*GLAUCOMAFifin Luthfia RahmiDepartment of OphthalmologyFaculty of Medicine Diponegoro University Dr . Kariadi Hospital Semarang

* setelah mengikuti mata kuliah ini mahasiswa dpt menyebutkan definisi, klasifikasi, gejala dan tanda serta pengelolaan glaukoma sehingga dapat mencegah terjadinya kebutaan akibat glaukomaTIU

* 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 T I K

*Referensi :Vaughan DG, Asbury T, Riordan-Eva P. General Ophthalmology, Appleton & Lange; Connectitut.Ilyas S. Ilmu Penyakit Mata; Balai Penerbit FKUI; Jakarta.6. mhs dpt menjelaskan ttg glaukoma sekunder, menyebutkan kelainan yg dapat menyebabkan glaukoma sekunder dan cara pengelolaannya shg dapat mencegah terjadinya kebutaan7. mhs dpt menjelaskan ttg glaukoma kongenital meliputi gejala, tanda dan pengelolaannya

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

* high intra ocular pressure ( IOP ) The 2nd cause of blindness, permanent Introduction

*Glaucomatous optic neuropathyNormal optic nerve

*Normal visual fieldVisual field in moderateglaucomaVisual field in advancestage glaucoma

* Risk factors :

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

* resistance of aqueous humor outflow Physiology of Aqueous Humor Resistance in outflow of aqueous humor IOPAqueous humorproductionEpiscleral vein pressure

* Aqueous humor :

liquid that fills the anterior and posterior chambers volume : 250 L production rate 1.5 2 L/ 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

*Aqueous humor outflow

*A. Primary Glaucoma 1. Primary open-angle glaucoma ( POAG )2. Primary Angle-closure glaucoma ( PACG )a. prodromal stage/ sub acuteb. acute stage( glaucomatous attack )c. Chronicd. Plateu iris

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

*C. Secondary Glaucoma because of ocular/ systemic diseases1. lens diseases2. uveal diseases3. trauma/ injury4. post ocular surgery5. neovascular glaucoma6. increase episcleral vein pressure ( in carotico-cavernous fistule )7. longterm steroid treatment8. etc..

* The pathology of glaucomaTwo 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

*2. Vascular blood perfusion not adequat ischemia risk factor : vascular/ cardiovascular disorder usually IOP not high

*Clinical Examination1. Tonometri measuring the IOP digitally using tonometer : Schiotz, Goldmann ApllanationSchiotz tonometer

*Application of Goldmann Applanation Tonometri

*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

*Gonioscopy using three-mirror Goldmann

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

*3. Visual field examination The simplest methode : confrontation test another methode : Campimetry Perimetry : Goldman, Humphrey

to evaluate impact of the disease on patients visual field to know the stage of the disease planning the treatment evaluation

*Confrontation test

* Goldmann perimeter

*Humphrey Visual Field Analyzer

*4. Optic nerve examination- evaluate the optic nerve- using ophthalmoscope or slit lamp and lens + 78 DOphthalmoscopy

* Result : Normal Optic NerveGlaucomatous Optic Nerve

*Optical Coherence Tomography ( OCT)

*Management of Glaucoma Medical treatment1. Supression of aqueous production - gol. - adrenergic blocker : timolol maleate, betaxolol - gol. 2 adrenergic agonis : apraclonidine, epinefrin - carbonic anhidrase inhibitor : asetazolamide, dorsolamid2. Facilitation of aqueous outflow- Parasympatomimetic : pilocarpine - adrenergic agonis : epinephrin- Prostaglandine analog : latanoprost, travoprost

*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

* 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

*Laser iridotomyColoboma iridis Post laser iridotomy

* Surgical treatment - Peripheral iridectomy laser iridotomyColoboma iridis post iridectomy

*- 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

*Glaucoma drainage device

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

* Clinical type of Glaucoma1. 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 Clinical sign : - IOP , no redness - chracteristic visual field defect - excavatio glaucomatosa

* Treatment : is began w/ medical treatment : -blocker, prostaglandin analog if IOP isnt sufficiently controlled laser trabeculoplasty / surgical treatment

*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 its detected early, most glaucoma patients can be successfully managed medically

*2. Primary Angle-closure Glaucoma usually occurs in eye w/ preexisting anatomic narrowing of the anterior chamber angle

* 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

*2. Primary Acute Angle-closure glaucoma is an ophthalmic emergency glaucomatous attack , sudden onset IOP raise rapidly severe pain, redness, blurring vision signs : congestive , very high IOP treatment : medicamentous surgery

*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

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

* 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

*Secondary glaucoma Clinical feature : primary disease, IOP management : - control IOP - appropriate w/ the primary diseasePhacomofic glaucomaSecondary glaucoma because of hyphema

*Congenital Glaucoma: Three type Clinical feature : epiphora, photophobia corneal opacity ( Haabs striae ) corneal diameter > 11.5 mm Treatment : surgical

*Contoh kasusSeorang wanita, 53 tahun, datang ke UGD karena sakit kepala hebat di sisi sebelah kanan sejak kemarin. Riwayat asma (+), riwayat hipertensi (+)Pada pemeriksaan saudara dapatkan :OD : Visus OD : 1/300tensi : 180/100 mmHg palpebra : blefarospasme konjungtiva : mixed injectie, kornea : edema COA : dangkal pupil : mid dilatasi, reflek pupil lambat TIO ( digital ) : N +2, dg tonometer Schiotz : 50 mmHg

Nyeri kepala disebabkan oleh : A. HipertensiB. Penurunan visus beratC. TIO tinggi mendadakD. Kongesti pembuluh darahE. Edema kornea

*2. Tindakan yang harus dilakukan untuk menyelamatkan fungsi penglihatan pasien adalah : A. mengatasi hipertensi B. Mengatasi edema kornea C. menurunkan tekanan intra okuler D. pemberian kacamata E. pemberian analgetikObat-obat yang dapat diberikan untuk menurunkan TIO : A. Beta-bloker tetes mataProstaglandin analog Asetazolamid steroid topikal anti inflamasi non steroid

*1. Ingat perjuangan ketika untuk masuk FK2. Ingat harapan & pengorbanan orang tua yang tiada duanya3. Ingat kesempatan yang sudah didapatkan4. Ingat tanggung jawab setelah kau sandang gelar dokter5. Ingat waktu yang telah pergi tak akan pernah kembaliSelamat belajar.

**