GLAUCOMA

Bagain Ilmu Kesehatan Mata

Fakultas Kedokteran
Universitas Hasanuddin

AQUEOUS HUMOUR
PRODUCTION
ACTIVE SECRETION FROM NON-PIGMENTED EPITHELLIUM OF
THE CILIARY BODY AS RESULT OF A METABOLIC PROCESS
( Na+/K+ ATPase PUMP, CARBONIC ANHYDRASE)

OUTFLOW
TRABECULAR MESHWORK :
- UVEAL MESHWORK
- CORNEOSCLERAL MESHWORK
- ENDOTHELIAL (JUXTACANALICULAR) MESHWORK

SCHLEMM CANAL, CONNECT IN/DIRECTLY EPISCLERAL

VEINS

.
DEFINITION
GLAUCOMA IS AN OPTIC NEUROPATHY
WITH CHARACTERISTIC APPEARANCE OF
OPTIC DISC AND SPECIFIC PATTERN OF
VISUAL FIELD DEFECTS THAT IS
ASSOCIATED FREQUENTLY BUT NOT
INVARIABLY WITH RAISED IOP

IOP (INTRAOCULAR PRESSURE)

RANGE 11-21 MMHG
MEASUREMENT BY TONOMETER:
- CONTACT TONOMETER :
= GOLDMANN APPLANATION TONOMETER
= PERKINS HAND-HELD APPLANATION TONOMETER
= TONO-PEN HAND-HELD TONOMETER
= SCHIOTZ INDENTATION TONOMETER
- NON CONTACT TONOMETER
= AIR PUFF NON-CONTACT TONOMETER
= PULSAIR 2000 KEELER

VISUAL FIELD
MEASSUREMENT BY HUMPHREY PERIMETRY
CHARACTERISTIC PATTERN OF THE GLAUCOMATOUS FIELD
DEFECT:
- PARACENTRAL SCOTOMA
- A NASAL (ROENNE) STEP SCOTOMA
- ARCUATE-SHAPED DEFECTS
- PERIPHERAL SCOTOMA
- END STAGE CHANGES

OPTIC NERVE HEAD

EVALUATION BY UN/DIRECT FUNDUSCOPY
1. The optic cup
2. The cup: disc ratio ( normally , vertical cup: disc ratio
<0,3)
3. The neuroretinal rim (the tissue between the outer edge of
the cup and the disc margin, normally broadest inferior rim
followed by sup, nas, temporal =ISNT)
4. The central retina artery & vein from centrally the disc of
the
optic nerve and then nasally following the edge of the cup

CLASSIFICATION

1. PRIMARY GLAUCOMA
= PRIMARY OPEN ANGLE GLAUCOMA
= PRIMARY ANGLE-CLOSURE GLAUCOMA, 6 CLINICAL
STAGES:
A. LATENT ANGLE-CLOSURE GLAUCOMA
B. SUBACUTE (INTERMITTEN) ANGLE-CLOSURE
GLAUCOMA
C. ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA
D. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA
E. CHRONIC ANGLE-CLOSURE GLAUCOMA
F. ABSOLUTE ANGLE-CLOSURE GLAUCOMA

2. SECONDARY GLAUCOMA
= SECONDARY OPEN ANGLE GLAUCOMA
A. PRETRABECULAR GLAUCOMA, WHICH AQUEOUS
OUTFLOW
IS OBSTRUCTED BY A MEMBRANE COVERING THE TRABECULUM
+ FIBROVASCULAR TISSUE (NEOVASCULAR GLAUCOMA)
+ ENDOTHELIAL CELLS (IRIDOCORNEAL ENDOTHELIAL
= ICE SYNDROME)
+ EPITHELIAL CELLS (EPITHELIAL INGROWTH)
B. TRABECULAR GLAUCOMA, WHICH THE OBSTRUCTION
OCCURS
AS A RESULT OF CLOGGING UP OF THE MESHWORK BY:
+ PIGMENT PARTICLES (PIGMENTARY GLAUCOMA)
+ RED BLOOD CELLS ( RED CELL GLAUCOMA)
+ DEGENERATED RED CELLS (GHOST CELL GLAUCOMA)
+ MACROPHAGES AND LENS PROTEINS ( PHACOLYTIC GLAU
+ PROTEINS ( HYPERTENSIVE UVEITIS)

+ PSEUDOEXFOLIATIVE MATERIAL
(PEX GLAUC)
.
+ OEDEMA (HERPES-ZOSTER IRITIS)
+ SCARRING (POST-TRAUMA ANGLE RECESSION GLAUC)
C. POST TRABECULAR GLAUCOMA, WHICH AQUEOUS
OUTFLOW
IS IMPAIRED AS ARESULT OF ELEVATED EPISCLERAL VENOUS
PRESSURE
+ CAROTID-CAVERNOUS FISTULAE
+ STURGER-WEBER SYNDROME
+ OBSTRUCTION OF THE SUPERIOR VENA CAVA
= SECONDARY ANGLE CLOSURE GLAUCOMA
A. POSTERIOR FORCED PUSH THE PERIPHERAL IRIS AGAINST
THE TRABECULUM (IRIS BOMBESECLUSIO PUPILLAE)
B. ANTERIOR FORCED PULL THE IRIS OVER THE TRABECULUM
BY CONTRACTION OF INFLAMMATORY (LATE NEOVASC GL)

3. CONGENITAL GLAUCOMA
A. TRUE PRIMARY CONGENITAL GLAUCOMA, WHICH IOP ELEVATED
DURING INTRAUTERINE LIFE
B. INFANTILE GLAUCOMA, WHICH MANIFESTS PRIOR TO THE 3TH
BIRTHDAY
C. JUVENILE GLAUCOMA, IOP RISED AFTER 3TH BIRTHDAY BUT
BEFORE
THE AGE OF 16 YEARS.
4. OCULAR HYPERTENSION
IOP MORE THAN 21 MMHG & ABSENCES OF DETACTABLE
GLAUCOMATOUS DAMAGE
5. NORMAL TENSION GLAUCOMA IS A VARIANT OF POAG,
CHARACTERIZED BY :
- IOP EQUAL TO OR LESS THAN 21 MMHG (DIURNAL TESTING)
- GLAUCOMATOUS OPTIC DISC DAMAGE & VISUAL FIELD LOSS
- OPEN ANGLE ON GONIOSKOPY
- ABSENCES OF SECONDARY CAUSES

PRIMARY OPEN ANGLE GLAUCOMA

(POAG)
SIN. CHRONIC SIMPLE GLAUCOMA
GENERALLY BILATERAL
CHARACTERIZED BY:
- ADULT ONSET
- IOP > 21 MMHG
- OPEN ANGLE OF NORMAL APPEARANCE
- GLAUCOMATOUS OPTIC NERVE HEAD DAMAGE
- VISUAL FIELD LOSS
PATOGENESIS
Elevation IOP, glutamine metabolism, Ca + influx into the cell
body increase in intracelluler nitric oxide retinal ganglion
cell death apoptosis

Cont.. POAG

AETIOLOGIES
1. The ischaemic theory, postulates that compromise of the microvasculature with resultant ischaemia in the optic nerve head
2. The direct mechanical theory, raised IOP directly damages the
retinal nerve fiber
RISK FACTORS
1. AGE . After the age of 65 years
2. RACE. More earlier & severe in black people than in white
3. FAMILY HISTORY with POAG
4. MYOPIA
5. RETINAL DISASES , central retinal vein occlusion, rhegmatogenous
retinal detachment, retinitis pigmentosa

CONT..POAG
.

CLINICAL FEATURES
SYMPTOMS. Asymptomatic until significant loss of visual field has
occurred
SIGN : - Raised IOP (> 21 mmHg ) & diurnal fluctuation in IOP (> 5
mmHg)
- Optic disc changes
- Typical visual field changes
- Gonioscopy shows a normal open angle
MANAGEMENT
- Medical therapy ( timolol maleat, prostaglandine analough )
- Laser trabeculoplasty
- Trabeculectomy

PRIMARY ANGLE-CLOSURE GLAUCOMA

(PACG)
Is a condition in which elevation of IOP occurs as a result of obstruction
of
aqueous outflow by partial or complete closure of the angle by the peripheral
Iris
RISK FACTORS
1. AGE , > 60 years
2. GENDER, females : males = 4:1
3. RACE, in caucasians, more common in South-East Asians
4. FAMILY HISTORY
ANATOMICAL PREDISPOSING FACTORS
1. Relatively anterior location of the iris-lens diaphragm
2. Shallow anterior chamber
3. Narrow entrance to the chamber angle (lens size, corneal diameter,
axial
length)

Cont.PACG

PATHOGENESIS
is incompletely understood.
1. The dilatator muscle theory postulates that contraction of
the dilator pupillae exerts a posterior vector.
2. The sphincter muscle theory postulates that the sphincter
pupillae is the prime culprit in precipating angle closure.

Cont PACG

CLASSIFICATION
1. LATENT ANGLE-CLOSURE GLAUCOMA
Clinical features
-Symptoms are absent
-Slit lamp biomicroscopy
+ Axial anterior chamber depth is less than normal.
+ Convex-shaped iris-lens diaphragm
+ Close proximity of the iris to the cornea
-Gonioscopy : Shaffer grade 1 or 0
Treatment
- Prophylactic peripheral laser iridotomy

Cont.PACG

2. SUBACUT (INTERMITTEN) ANGLE CLOSURE GLAUCOMA

A PREDISPOSED EYE WITH AN OCCLUDABLE ANGLE AN
ASSOCIATION
WITH INTERMITTENT PUPILLARY BLOCK.

CLINICAL FEATURES :
- BLURRING OF VISION ASSOCIATED WITH HALOES AROUND LIGHTS
- CORNEAL EPITHELIAL OEDEMA
- OCULAR DISCOMFORT
- FRONTAL HEADACHE
- THE ANGLE IS NARROW
TREATMENT
- PROPHYLACTIC PERIPHERAL LASER IRIDOTOMY

Cont.PACG

3. ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA

This is a sight threatening emergency.
CLINICAL FEATURE
- Symptoms : + rapidly progressive unilateral visual loss
+ periocular pain & congestion
+ nausea & vomiting
- Slit lamp biomicroscopy
+ injection the limbal & conjunctival blood vessels
+ corneal oedema
+ peripheral iridocorneal contact
+ pupil is fixed semi-dilated, vertically oval
+ IOP is 50-100 mmHg

Cont ..PACG

- Gonioscopy, perform until the corneal oedema resolved by

topical
glicerine or hypertonic saline ointment , shows complete
peripheral iridocorneal contact (Shaffer grade 0)
- Ophthalmoscopy, optic disc oedema & hyperaemia
IMMEDIATE TREATMENT
- Acetasolamide 500 mg/IV, 500 mg orally
- Topical therapy : + pilocarpine 2 %
+ beta blocker (timolol maleat 0,5 %)
- Glyserol 50 % (1g/Kg bw) orally or 20% mannitol IV
- Analgesia & anti-emetics
- YAG laser iridotomy : effective in relatively mild cases
- Trabeculectomy

Cont..PACG

4. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA

CLINICAL FEATURES
- Slit lamp biomicroscopy
+ Descemet membrane folds (if IOP reduced rapidly)
+ fine pigment granules (on the corneal endothelium & iris)
+ aqueous flare & cells
+ stroma iris atrophy (spiral like configuration)
+ fixed & semi-dilated pupil (paralysis sphincter & post
synechiae)
+ glaukomflecken
+ IOP normal, subnormal or elevated
- Gonioscopy , shows narrow angle, trabecular
hyperpigmentation
- Ophthalmoscopy, congestion or atropic optic disc, choroidal
folds

Cont.PACG

5. CHRONIC ANGLE-CLOSURE GLAUCOMA

PATHOGENESIS
1. Type 1 (creeping), gradual & progressive synechial angle closesure caused by anteriorly situated cilliary process plateau iris
2. Type 2, synechial angle closure as a result of intermittent (subacut) attacks secondary pupillary block
3. Type 3 (mixed), combination of POAG with narrow angle (the
long term use of miotics)
CLINICAL FEATURES
similar POAG , shows a variable degree of angle closure
TREATMENT
laser iridotomy combined with medical therapy

PRIMARY CONGENITAL GLAUCOMA (PCG)

Affecting 1:10.000 births, 65 % boys
Sporadic, 10 % autosomal recessive
PATHOGENESIS
Isolated trabeculodysgenesis absence of the angle recess with the
Iris inserted directly into the surface of the trabeculum :
1. Flat iris insertion, iris inserteds flatly and abruptly into the
thickened
trabeculum at or anterior to the scleral spur
2. Concave iris insertion, superficial iris tissue sweeps over the iridotrabecular junction and the trabeculum

Cont .PCG
.

CLINICAL FEATURES
- Corneal haze ( epithelial & stromal oedema) lacrimation,
photopho
bia, blepharospasm
- Buphthalmos, large eye as result of stretching due to elevated IOP
Scleral thinner ( blue appearance), AC deep, lens subluxasion (zonular fibres stretch), axial myopia (increase axial length)
- Breaks in Descemet membrane (Haab striae)
- Optic disc cupping
SURGERY
- Goniotomy
- Trabeculotomy
- Trabeculectomy

OCULAR HYPERTENSION (OH)

TERMINOLOGY
When the IOP is found to be > 21 mmHg on two consecutive occasions, in the absence of detactable glaucomatous damage
MANAGEMENT
do not require treatment
only high risk should be treated because its effective in delaying
or
preventing the development of POAG
1. High risk factors
- retinal nerve fiber layer defects
- parapapillary changes
- IOP 30 mmHg or more
- IOP 26 mmHg or more & central corneal thickness < 555 um
- vertical CDR 0,4 or more & CCT < 588 um

ContOH

2. Moderate risk factors

- IOP 24-29 mmHg without NFL defects
- Vertical CDR > 0,3 & CCT > 588 um
- Family history of POAG in a first degree relative
- high myopia
In these patients annual examination of the optic disc and
perimetry
is appropriate. Treatment is withheld until damage is
documented.

NORMAL TENSION GLAUCOMA (NTG)

SIGN
- IOP usually in the high teens, but rarely the low teens
- ONH
+ both glaucomatous cupping or parapapillary changes are identical
POAG
+ splinter haemorrhages at the disc margin progressive damage of
NFL
+ acquired optic disc pits (localized excavations of the lamina cribrosa}
- VF defects, to be closer to fixation, deeper, steeper and more localized.
- peripheral vascular spasm
- migraine
- Nocturnal systemic hypotension, over treated systemic hypertension
- Reduced blood flow velocity in the a. ophthalmic
- Paraproteinaemia

Cont.. NTG
.

TREATMENT
- progressive VF loss
- IOP to reduce by at least 30 %

1. Medical , betaxolol the drug of choice. Prostaglandin analoues tend

to greater ocular hypotensive effect
2. Trabeculectomy, in at least one eye, if progressive field loss occurs
3. Systemic calcium channel blockers (nifedipine) in younger patients
with peripheral vasospasm.
4. Monitoring of systemic blood pressure for 24 hours, if nocturnal drop
may be necessary to avoid anti-hypertensive medication