GLAUCOMA

dr.M.YUSRAN, SpM, MSc.

Department of Ophthalmology
Faculty of Medicine UNILA/RSAM
Glaucoma
A group of disease that have in common a characteristic optic
neuropathy with associated visual field loss for which
elevated IOP is one of primary risk factors.
Normal IOP: 10-22 mmHg.

Three risk factor determine the IOP:

- rate of aqueous humor production by ciliary body

- resistance to aqueous outflow across the
trabecular meshwork-Schlemms canal system
- the level of epischeral venous pressure
Classification
PRIMARY GLAUCOMA
not associated with known ocular or systemic disorders that
cause the
increased resistance to aqueous outflow
usually affects both eyes
may be inherited
SECONDARY GLAUCOMA
associated with ocular or systemic disorders responsible for
decreased aqueous outflow
the causal diseases are often unilateral
family occurrence is less common
OPEN-ANGLE GLAUCOMA
1. Primary open-angle glaucoma (POAG)
not associated with known ocular or systemic disorders that cause
increased resistance to aqueous outflow or damage to optic nerve
usually associated with elevated IOP
2. Normal-tension glaucoma
considered in continuum of POAG; often used when IOP is not
elevated
3. Juvenile open-angle glaucoma
used when open-angle glaucoma diagnosed at young age (typically
10-30 years of age)
OPEN-ANGLE GLAUCOMA
4. Glaucoma suspect
normal optic disc and visual field associated with elevated IOP
suspicious optic disc and/or visual field with normal IOP
5. Secondary open-angle glaucoma
increased resistance to trabecular meshwork outflow
associated with other conditions (e.g. pigmentary-,
phacolytic-, steroid-induced-)
increased posttrabecular resistance to outflow secondary to
elevated episcleral venous pressure (e.g. carotid cavernous
sinus fistula)
ANGLE-CLOSURE GLAUCOMA
1. Primary ACG with relative pupillary block
movement of aqueous humor from posterior chamber to anterior
chamber restricted
peripheral iris in contact with trabecular meshwork
2. Acute angle closure
occurs when IOP rises rapidly as a result of relatively sudden
blockage of the trabecular meshwork
3. Subacute angle closure (intermittent angle closure)
repeated, brief episodes of angle closure with mild symptoms and
elevated IOP, often a prelude to acute angle closure
4. Chronic angle closure
IOP elevation caused by variable portions of anterior chamber
angle being permanently closed by PAS
ANGLE-CLOSURE GLAUCOMA
5. Secondary ACG with pupillary block
e.g. swollen lens, secluded pupil
6. Secondary ACG without pupillary block
posterior pushing mechanism: lens-iris diaphragm pushed
forward (e.g. posterior segment tumor, scleral buckling
procedure, uveal effusion)
anterior pulling mechanism: anterior segment process pulling
iris forward to form PAS (e.g. iridocorneal endothelial
syndrome, neovascular glaucoma, inflammation)
CHILDHOOD GLAUCOMA

1. Primary congenital/infantile glaucoma

primary glaucoma present from birth to first few years of life
2. Glaucoma associated with congenital anomalies
associated with ocular disorders (e.g. anterior segment
dysgenesis, aniridia)
associated with systemic disorders (e.g. rubella, Lowe
syndrome)
3. Secondary glaucoma in infants and children
e.g. glaucoma secondary to retinoblastoma or trauma
RISK FACTORS for POAG

IOP, age, race and positive family history

Myopia, sex, various systemic factors (diabetes, systemic
hypertension, arteriosclerotic and ischemic vascular disease)
RISK FACTORS for PACG

Race: acute PACG is relatively uncommon in blacks

Sex: women develop acute PACG 3-4 times more often than
do men
Age: acute PACG is most common between the ages of 55 and
65 years
Refraction: PACG is typically associated with hyperopia
Inheritance: some of the anatomic features of the eye that
predispose to pupillary block (such as forward position of the
lens and greater than average lens thickness) are inherited.
Aqueous outflow
Posterior chamber pupil anterior chamber
trabecular meshwork Schlemms canal
collector channels venous system
 Aqueous outflow
Anatomy Physiology

a - Uveal meshwork a - Conventional outflow

b - Corneoscleral meshwork b - Uveoscleral outflow
c - Schwalbe line
d - Schlemm canal
c - Iris outflow
e - Collector channels
f - Longitudinal muscle of
ciliary body
g - Scleral spur
TRABECULAR OUTFLOW

Trabecular meshwork (uveal, corneoscleral,

juxtacanalicular) Schlemms canal venous system
Trabecular meshwork functions as a one-way valve that
permits aqueous to leave the eye by bulk flow but limits
flow in the other direction independently of energy.
UVEOSCLERAL OUTFLOW

Anterior chamber ciliary muscle supraciliary and

suprachoroidal spaces exits the eye through the intact
sclera or along the nerves and the vessels that penetrate it.
Pressure-independent.
Influenced by age

Increased by cycloplegic, adrenergic, and prostaglandin

agents and certain forms of surgery (e.g. cyclodialysis).

Decreased by miotics
Clinical examination
Funduscopy
Tonometry
Gonioscopy
Visual field (GOLDMAN PERIMETRI/HUMPREY
PERIMETRI)
Optical Coherence Tomography
Funduscopy
 Tonometers

Goldmann Perkins Schiotz

Contact applanation Portable contact applanation Contact indentation

Air-puff Pulsair 2000 (Keeler) Tono-Pen

Non-contact indentation Portable non-contact Portable contact applanation
 Goniolenses
Goldmann Zeiss

Single or triple mirror Four mirror

Contact surface diameter 12 mm Contact surface diameter 9 mm
Coupling substance required Coupling substance not required
Suitable for ALT Not suitable for ALT
Not suitable for indentation gonioscopy Suitable for indentation gonioscopy
 Indentation gonioscopy

Press Zeiss lens posteriorly Aqueous is forced into

against cornea periphery of anterior chamber
Goldman Perimetri
Humphrey perimetry
OCT optic nerve
PRIMARY OPEN-ANGLE GLAUCOMA
1. Definition and risk factor
2. Theories of glaucomatous damage
3. Optic disc cupping
4. Visual field defects
5. Medical therapy
6. Laser trabeculoplasty
7. Trabeculectomy
 Definition and risk factors

IOP > 21 mmHg Open angle of normal appearance

Glaucomatous disc damage Visual field loss

 Risk Factors
1. Age - most cases present after age 65 years

2. Race - more common, earlier onset and more

severe in blacks

3. Inheritance
Level of IOP, outflow facility and disc size are inherited
Risk is increased by x2 if parent has POAG
Risk is increased x4 if sibling has POAG

4. Myopia
 Theories of glaucomatous damage

Direct damage by pressure Capillary occlusion

Interference with
axoplasmic flow
Concentric excavation
1984

1994

Diffuse loss of nerve fibres

Excavation enlarges concentrically
Initially may be difficult to distinguish
from large physiological cup
Compare with previous record
 End-stage damage

All neural disc tissue is destroyed Atrophy of all retinal nerve fibres
Striations are absent
Disc is white and deeply excavated
Blood vessels appear dark and sharply defined
Progression of glaucomatous cupping
a. Normal (c:d ratio 0.2)

b. Concentric enlargement
(c:d ratio 0.5)

c. Inferior expansion with

retinal nerve fibre loss

d. Superior expansion with

retinal nerve fibre loss

e. Advanced cupping with nasal

displacement of vessels

f. Total cupping with loss of

all retinal nerve fibres
 Early visual field defects

Small arcuate scotomas Isolated paracentral scotomas

Tend to elongate circumferentially Nasal (Roenne) step
 Progression of visual field defects

Formation of arcuate defects Peripheral breakthrough

Enlargement of nasal step Appearance of fresh arcuate

inferior defects
Development of temporal wedge
 Advanced visual field defects

Development of ring scotoma Peripheral and central spread

Residual central island Residual temporal island
Drugs to treat glaucoma

1. Beta blockers
2. Sympathomimetics

3. Miotics
4. Prostaglandin analogues

5. Carbonic anhydrase inhibitors

Topical
Systemic
 Laser trabeculoplasty
Failed medical therapy
Primary therapy in non-compliant patients

Application of 50-100 burns Incorrect focus with oval

to junction of pigmented and aiming beam
non-pigmented trabeculum
Correct focus with round
aiming beam
 Indications for Trabeculectomy

1. Failed medical therapy and laser trabeculoplasty

2. Lack of suitability for trabeculoplasty

Poor patient co-operation
Inability to adequately visualize trabeculum

3. As primary therapy in advanced disease

 Technique (1)
a b
a. Conjunctival incision

b. Conjunctival undermining
c d

c. Clearing of limbus

d. Outline of superficial flap

e f

e. Dissection of superficial flap

f. Paracentesis
 Technique (2)
a b
a. Cutting of deep block -
anterior incision

b. Posterior incision

c d

c. Excision of deep block

d. Peripheral iridectomy

e f
e. Suturing of flap and
reconstitution of
anterior chamber

f. Suturing of conjunctiva
 Filtration blebs

Type 1 Type 2
Flat, thin and diffuse
Thin and polycystic Relatively avascular
Good filtration Microcysts present
Good filtration

Type 3 Encapsulated
Flat Localized, firm cyst
Engorged surface vessels Engorged surface vessels
No microcysts
No filtration No filtration
 Late bleb infection
Predispositions
Thin-walled, cystic bleb
Use of adjunctive antimetabolites
Bleb trauma
Blebitis Endophthalmitis

Subacute onset Acute onset

Milky bleb Hypopyon
No hypopyon
Guarded prognosis
Good prognosis
PRIMARY ANGLE-CLOSURE GLAUCOMA

1. Pathogenesis

2. Classification

3. Intermittent

4. Acute congestive

5. Post congestive
6. Chronic
 Anatomical predispositions

Convex iris-lens Shallow anterior Narrow entrance to

diaphragm chamber chamber angle
Pupil block

Increase in physiological
pupil block

Dilatation of pupil renders peripheral

iris more flaccid
Increased pressure in posterior
chamber causes iris bombe

Angle obstructed by peripheral iris

and rise in IOP
 Classification
1. Latent - asymptomatic
IOP may remain normal
May progress to subacute, acute or chronic
angle closure

2. Subacute - intermittent angle closure

May develop acute or chronic angle closure

3. Acute
Congestive - sudden total angle closure
Postcongestive - follows acute attack

4. Chronic - creeping or latent angle closure

Follows intermittent angle closure

5. Absolute
No PL following acute attack
 Acute congestive angle-closure glaucoma
Signs

Severe corneal oedema Ciliary injection Complete angle closure

(Shaffer grade 0)
Dilated, unreactive, Shallow anterior
vertically oval pupil chamber
Demographic risk factor of primary
angle closure glaucoma
Ras
Family history
Refraction
Hyperopic shallow AC
Gender
AC of the female eye is narrower than that of
men
Age
The depth and volume of the AC decrease with
age.
Ocular risk factors
Shallow anterior chamber
Decrease anterior chamber volume
Short axial length of the globe
Small corneal diameter
Increase thickness of the lens
Decrease corneal height
Increase of curvature of anterior lens surface
Anterior position of the lens with respect to the ciliary
body
 Pathophysiology of primary angle-
closure glaucoma
1. Pupillary block glaucoma

2. Plateu iris: configuration and syndrome

3. Phacomorphic glaucoma (lens induced

obstruction)
Pupilary block
 Acute primary angle closure
Defined by presence of at least two symptoms,
elevated IOP > 21 mmHg, at least three
finsding in examination
Symptoms
Periorbital or ocular pain
Diminished vision
Specific history of rainbow haloes with blurred
vision
Acute primary angle closure
Sign
IOP 21 mmHg
Ciliary flush
Corneal edema
Shallow anterior chamber
Cell and flare in anterior chamber
Middilated and sluggishly reactive pupil
Closed angel in gonoscopy
Hyperemic and swollen optic disc
Constricted visual field
 Findings suggesting previous
episodes of acute angle closure
glaucoma
Peripheral anterior synechiae
Posterior synechiae to the lens
Glaukomflecken
Sector or generalized iris atrophy
Optic nerve cupping and or pallor
Visual field loss
Signs of postcongestive angle-closure glaucoma

Folds in Descemet Stromal iris atrophy with

membrane spiral-like configuration

Posterior synechiae Fixed dilated pupil

Fine pigment on iris Glaukomflecken
Management of acute PACG
Immediate medical therapy
Protection of the fellow eye with
prophylactic iridotomy
Laser iridotomy in both eyes
Long-term glucoma surveillance and IOP
management of both eyes
 Treatment of Acute Congestive
Angle-Closure Glaucoma
1. Acetazolamide 500 mg i.v.
2. Hyperosmotic agents - if appropriate
Oral glycerol 1-1.5 g/kg of 50% solution in lemon juice
Intravenous mannitol 2g/kg of 20% solution

3. Topical therapy
Pilocarpine 2% to both eyes
Beta-blockers
Steroids

4. YAG laser iridotomy

To both eyes when cornea is clear
Sub acute or intermittent angle
closure
Sign

blurred vision, halos, mild pain, resolve

spontaneously ( during sleep-induced miosis )
Gonioscopy:

narrow angle with/without peripheral anterior

synechiae
can progress to chronic angle closure or acute attack

Management: peripheral iridectomy

 Intermittent angle-closure glaucoma
Signs Treatment

Epithelial oedema and closed angle Treatment - bilateral YAG laser

during attack iridotomy
Chronic angle closure
Mechanism: creeping angle closure ( slow formation
of PAS )
Sign
permanent PAS, rise IOP, progressive cupping, loss of
visual field
Management:
peripheral iridectomy

Anti glaucoma drug

 Chronic angle-closure glaucoma
Signs

Easily missed unless routine

Similar to POAG with gonioscopy performed
cupping and field loss
Variable amount of angle closure
Indication for Surgery in PACG
IOP not reaching target level
Progression optic nerve damage
Poor compliance or intolerant to medical treatment
Poorly controlled glaucoma at the time of planned
cataract surgery
Type of surgery
Trabeculectomy
Lens extraction alone
Combine cataract and trabeculectomy
Surgical iridectomy
Goniosynechialysis with cataract extraction
Glaucoma implant
Cyclodestructive procedure
 SECONDARY GLAUCOMAS

1. Pseudoexfoliation glaucoma
2. Pigmentary glaucoma
3. Neovascular glaucoma
4. Inflammatory glaucomas
5. Phacolytic glaucoma
6. Post-traumatic angle recession glaucoma
7. Iridocorneal endothelial syndrome
 Pseudoexfoliation glaucoma
Secondary trabecular block open-angle glaucoma
Affects elderly, unilateral in 60%
Prognosis less good than in POAG

Pseudoexfoliative material Iris sphincter atrophy Gonioscopy

Central disc with On retroillumination Trabecular hyperpigmentation

peripheral band - may extend anteriorly
(Sampaolesi line)
 Pigmentary glaucoma
Bilateral trabecular block open-angle glaucoma
Typically affects young myopic males
Increased incidence of lattice degeneration

Krukenberg spindle and very Fine pigment granules on

deep anterior chamber anterior iris surface

Mid-peripheral iris Trabecular hyperpigmentation

atrophy
 Causes of neovascular glaucoma
Common, secondary angle-closure glaucoma without pupil block
Caused by rubeosis iridis associated with chronic, diffuse retinal ischaemia

Ischaemic central retinal vein Long-standing diabetes (common)

occlusion (most common)

Central retinal artery Carotid obstructive

occlusion (uncommon) disease (uncommon)
 Signs of advanced
neovascular glaucoma

Severely reduced visual Severe rubeosis iridis

acuity, congestion and pain

Distortion of pupil Synechial angle closure

and ectropion uveae
Treatment options of neovascular glaucoma
Topical
Atropine and steroids to decrease inflammation
Beta-bockers

Panretinal photocoagulation Artificial filtering devices

- in early cases - in very advanced cases

Cyclodestructive procedures Retrobulbar alcohol injection

- to relieve pain - to relieve pain
Inflammatory glaucomas
Angle-closure with pupil block

Caused by seclusio pupillae

Anterior chamber is shallow
 Inflammatory glaucomas
Angle-closure without pupil block

Caused by progressive synechial angle closure

Anterior chamber is deep
 Phacolytic glaucoma
Pathogenesis Signs

Treatment

Control IOP medically

Deep anterior chamber
Remove cataract Floating white particles
Post-traumatic angle recession glaucoma

Pathogenesis Signs

Blunt traumatic damage to Irregular widening of ciliary body band

trabecular meshwork
Classification of Iridocorneal Endothelial Syndrome
Proliferation of abnormal corneal endothelial cells
Typically affects young to middle aged women
Three syndromes with certain overlap

1. Progressive iris atrophy

Iris atrophy in 100%

2. Iris naevus (Cogan-Reese) syndrome

Iris atrophy in 50%

3. Chandler syndrome
Iris atrophy in 40%
Corneal changes predominate
Progressive iris atrophy

Progressive stromal iris atrophy

Broad-based PAS Displacement of pupil

towards PAS
Iris naevus (Cogan-Reese) syndrome

Diffuse iris naevus Pedunculated iris nodules

 Chandler syndrome

Initially hammer-silver endothelial Later oedema which may cause halos

changes
CONGENITAL GLAUCOMA
 Primary congenital glaucoma
1:10,000 births, 65% boys
Most sporadic - 10% autosomal recessive
Absence of angle recess with iris inserted directly into trabeculum

Flat iris insertion Concave iris insertion

Clinical features of primary congenital glaucoma
Depend on age of onset
Bilateral in 75% but frequently asymmetrical

Corneal oedema associated with Buphthalmos if IOP becomes elevated

lacrimation and photophobia prior to age 3 years.

Breaks in Descemet membrane Optic disc cupping

 Management of primary congenital glaucoma

Measurement of IOP and

corneal diameters Goniotomy Trabeculotomy
Absolute glaucoma
The end result of any uncontrolled glaucoma is a hard,
sightless, and often painful eye.