Ocular hypertension Normal Tension Glaucoma 2ry open angle glaucoma

1. Elevated IOP with open angles, in the absence of identifiable ON damage or VF loss
and the absence of any ocular or systemic disorders contributing to the elevated IOP.
• Phasin
g
• Asymmet
ry
• Pachyme
try
• Asymmet
ry
• ONH
anomalies
• OCT ONH & PP
RNFL
• SWAP
• Search for other
causes of high
IOP e.g.
inflammation,
rubeosis,…

2. At 60 months, the cumulative
probability of developing
POAG was 4.4% in the
medication group and 9.5%
in the observation group.
Thus topical medications
were definitely shown to
reduce the risk of glaucoma
in patients with ocular
hypertension; however,
most untreated patients did
not get worse over a 5-year
period.

3. • Disturbance of the structural or functional integrity of the optic nerve, in which;
IOP constantly equal or < 21 mmHg
Glaucomatous ONH damage
Characteristic visual field changes
Open AC angle
Absent signs of 2ry glaucoma or a non glaucomatous cause of optic
neuropathy
• Phasin
g
• Pachyme
try
• Other ONH anomalies mimic glaucoma e.g. neurological,
congenital
• Other causes of field defects e.g. myopic degeneration

4. • More common in old age
• More common in Japanese
• Siblings, offspring
• Abnormal vaso regulation e.g. Raynaud
disease, Migraine
• Systemic hypotension
• Obstructive sleep apnoea
• Auto antibodies
• More common in females

5. • Brimonidine (neuro-protective effect)
• Betaxolol (Increase optic nerve blood flow)
• Prostaglandin derivatives (great ocular hypotensive effect)
• NB; topical beta blockers can have a dramatic effect on blood
pressure in some patients & may contribute to nocturnal dips
• Systemic: Calcium channel blockers (for vasospasm)
• Under trials (Neuro-protective agents);
A. Memantine
B. Gingko biloba

6. 1. Carotid Cavernous Fistula
2. Sturge Weber syndrome
3. Superior vena cava obstruction
1. Pigmentary glaucoma (Pigment)
2. Red cell glaucoma (RBCs)
3. Ghost cell glaucoma (degenerated RBCs)
4. Macrophages & lens protein (phacolytic glaucoma)
5. Pseudo exfoliation glaucoma
1. Neo vascular glaucoma (Fibro vascular tissue)
2. Epithelial ingrowth
3. Irido corneal endothelial syndrome

7. • Deposition of amyloid like material on various ocular structure including lens capsule,
zonules, TM, iris, …
• This substance is derived from abnormal extra cellular matrix metabolism

8. • PXF and pigment
deposited vertically
on the back of the
cornea

9. • Loss of pupillary ruff with deposition
of PXF on pupillary border
• Transillumination defects at
pupillary border

10. • Irregular pigmented
band anterior to
Schwalbe line

11. •The anterior lens
capsule typically
shows a central
disc and a radially
indented peripheral
layer of PXF
material, separated
by a clear zone
maintained by
pupillary abrasion

12. • Similar to POAG but failure is common
• ALT; More effective than with POAG due to more pigment content in the TM
• Same success rates with POAG

13. • Pigment shedding is precipitated by rubbing of the posterior
pigment layer of the iris against the zonule as a result of
excessive posterior bowing of the mid-peripheral portion of the
iris.

14. • PXF and pigment
deposited vertically
on the back of the
cornea

15. • Transillumination
defects at (radial,
spoke like)

16. • Heavily pigmented
TM

17. •Scheie line;
pigment granules
deposited on
anterior lens
capsule

18. •Acute IOP rise following the release of pigment
granules might particularly occur after physical
exercise.

19. • Similar to POAG but miotics are theoretically of particular benefit as they
decrease irido-zonular contact
• ALT; More effective than with POAG due to more
pigment content in the TM
• Laser Peripheral iridotomy, reverse iris concavity
& eliminate irido-zonular contact (equilibration of
abnormal pressure gradient between AC & PC)
• Same success rates with POAG

21. + signs of the cause
e.g. CRVO
Rubeosis irides

22. • Angle neo vascularisation

23. • Prostaglandin derivatives are used with caution due to their inflammatory promoting effect
• Atropine is used topically to resist synechia formation
• Topical steroids should be given if significant inflammation is present
• Pan retinal photocoagulation (PRP)
• Intra vitreal anti VEGF
• Cyclodestructive therapy e.g. Cyclo photo coagulation, cyclo diode
• SST + MMC
• if blind painful eye retro-bulbar alcohol, enucleation

24. • Trans scleral
cyclo-photo
coagulation

25. • Anterior uveitis causes plasmid aqueous. The inflammatory cells clog TM pores
increasing resistance to aqueous outflow.

26. • KPs

27. • AC cells & flare

28. • Hyper pigmented TM

29. • Prostaglandin derivatives are used with caution due to their inflammatory promoting effect
• Atropine is used topically to resist synechia formation
• Topical steroids are essential in treatment
• SST + MMC
• GDD
• Cyclodestructive therapy e.g. Cyclo photo coagulation, cyclo diode
• if blind painful eye retro-bulbar alcohol, enucleation