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POAG: Primary Open Angle Glaucoma Guide
1. Primary open angle glaucoma
Dr ANUPAMA MANOHARAN D.ophthal
1ST YEAR
Department of ophthalmology
Stanley medical college
2. DEFINITION
Chronic , progressive optic neuropathy caused by a
group of ocular condition which lead to damage of
optic nerve with loss of visual function
Components of POAG
1.Intraocular pressure >21mmHg
2.Glaucomatous optic nerve head changes
3.Visual field damage
4.Absence of secondary cause of glaucoma
3.
4. EtioPathogenesis of âIOP
Electro microscopic
⢠Change in trabecular
meshwork
⢠Collapse of canal of
Schlemm
⢠Sclerosis of intra-
scleral channel
Immunologically
⢠âgamma globulin &
plasma cells in
trabecular
meshwork
⢠Antinuclear
antibody âpositive
patients
5. Predisposing factor
Age factor 5th-6th decade
Sex equal
Ocular association
⢠High myopia
⢠Fuchs endothelial
dystrophy
⢠Retinitis pigmentosa
⢠Retinal detachment
⢠Central venous retinal
occlusion
Systemic association
⢠Diabetes
⢠Thyrotoxicosis
⢠Cardiovascular
abnormality
⢠Raynaud
⢠Phenomenon
Corticosteroid
responsiveness
⢠Chronic steroid
therapy with
significant increase in
iIOP
6. Genetic predisposing factor
â˘Autosomal recessive â commonest type
â˘Genetic expression analysis has found out 26
genetic loci in the region of long arm
chromosome1 (1q21-q31) associated with
POAG namely
⢠Myocilin (MYOC),
â˘Optineurin,
â˘WDR36
7. INCIDENCE
â˘One of the leading cause of blindness.
â˘Incidence- General population- About 1%
â˘International 14%
â˘India 4%
8. SYMPTOMS
⢠Painless , progressive , loss of vision
â˘Mild headache or eye ache
â˘Frequent changes in presbyopia glasses
-âdifficulties to accommodative failure due to constant
pressure on ciliary muscle & nerve supply.
Occasionally , an observant patient may notice a defect in visual
field.
â˘Delayed dark adaptation â later stage
â˘Significant loss of vision and blindness
10. Pathophysiology of disc changes
Mechanical effect
âIOP forces lamina
cribrosa backwards
Squeezes nerve
fibre within its
meshes to disturb
axoplasmic flow
Vascular factor
Ischemic atrophy of
nerve fibres
Without
corresponding â
of supporting glial
cells
11. Glaucomatous changes in optic disc
â˘CD ratio increased >0.6
â˘Neuroretinal thinning of rim
â˘Pallor
â˘Splinter haemorrhage
â˘Bayonetting sign
â˘Atrophy of retinal fibres
15. Visual defect field
â˘Paracentral scotoma (earliest clinical sign)
â˘Siedel scotoma paracental scotoma joins the blind
spot the blind spot to form a sickle shaped scotoma
known as siedel scotoma
â˘Arcuate or Bjerrum scotoma
â˘Ring or double arcuate scotoma :
â˘Roeneâs central nasal step when the 2 scotomas run in
different arcs & meets to form a sharp right angled
defect at the horizontal meridian
â˘Tubular vision
24. Schiotz tonometer
⢠Measures the depth of indentation of anaesthetized cornea, produced
by a weighted stylet & measured by a lever which travels over ascale
⢠The depth and volume of indentation are dependent on the intraocular
pressure and distensibility of ocular walls
⢠Not accurate in steep , thick or irregular cornea , vasodilator
vasoconstrictors , vitreoretinalsurgery
26. Applanation tonometry
â˘Based on Imbert âFick principle
â˘Asses the amount of force needed to flatten or
applanate a known area of cornea
â˘Use of applanation principle
ďGoldmann with Haag Streit slit lamp
ďMackay marg
ďNoncontact tonometers
ďPulse air tonometer
ďTon-pen
37. LASER TREATMENT
Argon or diode laser trabeculoplasty
⢠Increase outflow facility by collagen shrinkage on the inner
aspect of trabecular meshwork &opening the intratrabecular
spaces
38. Laser trabeculoplasty
ďSelective laser trabeculoplasty âtargets selectively
pigmented trabecular meshwork cell causing damage
to non pigmented cells or structures