1.
Introduction to Glaucoma: Terminology,
Epidemiology, and Heredity .
2. Intraocular Pressure and Aqueous Humor
Dynamics.
3. Clinical Evaluation
4. Open-Angle Glaucoma
5. Angle-Closure Glaucoma
6. Childhood Glaucoma
7. Medical Management of Glaucoma
8. Surgical Therapy for Glaucoma
Glaukoma
dr. Sahilah Ermawati, SpM
¨ a group of diseases that have in common a
characteristic optic neuropathy with associated
visual function loss. Although elevated
intraocular pressure (fOP) is one of the primary
risk factors. its presence or absence does not
have a role in the definition of the disease.
¨ a characteristic optic neuropathy consistent
with excavation and undermining of the neural
and connective tissue elements of the optic
disc and by the eventual development of
characteristic visual field defects.
¨ POAG was estimated at 2.4 million people per
year. Blindness prevalence for all types of
glaucoma was estimated at more than 8 million
people, with 4 million cases caused by POAG.
¨ Prevalence 7% in individuals older than 40 years.
Significant increase in the prevalence of
glaucoma in older individuals, with estimates for
persons in their 70s being generally 3 to 8
times higher than those fo r persons in their 40s
¨ blindness from POAG increasing to 15 times
higher for blacks in the age group 46- 65 years.
¨ Incidence the incidence increased
Significantly with age.
¨ Risk Factor POAG:
Age
thin corneal tickness
Family
- blacks
- Type 2 diabetes mellitus
¨ Prima ry Angle-Closure Glaucoma
-most Asian population groups have a prevalence
rate of PACG between that of whites and Inuits.
- in China suggested that a family history of
glaucoma increased by sixfold the ri sk of PACG
- more often in women than in men, and
- several population surveys demonstrate that
women are at increased risk of angle-closure
glaucoma.
- Acute angle-closure glaucoma is most common
between the ages of 55 and 65 years
- anterior chamber depth and volume are smaller in
hyperopic eyes
¨ Factors Influencing Intraocular Pressure :
time of day
heartbeat
respiration
exercise
fluid intake
systemic medications
topical medicat ions
¨ Goldmann applanation tonometer
¨ Noncontact (air-puff ) tonometers
¨ Schietz tonometry
1. The history should include the following:
patient's current complaint
symptoms, onset, duration, severity, location
ocular history
history of present illness
past ocular, medical, and surgical history
general medical history
past systemic medical history (including medications and
allergies)
review of systems
social history
history of alcohol and tobacco use
occupation, avocation, interests
family history
2. Refraksi
3. External Adnexae
4. Konjungtiva
5. Episklera
6. Sklera
7. kornea
Krukenberg spindle in pigmentary glaucoma
deposit ion of exfoliation material in exfoliation syndrome
keratic precipitates in uveitic glaucoma
guttae in Fuchs endothelial dystrophy
irregular and vesicular lesions in posterior polymorphous
dystrophy
a "beaten bronze" appearance in the iridocorneal endothelial
syndrome
8. Anterior chamber
9. Iris
10. Pupil
11. Lensa
12. funduskopi
¨ Two hypotheses
have emerged to
explain the
development of
glaucomatous optic
neuropathy, the
mechanical and
ischemic theories.
PRIMARY ANGLE-CLOSURE
GLAUCOMA
1. Pathogenesis
2. Classification
3. Intermittent
4. Acute
congestive
5. Post
congestive
6. Chronic
Anatomical predispositions
• Convex iris- • Shallow anterior • Narrow entrance to
lens chamber chamber angle
diaphragm
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
Intermittent angle-closure glaucoma
Signs Treatment
• • Treatment - bilateral YAG laser
Epithelial oedema and closed angle
during attack iridotomy
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
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
Signs of postcongestive angle-closure glau
• Folds in Descemet •Stromal iris atrophy
membrane with
spiral-like
configuration
• Posterior synechiae • Fixed dilated
• Fine pigment on iris pupil
• Glaukomflecken
Chronic angle-closure glaucoma
Signs
• Easily missed unless routine
• Similar to POAG with gonioscopy performed
cupping and field loss
• Variable amount of angle closure
Treatment of chronic
Angle-Closure Glaucoma
3. Topical therapy
• Pilocarpine 2% to both eyes
• Beta-blockers
• Steroids
4. YAG laser iridotomy
• To both eyes when cornea is clear
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. Trabeculectomt
• Indications
• Technique
• Filtration blebs
• Complications
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 inh
• 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 define
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
Indications
• Failed medical therapy
• Primary therapy in non-compliant patients
• Application of 50-100 burns• Incorrect focus with oval
to junction of pigmented andaiming beam
non-pigmented trabeculum
• Correct focus with round
aiming beam
Indications for Trabeculectomy
1. Failed medical therapy and laser trabeculop
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
SECONDARY GLAUCOMAS
1. Pseudoexfoliation glaucoma
2. Pigmentary glaucoma
3. Neovascular glaucoma
4. Inflammatory glaucomas
5. Phacolytic glaucoma
6. Post-traumatic angle recession glauco
Pseudoexfoliation glaucoma
• Secondary trabecular block open-angle glaucoma
• Affects elderly, unilateral in 60%
• Prognosis less good than in POAG
Pseudoexfoliative materialIris 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 veryFine pigment granules on
deep anterior chamber anterior iris surface
Mid-peripheral iris Trabecular hyperpigmentation
atrophy
Neovasculare glaucoma
• Common, secondary angle-closure glaucoma without pupil block
• Caused by rubeosis iridis associated with chronic, diffuse retinal isch
•Causes :
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 glaucom
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
