Glaucoma

1. By:
Dr.Ritu
Chaturvedi
HOD,Departm
ent of
Ophthalmolog
y
SRVS Medical
college

2. LEARNING OBJECTIVES
 Definition of glaucoma
 Classification of glaucoma
 Methods of examination – tonometry, gonioscopy,
ophthalmoscopy of the optic nerve head, visual field
examination, optical coherent tomography
 Primary open angle glaucoma – definition, risk factors, clinical
features, management
 Primary angle closure glaucoma – definition, predisposing
factors (anatomical and physiological), please pay special
attention to acute angle-closure glaucoma (clinical features
and management)
 Glaucoma surgeries – discuss briefly on the principles of
trabeculectomy and filtration surgery

3. DEFINITION
• Glaucoma is a group of disorders characterized by a
progressive optic neuropathy with involve
• Characteristic appearance of optic disc
• Specific pattern of irreversible visual field defects
• Associated frequently with increased Intraocular
Pressure(IOP)
• IOP is determined by balance of rate of aqueous
production and outflow (determined by trabecular
resistance and level of scleral venous pressure)
• normal value: 16mmHg (10-21mmHg)

4. ANATOMY

5. Aqueous Humor
• Clear, colourless, plasma-like balanced salt solution
produced by the ciliary body.
• It is structurally supportive medium providing nutrient to the
lens and cornea.
• Major components of the aqueous humor: organic and
inorganic ions, carbohydrates, glutathione, urea, amino acids
and proteins, oxygen, carbon dioxide and water.
• Contains no cell, less protein and glucose, and more lactic
acid and ascorbic acid.
• Function:
1. Maintains the intraocular pressure.
2. Nourishes the avascular cornea and lens.
3. Removes the excretory products from metabolism.

6. Aqueous Production and Drainage
•Secretion of aqueous humor
- Ciliary body ( Posterior Chamber )
•Route of drainage
- Primary (90%) through trabecular meshwork
- Uvo-scleral outflow (10%)

7. Aqueous Drainage(Primary)
Cavernous sinus
Sub-ophthalmic vein
Intrascleral venous plexus
Collector channels
Pass throughSchlemm’scanal
Filtering through trabecular meshwork
Outwards into angle (space between iris and cornea)
Flow through the pupil into the anterior chamber (space between
iris and cornea)
Filling the posterior chamber (space between iris and lens)
Ciliary body produce aqueous humor

8. Uveoscleral
Ciliary body
Suprachoroidal
space
Venous circulation
of ciliary body,
choroid and sclera

9. What went wrong?
• IOP is increased due to imbalance between secretion and
removal of aqueous humor.
• Raised IOP  Mechanical stretch on lamina cribrosa 
Altered capillary blood flow  Axonal deformation and
ischemia  Neurotrophins (growth factors) from the brain
unable to reach retinal ganglion cell(RGC) bodies 
damaging cascade initiated  RGC cell death
• RGC death of course is associated with loss of retinal nerve
fibres.
• Over time, the visual defects and optic disc changes become
apparent.

10. Ocular Hypertension (OHT)
• IOP >21mmHg without detectable glaucomatous damage
• Absence of angle closure
• no detectable causes of secondary glaucoma
• risk factor of developing glaucoma in OHT
• increase IOP
• older age
• lower central corneal thickness (CCT)
• higher Cup-Disc Ratio
• untreated OHT has 9.5% risk of developing Primary open
angle glaucoma in 5 years

11. Methods of examination
1. Visual field examination
• To map the patient’s field of vision

12. 2. Ophthalmoscope:
• Optic Disc
• Oval shape
• vertically orientated
• Diameter (horizontal)
1.5mm
• Neuroretinal rim: location of all axon
• Disc cup: space with no axon
• Oval shape with long axis horizontally orientated
• Larger diameter
• the larger diameter conferring relative mechanical weakness
and hence greater vulnerability to IOP-induced
displacement of the lamina cribrosa
• Normal cup-disc ratio: <0.4 (measured by vertical ratio)

13. 3. Optical Coherent tomography
• non-invasive imaging test that uses light waves to take cross-
section pictures of your retina, the light-sensitive tissue
lining the back of the eye.
• To measure the thickness of each retina’s layer
• Acquisition of 3D images of the ONH region enables accurate
and reproducible measurements of ONH parameters that
include: disc and rim area, cup to disc ratio, cup volume and
others

14. RNFL (retinal nerve
fiber layer)
ONH (optic nerve head)

15. 4. Tonometry
- to determine the intraocular pressure (IOP)
- Goldmann tonometry is considered to be the gold standard
IOP test and is the most widely accepted method

16. 5. Gonioscopy/Anterior chamber angle
examination
• to gain a view of the width of iridocorneal angle, or the
anatomical angle formed between the eye's cornea and iris
• To look for synechia (an eye condition where the iris adheres
to either the cornea (i.e. anterior synechia) or lens (i.e.
posterior synechia).
• Anterior chamber angle can be graded using several grading
system such as Shaffer, Scheie or Spaeth system.

17. Shaffer grading system (gonioscopy)

18. CLASSIFICATION
1. Primary glaucoma : i) Open angle glaucoma
ii) Angle closure glaucoma
2. Secondary adult glaucoma due to specific anomaly or
disease of the eye
3. Congenital glaucoma

19. Classification
Primary glaucoma Secondary glaucoma Congenital glaucoma
1. Chronic open
angle
2. Acute closed angle
3. Chronic closed
angle
1. Trauma
2. Ocular surgery
3. Raised episcleral
venous pressure
4. Steroid-induced
5. Associated with
other ocular
disease eg. uveitis
1. Primary
2. Rubella
3. Secondary to
aniridia (absence
of iris)

20. Epidemiology of Glaucoma
• affect 2-3% of people over aged over 40 years old
• Primary Open-Angle Glaucoma (POAG)  Commonest
glaucoma in Caucasian and Afro-Caribbean populations.
• Angle-Closed Glaucoma (ACG) have higher prevelance in
Asian descent

21. Primary Open Angle Glaucoma
• Most commonly bilateral disease of adult onset,
Over 90% of all glaucomas
•Characterized by:
• IOP >21 mmHg
• Glaucomatous optic nerve damage.
• An open anterior chamber angle.
• Characteristic visual field loss as damage
progresses. (Arcuate scotoma)
• Absence of signs of secondary glaucoma or a
nonglaucomatous cause for the optic
neuropathy.

22. POAG
• Increased resistance to aqueous humour outflow with a
normal anterior chamber angle
• How IOP is raised?
• Thickening and sclerosis of trabecular meshwork with
faulty collagen tissues
• Narrowing of intertrabecular spaces
• Collapse of Sclemm’s canal and absence of giant
vacoules in the cells lining it
• Usually insidious and asymptomatic

23. Mechanism of Primary Open Angle Glaucoma
There is increased resistance to the outflow of the
aqueous humor offered by:
1. The sclerosed trabecular meshwork—changes in the
trabecular meshwork. (i) Proliferation of endothelial
lining with thickening of the basement membrane. (ii)
Narrowing of intertrabecular spaces. (iii) Deposition of
amorphous material in the juxtacanalicular tissue.
2. The sclerosed endothelium lining of the canal of
Schlemm—This leads to narrowing or collapse of canal of
Schlemm.

24. Risk factors
• Elevated intraocular pressure (IOP) ( >21 mmHg)
• Thinner central corneal thickness (CCT)
•CCT <555μ had 3 fold risk of developing POAG compare to
CCT >588μ
• Age : prevalence at 40 years old is 1-2% and 80 years old is 10%
• Family history of POAG (first degree relatives-double the risk)
• Mutation
• MYOC gene- codes protein myocilin that is found in the trabecular
meshwork
• OPTN gene- codes for optineurin
• Race/Ethnicity:
•West African, Afro-Carribean, Hispanic/Latino ethnicity
•No studies for ethnic groups locally

25. Symptoms
• Asymptomatic initially as the intraocular pressure raises gradually
• Headache and eye ache of mild intensity
• Difficulty during close work
• Reading or close work is often difficult due to accommodative
failure as a result of pressure upon the ciliary muscle and its
nerve supply.
• Frequent changes in presbyopic glasses
• Visual field loss
• Painless, progressive loss of peripheral vision
• Arcuate scotoma, and nasal step are typical visual field defects
• late loss of central vision if untreated or late stage
• Delayed dark adaptation

26. Signs
• Optic disc changes (earliest sign)
• Marked cupping (size 0.7 – 0.9)
• Increased cup–disc ratio (vertical C:D >0.6)
• Significant cup–disc asymmetry between eyes (>0.2 difference)
• Thinning of neuroretinal rim
• Late stages(optic atrophy) - appears white and deeply excavated
• Anterior segment signs
• Shows normal angle
• IOP changes
• Diurnal variation in IOP changes
• Over 5mmHg suspicious
• Over 8 mmHg is diagnostic
• Visual field defects
• Late stages – central vision / tubular vision is spared

27. Management
•Medical therapy is initial therapy of choice
•Monotherapy
•Combination therapy
•If target IOP not reached with 1st choice monotherapy,
switching/adding another drug from different class
•Increase aqueous outflow
•Cholinergic drugs
•Prostaglandin derivatives
•Adrenergic agonists
•Decrease aqueous production
•Beta-blockers
•Carbonic anhydrase inhibitor
•Adrenergic agonists

29. 1. Prostaglandin Analogues
• Used as 1st choice monotherapy
• Have highest IOP lowering effect
• Lower risk of systemic adverse effects and
• E.g. Latanoprost, travoprost
• Action: increase uveoscleral outflow
• Side effects
a) iris pigmentation/lash changes
b) inflammation/cystoid macular edema
6 classes of anti-glaucoma
agents (according to CPG)

30. 2. Beta blockers (adrenergic antagonists)
• Non-selective (timolol, levobunolol, carteolol, metipranolol)
• Beta-1 selective (betaxolol)
• Action: reduce aqueous inflow
• Side effects
a. Bronchospasm
b. Bradycardia
c. Low blood pressure
d. Impotence
e. Confusion
f. Fatigue
g. Hallucinations

31. 3. Adrenergic Agonists
• Non-selective (epinephrine, dipivefrin)
• Alpha-2 selective (apraclonidine, brimonidine)
• Action: reduce aqueous inflow and increase uveoscleral outflow
• Side effects
i) Alpha-1 effects:
a. Mydriasis
b. Lid retraction
c. Vasoconstriction
d. Increased heart rate and blood pressure
ii) Alpha-2 effects:
a. Miosis in some
b. Hypotension
c. Fatigue

32. 4. Carbonic Anhydrase Inhibitors
• Oral (acetazolamide, methazolamide)
• Topical (dorzolamide, brinzolamide)
• Action: reduce aqueous inflow
• Side effects
i) Oral
a. nausea
b. fatigue
c. skin rash
ii) Topical
a. local irritation
b. same side effects possible as with oral

33. 5. Cholinergic drug
• Pilocarpine eyes drop no longer favoured due to its S/E and
the need for frequent dosing i.e 4 times a day
• Action: increase aqueous outflow through trabecular
meshwork
• Side effects:
a) Stinging
b) Pupillary constriction (miosis)

34. 6. Osmotic therapy
• Only available as systemic therapy
• Most effective IOP lowering agents
• Usually used preoperatively when rapid IOP reduction is desired
• Action—These agents increased the plasma tonicity or
osmolality to draw water out of the eyes. This results in lowering
the intraocular pressure.
• I.e Oral glycerol, Intravenous mannitol
• Systemic side effects:
a) Headaches
b) Unpleasant taste
c) Heart failure
d) Pulmonary edema

36. Surgical Management
• Indication:
i) Target IOP cannot be reached despite maximal
medical therapy
ii) Patient intolerant or non-compliant to medical
therapy
Trabeculectomy
• Primary surgery of choice
• Its lowering effect is as effective as medical therapy
• However, the development of scar tissue under the
conjunctive may lead to inadequate drainage
• Thus, anti-scarring or anti-metabolite agents
i.e 5-fluorouracil (5FU) & Mitomycin C (MMC) are used
to improved success rates of surgery

37. Trabeculectomy
• This is achieved by making a small hole in the eye
wall (sclera), covered by a thin trap-door in the
sclera.
• The fluid inside the eye known as aqueous
humour, drains through the trap-door to a small
reservoir or bleb just under the eye surface,
hidden by the eyelid.
• The trap-door is sutured (stitched) in a way that
prevents aqueous humour from draining too
quickly.
• By draining aqueous humour the trabeculectomy
operation reduces the pressure on the optic nerve
and prevents or slows further damage and further
loss of vision in glaucoma.
• Control of the eye pressure with a trabeculectomy
will not restore vision already lost from glaucoma.

39. • Laser trabeculoplasty
• Used as an adjunct to medical therapy or
as primary treatment in patients who are
intolerant or non-compliant to the
medical therapy
• This involves placing a series of laser
burns (50 μ m wide) in the trabecular
meshwork, to improve aqueous outflow.
• Increase outflow facility by producing
collagen shrinkage on the trabecular
meshwork
• And by opening the intratrabecular
spaces

40. Primary Angle Closure Glaucoma
• About 5% of all glaucoma cases
• Apposition of peripheral iris against the trabecular meshwork
resulting in obstruction of aqueous outflow
• sudden forward shift of the lens-iris diaphragm causes pupillary
block, and results in inability of the aqueous to flow from the
posterior chamber to the anterior chamber resulting in a
sudden rise in IOP

42. Iris has large arc of contact with anterior
surface of lens
Pupil dilates ,peripheral iris becomes more
flaccid and pushed anteriorly
Resistance toaqueuosflow from posterior to
anterior chamberwith resultant anterior
bowing of iris
Iris lies against trabecular meshwork lead to
impede aqueous humor drainage lead to
increase IOP
Physiological pupillary block

43. Risk Factors
• Hypermetropia (longsightedness)
• Age
• more common in elderly patients, particularly those with
significant increase in anteroposterior size of their lens as
their cataract develops.
• Women are usually affected (male: female ratio is 1:4)
• More common in people of Asian descent
• Pupil dilation (topical and systemic anticholinergics, stress,
darkness)

44. Symptoms
Acute onset of intense pain.
•The elevated intraocular pressure acts on the corneal nerves
(the ophthalmic nerve or first branch of the trigeminal
nerve) to cause dull pain.
•This pain may be referred to the temples, back of the head, and
jaws via the three branches of the trigeminal nerve which can mask
its ocular origin.
Nausea and vomiting due to irritation of the vagus nerve
Diminished visual acuity.
•obscured vision and colored halos around lights in the affected eye
•caused by the corneal epithelial edema precipitated by the
enormous increase in pressure.
Prodromal symptoms  transitory episodes of blurred vision or the
appearance of colored halos around lights prior to the attack.
•may go unnoticed or may be dismissed as unimportant by the
patient in mild episodes where the eye returns to normal.

45. Signs
• Oedema of the lids and conjunctiva (chemosis).
• Marked conjunctival and ciliary congestion (red eye).
• The cornea is dull and steamy with epithelial edema.
• Anterior chamber is very shallow as the iris gets pushed forwards.
• Angle of anterior chamber is completely closed
• Iris pattern is lost and may be discoloured. Atrophic patches (white
or grey coloured) may be seen due to ischaemia.
• Semidilated pupil, non reactive to both light and accommodation
• Markedly raised intraocular pressure (IOP).
• The fundus is generally obscured due to opacification of the corneal
epithelium. When the fundus can be visualized as symptoms
subside and the cornea clears, the spectrum of changes to the optic
disk will range from a normal vital optic disk to an ill-defined
hyperemic optic nerve.

46. Management
• The initial treatment is medical in order to control the raised tension.
• After controlling the raised intraocular pressure, surgical treatment
should be performed.
• Urgent treatment to reduce the IOP and prevent recurrences.
Acute angle closure glaucoma is an OCCULAR EMERGENCY
Immediate treatment
REFER OPHTHALMOLOGIST!

47. Surgical Treatment
• It is always indicated for permanent cure. However, the tension is
lowered by medical treatment before surgery to prevent
occurrence of expulsive haemorrhage.
• The choice of operation depends on the state of the angle of
anterior chamber.
• A careful gonioscopic examination is necessary in deciding the
percentage of angle closure by peripheral anterior synechiae (PAS)
before considering the type of surgery :
i. If the angle closure by PAS is less than 50%, then a laser iridotomy
or surgical iridectomy should be sufficient.
ii. If the angle closure by PAS is more than 50%, a filtration operation,
e.g. trabeculectomy is preferred.
Treat the second eye prophylactically.

48. Laser iridotomy (Nd:YAG) or surgical
peripheral buttonhole iridectomy (PBI)
• This is useful in cases where the peripheral anterior synechiae are present
in less than 50% circumference of the angle of anterior chamber.
• In general, Nd: YAG (neodymium yttriumaluminium-garnet) laser iridotomy
is superior to surgical iridectomy in the treatment of most forms of pupil-
block glaucoma.
• Nd: YAG is the best as it can be used in all types of irides.

49. Technique
• A drop of topical pilocarpine is instilled frequently 30 minutes before
laser therapy. This helps to keep the peripheral iris tight and straight
relatively.
• A crypt in the iris is noted. The laser with an anterior offset is then
used to make an opening measuring 150-200 microns in size is made in
the periphery of iris. The power used varies from 3 to 6 mJ.
• By making a hole in the periphery of iris, pupillary block is relieved
permanently. It re-establishes communication between posterior and
anterior chambers so it bypasses the pupillary
• block and controls the raised IOP. Posterior chamber aqueous pressure
is thus relieved by :
i. Aqueous flowing through this extraopening into the anterior chamber
ii. The peripheral iris falls away from the trabecular meshwork.
• Laser iridotomy is effective in about 75% of eyes. Unresponsive cases
may require trabeculectomy.
• Postoperative management—Steroids and anti-glaucoma treatment is
given for 5-7 days to control the inflammation and rise in IOP.

50. Advantages
• It is a non-invasive procedure and chances of infection are
nil
• It is a relatively painless, out-patient department procedure
• It is cheap in cost to the patient.
Disadvantages
• Laser is not widely available as it is costly
• It is difficult to perform iridotomy in presence of corneal
oedema and flat anterior chamber
• It may cause endothelial burns
• Iridotomy hole may be blocked by scar tissue later on.

52. Complications of surgery include:
• shallowing of the anterior chamber in the immediate
postoperative period risking damage to the lens and cornea;
• intraocular infection;
• possibly accelerated cataract development;
• failure to reduce intraocular pressure adequately.
• an excessively low pressure (hypotony) which may cause
macular oedema.

54. Secondary Glaucoma
• Rise in IOP
• Secondary open angle
• Secondary angle closure
• Causative primary disease
• Lens induced (Phacomorphic)
• Inflammatory (Uveitis)
• Neovascular
• Steroid induced glaucoma
• Traumatic (hyphaema)
• Intraocular tumours
• Symptoms depend on
• Underlying aetiology
• Rapidity of increase in
IOP
• Asymptomatic → pain,
photophobia, ↓ vision,
red eye, other systemic
symptoms

55. Congenital
• Present at birth or within the first year of life
• Developmental abnormalities obstructing drainage of
aqueous humour
• Usually treated surgically via goniotomy or trabeculotomy

56. Signs and Symptoms
• Classic triad of lacrimation, photophobia and blepharospasm
(involuntary tight closure of the eyelids)
• Corneal enlargement and oedema due to buphthalmos
(enlargement of the eyeball )
• Thin sclera appears to be blue due to underlying uveal tissue
• Deep anterior chamber
• Iridodonesis (agitated motion of the iris with eye movement)
• Flat or subxulate lens
• Axial myopia
• Variable cupping and atrophy of optic disc
• Raised IOP