO (stereo magnification)

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AQUEOUS HUMOUR DYNAMICS

• GOLDMAN EQUATION IOP (F/C)P
• PRODUCTION
• Rate 2-3 µl/min (1 turnover/min)
• Pigmentednon-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
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• IOP
• Mean 16mmHg SD3mmHg (10-22mmHg)
• Non Gaussian distribution, skew to R (gt40y)
• Diurnal variation/ Seasonal (WgtS)
• Heart beat/ respiration
• Exercise/ Posture
• Fluid intake
• Medication (systemic, topical, alcohol, caffeine,
  cannabis))
• Age
• FgtM after 40y
• Genetically influenced

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

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• 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?