STEP 7

FISIOLOGI HUMOR AQUOS

PRODUKSI : Aqueous humoris a clear, colorless, plasma-like balanced salt solution pro-duced by the
ciliary body. It is a structurally supportive medium providing nutrients to the lens and cornea. It
differs from plasma in having lower glucose (80% of plasma levels), low protein (assuming an intact
blood aqueous barrier), and high ascorbate. It is formed at around 2.5 μL/min by a combination of
active secre-tion (70%), ultrafi ltration (20%), and osmosis (10%). Active secretion is complex,
involving the maintenance of a transepithelial potential by the Na+K+ pump, ion transport by
symports and antiports (including the important Na+/K+/2Cl–symport), calcium- and voltage-gated
ion channels, and carbonic anhydrase.

OUTFLOW : While the trabecular route is the major outfl ow, the uveoscleral contribu-tion may be as
much as 30%. The outfl ow capacity through the trabec-ular route and uveoscleral route varies and
has been demonstrated to decrease with age.
Trabecular (conventional) route
Most aqueous humor leaves the eye by this passive, pressure-sensitive route. Around 75% of outfl
ow resistance is due to the trabecular mesh-work itself, the major component being the outermost
(juxtacanalicular) portion of the trabecular meshwork. This comprises several layers of endothelial
cells embedded in ground substance that appears to act as a fi lter, which is continually cleaned by
endothelial cell phagocytosis. Further transport into Schlemm’s canal is achieved via pressure-
dependent transcellular channels (seen as giant vacuoles of fluid crossing the endothe-lium) and
paracellular pores. Aqueous is then transported via collector channels to the episcleral veins and on
to the general venous circulation.
Uveoscleral (unconventional) route
The aqueous passes across the iris root and ciliary body into the supra-ciliary and suprachoroidal
spaces from where it escapes via the choroidal circulation
(OXFORD HANDSBOOK OF OFTALMOLOGY)

GARIS SCHWALBE?
- Sudut bilik mata depan terletak pada pertautan antara kornea perifer dan pangkal iris.
Ciri-ciri anatomis utama sudut ini adalah garis Schwalbe, anyaman trabekular (yang
terletak di atas kanal Schlemm) dan sclera spur (Paul, 2008).
- Garis Schwalbe menandai berakhirnya endotel kornea. Anyaman trabekular berbentuk
segitiga pada potongan melintang, dengan dasar yang mengarah ke korpus siliaris.
Anyaman ini tersusun atas lembar-lembar berlubang jaringan kolagen dan elastik, yang
membentuk suatu filter dengan pori yang semakin mengecil ketika mendekati kanal
Schlemm. Bagian-dalam anyaman ini, yang menghadap ke bilik mata depan, dikenal
sebagai anyaman uvea; bagian luar, yang berada dekat kanal Schlemm, disebut
anyaman korneosklera.
- Sclera spur merupakan penonjolan sclera ke arah dalam di antara korpus siliaris dan
kanal Schlemm, tempat iris dan korpus siliaris menempel. Saluran-saluran eferen dari
kanal Schlemm (sekitar 300 saluran pengumpul dan 12 vena aqueous) berhubungan
dengan sistem vena episklera (Paul, 2008). Pada anyaman trabekular juga terdapat
anyaman jukstakanalikula yaitu struktur yang berhubungan dengan bagian dalam kanal
Schlemm (Khurana, 2007).
 - Kanal Schlemm berbentuk oval dengan lapisan endotel dan dikelilingi oleh sulkus
skleral. Sel-sel endotel pada dinding bagian dalam tidak teratur dan berbentuk spindle-
shaped dan mengandung giant vacuoles. Bagian luar dinding kanal dilapisi oleh sel
datar yang halus dan berisi beberapa tempat masuknya collector channels (Khurana,
2007).

PROSES PEMBENTUKAN HUMOR AQUOS

Aqueous humor terbentuk dari plasma pada processus siliaris melalui tiga mekanisme yaitu
difusi, ultrafiltrasi dan transport aktif.
- Difusi adalah proses transport zat yang larut lemak melewati membran sel melalui
perbedaan gradient konsentrasi.
- Ultrafiltrasi adalah proses perpindahan air dan zat yang larut dalam air ke dalam
membran sel akibat perbedaan gradien osmotik atau tekanan hidrostatik.
- Transport aktif adalah zat yang larut air ditransport secara aktif melalui membran sel dan
memerlukan Na-K ATPase dan biasanya terdapat pada sel epitel yang tidak berpigmen
(Solomon, 2002).

PROSES OUTFLOW HUMOR AQUOS

Aqueous humor dari bilik anterior akan didrainase dengan dua rute yaitu aliran trabekular/
konvensional dan aliran uveoskleral/ nonkonvensional. Aliran trabekular merupakan jalur
utama keluar aqueous humor dari bilik anterior, sekitar 90% dari total. Aliran aqueous dari
anyaman trabekular masuk ke dalam kanal Schlemm yang menyebabkan resistensi aliran
keluar. Teori vakuolisasi merupakan mekanisme transport aqueous humor melewati dinding
dalam dari kanal Schlemm. Teori ini menyatakan bahwa jarak transelular yang ada di sel
endotel membentuk dinding dalam kanal Schlemm sehingga berbentuk seperti vakuola dan
pori-pori yang respon terhadap tekanan dan mentransport aqueous humor melalui jaringan
ikat jukstakanalikular ke kanal Schlemm. Dari kanal Schlemm, aqueous ditransport
melalui25-35 kanal-kanal pengumpul ke vena episklera melalui jalur direk maupun indirek
(Khurana, 2007).
SUMBER : KTI ONGKO NICOLAS XAVIER, HUBUNGAN GLAUKOMA DENGAN HIPERTENSI, 2013
2. Mengapa mata pasien sakit dan merah setelah mengoreksi ulangan harian murid-
muridnya?
KARENA AKOMODASI TERUS MENERUS
ACCOMMODATION.
In situations where miosis, whether physiologic or pharmacologic, is seen concurrently with
an angle-closure attack, the mechanism appears to be more related to accommodation than
to the pupil size. Contraction of the circular muscle of the ciliary body relaxes the zonules
and allows forward displacement of the lens. During accommodation, the central portion of
the lens becomes more curved while the peripheral zone of the lens surface flattens. In
young people, the radius of curvature of the central anterior surface of the lens changes
from 10 mm at rest to 5.3 mm in full accommodation. 32 There is a slight increase in the axial
length of the lens due to the forward bulge of the anterior surface. The coexistence of the
aforementioned physiologic mechanisms increases the lens-iris surface contact and
enhances the pupillary block phenomenon in predisposed eyes.
(http://www.eyecalcs.com/DWAN/pages/v3/v3c053.html)

3. Mengapa pasien mengeluh melihat warna warni seperti pelangi disekitar lampu?
Halo vision may occur due to edematous corneal epithelium. Acute angle closure glaucoma
may cause edema due to increase intraocular pressure that forces the fluid into corneal
tissue which is anterior to Bowman’s membrane. Edematous corneal epithelium may cause
blindness as well as halo vision (Taniguchi, Fumiko)
 PROSES PEMBENTUKAN WARNA PELANGI
Cahaya matahari adalah cahaya polikromatik (terdiri dari banyak warna). Warna
putih cahaya matahari sebenarnya adalah gabungan dari berbagai cahaya dengan
panjang gelombang yang berbeda-beda. Mata manusia sanggup mencerap paling
tidak tujuh warna yang dikandung cahaya matahari, yang akan terlihat pada
pelangi: merah, jingga, kuning, hijau, biru, nila, dan ungu.

Panjang gelombang cahaya ini membentuk pita garis-garis paralel, tiap warna
bernuansa dengan warna di sebelahnya. Pita ini disebut spektrum. Di dalam
spektrum, garis merah selalu berada pada salah satu sisi dan biru serta ungu di sisi
lain, dan ini ditentukan oleh perbedaan panjang gelombang.

Pelangi tidak lain adalah busur spektrum besar yang terjadi karena pembiasan
cahaya matahari oleh butir-butir air. Ketika cahaya matahari melewati butiran air,
ia membias seperti ketika melalui prisma kaca. Jadi di dalam tetesan air, kita
sudah mendapatkan warna yang berbeda memanjang dari satu sisi ke sisi tetesan
air lainnya. Beberapa dari cahaya berwarna ini kemudian dipantulkan dari sisi yang
jauh pada tetesan air, kembali dan keluar lagi dari tetesan air.

Cahaya keluar kembali dari tetesan air ke arah yang berbeda, tergantung pada
panjang gelombangnya. Perbedaan panjang gelombang ini, akan memunculkan
warna-warna pada pelangi yang tersusun dengan merah di paling atas dan ungu di
paling bawah pelangi.

Pelangi hanya dapat dilihat saat hujan bersamaan dengan matahari bersinar, tapi
dari sisi yang berlawanan dengan si pengamat. Posisi si pengamat harus berada di
antara matahari dan tetesan air dengan matahari dibekalang orang tersebut.
Matahari, mata si pengamat dan pusat busur pelangi harus berada dalam satu garis
lurus (http://blog.uad.ac.id)

4. Apa hubungan penyakit ini dengan riwayat darah tinggi?

- Berdasarkan penelitian yang dilakukan Christina Magdalena (2006) di Rumah Sakit
Umum DR. Soetomo Surabaya, menemukan bahwa penderita yang telah menderita
hipertensi ≥ 5 tahun berisiko mengalami glaukoma sebesar empat kali lebih besar.
- Kondisi hipertensi bukan hanya meningkatkan risiko untuk terjadinya serangan jantung
atau stroke tetapi juga dapat menyebabkan glaukoma (Langman, et al., 2005). Dari hasil
studi Baltimore menunjukkan hasil yang small-positive berkaitan dengan glaukoma dan
tekanan darah sistolik-diastolik. Hubungan keduanya adalah non linear dan batasan
sistolik untuk kasus ini adalah mmHg dan juga sering terjadi pada pasien yang berusia di
atas 70 tahun (Fraser, et al., 1999).
- Kondisi hipertensi menyebabkan meningkatnya retensi natrium. Meningkatnya retensi
natrium akan menyebabkan penumpukan cairan di mata yang juga menekan nervus
optikus. Hal ini dapat memicu peningkatan tekanan intraokuli akibat menumpuknya
cairan dan menyebabkan hilang atau gangguan penglihatan akibat penekanan pada
nervus optikus (Langman, et al., 2005).
- Kondisi hipertensi yang diakibatkan oleh perubahan epithelial sodium transport pada
distal ginjal dan epitel bersilia yang akhirnya menyebabkan retensi natrium yang
berlebihan. Meningkatnya ciliated epithelial sodium transport menyebabkan ekstrusi
natrium menuju aqueous humor. Hal ini akan menyebabkan rintangan pada aliran
aqueous humor sehingga terjadi penumpukan cairan yang akan menyebabkan
peningkatan tekanan intraokuli (Langman, et al., 2005).
- Kondisi peningkatan tekanan darah akan meningkatkan aliran darah pada mata (dengan
asumsi bahwa penderita telah mengalami hipertensi dalam jangka waktu yang lama).
Setelah peningkatkan tekanan darah berlangsung dalam jangka waktu yang lama,
terjadilah kerusakan pembuluh darah kecil dan meningkatnya resistensi aliran dan
pengurangan dari aliran darah pada mata disertai hilangnya sel-sel ganglion yang akan
mengakibatkan penahanan aliran dan terjadi penumpukan cairan sehingga terjadi
peningkatan tekanan intraokuli (Fraser, et al., 1999).
- Faktor terpenting untuk mengetahui perkembangan dari glaukoma adalah dengan
mengukur tekanan perfusi diastolik pada jaringan okular. Tekanan perfusi diastolik pada
mata dapat dihitung dengan cara: tekanan darah diastolik dikurangi dengan tekanan
pada bola mata. Berdasarkan penelitian yang ada, tekanan perfusi diastolik yang rendah
(kurang dari 55 mmHg) berhubungan dengan peningkatan progresifitas penyakit
glaukoma (Fraser, et al., 1999).
- Patofisiologi hubungan tekanan darah dengan tekanan intraokuli belum diketahui secara
pasti. Dikatakan bahwa ada korelasi positif antara tekanan darah sistolik dan tekanan
intraokuli yang berhubungan dengan peningkatan tekanan darah dan akan menyebabkan
peningkatan ultrafiltrasi aqueous humor dan peningkatan tekanan arteri siliaris yang
kemudian akan meningkatkan tekanan intraokuli (Deokule dan Weinreb, 2008).

HASIL PENELITIAN ONGKO NICOLAS XAVIER, HUBUNGAN GLAUKOMA DENGAN

HIPERTENSI, 2013 :
- Dari analisis hasil penelitian didapati responden paling banyak berjenis kelamin
perempuan (52.63%) dan kebanyakan responden yang berusia di atas 40 tahun (81.58%).
Selain itu, hanya ditemukan 21 orang (55.3%) yang mengalami hipertensi dan 3 orang
(7.9%) yang tekanan intraokulinya dalam batas normal.
- Dari analisis hasil, juga diperoleh 20 orang (52.6%) yang mengalami peningkatan
tekanan intraokuli, memiliki riwayat hipertensi sedangkan responden yang
tekanan intraokulinya dalam batas normal dan tidak memiliki riwayat hipertensi
ada sebanyak 2 orang (5.3%). Pada uji hipotesis dengan menggunakan Fisher’s
 exact test, diperoleh p > 0,05.
- Kesimpulan dari hasil penelitian ini adalah tidak ada hubungan yang
signifikan antara hipertensi dengan peningkatan tekanan intraokuli pada pasien
glaukoma.

SUMBER LAIN :

Diagnoses of glaucoma were more likely to be made in patients with hypertension than in
those without raised blood pressure. Odds ratios were low, but the numbers on which
calculations are based are large and confidence intervals tight, so that findings are unlikely to
be the result of chance. The tendency for glaucoma and hypertension to co-exist is plausible,
fitting with concepts of common causal mechanisms, through modulation of sodium transport
at receptors in ciliary and renal tubular epithelia,7 and agrees with the findings of others.8

Dysfunctional corticosteroid control of epithelial sodium transport in the distal nephron is

seen in several monogenic diseases, including glucocorticoid remediable hyperaldosteronism
(a cause of aldosterone excess), apparent mineralocorticoid excess, where cortisol acts as
mineralocorticoid in the absence of 11β-HSD, and Liddle’s syndrome caused by activating
mutations in EnaC.9 In the broader hypertensive population, primary aldosteronism is being
advocated as a common cause of essential hypertension,10 and approximately 40% of such
patients have reduced plasma renin activity, in keeping with enhanced renal sodium
reabsorption.

The ciliary epithelium, another corticosteroid target, acts as an “inverted” epithelium

producing aqueous humour through sodium transport. It also expresses mineralocorticoid and
glucocorticoid receptors, and 11β-HSD, together with EnaC.11–14 Our recent data have
additionally shown corticosteroid regulation of sgk in the ciliary epithelium.14 Administration
of aldosterone to rabbits increases intraocular pressure, while spironolactone, a
mineralocorticoid antagonist, and mefipristone (RU38486), a glucocorticoid antagonist,15,16
lower pressure. Furthermore, intraocular pressure is raised in Cushing’s syndrome17 and up to
40% of patients taking glucocorticoid therapy develop raised intraocular pressure.17–19 The
data in table 4 indicates an extra 500–600 cases of glaucoma occur in recipients of oral
corticosteroids in the population studied, equivalent to some 9000 overall in the United
Kingdom.

An association between glaucoma and hypertension might be found because of particular

attention to the possible retinal adverse effects of hypertension, a phenomenon in keeping
with Berkson’s bias.20 However, our findings of differential risk of glaucoma in takers of
ACE inhibitors and calcium channel blocking agents, from those taking β blocking agents,
are difficult to explain through bias. Lowered risk of glaucoma in takers of oral β blocking
agents is clinically plausible, and supported by reduced risk in current, but not ever takers but
our data do not allow us to determine whether any particular glaucoma type, notably primary
open angle, is responsive. Raised odds ratios in takers of ACE inhibitors or calcium channel
blocking agents are likely to represent failure to protect against a commonly associated
disease, rather than increased risk caused by treatment because odds ratios were virtually
identical in known current takers and ever takers of these drugs.

GPRD has a catchment population of some four million and, assuming equivalent disease
incidence elsewhere in the United Kingdom, there would be about 15 times 27 000 cases of
glaucoma in the United Kingdom, or some 400 000 cases overall, of whom about one fifth, or
80 000 would be expected to be hypertensive. Substantial numbers would be receiving
treatment by oral blockade, with possible beneficial change in glaucoma behaviour.

We conclude that systemic hypertension and glaucoma tend to be associated, that common
mechanisms related to sodium handling are responsible, and that systematic treatment with
corticosteroids and by β blockade may have clinically important and opposite effects on
glaucoma risk. (JURNAL : Hubungan Hipertensi dan Glaukoma, Langman, 2005)

SUMBER LAIN :

Higher systolic and diastolic blood pressures are associated with increased IOP. In the
Baltimore Eye Study, IOP was 1.5 mmHg higher for patients with a systolic blood pressure
over 160 mmHg when compared to systolic blood pressures lower than 110 mmHg. The same
study, however, did not find a statistically significant association between hypertension and
glaucoma. Likewise, no association was seen between POAG and hypertension in South
Indians or Southwest United States Hispanics.

The idea that insufficient perfusion of the optic nerve may contrib-ute to glaucoma led the
Baltimore Eye Study investigators to examine the relationship between POAG and diastolic
perfusion pressure (defined as the difference between diastolic blood pressure and IOP). They
found a significant increase in the rates of POAG for diastolic perfusion pressures under 50,
with a greater than sixfold odds of having POAG noted when the diastolic perfusion pressure
dipped below 30. More recently, similar findings were also reported for Caribbean and
Hispanic populations (Fig. 10-1-4). It is difficult to fully separate the influence of IOP from
perfusion pressure epidemiologically. There is no evidence to suggest that raising blood
pressure delays the progres-sion of glaucoma (Yanoff Duker)

5. Apa intepretasi pemeriksaan visus mata kanan 1/60 nc , mixed injection, kornea keruh,
pupil kesan melebar, TIO (digital) ++?
 VISUS MATA KANAN HIPEROPIA
GLAUKOMA SUDUT TERTUTUP : Work from multiple groups show that axial lengths in
eyes with PACG are 0.5–1.0 mm shorter than population-based con-trols, with even
shorter axial lengths found in AAC eyes. These shorter axial lengths translate into more
hyperopic refractions, with PACG eyes having a mean refractive error approximately 1 D
more hyperopic than normals.5,90,97–100,102

Hyperopia is a risk factor for PACG, and South Indians with hyperopia greater than 2 D
developed PACG 3.7 times as often as those whose refractive error was on the myopic
side of +2.0 D.18 White, black, Chinese, and South Indian women all have axial
lengths about 0.5 mm shorter than their male counterparts. Addi-tionally, an Eskimo
population with a high rate of ACG was noted to have a mean refraction 0.5 D more
hyperopic than the average refrac-tion for other races.

On the other hand, blacks, whites, and Chinese have similar mean refractions despite
highly dissimilar rates of PACG. Hyperopia > 2 D was actually found to be more common
among European-derived individuals than among Chinese in one study, even
though PACG rates were much higher among the Chinese.
 In a South Indian population, axial length and refractive error were not risk factors for
PACG when using a multiple regression analysis, suggesting that these factors may
predispose to PACG because of their association with other ocular biometric features,
such as anterior chamber depth. Indeed, strong correlations have been demonstrated
between ACD and refractive errors. (Yanoff Duker)

BEDA SAMA INI GLAUKOMA SUDUT TERBUKA : Numerous clinic-based studies show an
association between myopia and POAG, and population-based studies in different ethnic
groups found rates of open-angle glaucoma two to four times higher for myopes. The risk
of glaucoma appears greatest in persons with higher degrees of myopia. Longer axial
lengths and flatter corneas were also associated with a higher prevalence of POAG in
Hispanics. (Yanoff Duker)

Kelainan refraksi
Hipermetropia juga memiliki risiko peningkatan tekanan intraokular. Mata hipermetropia
mempunyai faktor predisposisi anatomi yaitu : sudut bilik mata depan sempit dan dangkal
sehingga mengakibatkan penurunan aliran humor akueus melalui sudut bilik mata depan.
Clinical Ophthalmology, J.J. Kanski, Seventh Edition, 2005

Terdapat hubungan antara miopia aksial dengan peninggian tekanan intraokular, dimana
bertambahnya panjang sumbu bola mata akan menyebabkan meningkatnya tekanan
intraokular.
Diagnosis and Therapy of the Glaucomas, 8th edition, Becker – Shaffer, 2009

 MIXED INJECTION
KARENA KONGESTIF
KONGESTI AKTIF : Kongesti aktif dapat terjadi karena kombinasi dari jaringan
hipoksia dan produksi metabolit vasodilator. Jaringan hipoksia adalah kondisi
dimana jaringan pembuluh darah yang menerima berkurangnya pasokan oksigen
dalam darah. Dan karena itu, mereka cenderung permintaan lebih banyak oksigen,
menyebabkan vasodilatasi. Vasodialti, di sisi lain, adalah proses pelebaran
pembuluh darah, yang dicapai melalui proses relaksasi otot polos ditemukan di
dalam dinding pembuluh. Zat disebut vasodilator dapat memicu proses ini.

KONGESTI PASIF :
Sesuai dengan namanya kongesti pasif tidak menyangkut tentang kenaikan jumlah
darah yang mengalir kesuatu daerah, tetapi lebih merupakan suatu gangguan aliran
darah dari daerah itu.Apapun yang menekan venule atau vena akan menimbulkan
kongesti pasif. Jadi dapat juga dikatakan bahwa kongesti pasif adalah penurunan
jumlah darah yang mengalir dari daerah yang disebabkan oleh adanya tekanan
pada venula-venula dan vena-vena yang mengalirkan darah dari jaringan. Selain
sebab lokal tadi, kongesti pasif juga dapat terjadi akibat sebab sistemik. Jika
seseorang telah mengalami itu (kongestif pasif), darah terkumpul dalam organ
tubuh tertentu sebagai respon terhadap vena yang tersumbat menyebabkan darah
tidak dapat bebas bergerak. Dan karena kondisi ini, kadar oksigen dalam darah
berkurang dan adanya limbah metabolisme dalam tubuh meningkat, yang juga
 dapat membangun di organ dan menyebabkan beberapa urat akan diblokir.
Kongesti Pasif, akibat berkurangnya aliran keluar dari vena.
(http://awaway.blogspot.com/2011/06/makalah-kongestif.html)

 KORNEA KERUH
POMPA ENDOTEL

(Ophtalmology Yanoff Duker)

HUBUNGAN GLAUKOMA DENGAN ENDOTEL KORNEA?

Glaucoma has been associated with endothelial cell loss. Compared with age-matched
controls, significantly lower endothelial cell counts were noted in patients with glaucoma
and ocular hypertension in one study. Cell counts were inversely proportional to the mean
intraocular pressure in the glaucoma and ocular hypertension groups. Mechanisms of cell
loss may include direct damage from intraocular pressure, con-genital alterations of
endothelium in glaucoma, and drug toxicity (Ophtalmology Yanoff Duker)

 DILATED PUPIL
PUPILLARY BLOCK MECHANISM : Pupillary block represents the most common
mechanism underlying angle closure. In pupillary block, iridolenticular contact at the
pupil limits the flow of aqueous from its site of production at the nonpig-mented ciliary
 epithelium to the anterior chamber, resulting in a pres-sure gradient between the
posterior and anterior chambers that further
pushes the iris anteriorly. Anterior bowing of the peripheral iris nar-rows the angle and
may then cause iridotrabecular apposition and angle closure. Laser iridectomy re-
establishes aqueous flow from the posterior to the anterior chamber and relieves the
pressure gradient, thereby allowing the iris to flatten and the angle to widen

(Pupillary Block)

NON PUPILLARY BLOCK MECHANISM : The variable efficacy of laser iridectomy in many
cases of angle closure as well as ultrasound biomicroscopy imaging suggests that
pupillary block may not be the only mechanism responsible. The role of angle
crowding, for example that caused by a thick peripheral iris roll, has been increasingly
recognized in many cases of angle closure. This has been added to Ritch’s classification,
for the sake of completeness. In many such cases, the peripheral iris stroma is thick.
Upon pupil dilata-tion, the peripheral iris bunches up. If the angle is already narrow, this
thick peripheral iris roll may become apposed to the trabecular mesh-work and result in
angle closure. (Yanoff Duker)

 TIO MENINGKAT (++)

- In the general population the mean IOP is 16 mmHg; two standard deviations on either
side of this gives a ‘normal’ IOP range 11–21 mmHg. The distribution is Gaussian with the
curve skewed to the right (Fig. 10.34).
- In the elderly the mean IOP is higher, particularly in women, and the standard deviation
greater than in younger individuals. This means that ‘normal’ IOP in elderly women may
range up to 24 mmHg and not 21 mmHg.
- It is estimated that 4–7% of the population over the age of 40 years have IOPs >21 mmHg
without detectable glaucomatous damage: ‘ocular hypertension’ (OHT).
- An absence of angle-closure is implicit, and there should be no detectable cause of
secondary glaucoma, though sometimes the term OHT is used to describe raised IOP in
these contexts. (Clinical Ophtalmology, Kanski)
 (Diagnosis and Therapy of Glaucoma, Becker-Shaffer)

6. Apa hubungan umur pasien dengan keluhan?

Increasing age is a major risk factor for primary open-angle glaucoma, as the disease seldom
occurs at ages younger than 40.13 Studies in Australia14,15 and the USA16 show that the
prevalence of the disease increases steadily with each decade over the age of 55. The
number of retinal ganglion cells is known to decrease gradually with age even in normal
human subjects17,18 and animal models.19 This decline in ganglion cell number will reduce
neural redundancy and impact on vision in older age. 20 One consequence of this reduced
neural capacity is that in older individuals fewer ganglion cells need to be lost before there is
detectable visual field loss. An alternative hypothesis is that ageing may increase the
inherent vulnerability of ganglion cells to IOP insult. 19 This is an area of intense interest for
glaucoma research. Age-related abnormalities in mitochondria may lead to increased
oxidative stress and reduce the capacity for cellular repair. 21 In addition, age-related changes
in the ability to maintain normal blood flow in the face of fluctuation of OPP (autoregulation)
can increase the vulnerability of ganglion cells to hypoxic and metabolic stress. A growing
number of studies22–24 has shown that ageing is associated with a progressive reduction in
ocular blood flow, which appears to occur in association with an insufficient capacity for
autoregulation. This is also supported by data from animal studies 25,26 showing that in
response to IOP elevation, older rats are less able to maintain normal blood flow than young
rats. The exact mechanisms by which older age causes a predisposition to glaucoma are
under investigation. (JURNAL : the role of blood pressure in glaucome, zheng, 2011)

SUMBER LAIN :
Several studies confirm that eyes with PACG or AAC, as well as fellow eyes in patients with
unilateral AAC, have lenses 0.2–0.6 mm thicker than controls. although work from South
 India showed very simi-lar lens thickness in normal eyes, PACG eyes, and eyes with
occludable angles. Groups that are more susceptible to angle closure tend to have
thicker lenses. Mean lens thickness in Eskimos is 0.3–0.4 mm greater than that of whites and
blacks, while mean lens thickness in Chinese is 0.1–0.2 mm thicker than in whites and blacks.
Lens thickness increases with age, and may be an important explanation for the pro-gressive
shallowing of the anterior chamber and increased prevalence of PACG observed in older age
groups (Yanoff Duker)

7. Mengapa pasien mengeluh penglihatan buram dan nyeri sampai kepala belakang sisi
kanan?
PENGLIHATAN BURAM  O.K. MEDIA REFRAKTA TIDAK JERNIH
Blurred vision generally results from corneal edema when the increased IOP forces
aqueous humor into the cornea. This can also cause the patient to note colored
haloes around lights, with the red part of the spectrum being more peripheral.
Corneal edema can often stimulate lacrimation.

Corneal edema that results from the effect of elevated IOP on the corneal
endothelium. Corneal edema can also result from breaks in Descemet’s
membrane due to enlargement and stretching of the corneal stroma (Fig. 17–1B).
These changes are more commonly seen in advanced cases.
Glaucoma Science and Practice, John C. Morrison, Irvin P. Pollack

NYERI SAMPAI KEPALA BELAKANG SISI KANAN

The ophthalmic nerve [V1] passes forward in the dura of the lateral wall of the cavernous
sinus (see Fig. 8.44), leaves the cranial cavity, and enters the orbit through the superior
orbital fissure The ophthalmic nerve [V1] carries sensory branches from the eyes,
conjunctiva, and orbital contents, including the lacrimal gland. It also receives sensory
branches from the nasal cavity, frontal sinus, ethmoidal cells, falx cerebri, dura in the
anterior cranial fossa and superior parts of the tentorium cerebelli, upper eyelid, dorsum of
the nose, and the anterior part of the scalp. (GRAYS ANATOMY)

(At a glance Anatomy)

8. Apa hubungan keluhan penderita dengan riwayat sakit serupa dalam keluarga?
 (Yanoff Duker)

9. Apa saja etiologi yang bisa menyebabkan penyakit pada pasien tersebut?

The following factors were significant on multivariate analysis:

1 Intraocular pressure. The risk increases with increasing IOP.

2 Age. Older age is associated with greater risk.
3 Central corneal thickness (CCT). The risk is greater in eyes with low CCT and lower
in eyes with higher CCT. This is probably due to resultant under- and over-estimation of
IOP although it has been proposed that associated structural factors, perhaps at the
lamina cribrosa, might also be important.
4 Cup–disc (C/D) ratio. The greater the C/D ratio the higher the risk. This may be
because an optic nerve head with a large cup is structurally more vulnerable, or it may
be that early damage is already present.
5 Pattern standard deviation (PSD). A greater PSD result represented a significant risk.
It is possible that this signified early glaucomatous field change.

The following factors were significant on univariate analysis only; they were not significant
in isolation but were over-ridden when the factors considered above were taken into account.
 1 African-American race was associated with a higher glaucoma risk.
2 Gender. Males were more likely to convert.
3 Heart disease was found to be significant.

Factors examined in the OHTS but not found to be significant are listed below.

1 Myopia, although it is suspected that myopic discs are more susceptible to

glaucomatous damage at a lower IOP than emmetropic discs.
2 Diabetes. An apparent protective effect of diabetes was initially found, but later analysis
with refreshed data did not confirm this.
3 Family history of glaucoma was not found to be a risk factor for conversion.
4 Other factors which were not examined in the OHTS but may be important include
retinal nerve fibre defects (though the presence of these may be taken to indicate pre-
perimetric glaucoma – see below) and specific peripapillary atrophic changes.
(Kanski)

INTINYA  SETIAP KLASIFIKASI ITU ADA ETIOLOGINYA MASING-MASING....

10. Pemeriksaan penunjang dari pasien?

- Pemeriksaan papil saraf optik : dengan oftalmoskop dilihat apakah mengalami degenerasi
atau atrofi serta cupping disk. Tanda atrofi papil adalah warna pucat, batas tepi tegas dan
lamina kribrosa tampak jelas. Tanda cupping : pinggir papil temporal menipis, eksavasasi
melebar, diameter vertikal lebih lebar daripada horizontal, pembuluh darah seolah
menggantung di pinggir dan terdorong ke arah nasal. Alat yang lebih sensitif adalah
Optical Coherence Tomography, Confocal Scanning Laser Ophtalmoscopy, Scanning Laser
Polarimetry (objectiv)
- Tonometri : palpasi (subjektif, dengan dua jari), Schiotz (kaya di skill, dipengaruhi oleh
kekakuan sklera), Applanasi Goldman (efek kekakuan sklera dapat dihilangkan sehingga
hasil lebih tepat)
- Gonioskopi : untuk memeriksa saluran pembuangan yaitu dengan memeriksa sudut
iridokornea dengan menggunakan lensa kontak khusus yang disebut gonioskop. Dapat
membedakan glaukoma sudut tertutup dan terbuka serta apakah ada perlekatan iris atau
tidak. Ada 2 : direct (langsung menggunakan lensa yang membelokkan sinar) indirect
(menggunakan cermin untuk memantulkan sinar)
- Lapang pandang : perimetri, tes konfrontasi
(Ilmu Kesehatan Mata, UGM, Prof. dr. Suhardjo, Sp. M(K))

11. Apa DD dari pasien?

GLAUKOMA
Ocular hypertension (OHT)
Ocular hypertension describes a condition of IOP >21 mmHg (represent-ing 2 SD above the
population mean) in the presence of a healthy optic
disc and normal visual fi eld. This population is positively skewed, with
5–7% of those aged >40 having an IOP >21 mmHg.
In the absence of glaucomatous damage, it is diffi cult to differentiate
those in whom such an IOP elevation is physiological from those in whom
it is pathological (i.e., will convert to POAG).
Risk of conversion to POAG
In the Ocular Hypertension Treatment Study (OHTS), the conversion
rate was found to be 9.5% over 5 years (untreated). If treated with topi-cal medication (to
reduce IOP by >20% and to achieve 24 mmHg), this
conversion rate was reduced to 4.4%.
Risk factors (and their hazard ratios [HR]) demonstrated in the OHTS
trial include the following:
Older age: HR 1.2 per decade. •
Higher IOP: HR 1.1 per mmHg. •
Larger cup–disc (C/D) ratio: HR 1.2 per 0.1. •
Greater pattern standard deviation (PSD): HR 1.3 per 0.2dB. •
Thinner central corneal thickness (CCT): HR 1.7 per 40 μm. •
While thin CCT is an independent risk factor for glaucoma, thinner CCT
also leads to underestimation of IOP; thus the true IOP may be higher
than the recognized IOP. Patients who have had corneal refractive proce-dures may also have
thin corneas and artifi cially low IOPs. Relatively thin
corneas (CCT < 555 μm) were associated with a three-fold greater risk of
conversion to POAG than that of thick corneas (>588 μm).
Some practitioners use a pachymeter routinely and correct the IOP for
corneal thickness. One estimate is that for every 20 μm that the CCT is
<550 μm (mean population CCT), the IOP is underestimated by 1 mmHg
(though the change is not truly a linear relationship). Interestingly, this
calculation reclassifi es many normal-tension glaucoma (NTG) patients as
high-tension POAG, and OHT patients as normal.
Other possible risk factors include abnormalities in corneal hysteresis,
African-Caribbean race, FH, myopia, and other suspicious disc or peripap-illary changes.
Whom to treat?
There is considerable variation in practice. Some practitioners treat all
patients >21 mmHg. Consider treating the following:
Isolated OHT if IOP >30 mmHg. •
OHT and suspicious disc if IOP >21 mmHg. •
OHT and thin cornea if IOP >21 mmHg.
Other factors that may suggest a lower threshold for treatment include
OHT and only eye. •
OHT and CRVO in either eye. •
OHT and an accumulation of risk factors, including thin CCT, FH of •
blindness, African or Hispanic heritage, large optic nerve head (ONH)
cupping, diabetes, age, and RNFL thinning on disc imaging.
There are calculators available that attempt to quantify a patient’s risks on
the basis of OHTS criteria.
Monitoring
For those not requiring treatment, follow up in 6–12 months (IOP, disc
appearance, RNFL analysis) and perform perimetry every 12 months.
For those requiring treatment, follow up as per POAG (p. 269).

Primary open-angle glaucoma (POAG)

This is an adult-onset optic neuropathy with glaucomatous disc and/or
field changes, open angles, and no other identifi able cause for glaucoma
(cf. secondary open-angle glaucomas). The term is usually reserved for
those with high-tension glaucoma, i.e., IOP >21 mmHg (cf. normal tension
glaucoma, NTG). POAG is present in 1% of the population over age 40.
Risk factors
Age: • increasing age (uncommon <40 years).
Race: African Caribbean: more frequent, younger onset, more vision loss •
FH: • fi rst-degree relative confers 1 in 8 risk; higher in siblings.
Steroid-induced IOP elevation is more common in POAG and those •
with a FH of POAG.
Other possible risk factors include diseases that reduce oxygen delivery to
the optic nerve, such as respiratory (COPD or sleep apnea) and vascular
disease (e.g., diabetes and hypertension), and myopia (the disc is believed
to be more vulnerable because of the scleral canal morphology).
Clinical features
Usually asymptomatic (rarely eye ache and halos—transient corneal •
edema if very high IOP). Decreased vision with central scotoma.
IOP >21 mmHg, often with high diurnal variability. •
Disc changes: C/D asymmetry, high C/D for disc size, vertical •
elongation of the cup, neuroretinal rim notch/thinning (does not follow
ISNT rule; p. 265), disc hemorrhage, vessel bayoneting/nasally displaced,
peripapillary atropy (B-zone). B-zone peripapillary atrophy describes
choroidal atrophy immediately adjacent to the disc; it may correspond
to areas of ganglion cell loss and fi eld defects. The A-zone is more
peripheral, irregularly pigmented, and less specifi c for glaucoma.
Retinal nerve fi ber layer loss is clinically identifi ed or detected by •
imaging analysis.
Visual fi eld defects: 1) focal defects respecting the horizontal meridian •
including nasal step, baring of the blind spot, arcuate defects, and
altitudinal defects; 2) generalized depression.

Normal-tension glaucoma (NTG)

NTG, also known as normal-pressure glaucoma and low-tension glau-coma, is generally
regarded as a subcategory of POAG, although some
have suggested a distinct pathogenesis, such as vascular anomalies, sys-temic hypotension,
and inherited abnormalities of the optic nerve.
NTG is present in at least one-third or more of all patients with open-angle glaucoma.
Risk factors
Age: NTG is more common in the elderly, but up to one-third of •
patients may be <50 years.
Race: NTG is more common in Japan (may constitute >50% of •
all OAG).
Sex: possible female preponderance. •
Clinical features
Usually asymptomatic. •
IOP <21 mmHg. •
Disc changes are as for POAG, although disc hemorrhages and •
acquired pits may be more common and the cup may be larger
and shallower.
Visual fi eld defects are similar to those in POAG, although 1) focal •
defects occur more often in the superior hemifield (especially
superonasal) and are said to be deeper, steeper, and closer to fixation;
2) generalized depression is less marked than in high-tension POAG.
NTG may be more common in patients with history of vasospasm •
(Raynaud’s), migraine, hypotension, systemic ischemia (vasculopathy,
respiratory disease), and automimmune disease.
Differential diagnosis and Investigations
POAG—perform diurnal curve to assess IOP range. •
Secondary glaucoma—clinical assessment. •
Compressive optic neuropathy—consider MRI optic nerves/chiasm •
if disc and fi eld defects do not correlate, if there is an atypical fi eld
defect, or if VA or color vision is affected.
Other optic neuropathies—consider sending blood for CBC, B • 12
,
folate, ESR, VDRL, TPHA, ACE, ANA, ANCA, CRP, Lebers Hereditary
Optic Neuropathy; get CXR (p. 338).
Previous history of OHT that caused optic nerve damage, with •
subsequent normal IOP and no progressive glaucoma damage
(postoperative IOP spikes, steroid-responsive glaucoma).

Primary angle-closure glaucoma (PACG)

PACG is a condition of elevated IOP resulting from partial or complete
occlusion of the angle by the iris. It is present in approximately 0.1% of
the general population over 40 years old, but up to 1.5% of the Chinese
population over 50.
Risk factors
Epidemiological
Age: >40 years old; mean age of diagnosis ± 60 years. •
Female sex. •
Race: Chinese, South East Asians, Inuits (i.e., Eskimos). •
Anatomical
Pupillary block mechanism
Narrow angle, shallow AC, relatively anterior iris–lens diaphragm, •
large lens (older, cataractous), small corneal diameter, short axial
length (usually hyeropic).
In pupillary block, apposition of the iris to the lens impedes aqueous fl ow
from the posterior chamber to the anterior chamber, causing a relative
buildup of pressure behind the iris, anterior bowing of the peripheral iris,
and subsequent angle closure.
Plateau iris mechanism
Plateau iris confi guration (anteriorly rotated ciliary body that apposes •
the peripheral iris to the TM; AC depth normal centrally, shallow
peripherally with fl at iris plane).
Mild forms of plateau iris confi guration are vulnerable to pupillary block,
but greater plateau iris configurations may result in plateau iris syndrome,
where the peripheral iris bunches up and blocks the TM directly. This
means that acute or chronic angle closure can occur despite a patent
peripheral iridotomy (PI).
Acute angle-closure glaucoma (AACG)
Clinical features
Pain (periocular, headache, abdominal), blurred vision, halos, nausea, •
vomiting.
Ipsilateral: • red eye, raised IOP (usually 40–80 mmHg), corneal edema,
angle closed, fi xed semidilated pupil; glaucomflecken; contralateral
narrow angle; bilateral shallow AC.
Differential diagnosis
Consider secondary angle closure (e.g., phacomorphic, inflammatory,
neovascular) or acute glaucoma syndromes such as Posner–Schlossman
syndrome (glaucomatocyclitic crisis) or pigment dispersion syndrome
(Table 10.2).
If there is no view to the posterior chamber, perform a B-scan ultra-sound to rule out
pathologies that shift the lens–iris diaphragm forward
(e.g., tumor, hemorrhagic choroidal)
Subacute and chronic angle closure glaucoma
Subacute
Incomplete closure of the angle may result in episodes of increased IOP
(causing blurred vision, halos, and red eye) that spontaneously resolve.
Treat with prophylactic Nd-YAG PI.
Chronic
This may occur from 1) synechial closure, which is either asymptomatic
(“creeping”) or follows repeated episodes of acute or subacute angle clo-sure, or 2) a POAG-
like mechanism of trabecular dysfunction in narrow
but clinically open angles. Treat with Nd-YAG PI plus medical therapy,
goniosynechiolysis, and/or drainage surgery, as required (Box 10.3).

RINGKASAN
 (Oxford Handbook of Ophtalmology)

12. Apa patofisiologi keluhan dari pasien?

Fig. 10-3-3 Mechanisms contributing to pathophysiology of glaucomatous
neurodegeneration.Intraocular pressure can cause blockade at the lamina cribrosa of axonal
protein transport, causing neuronal retinal ganglion cell death by trophic insufficiency. Other
implicated factors include local ischemia−hypoxia, excessive stimulation of the glutamatergic
system, alterations in glial cells or astrocytes, and aberrant immunity.
(Yanoff Duker)
AACG represents the end stage of processes resulting in the compromised egress of aqueous
humor circulation and the subsequent increase in IOP. Aqueous humor is produced by the
ciliary body in the posterior chamber of the eye. It diffuses from the posterior chamber,
through the pupil, and into the anterior chamber. From the anterior chamber, the fluid is
drained into the vascular system via the trabecular meshwork and Schlemm canal contained
within the angle.

Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals
to AACG. These include shallower anterior chambers, thinner ciliary bodies, a thinner iris,
anteriorly situated thicker lens,[2] and a shorter axial eye length. Recent studies have suggested
that increased iris thickness and cross-sectional area are associated with increased risk.[3] Of
the many predisposing anatomical variations, a narrow angle has the most devastating
consequences.

In the traditional model of AACG, the eye's natural response of dilation to environmental or
chemical stimuli results in a pathologic iris-lens apposition. The apposition and contact
between the lens and the iris is called pupillary block. Furthermore, pupillary block describes
a state in which the forward-most surface of the lens is anterior to the plane of the iris
insertion into the ciliary body. As a result, aqueous flow from the posterior chamber to the
anterior chamber is obstructed or altogether blocked. When pupillary block occurs in
conjunction with the iris, the increasing pressure in the posterior chamber causes the pliable
iris, particularly the peripheral region, to bow forward in a process termed iris bombé. Iris
bombé further closes the already narrow angle and compromises aqueous drainage, thus
increasing IOP.

Recent research has suggested an alternative pathophysiologic pathway for AACG.

Cronemberger et al propose that acute events can be traced to an autonomic imbalance in
individuals with AACG, specifically increased sympathetic tone. Furthermore, the iris dilator
muscles in these individuals have been found to be more developed and stronger. In instances
of increased ocular sympathetic tone, including emotional distress, low light conditions, or
after sympathomimetic drug use, contraction of the iris dilator muscles leads to pupil
dilatation and thickening of the middle-peripheral iris. This thickening can lead to angle
closure, thereby obstructing the outflow of aqueous humor.[4]

Other proposed mechanisms of AACG include plateau iris, lens swelling, and ciliary block.
Plateau iris is less common than pupillary block and is due to anterior insertion of the iris.
The superfluous and crowded iris tissue blocks the trabecular meshwork and again leads to
increased IOP.

Lens swelling and ciliary block are extremely rare. Lens swelling occurs in cases of cataracts
in which hydration forces cause enlargement of the lens and subsequent crowding of the
anterior chamber. Forces posterior to the lens can push the lens and iris forward causing
ciliary block or vitreous pressure. This can be seen in panretinal photocoagulation, scleral
buckles, and uveitis (MEDSCAPE)

13. Penatalaksanaan pasien pada skenario?

(Oxford Handbook of Ophtalmology)

Prostaglandin analogues
These analogues of PGF2A increase uveoscleral outfl ow (see Table 10.6).
- Ocular side effects: common: hyperemia, increased pigmentation of iris (and rarely lid
skin), thickening and lengthening of lashes; rare: uveitis, CME.
- Contraindications : may be associated with CME after complicated cataract surgery or if
used during active uveitis.
-
B-Blockers
These agents reduce aqueous production probably by acting on B-receptors on the
nonpigmented ciliary epithelium and vasoconstriction of the arterioles supplying ciliary
processes.
- Ocular side effects: • uncommon: allergic blepharoconjunctivitis, punctate keratitis.
- Contraindications: • asthma/COPD (bronchospasm may occur even with selective B1-
agents), heart block, bradycardia or cardiac failure. Try to avoid B-blocker in nursing
mothers as it is secreted in breast milk.
- Drug interactions: • concurrent use of cardiac-directed Ca2+antagonists such as
verapamil may compound bradycardia, heart block, and hypotension.

Carbonic anhydrase inhibitors

These agents reduce aqueous production by inhibiting carbonic anhydrase isoenzyme II (and
hence bicarbonate production) in the non-pigmented ciliary epithelium.
- Ocular side effects: • common: burning, tearing, allergic blepharoconjunctivitis (up to
10%).
- Contraindications: • sulfonamide sensitivity; renal failure, liver failure (systemic
acetazolamide).
- Drug interactions: • K+-losing diuretics (e.g., thiazide) may cause profound
hypokalemia if used concurrently with acetazolamide. K+supplementation is not usually
required for acetazolamide used alone.

Sympathomimetics
The highly A2-selective brimonidine is well tolerated for chronic use, and apraclonidine (A1+
A2) is useful for short-term use (e.g., after laser iridotomy). Nonselective sympathomimetics
such as adrenaline (epine-phrine), dipivefrin, and the adrenergic neuron blocker
guanethidine are now seldom used because of their frequent side effects.
- Ocular side effects: • common: allergic blepharoconjunctivitis (up to 15% for
brimonidine, 30% for apraclonidine); older agents: scarring, mydriasis, adrenochrome
deposits; uncommon: CME in aphakia (possibly pseudophakia).
- Contraindications: • heart block, bradycardia.
- Drug interactions: • monoamine oxidase inhibitors

Miotics (parasympathomimetics)
Muscarinic receptor agonist leads to ciliary muscle contraction, which pulls on the scleral
spur to open the trabecular meshwork. Pilocarpine is sometimes used as a fi rst-line agent in
narrow-angle glaucoma; it is some-times still used in POAG.
- Ocular side effects: • fl uctuating myopia, miosis (constricted visual field, worse night
vision).
- Contraindications: • infl ammatory or malignant glaucoma.

Combination agents : In the United States, two combination agents are available and have
been demonstrated to have more effective IOP lowering than either of the individual
components alone (but not more effective than each of the separate components alone).
Combination agents have benefi ts of increased convenience for patients as well as improved
patient adherence and compliance (since compliance decreases with each additional drop a
patient must use).Mechanism of action, contraindications, and side-effect profi les are the
same as for each individual agent. Dorzolamide/timolol: first fixed combination agent now
available in a • generic form.Brimonidine/timolol: most recently approved fi xed
combination agent. (Oxford Handbook of Ophtalmology)

PEMBAGIAN OBAT-OBAT GLAUKOMA

a) OBAT TOPIKAL
- Gol. Kolinergik : pilokarpin, karbakhol
- Gol. Agonis adrenergik : epinefrin, dipivefrin, brimonidin, apraklonidin,
- Gol. Penyekat reseptor beta : timolol, carteolol, betaxolol, levobunolol
- Gol. Analog prostaglandin : lataronoprost, travoprost, bimatoprost
- Gol. CAI : dorzolamid, brinzolamid
b) OBAT SISTEMIK
- Gol. CAI : acetazolamid, methazolamid
- Zat hiperosmotik : mannitol, gliserin, urea

OBAT TOPIKAL
- Pilokarpin : golongan kolinergik, menurunkan TIO dengan cara meniakkan kemampuan
aliran keluar cairan aquos melalui trabekulum meshwork, merangsang parasimpatik,
menyebabkan miosis  sudut iridokornea terbuka. Tidak boleh diberikan pada uveitis
Dosis : 1-2 tetes, 3-4x sehari. Durasi 4-6 jam
- Epinefrin : simpatomimetik, memacu reseptor adrenergik alfa dan beta mengakibatkan
turunnya produksi cairan aquos dan meningkatnya aliran keluarnya. Bisa menyebabkan
midriasis, makanya ga boleh diberikan pada glaukoma sudut tertutup akut
Dosis : 2x sehari
- Timolol Maleat : beta2 bloker, mengurangi produksi, unselective, Tidak boleh diberikan
pada yang punya penyakit jantung dan nafas.
Dosis : 2x sehari

OBAT SISTEMIK
- Acetazolamid : penghambat anhidrase karbonat, menurunkan produksi, KI ada di atas,
Dosis : sediannya 125, 250, 500 mg kapsul tiap 6 jam pada org dewasa, pada anak anak
diberikan 10-15 mg/kgBB/hari dosis terbagi 3-4. Bisa IV.
- Gliserol : obat hiperosmotik, mengurangi volume viterous, penting untuk keadaan akut
dimana TIO sangat tinggi, membuat osmotik darah tinggi sehingga air di vitreus bisa
terserap ke darah
Dosis : 2-3ml/kg diberikan per oral 3-4 kali sehari
KI : ginjal, DM

BEDAH :
- Iridektomi : pake alat, membuat lubang pada iris untuk mengalirkan cairan aquos dari
COP ke COA, mengobati blok pupil,
- Gonioplasti/ Iridoplasti : pake laser, memperdalam sudut iridokornea, misal pada iris
pletau. Dilakukan di stroma iris sehingga terjadi konstriksi yang akan menarik iris perifer
menjadi lebih datar dan sudut iridokornea menjadi lebih terbuka
- Trabekuloplasti : membuat sikatrik di trabekulu, yang kena laser jadi sikatrik diharapkan
yang tidak terkena laser akan tertarik sehingga celah trabekulumnya melebar
- Trabekulektomi : lubang pada COA dengan daerah subkonjungtiba atau subtenon (THE
MOST OPERATION YA)
- Goniotomi : untuk kongenital, hanya bisa bila kornea masih jernih, membuat irisan
pada permukaan depan trabekulum menggunakan jarum dengan bantuan lensa
gonioskop sehingga trabekulum terbuka, akibatnya cairan masuk ke canalis schlemm
- Trabekulektomi : untuk kongenital, alatnya dimasukan ke canalis schlemm
(Ilmu Kesehatan Mata, UGM, Prof. dr. Suhardjo, Sp. M(K))