Primary open angle glaucoma (POAG) is the most common type of glaucoma. It is characterized by a raised intraocular pressure, optic nerve damage, and visual field loss. Early signs include increased cupping of the optic nerve head and visual field defects like paracentral scotomas. Treatment aims to lower intraocular pressure through medications, laser therapy, or surgery to prevent further optic nerve damage and vision loss.

1. Primary Open angle Glaucoma
Dr. AR Rajalakshmi

2. • Glaucoma – Overview
• POAG clinical features
• Management

3. DEFINITION
• Glaucoma is a chronic, progressive optic
neuropathy caused by a group of ocular
conditions which lead to damage of the optic
nerve with loss of visual function.
• The most common risk factor known is a
raised intraocular pressure.

5. PATHOGENESIS
• MECHANICAL changes due to the rise of
intraocular pressure and
• VASCULAR perfusion of the optic nerve head.

6. MECHANICAL
mechanical pressure
on the lamina
cribrosa
mechanical pressure
on the lamina
cribrosa
altering capillary
blood flow
backward displacement
and compaction of the
laminar plates narrows
the openings through
which the axons pass
GANGLION CELL
DEATH

7. VASCULAR
rise in intraocular
pressure
mechanical
pressure on the
lamina cribrosa
decrease the
capillary blood
flow
mechanical
compression of
vessels at the
lamina cribrosa
GANGLION CELL
DEATH

9. Diagnosis
combination of clinical signs—characteristic
changes in
• the optic nerve head
• abnormalities in the visual field
• rise in intraocular pressure
• The type of glaucoma is determined by the
status of the anterior chamber angle as
determined by gonioscopy

10. Optic nerve head changes

11. OPTIC NERVE HEAD – EARLY SIGNS
Increase in vertical
c:d > 0.5
Asymmetry between the
two optic nerve heads of
more than 0.2

12. Baring of
circumlinear blood
vessel
Splinter
haemorrhages
Retinal nerve fibre layer defect

13. OPTIC NERVE HEAD – LATE CHANGES
MARKED CUPPING POLAR NOTCHING
Nasalisation of vessels

14. Peripapillary changes
Loss of NRR & disc pallor

15. VISUAL FIELD
• Portion of space in which objects are simultaneously
visible to the steadily fixating eye.

16. Visual field examination
Screening tests …
• Confrontational visual field testing
• Amsler grid (assesses the central 10° the
visual field ) .
Quantitative measurements using manual or
automated perimetry

17. DISTRIBUTION OF RETINAL NERVE FIBRES
BJERRUM’S AREA : an arcuate area extending
above and below the blind spot , 10 to 25 ̊
from fixation

18. Visual field defects
• Relative paracentral scotoma
• Roenne’s nasal step
• Seidel scotoma
• Arcuate scotoma
• Double arcuate / ring scotoma
• End stage / near total field defect

19. • RELATIVE PARACENTRAL
SCOTOMA – areas where
smaller / dimmer objects
are not visualised by patient
but larger & brighter objects
are seen
• SEIDEL SCOTOMA
• starts at the poles of the
blind spot , arches over the
macular area without
reaching the horizontal
meridian nasally

20. ARCUATE SCOTOMA
• Starts at superior or inferior
poles of blind spot
• Arches over macular area
• Ends as a horizontal line
nasally
• Does not cross the
horizontal divide of visual
field
DOUBLE ARCUATE / RING
SCOTOMA
• Two arcuate scotomas
expand to involve the
peripheral visual field
• Central(tubular vision ) and
temporal islands of vision
are left

21. ROENNE’S NASAL STEP
• Appearance of a horizontal
shelf in the nasal visual
field.
• Caused by asymmetrical
nerve fibre loss at the poles
END STAGE / NEAR TOTAL
FIELD DEFECT
• Small island of temporal
vision

22. Intraocular pressure
• IOP > 21mmHg on more
than one occasion
• Circadian Variation >
8mmHg
• Asymmetry in IOP
between 2 eyes of more
than 5 mmHg

23. GAT

24. Different types of tonometers

25. Gonioscopy

26. Grading of angles
van Herick
Shaffer system
Spaeth
Scheie

27. Schaffer’s grading
Grade 0
Grade 1
Grade 2
Grade 3
Grade 4
Grade 4 (35–45°) is the widest angle, the ciliary body can be visualized.
Grade 3 (25–35°) is an open angle, scleral spur is visible.
Grade 2 (20°) is an angle in which the trabeculum but not the scleral spur can be seen.
Grade 1 (10°) is a very narrow angle in which only the Schwalbe line and perhaps the top
of the trabeculum can be identified.
Slit angle is one in which there is no obvious iridocorneal contact but no angle structures
can be identified.
Grade 0 (0°) is closed due to iridocorneal contact.

28. Classification of the Glaucomas
• Open angle
• Angle closure
• Primary
• Secondary

29. Open-angle glaucomas
Primary open-
angle glaucoma
(POAG)
Not associated with known ocular or systemic
disorders that cause increased resistance to
aqueous outflow or damage to optic nerve;
usually associated with elevated I O P
Normal-tension
glaucoma ( NTG)
Considered in continuum of POAG;
terminology often used when I O P is not
elevated
Juvenile open-
angle
glaucoma (JOAG)
Terminology often used when open-angle
glaucoma diagnosed at young age (typically 4-
35 years of age)

30. Ocular
hypertension
Normal optic disc and visual field associated
with elevated I O P
Glaucoma suspect Suspicious optic disc or visual field regardless
of I O P
Secondary open
angle
glaucoma
Increased resistance to trabecular meshwork
outflow associated with other conditions (eg,
pigmentary glaucoma, phaco-lytic glaucoma,
steroid-induced glaucoma, exfoliation
syndrome, angle-recession
glaucoma)
Increased post-trabecular resistance to
outflow secondary to elevated
episcleral venous pressure (eg, carotid
cavernous sinus fistula)

31. POAG

32. DEFINITION
IOP > 21 mmHg Open angle of normal appearance
Visual field lossGlaucomatous disc damage

33. RISK FACTORS
• Genetics- multifactorial & polygenic – long arm of
chromosome 1
• Age : 6th-7th decade , rare before 40 yrs of age
• Sex : Both sexes equally affected
• Race: Blacks > Whites
• Family history: siblings 10% risk, offspring-4 %
• Diabetes mellitus
• Ocular associations
– Myopia ,CRVO, RRD, RP
• ↑ steroid responsiveness

34. Pathogenesis
Direct damage by pressure Ischemia
Interference with
axoplasmic flow

35. SYMPTOMS
• Insidious Onset/Nonspecific
• ‘Asymptomatic’ most of the time
• Painless Progressive Loss of Vision
• Dull Headache / eye pain
• Difficulty in Near Work
• Constant pressure on ciliary muscle
• Frequent change in presbyopic correction
• Difficulty in vision more at night (dark adaptation
delay )
• Dark areas (scotomas) in field of vision

36. Diagnosis
CLASSICAL TRIAD
• RAISED IOP
• OPTIC NERVE HEAD CUPPING
• VISUAL FIELD DEFECTS
• On Gonioscopy - the angle should be ‘normal’
and ‘open’

37. Management
Principle:
• Determine TARGET PRESSURE - the range of
IOP at which there is no further progression of
glaucomatous damage.
• Parameters to document:
• Baseline IOP at which damage occurred
• Extent/severity of damage
• Associated risk factors

38. Treatment
• Medical
• LASER
• Surgery

39. MEDICAL
 MECHANISM
• Decreased aqueous production
• Increased facility of outflow (trabecular / uveoscleral)
• Intraocular osmotic fluid reduction

40. LASER THERAPY
Argon laser trabeculoplasty
Selective laser trabeculoplasty

41. Surgical
TRABECULECTOMY
• Involves creation of
fistula between angle of
anterior chamber and
sub Tenon’s space

42. NORMAL TENSION GLAUCOMA
• Definition:
– Typical glaucomatous optic disc cupping
– Visual field loss
– A mean IOP ≤ 21mm of Hg on diurnal testing
– Open angles
– Absence of any contributing ocular / specific
systemic disorders

43. EPIDEMIOLOGY
• NTG accounts for 30% of the Glaucomas
• Age – significantly older than POAG
• Gender – females ≥ males – 2:1
• Race – Japan
• Family history – POAG is greater in families
of patients of NTG

44. PATHOGENESIS
• Controversy
• Vascular insufficiency
• Decreased optic disc resistance
• Optic nerve compression by normal carotid
arteries

45. CLINICAL FEATURES
• IOP
• In high teens
• Wide diurnal and postural IOP fluctuations
• Night and early morning spikes
• Visual field changes
• Closer to fixation
• Deeper
• Steeper
• Localised

46. CLINICAL FEATURES
• Splinter hemorrhage
• Acquired optic disc pits
• Focal notching

47. CLINICAL FEATURES
• OTHERS
• Peripheral vasospasm on cooling
• Migraine
• Nocturnal hypotension
• Reduced blood flow in ophthalmic & posterior ciliary
arteries
• Paraprotienaemias and presence of serum auto
antibodies

48. TREATMENT OF NTG
• Lower IOP by 30%
• Betaxolol- Increases the pulsatile ocular blood flow to the
optic nerve
• Brimonidine 0.2%:Neuroprotective
• Prostaglandin analogues –
• Latanoprost: 0.005% once daily
• Bimatoprost: 0.03%
• Travoprost: 0.004%
• Dorzolamide
• Improves blood flow and velocity in the vicinity of optic nerve
• Calcium channel Blockers

49. OCULAR HYPERTENSION
• Definition:
– IOP 22mm of Hg or greater
– Normal optic disc
– Normal Visual Fields
– Open angle
– Absence of any ocular or systemic disorder
contributing to elevated IOP

50. RISK FACTORS
• Increasing age
• Retinal nerve fibre layer defects
• Optic nerve head morphology
– Higher vertical C/D ratio
• Elevated IOP
• Peripapillary changes
• Central corneal thickness
• Positive family history -first degree relative
• High Myopia

51. MANAGEMENT
• 20% IOP reduction
• Medical
Other modalities less frequently
• LASER
• Surgery

52. • POAG clinical features
• ONH changes in POAG
• Visual field defects in POAG
• Management