GLAUCO

MA
Prepared
by:
Fazatin
Nadira

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

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)

ANATOM
Y

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.

Aqueous Production and Drainage

Secretion of aqueous humor
- Ciliary body ( Posterior Chamber )
Route of drainage
- Primary (90%) through trabecular
meshwork
- Uvo-scleral outflow (10%)

Aqueous Drainage(Primary)

Uveoscleral

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.

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

Methods of examination
1. Visual field examination
To map the patients field of vision

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)
asymmetry of >0.2 between the cup-disc ratio of both
eyes should be regarded as suspicious

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 retinas 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

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

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

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.

Shaffer grading system (gonioscopy)

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

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

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

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.

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 Sclemms canal and absence of
giant vacoules in the cells lining it
Usually insidious and asymptomatic

Mechanism of Primary Open Angle

Glaucoma
There is increased resistance to the outflow of the
aqueous humor offered by:
1. The sclerosed trabecular meshworkchanges 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
SchlemmThis leads to narrowing or collapse of
canal of Schlemm.

Risk factors
Elevated intraocular pressure (IOP) ( >21 mmHg)
Thinner central corneal thickness (CCT)

CCT <555 had 3 fold risk of developing POAG

compare to
CCT >588
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

Sympto
ms

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

Sign
s

Optic disc changes (earliest sign)

Marked cupping (size 0.7 0.9)
Increased cupdisc ratio (vertical C:D >0.6)
Significant cupdisc 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

Manageme
nt

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

6 classes of anti-glaucoma agents

(according to CPG)

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

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

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

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

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)

6. Osmotic therapy
Only available as systemic therapy
Most effective IOP lowering agents
Usually used preoperatively when rapid IOP reduction
is desired
ActionThese 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

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

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.

 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 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

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

Physiological pupillary
block

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)

Sympto
ms

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

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.

Managem
ent
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!

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.

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.

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 150200 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.

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.

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.

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

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

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