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.
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
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
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
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.
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)
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
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
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
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