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Hasil Anamnesis (Subjective)

Keluhan
Pasien datang dengan keluhan yang bervariasi dan berbeda tergantung jenis
glaukoma.
1.Gejala pada glaukoma kronik (sudut terbuka primer) adalah
kehilangan lapang pandang perifer secara bertahap pada kedua mata. Pasien
sering datang pada kondisi yang telah lanjut.
2. Gejala pada glaukoma akut (sudut tertutup) adalah rasa sakit atau nyeri
pada mata, mual dan muntah (pada nyeri mata yang parah),
penurunan visus mendadak, mata merah dan berair.

Faktor Risiko
a. Glaukoma akut : bilik mata depan dangkal
b. Glaukoma kronik :
1. Primer : usia di atas 40 tahun dengan riwayat keluarga glaukoma.
2. Sekunder :
Penyakit sistemik seperti Diabetes Melitus.
Pemakaian tetes mata steroid secara rutin.
Riwayat trauma pada mata

Hasil Pemeriksaan Fisik dan Pemeriksaan Penunjang


Sederhana (Objective)
Glaukoma adalah penyakit mata yang ditandai oleh trias glaukoma, terdiri dari:
a. Peningkatan tekanan intraokular.
b. Perubahan patologis pada diskus optikus.
c. Defek lapang pandang yang khas.
Pemeriksaan Fisik Oftalmologis
Pada glaukoma akut:
a. Visus menurun.
b. Tekanan Intra Okular meningkat.
c. Konjungtiva bulbi: hiperemia kongesti, kemosis dengan injeksi silier, injeksi konjungtiva.
d. Edema kornea.
e. Bilik mata depan dangkal.
f. Pupil mid-dilatasi, refleks pupil negatif.

Pada glaukoma kronik


a. Biasanya terjadi visus dapat normal.
b. Lapang pandang menyempit dapat diperiksa dengan tes konfrontasi
c. Tekanan Intra Okular meningkat (>21 mmHg).
d. Pada funduskopi, C/D rasio meningkat (N=0.3).
Pemeriksaan Penunjang
Tidak dilakukan pada pelayanan primer.

Penegakan Diagnosis (Assessment)


Diagnosis Klinis
Penegakan diagnosis dilakukan berdasarkan anamnesis dan pemeriksaan fisik
oftalmologis.
Glaukoma kronik
Penegakan diagnosis dilakukan berdasarkan tanda dan gejala trias glaukoma.

Berikut merupakan table 1, yang menunjukkan grading sistem Shaffer


Grade
Lebar sudut
Konfigurasi
Kesempatan
untuk menutup
IV
35-45
Terbuka lebar
Nihil
III
II

20-35
20

I
0

10
0

Terbuka
Sempit
(moderate)
Sangat sempit
Tertutup

Nihil
Mungkin
Tinggi
Tertutup

Struktur pada
Gonioskopi
SL, TM, SS,
CBB
SL, TM, SS
SL, TM
Hanya SL
tidak tampak
struktur

Keterangan :
SL : Schwalbes line, TM : trabecular meshwork, SS : scleral spur, CBB : ciliary body band.
Sistem aliran drainase aqueous humor, terdiri dari jalinan trabekular, kanal Schlemm, jembatan
pengumpul, vena-vena aqueous dan vena episkleral. Adapun jalinan trabekular terdiri dari tiga
bagian yakni jalinan uveal, korneoskleral, dan jukstakalanikular. Jalinan uveal merupakan jalinan
paling dalam dan meluas dari pangkal iris dan badan siliaris sampai garis Schwalbe. Jalinan
korneoskleral membentuk bagian tengah yang lebar dan meluas dari taji skleral sampai dinding
lateral sulkus skleral. Jalinan jukstakanalikular membentuk bagian luar, dan terdiri dari lapisan
jaringan konektif. Bagian ini merupakan bagian sempit trabekular yang menghubungkan jalinan
korneoskleral dengan kanal Schlemm. Sebenarnya lapisan endotel luar jalinan jukstakanalikular
berisi dinding dalam kanal Schlemm yang berfungsi mengalirkan aqueous ke luar.

Tekanan intra okuler normal


Tekanan intra okuler ( TIO ) yang normal berkisar antara 15-20 mmHg. Ini sangat individual, sebab
mungkin ada mata dengan tensi dalam batas-batas normal, tetapi menunjukkan tanda glaukoma. Karena
itu lebih baik disebut tekanan normatif, yaitu dimana TIO tidak menimbulkan akibat buruk. Umumnya
tekanan 24,4 mmHg masih dianggap sebagai batas tertinggi. Tekanan 22 mmHg dianggap High normal
sehingga kita harus waspada.

Tekanan intra okuler ini untuk satu mata tidak selalu tetap, tetapi :
- Pada bernafas ada fluktuasi 1-2 mmHg
- Pada jam 5-7 pagi paling tinggi, siang hari menurun, malam hari menaik lagi.
Hal ini dinamakan variasi diurnal, dengan fluktuasi 3 mmHg.

1.

KLASIFIKASI
Fase Prodorma ( Fase nonkongestif )
Sebelum penderita mendapat serangan akut, ia mengalami serangan prodorma, meskipun tidak selalu
demikian. Pada stadium ini terdapat pengelihatan kabur, melihat halo sekitar lampu atau lilin, disertai
sakit kepala, sakit pada mata dan kelemahan akomodasi. Keadaan ini dapat berlangsung - 1 jam.
Pada pemeriksaan stadium ini didapatkan :
Injeksi perikornea yang ringan
Kornea agak suram ( karena edema )
Bilik mata depan dangkal
Pupil sedikit melebar ( reaksi cahaya lambat )
Tekanan intra okuler meninggi
Bila serangan mereda, mata menjadi normal kembali, kecuali penurunan daya akomodasi tetap ada.
Karena itu bila terdapat penderita dengan kenaikan yang cepat dari presbiopinya, waspadalah terhadap
kemungkinan glaukoma sudut tertutup.
Stadium ini diperberat oleh :
Insomnia
Kongesti vena
Gangguan emosi
Kebanyakan minum
Pemakaian midriatika
Jarak antara serangan dapat terjadi setelah beberapa minggu atau bulan. Tetapi makin lama makin sering
dan serangannya berlangsung lebih lama. Stadium ini dapat berlangsung beberapa minggu, bulan,
bahkan beberapa tahun sebelum menjadi glaukoma akut.
Penatalaksanaan :
Medikamentosa
- Miotikum ( Pilokarpin 2-4 % tiap 20-30 menit )
- Penghambat karbonik anhidrase ( diamox, glaupax, glaukon, corotazol )
Operasi
- Iridektomi perifer : Menghubungkan bilik mata depan dengan bilik mata belakang.
- Operasi filtrasi : Bila pernah beberapa kali mengalami serangan sehingga terjadi sinekhia anterior
perifer ( goniosinekhia )
2. Akut ( Stadium Kongestif )
Pada stadium ini, penderita tampak sangat payah, memegangi kepalanya karena sakit hebat. Glaukoma
akut menyebabkan visus cepat menurun disertai sakit hebat didalam mata yang menjalar sepanjang N.V,
sakit di kepala, muntah-muntah, nausea dan dapat tampak halo disekitar lampu.
Manifestasi Klinis :
Glaukoma Sudut Tertutup Primer Akut adalah glaukoma yang ditandai oleh penutupan anyaman
trabekulum oleh pangkal iris atau sinekia anterior perifer sehingga menyebabkan obstruksi total aliran
keluar humor akuos secara tiba-tiba. Pada jenis ini TIO meningkat secara cepat sebagai akibat dari
penutupan trabekulum yang mendadak oleh iris perifer.
Gejala objektif :

Palpebra : Bengkak
Konjungtiva bulbi : Hiperemia kongestif, kemosis dengan injeksi silier, injeksi konjungtiva, injeksi
episklera
Kornea : keruh, insensitif karena tekanan pada saraf kornea
Bilik mata depan : Dangkal
Iris : gambaran coklat bergaris tak nyata karena edema, berwarna kelabu.
Pupil : Melebar, lonjong, miring agak vertikal, kadang-kadang didapatkan midriasis yang total, warnanya
kehijauan, refleks cahaya lamban atau tidak ada samasekali
Gejala Subjektif :
Nyeri hebat
Kemerahan ( injeksi siliaris )
Pengelihatan kabur
Melihat halo
Mual - muntah
Pemeriksaan Glaukoma :
Funduskopi : Papil saraf optik menunjukkan penggaungan dan atrofi
Tonometri : TIO lebih tinggi daripada stadium nonkongestif
Tonografi : Menunjukkan outflow yang baik. Tetapi bila sudah ada perlengketan antara iris dan trabekula (
goniosinekhia, sinekhia anterior posterior ), maka aliran menjadi terganggu.
Gonioskopi : Pada saat TIO tinggi, sudut bilik mata depan tertutup, sedang pada saat TIO normal,
sudutnya sempit.
Tes Provokasi : Dilakukan pada keadaan yang meragukan.
Tes yang dilakukan : Tes kamar gelap, tes midriasis, tes membaca, tes bersujud ( prone test )
Diagnosa Banding :
Iridosiklitis akut
Konjungtivitis akut
Keratitis
Skleritis
Bila serangan-serangan sudah berulang kali terjadi untuk waktu yang lama, maka terjadi lepasnya pigmen
dari iris yang masuk kedalam bilik mata depan, menimbulkan kekeruhan, juga dapat menempel pada
endotel kornea sehingga nampak seperti keratik presipitat. Dapat juga terjadi perlengketan antara lensa
dengan pupil ( sinekhia posterior ) sehingga pupil menjadi tidak teratur dan sering disangka menderita
uveitis. Iris nampak berwarna putih kelabu karena timbulnya nekrosis lokal. Lensanya menjadi katarak
yang tampak diatas permukaan kapsula lensa depan sebagai bercak-bercak putih ( glaukom flecke ), suatu
tanda bahwa pada mata itu pernah terjadi suatu serangan akut.Bila glaukoma akut tidak segera diobati
dengan baik, dapat timbul perlekatan antara iris bagian tepi dan jaringan trabekula yang disebut sinekhia
anterior perifer, yang mengakibatkan penyaluran keluar humor akuos lebih terhambat lagi.
Faktor resiko :
Hipermetrop ( terdapat penyempitan coa )
Usia lanjut ( pembesaran lensa kristalina )
Tujuan Penatalaksanaan :
Segera menghentikan serangan akut dengan obat-obatan (medikamentosa inisial)
Melakukan iridektomi perifer pada mata yang mengalami serangan sebagai terapi definitif (tindakan
bedah inisial)
Melindungi mata sebelahnya dari kemungkinan terkena serangan akut
Menangani sekuele jangka panjang akibat serangan serta jenis tindakan yang dilakukan.

Medikamentosa
1. Miotikum : Untuk mengecilkan pupil, sehingga iris lepas dari lekatannya di trabekula dan sudutnya
menjadi terbuka.
- Pilokarpin 2-4% 1 tetes tiap 30 menit-1 jam pada mata yang mengalami serangan dan 3 x 1 tetes pada
mata sebelahnya.
2. Penghambat karbonik anhidrase : Mengurangi produksi humor akuos
- diamox, glaupax, glaukon, dsb.
3. Obat Hiperosmotik
- Glycerin 50 % 3 x 100 - 150 cc ( sesuai dengan berat badan ) oral / hari.

4.

Obat pengurang rasa sakit


- Suntikan morfin 10-15 mg. Morfin juga dapat mengecilkan pupil.

Operasi
Tindakan operatif dilakukan bila TIO yang tinggi itu sudah dapat diturunkan. Bila operasi dilakukan pada
saat TIO masih tinggi, dapat menimbulkan glaukoma maligna, disamping kemungkinan timbulnya
prolaps dari isi bulbus okuli dan perdarahan.
1. Iridektomi perifer
Untuk stadium akut yang baru terjadi sehari dan belum ada sinekhia posteriornya. Juga dilakukan pada
mata sebelahnya yang masih sehat sebagai tindakan pencegahan. Dilakukan bila TIO dibawah 21 mmHg
dengan hasil tonografi C = 0,13 atau lebih.
2. Operasi filtrasi ( Iridenkleisis, trepanasi, sklerotomi, trabekulektomi )
Dilakukan bila TIO setelah pengobatan medikamentosa lebih tinggi dari 21 mmHg atau lebih kecil dari 21
mmHg disertai hasil tonografi C = lebih kecil dari 0,13.
2.

Subakut
Glaukoma subakut adalah suatu keadaan dimana terjadinya episode peningkatan TIO yang berlangsung
singkat dan rekuren. Episode penutupan sudut membaik secara spontan, tetapi terjadi akumulasi
kerusakan pada sudut di kamera okuli anterior berupa pembentukan sinekia anterior perifer. Kadangkadang penutupan sudut subakut berkembang menjadi penutupan akut.-Kunci untuk diagnosis terletak
pada riwayat. Akan dijumpai riwayat serangan nyeri unilateral berulang, kemerahan dan kekaburan
penglihatan yang disertai oleh halo disekitar cahaya. Serangan lebih sering pada malam hari dan sembuh
dalam semalam. 2,3,4,5
Gejala Subjektif

Sakit kepala sebelah pada mata yang sakit (timbul pada waktu sore hari karena pupil middilatasi
sehingga iris menebal dan menempel pada trabekulum out flow terhambat)

Penglihatan sedikit menurun

Melihat pelangi di sekitar lampu (hallo)

Mata merah
Gejala Objektif

Injeksi silier ringan

Edema kornea ringan

TIO meningkat
3. Kronis
Glaukoma jenis ini adalah glaukoma primer yang ditandai dengan tertutupnya trabekulum oleh iris
perifer secara perlahan. Bentuk primer berkembang pada mereka yang memiliki faktor predisposisi
anatomi berupa sudut bilik mata depan yang tergolong sempit.Selain sudut bilik mata depan yang
tertutup, gambaran klinisnya asimptomatis mirip glaukoma sudut terbuka primer. Glaukoma tersebut
dapat pula berkembang dari bentuk intermitten, subakut atau merambat ( creeping ) atau dari glaukoma
sudut tertutup primer yang tidak mendapat pengobatan , mendapat pengobatan yang tidak sempurna
atau setelah terapi iridektomi perifer / trabekulektomi ( Glaukoma residual) 2,3,4,5
Pemeriksaan fisik :

Peningkatan TIO

Sudut coa yang sempit

Sinekia anterior ( dengan tingkatan yang bervariasi )

Kelainan diskus optikus dan lapangan pandang.


Penatalaksanaan :
Terapi medikamentosa diberikan baik sebelum terapi iridektomi perifer maupun setelahnya
Tindakan bedah trabekulektomi bila TIO diatas 21 mmHg setelah tindakan Iridektomi perifer dan
medikamentosa.
Tindakan bedah kombinasi trabekulektomi dan katarak bila ada indikasi keduanya.

2.2 KLASIFIKASI
Klasifikasi Vaughen untuk glaukoma adalah sebagai berikut :1.
Glaukoma primer , tidak diketahui penyebabnya, didapatkan
bentuk :- G l a u k o m a s u d u t s e m p i t / t e r t u t u p ( c l o s e a n g l e g l a u c o
m a , a c u t c o n g e s t i v e glaucoma).- G l a u k o m a s u d u t t e r b u k a ( g l a u c o m
a s i m p l e k s , o p e n a n g l e g l a u c o m a , c h r o n i c simple glaucoma).2.
Glaukoma sekunder , t i m b u l s e b a g a i a k i b a t p e n y a k i t l a i n d a l a m
b o l a m a t a , disebabkan :- Perubahan lensa.- Kelainan uvea.- Trauma.- Bedah.Rubeosis.- Steroid dan lainnya.3.
Glaukoma kongenital
- Primer atau infantile.- Menyertai kelainan kongenital lainnya.4.
Glaukoma absolute
, keadaan terakhir suatu glaucoma, yaitu dengan kebutaan totaldan bola mata
nyeri.2
G l au ko m a s u du t t e r t u t u p p ri m e r s e nd i r i d ap at d i b agi d al am 5 t in g k
atand e n g a n p e r j a l a n p e n y a k i t n y a y a n g o v e r l a p p i n g d a n t i d a k
s e l a l u d i m u l a i d a r i progresifitas tingkat awal ke tingkat selanjutnya.
Kombinasi ini dibagi sesuai dengantingkatan klinis, yaitu:1.
Glaukoma sudut tertutup suspek
2.
Glaukoma sudut tertutup intermitten (subakut)
: e p i s o d e s e r a n g a n s i n g k a t d a n rekuren3.
Glaukoma sudut tertutup akut
: kongesti dan post-kongesti4.
Glaukoma sudut tertutup kronik

: tanpa atau dengan glaucomatous damage5.


Glaukoma sudut tertutup absolut
: merupakan tingkat terakhir dari glaukoma akut, pada tingkatan ini mata sudah
mengalami kebutaan total.
2,5

Penting untuk diketahui, jika sudut bilik mata tidak sempit atau sudut terbukaluas, perifer iris
tidak kontak dengan perifer kornea, sehingga sudut bilik mata depan
tidak tertutup dan glaukoma sudut tertutup tidak akan terjadi. Ini
m e r u p a k a n perbedaan dasar antara glaukoma sudut terbuka dengan glaukoma sudut
tertutup.Ketika dislokasi lensa sebagai penyebab tertutupnya sudut bilik mata
makakeadaan ini dikenal dengan glaukoma sudut tertutup sekunder .
Jika glaukoma suduttertutup tidak diketahui penyebabnya, kondisi ini dikenal dengan
glaukoma sudut tertutup primer.
Apabila sudut bilik mata depan tertutup secara cepat dan berat, ini
dikenaldengan glaukoma akut y a n g d i s e r t a i d e n g a n b a n y a k g e j a l a d a n t a n d a .
A p a b i l a penutupan sudut bilik mata depan tidak sempurna dan kadang-kadang saja terjadi,
inidikenal dengan glaukoma sudut tertutup intermittenatau glaukoma sudut tertutupkronik
dan disertai dengan sedikit gejala. Apabila glaukoma sudut tertutu
p i n t e r m i t t e n y a n g t i d a k m e m p u n y a i g e j a l a , i n i d i k e n a l d e n g a n glaukoma su
dut tertutup kreeping .Satu hal penting untuk diketahui bahwa tidak semua sudut bilik
mata sempitakan berkembang menjadi glaukoma akut, dapat terjadi hanya sebagian
kecil
saja,t e r u t a m a p a d a m a t a y a n g p u p i l n y a b e r d i l a t a s i s e d a n g ( 3 , 0 - 4 , 5 m m )
y a n g d a p a t memungkinkan terjadinya blok pupil sehingga dapat berlanjut menjadi sudut
tertutup.Akibat terjadinya blok pupil, maka tekanan intraocular lebih tinggi di
bilik m a t a b e l a k a n g d a r i p a d a b i l i k m a t a d e p a n . J i k a b l o k p u p i l s e m a k i n
b e r a t t e k a n a n intraokuler di bilik mata belakang semakin bertambah, sehingga
konveksivitas irissemakin bertambah juga, ini dikenal dgn iris bombe
, yang membuat perifer iris kontak dengan jalinan trabekuler, dan menyebabkan sudut
bilik mata depan tertutup. Jikatekanan intraokuler meningkat secara drastic akibat sudut
tertutup komplit maka akanterjadi glaukoma akut.Mekanisme lain yang dapat menyebabkan
glaukoma akut adalah: plateau iris dan letak lensa lebih ke anterior. Pada keadaan
seperti ini juga sering terjadi blok pupil.
Slit-lamp Biomikroskopi
Konjungtiva bulbi: hiperemia kongestif, kemotis dengan injeksi silier,injeksi konjungtiva,
injeksi epislera.
Kornea: edema dengan vesikel epithelial dan penebalan struma, keruh,insensitif karena tekanan
pada saraf kornea.
Bilik mata depan: dangkal dengan kontak iridokorneal perifer. Flare dan sel akuos
dapat dilihat setelah edem kornea dapat dikurangi.
I r i s : g a m b a r a n c o r a k b e r g a r i s t a k n y a t a k a r e n a e d e m a , b e r w a r n a kelabu,
dilatasi pembuluh darah iris.

Pupil: oval vertikal, tetap pada posisi semi-dilatasi, kadang-kadang


didapatmidriasis yang total, warna kehijauan, tidak ada reaksi terhadap cahaya
danakomodasi b . T o n o m e t r i S c h i o t z : ( N o r m a l T I O : 1 0 - 2 1 m m H g )
p a d a g l a u k o m a a k u t d a p a t mencapai 50-100 mmHg.c . F u n d u s k o p i : p a p i l s a r a f
o p t i k m e n u n j u k a n p e n g g a u n g a n d a n a t r o f i , s e p e r t i p a d a glaukoma simpleks.
Sehingga cup disk ratio membesar (N = <0,4) (gambar 3 dan4).Sering juga ditemukan optic-disk
edema dan hiperemis.

Gambar 3: saraf optik normal (kiri), penggaungan saraf optik pada glaukoma
akibat peningkatan TIO (kanan)

Gambar 4:
terlihat cup-disk ratio membesar akibat penggaungan saraf optik pada funduskopi
(kanan)
d.Gonioskopi

P e m e r i k s a a n g o n i o s k o p i a d a l a h t i n d a k a n u n t u k m e l i h a t s u d u t b i l i k m a t a den
gan goniolens. Gonioskopi adalah suatu cara untuk melihat langsung keadaan patologik sudut
bilik mata, juga untuk melihat hal-hal yang terdapat pada sudut bilik mata seperti
benda asing. Dengan gonioskopi dapat ditentukan klasifikasiglaukoma penderita
apakah glaukoma terbuka atau glaukoma sudut tertutup dan mungkin dapat menerangkan
penyebab suatu glaukoma sekunder.1
Pemeriksaan gonioskopi ditunda sampai edem kornea berkurang, salah satunya
d e n g a n o b a t y a n g d a p a t m e n u r u n k a n t e k a n a n i n t r a o c u l a r, m i s a l n y a d e n g a n
gliserin topical atau saline hipertonik salap mata.
e . P e m e r i k s a a n l a p a n g p a n d a n g Penting, baik untuk menegakkan diagnosa maupun
untuk meneliti perjalanan penyakitnya, juga bagi menetukan sikap pengobatan
selanjutnya. Harus selaluditeliti keadaan lapang pandangan perifer dan juga sentral.
Pada glaukoma yangmasih dini, lapang pandangan perifer belum menunjukkan kelainan,
tetapi lapang pandangan sentral sudah menunjukkan adanya bermacam-macam
skotoma. Jikaglaukomanya sudah lanjut, lapang pandangan perifer juga memberikan
kelainan berupa penyempitan yang dimulai dari bagian nasal atas. Yang kemudian
akan b e r s a t u d e n g a n k e l a i n a n y a n g a d a d i t e n g a h y a n g d a p a t m e n i m b u l k a n t
u n n e l vision, seolah-olah melihat melalui teropong untuk kemudian menjadi buta.
f . Tes p r o v o k a s i , d i l a k u k a n p a d a k e a d a a n y a n g m e r a g u k a n . Tes yang
dilakukan : tes kamar gelap, tes midriasis, tes membaca, tes bersujud(prone test).
Untuk glaucoma sudut tertutup, yang umum dilakukan adalah tes kamar gelap (karena
pupil akan midriasis dan pada sudut bilik mata yang sempit,ini akan menyebabkan
tertutupnya sudut bilik mata). Caranya adalah ukur TIO awal, kemudian pasien masuk
kamar gelap selama 60-90 menit. Ukur segera TIOnya. Kenaikan 8 mmHg, tes provokasi (+)

Diagnosis Banding:
Glaukoma akut:
a. Uveitis anterior
b. Keratitis
c. Ulkus kornea
Glaukoma kronis:
a. Katarak
b. Kelainan refraksi
c. Retinopati diabetes/hipertensi
d. Retinitis pigmentosa

Pembagian glaukoma sudut tertutup :


a. Stadium prodromal/subakut :

Gejala : sakit kepala sebelah pada mata yang sakit ( timbul pada waktu
sore hari/ ditempat gelap), penglihatan sedikit menurun, melihat hallo
disekitar lampu, mata merah
Tanda : injeksi silier ringan, edema kornea ringan, TIO meningkat
b. Stadium akut/ inflamasi
Gejala : sakit kepala hebat sebelah pada mata yang sakit, kadang
disertai mual muntah, mata merah, penglihatan kabur, melihat hallo
Tanda : injeksi silier, edema kornea, COA dangkal, Tyndall effect (+),
pupil melebar/lonjong, reflek pupil (-), TIO sangat tinggi
c. Stadium kronis
Gejala : sakit kepala hebat sebelah pada mata yang sakit, kadang
disertai mual muntah, mata merah, penglihatan kabur, melihat hallo.6

Tanda : terdapat sinekia closure persisten, injeksi silier, edema kornea,


COA dangkal, Tyndall effect (+), pupil melebar/lonjong, reflek pupil
(-), TIO sangat tinggi
d. Absolut
Gejala dan tanda : penglihatan buta (visus = 0), sakit kepala, mata
merah, TIO sangat tinggi, kesakitan
e. Degenerative
Gejala dan tanda : visus = 0, degenerasi kornea ( bullae,vesikel), mata

perih sekali, TIO tinggi tanpa rasa sakit.

Glaukoma fakolitik
Sebagian katarak stadium lanjut dapat mengalami kebocoran kapsul lensa
anterior dan
memungkinkn protein-protein lensa yang mencair masuk ke dalam bilik mata
depan.
Terjadi reaksi peradangan di bilik mata depan, anyaman trabekular menjadi
edema
dan tersumbat sehingga terjadi peningkatan tekanan intraokular.
Ekstraksi lensa
merupakan terapi definitif, dilakukan segera setelah tekanan intraokular
terkontrol
secara medis dan terapi steroid topikal telah mengurangi peradangan
intraokular.
Tindakan bedah pada mata yang menimbulkan peningkatan tekanan
intraokular yang
bermakna dan sudut sempit atau tertutup dapat menyebabkan glaukoma
sumbatan
siliaris. Segera setelah pembedahan, tekanan intraokular meningkat hebat
dan lensa
terdorong ke depan akibat penimbunan aqueous di dalam dan di belakang
korpus
vitreus. Pasien awalnya merasakan penglihatan jauh yang kabur, tetapi
penglihatan
dekatnya membaik serta diikuti oleh nyeri dan peradangan. Terapi
terdiri atas
siklopegik, midriatik, penekanan aqueous humor dan obat-obat hiperosmotik.
Target IOP may be a percent reduction from a baseline IOP or
may be an absolute IOP reduction. It is generally assumed that aiming to
achieve a target
IOP of at least a 20% reduction from the initial pressure at which damage
occurred is a
useful starting point. For moderate and advanced damage, a 30 and 40%
decrease of IOP

from baseline, respectively, is proposed.

Test how quickly the dark spot in the center of your eye (pupil) closes (constricts)
when bright light is shined on it. If the pupil does not react to light, closed-angle
glaucoma may be suspected.
Look at your eyes for signs of redness or excessive tearing. Redness and
excessive tearing could indicate closed-angle glaucoma. But glaucoma most
often has no symptoms.

Diagnosis

[edit source]

Presentation of glaucoma in aphakic/pseudophakic eyes could be the same as in phakic


glaucoma and thus, collection of good patient history is necessary. Some of the ways to
evaluate the patient presenting with glaucoma include utilizing gonioscopy, optical
coherence tomography, ultrasound biomicroscopy (UBM) and Scheimpflug video
imaging[7][8]. Piette et al. have published UBM findings in a series of UGH patients. Eight
of total nine study patients had posterior chamber intraocular lens. In 5 cases, UBM
showed at least one of lens haptics was in contact with posterior iris pigment epithelium
and in remaining, one of the haptics was embedded into ciliary body [7].

Differential diagnosis[edit source]


At 1-7 days. Pre-existing open angle glaucoma, Retained viscoelastic, Trabecular
edema or angle distortion, Surgical hyphema, Pigment Dispersion, Inflammation,
Pupillary Block, Aqueous Misdirection, Choroidal hemorrhage or effusion.
At 1-7 weeks. Pre-existing open angle glaucoma, Vitreous in the anterior chamber,
Steroid-induced glaucoma, Ghost cell glaucoma, Lens particle glaucoma, Neovascular
glaucoma.
After 2 months. Pre-existing open angle glaucoma, Ghost cell glaucoma, Lens particle
glaucoma, Uveitis-Glaucoma-Hyphema syndrome, Pigment Dispersion, Chronic uveitis,
Epithelial downgrowth or fibrous ingrowth, Pupillary block [10].

Chronic Angle-Closure Attacks


Developed for the use in prevalence surveys, it identifies 3 stages in the natural
history of angle closure:
Primary angle-closure suspect: an "occludable angle" with normal IOP,
optic disc, and visual field, without evidence of peripheral anterior
synechiae (PAS)
Primary angle closure: an "occludable angle" with either raised IOP and/or
primary PAS; optic disc and field normal
Primary angle-closure glaucoma: primary angle closure with evidence of
glaucomatous damage to optic disc and visual field

Mekanisme yang paling berkontribusi dalam kehilangan visual pada


glaukoma adalah atrofi sel ganglion retina yang menyebabkan penipisan
lapisan nervus dan nuklear dalam pada retina dan hilangnya akson pada
nervus optikus.
Optic disc mengalami atrofi dan optic cup membesar. Iris dan korpus
siliaris juga mengalami atrofi, dan prosesus siliaris mengalami degenerasi hia
lin.
Efek peningkatan tekanan intraokular dipengaruhi waktu dan besarnya
peningkatan tekanan. Pada glaukoma sudut tertutup akut,tekanan intraokular
mencapai 60-80 mm Hg, menyebabkan kerusakan iskemik akut pada iris denganedema
kornea dan kerusakan nervus optikus. Pada glaukoma sudut terbuka primer, tekanan
intraokular biasanya tidak meningkat di atas 30 mm Hg dan kerusakan sel
ganglion retina terjadi pada jangka waktuyang lama (beberapa tahun).

Glaucomatous optic nerve demonstrating notching of the disc rim superiorly.


There is also sloping of the temporal disc rim.

Clinical evaluation of the optic disc can be performed via indirect or direct
ophthalmoscopy techniques

Slit lamp indirect ophthalmoscopy is associated with use of a 78 or 90 diopter


handheld lens, a Hruby lens, or a posterior pole contact lens

Photographic documentation of the optic disc and retinal nerve fiber layer is useful
for baseline comparison

Newer disc and/or nerve fiber layer imaging techniques (e.g. OCT, HRT, GDx) are
promising and may assist in clinical evaluation

Characteristic features of glaucomatous optic nerve include:


o

Generalized or focalized increase in the optic cup size and in the cup-disc ratio

Vertical enlargement of the optic cup as a result of retinal nerve fiber loss
and/or disc rim loss (especially at the superior and inferior poles)

Asymmetric cupping ( 0.2 cup-disc ratio difference) between the two eyes

Changes in vessel configuration and caliber

Splinter hemorrhages

Increased visibility and thinning of the lamina cribrosa

Narrowing or notching of the neural rim

Glaucomatous cupping of the optic nerve.

Comments on the above two disc photographs (from the same patient):
o

Noticeable asymmetry of optic discs

Advanced glaucomatous cupping of the right optic nerve

Localized rim loss inferiorly and baring of the circumlinear vessel (left eye)

Nasalization and bayoneting of the vessels (more apparent in the right eye)

Baring of the lamina cribrosa (right eye)

Open -Angle

Phacolytic glaucoma in a patient with mature cataract.

A form of lens-induced open-angle glaucoma.

Caused by the leakage of lens protein (from a mature or


hypermature cataract) into the aqueous humor, thereby
causing obstruction of aqueous outflow.

Clinical features:
o

Symptoms: may present as sudden or insidious onset


of ocular pain and worsened vision

Signs:

Occurs unilaterally (majority of cases)

Conjunctival hyperemia (associated)

Acutely elevated intraocular pressure (may


reach as high as 80 mmHg)

Diffuse corneal edema

Inflammatory cells in the anterior chamber

Presence of white patches on the anterior lens

capsule probably representing phagocytosis of


lens protein by macrophages

On gonioscopy evaluation, the anterior


chamber angle appears open

Management:
o

Anti-inflammatory therapy

Anti-glaucoma medication(s)

Cataract removal surgery (the IOP usually returns to


normal in several days)

Lens damage subluxation or


dislocation
Partial zonular rupture results in lens subluxation and complete rupture in lens
dislocation, either anteriorly into the AC or posteriorly into the vitreous. These
ruptures result from blunt or penetrating injuries and suggest a significant injury.
However, in children with underlying zonular fragility (such as Marfan syndrome
and homocystinuria, or in buphthalmic eyes) trivial trauma can dislocate the lens.

Mechanism of glaucoma
A subluxed lens leads to angle-closure glaucoma by forward displacement of the
lens-iris diaphragm narrowing the angle, and/or by a secondary pupillary block
mechanism. Anterior dislocation can result in the lens becoming trapped in the
pupil, causing acute angle closure from secondary pupillary block or, if
completely dislocated into the AC, may cause raised IOP by reverse pupil block.
Posterior dislocation is less likely to lead to glaucoma. However, there is still a
possibility that vitreous can occlude the pupil and cause acute angle closure, or
that if the lens capsule has been breached, leached proteins can cause an
inflammatory response leading to a secondary uveitic glaucoma

(phacoanaphylactic glaucoma). A posteriorly dislocated lens that becomes


cataractous can also lead to phacolytic glaucoma if it leaks lens proteins.
Repeated episodes of raised IOP result in angle damage. So even in the
presence of normal IOP, finding PAS on gonioscopy and other signs of glaucoma
is highly suggestive of intermittent raised IOP from angle closure secondary to
lens subluxation/dislocation. However, it may be difficult to distinguish this from
previous angle damage in an eye that has had significant previous trauma.
Children are often not able to describe the symptoms of intermittent angle
closure with raised IOP, and a careful history from parents probing for symptoms
suggestive of episodic eye pain, headaches, and photophobia may help.

Management
Topical and systemic glaucoma medications are used in the acute situation.
Following anterior lens dislocation, pilocarpine may be helpful to keep a mobile
lens in the posterior segment as a temporizing measure. However, treating the
underlying cause of the secondary glaucoma is required, so lens extraction might
be necessary. If elevated IOP remains an issue, further glaucoma surgery, such
as implantation of a glaucoma drainage device (GDD) may be required. For a
more detailed approached to management of lens subluxation /dislocation, refer
to connective tissue disorders in section 2 (See Lens damage subluxation or
dislocation.) .
Pearl: Temporizing measures for a child presenting with a dislocated crystalline
lens in the AC: dilate the pupil with a short-acting mydriatic eye drop, keep the
child supine and face up until the lens has dropped back into the vitreous cavity,
then instill pilocarpine to constrict the pupil.

Trauma
Definition and incidence
Trauma is usually classified as blunt or penetrating both types can lead to
secondary glaucoma. The presentation may be immediate at the time of the
injury (acute or delayed), or develop over a period of time after the injury
(chronic). Most chronic presentations are painless and slow in onset so patients
at high risk of glaucoma should have regular lifelong monitoring of their
intraocular pressure (IOP). Occasionally a later-onset form may present with
sudden onset of pain and photophobia from raised IOP (classically seen after
surgical closure of a cyclodialysis cleft, or in some neovascular glaucoma
patients).

Mechanism of glaucoma
A variety of mechanisms may contribute to secondarily raised IOP; they are
determined by the nature and severity of the injury, as well as its management.
Predictors for the development of chronic glaucoma after injury are increased
angle pigmentation, higher baseline IOP, absence of cyclodialysis cleft,
hyphema, angle recession greater than 180 degrees, and lens injury.1 The
various mechanisms for glaucoma and approaches to their management are
discussed below.

Hyphema
Hyphema can be caused by either blunt or penetrating injury, but when it is a
result of penetrating trauma, its management and role in glaucoma are dictated
by the overall globe injury. In blunt trauma situations hyphema is caused by tears
of the iris, iris root, and ciliary body. There may also be recurrent hemorrhage
(re-bleed) from the original site, which can exacerbate existing ocular
hypertension (OHT) or cause acutely raised IOP a few days (typically 3-5 days)
after the injury.

Mechanism of glaucoma
This is an open-angle glaucoma mechanism with pre-trabecular meshwork (TM)
obstruction by red blood cells (RBCs), accompanying inflammatory mediators,
and/or clot. The likelihood and severity of IOP elevation is proportional to the
degree of hyphema2 and can be extremely high, requiring urgent attention.
Concomitant damage to the angle structures, if present, may compound the
elevated IOP, or mitigate it if there is a cyclodialysis cleft or ciliary body damage.
Be aware that in cases of sickle cell disease and trait, significantly elevated IOP
can accompany a relatively benign-appearing hyphema. (See Special
considerations in sickle cell disease (SCD) and sickle cell trait (SCT).) .
More rarely, an acute angle-closure situation can develop from secondary
pupillary block by a large blood clot. Posterior synechiae (PS) and peripheral
anterior synechiae (PAS) may develop from prolonged or more severe hyphema,
which can also predispose to angle closure.

Management
Management in the acute situation is directed at globe integrity and controlling
underlying risks of hemorrhage or re-bleed. Close monitoring and medical
treatment of raised IOP will be sufficient in most cases. Cycloplegia, topical
steroids, and limitation of physical activity are also advised. If, despite
medications, IOP is considered too high for the safety of the optic nerve or it risks
blood staining of the cornea, surgery may be required. The World Glaucoma
Association (WGA) Childhood Glaucoma consensus group found general
agreement that situations requiring prompt surgery are total hyphema, partial
hyphema with IOP sustained at greater than 30 mmHg on maximally tolerated
medical therapy, and development of corneal blood staining.3 There was,
however, less consensus on the surgical procedure of choice. Although anterior
chamber (AC) washout of the hemorrhage is agreed by many, the role of
trabeculectomy at the time of washout is less clearly defined. Angle surgery in
the form of gonioaspiration has also been reported for small hypertensive
hyphemas.4 One disadvantage of early surgery, however, is that deflating the
globe and introducing irrigation or instruments into the eye may disturb the clot

and precipitate fresh bleeding. These risks must be weighed against each other
when determining the most suitable approach for each case.

Pemeriksaan pada mata selanjutnya memberikan gambaran kornea yang


jernih, ini menandakan gejala penglihatan kabur yang mungkin disebabkan
oleh terganggunya fungsi korena sebagai media refraksi, dapat
disingkirkan. Kemudian lebih dalam lagi terlihat opasitas pada lensa.
Kemudian secara sederhana, dilakukan pemeriksaan shadow test untuk
mengetahui fase opasitas lensa tersebut, serta mengarahkan kemungkinan
diagnosis ke arah katarak. Hasil pemeriksaan yaitu shadow test negatif,
dimana masih dapat terlihat bayangan iris pada sebagian permukaan
lensa. Hal ini pada katarak menunjukkan fase imatur. Kemudian untuk
mengetahui lokasi terjadinya opasitas lensa tersebut, dilakukanlah
pemeriksaan dengan menggunakan slit lamp. Kemudian diadapatkan
bahwa opasitas terdapat pada bagian nukleus dan subkapsular lensa, yang
umum terjadi pada proses degeneratif. Juga pada pemeriksaan funduskopi
langsung, media tampak keruh yang sering terjadi pada pemeriksaan
funduskopi pada mata katarak. Hal ini membantu penegakan diagnosis
mata kanan pasien ke arah katarak imatur.

Indications for Glaucoma Surgery


(http://www.worldglaucoma.org/consensus-2/)

The decision for surgery should consider the risk/benefit ratio. Although
a lower IOP is generally considered beneficial to the eye, the risk of vision
loss without surgery must outweigh the risk of vision loss with surgery.

Surgery for glaucoma is indicated when:


a. Optimum medical therapy and/or laser surgery fails to sufficiently lower

IOP.
b. A patient does not have access to or cannot comply with medical therapy.

Clinicians should generally measure IOP more than once and preferably at
different times of day when establishing baseline IOP prior to surgery. When
IOP is markedly elevated, a single determination may be sufficient.

Progression of glaucoma, considering both the structural and functional


integrity of the optic nerve, is clearly a threat to vision and strongly influences
the threshold for surgery.

Ongoing care of the patient with glaucoma requires careful periodic evaluation
of structure and function.

Efforts should be directed at estimating the rate or risk of progression.


A greater rate or risk of progression may lower the threshold for surgery but
must be balanced against the risk and benefits of surgery and the life expectancy
of the patient.
Comment: An elderly patient with slow progression may suffer no effect
on quality of life during his/her lifetime.
Comment: Advancing glaucomatous optic disc damage or retinal nerve fiber
loss without detected visual loss is progression and can in certain circumstances
be an indication for surgery.

Risk factors for progression of glaucoma are emerging from prospective studies.
(AGIS-older age, lower education, male sex, diabetes; CNTGS-female sex, migraine;
EMGT- high IOP, pseudoexfoliation, worsening visual fields during follow up,
disc hemorrhage, advanced stage of disease.) Presence of these risk factors
may alter target IOP or lower the threshold to surgery.

Comment: Fellow eye vision loss from glaucoma may lower the threshold
IOP for consideration of surgery. It is not clear that it is a risk factor for
threat to vision.
Comment: Family history of blindness from glaucoma is not a known risk
factor for vision loss, but such patients warrant close observation.

Primary surgery may be indicated on the basis of socioeconomic or logistic


constraints.

Comment: There is insufficient evidence to recommend primary surgery


in all patients.

Patients who are unable or unwilling to use their medical therapy as prescribed
represent failures of treatment efficacy and may need surgery to achieve consistent
IOP reduction, even when isolated IOP measurements appears normal at office
visits.

The extent and location of damage may alter the threshold for surgery. Patients
with advanced damage or damage threatening central vision may require lower
IOP than those with early disease.

In fact, Baum et al found digital palpation to yield


a moderate success rate for identifying elevated
IOP and concluded that although this technique is
perceived to be inaccurate, it can definitely alert
physicians to marked increases in IOP (.30 mm
Hg).7 (file:///C:/Users/Win7/Downloads/OPTO14096-importance-of-digital-palpation-as-aroutine-technique-for-i_092410.pdf)

Target IOP in Clinical Practice


(http://www.worldglaucoma.org/consensus-4/)
1. The target IOP is the IOP range at which the clinician judges that progressive
disease is unlikely to affect the patients quality of life.
Comment: The burdens and risks of therapy should be balanced against
the risk of disease progression.
2. The determination of a target IOP is based upon consideration of the amount
of glaucoma damage, the IOP at which the damage has occurred, and the life
expectancy
of the patient, and other factors including status of the fellow eye and family
history of severe glaucoma.

Comment: At present, the target IOP is estimated and cannot be determined


with any certainty in a particular patient.
Comment: There is no validated algorithm for the determination of a target
IOP. This does not, however, negate its use in clinical practice.
3. It is recommended that the target IOP be recorded so that it is accessible
on subsequent patient visits.
4. The use of a target IOP in glaucoma requires periodic re-evaluation.
Comment: This entails examination of the optic nerve and assessment of
visual function to detect glaucomatous progression, the effect of the therapy
upon the patients quality of life, and whether the patient has developed any
new systemic or ocular conditions that might affect the risk/benefit ratio of
therapy.
Comment: During the re-evaluation, it is essential to determine whether
the IOP target is appropriate and should not be changed, or that it needs to
be lowered or raised.

Laser iridoplasti
Merupakan tindakan alternatif jika tekanan intraokular gagal
diturunkan secara intensif dengan terapi medika mentosa. Bila tekanan
intraokularnya tetap sekitar 40 mmHg, visus jelek, kornea edema dan
pupil tetap dilatasi. Pada laser iridoplasti ini pangaturannya berbeda
dengan pengaturan pada laser iridektomi. Disini pengaturannya dibuat
sesuai untuk membakar iris agar otot spingter iris berkontraksi, sehingga iris
bergeser kemudian sudutpun terbuka. Agar laser iridoplasti berhasil maka titik
tembakan harus besar, powernya rendah dan waktunya lama.
Aturan yang digunakan ukurannya 500 ?m (200-500 ?m), dengan power
500 mW (400-500 mW), waktunya 0,5 detik (0,3-0,5 detik). Pada
penelitian ahli terhadap 20 mata penderita glaukoma akut, dari tekanan
intraokular rata-rata sebelum iridoplasti 43,2 mmHg turun menjadi rata-rata 17
mmHg, pada 2 jam setelah dilakukan iridoplasti laser. 1,2,5,11
Iridektomi insisi dilakukan pada pasien yang tidak berhasil dengan
tindakan laser iridektomi. Seperti;

? Pada situasi iris tidak dapat dilihat dengan jelas karena edema
kornea, hal ini sering terjadi pada pasien glaukoma akut berat yang
berlangsung 4 - 8 minggu.
? Sudut bilik mata depan dangkal, dengan kontak irido-korneal yang
luas.
? Pasien yang tidak kooperatif.
? Tidak tersedianya peralatan laser.1,6
5.1. Iridektomi bedah insisi
Jika iridektomi bedah insisi yang dipilih, maka pupil dibuat semiosis
mungkin, dengan menggunakan miotik tetes atau asetilkolin intrakamera. Peritomi superior 3 mm, walaupun beberapa ahli mata memilih
tidak melakukan peritomi. Kemudian dilakukan insisi 3 mm pada korneasklera 1 mm di belakang limbus. Insisi dilakukan agar iris prolap.Bibir
insisi bagian posterior ditekan, sehingga iris perifer hampir selalu prolaps
lewat insisi, dan kemudian dilakukan iridektomi. Bibir insisi bagian
posterior ditekan lagi diikuti dengan reposisi pinggir iridektomi. Luka
insisi kornea ditutup dengan satu jahitan atau lebih, dan bilik mata depan
dibentuk kembali dengan NaCl 0,9% melalui parasintesis. Setelah
operasi selesi, fluoresen sering digunakan untuk menetukan ada
tidaknya kebocoran pada bekas insisi. Oleh karena kebocoran dapat
meningkatkan
seperti bilik mata depan dangkal.
1,2,7,14
Ad. 6. Ekstraksi lensa
Apabila blok pupil jelas terlihat berhubungan dengan katarak,
ektraksi lensa dapat dipertimbangkan sebagai prosedur utama.
Walaupun iridektomi laser dapat menghentikan serangan akut akibat
blok pupil, namun operasi katarak baik dilakukan agar lebih aman untuk
waktu yang akan datang.4,5,8
Relative afferent pupillary defect (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3588123/)

Although glaucoma usually affects both eyes, it is sometimes asymmetric. This can
be detected with the relative afferent pupillary defect (RAPD) test see article on
page 58. As other diseases of the retina or optic nerve can also cause a RAPD (e.g.
optic atrophy), all patients with RAPD should always be referred for further
assessment. Remember: a RAPD is not only caused by a cataract.

7th Consensus Meeting:


Medical Treatment of Glaucoma
Fort Lauderdale, FL, May 1, 2010

(http://www.worldglaucoma.org/consensus-7/)
Section 1 Who should be treated?

In general, treatment is indicated for patients with glaucoma or glaucoma


suspects who are at risk for developing functional impairment or decrease
in vision-related quality of life from the disease.
Comment: Treatment is generally indicated when the risks of progressive
disease outweigh the risks and potential side effects of treatment.

All treatment decisions should take into account the presence of coexisting
ocular conditions, the patients life expectancy and general health status,
as well as his/her perceptions and expectations about treatment.

The rate of disease progression is of fundamental importance in considerations


of treatment for glaucoma patients. Treatment is indicated for patients
whose rates of progression will most likely result in loss in vision-related
quality of life over the projected remaining years of life.

Treatment is generally indicated for patients with definitive glaucomatous


visual field loss, particularly in circumstances when such loss has been
determined to be progressive at a measurable rate.

Changes of the optic nerve and/or retinal nerve fiber layer (RNFL) characteristic
of glaucoma predict functional vision loss in glaucoma and thus patients
with such documented structural evidence of progressive damage should generally
be treated with intraocular pressure lowering therapy.

The decision regarding whether or not to treat glaucoma suspects should


involve a consideration of risk factors for disease development, including
age, family history of glaucoma, intraocular pressure, central corneal thickness,
presence of pseudoexfoliation, disc hemorrhages and measures of structural
and functional integrity of the optic nerve head and retinal nerve fiber
layer.
Comment: While it is clear that progress has been made in establishing
risk factors for glaucoma progression, much work remains to be done to better
refine risk models. Nonetheless, the factors that affect the risk of progression
help decide the expected prognosis of the individuals untreated disease
and thereby the frequency of follow-up and aggressiveness of the therapy
to be undertaken.

Imaging of the optic nerve head and retinal nerve fiber layer can provide
useful predictive information about the risk of developing functional loss
from glaucoma and thus can serve as a surrogate predictor of such vision
loss.

Selective visual function tests may be predictive of functional loss


in glaucoma patients and thus may be used as complementary tests to assist
in treatment decisions.

Predictive models or risk calculators may assist clinicians in providing


more objective estimates of the risk of glaucoma development for individual
patients.
Comment: Predictive models are based on restricted populations of
patients that were selected based on strict inclusion and exclusion criteria
and that may not be representative of all patients seen in everyday clinical
settings. Use of these models should be restricted to those patients who
are similar to the ones included in the studies used to develop and validate
such models and calculators.

Section 2 Treatment goals

The target IOP is the IOP range at which the clinician judges that the
estimated rate of progression is unlikely to affect the patients quality
of life.
Comment: Although recommended by most experts, there is insufficient
evidence that using target IOP is associated with better clinical outcomes.

The determination of a target IOP is based upon consideration of the


amount of glaucoma damage, the rate of progression, the IOP at which the
damage has occurred, the life expectancy of the patient, and other factors
including status of the fellow eye and family history of severe glaucoma.

The use of a target IOP in glaucoma requires ongoing re-evaluation and


adjustment.

The benefits and risks of escalating treatment to reach a target IOP


must be balanced.
Comment: Uncertainties regarding the short- and long-term variations
of IOP, accuracy of tonometer readings, patients life expectancy, adherence
to therapy and estimated progression rates remain unresolved.

Treatment goals include IOP, visual function and structural (optic disc,
RNFL) outcomes and QOL.
Comment: It is uncertain whether patient reported outcomes of glaucoma
can be applied in clinical practice, and whether they capture clinically
meaningful progressive changes.

Section 3 Drugs

All eye drops have the potential for systemic effects, which may be
decreased with a lower concentration, reduced frequency of administration
and using nasolacrimal occlusion or gentle eyelid closure.
Comment: During pregnancy and lactation, the risks and benefits of
these medications should be evaluated for each patient.

Topical cholinergic agents can effectively reduce intraocular pressure.

Comment: In open-angle glaucoma, cholinergics enhance aqueous outflow


through the trabecular meshwork by means of ciliary muscle contraction.
Comment: Cholinergics may open the drainage angle in certain instances
of angle closure by stimulating the iris sphincter muscle.
Comment: The effects of pilocarpine are representative of this class.
Pilocarpine has an additive hypotensive effect to -blockers, alpha-2 adrenergic
agonists, and carbonic anhydrase inhibitors. It can be additive to prostaglandin
analogues in some patients.
Comment: Common ocular side effects of pilocarpine, which limit its
use, include brow-ache, induced myopia, and dimness of vision. Comment:
TID or QID dosing is associated with poor adherence.

Indirect cholinergic agents are reserved for open-angle glaucomas in


aphakic or pseudophakic eyes.
Comment: Indirect cholinergic agents are cataractogenic and also
may cause adverse systemic effects.

Topical -blockers are effective IOP-lowering agents.


Comment: Topical -blockers decrease IOP by reducing aqueous humor
formation. All non-selective -blockers have comparable IOP-lowering efficacy.

Comment: Topical and systemic -blockers are poorly additive with


respect to lowering IOP.
Comment: Although some -blockers have intrinsic sympathomimetic
activity (ISA) or -blocking properties, their clinical properties are similar
to those of other non-selective -antagonists. However, ISA may reduce
respiratory
and cardiovascular side-effects related to -blockade.

Timolol, and possibly all other -blockers, have minimal IOP-lowering


efficacy during sleep.
Comment: Non-selective topical -blockers are contraindicated in
patients with asthma, chronic obstructive pulmonary disease (emphysema and
bronchitis) some cases of congestive heart failure, bradycardia, and heart
block.

The IOP-lowering efficacy of betaxolol, a relatively selective -1-blocker,


is less than that of non-selective -blockers.
Comment: Betaxolol is relatively safer than a non-selective -blocker
in patients with known reactive airway disease.

Carbonic anhydrase inhibitors (CAIs) are effective IOP-lowering agents.

Comment: CAIs reduce IOP by suppressing aqueous humor production


through inhibition of the isoenzyme carbonic anhydrase II.
Comment: CAIs are the only category of drugs available commercially
in both topical and systemic formulations to lower IOP.
Comment: For systemic CAIs, major side effects include paresthesia,
malaise, gastrointestinal disturbances, renal disorder, blood dyscrasia,
and metabolic acidosis.
Comment: For topical CAIs, side effects include
ocular burning, stinging, bitter taste, superficial punctuate keratopathy,
blurred vision, tearing, headache, and transient myopia.
Comment: CAIs may increase ocular blood velocity; however, there
is insufficient evidence for any clinical benefit of this effect for glaucoma
patients.
Comment: Topical CAIs and systemic CAIs are poorly additive with
respect to lowering IOP.

Systemic CAIs are contraindicated with sulfonamide allergy, with depressed


sodium and/or potassium blood levels, and in metabolic acidosis.

The non-selective adrenergic agonists, epinephrine and its pro-drug


(dipivefrin) are effective IOP-lowering agents.
Comment: Adrenergic agonists reduce IOP by decreasing aqueous formation
and increasing outflow.
Comment: Adrenergic agonists are contraindicated in infants and children
because of systemic side effects.
Comment: IOP-lowering efficacy of adrenergic agonists is less than
that with timolol. This class is often additive to prostaglandin analogues
but not to non-selective -blockers.
Comment: Local side effects
include hyperemia and blepharoconjunctivitis. Systemic circulatory effects
include hypertension and tachyarrhythmias.

Selective alpha-2 adrenergic agonists reduce IOP by suppressing aqueous


inflow and increasing outflow. They also may affect episcleral venous pressure.

Comment: Systemic side effects with selective alpha-2 adrenergic


agonists include dry mouth, drowsiness and hypotension.

There is insufficient evidence for neuroprotection by selective alpha-2


adrenergic agonists in humans.

Bunazosin, a selective 1A antagonist, increases uveoscleral outflow.

Comment: Although it is well-tolerated, the hypotensive effect of


topical bunazosin is weaker than that of topical timolol.

Prostaglandin analogues (PGAs) are the most effective IOP-lowering agents


of all topical glaucoma medications, and generally are first line therapy.

Comment: PGAs lower IOP by increasing uveoscleral aqueous humor outflow,


and may also have an effect on outflow facility.
Comment: Common side effects of prostaglandin analogue drops include
conjunctival hyperemia, reversible increase of eyelash length, thickness
and pigmentation, irreversible increase of iris pigmentation, and increase
of eyelid skin pigmentation. Rare side effects include uveitis, reactivation
of herpetic keratitis and cystoid macula edema.
Comment: PGAs are systemically safe, but are relatively contraindicated
in pregnancy, as are all glaucoma medications.

Preservatives used for multi-dose topical ophthalmic medications can


cause ocular surface changes.
Comment: Benzalkonium chloride (BAK), in particular, has been associated
with ocular surface changes in chronic use. Alternative preservative systems
are increasingly used in multi-dose bottles in an effort to decrease the
potential for deleterious effects on ocular surface. However, direct comparisons
between these agents are lacking.
Comment: Preservative free systems, in the form of unit dose packages,
are a viable alternative to traditional multi-dose bottles. In theory, they
may have fewer ocular surface effects, however, direct comparisons with
preserved agents are lacking.

Section 4 Selection of drugs

Only the IOP lowering effect should be considered to define the comparative
efficacy of an ocular hypotensive agent.

Initiation of therapy: prostaglandin analogues (PGA) are recommended


as first choice agents for most eyes with glaucoma.

IOP reduction with initial monotherapy should be at least 20% from baseline.

Comment: IOP reduction of less than 10% should be considered as


nonresponse.
Comment: Switching drugs within the PGA class may, upon occasion,
provide greater IOP lowering.

Adjunctive therapy is indicated when existing therapy fails to reach


the target IOP.
Comment: Adjunctive therapy should be limited to
one drug from each class.
Comment: The efficacy of a drug when used as monotherapy is usually
less when used as an adjunctive agent.

Provided the use of the combination product is as efficacious as the


two components administered independently, fixed-combinations are preferred
when possible over the use of two separate bottles due to convenience, reduced
amount of preservative instillation and possible improved adherence.
Comment: Evidence is lacking that fixed combination products provide
better outcomes than the individual components delivered separately.

Surgery is indicated when medical therapy fails to adequately lower


the intraocular pressure or prevent progression, the risk of progression
remains too high despite the use of medical therapy, or is not possible
due to allergy, intolerance, poor adherence or lack of availability.

Section 5 Medical treatments of other types of


open-angle glaucomas

PG analogs are first choices for monotherapy in pseudoexfoliative glaucoma


and pseudoexfoliation syndrome with ocular hypertension when treatment is
required.
Comment: Pilocarpine can reduce iris movements in eyes
with pseudoexfoliation and, therefore, may reduce deposition of exfoliation
material or pigment in the trabecular meshwork.

PGAs are first choices for monotherapy in pigmentary glaucoma.


Comment: Pilocarpine can be effective in pigmentary glaucoma in reducing
reverse pupillary block and diminishing iris movements.

Medical treatment of inflammation is first line treatment for uveitic


glaucoma.

Section 6 Drug delivery

Poor adherence / perseverance / dyscompliance are major problems in


glaucoma. Patients taking fewer doses than prescribed are at risk of having
worse outcomes than those taking a higher proportion.
Comment: On average, most studies of glaucoma patients estimate that
about 70% of doses are taken. This may vary depending on duration of treatment,
number of medications taken and severity of the disease.

Patient self-report of adherence is often overestimated.


Comment: Physicians do not accurately predict which patients are
poorly compliant.
Comment: While not readily available, better systems
to reliably and easily monitor patient drop taking behavior are desirable

since they would provide feedback for physicians to better identify patients
with difficulty adhering to drop regimens.

Risk factors for lower adherence rates have been identified and include
younger and older age, race/ethnicity, and depression.
Comment: While poor adherence can occur in all patients, additional
efforts may be required in patients with these risk factors.

Patients often have difficulty properly administering drops to their


eyes.
Comment: Efforts to improve adherence should address physical barriers.

Comment: Observation of patient eye drop administration can detect


patients that are unable to instill them.

For at least the next several years, topical IOP-lowering medication


will remain the mainstay for glaucoma treatment.
Comment: Despite limitations (inconvenience, dependence on the compliance
of the patients and well-described adverse events in particular on the conjunctiva),
topical anti-glaucomatous medication is (relatively) cheap, easily available,
and generally safe, and it is reversible, should side effects arise.

A change in the preservatives of eye drops to a less toxic and more


tissuefriendly formulation, and/or the development of preservative free
drug delivery systems is needed to reduce the preservative related side-effects
and tissue toxicity while delivering enough drug to control the intraocular
pressure.

Non-IOP dependent therapy for glaucoma and also new drug delivery systems
remain a high priority unmet medical need in glaucoma management.

Section 7 Health economics

There are wide variations in reported costs of glaucoma therapy across


nations.
Comment: There is little information from developing countries.

Comment: With the exception of the US, the differences in costs of


therapy are largely related to the level of economic development in various
regions of the world.

Cost of one time surgery is substantially greater than medication in


the short term, but lower in the long term.
Comment: Changes in medication costs may alter this.
Comment: Surgical failure may alter this because of the need for
additional medication and/or surgery.

Generic drugs potentially can reduce direct treatment costs.


Comment: More studies are needed comparing generic and branded drugs.

Side effects of glaucoma medications have minimal economic impact.

There do not appear to be significant differences in the cost of fixed


combination products compared with individual components.

Failed medical therapy is defined differently in each country and depends


on the cost and availability of medical therapy and surgical alternatives
in that country.
Comment: Pricing of glaucoma medications is not transparent.

Section 8 Non-pharmaceutical medications and


approaches

There is a paucity of clinical trial information examining neuroprotective


effects of non-pharmaceutical compounds (alternative or complementary therapies)
for glaucoma.

Comment: Bio-availability of these natural compounds has not been


well studied, and clinical studies of their efficacy and safety are needed.

Exercise reduces IOP, but the extent, duration and clinical significance
are unclear.
Comment: Exercise also can increase ocular blood flow, but the significance
of this is unknown.

Acupuncture has been reported to lower IOP and increase ocular blood
flow.
Comment: The reported results are inconsistent and additional studies
are needed before it is employed in clinical practice.

Section 9 Neuroprotective therapies

A neuroprotective strategy for glaucoma is defined as a therapy that


prevents the occurrence or progression of optic neuropathy and preserves
visual function by mechanisms other than IOP lowering.

Agents that lower IOP have been shown to protect the optic nerve from
glaucoma progression.
Comment: Some agents that lower IOP might additionally confer protection
to the optic nerve through mechanisms that are independent of IOP lowering,
but there is insufficient evidence for this dual effect with any agent at
the present time.

Therapeutic approaches for preventing RGC death may aim to prevent primary
or secondary degeneration of retinal ganglion cells.

Evidence from experimental models suggests that neuroprotection could


be conferred by:
a. Inhibiting the pathogenic mechanisms that injure or kill RGCs.

b. Rendering the optic nerve more resistant to injury.

Numerous studies have demonstrated neuroprotection in experimental models


of glaucoma or optic nerve injury, but good evidence demonstrating neuroprotection
in clinical studies is lacking.

Challenges in translating experimental evidence of neuroprotection into


clinical proof may be due to:
a. The therapy may not be effective in humans.
b. The lack of sufficiently robust tools to assess clinically
the state of optic nerve
health.
c. The lack of animal models that are good representatives of
human glaucoma.
d. The lack of well-designed and well-conducted clinical studies.

Current testing paradigms are insufficiently sensitive and specific


to detect change in a logistically feasible time frame. The development
of accurate, sensitive, specific and reproducible clinical tests that provide
information on the current state of health of the optic nerve are required
to increase the feasibility of clinical development of neuroprotective agents.

Comment: A desired embodiment of such clinical testing would allow


detection of progression before the damage is irreversible.

Section 10 Medical management of glaucoma in


infants and children

The primary treatment of glaucoma in infants and young children is surgery.

Comment: In many situations, however, the clinician must treat elevated


IOP medically while awaiting surgery or after a partially-successful procedure.
Comment: Only rarely should medical therapy be the primary treatment
of glaucoma in infants and young children.

Comment: A young child is not a small adult: systemic adverse reactions


rarely seen in adults can occur in young children.

Outflow medications (pilocarpine and prostaglandin analogues) are variably


effective in pediatric glaucomas, whereas aqueous suppressants lower IOP
more consistently.
Comment: Systemic and topical carbonic anhydrase
inhibitors can be safe and effective. If possible, systemic use should be
monitored by a pediatrician.
Comment: Topical beta-blockers are effective; systemic safety is
the major concern. Betaxolol is safer than timolol.
Comment: Topical brimonidine is absolutely contraindicated in children
under two years, and must be used with great caution in older children.
Apraclonidine may be safer, for short-term use, but clinical data is lacking.

Comment: Prostaglandin agonists are less effective in children than


in adults, and are more likely to be effective in older children.
Comment: Miotics are rarely used in phakic children.

Section 11 Treatment of glaucoma in pregnancy

Appropriate management of the pregnant/lactating glaucoma patient requires


balancing the risk to the fetus of treatment against the risk to the mother
if treatment is reduced or suspended.
Comment: While a complete lack of prospective human data complicates
this decision-making process, publications provide a guide.

Like all systemically-absorbed medications that are used during pregnancy


and lactation, the maternal use of topical anti-glaucoma medications carries
risks of teratogenicity, of interference with establishment or maintenance
of pregnancy, or of side effects in the neonate.
Comment: Prostaglandin analogues may be associated with uterine contraction.
Comment: Beta-blockers and alpha agonists can cause serious toxicity
(re spiratory and CNS depression) When possible, these agents should be

withdrawn during the last few weeks of pregnancy.


Comment: Topical CAIs are generally well tolerated.

Laser trabeculoplasty can be a reasonable initial or adjunctive intervention


in pregnant and nursing women.

Filtering surgery, preferably without anti-fibrosis chemotherapy, can


be considered in certain cases.

Section 12 Unmet needs

Identification of biomarkers of retinal ganglion cell dysfunction:

A more reliable tool for measuring the health of retinal ganglion cells
is needed for more effective evaluation of treatment outcome.
There is a need to identify new models to test drugs.

Identification of novel targets for glaucoma treatments that lower IOP


and preserve retinal ganglion cell function should be sought.
Comment: Structural changes in the optic disc or retinal nerve fiber
layer often precede functional changes and could be useful for primary endpoints
in clinical trials.

New agents need not necessarily have enhanced pressure-lowering efficacy


compared with prostaglandin analogues, particularly if they have an additive
effect when used with existing medications.

Continuous IOP monitoring and home tonometry: There are currently no


commercially available devices that allow continuous monitoring of IOP in
humans. Comment: There is insufficient evidence at this time to show that
home tonometry with any device provides accurate and reliable IOP measurement.

Comment: Drugs that provide sustained lowering of IOP throughout


the 24-hour day may be advantageous.
Comment: However, it still is uncertain if additional IOP data from

continuous IOP monitoring or home tonometry provides additional clinical


information to the current measures of IOP peak, mean and fluctuation.

Objective measurement of patient adherence to glaucoma medication: Nonadherence


to treatment regimens is common in glaucoma patients. Addressing the risk
factors for poor adherence and developing new methods to improve adherence
are pivotal to effective delivery of glaucoma treatment.

There is insufficient information regarding current treatment practices


and the most appropriate glaucoma treatment strategies for developing countries.

Regulatory agencies should develop uniform standards for preservatives


and unpreserved medications that could be applied worldwide.

A worldwide color-coding scheme for caps of classes and fixed combination


of glaucoma medications is recommended.

Additional studies of the effects of different treatments on ocular


blood flow and its relationship to glaucoma are needed.

Biomarkers for glaucoma diagnosis and progression are needed.

Improved delivery methods for drug therapies are needed.

A medical treatment is needed to restore retinal ganglion cell function


or regenerate the optic nerve.

Penyebab glaucoma sekunder pasca


bedah katarak intrakapsular atau
ekstrakapsular yang mengakibatkan
terbentuknya goniosinekia pada bibir luka
bedah dan terbentuknya blockade pupil
akibat iridektomi yang tidak adekuat dan
seklusi pupil akibat radang di daerah
pupil.

8. Lensa
Kerusakan yang terjadi pada lensa paska-trauma adalah kekeruhan, subluksasi dan
dislokasi lensa. Kekeruhan lensa dapat berupa cincin pigmen yang terdapat pada kapsul anterior
karena pelepasan pigmen iris posterior yang disebut cincin Vosslus. Kekeruhan lain adalah
kekeruhan

punctata,

diskreta,

lamelar

aau

difus

seluruh

massa

lensa.

Akibat lainnya adalah robekan kapsula lensa anterior atau posterior. Bila robekan kecil,
lesi akan segera tertutup dengan meninggikan kekeruhan yang tidak akan mengganggu
penglihatan. Kekeruhan ini pada orang muda akan menetap, sedangkan pada orang tua dapat
progresif menjadi katarak presenil. Dengan kata lain, trauma dapat mengaktivasi proses
degeneratif lensa.
Subluksasi lensa dapat aksial dan lateral. Subluksasi lensa kadang-kadang tidak
mengganggu visus, namun dapat juga mengakibatkan diplopia monokular, bahkan dapat
mengakibatkan reaksi fakoanafilaktik. Dislokasi lensa dapat terjadi ke bilik depan, ke
vitreus, subskleral, ruang interretina, konjungtiva, dan ke subtenon. Dislokasi ke bilik
depan sering menyebabkan glaukoma akut yang hebat, sehingga harus segera diekstraksi.
Dislokasi ke posterior biasanya lebih tenang dan sering tidak menimbulkan keluhan,
tetapi dapat menyebabkan vitreus menonjol ke bilik depan dan menyebabkan blok pupil
dan

peninggian

TIO.

SECONDARY
Secondary angle closure glaucoma is caused by a myriad of other eye diseases (see
Differential Diagnosis section). There are several secondary causes of angle closure
that involve relative and absolute pupillary block. In phacomorphic glaucoma, the mass
effect of a thickened or intumescent cataract pushes the iris forward and causes
pathological angle narrowing. Forward displacement of the lens in ectopia

lentis or microspherophakia can also push the iris forward and


shallow the angle. Absolute pupillary block occurs when there is no movement of
aqueous through the pupil because of 360 o posterior synechiae between the iris and a

crystalline lens, an intraocular lens, capsular remnants, or the vitreous face. In


secondary angle closure glaucoma without pupillary block, angle closure is due to either
a.) contraction of an inflammatory, hemorrhagic, or vascular membrane in the angle
leading to PAS, or b.) forward displacement of the lens-iris diaphragm, often associated
with ciliary body swelling and anterior rotation.

Mechanisms that push the iris forward from behind


Relative pupillary block (primary angle closure)
Plateau iris configuration (primary angle closure)
Absolute pupillary block 360o posterior synechiae secluding pupil
Aqueous misdirection or malignant glaucoma
Ciliary body swelling, inflammation or cysts
Choroidal swelling, effusions, or detachments
Posterior segment tumors or space-occupying substances (silicone oil or
gas bubble)
Contracting retrolental tissue as seen in retinopathy of prematurity
Anteriorly displaced lens
Encircling retinal bands/buckles
Mechanisms that pull the iris forward into contact with the trabecular
meshwork
Contraction of inflammatory membrane or fibrovascular tissue
Iridocorneal endothelial (ICE) syndrome with migration of corneal
endothelium
Fibrous ingrowth
Epithelial downgrowth
Iris incarceration in traumatic or surgical wound

Diagnosis

[edit source]

Diagnosis of both primary and secondary angle closure glaucoma is based on history
and eye exam. Gonioscopy is the gold standard for evaluating the anterior chamber
angle, but imaging modalities assist in quantifying and objectifying angle characteristics.
To distinguish between primary and secondary causes, the clinician must actively look
for signs and symptoms of possible secondary causes and rule each out before the
patient can be diagnosed with primary angle closure glaucoma .

History[edit source]
History of present illness typical signs and symptoms of acute or subacute angle
closure attacks (see Signs and Symptoms sections) and if patient was upset or in the
dark when symptoms started
Past ocular history
o Trauma can cause zonular weakness or dehiscence allowing lens to displace
anteriorly
o Incisional or laser surgery can cause anterior chamber inflammation or
predispose to epithelial/fibrous ingrowth; may also lead to aqueous misdirection (e.g.
after LPI) or ciliary body engorgement (e.g. after extensive panretinal
photocoagulation).
o History of prior retinal vein occlusion can cause angle neovascularization or
ciliary body engorgement rotating lens forward
Past medical history history of diabetes or carotid stenosis disease that can
cause angle neovascularization
Medications use of systemic medications, such as sulfonamide, topiramate, and
phenothizaines, that may cause ciliary body engorgement or suprachoroidal effusion;
use of medications to treat allergy, bladder dysfunction,
or depression; use of anticholinergics or sympathomimetics that can dilate pupil
Family history of acute angle glaucoma

Physical examination[edit source]


Refractive status hyperopic eyes tend to have shallower anterior chamber angles
which places them at risk for angle closure
Pupil size and reactivity
Slit lamp exam
o Conjunctiva injection
o Cornea clarity, presence of edema, evidence of surgical or traumatic wounds
o Anterior chamber central and peripheral depth, inflammation
o Iris areas of atrophy, mass, neovascularization, or posterior synechiae
o Lens thickness, phacodonesis, subluxation, glaucomflecken (necrosis of
anterior lens capsule; may indicate previous attacks)
Intraocular pressure measurement, preferably with applanation prior to gonioscopy
Gonioscopy of both eyes with indentation to evaluate for appositional versus
synechial angle closure
Evaluation of fundus and optic nerve dilation is often not advisable in primary
angle closure attack until an iridotomy has been performed and/or the acute attack has
resolved as dilation can exacerbate the condition. In contrast, dilation may be
permissible as the appropriate treatment in certain forms of secondary angle
closure. The fundus should be examined for underlying causes leading to the angle
closure.

Signs[edit source]
Signs of a primary anatomic narrow angle on slit lamp exam can be subtle and include a
shallow anterior chamber and an anteriorly bowed iris.

Both primary and secondary forms of angle closure can cause acute angle closure
attacks. The intraocular pressure usually exceeds 40 mmHg and may rise to as high as
80 mmHg. The conjunctiva is significantly injected. The cornea develops stromal and
microcystic edema in response to the acute rise in eye pressure and decompensation of
the endothelial pump mechanism. Iris sphincter ischemia leads to a fixed, mid-dilated
pupil. Sectoral iris atrophy may occur, releasing pigment into the anterior chamber that

dusts the corneal endothelium and anterior lens capsule. The overall anterior chamber
is shallow. The center is usually formed, but the mid-peripheral iris bows forward and
may touch the peripheral cornea. Often there is anterior chamber inflammation. The
fundus is typically difficult to examine because of corneal edema. If visualized, the optic
nerve head may be hyperemic and edematous. The angle is often difficult to examine
with gonioscopy because of corneal edema, but if visualized, reveals contact of the
peripheral iris with cornea.

In the aftermath of an acute attack, pupillary distortion may result if there is permanent
sphincter damage and/or iris atrophy. Anterior lens capsule opacities, known as
glaukomflecken, may result from damage to the anterior lens epithelium from high
intraocular pressure. The angle may have permanent synechiae formation. Intraocular
pressure may be low if the ciliary body is so ischemic that aqueous humor production is
compromised. As the ciliary body recovers, normal aqueous humor production resumes
and the intraocular pressure rises.

ACG exhibits signs of optic neuropathy in the typical glaucomatous pattern with
increased cupping of the optic nerve and retinal nerve fiber layer dropout.

Summary of Clinical Findings in Various Types of Secondary Angle Closure Glaucoma

Neovascularization of the angle blood vessels from iris that cross scleral spur to arborize
along trabecular meshwork, PAS

Anterior chamber inflammation keratic precipitates, posterior synechiae, iris bomb,


inferior PAS (as opposed to primary angle closure where PAS tend to develop superiorly)

Iridocorneal endothelial (ICE) syndrome beaten-bronze corneal endothelium, corneal


edema, high PAS that can extend anterior to the Schwalbe line, iris atrophy, corectopia

Drug induced (e.g. systemic topiramate) acute bilateral disease, acute myopic shift,
uniformly shallow chamber with anterior iris and lens displacement, ciliochoroidal effusion or
detachment

Aqueous misdirection (malignant glaucoma) flattening of central and periperhal anterior


chamber, anterior displacement of lens (cystralline or intraocular lens) or vitreous face, clear
aqueous zones in vitreous

Lens-induced angle closure thick cataract, unstable or subluxed lens

Nanophthalmos small but normal eye with short axial length, microcornea, large lens, and
thickened sclera; choroidal effusion

Retinopathy of prematurity or persistent hyperplastic primary vitreous contracting retrolental


tissue

Iris or ciliary body mass lesions or cysts irregular contour of iris or neovascularization,
hyphema or vitreous hemorrhage, episcleral sentinel vessel, ciliary body mass through dilated
pupil or on ultrasound biomicroscopy

Posterior segment mass or large serous retinal detachment signs of each on funduscopic
exam

Epithelial and/or fibrous downgrowth wound dehiscence or gape, epithelial cysts in anterior
chamber adjacent to wound, gray sheetlike membrane covering anterior segment structures
that whitens with argon laser

Pseudophakic or aphakic pupillary block pupilary obstruction or synechiae to anterior


hyaloid surface, the intraocular lens, or posterior capsule

Ciliary body engorgement associated with retinal vascular occlusion or panretinal


photocoagulation anterior rotation of iris and lens; retinal signs of each underlying etiology,
e.g. retinal hemorrhages for vein occlusion and extensive retinal laser scars from
photocoagulation.

Retinal surgery
o Encircling scleral buckle relatively deep central anterior chamber with peripheral iris
flattening, choroidal effusion
o Pars plana vitrectomy - pupillary block from expansile gases pushing iris and lens forward,
silicone oil in the anterior chamber, non-patent iridotomy

Symptoms[edit source]
Patients with anatomic narrow angles without acute angle closure are typically
asymptomatic in both the primary and secondary forms. Similarly, primary and
secondary chronic angle closure patients often experience no symptoms unless they
develop end-stage glaucoma, in which case they may complain of decreased vision or
reduced peripheral vision.

Acute angle closure, on the other hand, usually presents with dramatic symptoms from
the quick rise in intraocular pressure. Patients complain of blurred vision, rainbows,
halos around lights, or even transient loss of vision. They often have intense pain that

may be localized to the eye, may follow the trigeminal distribution, or may be described
as diffuse discomfort. Nausea and vomiting are common.

Subacute or intermittent angle closure attacks are brief episodes of angle closure that
resolve spontaneously. Patients experience the above symptoms of acute angle closure,
but on a milder scale. They will typically experience some blurring of the vision or halos
with mild to moderate eye pain, brow ache, or headache. These attacks are often
resolved by entering a well lit room which may cause miosis or sleep as sleep-induced
miosis ameliorates the lesser degree of pupillary block in these patients.

Clinical diagnosis

[edit source]

GONIOSCOPY
[edit source]

The key to diagnosis of anatomic narrow angle or angle closure is gonioscopy, which is
still the gold standard method of angle evaluation. The ideal way to perform gonioscopy
is in a dark room using a small rectangle of light only as bright as necessary to view the
angle structures, as light can open an appositionally closed angle in about one-third of
cases.[25][26] Dynamic or compression or indentation gonioscopy is essential to
differentiate appositional closure from synechial closure. Gentle pressure on the cornea
with the goniolens pushes back the iris and reveals whether the angle can be opened
any further; if not, synechial closure is present. This maneuver can also help break
acute attacks by forcing fluid into the periphery and opening areas of appositional
closure.
Occludable angles are typically described as eyes in which the posterior, usually
pigmented, trabecular meshwork is seen for less than 90 of the angle circumference or
if the angle width is less than 20.[27]

Angle Grading and Classification Systems[edit source]


A. Scheie system (R)
0 entire angle visible with wide ciliary body band
I last roll of iris obscuring part of the ciliary body
II nothing posterior to trabecular meshwork visible
III posterior portion of trabecular meshwork not visible
IV no structures posterior to Schwalbes line visible
Pigmentation graded 0 (no pigmentation) to 4 (heavily pigmented)

B. Shaffer system (R)


0 closed or slit
1 extremely narrow, 10 degrees
2 narrow, 20 degrees
3 open, 20-35 degrees
4 wide open, 35-45 degrees

C. Spaeth system (R)


Level of iris insertion:
A anterior to trabecular meshwork
B anterior to posterior limit of trabecular meshwork
C posterior to scleral spur
D into the mid-ciliary body face (anterior ciliary body band visible)
E posterior ciliary body (wide band of ciliary body band visible)

Angle width estimated in degrees from line tangential to the trabecular meshwork to
line tangential to the iris surface one third of the way from the periphery (ranges from 0 40 degrees)

Curvature of iris:

r regular configuration, no significant forward or backward arching of iris


s steep or forward bowing (convex) curve
q queer or posterior bowing (concave) curve

Pigmentation: 0 (no pigment) to 4 (heavy pigmentation)

Change in angle configuration after indentation performed described by putting the


original insertion in parenthesis, followed by the insertion after indentation. For
example, if indentation shows that the insertion is actually a D when it originally
appeared to be a C, it is indicated as a (C)D.

Photos Courtesy of Sarwat Salim, MD, University of Tennessee

Chronic Angle Closure Glaucoma

Combined Mechanism Glaucoma with Scattered PAS

PAS in a patient with ICE Syndrome

PROVOCATIVE TESTS
[edit source]

Various provocative tests have been developed in an attempt to separate out patients
who may be at higher risk of angle closure. In these tests, different maneuvers are used
in an attempt to induce pupillary block, and then the pressure is rechecked and the

angle is examined for narrowing. A test is considered positive if the IOP increases by 8
or more mmHg. In the dark room test, patients are placed in a dark room for 1-2 hours
to dilate the pupil and increase resistance at the lens-iris channel.

The prone test involves placing the patient in the prone position for 1-2 hours without
sleeping to anteriorly displace the lens and increase pupillary block. These tests have
not been found to be very predictive of angle closure. [28] Combining anterior chamber
imaging (e.g. ultrasound biomicroscopy) with provocative testing assists in detecting
apposition and allows measurement of various parameters of the angle, [29] [30] but their
ability to predict future angle closure is not well established.
Pharmacologic provocative tests using mydriatic eye drops to increase pupillary block
via pupil dilation have fallen out of favor as they carry a significant risk of angle closure
in and of themselves.

IMAGING MODALITIES[edit source]


To supplement information obtained through gonioscopy, there are several anterior
segment imaging devices available that provide detailed images of structures and
quantitative measurements. They are useful in primary angle closure but can also help
detect secondary cases of angle closure, such as ciliary body masses or anterior
rotation. At this time, there are no widely agreed upon quantitative measurement cutoffs
obtained from these devices that distinguish a narrow angle from an open one.

Ultrasound biomicroscopy (UBM)


[edit source]

This high-frequency B scan ultrasound provides high-resolution cross-sectional images


of the anterior segment of the eye to the anterior vitreous. Because it uses sound, it can
pass through opaque structures to visualize structures hidden from direct clinical
examination, such as the ciliary body.[31] It is particularly helpful for evaluating plateau iris
and other ciliary body pathology. The disadvantages of UBM include: requirement of a

water bath immersion, specialized equipment, and a skilled technician to operate; it is


also relatively costly and time consuming.

Anterior segment OCT (AS-OCT)


[edit source]

This modality uses a diode light source instead of sound to produce highly detailed
images of the cornea, angle region, and anterior ciliary body similar to those seen with
UBM. Compared to UBM, AS-OCT is unable to image structures posterior to the iris
plane well because of posterior pigmented iris shadowing and scleral light scattering.
[31]
The advantages of AS-OCT are that it is a noncontact exam: the patient can be
imaged in an upright position avoiding positional lens changes, and all four quadrants
can be scanned at once.

Scheimpflug photography
[edit source]

Digital images of the anterior chamber angle can be obtained using a Scheimpflug
camera. Rotating versions of the camera provide three-dimensional photos that can be
analyzed by computer software to measure specific parameters of the angle. The
camera has an easy-to-use slit lamp type configuration but is expensive and requires
special equipment. It cannot image the ciliary processes or body behind the iris.

Optic nerve assessment and imaging, retinal nerve fiber layer analysis, and visual field
testing should be preformed to assess for signs of glaucomatous optic neuropathy in
any patient with angle narrowing or angle closure glaucoma.

Laboratory test
Not applicable

[edit source]

Differential diagnosis

[edit source]

The main entities to distinguish are primary angle closure versus secondary causes of
angle closure because treatment may differ depending on the etiology. Primary disease
tends to be bilateral, while disease caused by a secondary etiology may be unilateral or
bilateral. Please refer to the previous tables for various causes of secondary angle
closure glaucoma.

Management
[edit source]

The overall goals for management are to reverse or prevent the angle closure process,
control intraocular pressure elevation, and prevent damage to the optic nerve. Some
primary and secondary forms of angle closure may be treated similarly, while others
require very different treatment approaches based on their underlying
pathophysiology. IOP is lowered with glaucoma medications. Iridotomy is an essential
part of treatment in PAC, but may not be indicated in some forms of secondary angle
closure glaucoma. Trabeculectomy and tube shunts may also not be indicated for
certain secondary forms of angle closure glaucoma.

Medical therapy[edit source]


ACUTE ANGLE CLOSURE GLAUCOMA[edit source]
The role of medical therapy in acute angle closure attacks is to lower IOP, reduce pain,
and clear corneal edema in preparation for iridotomy. The medications below can be
used, provided the patient has no condition contraindicating them:

Topical

Beta blockers
Selective alpha agonists
Carbonic anhydrase inhibitors
Miotics (e.g., pilocarpine 2%) may help break an early angle-closure attack, but
may be ineffective if the iris is already ischemic. High-concentration miotics (e.g.,
pilocarpine 4%) should be avoided because of the potential for forward displacement
iris-lens diaphragm.
Prostaglandin analogues unreliable effect in acute attack because of slow onset
of action
Hyperosmolar agent (e.g. 5% sodium chloride) assists in clearing corneal edema
Prednisolone 1% - decreases inflammation

Systemic

Carbonic anhydrase inhibitors oral acetazolamides maximum IOP reduction is


reached in 2-4 hours and lasts for 6-8 hours. Intravenous acetazolamide drops the IOP
within 2 minutes with a peak effect noted by 10-15 minutes. In acute
situations, a single dose of 500 mg acetazolamide should be given orally if the
patient is not vomiting. Regular acetazolamide is preferred over the sustained-release
sequel form because of quicker onset of action. If the patient is vomiting,
acetazolamide can be given intravenously.

Osmotic agents
1. Mannitol can decrease the IOP 30 mm Hg or more within 30 minutes of
administration. The recommended intravenous dose is 0.5-1.5 g/kg body weight as a
15% or 20% solution, delivered at 3 to 5 mL/minute. Frail patients with cardiac or

renal conditions may develop circulatory overload, pulmonary edema,


congestive heart failure, and electrolyte imbalance. A rapid reduction in cerebral volume
may result in subdural hematomas from vein rupture between the sagittal sinus and
cerebral cortical surface. Therefore, patients receiving IV mannitol should be
monitored in a hospital setting.
2. Oral osmotic agents:
Glycerin: 1 to 1.5 g/kg body weight of a 50% solution. Onset of pressure
reduction is typically 10 to 30 minutes. Avoid in diabetics because the increased caloric
load can cause ketoacidosis.
Isosorbide is commercially available as a 45% (45 g/100 mL) solution (Ismotic;
Alcon Surgical). The recommended dose is 1 to 1.5 g/kg body weight. Its effect is similar
to glycerins but is safe for use in diabetics because
it is not metabolized. Although less common, oral agents can also cause
subdural hematomas. Headache and gastrointestinal upset are common adverse
reactions.

Paracentesis
can be perfomed in an acute setting. Technically, it can be difficult to perform on a
phakic eye in pain with a shallow chamber, and there is a risk of permanent damage to
the cornea, lens, and iris. Devastating complications such as endophthalmitis and
choroidal hemorrhage from a rapid pressure drop may occur. Also the effects are
typically short-term, because, as the ciliary body begins to form aqueous again, the IOP
will inevitably rise. This procedure can be used in cases of extreme IOP elevation to
buy time until medications take effect or iridotomy can be performed.

Laser Iridotomy
should be performed as soon as possible in the affected eye and in the contralteral eye
to avoid an attack of acute angle closure glaucoma in the future.

CHRONIC ANGLE CLOSURE GLAUCOMA


[edit source]

Very few studies exist to address medical therapy in chronic angle closure glaucoma
after laser iridotomy. In cases where elevated IOP becomes an issue, aqueous
suppressants are helpful in reducing IOP. [32] Prostaglandin analogues have been shown
to be effective in lowering IOP, even in angles that are partially closed. [32] [33] Evidence is
not conclusive, however, regarding their effectiveness in cases of 360 degrees of
synechial closure.[34] The role of PI and other surgical interventions are described below.

PERIPHERAL IRIDOTOMY[edit source]


See Primary prevention section for information regarding prophylactic LPI for narrow
angles.

Acute Angle Closure and Fellow Eyes[edit source]


In angle closure secondary to pupillary block, an iridotomy is the definitive treatment.
Laser peripheral iridotomy (LPI) is considered an effective and safe treatment. It often
breaks an attack of acute angle closure and can prevent future attacks. An incisional
iridectomy may be necessary in cases of cloudy corneas, flat anterior chamber, poor
patient cooperation at the laser, or inability to substantially lower the IOP with
medications after a failed LPI attempt.
The fellow eyes of patients that have undergone primary acute angle-closure are
generally at significant risk for an acute attack and should receive an iridotomy. [35] [36] An
untreated fellow eye has a 40% to 50% chance of developing an acute PAC attack over
the next 5 to 10 years.[35] [37] [38] Chronic miotic therapy is not an acceptable alternative, as
50% of contralateral eyes of individuals suffering acute PAC developed acute attaks
when treated with pilocarpine alone. This is in contrast to the 1.8% of patients treated

with prophylactic incisional iridectomy who developed an attack during this same time
period.[39]

Chronic Angle Closure and Angle Closure


Glaucoma[edit source]
LPI relieves the pupillary block component in chronic disease and may halt the
progression of synechial closure and progressive IOP elevation. [40] Its ability to control
IOP, however, may not be long-lasting, especially in eyes where glaucomatous optic
neuropathy has already developed. Additional medications or surgical treatment is often
necessary.[41] In cases where LPI does successfully lower IOP, eyes still need to be
monitored routinely as IOP can increase months or years after the procedure. [38]

Persistent or progressive rise in IOP after LPI[edit source]


Damage to trabecular meshwork and/or formation of PAS has occurred when
iridocorneal apposition present
Pupillary block may recur if iridotomy becomes occluded
Factors other than pupillary block causing angle closure may have gone
unrecognized until after the LPI (e.g. plateau iris syndrome)
Angle closure may have been superimposed on pre-exisitng open angle glaucoma
or another eye condition causing IOP elevation, such as pseudoexfolation
There may be co-existing chronic open angle glaucoma

Complications of LPI
[edit source]

The most common complications of LPI are transient bleeding at site of treatment,
hyphema, postoperative pressure spike, and anterior chamber inflammation.
Occasionally, patients may complain of a seeing a double image if the lid does not cover
the iridotomy site. More severe but rare complications include aqueous misdirection and
injury to the cornea, lens, or retina.

IRIDOPLASTY[edit source]
In laser iridoplasty, contraction burns of long duration, low power, and large spot size are
placed on the peripheral iris to contract the iris stroma and physically pull the iris from
the drainage angle in an attempt to open the angle. In acute angle closure, iridoplasty
has been found effective and safe in short-term lowering of IOP. [42] [43] It can be used in
cases that are medically unresponsive, in which systemic carbonic anhydrase inhibitors
must be avoided, when immediate iridotomy is not possible, or rarely when the attack
continues despite a successful LPI. It is the procedure of choice for plateau iris
syndrome when the angle fails to open and IOP remains elevated despite a patent
peripheral iridotomy. In chronic cases of angle closure, iridoplasty may slightly decrease
the formation of PAS.[44]

It is important to note that iridoplasty does not eliminate pupillary block, so iridotomy
remains necessary if pupillary block is the mechanism of angle closure.
[34] [45] [46] [47]
Potential complications include IOP spike, iris atrophy from destruction of iris
vessels, corneal burns, marked anterior chamber inflammation, and corneal endothelial
damage.[34]

CATARACT EXTRACTION[edit source]


In PAC, since the lens is a key player in development of relative pupillary block, it makes
sense that cataract extraction can lower IOP in both acute and chronic angle closure.
Removal of the lens from an eye with a crowded anterior chamber opens the angle and
may prevent or reduce PAS formation. In one study, early phacoemulsification was
found to be better than LPI at preventing IOP rise after an acute angle closure event
was controlled medically.[48] Cataract extraction in the setting of an acute angle-closure
attack, however, is technically difficult. The eye is inflamed with significant corneal
edema, a shallow anterior chamber, an atrophic and atonic iris that is difficult to dilate,
and possible zonular weakness. It may be more prudent to control the acute attack with

medications and LPI first and then wait to perform surgery when the eye has recovered
and is less inflamed.

In the chronic phase when patent laser iridotomy and medical treatment have failed to
adequately control IOP, lens extraction many months after the initial attack has been
found to reduce IOP and reduce the need for IOP medications. [49] [50] [51] Cataract
extraction can be combined with goniosynechialysis to further improve IOP control in the
short term.[52] Methods of goniosynechialysis include breaking synechiae with a heavy
viscoelastic (viscogonioplasty), forceps, or a cyclodialysis spatula.

In lens-induced ACG, which includes phacomorphic glaucoma and angle closure due to
forward subluxation of the lens, the definitive treatment is lensectomy. Acute attacks can
be first controlled with medical therapy and/or LPI with lens extraction performed when
the eye is quiet.

FILTRATION SURGERY [edit source]


Filtration surgery has been performed for both acute and chronic angle closure
glaucoma.[53] The indications to perform filtration surgery in PACG are similar to those for
surgery in POAG. In chronic cases, surgery is considered if the optic neuropathy is
progressing and IOP is at a level believed to be contributing to the progression.
Reasons for performing filtration surgery in the setting of an acute closure attack include
medical unresponsiveness, lack of laser availability, or signs of glaucomatous optic
neuropathy already present.[54]The same techniques of filtration surgery are used as in
POAG, although some surgeons advocate tighter suturing of the trabeculectomy flap to
avoid low IOP in the immediate postoperative period. A low IOP may contribute to
further anterior chamber shallowing, which may lead to a higher rate of malignant
glaucoma postoperatively.[20] [55] [56] [57]

Whether to perform filtration surgery versus a tube shunt procedure for secondary angle
closure glaucoma depends on the underlying etiology. In most cases, dealing with the
underlying pathology (e.g. stopping topiramate in drug-induced glaucoma, removing the
lens in lens-induced glaucoma) will slow or stop the progression of disease. If medical
therapy is not sufficient to control IOP, even when the primary pathology has been
addressed, glaucoma surgery may be necessary and filtration surgery may be
appropriate. Conditions such as neovascular glaucoma and ICE, however, tend to do
better with glaucoma drainage implants. (see below).
It has been proposed that combined phacotrabeculectomy may be more effective at
controlling IOP than cataract extraction alone. Recent study results have been mixed,
with some showing phacoemulsification as being superior for deepening the chamber,
[58]
the two procedures being equal in terms of IOP control, [59] and combined procedures
being superior for IOP control.[60] Of note, one randomized control trial found that patients
who undergo combined procedures have more postoperative complications and
progression of their optic neuropathy compared to the phacoemulsification alone group,
[61]
so the risks and benefits of each procedure need to be carefully considered in each
case until more definitive evidence is available.

GLAUCOMA DRAINAGE IMPLANTS


[edit source]

A limited number of studies look at the use of tube shunt devices in PACG. PACG eyes
are often placed into the category of refractory glaucoma along with other types of
glaucoma and thus are not separately evaluated. Based on the limited data available in
these studies, tube implants appear effective in controlling IOP in PACG.[62] Drainage
implants are considered more effective than filtering procedures in neovascular
glaucoma and ICE syndrome because, in these diseases, a fibrovascular membrane
often grows over the sclerostomy site causing bleb failure.

OTHER SURGICAL PROCEDURES


[edit source]

May be required depending on the etiology of the underlying disease.

Aqueous misdirection: Nd:YAG laser can be used to disrupt the anterior vitreous in
aphakic and pseudophakic eyes. If that is not successful, definitive surgical treatment in
the form of vitrectromy with anterior hyaloid disruption combined with an anterior
chamber deepening procedure may be indicated.

Epithelial and/or fibrous downgrowth: radical surgery to remove the intraocular


membrane and affected tissues may be necessary.

Angle closure that develops after retina surgery may require removing or loosening
encircling bands, opening up iridectomy sites, or removing silicone oil.

Surgical follow up[edit source]


Patients typically need to be watched closely in the immediate postoperative period,
sometimes weekly for several months. Once IOP control is achieved and the eye is
stabilized, follow up can follow the schedule of routine PACG patients.

Complications[edit source]
Complications of acute angle attacks are the result of a rapid, extreme rise in IOP.
Possible sequelae include corneal decompensation, cataractous lens changes, iris

ischemia resulting in atrophy and distortion, ciliary body shutdown with resultant
hypotony, central retinal vein occlusion, optic nerve ischemia, and acute permanent
vision loss.

Complications of chronic disease include all the same ones that can be seen in acute
disease. The difference in chronic disease is that these conditions develop in a more
insidious fashion over a longer period of time. These patients typically have
asymptomatic progression of glaucomatous optic neuropathy with corresponding visual
field defects developing over time.

Prognosis

[edit source]

PRIMARY ANGLE CLOSURE SUSPECTS[edit source]


The overall likelihood of an individual with a narrow angle developing acute angle
closure in the United States is less than 10%. [63] A prospective multicenter study,
however, found that patients judged to be at risk for developing ACG by experienced
ophthalmologists through careful slit lamp exam and gonioscopy had a 30% risk of
developing angle closure within 5 years when no prophylactic intervention was
performed.[28] See Primary Prevention for recommendations regarding prophylactic LPI
in PACS.

In contrast, fellow eyes in which the other eye has already suffered an acute angle
closure attack have a much worse prognosis without prophylactic treatment. An
untreated fellow eye has a 40% to 50% chance of developing an acute PAC attack over
the next 5 to 10 years.[35] [37][38]An iridectomy or iridotomy virtually eliminates the risk.
[35] [36]
The long-term fate (46 years) in terms of IOP and glaucomatous optic neuropathy
is good for most fellow eyes after LPI with the majority not requiring any additional

glaucoma treatment and retaining good vision.[64] <span


id="fck_dom_range_temp_1278270701009_222" />

ACUTE ANGLE CLOSURE[edit source]


In an eye suffering an acute angle-closure attack, the long-term outcomes vary
depending on ethnicity (which may be a reflection of mechanism of angle closure),
duration of attack, and severity of attack in terms of whether or not it can be aborted by
medical treatment alone. If promptly treated, most (60%75%) symptomatic episodes of
angle closure recover without visual field or optic disc damage in the short term. [65] [66] Six
months post-attack, one study reported 38% of eyes to have visual field loss secondary
to nerve fiber bundle loss.[66] In another study, 2 - 16 weeks after an attack, changes
were noted in optic disk morphology, with preferential loss in the superotemporal and
inferotemporal areas.[67]

The longer the duration of an attack and the more difficult to manage, the worse the
outcome for the eye, regardless of the initial IOP measurement. [68] [69] [70] Patients with a 24
to 72 hour delay in presentation had a relative risk of 2.78 for developing chronic
glaucoma, whereas those requiring laser iridotomy to control IOP or a trabeculectomy
had relative risks of 3.63 and 4.83, respectively.[70] In Singapore, risk of visual field loss
was significant if the duration of symptoms was longer than 7 days. [66]
Even despite successful termination of an acute attack by surgical iridectomy, late IOP
increase is reported in 19% to 24% of cases.[71] [72] There may be ethnic differences in the
rate of IOP control by LPI alone.[7] A greater extent of PAS, a high presenting IOP, and a
larger cup to disc ratio have been reported as predictors of poor pressure control
following iridotomy in Asian and African eyes.[73] [74] A significant portion of patients go on
to develop PACG and require further medical or surgical intervention in an attempt to
control their disease. Unfortunately, up to 20% these patients deteriorate to lose
significant vision and are classified as blind in that eye. [75]

CHRONIC ANGLE CLOSURE GLAUCOMA


[edit source]

Asymptomatic angle-closure patients present with more severe visual field defects than
symptomatic patients.[65] [76] In one study which examined visual field loss on presentation,
52.8% of asymptomatic PACG had end stage visual field loss by Advanced Glaucoma
Intervention Study criteria compared to only 17.5% of symptomatic PAC cases. Although
presenting IOP was considerably higher in the symptomatic group, the level of IOP was
not found to be a significant predictor for visual field outcome. [77] It is likely that the
duration of elevated IOP has a major influence in causing optic nerve damage in PACG,
possibly more so than the level of IOP. Once glaucomatous optic neuropathy has
developed, almost all cases will require further treatment to control IOP (94%100%).
[78]
Closer monitoring of IOP is recommended in CACG compared to POAG, despite the
efficacy of medical therapy. Chronic angle-closure glaucoma tends to progress more
quickly and fail medical therapy sooner than POAG. [79] [80] [14]With aggressive management,
however, chronic ACG patients can maintain stable fields and long-term IOP control. [14]

Secondary Angle Closure[edit source]


The prognosis for secondary angle closure patients depends on the underlying etiology.
Early recognition of the underlying pathology and timely directed treatment helps to
improve outcomes.

It is possible that a peaked pupil results damage to an iris by a


phaco probe or a chopping instrument. The inadvertent chaffing
of the iris may (1) cause entrapment of some strands of the iris at
the wound and (2) affect the shape of the pupil. A repeated
prolapse of the iris from the main wound during surgery, may
cause such an occurance.
To address this, a small amount of intracameral Miochol at the

end of the surgery constricts the pupil and brings it to its


physiological size. That can be helpful in keeping the iris away
from the wound side. Air can also be injected into the anterior
chamber at the end of the surgery and using a thin iris spatula
from the side port, can sweep the strands of iris away from the
wound site.
Acute angle closure glaucoma in aphakia and pseudophakia may take several
forms (Table 1). Corneal edema and haze, anterior chamber reaction, and iris
congestion may make argon laser iridectomy impossible. Argon laser iridectomy
may not relieve the glaucoma because of the role of the vitreous. The Nd:YAG
laser better treats these conditions and is the treatment of rst choice. Success
of the Nd:YAG laser "anterior hyaloidotomy" in curing ciliovitreal block glaucoma,
demonstrates the pathophysiologic role of the anterior hyaloid face in many
cases of pupillary block glaucoma.
Table 1. Classication of acute aphakic and pseudophakic glaucoma
Pupillary block (iridovitreal block)

Absent, imperforate, or secluded

Aphakic malignant glaucoma (ciliovitreal


block)
Posterior diversion of aqueous

peripheral iridectomies
Inflammatory adhesion of intact
hyaloid face to iris
Anterior chamber hemorrhage and
exudate
Figure 1 illustrates a case of pupillary block in a patient who had an iridectomy
and antibiotic therapy for endophthalmitis after complex extracapsular cataract
extraction with an anterior chamber IOL (AC IOL). The surgical iridectomy
became occluded postoperatively, but an argon laser iridotomy relieved the

resultant iris bomb. The argon laser iridotomy closed within weeks, and the iris
bomb recurred with an intraocular pressure (IOP) of 50 mm Hg. The Nd:YAG
laser at 4 mJ created new iridotomies with permanent relief of the iris bomb and
pressure elevation. The pupillary membrane was cleared by the Nd:YAG laser.
Pseudophakic block is most common after AC IOL placement, typically after
complicated extracapsular cataract extraction or phacoemulsication. Risk of
pupillary block rises when the surgeon fails to place a large surgical iridectomy.
Further vitreous may prolapse and occlude the pupil against the optic of the AC
IOL. Large surgical iridectomy may be occluded by prolapsing vitreous and by
capsular and cortical remnants.
The role of the hyaloid face in aphakic malignant glaucoma is illustrated in
Figure 2. Three months after cataract extraction and IOL removal in a patient with
a large superior loss of iris, the chamber became shallow, and the pressure rose
to 34 mm Hg over several days, with the onset of deep pain. A thin, intact hyaloid
face or inflammatory membrane was present. The patient was treated with the
Nd:YAG laser, focused and red at 3 mJ on the hyaloid face through the mild
corneal edema despite less than 1 mm of residual anterior chamber depth. The
anterior chamber immediately deepened.