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GLAUCOMA

Fifin Luthfia Rahmi

Department of Ophthalmology
Faculty of Medicine Diponegoro University
Dr . Kariadi Hospital
Semarang

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TIU

 setelah mengikuti mata kuliah ini mahasiswa dpt


menyebutkan definisi, klasifikasi, gejala dan tanda
serta pengelolaan glaukoma sehingga dapat
mencegah terjadinya kebutaan akibat glaukoma

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TIK

1. mhs dpt menyebutkan definisi glaukoma


2. mhs dpt menyebutkan klasifikasi glaukoma
3. mhs dpt menjelaskan gejala, tanda dan
pengelolaan glaukoma primer sudut terbuka
4. mhs dpt menjelaskan gejala, tanda dan
pengelolaan glaukoma primer sudut tertutup
5. mhs dapt menjelaskan keadaan darurat mata
akibat glaukoma, cara penanganan pertama
dan tahu kapan hrs merujuk shg dpt mencegah
kebutaan akibat glaukoma

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6. mhs dpt menjelaskan ttg glaukoma sekunder,
menyebutkan kelainan yg dapat menyebabkan
glaukoma sekunder dan cara pengelolaannya
shg dapat mencegah terjadinya kebutaan
7. mhs dpt menjelaskan ttg glaukoma kongenital
meliputi gejala, tanda dan pengelolaannya

Referensi :
1. Vaughan DG, Asbury T, Riordan-Eva P. General Ophthalmology,
Appleton & Lange; Connectitut.
2. Ilyas S. Ilmu Penyakit Mata; Balai Penerbit FKUI; Jakarta.
3. Berson FG. Basic ophthalmology – for medical students and
Primary care Residents. American Academy of Ophthalmology

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Introduction

• Glaucoma  the 2nd cause of blindness, permanent

• Definition :
Glaucoma is a syndrome of :
* optic neuropathy  cupping/ excavation
* characteristic visual field defect

* high intra ocular pressure ( IOP )

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Glaucomatous Normal optic nerve
optic neuropathy

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Normal visual field

Visual field in moderate


glaucoma

Visual field in advance


stage glaucoma

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• Risk factors :

- gender
- race : black > white
- age : 70 y o  7 x >
- family history
- refraction state : myopia, hypermetropia
- systemic disease : diabetes mellitus,
hypertension

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Physiology of Aqueous Humor

Aqueous humor
production

Resistance in outflow IOP


of aqueous humor

 resistance of aqueous
Episcleral vein
humor outflow
pressure

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 Aqueous humor :

liquid that fills the anterior and posterior chambers


volume : ± 250 µL
production rate 1.5 – 2 µL/ min, by ciliary body
osmotic pressure slightly higher than plasma
composition ≈ plasma
> ascorbat, pyruvate and lactate
< protein, urea and glucose
intraocular inflamation/ trauma cause an increase
in the protein concentration  plasmoid

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Aqueous humor outflow

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Classification of glaucoma
A. Primary Glaucoma
1. Primary open-angle glaucoma ( POAG )
2. Primary Angle-closure glaucoma ( PACG )
a. prodromal stage/ sub acute
b. acute stage( glaucomatous attack )
c. Chronic
d. Plateu iris

B. Congenital glaucoma
- primary congenital glaucoma
- associated w/ other developmental ocular
abnormalities
- associated w/ extraocular developmental
abnormalities

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C. Secondary Glaucoma
 because of ocular/ systemic diseases
1. lens diseases
2. uveal diseases
3. trauma/ injury
4. post ocular surgery
5. neovascular glaucoma
6. increase episcleral vein pressure ( in
carotico-cavernous fistule )
7. longterm steroid treatment
8. etc..

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The pathology of glaucoma

Two major theories :


1. Mechanical
chronic high IOP  glaucomatous optic neuropathy
 The effect of raised IOP are common to all forms
of glaucoma
 being influenced by the time course and magnitude
of rise in IOP

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2. Vascular

 blood perfusion not adequat  ischemia


 risk factor : vascular/ cardiovascular disorder
 usually IOP not high

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Clinical Examination

1. Tonometri  measuring the IOP


• digitally
• using tonometer : Schiotz, Goldmann Applanation

Schiotz tonometer
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Application of Goldmann Applanation Tonometri

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2. Gonioscopy

 examine the iridocorneal/ anterior chamber angle


 to know the structure of iridocorneal angle as
a basic in :
# diagnosis
# treatment
# evaluation

 using goniolens : three-mirror Goldmann,


two mirror goniolens

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Gonioscopy using three-mirror Goldmann

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 predicting the deep of anterior chamber using
a pen light : shalow AC if < 2 mm in the central

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Imaging of anterior chamber depth

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3. Visual field examination

• The simplest methode : confrontation test


• another methode : Campimetry
Perimetry : Goldman, Humphrey

• to evaluate impact of the disease on patient’s


visual field  to know the stage of the disease
 planning the treatment
 evaluation

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Confrontation test

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Goldmann perimeter

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Humphrey Visual Field Analyzer

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4. Optic nerve examination

- evaluate the optic nerve


- using ophthalmoscope or slit lamp and lens + 78 D

Ophthalmoscopy

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Result :

Normal Optic Nerve Glaucomatous Optic Nerve

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Optical Coherence Tomography ( OCT)
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Management of Glaucoma

Medical treatment

1. Supression of aqueous production


- gol. β- adrenergic blocker : timolol maleate, betaxolol
- gol. α 2 – adrenergic agonis : apraclonidine, epinefrin
- carbonic anhidrase inhibitor : asetazolamide, dorsolamid

2. Facilitation of aqueous outflow


- Parasympatomimetic : pilocarpine
- α – adrenergic agonis : epinephrin
- Prostaglandine analog : latanoprost, travoprost

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3. Reduction of vitreous volume
- Hyperosmotic agents  blood hypertonic 
drawing water out of the vitreous shrink
- decreasing aqueous production
- agents :
@ oral glycerin ( glycerol ) 1 mL/ kgbw +
lemon juice
@ oral isosorbid
@ intravenous urea or mannitol

4. Miotics, mydriatics and


cycloplegics

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Laser and Surgical Treatment

 Laser treatment

- Iridotomy :
 forming a direct communication between the
anterior and posterior chambers remove
the pressure different between them
 indication : angle-closure, pupillary block

- Trabeculoplasty:
 enhance the function of the meshwork
 indication : open- angle

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Laser iridotomy (for angle-closure)

Coloboma iridis
Post laser iridotomy

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Laser Trabeculoplasty (for Open-angle)

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 Surgical treatment

- Peripheral iridectomy
 ≈ laser iridotomy

Coloboma iridis post iridectomy

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- Glaucoma drainage surgery
 forming communication between anterior chamber
and sub conjunctival area  direct access of
aqueous from anterior chamber to subconjuctival
 trabeculectomy, implantation silicon tube ( glaucoma
drainage device = GDD )

trabeculectomy
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Glaucoma drainage device

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- Cyclodestructive surgery
 destuction of cyliary bodies  decrease aqueous
production  IOP ↓↓
 indication : absolut glaucoma + pain >>

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Clinical type of Glaucoma

1. Primary Open-Angle Glaucoma


• familial tendency
• pathologic feature :
 a degenerative process in the trabecular
meshwork, deposition extracellular material 
reduction in aqueous drainage  ↑↑ IOP
• chronic progressive, incidious
• sometimes w/o symptoms until relatively late
 patient not realize – ‘the thief of sight’
• Clinical sign : - IOP ↑↑, no redness
- chracteristic visual field defect
- excavatio glaucomatosa

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• Treatment :
 is began w/ medical treatment : β-blocker,
prostaglandin analog
 if IOP isn’t sufficiently controlled  laser
trabeculoplasty / surgical treatment

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Patient/ family must be educated to understand :
 The treatment of POAG is a lifelong process
 Regular reassesment is essential

• Course & Prognosis


 w/o treatment  incidiously progressive to blind
 if it’s detected early, most glaucoma patients can
be successfully managed medically

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2. Primary Angle-closure Glaucoma

 usually occurs in eye w/ preexisting anatomic


narrowing of the anterior chamber angle

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1. Sub acute ( prodromal )

 episode of elevated IOP are of short duration,


resolve spontaneously but potentially recurrent

 the key to diagnose : history


short episode of : unilateral pain, redness,
blurring vision + halos around the light

 treatment : medicamentous  preparing


iridotomy/ iridectomy

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2. Primary Acute Angle-closure

 is an ophthalmic emergency
 glaucomatous attack , sudden onset
 IOP raise rapidly  severe pain, redness,
blurring vision
 signs : congestive , very high IOP
 treatment : medicamentous  surgery

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3. Chronic angle-closure glaucoma

 Two types :
 patients with predisposition to an anterior chamber
angle closure, never develop acute rise in IOP but
form an extensive peripheral anterior synechia ( PAS)
Clinical feature ≈ POAG

 chronic episode after glaucomatous attack w/o


adequate treatment

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Another condition

 Absolut glaucoma :
 the end result of any uncontrolled glaucoma
 clinical appearance :
- hard ( IOP still high ), redness
- sightless eye ( visual acuity : 0 )
- often painfull
- optic nerve atrophy
 treatment :
- enucleation of the bulbi
- cyclocryotherapi
- retro bulbair alcohol injection

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 Degenerative glaucoma :

- clinical appearance:
sightless ( visual acuity : 0 )
signs of degenerative condition :
- bullous keratopathy  often painfull
- atrophy of the iris
- atrophy of the ciliary body  decrease
of aqueous humor production  IOP ↓
- Cataract in glaucoma

- Treatment : enucleation of the bulbi


retobulbair alcohol injection,
bandage contact lens

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Secondary glaucoma

 Clinical feature : ≈ primary disease, IOP ↑


 management : - control IOP
- appropriate w/ the primary disease

Secondary glaucoma because of


Phacomofic glaucoma hyphema
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Congenital Glaucoma:

• Three type
• Clinical feature : epiphora, photophobia
corneal opacity ( Haab’s striae )
corneal diameter > 11.5 mm
• Treatment : surgical

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1. The characteristic of glaucoma is optic disc cupping
2. Glaukoma sudut terbuka seringkali disebut sebagai ‘pencuri
penglihatan karena sifat serangannya yang akut dan berulang
3. Longterm treatment with steroid will cause secondary glaucoma
4. Kelainan mata yang dapat menyebabkan glaukoma sekunder
diantaranya adalah hifema traumatika.
5. Prinsip pengelolaan glaukoma sudut tertutup adalah medikamentosa
6. Efek golongan obat beta- blocker pada glaukoma adalah
menurunkan out flow humor aquos.

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