Glaucoma

Dr. Yang Mochi

Review

 1.anatomy of the angle

 2.aqueous humor outflow

Anatomy of the angle

 The anterior chamber is bounded

anteriorly by the posterior surface
of the cornea and the anterior
surface of the iris.
 2.5mm deep in the center
Anatomy of the angle
 Aqueous humor

 Aqueous humor is produced by the ciliary body.

 0.15~0.3ml

 Entering the p.c, it passes through the pupil into

the a.c and then peripherally toward the a.c

angle.

 Aqueous humor outflow occurs by two routes:

 Trabecular outflow

 75%~90%
 Trabeculum is the site for
pressuredependent aqueous outflow

functioning as a one-way valve that

allows aqueous to leave the eye but
does not allow the flow inside it.
 Trabecular outflow

Trabecular mashwork is anatomically

divided into 3 parts:
 Uveal mashwork: innermost,larger
opennings
 Corneoscleral mashwork: larger
part,small opennings
 Juxtacanalicular mashwork: outermost,
the major site of outflow resistance
Uveoscleral outflow
 Nearly 5%~15%
 The aqueous passes across the
ciliary muscles into the
supraciliary and suprachoroidal
spaces and drained into the
venous circulation.
 pressure-dependent.
a. Trabecular outflow
b. Uveoscleral outflow
c. Absobed by recess of iris
Glaucoma

Glaucoma is in many ways a

mysterious disease process.

It is more than merely the

reflection of an intraocular
pressure, or a field defect, or
a change in the optic nerve
head.
Glaucoma affects approximately 4%
of the population above the age of
40.

It can also affect younger people,

and measurement of eye pressure
is an important part of routine eye
examination.
Glaucoma is the second
blindness disease behind
cataract.

First blindness disease can

not recover ----glaucoma
Risk factors of glaucoma
 positive family history
 high intraocular pressure
(IOP)
 myopia
 old age
 black race
 diabetes mellitus
 high blood pressure
 IOP is a major risk factor,
but not always, especially for
open angle glaucoma & normal
tension glaucoma.

 Vascular or ischemic factors

Definitio
n
Glaucoma

Sufficiently high intraocular

pressure will result in damage to
the optic nerve and ultimately
loss of visual field and visual
acuity.
 Concept:
Those suffer from pathologic
high IOP which is sufficient to
cause excavation of optic disc,
optic nerve atropy and
characteristic loss of visual field
are called glaucoma.
Normal fundus
 Glaucomatous cupping

The nasal displacement of the vessels and hollowed-out

appearance of the optic disk except for a thin border.
Peripheral field loss
Glaucoma’s Physiologic
Mechanisms
Physiology of Aqueous
Humor
The intraocular pressure is
determined by the rate of
aqueous production and the
resistance to outflow of
aqueous from the eye. Some
knowledge of the physiology of
aqueous humor is necessary
for understanding glaucoma.
aqueous humor
- produced by the
ciliary process
- returned to blood
supply via canal of
Schlemm
- helps control intra-
ocular pressure
 Circulation of aqueous
humor

It exits from the anterior chamber at the angle of the

anterior chamber, flowing through the trabecular
meshwork of the sclera, into schlemm’s canal.
 Intraocular Pressure (IOP)

IOP(10-21mmHg)
The amount
The rate of
of resistance
aqueous to aqueous
humor flow out of
productio the anterior
n chamber
Pathophysiology of
Glaucoma

The pathophysiology of
intraocular pressure elevation
---whether due to open-angle
or angle-closure mechanisms is
considered.
 The effects of raised intraocular
pressure within the eye are common to
all forms of glaucoma, their
manifestations being influenced by the
time course and magnitude of the rise
in intraocular pressure.
The major mechanism of visual
loss in glaucoma is ganglion
cell atrophy, leading to
thinning of the inner nuclear
and nerve fiber layers of the
retina and axonal loss in the
optic nerve.
 The optic disk
becomes atrophic,
with enlargement of
the optic cup.
The iris and ciliary
body also become
atrophic, and the
ciliary processes
show hyaline
degeneration.
Raise IOP cause damage
of the RNFL
Raise IOP cause damage
of the optic never
 Raise IOP cause
damage of the optic
never
① Bjerrum scotoma isolated
from blind spot
② arcuate scotoma(fully
developed nerve fiber
bundle defect with nasal
step)
③ Double arcuate scotoma
with peripheral
breakthrough and nasal
step
④ End stages in glaucoma
field loss. Renmnant of
Classification
A generally accepted
classification of glaucoma
is as follows:
(1) Primary glaucoma
Angle-closure glaucoma:
Iris bombe:
Acute angle-closure
glaucoma
Chronic angle-closure
glaucoma
Plateau iris
Open-angle glaucoma:
Chronic simple glaucoma
Normal tension glaucoma
Ultrasound biomicroscope image showing anterior convexity of the iris in primary angle-
closure glaucoma
(2) Secondary glaucoma
(3) Congenital glaucoma
Infantile glaucoma
Juvenile glaucoma
Glaucoma associated
with
congenital anomalies
Congenital glaucoma (buphthalmos)
 Primary
Angle-closure
Glaucoma
Etiology:
blockage or permanent synechia
of
trabecular meshwork by
peripheral iris.
narrow angle,
small eye,
shallow anterior chamber
 Mechanism of angle-closure
glaucoma

The underlying
mechanism is
pupillary block, in
which aqueous
egress through the
pupil is limited
causing forward iris
displacement.
Mechanism of angle-closure
glaucoma

Primary angle-closure
glaucoma results from
obstruction of aqueous
humor outflow through
the trabecular
meshwork by
peripheral iris
apposition to the
cornea with
consequent elevation
in intraocular
Factors leading to its occurrence
include a shallow anterior chamber
with narrow angle, which is more
likely with age, due to enlargement
of the lens, and a semi-dilated pupil
as occurs in the evening, or with
dilating drops. Intumescent cateract

It occurs mainly in the elderly, more

commonly in females and
hypermetropic individuals.

It also has a familial tendency.

Angle-closure glaucoma can
occur in subacute, acute, and
chronic forms and is associated
with an anatomically narrow
anterior chamber angle.
In its acute form, primary angle-
closure glaucoma is an
ophthalmic emergency with a
natural history of severe visual
loss.
Acute angle-
closure
Glaucoma
Risk factors of acute angle-closure
glaucoma
small or crowded eye
short axis of the globe
Anatomica small cornea
l
shallow anterior chamber
narrow angle
factors ： thick lens

fatigue
Induced anxiety
anger
factors ：
dark circumstance
 Staging:

1. Preclinical stage
2. Premonitory stage
3. Acute attack
4. Remission stage
5. Chronic stage
6. Absolute stage
Clinical Findings of

Acute attack
Symptoms
excruciating pain localized in
or
around the eye
often in association with
headache

 characterized by
a sudden onset of
blurred vision
Symptoms
 a rainbow-colored halo
is seen around lights.

 Nausea
vomiting
 Signs

markedly
increased IOP （ 50-
100mmHg ）
measured by
applanation
tonometry
 Signs

ciliary injection

an edematous
cornea

a fixed,
moderately
dilated pupil
 Signs
Slit lamp examination
shallow anterior chamber
 Signs

Gonioscopy shows a very narrow

angle or complete angle closure.
 Gonioscopic view
of the normal angle
structure

Iris root
Ciliary
body
Scleral spur
Trabecular
meshwork
Schwalbe’s line
 Signs
Glaukomflecke
n

Sector atrophy of
the iris

Pigmental KP
 Diagnosis
typical symptoms and
signs
of acute attack

Definitive diagnosis__
angle closure
Diagnosis
 Acute attack :
nausea, vomitting, headache
 High IOP
 Reduced vision
 Congestion
 Edematous cornea
 Shallow chamber
 Pupil dilated
Differential diagnosis
1. Acute conjunctivitis
2. Acute iridocyclitis
3. Acute angle-closure glaucoma
Identification points:
Vision acuity,Cornea ,anterior chambe
iris, pupil, IOP
Treatment

 Medicine
 Surgery
Treatment

1. IOP controled with

20% mannitol, 1% pilocarpine
0.25% timolol, diamox, etc
2. Peripheral iridectomy
laser iridotomy
3. Trabeculectomy
If there is extensive angle damage or if
the pressure fails to be controlled on
Pilocarpine, a drainage procedure, e.g.
trabeculectomy, is required.

If the pressure is down to normal, a

laser iridotomy or surgical peripheral
iridectomy is performed on the affected
eye.

A prophylactic laser iridotomy is

performed on the other eye a few days
later.
 Chronic angle-closure
glaucoma

Etiology: still unknown

shallow chamber
narrowed angle
Clinical manifestation
 IOP increase
progressively
 Excavation of optic cup
 Visual field loss

Seidel’s scotoma
nasal step
arcuate scotoma
circuit scotoma
severe
tubular vision
Treatment
1. Medical treatment
0.25% pilocarpine
0.5% timolol
diamox
mannitol if necessary
2. Peripheral iridectomy
or
trabeculectomy
according to
gonioscopy
 Primary
Open-angle Glaucoma
Primary open-angle glaucoma
is the most common form of
glaucoma in the community,
affecting over 1 in 200 of the
population over 40 years of
age.
In primary open-angle
glaucoma, aqueous secretion
by the ciliary body is normal,
and its flow between the lens
and the iris through the pupil
into the anterior chamber is
normal.
However, the trabecular
meshwork does not permit
adequately rapid egress of
aqueous with a resultant
pressure elevation.
Primary open-angle glaucoma
consists of progressive loss of
visual field due to optic nerve
damage through raised
intraocular pressure.

It is insidious in onset and

entirely asymptomatic until
pronounced field loss is
evident in the end stages.
Etiology: still unknown
Characteristics:
high IOP
open angle
pathologic findings on trabecular
meshwork
& Schlemm’s cannal
 Clinical findings
Symptoms:
usually no symptoms
usually found at late stage
few blurred vision, pain of the eye
IOP:
fluctuated at early stage
high at late stage
24-hour IOP curve is important for abnorm
findings
 Clinical findings
Anterior Segment of Eye:
usually no abnormal findings
Fundus Examination (key tips):
1. optic cup enlarged and
deepened
2. narrowing of neuroretinal rim
3. larger C/D ratio
4. unsymmetric C/D ratio
5. hemorrhage on or near optic disc
6. loss of optic nerve fiber
Clinical findings

visual function: loss of visual

field
1. paracentral scotoma
2. arcuate scotoma
3. quadrant field loss
4. tubular visual field
It is usually bilateral and there is a strong familial
tendency.

In order to make the diagnosis four factors

are important:
(1) Raised intraocular pressure, low tension glaucoma,
ocular hypertension;
(2) Open angle on gonioscopy;
(3) Cupping of the optic disc: This is due to a loss in the
number of nerve fibres passing through the disc.
C/D;
(4) Glaucomatous field loss: paracentral
or arcuate scotomata, peripheral field loss, altitudinal
defects, entire peripheral field loss, central island.
Diagnosis

IOP: 24-hour IOP curve important

Optic cup changes:
Visual field loss:

any patient with either 2 of the 3

signs mentioned above plus an
open angle,
diagnosis can be made.
Treatment

 Medical:
target IOP: various, individual
beta-blockers or alpha-excitors
diamox (carbonic anhydrase
inhibitor)
latanoprost
 Laser : trabeculoplasty
 Filtering surgery
trabeculectomy
nonpenetrating trabecular
surgery
reversed trabeculectomy
 Management

Referral is urgent if there is extensive

field loss or cupping of the disc, or an
intraocular pressure over 30 mmHg.

The mainstay of treatment is using

drops to reduce intraocular pressure.
The principal ones used are:
(1) Beta-blocks, e.g. Timolol drops,
which reduce aqueous secretion,
0.25% to 0.5%.
(2) Cholinergic agonists, e.g.
Pilocarpine, which increase
aqueous outflow, 1%, 2%, or 4%.
(3) Alpha adrenergic agonists, which
increase aqueous outflow.
(4) Carbonic anhydrase inhibitors, e.g.
Acetazolamide 250 mg b.i.d. to
t.i.d. p.o., are used reduced
aqueous secretion.
(5) Surgical treatment consists of
trabeculectomy, which creates an
artificial drainage channel from the
posterior chamber to the
subconjunctival space via a filtering
bleb, or laser trabeculoplasty,
which open up the trabecular
meshwork to facilitate drainage.
Secondary
Glaucoma
Glaucoma secondary to anterior
uveitis,
when there is marked anterior
chamber activity, an open angle
and
the intraocular pressure is
generally not as high, e.g. 35-45
mmHg.
Acute anterior uveitis

when the cornea may appear

hazy to the naked eye, but this
is due to keratic precipitates,
the pupil is small and posterior
synechiae are present,
together with marked anterior
chamber activity.
Posterior synechiae &
seclusio pupillae
Phakolytic glaucoma

when there is a mature cataractous

lens and protein cause a uveitic
glaucoma. Treatment is to lower
pressure and then perform cataract
extraction.
Phakomorphic glaucoma

when a swollen, cataractous lens

causes pupil block and angle-closure
glaucoma.
Treatment is prompt cataract
extraction.
 Neovascular glaucoma
when there is a history of
diabetes or central retinal
vein occlusion.
Rubeosis

with blood vessels in

the angle, is seen on
examination.
Congenital glaucoma
 Infantile glaucoma
 Juvenile glaucoma
abnormalities of angle
 Surgery
trabeculotomy
goniotomy
 Homework
 Definition of glaucoma?
 Classification of glaucoma
 Circulation of aqueous humor
 Mechanism of angle-closure glaucoma
 Mechanism of open angle glaucoma
 Clinical Findings of Acute attack of
acute angle-closure glaucoma
 Differential diagnosis of glaucoma
 Treatment of glaucoma
Thanks
to every
one