DR. MD.

YEAMLI KHAN
MBBS(DHAKA) DO(DU) FCPS (OPHTH)
Associate professor
Department of ophthalmology
Shahid Syed Nazrul Islam Medical College
GLAUCOMA
Sometimes Bluish
 Glaucoma
1. Gross Anatomy
2. Physiology
a) Production, circulation and outflow of the
aqueous humor.
b) Intra ocular pressure and factors
influencing IOP.
3. Classification of glaucoma.
4. Disease.(gross aspect)
a) Primary angle closure glaucoma i) Risk
factors ii) Symptoms iii) Signs iv) 4 hrs
Management
b) Primary open angle glaucoma: i) Risk
factors ii) Symptoms
c) Congenital glaucoma
i) Genetics ii) Symptoms iii) Signs
d) Secondary Glaucoma: Causes
6. Principles of Management:
a. Pharmacological treatment. b. Surgical
Management: c. Laser treatment
 DEFINITION
Glaucoma is defined as an acquired
optic neuropathy characterized by
loss of retinal ganglion cells and
retinal nerve fibre layer (RNFL).
 GLAUCOMA

Etiology
The most important factor which is
obstruction to the drainage of the
aqueous humor through the:
i. Angle of the anterior chamber
ii. At the pupil.
 PATHOGENESIS

Retinal ganglion cell death in glaucoma occurs predominantly through

apoptosis (programmed cell death).The glaucomatous damage is due to
the factors which affect perfusion of optic nerve head.

1. Direct Mechanical damage—The raised intraocular pressure pushes

the lamina cribrosa backwards, which squeezes the nerve fibres and
disturb the axoplasmic flow.
 PATHOGENESIS CONTD.

2. Ischamic damage—The perfusion of optic nerve head may be

affected due to decreased blood flow in the capillaries and in annulus
of Zinn which supply nutrition to the laminar and postlaminar optic
nerve head.
Both mechanisms might lead to a reduction in axoplasmic flow,
interference with the delivery of nutrients or removal of metabolic
products, deprivation of neuronal growth factors, oxidative injury and
the initiation of immune-mediated damage.
 CLASSIFICATION
Glaucoma may be
A. According to age of onset
a) congenital (developmental)
b) acquired.
B. On configuration of angle of the anterior chamber-
a) Open-angle
b) Angle-closure
C. Distinction is also made
a) primary
b) secondary glaucoma - in the latter a recognizable ocular or non-
ocular disorder contributes to elevation of IOP.
PRIMARY ANGLE-CLOSURE
GLAUCOMA (PACG)
 PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG)

This is a condition in which the intraocular tension is raised due to the

narrow or closed angle of the anterior chamber. There is obstruction to
the outflow of the aqueous humor.
 ETIOLOGY
It has a genetic basis. It is typically seen in eyes which are:
i. Small and hypermetropic eye
ii. Anatomical narrow angle of the anterior
chamber
iii. Shallow anterior chamber
iv. Iris—lens diaphragm is pushed forwards.
 Incidence
i. Age—It affects mainly in the 5th-6th decade
ii. Sex—Women are usually affected (male: female
ratio is 1:4)
iii. It is usually bilateral but one eye is involved first
iv. Personality—Highly strung, anxious persons with
unstable vasomotor system
v. Race—It is common among Asians and Eskimos
but rare in Africans and Caucasians.
MECHANISM OF ANGLE-CLOSURE GLAUCOMA
1. Relative pupil block—Normally pupillary margin just touches the
anterior surface of the lens.
MECHANISM OF ANGLE-CLOSURE GLAUCOMA CONTD.
2. Physiological iris bombe—On dilatation of the pupil there is crowding of
the iris in the angle of anterior chamber causing obsruction to the flow of
aqueous from the posterior to the anterior chamber at the level of the
pupil. The iris bows forwards due to the increased pressure in the posterior
chamber.
MECHANISM OF ANGLE-CLOSURE GLAUCOMA CONTD.
3. Irido-trabecular contact—It totally cuts off the drainage channel by
forming a false angle. It
precipitates an attack of raised intraocular pressure (acute congestive
attack).
 CLASSIFICATION

• Primary angle closure suspect (PACS)

• Primary angle closure (PAC)
• Primary angle-closure glaucoma (PACG)
 RISK FACTORS
• Age. The average age of relative pupillary block is about 60
years at presentation.
• Gender. Females are more commonly affected than males.
• Race. prevalent in Far Eastern and south east asian
• Family history. an increased prevalence of angle closure in
family members.
• Refraction. Eyes with ‘pure’ pupillary block are typically
hypermetropic, Up to one in six patients with
hypermetropia of one dioptre or more are primary
angle closure suspects
• Axial length. Short eyes tend to have a shallow AC
 SYMPTOMS
• Most patients with angle closure are asymptomatic, including a majority
of those with intermittently or chronically elevated IOP.
• Presentation can be with intermittent mild symptoms of blurring
(‘smoke-filled room’) and haloes (‘rainbow around lights’) due to corneal
epithelial oedema
• acutely with markedly decreased vision, redness and
ocular/periocular pain and headache; abdominal pain and other
gastrointestinal symptoms may occur.
 SYMPTOMS CONTD.
• Precipitating factors include
- watching television in a darkened room,
- pharmacological mydriasis or rarely miosis,
- adoption of a semiprone position (e.g. reading),
- acute emotional stress and
- occasionally systemic medication: parasympathetic antagonists or
sympathetic agonists including inhalers, motion sickness patches and
cold/flu remedies (mydriatic effect), topiramate and other sulfa derivatives
(ciliary body effusion).
 SIGNS
• Chronic presentation
○ VA is normal unless damage is advanced.
○ The AC is usually shallower in relative pupillary block than non-pupillary block.
○ IOP elevation may be only intermittent.
○ ‘Creeping’ angle closure is characterized by a gradual band-like anterior
advance of the apparent insertion of the iris. It starts in the deepest part of the
angle and spreads circumferentially.
○ Intermittent ITC may be associated with the formation of discrete PAS,
individual lesions having a pyramidal (‘saw-tooth’) appearance.
○ Optic nerve signs depend on the severity of damage.
 ACUTE PRIMARY ANGLE CLOSURE (APAC)
• VA is usually 6/60 to HM.
• The IOP is usually very high (50– 100 mmHg).
• Conjunctival hyperaemia with violaceous
circumcorneal injection.
• Corneal epithelial oedema
• The AC is shallow, and aqueous flare is usually
present.
• An unreactive mid-dilated vertically oval pupil is
classic .
• The fellow eye typically shows an occludable
angle; if not present, secondary causes should be
considered.
 RESOLVED APAC
○ Early: - low IOP,
- folds in Descemet membrane if IOPhas reduced
rapidly ,
- optic nerve head congestion,
glaukomflecken, spiral-shaped
- choroidal folds. atrophic iris, dilated pupil and
posterior synechiae
○ Late: - iris atrophy with a spiral-like configuration,
- glaukomflecken and other forms of cataract,
- irregular pupil due to iris sphincter/dilator damage
and posterior synechiae
-the optic nerve may be normal or exhibit varying
signs of damage, including pallor and/or cupping optic atrophy
– combined pallor and
cupping
NORMAL PUPILLARY RUFF
LOSS OF PUPILLARY RUFF
SECTORIAL IRIS ATROPHY
 SUBACUTE ANGLE CLOSURE

is intermittent episodes of spontaneously resolving mild/moderate

APAC, usually in patients with predominant pupillary block. The clinical
course may be chronic, or may culminate in a more severe/unresolving
episode of APAC.
 INVESTIGATION
• Anterior segment OCT
• Anterior chamber depth measurement
• Provocative testing.
• Gonioscopy
• IOP measurement
OCT
FLASHLIGHT TESTS TO MEASURE THE ANTERIOR CHAMBER
DEPTH
GONIOSCOPY ON THE SLIT LAMP TO MEASURE THE ANGLE
OF ANTERIOR CHAMBER
GONIOSCOPY: NORMAL ANTERIOR CHAMBER ANGLE
DARK ROOM-PRONE PROVOCATIVE TEST
IOP MEASUREMENT IN PACG BY APPLANATION
TONOMETER
IOP MEASUREMENT IN PACG BY NONCONTACT
TONOMETER (NCT)
 TREATMENT
PACS
• Laser iridotomy .
• If significant ITC persists after iridotomy,
- observation (most),
- laser iridoplasty, and
- long-term pilocarpine prophylaxis, e.g. 1% twice
daily; provocative testing may be helpful in some
patients.
• If symptomatic cataract is present, lens extraction
usually definitively opens the angle.
• If IOP is elevated, then by definition PAC is present.
ND:YAG LASER MACHINE 1064 FOR YAG PI
FIGURE- LASER IRIDOTOMY
.
LASER PERIPHERAL IRIDOPLASTY DONE
BY GREEN LASER 532
LPI DONE BY RESIDENT DOCTOR
GREEN LASER PARAMETER FOR LPI
ABRAHAM PI LENS FOR LPI
LASER PERIPHERAL IRIDOPLASTY
 PAC AND PACG

• Management is as for PACS, but further intervention

- If angle widening is inadequate after iridotomy,
- If IOP remains elevated.
• Urgency and intensity of treatment, and frequency of
review is tailored to the individual patient, taking into account
- IOP,
- extent of angle closure and
- glaucomatous damage, if present.
• Medical treatment as for POAG may be required for eyes
with substantial synechial closure or with persistently
elevated IOP despite an opened angle.
 APAC
• Initial treatment
○ The patient should assume a supine position.
○ Acetazolamide 500 mg is given intravenously or orally .
○ A single dose of each of
1%,timolol 0.5%, and -
- prednisolone 1% or dexamethasone 0.1%
○ Pilocarpine 2–4% one drop to the affected eye, repeated
after half an hour; one drop of 1% into the fellow eye.
○ Analgesia and an antiemetic may be required.
 RESISTANT CASES

○ Central corneal indentation to force aqueous into the angle;

epithelial oedema can be cleared first with topical 50% glycerol
to improve visualization and avoid abrasion.
○ Further pilocarpine 2–4%, timolol 0.5%, apraclonidine 1% and topical
steroid.
○ Mannitol 20%, 1–2 g/kg intravenously over 1 hour, oral glycerol
50% 1 g/kg, or oral isosorbide 1–1.5 g/kg,
 RESISTANT CASES CONTD.
○ Early laser iridotomy or iridoplasty after clearing corneal oedema with
glycerol.
○ Paracentesis can be performed, but carries significant risks.
○ Surgical options:
- peripheral iridectomy,
- lens extraction,
- goniosynechialysis,
- trabeculectomy and
-cyclodiode
SUBSEQUENT MEDICAL TREATMENT
○ Pilocarpine 2% four times daily to the affected eye
and 1% four times daily to the fellow eye.
○ Topical steroid (prednisolone 1% or Dexamethasone
0.1%) four times daily if the eye is acutely inflamed.
○ Any or all of the following should be continued as
necessary according to response:
- timolol 0.5% twicedaily,
- oral acetazolamide 250 mg four times daily.
SUBSEQUENT MEDICAL TREATMENT CONTD.
• Bilateral laser iridotomy is performed once an
attack has been broken.
• Subsequent management
- as for post-iridotomy chronic PAC/PACG. - A
low threshold may be adopted for
cataract surgery
- Trabeculectomy is occasionally necessary
for persistent IOP elevation despite a
successfully opened angle.
TRABECULECTOMY
THANK YOU