-Is optic neuropathy xtised by
- A pale cupped optic disc
- specific pattern of visual field defects
- + a raised intraocular pressure (IOP)
-Normal tension glaucoma is characterised by cupped optic disc
and glaucomatous visual field pattern and normal IOP.
-Ocular hypertension- intraocular pressure is consistently
elevated in the presence of normal optic discs and visual
-Malignant glaucoma occurs post operatively i.e. following
cataract extraction, aqueous flows posteriorly into vitreous,
leading to rise in IOP, with a shallow anterior chamber.
2. Applied anatomy and physiology
-Angle of anterior chamber
-Trabecular mesh work
-Carbonic anhydrase enzyme.
3. Intraocular pressure depends on;
-Rate of secretion of aqueous
-Rate of aqueous out flow
Distribution of IOP
-Ranges between 10-21 mmHg, no absolute cut off but
21mmHg is an upper limit
- Levels of IOP is inherited
Normal IOP varies
- Time of the day
- Blood pressure
14. Classification of glaucoma
-Primary glaucoma-elevation of IOP not associated
with any ocular or non-ocular disorder.
-Secondary glaucoma there is an ocular or non-
ocular disorder which alters aqueous out flow and
results in elevated intraocular pressure.
-open or angle closure glaucoma
15. • Primary open angle glaucoma (chronic simple
-The angle is open, aqueous fluid produced circulates
normally but for reasons which are not clear, the
aqueous cannot drain through the trabecular mesh
work properly so causes gradual rise in IOP.
-1% of the world population affected, incidence rises
age, uncommon below 30yrs but common after 60
16. -Race; common and severe in blacks and
develops at a young age
-inheritance runs in family
-Use topical Steroids; can be induced by steroid
17. Signs and symptoms
-The rise in IOP does not cause pain
-Very gradual loss vision from optic nerve atrophy
- Pale cupped optic disc/glaucomatous optic atrophy
-Visual field defects arcuate shaped defects(scotoma)
-Nasal shifting of vessel of the optic disc
-Haemorrhage at optic disc
-Sphincter muscles of the iris atrophies, so pupil is
dilated and non-reactive.
-Discomfort in eyes
18. Treatment of primary open angle
• The aim of treatment is to lower IOP to normal level
and prevent further damage to optic nerve
• Medical treatment
- Timolol eye drops 0.25%-0.5% BD
- Metipranolol 0.1-0.6%
Miotics- Act by stimulating the parasympathetic
system and cause contraction of ciliary M.
19. Pilocarpine 1-4% 6-8hourly, side effects include
miosis, brow head ache, worsen defects from
Carbonic anhydrase inhibitors decrease the
production of aqueous
-Acetazolamide tabs Diamox 250mg 8hourly
Topical carbonic anhydrase inhibitors
-Dorzolamide drops 0.2%
-Brinzolamide eye drops 1%
Hyperosmotic agent ie glycerol, mannitol and
20. Prostaglandins analogues reduce IOP by
facilitating uveal scleral out flow.
• Alpha2 agonists decrease IOP by decreasing
aqueous production and increase aqueous
outflow the uveal scleral route.
-Brimonidine 0.2% x2/day
21. Surgical treatment
-Drainage operations; trabeculoctomy which is anastomosis
between the anterior chamber and conjuctival sac.
-Fibrosis and scarring of the bleb
Other treatment modalities
-Argon laser trabeculoplasty
-Cryotherapy and diathermy reduce aqueous production
Follow up of patients
Patients on medical and surgical treatment should be
followed up to monitor the IOP and visual fields.
22. • Primary angle closure glaucoma or acute closure
-IOP rises as result of obstruction aqueous out flow by
closure of the anterior chamber angle by periphery iris.
-Iris bows forward so that the iris root touches the back
of the cornea; this closes the A/C angle and prevents
aqueous reaching the trabecular mesh work.
-Shallow anterior chamber
-Age, lens grow with age hence making the angle shallow
-Females affected than males
-Seeing in dark
23. Symptoms and signs
-Sudden visual loss
-Acute on set of painful eye
-Nausea and vomiting
-Signs- dilated ciliary vessels/ciliary injection
-Shallow anterior chamber
-Semi dilated and non-reactive pupil
-Iris atrophy in recurrent attacks
-High intraocular pressure stony hard eye ball
-NB At times angle closure does not present acutely
leading ocular discomfort, minor attacks with
spontaneous recovery, blurred vision with haloes
24. • Treatment
-The aim of treatment is to lower IOP as quickly as
possible by medical means.
-Initial treatment is medical
-Pilocarpine 2-4% very 5mins for 1 hour and then
1hourly for 12hours
-Acetazolamide IV or orally
-Dexamethosone eye drops to reduce inflammation
-Osmotic diuretics like urea, mannitol, and glycerol
-Treat the normal eye with pilocarpine 4hourly
25. • Congenital glaucoma
• It’s a rare condition in which the angle of A/C does
not develop normally in the embryo.
• Amesodermal membrane covers the trabecular MW
and IOP rises excessively.
• Boys are affected more than girls.
• True congenital glaucoma pressure is elevated
during intrauterine life 40%
• Infantile glaucoma manifest prior to 3rd to birth
• Juvenile glaucoma pressure develops after 3rd birth
day but before 16yrs
26. Clinical features
• Both eyes affected in 75%
• Hazy cornea associated lacrimation and photophotobia
• Bulphthalmos - big eye, blue appearance
• Breaks in descement membrane line across the cornea
• Optic cupping
• Cloudy cornea at birth – birth trauma
• -Intrauterine rubella
• Large cornea – megacornea
• Secondary infantile glaucoma- Retinoblastoma
• -Intraocular inflammation
• Medical to lower intraocular pressure before surgery
• Surgical Goniotomy
• Trabeculotomy and trabeculectomy
29. CONGENITAL GLAUCOMA
• Glaucoma is due to an increase in intraocular
• This is to due to congenital anomalies in the eye.
• Early surgery is very crucial otherwise the eyes
become very big and blind irreversibly.
30. • Secondary open angle glaucoma
-An ocular or non-ocular disorder alters aqueous out
flow and leads to arise in IOP.
-Fibrovascular tissue - neovascular glaucoma
-Epithelial cells –epithelial in grow following operation
-Red blood cell - glaucoma following trauma
-Degenerated cells- ghost cell glaucoma
-Lens proteins - phacolytic glaucoma
-Pseudoexofoliative material from the iris -
32. -Trabecular inflammation ie herpes zoster, iritis,
scarring of trabecular mesh work
-Carotid carvenous fistulae
Secondary angle closure glaucoma
-It’s caused by impairment of aqueous out flow
secondary to apposition between the periphery iris
and trabeculi caused by either posterior or anterior
- Posterior forces push the peripheral iris against the
trabecular mesh work
-pupil glaucoma/iris bombe’ /inflammatory