GLAUCOMA
AQUEOUS SECRETION
Aqueous humor is produce in two
steps:
- Formation of a plasma filtrate within
the stroma of the ciliary body.
- Formation of aqueous from this
filtrate across the blood-aqueous
barrier.
Two mechanisms are nvolved:
- Active secretion
- Passive secretion
AQUEOUS OUTFLOW
Anatomy
1. The trabecular meshwork
a. The uveal meshwork
b. The corneoscleral meshwork
c. The juxtacanalicular (cribiform)
meshwork
2. Schlemm canal
Physiology
1. Trabecular (conventional)
2. Uveoscleral (unconventional)
INTRAOCULAR PRESSURE
- The IOP is determined by the
balance between the rate of
aqueous secretion and secretion
outfllow.
- The distribution of IOP within the
general population has a range of
11-21 mmHg.
- Normal IOP varies with the time of
the day, heartbeat, blood pressure
level and respiration.
- The diurnal pattern varies, with a
tendency to be higher in the
morning and lowering the afternoon
and evening.
OVERVIEW OF GLAUCOMA
- potentially progressive and
characteristic optic neuropathy
which is associated with visual field
loss as damage progresses, and in
which intraocular pressure is usually
a key modifying factor
- Glaucoma affects up to 2% of those
over the age of 40 years globally,
and up to 10% over the age of 80;
50% may be undiagnosed.
Classification
- Glaucoma may be congenital
(developmental) or acquired.
- Sub-classification into open-angle
and angle-closure types is based on
the mechanism by which aqueous
outflow is impaired with respect to
the anterior chamber angle
configuration.
PATHOLOGICAL FINDINGS
1. Peripheral anterior synechiae
 Primary angle-closure glaucoma.
 Anterior uveitis.
 Iridocorneal endothelial (ICE)
syndrome.
2. Neovascularization
 Neovascular glaucoma.
 Fuchs heterochromic cyclitis.
 Chronic anterior uveitis.
3. Hyperpigmentation
 Pigment dispersion syndrome.
 Pseudophakic pigment
dispersion.
 Pseudoexfoliation syndrome.
 Blunt ocular trauma.
  Anterior uveitis. CHANGES IN GLAUCOMA
 Following acute angle-closure Glaucomatous damage results in
glaucoma characteristic signs involving:
 • Following YAG laser iridotomy. Peripapillary changes: Peripapillary atrophy
 Iris melanoma. surrounding the optic nerve head may be of
 Iris pigment epithelial cysts. significance in glaucoma and may be a sign
 Naevus of Ota. of early damage in patients with ocular
4. Trauma hypertension.
 Angle recession. Optic nerve head: The spectrum of disc
 Trabecular dialysis. damage in glaucoma ranges from highly
 Cyclodialysis. localized tissue loss with notching of the
 Foreign bodies. NRR to diffuse concentric enlargement of
5. Blood in the Schlemm canal the cup, as well as changes in vasculature.
 Carotid-cavernous fistula and
dural shunt. Subtypes of glaucomatous damage:
 Sturge–Weber syndrome. 1. Focal ischemic discs
 Obstruction of the superior vena 2. Myopic disc with glaucoma
cava. 3. Senile sclerotic discs.
 Physiological variant. 4. Concentrically enlarging discs

EVALUATION OF OPTIC NERVE HEAD NON-SPECIFIC OF GLAUCOMATOUS

DAMAGE
Normal optic nerve head Other disc signs of glaucomatous damage,
Neuroretinal rim though of variable specificity, include:
1. Baring of circumlinear blood vessels
 The neuroretinalrim (NRR) is the
is a sign of early thinning of the NRR.
tissue between the outer edge of
2. Bayoneting is characterized by
the cup and the optic disc margin.
double angulation of a blood vessel
 The normal rim has an orange or
3. Collaterals between two veins at the
pink color and a characteristic
disc
configuration in most healthy eyes.
4. Loss of nasal NRR
Optic disc size
5. Lamina dot sign
Optic disc size is important in deciding if a
6. Disc hemorrhages often extend from
cup-disc (C/D) ratio is normal. Normal
the NRR onto the retina, most
median vertical diameter for non-
commonly inferotemporally.
glaucomatous discs is 1.50 mm in a
7. ‘Sharpened edge’ or ‘sharpened rim’
Caucasian population.
is a sign of advancing damage.
Cup–disc ratio
The C/D ratio indicates the diameter of the
CHANGES IN GLAUCOMA
cup expressed as a fraction of the diameter
Retinal nerve fiber layer
of the disc; the vertical rather than the
In glaucoma subtle retinal nerve fiber layer
horizontal ratio is generally used in clinical
(RNFL) defects precede the development of
practice.
detectable optic disc and visual field
changes; their onset often follows disk
hemorrhages.
(a) localized wedge-shaped defects
(b) diffuse defects that are larger and have
indistinct borders
OCULAR HYPERTENSION
It is estimated that 4–7% of the population
over the age of 40 years have IOPs >21
mmHg without detectable glaucomatous
damage: ‘ocular hypertension’ (OHT).
Risk factors for developing glaucoma:
1. IOP
2. Age
3. Central corneal thickness (CCT)
4. Cup–disc (C/D) ratio
5. Pattern standard deviation (PSD)
PRIMARY OPEN-ANGLE GLAUCOMA
 also referred to as chronic simple
glaucoma, is a generally bilateral
disease of adult onset.
 An IOP >21 mmHg at some stage.
 Glaucomatous optic nerve damage.
 An open anterior chamber angle.
 Characteristic visual field loss as
damage progresses.
 Absence of signs of secondary
glaucoma or a non-glaucomatous
cause for the optic neuropathy.
RISK FACTORS:
 IOP
 Age
 Race
 Family History
 Diabetis mellitus
 Myopia
 Vascular Disease
Examination
1. Visual acuity
2. Pupils. Exclude a relative afferent
pupillary defect (RAPD)
3. Colourvision assessment such as
Ishihara charttesting if there is any
suggestion of an optic
neuropathyotherthan glaucoma.
4. Slit-lamp examination. Exclude
features of secondaryglaucomas
such as pigmentary and
pseudoexfoliative.
5. Tonometry, prior to pachymetry,
noting the time ofday.
6. Pachymetry for CCT.
7. Gonioscopy.
8. Optic disc examination should
always be performedwith the pupils
dilated.
9. Perimetry
10. Optic disc or peripapillary RNFL
POAG VISUAL FIELD DEFECTS
 Paracentral, small, relatively steep
depressions
 Nasal (Ronne) step represents a
difference in sensitivity above and
below the horizontal midline in the
nasal field
 Arcuate-shaped defects develop as a
result of coalescence of paracentral
scotomas.
 Enlargement of scotomas due to
damage to adjacent fibres.
 A ring scotoma
 End-stage changes are characterized
by a small island of central vision
typically accompanied by a temporal
island.
NORMAL-PRESSURE GLAUCOMA
 also referred to as normal- or low-
tension glaucoma, is a variant of
POAG.
It is characterized by:
  IOP consistently equal to or less than
21 mmHg.
 Signs of optic nerve damage in a
characteristic glaucomatous pattern.
 An open anterior chamber angle.
 Visual field loss as damage
progresses, consistent in pattern
with the nerve appearance.
 No features of secondary glaucoma
or a non glaucomatous cause for the
neuropathy.
RISK FACTORS
1. Age. Patients tend to be older than
those with POAG, though this may
be due to delayed diagnosis.
2. Gender. Some studies have found a
higher prevalence in females.
3. Race. NPG occurs more frequently in
Japan than in Europe or North
America.
4. Family history. The prevalence of
POAG is greater in families of
patients with NPG than in the
normal population.
5. CCT is lower in patients with NPG
than POAG.
6. Abnormal vasoregulation
PRIMARY ANGLE-CLOSURE GLAUCOMA
term ‘angle-closure’ refers to occlusion of
the trabecular meshwork (TM) by the
peripheral iris (iridotrabecular contact –
ITC), obstructing aqueous outflow.
CLASSIFICATIONS:
1. Primary angle-closure suspect (PACS)
2. Primary angle-closure (PAC)
3. PrimaRy angle-closure glaucoma
(PACG)
MECHANISM
1. Pupillary block: Failure of aqueous
flow through the pupil (relative
pupillary block
2. Non-pupillary block relating to the
iris: Specific anatomical factors
include plateau iris (anteriorly
positioned ciliary processes), and a
thicker or more anteriorly-
positioned iris.
3. Lens-induced angle-closure:
Includes only those cases in which a
sudden change in lens volume
and/or position leads to an acute or
subacute IOP rise.
4. Retrolenticular causes: Malignant
glaucoma (‘ciliolenticular block’)
5. ‘Combined mechanism’ describes
the combination of angle-closure
and open-angle elements.
RISK FACTORS
1. Age: The average age at
presentation is about 60 years and
the prevalence increases thereafter.
2. Gender:Females are more
commonly affected than males.
3. Race.
4. Family history: First degree relatives
are at increased risk.
5. Refraction: Eyes with ‘pure’ pupillary
block are typically hypermetropic
6. Axial length
CLASSIFICATION OF SECONDARY
GLAUCOMA
Open-angle
1. Pre-trabecular glaucoma in which
aqueous outflow is obstructed by a
membrane covering the trabeculum.
2. Trabecular glaucoma in which the
obstruction occurs as a result of
‘clogging up’ of the meshwork.
3. Post-trabecular glaucoma in which
the trabeculum itself is normal but
 aqueous outflow is impaired as a
result of elevated episcleral venous
pressure.
Angle-closure
Secondary angle-closure is caused by
impairment of aqueous outflow secondary
to apposition between the peripheral iris
and the trabeculum.
1. With pupillary block
2. Without pupillary block
PSEUDOEXFOLIATION
Pseudoexfoliation syndrome
known as exfoliation syndrome, is a
relatively common cause of chronic open-
angle glaucoma, though subtle signs are
easily overlooked.
Pseudoexfoliation glaucoma
Trabecular blockage due to a combination of
‘clogging up’ of the trabeculum by PXF
material and/or pigment released from the
iris.
PIGMENT DISPERSION
Pigment dispersion syndrome:
 bilateral condition characterized by
the liberation of pigment granules
from the iris pigment epithelium and
their deposition throughout the
anterior segment.
 Pigment shedding is caused by the
mechanical rubbing of the posterior
pigment layer of the iris against
packets of lens zonules as a result of
excessive posterior bowing of the
mid-peripheral portion of the iris.
PIGMENTARY GLAUCOMA
 Elevation of IOP appears to be
caused by pigmentary obstruction of
the intertrabecular spaces and
damage to the trabeculum
secondary to denudation, collapse
and sclerosis.
 Presentation is usually with chronic
glaucoma most commonly in the 3rd
and 4th decades although in women
it tends to develop around 10 years
later.
NEOVASCULAR GLAUCOMA
 is an aggressive condition which
occurs as a result of iris
neovascularization (rubeosis iridis).
 The common etiological factor is
severe, diffuse and chronic retinal
ischaemia.
Causes of rubeosis iridis
1. Ischaemic central retinal vein
occlusion
2. Diabetes mellitus
3. Arterial retinal vascular disease
Classification
 Despite a degree of overlap it is
convenient to divide
 NVG into the following three stages:
(a) rubeosis iridis,
(b) secondary open-angle glaucoma
(c) secondary synechial angle-
closure glaucoma.
RUBEOSIS IRIDIS
 Tiny dilated capillary tufts or red
spots develop at the pupillary
margin
 The new vessels grow radially over
the surface of the iris towards the
angle.
 Angle neovascularization in the
absence of pupillary involvement.
SECONDARY OPEN-ANGLE GLAUCOMA
NEOVASCULAR tissue proliferates across the
face of the ANGLE & the new blood vessels
arbourize and form a fibrovascular
membrane which blocks the trabeculum,
giving rise to secondary open-angle
glaucoma. TRAUMATIC GLAUCOMA
Hyphaema: may be associated with IOP
elevation due to trabecular blockage by red
TX: blood cells.
 Topical atropine 1% and intensive Pupillary occlusion by a blood clot may be
topical steroids should be given if superimposed on an angle-closure
significant inflammation is present. component.
 Intravitreal VEGF inhibitor injection
Angle recession glaucoma: rupture of the
SECONDARY ANGLE-CLOSURE GLAUCOMA face of the ciliary body, the portion that lies
rubeosis continues to progress the angle between the iris root and the scleral spur,
becomes progressively closed by due to blunt trauma.
contraction of fibrovascular tissue with
pulling of the peripheral iris over the PRIMARY CONGENITAL GLAUCOMA (PCG)
trabeculum.  Most cases are SPORADIC, 10%
approx inheritance is AR w/
INFLAMMATORY GLAUCOMA incomplete penetrance.
Elevation of intraocular pressure (IOP)  Caused by maldevelopment of the
secondary to intraocular inflammation angle of the anterior chamber,
frequently presents a diagnostic and unassociated with any other major
therapeutic challenge. ocular anomalies (isolated
trabeculodysgenesis).
CLASSIFICATION
1. Angle-closure with pupillary block. CLASSIFICATION
2. Angle-closure without pupillary TRUE
block. INFANTILE
3. Open-angle. JUVENILE
4. Posner–Schlossman syndrome.
SIGNS
LENS-RELATED GLAUCOMA Corneal haze
Phacolytic glaucoma: Buphthalmos
 (lens protein glaucoma) is open Breaks in Descemet membrane
angle glaucoma occurring in Optic disc cupping
association with a hypermature
cataract. ANIRIDIA
 Once the IOP is controlled medically,  a rare bilateral condition that may
the proteinaceous material is have life-threatening associations
flushed out and the cataract  typically at birth with nystagmus and
removed. photophobia.
Phacomorphic glaucoma:  The parents may have noticed
an acute secondary angleclosure glaucoma absence of irides or ‘dilated pupils
precipitated by an intumescent  Can vary to MINIMAL, PARTIAL &
cataractouslens. TOTAL.
  Glaucoma occurs in approximately water is ‘drawn out’ from the
75% of patients vitreous.

GLAUCOMA MEDICATIONS
 Most glaucoma medications are
administered topically.
 The decision on which medication to
prescribe depends not only on the
type of glaucoma, but also on the
patient’s medical history.
 Beta-blockers: Adrenergic neurons
secrete noradrenaline at
sympathetic postganglionic nerve
endings.
 Reduce IOP by decreasing aqueous
secretion and are therefore useful in
all types of glaucoma,irrespective of
the state of the angle.
 Alpha-2 agonists: decrease IOP by
both decreasing aqueous secretion
and enhancing uveoscleral outflow.
 Prostaglandin analogues: sustained
IOP-lowering effect which probably
extends for several days in most
patients.
 Topical carbonic anhydrase
inhibitors: chemically related to the
sulphonamides they lower IOP by
inhibiting aqueous secretion.
 Miotics: parasympathomimetic
drugs that act by stimulating
muscarinic receptors in the sphincter
pupillae and ciliary body.
 Combined preparations: similar
ocular hypotensive effects to the
sum of the individual components
improve convenience and patient
compliance
 Systemic carbonic acid inhibitors:
Osmotic agents: lower IOP by
creating an osmotic gradient
between blood and vitreous so that