Primary Glaucoma

3.
1 Primary Glaucoma
3.1.1 Primary Angle Closure Glaucoma (PACG)
A. Pathogenesis
Primary Angle Closure Glaucoma (PACG) is an anatomical disorder in which the
anatomical closure (occlusion) of the iridocorneal angle (which is normal but narrow) by the
peripheral iris occurs. An asposition can occur between the peripheral iris with trabecular
meshwork or with the peripheral cornea, it can bereversible or permanent due to the presence of
synecemia. The peripheral iris can be pulled forward (anterior mechanism) or pushed forward
(posterior mechanism). Some of the factors that can be a risk factor for PACG include shallow
front eye chambers, narrow iridocorneal angles and increasing age. 1
The most frequent mechanism of occurrence of PACG is the obstruction of the flow of
aquaeous humour from the rear eye chamber to the front eye chamber which is referred to as the
pupil block. The concept was first proposed by Curran and Banziger in the early 1920s, and was
developed by Chandler who stated that if there is a shallow front eye chamber, the contact
between the iris and the anterior surface of the lens is wider. Chandler states that mid- dilated
pupils (diameter 3.0 - 4.5 mm) are the size of pupils that can cause acute attacks. The mid-dilated
pupil causes pupil block and peripheral iris relaxation so that the iris root closes the angle of the
iridocornealis. Mid-dilatation of the pupil can occur due to fatigue, emotion, acute taste, stress
or use of the mydriatic. Some mechanical factors related to pupil block include: the position of
the lens too much, dilatation / constriction of the pupil, elasticity of the iris, thickness of the iris,
stability of the lens, elasticity of the zonula and changes in the corpus siliarys. 1
The increase in age causes the antero-posterior diameter of the lens to increase so that
the iris-lens diaphragm is pushed to the anterior and causes the pupil block. If a pupil block
occurs, the flow of aquaeous humour is blocked and causes the accumulation of aquaeous
humour in the back eye chamber, this will cause the peripheral part of the iris to be pushed to the
anterior and cause the angle of the iridocornealis to become narrow. As long as the flow of
aquaeous humour still smoothly passes through the pupil, the angle of iridocornealis remains
terbuka. 1
Relative pupillary block usually does not cause complaints, but can cause partial closure
of the iridocorneal angle without an increase in intraocular pressure, slowly peripheral anterior
synechiae (PAS) will form, causing a chronic closed angle. If this condition does not get
treatment
the right one will be an absolute pupillary block, PAS will more widely close the trabecular
meshwork, trigger an increase in intraocular pressure and an acute attack or Acute Primary Angle
Closure (APAC) occurs. 2
The lens, zonula fibers and iris have a very important role in the closure of the
iridocorean angle. In conditions of shallow front eye chambers, the lens surface protrudes more
anteriorly than the normal eye, and is very convex, the lens size is larger with a small eyeball so
that the peripheral area of the front eye chamber is shallow and the lens surface is close to the
peripheral cornea. The lens pushes the iris anterior causing the aquous flow resistance to
increase. 3
The stability of the lens position is influenced by the integrity of the zonula fibers. The
movement of the lens to the anterior or the position of the lens pushed to the anterior caused by
lens subluxation or lens thickening increases the risk of pupil blockage. 4.5
The clinical picture of PACG varies greatly, depending on the extent and speed of
closure of the corners. If the closure of the corner occurs suddenly and expansively (extensive),
an acute attack picture will be obtained. If the angular closure is not too wide, a sub-acute
PACG picture will be obtained and if the angular closure is slow or creeping, a chronic PACG
picture will be obtained. If one eye has an acute attack of glaucoma, then the other is at risk of
developing an acute attack in 1 year. More than 50% of sufferers experience an attack on the
other eye within 5 years. This is because in general both eyes have a similar biometric structure.
4-6
B. Diagnosis Enforcement
Based on the APGS guidelines, the diagnosis of theclosed angle is divided into:2
1. Primary angle closure suspect (PACS): In gonioscopy, trabecular is seen to be less
than 180, TIO does not increase and there is no PAS.
2. Primary Angle Closure (PAC): In gonioscopy, the trabeclum is less than 180,
and is accompanied by an increase in TIO and/or the presence of PAS.
PAC can be in an acute state when a sudden increase in TIO occurs (APAC).
3. Acute or chronic PACG (PACG): Optics of glaucomatose neuropathy and field of
view defects accompanied by an increase in acute intraocular pressure due to
simultaneous and sudden closure of trabecular webbing by the base of the iris or an
increase in chronic intraocular pressure (more than 1 month).
B.1. Acute Primary Angle Closure (APAC) Diagnosis
Acute closed-angle diagnosis is based on signs and symptoms. Meanwhile,
confirmation of the diagnosis and differential diagnosis is established based on several
follow-up examinations. 5
 Signs and Symptoms
Acute primary closed corners have quite characteristic complaints. This attack
occurs as a result of a rapid increase in intraocular pressure caused by a sudden
trabecular block of meshwork by an extensive iris. In general, these complaints occur
suddenly and severely. Usually the manifestations thatoccur are blurred vision, there
is a rainbow-like colored halo that appears around the light, pain in the eyeballs,
headaches especially in the front on the side of the eye concerned with varying
degrees, nausea and vomiting. Most acute angle-closure attacks are unilateral, only
5% to 10% occur bilaterally. 5-8
Symptoms of an acute closed angle are associated with a significant increase in
intraocular pressure. This intraocular pressure test can be measured at most atime
using an aplanatory tonometer from Goldmann. Pain in the eyeball is caused by the
expansion of ocular tissue, including the cornea, iris and the entire eyeball. This
increase in intraocular pressure affects the function of the corneal endothelium, which
causes edema d the cornea with a stretched layer of the stroma, responsible for the
occurrence of visual complaints, namely blurred eyes and the presence of halo around
the light, with a turquoise central halo and a reddish-yellow peripheral halo. 5,7,8
Headaches generally appear along with the appearance of eyeball pain as a form
of radiant pain. Nausea and vomiting are symptomatic characters of increased
intraocular pressure. Activation of the vomiting center in the medulla may be caused
by anafferent input trigger from peripheral pain receptors. Other vasovagal responses
such as bradycardia and sweating may appear. Other responses such as abdominal
cramps are also sometimes complained of by patients. 5,7,8
 Supporting Examinations
There are several tests to establish an acute primary closed-angle diagnosis, some of
which are basic examinations.
1. Field inspection
Field checks at the time of the attack cannot be carried out practically and ethically.
This check can be done after the attack has improved and the risk factors for the
attack have disappeared. The results of the field examination were related to the
findings of the optic nerve papillary examination. 5
2. Pressure Check intraocular
At an acute primary closed angle, an increase in intraocular pressure above 21
mmHg will be obtained, often up to 50-80mmHg. There are several tools for
measuring intraocular pressure including Schiotz tonometry, Goldmann aplanatory
tonometry, pneumotonometry, non-contact tonometry, tonopen, Pascal Dynamic
Contour tonometer, and rebound tonometry. The gold standard is an examination
using Goldmann aplanatory tonometry. 7.9
3. Flashlight and Magnifying Glass
On a simple inspection using a flashlight and a magnifying glass, irregular
corneal light reflexes can be found. This is due to the presence of edema in the
corneal epithelium. The eyes appear red, the eyelids appear swollen. This is due to
the presence of an injective of the conjunctiva and leakage from the blood vessels
of the conjunctiva. 5
This simple examination can also replace the function of the slit lamp to measure
the depth of the front eye chamber if the tool is not available. How to judge by
illumination flash light pa da the surface of the iris through rays from the temporal
side of the eye. If the flat iris will be illuminated on the temporal and nasal sides of
the pupil while if the iris is more pushed forward it will appear shadows on the
nasal side or called eclipse sign. This examination has a sensitivity of 80-86 %
and a specificity of 69-70%. 6.10
4. Biomicroscopy slit lamp
On the slit lamp examination, conjunctival and episcular vascular congestion will
be found. Conjunctival injection begins around the limbus (siliary injection)
associated with congestion of the siliary body. In addition, it also gets congestion
from the veins. Other symptoms that are often found are epiphora (watery eyes) and
corneal edema especially the epithelial layer. 5,7,8
Theangle of the central front eye chamber can be estimated by examining this slit
lamp. In general, the angle of the front eye chamber is shallow or flat. Several
techniques for the measurement of this parameter have been proposed. After all,
the depth of the bibi lik of the front eye of the central part is only
Weakly correlated with the angular width of the chamber of the eye, and a larger
parameter of diagnostic value in the context of the closed angle is the depth of the
angle of the front chamber of the eye. 5-8
Van Herick et al. developed a technique toestimate the measurement of this
parameter with a slit lamp, by comparing the depth of the angle of the front eye
chamber with the thickness of the adjacent cornea. This is commonly referred to as
the van Herick technique. When the depth of the front eye chamber of the peri fer
part is less than a quarter of the thickness of the cornea, the angle of the front eye
chamber may be potentially occludable. 5-8
Depth examination of the front eye chambers can also be done using a technique
called optical pachymetry, where a special eyeroom depth measuring device called
pachymeter II is needed, which is installed on two steel pins above the microscope,
and also a special eyepiece or ocular lens is needed, so that with this examination an
angular depth value will be obtained internal front eye chambers (excluding the
thickness of the cornea). 11th
On examination of the pupils, the pupils are mid-dilated, with light reflexes that are
descending or not reactive. This is due to ischemia which results in damage to the
spingter muscles. If thespingter collapse occurs partially or sectorally, the shape of
the dilated pupil can be oval or iregular. In some cases, iris blood vessels may also
undergo dilatation which is often mistaken for neovascular glaucoma. 5.8
Recurrent acute attacks indicate a characteristic condition. The iris shows atrophic
changes from depigmentation and thinning in the previous ischemic region of the
border area of the pupil and stroma iris. A severe attack can make a hole in the
stroma of an atrophied iris. The pupil edge line may show a spiral or circle pattern
(whorl) due to irregular contractions between areas experiencing sectoral damage.
Examination of the lens shows a white anterior sub-capsular turbidity referred to as
'glaukom-flecken' and represented as small multiple white spots in the pupil
region, as a result of anterior lens fibre ischemia. 5
5. Gonioskopi
If the peripheral front eye chamber is considered shallow (less than aquarter of the
thickness of the cornea by slit lamp examination using the van Herick technique), a
thorough gonioscopy examination is required. The gonioscopy methodology has
been used for decades and has proven to be effective and reliable.
Coffee goniosrequire goniolens due to the fact that it is impossible to visualize the
angle of the eye chamber directly through the cornea, at an angle where the light
beam of the slit lamp radiating from the corner of the eye chamber will be
completely reflected internally. This examination can be performed using Zeiss
four-mirror lenses or other similar goniolens. 5,6,8,11,12
At an acute closed angle, iridotrabecular contact will be obtained 360 degrees.
Angular closures of 180 degrees or more (trabecular meshwork is not visible)
indicate an occludable angle, so it is important to do a gonioscopy compression to
distinguish whether the closure is positional or synecial. 5,6,8,11,12
The patient is best examined in a darkened room by means of rays through narrow
and short gaps, in order to avoid constriction from the pupils and the opening of
false corners. The examiner should avoid over-pressing the cornea so that the angle
does not become falsely deep (artifactually). If needed, the burlap irror on the
Goldmann three-mirror can be used to avoid the depth of the false front eye
chamber. If the iris is peripheral prominent, or when the iris is very convex and
difficult to see the angular structure, the patient may be asked to look towards the
mirror being examined
or viewed. This can go a long way in obtaining an accurate assessment of the
angular structure. 5,6,8,11,12
In the acute stage where corneal edema is obtained, examination of the angle of the
front eye chamber using gonioscopy becomes difficult. The application of glycerol
or NaCl 5% topically will make the cornea appear temporarily clear so that an
examination of the angle of the front eye chamber can be carried out. Gonioscopy
examination of the jiran eye can provide several clues, because basically the
cofiguration of the angle of the eye chambers in both eyes is almost the same,
especially if the corneal edema that occurs in the affected eye makes it difficult to
do an angular examination. Focal peripheral anterior synecia and
hyperpigmentation of the iris contact area duringmoaning can be observed also with
gonioscopy. 5.8
6. Funduskopi
In acute attacks, the fundus cannot be examined clearly due to the presence of
corneal edema. Ophthalmoscopy of indirek with the brightest light can help in the
examination of the fundus and papill saraf optics. In new and mild acute angle-
closure attacks, the papill may not show any changes. In severe and prolonged
attacks with congestion of the entire eyeball, the papillae will show edema and
hyperemia, with venous congestion and splinter
hemorrhages. If an acute attack occurs during chronic angular closure or creeping,
the papill may show atrophy and there is cupping glaucomatus due to previous
accumulation of damage. There is also the possibility of occurrence of central
retinal vein occlusion (CRVO) during an attack, and nonarteritic anterior ischemic
optic neuropathy (NA-AION) which occurs bilaterally about 2.5 weeks after the
patient has an attack. 5,7,8
If there is a change in the papill of the optic nerve, the diagnosis needs to be
changed from acute closed angleto acute closed-angle glaucoma. However, at acute
closed angles, optic nerve papill damage is relatively rare due to the short duration
of intraocular pressure elevation, unless it is missed ordevelops into a chronic
closed angle. 5
7. Anterior Segment Optical Coherence Tomography (ASOCT)

Optical Coherence Tomography was reported for the first time in 1991 and was
used as a posterior segment of imaging which later evolved into the anterior
segment imaging. Anterior Segment Optical Coherence Tomography (ASOCT) is a
useful device for detecting anatomically narrow angles of the eye chambers,
anterior segment structure and also for measuring the thickness of the cornea
quickly and relatively conveniently for patients. Nolan et al evaluated ASOCT's
ability to detect primary angles of closure when compared to gonioscopy, in Asian
subjects. ASOCT is known to be very sensitive anddetects angular closure when
compared to gonioscopy. More people were found to have a closed angle with
ASOCT examination compared to gonioscopy. Evaluation of structural causes of
closed angles such as iris plateau syndrome, malignant glaucoma, and pupil block
can be performed. 5,13,14
8. Scheimpflug Photographers (Pentacam)
Scheimpflug photography is a technique that has been used for quantitative
evaluation of the angle of the front eye chamber, in particular the depth of the front
eye chambers both central and peripheral, the volume of the front eye chambers
and the thickness of the cornea. 15.16
However, the actual angle recess cannot be visualized with this technique and the
important structural information contained in this area can be missed. 15.16
9. Biometri eyepiece
Ocular biometry is a study that analyzes eye measurements. When compared to a
normal eye, an eye with a primary closed angle exhibits the following biometric
characteristics: (a) a smaller corneal diameter and a smaller corneal curve, (b) a
shallower depth of the front eye chamber and a smaller volume of the front eye
chamber, (c) a thicker lens with a steeper anterior lens surface curve; (d) a larger
lens position anterio r, (e) a greater ratio of lens thickness/axial length factor, and
(f) a shorter axial length. 15.17
The flat depth of the eye with a closed angle is about 1.0 mm shallower than a
normal eye. The thickness of the lens increases by about 0.35 mm and thelens side
is more to the anterior by about 0.65 mm. The jiran eye in patients suffering from
unilateral acute attacks has almost the same depth of the front eye chambers as the
eye that has an attack. The depth of the front eye chambers and the volume of
hypermet eyes are lower when compared to normal eyes. 15
10. Ultrasound Bio Microscope (UBM)
UBM is an ultrasound examination of the anterior segment of the eye using high
frequencies that serve as sufficient magnification to assess the details in the front
and rear eye chambers. Its penetration depth is only up to 4 mm, due to which this
examination cannot show retrolenticular details. This method has created the
possibility of a better understanding of pathogenesis for some diseases of the
anterior segment of the eye, including in the field of glaucoma diseases (primary
and secondary closed angles, pigmentation glaucoma, ciliary block (glaucoma
maligna). 5.11
This UBM method has proven to be ideal for the examination and interpretation of
pathoanatomy present in the primary closed angle and in particular the condition of
the iris plateu at the primary closed angle. UBM is appropriate for determining
pathogenesis in difficult closed-angle cases. However, it should be emphasized that
this examination is not easy to perform precisely (at a high anglefrom the surface of
the eye) and this examination sometimes causes some discomfort to the patient. 5.11
B.2. Primary Angle Closure Glaucoma (PACG) Diagnosis
The basis for the diagnosis of establishing PACG from anamnesis is obtained a
history of having experienced acute, sub-acute or intermittent attacks with symptoms of red
eyes accompanied by headaches on the same side, blurred eyes, seeing halo, history of
glasses, with drugs attacks can be resolved. In cases that have experiencedacute attacks,
they may have undergone peripheral iridotomy. 18
The decision to establish a diagnosis for PACG is the obtaining of a narrow-angle
anatomical state and the presence of a closed-angle pathological condition on examination.
Gold standard diagnostic procedure todetermine the angle of closure is a gonioscopy
examination that must always be done in every glaucoma patient. In addition, the closed
angle can also be determined by assessing the depth of the front eye chamber with shallow
Van Herrick grading (VH 1 and VH 2) using a slit lamp, with UBM or AS-OCT the angle
depth of the front eye chamber can be assessed the shape of the cross section and the
quantitative width of the angle. With UBM it can be in the value of the cornea, the
configuration of the iris and the lens and the organ behind the i ris such as the siliary
corpus, while with AS-OCT it can be in a better resolution value what is the width of the
angle. 18.19
In the dynamic gonioscopy examination, it can be identified the presence of PAS
(Peripheral Anterior Synechia) which plays a role in increasing pressure intraocular.
Indentation can be performed using a four mirror gonioscope or by using a rim on the
goldmann gonioscope to determine whether a PAS is formed or just a trabeculae position
with iris, ITC (Iridotrabecular Contact) and iris plateu configuration. In PAPG, the
presence of a PAS of >180 degrees will determine the management to move to surgical
procedures to control TIO. In chronic PACG cases, a serial gonioscopy examination is
performed to assess the number of PAS formed in this creeping angle. 18
In cases with a young age it is necessary to identify other pathological
abnormalities in the COA angle such as membranes that have been formed since birth,
such as embryotoxon and Barkan membranes. Examination of fellow eye is essential in
acute glaucoma, perform gonioscopy to assess the angle, and perform preventive Laser
Peripheral Iridotomy. 3
Examination of the optic nerve papill using a 78 or 90D lens to determine the stage
of glaucoma and the target of intraocular pressure to be achieved by medicamentous or
surgical. To assess the visual function is determined by perimetry results that give an idea
of how much ganglion cell damage is heavy and a serial examination is carried out to
assess the progressiveness of the decrease in the field of view. 12
 Clinical Symptoms 6.18
- Acute symptoms : Sudden pain around the eyes, can be accompanied by nausea to
vomiting, headaches, red eyes, and blurred vision.
- Chronic symptoms : Asymptomatic or
sometimes accompanied by mild pain
around the eyes, red eyes/ sometimes red and
headaches
 Routine Checkup 6.18
a. Visus to assess sharp vision
Acute: Sharp vision decreases suddenly Chronic :
Sharp vision decreases slowly
b. Tonometry (Measuring eyeball pressure )
Applanation tonometer for measuring intraocular pressure (gold standard)
It can also be done with a schiotz tonometer, noncontact tonometer, or tonopen
Acute : There is a significant increase in eyeball pressure, more than 21mm
Hg and often even reaches 50-80 mm Hg
Chronic : Sometimes there is an increase in eyeball pressure even if it is not too
high
 Biomicroscopy of gap lamp for evaluation of anterior segment 6.18
Acute : - Conjunctival hyperemi
- Cornea edema, cloudiness
- Shallow Front Eye Chamber , van Herick 0-1
- Iris details are difficult to evaluate because of the cloudy cornea,
appearing atrophic iris when it has experienced several recurrent
acute attacks
- Pupil : mid dilatation, not reactive to light,
oval / irregular shape
- Lens : glaucoma flecken
Chronic : - Conjunctiva no hyperemic
- Clear cornea
- The front eye room is shallow
- Iris normal
- Round pupils, good light reflexes
- Lens: clear
c. Funduscopy to assess the papill of the optic nerve and retina
Acute : performed on an undilated pupil, often it cannot be evaluated due to a
turbid medium
Chronic : visible glaukomatous optic neuropathy
d. Gonioscopy is a gold standard procedure for assessing closed angles, visible angles
of closed eye chambers that depend on gradation (use gonioscopy indentation d
examination), gonioscopy can be performed when the media is clear. There is a
focal contact iridotrabecular of 270-360 degrees, focal PAS (peripheral anterior
synecia) and hyperpigmentation of the iris contact area during an attack.
To distinguish the closure of the angle is the synecial positional performed examination
with indented dynamic gonioscopy.
e. Perimetry obtained field defects typical of glaucoma The
perimetry examination is performed when the acute phase has
passed
f. Supporting and additional checks
Anterior OCT : to assess the angle of the front eye chamber
Posterior OCT : to assess the thickness of Retinal Nerve Fiber Layer Imaging
g. Biometrics to assess the depth of the front eye chambers, axial length of the eyeball
C. PACG Management
PACG management aims to prevent or revise closed-angle processes, control intraocular
pressure, and prevent damage to the optic nerve with the aim of maintaining the patient's vision
function and quality of life. 2.18
A. Tatalaksana Primary Angle Closure Suspect (PACS)2,12,18

1. Prophylactic iridotomy in PACS needs to be performed on the circumstances:
a. Patients taking medications that may be at risk of pupillary block
b. There are signs of suspicion of an acute attack before
c. Patients who have difficulty reaching health centers
d. Next eye there is PAC or PACG
2. It remains to be informed of the possibility of acute PAC and PACG attacks
B. Primary Closed Angle Management (PAC)2,12,18

1. Peripheral laser iridotomy/surgical iridectomy
2. In the event of an increase in intraocular pressure, medicamentose can be given:
a. Beta blocker (thymolol maleate 0.5%) 2 x 1 drop
b. Carbonic anhidrase inhibitor topikal (Dorzolamide/Brinzolamide) 3 x 1 tetes
c. Prostaglandine analog (latanoprost/travoprost/tafluprost) 1 x 1 tetes
d. Alfa adrenergic (brimonidine) 3 x 1 tetes
e. Carbonic anhidrase inhibitor oral 3 x 250 mg
3. Lens extraction (phacoemulsification) and implantation of intraocular implanted
lenses with or without goniosinechiolysis.
4. Filtration surgery (trabeculectomy) without or with antifibrotic agents (Mitomycin C
/ 5-fluorouracil)
C. PACG Management (PACG)2,12,18
1. Peripheral laser iridotomy/surgical iridectomy
2. In the event of an increase in intraocular pressure, medicamentose can be given:
a. Beta blocker (thymolol maleate 0.5%) 2 x 1 drop
b. Carbonic anhidrase inhibitor topikal (Dorzolamide/Brinzolamide) 3 x 1 tetes
c. Prostaglandine analog (latanoprost/travoprost/tafluprost) 1 x 1 tetes
d. Alfa adrenergic (brimonidine) 3 x 1 tetes
e. Carbonic anhidrase inhibitor oral 3 x 250 mg
3. Filtration surgery (trabeculectomy) with or without IOL phacoemulsification

4. Filtration surgery (trabeculectomy) without or with antifibrotic agents (Mitomycin C
/ 5-fluorouracil)
5. Glaucoma tube implant can be performed in refractory cases
6. The next follow-up is like the handling of glaucoma cases generally: TIO
evaluation, gonioscopy and static/dynamic perimetry
D. Tatalaksana Acute Primary Angle Closure (APAC)2, 10,12,18

1. The patient is hospitalized.
2. Lower immediately TIO (Intraocular pressure) with medications and evaluate
within 24 hours
a. Oral carbonic anhydrase 500 mg further 3-4 x 250 mg (accompanied by
potassium supplement tablets)
b. Pilocarpine 2% 4x1 tetes
c. Timolol 0,5% 2 x 1 tetes
d. Oral hyperosmotics / infusion when necessary, oral glycerin dose 50% 1 – 3
mL / KgBB , while mannitol IV 20% 2.5 - 7 mL / KgBB by giving 60 drops per
minute when surgery is to be performed with a TIO > of 30 mmHg
3. Give drugs that lower the inflamed reactionand corneal edema: topical steroids 6 x
1 drop
4. Laser iridoplasty (when the cornea is still edema) with or without iridotomy
5. If the TIO has dropped relatively and the eye condition becomes calmer (corneal
edema decreases or disappears) then laser peripheral / surgical tomi iridek is
performed
6. Trabecectomy without or with antifibrotic agents (Mitomycin C/5-fluorouracil)
may be considered when TIO is unresponsive to the drug
7. Cataract extraction can be performed when the eye condition has calmed down
8. For the fellow eye, laser /surgical peripheral iridectomy is performed to prevent an
attack.
9. The next follow-up is like the handling of glaucoma cases generally: TIO
evaluation, gonioscopy, Humphrey static campimetry and OCT / Imaging
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Opththalmology Staff, editors. Fundamentals and Principles of Ophthalmology. Section 10.
AAO: San Fransisco; 2011-2012.
19. Foster P, Day A, Low S. Primary Angle Closure Glaukoma, Glaukoma Medical
Diagnosis &Therapy editor Shaarawy TM at al, Elsevier Saunders, London; 2015; 346-353
3.1.2 Primary Open Angle Glaucoma (POAG)
Primary Open Angle Glaucoma has a gradual onset, slow progressive, and painlessness.
The disease is generally bilateral but can be asymmetrical. There is damage to retinal ganglion
cells and narrowing of the field of view from the central hin gga peripheryin the late stages of the
disease. Asymptomatic to sharp central vision is affected in advanced stages. 1.2
A. Pathogenesis
Trabecular outflow is the main pathway of aquaeous humour flow from the front eye
chamber. Approximately 90% of aquaeous humour comes out of the eyes through this pathway.
From the front eye chambers of the aquaeous humour sequentially exit through the trabecular
meshwork, Schlemm canal, collector canal, episclera vein, towards the systemic circulation.
Trabecular mes hwork consists of three components, namely uveal, corneal, and
juxtacanalikeler. The mechanism of changes in trabecular meshwork occurs in the increase in
age. Trabecular cells are lost on average about 0.5% per year. There are major changes that occur
with respect to the increase in age, namely the loss of trabeclar cells, the thickening of the
trabecular lamella, and the thickening of the elastic fiber sheath. The main detention location is
in the juxtacanalikuler area. 1.2
There is a positive correlation between the intensity and duration of the increase in TIO
with SGR mortality. SGR mortality due to high TIO exposure occurred in 2 stages. The first
phase ends in 3 months where as much as 12% of SGR is lost per week. This process is then
followed by the second stage in the form of slower neuron loss. The primary phase of neuron
loss is the initial phase of apoptosis, followed by the secondary phase in the form of toxic
effects due to ongoing neuron damage due to high TIO exposure. 1.2
In theory, there are two major theories regarding the occurrence of nerve damageo ptik
due to increased TIO, namely mechanical theory and ischemia. In mechanical theory, it is
explained that an increase in TIO can result in direct suppression of SGR axon fibers,
suppression of the anterior structure of the optic nerve and distortion of the lamina cribrosa
resulting in the death of retinal ganglion cells. Meanwhile, based on the theory of ischemia, an
increase in TIO results in suppression of blood flow in the optic nerve so that there is a decrease
in perfusion of the optic nerve and intraneural ischemia. Today's n thinkers recognize that
various
Vascular and mechanical factors may combine, together damaging the optic nerve lamina.
Glaucoma is a heterogeneous clump disorder and SGR death seen in optic nerve papillary
neuropathy, likely mediated by multiple factors. Active research continues to be conducted to
examine the role of various processes such as excitotoxicity, molecular biological abnormalities,
apoptosis, and auto-immunity as the cause of SGR death. 1.2
B. Penegakan Diagnose
Clinical signs 2.3 :
 Excavation glaucomatous Papil N. II

Examined using a biomicroscope slit lamp and a 78 or 90 dioptri lens to get a
stereoscopic picture
 Arcuate-shaped retinal nerve fiber layer defects
 Open iridocorneal angle on gonioscopy examination
 High eyeball pressure without any other secondary causes
Risk factor 1,2 :
 Intra-ocular pressure
Risk factors that play an important role in progressiveness and that can be modified to
prevent progressiveness. The higher the intraocular pressure, the higher the risk for the
occurrence of progressiveness. In patients without glaucoma, there can be variations in
TIO fluctuations of 2-6 mmHg, while in glaucoma patients, TIO fluctuations reach
10mmHg or more.
 Central Corneal Thickness (CCT)

The thickness of the central cornea can affect the results of intraocular pressure
measurements. A thick central cornea will produce ostensibly high intraocular pressure
and vice versa.
 Ras
Racejug a is an important risk factor for POAG. The prevalence of POAG is 3-4 times
greater in blacks and Hispanics than non-Hispanic whites. Blindness due to glaucoma is 4
times more common in blacks than in people with disabilities
 Age
The prevalence of glaucoma increases with age
 Family history
The presence of a family history is also a risk factor for POAG. The Baltimore Eye Study
states the relative risk of POAG increases up to 3.7 times in individuals who have
relatives with POAG
 Myopia
Higher prevalence of myopia in POAG
 Vascular abnormalities
Examples: central retinal vein occlusion, hypertension, diabetes mellitus
Supporting examination 1,2 :
 Tonometri
Tonometry is a measurement of intraocular pressure. Tonometry applanation is the most
commonly used method. TIO measurement using aplanation is a safe, easy to do,
relatively accurate method in various clinical conditions. Among the tools available,
Goldmann's aplanatory tonometry is the most valid (correct) and trustworthy because it
does not move much fluid (approximately 0.5 μL) or increase eyeball pressure, and this
method is not affected by ocular rigidity.
 Gonioskopi
In POAG, an open angle is obtained on gonioscopy examination.
 Photo fundus colour
POAG diagnosis is based on the appearance of the opticus disc and the assessment of visual
function
 Optical Coherence Tomography (OCT)
To find out the thickness of the lining of the nerve fibers of the retina. OCT
examination is currently widely used in detecting and evaluating the progressivity
of glaucoma
 Field of view inspection
Field of view can be checked using both Goldmann static perimetry and Humphrey's
standard automatic perimetry. Thefield of view def in glaucoma that is often found is
general depression, paracentral skotoma, arcuate or Bjerrum skotoma, nasal step,
altitudinal defect, and temporal wedge.
Normotension Glaucoma (NTG) / Low tension Glaucoma1,2
NTG is a form of open-angle glaucoma where the pressure of the eyeball is within
normal limits but there is a glaucomous papillary disorder. Most are asymptomatic unless field of
view abnormalities have reached the center, and are commonlydetected during routine eye
exams.
Clinical signs :
 Intraocular pressure within normal limits

 The anterior segment is calm / without any acute signs
 Open iridocorneal angle
 Excavatio papill glaucomatose (hemorrhage on papillaries, notching)
 Retinal nerve fiber layer defects
 Narrowing of the field of view
Risk factors :
 Vascular abnormalities (eg: migraine)

 Ischaemic vascular dissease
 Autoimmune diseases
 Postural hypotension
 Sleep apnea
 Koagulopati
Supporting examinations:
 Intraocular pressure
 Gonioskopi
At NTG open iridocorneal angle
To find out the thickness of the lining of the retinal nerve fibers
To diagnose whether there is a baseline defect and then it is used to find out whether
there is progressiveness
To find out if it is actually intraocular, whether it is within normal limits or because of the
thin CCT so that it seems normal but actually high
Ocular Hypertension (OHT)1,2
Ocular Hypertension is not actually a form of glaucoma, because there has been no
damage to the glaucomatose papill and narrowing of the field of view. However OHT if left
untreated can develop into glaucoma.
Clinical signs :
 Intraocular pressure above normal

 Papill nervus II within normal limits
 There has been no defect of the retinal nerve fiber layer
 There has been no narrowing of the field of view
Risk factors :
 High intraocular pressure

The higher the intraocular pressure the higher the risk of becoming a POAG
 Thin CCT
 Age
 Family history
 Gonioskopi
Glaucoma Suspect 1,2
Asymptomatic and usually detected during routine eye exams
Clinical signs:
 Normal intraocular pressure

 Papill nervus II suspected glaucomatose
 Gonioskopi
C. Management
The management of primary open-angle glaucoma includes medicamentous and non-

medicamentous. Medicamentous therapy aims to inhibit the formation of aquaeous humour,
increase trabecular flow, and increase uveoscleral flow. Medicamentous therapy is an option for
open-angle glaucoma. Surgical therapy is performed only when medicamentous therapy fails.
Decreased TIO is still an option in the treatment of glaucoma patients. The administration
of therapy to patients with increased TIO will reduce the occurrence of glaucoma or reduce the
progressiveness of glaucoma. When we decide that a glaucoma patient needs to get therapy, then
we must determine what TIO (target pressure) target to achieve2
 Medicamentous therapy
In POAG, it begins with monotherapy. It is recommended to choose glaucoma
drugs according to the percentage of effectiveness of their decrease, so that the target
pressure can be achieved. According to meta-analysis research, prostaglandin analogues
(PGA) were the agents with the greatest decrease in TIO, followed by non-selective beta
blockers, alpha adrenergic agonists, selective beta blockers, and topical carbonic
anhydrase inhibitors. 2.3
If with monotherapy the intra-ocular pressure still does not reach the target
pressure after a 2-week evaluation, then combination therapy can be given. Current
combination therapies include the combination of beta blockers with prostaglandin
analogues such as timolol maleate – latanoprost, timolol maleate – travoprost. Beta
combinations
blockers with CAI inhibitors e.g. thymolol maleate – dorzolamid or brinzolamid and other
combinations such as brimonidin – brinzolamide. 1-3
 Non-medicamentous Therapy
o Laser Trabekuloplasti 1-3
Initially laser trabeculatation is indicated in patients with glaucoma to have
maximum tolerance to Medikamentous therapy, and have an open angle on
gonioscopy examination. Recently, many clinicians give some Medicamentosa
therapy before performing laser trabeculoplasty, but laser therapy can be
considered as the first step in the management of glaucoma. Patients with poor
tolerance to Medicamentosa and lack of compliance in the use of drugs can be
candidates for laser trabecyloplasty.
The Glaucoma Laser Trial (GLT) states that in the first 2 years, the loplastic
trabecue laser used as the initial therapy has the same effectiveness as
Medikamentosa. However, after 2 years more than half of the laser-treated eyes
require an additional 1 or more medicamentose to control TIO. The lasti
trabeculate laser is expected to lower TIO by 20-25%.
o Surgical Therapy
Surgical therapy is indicated in open-angle glaucoma when other
therapeutic modalities are unable to keep the TIO low enough to prevent damage
to the opticus nervus or a decrease in field of view. Uncontrolled glaucoma occurs
due to several causes:
 Maximum tolerance to medicamentous therapy and unable to adequately

lower TIO
 Glaucomatose optic neuropathy or field of view reduction remains
progressive even thoughTIO's deposition with medicamentous therapy
appears adequate
 Patients are less compliant in using medicamentous therapy
Surgical therapy options:
 Filtering surgery without or with antifibrotic agents (Mitomycin C/5-
fluorouracil )
 Installation of implant tube drainage
 Cyclodestructive
 Combination of filtering surgery with cataract surgery in patients if there is
also a significant cataract with a sharp decrease in vision
Based on a summary of publication studies from 1964 to 2000 for the treatment of
glaucoma accompanied by cataracts, it is concluded as follows: 4-7
a. Phacoemulsification surgery will reduce intraocular pressure by 2-4 mmHg within 1-2
years (weak evidence) (Evidence level: I)
b. Two-side phycoemulsion-trabecectomy combination surgery will lower intraocular

pressure 1-2 mmHg lower than 1-2 mmHg lower than 1-sided one-site surgery (modest
evidence) (Evidence level: I)
c. Trabecectomy surgery alone will reduce low intraocular pressure to 2-4 mmHg
compared to phacoemulsification combination trabeculectomy (strong evidence) surgery
(Evidence level : I)
Recommendations for surgical measures in case of glaucoma accompanied by

cataracts: 4-7
- Patients with mild and moderate glaucoma controlled with 1-2 anti-glaucoma drugs, it
is recommended to perform phacoemulsification surgery only (Evidence level: I)
- Patients with advanced glaucoma with optic neuropathy (advanced glaucoma)

accompanied by mild cataracts to sedang, trabecectomy surgery is recommended first,
then cataract extraction surgery can be performed (if vision is disturbed due to cataracts)
at least 6 months later. (Evidence level: I)
- Uncontrolled glaucoma or controlled glaucoma incataract with more than 2 types of

anti-glaucoma drugs is recommended to perform a combination operation of
phacoemulsification – trabeculectomy. (Evidence level: I)
In NTG, although intraocular pressure is still within normal limits, according to the
Collaborative Normal-tension Glaucoma Study (CNTGS) by lowering intra-ocular pressure by
30% from the initial intraocular pressure can reduce the risk of progressiveness for 5 years
from 35% to 12%. 1-3
According to the results of a large-scale study of the Ocular Hypertension Study (OHTS),
with the administration of medicamentous topical therapy until the intra-ocular pressure < 24
mmHg or 22.5% of the initial intraocular pressure, after 5 years only 4.4% in the therapy group
9% of the control group experienced a 50% reduced risk of becoming POAG. After 13 years,
22% of the control group became POAG while in the therapy group only16%. 1-3
Evaluations are
recommended every 12 – 24 months. 3
The risks and benefits of administering therapy to glaucoma suspects need to be

considered based on the presence or absence and how manyrisk factors for developing glaucoma
suspects into glaucoma. Laser trabeculoplasty is not always indicated and surgical therapy is not
indicated. 3
BIBLIOGRAPHY
1. Cioffi GA, Durcan FJ, Girkin CA, Gupta N, Piltz-Seymour JR, Samuelson TW, et al.
Basic and clinical science course: Glaucoma section 10. San Fransisco: American
Academy of Ophthalmology; 2014. p 73-78, 166, 180.
3. Krishnadas SR. Primary open angle glaucoma. In: Krishnadas SR, Ramakrishnan R,
Khurana Mona, Robin AL. Diagnosis and management of glaucoma. New Delhi :
Jaypee Brothers Medical Publishers; 2013. P 301-14
4. European Glaucoma Society, Glaucoma Guideline. 2014

5. Fridman DS, Jampel HD, Lubomsky LH, et al. Surgical strategies for coexisting
glaukoma and cataract. An evidence-based update. Ophthalmology 2002; 109: 1902-
1915
6. Jampel HD, Fridman DS, Lubomski LH et al. B. Effect of technique on Intra

okular pressure after combined cataract and glaukoma surgery. An evidence-base
review. Ophthalmology 2002; 109: 2215-2224
7. Buys YM. Surgical Management of coexisting cataract and glaukoma. Ophthalmology

Rounds 2004; 2:1-5
3.2 Secondary glaucoma
3.2.1 Neovascular glaucoma
Neonascular glaucoma (GNV) is a secondary glaucoma caused by an underlying ocular

or systemic disease. The most frequent ocular causes are ischemic and retinal hypoxia. If left
untreated GNV may cause advanced optic neuropathy and irreversible blindness. Early diagnosis
and aggressive management are necessary to prevent blindness. 1.2
The prevalence rate of GNV is around 3.9%. The most commonly associated states
associated with the incidence of GNV are Central Retinal Vein Occlusion (CRVO), Diabetic
Proliferative Retinopathy (PDR), and other ischemic states and tumors. Thirty-six percent of
GNV occurs after CRVO, 32% occurs after PDR, and 13% occurs after carotid artery
obstruction. 3.4 pm
A. Pathogenesis
Neonaccular glaucoma is a secondary gluacoma associated with the formation of new
blood vessels that can develop into a fibrovascular membrane on the anterior surface of the iris
and the angle of the front eye chamber. The presence of this membrane causes humour aquaeous
obstruction in the early and advanced stages will result in the formation of peripheral anterior
synechia (PAS) which will cause high intraocular pressure. 4.5
The formation of new blood vessels occurs due to an imbalance between pro- angiogenic
ic factors (one of which is Vascular Endothelial Growth Factors / VEGF) and anti-angiogenic
factors (one of which is pigment epithelial derived factors). 4.5
VEGF is an important mediator against the occurrence of intra-ocular neovascularization

in patients with retinal ischemic. In addition to VEGF, there is another pro-angiogenic that plays
a role in the occurrence of iris neovascularization, namely inflammatory cytokine IL-6 yang
correlated with staging iris neovascularization. 4.5
Risk Factors
Oklusi Vena Retina Sentral (Central Retinal Vein Occlusion/CRVO)
The dominant risk factors in CRVO that become GNV are the extent, location and
duration of the retinal ischemia state. The incidence of neovascularization of the iris occurs up to
60% in ischemic eyes and occurs usually 3-5 months after CRVO. 2.3
The Central Vein Occlusion Study (CVOS) showed that 15% of CRVO non ischemic
patients developed into CRVO chemic in the first 4 months. Neovascularization of the iris for at
least 2 hours and/or neovascularization of the angle of the front eye chamber appears in 16% of
the eyes. The main predictive risk factor in iridist rubeosis is sharp poor eyesight. 3.4 pm
In the study of the effective prospof CRVO patients about 20% became neovascular
glaucoma. The risk of neovascular glaucoma is about 60% in eyes with extensive ischemic
retina. The tendency of rapid progressiveness in neovascularization of the iris and neovascular
glaucoma makes early detection in m ata with a high risk of neovascular glaucoma become
essential. 2.4
Diabetic Retinopathy
About one-third of patients with iridis rubeosis are diagnosed as patients with diabetic
retinopathy. The Diabetes Control and Complication Trial (DCCT) showed that strict control
of blood sugar slows the onset of the incidence of diabetic retinopathy and slows the
progressiveness of proliferative retinopathy. 3.4
pm
The prevalence of GNV in diabetic retinopathy is about 2% and increases to 21%
inproliferative diabetic retinopathy. When a patient with diabetes has GNV in one of his eyes,
the unaffected eye has a high risk of GNV if no prophylactic photocoagulation panretinal laser is
performed. 2.4
Ocular Ischemic Syndrome

Ocular ischemic syndrome occurs in severe and chronic obstruction of the carotid artery.
Ninety percent or more of the obstructions that occur in ipsilateral are associated with ocular
ischemic syndrome. Iridist rubeosis occurs up to 66% in these patients. In this case Doppler
sonography of the carotid artery should be performed. Good cooperation between
ophthalmologists,
radiology, and vascular surgery are essential for the handling of the case so that its progressiveness can
be slowed down. 3.4 pm
Central Retinal Artery Occlusion (CRAO)

The occurrence of ischemic in the retina after CRAO is at risk of causing rubeosis iridis
in 18% of cases within 3 months. 2.3
B. Diagnosis Enforcement
A full examination should be carried out in patients with GNV risk factors. Examination
of signs of pupil dilatation with attention to the edges of the pupils is carried out for
neovascularization of the iris. Gonioscopy is performed for examination of the meovasularization
of the angle of the front eye chamber. 2.4
The signs and symptoms that arise depend on the severity of the neovascular glaucoma
that is affected. Sharp vision may decrease accompanied by photophobia. There is corneal
edema, ciliar and conjunctival injections, rubeosis, increased intraocular pressure, inflammation,
hyphema, vitreous hemorrhage. When the increase in introcular pressure occurs suddenly and
very high, complaints may be accompanied by severe headaches, nausea, and vomiting. 2-4
Staging Glaukoma Neovaskular4

a. Rubeosis Iridis
Mild neovascularization of the iris (pupil edge area) and/or the angle of the front eye
chamber, intraocular pressure is usually still normal.
b. Open-angle glaucoma
Mild to moderate neovascularization of the iris and/or angle of the front eye chamber.
Intraocular pressure begins to increase, on gonioscopy examination an open angle of the front
eye chamber is obtained. Hifema can be found in this phase.
c. Closed-angle glaucoma
Moderate to severe neovascularization of the iris and angle of the front eye chamber. The
fibrovascular tissue proliferates and contracts so that it pulls the corner of the front eye chamber
into a disarray. Intraocular pressure can reach 60-70 mmHg. It can be found inflammation and
hifema.
Neovascularization Management
The main objective in managing neovascularization is to reduce the ischemic state that
triggers neovascularization. Pan Retinal Photocoagulations (PRP) is an excellent measure to
shut down the ischemic retinal region, minimize oxygen demand, and reduce the vascular
endothelial growth factors (VEGF) released. Pan Retinal Photocoagulation before filtration
surgery increases the success rate. Neovascular iris can regression in a matter of days to weeks
after PRP is performed, the recommended time to perform filtation surgery 3-4 weeks after PRP
procedure. 4.5
Anti VEGF has afairly fast response to the resolution of vascular leakage resulting in
regression of the neovascular formed. Intravitreal Bevacizumab 1.25 mg/0.05 ml may result in
neovascularized iris regression in a median of 8 days (1-10 days) on some case reports. Although
the long-term effects are not yet known, they can produce transient effects that can make the
right time to perform filtration surgery. 4.5
Management of Neovascular Glaucoma

a. Medicamentosa
Intraocular pressure-lowering drugs can be administered single or a combination of
carbonic anhydrase inhibitor groups (topical or oral), topical beta blockers, alpha two agonists.
Analog prostaglandins are not recommended in this state. It can be addedtopical and cycloplegic
steroids to coping states of inflammation and pain. 3-5
Another therapy to reduce neovascularization in the retina and iris is to give intravitreal
anti-VEGF injections. Drugs that can be given include bevacizumab, ranibizumab, and
aflibercept. 6
b. Surgical procedures
Filtration surgery (trabeculectomy) has a low success rate. The addition of an anti-
fibrotic agent (Mytomicin C/MMC) increases the success rate.
This procedure is performed pthere is a fairly calm state of the eye, but the risk of intraoperative
or postoperative bleeding can still occur. 4-6
Glaucoma Drainage Device (GDD) is the choice of primary surgical procedure in the
state of refractory glaucoma or failure of previous surge ry filtering procedures. Further GNV
management has the possibility of trabecectomy failure so that primary GDD can be performed
in this case. 4-6
The symdestructive procedure can be performed on end-stage GNV patients with very
poor visual acuity and isnot indicated for surgical procedures, so the main purpose of this
procedure is to reduce pain. Trans Scleral Cyclo Photo Coagulation (TSCPC) is a
cyclodestructive method that is often used today because inflammation and pain aremilder. 4-6
BIBLIOGRAPHY
1. AAO Section 10. Glaucoma. 2011-2012
2. Shield’s Glaucoma Textbook. 2011
3. Becker Shaffer’s Glaucoma Textbook. 2009
4. Glaucoma Medical & Diagnosis Therapy. 2009
5. Rodrigues GB, Abe RY, Zangalli C, Sodre SL, Donini FA, Costa DS, Leite A, et.al. Neovascular
glaucoma: a review. 2016. Int J Retin Vitr:2; 1-10
6. Dubey S, Pegu J. Management of Neovascular Glaucoma. Journal of Current Glaucoma and Practice.
2009; 3(3):27-34
3.2.2 Lens-Related Glaucoma
Lens-induced glaucoma is secondary glaucoma caused by lens factors that can result in
secondary glaucoma both closed and open angles. Open-angle types can be divided into
phacolithic glaucoma, lens- particle, and antigenic glaucoma (phacantigenic glaucoma). The
closed-angle type is divided into phacomorphic and ectopia lentis. 1
3.2.2.1 Lens-induced glaucoma, Open Angle
3.2.2.1.1 Facololitic glaucoma
A. Pathogenesis
Facololitic glaucoma occurs as a result of the blockage of trabecular webbing by large
molecular weight lens protein cells, which exit into the front eye chambers as a result of leakage
of the lens capsule that is maturing or hypermaturized. This condition is accompanied by
inflammation of the front eye chambers. 1 It is generally complained of in elderly patients who
are suspected of having cataracts for months or years accompanied by a long history of
complaints of blurry vision. 1.2
B. Diagnose enforcement
Common complaints include eye pain on the one hand, redness, and a sharp decrease in
vision that gets worse, which occurs suddenly. Intraocular pressure is very high, accompanied by
corneal edema and conjunctival and ciliary injections, open corners of the eye chambers, and
cells in the front eye chambers. 1.2
C. Management
The definitive treatment is surgery to extract cataracts. Before surgical action,

intraocular pressure and inflammation need to be lowered with glaucoma drugs and anti-
inflammatory corticosteroids. Glaucoma drugs that can be given are acetazolamide oral as well
as topical. If the intraocular pressure is still very high then hyperosmotic agents such as glycerin
and infusion i.v Mannitol sometimes need to be given as a quick effort
decrease in intraocular pressure on the perioperative, in situations where vital signs can be properly
monitored. 1-3
3.2.2.1.2 Lens-particle
A. Pathogenesis
Glaucoma occurs as a result of lens particles physically causing obstruction of the angle
of the front eye chamber and trabecular webbing. 1 The detachment and retention of lens particles
in the front eye chambers occurs due to rupture or disruption of the lens capsule after cataract
surgery, capsuleotomy or ocular trauma. 1,2
May occur after a few weeks to years after surgery
or trauma. 1
B. Diagnosis enforcement
Patients generally complain of pain, red eyes and a sharp decrease in vision. On
examination there is high intraocular pressure, corneal edema and a decrease in visus. Lens
particles in the form of chunks of varying sizes are found in the front chamberswith cells and
flares and open angles. If the condition has been long enough then anterior or posterior synecia
can be found. 2.3
C. Management
Treatment of secondary glaucoma due to lens particles is similar to phacolithic
glaucoma. The administration of glaucoma and anti-inflammatory drugs is the initial treatment
followed by surgical evacuation of the lens particles. 1.3
If the lens particles are already in the
vitreus, it is necessary to perform a vitrectomy. 3
3.2.2.1.3 Phacoangenic glaucoma
A. Pathophysiology
Another known term is phacanoanphylactic glaucoma, which is caused by an immune

reaction of the body that becomes sensitized to the protein antigen of its own lens so that
granulomatous inflammation occurs. Exposure to lens proteins due to previous surgical procedures or
ocular translucent trauma. 1-3
Inflammation of the front eye chambers with granulomatous cells as well as keratic
precipitate accompanied by an increase in intraocular pressure was found. 1
C. Management
The main management is to reduce inflammatory reactions in the front eye chambers
and lower intraocular pressure with topical corticosteroid drugs and glaucoma. If the treatment is
not successful then surgery is needed to remove thelens residue as well as irrigate the front eye
chambers. 1.2
3.2.2.2 Lens-induced Glaucoma, Closed Angle
3.2.2.2.1 Fakomorfik
A. Pathophysiology
Glaucoma occurs as a result of lenses being subjected to bending. The swelling of the
lens is a significant component that causes the narrowness of the angle of the front eye chamber.
This swelling of the lens occurs as a result of natural development in the direction of cataracts
(cataract intumesens), or traumatic cataracts. This circumstance causes a blockade of aquous
fluid flow in the area of the iris diaphragm -lens and the angle of the front eye chamber is closed.
1-3
Narrowing of the angle of the front eye chamber can occur slowly according to the
development of cataracts, and also occurs acutely when the lens becomes intumescent and pupil
block occurs in the eye without a certain anatomical predisposition that allows closed-angle
glaucoma. 1.3
B. Diagnose enforcement
The complaints that arise are red eyes, pain and a sharp decrease in vision. There is an
injection of conjunctiva, episclera and corneal edema. Intraocular pressure increases and the eye
chambers are shallow, accompanied by bulging lenses and intumesants found only in diseased
(unilateral) eyes. Generally, it is over the age of 64, and the ratio of women is slightly higher
than that of men. 1-3
One of the differential diagnoses of facomorphic glaucoma is closed-angle primary

glaucoma. To distinguish from the primary condition, on examination an asymmetry was found
at the depth of the front eye chambers of both eyes of the patient. In patients with facomorphic
glaucoma,the painless mat a has a deep front eye chamber and an open angle on gonioscopic
examination. 2.3
C. Management
The goal of therapy in facormorphic glaucoma is to lower intraocular pressure by

reopening theclosed corners of the eye chambers. Initial therapy can be done by administering
oral glaucoma medications or drops. If significant inflammation is found, it is also given
steroidal or non-steroidal anti-inflammatory topically. Once the pressure is sufficientlycontrolled
and the corneal edema is reduced, cataract extraction can be performed as the definitive surgical
therapy. If it is not possible to extract cataracts, laser iridotomy can be carried out beforehand.
Trabecectomy can be performed withwishful thinking when intraocular pressure is not
controlled. 1-3
3.2.2.2.2 Ectopia Lentis
A. Pathophysiology
Lenses that shift to a position that does not match their anatomical location can cause
closed-angle secondary glaucoma. If the shift occurs in the anterior direction, it is blocked by
thepupil and iris bombe so that the front eye chamber is shallow and the corner of the front eye
chamber is closed. 1.3
Ectopia lentis can occur under conditions as seen in the following table:
Table. Causes of Ectopia Lentis 1
Causes of Ectopia Lentis
Traumaic Pseudoexfoliation Syndrome

Marfan Homosisteinuria Mikrosferofakia syndrome
Syndrome Weill-‐Marchehisnor Syndrome Ehlers-‐D a NLos Deficiency sulfit -
‐oKsidasi on
There is an increase in intraocular pressure accompanied by the position of the lens that is
subluxated or total luxation (dislocation) either to the anterior, posterior, or to one of the
quadrants/ sides. If there is a luxation to the anterior and a lenticulocornea touch occurs then
corneal edema can be found. 1.2
C. Management
The purpose of management is to prevent an increase in intraocular pressure and contact

lenses to the corneal endothelium. 1.2
Under initial conditions, the supination position is good for
positioning the subluxation lens in the posterior direction. Applying myoticum drops will keep
agar lens in the back position of the pupil. When the lens has dislocated to the anterior, the
myoticum becomes counterindicative because it causes weak contractions of the Zinn zonula,
making dislocation easier to occur. 2.3
Indications of mainly lens extraction surgical procedure
if there has been a complete anterior dislocation to the front eye chamber, or cataracts and other
recurrent problems have been formed. 1-3
BIBLIOGRAPHY
1. American Academy of Ophthalmology. Glaucoma. Basic and clinical science course

(BCSC). San Francisco: American Academy of Ophthalmology, 2016-2017
2. Oxford American Handbook of Ophthalmology. Tsai JC, Denniston AKL, Murray PI,
Huang JJ, Aldad TS (eds). Oxford University Press, 2011.
3. Becker- Shaffer’s Diagnosis and therapy of the glaucomas, 8th edition. Stamper
RL, Lieberman MF, Drake MV (eds). Mosby Elsevier, 2009.
3.2.3 Glaucoma Pseudoexfoliation
A. Pathogenesis
Pseudoexfoliation syndrome or abbreviated as PES, is an age-related systemic
microfibrilopathy, caused by the presence of progressive accumulation and periodic buildup of
gray and white extracellular material in various tissues. This disorder is suffered by 30% of the
human populationover 60 years of age with a thorough distribution in different parts of the
world.
Research shows that 44% of PES sufferers develop into glaucoma pseudoexfoliation
(PEG) within 15 years. In addition, PES patients have a 5-10 times greater risk of menderita
PEG. PES is mainly characterized by the accumulation of fibrillar material on the anterior
segment of the eye. Histologically, the material can be found in the epithelium of the lens as well
as the capsule, the edge of the pupil, the epithelium of the ciliar body, the pigment epithelium of
the iris, the stroma of the iris, the blood vessel of the iris, and the subconjunctival tissue. 1-6
B. Etiology
The role of genetic and environmental factors in the pathogenesis of PES is not yet
clearly known even though a genetic predisposition is often found. High incidence rates in
Scandinavian countriesindicate that northern latitude, cold air, and sunlight can contribute but
there is no solid evidence. PES was obtained in the younger age group in patients living in
countries with low latitudes (Greece/Saudi Arabia/Iran). People who do activities outside more
often are found to be more at risk of suffering from PES compared to those who do activities
more often indoors. 3
Analysis of the relationship between genetic factors and PES began to identify3
suspected gene loci, namely 2p16, 2q35-36, and 3q13-24. The genetic basis is strongly suspected
to have an effect on both PES and PEG as it is known that both show strong familial aggregation
and are associated with inherited abnormalities. However, the pattern of gene inheritance in this
case remains unclear. PES is suspected to be an autosomal dominant inherited disorder with
incomplete penetration. 2.3
Several non-genetic environmental factors are also thought to be related to the
pathogenesis of PES, including exposure to ultraviolet rays, dietary factors, autoimmune,
infectious agents, and trauma. Ultimately, PES is a complex, multifactor, and late-onset
disorder
which is influenced by both genetic and non-genetic factors. 2.3
C. Enforcement of
diagnosis of Symptoms
and Signs
The clinical diagnosis of PEG is based on the clinical detection of pseudoexfoliative
material. The classic sign of PES is the presence of a shape resembling 'dandruff' (dandruff like
or flake like deposits) on the anterior surface of the lens which generally appears in the late
stages of the disease, which is a chronic symptom. Early clinical signs that are still unclear are
often undetectable. These signs can appear without an increase in TIO or signs of full-blown and
can be detected by careful examination of the condition of the dilated pupils. PES is generally
bilateral and asymmetrical. It is stated in the study that in 10 years, one-third of unilateral PES
cases will develop intobilateral ones. 3.4 pm
In the early stages of the disease where classical signs have not yet appeared, the
pseudoexfoliative material can only be seen in the peripheral part of the anterior capsule of the
lens. Detection of early signs of PES can be done using low intensity slit-lamp irradiation. The
highlight of the lamp should be positioned at an angle of 45. Striking early signs include:
 pseudoexfoliative material at the edge of the dilated pupil
 uniform, homogeneous, or ground glass appearance material on the anterior
surface of the lens
 Red flags due to atrophy in the pigment epithelium of the iris
 tidak adanya pupillary ruff
 pigment dispersion after the pupil is dilated
 increased trabecular pigmentation
 hard pupils wide
Eye jirant in unilateral cases with signs of pigment dispersion as well as the absence of
pupillary ruff without pseudoexfoliative material detected is called "exfoliation suspects". The
ciliary processus can be the initial observed part in search ofpseudoexfoliative terial ma. The
material can be obtained at the earliest in the ciliary process with the help of indirect
ophthalmoscopy at the grave. In the afactia eye, pseudoexfoliative material can be seen on the
anterior surface of the glass body, as well as on the posterior chamber IOL as well as in the
posterior capsule in the pseudophic eye. 3.4
pm
In full-blown PES, pseudoexfoliative material appears on the anterior surface of the lens
in a distinctive shape, consisting of 3 zones or known as "Bull's eye" that appear after the pupil is
dilated, that is, a relatively homogeneous central disc with a size corresponding to the size of the
undilated pupil, which is surrounded by a clear intermediate zone 1-2 mm wide (located between
the central disc and the zo na peripheral). The peripheral zone is granular, appearing as a layered
ring of pseudoexfoliative material, which is the result of friction of the pseudoexfoliative
material on the iris with the lens surface during pupil movement. It also finds a pre-equatorial
zone that is generally hidden behind the iris and corresponds to the proliferative zone of the
epithelium of the lens. In this zone there is a lot of debris that covers the zonula and its
attachment. These classic clinical findings are not always apparent. You can get a tanda-sign that
is almost invisible before the appearance of the classic sign. Please be aware that although these
clinical findings generally appear, sometimes PES cannot be diagnosed in unablatated pupil
codition. 3.4 pm
Fine pseudoexfoliative material can generally be seen at the edge of the pupil and less
often on the iris, endothelial cornea, and can sometimes be seen above trabecular meshwork by
gonioscopy. Due to degenerative changes in this condition, the iris becomes atrophied, with
transillumination defects, and there is a moth-eaten formation at the edge of the pupil due to loss
of pigment. Scattered and accumulated iris pigments are an early and distinctive sign of PES and
PEG conditions. Pigment granules sometimes appear to be deposited on the anterior surface of
the lens after the pupil has been dilated. Fine pigment deposits appear on the surface of the iris
and rarely appear on the corneal endothelium. The accumulation of pigment at the angle of the
front eye chamber is a sign of pathognomonis in this condition and is seen as a pile of
undulating pigments above the Schwalbe line (called Sampaolesi's line) as well as as thick and
dark pigments accumulated in trabecular meshwork. The number of pigment granules depends
on as well as correlates with the severity of the disease. 4
Studies with fluorescein angiography showed damage to the blood aqueous barrier. This
is especially true in the iris and in some cases extends to the ciliar body. This damage has a direct
influence on the early postoperative period resulting in the eye being more susceptible to
fibrinoid reactions. It can also result in the formation of posterior synecia, glaucoma due to
pupillary block, as well as neovascularization of the iris. 3
Eyes with PES are difficult to dilate. The pupil in the eye with PES has more diameter
small when compared to eyes that do not suffer from PES. The same is true of attempts to
constrict pupils with pilocarpines. This can occur due to fibrotic and degenerative changes in
theiris sphinc and dilator muscles. This is important for consideration of surgical management in
PES. 3
Pseudoexfoliative material can initially be detected in ciliary and zonular processes. A
buildup of pseudoexfoliative material was found inthe damaged zonu la. This explains the
tendency to subluxate lenses in PES. 3
Increased trabecular pigmentation is a clear sign of gonioscopy. The pigmentation that
occurs is generally patchy, in contrast to the formation of the mascara linea in PDS. This can be a
sign for early diagnosis of the development of pseudoexfoliative material in the lens or iris.
RNFL was found thinner in the eyes with PES. 3
In PEG, there are all signs in PES accompanied bytio tightening and depletion of the
neuroretinal rim on the optic nerve papill which indicates glaucomatose damage. Diffuse optic
nerve papill damage is caused by high TIO as a characteristic of PEG, where TIO can reach 60
mmHg. PEG is characterized by uglier 24-hour TIO characteristics compared to POAG. In
addition to high TIO, PEG is generally asymptomatic and not associated with pain. Patients
generally do not feel a sharp decrease in vision in unilateral cases or due to the different degrees
of disease between the two eyes. In the presence of large TIO fluctuations within 24 hours on the
PEG, TIO measurements should be carried out periodically; ideally TIO measurements in 24
hours are carried out three times, namely morning, evening, and evening. 4
Proper diagnosis enforcement as well as peak identification of TIO improvement is
important in PEG management. The TIO curve is also important for evaluating the magnitude of
the TIO decrease in PEG, as proper diagnosis and management cannot be obtained with just one
measurement. 4
In PES and PEG, when the pupil is pharmacologically latated, usually the pigment
appears detached from the posterior iris layer. This can lead to an acute increase in TIO. To
prevent acute damage from a sharp TIO increase, TIOshould be measured every 2-3 hours after
dilatation and if necessary, medications to lower TIO. 4
The symptoms and signs of PEG can be a form of mechanism of glaucoma
open angle, PEG 'normal tension', or closed-angle glaucoma . 3
 PEG can be a secondary open-angle glaucoma that occurs due to the buildup of
pseudoexfoliative material in the trabecular meshwork. The most common finding is
pseudoexfoliative material in the eye. The clinical interest in this regard is open-angle
glaucoma due to the pseudoexfoliative material being more often uncontrolled, with
higher TIO rates and requiring regular and periodic follow-ups. Early failure of
medicamentous therapy and failure of laser trabeculonplasty generally occur and such
cases require early surgical therapy. Surgery is associated with an increased risk of
durante and postoperative complications. 3
 Acute open-angle glaucoma can alsobe one of the forms of glaucoma in PEG. Dispersion
of pigment granules and pseudoexfoliative material in the front eye chambers is generally
found after pupil dilatation and can result in increased TIO which sometimes leads to dif
us corneal edemathat resembles clinical manifestations in PACG. Such increased TIO can
also resemble acute pupil blocks with symptoms of red eyes, corneal edema, an increase
in TIO of more than 50 mmHg despite a form of open-angle glaucoma. There is a posit if
correlationbetween the degree of increase in TIO and the release of pigment, both of
which take a maximum of 2 hours after the mydriatic process, then return to normal after
12-24 hours. This is important to distinguish from acute closed angles where peripheral
iridotomy actually worsens the condition due to pigment deposits. In rare cases,
spontaneous subluxation of the lens into the vitreus can trigger facololitic glaucoma. 3
 In normal TIO states the cause of glaucomast optic neuropathy isocular and retrobulbar
perf usi disorders and abnormalities of the elastic tissue of the lamina cribosa. This is
supported by the presence of ultrastructural and immunohistochemical images in
exfoliating fibers in the vortex vein, ophthalmical artery, centralist retinal vein, and iris
stroma. In addition, elastosis of the expanding blood vessels is also found in the eyes with
PEG. Disrupted autoregulation mechanisms relate to microvascular changes or changes
in the lamina cribosa that may result in increased susceptibility to minimal changes in TIO
within the normal TIO value range. 3
 Other mechanisms of closed-angle glaucoma include the formation of posterior synecia
due to disturbances in the blood aqueous barrier which results in an increase in protein
concentration in the acu humor, stiffness and decreased motility of the iris resulting in
pupil block as well as neovascularization in the iris. In rare cases, aqueous misdirection
syndrome can occur due to zonula weakness as well as subluxation of the lens to the
anterior and ciliary musculus contractions can cause closed-angle glaucoma due to the
ciliary block. 2.3
PES is known to be related to a higher prevalence of cataracts and the exact etiology of
this is still unknown. Ischemia of the eyeball as well as oxidative damage are suspected to be the
cause of cataracts. Nuclear cataracts and subcapsulesare reported to occur in many patients with
PES and PEG. In some cases, phasianderesis, subluxation, or even lens luxation may occur as a
result of zonula damage. 3.4 pm
MANAGEMENT
Medicamentous Therapy
Medicamentous therapy in PEG is in accordance with the stages of medicamentous
therapy in POAG. Such therapies include β- adrenergic antagonists, α-adrenergic agonists,
myotics, carbonic inhibitors of anhydrose, as well as analogous prostaglandins. There was a poor
response to monotherapy treatment in PEG, which often required more aggressive therapy along
with diurnal TIO monitoring and examination at shorter intervals compared to POAG patients.
Any therapy should aim to reduce the average TIO and 24-hour TIO fluctuations. To date, the
impact of the latest medicamentous therapies on the long-term prognosis of PEG is unknown. 2.4
The fixed combination of dorzolamide/thymolol has been evaluated as an initial therapy
in PEG and expressedas one of the applicable options. On a crossover study, Konstas et al.
applied a fixed combination of the two drugs to 65 newly diagnosed patients with PEG with a
mean TIO before therapy of 31.2 mmHg. After receiving therapy for 2 months, the average
decrease in TIO at its peak was obtained by
13.1 mmHg (42%). 2,4
There is little information regarding the response and success rate of therapy using
prostaglandin analogues on PEG. In a recent parallel diurnal study, latanoprost was slightly more
effective compared to monotherapy using thymolol to lower TIO in the eye with PEG. In a
multicenter study, latanoprost was said to be slightly more effective than monotherapy with
timolol for lowering the TIO of patients with PEG as well as showing lower diurnal fluctuations
and mean peaks of TIO. 2,4,7
Additional therapy with latanoprost is declared safe and has good tolerance as a long-
term therapy of patients with PEG. Sebuah studies report that latanoprost is more effective as an
adjunct therapy when used simultaneously with timolol compared to dorzolamide. In some cases
of PEG with high basal TIO and severe damage, treatment with a combination of te tapscan be
the best choice as an initial therapy. Initial therapy with fixed combinations was stated to have
better TIO control compared to non-combination therapies administered together, as well as
reducing drug side effects. In PEG, rice combi should still be used earlier and more frequently in
PEG management given the characteristics of a worse 24-hour TIO, faster disease progression,
and a worse prognosis in PEG. 4
Myotic agents have asignificant effect on reducing TIO, but there are several
disadvantages of using myoticum including increased damage to the blood- aqueous barrier,
decreased pupil movement which increases the risk of posterior synecia, the formation of
cataracick, increased lens turbidity, and triggers closed-angle glaucoma due to pupil block or
siliar block in the eye with unstable zonula, Thus myotic agents become relatively
contraindicated therapies. 2.7
Laser Argon Trabekuloplasti (ALT)

Laser argon trabeculatlasty (ALT) is a photocoagulative procedure that aims to lower the
TIO in PEG, which has a high success rate and is well developed. Most studies show a better
response to PEG compared to POAG. Nevertheless, long-term failures generally occur in PEG.
ALT is recommended when TIO cannot be properly controlled with maximum tolerance of
medicamentose, as an option before breast milk filtr surgical procedures. However, when there
are contraindications to the use of medicamentosa as well as in elderly patients or patients
who do not comply with the rules of treatment, ALT can be the first choice in the management of
PEG. 3.4 pm
PEG is characterized by thick pigmentation in trabeculae, so in PEG patients with an
open angle of the front eye chambers is especially appropriate when ALT is performed. Because
the amount of pigmentation in trabecular meshwork directly affects the results of therapy in
PEG, trabecular meshwork generally experiences heavier pigmentation, should the ALT strength
be set lower than the selected ALT strength on POAG. The optimal laser strength setting is
determined by the heat-induced reaction of the trabecular meshwork, which indicates the
suitability of the laser power setting. Ideally, TIO is measured within the first 6 hours post-
action. If not possible, initial therapy using topical apraclonidine as well aspost-action oral
acetazolamide treatment is recommended to prevent ALT-triggered thio depletion. Topical
steroids or non-steroidal anti-inflammatory drops are used 4 times a day for 7 days. Strict
monitoring is recommended in cases with direct stage glaucoma, patients with one-eye status,
high TIO before laser, as well as recurrent trabeculoplasty. The results of the action of ALT
cannot be evaluated before 4-6 weeks. ALT has minimal complications, the most frequent of
which is a temporary increase in TIO, which is more common in patients with PEG than in
POAG patients. In some eyes, small peripheral anterior synecia formation is obtained
(especially after laser placement in the posterior or patients with a narrow front eye chamber
angle). Slow increase in TIO as a long-term complication is also common. 4
Postlaser complications are more common in PES including temporary inflammatory
reactions and TIO depletion, which require careful further management with flamacy anti-
inflammatory therapyand TIO control in the early postlaser phase. Apraclonidine hydrochloride
is reported to have potent effects as a temporary drug to prevent as well as reduce TIO
congestion after ALT procedures. 2.5
Selective Trabeculoplasty Laser (SLT)

Selective laser trabeculoplasty (SLT) can be a safe and effective alternative measure
compared to ALT in PEG patients although further studies are still needed. SLT can be
considered a repeatable procedure as well as more powerful than ALT. A recent study conducted
by Goldenfeld et al. showed a decrease in TIO of up to 31.6% and a decrease in the average
use of medicamentose
significant in each patient within 1 year. The low success rate of SLTcan be attributed to the
magnitude of the angle treated. 2.5
Surgical Management
Filtration surgery may be needed earlier and is more commonly used in PEG
management compared to other types of glaucoma. In cases withn extreme TIO fluctuations,
primary trabecectomy action can be considered. In addition, another alternative filtration surgery
that can be done is ExPress. Whichever filtration surgical technique is chosen, antifibrotic agents
can help reduce the risk of postoperative scar tissue formation. Drainage implantation may also
be indicated when a failure of the trabecectomy action occurs once or more. 2
Trabekulektomi
Trabecectomy is still a surgical procedure that is often performed in the management of
PEG patients with severe glaucoma or failure of TIO control with medicamentous or laser.
Shaheen et al. stated in their study that the effect of reducing TIO during 6 months postoperative
trabeclectomy in PEG reached 92% without medicamentous and 98% with medicamentous. The
study proved that trabecectomy is an effective modality in controlling the TIO of patients with
PEG. 8
Implantasi Aqueous Shunt

In 2012, a controlled randomization clinical trial (RCT) study showed greater
effectiveness in aqueous shunt implantation than surgical trabecectomy. 211 patients with
intraocular lens and/or surgical failure of filtration were studied and treatedwith aqueous shunt
or trabecectomy surgery. Similar TIO values were obtained from both groups, but the likelihood
of failure and complications sooner or later was higher in the trabecectomy group compared to
the shunt impl antasi group. 5
Cataract Surgery
In the evaluation of a cataract surgical procedure in patients with PEG, control over
the depletion of TIO and the severity of glaucoma should be taken into consideration in addition
to corneal endotheliopathy, poor mydriasis, lens subluxation, and zonula instability. An increase
in the number of complications during the extraction of extra-capillary cataracts in the eye with
PEG compared to cataracts in the normal eye has been suggested previously, although some
researchers found no difference between the two. Currently, phacoemulsification is the most
frequent procedure performed in cases of pseudoexfoliative cataracts and has a lower recurrence
rate. 5
Good results in cataract procedures can be influenced by several factorssuch as good
pupil dilatation as well as wider capsules. In lens capture several techniques have been put
forward to reduce stress on weak zones. In addition, in the selection of intraocular implantation,
3-piece type intraocular lenses are considered a better option for PEG patients. However, the
incompleteness of the zonula and the tightening of the capsules in the eyes of PEG who are
pseudophacic are more at risk of luxation or dislocation to the vitreus and resultin acute sharp
loss of vision. Pars plana vitrectomy is the most suitable surgical approach to taking a
dislocated intraocular lens. However, in elderly patients, in order to maintain sharp vision,there
is no need to perform any surgical procedures due to the increased risk of intraoperative and
postoperative complications. 5
Combination of Cataract and Glaucoma Surgery

The combination of cataract and glaucoma surgical procedures can be a good choice for
patientswith PEG. Tran reported that approaches with pseudoexfoliative material cleaning
techniques at both iridocorneal and trabecular meshwork angles significantly reduced TIO and
reduced the use of postoperative medicamentous therapy. This techniqueavoids incision and the
need for suturing, so as to maintain the anatomical structure of the eyeball. 5.9
Cataract surgery should be performed when a sharp decrease in vision interferes with a
person's quality of life and is sufficient to guarantee the risk of surgery. The increased risk of
complications associated with PEG should be balanced with the surgeon's experience. The
decision to perform or postpone surgery and the existence of more advantages than losses to the
patient should be considered first by a surgeon. 10
Complications during the phacoemulsification procedure are mostly related to the
weakness of the zonula so it requires special attention. Based on the weakness of zonula and
dialysis, capsular tension ring (CTR) can be installed before phacoemulsification or after
phacoemulsification of the nucleus and before irrigation-aspiration of the cortex.
The selection of intraocular lens type is also important in the eye with PES. Heparin
surface modified posterior chamber in traocular lenses is associated with fewer postoperative
fibrinoid reactions, pigments and cell build-ups in less frequent lenses, as well as a reduced
incidence of posterior synecia when compared to other types of intraocular lenses. In addition,
intraocular lenses with flexible silicone should not be used to prevent capsular contraction
syndrome. Although unfolding one-piece acrylic posterior chamber intraocular lenses are more
commonly used by surgeons as the best option to reduce the risk of stress in both capsules and
zonulas, three-piece posterior chamber IOL (with haptics made of PMMA) is more often used as
a procedure with a comparable level of safety. 11th
Bibliography
1. Nagar, Madhu. SLT a New Option for Pseudoexfoliation Glaucoma. Ophthalmology Times Europe.
2008.
2. Schlötzer-Schrehardt, U & Naumann, GOH. Trabecular Mechanisms of Intraocular Pressure
Elevation: Pseudoexfoliation Syndrome, dalam J Tombran-Tink, CJ Barnstable & MB Shields (eds.).
Mechanisms of the Glaucomas. Humana Press, Totowa, New Jersey. 2008
3. Khurana, M & Ramakrishnan, R. Exfoliation Syndrome and Exfoliation Glaucoma, dalam R
Ramakrishnan, SR Krishnadas, M Khurana & AL Robin (eds.). Diagnosis and Management of
Glaucoma. Jaypee Brothers Medical Publishers. New Delhi. 2013
4. Konstas, AP, Hollo, G, Teus, MA & Ritch, R. Exfoliation Syndrome and Glaucoma, dalam JR
Samples & PN Schacknow (eds.). Clinical Glaucoma Care. Springer. Heidelberg. 2014
5. Plateroti, P, Plateroti, AM, Abdolrahimzadeh, S & Scuderi, G. Pseudoexfoliation Syndrome and
Pseudoexfoliation Glaucoma: A Review of the Literature with Updates on Surgical Management.
Journal of Ophthalmology. 2015;vol. 2015.
6. Girkin, CA, Bhorade, AM, Giaconi, JA, Medeiros, FA, Sit, AJ, Tanna, AP & Crowston, JG.
Glaucoma. American Academy of Ophthalmolog section 10. San Fransisco. 2016
7. Ritch, R, Barkana, Y & Liebmann, JM. Special Therapeutic Situations, dalam PA Netland (ed.).
Glaucoma Medical Therapy Principles and Management Second Edition, Oxford University Press.
Oxford. 2008
8. Shaheen, N, Rashid, W, Rasool, F, Mir, AM, Saleem, T & Rashid, A. Intraocular Pressure Control in
Post Trabeculectomy Patients with Pseudoexfoliation Syndrome: A Prospective Study. International
Journal of Scientific Study. 2016;vol. 4,no. 1,hal. 228-230.
9. Tran, VT. Washout of Pseudoexfoliation Material Combined with Cataract Surgery: A New Surgical
Approach to Lower Intraocular Pressure in Pseudoexfoliation Syndrome. International
Ophthalmology. 2014;vol. 35, p. 209-214.
10. Rand, WJ, Velázquez, GE & Schechter, BA. Cataract Surgery in Pseudoexfoliation Syndrome, dalam
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Incorporated, New Jersey. 2004
11. Kaštelan, S, Tomić, M, Kordić, R, Kalauz, M & Salopek-Rabatić, J. Cataract Surgery in Eyes
with Pseudoexfoliation Syndrome. Journal of Clinical and Experimental Ophthalmology. 2013
3.2.4 Glaukoma Pigmentary
A. Pathophysiology
Pigment Release Mechanism
There are three factors that play a role in the pathophysiological process of pigment
release, namely mechanical, genetic, and environmental. 1.2
The curvature of the iris to the posterior is due to the presence of several distinctive
anatomical features, namely the presence of a more posterior insertion of the sclera, a concave
shape that coincides with the presence of a deeper than normal peripheral front eye chamber
condition, and a more floppy stromal condition causing a lower resistanceto the vectorial
dynamic power of the aculot humor. Each such anatomical picture is confirmed by analysis by
UBM examination. The distance between the trabecular base of the meshwork and the iris
insertion proved to be larger, the concave shape of the iris with the deep front eye chambers
is often described in the eye with PDS and PG, and the radial width of the iris proved to be
greater in the PDS eye than normal causing the possibility of occurrence Flattening on
midperipheral irises with a complex of lenses- zonulas. At the histopathological level, atrophy
and dysplasia of the iris epithelium, the presence of poor differentiation of the dilator muscles
and abnormal iris stroma has been reported and is suspected to be a primary abnormality in PDS.
1-4
Iris-lens contact that is moreintense than usual will hinder the process of balancing the
humor between the front and back eye chambers. Therefore, the iris will be more concave in
shape and the friction with the zonula will be greater. This is called a reverse pupillary block.
Accommodation and exercise bikes will also increase the concavity of the lens and form a
reverse pupillary block. The occurrence of accommodation causes the lens to move more
anterior and increases the pressure on the front eye chambers. In addition, accommodation
causesan increase in iris concavity. Contractions in the ciliary ring cause siltation of the front
eye chambers, movement of the anterior lens and increased iridolenticular contact. The akuos in
the front eye chamber is forced into the angle recess andthe peripheral iris becomes more
concave. When accommodation is validated, the iris returns to its original shape. In addition to
the curving of the posterior iris during accommodation, the pupil is subject to constriction.
Relaxation of the accommodation followed by dilatation of the dap pupil causes additional
friction in the iridozonular. Movements, especially sudden ones, can cause the zonula to rub
against the posterior part of the iris. It is more severe in sports
which contains jumps such as basketball and volleyball. The release of pigments associated with
pupil dilatation is one of the contributing factors. Another theory says that exercise causes an
increase in systolic volume in choroid vascularization. This is one of the mechanisms by which
akuos at the beginning ofits back eye chamber and increases iridolentical contact causing reverse
pupillary block. Dilatation of the pupils leads to increased release of pigments and an increase in
intraocular pressure. The type of exercise that triggers the release of pigment may differ between
patients. Tello and friends said one patient who was a football player came after training that
included running and kicking and his intraocular pressure was normal. However, when the
suffereris challenged after a football match, his intraocular pressure increases. Tello and friends
concluded that the usual act of heading the ball during the game, was allegedly responsible for
the release of pigment in this case. 1-4
This mechanical theory has been widely validated by studies using UBM in related
sufferers. But the posterior curvature of the iris is actually not enough to explain the loss of
pigment of the epithelium of the iris.
Milieu
Although currently there has been a development of knowledge and understanding of
genetic factors in PDS, the contribution of environmental factors is still not understood. Factors
such as accommodation, exercise, pupill dilatation, and blinking increase the concavity of the
osterior p part of theiris causing pigment release. Accommodation may explain the onset of PG
at a younger age than other types of glaucoma, but the effect of this accommodation on iris
profile in PDS/PG varies widely, where some irises will increase concavity, others have no
change and some actually decrease it. Pupillary dilatation with drugs is believed to trigger a
meaningful release of pigment and an increase in intraocular pressure. La innya environmental
factors, such as ultraviolet light, are known to trigger melanogenic pathways and accelerate the
release of iris pigment acutely, but this hypothesis has not been clinically validated. 5
Intraocular pressure enhancement mechanism

The development ofPDS into PG is a consequence of the release of melanin granules
from the pigment of the iris epithelium which then causes obstruction of the trabecular
webbing. Pigment particles from the iris and the ciliar body of the donor monkey's eye when
injected in the front mat chamberof the healthy monkey's eye show an increase in intraocular
pressure in a short period of time and the resistance from the outflow flow will return to normal
after one week.
The release of pigment has been found to accumulate in the endothelial cells ofthe laric
trabeku, cells in the connective tissue and the endothelial layer on the outer wall of the Schlem
canal. Obstruction of the akuos drainage path is obtained as a result of a combination of various
factors. The pigment is phagocytosed by trabecular endothelial cells and macrophages.
Trabecular e ndotel cells will ingest melanin, which will then lead to cell sequencing and death
due to excessive phagocytosis processes. Because melanoproteins are only partially digested, the
rest is trapped in intracellular storage vacuoles, where these proteins will produce free radicals.
Macrophages migrate to necrosed trabecular cells, likely in response to the release of cytokines
by injured cells, and carry pigments and residual cells through the Schl emm canaland into
circulation. The loss of trabecular cells makes this layer open and prone to fusion, causing the
loss of the aqueous canals. The trabecular layers of the corneosclea and uveosklera that have
been reduced layer are destroyed and disintegrated and then add to the obstruction of the
intertrabecular spaces. These changes have been documented in the human eye with PDS
performed enucleation. In the end, at the end of the aqueous drainage path, the internal boundary
of the juxtanalicular network is affected by a reduction in the surface area and increases the
resistance of the outflow. These factors that affect the facility of outflow, resulting in increased
intraocular pressure. As a result, although the release of pigment has decreased or even stopped,
intraocular pressure remains high due to permanent dysfunction of trabecular webbing and
decreased outflow facilities. 1.4
Clinicians should find glaucoma-related symptoms, such as pain, redness, rainbows around
light, changes in vision, and sharp loss of vision. A history of the disease should also include
diseases that can have manifestations in the eyes or that may affect the patient's ability to
tolerate treatment that
Given. These conditions include diabetes, heart and lung disease, hypertension, oddynamic hem
shock,hypotensive shock, sleep apnea, Raynaud's phenomenon, migraine and other neurological
diseases, and kidney stones. Clinicians should also ask for a history of corticosteroid use. 6
The onset of PDS is estimated to occur in most sufferers in the third decade of life. The
course of PDS/PG disease can be divided into three phases namely:2,7
1. Active phase of pigment release
 Begins in the middle of adolescence
 Pigment is actively released and accumulates on the anterior segment of the eye
 Asimtomatis
 Intraocular pressure remains normal
 The release of pigments can be accelerated by the presence of environmental
factors such as physical exercise, emotional stress, and mydriasis both normally
occurring and induced by medicamentous administration
 Happened over the years
2. Conversion phase to glaucoma
In a population-based retrospective study, it was estimated that about 10% of PDS
sufferers would become PG after 5 years, this incidence increased to 15% after 15 years. Another
study cited a PDS-PG conversion rate as high as 35% over a span of 5-35 years. Another series
of cases mentioned only two of the 43 points that showed the occurrence of PDS-PG conversion
after 6 years. Most studies approve the active release of pigment asan important risk factor in the
conversion from PDS to PG.
3. Regression phase
 After aging, the pigment begins to disappear from the trabecular meshwork, the
iris defect slowly disappears, and in some sufferers the intraocular pressure
improves to within normal limits
 Pada eye still obtained glaucomatous optic neuropathy (GON) with or without
field of view defects, but intraocular pressure was obtained low
 Gonioscopy examination can show a pigment reversal sign where
normal pigmentation pattern becomes reversed, becoming darker in superior
than inferior, indicating a history of pigment dispersion but not specific to PG
Open-angle glaucoma is usually asymptomatic until the disease reaches an advanced

stage. Namun sufferers of PG are slightly different, conditions that can trigger an acute pigment
dispersion, for example physical exercise, being in the dark for a long time, looking closely for a
long time, driving at night, and others can cause an acute and intense increase in intraocular
pressure. This can lead to complaints such as seeing rainbows around light sources and blurred
vision caused by corneal edema. Meanwhile, people with PDS where they have normal
intraocular pressure, do not report these complaints regarding their condition. However, because
patients with PDS usually suffer from myopia, so they often have their eyes checked to get
corrections for glasses or contact lenses, then theexamination can be noticed an increase in
intraocular pressure or pigment dispersion. PDS itself can appear asymptomatic. The classic
presentation of a PDS sufferer is a young man, aged between 20 to 40 years who complains of
blurredvision or pain in the eyes after exercise. 2.8
Ophthalmology Examination
 Sharp vision
 Intraocular pressure: Fluctuations of extensive daily intraocular pressure are thought to
arise more frequently in PG and can be high enough to cause corneal edema, blurred
vision and rainbow viewing around light. In patients with PG, there can be a sudden
release of pigment after pupil dilatation or exercise, this can lead to an increase in
intraocular pressure, and cause complaints such as seeing rainbows around light,
intermittent blurred vision, and pain in the oculi. 6.9
 Examination of the anterior segment with biomicroscopic slitlamp is carried out to look
for signs of basic or associated eye diseases
o Preferably done with a large magnification and in the dark
to detect the presence of pigments in the anterior segment and defects in the
transillumination of the iris.
o Imaging support examinations in the anterior segment such as UBM and anterior
segment optical coherence tomography are useful for documenting the
configuration of the iris and angle of the front eye chamber and comparing
between before and after laser iridotomy. 4.8
o Krukenberg spindle is an accumulation of pigments on the posterior surface of the
central cornea in a vertical, spindle-shaped pattern.
o On examination using a specular microscope, it is obtained in the corneal
endothelium of a pleomorphism and polymegathism, namely abnorm ality in the
size and shape of the cell. In addition to this phenomenon, there were no reports
of abnormalities in the endothelial cell count and central sufferers of PDS / PG.
2,4,8
 Iris transillumination examination is an important clinical picture for the diagnosis of PG

because with this examination can be seen areas where the pigment is dispersed. The
characteristic picture is a radial spoke-like pattern on the midperipheral iris. This picture
can be seen on examination with slit lamp by directing the rays through the pupil
perpendicularly to the plane of the iris and observing the retinal light reflex through the
defect in the iris. In some sufferers, however, dark and thick iris stroma may prevent
transillumination of pad a defect, and therefore the absence of this finding does not rule
out PG as a differential diagnosis. 4.10
Pigment granules are often dispersed in the iris
stroma, which can make the iris appear progressively darker or create heterochromia in
asymmetric cases. Patients with PDS can have anisochoria, where the eye with a more
intense pupilis the eye with a larger iris transillumination defect. Iris heterochromia and
anisokoria in people with PDS can resemble Horner syndrome. 4.8
Peripheral irises can
have a concave configuration that can be seen using a slit lamp or by gonioscopy. 9
 Lens: The pigment can be depositioned on the zonula, the posterior surface of the lens, on
the insertion region of the zonula fibers (Zentmayer ring), on the posterior region of the
central lens of the Weigert ligament (Scheie line), and the anterior iris surface. This
disorder can only be
seen when the pupils of the sufferer are dymidriasis. 2.8
 Front Eye Chambers: The front eye chambers in PDS/PG sufferers are obtained deeper
than normal. The corner of the front eye chamber is wide open with iris insertion that is
more to thesterior po. 2
 Gonioscopy has an important role in the evaluation of patients with PDS / PG. In
gonioscopy, an open angle is usually obtained, with the iris inserted posteriorly from the
siliar body, and the peripheral iris configuration in the form of a concave. The amount of
pigmentasi in trabecular meshwork should be graded and documented separately at
superior and inferior angles in both eyes. Pigments can also be deposited on the Schwalbe
line. In the early cases of PG, trabecular meshwork was modera well pigmented, with
pigmentation varying from one part to another. In advanced cases, trabecular meshwork
appears as a similarly visible dark brown band along the angular circle of the front eye
chamber. Pigments can penetrateall angles from the surface of the siliar to the peripheral
cornea, the pigmentation line that resides anteriorly from the Schwalbe line known as the
Sampaolesi line. 8.9
 Posterior segment examination: Peripheral retinas are found to be mostly abnormal in
both PDS and PG patients. Peripheral retinal degeneration is found more frequently in
people with myopia with PDS/PG compared to people with myopia without PDS/PG.
Examination of the optic nerve papill with careful documentation needs to be carried out
in all patients, by paying attention to the presence or absence of signs of GON such as the
size of the optic nerve papillary, the presence or absence of peripapillary atrophy, defects
in the lining of nerve fibers, papillary bleeding, or narrowing of the neuroretinal rim.
2,3,8,11
 Field of view examination: Lapang view quantitatively measures the loss of vision
function. This examination is important for the evaluation of the patient's quality of life
and the effectiveness of the therapy. The age of onset of the disease is younger when
compared to POAG. In additionto the release of pigments, PG resembles POAG in many
aspects, including a decrease in outflow facilities, cupping of the optic nerve papill, and
field of view defects. Nilforushan and colleagues conducted a study to compare field
view defects between PG sufferers and POAG. The results of the study showed that the
temporal area of the field of view associated with the nasal sector of the optic nerve
papill is more prone to injury in POAG sufferers compared to PG sufferers. The study
has not been able to explain the reasons
the occurrence of this. 6,9,12
MANAGEMENT
PDS is a risk factor for the occurrence of occuli hypertension, all sufferers must have
regular eye examinations, especially when they are in the active phase of pigment release. The
therapeutic algorithm of PG can be equated with therapy on POAG. Medicamentous therapy is
usually the initial approach in PG therapy. A more aggressive approach is considered when
therapy with drugsan unsuccessful in controlling intraocular pressure. Eyes with PG have
phenotypic characteristics that can influence both the selection of therapy and the timing of non-
medicamentous therapy strategies. The principle of therapy is to lower the releasen pigment and
its dispersion, remove concavity from the iris and iridozovicular contact, lower intraocular
pressure, and prevent disease progression. Consideration of therapeutic selection should keep in
mind the pathogenesis of pigment dispersion so that therapy can lead to elimination from acute
pigment release rather than simply treating an increase in intraocular pressure. 1.2
 Changes in Sports Lifestyle are associated with acute iris pigment release and it is
advisable to avoid activities such as running and taking toursun-stairs. Pylocurin can have
a prophylactic effect on sports. 11th
 Medicamentous Therapy
o This beta-blocker agent causes an emphasis on the production of humor and has a
relatively easy way of use with minimal ocular side effects. 1
o Prostaglandin Analogues is reported to have high effectiveness in lowering
intraocular pressure in the eye with PG, but the use of latanoprost is more
effective than timolol in the eye with PG. 2
o Pyrerexine can reduce the release ofpigments by inhibiting the occurrence of
pupil blocks where this effect is obtained by making the pupils myotic, and
lowering intraocular pressure by increasing the flow of akuos through the
trabecular tissue. 1.2
o Α1 receptor antagonist drugs such asdapiprazole and thymosamin have been
considered as therapeutic options to avoid mydriasis
physiological in the eye affected by PDS/PG. This drug has a therapeutic
advantage by not involving the ciliary muscles and works by relaxing the dilator
muscles so that it does not affect the refraction of the sufferer. But the
effectiveness on long-term use of both intraocular pressure control and pigment
release remains controversial. The incidence of side effects on topical use such as
a burning sensation and intolerable hyperemia has never been reported on long-
term use of this drug. 1.2
o Alpha-Adrenergic Agonists. The drug can be used as a second-line therapy in
combination with other aqueous humor production suppressors or prostaglandin
analogues. The limitation of the use of this drug is the development towards
allergies in long-term use in about 50% of patients. 1
o Carbonic Anhydrase Inhibitors (CAI). CAI group drugs in topical preparations
are effective in lowering intraocular pressure on PG and are generally well
tolerated. Drugs of this class cause an additional decrease in intraocular pressure
when combined with beta blockers, prostaglandin analogues and alpha agonists.
1.2
Laser Trabekuloplasti
Laser trabeculoplasty is a procedure to lower intraocular pressure with the direct
application of laser energy to trabecular tissues. Argon and explanatory trabecoleplastylasers can
be used for people with PG. In contrast to that observed in POAG, laser trabeculatation appears
more effective in young individuals with PG. The response to laser trabecoliplasty depends on
the duration of the disease where the longer the duration, the worse the response. This is
consistent with histological data showing the majority of the released pigments are found far
from the trabecular tissue in young sufferers and the early phases of the disease. Patients with PG
require a laser with a minimum energy of as low as 300 mW/spot on argon or 0.4 mJ/spot on
selective. The greater the amount of pigment present at the angle of the front eye chamber, for
example in patients with older age, the lower the energy used, this is aimed at minimizing the
risk of increased post-laser intraocular pressure caused by energy absorption
excess and the occurrence of extensive scarring of trabecular tissue. In the interventional,
prospective, non-randomi studiesof the eye with PG, an increase in intraocular pressure of 2.7
mmHg was reported as an initial response after selective laser trabeculonplasty that occurred in
the first 6 months after therapy. A study by Ayala said the probability of success of selective
trabeculoplasty lasers in PG sufferers in the first year was 85%. Success is influenced by large
angle of the front eye chambers, pigmentation and initial intraocular pressure. The study reported
a decrease in raocular int pressure after selective laser trabeculatlasty in PG sufferers could
persist for two years then the effects of this laser therapy decreased. 1,2,13-15
Peripheral Iridotomy Laser

Peripheral laser iridotomy causes a pressure balance between the front and rear chambers
of the eye. After iridotomy, the concave iris will flatten out, thus making a narrower angle and
thus lowering the possibility of iridolenticular contact. This can prevent further release of
pigmen. In addition, Nd:YAG laser iridotomy resulted in a significant decrease in the number of
melanin granules in the aqueous humor of the eye with PDS which was about 65%. 1.2
Laser iridotomy can result in the release of large amounts of pigment into the front eye
chambers. Before carrying out this procedure, it is necessary to consider the possible benefits
that can be obtained and the possibility of theoretical increase in the severity of the disease. In a
randomized, prospective, controlled, clinical trial study it was reported that laser iridotomy
lowered the incidence of significantly increased intraocular pressure over 10 years in the eye
with PDS. 2
The effect of laser iridotomy is greater in patients under the age of 40. This corresponds
to the widely known incidence of exacerbations of reverse pupillay blocks triggered by
accommodation. If iridotomy proves effective in the eye with PDS then it shows still good
trabecular function, which can be estimated with still normal intraocular pressure. When the
trabecular tissue has been disturbed, characterized by an increase in intraocular pressure, the
result of the conduct of the iridotomy procedure is controversial. The iridotomy procedure
should be performed on patients under the age of 45 years who show a well-documented
concave-shaped iris , the release of pigment
which is numerous and clinically detectable in the front eye chambers when pupil dilatation is
performed with medication, and ya ng trabecular tissueis functioning properly, as evidenced by
intraocular pressure that can still be controlled without drugs. When trabecular tissue is
damaged and intraocular pressure increases, then the advantage of the absence of excess pigment
in the gan jarin is questionable and this is supported by the current scientific evidence. The
effectiveness and indications of peripheral laser iridotomy are still a matter of debate. This
procedure is not an ideal option in at least two groups of patients, namely PDS tanpa ocular
hypertension with minimal risk for progressivity towards PG, patients with severe glaucoma
damage although with a variety of drugs where peripheral laser iridotomy triggers pigment
release and increased pressure intraocular can add to the damage already present. 1.2
Filtration Surgery
The surgical management carried out has the same principles as the management in the
POAG. Surgery is indicated when there is progression in the field of view defects or changes in
the papills of the optic nerve even though medicamentous or laser therapy has been carried out.
Progressivity in optic nerve papill damage along with field of view defects should be the main
guide used to determine the indications of differentiatorn.1
The recommended surgical procedure option is trabecectomy. Patients with PG are
mostly young, therefore the risk of major failures. The use of antimetabolites must be done
vigilantly because of the risk of hypotony in young patients with myopia. In addition, it is
important to minimize the risk of intraoperative silting of the front eye chambers to avoid
traction at the vitreous base of the peripheral retina. Eyes with PG have a higher prevalence of
peripheral retinal degeneration and dystrophy, therefore the risk of retinal tears and detachment
is greater. Careful postoperative supervision of the peripheral retina is necessary.
1,2
Bibliography
1. Khurana, M, Pilai, M & Ramakrishnan, R. Pigment dispersion syndrome and pigmentary glaucoma,
in R Ramakrishnan, SR Krishnadas, M Khurana & AL Robin (eds). Diagnosis and Management of
Glaucoma. Jaypee Brothers Medical Publishers. New Delhi. 2013
2. Gandolfi, SA, Ungaro, N, Moro, P & Sangermani, C. Pigmentary glaucoma, in T Sharaawy, MB
Sherwood, RA Hitchings, JG Crowston (eds.). Glaucoma. Elsevier, New York. 2015; edisi 2
3. Tello, C, Radcliffe, N & Ritch, R. Pigmentary dispersion syndrome and glaucoma, in PN Schacknow,
JR Samples (eds.). The Glaucoma Book. Springer, New York. 2010
4. Allingham, RR. The clinical forms of glaucoma, in RR Allingham, SF Freedman, SE Moroi, DJ Rhee
(eds.). Shields Textbook of Glaucoma. Lippincott Williams & Wilkins, Philadelphia. 2011; edisi 6
5. Lascaratos, G, Shah, A & Garway-Heath, DF. The genetics of pigment dispersion syndrome and
pigmentary glaucoma. Survey of Ophthalmology. 2013; vol. 56, no. 2, hal. 164-175.
6. Cioffi, GA, Durcan, JF, Girkin, CA, Gupta, N, Piltz-Seymour, JR, Samuelson, TW, Tanna, AP,
Barton, K & O’Connel, SS. Glaucoma. American Academy of Ophthalmology. San Fransisco. 2016
7. Whitson, JT. Pigmentary glaucoma, in TJ Zimmerman & KS Kooner (ed.). Clinical Pathways in
Glaucoma. Thieme, New York. 2001
8. Park, SC, Tello, C, Radcliffe, N & Ritch, R. Pigment dispersion syndrome and pigmentary glaucoma,
in JR Samples & PR Schacknow (eds.). Clinical Glaucoma Care. Springer, New York. 2014
9. Stamper, RL, Lieberman, MF & Drake, MV. Becker-Shaffer’s Diagnosis and Therapy of The
Glaucomas. Mosby Elsevier, San Fransisco. 2009; edisi 8
10. Hawkins, AS. Intraocular inflammation and glaucoma, in DP Edward & TS Vajaranant (eds),
Glaucoma. Oxford University Press, New York. 2013
11. Bowling, B. Kanski’s Clinical Opthalmology A Systematic Approach. Elsevier, New York. 2016;
edisi 9
12. Nilforushan, N, Yadgari, M & Jazayeri, A. Comparison between visual field defect in pigmentary
glaucoma and primary open-angle glaucoma. International Ophthalmology. 2016; vol.36, no. 5, hal.
637-642.
13. Khan, AM. Laser treatment for glaucoma, in DP Edward & TS Vajaranant (eds). Glaucoma. Oxford
University Press, New York. 2013
14. Wong, MOM, Lee, JWY, Choy, BNK, Chan, JCH & Lai, JSM. Systematic review and meta- analysis
on the efficacy of selective laser trabeculoplasty in open-angle glaucoma. Survey of Ophthalmology.
2014; vol. 30, hal. 1-15.
15. Ayala, M. Long-term outcomes of selective laser trabeculoplasty (SLT) treatment in pigmentary
glaucoma patients. J Glaucoma. 2014; vol. 23, no. 9, hal. 616- 619.
3.2.5 Inflammation-Related Glaucoma
Glaucoma can occur secondary to inflammation of the eye. Glaucoma that occurs
inconjunction with eye inflammation is called glaucoma uveitis or inflammatory glaucoma. As
many as 20% of eyes with uveitis are accompanied by secondary glaucoma. 1.2
A. Pathogenesis
Increased intraocular pressure on inflammation is quite complex. Eye pressure may

increase when the decrease in aqueous humour flow through trabecular meshwork is greater than
the decrease in aqueous humour production that is common in uveitis. 3
Somemekan isms that can cause an increase in intraocular pressure (TIO) in glaucoma uveitis
are:3,4
1. Inflammation of the trabecular meshwork (trabecitis), resulting in swelling

lamellae trabeculae and decreased filtration function.
2. An increase in inflammatory cells in the anterior ocular camera leads to blockage of the
trabecular ducts by inflammatory cells.
3. The occurrence of pupil adhesion with the anterior capsule of the lens causes pupil block,
iris bombe, peripheral anterior synecia and closure of the anterior oculi camera angle.
4. TIO enhancement can also occur as a result of steroid therapy used for uveitis therapy
(steroid induced)
Acquired symptoms of glaucoma uveitis include blurred vision, red eyes, pain in the eyes
and temples, and sometimes visible signs of halo. A history of onset of symptoms of eye
inflammation or uveitis can be experienced as early as a few days or weeks before symptoms of
increased TIO arise. A complete eye examination needs to be performed covering the visus,
anterior segment with slit lamp, gonioscopy, and intraocular pressure examination. The
posterior segment can be examined with direct ophthalmoscopy or biomicroscopic slitlamp with
a 78D or 90D lens. Examination of the field of view (perimetry) and ocular cohorence
tomography (OCT) for the posterior segment should be performed when the eye condition is
calm. 1.3
Increased TIO in glaucoma uveitis can occur quickly and high. In the secondary closed-angle
mechanism there will appear the presence of pupillary miosis, posterior synecia, with iris bombe
and silting of the front eye chambers as well as angular closure and PAS seenin gonioscopy. 3
Some types of uveitis that have the potential to cause glaucoma uveitis are as follows:4
1. Fuch’s heterochromic iridocyclitis,

2. Glaucomatocyclitic crisis (Posner-Schlossman syndrome)
3. Juvenile rheumatoid arthritis
4. Herpetic keratouveitis
5. Postoperative uveitic glaucoma
Additional Checks
In patients with recurrent or bulateral glaucoma uveitis, it is necessary to explore to find

the background of the causes of inflammation both ocular and systemic. A complete blood test,
examination for arthritis, infections, as well as skin and mucosal lesions need to be carried out. 3.4
pm
1. Management
The first step in treating glaucoma uveitis is to relieve inflammation so that it can reduce its
detrimental effects. In some cases a decrease in inflammation can lead to a significant decrease
in TIO. Patients with aggressive inflammatory treatment will have a better prognosis and course
of the disease. 1,3,4
Corticosteroids are the anti-inflammatory of choice in cases of glaucoma uveitis. Strong topical
steroids are indicated to be administered such as dexamethasone or betamethasone. In refractory
cases sometimes periocular or systemic steroids are required. In steroid responders or who tend
to experience a tio tan reduction with steroid administration, can be given
immunosuppressants such as cyclosporine, methotrexate, or azathioprine. In this case
coordination with a uveitis specialist or an experienced rheumatologist can help. 4
Antiviral therapyis given in cases of glaucoma uveitis associated with infection with the herpes
simplex virus or varicella zoster. 1.4
Cycloplegic needs to be administered to release posterior synecia to avoid the occurrence of

permanent synecia and pupil block. This plegic cyclo therapy can also reduce complaints of
photophobia and pain in the eyes. 3
Antiglaucoma therapy
Topical antiglaucoma needs to be administered to lower the TIO of glaucoma uveitis

sufferers. Topical beta blockers are one of the first-line drugs. Topical Carbonic anhydrase
inhibitors (CAI) can also be administered singly or in combination with topical beta blockers.
1,3,4
If the decrease in TIO has not achieved the expected results, systemic CAI administration can
be considered.
The use of topical analog prostaglandins (PGA) in glaucoma uveitis is controversial.

There are concerns that the side effects of these drugs may aggravate existing inflammatory
reactions. However, some sources say that PGA has a fairly good effectiveness in lowering TIO
and can be given in cases of calm glaucoma uveitis. 1,3,4
Surgical therapy
Surgery is a therapy that sometimes needs to be done when eye pressure cannot be
controlled with other therapies. Laser iridotomy can be performed on patients with posterior
synecia acicit pupil block. Sometimes it takes more than one laser location to relieve the iris
bombe. 3.4 pm
Trabecectomy filtration surgery can benefitfrom glaucoma uveitis both at an open angle
and a closed angle with uncontrolled TIO. Protection with systemic steroid doses of
immunosuppressants is recommended for cases of feared postoperative inflammatory
exacerbations. 1.3
Glaucoma tube implant can be considered in cases of glaucoma uveitis because some reports say
the complication rate is lower than trabecectomy. The installation of this tool can be done as a
primary surgical therapy as well as on the cassetteof trabeclectomy failure. 4
Bibliography
1. American Academy of Ophthalmology. Glaukoma. In: American Academy of

Opththalmology Staff, editors. Fundamentals and Principles of Ophthalmology. Section
10. AAO: San Fransisco; 2011-2012
2. Quigley HA, Broman AT. The number of people of glaukoma worldwide in 2010 and
2020. Br J Ophthalmol 2006; 90: 262-7
4. Francisco J. Muñoz-Negrete, Javier Moreno-Montañés, Paula Hernández-Martínez, and
Gema Rebolleda Current Approach in the Diagnosis and Management of Uveitic
Glaucoma. BioMed Research International. Volume 2015
3.2.6 Secondary glaucoma due to increased pressure of the episclera vein
Glaucomasekun der is glaucoma associated with ocular or systemic abnormalities that

cause a decrease in aqueous outflow. . Aqueous outflow through the conventional outflow path
depends on the pressure difference between intraocular pressure (TIO) and isclera ep vein
pressure (TVE), so an increase in TVE that is not compensated by reduced aqueous inflow or
increased aqueous outflow will lead to an increase in TIO. 1.2
Some of the conditions that cause an increase in episclera venous pressure areobstruction
of venous flow, arterivenous fistulas, and idiopathic enhancement. All of these conditions will
appear in a variety of clinical symptoms followed by an increase in TIO and lead to
glaucomatous cupping and field of view abnormalities. 3
Orbital tumors can also causeincreased intraocular pressure through several mechanisms
so that they can also cause secondary glaucoma. 4.5
This secondary glaucoma therapy aims to
lower TIO and therapy against its underlying disease.
A. Pathogenesis
Conditions that cause an increase in episclera venous pressure divided into three
categories: 6
 Obstruction of venous flow, including thyroid eye disease, retrobulbar tumors,
cavernous sinus thrombosis or venous platelet orbita, orbital vein vasculitis,
superior vena cava obstruction
 Arterivenous anomalies, including cavernous carotid-sinus artery fistula, verises orbita,
shunts dural dan Sturge-Weber syndroma
 Idiopathic.
All conditions that increase the pressure of the episcleral vein will also increase the TIO
due to obstruction of the flow of aqueous post trabecular. The clinical picture of increased
episcleric venous pressure depends on the disease and underlying conditions, including
chemosis, proptosis, bruit orbita, and eksoftalmus pulsating. Dilated episclera veins, tortous,
and corkscrew images with mild to severe variations. The corner of the COA was open, and
blood was visible in the Schlemm canal. Outflow flow is usually normal in most cases. In
chronic cases, there can be changes in trabecular meshwork and cause reduced outflow. 3
Table 1. Causes of Increased TVE6
Venous Congestion Arteriovenous Fistulas Idiopathic (Radius

Maumenee Syndrome)
Thyroid-associated Carotid-cavernous sinus Diagnosis of exclusion

Opthalmopathy fistula
Sindorm vena kava superior Dural arteriovenous shunts
Tumor retrobulbar Varicose veins orbitals
Cavernous sinus thrombosis Sindrom Sturge-Weber
Orbital amyloidosis
Venous Flow Obstruction

Superior vena kava
obstruction
A variety of conditions can cause superior vena kava obstruction, including tumors,
aortic aneurysms, mediastinum tumors, and intra-thoracic goiter. This obstruction causes
edema and cyanosis of the face and neck, and causes dilatation of blood vessels in the head, le
her, chest, and upper extremities. Superior vena kava obstruction also increases intra-cranial
pressure which will cause headaches, stupor, vertigo, and mental changes. On ocular
examination will be found ecsoftalmus, papilledema, dilated blood vessels in the conjunctiva,
episclera, and retina. TIO increases, and the increase is higher when the patient is in the supine
position. In this superior vena kava obstruction glaucomatous cupping is rare, some researchers
believethis is due to TIO offset by an increase in intracranial pressure. During this period of
increased TIO is treated with drugs that decrease aqueous production , such as B blockers and
topical or systemic CAIs. 3.7
Thyroid Eye Disease

Thyroid eye disease is known by various names, including endocrine ecsoftalmus,
Graves' disease. Hormonal abnormalities in this condition are still unclear, and the patient can be
hypothyroid, euthyroid, or hyperthyroid when problems in his eyes appear. In thyroid eye disease
there is an increase in episcleral venous pressure which causes an increase in TIO. 3,6,7
Clinical symptoms are varied and include ecsoftalmus, chemosis, palpebral retraction,
lid lag, dilatation of the conyungtiva and episclera blood vessels, tortosity of the veins of the
episklera, exposure to the cornea, limitation of eye movement, papillary atrophy. 6
In patients with increased pressure of the heavile veins, cholinergic drugs have a
minimal effect. Aqueous humour suppression drugs such as beta-adrenergic blockers, alpha-
adrenergic blockers, and carbonic anhydrase inhibitors provide better results. 3.6
Anomali Arterivena
Fistula arteriovenous
Carotid-cavernous fistulas cause a connection between the internal carotid artery and the
surrounding cavernous sinuses, causing high blood flow and high pressure in the shunt. Reverse
blood flow in blood vessels causes congestion of the orbital veins and soft tissues. This leads to
ocular ischemic and possibly the passage of arterial pulsation to the eyeball. Carotid-cavernous
fistula patients often have a history of previous trauma. The clinical picture is in the form of
ecsoftalmus pulsating, palpebral edema chemosis, limited movement of the eyeball. The
conjunctival and episclera veins are noticeably dilated and corkscrew. Most cases are treated
with embolization, and sometimes a more invasive approach such as orbital decompression may
be required. The increase in TIO is generally due to an increase inatan
episclera pressure, although it can also be caused by angular closure and neovascular. Increased
TIO treated with -adrenergic topical antagonists and CAI. 3,6,7
Sturge-Weber Syndrome
Sturge-Weber Syndrome is a congenital disorder characterized by a classical triassic
consisting of dilatation of the facial vein or port-wine stain (PWS), leptomeningen vascular
malformations, and ocular abnormalities.
A. Pathogenesis
SWS is thought to originate from the embryonic phasewhere there are residues of
embryonal blood vessels with their secondary effects on brain tissue. Vascular plexuses form
around the cephalic part of the neural tubes, under the ectoderm that will insect the skin of the
face. Normally, this vascular plexus is formed in the sixth week and undergoes regression around
the ninth week of pregnancy. Normal regression failures that occur in this vascular tissue, will
form angiomas in the leptomeningen, face, and ipsilateral eyes. 8.9
Glaucoma in SWS can occur at the time of newborn (early-onset) or appear at the age of a
child or adult (late-onset). Early onset glaucoma is caused by a combination of COA angular
abnormality and increased epocleral vein pressure, while episcleral vein pressure enhancer is the
primary mechanism in late-onset glaucoma. 10.11
pm
Ocular manifestations in SWS are usually abnormalities of the eyelid blood vessels,
conjunctiva, episclera, siliary corpus, retina and choroid. On examination of the erythropic ant
segment, malformations of the episclera blood vessels and dilatation of conjunctival blood
vessels (figure 2) are usually found. Choroid hemonoids occurs in 50% of patients with SWS. Iris
heterochromia can also be found in SWS patients according to the part of the face that is
affected. 4, 12
Management
Glaucoma management in SWS is still controversial today because it is quite difficult to
treat with medicamentous and has a low success rate with a high risk of surgical complications.
Glaucoma management usuallydepends on the onset
the occurrence of glaucoma. In early-onset glaucoma, a goniotomy procedure is usually required
as the main option. Surgical therapy has such a low success rate that ..? Procedures typically
chosen in glaucoma early onset are trabecectomy and drainage implants such as Ahmed Valve or
Baerveldt's two-staged procedure. 8
Idiopathic Episclera Vein Pressure Increase

An increase in idiopathic episcleric venous pressure is diagnosed when all intraorbital
and intracranial abnormalities have been removed. The diagnosis was based on clinical findings
of dilated episclera veins (pictured), an increase in TIO that led to glaukomatous optic
neuropathy and/or changes in the field of view and in gonioscopy an open angle (mustard) was
found. Several cases of dioptic elevation of episcular venous pressure and TIO have been
reported. These conditions can be unilateral or bilateral and sporadic or familial. 3.7
The diagnosis is established on the basis of a complete eye examination, radiologi

examination such as MRI to rule out cerebrovascular abnormalities. 13
Increased TIO treated with topical and systemic drugs that reduce aqueous production,
cholinergic groups can also be useful, especially in patients with reduced outflow outflow. Argon
laser trabeculplasty can also help in patients. Filtration surgery may also be required, but be
careful with complications. 3
Table 2. Differences between idiopathic TVE enhancement and Arteriovenous Fistula
Idiopatik Elevated EVP Arteriovenous Fistula
Onset Maybe as congenital (maybe Herediter (often acquired)

congenital)
Predisposing factors Family (possibly familial) Trauma, hypertension
Symptom Tidak ada Pulsatile bruit/tinnitus,

pain,diplopia
Signs of neurology Tidak ada Unilateral atau bilateral,

cranial nerve VI paresis,
cranial nerve III paresis
External signs Dilated episceral vessels, Dilated corkscrew episcleral

conjunctival vessels can be and conjunctival vessels,
under normal circumstances Chemosis, eyelid edema
Orbital signs Tidak ada Bruit, Proptosis
Imaging Normal Dilated superior ophthalmic

vein or cavernous sinus
Angiography catheter Normal Arteriovenous fistula

BIBLIOGRAPHY
1. Skuta GL, Cantor BL. Glaucoma. American Academy Ophthalmology. Section 10. San Fransisco;
2011.
2. Ministry of Health of the Republic of Indonesia. Sensory health survey. Ministry of Health of the Republic of
Indonesia. Jakarta; 1997.
3. Becker- Shaeffer’s. Secondary open angle glaucoma. In: Diagnosis and Therapy of the Glaucoma 8 th
edition. Ed. Stamper RL, Lieberman MF, Drake MV, Mosby St. Louis, Philadelphia;2009.p.266-286
4. Shaarawy TM, Sherwood MB, Hitching RA, Growston JG. Childhood Glaucoma. Glaucoma : Medical
Diagnosis & Therapy. New York: Elsevier; 2015. p. 387-400.
5. Allingham RR. Glaucomas associated with elevated episcleral Quigley HA, Broman T. Number of People
With Glaucoma Worldwide in 2010 and 2020. British Journal of Ophthalmology;2006. 90; 262-267
6. Moster M, Ichhpujani P. Episcleral Venous Pressure and Glaucoma. Journal of Current Glaucoma
Practice. 2009;(1):5-8
7. Skuta GL, Cantor LB, Weiss JS. Glaucoma . American Academy of Ophthalmology. San
Fransisco.2011
8. Wen JC, Johnstone M. Increased Episcleral Venous Pressure As An Etiology Of Glaucoma. Glaucoma
Today.2017;53-55
9. Abdolrahimzadeh S, Scavella V, Felli L, Cruciani F, Contestabile MT, Recupero SM. Ophthalmic

Alterations in the Sturge-Weber Syndrome, Klippel-Trenaunay
10. Stamper RL, Lieberman MF, Drake MV. Developmental and Childhood Glaukoma. Becker-
Shaffer's Diagnosis and Therapy of the Glaucoma. US: Elsevier; 2009. p. 294-329.
11. Crowston J, Weinreb R, Minckler D, Medeiros F. Glaucoma Secondary to Sturge-Weber Syndrome.
Glaucoma Today. 2005;12:19-22.
12. Syndrome, and the Phakomatosis Pigmentovascularis: An Independent Group of Conditions?
BioMed Research International. 2015;2015:786519.
13. Akhter K, Salim S. Sturge-Weber Syndrome and Secondary Glaucoma. Ophtahlmic Pearls Glaucoma.
2014;17:49-51.
14. Nassr MA, Morris CL, Netland PA, Karcioglu ZA. Intraocular Pressure Change in Orbital Disease.
Survey of Ophthalmology.2009;(54):519-544
15. Audren F, Abitbol O, Dureau P, et al. Non-penetrating deep sclerectomy for glaucoma associated with
Sturge-Weber syndrome. Acta Ophthalmol Scand. 2006;84(5):656-660.
3.2.7 Glaucoma due to Tumor (Orbital Tumor that gives rise to Glaucoma)
Different types of ocular tumors can cause glaucoma through various mechanisms
3.2.7.1 Hemangioma Kavernosus

In one study of 66 patients with cavernous hemangioma, the TIO was about 6 mmHg
higher than the next eye. Intraconal vascular lesions can cause an increase in TIO due to direct
compression or due to secondary bleeding that causes a sudden increase in TIO. 1
3.2.7.2 Ocular malignant melanoma

A. Pathogenesis
Ocular malignant melanoma can cause glaucoma through several mechanisms, including
direct extension of the tumor to trabecular meshwork, entry of tumor cells into the outflow
channel, pigment dispersion, inflammation, bleeding, including hemolytic glaucoma and
suprakoroid hemorrhage causing closed-angle glaucoma, neovascularization in the corner, closed
angle due to shift of the lens-iris diaphragm to the anterior, peripheral anterior synechiae or
posterior synecia, trabecular obstruction of meshwork by macrophages consisting of melanin
released by necrotic tumors. 1.2
Management by lowering eyeball pressure with topical, oral medications and eyeball removal. 1
3.2.7.3 Cysts of irises and siliar

A. Pathogenesis
Iris and ciliar cysts can also cause glaucoma, the mechanism of which is similar to that of
the plateu iris, there is a blockage of the trabeculae by an enlarged cyst, causing the pressure of
the eyeball to increase. 2
B. Management
Decrease in intra-ocular pressure with topical and oral medicamentosa , when not controlled
can be performed filtration surgery (trabeculectomy) and in refractory cases can use glaucoma
implant. 2
3.2.7.4 Choroid melanoma and ciliar bodies
A. Pathogenesis
Choroid melanoma strongly causes secondary glaucoma, Shields et al report only 2% of
eyes with choroid melanoma give rise to secondary glaucoma. 21
Choroid melanoma and ciliar
bodies can cause glaucoma through several mechanisms, namely neovascularization, shift to the
anterior of the iris lens diaphragm by the tumor mass with the onset of PAS and causing closed-
angle glaucoma, direct tumor extension to trabecular meshwork, pigment dispersion, seeding
tumor cells to outflow,inflammation, bleeding. 3
Diagnosis by finding iris nodules of various sizes, the enlargement of the nodules can grow
to the anterior chamber or to the posterior chamber, heterochromia can be found without iris
thickening. Iris melanoma can metastasize considerably at diffuse 13%. 1, 4
B. Penatalaksanaan
Glaucoma is controlled with the drug if the tumor does not infiltrate the corners. Surgical
procedures can be performed iridocyclectomy, radiotherapy, finally can be performed
enucleation. 4
3.2.7.5 Retinoblastoma
Retinoblastoma also often causes glaucoma through neovascularization mechanics,
passage to corners, iridocyclitis and hyphemas. Retinoblastoma can also appear as a mass in the
posterior that develops rapidly and pushes the lens of the iria and causes glaucoma to close
without pupil block. 5
Tumor management is in accordance with the retinoblastoma procedure, namely the

removal of the eyeball (enucleation or exenteration). 5
3.2.7.6 Tumor metastasis

Metastatic tumors to the eye are also often associated with glaucoma, especially when the
tumor involves the anterior segment of the eyeball. Glaucoma arises through several
mechanisms, including direct tumor extension to trabecular meshwork, iridosilklitis, hyphema,
neovascularization, and PAS. Tumor metastasis can also appear as a mass in the posterior
It develops rapidly and pushes the lens-iris and causes closed-angle glaucoma without pupil
blocking. 2
Management by lowering intraocular pressure with oral and topical therapy, primary
tumor treatment and more frequent enucleation due to rapid tumor growth. 2
3.2.7.7 Intraocular limpo ma and leukemia

Intraocular lymphoma and leukemia can cause glaucoma by seeding outflow channels or
cause closed-angle glaucoma.
Drugs that lower the production of aquous humor are more effectively administered.
5,9,11
. If TIO is not controlled with drugs, then surgical action is an option to control TIO
increase. Some case reports report that trabecectomy can cause intraoperative or postoperative
complications in the form of uveal effusion. Some experts recommend tight trabeculotomy with
multiple sutures around the sclera flap for a slow decrease in TIO in the postoperative period. 7
Libre et al performed surgery on the eye with idiopathic increase in TVE by performing non
penetrating filtering surgery followed by goniopuncture ( a staged trabeculectomy ) to prevent
the occurrence of choroid effusion. 7
Nonpenetrating deep sclerotomies also causes low
complication rates, but is not good at controlling the TIO of the extended period. 8
BIBLIOGRAPHY
1. Skuta GL, Cantor BL. Glaucoma. American Academy Ophthalmology. Section 10. San Fransisco;
2011.
2. Becker- Shaeffer’s. Secondary open angle glaucoma. In: Diagnosis and Therapy of the Glaucoma 8 th
edition. Ed. Stamper RL, Lieberman MF, Drake MV, Mosby St. Louis, Philadelphia;2009.p.266-286
3. Shields Textbook of Glaucoma.Lippincott Williams & Wilkins.2011
4. Thakur SKD, Sah SP, Kaini KR. Choroidal Melanoma With Secondary Glaucoma. Southeast Asian
J.2003; (34): 424-426
5. Leon JM, Mercado GV, Walton D. Secondary glaucoma in retinoblastoma. Philippine Journal of
Ophthalmology.2005:124-128
6. Ministry of Health of the Republic of Indonesia. Sensory health survey. Ministry of Health of the Republic of
Indonesia. Jakarta; 1997.
7. Pradhan ZS, Kuruvilla A, Jacob P. Surgical management of glaucoma secondary to idiopathic elevated
episcleral venous pressure. Oman J Ophthalmol. 2015;8( 2):120-121.
8. Libre PE. Nonpenetrating filtering surgery and goniopuncture (staged trabeculectomy) for episcleral
venous pressure glaucoma. Am J Ophthalmol. 2003;136(6):1172-1174.
3.2.8 Open-angle secondary glaucoma due to trauma
Post-traumatic secondary glaucoma is glaucoma caused by injury to the eye. This type of
glaucoma can occur either shortly after an eye injury or years later. It can be caused by a "bruise"
of the eye (called blunt trauma) and a wound that penetrates the eye. Conditions such as severe
nearsightedness, injury, infection or previous surgery can also make the eye more susceptible to
serious eye injury. 1.3
As a result of an imminent injury, traumatic glaucoma is most often caused by blunt

trauma, that is, a wound that does not penetrate the eye, such as a blow to thehead or a direct
wound to the eye. The most common causes are from sports-related injuries, such as baseball or
boxing. Normally, eye fluid flows out of the front of the eye through the pupil and is then
absorbed into the bloodstream through a mesh drainage channel around the outer edge of the
iris. 1.3
The most common cause is the ciliary body, the part of the eye that produces eye fluid,
inside the eye is torn. This can cause bleeding inside the eye. Excessamounts of blood, plasma
and dirt can accumulate and clog the drainage system. This can lead to an increase in eye
pressure, which can damage the optic nerve. 3
Increased eye pressure due to blunt trauma is treated by keeping eye pressure on asafe
level while the eye drains excess blood. Glaucoma medications to control eye pressure are
usually treated first. If this is not enough to control eye pressure, surgery may be required.
Increased eye pressure aftera blunt t is temporary in most cases. But it's important to make sure
to have regular follow-up eye exams. 1.3
In some cases, a damaged drainage canal in the eye can build up excessive scarring. Grate
ini inhibits the flow of fluid and can cause glaucoma. This type of glaucoma, called recession-
angle glaucoma, can occur years after the initial injury. 3
Angle recession is seen as a tear at the base of the iris where the drainage canal is located.
Glaucomaa angle recession can be difficult to treat. Treatment may include medications that
reduce fluid production in the eye, laser surgery or screening surgery. 3
Blunt trauma, can cause various injuries of the anterior segment: 1,4
• hifema
• angle recession
• iridodialisis
• siklodialisis
• lens subluxation
The combination of posttraumatic inflammation, the presence of blood, and direct injury
to the trabecular tissue often results in a high TIO that initially occurs after the trauma. This
increase in TIO tends to be of short or sustained duration, with the risk of hemosiderosis and
damage to the glaukomatous optic nerve. 1.4
Glaucoma due to trauma can also be caused by a penetrating wound in the eye. Eye
pressure is usually lower after an injury occurs. Once the wound is closed, the tissues inside the
eye can develop inflammation andattachment, which causes eye pressure to increase. Glaucoma
due to a penetrating eye injury is best treated with precautions when the initial injury occurs.
Corticosteroid therapy to help prevent tissue and scar damage and is an importantcomponent of
early treatment. If glaucoma develops in the long term, drugs that reduce the production of eye
fluid are usually the first method of treatment, followed by filtration surgery. 1.3
3.2.8.1 Hifema
Increased TIO can occur as a result of hyphemas through several mechanisms. Increased
TIO is more common as a result of re-bleeding after hyphema. The frequency of re-bleeding
reported after hifema varies greatly in the literature, due to differences in the study population,
with an average incidence between 5%-10%. Re-bleeding usually occurs within 3-7 days of the
initial hyphema and is associated with normal clot retraction and lysis. In general, the larger the
hyphema, the higher the incidence of increased TIO, althoughsmall bleeding is also associated
with TIO elevation. The increase in TIO is due to blockage of trabecular tissue with red blood
cells, inflammatory cells, debris, and fibrin, as well as direct injury to the trabecular tissue due
to blunt trauma. 1,3,5
Topical and systemic corticosteroids can reduce inflammation, although their effects on
re-bleeding are debatable. If ciliary or photophobic spasms occur significantly, cycloplegic
agents may be helpful, but they do not have proven benefits for the prevention of re-bleeding. 1
Eye restraint and bed rest are recommended by some authors, although these precautions
have not been shown to be effective. If TIO is improved, manufacturing agents of manureof
aquaeous hu mour and hyperosmotic agents are recommended. 1.4
If surgery to lower the TIO is required, the irrigation procedure of the front eye chambers
is usually performed first. If the TIO remains uncontrolled, trabecectomy surgery can be
performed. 1.5
3.2.8.2 Hemolytic glaucoma or ghost cell glaucoma

Hemolytic glucoma or ghost cells can develop after vitreous hemorrhage. In hemolytic
glaucoma, the macrophage hemoglobin blocks the trabecular outlet. Red-colored cells are seen
floating in the anterior space, and reddish-brown discoloration of trabecular meshwork is often
seen. Ghost cells are red blood cells that have lost intracellular hemoglobin and appear small,
khaki-colored cells that block trabeculae tissue, leading to increased TIO. 1.4
Hemolytic glaucoma can occur within 1-3 monthsd of vitreous bleeding. They gain
access to the anterior space through hyaloid tissue torn as a result of previous surgery (pars
plana vitrectomy, cataract extraction, or capsuleotomy), trauma, or spontaneously. 1.4
Hemolytic glaucoma is generally as longas the bleeding is cleared. Medical therapy with
suppressors of the production of aquaeous humour is a frequent initial approach. If medical
therapy fails to control TIO, some patients may require frontal eye chamber irrigation, pars plana
vitrectomy, and/or trabecectomy. 1.2
3.2.8.3 Glaucoma due to trauma or angle recession

Angle recession is due to a tear in the ciliary body, usually between longitudinal and
circular muscle fibers. Glaucoma angle recession is a unilateral and chronic secondary open-
angle glaucoma that can occur immediately after eye trauma or may develop months to years
later. Similar to primary open-angle glaucoma in the clinical picture but usually distinguishable
by gonioscopic findings: 1,2,4
• Wide and brown angle recession
• Iris processus is absent or torn
• Scleral Spur looks shiny white
• Depression of the trabecular tissue
• PAS on the edge of recession area
Glaucoma angle recession should be considered in patients who have unilateral increased
TIO. The patient's anamnesis can reveal a history of previous trauma, although it is sometimes
forgotten. The examination can show findings consistent with previous trauma history, such
ascorneal scars, iris wounds, angular changes as previously mentioned, anterior focal subcapsular
cataracts, and phagodonesis. Comparing the findings of gonioscophisis in the affected eye with
the next eye can help clinicians identify thoseexperiencing recession. Although the risk of
glaucoma decreases after a few years, an increase in TIO can still occur within 25 years or more
after injury. 1.4
Treatment of glaucoma angle recession often begins with aquaeous humour production
suppressants, prostaglandin analogues, and α2-adrenergic agonists. Trabeculoplasty lasers have a
limited role. Filtration surgery or implantable glaucoma is necessary to control TIO in patients
who are not responsive to medical therapy. 1.4
BIBLIOGRAPHY
1. Cioffi GA, Durcan FJ, et al. Glaucoma. American Academy of Opthalmology. 2015
2. Singh K, Dangda S. Post Traumatic Glaucoma. Ocular Trauma. New delhi : 2015
3. George T, Sunil. Trauma related Glaucoma. Kerala Journal of Ophthalmology. Vol XXII no 3, Sept 2010
4. Girkin CA, Mcgwin G, et al. Glaucoma Following Penetrating Ocular Trauma: A Cohort Study of the
United States Eye Injury Registry. Elsevier. 2005
5. Purvi R. Bhagat, Priyanka Gupta, Nitesh Agrawal, Mariam N. Mansuri. “Glaucoma Following Blunt
Trauma : An Epidemiological and Clinical Study”. Journal of Evolution of Medical and Dental Sciences
2014; Vol. 3, Issue 11, March 17; Page: 2926-2943
3.2.9 Drug-induced Secondary Glaucoma
Drug-induced glaucoma can be both open-angle and closed-angle glaucoma. Topiramate

is a sulfamate monosaccharide substitution prescribed orally for the management of epilepsy,
depression, headaches, and cerebri pseudotumors. 1
Drugs that induce an increase in TIO generally give rise to an open-angle mechanism.
Corticosteroids are a type of drug that often gives rise to this mechanism. Risk factors for this
type of glaucoma are a family history of glaucoma, high myopia, diabetes mellitus, and a history
of tissue disease. 1
The risk of glaucoma increases with topical use of corticosteroids.
Corticosteroids increase TIO after a few weeks of use. 1
Some categorized drugs have the side effect of causing acute closed-angle glaucoma. The
drug initiates attacks mainly on individuals that have a relatively narrow angle. Some drugs
capable of causing closed-angle acute glaucoma include topical or sympathomimetic
anticholinergics, tricyclic antidepressants, axidase monoamine inhibitors, antihistamines,
antiparkinsonian drugs, antipsychotics, and antispasmolytics. 1
3.2.9.1 Steroid-Induced Secondary Glaucoma Drugs

Steroids are a group of anti-inflammatory drugs, commonly used to treat diseases of the
eyes and systemic. Steroid use is not monitored especially in over-the-counter eye drop
formulations, resulting in unwanted side effects. 1-3
Among the ocular side effects, cataracts and glaucoma are common. Steroid-induced
ocular hypertension was reported in 1950, when long-term systemic steroid use was shown to
increase intraocular pressure (TIO). Chronic administration of steroids in any form with
increased TIO can lead to optic neuropathy that causesglaucoma due to steroids. 2
Corticosteroids can give rise to increased TIO with an open-angle mechanism. Not all
patients who take steroids will cause glaucoma. Risk factors include pre-existing primary
open-angle glaucoma, family history of glaucoma, history of high TIO, diabetes mellitus, and
young age. There are 18-36% of the general population and 46-92% of patients with open-angle
glaucoma caused by the administration of corticosteroids with a TIO elevation, usually within
2-4 minggu after therapy has been administered. 1-3
Steroid eye drops and topical creams into the periorbital area and intravitreal injections
are more likely to cause an increase in TIO than intravenous, parenteral and inhaled forms.
Increased TIO can bep-orous and asymptomatic, patients with chronic corticosteroid therapy
may remain undiagnosed, which can lead to damage to the optic nerve glaucomatosus. An
increase in TIO usually occurs within a few weeks of starting steroid therapy. In most cases, TIO
returns spontaneously to the baseline within a few weeks to a few months after stopping steroids
(steroid responders). In rare situations, TIO remains high (steroid-induced glaucoma) which may
requireprolonged glaucoma removal or even surgery. 1.3
Steroid-induced glaucoma is an open-angle form of glaucoma. The exact mechanism for
increasing TIO after steroid use is not so obvious, but mainly occurs due to reduced water
outflow. Some theories of increased TIO due to steroids include:1,2
1. Steroids cause stabilization of lysosomal membranes and accumulation of
glycosamino- glycans (GAGs) polymerized in trabecular meshwork. This
polymerized GAG becomes hydrated, resulting in "biological edema" and
increasing exit resistance.
2. Glucocorticoids also increase the expression of fibronectin extracellular matrix
proteins, GAG, elastin, and laminin in trabecular meshwork cells causing
trabecular meshwork resistance to increase. Ultrastructurally, in steroid-induced
glaucoma, the accumulation of basic membranes such as staining of the material
occurs. for type IV collagen.
3. Corticosteroids cause inhibition of the phagocytic properties of endothelial cells
lining the trabecular web causing the accumulation of watery debris.
4. Glucocorticoids have been shown to alter the morphology of meshwork trabecular
cells by causing an increase in nuclear size and DNA content. Zhang et al have
suggested bahwa FKBP51 binding to FKBP06 mediate the transport of nuclear
beta receptors of beta glucocorticoids, which suggests that this may play a role in
improving the glucocorticoid response. A series of recent cases suggest that the
obstruction of the outflow of the bekular tra can
occurs due to crystalline steroid particles after receiving intravitreal injection of
triamcinolone acetonide (IVTA) for diabetic macular edema.
5. Glucocorticoids lower the synthesis of prostaglandins, which regulate the outflow
of water.
6. The influence of genetika.
Several genes have been found to be associated with trabecular meshwork cells
that protect and damage glucocorticoids. Glucocorticoids can drive their effects by
increasing the expression of the MYOC gene [Streptococcericoid response-
induced glucocorti coid(TIGR)] gene at the GLC1A locus. However, recent
studies in monkeys failed to show a significant association between the myocline
gene and steroidal ocular hypertension. In addition to the antigenimotrypsin gene,
myocilin gene antigen, epithelial pigment derivative factors, ditprescriptions from
cornea 6, prostaglandin D2 synthetase, specific growth catch 1, decorators,
insulin-like protein booster protein 2, ferritin light chain, and fibulin-1C are other
genes that have been postulated to play a role in the ster oid response but more
research is needed to confirm their role in the steroid response.
In steroid-responsive patients, an increase in TIO usually develops within the first few
weeks of steroid administration. However, it can increase withinan hour or a few years after
chronic steroid use. Once the steroid is discontinued, TIO is typically normal within 1 to 4
weeks. 1.2
3.2.9.2 Secondary Glaucoma Induced Alpha Adrenergic Agonist Drug

Adrenergic alpha agonists can give rise to closed-angle acute glaucoma through the pupil
block resulting from pupil dilatation, especially in individuals who have a narrow iridocornal
angle. Fenylephrine eye drops often used for ophthalmology examination often give rise to
iatrogenic acute glaucoma by 0.03%. 1.2
Systemic ephedrine as a treatment of hypotension is often used in general anesthesia.
There were reports of cases of closed-angle glaucoma after surgery. This may be due to the use
of ephedrine or it may be causedby psychic stress. 2
3.2.9.3 Induced Secondary Glaucoma Non-Catecholamine Adrenergic Agonist Drug
There were reports of glaucoma events after the use of nasal ephedrin and napazolin as an
epistaxis treatment. There is a hypothesis of reflux through the nasolacrimal duct or through
absorption of the nasal mucosa because it is often bilateral. 1.2
Non-catecholamine adrenergic agonists e.g. salbutamol, stimulate beta receptor 2
agonists to secrete humorous aqueous. P-angle glaucomacan be exacerbated due to pupil
dilatation as a parasympathetic effect. 1.2
3.2.9.4 Drug-Induced Secondary Glaucoma Anticholinergic Agent

Tropikanamide eye drops are often used as a drug that helps to dilate the pupils on
examination of the fundus. Other jenis drugs of this anticholinergic agent e.g. atropine sulfas and
cyclopenpentolat which can spur closed-angle glaucoma. 1.2
Ipatropium bromide is an antimuscarinic agent that is often combined with salbutamol.
This agent gives rise to closed-angle acute glaucoma due to increasing the diffusion of oxygen to
the cornea giving rise to pupil dilatation. 1,2,6
Antihistamines (H1 and H2 receptor blockers) also induce the occurrence of closed-angle
acute glaucoma due to their anticholinergic effects. Prometazine is said to cause edema in the
lens, causing pupil blockage. Ranitidine and cimetidine other than as management of esophageal
reflux can cause an increase in TIO so as to induce glaucoma. 1,2,6
3.2.9.5 Secondary Glaucoma induced by Botulinum Toxin

Botulinum toxin can induce the occurrence of closed-angle acute glaucoma due to its
anticholinergic effect. Botulinum exerts an effect on the sympathetic ganglia, preganglion, and
post ganglion nervus triveminus. This gives a paratic effectso that it causes pupil dilatation and
causes pupil blockage. It is necessary to conduct a gonioscopy examination before the use of
botulinum toxin. 1,2,7
3.2.9.6 Secondary Glaucoma Induced Cholinergic Agent

Pylokarpin is used as an agonist of the parasympathetic that gives rise to constrictions in
the pupil. Pylocarprine is used as a treatment in closed-angle acute glaucoma due to
its myotic effect. Pilokarpin also enhances the flow of aquaeous humor. However, pylocarprine
also has the potential to cause closed-angle acute glaucoma through its mechanism of changing
the diphragm between the iris and the lens. 1.2
In narrow-angle eyes, pilocarpin increases the angular width because it reduces the
thickness of the iris and iris body due to the forward movement of the iris-lens diaphragm due to
the contraction of the ciliary muscles. But there are exceptions. Acute angular closure after
administration of pylocarpine has been reported in patients with spherophakia (as in Weill-
Marchesani syndrome, WMS) but may also occur in patients whodo not have known systemic
abnormalities. In spherophakia, a highly convex lens is supported by a weak zonula that allows
greater anterior movement of the lens-iris diaphragm. Acute angular closure in this situation can
be reduced byn pilocarpine. Other conditions associated with paradoxical reactions to pilocarpin
include exfoliating syndrome, facomorphic glaucoma and progressive glaucoma. 8
3.2.9.7 Anti-Depressant-induced Secondary Glaucoma

Tricyclic antidepressants e.g. clomipramine, imipramin, amitriptilin, and selective
serotonin reuptake inhibitor (SSRI) groups e.g. venlafaxin, citalopram. Fluoxetin, and paroxetine
are said to give rise to closed-angle acute glaucoma. This is due to the induced pupil block.
Theoccurrence of pupil blocks due to the use of antidepressant drugs remains unclear. 1.2
The main classes of antidepressants that cause angular closure are tricyclic
antidepressants (TCA) and serotonin-specific reuptake inhibitors (SSRIs). TCA has historically
been associatedwith a high incidence of anticholinergic (muscarinic) effects such as dry mouth
and constipation. The latest tricyclic-related drugs such as trazodone have a lower side effect
profile. AAC has been widely reported among patients whouse clomipramine and imipramine, a
less sedative sedative. Although trazodone has fewer anticholinergic (muscarinic) side effects
than older tricyclic , chronic low-dose use in patients known to havePACG ki results in poor
TIO control. 9
From other SSRIs, both citalopram and escitalopram have been reported to be associated
with AAC. The mechanism of angular closure for escitalopram is through the production of
ciliochoroidal effusions and ciliary bodies as well as the rotation of the angle of the front eye
chambers. It is diagnosed before glaucomatous disc damage occurs and is completed after
topical administration of cycloplasmos and cessation of escitalopram, fluvoxamine, or other
SSRIs involved in provoking AAC in acidic pitsknown to have narrow angles and glaucoma.
The patient's symptoms disappear when stopping treatment. 9
Venlafaxine is a serotonin and noradrenaline re-uptake inhibitor, widely used for
depression because it is thought to have fewer sedative effects dan antimuscarinic than
tricyclic. It is also used to treat irritable bowel syndrome, where it is considered to function well
by modulating central and peripheral sensory mechanisms and by reducing associated
depression. However,there have been some reports of AAC with venlafaxine through a
privileged mechanism with supracili effusion. It remains unclear whether this is due to
serotoninergic effects, anticholinergic effects or weak adrenergic effects. 9
Serotinergic agents also used as appetite suppressants and dexfenfluramine prescribed for
this are associated with AAC by inducing pupil block. 9
3.2.9.8 Secondary Glaucoma Induced Sulfa Agent

Sulfa agents such as topiramate, acetazolamid, and hydrochlorothiazide are drugs that
cause closed-angle acute glaucoma that is not caused by pupil block. Sulva agents are said to be
able to shallow the front eye chambers, give rise to choroid effusions, increase TIO, edema of the
lens and retina. 1.2
LIST OF PUSTAKA
1. Cioffi G.A., Durcan F,J., dll. American Academy of Opthalmology. Section 10. Glaucoma. 2015-
2016.
2. Elliott Yann Ah-kee, , Eric Egong, Ahad Shafi, Lik Thai Lim, dan James Li Yim. A review of drug-
induced acute angle closure glaucoma for non-ophthalmologists. National Center British Information.
2015
3. Sonia Phulke, Sushmita Kaushik, Savleen Kaur, and SS Pandav. Steroid-induced Glaucoma: An
Avoidable Irreversible Blindness. National Center British Information. 2017
4. Stella Arthur, Louis B. Cantor. Update on the role of alpha-agonists in glaucoma management.
Elsevier. 2011
5. Yukie Nitta, DDS, PhD, Nobuhito Kamekura, DDS, PhD, Shigeru Takuma, DDS, PhD, and
Toshiaki Fujisawa, DDS, PhD. Acute Angle-Closure Glaucoma After General Anesthesia for Bone
Grafting. National Center British Information. 2014.
6. Nicola Pescosolido, Francesco Parisi, Paola Russo, Giuseppe Buomprisco, and Marcella Nebbioso.
Role of Dopaminergic Receptors in Glaucomatous Disease Modulation. Elsevier. 2014
7. P Corridan, S Nightingale, N Mashoudi, A C Williams. Acute angle-closure glaucoma following
botulinum toxin injection for blepharospasm. British Journal of Ophthalmology. 2012.
8. Alexander C Day, Winnie Nolan, Aeesha Malik, Ananth C Viswanathan, and Paul J Foster.
Pilocarpine induced acute angle closure. National Center British Information. 2012.
9. Vincent Chin-Hung Chen, Mei-Hing Ng, Wei-Che Chiu , dkk. Effects of Selective Serotonin
Reuptake Inhibitors on Glaucoma: A Nationwide Population-Based Study. British Journal of
Ophthalmology. 2015
10. Anvesh C. Reddy, MD, and Sarwat Salim, MD, FACS. Choroidal Effusions. Academy American of
Opthalmology Journal. 2012
3.2.10 Secondary Glaucoma due to Surgery
Surgical procedures such as cataract surgery, corneal transplantation, vitrectomy can

cause an increase in eye pressure. This is similar to occur in laser surgeries including
trabeculoplasty, iridectomy and posterior capsulotomy. The increase in ball pressure canreach 50
mmHg or more. This increase in eyeball pressure is transient which can last several hours to
several days. The exact mechanism is unknown but the presence of pigment release,
inflammatory cells, debris, trabecular deformation of meshwork, and angle closure can be the
cause. 1.2
This increase in eyeball pressure can cause damage to the opticus nervus papill,
especially in patients who have a tendency to glaucoma. If the increase in eyeball pressure is
sedentary then itneeds to be applied. Both medicamentous therapy and surgical therapy. 1.2
3.2.10.1 Secondary Glaucoma due to cataract surgery
Secondary glaucoma often occurs after cataract surgery through various mechanisms. A
temporary increase was reported to be 33 percent of all cataract surgeries depending on the
surgical technique and operator. The increase in pressure can go undetected because it occurs a
few hours after surgery and can return to near nomal the next day. This ocular hypertensi can
cause complaints of nausea, vomiting, corneal oedema, and damage to the opticus nervus,
especially in patients who have a history of glaucoma. TIO measurements are important to do
immediately after laser or surgery. When there is an increase in ball pressure mata therapy is
indispensable. The mechanism for increasing eyeball pressure is complex and includes the
following conditions:1
1. Inflammation with the release of active substances including prostaglandins

2. Very tight surgical wound closure watertight wound closurewith multiple sutures
3. Trabecular meshwork blockage by pigment, blood, lens particles, inflammatory
cells, and viscoelastics
Implantation of the IOL can cause various variations of secondary glaucoma. Some of
the mechanisms found include, uveitis glaucoma-hyphema syndrome (UGH-
Syndrome), secondary pigmentary glaucoma, pseudophakic pupillary block. UGH syndrome is a
secondary inflammatory form of glaucoma caused by chronic irritation due to malposition or
rotation of the IOL. Characteristic of this condition are chronic inflammation,
neovascularization of the secondary iris, recurrent hyphema. This condition is followed by iris
irritation by IOL or erosion rather than haptic lens in the iris or siliary corpus. Sedentary cases
require repositioning or lens turnover. This is very difficult to do because there is already a
synagogue. 2
Patients can be treated with the administration of topical and systemic anti-glaucoma
therapy. Therapies typically used are β-adrenergic antagonists, 2-adrenergic α agonists, or
carbonic anhydrase inhibitors. In therapy, sometimes hyperosmotic agents and paracentesis are
also required. Persistent eyeball pressure requires filtration surgery. 2
3.2.10.2 Secondary glaucoma after penetrating keratoplasty
Secondary glaucoma isa frequent complication after penetrating keratoplasy. It can

occur in patients with afakia or pseudophhia with recurrent grafts. Distortion of trabecular
meshwork, and closed-angle progressivity conditions are the causes of increased tenetratingn
eyeballs. Attempts or ways to minimize the occurrence of secondary glaucoma by using grafts of
different sizes, peripheral iridectomy and iris spingter repair did not give satisfactory results.
Alternative procedures such as lamellar stromal atau endothelial graft are associated with a
smaller percentage for the occurrence of increased eye pressure. 2
3.2.10.3 Secondary glaucoma after vitrectomy
Increased eye pressure is a frequent complication post-vitreoretina procedures and

treatment of other retinal abnormalities. This occurs due to various mechanisms including
corticosteroid induced ocular hypertension, closed-angle secondary glaucoma, and increased
pressure of the hefclera vein. It is important to measure post-action TIO. Intravitreal injection
ofriamcinolone t is very closely related to corticosteroid induced ocular hypertension. Scleral
buckle surgery can make anterior oculi cameras shallower and cause closed-angle secondary
glaucoma. Usually COA will improve in daysto several weeks with cycloplegic administration,
anti-inflammatory agents, β- adrenergic antagonists, β-adrenergic antagonists, α 2-adrenergic
agonists, or carbonic anhydrase inhibitors,
Carbonic anhydrase inhibitors, and hyperosmotic agents. If treatment with medicamentosa is not
successful, argon laser iridoplasty, supracoroidal fluid drainage or readjustment of sclera
buckle. Iridectomy provides minimal advantagesal in this condition. Sclera buckle can interfere
with venous drainage by pressing on the vortex vein, increasing the pressure of the episclera and
TIO veins. Some cases simply respond by moving the buckle sclera or reducing its voltage. 1,2,3,4
Air injection, long-acting gases (sulfur hexaflouride and perflorocarbon), silicon oil, can
increase eyeball pressure and cause closed-angle secondary glaucoma. This substance is less
dense than water and accumulates at the top of the eye and iridectomy is very important. An
increase in eyeball pressure was reported to be nearly 50 percent in patients undergoing pars
plana vitrectomy procedure by injection of silicon oil. Silicon oil used in patients with complex
retinal detachment can cause secondary glaucoma atan open or closed angle. Tamponade rather
than pupil can cause pupil block which can be prevented or treated by making inferior
iridectomy. If silicone oil spreads on aquaeous humour, silicon oil can clog trabecular meshwork
and will cause open-angle secondary glaucoma. If inferior prophylactic iridectomy does not
succeed in lowering eyeball pressure then TIO can be lowered through surgical therapy with
glaucoma drainage device, cyclodestructive procedure, removal of expansion gas, release of
encircling elements, or removal of silicon oil. 1,2,3,4
The end result of retinal pan photo coagulation causes an increase in TIO because it
triggers angular closure. The ciliary body will thicken and rotate anteriorly and choroid release
may occur. In general, secondary glaucoma is self-limited and temporary treatment is required
with cycloplegic agents, topical corticosteroids dan aquos suppresant. 1
BIBLIOGRAPHY
1. Stamper,R.L Lieberman,M.F. Drake,M.V. 2009. Becker-ShafferDiagnosis and Therapy of the

Glaucomas. 8th ed. Mosby Elsevier p.273-281
2. American Academy of Ophthalmology.2014. Basic and Clinical Science Course ; Glaucoma. San
Fransisco.p.118-120, 149-151
3. Shaarawy,T.M, Sherwood, M.B.Hitching, R.A.Crowston.J.G. 2009. Glaucoma, Medical
Diagnosis and Therapy . Saunders Elsivier. (1):p.428
4. Boyd B.F,Luntz. 2002. Innovations in the Glaucomas, Etiology, Diagnosis, and Management.
Highlight of Ophthalmology. P381-384
3.2.11 Glaucoma in Iridocorneal Endothelial Syndrome
Iridocorneal Endothelial Syndrome (ICE Syndrome) is a group of secondary closed-

angle glaucoma that contains 3 variations of overlapping disorders, namely: progressive iris
atrophy, iris nevus (Cogan-Reese Syndrome), Chandler syndrome. 1,2,3,4
Patients with ICE syndrome usually occur in young women. More often in the
Caucassians, and there is no family history of this disorder. It occurs unilaterally but has also
been found bilateral. 1,4,5
From clinical research and pathology, Campbell and friends as well as Eagle and friends,
put forward a hypothesis thata fundamental abnormality of ICE syndrome is the abnormality of
the endothelial cornea. Abnormally it is this endothelium that does not appear to be a "beaten
meal appearance" with a slitlamp biomicroscope. If the patient is examined at an early stage of
the disease, tampak demarcation between the corneal endothelium is normal and abnormal. Over
time, this abnormal endothelial area will enlarge, until the entire corneal endothelium is
involved. The epithelial and stromal layers around the abnormal endothelium can be clean or
become edematous. 6
Therapy is aimed at corneal edema and secondary glaucoma that occurs. Hypertonic
solutions and drugs are used to reduce TIO, when it rises, it will be effective by controlling the
corneal edema that occurs. Closed-angle glaucoma that occurscan t be in therapy with aqueous
suppressants. Myotium is useless. When drug therapy fails filtration surgery (trabecectomy or
tube shunt procedure) can be effective. 1
Definsi ICE Syndrome

Iridocorneal Endothelial Syndrome is a disorder characterized by corneal endothelial
abnormalities that cause atopic iris, secondary angle closure glaucoma, and corneal edema.
There are 3 clinical changes that can be described as : 1.9
 Chandler Syndrome
 Progressive iris atrophy
 Nevus iris/Cogan-Reese syndrome
The specific iris abnormalities are: 4
 Essential iris atrophy – there are areas that are thinned and result in pupil deformity due
to the endothelial membrane contracting, pulling the iris occurs peripheral anterior
synekhia.
 Chandler syndrome – similar to iris changes in essential iris atrophy, but there is a
more severe degree in corneal edema.
 Cogan-Reesse Syndrome – The iris appears flat with small nodules in normal iris tissue
thatpush past the hole in the endothelial layer giving it a 'mushroom patch' appearance
A. Incidence
Arises at the age of between 20-50 years, and more often in women. Patients with ICE
syndrome usually occur in 3-5 decades of life, sufferers complain of visual impairment or
discomfort that occurs due to corneal edema or increased TIO. It occurs sporadically and almost
all of it happens on whites. 1.6
B. Pathogenesis
The obvious pathogenesa of ICE syndrome is unknown but there appears to be abnormal
endothelial cells. This state arises from the presence of maldifferentiation of a number of
endothelial cells, although these abnormal clones originate from birth or before. The degree of
endothelialization occurs at an angle of bile of the front eye and the surface of the iris. DNA
Herpes virus was once identified in corneal specimens after keratoplation in the patient's aqueous
tumor. It is suspected that a possible infection with the herpes simplex virus induces this
alteration. 2,9,11
The corneal endothelium isabnormally at the corner of the anterior eye chamber covering
the iris. The corner of the front eye chamber is open but occlusion (blocked). The endothelial
membrane contracts, closes the corners and changes the shape of the pupil and iris. 10
The similarity between the 3 variants of ICE syndrome is the wipe of thecorneal
endothelial cells in their proliferation capacity and their displacement along the corners to the
surface of the iris. The term "proliferative endotheliopathy" allegedly describes this disorder.
ICE syndrome can be
It continues to be glaucoma, decompensation of theNEA corps, or both. Glaucoma arises
secondary because the synekhia closes the angle that contracts this abnormal tissue.
Polymeration chain reaction indicates the presence of herpes simplex virus DNA from a corneal
specimen of ICE syndrome, suspected to be derived from the virus. 4,5,11
C. Clinical Symptoms
The iris, cornea and angle of the front eye chamber will be involved in patients with ICE
syndrome.
3.2.11.1 Essential / Progressive Atropy Iris

Typical of iris atrophy, with thinning the iris stroma that will continue to be a "full-
thickness iris hole". At first there will be anterior peripherals of synekhia, and subsequently will
continue around all the corneal circles. Pupillary distortion occurs, uvea ectropion, the most
characteristic and important of which is the presence of PAS.
Sometimes the iris ishollow and attracted, there appears to be iris traction between the
PAS in the opposite direction to the eyeball. A smaller oval hole will form a PAS. This hole will
cause iris ischemia arising from the obstruction of the iris blood vessels in the synechia. Strictly
delimited and pedunculated multiple iris nodules can be found, which arise at the end of the
disease process.
The corneal endothelium of the eye involved undergoes a metal-like irregularity, which
sometimes arises in the local area. 6.9
3.2.11.2 Chandler syndrome

The main feature in this variant of ICE syndrome is usually corneal edema, often with a
normal or moderate increase in TIO. Chandler described the corneal endothelium as a "fine
hammered silver appearance". An atrophied iris is less pronounced in Chandler syndrome than
an iris atrophy and when detected it is often confined to the anterior iris stroma it is usually
round or slightly oval. 6,9,12
3.2.11.3 Cogan-Reese syndrome
Characterized by pigmented lesions of irises that are multiple, pedunculated, nodular
lesions become more diffuse, smooth, velvety edging irises. The surface of the iris tends to be
lost than normal, and appears darker than the next eye. Uvea ectripyons, damage to the iris
stroma, and pupillary ectopics often appear. PAS, corneal edema, labile glaucoma are special
features. 6.9
The clinical manifestations of progressive iris atrophy, Chancler syndrome, and Cogan-
Reese syndrome are all explained in the presence of this abnormal endothell proliferation. The
cause of this endothelial proliferation is unknown. Ultrastructural membrane secemet's research
in cases of ICE syndrome shows the presence of normal anteriror banded and posterior non
banded zone, p[osterior is an abnormal posterior collagen layer thought to be due to endothelial
function decreasing suddenly after initially normalizing some time after birth. It is this
endothelial damage that results in proliferation. Bahn and friends suspect that primary crest
neural abnormalities are the cause of this endothelial proliferation. 6
Glaucoma in ICE syndrome arises as a result of progressive loss of the corners of the eye
chambers. PAS that has arisen increases in weight over time. Intraocular pressure can
increasedue to the formed PAS. Histologic research states that abnormal endothelium and
basement membranes are often squashed with trabecular meshwork. This membrane blocks the
flow of aqueous humour and develops into synekhia, increasing intraocular pressure. 6
Corneal edema arises from subnormal endothelial pump function, called the chandler
variant of the Ice Syndrome. The boundary between normal and abnormal endothelium appears
with a slit lamp using specular reflexes. When an abnormal endothelium moves to the corner of
the front eye chamber, the presence of PAS and flow obstruction gives rise to glaucoma. When
the abnormal endothelium spreads to the surface of the iris, membrane contractions arise that
cause atopic irises, correctopia, and polychoria, a clear sign of an essential atropy iris variant of
ICE syndrome. Cogan-Reese syndrome indicates multiple iris pigmentation nodules, caused by a
contractionary endothelial mebran. 2
Clinically unilateral, no other ocular or systemic abnormalities were found. Patients
complain of decreased performance, pain due to corneal edema or angular glaucoma
closed secondary, abnormal image of the iris. Abnormal corneal endothelium shows 'beaten
bronze appearance' similar to cornealguttae in Fuchs corneal endothelial dystrophy, Microcytic
corneal edema can occur without increased intra-occuli pressure, cornea without other
manifestations of the disorder. 1
The high PAS (Peripheral anterior sinechyae) is characteristic of ICE syndrome, and
often extends anteriror to Schwalbe's line.
The PAS is caused by the contraction of the layers of endothelial cells and around the
collagen fibril tissue that extends from the peripheral cornea trabecular meshwork and iris. The
PAS caused closure on the anterior ocular camera which then caused closed-angle glaucoma.
Similar to neovascular glaucoma, the degree of angular closure is not necessarily associated with
an increase in TIO, since some angles sefunctional means are closed by the endothelial
membrane in the absence of synechhia. 1
A variety of degrees of atrophic irises and corneal changes distinguish their clinical
differences. Progressive atropy irises are typical in the presence of heavy iris atropies that give
rise to heterochromia, correctopia, uvea ectropion, pigment epithelial atropy and iris stroma, and
the presence of hole formation. In Chandler Syndrome, iris atrophy is minimal and the presence
of correctopia, as well as corneal and angular abnormalities are more pronounced. Chandler
syndrome is the one that shows the most abnormalities in pada almost 50% of cases of ICE
syndrome. This state is distinguished by brown nodules or diffuse pigment lesions on the surface
of the anteriror iris. 1
Glaucoma occurs in 50% of patients with ICE syndrome, and glaucoma that occurs tends
to be more severe in atrophy iris progresif and Cogan-Reese syndrome. The clinical state is a
noticeable abnormality of the corneal endothelium, as well as a metallic image of the posterior
cornea. In this state the corneal endothelium passes posterior to the descemet's membrane. With
an electron microscopedesignate a layer of endothelium of different thickness. Unlike normal
corneal endothelium, here appear filopodial processes and cytoplasmic actin filaments. Viral is
thought to be the mechanism of ICE syndrome after the discovery of lymphocytes that appear in
the endothelium of the patient's corne. Based on serological results, it is suspected that Epstein-
Barr virus and herpes simplex are also involved. 1
Biomicroscope
Examination of
Slitlamp4
Slit Lamp examination is an instrument consisting of a high-intensity light source that
can be focused on shining into thin sheets from light to eye.
Abnormalities of the corneal endothelium are typical with a "hammered-silver" shape
similar to Fuchs dystrophy when viewed with specular light reflection. Secondary corneal edema
becomes endothelial decompensation in advanced cases. The endothelial layer of the cornea
looks like a "beaten metal appearance" on the unilateral eye.
Gonioskopi
At the beginning of the abnormality of the disease, gonioscopy shows a normal anterior
oculi camera angle. Then came PAS and it seemed to cover all the corners. The posterior polus
appears normal but there is 'glaucomatous optic nerve cupping' and there is an intraocular
increase. Gonioscopy exhibits anterior peripheral synechia that extends up to Scwalbe's line. 4
Microscope Specular
With a specular microscope, it can clearly distinguish the state of the corneal endothelium
in ICE syndrome from the state of the endothelium in other disorders. The earliest apparent
change is the loss of the hexagonal form of endothelial cells.
The darkened regions begin to appear on single cells. In the affected cornea there is an
increase in cellular pleomorphism and dark areas of the affected eye, with a specular microscope
showing a normal endothelial mosaic but smallerthan usual s el size. The cause of this is not yet
known. In some cases the uninvolved eye showed an abnormal pleomorphic endothelial cell with
a lower cell count. The corneal endothelium and basement membrane spread from the cornea to
the trabecular meshwork and the surface of the iris. This contraction of the membrane triggers
the appearance of PAS in areas where previously the angle was open and gives rise to uvea
ectropion. Iris atrophy and "full thickness hole" arise because there is a pull between the iris and
the synerchia. Nodul iris arises on the area involved with the endothelial-basement membrane
complex . It is suspected that the shape of the nodules arises from the siege and
"pinch" of the iris by the cellular membrane. The nodule is a sign of the endothelialization region
of the iris. 6
Diagnosis of ICE syndrome is always suspected in middle-aged patients with unilateral
angle-closure glaucoma. With a specular microscope can confirm the diagnosis in the presence
of missing endothelial cells and the morphology of atypical endothelial cells in the eye involved.
1
Management
In the early stages, glaucoma is treated with drugs. The increase in TIO is aggravated by
synechia occurring or being covered by abnormal membranes, drugs that decrease aqueous
production are more effective than myotics. Laser trabeculoplasty is also not entirely effective.
Thus, intraoculous pressure is not controlled with drugs, hence filtration surgery is performed.
The success of trabecectomy in ICE syndrome is comparable to trabecectomy in primary open-
angle glaucoma. Failure occurs when abnormal endothelial proliferation enters the filtering bleb.
In such cases, filtration procedures are recommended at different locations appropriately. This
recurrent trabeclectomy is also comparable in success rates to those performed in patients with
primary open-angle glaucoma. Filtration surgery is not aimed at corneal edema by a reduction in
TIO. However corneal edema may decrease with TIO at a low rate. Drops of hypertonic solution
can be useful in mild epithelial edema. If corneal edema still appears significantly even though
TIO has been lowered with medications, then keratoplasty penetrating is recommended. A
controlled TIO determines the success of the corneal graft. Recurrence of endothelial
abnormalities in ICE sindrom does not mean that it also occurs in the donor cornea. 6.15
Penetrarting keratoplasty is the most effective therapy for the cornea in this syndrome.
Glaucoma is an important symptom in ICE syndrome. Long-term graft depends on handling
TIO, which can complicate its success. 2.5
Therapy with drugs is not adequate to deal with TIO. Surgical intervention is required.
Options include trabecectomy with antifibrotic agents, glaucoma drainage implant device, and
an esstructive cyclod procedure. Corneal transplantation that severely impairs the patient's
vision.
Glaucoma Treatment 4,9,15
1. Drugs, often ineffective
2. Trabecectomy, when combined with metabolite therapy often does not work because in the
end bleb occurs
3. Glaucoma implants are often successful
BIBLIOGRAPHY
1. American Academy of Ophthalmology : Glaucoma, Section 10, Basic and Clinical Science
Course, 2014-2015, p: 128-130
2. American Academy of Ophthalmology : External Disease and Cornea, Section 8, Basic and
Clinical Science Course, 2014-2015, p: 195-196
3. Crick and Khaw, A Textbook of Clinical Ophthalmology 3rd Edition, A Practical Guide to
Disorders of the Eyes and Their Management, 2003, p: 515-516
4. Kansky JJ, Clinical Ophthalmology, A Systemic Approach, Eighth Edition, Butterworth
Heinemann, China, 2016, p: 381-383
5. Ilyas S, Ophthalmology third edition, Faculty of Medicine, University of Indonesia, Jakarta,
Sagung Seto, 2010, p.4-6
6. Paul R,Vaughan & Ashbury’s General Ophthalmology 18th, The McGraw-Hill Companies,
United Kingdom, p 216
7. Schlote. T, Pocket Atlas of Ophthalmology, Thieme, Stuttgart, 2009, p: 164
8. Stamper L.S, Becker-Shaffer’s Diagnosis and Theraphy of the Glaucomas 8 th Edition, Elsevier,
USA, p 218-220
9. Tsai.J.C, Oxford American Handbook Of Ophthalmology, Oxford University Press, New York,
USA, 2011, p: 288
10. AK Khurana, Comprehensive Ophthalmology 4th edition, 2007, p:237
11. Yanoff M, Duker J.S, Ophthalmology 4th, Saunders Elsevier, Philadepia, USA, 2014 p: 1095-
1096
12. Sacchetti M, Mantelli F, Diagnosis and Management of Iridocorneal Endothelial Syndrome,
Biomed Research International, Milan, Italy, 2015
13. Estacia C.T, Filhio A.R, Iridocorneal Endothelial Syndrome: Case Report of Chandler’s Variant,
Rev Brasil Ophthalmology, Brasil, 2017
14. Ritch.R, MD; Teekhasaenee. C, MD; Iridocorneal Endothelial Syndrome in Thai Patients, Journal
American Medical Association Ophthalmology, 2000
15. Levy, S.G; Mohammad H.B, Pathology of the Iridocorneal Endothelial Syndrome, Investigative
Ophthalmology & Visual Science, 1995
16. Sidoti P.A; Schulhof J, Managing Glaucoma with ICE syndrome, available at
www.reviwofopthalmology.com/article/managing-glaucoma-with-ice-syndrome, New York,
2016
3.2.12 Malignant glaucoma
Malignant glaucoma is the silting of the front eye chambers in the eye followed by an
increase in intraocular pressure with a history of intraocular surgery. The pathophysiology of
glaucoma maligne is the result of anterior rotation of the ciliary body and posterior misdirection
of the aqueous fluid. There is a relative block of aqueous flow at the equator of the lens, the
vitreous surface and the ciliary processus. In the anamnesis there is a sharp decrease in visus, red
eyes, pain, history of intraocular surgery, nausea / vomiting. From the physical examination, it
was found that the level of the peripheral and central anterior oculi camera, it appeared that the
lens advanced to the anterior or there was intraocular or vitreous implantation, the aqueous fluid
was trapped behind the posterior capsule or in the anterior vitreus, and the TIO increased.
The diagnosis of malignant glaucoma is established when red eyes are obtained, sudden visus
drops accompanied by shallow front eye chambers and increased TIO despite patent iridectomy,
and there is a history of intraocular surgery. Differential diagnoses of this condition include
pupillary block glaucoma, choroidal detachment, and suprachoroidal hemorrhage. A
supporting examination that can help the diagnosis is ultrasound biomicroscopy.
The management of malignant glaucoma is with medicamentose, atropine 1% every 6 hours, α2

adrenergic agon ist, oralglycerol (1ml / kgBB) or mannitol (2g / kgBB) oral / 1-2x daily, and oral
acetazolamide. Operative management includes: Nd-YAG laser capsulotomy and hyaloidotomy,
pars plana vitrectomy, glaucoma drainage implant, and cyclodestruction procedures.
Refersto nsi
1. American Academy of Ophthalmology. Staff. Basic and Clinical Science Course. Section
10. Glaucoma. San Fransisco, 2015-2016
2. Stemper et al. Becker-Shaffer’s Diagnosis and Therapy of the Glaucomas. 2009
3. Foreman-Larkin et al. Clinical Management of Malignant Glaucoma. J
Ophthalmol. 2015; 283707
4. Quigley HA, Friedman DS, Congdon NG. Possible mechanisms of primary angle-
closure and malignant glaucoma. J Glaucoma. 2003;12(2):167–180.
3.2.13 Schwartz-Matsuo syndrome
Rhegmatogen retinal detachment is usually associated with the occurrence of a decrease

in intraocular pressure. However, Schwartz describes different conditions in which there is an
increase in intraocular pressure, retinal detachment, open angles and the presence of cells and
flares in the COA. This condition in 1973 was introduced by Schwartz so it was called
Schwartz syndrome. 5
In 1986 Matsuo and colleagues investigated seven similar patients ranging in age from
11-31 years. In these cases 'uveitis' is resistant to topical corticosteroids, but is resolved
completely after retinal surgery. After paracentesis was performed on this patient and examined
using a transmission electron microscope, inflammatory cells were found. Such cells have a
lamellar structure of fragments derived from retinal photoreceptor cells. This is thought to be the
result of a peripheral retinal tear that allows for a direct connection between the subretinal space
and the front eye chamber. The cells then enter the aqueous and clog the trabecular meshwork.
3,5,6
To diagnose a patient with Schwartz- Matsuo Syndrome, one of the things to know is
through a previous history anamnesis. Usually this condition is found in patients who have had
blunt trauma, postopeye eration, have had retinal detachment and in patients with atopic
dermatitis. Patients complain of eye pain, blurred eyes, headache, nausea, or vomiting. Other
complaints are related to the presence of retinal detachment, such as fieldof view disturbances,
photopsia, floater and decreased visus. 3.4 pm
Based on the anamnesis, it can be continued with the examination that needs to be done.
Systemic physical examination can be done, to see the risk factors that can result in retinal
detachment, such as in Marfan syndrome or in atopic dermatitis. In ophthalmology examination,
what needs to be done is visus examination, intraocular pressure measurement, slit lamp and
gonioscopy. Visus examination is carried out to determine the extent of the reduced visual acuity
of the patient. Examination using a slit lamp appears the presence of cells and flares. 4.5
Based on the above examination, the signs that can be found are 3 major signs. In this
syndrome can be the presence of cellsd an flare in the front chamber of the eye, an increase in
fluctuating intraocular pressure, rhegmatogenous retinal detachment. In addition to this
syndrome the angle is usually open. 1,3,4
As a differential diagnosis of Schwartz Matsuo syndrome can berupa :4,5,6
a. Iritis : the presence of anterior synecia and keratic precipitate indicates the presence of an
inflammatory process, in contrast to Schwartz-Matsuo Syndrome. The aqueous cells
found in Schwartz Matsuo Syndrome do not respond to corticosteroids.
b. Open-angle glaucoma : can be considered, especially when it occurs in patients with a
history of the presence of blunt trauma.
c. Posner Schlossman syndrome : shows very mild inflammation in the COA, with the
presence of few cells and flares, some clear keratic precipitate, and responds to
corticosteroid therapy.
Treatment in Schwartz Matsuo Syndrome, the same as treatment of Rhegmatogenous Retina
Detachment and glaucoma. Eyeball pressure can be lowered with mat ball pressure lowering
drugsa.4
BIBLIOGRAPHY
1. Sebastian Wolf, Martin Zinkernagel. Pathogenetic Mechanisms of Retinal Detachment. Ryan’s retina
6Th ed. 2017;98:1821-1827.
2. McCannel C A, Atebara N H, Kim S J, Leonard B C, Rosen R B, Sarraf D, Cunningham E Jr.
Rhegmatogenous retinal detachment. Retina and vitreous, Basic and clinical science course, Section
12.2017;13:286-290
3. Cioffi G A, Durcan F J, Gupta N, Salmuelson T W, Tanna A P, Barton K, O'Connell S S. Open- angle
Glaucoma. Glaucoma, Basic and clinical science course, Section 10.2017;4:102 – 103
4. Allingham R R. Classification of the Glaucomas. Shields Textbook of Glaucoma, 6th Edition.
2011;7:288-289
5. Callender D, Jay J L (1997): Schwartz-Matsuo syndrome: atypical presentation as acute open angle
glaucoma. Br J Ophthalmol 81: 609-610.
6. Heatley G, Michael Pro, Harasymowicz P (2006): Schwartz - Matsuo syndrome. J Glaucoma 15: 562
- 564.
3.3 Congenital glaucoma
Glaucoma in children occurs less frequently than glaucoma in adults. Glaucoma in

children itself is a rare pediatric condition and is associated with significant visus disorders.
Although glaucoma can cause visual impairment of a permanent nature, the consequences of the
disease are often more severe in children due to the presence of additional damage that can occur
to the developing visual system. Ambliopia and refractive disorders associated with this disease
are often found. Current glaucoma surgery has significantly improved the visual prognosis in
children suffering from glaucoma. However, a late diagnosis can lead to permanent and severe
visual morbidity. (1)
3.3.1. Classification
3.3.1.1 Primary glaucoma in Children
A. Glaukoma Kongenital Primer (Primary Congenital Glaucoma/PCG)

Primary congenital glaucoma (PCG) or primary congenital glaucoma generally occurs in
the first 2 years of life, although the cases found are mostly at the age of 1 year. The incidence of
PCG is estimated to be 1 in 10,000 births and more inmen than in women. It is generally
sporadic, but 10% of cases that occur are familial. Pathology analysis of the eye with PCG
showed a consistent feature in the form of stopping the development of the angle of the front eye
chamber. This is the location of the iris root and the ciliary corpus which is more in front or
sometimes the location of the scleral spur that is too forward so as to close the trabecular
meshwork either partially or completely. In the end, trabecular meshwork is depressed and does
not develop properly. (2.3)
The iris and the ciliary corpus failed to move backwards so they were both directly in
front of the trabecular posterior part of the meshwork. This is more similar to the eye condition at
7 or 8 months of gestation than at the age of aterm that should be. A more anterior ciliary corpus
musculus insertion was also found. Longitudinal and circular musculus can be insertion
into the skeral spur. The roots of the iris can also be inserted directly into the trabecular
meshwork. Malinsertion at the corner of the front eye chamber will result in a dam of humor. (2,3,4)
The most common defects are believed to stem from the cessation ofthe process of tissue
development originating from neural crest cells at the age of 3 months of gestation. The
mechanism by which this developmental defect can cause obstruction of aqueous humor may be
due to the presence of trabecular collapse of meshwork and paradoxical Schlemm canals that
occur akibat contraction of the muscles, although in some patients there may be other aqueous
drainage development defects that can be the cause of glaucoma.
The obstruction of acuus humor that occurs due to the defect of the development of the
angle of the front eye chamber in PCG isnot related to other ocular anomalies or commonly
called isolated trabeculodysgenesis.
Clinically, trabecuelodisgenesis is characterized by loss of angle recess, with the
insertion of the iris into the surface of the trabeculae with one of 2 konfigurations:
a. Flat iris insertion: flat insertion of the iris into the thick trabeculae on or anterior of
the skeral spur.
b. Convex insertion of the iris: this is rarely found. The iris plain is more posterior than
the normal position of the skeral spur. Stroma anterior iris runs up the trabecular
tissue, covering the skeral spur and the angular structure of the front eye chamber.
The mechanisms involved in the pathophysiology of PCG are actually not known for
certain. However, in principle, the defect that occurs is a failure of one or more stages of
development of the angle of the front eye chamber. If the genes related to PCG can be further
studied and the physiological role and role in the developmental process of the proteins encoded
by those genes can be further explored, then the pathophysiology in terms of molecular, cellular
and embryology will become clearer. (3,4,5)
B. Juvenile Open-Angle Glaucoma (JOAG)

JOAG is a form of primary open-angle glaucoma that occurs due to increased intraocular
pressure at the age of 3 to 35 years. Since almost all cases of JOAG are inherited as autosomal
dominant, families who are worried about the risk of suffering from this disease should do
screening and examination earlier. Although the intraocular pressureof ar increases, it does not
usually cause enlarged cornea or Haab striae; Instead
Progressive myopia will probably continue to develop until the age of 10. This JOAG is almost
the same as primary open-angle glaucoma in adults because the angles of the front eye chambers
and trabecular meshwork appear normal. (3,4,6)
Genetic analysis found a defective gene in the long arm of chromosome 1 of some
patients, and the presence of specific mutations that may be related to the severity of this
disorder. This defective gene is associated withmutations in the TIGR/MYOC gene, and most
patients with this gene have a high IOP and respond poorly to treatment. These patients seem to
be best treated in the early stages and with surgery. (1.7)
C. Developmental Glaucoma Associated with Ocular Or Systemic Abnormalities

1. Sindrom Axenfeld-Rieger
Axenfeld-Rieger syndrome (A-R) is a collection of abnormalities characterized by the
presence of bilateral anterior segment developmental defects that Shield said are likely the result
of cessation of neural-crest development. The structures involved include the angle of the front
eye chamber, iris and trabecular meshwork. (2.3)
The Axenfeld anomaly is aimed at the presence of embryotoxone with iris adhesions that
vary fromthread-like tips to thick ribbon-shaped. Rieger's anomaly is the Axenfeld anomaly
accompanied by congenital abnormalities in the iris including hypoplasia, correctophilia and
pseudopolychoria. Meanwhile, Rieger syndrome is a Rieger anomaly accompanied by systemic
developmental disorders, namely teeth, face and umbilicus. (2.3)
Genetic analysis shows a link between A-R syndrome and several loci, a gene that
appears to be important in the process of forming the angle of the front eye chamber. In
glaucoma-related cases, inhibition of the formation of the front eye chamber angle also leads to
characteristic congenital glaucoma, including poorly developed trabecular meshwork and overly
anterior iris insertion. Several reports documented significant changes in the shape of the
trabecular meshwork and Schlemm canals. These include trabecular meshwork and Schlemm
canals that thicken and solidify. These changes may also be accompanied by peripheral insertion
of the iris and ciliary corpus into the trabecular meshwork. Normal Schlemmm canals are
usually absent. (2,3,4,5,6)
2. Peters Anomaly
Von Hippel was the first to find patients with opacity in the central cornea accompanied
by iris adhesions and galukoma. He attributed this to infection and perforation of the intrauterine
cornea, which leads to adhesions of the iris (internal corneal ulceral von Hippel). This
abnormality is the result of an imperfect development process and a wrong separation process
between the lens and the lens vesicle and the surface ectoderm. Later in some cases it was found
that the defects that occurred were hasil of abnormal migration from neural crest cells to form
anterior segments. (2.3)
Peters anomaly it is a developmental condition characterized by the presence of an

anular corneal opacity (leucoma) in the central visual axis. Leucoma is the result of defects in
the endothelium cornea and descemet membrane, as well as the posterior stroma. There is
usually an attachment of the iris extending from the cholaret to the opacity of the cornea. The
lens may be in the normal position, with or without cataracts, or the lens may passt to the back
layer of the cornea. Patients with corneolenticular adhesions have more complex ocular
abnormalities, such as microcorneas and anomalies of the angle of the front eye chamber, and are
accompanied by systemic abnormalities, including heart defects, genitourinary tract,
musculoskeletal sist em, ear, palate and vertebrae. (2.4)
There are 3 types of anomaly peters, namely type 1 is a posterior corneal defect with
leucoma without any abnormalities of the anterior segment, type 2 is a posterior corneal defect
accompanied by leucoma and iris lengthen and type 3 is a posterior corneal defect along with
iris adhesions and keratolenticular or catarrhal contact.
3. Aniridia
Aniridia is a congenital disease characterized by hypoplasia of irises. Generally, patients
with aniridia only have arudimentary iris piece; however, the appearance of irises is very diverse,
some patients also have almost perfect but very thin irises. Aniridia is usually associated with
other ocular abnormalities including a small cornea, cataracts that occurat birth or in infancy, and
hypoplasia of the optic and fovea nervus that leads to a penular nystagmus and a decrease in the
visus. (2,3,5,6)
About 50%-75% of patients with aniridia suffer from glaucoma. Although sometimes
associated with congenital glaucoma, glaucoma in aniridia usually develops after
The rudimentary iris rotates towards the anterior and then closes the trabecular tissue causing the
closure of the corner of the front eye chamber. This process occurs gradually, and glaucoma can
occur in the second decade or more. The main developmental abnormalities in the corners of the
front eye chambers can also lead to increased intraocular pressure at a younger age. Patients with
aniridia may have a stem cell abnormality of the lim bal which will eventually lead to the
occurrence of a cordal pannus that starts from the peripheral cornea and extends slowly in the
central direction.
Generally anides are familial and autosomal dominant, but about 1/3 of the cases are
isolated sporadic mutations. About 20% of sporadic cases are linked to Wilm's tumors. The locus
of the aniridia gene, both familial and sporadic forms, is a mutation of the PAX6 gene on
chromosome 11p3. (2,3,6)
4. Sturge-Weber Syndrome
Sturge-Weber syndrome (also known as encephalotrigeminal angiomatosis) is a
factomatosis with ipsilateral fascial quadantius hemangioma (nevus flammeus or port- wine
stain), ipsilateral choroid cavernous hemangioma, and ipsilateral leptomeningeal angioma.
Glaucoma occurs in 30%-70% of patients suffering from this syndrome. Nevus flammeus
involving palpebral is the most common case. In infants, glaucoma that occurs is suspected to be
the result of congenital anomalies of the front eye chambers. In alarger son , the glaucoma
that occurs is associated with an increase in the pressure of the episcleral vein. (2,3,5)
5. Neurofibromatosis
Neurofibromatosis also known as von Recklinghausen disease is a dominant
autosomal disease characterized by the presence of multiple café-au-lait spots,
neurofibromatomamas on the skin, central and peripheral nervous system, as well as loss of os
spheoid parts or other bone abnormalities. Emerging ocular abnormalities cover i nodules in the
iris (Lisch nodules) and palpebral, uvea ectropion, optical nervus glioma, retinal astrocytocyte
hamartoma and proptosis that occur both due to glioma nervus optics maupum harniation of
brain tissue to the eye.
Glaucoma associated withomatosis neurofibr is commonly seen in neuromas involving
the superior palpebral or the eye itself. Stand-alone trabeculodisgenesis or synecia that occurs as
a result of neurofibromatous tissue can be a mechanism
pathology of the occurrence ofglaucoma. A dense sheet of avascular tissue can emerge from the
edge of the iris and extend to the front of the front chamber of the eye. (2,3,4,6)
3.3.1.2 Secondary Glaucoma in Children

Generally, the causes of secondary glaucoma in infants and children are almost the same
as the causes ofsecondary glauko ma in adults. Trauma, inflammation, steroid use and
topiramate-induced angle closure glaucoma are the most frequent causes in all age groups. Lens
abnormalities that can cause closed-angle glaucoma include Mar fan syndrome, homocystinuria,
Weill-Marchesani syndrome and microsferofakia. Abnormalities in the posterior segments such
as persistent fetal vasculature (PFV), retinopathy of prematurity (ROP) and familial exudative
vitreoretinopathy (FEVR), as well as tumors in the re-tina, iris and siliary corpus.
Retinoblastoma, juvenile xanthogranuloma and medulloepithelioma are some of the tumors
known to cause secondary glucoma in infants and children. Rubella and congenital cataracts are
conditions that are also associatedwith secondary glaucoma in children.
Secondary inflammatory glaucoma is usually associated with chronic anterior uveitis, and
lenses with other inflammatory conditions. Glaucoma in this condition can occur through various
mechanisms, either acute (for example: trabeculitis, trabecular obstruction,iris bombe and pupil
block) or chronic (anterior peripheral synecia, scar trabeculae or trabecula dysfunction, steroid-
induced trabeculae obstruction). (2,3,4,6,7)
Corticosteroids themselves are topical and systemic drugs that most often cause a
hypertensive response. The higher the potential of the corticosteroid the higher the resulting
increase in intraocular pressure. Children had a stronger response to corticosteroids than people
a. Topical administration is the most frequent route of administration in children so it is more
likely to be a route that induces an increase in intraocular pressure in children.
A. Afghan glaucoma
Glaucoma can occur in 15%-50% of pediatric patients who have undergone congenital
cataract surgery. Although almost all aphaxian glaucoma appears after 3 years after surgery,
patients have a risk of suffering from glaucoma throughout their lives, so
they alsoneed follow-ups throughout their lives. Risk factors for suffering from aphaxial
glaucoma include cataract surgery in the first year of life, postoperative complications, and
corneas with a small diameter. Although the underlying mechanisms of the disease are not yet
jelas, congenital abnormalities, inflammation due to surgery and postoperative intraocular
anatomical changes may play a role. Cleaning of residual cortex during cataract surgery can
reduce the occurrence of aphaxial glaucoma in a child. (1,3,5,6)
3.3.2 Diagnosis
Accurate diagnosis requires a thorough anamnesis and a good examination. This
examination is often difficult and depends on the age of the child and his ability to be
cooperative during the examination. In the group of children with a younger age (4 years or
young) light sedatives such as chloral hydrate syrup (25 to 50 mg / kgBB) can be used to
perform slit lamp examinations, gonioscopy of aplanation and funduscopy. This doesn't always
work, and when it doesn't work it's often necessary to have a general psyche to perform a more
precise examination. Examination under general anesthesia may be avoided if the diagnosis of
glaucoma can be ruled out with certainty (in infants or younger children) or if it would be more
beneficial for older children ifgiven trial treatment only. If necessary, examination under general
anesthesia allows for a more detailed examination of gonioscopy and optic nervus, as well as
corneal diameter and paximetry, axial length, andwhether operative intervention is then needed.
It is important to know that almost all general anesthesia causes a decrease in intraocular
pressure, so the examination should be carried out as carefully as possible when the child begins
to fall asleep.
Infants andyoung children suffering from glaucoma usually come for an examination
because the pediatrician or his parents notice any unusual images in the child's eyes or in his
behavior. Corneal turbidity and or a more bes ar size of the corneaare the most frequently found
early symptoms and usually both of these signs appear in the first 2 years of life if intraocular
pressure continues to increase. Buphthalmos is a term used to describe the enlargement of a
baby's eyes that are not affectedby an increase in intraocular pressure.
The classic triassic that is often found in the form of epiphora, photophobia and
blepharospasm is the result of corneal edema associated with damage to the descemet membrane
called Haab striae. This descemet membrane damage usually occurs in the first 2 years of life. In
conditions where optic nerve atrophy does not occur, cupping can be significantly reduced by
lowering intraocular pressure and will re-enlarge if intra-ocular pressureis not controlled. Optic
nerve atrophy due to increased chronic and severe intraocular pressure is irreversible.
For older children, it usually comes with complaints of decreased visus or conditions
where glaucoma sekund er may occur. Although optic nerve papillary abnormalities are not a
definitive indicator of glaucoma, this sign will encourage a thorough examination. Loss of visus
in infants and children suffering from glaucoma occurs as a result of pathological changes in the
co-rnea and damage to the optic nerve. In addition, it can also occur due to refractive disorders.
(2,3,4,6,7)
3.3.3 Management and Therapy

The ophthalmologist must be able to determine the ideal treatment by paying attention to
case by case. Generally, children suffering from glaucoma will eventually need intervention,
either medication administration, surgery, or both.
3.3.3.1 Operative Handling

Congenital glaucoma is basically an operative disease in which surgery must be
performed as soon as possible. Surgical intervention is a therapeutic option in primary congenital
glaucoma. If the cornea is clear, goniotomies or trabeculotomy can bean option. If visualization
through the cornea is disturbed, trabeculotomy or a combination of trabeculatomy-trabecectomy
can be performed. About 80% of babies with congenital primary glaucoma from 3 months- 1
year, TIO controlled with 1 or 2 sud ut surgery. If the first operation was unsuccessful, at least 1
additional angular surgery was performed before replacing with a different procedure. (6.7)
A. Goniotomi
The goal of goniotomy is to eliminate network obstruction on the Schlem canal that
causes akuous humor flow resistance, thereby restoring access to the Schlemm canal and
increasing outflow. Chen and Walton (2000) used a modified goniotomy technique, namely with
a 20o angle had a success rate of about 89% in lowering the intraocular right te, the remaining
11% received advanced anti-glaucoma therapy. Mandal (2011) states that goniotomies are often
successful in pediatric glaucoma patients diagnosed and treated in the first month to the first year
of birth. (4,6,7)
B. Trabecuelotomi and Trabecectomy

Similar to goniotomi, the success rate of this action is reported to be around 70- 90%
during the 2-9 year follow up period after the action. Trabeculotomy has several advantages over
goniotomies. Among them, trabeculotonoodles can be done even though the cornea is not clear
(cloudy), there is a rupture of the inner wall of the Schlem canal and if the trabecular meshwork
is not in normal anatomy. Does not require special instruments, performed as a minor operation
(microsurgical) without the use of lensa goniotomi. According to Mandal (2011) the success of
trabeculotomy surgery depends on the type of pediatric glaucoma angle disorder, not on the
severity of glaucoma or the size of the corneal diameter. Compared to goniotomies that can
reduce TIO by 64-77%, PRosedur trabeculotomy can reduce TIO by up to 90%.
(2,7,8)
The trabecectomy procedure is preferred for most ophthalmologists, as it is easier than

goniotomy and trabeculotomy. However, many researchers do not recommend it to be used as a
first-line procedure in the treatment of pediatric glaucoma due to high complication rates and
low success rates. Finally developed a combined procedure of trebecutomy and trabeculectomy.
Where after the trabeculotomy procedure is carried out, followed by trabeculectomy. (6,7,8)
Trabecectomy and MMC therapy show success in 50-95% of glaucoma cases in a child.
The results obtained do vary. In children under the age of 1 tyear and in children with afakia the
results obtained were not satisfactory, there were even some who failed therapy. Although the
success rate of trabecectomy and MMC is quite high,
But the rate of infection in bleb, bleb leakage, and long-term complications of trabeclectomy is
also increasing. So the use of MMC is still being considered. (4.7)
Implant insertions performed by Molteno, Bearveldt and Ahmed (2000) in pediatric
patients withglaucoma had a success rate of 80-85%. But after implant installation, TIO should
be periodically controlled with the addition of topical or oral anti-glaucoma adjuvant therapy.
Compared to children undergoing trabecectomy + MMC, leakage and infection rates in blebs
were lower. Complications of implantation include hypotony due to shallowness of the front eye
chambers, attachment of the cornea with tubes, obstruction tubes, exposed tubes and retinal
detachment. (7.9)
3.3.3.2 Medicamentosa
It is usually carried outas a supporting therapy to lower the TIO temporarily, to clear the
cornea, and facilitate surgical intervention: (2,4,5,6)
a. Topical Beta Blockers: this drug is administered under close supervision in infants for
possible apnea and other systemic side effects. Cardiac abnormalities and bronchial
asthma should be ruled out first before use. The use of the preparation 0.25% more
is recommended so that the side effects can be reduced.
b. Oral Carbonic Anhydrase Inhibitors (CAIs): Systemic administration of CAIs in
children has the same side effects as administration in adults. In addition, growth
suppression has been linked to oral use of acetazolamide, and can give rise to severe
metabolic acidosis in infants. Oral administration of acetazolamide at a dose of 10
(between 5-15) mg/kg/day at a dose of 3 times a day was rated safe and tolerable.
c. Topical prostaglandin analogues: latanoprost 0.005% (xalatan) and travoprost 0.004%
(travatan) and prostamide bimatoprost 0.03% (Lumigan) are effective in pediatric
patients. Side effects include increased pigmentation of the iris and eyelash growth.
The drug should not be used in uveitic glaucoma patients.
d. Topical alpha-2-agonist: brimodinine can decrease TIO by as much as 7% in 30
patients with an average age of 10 years. It can cause systemic side effects and
disorders of the central nervous system so its use is recommended in older children.
e. Oral carbonic anhydrase inhibitor: effectively used in children, especially in children
who want to postpone surgery. In children with low body weight, lethargy and
metabolic acidosis, oral administration of carbonic anhydrase inhibitors needs to be
considered. Examples of acetazolamide, methazolamide. (2,4,5,6)
Osmotic drugs such as mannitol dapat are used to lower TIO before surgery in patients
with developmental glaucoma who have increased TIO and do not respond to standard therapy.
(2,5,6)
3.3.3.3 Other Handling

A. Laser Therapy
In cases that are resistant or cannot be surgically performed, cyclodestruction using
Nd:YAG laser, diode laser or cyclocryotherapy can be used as an option in the treatment of
glaucoma in children. These techniques would reduce the production of humor akuous by the
procession. The success rate of cyclocryotherapy (processus siliar frozen via skera) is about 33%
with a high degree of complications. This cyclocryotherapy needs to be done periodically. The
risk of ptisis and blindness can reach 10%. Cycloablation transcleral lasers with Nd:YAG or
laser diodes, have a smaller risk of complications. Success
short-term is about 50%. It also requires an iterative process, not just a single therapy. (2,4,6,8)
Bibliography
1. AAPOS. Glaucoma for Children. 2014.
2. The American Association of Ophthalmologists. Glaucoma in children and adolescents, Glaucoma;
chapter 6. USA: AAO; 2017.
3. The American Association of Ophthalmologists. Pediatric Glaucomas, Pediatric Ophthalmology and
Strabismus; chapter 22. USA: AAO; 2017.
4. Kanski JJ, Bowling B. Ophthalmology: A Systematic Approach 7th ed. New York: Elsevier/Saunders;
2011.
5. Khurana, AK. Comprehensive Ophthalmolog. UK:Anshan Publishers.
6. Jackson,T. Moorfields Manual of Ophthalmology Second Edition. UK: JP Medical Ltd; 2014.
7. Khan,Arif. A Surgical Approach to Pediatric Glaucoma. Open Ophthalmol J. 2015; 9: 104–112.
8. Gutiérrez-Díaz E, Mencía-Gutiérrez E , Tejada-Palacios P. The role of Glaucoma Drainage Devices in
Paediatric Glaucoma. European Ophthalmic Review, 2012;6(4):208-213 DOI:
http://doi.org/10.17925/EOR.2012.06.04.208
9. Mandal AK, Chakrabarti D. Update on congenital glaucoma. Indian J Ophthalmol 2011;59, Suppl
S1:148-57
Appendix
A. Indications of Hospitalization in Glaucoma Patients
Patients with glaucoma are hospitalized with the following indications :

1. Acute glaucoma sufferers.
2. Surgery under general anesthesia.
3. There are complications of intasurgery that require monitoring, for example intraocular hemorrhage,
glaucoma maligna, or systemic disorders during surgery or perioperative.
4. Patients with postoperative pain in the VAS >4 category.
B. Recommendations for the management of closed-angle glaucoma based on the

level of health care facilities
Primary Secondary Tertiary Services

Services Services
Medicamentosa In In In
Laser iridotomi / iridektomi In In
Phacoemulsifikasi In In
Trabekulektomi In In
Phaco + Trabekulektomi In
Phaco post trabecectomy In
Glaucoma implants In
C. Recommendations for the management of open-angle glaucoma based on the level of

health care facilities
Primary Secondary Tertiary Services

Services Services
Medicamentosa In In In
Laser trabekuloplasti In
Phacoemulsifikasi In In
Trabekulektomi In In
Phaco + Trabekulektomi In
Phaco post trabecectomy In
Glaucoma implant In
CHAPTER IV
CONCLUSIONS AND RECOMMENDATIONS
4.1 Conclusion
To reduce the prevalence and rate of blindness due to glaucoma, it is necessary:
Early detection of glaucoma sufferers.
Periodic control of glaucoma sufferers includes intraocular pressure, optic nerve compartmentality and field of vision
Control intraocular pressure with medicamentous, laser, or surgical to slow down the progressiveness of glaucoma, an
Education for sufferers and families.
4.2 Recommendations
The management of glaucoma sufferers is carried out in accordance with the PNPK glaucoma.
Glaucoma management is adjusted to the competence of doctors and available health service facilities.
Cases requiring further action may be referred to a service center with facilities
the higher one .

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3.

7. Anterior Segment Optical Coherence Tomography (ASOCT)

A. Tatalaksana Primary Angle Closure Suspect (PACS)2,12,18

2. It remains to be informed of the possibility of acute PAC and PACG attacks

B. Primary Closed Angle Management (PAC)2,12,18

e. Carbonic anhidrase inhibitor oral 3 x 250 mg

3. Filtration surgery (trabeculectomy) with or without IOL phacoemulsification

D. Tatalaksana Acute Primary Angle Closure (APAC)2, 10,12,18

Clinical signs 2.3 :

 Excavation glaucomatous Papil N. II

Risk factor 1,2 :

 Central Corneal Thickness (CCT)

Supporting examination 1,2 :

Normotension Glaucoma (NTG) / Low tension Glaucoma1,2

 Intraocular pressure within normal limits

 Vascular abnormalities (eg: migraine)

Ocular Hypertension (OHT)1,2

 Intraocular pressure above normal

 High intraocular pressure

Glaucoma Suspect 1,2

Asymptomatic and usually detected during routine eye exams

 Normal intraocular pressure

The management of primary open-angle glaucoma includes medicamentous and non-

 Maximum tolerance to medicamentous therapy and unable to adequately

b. Two-side phycoemulsion-trabecectomy combination surgery will lower intraocular

Recommendations for surgical measures in case of glaucoma accompanied by

- Patients with advanced glaucoma with optic neuropathy (advanced glaucoma)

- Uncontrolled glaucoma or controlled glaucoma incataract with more than 2 types of

The risks and benefits of administering therapy to glaucoma suspects need to be

4. European Glaucoma Society, Glaucoma Guideline. 2014

6. Jampel HD, Fridman DS, Lubomski LH et al. B. Effect of technique on Intra

7. Buys YM. Surgical Management of coexisting cataract and glaukoma. Ophthalmology

Neonascular glaucoma (GNV) is a secondary glaucoma caused by an underlying ocular

VEGF is an important mediator against the occurrence of intra-ocular neovascularization

Ocular Ischemic Syndrome

Central Retinal Artery Occlusion (CRAO)

Staging Glaukoma Neovaskular4

Management of Neovascular Glaucoma

3.2.2.1 Lens-induced glaucoma, Open Angle

3.2.2.1.1 Facololitic glaucoma

The definitive treatment is surgery to extract cataracts. Before surgical action,

3.2.2.1.3 Phacoangenic glaucoma

Another known term is phacanoanphylactic glaucoma, which is caused by an immune

3.2.2.2 Lens-induced Glaucoma, Closed Angle

One of the differential diagnoses of facomorphic glaucoma is closed-angle primary

The goal of therapy in facormorphic glaucoma is to lower intraocular pressure by

3.2.2.2.2 Ectopia Lentis

Causes of Ectopia Lentis

Traumaic Pseudoexfoliation Syndrome

The purpose of management is to prevent an increase in intraocular pressure and contact

1. American Academy of Ophthalmology. Glaucoma. Basic and clinical science course

Laser Argon Trabekuloplasti (ALT)

Selective Trabeculoplasty Laser (SLT)

Implantasi Aqueous Shunt

Combination of Cataract and Glaucoma Surgery

Intraocular pressure enhancement mechanism

Open-angle glaucoma is usually asymptomatic until the disease reaches an advanced

 Iris transillumination examination is an important clinical picture for the diagnosis of PG

Peripheral Iridotomy Laser