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Diagnostic and treatment of glaucoma
Małgorzata Seredyka-Burduk
Introduction
Physiology and anatomy
Aqueous secretion
Active secretion accounts for approximately 80%
of aqueous production.
The aqueous is secreted by the non-pigmented
ciliary epithelium via an active metabolic
process that is dependent on number of
enzymatic systems.
Introduction
Physiology and anatomy
Aqueous secretion
Passive secretion accounts for the remaining 20%.
Aqueous is produced by passive processes such as
ultrafiltration and diffusion which are dependent
on the level of blood pressure in the cilliary
capillaries, the plasma oncotic pressure and the
level of intraocular pressure.
Introduction
Physiology and anatomy
Aqueous outflow
Aqueus humour leaves the eye by trabeculum. The
trabeculum (trabecular meshwork) is a sieve-like
structure.
Introduction
Physiology and anatomy
The trabeculum consists of three portions:
1. The uveal meshwork (a) is the innermost portion
which consists of cord-like meshes that extend
from the root of the iris to the Schwalbe’s line.
The intertrabecular spaces are relatively large and
offer little resistance to the passage of aqueous.
Introduction
Physiology and anatomy
2. The corneoscleral meshwork (b) forms the larger
middle portion which extends from the scleral
spur (g) to Schwalbe’s line (c).
The meshes are sheet-like and the intertrabecular
spaces are smaller than in the uveal meshwork.
Introduction
Physiology and anatomy
3. The endothelial meshwork is the narrow outer
part of the trabeculum which links the
corneoscleral meshwork with the endothelium
on the inner wall of Schlemm’s canal (d).
Introduction
Physiology and anatomy
Schlemm’s canal is a circumeferential channel
bridged by septa.
The inner wall of the canal is lined by irregular
spindle-shape endothelial cells which contain
giant vacuoles.
The outer wall of the canal is lined by smooth flat
cells and contain the openings of the collector
channels.
Introduction
Physiology and anatomy
Aqueous flows from the posterior chamber into the
anterior chamber through the pupil and is drained
by the two routes:
 The trabecular (conventional) route (accounting
90% of aqueous outflow) is through the trabaculum
into Schlemm’s canal and episcleral veins.
Introduction
Physiology and anatomy
 The
uveoscleral (unconventional) route accounts
10%. The aqueous passes across the cilliary body
into the suprachoroidal space and is drained by the
circulation in the cilliary body, choroid and sclera.
Some aqueous also drains via the iris.
Introduction
Physiology and anatomy
The following factors determine IOP:
 rate of aqueous secretion,
 resistance encountered in the outflow channels,
 level of episcleral venous pressure
The normal IOP varies between 10mmHg and 21 mmHg.
Although there is no absolute cutoff point, 21 mmHg is
considered the upper limit of normal, and levels above this
are viewed with suspicion.
Introduction
Physiology and anatomy
Fluctuations of IOP occur with the time of day,
heartbeat, blood pressure level and respiration.
Normal eyes have a smaller diurnal fluctuations (<4mmHg)
than eyes with glaucoma in which the fluctuation may be
10mmHg or more.
Introduction
Pathogenesis of glaucomatous damage of optic nerve
1. The ischaemic theory postulates that raised IOP
causes death of nerve fibres because of too low
perfusion pressure (difference between the IOP
and the intracapillary pressure).
2. The mechanical theory suggests that elevated IOP
directly damages the retinal nerve fibres as they
passed through the optic nerve head.
It seems likely that both mechanisms
play a role in most cases.
Introduction
Classification of the glaucomas
1. Open-angle glaucomas
2. Angle-closure glaucomas
1. Primary glaucomas (the elevation of IOP is not
associated with any other ocular disorder)
2. Secondary glaucomas (an ocular or non-ocular
disorder alters aqueous outflow – this results in
elevation of IOP).
Introduction
Classification of the glaucomas
There are the following secondary open-angle
glaucomas:
 pre-trabecular (aqueous outflow is obstructed by
a membrane covering the trabeculum)
 trabecular (the obstruction occurs within the
trabeculum itself)
Introduction
Classification of the glaucomas
There are the following secondary open-angle
glaucomas:
 post-trabecular (the trabeculum by itself is
normal but aqueous outflow is impaired as a
result of elevation of pressure in episcleral veins)
Introduction
Classification of the glaucomas
Secondary angle-closure glaucomas are those in
which aqueous outflow is impaired by apposition
between the peripheral iris and the trabeculum.
This may be the result of:
 posterior forces which push peripheral iris against
the trabeculum
 anterior forces which pull the peripheral iris over
the trabeculum
Introduction
Classification of the glaucomas
In generally, primary open-angle glaucoma (POAG)
is most common and accounts for 55% of cases,
secondary glaucomas are next (30%), followed by
primary angle-closure glaucoma (PACG) – 12%
and congenital – 3%.
Methods of examination
Tonometry
The two main methods of measuring IOP are by
applanation (The Goldmann tonometer, The Perkins
tonometer, The air-puff, The Pulsair, The TonoPen) and indentation (The Schiotz tonometer).
Both are based on the principle that the applied force
either flattens (applanates) or indents the cornea.
Methods of examination
Gonioscopy
The main purposes of gonioscopy:
 identification of abnormal angle structures
 estimation of the width of the chamber angle
 visualization of the angle during procedures
such us laser trabeculoplasty and goniotomy
Methods of examination
The angle of the anterior chamber cannot be
visualized directly through an intact cornea
because light emitted from angle structures
undergoes total internal reflection.
A goniolens eliminates this by replacing the
cornea/air interface with a new interface which
has a refractive index greater than that of the
cornea and tears.
Methods of examination
The two main types of goniolenses are:
1. indirect (provide a mirror-image view of the
opposite angle and can be used only with
conjunction with a slitlamp) – the Goldmann
goniolens, the Zeiss goniolens
Methods of examination
The two main types of goniolenses are:
2. direct (provide a direct view of the angle and is
usually used with the patient in the supine
position during operations on the angle) – the
Koeppe goniolens, the Swan-Jacob goniolens,
the Barkan goniolens
Methods of examination
The Goldmann goniolens gives an excellent view of
the angle structures, stabilizes the globe, is
suitable for laser trabeculoplasty.
The curvature of the contact surface of the lens is
steeper than that of the cornea, so a viscous
coupling substance, with the same refractive index
as the cornea, that bridges the gap between the
cornea and the goniolens is required.
Methods of examination
The Zeiss goniolens has four mirrors, so the entire
extent of the angle may be visualized with
minimal rotation.
As the curvature of the contact surface of the lens is
flatter than that of the cornea, coupling substance
is not required.
Methods of examination
The Zeiss goniolens does not stabilize the globe, but
if the lens is pushed hard against the cornea, it
will distort it and impair visualization of the
angle.
This will also displace aqueous humour to the
periphery of the angle, so that a narrow angle may
appear artificially wide.
indentation gonioscopy
Methods of examination
Identification of angle structures during gonioscopy
Schwalbe’s line is the most anterior structure
appearing as an opaque line. It represents the
peripheral termination of Descemet’s membrane
and the anterior limit of the trabeculum.
In locating Schwalbe’s line is useful the corneal
wedge. Using a narrow slit beam, two linear
reflections can be seen: one from the external
surface of the cornea and its junction with sclera,
the other from the internal surface of the cornea.
The two reflections meet at Schwalbe’s line which
forms the apex of the corneal wedge.
Methods of examination
Identification of angle structures during gonioscopy
The trabeculum has a ground-glass appearance and
appears to have a depth.
It consists of the two parts:
 the anterior, non-functional, non-pigmented, lies
behind the Schwalbe’s line, has a whitish colour.
 the posterior, functional, pigmented, lies between
the anterior trabeculum and scleral spur, has a
greyish-blue colour.
Methods of examination
Identification of angle structures during gonioscopy
Pigmentation of the trabeculum is very rare before
puberty.
In senile eyes it involves the trabeculum to a variable
extend and is most marked inferiorly.
Pathological trabecular hyperpigmentation is caused
by excessive shedding of pigment from the
posterior layer of the iris.
In eyes without trabecular pigmentation Schlemm’s
canal can occasionally be identified as a slightly
darker line deep to the posterior trabeculum.
Methods of examination
Identification of angle structures during gonioscopy
The scleral spur is the most anterior part of the
sclera and the site of attachment of the
longitudinal muscle of the ciliary body.
It appears as a narrow, dense, shiny, whitish band.
The scleral spur is the most important landmark
because it has relatively consistent appearance in
different eyes.
Methods of examination
Identification of angle structures during gonioscopy
The ciliary body stands out just behind the scleral
spur as a dull-brown or slate-grey band.
Its width depends on the position of the iris insertion
and tends to be narrower in hypermetropic eyes
and wider in myopic eyes.
Methods of examination
Identification of angle structures during gonioscopy
Iris processes are small extensions of the anterior
surface of the iris which are inserted at the level of
scleral spur and cover the ciliary body.
Iris processes are present in about one-third of
normal eyes and are most prominent during
childhood and in brown eyes.
Iris processes should not be confused with peripheral
anterior synechiae, which are adhesions between the iris
and the angle structures!
Methods of examination
Grading of angle structures
Its main aims are to evaluate the functional status of
the angle, its degree of closure and the risk of
future closure.
Methods of examination
Grading of angle structures
In the Shaffer system, an estimation of the angle
width is achieved by observing the amount of
separation between two imaginary lines,
constructed to the inner surface of the trabeculum
and the anterior iris surface.
Methods of examination
Grading of angle structures
Grade 4 (35°-45°) is the widest angle
characteristic of myopia and aphakia in which the
ciliary body can be visualized. It is incapable of
closure.
Methods of examination
Grading of angle structures
Grade 3 (20°-35°) is an open angle in which at
least the scleral spur can be identified. It is
incapable of closure.
Methods of examination
Grading of angle structures
Grade 2 (20°) is moderately narrow angle in which
only the trabeculum can be identified. Angle
closure is possible but unlikely.
Methods of examination
Grading of angle structures
Grade 1 (10°) is a very narrow angle in which only
Schwalbe’s line and the top of the trabeculum can
be identified. The risk of angle closure is high.
Methods of examination
Grading of angle structures
Grade 0 (0°) is a closed angle resulting from
iridocorneal contact.
Indentation gonioscopy with the Zeiss goniolens is
neceserry do differentiate between „appositional”
and „synechial” angle closure.
Methods of examination
Ophthalmoscopy of the optic nerve head
The key to the interpretation of visual field loss in
relation to optic nerve cupping in glaucoma is an
understanding of the distribution of the 1,2 million
axons.
Fibres arising from the macula an from the nasal
retina follow a straight course to the optic nerve
head. Those from macula form a spindle-shape
area (papillomacular bunge).
Methods of examination
Ophthalmoscopy of the optic nerve head
Fibres arising from the retina temporal to the macula
follow an arcuate path around the papillomacular
bundle to reach the optic nerve head.
Methods of examination
Ophthalmoscopy of the optic nerve head
The arcuate fibres reaching the superotemporal and
inferotemporal parts of the optic nerve head are
most vulnerable to damage in glaucoma and the
fibres of the papillomacular bundle are the most
resistant.
Methods of examination
Ophthalmoscopy of the optic nerve head
The scleral canal is an opening through which nerve
fibres leave the eye.
The diameter of this canal is related to the size of the
optic disc – eyes with small canals have small
optic discs (hypermetropia), with large canals –
large discs (myopia).
Methods of examination
Ophthalmoscopy of the optic nerve head
The optic cup is a pale depression in the centre of the
optic nerve head which is not occupied by neural
disc tissue. Cupping is best evaluated by observing
the bending of the small blood vessels as they
cross the disc.
Methods of examination
Ophthalmoscopy of the optic nerve head
The size of the cup is related to the diameter of the
disc – a small disc have a small cup because the
nerve fibres are bunched and crowded up as they
leave the eye.
Methods of examination
Ophthalmoscopy of the optic nerve head
In adult glaucoma, pathological cupping is caused by
a decrease in the number of nerve fibres, glial cells
and blood vessels.
In young children, cupping may be caused by an
increase in the diameter of scleral canal and be
reversible with early treatment.
Methods of examination
Ophthalmoscopy of the optic nerve head
The neuroretinal rim is a tissue between the outer
edge of the cup and the outer margin of the disc.
A normal rim should be orange or pink and constant,
irrespective of the overall diameter of the disc.
Methods of examination
Ophthalmoscopy of the optic nerve head
The normal c/d ratio in the horizontal meridian in
most eyes is 0,3 or less. Only 2% of normals have
a ratio of more than 0,7.
In 70% of patients with early glaucoma the
difference between two eyes is more than 0,1.
Methods of examination
Ophthalmoscopy of the optic nerve head
The spectrum of disc damage in glaucoma ranges
from highly localized tissue loss with notching of
the neuroretinal rim to diffuse concentric
enlargement of the cup.
Concentric expansion of the optic cup is caused by a
diffuse loss of nerve fibres. When this occurs the
excavation simply enlarges concentrically without
associated localized notching of neuroretinal rim.
Methods of examination
Ophthalmoscopy of the optic nerve head
Localized expansion of the optic cup is caused by
localized damage to the neuroretinal rim at the
superior or – more commonly – inferior poles of
the optic disc.
Methods of examination
Ophthalmoscopy of the optic nerve head
In advanced cupping occurs the double angulation of
the blood vessels – they dive sharply backwards
and then turn along the steep wall of the
excavation before angling again onto the floor of
the disc –
bayonetting sign
Methods of examination
Ophthalmoscopy of the optic nerve head
Progression of glaucomatous damage of optic disc
Methods of examination
Visual fields
The visual field is an island of vision surrounded by
a sea of darkness.
Methods of examination
Visual fields
The outer aspect of the visual field extends:
 60° nasally,
 90° temporally,
 50° superiorly,
 70° inferiorly.
Methods of examination
Visual fields
The visual field isn’t a flat plane but a
three-demensional structure.
The visual acuity is sharpest at the top of the island
and then declines progressively towards the
periphery. The nasal slope is steeper than the
temporal.
The blind spot is located temporally between 10° and
20°.
Methods of examination
Visual fields
An isopter enclosses an area within which a target of
a given size is visible.
As a size of target is decreased, the area within
which it can be perceived becomes smaller, so a
series of isopters is formed.
Methods of examination
Visual fields
A scotoma is either an absolute or a relative defect in
the visual field.
Absolute scotoma represents total loss of vision.
Relative scotoma is an area of partial visual loss
within which some targets can and others cannot
be seen.
Sometimes an absolute scotoma is surrounded by a
relative scotoma.
Methods of examination
Visual fields
Perimetry is a method of evaluating the visual field.
Kinetic perimetry involves the presentation of a
moving stimulus of known intensity from a nonseeing area to a seeing area, until the patients
reports that the stimulus has been perceived.
It can be performed by simple confrontation, as well
as using perimeters, such as the tangent screen, the
Lister and the Goldmann.
Methods of examination
Visual fields
Static perimetry involves the presentation of stimuli
of varying intensity in the same position to obtain
vertical boundary of the visual field.
Although it is slower than kinetic perimetry, it is
much better suited to quantitative testing.
It can be performed by an automatic perimeters, such
as the Humphrey, the Octopus, the Optopol.
Methods of examination
Visual field defects in glaucoma
Early defects:
1. The earliest clinically significant field defect is a
scotoma that develops between 10° and 20° of
fixation. Initially the defects do not connect with
the blind spot itself but, with the passage of time,
they tend to elongate circumferentially along the
distribution of arcuate nerve fibres.
Methods of examination
Visual field defects in glaucoma
2. Baring of the blind spot may occur in association
with other nerve fibre bundle defects, but it is too
non-specific a sign to be of diagnostic importance by
itself.
Methods of examination
Visual field defects in glaucoma
3. Isolated paracentral nasal scotomata may also be
find. Although they are frequently absolute when
first detected, they may ocassionally disappear
after normalization of IOP.
Methods of examination
Visual field defects in glaucoma
4. A nasal (Roenne) step or a temporal wedge is
frequently associated with other defects and may
rarely be present by itself.
Methods of examination
Visual field defects in glaucoma
Late defects
1. The scotomata in Bjerrum’s area (between 10°
and 20° of fixation) change to form an arcuateshaped defect which arches from the blind spot
around the macula, reaching to within 5° of
fixation nasally.
Methods of examination
Visual field defects in glaucoma
2. A ring of double arcuate scotoma develops when
defects arising in opposite halves of the visual
field join together.
Methods of examination
Visual field defects in glaucoma
3. The visual field loss gradually spreads to the
periphery and also centrally, so that eventually
only a small island of central vision and a temporal
island are left.
Methods of examination
Visual field defects in glaucoma
4. The temporal island is usually extinguished before
the central island, although occasionally this
sequence is reversed.
Types of glaucomas
1. Primary glaucomas (the elevation of IOP is not
associated with any other ocular disorder)
2. Secondary glaucomas (an ocular or non-ocular
disorder alters aqueous outflow – this results in
elevation of IOP).
Primary open-angle glaucoma
Primary open-angle glaucoma (POAG) is generally a
bilateral, although not necessarily symmetrical,
disease characterized, in least one eye, by the
following:
o glaucomatous optic nerve damage
o glaucomatous visual field defects
o repeated IOP>21 mmHg (in 15% IOP<21 mmHg)
o adult onset
o open and normal appearing angle
o absence of secondary causes of open-angle
glaucoma
Primary open-angle glaucoma
POAG is the most prevalent of all glaucomas,
affecting 1 in 200 of the general population over
the age of 40 years.
It increases with age.
It affects both sexes equally.
It is more common in black than in white
individuals.
Primary open-angle glaucoma
POAG is freqently inherited.
First-degree relatives of patients with POAG are at
increased risk of developing it.
In general risk is 10% in siblings (brothers and
sisters) and 4% in offspring (parents).
Primary open-angle glaucoma
Ocular risk factors of POAG:
 high myopia
 central retinal vein occlusion
 Fuchs’ endothelial dystrophy
 rhegmatogenes retinal detachment
 retinitis pigmentosa
Primary open-angle glaucoma
Systemic risk factors of POAG:
 increasing age
 diabetes
 elevated systolic blood pressure
Primary open-angle glaucoma
POAG is a chronic, slowly progressive, usually
bilateral but asymmetrical disease with an
insidious onset.
It is usually asymptomatic until it has caused a
significant loss of visual field. Patients
frequently present with significant visual field
loss in one eye and less advanced or without any
damage in the other.
Primary open-angle glaucoma
Ocassionally, patients with very high IOPs may
complain of eye ache, headache and even haloes
caused by transient corneal epithelial oedema.
Primary open-angle glaucoma
Treatment
There should be a treatment goal in terms of ideal
IOP level.
Unfortunately, the actual safe level of IOP is still
unknown, although, in general, the more
advanced the damage the lower the IOP required
to halt a progression of the disease.
Primary open-angle glaucoma
Treatment
Only the long-standing stability of visual fields,
and the appearance of the optic nerve head, are
proof that the IOP is at a safe level.
If control is good and the appearance of the optic
disc stable, twice-yearly perimetry is sufficient.
Primary open-angle glaucoma
The initial therapy is usually medical, except in
advanced cases.
We use:
 β-blockers
 α2-sympathomimetics
 carbonic anhydrase inhibitors
 prostaglandins
 miotics
Primary open-angle glaucoma
The chosed drug should be used at its lowest
concentration, as infrequently as possible, to
achieve the desire effect.
If possible, the drug with the fewest potential side
effects should be chosen.
Primary open-angle glaucoma
If the IOP is not reduced to satisfactory level the
following options should be considered:
 increase the strength of the drug,
 withdraw the initial drug and substitute to another,
 add another drug (when a combination of drugs is
used, the patient should be instructed to wait 10
minutes before instilling the second drug to
prevent washout)
Primary open-angle glaucoma
If the decrease of IOP is not reduced to a satisfactory
level laser trabeculoplasty or filtration surgery
should be considered.
Laser trabeculoplasty is a method of lowering IOP
by the application of discrete laser burns to the
trabeculum.
We use two types of lasers to realize trabeculoplasty:
 argon laser (ALT – argon laser trabeculoplasty)
 Nd:YAG Q-switch (SLT – selective laser
trabeculoplasty)
Primary open-angle glaucoma
Indications to a trabeculoplasty:
 open-angle glaucomas which are uncontrolled
despite maximal tolerated medical therapy,
 primary therapy in patients with open-angle
glaucoma who do not comply with medical
therapy,
 open-angle glaucoma following filtration surgery
in which a further lowering of IOP is required
Primary open-angle glaucoma
Contraindications to a trabeculoplasty:
 closed of extremely narrow angle (trabeculum is
not visible)
 corneal clouding
 advanced and rapidly progressive glaucoma–there
is insufficient time to assess the response to LT
 active intraocular inflammation or blood in AC
 bad cooperation with patient
Primary open-angle glaucoma
During trabeculoplasty, the burns are applied to the
junction of the non-pigmented with the pigmented
trabeculum.
The pigmented Schwalbe’s line should not be
confused with posterior pigmented trabeculum!
Primary open-angle glaucoma
It is extremely important to identify the scleral spur
because the application of burns posterior to it will
result in greater inflammation and therefore
increased risk of early post-laser rise in IOP, as
well as the formation of peripheral anterior
synechiae.
Primary open-angle glaucoma
Trabeculectomy is a surgical procedure which
lowers the IOP by the creation of a new channel
for aqueous outflow between the anterior
chamber and sub-Tennon’s space.
Primary open-angle glaucoma
Technique of trabeculectomy:
1. A conjunctival flap is fashioned superonasally. It
may be based at limbus or at fornix.
Primary open-angle glaucoma
2. The scleral flap is cut by first outlining a rectangle
based at the limbus (some surgeons make a square or
triangular flap). Than incisions are made along the
marks through two-thirds of sleral
thickness and the flap is prepared.
Primary open-angle glaucoma
3. The deep block of slera and trabeculum is excised.
Primary open-angle glaucoma
4. A peripheral iridectomy is performed to prevent
blockage of the internal opening by the peripheral
iris.
Primary open-angle glaucoma
5. The superficial scleral flap and the conjunctival
flap are sutured.
Primary angle-closure glaucoma
Primary angle-cosure glaucoma (PACG) is a
condition in which aqueous outflow is
obstructed solely as a result of closure of the
angle by the peripheral iris.
It occurs in anatomically predisposed eyes and is
frequently bilateral.
It affects 1 in 1000 individuals over the age of 40.
Its prevalence increases with age.
Women are affected more commonly than men by
a ratio of 4:1.
Primary angle-closure glaucoma
Anatomical predisposition to the disease is
inherited and consist of the following three
factors:
1. A relatively anterior location of the iris-lens
diaphragm
2. A shallow anterior chamber
3. A narrow entrance to the chamber angle
Primary angle-closure glaucoma
The proximity of the cornea to the peripheral iris
enables angle closure to occur more easily than in
a normal eye.
The following three interrelated factors are
responsible for these characteristics:
1. axial growth of the lens
2. small corneal diameter
3. short axial length
A short eye, which is also frequently hypermetropic,
has a small corneal diameter, and a thick lens that is
located in an anterior position.
Primary angle-closure glaucoma
Mechanism of angle closure in PCAG
1. the dilator muscle of the iris contracts, which
increases the amount of apposition between the
iris and the anteriorly located lens (reliative pupil
block)
Primary angle-closure glaucoma
Mechanism of angle closure in PCAG
2. increase the pressure in posterior chamber and
the flaccid peripheral iris bows anteriorly (iris
bombe)
3. the angle becomes obstructed by the peripheral
iris and the IOP raises
Primary angle-closure glaucoma
PACG can be divided into five overlapping stages:
 latent PACG
 subacute (intermittent)
 acute
 chronic
 absolute
The condition does not necessarily progress from
one stage to the next in an orderly sequence.
Primary angle-closure glaucoma
Latent PACG
Examination shows a shallow anterior chamber, a
convex-shaped iris-lens diaphragm, close
proximity of the iris to the cornea, a normal IOP
and a narrow angle capable of closure.
Without treatment, an eye with latent PACG may
remain normal or it may develop subacute, acute
or chronic angle closure with or without passing
through the other stages.
Primary angle-closure glaucoma
Treatment of latent PACG depends on the state of
fellow eye.
If it has had acute or subacute PACG, treatment is
by a laser iridotomy.
It lowers the risk of an acute angle closure.
Primary angle-closure glaucoma
Subacute PACG
It occurs when the angle is narrow in only one part.
A rapid partial closure and reopening the angle
occurs. The level of elevation of IOP is
proportional to the extend of angle closure.
Primary angle-closure glaucoma
Subacute PACG
The attacks may be precipitaded by:
 physiological mydriasis (watching TV in a dark
room, stress)
 physiological shallowing of the anterior chamber
(when the patient assumes a prone or semiprone
position to see or read)
Primary angle-closure glaucoma
Subacute PACG
The attacks are recurrent and usually broken after
1-2 hours by physiological miosis (exposure to
bright sunlight or sleep).
Presentation is with transient blurring of vision
associated with haloes around lights resulting
from corneal epithelial oedema.
They may also be some eye ache or frontal
headache.
Primary angle-closure glaucoma
Subacute PACG
Examination during an attack shows corneal
epithelial oedema.
In some cases pupil may be semidilated but the
globe itself is uncongested.
In between attacks the eye looks
perfectly normal although
the angle is narrow.
Primary angle-closure glaucoma
Subacute PACG
Treatment is with intensive miotic therapy of both
eyes.
Also bilateral laser peripheral iridotomies should
be performed.
Primary angle-closure glaucoma
Acute congestive angle-closure glaucoma
Acute congestive PACG is characterized by a
sudden and severe elevation of IOP as a result of
total closure of the angle.
Presentation is with rapidly progressive impairment
of vision associated with periocular pain and
congestion.
In severe cases nausea and vomiting may occur.
Primary angle-closure glaucoma
Acute congestive angle-closure glaucoma
Examination during the acute stage shows a ciliary
flush caused by injection of the limbal and
conjunctival blood vessels.
The IOP is elevated and the cornea is oedematous.
Primary angle-closure glaucoma
Acute congestive angle-closure glaucoma
The anterior chamber is shallow with peripheral
iridocorneal contact.
The pupil is vertically oval, fixed in the semidilated
position. It is unreactive to both light and
accommodation.
Primary angle-closure glaucoma
Acute congestive angle-closure glaucoma
After the corneal oedema has cleared, examination
shows:
 aqueous flare and cells
 dilated and congested blood vessels on the iris
 oedema of optic nerve head
 iridocorneal contact in gonioscopy
Primary angle-closure glaucoma
Acute congestive angle-closure glaucoma
Initial treatment is aimed primarily at lowering IOP
through systemic medication with hyperosmotic
agents (glycerol p.o., mannitol i.v.).
Hyperosmotic agents lower IOP by increasing blood
osmolality, thereby creating an osmotic gradient
between the blood and vitreous, and drawing water
from the vitreous.
Primary angle-closure glaucoma
Acute congestive angle-closure glaucoma
Subsequent treatment is aimed at re-establishing the
communication between the posterior and anterior
chambers by making an opening in the peripheral
iris.
A peripheral iridotomy is successful only if no more
than 50% of the angle is permanently closed by
peripheral anterior synechiae.
If more than half the angle is permanently closed, the
filtration surgery is usually required.
Primary angle-closure glaucoma
Acute congestive angle-closure glaucoma
After lowering the IOP topical therapy with antiglaucomatous drops, especially miotics may be
helpful in reducing IOP and topical steroids may
be useful in decongesting the eye.
Primary angle-closure glaucoma
Acute congestive angle-closure glaucoma
It is very important to treat the fellow eye
prophylactically with pilocarpine drops until a
prophylactic iridotomy has been performed.
Primary angle-closure glaucoma
Postcongestive angle-closure glaucoma
Examination shows a combination of the following signs:
 the IOP is normal, subnormal or elevated
 folds in Descemet’s membrane
 pigment granules on the corneal endothelium and iris
Primary angle-closure glaucoma
Postcongestive angle-closure glaucoma

stromal iris atrophy
 semidilated pupil
 small, grey-white anterior capsular or subcapsular
opacites (glaukomflecken)
 in gonioscopy - open angle or varying degrees of angle
closure
Primary angle-closure glaucoma
Chronic angle-closure glaucoma
The clinical features of chronic PACG are those of
POAG except that gonioscopy shows a variable
amount of angle closure.
Primary angle-closure glaucoma
Chronic angle-closure glaucoma
The management depends on the mechanism of
angle closure:
1. A gradual and progressive synechial angle
closure, usually starting superiorly and spreading
inferiorly.
Treatment is by laser iridotomy to eliminate any
element of pupil block, prevent the development
of new peripheral anterior synechiae and make
medical control easier.
Primary angle-closure glaucoma
Chronic angle-closure glaucoma
2. angle closure is a result of subacute attacks
These cases will already have had a laser iridotomy
so that the medical therapy should be added as
necessary.
Primary angle-closure glaucoma
Absolute angle-closure glaucoma is the end stage
of acute congestive PACG in which the eye is
completely blind.
Secondary glaucomas:
1. Common secondary glaucomas:
 pseudoexfoliative glaucoma
 pigmentary glaucoma
 neovascular glaucoma
 inflammatory glaucomas
Secondary glaucomas:
2. Uncommon secondary glaucomas:
 phacolytic glaucoma
 lens-related pupil block glaucomas
 red cell glaucoma
 angle-recession glaucoma
 ghost cell glaucoma
 iridocorneal endothelial syndromes
Common secondary glaucomas
Pseudoexfoliative glaucoma
Pseudoexfoliative glaucoma is chronic trabecular –
block open-angle glaucoma, caused by
pseudoexfoliation syndrome (PXS, PEX).
PXS typically affects elderly patients and is bilateral
only in about one-third cases.
In patients with unilaterated PXS, the propability of the
normal fellow eye also developing PXS after 10
years is 20%.
More than 50% of patients with PXS present with
glaucoma which is usually unilateral.
Common secondary glaucomas
Pseudoexfoliative glaucoma
PXS is characterised by the secretion of a greywhite fibrillogranular material by ageing
endothelial cells in anterior segment of the eye.
This material is abnormal basement membrane and
is histologically similar to amyloid.
Common secondary glaucomas
Pseudoexfoliative glaucoma
The most commonly recognized feature of PXS is
pseodoefoliation material (PXM) on pupillary
border and anterior lens surface.
The constant rubbing of the pupil scrapes the PXM
off the midzone of the lens, giving rise to a
central disc, a peripheral band and a clear zone
in between.
Peripheral band can be detected
only after the pupil has been dilated.
Common secondary glaucomas
Pseudoexfoliative glaucoma
Iris changes consist of PXM on the pupillary border,
pigment dispersion and atrophy of the sphincter
pupillae, which gives rise to transilumination
defects (sphincter has ‚moth-eaten’ pattern).
Common secondary glaucomas
Pseudoexfoliative glaucoma
The cornea may show deposits of both PXM and
pigment. The pigment is usually distributed
diffusely.
The zonules and cilliary processes are covered by
PXM and zonules themselves may be weak
(high risc of development of a zonular dialysis
during cataract surgery!).
Common secondary glaucomas
Pseudoexfoliative glaucoma
Gonioscopy shows hyperpigmentation of
trabeculum (pigment lies on the surface of
trabeculum).
Also Schwalbe’s line is pigmented and is called
Sampaolesi’s line.
Common secondary glaucomas
Pseudoexfoliative glaucoma
Other gonioscopic findings consist of deposits of
PXM which have been rubbed off the anterior
lens capsule by the iris float in the aqueous and
come to rest in the inferior trabecular meshwork.
On gonioscopy the PXM has a dandruff-like
appearance.
Common secondary glaucomas
Pseudoexfoliative glaucoma
The prognosis of pseudoexfoliative glaucoma is
not as good as in POAG because:
 the IOP is usually higher and more difficult to
control
 visual field loss may develop more rapidly.
Common secondary glaucomas
Pseudoexfoliative glaucoma
All patients with PXS and raised IOP should be
treated even in the presence of normal fields and
disc, because, if untreated, a large percentage of
cases will develop damage.
(medical treatment, laser trabeculoplasty, filtration
surgery)
Common secondary glaucomas
Pigmentary glaucoma
Pigmentary glaucoma is chronic trabecular block
open-angle glaucoma, caused by the pigment
dispersion syndrome (PDS).
PDS is a bilateral condition characterized by the
deposition of pigment granules throughout the
anterior segment. Glaucoma develops in 10% of
patients with PDS.
Affected individuals are typically myopic men in
the third or fifth decades of life.
The male:female ratio is 5:1.
Common secondary glaucomas
Pigmentary glaucoma
PDS is caused by shedding of pigment, resulting
from mechanical rubbing between the posterior
pigment layer of the iris and the anterior surface
of the zonular fibrils.
This state is caused by excessive posterior bowing
of the peripheral portion of the iris.
The pigment granules are released into the aqeous
humour and deposited on all anterior chamber
structures, including trabecular meshwork.
Common secondary glaucomas
Pigmentary glaucoma
Slitlamp examination shows:
1. Krukenberg’s spindle, which consists of pigment
deposits on the corneal endothelium. The size and
density of deposits are usually proportional to the
extent of associated iris atrophy.
2. The anterior chamber is very deep, particularly in
the midperiphery where the iris tends to bow
posteriorly.
Common secondary glaucomas
Pigmentary glaucoma
3. The anteror surface of iris is coated with
pigment granules. The loss of pigment from the
midperiphery of the iris gives slit-like iris
defects seen on transillumination.
4. The lens and extreme periphery of the retina
also show pigment deposits.
Common secondary glaucomas
Pigmentary glaucoma
Gonioscopy shows a wide open and heavily
pigmented angle.
The peripheral iris root shows a mild concavity
close to its insertion.
Common secondary glaucomas
Pigmentary glaucoma
The symptoms and treatment of pigmentary
glaucoma are usually those of POAG, but in some
patients the IOP may initially be very unstable.
In general, the long-term prognosis is relatively good
but some patients have very high levels of IOP so
that, at the time of diagnosis, it is common for
advanced visual field to be present in one eye and
relatively mild damage in the other.
Common secondary glaucomas
Neovascular glaucoma
In neovascular glaucoma (NVG) elevation of IOP
is caused by synechial angle closure through
contraction of fibrovascular tissue.
The common factor in all eyes with NVG is
severe, diffuse and chronic retinal ischaemia,
caused by:
 ischaemic retinal vein occlusion,
 proliferative diabetic retinopathy,
 carotid obstructive disease, carotid-cavernous
fistula, intraocular tumours, chronic intraocular
inflammation, ROP (rare causes).
Common secondary glaucomas
Neovascular glaucoma
NVG is divided into three stages:
1. rubeosis iridis
2. secondary open-angle glaucoma
3. synechial angle-closure glaucoma
Common secondary glaucomas
Neovascular glaucoma
1. rubeosis iridis
Slitlamp examination of early stage of rubeosis
iridis shows tiny dilated capillary at the pupillary
margin.
The new blood vessels grow radially over the
surface of the iris towards the angle.
At this stage the IOP is usually
normal and neovascularization
may regress (spontaneously or with
treatment).
Common secondary glaucomas
Neovascular glaucoma
Treatment of rubeosis iridis:
1. panretinal laser photocoagulation (PRP)
2. ppV (especially in eyes with residual retinal
detachment)
Common secondary glaucomas
Neovascular glaucoma
2. secondary open-angle glaucoma
Slitlamp examination shows continued growth of
new blood vessels across the iris surface, across
the face of ciliary body and scleral spur to the
angle.
Gonioscopy shows the formation of a fibrovascular
membrane which blocks the trabeculum, giving
rise of IOP.
Treatment options include: medical
therapy and PRP even if IOP is
controlled adequately by eye drops).
Common secondary glaucomas
Neovascular glaucoma
3. synechial angle-closure glaucoma
The fibrovascular tissue in the angle contracts and
pulls the peripheral iris over the trabeculum in a
zipper-like fashion.
Common secondary glaucomas
Neovascular glaucoma
Examination shows:
 reduced visual acuity,
 very high IOP with pain of the globe,
 congestion of the eye, corneal oedema, aqueous
flare, severe rubeosis iridis, distorted pupil with
ectropion uveae (caused by contraction of
fibrovascular tissue).
Common secondary glaucomas
Neovascular glaucoma
Gonioscopy shows synechial angle-closure with
inability to see any of the angle structures
posterior to Schwalbe’s line.
Common secondary glaucomas
Neovascular glaucoma
Visual prognosis is extremely poor!!!
Treatment is mainly to relieve pain and congestion
of the eye by the following methods:
 PRP (if media are clear) or peripheral retinal
cryotherapy (if media are hazy),
 medical therapy (the same as that for POAG, steroids and
atropine) – may make the eye more comfortable and
less congested,
 artificial filtering shunts,
 cyclodestructive procedures,
 enucleation (if all else fails)
Common secondary glaucomas
Inflammatory glaucomas
There are three main types of inflammatory
glaucomas:
1. angle closure with pupil block
2. angle closure without pupil block
3. open angle
Common secondary glaucomas
Inflammatory glaucomas
1.angle-closure glaucoma with pupil block
Secondary angle closure is caused by 360
iridolenticular adhesions – seclusio pupillae.
The pupil block obstructs the passage of aqueous
humour from the posterior to the anterior chamber,
and the increased pressure in the
posterior chamber causes an anterior
bowing of the peripheral iris –
iris bombe.
Common secondary glaucomas
Inflammatory glaucomas
If iris bombe occurs in an eye with active
inflammation, the iris sticks to the trabeculum and
iridocorneal contact becomes permanent with the
development of peripheral anterior synechiae (PAS).
Slitlamp examination shows seclusio pupillae, iris
bombe and very shallow anterior chamber.
Gonioscopy shows angle closure from
iridotrabecular contact.
Common secondary glaucomas
Inflammatory glaucomas
Treatment involves the following measures:
 prevention of synechial angle closure (intensive
topical steroids),
 lowering of IOP (B-blockers, sympathomimetics,
carbonic anhydrase inhibitors),
 laser iridotomy ( will be effective in lowerring
IOP, if at least 25% of angle is open)
Common secondary glaucomas
Inflammatory glaucomas
2. angle closure glaucoma without pupil block
The deposition and subsequent contaction of
inflammatory debris in the angle (during chronic
anterior uveitis) pull the peripheral iris over the
trabeculum, causing a gradual and progressive
synechial angle closure.
The rise of IOP is usually
gradual and even severe
elevations of IOP may be
asymptomatic!!!
Common secondary glaucomas
Inflammatory glaucomas
Slitlamp examination shows a deep anterior
chamber and variable amounts of angle closure
by peripheral anterior synechiae are found in
gonioscopy.
Exacerbations of intraocular inflammation in eyes
with chronic iridocyclitis are frequently
associated with lowering IOP!!!
Common secondary glaucomas
Inflammatory glaucomas
Treatment options:
 medical therapy (the same as that for secondary
angle closure caused by pupil block),
 filtration surgery, combined with anti-metabolites
or artificial filtering shunts,
 cyclodestructive procedures
Common secondary glaucomas
Inflammatory glaucomas
3. open angle glaucoma
In acute anterior uveitis the trabecular-block
may be caused by either inflammatory cells and
debris or acute trabeculitis.
In chronic anterior uveitis the facility of outflow
is impaired by trabecular scarring and sclerosis
secondary to chronic trabeculitis.
Common secondary glaucomas
Inflammatory glaucomas
Definitive diagnosis of inflammatory open angle
glaucoma is difficult because of the variable
appearance of the angle.
In theory, the angle should be open with
gelatinous exudate on the trabeculum – ‚mashed
potatoes’.
Treatment is the same as that for secondary
synechial angle-closure glaucoma.
Uncommon secondary glaucomas
Phacolytic glaucoma
This is trabecular-block open-angle glaucoma which
occurs in eyes with hypermature cataracts.
It is caused by trabecular obstruction with highmolecular, soluble lens proteins which have leaked
through an intact capsule into the aqueous humour.
Macrophages that have phagocytosed some of the
proteins may also contribute to trabecular
blockage.
Uncommon secondary glaucomas
Phacolytic glaucoma
Phacolytic glaucoma should not be cofused with
phacoanaphylactic uveitis which is an
autoimmune granulomatous reaction to lens
proteins occuring in eyes with ruptured
capsules.
Uncommon secondary glaucomas
Phacolytic glaucoma
Slitlamp examination shows an eye with a
hypermature cataract.
The anterir chamber is deep and contain floating
white particles, some of which may settle
inferiorly to form a ‚pseudohypopyon’.
Gonioscopy shows an open angle
with white particles in trabeculum.
Uncommon secondary glaucomas
Phacolytic glaucoma
Treatment –
cataract extraction!
Uncommon secondary glaucomas
Ghost cell glaucoma
Trabecular obstruction is caused by degenerated
red blood cells.
2 weeks after haemorrhage into the vitreous, the
haemoglobin leaks out of the red blood cells,
turning them into ‚ghost cells’.
They pass through a defect in the anterior vitreous
face into the anterior chamber and obstruct
aqueous outflow.
Uncommon secondary glaucomas
Ghost cell glaucoma
Slitlamp examination shows reddish-brown or
khaki particles in anterior chamber.
Treatment is initially medical. If this is ineffective,
irrigation of the anterior chamber should be
performed and the ghost cells washed out.
Congenital glaucomas
Congeniatal glaucomas are divided into:
1. Primary congenital glaucoma
2. Secondary congenital glaucoma
Primary congenital glaucoma (PCG)
PCG affects 1 in 10 000 births, with 65% patients
being boys. In 75% of cases both eyes are affected.
Aqueous outflow is impaired as the result of a
maldevelopment of the trabeculum and the
iridotrabecular junction, which is not associated
with other major ocular anomalies –
isolated trabeculodysgenesis.
Primary congenital glaucoma
Clinically, trabeculodysgenesis is characterised by
the absence of the angle recess, with the iris
inserted directly into the surface of the
trabeculum.
The iris insertion can be either flat or concave.
Primary congenital glaucoma
The clinical features depend on the age of onset and
the level of IOP.
Examination of patients shows the following:
1. Corneal haze – resulting from epithelial oedema
and corneal clouding is an important sign of
elevated IOP. It is often associated with
lacrimation, photophobia and blepharospasm.
Primary congenital glaucoma
2. Buphthalmos – occurs if the IOP becomes
elevated before the age of 3 years.
As the sclera enlarges, it also becomes thinner and
takes on a blue appearance as a result of enhanced
visualisation of the underlying choroid.
In advanced cases, when the anterior chamber
deepens the zonules become stretched and the lens
may subluxate.
The ocular enlargement
causes axial myopia.
Primary congenital glaucoma
3. Breaks in Descemet’s membrane may be
associated with endothelial decompensation and a
sudden influx of aqueous into the corneal stroma.
Healed breaks in Descemet’s membrane are called
Haab’s striae and appear as a horizontal lines in
cornea.
Primary congenital glaucoma
4. Glaucomatous cupping in infants may occur
early, although it may regress once the IOP is
normalized.
In contrast to adults eyes, the scleral canal in
infants enlarges with high IOPs because of the
generalized enlargement of the globe. The lamina
cribrosa may also bow posteriorly.
In infants, the cup/disc ratio may
be increased from either neuronal
loss or enlargement of the scleral
canal, or both.
Primary congenital glaucoma
Treatment of PCG:
1. Goniotomy – should be done as soon as it’s
possible!
In this procedure an incision is made in the angle to
establish a communication between the anterior
chamber and Schlemm’s canal.
Although goniotomy may have to
be repeated, the eventual success
rate is about 85%.
Primary congenital glaucoma
2. Trabeculotomy may be necessary if either corneal
clouding prevents visualization of the angle or
goniotomy has failed.
In this procedure, part of the trabecular meshwork is
removed to establish a communication between
the anterior chamber and Schlemm’s canal.
Primary congenital glaucoma
The prognosis is good in about 60% of cases.
The remainder develop visual loss from a
combination of:
 optic nerve damage,
 anisometropic amblyopia (myopia!),
 corneal scarring,
 cataract,
 lens subluxation.
A buphthalmic eyes are also susceptible to traumatic
damage!!!
Congenital glaucomas
Secondary congeniatal glaucomas occur in patients
with congenital disorders involving the cornea and
iris - iridocorneal disgenesis.
Rare conditions which may be associated with
glaucoma are:
o
o
o
o
o
o
o
Axenfeld’s anomaly,
Rieger’s anomaly,
Rieger’s syndrome,
Peter’s anomaly,
aniridia,
nanophthalmos,
phacomatoses.
Thank you